Anaesthesia Resident's Handbook

Abouleish
ANZCA
Bader
Bellhouse
Blackshear
Boyle
Brown
Burm
Camann
Carden
Carrie
Chan
Chantigian
Chester
Collier
Cooper
Crooke
Crowhurst
Datta
Deacon
Douglas
Doyle
Feldman
Finucane
Gambling
Gatt
George
Gielen
Goulding
Halpern
Hanaoka
Harrington
Harrison
Hughes
Keast
Lah
Leeson
Lema
Liberman
Lim
Lynch
Marcus
Morgan
Neilson
Neumark
O'Sullivan
Paech
Paull
Pavy
Porter
Pybus
Redick
Reed
Reynolds
Ross
Russell
Sage
Sandler
Scarf
Scott
Stienstra
Torda
Turner
Van Aken
Van Zundert
Vartis
Volpe
Watanabe
Watterson
Wildsmith
Writer
Ezzat I. Abouleish.
MB.,Ch B., DA., DM., MD.
Professor of Anesthesiology,
Medical Director of Obstetric Anesthesia,
University of Texas,
Houston Health Science Center.
Houston,
Texas.
United States.
Contributions:
Post-partum Alternatives to a Spinal
Spinal Anesthesia in the Post-delivery Period
Australia and New Zealand College of Anaesthetists:
Policy Documents.
The following documents have been reproduced with the kind permission of the
Australian and New Zealand College of Anaesthetists.
P3 Major Regional Anaesthesia
T6 Recommended Minimum Facilities for Safe Anaesthetic Practice in Delivery
Suites
Angela M. Bader,
MD.
Assistant Professor of Anesthesia,
Harvard Medical School
Staff Anesthesiologist,
Director, Pre-Admitting Test Center,
Brigham and Women's Hospital,
Boston, Ma 02115
United States.
Contribution:
Thermoregulation during regional analgesia
Paul Bellhouse,
MB, BS, FANZCA. Specialist Anaesthetist,
Murwillumbah Hospital,
NSW 2484
Australia.
Contribution:
Regional Anaesthesia and the difficult airway
Robert Blackshear.
MD. United States.
Contribution:
Tensile strength of epidural catheters
Rhonda Boyle,
MB. BS. FANZCA.
Staff Anaesthetist.
Royal Women's Hospital Brisbane,
Bowen Bridge Road,
Herston,
Queensland.
Australia.
Contribution:
Effect of analgesia on labour
Mark Brown,
MB, BS, FRACP, MD.
Associate Professor of Medicine,
University of New South Wales,
Senior Staff Specialist, Renal Medicine,
St George Hospital,
Belgrave St.
Kogarah.
NSW 2217
Australia.
Contributions:
Pre-Eclampsia: Management
Pre-Eclampsia: Pathophysiology
Rudolf Stienstra,
MD, PhD.
Vice-Chairman.
Department of Anesthesiology,
University Hospital Leiden.
and
Anton G. L. Burm,
MSc, PhD.
Associate Professor of Anesthesiology,
University of Leiden,
University Hospital Leiden.
Leiden
Netherlands.
Contribution:
Placental transfer of local anaesthetic agents
William Camann,
MD.
Harvard Medical School,
Director - Obstetric Anesthesia Education,
Boston,
Mass.
United States.
Contribution:
Cesarean Section Rates and Regional Block
Jennifer Carden,
MB, BS, FANZCA.
Staff Anaesthetist,
Monash Medical Centre,
Melbourne,
Victoria.
Australia.
Contribution:
Management of Pulmonary Acid Aspiration
Len Carrie,
FRCA.
Consultant Anaesthetist.
Nuffield Department of Anaesthetics.
The John Radcliffe Hospital,
Headley Way,
Headington,
Oxford OX3 9DU.
United Kingdom.
Contribution:
Extradural Space
YK Chan,
MB. BS. (Mal)., FFARCS(Ireland)
Associate Professor,
University of Malaya,
Consultant Anaesthetist,
University Hospital.
Kuala Lumpur. Malaysia.
Contribution:
Aspiration Prophylaxis
Robert Chantigian,
MD.
Director of Obstetric Anesthesia,
Consultant in Anesthesiology,
Mayo Clinic.
Assistant Professor of Anesthesiology,
Mayo Medical School.
United States.
Contribution:
Treatment of PDPH (excluding blood patch)
Stephen Charles Chester,
MB, BS, FANZCA, D Obs RCOG, GDHSM.
Director of Anaesthesia,
The Royal Women's Hospital,
132 Grattan Street,
Carlton,
Victoria.
Australia.
Contribution:
Role of Caudal, Pudendal and Paracervical blocks
Clive Collier,
MD, MRCP, FRCA, FANZCA.
Senior Visiting Specialist,
Royal Hospital for Women,
Sydney
Australia.
Contributions:
Additives to Local Anaesthetics
Caesarean Section in the Morbidly Obese
Caudal Analgesia
CNS Toxicity of local anaesthetics
CSE: Development and Equipment
CSE: Technique
Epidural catheter design
Epidural Technique
General Anaesthesia in Obstetrics
Multicompartment Block
Neonatal effects of local anaesthetics
Neonatal Outcome
Paramedian epidural approach
Regional block in the presence of spinal deformity
Regional Blockade and Heart Disease - Principles
Regional blocks and neurological disease
Relative Toxicity of Local Anaesthetics
Spinal Block Technique
Subdural Space
Therapy of accidental dural puncture
Michael Cooper,
MB, BS,FANZCA.
Senior Visiting Anaesthetist,
St George Hospital,
Sydney.
Honorary Historian,
Australian and New Zealand College of Anaesthetists.
Australia.
Contribution:
Infiltration anaesthesia for Caesarean Section
David Keith Crooke,
MB, BS, M Biomed E, FANZCA.
Director of Obstetric Anaesthesia,
Liverpool Hospital,
Lecturer,
University of New South Wales,
Sydney.
Australia.
Contributions:
Practical aspects of resuscitation after major block
Theoretical aspects of resuscitation after major block
John Crowhurst
AUA (Pharm.), MBBS. D(Obst.)RCOG, FANZCA
Senior Consultant
Department of Anaesthesia,
Queen Charlotte's and Chelsea Hospital,
London.
United Kingdom.
Contribution:
The block which does not wear off
Sanjay Datta,
M.D., FFARCS (Eng)
Professor of Anaesthesia,
Boston, Massachusetts,
U.S.A.
Contribution:
Diabetes and Major Regional Blockade
Gregory J. Deacon,
MBBS, FANZCA, Dip ABA
Visiting Specialist Anaesthetist,
St Vincent's Hospital.
Prince of Wales Hospital,
Sydney.
Australia.
Contribution:
Factors affecting spread of spinal anaesthesia
M. Joanne Douglas,
MD, FRCPC.
Head, Department of Anaesthesia,
British Columbia Women's Hospital,
Head, Division of Obstetric Anaesthesia,
University of British Columbia,
Vancouver,
British Columbia,
Canada.
Contribution:
Placental transmission of local anaesthetics
D. John Doyle,
MD, PhD, FRCPC.
Staff Anaesthetist,
The Toronto Hospital.
University of Toronto.
and
Alan N. Sandler,
MB, ChB, MSc, FRCPC.
Anaesthetist-in-Chief,
The Toronto Hospital.
Canada.
Contribution:
Inadvertent IV injection of Local Anaesthetics
Hal. S. Feldman,
BSc, DSc.
Associate Director of Research,
Department of Anesthesia,
Brigham & Women's Hospital.
Boston.
Mass.
United States.
Contribution:
Acute Systemic Toxicity of Local Anaesthetics
Brendan T. Finucane,
MB, BCh, FRCA, FRCPC.
Professor and Chair,
University of Alberta,
Chief, Department of Anaesthesia,
University of Alberta Hospital,
Edmonton,
Alberta.
Canada.
Contribution:
Hemodynamic effects of Local Anaesthetics
Dr David R. Gambling
MB, BS, DRCOG, FRCPC.
Associate Clinical Professor
Co-Director Obstetric Anesthesia
University of California, San Diego
San Diego,
California.
United States.
Contribution:
PCEA: Should we use a background Infusion?
Stephen Gatt,
LRCP,MRCS, FANZCA, FFICANZCA.
Sydney.
Australia.
Contributions:
Epidural Blood Patching
Indications for Epidural Blockade
Natural Childbirth
Non-Pharmacological Analgesia
Pharmacological Rx of PPH
Removing a trapped epidural catheter
Ropivacaine in Obstetric Anaesthesia
The severed epidural catheter
Uterine relaxation
Uterine Relaxation: Treatment Protocol
Lenore M. George,
MB, BS.
Registrar,
Prince of Wales Hospital,
Sydney.
Australia.
Contribution:
Peripartum Cardiomyopathy: Regional Blockade
Mathieu Gielen,
PhD, MD.
Radboud University Hospital,
University of Nymegen,
Nijmegen.
Netherlands.
Contribution:
Spinal needles in obstetrics
Genevieve Goulding,
MB, BS, FANZCA.
Sydney.
Australia.
Contributions:
Consent for epidural analgesia
Epidural Analgesia Fact Sheet Design
Experience with Ropivacaine for labour analgesia
Steven Halpern,
MD, FRCPC.
Director of Obstetrical Anaesthesia,
Women's College Hospital.
Canada.
Contribution:
Uterine blood flow during regional blockade
Kazuo Hanaoka,
MD.
University of Tokyo,
Tokyo,
Japan.
Contribution:
Combined Spinal-Epidural Needle
Phillip Harrington
MB, BS, FANZCA, Dip ABA.
Southport,
Queensland.
Australia.
Contribution:
Needle Size and Post-dural Puncture Headache
Patricia Harrison,
MD
Pain Service Director,
and
Mark J. Lema.
MD, PhD
Chairman,
Roswell Park Cancer Institute
Clinical Assistant Professor,
State University of New York at Buffalo
United States.
Contribution:
Respiratory depression from neuraxial opioids
Samuel C Hughes,
MD.
San Francisco General Hospital.
Professor of Anesthesia,
University of California,
San Francisco,
California.
United States.
Contribution:
Chloroprocaine and Obstetric Anesthesia
Peter Keast,
FANZCA.
Monash Medical Centre,
Melbourne.
Australia. and
Andy Pybus
FANZCA
Cardiac Anaesthetist and Perfusionist,
St. George Hospital and
Royal North Shore Hospital,
Sydney.
Australia.
Contribution:
Reducing the Risk of Aspiration during Anaesthesia
Frank Lah,
MB, BS, FANZCA.
Woden Valley Hospital,
Woden,
A.C.T.
Australia.
Contribution:
Cardiotocography and regional blockade
Stan Lee-Son,
MD.
Boston,
Mass.
United States.
Contribution:
Site of action of local anaesthetics
Henry Liberman,
MB, BS, FFARACS, FANZCA.
Sydney.
Australia.
Contribution:
Effect of posture on spread of local anaesthetics
Saywan Lim,
President,
WFSA Pantai Medical Centre,
59100 Kuala Lumpur,
Malaysia.
Contribution:
Regional Anaesthesia Worldwide
Judith C. Lynch,
MB, BS (Hons), FANZCA
Visiting Anaesthetist,
Royal Prince Alfred Hospital.
Visiting Anaesthetist,
Sutherland Hospital,
Sydney.
Australia.
Contribution:
Distant effects of epidurally administered drugs
Marco A.E Marcus.
MD
Assistant Professor,
Dept of Anesthesiology,
University Hospitals,
Katholieke Universiteit Leuven,
Leuven.
Belgium.
and
Hugo Van Aken,
MD PhD.
Direktor: Univ.-Prof. Dr. med,
Anesthesiologie u. operative intensiv medizin,
Westfalische Wilhelms-Universitat
Munster.
Republic of Germany.
Contribution:
Prevention of local anaesthetic toxicity
Pamela J. Morgan,
MD, CCFP, FRCP(C).
Staff Anaesthetist,
Mount Sinai Hospital,
Assistant Professor,
University of Toronto,
Toronto.
Canada.
Contribution:
Vasopressors and regional blockade
Anton Neilson,
MB, BS (Qld), FANZCA.
Director of Anaesthetic Services,
Royal Women's Hospital.
Clinical Senior Lecturer,
University of Queensland,
Brisbane.
Australia.
Contribution:
Mechanism of action of local anaesthetics
Julius Neumark
MD. FACA.
Professor & Chairman,
Dept. of Anaesthesiology.
Donauspital,
Vienna.
Austria.
Contribution:
Drug interactions and regional blockade
Geraldine O'Sullivan,
MD, FRCA
Department of Anaesthetics,
St. Thomas' Hospital,
London SEI 7EH
United Kingdom.
Contribution:
Fasting During Labour
Michael Paech,
MB, BS, DRCOG, FRCA, FANZCA.
Head, Department of Anaesthesia,
King Edward Memorial Hospital,
West Australia.
Contributions:
Choice of drug(s) for CSE
Choice of epidural agent
John Paull,
MB, BS, FANZCA, Dip Ed (Monash)
Director of Anaesthetics and OT Services,
Box Hill Hospital,
Melbourne.
Australia.
Senior Lecturer,
Universiti Kebangsaan Malaysia,
Kuala Lumpur.
Malaysia.
Contribution:
Contribution of regional analgesia to safety
Timothy J G Pavy,
MBBS, FANZCA, FRCA, DA, DIP.MID.COG
Staff Anaesthetist,
King Edward Memorial Hospital for Women.
Clinical Instructor,
University of West Australia.
West Australia.
Australia.
Contribution:
Sensory-motor splitting by epidural blockade
Jackie Porter,
MB, BS, FRCA.
Research Associate in Anaesthetics,
and
Felicity Reynolds,
MB, BS, MD, FRCA, FRCOG.
Professor of Obstetric Anaesthesia,
Division of Anaesthetics,
St Thomas's Hospital,
London.
United Kingdom.
Contribution:
Maternal Hypoxaemia after regional blockade
Lloyd Franklin Redick,
MD.
Duke University Medical Centre,
Professor of Anesthesiology and
Associate Professor of Obstetrics and Gynecology,
Duke University,
Durham, NC.
United States.
Contributions:
Management of a failed epidural
Management of a failed spinal
Justin M. Reed,
MB, BS, DA (UK)
Provisional Fellow,
The New Childrens Hospital,
Westmead,
NSW.
and
Michael G. Scarf,
MB, BS, FFARACS, FANZCA
Visiting Medical Officer,
St Vincent's Hospital.
Sydney.
Australia.
Contribution:
Epidural Blood Patch in HIV Patients
Andrew Ross,
MB, BS, FANZCA.
Senior Staff Specialist,
Mercy Hospital for Women.
Visiting Intensivist,
Alfred Hospital.
Melbourne.
Australia.
Contribution:
Intravenous PCA following Caesarean Section
Robin Russell,
MB, BS, FRCA.
Department of Anaesthetics,
St Thomas' Hospital,
London.
United Kingdom.
Contributions:
Backache and regional analgesia in labour
Site of action of epidurally administered drugs
David John Sage,
MB, ChB, Dip Obstet, FANZCA.
Clinical Director of Anaesthesia,
Auckland Hospital,
Auckland.
New Zealand.
Contribution:
Aspirin, Heparin and Regional Blocks
David A Scott,
MB, BS, FANZCA
Deputy Director of Anaesthesia,
St. Vincents Hospital,
Melbourne
Australia.
Contributions:
Spinal Anaesthesia and CV Disease - Pathophysiology
Spinal Anaesthesia and Specific CV Conditions
Tom Torda,
MD, FANZCA
Professor of Anaesthesia,
Prince Henry & Prince of Wales Hospital,
Sydney.
Australia.
Contribution:
Analgesia following caesarean section
Robert Turner,
MB. BS.
Sydney.
Australia.
Contribution:
Regional techniques compared
Andre van Zundert
Anesthesiologist, Intensivist,
Intensive Care & Pain Therapy.
Catharina Hospital,
Michelangelolaan,
Netherlands.
Contribution:
Intensity and prevalence of labour pain
Arthur Vartis
MB. BS.
Provisional Fellow,
Sydney.
Australia.
Contribution:
Epidural to subarachnoid space leakage after CSE
Nicola G. Volpe
University of Turin,
Ospedale "Maggiore della Carita"
Novara
Italy.
Contribution:
Management of Specific Heart Diseases in Obstetrics
Seiji Watanabe,
MD, PhD.
Anesthetist-in-Chief,
Mito Saiseikai General Hospital
Japan.
Contribution:
Regional Anaesthesia and Coagulopathy
Leonie Watterson
MB, BS.
Fellow in Anaesthesia,
Royal North Shore Hospital,
Sydney.
Australia.
Contributions:
Aortocaval Compression
Assessing the quality of a block
Epidural analgesia and the progress of labour
Hypotension complicating regional blockade
Monitoring epidural blockade
Multiple Gestations: - Caesarean Section
Multiple Gestations: - Obstetric Considerations
Multiple Gestations: - Vaginal delivery
Paracervical Block
Preparation and Monitoring for Regional Blockade
Pudendal Nerve Block
Regional Anaesthesia for Breech Presentation
Subarachnoid space
John Anthony Winston Wildsmith
MD, FRCA.
Professor of Anasethesia,
University of Dundee.
Honorary Consultant Anaesthetist,
Dundee Teaching Hospitals NHS Trust.
Dundee,
Scotland.
United Kingdom.
Contribution:
Anaphylactic and histaminoid reactions
Desmond Writer,
MB, FRCA, FRCPC.
Professor of Anaesthesia.
IWK - Grace Health Centre,
Halifax,
Nova Scotia.
Canada.
Contribution:
Breech Presentation
Ezzat Abouleish
I. Epidural Anesthesia (E.A): Epidural anesthesia offers no advantages over spinal
anesthesia (Chapter 67) and should not be considered for a short procedure like
post-partum tubal ligation unless an epidural catheter is already in place after its use
for delivery. When E.A. is reinstated many hours after the delivery, certain
precautions should be taken:
1) A history of the reliability of E.A. for labor should be confirmed.
2) The patient's back should be examined to ensure that an appropriate length of the
catheter is still present. The catheter may be displaced by too much movement of the
patient, inadequate taping or perspiration.
3) The first 10 ml of the local anesthetic should be injected with the patient on her
side to exclude leakage of the catheter or superficial position of its tip, which can lead
to subcutaneous crepitus or swelling.
4) If epidural injection of an adequate dose of a local anesthetic (e.g. 20 to 30 ml of
3% chloroprocaine) cannot achieve an adequate bilateral level of block (i.e. at least
T6 dermatomal level), spinal anesthesia should be considered rather than struggling
with an inadequate block and exposing the patient to its dangers.
The use of spinal anesthesia immediately after verification of inadequate E.A. and
after administration of a large dose of a local anesthetic sometimes leads to an
excessively high block. The mechanism of this occurrence is multifactorial. C.S.F.
volume may have decreased owing to its compression by the epidurally injected large
volume of local anesthetic; both techniques may have had an additive effect; or
leakage of the epidurally injected local anesthetic into the subarachnoid space
through the hole created in the dura. The dose of spinal should be reduced by one
third, or the epidural block should be allowed to wear off before administering a spinal
anesthetic.
II. Combined Spinal and Epidural Technique (CSE) (Chapter 62): This technique for
both delivery and tubal ligation is an excellent alternative. The analgesia for early
labor can be conducted using intrathecal 10 mcg sufentanil with or without 2.5 mg
bupivacaine (1ml 0.25%). (1, 2) The analgesia begins almost instantaneously.
Although the addition of a small dose of bupivacaine (2.5 mg) does not have any
significant effect on motor power, it does prolong the duration and improve the quality
of analgesia . After the spinal component of the block wears off, the epidural part can
be initiated in the regular manner. To avoid a period of pain between the two parts of
the technique, the epidurally injected local anesthetic should be started as soon as
the patient feels discomfort. After delivery, E.A. can also be used for tubal ligation as
described earlier.
III. Continuous Spinal Anesthesia (C.S.A): With C.S.A, analgesia for labor can be
obtained by the use of an intrathecal narcotic with or without a local anesthetic as
described above for C.S.E. After delivery, the level and intensity of the block can be
achieved by titrating hyperbaric bupivacaine dosage (0.75% in 8.25% dextrose) to
achieve a T4 dermatomal level. C.S.A. can be initiated from the start or an attempted
E.A. can be converted to C.S.A. after inadvertent dural puncture. This alternative is
simpler and safer than a repeated attempt to perform E.A.
References:
1. Abouleish A., Abouleish E, Camann W: Combined spinal-epidural analgesia in
advanced labour. Can J Anaesth 1994; 41: 575-578.
2. Campbell DC, Camann WR, Datta S: The addition of bupivacaine to intrathecal
sufentanil for labor analgesia. Anesth Analg; 81: 305-309.
Ezzat Abouleish
Introduction: Obstetric patients are at increased risk of aspiration of gastric contents
secondary to gastric stasis caused by pain, stress, and narcotics, as well as
mechanical and hormonal factors. This risk decreases after delivery (1). However,
the exact time that gastric emptying returns to the non-pregnant state is still not clear.
There are no contraindications to tubal sterilization in the immediate postpartum
period if a woman has had a major anesthetic for delivery and the anesthetic can be
continued safely. Nonetheless, a major anesthetic (conduction, regional, or general
inhalation) to accomplish a tubal sterilization should be continued only after careful
evaluation by the anesthesia service. Because the parturient may have an increased
risk of regurgitation and aspiration of acidic gastric contents, it is preferable to wait 8
hours after delivery before initiating a major block to allow for:
1) decreased risk of aspiration,
2) increased maternal cardiovascular stability and
3) more assurance of the neonatal condition.
A sensory level to T4 (as determined by pin-prick) is required for any intra-abdominal
operation including tubal ligation (2). With a lower dermatomal level, for example,
T10, skin incision may be tolerable but intra-abdominal manipulation and pulling on
the Fallopian tubes can cause pain. In a patient with cardiovascular disease in whom
a relatively high block to T4 is risky (Chapter 83), a lower level is acceptable and
anesthesia is supplemented by intraperitoneal instillation of 80 ml of 0.5% lidocaine 5
minutes earlier (3).
The local anesthetic requirement for each spinal segment block after spinal
anesthesia is less in cesarean section than in gynecologic operation, the ratio being
1:1.5. During the postpartum period, the doses of local anesthetic lie between that for
cesarean section and gynecologic operation. For example, with spinal or epidural
anesthesia the dose requirement per segment with cesarean section compared with
Post-partum Tubal Ligation (PPTL) is 1:1.3 (4, 5).
The types of regional anesthesia techniques available for PPTL are spinal, epidural,
combined spinal and epidural, continuous spinal, or local (Chapter 68).
Spinal Anesthesia: Spinal anesthesia is the simplest and safest technique. The
cardiotoxicity and neurotoxicity of local anesthetic drugs arising from inadvertent
intravascular or subarachnoid injection associated with epidural anesthesia are
eliminated with spinal anesthesia. Moreover, with a spinal block, the onset of action is
fast, the analgesia is superb, and the recovery is smooth. The incidence and severity
of hypotension and the occurrence of nausea and vomiting under spinal anesthesia
are much less with PPTL than with cesarean section (4). Intravenous infusion of
lactated Ringer's solution, 15 ml/kg, is administered within 20 minutes of the spinal
block. While monitors are being applied, i.v. sedation of the patient is performed.
L2-3 may be preferable to L3-4 because of the more predictable level associated with
the former interspace. The dose of local anesthetic should be based on patient's
height (Table 67.1). The addition of 0.2 mg epinephrine intensifies the block and
prolongs its duration of action (6). The addition of 0.2 mg morphine to hyperbaric
bupivacaine also intensifies the spinal block and prolongs the postoperative
analgesia (7). The combination of epinephrine and morphine to bupivacaine provides
better analgesia than the addition of either one alone (8). For PPTL only morphine is
added to the local anesthetic. Using a small gauge (Chapter 97), pencil-tip needle
(Chapter 59) is advisable as this will reduce the incidence of post-dural puncture
headache.
References:
1. Whitehead BEM, Smith M, O'Sullivan G: An evaluation of gastric emptying times in
pregnancy and parturim. In Abstracts of Scientific Papers, Society of Obstetric
Anesthesia and Perinatology, Annual Meeting, 1990.
2. Abouleish E: Subarachnoid block: In Abouleish E, editor: Pain Control in
Obstetrics, Philadelphia, 1977, JB Lippincott.
3. Cruikshank DP, Laube DW, DeBaker LF. Intraperitoneal lidocaine for postpartum
tubal ligation, Obstet Gynecol 1973; 42:127.
4. Abouleish E. Postpartum tubal ligation requires more bupivacaine for spinal
anesthesia than does cesarean section. Anesth Analg 1986; 65:897.
5. Brooks GZ, Mandel ALZ: The early postpartum dermatomal spread of epidural
2-chloroprocaine. In Abstract of Scientific Papers, Society for Obstetric Anesthesia
and Perionatology, Annual Meeting, San Antonio, Texas, 1984.
6. Abouleish E: Epinephrine improves the quality of spinal hyperbaric bupivacaine for
cesarean section. Anesth Analg 1987; 66:395.
7. Abouleish E, Rawal N, Fallon K, Hemandez D: Combined intrathecal morphine and
bupivacaine for cesarean section. Anesth Analg 1988; 67:370.
8. Abouleish E, Rawal N, Tobon-Randal B, et al: A clinical and laboratory study to
compare the addition of 0.2 mg morphine, 0.2 epinephrine or their combination to
hyperbaric bupivacaine for spinal anesthesia in cesarean section. Anesth Analg
1993; 77:457.
Review P3 (1993)
Major Regional Anaesthesia
1. GENERAL PRINCIPLES
1.1 Major Regional Anaesthesia is an anaesthetic technique which can produce
significant physiological changes or local anaesthetic toxicity and which may
cause patient morbidity or mortality (eg epidural or spinal blockade, plexus
blockade, intravenous regional blockade).
1.2 Major regional anaesthesia should be undertaken only by medical
practitioners with adequate experience in the technique or by those in a
supervised training programme. Such persons must understand the relevant
anatomy, physiology, pharmacology and complications of the particular block.
They must be able to recognise and promptly treat any complications of the block.
1.3 The Australian and New Zealand College of Anaesthetists does not approve
of one person assuming the dual responsibility of both the operator and the
anaesthetist for any forms of major regional anaesthesia.
1.4 Management of major regional anaesthesia should include secure intravenous
access, patient monitoring in accordance with Policy Document P18 "Monitoring
During Anaesthesia" and appropriate sedation.
1.5 The anaesthetist should be in attendance throughout the procedure, or until
the block is successful, the condition of the patient is stable and the potential for
acute toxicity of the local anaesthetic has passed.
1.6 To ensure that standards of patient care are satisfactory, equipment and
staffing of the area in which the patient is being managed should satisfy the
requirements of the following Australian and New Zealand College of
Anaesthetists Policy Documents:
T1 "Recommended Minimum Facilities for Safe Anaesthetic Practice in
Operating Suites"
T6 "Recommended Minimum Facilities for Safe Anaesthetic Practice in
Delivery Suites"
P2 "Privileges in Anaesthesia"
P4 "Guidelines for the Care of Patients Recovering from Anaesthesia"
P9 "The Use of Sedation for Diagnostic and Minor Surgical Procedures"
2. SPECIFIC PRINCIPLES FOR POSTOPERATIVE EPIDURAL ANALGESIA
MANAGEMENT
The placement of an epidural catheter and the administration of the initial dose of
local anaesthetic or opiod is the responsibility of the anaesthetist performing the
procedure.
2.1 Should the anaesthetist delegate the further administration of epidural
analgesia to another person it is the responsibility of the anaesthetist to hand over
properly the patient's management to that person and to satisfy himself or herself
of the competence of that person to manage the epidural analgesia and carry out
the administration procedures. Adequate medical records documenting the time,
dose and subsequent effects must be kept.
2.2 Competency should be established by:
2.2.1 a form of accreditation which certifies that the person who will be
performing the epidural administration has carried out a sufficient number of
similar administrations satisfactorily under supervision,
and
2.2.2 enquiry of the person to establish familiarity with and knowledge of the
procedure and subsequent management, including the management of
complications.
2.3 No person should be required to carry out any such procedure if uncertain of
their competence to do so.
2.4 All patients must have secure intravenous access throughout the duration of
the epidural analgesia.
February 1993
This document is copyright and cannot be reproduced in whole or in part without
prior permission.
Review T6 (1995)
Recommended Minimum Facilities for Safe
Anaesthetic Practice in Delivery Suites
The safe provision of anaesthesia requires appropriate staff, facilities and equipment
for proper patient safety. These are specified in this Document.
1. PRINCIPLES OF ANAESTHETIC CARE
1.1 Anaesthesia should be administered only by medical practitioners with
appropriate training in anaesthesia or by trainees supervised according to College
Policy Documents "The Supervision of Trainees in Anaesthesia" (E3) and
"Privileges in Anaesthesia" (P2).
1.2 Every patient presenting for anaesthesia should have a pre-anaesthetic
consultation by a medical practitioner who has appropriate training in anaesthesia.
See College Policy Document "Pre-anaesthetic Consultation" (P7).
1.3 Appropriate monitoring of physiological variables must occur during
anaesthesia. See College Policy Document "Monitoring During Anaesthesia"
(P18).
2. STAFFING
2.1 In addition to the nursing staff required by those carrying out the obstetric or
the operative procedure, there must be:
2.1.1 An assistant to the anaesthetist. See College Policy Document
"Minimum Assistance for the Safe Conduct of Anaesthesia" (P8).
For the establishment and management of epidural blockade for analgesia in
labour, the presence of a midwife trained and competent in obstetric epidural
management is required.
2.1.2 Adequate assistance in positioning the patient.
2.1.3 Adequate technical assistance to ensure proper servicing of all
equipment used.
2.1.4 At the time of delivery, there must be a medical practitioner with
appropriate training in the resuscitation and care of the neonate with sole
responsibility for that task.
3. DELIVERY SUITES
3.1 Anaesthetic Equipment
3.1.1 Where general anaesthesia, sedation or major regional blockade are
utilised, equipment must comply with the requirements set out below as well
as with College Policy Document "Sedation for Diagnostic and Minor Surgical
Procedures" (P9). Where a range of equipment is recommended, the hospital
is expected to provide the type most suitable to its needs. Where patients are
transferred to another facility for operative delivery, anaesthetic and
resuscitative equipment is still essential for the management of complications
of epidural and other major regional blockade.
3.1.2 Each hospital must designate:
3.1.2.1 One (or more) specialists to advise on the choice and maintenance
of anaesthetic equipment.
3.1.2.2 One (or more) of its nursing or technical staff to be responsible for
the organisation of cleaning, maintenance and servicing of anaesthetic
equipment.
3.1.3 There must be an anaesthetic machine for each anaesthetising location
which is capable of delivering air, oxygen, nitrous oxide as well as other
anaesthetic agents which are in common use. Essential equipment includes:
3.1.3.1 Suitable calibrated vaporisers for the delivery of inhalational
anaesthetic agents.
3.1.3.2 A range of suitable breathing systems.
3.1.3.3 Medical air where this is clinically necessary.
3.1.4 Safety devices which must be present on every machine include:
3.1.4.1 An indexed gas connection system.
3.1.4.2 A reserve supply of oxygen.
3.1.4.3 An oxygen supply failure warning device (see College Policy
Document "Monitoring During Anaesthesia" (P18).
3.1.4.4 A breathing system high pressure relief valve.
3.1.4.5 An oxygen concentration analyser with appropriate alarm limits (see
College Policy Document "Monitoring During Anaesthesia" (P18).
3.1.4.6 Every anaesthetic machine purchased after 1 January 1996 shall
have a device to prevent the supply of a hypoxic gas mixture whenever
nitrous oxide is administered.
3.1.4.7 Every anaesthetic machine purchased after 1 January 1996 shall
have an approved non-slip connection for the common gas outlet
whenever a circle system is in use.
3.1.5 A separate means of inflating the lungs with oxygen must be provided in
each anaesthetising location. This apparatus should comply with the current
requirements of the relevant national Standards. Its oxygen supply should be
independent of the anaesthetic machine.
3.1.6 Suction apparatus must be available for the exclusive use of the
anaesthetist at all times together with appropriate hand pieces and
endotracheal suction catheters. This apparatus should comply with the current
requirements of the relevant national Standards. Provision must be made for
an alternative suction system in the event of primary suction failure.
3.1.7 In every anaesthetising location there should be:
3.1.7.1 Appropriate protection for the anaesthesia team against biological
contaminants. This shall include disposable gloves and eye shields.
3.1.7.2 A stethoscope
3.1.7.3 A sphygmomanometer
3.1.7.4 Monitoring equipment complying with College Policy Document
"Monitoring During Anaesthesia" (P18).
3.1.7.5 An appropriate range of face masks.
3.1.7.6 An appropriate range of oropharyngeal, nasopharyngeal and
laryngeal mask airways.
3.1.7.7 Two laryngoscopes with a range of suitable blades.
3.1.7.8 An appropriate range of endotracheal tubes and connectors.
3.1.7.9 A range of endotracheal tube introducers.
3.1.7.10 Inflating syringe and clamps.
3.1.7.11 Magill's forceps.
3.1.7.12 A suitable range of adhesive and other tapes.
3.1.7.13 Scissors.
3.1.7.14 Sterile endotracheal lubricant.
3.1.7.15 Vascular tourniquets.
3.1.7.16 Intravenous infusion equipment with an appropriate range of
cannulae and solutions.
3.1.7.17 Means for the safe disposal of items contaminated with biological
fluids as well as of "sharps" and waste glass.
3.1.7.18 Equipment suitable for the establishment of sub-arachnoid,
epidural or regional nerve blocks.
3.1.7.19 Provision for scavenging of anaesthetic gases and vapours with
interface equipment which precludes over-pressurisation of the
anaesthesia breathing circuit.
3.1.7.20 A cardiac defibrillator with capacity for synchronised
cardioversion.
3.1.8 In every anaesthetising location there should be available:
3.1.8.1 Equipment for managing difficult intubations .
3.1.8.2 Equipment for automatic ventilation of the lungs incorporating
alarms as specified in College Policy Document "Monitoring During
Anaesthesia" (P18).
3.1.8.3 Equipment for the direct measurement of arterial and venous
pressures.
3.1.8.4 Equipment for the rapid infusion of fluids.
3.1.8.5 Equipment to minimise patient heat loss by warming of infused
fluids and the body surface.
3.1.8.6 Equipment to warm and humidify gases administered during
anaesthesia.
3.1.8.7 Interpleural drainage sets.
3.1.9 Other requirements for safe anaesthesia include:
3.1.9.1 Appropriate lighting for the clinical observation of patients which
complies with the current requirements of the relevant national Standards.
3.1.9.2 Emergency lighting.
3.1.9.3 Telephone/Intercom to communicate with persons outside the
anaesthetising location.
3.1.9.4 Refrigeration facilities for the storage of drugs and biological
products.
3.1.9.5 The means to maintain room temperature in the anaesthetising
location within the range of 18 - 28oC.
3.1.9.6 Patient transfer trolleys/beds as specified in College Policy
Document "Guidelines for the Care of Patients Recovering from
Anaesthesia" (P4).
3.1.10 In each delivery room there must be:
3.1.10.1 Apparatus for the administration of inhalational analgesia with a
minimum of 30% oxygen.
3.1.10.2 Suction apparatus for the exclusive use of the anaesthetist which
is separate from that required for the resuscitation of the neonate.
3.1.10.3 Separate oxygen outlets and suitable attachments for
administering oxygen to the mother and to the neonate.
3.2 Drugs
3.2.1 In addition to the drugs and agents commonly used in anaesthesia,
drugs necessary for management of conditions which may complicate or
co-exist with anaesthesia must also be available:
Anaphylaxis
Cardiac arrhythmias
Cardiac arrest
Pulmonary oedema
Hypotension
Hypertension
Bronchospasm
Respiratory depression
Hypoglycaemia
Hyperglycaemia
Adrenal dysfunction
Raised intracranial pressure
Uterine atony
Blood coagulopathy
Malignant hyperpyrexia
3.2.2 In making an appropriate selection of drugs for the management of these
conditions, advice should be sought as in 3.1.2.1.
3.2.3 Appropriate mechanisms must exist for the regular replacement of these
drugs after use and/or their expiry date has been reached.
3.2.4 A basic supply of dantrolene should be rapidly available to all
anaesthetising locations with further doses being available on request.
3.3 Routines for Checking, Cleaning and Servicing Equipment
3.3.1 Regular sterilising, cleaning and housekeeping routines for the care of
equipment should be established.
3.3.2 Documented servicing of the anaesthetic machine and medical gas
equipment by an appropriate organisation must be carried out at least twice a
year. After any modification to the gas distribution system, gas analysis and
flow measurement must be carried out and documented before use.
3.3.3 A copy of the College Policy Document "Protocol for Checking an
Anaesthetic Machine Before Use" (T2) or a similar document should be
available on each anaesthetic machine.
3.4 Recovery Area
3.4.1 Recovery from anaesthesia should take place under appropriate
supervision in a designated area which conforms with College Policy
Document "Guidelines for the Care of Patients Recovering from Anaesthesia"
(P4).
3.4.2 Contingency plans should exist which would allow rapid patient transfer
in an emergency from the delivery suite or recovery areas to another
appropriate area under adequate medical supervision.
3.5 Neonatal Resuscitation Equipment
3.5.1 A suitable range of equipment must be available for:
3.5.1.1 Administration of oxygen to the neonate.
3.5.1.2 Intubation and ventilation of the neonate.
3.5.1.3 Clearing of the airway of the neonate.
3.5.1.4 Administration of intravenous fluids and drugs.
3.5.1.5 Maintenance of the neonate's temperature.
3.5.2 An appropriate range of drugs must be available.
3.5.3 It is recommended that each hospital designate:
3.5.3.1 One (or more) medical practitioners with appropriate training and
qualifications to advise on the choice and maintenance of equipment and
drugs required for the resuscitation and care of the neonate.
3.5.3.2 One or more of its nursing or technical staff to be responsible for
the organisation of cleaning, servicing and maintenance of this equipment.
This policy document has been prepared having regard to general circumstances,
and it is the responsibility of the practitioner to have express regard to the particular
circumstances of each case, and the application of this policy document in each
case.
Policy documents are reviewed from time to time, and it is the responsibility of the
practitioner to ensure that the practitioner has obtained the current version. Policy
documents have been prepared having regard to the information available at the time
of their preparation, and the practitioner should therefore have regard to any
information, research or material which may have been published or become
available subsequently.
Whilst the College endeavours to ensure that policy documents are as current as
possible at the time of their preparation, it takes no responsibility for matters arising
from changed circumstances or information or material which may have become
available subsequently.
Promulgated: 1989
Reviewed: 1994
Date of current document: Oct 1995
This document is copyright and cannot be reproduced in whole or in part without
prior permission.
Content &COPY 1996, Australian and New Zealand College of Anaesthetists.Design &COPY 1996 Med-E-Serv Pty Ltd.
All Rights Reserved. Revised 23 Oct 1996
Angela Bader
Close monitoring of maternal temperature is performed during labor because
maternal infection is associated with significant maternal and neonatal morbidity.
An association between the use of epidural analgesia during labor and an elevation in
maternal temperature was first noted in 1989, when Fusi (1) reported that the vaginal
temperatures of 18 parturients receiving epidural analgesia increased by about 1
degree Centigrade over 7 hours when compared to women receiving intramuscular
narcotics. Since detrimental fetaI effects had been demonstrated in animals warmed
to a temperature of about 42 degrees Centigrade (2), Fusi's article raised concern
regarding the effects of epidural anesthesia on maternal temperature. Perhaps
decreases in sweating and hyperventilation contribute to the association between
epidural analgesia and increasing temperature in the parturient. However, increased
lower extremity blood flow during epidural analgesia renders vaginal or rectal
temperatures unreliable, and tympanic membrane temperature will more accurately
reflect core temperature.
Camann et al (3) studied tympanic temperature measurements in laboring parturients
in a controlled temperature environment and found no difference in temperature in
the groups receiving either epidural or intravenous analgesia up to four hours after
epidural placement. At five hours, the parturients receiving epidural analgesia with
either plain bupivacaine or bupivacaine plus fentanyl showed a small but significant
increase in temperature from 36.6 degrees C to 37.1 degrees C (3). These authors
felt that this degree of temperature increase was not sufficient to result in an adverse
intrauterine environment and fetal compromise. Macaulay then studied intrauterine
fetal skin temperature directly and noted a maximum fetal skin temperature greater
than 38.0 degrees C in 10 of 33 parturients in the epidural group but in none of those
not receiving epidurals (4). There were no differences in neonatal acid base
measurements or Apgar scores (Table 35.1). The ambient room temperatures in this
study, however, ranged as high as 29.0 degrees C. These authors suggested
maintaining cooler ambient temperatures and frequent sponging in women receiving
epidural analgesia for prolonged periods of time.
In conclusion, although epidural anesthesia maintained for longer than five hours is
associated with an increase in maternal temperature, it is unlikely that epidural
anesthesia causes increases in temperature of sufficient severity to cause fetal
compromise. There is no evidence of adverse fetal effects based on Apgar scores
and acid base status. Altered thermoregulatory transmission from the periphery to the
hypothalamus may be postulated as a possible mechanism for the increase in
temperature seen during epidural analgesia.
References:
1. Fusi et al, Lancet 1989;1:1250-1252.
2. Morishima et al, Am J Obstet Gynecol 1970; 121:531-8
3. Camann et al, Br J Anaesth 1991;67:565-568
4. Macaulay et al, Obstet Gynecol 1992;80:665-669
Paul Bellhouse
The place of regional anaesthesia in the patient with a difficult airway.
There is a place for regional anaesthesia in the patient with the difficult airway when it
is used by a clinician who has a clear understanding of the risks involved and a clear
definition of the type and likelihood of difficulty which may be experienced with
intubation or ventilation. The anaesthetist must also be both proficient in regional
anaesthesia and be prepared to maintain ventilation in a patient with a difficult airway
who has become accidentally paralyzed.
Specifically, the risk is that a regional anaesthetic (eg subarachnoid block) may
extend high enough to cause respiratory paralysis lasting for a prolonged period in a
patient who cannot be intubated or ventilated.
Every candidate for major regional anaesthesia or muscle relaxation anaesthesia
must be assessed with regard to the likelihood of difficult intubation. Emphasis should
be placed on reduced mouth opening, enlarged tongue and restricted head extension
(1, 2, 3, 4, 5).
As only about 10% of difficult or impossible intubations can be predicted with
certainty, the possibility of a difficult intubation should be kept in mind even in those
patients for whom regional anaesthesia is planned. Because the parturient is at
particular risk of oesophageal reflux, all the equipment required to deal with a difficult
intubation or airway soiling should be functional and immediately available.
Respiratory embarassment is possible following epidural or spinal anaesthesia. Low
spinal (eg. saddle block) and mid-spinal (eg. to T10) have a lower risk of respiratory
compromise.
Measures to reduce the risk of respiratory impairment include:
1. test dosing if an epidural is to be used,
2. care with the dose of the drug used for subarachnoid anaesthesia and,
3. appropriate posturing of the patient.
If an airway emergency occurs during regional anaesthesia in a woman with a difficult
airway, there are many alternatives to intubation with the Macintosh laryngoscope.
These include:
1. Belscope angulated laryngoscope (6),
2. Bullard laryngoscope,
3. flexible fibreoptic laryngoscope,
4. light wand (not practical in the emergency case),
Other intubation aids such as a flexible copper wire introducer or gum elastic bougie
may also be useful.
Measures which permit ventilation of the patient without the benefit of a cuffed
endotracheal tube include:
1. bag and mask,
2. laryngeal mask airway,
3. crico-thyroid puncture and
4. tracheostomy.
None of these methods should be used in an emergency by someone who is not
skilled in their use.
References:
1. Bellhouse CP, Dore C. Criteria for estimating likelihood of difficulty of endotracheal
intubation with the Macintosh laryngoscope. Anaesthesia and Intensive Care
1988;16:329- 337.
2. Rocke DA, Murray WB, Rout CC, Gouws E. Relative risk analysis of factors
associated with difficult intubation in obstetric anesthesia. Anesthesiology
1992;77:67-73.
3. Wilson ME, Spiegelhalter D, Robertson JA, Lesser P. Predicting Difficult
Intubation. British Journal of Anaesthesia, 1988; 61:211-216.
4. Frerk, CM. Predicting difficult intubation. Anaesthesia, 1991;46:1005-1008.
5. Pottecher T, Velten M, Galani M, Forrler M. Valeur comparee des signes cliniques
d'intubation difficile chez la femme. Ann Fr Anesth Reanim 1991;10:430-5.
6. Bellhouse CP. A new laryngoscope for routine and difficult intubations.
Anesthesiology 1988;68:126-129.
R Blackshear
The Tensile Strength of Epidural Catheters and Spinal Micro-Catheters: Implications
for Clinical Anaesthesia.
Complications related to regional anesthesia using either epidural or spinal catheters
are well described and are generally associated with unintentional intrathecal
injection of drugs meant to be administered in the epidural space, or in the case of
intrathecal catheters, unintentional injection of medicines which should not be
delivered into the spinal canal (1, 2, 3). However, a described, but uncommon,
complication of both epidural and intrathecal catheterisation is separation of the
catheter tip during removal (4, 5, 6).
Currently, the standard of care which applies to retention of a segment of epidural
catheter within the epidural space is to leave the broken segment in place if no
symptoms occur and then follow up with neurologic examination (Chapter 104).
However, if a small-diameter continuous spinal catheter becomes separated within
the intrathecal space, it is not unreasonable to perform an exploration of the
intrathecal space and to retrieve the broken segment of the spinal catheter (11). As
intrathecal catheters have become smaller and smaller in diameter, not only has the
use of these catheters increased in popularity, but so has the chance of separation of
the catheter tip when the device is withdrawn.
Of the studies relating to the tensile strength of catheters, three are of relevance to
those who perform regional anesthesia (8, 9, 10):
Study 1. Tensile strengths of epidural catheters in vitro.
Study 2. Tensile strengths of micro-catheters used for continuous spinal anesthesia
in vitro.
Study 3. Force necessary to withdraw an epidural catheter in vivo.
Study 1. The tensile strength and elongation before failure of six commonly used
epidural catheters was investigated. This test was performed using an 'Instron'
universal testing instrument and both load-to-failure as well as catheter elongation
were measured (Table 42.1). It should be noted that a 19 Gauge (ga) nylon catheter
by Pharmaseal gave the greatest margin of safety when considering separation of a
catheter tip. In fact, the 19ga Pharmaseal nylon catheter offered nearly a 2kg margin
of safety before breakage when compared with a 20ga Teflon epidural catheter. Also
of note was the elongation factor where, once again, the 19ga Pharmaseal catheter
performed best in that it had a greater than 1,000 percent elongation before failure
occurred. This adds to the margin of safety of the catheter in that once it is seen to
stretch, the patient can be repositioned in order to permit removal of an intact
catheter.
Study 2. The second evaluation involved seven continuous spinal micro-catheters
including 24ga, 28ga and 32ga devices. Testing done on these particular catheters
was the same as for the epidural catheters described in Study 1. There was no
significant difference in the tensile strength or extent of elongation of any of the
catheters tested. The range in which breakage occurred was 0.45 - 0.51 kg. The
force needed to break a 20ga epidural catheter measured nearly 3kg indicating a
six-fold difference in break forces between spinal micro-catheters and conventional
20ga epidural catheters.
Study 3: This study was an in vivo determination of the force of manual extraction of
lumbar epidural catheters in postpartum patients. Results of this study indicated that
there was a considerable margin of safety between actual in vivo force needed to
extract lumbar epidural catheters and measured in vitro tensile strengths. The in vitro
breaking strength of a 20ga nylon epidural catheter has been measured at 3kg which
was more than 1.4kg greater than the highest level recorded in the in vivo manual
extraction study. However, the in vitro breaking force in spinal micro-catheters has
been measured at 0.4 - 0.5kg. This breaking point lies within the in vivo ranges noted
in this study regardless of body position when an epidural catheter is removed.
Furthermore, body position during catheter removal must be considered because the
force needed to remove an epidural catheter in the sitting position is considerably
greater than that for the lateral decubitus position. Figure 42.1 describes ounces of
pull needed to extract catheters in the lateral decubitus and sitting positions. These
forces are also compared to those required to break a spinal microcatheter.
Figure 42.2 integrates all the data from the three studies described and supports the
following recommendations: (1) Care must be used when spinal micro-catheters are
being extracted from a patient because the chance for breakage is real;
(2) Using the lateral decubitus position when removing an epidural catheter is
recommended as this results in the least force of extraction (Chapter 75); and finally,
(3) if the catheter separates within the epidural space, leave the broken segment in
place and follow up with neurological examination as needed. However, if a spinal
microcatheter separates within the intrathecal space, surgical exploration with
retrieval of the tip of the catheter is required to avoid future neurologic problems
(Chapter 104).
References:
1. Murphy TM: Spinal, epidural, and caudal anesthesia. In: Miller RD (ed).
Anesthesia, 2nd edition. New York, Churchill Livingstone. 1986
2. Bromage PR: Epidural Analgesia. Philadelphia. WB Saunders, 1978, pp 664-666
3. Cousins MJ. Bromage PR: Epidural neural blockade. In: Cousins MJ, Bridenbaugh
PO (eds). Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed,
JB Lippincott Co, Philadelphia,1988. p 336
4. Moerman N. Porcelijn T, Deen L: A broken epidural catheter. Reg Anesthesie
(Springer-Verlag) 3:17-18, 1980.
5. Hurley R J, Lambert DH. Continuous spinal anesthesia with a microcatheter
technique: preliminary experience. Anesth Analg 1990:70:97-102
6. Tio TO, Macmurdo SD, McKenzie R: Mishap with an epidural catheter.
Anesthesiology 1979;50:260-262
7. Ley SJ, Jones BR: Strength of continuous spinal catheters. Anesthesia and
Analgesia 1991:394-6
8. Blackshear RH, et al. Comparison of tensile strength of seven types of epidural
catheters. Anesthesiology 1990;73(3A);A961
9. Wissler RN, Blackshear RH: Tensile strength of spinal microcatheter.
Anesthesiology 73:A505, 1990.
10. Blackshear RH, Gravenstein N, Radson E: Tension applied to lumbar epidural
catheters during removal is much greater with patient sitting versus lying.
Anesthesiology 1991; 75:A833
11. De Vera HV, Ries M. Complication of continuous spinal microcatheters: Should
we seek their removal if sheared? (Letter) Anesthesiology 1991 74:794
Rhonda Boyle
The effect of analgesia on the stress of labour: The pain of labour and delivery
involves local segmental, suprasegmental and cortical stress responses. Properly
administered analgesia makes labour safer.
Respiration.
Epidural analgesia prevents transient hyperventilation during, and hypoventilation
between, uterine contractions, so that maternal PaCO2 remains 28-32mmHg and
PaO2 about 100mmHg (1). The incidence of hypoxaemia during first or second stage
labour is 3 times greater with no analgesia, or 1.4 times greater with intramuscular
pethidine, than when epidural analgesia is provided by bupivacaine 0.125% without
fentanyl (2) (Chapter 87). Maternal hypoxia during labour has not correlated with non
reassuring cardiotocography . Some studies have (3) and others (4, 5) have not
correlated maternal hypoxia with low neonatal Apgar scores (Table 35.1) or abnormal
umbilical cord blood gases.
Reduced Neuroendocrine Effects of Pain
The relief of pain and associated anxiety with continuous epidural analgesia reduces
maternal catecholamine, beta endorphins, ACTH and cortisol. (6, 7, 8, 9) Total work
of labour, maternal metabolism and oxygen consumption are reduced. Maternal and
fetal acidosis are reduced (10) though active pushing during second stage sustains
some metabolic acidosis whether or not epidural analgesia is administered.
Reduced Cardiovascular Effects of Pain
Epidural analgesia eliminates the increase in cardiac output, heart rate and blood
pressure caused by pain.
Uterine Activity
Catecholamine alpha receptor stimulation causes uterine hypertonus, and beta
receptor stimulation decreases uterine tone and contractility. Epidural analgesia
without adrenaline may (a) reduce effect of circulating catecholamines causing
uterine hypo and hyper activity, and (b) change incoordinate uterine activity to a
normal labour pattern. Allowing an epidural to wear off during second stage increases
circulating catecholamines, leading to impairment of uterine activity and a longer
second stage. (11)
Effect of analgesia on duration of 2nd stage of labour and mode of delivery
Studies of the effects of epidural analgesia can be classified into those in which a
particular epidural drug or administration
1. Slows labour, increasing the rate of instrumental deliveries (12, 13, 14, 15, 16, 17,
18, 19) or has no effect (14, 20, 21, 22, 23, 24, 25, 26), and
2. Improves the progress of labour (11, 22, 25, 27, 28, 29)
Why do studies give conflicting results ?
There are many unanswered questions with regard to effects of epidural analgesia on
second stage of labour and mode of delivery. When designing a study, particular
attention should be paid to the following areas:
1. Patient matching:
Patients studied are not always comparable to controls in proportion of primigravidae
/ multigravidae, age, pre-existing medical or obstetric complication, maternal height,
fetal size. When groups not receiving epidurals are compared with those undergoing
epidural analgesia, the process of randomization should occur before analgesia is
requested.
2. Conduct of labour:
Labours are not always comparable to controls. Onset of labour before or after 37
weeks, duration of active stage, posture of mother during second stage (30), timing
and dose of oxytocin, prostacyclin, rupture of membranes all affect duration of
second stage. Similar definitions are required between study and control groups of
beginning of second stage (full cervical dilatation, or appearance at introitus of
presenting part).
3. Obstetric Management:
The extent of labour monitoring, indications for augmentation and rates of
instrumental and operative delivery are sometimes not specified or are not
supervised by someone other than the provider of epidural analgesia.
4. Anaesthetic management:
Anaesthetic end-points and outcomes are not always consistent. Investigators should
report the incidence of spontaneous vaginal delivery, quality of analgesia in both first
and second stage, degree of motor block, rate of perineal trauma (31) and extent of
maternal expulsive efforts. Studies do not always specify adverse effects on gastric
emptying, fetal acidosis or respiratory depression. Among a large group of patients
with a uniform sensory level, epidural analgesia will have different effects on labour
haemodynamics.
5. Statistical power:
The size of groups may not be large enough to detect significant differences (32).
The mechanisms of prolongation of labour by epidural analgesia:
I. Somatic motor blockade increases dystocia.
Removal of the urge to push and perineal muscle relaxation may slow internal
rotation and descent of the fetal head.
A. The use of dilute concentrations of local anaesthesia with/without opioids provides
less motor blockade.
B. Some local anaesthetics (Chapter 4) preferentially block motor over sensory fibres
(Chapter 88) (33).
C. Opioids alone (epidural or parenteral) reduce somatic block but provide
inadequate maternal analgesia, increase gastric stasis and fetal depression. Epidural
opioids increase duration of active phase of stage 1 (34).
D. Epidural clonidine and fentanyl, when used alone, preserve motor function but
analgesia is inadequate (35).
E. Predictably, intrathecal bupivacaine in addition to or instead of, epidural
bupivacaine reduces the required dose for labour analgesia but does not reduce the
degree of motor blockade or the duration of the second stage (36).
II. Epidural blockade of pelvic autonomic nerves may abolish the increment in
oxytocin levels that occurs normally between full cervical dilatation and crowning of
the fetal head (37). Oxytocin is claimed to be crucial to correct rotation and descent
of fetal head but does not correlate with uterine contractility or spontaneous delivery.
Plasma oxytocin levels have questionable clinical significance (38).
III. Aortocaval compression, not epidural blockade, reduces uterine perfusion and
contractility even in the absence of demonstrable hypotension (39).
IV. If the intravenous fluid load prior to an epidural is administered as a bolus, rather
than at a maintenance infusion rate, a 20 minute decrease in uterine activity results
(22). The bolus transiently inhibits posterior pituitary production of antidiuretic
hormone and perhaps of oxytocin.
V. Medico legal climate (40).
Legal notions regarding the appropriate duration of the various stages of labour may
influence obstetric management.
VI. An arbitrary time limit, not maternal or fetal well being, may be used to terminate
labour and justify operative delivery.
VII. Epidurals (41) account for only 8.3% of total variability in the duration of second
stage of labour. 75% of variability in the length of second stage cannot be accounted
for (Figure 33.3). It is no wonder that an improvement in spontaneous delivery rate
has not been shown despite absence of motor block in majority of parturients (32, 42,
43, 44). While the need for instrumental vaginal delivery will decline as motor power
is retained, this effect can exert only a minor influence until all other factors
influencing second stage duration are better understood.
Summary
Labour is unpredictable and influenced by many factors. Anaesthetic technique can
affect the course of fetal descent and delivery but judicious obstetric and anaesthetic
management provide safe maternal and fetal care without excessive prolongation of
labour.
References:
1. Fisher A, Prys-Roberts C: Maternal pulmonary gas exchange. Anaesthesia 1968;
23:350.
2. Griffin R, Reynolds F: Maternal hypoxaemia during labour and delivery. The
influence of analgesia and effect on neonatal outcome. Anaesthesia 1995; 50:151 -
156.
3. Porter KB, Goldhamer R, Mankad A, Gaddy J, Peery J, Spinnato JA: Evaluation of
arterial oxygen saturation in pregnant patients and their newborn. Obstet Gynecol
1988; 71:354 - 357.
4. Reed PN, Colquhoun AD, Hanning CD: Maternal oxygenation during normal
labour. Br J Anaes 1989; 62:316 -18.
5. Deckardt R, Fembacher PM, Schneider KTM, Graeff H: Maternal arterial oxygen
saturation during labour and delivery. Pain - dependent alterations and effects on the
newborn. Obstet Gynecol 1987; 70:21 - 25.
6. Browning AJ, Butt WR, Lynch SS, Shakespear RA et al: Maternal and cord plasma
concentrations of beta-lipotrophin, beta-endorphin and gamma-lipotrophin at delivery;
effect of analgesia. Br J Obstet Gynaecol 1983; 90:1152.
7. Fettes I, Fox J, Kuzniak S, Shime J, et al: Plasma levels of immunoreactive
beta-endorphin and adrenocorticotropic hormone during labour and delivery. Obstet
Gynecol 1984; 64:359.
8. Jouppila R, and Hollmen A: The effect of segmental epidural analgesia on
maternal and foetal acid-base balance, lactate, serum potassium and creatine
phosphokinase during labour. Acta Anaesthesiol Scand 1976; 20:259.
9. Maltau JM, Eilson OV, Stokke KT: Effects of stress during labour on the
concentration of cortisol and estriol in maternal plasma. Am J Obstet Gynecol 1979;
134:681.
10. Pearson JF, Davies P: The effect of continuous lumbar epidural analgesia on
maternal acid-base balance and arterial lactate concentration during second stage of
labour. J Obstet Gynaecol Br Common W 1973; 80:225.
11. Phillips KC, Thomas TA: Second stage of labour with or without extradural
analgesia 1983; 38:972-976.
12. Abboud TK, Afrasiabi A, Sarkis F et al Continuous infusion epidural analgesia in
parturients receiving bupivacaine, chloroprocaine, or lidocaine: Maternal, fetal and
neonatal effects. Anesth Analg 1984; 63:421 - 428.
13. Chestnut DH, Vandewalker GE, Owen CL, Bates JN, Choi WW: The influence of
continuous epidural bupivacaine analgesia on the second stage of labour and method
of delivery in nulliparous women. Anethesiology 1987; 66:774 - 780.
14. Lysak SZ, Eisenach JC, Dobson CE: Patient-controlled epidural analgesia during
labour: A comparison of three solutions with a continuous infusion control.
Anesthesiology 1990; 72:44-49.
15. Robinson JO, Rosen M, Evans JM, Revill SI, David H, Rees G: Maternal opinion
about analgesia for labour: A controlled trial between epidural block and
intramuscular pethidine combined with inhalation. Anaesthesia 1980; 35:1173-1181.
16. Smedstad KG, Morison DH: A comparative study of continuous and intermittent
epidural analgesia for labour and delivery. Can J Anaesth 1988; 35:234-241.
17. Studd JWW, Crawford JS, Duigan NM, Rowbotham CJF, Hughes AO: The effect
of lumbar epidural analgesia on the rate of cervical dilatation and the outcome of
labour of spontaneous onset. Br J Obstet Gynaecol 1980; 87:1015-1021.
18. Thorp JA, Parisi VM, Boylan PC, Johnston DA: The effect of continuous epidural
analgesia on cesarean section for dystocia in nulliparous women. Am J Obstet
Gynecol 1989; 161:670-675.
19. Walton P, Reynolds F: Epidural analgesia and instrumental delivery. Anaesthesia
1984; 39:218-223.
20. Bailey PW, Howard FA: Epidural analgesia and forceps delivery: Laying a bogey.
Anaesthesia 1983; 38:282-285.
21. Celleno D, Capogna G: Epidural fentanyl plus bupivacaine 0.125 per cent for
labour: Analgesic effects. Can J Anaesth 1988; 35: 375-378.
22. Cheek TG, Samuels P, Tobin M, Gutsche BB: Rapid intravenous saline infusion
decreases uterine activity in labour: Epidural analgesia does not. Anesthesiology
1989; 71:A884.
23. Chestnut DH, Bates JN, Choi WW: Continuous infusion epidural analgesia with
lidocaine: Efficacy and influence during the second stage of labor. Obstet Gynecol
1987; 69:323-327.
24. Gribble RK, Meier PR: Effect of epidural analgesia on the primary cesarean rate.
Obstet Gynecol 1991; 78:231-234.
25. Naulty JS, Smith R, Ross R: Effect of changes in labour analgesic practice on
labour outcome. Anesthesiology 1988; 69:A660.
26. Philipsen T, Jensen N-H: Epidural block or parenteral pethidine as analgesic in
labour: A randomized study concerning progress in labour and instrumental
deliveries. Eur J Obstet Gynecol Reprod Biol 1989; 30:27-
27. Floberg J, Belfrage P, Ohlsen H: Influence of the pelvic outlet capacity on fetal
head presentation at delivery. Acta Obstet Gynecol Scand 1987; 66:127-130.
28. Hawkins JL, Skjonsby BS, Joyce TH III, Hess KR, Morrow DH: The association of
epidural analgesia and forceps delivery. Anesth Analg 1990; 70:S150.
29. Vertommen JD, Vandermeulen E, Van Aken H et al The effects of the addition of
sufentanil to 0.125 % bupivacaine on the quality of analgesia during labour and on
the incidence of instrumental deliveries. Anesthesiology 1991; 74:809-814.
30. Chen SZ, Aisaka K, Mori H, Kigawa T: Effects of sitting position on uterine
activity during labour. Obstet Gynecol 1987; 69:67-73.
31. Walker MPR, Farine O, Rolbin SH, Ritchie JWK: Epidural anaesthesia
episiotomy and obstetric laceration. Obstet Gynecol 1991; 77:668.
32. Russell R, Reynolds F: Epidural infusions for nulliparous women in labour. A
randomized double blind comparison of fentanyl/bupivacaine and
sufentanil/bupivacaine. Anaesthesia 1993; 48:856-861.
Cousins MJ, Bridenbaugh PO. In: Cousins MJ, Bridenbaugh PO (eds). Neural
Blockade in Clinical Anesthesia and Management of Pain, 2nd ed, JB Lippincott Co,
Philadelphia,1988.
34. Abouleish MD, Rawal N, Shaw J, Lorenz T, Rashad MN: Intrathecal morphine
0.2mg versus epidural bupivacaine 0.125 % or their combination. Anesthesiology
1991; 74:711 - 716.
35. Husaini SW, Russell IF: Epidural clonidine-fentanyl combination for labour
analgesia a comparison with bupivacaine-fentanyl. Int J Obstet Anes 1995; 4:150 -
154.
36. Graham CM, Cooper GM: Comparison of continuous spinal and epidural
analgesia for pain relief in labour. Int J Obstet Anes 1995;4:219 - 224.
37. Goodfellow CF, Hull MGR, Swaab DF, Dogterom J, Buijs RM: Oxytocin
deficiency at delivery with epidural analgesia. Br J Obstet Gynaecol 1983; 90:214 -
219.
38. Amico JA, Seitchik J, Robinson AG: Studies of oxytocin in plasma of women
during hypocontractile labour. J Clin Endocrinol Metab 1984; 58:274 -279.
39. Schellenberg JS: Uterine activity during lumbar epidural analgesia with
bupivacaine. Am J Obstet Gynecol 1977; 127:26 - 31.
40. Neuhoff D, Burke MS, Porreco RP: Cesarean birth for failed progress in labour.
Obstet Gynecol 1989; 73:915 - 920.
41. Piper JM, Bolling DR, Newton ER: The second stage of labour: factors
influencing duration. Am J Obstet Gynecol 1991; 165:976 - 979.
42. Bailey CR, Ruggier R, Findley IL: Diamorphine-bupivacaine mixture compared
with plain bupivacaine for analgesia. Br J Anaesth 1994; 72:58 - 61.
43. Murphy JD, Henderson K, Bowden MI, Lewis M, Cooper GM: Bupivacaine versus
bupivacaine plus fentanyl for epidural analgesia: effect on maternal satisfaction. Br
Med J 1991; 302:564 - 567.
44. Phillips GH: Continuous infusion epidural analgesia in labour: effect of adding
sufentanil to 0.125% bupivacaine. Anesth Analg 1988; 67:462 - 465.
Mark Brown
Acute management of severe pre-eclampsia prior to initiation of a major regional
block.
The principles of treatment are:
1. Assessment of the extent of maternal organ system involvement,
2. Assessment of the fetus,
3. Correction of the underlying patho-physiologic changes.
1. The first aim is rapidly achieved by
(a) checking the blood pressure (an appropriate sized cuff and a sphygmomanometer
remain the gold standard for this),
(b) examining for hyperreflexia and clonus (signs of central nervous system
involvement), epigastric tenderness (subcapsular liver swelling due to ischaemia) and
pulmonary oedema, and
(c) measuring the haemoglobin and haematocrit (a haematocrit above 0.40 is
probably abnormal; certainly > 0.45 reflects plasma volume contraction) (1), platelet
count and coagulation studies (the latter are rarely abnormal when the platelet count
is normal) (2), liver enzymes, plasma creatinine concentration (greater than 90
micromol/L is abnormal for pregnancy).
2. The fetus can be assessed rapidly by examining fundal height, fetal heart rate and
CTG. Check whether steroids have been given in cases of severe prematurity as
these will have aided fetal lung maturity.
3. Hypertension is generally treated when BP is persistently above 160 mmHg
systolic and/or 90 mmHg diastolic. Chronic treatment centres around medications
such as oxprenolol, methyldopa, labetalol, clonidine, prazosin, hydralazine and
nifedipine (3). In the acute setting, BP should be lowered if systolic BP &gt170 mmHg
and/or diastolic > 110 mmHg, using sublingual nifedipine 10 mg or intravenous
hydralazine 5 mg boluses. If hypertension is refractory to 3 such doses at 20 minute
intervals then a hydralazine infusion (5mg/hr) is often successful. If this fails sodium
nitroprusside should be used and delivery effected quickly.
Convulsion prophylaxis is required when there is evidence of central nervous system
involvement, ie. following a convulsion or else prophylactically when there is
hyperreflexia with clonus, severe headaches with hyperreflexia or repeated visual
scotomata. Magnesium sulphate (there are many regimens but a 4gm intravenous
loading dose followed by 1.5gm/hr until 48 hours post delivery is one useful method)
is now thought to be superior to phenytoin for convulsion prophylaxis (4, 5).
Thrombocytopenia is generally treated (with 6 to 8 units of platelets) if the platelet
count is below 40,000 as the accompanying severe hypertension makes intracerebral
haemorrhage a very real risk. Coagulation abnormalities are uncommon but should
be corrected with fresh frozen plasma.
Volume expansion remains a controversial area of management. In severe
pre-eclampsia, the plasma volume is likely to be contracted. Particularly when
vasodilators have been given or an epidural anaesthetic is about to be administered,
preloading with 500 ml (approximately the plasma volume deficit in most cases) of a
colloid containing solution (125 ml/hr) is a safe technique which helps prevent sudden
hypotension and is very unlikely to induce pulmonary oedema. Oliguria is very
worrying and should be treated initially with careful volume restoration (up to 1000 ml
of a colloid solution is adequate). If there is no response to volume restoration, a
diuretic (20 mg frusemide intravenously is often enough) can be administered after
collecting blood and urine to check the fractional sodium excretion. Invasive
haemodynamic monitoring is unnecessary in most cases and should be reserved for
the pre-eclamptic woman with continuing oliguria or pulmonary oedema (3).
In general, it must be remembered that the best treatment of severe pre-eclampsia is
delivery of the placenta. This should be effected quickly but the best outcomes are
obtained when the pre-eclamptic woman has been adequately prepared for delivery,
as outlined above.
References:
1. Brown MA, Zammit VC, Mitar DM. Extracellular fluid volumes in
pregnancy-induced hypertension. J. Hypertension. 1992; 10: 61-68.
2. Barker P, Callandar CC. Coagulation screening before epidural analgesia in
pre-eclampsia. Anaesthesia. 1991; 46: 64-67.
3. Australasian Society for the Study of Hypertension in Pregnancy. Management of
hypertension in pregnancy: Consensus summary. Med J Aust. 1993; 158: 700-702.
4. Eclampsia Trial Collaborative Group. Which anticonvulsant for women with
eclampsia? Evidence from the collaborative eclampsia trial. Lancet. 1995;
345:1455-1462.
5. Lucas M, Leveno K, Cunningham G. A comparison of magnesium sulfate with
phenytoin for the prevention of eclampsia. New Engl J Med. 1995; 333: 201-205.
Mark Brown
Pathophysiology of pre-eclampsia as it applies to acute resuscitation prior to regional
anaesthesia:
It is impossible to resuscitate a pre-eclamptic woman without proper knowledge of
the underlying pathophysiology.
Whereas all hypertensive disorders in pregnancy (pre-eclampsia, essential
hypertension, 'secondary' hypertension) share high blood pressure as a common
theme (probably mediated by inappropriate vasoconstriction), pre-eclampsia is the
only disorder with multisystem abnormalities (1).
The triad of physiological derangements in pre-eclampsia is:
1. Intense vasospasm,
2. Local or disseminated intravascular coagulation,
3. Plasma volume contraction.
Although the cause of pre-eclampsia is unknown the placenta appears to be the
culprit - delivery of the placenta is the only known cure and the disorder is more
frequent with large placental mass, eg. twins (2), or abnormal placentae (3). Current
hypotheses propose release of a toxic factor from the placenta which alters maternal
endothelial cell functions (4), though this is unproven.
Vasospasm follows due to excess production or sensitivity to vasoconstrictors
(angiotensin II, serotonin and endothelin are the most popular candidates) and/or
decreased production or sensitivity to vasodilators (prostacyclin and nitric oxide are
the current candidates here). This issue is by no means resolved.
Intravascular coagulation is associated with platelet activation (5), thrombocytopenia
and, often, reduced production of anti-thrombin III (6).
Plasma volume contraction follows vasospasm, capillary leakage (7) and, in more
severe cases, reduction in plasma oncotic pressures (8). There is redistribution of
fluid from the intravascular to interstitial fluid spaces so that total extracellular fluid
volume remains unaltered (9). These are important considerations as intravascular
volume correction may result in pulmonary oedema when capillary permeability is
high and plasma oncotic pressure low.
The net result of this triad of abnormal physiology is organ hypoperfusion. Systems
most commonly affected are the kidney (manifested by reduced GFR, proteinuria,
hyperuricaemia and occasionally oliguria), the liver (manifested by elevated aspartate
transaminase with or without epigastric and right upper quadrant pain), the brain
(manifested most commonly by transient visual scotomata due to occipital lobe
ischaemia, severe headaches and rarely convulsions, ie. eclampsia) and the placenta
(manifested by intrauterine fetal growth retardation and less commonly placental
abruption (Table E.3) or fetal death in utero). Peripheral oedema is common but is
not a useful clinical sign; pulmonary oedema is rare and when it occurs is usually
iatrogenic.
References:
1. Brown MA, Pregnancy induced hypertension: pathogenesis and management.
Aust. NZ J Med. 1991; 21: 257-273.
2. Long PA, Oats JN. Pre-eclampsia in twin pregnancy -severity and pathogenesis.
Aust. NZ Obstet Gynecol. 1987; 27: 1-5.
3. Newman RB, Eddy GL. Association of eclampsia and hydatidiform mole. Obstet
Gynecol Survey. 1988; 43: 185-190.
4. Roberts JM, Redman CWG. Pre-eclampsia: more than pregnancy -induced
hypertension. Lancet. 1993; 341: 1447-1450.
5. Janes SL, Goodall AH. Flow cytometric detection of circulating activated platelets
and platelet hyper-responsiveness in pre-eclampsia and pregnancy. Clin Science.
1994; 86:731-7
6. Horn EH. Platelets in normal and hypertensive pregnancy. Platelets. 1991;
2:183-195.
7. Brown MA, Zammit VC, Lowe SA. Capillary permeability and extracellular fluid
volumes in pregnancy-induced hypertension. Clin Science. 1989; 77: 599-604.
8. Oian P, Maltau JM, Noddeland H, Fadnes Ho. Transcapillary fluid balance in
pre-eclampsia. Br J Obstet Gynaecol. 1986; 93: 235-2
9.Brown MA, Zammit VC, Mitar DM. Extracellular fluid volumes in pregnancy-induced
hypertension. J. Hypertension. 1992; 10: 61-68.
See also:Brown MA, de Swiet M: Classification of hypertension in pregnancy.
Baillieres Best Pract Res Clin Obstet Gynaecol. 1999 Mar;13(1):27-39.
Rudolf Stienstra and Anton Burm
The placental transfer of local anaesthetic agents is largely perfusion-limited. Being
lipophilic drugs, local anaesthetics can easily cross the placenta by passive diffusion
(1, 2, 3). This ensures rapid equilibration between umbilical venous and maternal
blood, even though the rate of transfer may be affected by placental uptake and large
maternal/fetal protein binding or pH differences. Clinical studies also indicate that
umbilical venous concentrations approach those in maternal blood rapidly (4). In
addition, local anaesthetic concentrations in umbilical arterial blood have been shown
to approach those in umbilical venous blood in approximately 30 minutes, indicating
rapid tissue/blood equilibration in the fetus (4, 5).
Total umbilical venous/maternal venous (UV/MV) concentration ratios may differ
considerably from unity, even after equilibrium has been achieved. For example,
UV/MV ratios of bupivacaine and etidocaine at delivery are usually in the range of 0.2
- 0.4, whereas UV/MV ratios of lidocaine and mepivacaine are generally in the range
0.5 - 0.7. The low UV/MV ratios reflect a considerably smaller degree of plasma
protein binding in the fetus compared to the mother and are related to the lower fetal
concentrations of alpha1-acid glycoprotein. At equilibrium, free (unbound) blood
concentrations on either side of the placenta are likely to be similar, or possibly
somewhat higher, on the fetal side, due to ion trapping when the fetus is acidaemic.
A lower UV/MV ratio does not necessarily imply a greater margin of safety for the
fetus, since toxicity is likely to be more closely related to free than to total blood
concentrations. The important factor in this respect is the ratio of the free drug
concentration that is associated with toxicity to the free drug concentration that is
achieved in the fetus after maternal dosing. This ratio is in all likelihood greater for
bupivacaine and etidocaine than for lidocaine and mepivacaine, indicating the greater
safety margin of the former agents (6).
Placental transfer of local anaesthetic agents after epidural administration may yield
depressed neurobehavioural scores in the newborn, especially when hypotension
occurs. However, in the absence of hypotension or other complicating factors,
neurobehavioural scores in infants born with epidural anaesthesia are mostly better
when compared with general anaesthesia (7). There is now general agreement that
properly conducted epidural anaesthesia does not cause neurobehavioural changes
in the newborn.
References:
1. Hamshaw-Thomas A, Rogerson N, Reynolds F. Transfer of bupivacaine,
lignocaine and pethidine across the rabbit placenta: Influence of maternal protein
binding and fetal flow. Placenta 1984; 5: 61-70.
2. Hamshaw-Thomas A, Reynolds F. Placental transfer of bupivacaine, pethidine and
lignocaine in the rabbit: Effect of umbilical flow rate and protein. Br J Obstet
Gynaecol 1985; 92: 706-713.
3. Johnson EF, Herman N, Arney TL, Gonzalez H, Johnson V, Downing JW.
Bupivacaine transfer across the human term placenta: A study using the dual
perfused human placental model. Anesthesiology, 1995; 82: 459-468.
4. Reynolds F, Laishley R, Morgan B, Lee A. Effect of time and adrenaline on the
feto-maternal distribution of bupivacaine. Br J Anaesth 1989; 62: 509-514.
5. Tucker GT, Boyes RN, Bridenbaugh PO, Moore DC. Binding of anilide-type local
anesthetics in human plasma: Implications in vivo, with special reference to
transplacental distribution. Anesthesiology 1970; 33: 304-314.
6. Tucker GT. Pharmacokinetics of local anaesthetics. Br J Anaesth 1986; 58:
717-731.
7. Abboud TK, Nagappala S, Murakawa K et al. Comparison of the effects of general
and regional anesthesia for cesarean section on neonatal neurologic and adaptive
capacity scores. Anesth Analg 1985; 64: 996-1000.
William Camann
It is widely agreed that epidural analgesia during labor is associated with an
increased risk of operative delivery (forceps or cesarean section). However, many
patients during labor will have confounding factors that predispose to both operative
delivery and also to the patient receiving epidural analgesia. Such factors include
dysfunctional labor requiring oxytocin augmentation, fetal malpresentation, large fetal
size, presence of non-reassuring fetal heart rate patterns, or maternal exhaustion
following long labor. Thus, it is crucial that such confounding variables be considered
whenever the incidence of operative delivery is related to epidural analgesia.
Retrospective studies usually fail to account for all confounding variables.
Prospective, randomized trials are particularly difficult to perform, as random
allocation of the method of pain relief is generally not well accepted.
Several recent studies have attempted to address this issue. In a prospective trial,
Thorp et. al. (1) studied 93 women randomized to receive either epidural (n=48) or
systemic narcotic analgesia (n=45). All subjects were healthy nulliparous women with
a singleton fetus in spontaneous labor. The cesarean section rate (mostly for
dystocia) was 2% in the narcotic group vs. 25% in the epidural group. The epidural
group also had more requirement for oxytocin augmentation and a prolonged first and
second stage of labor. However,
(a) dystocia was poorly defined,
(b) the station of fetal descent was never mentioned,
(c) the obstetricians were not blinded to the anesthetic management ,
(d) most epidurals were placed very early in labor, and
(e) the dose of oxytocin was relatively low.
In contrast, Chestnut (2, 3) randomized women to receive either early (<5 cm) or late
(>5 cm) epidural analgesia. Separate analyses were performed for women in
spontaneous labor and those receiving oxytocin augmentation. Neither study found a
difference in operative delivery between early and late epidural administration.
Important points here include:
(a) all patients had epidural analgesia (cf. Thorp's study (1) where a narcotic - only
group was included),
(b) group separation was relatively unclear, i.e. "early" and "late" groups may have
been actually quite similar, and
(c) the study may lack adequate power to support a finding of no difference between
groups.
At present, the answer to this important question remains elusive. The obstetrical
management of patients with epidural analgesia is likely to be an important
determinant of mode of delivery (4). Even the individual obstetrician may be of
importance in determination of outcome (5).
In summary, a recent American College of Obstetrics and Gynecology Committee
opinion is relevant here: "Labor results in severe pain for many women. There is no
other circumstance where it is considered acceptable for a person to experience
severe pain, amenable to safe intervention, while under a physician's care. Maternal
request is a sufficient justification for pain relief during labor" (6).
References:
1. Thorp JA, Hu DH, Albin RM, et. al. The effect of intrapartum epidural analgesia in
nulliparous labor: A randomized, controlled, prospective study. Am J Ob Gyn 1993;
169: 851-8.
2. Chestnut DH, McGrath JM, Vincent RD, et. al. Does early administration of
epidural analgesia affect obstetric outcome in nulliparous women who are in
spontaneous labor? Anesthesiology 1994; 80: 1201-1208.
3. Chestnut DH, Vincent RD, McGrath JM, et. al. Does early administration of
epidural analgesia affect obstetric outcome in nulliparous women who are receiving
oxytocin? Anesthesiology 1994; 80:1193-1200
4. Carli F, Creagh-Barry P, Gordon H. Does epidural analgesia influence the mode of
delivery in primiparae managed actively? Int J Obstet Anesth 1993; 2: 15-20.
5. Goyert GL, Bottoms SF, Treadwell MC, Nehra PC. The physician factor in
cesarean birth rates. N Engl J Med 1989; 320: 706-709.
6. American College of Obstetricians and Gynecologists: Committee opinion: Pain
relief during labor. Number 118. 1993.
Jennifer Carden
The management of Pulmonary Acid Aspiration during regional anaesthesia:
It is well known that the risk of morbidity and mortality from aspiration pneumonitis is
high in the obstetric patient. The risk has theoretically increased over the last
decades due to the ageing maternal population, multiple births associated with IVF
and an increasing caesarean section rate (1). However there has been a significant
decline in the anaesthetic contribution to perinatal deaths over the last two decades
(2) which has been partially attributed to the increased use of regional anaesthesia
and a better appreciation of airway protection in the parturient (3). Nevertheless, the
use of regional techniques does not eliminate the risk of aspiration. There is still the
possibility of aspiration with loss of airway protection in such circumstances as fitting,
local anaesthetic toxicity (Chapter 89), high or total spinal anaesthesia (Chapter 11),
severe hypotension and associated pathology such as aortocaval compression
(Chapter 28), anaphylaxis (Chapter 69) or amniotic- or thrombo-embolism.
PROPHYLAXIS
a) Fasting regimens:
Fasting during labour has become controversial (4, 5). Interventions that put a
mother at risk of aspiration are to a certain extent unplanned. Only 87% of parturients
coming to caesarean section can be predicted; the remaining 13% are completely
unforseen.
The outcome, in the rare event of aspiration of stomach contents, is dependent on
the type of matter aspirated (ie particulate vs non particulate) and the pH and volume
aspirated. As a consequence, it is reasonable to fast parturients at high risk of
anaesthetic intervention in labour. Should we also fast "low risk" labouring parturients
(for the sake of those who will go on to an unpredicted intervention) or should we fast
only those at high risk (Chapter 26)? To date, this issue remains unresolved.
b) Pharmacological:
Non particulate antacid prophylaxis (eg. 30 ml 0.3 Molar Sodium citrate) aimed at
raising gastric pH prior to epidural insertion or other anaesthetic intervention, or,
indeed, in some institutions, throughout labour, is practised in the belief that if
aspiration does occur then its severity will be reduced by raising pH of the aspirate.
Whilst this is certainly true theoretically, the practicalities are that antacids are
unreliable because their effect is variable both in duration (which may be as low as
1-2 hours) and in efficacy.
The additional administration of H2 antagonists (eg cimetidine or ranitidine) either
orally or parenterally to the antacid provides longer prophylaxis.
Neither antacid nor H2 antagonist therapy reduces the gastric volume, so drugs such
as metoclopramide can be added.
c) Protection of the airway:
Avoid general anaesthesia or depression of the airway reflexes (eg. by sedative
drugs) in patients not afforded airway protection by a cuffed endotracheal tube.
MANAGEMENT OF ASPIRATION IN THE AWAKE PATIENT (6)
If the parturient has aspirated as a result of an alteration in the conscious state, the
airway should be immediately protected with a cuffed endotracheal tube.
There is a clinical spectrum of presentation of aspiration ranging from immediate
asphyxiation due to large airway obstruction or reflex airway closure through to more
delayed ARDS. The resultant reduction in surfactant activity and interstitial and
alveolar oedema leads to a large Alveolar-arterial gradient, venous admixture and
hypoxaemia. Chest X-ray may show no early changes. Serial arterial blood gas
analysis may help define the severity of the injury.
Treatment in the awake patient is aimed at maintaining tissue oxygen delivery by
administering supplemental oxygen by mask, or, in more severe cases, intubation
and modes of ventilation which are aimed at optimising oxygenation by recruiting
non-ventilated alveoli (eg PEEP, CPAP). Unnecessarily high airway pressures should
be avoided because reductions in cardiac output will compromise tissue oxygen
delivery. Maintenance of optimal vascular filling is also important because severe
aspiration pneumonitis may cause major fluid shifts in much the same way as can
major burns. Consideration should be given in these severe cases to the use of a
pulmonary artery catheter.
As dispersion of gastric acid is rapid, manoeuvres such as bronchial lavage with
bicarbonate are not indicated. Airway suction as an initial manoeuvre may prevent
further soiling. Bronchoscopy has a limited role in the management of particulate
aspiration or severe atelectasis.
The use of steroids is controversial (with some authorities suggesting that the
inflammatory response is modified). Steroids do not alter the course of the disease
and may have a deleterious effect on healing and increase the risk of secondary
infection. The use of antibiotics is only indicated if infection supervenes.
References:
1. Annual Report for the Year 1993 Consultative Council on Obstetric and Paediatric
Mortality and Morbidity in Victoria
2. Report on Confidential Enquires into Maternal Deaths in the United Kingdom
(1988-1990) London HMSO 1994
3. Benhamou D. Complications of Obstetric Anaesthesia. Current Opinion in
Anaesthesiology 1995 8: 3; 216-219
4. Ludka L, Roberts. CC Eating and Drinking in Labour Journal of Nurse Midwifery
38:4;July-August 1993
5. Elkinton KW At The Waters Edge Where Obstetrics and Anaesthesia Meet.
Obstetric and Gynaecology 1991: 67; 54-57
6. Gibbs CP Aspiration risk in parturients. In: Common Problems in Obstetric
Anaesthesia, Datta S (Ed), 2nd Edition, Mosby, Boston, 1995 pp 15-38
Extradural Space
Len Carrie
Increased popularity of extradural techniques has led to renewed interest in the
detailed anatomy of the extradural region.
Standard texts agree that:
1. The cephalad limit of the extradural space is at the foramen magnum;
2. the inferior limit is the sacro-coccygeal membrane;
3. anteriorly, the posterior longitudinal ligaments separate the extradural space from
the bodies of the vertebrae and the intervertebral discs;
4. posteriorly, lie the laminae of the vertebrae and the ligamenta flava; and
5. laterally, the pedicles and intervertebral foraminae (Figure E.2).
The extradural space contains the dural sac, nerve roots, blood vessels, lymphatics
and connective and fatty areolar tissue.
Because of the potential effect of the geometry of the epidural space on technique
and spread of drugs, interest has centred on
1. the amount and distribution of fat in extradural space,
2. the presence or absence of a median dorsal fold of the dura mater,
3. the presence of connective tissue bands or septa, and
4. the detail of the ligamenta flava.
This information is absent or inaccurate in older texts derived almost entirely from
cadaveric dissection - which is much subject to artefact. Unfortunately, most modern
methods of investigation also induce some degree of artefact, for example, by
opening the epidural space during surgery (1), by introducing air for epiduroscopy (2,
3), or by injecting radiological contrast (4) or resin (5) into the epidural space.
Cryomicrotome sectioning (6) is less disruptive of the epidural contents and magnetic
resonance imaging (7) is probably the only technique not to introduce artefact.
From these studies it appears that the extradural space is divided into metamerically
repeating segments, being little more than a potential space posteriorly at the level of
each lamina and widening to a 4 to 6mm space opposite the ligamenta flava. Still
controversial is the existence of a dorsal median fold of the dura mater (plica
mediana dorsalis) and connective tissue bands (dorso-lateral extensions) with those
advocating its presence being opposed by those insisting it is an artefact. Whichever
is correct, epidurally injected drugs sometimes behave as if there is a variable degree
of epidural space compartmentalisation, and, from a clinical point of view, the
question of whether the anatomical details are artefactual or not is largely academic.
References:
1. Luyendijk W. The plica mediana dorsalis of the dura mater and its relation to
lumbar peridurography (canalography). Neuroradiology 1976; 11:147-149.
2. Blomberg R. The dorsomedian connective tissue band in the lumbar epidural
space of humans: an anatomical study using epiduroscopy in autopsy cases.
Anesthesia and Analgesia 1986;65:747-752.
3. Blomberg RG, Olsson SS. The lumbar epidural space in patients examined with
epiduroscopy. Anesthesia and Analgesia. 1989; 68:157-160.
4. Savolaine E R, Pandya J B, Greenblatt SH, Conover S R. Anatomy of the human
lumbar epidural space: new insights using CT-epidurography. Anesthesiology
1988;68:217-220.
5. Harrison G R, Parkin I G, Shah J L. Resin injection studies of the lumbar
extradural space. British Journal of Anaesthesia 1985; 57:333-336.
6. Hogan Q H. Lumbar epidural anatomy. A new look by cryomicrotome section.
Anesthesiology. 1991; 75:767-775.
7. Westbrook JL, Renowden SA, Carrie LES. Study of the anatomy of the extradural
region using magnetic resonance imaging. British Journal of Anaesthesia
1993;71:495-498.
YK Chan.
Aspiration Prophylaxis:
Is it needed for Caesarean section and vaginal delivery under regional block?
What prophylaxis should we use?
Aspiration of gastric contents is still a major cause of anaesthesia-related death in
obstetric practice (1, 2, 3). It usually occurs during the course of a general
anaesthesia, more so when intubation is difficult (4).
Most mothers in labour are unlikely to receive general anaesthesia (5). In those with
a regional block placed during labour this can usually be extended cephalad for use
during Caesarean section (CS). Since the probability of general anaesthesia and thus
aspiration is relatively low in parturients, it is difficult to justify the use of acid
aspiration prophylaxis in labouring women (5). In 1988 in the United Kingdom, it was
shown that up to 25% of 288 departments surveyed (6) did not administer aspiration
prophylaxis to mothers in labour. Besides the drug costs and discomfort to the
mother (5, 6) the H2 receptor antagonists can alter local anaesthetic metabolism (7).
This creates a risk of local anaesthetic toxicity (Chapter 89) in mothers with ongoing
epidural block, who are given regular doses of these drugs. Prophylaxis should be
limited to those at high risk of requiring a CS, and this should be in the form of
regular oral ranitidine.
All mothers for CS be it elective or emergency, require aspiration prophylaxis (8)
(Chapter 45). Despite the increasing trend towards CS under regional anaesthesia,
an epidural failure rate of up to 20% (9, 10, 11) still necessitates preparation of all
these mothers as for general anaesthesia as this is a sizeable group at risk. The
1988 survey in the United Kingdom (6) showed that this is religiously given in all the
departments and there is no relaxation of this practice.
Many obstetric units recommend a regimen along the following lines:
(a) Elective Caesarean section (6) - 150 mg oral ranitidine the night before and again
on the morning of the operation. This is followed by 30 mls of 0.3 molar sodium
citrate before the commencement of the regional block.
(b) Emergency Caesarean section (6, 12) - slow intravenous ranitidine, 50 mg at the
time the need for CS is determined if this has not been given regularly during labour.
Sodium citrate is given immediately before commencement of surgery.
References:
1. Tomkinson J, Turnbull A, Robson G, et al. Report on confidential enquiries into
maternal deaths in England and Wales 1976-1978. London: Her Majesty's Stationery
Office, 1982.
2. Turnbull A, Tindall VR, Robson G, et al. Report on confidential enquiries into
Office, 1986.
3. Turnbull A, Tindall VR, Beard RW, et al. Report on confidential enquiries into
Office, 1989.
4. Macdonald AG. The gastric acid problem. Recent Advances in Anaesthesia and
Analgesia. 15: 8: 107-131.
5. Thorburn J, Moir DD. Antacid therapy for emergency Caesarean section.
Anaesthesia 1987; 42; 352-355.
6. Tordoff SG, Sweeney BP. Acid aspiration prophylaxis in 288 obstetric anaesthetic
departments in the United Kingdom. Anaesthesia 1990; 45; 776-7
7. Wilson CM, Moore J, Ghaly RG et al. Plasma bupivacaine concentration
associated with extradural anaesthesia for Caesarean section: Influence of
pretreatment with ranitidine. British Journal of Anaesthesia 1986; 58; 1330P-1331P.
8. May AE. The confidential enquiry into maternal deaths 1988-1990. British Journal
of Anaesthesia Editorial 1. 1994; 73; 129-131.
9. Milne MK, Murray Lawson JI. Epidural analgesia for Caesarean section. British
Journal of Anaesthesia 1973; 45; 1206-1210.
10. Thorburn J, Moir DD. Epidural analgesia for elective Caesarean section:
Technique and its assessment. Anaesthesia 1980:3 5:3-6.
11. Chamberlain G, Wright A, and Steer P. Pain and its relief in labour: Report of the
1990 NBT survey. (1993) Churchill Livingstone, Edinburgh.
12. Rout CC, Rocke DA, Gouws E. Intravenous ranitidine reduces the risk of acid
aspiration of gastric contents at emergency Caesarean section. Anaesthesia and
Analgesia 1993; 76; 156-61.
Robert Chantigian
The treatment of Post Dural Puncture Headache (PDPH) - excluding epidural blood
patch (Chapter 110).
The cause (CSF leakage through a dural hole producing a low CSF pressure) (1),
mechanism (traction on the pain sensitive structures in the brain and vasodilation of
the cerebral vessels when the patient is upright) (2), and duration (until the hole
spontaneously heals and CSF pressure is restored; typically lasts a few days and
rarely more than one week) (1) helps to define the condition known as PDPH and to
suggest an approach to treatment.
Therapeutic alternatives to epidural blood patching include:
1. Bedrest
The symptoms of PDPH are alleviated by assuming the horizontal position. Attempts
at prophylactic treatment by placing the patient horizontal for a period of time (eg. 24
hours) after a dural puncture have no effect on the incidence or duration of a PDPH;
it only delays the onset of the PDPH until the patient ambulates (1).
2. Hydration
Normal hydration of the patient should be maintained. Extra hydration to help the
body make more CSF does not alleviate the headache. Dehydration may make
symptoms worse.
3. Analgesics
Narcotic analgesics and, in some instances, non-steroidal anti-inflammatory agents
are often administered for symptomatic treatment of the headache.
4. Caffeine
Caffeine has been suggested as a mode of therapy to help constrict the vasodilated
cerebral vessels. It is best administered early in the day so that patients can sleep at
night. The dose of caffeine sodium benzoate is 500 mg intravenously which can be
repeated once two hours later if the first dose does not have the desired effect (2).
5. Epidural saline injection
Boluses or infusion of epidural normal saline can help to transiently increase the
epidural pressure, slowing the speed at which CSF leaks through the dural hole (3).
This may speed the natural healing process. The bolus dose is 30-60 mls given 6
hourly for 4 doses. The rate of infusion is 1000 mls administered over a 24 hour
period. Although epidural saline can be a useful technique, higher success rates are
often achieved with epidural blood patches (4).
References:
1. Jones R J: The role of recumbency in the prevention and treatment of postspinal
headache. Anesthesia and Analgesia 53:788-796, 1974
2. Sechzer PH: Post-spinal anesthesia headache treated with caffeine. Part II:
Intracranial vascular distension, a key factor. Current Therapeutic Research
26:440-448, 1979
3. Usubiaga JE: Effect of saline injections on epidural and subarachnoid space
pressures and relation to postspinal anesthesia headache. Anesthesia and Analgesia
46: 293-296, 1967
4. Bart AJ: Comparison of epidural saline placement and epidural blood placement in
the treatment of post-lumbar-puncture headache. Anesthesiology 48:221-223, 1978
Stephen Chester
Caudal, Paracervical and Pudendal nerve blocks: Their place in modern obstetric
anaesthetic practice.
CAUDAL BLOCK (Chapter 22)
Caudal epidurals in labour have become less popular because better perineal
analgesia can be achieved by the use of epidural infusions and primigravidae are
more likely to receive an epidural block. Also, there have been recent concerns about
the risks of inadvertent intravenous and fetal injection.
A modified caudal epidural technique can provide rapid onset perineal anaesthesia
without cardiovascular disturbance and with relatively little loss of expulsive power. If
used for perineal anaesthesia only, caudal block is a useful, safe technique for
experienced anaesthetists provided that the volume of local anaesthetic is limited to a
maximum of 10 mls, injected slowly (with multiple aspirations). It should be noted that
this dose is less than half that which is required to achieve full labour analgesia. The
block should be inserted before the head is on the perineum (Figure 22.1).
Since it has been shown that pencil point spinal needles have a low incidence of
headache (0 to 0.66% with 27G and 25G Whitacre needles) (1, 7) spinal anaesthesia
is often more appropriate than lumbar or caudal epidural anaesthesia for rotational
forceps, manual removal of placenta and, at times, low forceps delivery.
INDICATIONS
1. Unrelieved perineal pain.
2. Premature urge to push.
3. Low forceps delivery.
4. When lumbar epidural analgesia is contraindicated.
INCIDENCE
In most Australian hospitals, caudal blocks are being used less frequently in labour
as the number of spinals has increased (Table 2.1). The major indications for caudals
are perineal pain, labour pain, forceps delivery, and manual removal of placenta.
Less commonly, caudals can provide anaesthesia for artificial rupture of the
membranes, suturing of episiotomies and repair of vaginal lacerations.
CAUDAL ANALGESIA IN COMBINATION WITH OTHER MAJOR REGIONAL
BLOCKS
At the Royal Women's Hospital, of those women who had a caudal, at least 62% also
had a lumbar epidural. The lumbar epidural was either already in situ or was inserted
at the same time as the caudal.
It has been shown that for the lumbar epidural route, increasing the volume of
anaesthetic is more likely to secure good sacral blockade (3) than injection in the
sitting position (4). However, in our experience sacral blockade can occasionally only
be achieved with a caudal or spinal block.
COMPLICATIONS
l. Vascular tap and intravascular injection of local anaesthetic (Table 36.3).
2. Failed block (8%) - the sacral hiatus is absent in 5% of adults. (2, 9)
3. Subarachnoid injection - the dural sac reaches S2 .
4. Infection.
5. Fetal injection (Figure 22.1).
Modified caudal block is a safe technique with a limited specific place in modern
obstetric anaesthesia.
PARACERVICAL BLOCK (Chapter 46)
The risk of complications, particularly fetal bradycardia, generally make this
technique an unsuitable form of anaesthesia for obstetric patients. However, if used,
it should be avoided in the presence of fetal distress or uteroplacental insufficiency
and the fetal heart rate should be monitored continuously (Table 3.1) during and after
insertion of the paracervical block (Figure 46.2).
COMPLICATIONS
1. Vaginal trauma.
2. Systemic local anaesthetic toxicity due to excessive dosage or intravenous
injection (Table 36.3).
3. Parametrial haematoma.
4. Sacral plexus trauma.
5. Infection and deep abscess formation.
6. Fetal scalp injection of local anaesthetic.
7. Fetal bradycardia probably caused by decreased uteroplacental perfusion.
8. Needle stick injury.
PUDENDAL NERVE BLOCK (Chapter 21)
Pudendal nerve block provides anaesthesia for spontaneous vaginal delivery or low
forceps delivery. The pudendal nerve (S2 - S4) (Figure 21.1) is the major sensory
innervation of the lower vagina, vulva and perineum and provides motor fibres to the
external anal sphincter and the perineal muscles.
Pudendal nerve block was first reported for vaginal delivery in 1916 (7). It is
inadequate for rotational forceps delivery and manual removal of the placenta. Either
a transvaginal or transperineal approach can be used. The bilateral success rate has
been reported as 50% after the transvaginal approach and 25% after the
transperineal approach. (6).
INDICATIONS.
1. Low forceps delivery.
2. Vaginal and perineal pain when lumbar or caudal epidural or spinal analgesia is
unavailable, contraindicated or declined.
COMPLICATIONS
1. Vaginal trauma.
2. Systemic local anaesthetic toxicity due to excessive dosage or intravenous
injection.
3. Vaginal or ischio-rectal haematoma.
4. Infection and deep abscess formation.
5. Fetal trauma or direct local anaesthetic injection.
6. Needle stick injury.
References:
1. Campbell DC, Douglas MJ, Pavy TJG, Merrick P et al. Comparison of the 25
gauge Whitacre with the 24 gauge Sprotte needle for elective caesarean section:
cost implications. Can J Anaesth 1993; 40:1131-5.
2. Dawkins CJM. An analysis of the complications of extradural and caudal block.
Anaesthesia 1969; 24: 554-563.
3. Erdemir HA, Sopper LE, Sweet R.B, Studies of factors affecting peridural
anesthesia. Anesth Analg 1965; 44:400-404.
4. Park WY. Factors influencing distribution of local anesthetics in the epidural space.
Reg Anesth 1988; 13:49-57.
5. Robson M, Boylan P, McParland P. Epidural analgesia need not influence the
spontaneous vaginal delivery rate (abstract). Am J, Obstet Gynecol 1993; 168:364.
6. Scudamore JH, Yates MJ. Pudendal block - a misnomer? Lancet 1966; 1:23-4..
7. Smith EA, Thorburn J, Duckworth RA, Reid JA. A comparison of 25G and 27G
Whitacre needles for caesarean section. Anaesthesia 1994; 49: 859-862.
8. Thompson JE. An anatomical and experimental study of sacral anaesthesia Ann
Surg 1917; 66: 718-727.
9. Trotter M. Variations of the sacral canal: their significance in the administration of
caudal anaesthesia. Anesth Analg 1947; 26: 192-202.
Clive Collier
Various agents have become popular as adjuncts to the local anaesthetic solutions
for use in intraspinal (epidural and subarachnoid) blocks.
ADRENALINE (EPINEPHRINE).
Adrenaline was probably first used by Braun in 1903 to prolong the action of cocaine
by reducing the local blood supply and delaying its uptake.
When adrenaline is absorbed slowly from the maternal epidural space, it usually
causes a rise in cardiac output and heart rate with a concomitant fall in peripheral
vascular resistance, leaving the mean arterial pressure unchanged or slightly
reduced.
The use of adrenaline in obstetrics is somewhat controversial because it can cause a
reduction in utero-placental blood flow (Chapter 76). This is particularly true in
pregnancy induced hypertension where vasospasm may already be present (1, 2)
(Chapter 39).
Advantages: Adrenaline increases the speed of onset of epidural block and, in most
of the studies performed, enhances both the spread and quality of the block. It also
prolongs the effects of lignocaine and reduces peak local anaesthetic blood levels
and toxicity (3, 4, 5) (Table 36.3).
Disadvantages: Uterine contractile activity may be diminished for up to 60 minutes
(6). Uterine blood flow may be reduced (7) and labour slowed (8) when adrenaline
has been added to the epidural local anaesthetic solution.
It has been suggested that adrenaline may exert an independent analgesic effect at
spinal cord level as a consequence of its anti-nociceptive effect at spinal
alpha-adrenoreceptors (9).
The effective epidural dose of adrenaline for obstetrics is approximately 5mcg/ml.
This can be added fresh by the operator. Solutions premixed by the manufacturers
are available in concentrations ranging from 1:400,000 (2.5mcg/ml) to 1:200,000
(5mcg/ml).
Subarachnoid adrenaline (200mcg) does prolong the action of spinal anaesthetics,
but is rarely used, partly out of concern for the potential to cause spinal cord
ischaemia.
BICARBONATE.
This is not a new additive. Bignon, in 1892, reported that making cocaine alkaline
greatly increased its anaesthetic potency. Commercial supplies of amide-type local
anaesthetics have a pH between 3.2 and 6.5 (20), but with the pKa of these solutions
being between 7.5 and 9.0, less than 3% of the local anaesthetic will be present as
the nonionized free base (10). As it is the nonionized form of the local anaesthetic
that crosses nerve sheaths and membranes, it follows that if the pH of the agents
could be made less acidic (or closer to the pKa) then, in the body, more of the
nonionized form will be present and the onset of nerve-block will be more rapid.
Studies of epidural block in obstetric patients using small doses of sodium
bicarbonate have produced conflicting results. Tackley and Coe (11) demonstrated
that 0.15ml of an 8.4% solution of sodium bicarbonate added to 10ml bupivacaine
0.5% for Caesarean section can produce a more rapid onset of both sensory and
motor blockade as well as a prolongation of duration of action. This effect has been
confirmed by some (12) but not by others (13, 14).
If too much bicarbonate is added, however, precipitation of the free base may occur
because the nonionized form is only slightly soluble in water. An alternative to
bicarbonate is to add carbon dioxide to the local anaesthetic ampoule to achieve a
pCO2 of about 600mm Hg. These solutions, of which carbonated lignocaine is the
most widely used, have been shown to produce a better quality and quicker onset of
sensory blockade than similar 'non-gassed' solutions in obstetric patients (15).
NARCOTICS.
Opioids are now routinely added to many intraspinal solutions. In some cases,
intraspinal narcotics have become the sole analgesic agent (Chapter 60).
DEXTROSE.
Dextrose, in a concentration ranging from 3% to 5%, is frequently added to
subarachnoid local anaesthetic solutions to adjust the baricity of the solution in
relation to cerebro-spinal fluid (Figure 30.1).
PRESERVATIVES AND ANTIMICROBIALS.
The widely used amide-type local anaesthetic agents are extremely stable chemical
compounds and, if stored in glass or plastic containers, will not deteriorate over an
almost indefinite period. Adrenaline, however, will break down in solution and the
antioxidant sodium metabisulphite (0.1%) is added as a stabilizer, increasing the
shelf-life to 2 years. If the adrenaline is to maintain its potency, these ampoules or
vials may only be autoclaved once .
Although multidose vials are currently being phased out in many countries, some still
remain in use and frequently contain an antimicrobial agent. Methylparaben has been
used in epidural and spinal solutions over many years and is effective as both an
antibacterial and an antifungal agent, although it may be responsible for some of the
rare cases of "allergic" reactions to local anaesthetics (16) (Chapter 69). Chlorocresol
is a more effective antimicrobial agent but is neurotoxic and unsuitable for use in
solutions for major nerve-blocks. It is used solely in solutions for local infiltration. It is
anticipated that, in the near future, most local anaesthetics will be supplied in
single-use plastic (polypropylene) vials without preservatives.
Narcotics for intraspinal use and, even the normal saline diluent, should be specified
as "preservative-free" by the manufacturers. Some morphine products still contain
metabisulphite and fentanyl may include citric acid. Benzyl alcohol has, in the past,
been occasionally added to saline.
OTHER (NEWER) AGENTS.
As the cellular mechanisms involved in the physiological responses to pain at the
spinal cord level are being revealed, the search for alternative analgesics has
intensified. Intraspinal alpha2-adrenergic agonists (clonidine and dexmedetomidine)
induce analgesia by a pathway involving nitric oxide and acetylcholine release and
are potentiated by intrathecal neostigmine (17). Their use as sole agents in labour is
limited by the production of excessive sedation or hypotension. Synergistic reactions
with other analgesics, which will allow a reduced dosage and diminished side-effects,
are being investigated.
Other prospective intraspinal agents under review include:
adenosine A1 agonists,
ketorolac (18),
GABA (gamma aminobutyric acid) agonists,
midazolam,
ketamine,
somatostatin, and
MDA (n-methyl D-aspartate) antagonists (19).
CARRIER VEHICLES
The search for a suitable carrier vehicle to prolong the duration of intraspinal local
anaesthetics has been under way for many years. The latest candidate is 50%
glycerin which has been combined with 0.125% bupivacaine (18). This mixture might
be suitable for post-Caesarean section analgesia. An alternative is the encapsulation
of bupivacaine into liposomes.
References:
1. Holdcroft A. Use of adrenaline in obstetric analgesia. Anaesthesia 1992
47:987-990.
2. Alahuhta S, Rasanen J, Jouppila P, Jouppila R, Hollmen AI. Uteroplacental and
fetal circulation during extradural bupivacaine for caesarean section in hypertensive
pregnancies with chronic fetal asphyxia. British Journal of Anaesthesia 1993
71:348-353.
3. Laishley RS, Morgan BM, Reynolds F. Effect of adrenaline on extradural
anaesthesia and plasma bupivacaine concentration during Caesarean Section.
British Journal of Anaesthesia 1988 60:180-186.
4. Scott DB, Jebson PJ, Braid DP, Ortengren B, Frisch P. Factors affecting plasma
levels of lignocaine and prilocaine. British Journal of Anaesthesia 1972
44:1040-1049.
4. Abboud TK, Sheik-ol-Eslam A, Yanagi T et al. Safety and efficacy of epinephrine
added to bupivacaine for lumbar epidural analgesia in obstetrics. Anesthesia and
Analgesia 1985 64:585-591.
6. Craft JB Jr, Epstein BS, Coakley CS. Effect of lidocaine with epinephrine versus
lidocaine (plain) on induced labor. Anesthesia and Analgesia 1972 51:243-246.
7. Wallis KL, Shnider SM, Hicks JS, Spivey HT. Epidural anesthesia in the
normotensive pregnant ewe; effects on uterine blood flow and fetal acid base status.
Anesthesiology 1976 44:481-487.
8. Gunther RE, Bauman J. Obstetrical caudal anesthesia. I. A randomized study
comparing 1% lidocaine with 1% lidocaine plus epinephrine. Anesthesiology 1969
31:5.
9. Collins JG, Matsumoto M, Kitahata LM. Suppression by spinally administered
epinephrine of noxiously evoked dorsal horn neuron activity in cats; evidence for
spinal epinephrine analgesia. Anesthesia and Analgesia 1983 62:253-254
10.DiFazio CA, Carron H, Grosslight KR et al. Comparison of pH-adjusted lidocaine
solutions for epidural anesthesia. Anesthesia and Analgesia 1986; 65:760-764.
20. Moore DC The pH of local anesthetic solutions. Anesth Analg 60:833-834, 1981
11. Tackley RM, Coe AJ. Alkalinised bupivacaine and adrenaline for epidural
Caesarean section. Anaesthesia 1988; 43:1019-1021.
12. Capogna G, Constantino P, Muratori A et al. The addition of bicarbonate
improves the quality of intraoperative analgesia of lidocaine-fentanyl epidural
anesthesia for cesarean section. Regional Anesthesia 1992 ;17:S32.
13. Stevens RA, Chester WL, Grueter JA, Schubert A, Brandon D, Clayton B, Spitzer
L. The effect of pH adjustment of 0.5% bupivacaine on the latency of epidural
anesthesia. Regional Anesthesia 1989; 14:236- 239.
14. Benhamou D, Labaille T, Bonhomme L, Perrachon N. Alkalinisation of epidural
0.5% bupivacaine for cesarean section. Regional Anesthesia 1989 14:240-243.
15. Bromage PR. Unblocked segments in epidural analgesia for relief of pain in
labour. British Journal of Anaesthesia 1972; 44:676-679.
16. Aldrete JA, Johnson DA. Evaluation of intracutaneous testing for investigation of
allergy to local anesthetic agents. Anesthesia and Analgesia 1970 49:173
17. Bouaziz H, Hewitt C, Eisenach JC. Subarachnoid neostigmine potentiation of
alpha2-adrenergic agonist analgesia. Dexmedetomidine versus clonidine. Regional
Anesthesia 1995:20:1 21-127.
18. Arkoosh VA. What's new in obstetric anesthesia, 1993? International Journal of
Obstetric Anesthesia 1994; 3:21 9-226.
19. Information partly supplied by Astra Pharmaceuticals Pty Ltd.
Stephen Gatt and Clive Collier.
Regional Anaesthesia for Caesarean Section in the Morbidly Obese Patient.
Major regional blockade in the morbidly obese is complicated by a number of factors:
1. Psychological 'make-up' of the morbidly obese.
Contrary to the popular image of the plump, jovial matron these women often feel
guilty about their physical condition and body configuration, depressed about
anticipated problems with childbirth and infant rearing and, sometimes, hostile and
defensive to an anaesthetist encountering genuine technical difficulty.
2. Effect of associated diseases.
Fatty accumulation in the liver can produce a pro-coagulant deficiency coagulopathy.
These patients are also more prone to pregnancy-induced hypertension, gestational
diabetes, failure to progress, shoulder dystocia, hiatus hernia, coronary artery
disease and diabetes (Chapter 81) (2).
3. Difficulty may be encountered in gaining vascular access, in non-invasively
measuring systemic arterial pressure, in assessing the airway and in adequately
monitoring these parturients (2, 8, 11).
4. Inability to identify landmarks.
Often, it is impossible to identify any bony landmarks whatsoever in the lumbar area
because of the presence of a lumbar fat pad. If the left lateral position is to be used,
the location of any vertebral spinous processes (even C7) should be marked prior to
scrubbing as this will assist in identifying the midline. It may also be preferable to
dispense with drapes (and to 'prep' a wider area than usual) to allow better
recognition of the midline. An assistant may be required to pull the right lumbar fat
pad upwards to reveal the midline.
5. Difficulty with appropriately positioning the parturient (2).
As it may be difficult to move these patients once motor block has been established,
it may be appropriate to place the epidural catheter but not inject any local
anaesthetic, until the patient has assumed an appropriate position. Sometimes, the
sitting position is preferable because this allows the back and buttock fat to fall away
from the midline and to gain an idea of where the midline lies in the absence of bony
landmarks.
6. Technical difficulty with placement of the regional blocks, (5, 10)
Obese women have a tendency to thoraco-lumbar Iordosis which can make an
already technically difficult block even more difficult.
7. Erratic spread of the local anaesthetic solution. (1)
For any given dose of local anaesthetic, a higher level of epidural block (in proportion
to the degree of obesity) can be anticipated (1).
8. Insufficiently long spinal, CSE and epidural needles.
Long (12cm) or extra-long (18 and 20cm) needles may be necessary to gain access
to the epidural or subarachnoid spaces. In the massively obese, the effective length
of a standard epidural needle is reduced by ~0.5-1.0cm if the Weiss flange wings are
attached to the Tuohy-Borst epidural needle.
Even after a satisfactory regional block is achieved, Caesarean Section is not without
hazard because of:
1. Difficulty breathing in the supine 'wedged' position, especially if head down tilt or
Trendelenburg is employed (6). These patients already have increased oxygen
requirement, increased work of breathing and abnormal chest wall compliance and
reduced expiratory reserve volume and functional residual capacity. Pregnancy
produces a worsening of respiratory function and the assumption of the supine
position reduces the functional residual capacity even further (2, 3). Hypoxaemia is
common (3) (Chapter 87). Administration of supplemental oxygen, 5-10 degrees
reverse Trendelenburg and a large pillow under the head will go a long way towards
reversing some of the respiratory abnormalities.
2. Inability to position the patient on a standard operating table (7, 9).
Two anchored standard width 50cm operating tables with arm boards may be
necessary before caesarean section can commence.
3. Reluctance of staff to shift or lift these patients once they are unable to move
themselves when the regional block takes effect (2).
4. Difficulty with surgical access produced by a large panniculus (4). There is still
considerable debate as to whether a transverse incision or a vertical Caesarean
incision is best, but most agree that a low suprapubic transverse incision (in the skin
fold) is contraindicated (1).
5. Postoperative complications including bleeding, inadequate analgesia, deep vein
thrombosis, hypoxaemia and myocardial ischaemia (6, 7, 8, 9).
The morbidly obese parturient should always be considered to be at high risk.
References:
1. Hodgkinson R, Husain F; Obesity and the Cephalad Spread of Analgesia following
Epidural Administration of Bupivacaine for Cesarean Section. Anesth & Analg
59:89-92,1980.
2. Wilson A, Reilly C; Anaesthesia and the Obese Patient. Intl J Obesity Related
Metabolic Disorders 17:8:427-435, 1993.
3. Jense H, Dubin S, Silverstein P, O'Leary-Escolas U. Effect of Obesity on Safe
Duration of Apnea in Anesthetised Humans. Anesth & Analg 72:1:89-93, 1991.
4. Pasulka P, Bistrian B, Benotti P, Blackburn G. The Risks of Surgery in Obese
Patients. Ann Int Med 104:4:540-546, 1986.
5. Robertson I, Eltringham R. Anaesthetic Management of the Morbidly Obese. Br J
Hosp Med 34:4:224-228, 1985.
6. Chi I, Wilkens L. Interval Tubal Sterilisation in Obese Women - An Assessment of
Risks. Am J Ob Gyn 152:3:292-297, 1985.
7. Graves D, Batenhorst R, Bennett R, Wettstein J, et al. Morphine Requirements
using Patient-Controlled Analgesia: Influence of Diurnal Variation and Morbid
Obesity. Clin Pharm 2:1:49-53, 1983.
8. Vaughan R: Anesthetic Management of the Morbidly Obese Patient. Contemp
Anes Practice 5:71-94, 1982.
9. Sicuranza B, Tisdall L: Cesarean Section in the Massively Obese. J Reprod Med
14:1:10-11,1975.
10. Ogden P: Failure of Intravenous Regional Analgesia using a Double Cuff
Tourniquet. Anaes 39:5:456-459, 1984.
11. Burch GE: Sphygmomanometric Cuff Size and Blood Pressure Recordings.
JAMA 225:1215, 1973.
Caudal Analgesia
Clive Collier
Although the caudal route was the first widely used approach to the epidural space
for continuous block in labour (Hingson and Edwards, 1942), and remained in
frequent use in a few centres until the late 1970's (McCaul), its present role is very
limited. Apart from providing good analgesia for low instrumental deliveries and
perineal repair, the use of caudal block is usually restricted to a very few enthusiasts
and to those cases in which a lumbar epidural is anatomically impossible or
contraindicated by local infection (Chapter 70). (However, local sepsis may also
preclude the use of caudal block) (Chapter 2).
The patient should be prepared according to the guidelines shown in Chapter 44.
Following the provision of secure venous access and preloading with crystalloid, the
patient is either turned into the left lateral position with both knees flexed and forward
tilt of the upper hip, or (occasionally) the knee-elbow position according to patient or
operator preference. The skin of the lumbosacral area is prepared with a bactericidal
solution and sterile drapes are applied. A bleb of local anaesthetic is raised in the
skin overlying the sacral hiatus, between the sacral cornua, at a site deep to the
proximal extremity of the natal cleft. A 21- gauge needle may then used to infiltrate
the deeper tissues, but this is not essential.
A variety of needles and cannulae may be used for the block itself, including a:
1. 7.6 cm 19-gauge caudal needle,
2. disposable 3.8 cm 19-23g hypodermic needle,
3. 20-24-g intravenous catheter for a "single-shot" technique, or
4. Tuohy needle (17 or 18g) and catheter for a continuous technique.
Whichever needle is used, it is gently inserted at an angle of 70-80degrees to the
skin and slowly advanced until the bony resistance of the sacrum is detected (Figure
22.1). The needle is withdrawn slightly, the entry angle reduced by about half, and
then reinserted until the resistance of the sacrococcygeal ligament is felt at a depth of
1.5-3.8 cm. The ligament is then penetrated and the needle or catheter inserted to a
depth of 2-3 cm, bearing in mind that the dural sac terminates at the S2 level, and
that dural puncture should be avoided (Figure 16.1).
Test aspiration for blood or CSF is performed. If the test is negative, this is followed
by the injection of a 3ml test dose of local anaesthetic, with a hand positioned over
the sacrum to detect any tissue swelling, resulting from malposition of the needle or
catheter either subperiosteally or along the dorsal surface of the sacrum. Following a
negative test dose and in the absence of pain on injection, the definitive dose may be
injected slowly in small, repeated increments (Chapter 91). If CSF is aspirated or if
blood continues to be aspirated after repositioning of the needle or catheter the block
should be abandoned.
Single-shot needles or cannulae are withdrawn following injection. Catheters are
affixed to their connectors and filters and strapped in position.
Lignocaine is preferred to bupivacaine in view of the potential for large doses of
bupivacaine to produce cardiovascular collapse and intractable ventricular
dysrhythmias (Table 36.6) should intravascular injection occur into one of the
abundant epidural veins (1, 2). The dose and concentration of lignocaine depends on
the indication for the block. A recommended dose for outlet forceps delivery would be
15 to 20mls of 1.5% lignocaine with adrenaline. For perineal analgesia, a dose of 10
to 15mls of 1.0% lignocaine with adrenaline would suffice (Chapter 2).
References:
1. Albright GA Cardiac arrest following regional anesthesia with etidocaine or
bupivacaine Anesthesiology 1979; 51:285-287
Clive Collier
Injection of local anaesthetic into an epidural vein may lead to signs of CNS toxicity
within 15 to 30 secs, depending on the dose and speed of injection (Table 36.2)
(Chapter 36). The picture is of initial CNS stimulation followed by depression.
A relatively small dose (5 to 10ml lignocaine 1%) may cause ringing in the ears, a
metallic taste in the mouth, numbness of the tongue, blurring of vision, drowsiness
with decreased awareness, muscular twitching, restlessness and apprehension. With
a larger dose, delirium may ensue and progress to grand mal convulsions (Table
36.6). Asphyxia may develop if the convulsions are not treated rapidly and
adequately, leading to metabolic and respiratory acidosis with cardiac depression,
and eventually fatal cardiac arrest (Table E.2). Some of the manifestations of cardiac
toxicity may, in fact, be directly due to brain-stem toxicity (1) (Chapter 89).
The presence of added adrenaline in the local anaesthetic will usually lead to the
immediate development of palpitations following intravenous injection, and this may
be the first symptom.
The treatment of convulsions is aimed at maintaining the airway and oxygenation.
Seizure activity can be controlled with diazepam or thiopentone (Table 36.5).
Toxicity arising from an excessive total dose of local anaesthetic in the epidural
space usually produces similar signs and symptoms to those seen following
intravascular injection but occurs after a delay of 5 to 20 minutes.
References:
1. HEAVNER JE. Cardiac dysrhythmias induced by infusion of local anesthetics into
the lateral cerebral ventricle of rats. Anesthesia and Analgesia 1986; 65:133-138.
Clive Collier
Development:
The technique of combined spinal epidural (CSE) was first described by Soresi in
1937 using his "episubdural" method, consisting of a single shot of local anaesthetic
epidurally followed by advancment of the needle through the dura and injection of a
subarachnoid dose (1). This method was short lived.
Brownridge, in 1979, described the double-segment technique for Caesarean section.
This involved the introduction of an epidural catheter and test dose, followed by a
standard subarachnoid puncture one or two segments distally using a 26-gauge
spinal needle (2).
Carrie and O'Sullivan (1984) reported a single-space technique for Caesarean
section, where epidural puncture was performed with a 16-gauge Tuohy needle,
through which a spinal needle was inserted and subarachnoid block initiated (Figure
54.2). Following removal of the spinal needle an epidural catheter for later use was
inserted (3). This forms the basis of the currently popular techniques.
Equipment:
Packaged sets for CSE are now available from several manufacturers. These kits
include various gauges of spinal needles which are usually 10-13mm longer than the
Tuohy needle (Figure 51.1).
The main advantages claimed for these sets are:
1. improved fit of the spinal needle within the Tuohy needle,
2. reduced friction between the needles,
3. diminished likelihood of damage to the tip of the spinal needle, and
4. reduced potential for the generation of injectable metal fragments.
Innovative designs have been described. One includes a "back eye" in the Tuohy
needle (Figure 54.1) for easier spinal needle insertion (Chapter 54), and another
incorporates a second lumen alongside the shaft of the Tuohy needle (1).
References:
1. FELSBY S, JUELSGAARD P. Combined spinal and epidural anesthesia. Anesth
Analg 1995 80:821-826.
2. BROWNRIDGE P. Central neural blockade and caesarean section. Part I: review
and case series. Anaesth Intensive Care 1979 7:33-41
3. CARRIE LES, O'SULLIVAN GM. Subarachnoid bupivacaine 0.5% for Caesarean
section. Eur J Anaesthesiol 1984 1:275-283.
CSE: Technique
Clive Collier
Use of a pre-packaged set is recommended for a single-space combined spinal
epidural (CSE) technique. A vasopressor (eg. ephedrine) should be at hand to treat
any hypotension that may develop.
1. Following the intravenous infusion of at least 1 to 2 litres of crystalloid solution, the
mother is placed in the left lateral position, and a 16G 105mm length Tuohy needle is
inserted into the epidural space at the L2 - L3 or L3 - L4 interspace, using loss of
resistance to air or saline (Figure E.2).
2. A spinal needle of 26G or 27G and approximately 118 mm in length and with a
Whitacre or pencil point (Figure E.1) (Chapter 59) is introduced through the Tuohy
needle into the subarachnoid space (Figure 54.2). Slight resistance is detected as
the spinal needle emerges through the tip of the Tuohy needle, and stronger
resistance as the dura is pierced with a slight "pop".
3. After 5 to 10 secs, CSF appears at the needle hub and appropriate subarachnoid
injection is made, taking care to stabilize the spinal needle. For labour ward
analgesia, 25mcg (0.5ml) fentanyl may be added to 0.5ml bupivacaine 0.5% and
made up to a volume of 2.0ml with normal saline. For caesarean section, 2.0 to
2.8mls bupivacaine 0.5% may be suitable. A similar dose of fentanyl (25mcg, 0.5ml)
may be added if desired (Chapter 61).
4. The spinal needle is then removed and an epidural catheter is inserted to leave 3
to 4cms in the epidural space. Following secure fixation of the catheter, the patient is
assisted into the right lateral position.
5. Careful patient monitoring is required as CSE can produce a more extensive block
than either block alone (1).
6. The epidural catheter is available if extension of the block is required. Injection
may be performed following negative aspiration and a negative test dose. It has been
suggested that between 1.5 and 3ml of epidural local anaesthetic is required to
extend the subarachnoid block by one segment; less volume than that required for a
standard epidural block (1).
References:
1. RAWAL N, SCHOLLIN J, WESTROM G. Epidural versus combined spinal epidural
block for cesarean section. Acta Anaesthesiol Scand 1988 32:61-66.
Clive Collier
Almost fifty years elapsed between the first nerve-block with cocaine by Halsted and
Hall in 1884 and the initial successful attempts at continuous regional anaesthesia in
1931 by Aburel. For many years, the catheters used were simply "plain tubes" made
of currently available industrial compounds, and development was largely empirical.
Nowadays, there are many catheter designs available with various orifices in different
positions, but there has been little scientific study as to the advantages and
disadvantages of each type.
In the fifties and early sixties, a very common practice was for the epidural enthusiast
to cut a suitable length of industrial polyvinyl chloride (PVC) or nylon tubing of
approximately 1mm external diameter from a large (100 foot) roll and to have this
sterilized with the other epidural equipment. Some departments added their own
markings prior to sterilization. This latter process usually increased the stiffness of
the catheter. Furthermore, the cut end of the catheter was relatively traumatic to the
tissues and more likely to penetrate vessels. Later, such catheters could be supplied
sterilized and packaged, although they were often reused on 4 or 5 occasions! Lee's
catheter (3) was one of the first with a smooth non-patent tip and a single lateral eye
(Figure 9.1).
Later catheter developments (Figure 9.1) included two eyes in various configurations
(5). By 1980, these had been superseded. Today, the two types of epidural catheter
most commonly used world-wide are the terminal eye variant and the one with three
lateral eyes (Figure 9.1). Whereas about 90% of the Australasian and European
market consists of the three lateral-eye model, the reverse is true in the U.S.A. where
some 90% of catheters have only the terminal eye. This difference in usage remains
unexplained.
Some catheters are supplied with stylets, others are reinforced (Figure 9.5) and most
are constructed of polyamide nylon. Silicone catheters have been introduced for
long-term use with multiple holes at the tip. Catheter types are manufactured in the
size range of 16-21G and may or may not be radio-opaque.
In Australia, the typical catheter has three lateral eyes arranged in a helix, with either
3 or 4mm between the eyes, and the distal eye being 5-8 mm away from the tip (2).
The reason for the introduction of three lateral eyes has never been explained in the
literature, but the following information was supplied by one manufacturer (Portex):
"In the late 1970's, the manufacturing technology was developed to allow the drilling
of small holes in the catheters, without producing any debris. The diameter of the
holes related to the maximum size that could be drilled without weakening the tube.
The number of holes was then determined by that which gave equivalent to full-bore
flow."
For the Portex 16G catheter, the eye-discharge area is larger than the
cross-sectional area of the tube bore and the flow rate through the three eyes is the
same as that through an open-ended catheter at the same injection pressure. The
exact spacing of the eyes was not thought to be critical but was largely related to
manufacturing practicalities, with the aim of siting the eyes as close together as
possible to reduce the incidence of multicompartment block (Chapter 11). Current
technology has allowed the holes to be positioned much closer together (1mm
separation) and much closer to the tip (1) (Figure 9.1).
The choice of epidural catheter for non-obstetric work does not appear to be critical,
but the lateral-eye catheter produces improved results in obstetric patients (1, 2, 4).
In one series, unsatisfactory blocks requiring remedial action were recorded with 32%
of the terminal eye catheters compared with 11% of the lateral eye catheters and 8%
of the former had to be replaced compared to 2% of the latter (2).
References:
1. COLLIER CB, GATT SP. A new epidural catheter. Closer eyes for safety?
Anaesthesia 1993 48:803-806.
2. COLLIER CB, GATT SP. Epidural catheters for obstetrics; terminal hole or lateral
eyes. Regional Anesthesia 1994 19:378-385.
3. LEE JA. A new catheter for continuous extradural analgesia. Anaesthesia 1962
17:248-250.
4. MICHAEL S, RICHMOND MN, BIRKS RJS. A comparison between open-end
(single hole) and closed-end (three lateral holes) epidural catheters. Anaesthesia
1989 44:578-580.
5. SKINNER BS. A new epidural cannula. Canadian Anaesthetists' Society Journal
1966 13:622-623.
6. WARD CF, OSBORNE R, BENUMOF JL, SAIDMAN LJ. A hazard of double-orifice
epidural catheters. Anesthesiology 1978 48:362-364.
Epidural Technique
Clive Collier
1. Following placement of secure venous access, and the infusion of at least 500 ml
of a crystalloid solution, the patient is positioned on her left side with neck flexed and
knees drawn up as far as possible (Chapter 44). Some operators prefer the sitting
position, particularly for the obese parturient (Chapter 105).
2. A appropriate vasopressor, such as ephedrine, should be close at hand (Chapter
79). An aseptic technique should be adhered to. A midline or paramedian approach
may be used.
3. For the midline approach, the skin and underlying tissues are infiltrated with local
anaesthetic in the midline at the mid-point of either the L2 - L3 or L3 - L4 interspace.
(The spinal cord ends at L3 or above in at least 97% of the population (Figure 16.1)).
The bony and ligamentous structures of the region are shown in Figure E.2. An
epidural (Tuohy) needle is inserted in the sagittal plane, with its bevel pointing
cephalad. After traversing the supraspinous ligament, the needle is then passed into
the interspinous ligament which grips it tightly. The stylet is removed from the Tuohy
needle and the loss-of-resistance syringe attached. The syringe may contain saline,
air or both according to preference. The Tuohy needle may then be advanced slowly
using either a continuous or intermittent movement. Loss-of-resistance is detected by
applying gentle pressure to the plunger of the syringe (Figure E.3). When the needle
is in the ligamentum flavum, increased resistance is transmitted to the plunger, only
to disappear when the epidural space has been entered (Chapter 32).
4. For the paramedian approach, local anaesthetic is infiltrated 15mm lateral to the
cephalad end (upper border) of the vertebral spinous process below the selected
interspace. The Tuohy needle is inserted at 900 to all skin planes. The paravertebral
muscles are penetrated until the bone of the vertebral lamina is encountered. The
depth of needle insertion is noted. The needle is partially withdrawn and redirected
cephalad and towards the midline until the previous depth is attained. Once the
ligament is entered, the syringe is attached and the needle is slowly advanced while
searching for loss-of-resistance.
5. Whichever approach has been used, the depth to which the needle has been
inserted is noted. Following negative aspiration for blood or CSF, a small volume of
local anaesthetic (3-4 ml) may be injected into the epidural space to aid the
subsequent catheter insertion. The catheter is advanced 3-4cms (Figure E.5)beyond
the previously-noted distance between the skin and epidural space. If too much
catheter is threaded into the epidural space, it may emerge through an intervertebral
foramen causing failure of the epidural.
6. The Tuohy needle is gently removed and the catheter is fixed to the skin under a
transparent adhesive dressing. A test dose (Chapter 91) of local anaesthetic is given
through the catheter before the main dose is administered in increments (Chapter
60).
7. Use of a continuous catheter is generally preferable to a single-shot technique to
cover most obstetric eventualities.
The Australian and New Zealand College of Anaesthetists has outlined the
requirements for the safe conduct of epidural analgesia (P14).
Clive Collier
There remain very few obstetric situations where general anaesthesia (GA) is
essential. The majority of patients undergoing general anaesthesia will have refused
or been unsuitable for a regional technique, or there may have been insufficient time
for insertion of a block in the emergency situation. The incidence of usage of the
various techniques of anaesthesia for caesarean section in a modern obstetric
hospital is shown in Figure 73.1.
Urgent general anaesthesia may be requested for breech extraction or to provide
uterine relaxation for intrauterine manipulation, particularly of a second twin, although
intravenous glyceryl trinitrate is a possible alternative in this situation (Chapter 52).
GA will usually be preferred for emergency Caesarean section following uterine
rupture, antepartum haemorrhage, placental abruption (Table E.3), acute fetal
distress (Table 3.1) or cord prolapse. GA may also be requested in the presence of
intra-uterine fetal death. While lesser degrees of placenta praevia can be
satisfactorily managed under regional block, the method of anaesthesia for a grade
IV placenta praevia remains controversial. Many anaesthetists fear the combination
of massive maternal haemorrhage and impairment of cardiovascular reflexes in an
awake patient.
General anaesthesia may also be administered for removal of a cervical suture prior
to labour, manual removal of the placenta or products of conception, treatment of an
acute inversion of the uterus and repair of a third degree tear. A suggested sequence
for elective Caesarean section GA follows:
- ANTACIDS: Ranitidine 300mg orally (or cimetidine 400mg orally), 8 hours and 2
hours prior to induction, and/or 0.3 Molar sodium citrate solution 30ml orally 30
minutes preoperatively.
- FASTING: for 6 to 8 hours.
- POSITION: Left lateral tilt on a wedge under the right hip.
- MONITORING: Pulse oximetry, ECG, blood pressure, capnography, oxygen
analysis, inspiratory pressure monitoring, peripheral nerve stimulation.
- HYDRATION: An intravenous crystalloid solution delivered through a 14 or 16
gauge cannula.
- PREOXYGENATION: With 100% oxygen for 3 minutes.
- INDUCTION: Rapid sequence with cricoid pressure using thiopentone 4 to 5mg/kg,
followed by suxamethonium 1.0 to 1.5 mg/kg prior to intubation with a cuffed
endotracheal tube.
- MAINTENANCE: Fresh gas flow of 8 litres/min with oxygen 50% in nitrous oxide
and isoflurane 0.75% until delivery. (As an alternative, 33% oxygen in nitrous oxide
may be used in an attempt to ensure that there is no patient awareness. Neonatal
outcome does not appear to be adversely affected by this reduction in inspired
oxygen concentration (1, 2) provided that maternal oxygenation is maintained).
Atracurium (0.3 mg/kg) may be used to maintain relaxation.
- POST-DELIVERY: Once the cord is clamped, 10 units of synthetic oxytocin are
given intravenously, and an infusion is commenced with 40 units oxytocin in 1000ml
compound sodium lactate (lactated Ringer's) solution. A narcotic of choice (eg.
pethidine 1.5 mg/kg) is given, with or without an antiemetic (eg. droperidol 0.05
mg/kg), and the gas flow is adjusted to produce an FiO2 of 0.33.
- RECOVERY: Following adequate reversal with neostigmine/atropine, the patient
should be extubated in the lateral position and transferred breathing oxygen to a
recovery room.
A similar induction technique should be used for all emergency general anaesthetics,
both prior to delivery and in the first 24 hours postpartum.
References:
1. Lawes EG, Newman B, Campbell MJ, et al. Maternal inspired oxygen
concentration and neonatal status for caesarean section under general anaesthesia.
Comparison of effects of 33% or 50% oxygen in nitrous oxide. British J Anaesthesia
1988 61:250-254.
2. Hodgson CA, Wauchob TD. A comparison of spinal and general anaesthesia for
elective caesarean section: effect on neonatal condition at birth. International J of
Obstetric Anesthesia 1994 3:25-30.
Clive Collier
The concept of a "dual compartmental" block was first investigated by Beck et al (1)
who demonstrated that the three widely-spaced holes of lateral eye epidural
catheters (Figure 9.1) could accidentally come to rest in two of the four neighbouring
compartments - the epidural (Chapter 32), subdural (Chapter 15) or subarachnoid
(Chapter 16) spaces or the epidural venous plexus.
Beck et al studied 113 patients with three-holed catheters in situ, and reported 14
catheters (12%) to be misplaced, with 13 invading veins and the other located
epiduro-subarachnoid. Their incidence of dual compartment block would seem to be
excessively high, compared to other published figures (eg 0.2% (14)), and may be
largely attributed to the rigid catheters they used. It is of interest that blood could only
be aspirated in 5 of the 13 cases of proven vascular invasion and that signs of
toxicity were only obvious in 6 of the 9 patients in those who were given a local
anaesthetic.
It has been demonstrated with computerised tomographic scanning that it is possible
to insert an epidural catheter with the eyes in three spaces. The clinical picture
produced when a drug is injected into more than one compartment has been named
"Multicompartment Block" (19) (Figure 11.1).
The current multi-holed catheter design with eyes 3 to 4mm apart may predispose to
the occurrence of multicompartment block especially when one bears in mind that the
lumbar dura has a mean thickness of 0.5 mm.
Catheter misplacements and multicompartment block may be defined as "primary",
when the catheter is initially inserted incorrectly (1, 2), or "secondary" when a
correctly positioned catheter subsequently migrates into a blood vessel or through
the dura into subdural or subarachnoid spaces (3) (Figure E.2).
Attempts to assess the clinical significance of multicompartment block are
complicated by the finding that, in many reports of misplaced catheters, the eye
configuration was not stated and it is difficult to know whether the misplacement was
primary or secondary.
The development of multicompartment block may also be determined by the injection
technique as it has been suggested that, when multi-holed catheters are used, the
differential outflow through the individual eyes may be a function of both the injection
pressure and the speed of injection (4).
Several cases of convulsions caused by inadvertent intravascular injection of local
anaesthetic secondary to vascular invasion by catheters have been reported
(Chapter 36). This has occurred with both a two-hole (after the first top-up) (5) and a
three-hole (after the sixth top-up) catheter (6).
Invasion of the subarachnoid space has also been described. Hartley (7) and Ward
et al (9) both recorded perforation of the dura with a two-hole catheter, with the latter
proving fatal. Intrathecal spread of a second top-up was reported by Philip and Brown
(10) with a terminal eye catheter and by Barnes (11) with a lateral eye catheter.
Robson and Brodsky (12) were able to aspirate CSF only at the time of the third
top-up.
Multicompartment block is seen not only with lateral eye catheters, but also with the
Tuohy needle itself where mixed epidural-subdural block developed during a single
injection (13).
A terminal eye catheter can also produce a mulitcompartment block. A single top-up
of local anaesthetic produced classical symptoms of intravascular injection (Table
36.4) followed by an effective epidural block 5 minutes later (14) (Chapter 7). Test
aspiration for blood had been negative. Two mechanisms can be proposed to explain
this sequence of events. Either, the terminal eye was in both the vein and the
epidural space, or, the catheter had previously punctured an epidural vein allowing
entry into the circulation of part of the subsequent dose of local anaesthetic.
A worrying aspect of these cases of multicompartment block is that late collapse can
develop following previously "normal" top-ups when the anaesthetist may have left
the immediate vicinity of the patient. Delayed collapse is of even greater concern in
those obstetric units where the top-ups are performed by midwives and the arrival of
medical assistance may be delayed.
A recent strategy designed to reduce the occurrence of inadvertent multicompartment
block has been the introduction of closer eye epidural catheters. This new catheter
has 3 lateral eyes, with a 1mm eye separation, close to its tip (Figure 9.1) (19).
While the incidence of accidental multicompartment spread is low, the use of planned
multicompartment block (as in a combined spinal-epidural technique) (Chapter 62) is
growing rapidly. Even with deliberate multicompartment block there have been some
unexpected complications (16, 17, 18).
References:
1. BECK H, BRASSOW F, DOEHN M, DZIADZKA A, SCHULTE Am ESCH J.
Epidural catheters of the multi-orifice type: dangers and complications. Acta
Anaesthesiologica Scandinavica 1986; 30:549-555.
2. Reynolds F and Speedy HM. The subdural space: The third place to go astray.
Anaesthesia 1990: 45:120-123
3. GREGORETTI S. Uneventful extradural analgesia after unrecognized perforation
Canadian Anaesthetists Society Journal 1978; 25:509-5
4. POWER I, THORBURN J. Differential flow from multi-hole epidural catheters.
Anaesthesia 1988 43:876-878.
5. RYAN DW. Accidental intravenous injection of bupivacaine: a complication of
obstetrical epidural anaesthesia. Anaesthesia 1973 45:907-908.
6. CRAWFORD JS. Some maternal complications of epidural analgesia for labour.
Anaesthesia 1985; 40:1 21 9-1225.
7. HARTLEY M. The strange case of the inadvertent spinal. British Journal of
Anaesthesia 1975 47:420.
9. WARD CF, OSBORNE R, BENUMOF JL, SAIDMAN LJ. A hazard of double-orifice
epidural catheters. Anesthesiology 1978 48:362-364.
10. PHILIP JH, BROWN WU. Total spinal anaesthesia late in the course of obstetric
bupivacaine epidural block. Anesthesiology 1976 44:340-341.
BARNES PK. Delayed subarachnoid migration of an epidural catheter. Anaesthesia
and Intensive Care 1990 18:564-566.
12. ROBSON JA, BRODSKY JB. Latent dural puncture after lumbar epidural block.
Anesthesia and Analgesia 1977 56:725-735.
13. MEHTA M, SALMON N. Extradural block, confirmation of the injection site by
X-ray monitoring. Anaesthesia 1985 40:1009-1012.
14. Collier CB and Gatt SP Epidural Catheters for obstetrics. Terminal hole or lateral
eyes. Regional Anesthesia 1994; 19:378-385
16. MYINT Y, BAILEY PW, MILNE BR. Cardiorespiratory arrest following combined
spinal epidural anaesthesia for Caesarean section. Anaesthesia 1993 48:684-686.
17. BOUGHER R J, RAMAGE D. Spinal subdural haematoma following combined
spinal-epidural anaesthesia. Anaesth Intens Care 1995 23:111-113.
18. HARDING SA, COLLIS RE, MORGAN BM. Meningitis after combined
spinal-extradural anaesthesia in obstetrics. Brit J Anaesth 1994 73:545-547.
19. Collier CB; Gatt SP A new epidural catheter. Closer eyes for safety?
Anaesthesia. 1993 48(9): 803-6
Clive Collier
The use of neurobehavioural scoring techniques by Scanlon et al in 1974 found that
neonates born vaginally to mothers who had received epidural lignocaine and
mepivacaine, but not bupivacaine, in labour were "floppy but alert" (1) (Table 35.2).
Until further work, ten years later, was found not to confirm the original findings,
bupivacaine became the drug of first choice for obstetric epidural analgesia (2).
Lignocaine then came back into widespread use for caesarean section anaesthesia,
although bupivacaine remained the agent of choice in labour. Both lignocaine and
bupivacaine, in standard doses (Table 36.3), produce minimal direct neonatal
depression or neurobehavioural effects, provided that adequate placental circulation
is maintained. Bupivacaine, when used to excess, can compromise fetal well-being.
Local anaesthetics are basic drugs that, in plasma, bind predominantly to alpha1-acid
glycoprotein. The extent of placental transfer is dependent on the pKa of the drug,
the maternal and fetal pH and the degree of protein binding. Fetal hypoxia and
acidaemia increase the transfer of these weak bases, producing higher fetal:maternal
drug ratios. Acidosis also increases the magnitude of the toxic effects of local
anaesthetics in both fetus and neonate.
Bupivacaine is more than 80% protein bound and its placental transfer is relatively
less than that of lignocaine, which is 70% protein bound. After epidural
administration, the mean Umbilical Vein:Maternal Vein ratio is approximately 0.3 for
bupivacaine, and 0.57 for lignocaine (Chapter 50). Spinal anaesthesia (Chapter 63)
results in only negligible maternal blood levels of local anaesthetics and is not
accompanied by neonatal drug depression.
Groups of mothers receiving epidural analgesia with bupivacaine, when compared to
non-epidural groups, have been shown to have improved neonatal outcomes in the
following situations: twins (3), Iow-birthweight (4) and pregnancy-induced
hypertension (5). In one series of vaginal deliveries, the epidural group of patients
scored far better in the majority of neonatal outcome tests than a group given
intramuscular pethidine and even outperformed a group given no analgesia (6).
Subarachnoid block for Caesarean section has been reported to result in higher one
minute Apgar scores and mean umbilical venous pHs than general anaesthesia in a
similar group of patients (7).
It is generally believed that neonates delivered by Caesarean section are more alert,
quicker to establish spontaneous respiration and less likely to require endotracheal
intubation if regional, rather than general anaesthesia, has been used (8, 9), provided
that hypotension has been avoided. A fall in blood pressure may reduce placental
blood flow (10) and result in depressed neonatal reflexes (11).
In this context, a statement by Reynolds is worthy of repetition: "Provided the
maternal circulation is well maintained, both epidural analgesia in labour and regional
block for Caesarean section are, if anything, actually beneficial to the baby. It is a pity
that women are not told more often of the benefits to the baby of epidural analgesia"
(12).
References:
1. Scanlon JW, Brown WU, Weiss JB, Alper MH. Neurobehavioral responses of
newborn infants after maternal epidural anesthesia. Anesthesiology 1974 40:1
21-128.
2. Abboud TK, Kim KC, Nouheid R et al. Epidural bupivacaine, chloroprocaine or
lidocaine for Cesarean section: maternal and neonatal effects. Anesthesia &
Analgesia 1983 62:914-91 9.
3. Crawford JS. A prospective study of 200 consecutive twin deliveries. Anaesthesia
1987 42:33-43.
4. Osbourne GK, Patel NB, Howat RCL. A comparison of the outcome of low
birthweight pregnancy in Glasgow and Dundee. Health Bulletin (Edinburgh) 1984
42:68-77.
5. Abboud T, Artal R, Sarkis F et al. Sympathoadrenal activity, maternal, fetal and
neonatal responses after epidural anesthesia in the pre-eclamptic patient. American J
of Obstetrics and Gynecology. 1982 144:915-918.
6. Corke BC. Neurobehavioural responses of the newborn. The effects of different
forms of maternal analgesia. Anaesthesia 1977; 32:539-543.
8. James FM, Crawford JS, Hopkinson R et al. A comparison of general anesthesia
and lumbar epidural analgesia for Cesarean section. Anesthesia and Analgesia 1977
56:228-235.
9. Ong BY, Cohen MM, Palahniuk RJ. Anesthesia for Cesarean section - effects on
neonate. Anesthesia and Analgesia 1989 68:270-275.
10. Jouppila R, Jouppila P, Kuikka J, et al. Placental blood flow during Caesarean
section under lumbar extradural analgesia. British Journal of Anaesthesia 1978
50:275-279.
11. Hollmen AI, Jouppila R, et al. Neurologic activity of infants following anesthesia
for Cesarean section. Anesthesiology 1978 48;350-356.
12. Reynolds F. Effects on the baby of conduction blockade in obstetrics. In: Epidural
and spinal blockade in obstetrics. Editor: Reynolds F, London: Balliere Tindall p215
1990.
Neonatal Outcome
Clive Collier
Neonatal outcome and the influence of different anaesthetic techniques and modes
of delivery
Early neonatal assessment usually consists of:
1. Apgar score (Table 35.1),
2. time to sustained respiration (TSR), and, occasionally,
3. biochemical status, and
4. neurobehavioural testing (usually for research purposes).
Long-term outcome is rarely studied.
The infant's Apgar score (up to a maximum of 10 points) is evaluated at 1 and 5
minutes. A 1 minute score of 4-6 is taken to signify moderate depression and
ventilation of the neonate with oxygen is recommended. A score of 0-3 indicates
severe depression (or cardiac arrest) and urgent resuscitative measures should be
instituted immediately.
Prior to the advent of continuous epidural block, repeated large doses of
intramuscular pethidine, often combined with sedatives (eg promazine), were
standard maternal pain relief in most labour wards. Neonatal depression was
frequently evident even on cursory examination. The use of lignocaine and
mepivacaine in the early days of continuous epidural block were associated with
"floppy but alert" neonates (1) (Chapter 77).
Today, few neonates are delivered in a depressed condition as a result of the choice
of maternal analgesia. This reduction in incidence can be attributed to the:
1. decreased use of intramuscular pethidine,
2. availability of naloxone to reverse narcotic effects,
3. almost universal use of bupivacaine for continuous epidural block in labour
(Chapter 25).
The Apgar score is not an appropriate tool for the detection of subtle changes in early
infant behaviour. These assessments can be made using methods such as the:
1. Brazelton Neonatal Behavioural Assessment Score,
2. Early Neonatal Neurobehavioural Scale, and
3. Neurologic and Adaptive Capacity Score (Table 35.2).
Concern has been expressed that neonatal depression can occur as a result of large,
repeated doses of epidural fentanyl given just before delivery (especially if fentanyl is
"trapped" in an acidotic fetus). Scientific evidence for this is lacking.
In the case of general anaesthesia for caesarean section, the induction to delivery
(I-D) time may be important. If I-D interval is prolonged beyond about 10 minutes,
placental transfer of anaesthetic agents may contribute to neonatal depression (2)
(Chapter 50). Similarly, the time from uterine incision to delivery (U-D) may be critical.
Fetal acidosis can be anticipated if the U-D interval is greater than 90 seconds in
patients under general anaesthesia (3).
These time constraints are of lesser importance when epidural or spinal anaesthesia
is used (4).
Intrapartum and early neonatal death rates provide a reliable, if crude, measure of
neonatal outcome. One survey showed that epidural analgesia was associated with a
marked reduction in neonatal mortality in low birthweight babies (5). A study of
neonatal outcome following 3940 caesarean sections showed a doubling of the
mortality rate when general, as opposed to regional, anaesthesia was used (6).
References:
1. Scanlon JW, Brown WU, Weiss JB, Alper MH. Neurobehavioral responses of
newborn infants after maternal epidural anesthesia. Anesthesiology 1974
40:121-128.
2. Warren TM, Datta S, Ostheimer GW. Comparison of the maternal and neonatal
effects of halothane, enflurane and isoflurane for cesarean delivery. Anesthesia and
Analgesia 1983 62:516-520.
3. Datta S, Ostheimer GW, Weiss JB, et al. Neonatal effect of prolonged anesthetic
induction for cesarean section. Obstetrics and Gynecology 1981 58:331-335.
5. David H, Rosen M. Perinatal mortality after epidural analgesia. Anaesthesia 1976
31:1054-1059.
6. Ong BY, Cohen MM, Palahniuk RJ. Anesthesia for Cesarean section - effect on
neonates. Anesthesia and Analgesia 1989 68:270-275.
Clive Collier
The paramedian (paraspinous or lateral) approach.
While the paramedian approach is the favoured epidural technique of many
anaesthetists, it tends to be used less than the midline approach (1) (Chapter 1).
Some of the claimed advantages of the paramedian route are:
1. reduced incidence of technical and catheter-related problems - extreme flexion of
the back to open up the interlaminar space is not required;
2. reduced risk of trauma to the epidural veins;
3. lower incidence of epidural vein cannulation;
4. easier catheter insertion - the needle is angulated substantially more cephalad
resulting in less "tenting" of the dura and a straighter catheter path;
5. lower incidence of dural puncture with a reduced incidence of headache after dural
puncture (2) (Chapter 97);
6. less paraesthesiae on catheter insertion;
7. less trauma to the ligaments of the back, with fewer complaints of postpartum
backache (Chapter 84);
8. less incidence of initial failure;
9. the technique is said to be easier to teach.
It should be stressed that many of the claimed advantages are unconfirmed. The
approach may be extremely useful for patients with a midline scar or for those with a
rigid spine (eg following back trauma, ankylosing spondylitis).
References:
48.1. GAYNOR A. The epidural region: anatomy and approach. In; Reynolds F, ed.
Epidural and spinal blockade in obstetrics. London: Balliere Tindall,1990: 3-18.
48.2. HATFALVI BI. The dynamics of post-spinal headache. Headache 1977;
17:64-67
Clive Collier
Regional block in the presence of spinal deformities
Although severe spinal deformities may make epidural or spinal puncture impossible,
lesser degrees of scoliosis, kyphosis, kyphoscoliosis, increased lumbar Iordosis or
disc disease usually allow satisfactory access to the epidural (Chapter 1) or
subarachnoid space (Chapter 68). However, the resulting block may fail (3) or
produce only patchy analgesia (4). Moderately severe scoliosis may be associated
with persistent unilateral epidural analgesia (9) and kyphosis frequently predisposes
to an excessively high level of sensory block.
Similarly, blocks may be difficult to insert and spread may be inadequate in patients
who have undergone surgical correction of these spinal deformities (5). Scar tissue
and bone grafts may disrupt the ligamentum flavum or impede the spread of local
anaesthetic. The epidural space may even be obliterated by adhesions.
The presence of Harrington rods or similar instrumentation provides another
challenge. One group of workers were only able to satisfactorily overcome the
technical difficulties in 5 out of 9 parturients receiving epidural block and one of these
parturients suffered an inadvertent dural puncture (6). These patients are unable to
flex their spines making any approach technically more difficult. In those patients who
have not had a laminectomy, insertion of a block needle may be attempted adjacent
to a single rod or between the two rods. In one patient with a Harrington rod, a
subdural block followed an L5 - S1 epidural puncture (7).
In patients who have undergone laminectomy, insertion of a block needle may be
attempted above or below, but not through, the scar. In these individuals, fibrous
tissue has completely replaced the epidural space. A midline or paramedian
approach may be used but caution is always required.
In those with spinal deformity, a planned subarachnoid block may be undertaken, but
this can result in a patchy block (Chapter 98). This may necessitate the use of either
a continuous technique or repeated subarachnoid puncture (4). The presence of
abnormal spinal curves makes the effect of posture on the distribution of a spinally
administered drug difficult to predict (Chapter 30). Caution is required because
excessively high levels of block, with respiratory insufficiency, have been reported.
This is especially so when a subarachnoid injection is used to correct an inadequate
epidural block (8). In one case, the spinal component ascended rapidly even though
only normal saline was injected into the epidural space (8).
Two epidural catheters may be inserted at different levels to overcome the poor
spread of epidural solutions in patients with spinal deformity (4). There is a minor
theoretical concern that the catheters might become knotted together, or that the
second epidural needle insertion might damage the first catheter. An alternative to
the double lumbar catheter technique is the addition of a caudal (Figure 22.1), low
spinal or, very occasionally, paravertebral block to provide analgesia for delivery.
A combination of various techniques together with some ingenuity is required for
these difficult patients!
References:
3. MORAN DH, JOHNSON MD. Continuous spinal anesthesia with combined
hyperbaric and isobaric bupivacaine in a patient with scoliosis. Anesthesia and
Analgesia 1990; 70:445-447.
4. SCHACHNER SM, ABRAM SE. Use of two epidural catheters to provide analgesia
of unblocked segments in a patient with lumbar disc disease. Anesthesiology 1982;
56:150-151.
5. PASCOE HF, JENNINGS GS, MARX GF. Successful spinal anesthesia after
inadequate epidural block in a parturient with prior surgical correction of scoliosis.
Regional Anesthesia 1993; 18:1 91-192.
6. CROSBY ET, HALPERN SH. Obstetric epidural anaesthesia in patients with
Harrington instrumentation. Canadian J Anaesthesia 1989; 36:693-.
7. LEE Y-S J, BUNDSCHU RH, MOFFAT EC. Unintentional subdural block during
labor epidural in a parturient with prior Harrington rod insertion for scoliosis. Regional
Anesthesia 1995; 159-162.
8. BECK GN, GRIFFITHS AG. Failed extradural anaesthesia for caesarean section:
complication of subsequent spinal block. Anaesthesia 1992; 47:690-692.
9. COLLIER CB Why obstetric epidurals fail. International Journal of Obstetric
Anaesthesia. 1996 5:19-31
Clive Collier
General Principles in the Management of Major Regional Blockade in the Parturient
with Significant Heart Disease.
General Principles:
The incidence of significant congenital or acquired heart disease in women
presenting to obstetricians is approximately 0.5 to 2.0%. Cardiac output rises by
40-50% prior to the onset of labour and is further increased by the pain of labour and
expulsive efforts by the mother in the second stage. The presence of significant
cardiac disease can pose particular problems for both the patient and the
anaesthetist.
Early, continuous epidural analgesia, cautiously administered using small incremental
doses or an infusion, is recommended for most patients with cardiac disease
(Chapter 83). Effective analgesia abolishes pain and, sometimes, the bearing down
reflex, both of which can increase right heart pressures and induce tachycardia
reducing the time available for cardiac filling and coronary perfusion. Monitoring for
NYHA Class I and II patients (Table 108.1) should include continuous
electrocardiography and pulse oximetry. In addition, invasive systemic and pulmonary
arterial pressure monitoring should be considered for NHYA III and IV patients.
Epidural morphine and fentanyl have been shown to produce adequate, but
incomplete, analgesia for first stage labour in patients with significant heart disease
with minimal cardiovascular instability (1). The addition of low concentrations of
bupivacaine will usually ensure satisfactory analgesia. In the second stage, a low
subarachnoid or "saddle block" may be useful for delivery as an alternative to
epidural block.
In compromised patients, the volume of crystalloid infused must be kept under tight
control and titrated against the central venous or pulmonary capillary wedge (or
pulmonary artery diastolic) pressure. Special care must be taken to avoid aortocaval
compression and supine hypotension at all times (Chapter 28). Oxygen should be
administered throughout labour (Chapter 87).
If hypotension secondary to a reduced systemic vascular resistance occurs,
phenylephrine may be preferable to ephedrine. Phenylephrine exhibits less
beta-agonist activity than ephedrine and has a lesser tendency to increase cardiac
work and to cause tachycardia (Chapter 79). The potential cardiovascular benefits of
the use of phenylephrine should be weighed against the possible detrimental effect of
phenylephrine on utero-placental blood flow although recent work suggests that
phenylephrine can, in fact, be used with safety (3).
In those patients with prosthetic cardiac valves or conduits, congenital malformations,
mitral valve prolapse or other valvular disease, broad-spectrum antibiotic prophylaxis
against subacute bacterial endocarditis should be commenced antepartum and
should be continued for 3 to 4 days after delivery.
Anticoagulant therapy with heparin may have been prescribed in the latter half of
pregnancy to patients with prosthetic valves, conduits, atrial fibrillation or a history of
thrombo-embolism. Full-dose heparin should be stopped prior to labour or at least
three hours before institution of a major regional block (Chapter 72).
General Principles: Specific Cardiac Conditions (Chapter 82 and Chapter 83):
Acquired Disease:
Rheumatic heart disease is probably the commonest (75%) form of heart disease
encountered in pregnancy. Mitral stenosis in particular, may be associated with a
relatively low, fixed, cardiac output and it is particularly important to avoid
hypotension, hypervolaemia and tachycardia. The latter two, if uncontrolled, can lead
to congestive cardiac failure.
Ischaemic heart disease and peripartum cardiomyopathy occur less commonly
(Chapter 41). These mothers may also benefit from the judicious use of continuous
epidural block and intensive monitoring.
Congenital heart disease:
Unless shunt reversal occurs, parturients with a left-to-right shunt (commonly an atrial
or ventricular septal defect) usually experience labour and delivery without major
problems.
If a right-to-left shunt is already present or develops as a result of shunt reversal, the
outcome for mother and baby is, generally, poor. The anaesthetist should be aware
of the specific problems of right-to-left shunting which relate to:
1. central cyanosis (which is relatively unresponsive to supplemental oxygen),
2. the effect of changing the balance between pulmonary and systemic vascular
resistances - particularly the effect of pulmonary hypertension and/or systemic
hypotension on this relationship,
3. the effect of a reduction in cardiac output on arterial oxygen saturation,
4. the potential for air embolism (particularly from intravenous lines), and
5. the impairment of platelet function which is a feature of cyanotic heart disease.
Shunt reversal is typically seen in Eisenmenger's syndrome and Ebstein's anomaly.
Eisenmenger's (3% of congenital heart disease) consists of a right-to-left or
bi-directional shunt at atrial, ventricular or aortopulmonary level, with cyanosis. The
syndrome is associated with a high maternal (12-30%) and fetal (50%) mortality rate
(2). Right-to-left shunting is also a feature of Fallot's Tetralogy which, however, is
very rarely seen in the obstetric patient (Figure E.4).
References:
1. Macdonald R. Indications and contraindications for epidural blockade in obstetrics.
In: Reynolds F, ed. Epidural and spinal blockade in obstetrics. London: Balliere
Tindall,1990:19-32.
2. Rocke DA, Rout CC, Orlikowski CEP. Anesthesia and coexisting maternal
disease; Part 1. Cardiac and hematologic disease. In: Norris MC, ed. Obstetric
Anesthesia. Philadelphia: J.B.Lippincott, 1993: 447-473.
Clive Collier
The use of major regional techniques in this group of patients remains contentious.
However, the decision whether or not to offer the option of a block to the individual
patient, must be based on sound knowledge of their medical history and the natural
history of their condition (where possible). In discussion with the patient, the potential
for deterioration of their neurological condition as a consequence of pregnancy,
labour, delivery and anaesthesia should be stressed.
Lumbar disc disease.
This group comprises the majority of patients with a neurological disorder presenting
to the obstetric anaesthetist, yet little appears in anaesthetic textbooks. Exacerbation
of disc disease is common in pregnancy, with mothers limping into antenatal clinics
and complaining of sciatic pain, partly as a result of the postural changes of
pregnancy. These patients are often denied the choice of an epidural or
subarachnoid block at the insistence of their attending neurosurgeon who fears a
deterioration in their condition. There appears to be little scientific evidence to
support this view. In fact, epidural injections of local anaesthetics, with or without
steroids, have been used successfully in the treatment of disc prolapse for many
years.
Post-laminectomy and spinal fusion patients are sometimes referred to the obstetric
anaesthetist in early pregnancy and often carry a letter from their neurosurgeon
counselling against regional block in labour (Chapter 115). Except in rare and specific
cases, this prohibition of regional anaesthesia would appear to be unjustified.
Nevertheless, epidural block in patients with disc disease, including post-surgical
cases, may be technically difficult, time-consuming and require a paramedian
approach or special technique (Chapter 48). The resulting block may initially be
patchy but perseverance usually results in satisfactory analgesia without neurological
sequelae (1, 2). The avoidance of adrenaline-containing solutions may be wise if it is
considered that there might be an ischaemic element in the symptomatology of disc
prolapse.
Many patients with marked disc disease are now managed with elective caesarean
section in order to avoid back strain in labour. It seems unreasonable not to allow
most, if not all, of these women the option of regional techniques (Chapter 84).
Multiple Sclerosis (MS).
This disease of uncertain aetiology is characterized by plaques of nerve
demyelination which can produce widespread symptoms including visual
disturbances, muscle weakness, paraplegia, neurogenic bladder and emotional
lability. It is classically a relapsing and remitting condition. Infection, fatigue,
emotional trauma, pregancy and labour may all precipitate a relapse. In general,
pregnancy is usually well tolerated and, if relapses develop, they tend to occur in the
first 3 months postpartum.
Theoretical concerns about the use of regional techniques in MS include the
possibility that:
1. exacerbation of symptoms may, coincidentally, follow a satisfactory block and
blame may be wrongly attributed to the technique; and
2. local anaesthetics may be toxic to demyelinated nerves. For this reason,
subarachnoid block (Chapter 63) is not recommended in this condition.
Epidural analgesia is said not to be contraindicated in MS, but adrenaline-containing
solutions should be avoided because local ischaemia may be deleterious in this
situation. In practice, there have been several individual case reports and one series
describing the safe use of epidural block for labour analgesia and caesarean section
(3). In this review, of the 14 patients who received epidural block, 5 (36%) relapsed in
the first 12 weeks postpartum, as compared to 4 (22%) of 18 patients who received
general or local infiltration anaesthesia. High concentrations of local anaesthetics
may be associated with a greater relapse rate and the use of a low as concentration
as necessary seems wise.
A discussion with the patient regarding the choice of technique for labour, delivery
and/or caesarean section should, preferably, occur early in the pregnancy.
Myasthenia gravis.
In this condition, auto-antibodies to acetylcholine (ACh) receptors produce a
diminution in the number and size of post-synaptic ACh receptor sites and motor
end-plates. The symptoms include weakness and easy fatiguability of voluntary
muscles.
Epidural block may be used for labour or caesarean section provided that high levels
of block are avoided. Excessively high blocks have the potential to further impair
ventilatory function. For vaginal delivery, low spinal block may also be suitable.
Dosage levels of anticholinesterases may have to be adjusted.
Paraplegia.
On the surface, it would seem that an obstetric patient who is paraplegic (or
quadriplegic) with a sensory level above T10 should not require analgesia for labour.
However, because autonomic hyperreflexia can be life-threatening to these patients,
some form of neuraxial block is mandatory. Autonomic dysreflexia occurs in the
majority of patients with lesions above T7 and occurs when the skin or viscera below
the lesion are stimulated. The autonomic dysfunction may range from sweating and
facial flushing to bradycardia with severe hypertension (10% of patients) and
headache. The hypertension may be severe enough to produce convulsions or
subarachnoid or cerebral haemorrhage (4).
Other conditions.
Epileptic patients may benefit from a tranquil labour under continuous epidural
blockade.
Epidural analgesia would also benefit patients with most neuromuscular disorders in
the absence of any marked cardiomyopathy or respiratory embarrassment.
In myotonic conditions, the addition of fentanyl to the epidural solution may have the
added benefit of reducing "epidural shivering" which may precipitate the characteristic
attacks.
Opinions differ as to the advisability of attempting epidural blockade in patients with
an intracranial tumour or raised intracranial pressure. Provided the considerable risk
of cerebral herniation and sudden death associated with dural puncture in these
patients is realized, and the utmost care is taken by an experienced anaesthetist,
epidural blockade may be invaluable in the management of labour.
Benign intracranial hypertension (pseudo-tumour cerebri) is a different proposition, as
there is generalized, not localized, cerebral oedema. Epidural or subarachnoid blocks
may be safely undertaken.
Cases of peripheral neuropathy are usually suitable for regional techniques, following
detailed discussion with the patient. Prolonged motor and sensory blocks, lasting up
to 12 hours following epidural bupivacaine 0.5%, have been observed in patients with
diabetic neuropathy.
With poliomyelitis on the wane, it is increasingly unusual to encounter women with
residual paralysis in labour. However, those with polio affecting a lower limb should
be warned that, occasionally, motor block may be prolonged in the affected leg.
References:
1. Daley MD, Morningstar BA, Rolbin SH et al. Epidural anesthesia for obstetrics after
spinal surgery. Regional Anesthesia 1990 15:280-284.
2. Crosby ET, Halpern SH. Obstetric epidural anesthesia in patients with Harrington
instrumentation. Canadian J Anaesth 1989 36:696.
3. Bader AM, Hunt CO, Datta S et al Anesthesia for the obstetric patient with multiple
sclerosis. J. Clin Anesth 1988; 1:21-28
4. Stirt JA, Marco A, Conklin KA. Obstetric anesthesia for a quadriplegic patient with
autonomic hyperreflexia. Anesthesiology 1979;51:560-562.
Clive Collier
Relative Cardiovascular and Central Nervous System Toxicity of Local Anaesthetics:
Relative CVS:CNS toxicity ratios.
The cardiovascular system (CVS) appears to be more resistant to the toxic effects of
local anaesthetic agents than the central nervous system (CNS). 'Toxicity' symptoms
occurring subsequent to injection into the epidural space are due to: 1. accidental
intravenous injection producing immediate, high plasma levels of local anaesthetic.
This produces mainly CVS symptoms; or
2. slower systemic absorption of an excessive dose of correctly-placed local
anaesthetic. Here, the CNS toxicity symptoms predominate (Table E.2).
Animal experiments have been undertaken to investigate the relative toxicity of
several local anaesthetics. Their CVS and CNS toxicity thresholds are usually
expressed as a ratio (Table 37.2) (1, 2). The CVS:CNS toxicity ratio is obtained by
administering the local anaesthetic until convulsions ensue and then continuing until
circulatory collapse follows. The lower the ratio, the greater the likelihood of selective
cardiotoxicity.
In non-pregnant sheep, the CVS:CNS toxicity ratio is low following bupivacaine (3.7)
but not lignocaine (7.1).
Ropivacaine may be less cardiotoxic than bupivacaine because it has a higher ratio.
References:
1. LAISHLEY RS. Local Anaesthetic Toxicity.In:
Reynolds F Editor. Epidural and Spinal Blockade in Obstetrics. London: Bailliere
Tindall 1990: 81-94
2. Reynolds F. In defence of bupivacaine. Int. Journal of Obstetric Anesthesia 1995;
4:93-108
Clive Collier
1. The patient should be prepared according to the guidelines shown in Chapter 44.
The equipment required is shown in Table 44.2. Subarachnoid block may be
performed in either the sitting or lateral position, following the administration of 1-2
litres of crystalloid solution, and with a suitable vasopressor agent (e.g. ephedrine)
close at hand (Chapter 79).
2. Skin infiltration with local anaesthetic (Figure 16.1) should be performed at the
L2-3 or L3-L4 interspace.
3. A wide variety of needles are available (Figure E.1) but, for obstetric use, a
non-cutting, dural-fibre-splitting needle such as a 24G Sprotte or a 26G Whitacre is
preferred because of the lower incidence of post dural puncture headache (Chapter
97). If a cutting needle has to be used (eg 26G Quincke) it should be inserted with
the bevel pointing laterally.
4. A spinal needle introducer (eg. Sise) may facilitate insertion of the spinal needle. If
an introducer is not available, an 18G hypodermic needle may suffice.
5. The needle traverses the skin, subcutaneous tissue, supraspinous and
interspinous ligaments and ligamentum flavum before crossing the epidural space
and perforating the dura with a characteristic "pop" (Figure E.3).
6. Withdrawal of the stylet should allow CSF to appear at the hub of the needle within
a few seconds. Failing this, gentle aspiration with a syringe and, sometimes, rotation
of the needle may confirm that the needle tip is located within the subarachnoid
space. It should be remembered that the flashback time for very fine needles may be
quite long. For example, for a patient lying in the lateral position, with a typical CSF
pressure of 5cm of water, the time taken for CSF to appear in the hub of a 90mm,
0.32mm internal diameter Pajunk needle is quoted as 12 seconds.
7. The syringe containing the local anaesthetic or opioid solution is now attached to
the needle and, following further aspiration, the drug is injected slowly over 10 to
15secs. The needle is now removed and a sterile dressing applied.
8. Patients who were in the lateral position are now turned onto the opposite side.
Seated patients are placed in a supine, lateral position.
9. Close monitoring of the extent of block is commenced (Chapter 10). If hyper- or
hypo-baric solutions are used, posture can be used to control the spread of
anaesthesia (Figure 30.1) (Chapter 30).
Subdural Space
Clive Collier
The classic anatomical description of the subdural space is of "a potential cavity
between the dura and arachnoid mater, containing a small volume of serous fluid"
(1). The space runs up from the lower border of the second sacral vertebra into the
cranial cavity as high as the diaphragma sellae in the floor of the third ventricle (2)
but does not communicate with the subarachnoid space. It is continued onto the
cranial and spinal nerves for a short distance. The space appears to be widest in the
cervical region (3).
Contemporary anatomists have suggested, however, that the spinal subdural space
is not a "potential" space at all, but that it occurs as a result of tissue damage which
creates a cleft in this area of the meninges (4). These anatomists contend that there
is no natural space between the arachnoid barrier cell layer and the dural border cell
layer. When tissue damage occurs, it results in a cleaving open of the dural border
cell layer.
The force required to enter the subdural space or produce this cleavage is usually
small. Blomberg (5) reported little difficulty in inserting an endoscope and viewing the
cavity in the majority of his autopsy studies.
Entry into the subdural space in the course of attempted epidural block appears to
result from:
1. the bevel of an epidural needle perforating the dura, particularly if the bevel has
been rotated in the epidural space (6),
2. invasion by an epidural catheter at the time of its insertion, or
3. subsequent migration of the catheter.
The subdural space is well known to radiologists as a place to go astray when
attempting subarachnoid contrast injection (6, 9). This is particularly likely to occur
following previous subarachnoid block, or lumbar puncture, and is recognized on
fluoroscopic screening by the sluggish flow of contrast away from the injecting
needle, which is little improved by tilting the patient.
Injection of local anaesthetic into the subdural space usually results in an
unexpectedly high level of sensory block - as little as 3.5 ml bupivacaine 0.5% has
produced a block as high as the C5 level (7). The high sensory block is usually
evident between 10 and 35 minutes following injection (Chapter 8). It may spread
intracranially producing apnoea and unconsciousness. Accompanying hypotension is
gradual in onset and systolic blood pressure is rarely below 60 mm Hg. (8).
References:
1. GRAY'S ANATOMY. Neurology pp 1044-1102 33rd edition, Editors: Davies DV,
Davies F. London,Longmans, 1964
2. Jones MD, Newton TH. Inadvertent extra-arachnoid injections in myelography.
Radiology 1963 80:818-821.
3. Mehta M, Maher RM. Injection into the extra-arachnoid subdural space.
Anaesthesia 1977 32:760-766.
4. Haines DE. On the question of a subdural space. The Anatomical Record 1991
230:3-21.
5. Blomberg RG. The lumbar subdural extra-arachnoid space of humans; an
anatomical study using spinaloscopy in autopsy cases. Anesthesia and Analgesia
1987 66:177-180.
6. Schultz EH, Brogdon BG. The problem of subdural placement in myelography.
Radiology 1962 79:91-95.
7. Brindle-Smith G, Barton FL, Watt JH. Extensive spread of local anaesthetic
solution following subdural insertion of an epidural catheter during labour.
Anaesthesia 1984 39:355-358.
8. Collier CB. Accidental subdural block: four more cases and a radiographic review.
Anaesthesia and Intensive Care 1992 20:215-232.
9. Reynolds F and Speedy HM. The subdural space: The third place to go astray.
Anaesthesia 1990: 45:120-123
Clive Collier
Immediate treatment of accidental dural puncture.
1. Loss of CSF should be minimized by replacing the stylet of the Tuohy needle or by
immediate, complete withdrawal of the needle.
2. Partial withdrawal of the Tuohy needle through the dura until CSF flow stops is not
recommended because the subdural space, rather than the epidural space, may be
entered (1).
3. If a subsequent subarachnoid block is undertaken (Chapter 63), there may be an
increased risk of a high block, particularly if any fluid has been injected into the
epidural space (2). It is thought possible that an increased hydrostatic pressure in the
epidural space may encourage spread of local anaesthetic in the subarachnoid
space.
4. Epidural puncture may be repeated in an adjacent interspace, although there is an
increased risk of a second dural puncture. The local anaesthetic dose should be
decreased by 25% and given in small increments because of the potential for
leakage of local anaesthetic through the dural hole into the subarachnoid space (3)
(Chapter 114).
5. A normal vaginal delivery with bearing-down is to be permitted. This is in contrast
to earlier recommendations that delivery be forceps-assisted so as to avoid straining
and increased CSF loss.
6. The epidural catheter may be left in position for prophylactic saline infusion or
blood injection through the catheter but these techniques have met with little success
(4).
7. Bedrest post-puncture is not effective in the prevention of headache although it will
relieve symptoms once they occur. A temporary abducent (Vlth cranial) nerve palsy
and diplopia may follow early, energetic ambulation.
8. The management of post-dural puncture headache by blood patching and other
means is discussed in Chapter 110 and Chapter 85.
References:
1. COLLIER CB. Collapse after epidural injection following inadvertent dural
perforation. Anesthesiology 1982 57:427-428.
2. BECK GN, GRIFFITHS AG. Failed extradural anaesthesia for caesarean section:
Complication of subsequent spinal block. Anaesthesia 1992 47:690-692.
3. LEACH A, SMITH GB. Subarachnoid spread of epidural local anaesthetic following
dural puncture. Anaesthesia 1986 43:671-674.
4. GUTSCHE BB. Lumbar epidural analgesia in obstetrics: taps and patches. In:
Reynolds F, Editor. Epidural and spinal blockade in obstetrics. London: Balliere
Tindall,1990: 95-106.
Michael Cooper
Indications:
Local anaesthetic infiltration for caesarean section (CS) is a rarely used technique. It
has application in the rare situation where both general and regional anaesthesia is
contraindicated and in countries with limited health resources. There are few
contemporary reports of this technique (1, 2) and most descriptions come from
countries (3, 4) where:
1. anaesthetic expertise is lacking, or limited,
2. anaesthetic equipment or gas supplies are unavailable, or
3. a single individual is required to both operate and anaesthetise.
Local anaesthetic infiltration has also been used in rare situations such as:
1. Myotonic dystrophy where it has been used in conjunction with spinal anaesthesia
for CS with bupivacaine applied directly to the myometrium to relieve incoordinate
cycles of uterine spasm / atony (5)
2. Familial dysautonomia (Riley-Day syndrome) (1)
Advantages of local anaesthetic infiltration:
1. Allows for immediate commencement of surgery in emergency situations.
2. Useable when central neural blockade (CNB) is technically difficult,
eg. kyphoscoliosis (2) , unpredictable in result or contraindicated.
3. Retains the patient's protective airway reflexes.
4. Avoids the sudden haemodynamic changes that may occur with CNB.
Technique:
A long (18 cm) spinal needle minimises the number of individual injections required.
Skin:
The skin of the anterior abdominal wall is supplied by the anterior and lateral
cutaneous branches of the lower six intercostal nerves and the iliohypogastric and
ilioinguinal nerves. For a transverse suprapubic (Pfannensteil) incision simple
subcutaneous infiltration is adequate.
Fat:
The fat layer is relatively devoid of innervation and a large amount of local
anaesthetic may be wasted by infiltrating this layer, which is relevant to the often
large total dose used.
Fascia:
Direct infiltration can be used; other authors have recommended bilateral rectus
sheath blocks (6, 7).
Retropubic space:
This can be a difficult area to anaesthetise and may require additional infiltration
retropubically and into the pyramidales muscles.
Parietal peritoneum:
Many authors report this to be a difficult area to anaesthetise and several techniques
have been described.
1. The injection of several mls of solution through the fascia (before its division) helps
to separate the layers and to anaesthetise the parietal peritoneum.
2. Once the peritoneum is opened, the instillation of 10-15ml of local anaesthetic into
the peritoneal cavity.
3. Once the peritoneum is opened, radiate intraperitoneal injections.
Visceral peritoneum / uterus:
These do not need infiltration, but doing so separates the visceral layer of the
peritoneum from the lower uterine segment.
Some authors (7, 8) have described field block anaesthetic techniques for vertical
classical skin incisions which involve multiple injections and increased discomfort for
the patient. They may take longer and require greater skill and use a greater volume
of local anaesthetic than simple direct infiltration. These papers, which described the
authors personal experiences in the 1950s and 60s cite local anaesthesia as giving
better neonatal outcomes than general anaesthesia for CS.
Macintosh (9) warns of the risk of rectus sheath block in a patient with abdominal
distension (from whatever cause). As the anterior and posterior layers of the sheath
are almost in apposition, the needle may pass through both structures giving the
false impression that only the anterior layer has been penetrated.
Drugs, vasoconstrictor and volume:
Many different agents have been used depending on the availability of the drug and
the familiarity of the operator with the agent.
Bearing in mind the maximum recommended doses of local anaesthetic agents
(Table 36.3), the volume required may be as high as 100ml. Not all of this may be
required initially, and further infiltration may be necessary after delivery to close the
superficial layers.
Obviously, local anaesthetic toxicity (Chapter 89) to mother and fetus is a significant
risk. This should influence the choice of agent in terms of :
1. The concentration which is required for effective infiltration anaesthesia.
2. The decision to add a vasoconstrictor in order to increase the amount of drug that
can be used with safety.
3. The toxicity and metabolism profile of the local anaesthetic.
4. The fetal / maternal ratio of the local anaesthetic. Substantial uptake of lignocaine
in the fetal liver can occur (10). Ester local anaesthetics such as 2-chloroprocaine
have a half-life in neonatal blood of 43 secs (11). Fetal acidosis favours drug
ionisation, retention of local anaesthetic within the fetus and increased risk of fetal
toxicity.
Choice of agent:
Lignocaine 0.5% or chloroprocaine 1% with 1:200,000 adrenaline is adequate for
infiltration anaesthesia and both agents are rapid in onset. The addition of adrenaline
allows for the use of a greater overall dose. Longer acting agents such as
bupivacaine have a slower onset time and a lower free drug concentration in the fetal
blood (12). The addition of hyaluronidase has been described (8) but may increase
absorption.
Surgical technique:
Gentle tissue handling is required and retractors are generally not well tolerated. If
adequate retropubic anaesthesia has been obtained, a Doyen retractor can be used.
Adequate exposure of the uterus can be obtained by using corner stitches to rotate
the uterus (4). Manoeuvres that can cause significant pain are:
1. Disengagement of the fetal head from the pelvis.
2. Peritoneal traction (may also cause vagal effects).
3. Externalisation of the uterus.
Blood loss is not increased using this technique (4).
In their series of 141 caesarean sections, Ranney and Stannage (7) reported 61
patients having a second, 14 a third and 2 a fourth operation. Only three patients
wanted to have general anaesthesia for their repeat procedure.
References:
1. Leiberman JR, Cohen A, Wizniter A, Maayan C, Greemberg L. Cesarean section
by local anesthesia in patients with familial dysautonomia. American Journal of
Obstetrics and Gynecology 1991;165:110-1.
2. Cooper MG, Feeney EM, Joseph M, McGuinness JJ. Local anaesthetic infiltration
for caesarean section. Anaesthesia and Intensive Care 1989; 17: 198-201.
3. Barker A, Barker M. Caesarean section under local analgesia. Tropical Doctor
1976; 6:23-25.
4. Larsen JV, Barker A, Barker M, Brown RS. A technique combining
neurolept-analgesia with local analgesia for caesarean section. South African Medical
Journal 1971; 45: 750-751.
5. Cope DK, Miller JN. Local and spinal anaesthesia for cesarean section in a patient
with myotonic dystrophy. Anesthesia & Analgesia 1986; 65:687-90.
6. Mackey R. Local anaesthesia in obstetrics. Medical Journal of Australia. 1947; 2:
593.
7. Ranney B, Stannage WF. Advantages of local anesthesia for cesarean section.
Obstetrics & Gynecology 1975; 45: 163-167.
8. Busby T. Local anesthesia for cesarean section. American Journal of Obstetrics &
Gynecology 1963; 87:399-404.
9. Macintosh RR, Bryce-Smith R. Local analgesia: Abdominal Surgery. ES
Livingstone Ltd, Edinburgh, 1953; 74-5.
10. Finster M, Morishima HO, Boyes RN, Covino BG. The placental transfer of
lidocaine and its uptake by fetal tissues. Anesthesiology 1972; 36: 159-163.
11. Finster M, Perel JM, Hinsvark ON, et al. Pharmacodynamics of 2-chloroprocaine.
Fourth European Congress of Anesthesiology, 1974;330:189.
12. Tucker GE, Mather LE. Properties, absorption, and disposition of local anesthetic
agents. In: Cousins MJ, Bridenbaugh PO (eds). Neural Blockade in Clinical
Anesthesia and Management of Pain, 2nd ed, JB Lippincott Co, Philadelphia,1988.
David Crooke
Practical aspects of resuscitation following collapse in the labour room after a major
block
BASIC LIFE SUPPORT (BLS) strategies are applicable with little modification, but in
addition, minimisation of aortocaval compression (ACC) (Chapter 28) using
manoeuvres such as a Human Wedge (1), Cardiff Resuscitation Wedge (2), or
simply a rolled up towel or pillow under the right abdominal flank should be carried
out (Figure 28.2).
ADVANCED LIFE SUPPORT (ALS) strategies (3) are also applicable with little
modification, except that urgent consideration should be given to the possibility of
delivery by caesarean section (CS) while CPR continues unabated (Chapter 12).
Additional points of note are:
AIRWAY
The application of early cricoid pressure by a skilled operator may be appropriate and
facilitate mouth-to-mouth ventilation or the use of a resuscitator device. Inappropriate
cricoid pressure can obstruct the airway or stimulate vomiting. Early securement of
the airway with a cuffed tracheal tube is ideal and in the absence of this, airway
difficulties can supervene at any time and convert an effective resuscitation into an
unmanageable situation. Problematic airways occur frequently in obstetrics.
Management plan:
A. Have in your mental foreground a planned, controlled approach to the possibility of
"failed intubation".
B. Be mindful of where you are and be prepared:
1. to modify the cricoid pressure;
2. to use different laryngoscope blades (Chapter 38);
3. to cease attempts at tracheal intubation and ventilate;
4. to use the laryngeal mask;
5. to seek a surgical airway (crico-thyrotomy).
C. Remember that:
1. physiological goitre of pregnancy may complicate attempts at a "surgical airway';
2. gastric decompression using an oral rather than a nasal approach is preferable
because the risk of epistaxis during instrumentation of the unprepared nose is great.
BREATHING
Low arterial PC02 may further compromise uteroplacental flow.
Venous embolic events may be responsible for a large alveolar dead space.
The pattern of IPPV may contribute to a complex interplay of multiple pathological
factors, such as can occur in cardiopulmonary arrest after major regional block in a
parturient. Aortocaval compression, "high epidural" with reduced cardiac and
vascular sympathetic tone, and high intrathoracic pressures from IPPV or coughing
can all contribute towards reducing venous return during resuscitation.
CIRCULATION
Intraabdominal complications of CPR are more likely in late pregnancy. When
performing cardiac massage, these can be minimised by carefully placing the hands
over the sternum above the xiphoid.
Monitoring of the massage by arterial palpation may be made more difficult by ACC
(Figure 28.1) and by the low systemic vascular resistance (SVR) which can render
the pulse impalpable.
When, and if, CS is performed the newborn will need immediate advanced life
support.
After delivery of the infant, the distal aorta can be occluded so as to control bleeding
and improve cardiac afterload and perfusion (although reperfusion injury may occur).
Once the uteroplacental circulation is closed, the SVR will increase and
responsiveness to beta agonists may be less blunted.
SUBSEQUENT MANAGEMENT
Establish the diagnosis because this will alter further management.
Some life-threatening conditions require different treatment in the non-pregnant and
pregnant states (eg. pulmonary embolectomy, rather than thrombolysis, is preferable
after massive obstetric pulmonary embolism). If resuscitation is rapidly successful
(before CS has been performed) the fetus requires careful monitoring until delivery.
Crisis management, team debriefing and bereavement issues may also need to be
addressed.
References:
1. Goodwin APL. The Human Wedge - a manoeuvre to relieve aortocaval
compression during resuscitation in late pregnancy Anaesthesia 1992 47:433-434.
2. Rees GAD, Willis BA. Resuscitation in late pregnancy Anaesthesia 1988
43:347-349.
3. American Heart Association 'Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiac Care' JAMA, OCT 28, 1992 268:16; 2171-2302, (see p 2249)
David Crooke
Theoretical aspects of resuscitation following collapse in the labour room after a
major block
Cardio-puImonary arrest (CPA) complicating major regional blockade (MRB) in late
pregnancy is uncommon. The cause(s) of the arrest and the timeliness of basic and
advanced life support affect the outcome. Three causal patterns exist, all with
common initial resuscitation requirements:
1. CPA causally related to the MRB, eg. total spinal block and primary respiratory
arrest; local anaesthetic CNS and CVS toxic effects (1).
2. CPA causally related to obstetric or medical factors, with the MRB complicating
management of the CPA, eg. haemorrhage; vagotonia (uterine inversion);
anaphylaxis; complications of pregnancy induced hypertension; peri-partum
cardiomyopathy; venous gas-, amniotic fluid- and thrombo-embolism (2); arrhythmia
or congestive cardiac failure secondary to valvular or congenital heart disease (mitral
stenosis, ASD).
3. CPA related to a complex interplay of multiple factors, eg. aortocaval compression
(ACC) (Figure 28.1) with a "high epidural" on a background of hypovalaemia; MRB
mediated hypotension and idiopathic hypertrophic subaortic stenosis; MRB with ACC
mediated hypotension or a minor pulmonary embolism causing reversal of a left to
right cardiac shunt in an otherwise asymptomatic atrial septal defect; primary cardiac
tachyarrhythmia with a MRB and ACC.
Cardiac arrest complicating major regional blockade is associated with unexpectedly
poor neurological outcomes (4). The physiological changes of pregnancy further
complicate the situation. ACC can confound both the diagnosis of CPA and the
monitoring of CPR because femoral pulses can be unreliable. A carotid pulse,
apnoea and unconsciousness are more reliable clinical markers (Chapter 13).
Reports such as "Post-mortem caesarean section with recovery of both mother and
offspring" (5, 6, 7) and cases of ACC masquerading behind esoteric diagnoses
indicate that vigilance in avoiding ACC is required (8). ACC is treated by:
1. Lateral patient positioning and uterine displacement,
2. Elevation of the legs,
3. Appropriate fluids, and
4. IV vasopressor.
Delivery of the fetus is ultimately the only way to eliminate ACC as a component of
haemodynamic instability. Late term pregnancy is associated with a propensity for
arterial hypoxaemia, airway management difficulty and pulmonary aspiration.
Local anaesthetics (LA) may directly cause circulatory instability via several
mechanisms:
1. MRB related - denervation of vascular tree and venous pooling, attenuated cardiac
sympathetic neural traffic, impaired sympathetic compensation for the ACC and in
asymmetric blocks, QT interval changes;
2. CNS toxicity (Chapter 7);
3. Cardiac toxicity (Chapter 36). "Prevention" of LA toxicity with interval dosing of
epidural LA etc is preferable to the "cure". Bupivacaine is more prone to induce
complex arrhythmias than either lignocaine or ropivacaine (Table 36.6).
In true CPA during pregnancy, the usual resuscitation drugs are indicated. Pregnancy
is associated with blunted responsiveness to beta-agonists. Adrenaline will reduce
uteroplacental blood flow, but this must be weighed against the systemic effect of
supporting cardiac perfusion and output. Drugs can have unexpected effects, eg.
magnesium and verapamil can cause uterine atony. Bretylium may be the
anti-arrhythmic of choice in LA toxicity with refractory ventricular tachyarrhythmia.
Lateral patient positioning simplifies electrical cardioversion with anterior-posterior
paddle placement.
References:
1. Dawson P. Cardiac Arrest following Epidural Overdose Anaesthesia and Intensive
Care 23: 5; 650 1995.
2. Noble WH, St-Amand J. Amniotic Fluid embolism [review] Can J of Anaesthesia
40(10):971-980 1993.
3. Brown MA Pregnancy induced hypertension: pathogenesis and management Aust
NZ J Med 1991 21:257-273.
4. Caplan PA. et al. Unexpected Cardiac arrest during spinal anesthesia: A closed
claims analysis of predisposing factors Anesthesiology 68:5-11, 1988.
5. DePace NL, et al; 'Post-mortem' Caesarean Section with recovery of both mother
and offspring JAMA 1982 248: 971-973.
6. Weber CE Post-mortem caesarean section: Review of the literature and case
reports Am J Obst Gyn 1971 110: 2; 158-165
7. Strong TH, Lowe RA. Peri-mortem Caesarean Section Am J of Emergency
Medicine 7: 5: 489-494 Sept 1989.
8. Sutherland SK, Duncan AW, et al 'Death from snake bite associated with the
supine hypotensive syndrome of pregnancy' Med J Aust 1982 2: 238-239.
John Crowhurst
Persistent neurological deficit is arguably one of the greatest fears of the regional
anaesthetist. Athough post-anaesthesia neurological deficit or persistent blockade is
not uncommon, permanent neurological sequelae are rare (1) (Chapter 103).
Detailed statistics on neurological complications are not available for contemporary
practice but in the literature are many individual case reports, closed
medical-insurance claim reviews and other reports which provide some hints as to
the incidence of such sequelae.
Unfortunately, the attitude of many anesthesiologists continues to be swayed by
anecdotal reports of the complications of regional blockade. This clouds their
decision-making with regard to their choice of technique. A good example is the
Woolley and Roe case in the United Kingdom (2) after which spinal anaesthesia fell
into disfavour in that country for almost a generation. It is to be hoped that in the
future evaluation of techniques and drugs will be more scientific, unbiased and
evidence-based (1).
In obstetric practice, neurological symptoms are usually reported by a nurse or
surgical colleague some hours or days after the procedure. This is unfortunate
because successful resolution of some neurological complications requires urgent
treatment (eg. spinal epidural haematoma and abscess; meningitis; compressive and
ischaemic neuropraxias).
Almost invariably, obstetricians, midwives and patients assume that the block is the
cause of the symptoms although this is rarely the case.
A: INITIAL ENQUIRIES.
1 . THE PATIENT:
A detailed neurological history should be obtained and any conditions pre-disposing
to neuropathy should be viewed with suspicion. These conditions include:
backache,
obesity,
disc disease,
local or systemic infection,
coagulopathy,
diabetes mellitus,
neurofibromatosis,
malignancy,
previous trauma.
Pregnancy and labour (particularly prolonged active second stage, abnormal posture
and instrumental delivery) can, by themselves, produce nerve trauma (5) and
backache (Chapter 84).
A comprehensive drug history (particularly with regard to the use of salicylates,
NSAIDs, anti-coagulants, B12, anti-thyroid medications, hypoglycaemic agents,
steroids and anti-metabolites) should be taken (Chapter 34).
A complete physical and neurological examination should be carried out without delay
and the details carefully recorded. Because the interpretation of many neurological
signs is subjective, it may be necessary for a second clinician to re-examine the
patient.
2. THE LABOUR AND MODE OF DELIVERY:
Factors which have been implicated in the aetiology of nerve damage include:
mode of delivery;
posture during labour;
use of retractors or diathermy;
injections of local anaesthetic or vasopressors by the obstetrician;
major blood loss and other causes of hypotension (which may cause spinal cord
ischaemia) (6) (Chapter 6).
It may be necessary to ascertain details of patient positioning or equipment usage
from staff who were present in the operating or delivery room.
3. THE ANAESTHESIA:
Critically review the anaesthetic technique with particular reference to:
type of block (Chapter 70),
degree of technical difficulty (Chapter 105),
possibility of inadvertent dural puncture (Chapter 31),
distribution and severity of paraesthesiae at the time of insertion of block,
occurrence of a 'bloody' tap,
type, baricity and concentration of anaesthetic (eg. chloroprocaine) (Chapter 106),
additives to the anaesthetic (eg. adrenaline, clonidine, preservatives),
other drug usage (eg. sodium nitroprusside, diazoxide),
equipment usage (eg. continuous micro-catheter spinal),
details asepsis/antisepsis precautions taken (7),
possibility of incorrect drug usage,
experience of the operator,
difficulty with removal of the catheter (Chapter 75),
integrity of the removed catheter or spinal needle tip (Chapter 42), and
site of injection (eg. epidural above L2 - L3).
Spinal cord injury has been caused by lumbar puncture performed above L2-3
(Figure 16.1). Check the needle or catheter insertion site for signs of infection or
other inflammation. The possibility that unsterile equipment has been used should be
considered and needles and catheters from the same batch should be checked
(microbiologically if thought appropriate).
Retained segments of fractured catheters may cause nerve irritation and damage
(Chapter 104).
If parasthesiae or bleeding were noticed during the procedure, their significance
should be evaluated in the context of the injury being investigated. The distribution of
a parasthesia is most important when evaluating a neurological injury later on.
Many blocks are induced and/or maintained with mixtures of drugs and adjuvants
prepared in the delivery room or at the bedside. Strict protocols for checking, diluting
and mixing of drugs and for rechecking of ampoules and packaging should be
adhered to (8).
If a wrong drug has been injected, its potential for causing nerve damage should be
evaluated. The cause of the mistake should be reviewed and recommendations
made to prevent its recurrence.
If infection has occurred, it should be borne in mind that many mixtures are prepared
using sterile solutions obtained from ampoules which may not be sterile on the
outside. Enquire whether:
1. drug mixing has occurred (eg opioids and adrenaline),
2. local anaesthetic contains an anti-microbial adjuvant (Chapter 5),
3. multi-dose vials have been used, or
4. solutions were drawn up using a sterile bacterial/viral filter.
The use of these filters may also reduce the potential for neurological damage
caused by foreign matter such as crystals, shards of glass or fragments of rubber.
Under some circumstances, neurotoxicty has been associated with the use of certain
local anaesthetic agents. For example, hyperbaric, concentrated (5%) lignocaine
solutions have been associated with sacral nerve root damage when administered by
slow injection through microspinal catheters (9).
Ideally, all drug mixtures should be prepared under sterile conditions in a laminar flow
facility but this is often not possible. It is appropriate to have a hospital pharmacist
review all dilution and mixing procedures before they are adopted.
Some local anaesthetics, such as etidocaine and bupivacaine, may cause prolonged
neural blockade. This cause of prolonged blockade should only be proposed after all
other possible causes have been excluded.
B. SITE AND NATURE OF THE INJURY
The anatomical site of the injury should be determined as accurately as possible in
case the location of the neurological lesion is incompatible with the site of block
placement (eg. prolapsed thoracic disc in a patient who received a lumbar epidural)
(10).
The nature of the lesion should be described in terms of:
1. type: upper or lower motor neuron,
2. loss of function or modality: complete or partial, and
3. laterality.
C. DIAGNOSIS CONFIRMATION
If nerve damage is suspected, the clinical findings should be confirmed and
documented by an appropriately-qualified colleague (neurologist, neurosurgeon).
Further investigations may be required in order to establish a firm diagnosis. These
may include magnetic resonance imaging, computed tomography and
nerve-conduction or electromyographic studies.
D. DOCUMENTATION AND FOLLOW-UP
All findings and investigations should be recorded and, ideally, reported to a central
data-base or journal. The patient and her obstetrician should be informed of the
diagnosis and of the investigation and management plan. It is prudent to contact the
medical insurer if there is any hint that litigation may follow.
It is important to remain in contact with the patient during the period of investigation
and treatment and to reassure them about anaesthesia in the future. A letter to the
patient, and the patient's primary doctor or physician with full details of the
complication, investigations, treatment and recommendations about future
anaesthesia care should follow.
References:
1. Ong BY, Cohen MM, Esmail A, et al: Parasthesia and motor dysfunction after labor
and delivery. Anesth Analg 1987 66:18-22.
2. Cope RW: The Woolley and Roe Case. Anaesthesia 1954 9:275-283.
3. Sprotte G, Schedel, Pajunk H, Pajunk H: An atraumatic needle for single-shot
regional anesthesia. Reg Anaesth 1987 10:104-108.
4. Vines G: Is there a database in the house? New Scientist 1995 145;1961;14-15.
5. Redick LF: Maternal perinatal nerve palsies. Postgrad Obstet Gynecol 1992
12:1-6.
6. Bromage PR: Spinal thrombophlebitis after hypotensive anaesthesia. NZ Med J.
1974 80:519-520.
7.Philips BJ, Fergusson S, Armstrong P, et al: Surgical face masks are effective in
reducing bacterial contamination caused by dispersal from the upper airway. Br. J.
Anaesth 1992 69:407-408.
8. Crowhurst JA, Simmons SW: Safety of Epidural Infusion Systems. Anaesth Intens
Care 1994 22:6:741-743.
9. Bensons JS: FDA Safety Alert: Cauda equina syndrome associated with
small-bore catheters in continuous spinal anesthesia. Food and Drug Administration.
Rockville, Md. May 29, 1992.
10. Mills GH, Howell SJ, Richmond MN. Spinal cord compression immediately
following, but unrelated to, epidural analgesia. Anaesthesia. 1994 Nov;49(11):954-6.
Sanjay Datta
Diabetes is one of the most common medical problems during pregnancy. It occurs
once in every 700-1,000 gestations. Regional analgesia and anesthesia are popular
and commonly used techniques for labor, delivery and cesarean section. However,
for safe administration of regional analgesia and anesthesia, a few important
pathophysiological changes associated with this disease should be mentioned.
Diabetic parturients can be classified either:
(1) according to White's classification (Table 81.1) (1), or
(2) according to the universal classification
(Type 1: insulin dependent, Type 2: non-insulin dependent).
Because White's classification is based mainly on the duration of diabetes and the
extent of organ involvement it immediately conveys to anesthesiologists the nature
and severity of the diabetic state.
Major maternal problems include:
(1) Hypertension with associated nephropathy or pre-eclampsia,
(2) Impairment of the normal hemodynamic adjustments to pregnancy due to
preclinical diabetic cardiomyopathy and subclinical autonomic neuropathy (2),
(3) Impairment of uteroplacental blood flow (UPBF) in diabetic parturients. UPBF can
be further decreased in the presence of a high blood glucose. Aggressive treatment
of maternal hypotension is very important, and,
(4) Prolonged exposure to an elevated blood sugar level leads to an increased
hemoglobin A1C (Hb A1C) in diabetic parturients (3). The correlation between Hb
A1C and Fasting Blood Sugar (FBS) is illustrated in Figure 81.1. Hb A1C is a poor
oxygen carrier and the chances of hypoxia in the fetus will increase if the maternal
diabetes is not properly controlled.
Major fetal problems include:
(1) The occurrence of severe intrauterine growth retardation (lUGR) due to
decreased placental perfusion as well as increased maternal HbA1C. These babies
may be very sensitive to reduced placental perfusion due to maternal hypotension. At
the other extreme, management of fetal macrosomia may be a real challenge (4).
Shoulder dystocia can complicate vaginal delivery and accidental extension of the
uterine incision can occur during difficult abdominal delivery. These extremes of
growth abnormality are shown in Figure 81.2. The infant on the left has severe IUGR
(470g) and the one on the right has macrosomia (5100g).
(2) Major fetal congenital anomalies may be associated with uncontrolled maternal
diabetes.
Anesthetic Management:
Labor and Delivery
Epidural analgesia for labor and delivery is associated with obvious advantages:
(1) It can indirectly increase uteroplacental blood flow by decreasing the endogenous
catecholamine concentrations,
(2) It will reduce the maternal lactic acid production, and, hence, reduce fetal
acidosis,
(3) It will provide excellent pain relief during the first, as well as the second, stage of
labor, especially during a difficult delivery, and
(4) The existing epidural catheter can be used should an emergency cesarean
section be necessary.
Cesarean Section
Although both spinal and epidural anesthesia can be used with good neonatal
outcome, epidural anesthesia may be preferable in patients with longstanding
diabetes for maintenance of cardiovascular stability. Regional anesthetic
management for cesarean section for diabetic parturients should include:
(1) acute hydration with non-dextrose solution,
(2) routine left uterine displacement,
(3) prompt treatment of hypotension with intravenous ephedrine (5).
Because there are some suggestions of abnormal hemodynamic adjustments from
associated diabetic cardiomyopathy and autonomic neuropathy in long-standing
diabetic parturients, careful volume expansion may be necessary. Epidural
anesthesia may be the preferable technique for cesarean section.
Stiff joint syndrome (diabetic scleredema) is a recognised cause of difficult intubation
and has been associated with anterior spinal artery syndrome following administration
of epidural anesthesia in a parturient with this condition (6). A rigid epidural space
associated with reduced spinal cord circulation from administration of a large volume
of local anesthetic was the postulated mechanism. Judicious use of a reduced
volume of epidural local anesthetic is indicated in these cases.
References:
1. White P. Pregnancy complicating diabetes. Am J Med 1949; 7:609-616.
2. Airaksinen KEJ, Ikaheimo MJ, Slmea PI, et al. Impaired cardiac adjustment to
pregnancy in Type I diabetes. Diabetes Care 1986; 9:376-382.
3. O'Shaughnessy R, Russ J, Zuspan FP. Glycosylated hemoglobins and diabetes
mellitus in pregnancy. Am J Ob Gyn 1979; 135:783-790.
4. Landon MB. Diabetes mellitus and other endocrine diseases. In Gabbe SG, Niebyl
JR, Simpson JL (eds): Obstetrics: normal and problem pregnancies. New York 1991,
pp. 100.
5. Datta S, Kitzmiller JL, Naulty JS, et al. Acid-base status of diabetic mothers and
their infants following spinal anesthesia for cesarean section. Anes Analg 1982;
61:662.
6. Eastwood DW. Anterior spinal artery syndrome after epidural anesthesia in a
pregnant diabetic patient with scleredema. Anes Analg 1991; 73:90-91.
Gregory Deacon
The spread of sensory blockade during spinal anaesthesia is influenced by the
following factors:
PATIENT FACTORS:
Height:
There is evidence to support the opinion that the taller the patient, the lower the
dermatome level of analgesia for a given dose of local anaesthetic (1, 2, 3, 4, 5, 40).
Vertebral column length rather than height may be more important in determining
anaesthetic spread (41).
Weight:
There is a correlation between height of blockade and the degree of obesity, A high
level of block may be anticipated in obese patients (2, 7, 8, 9, 42).
Age:
There appears to be a correlation between age and the height of spinal anaesthesia
(3, 10, 11, 43).
Cerebrospinal Fluid Volume:
In patients with a decreased volume of CSF (such as parturients, women in the 2nd
or 3rd trimester of pregnancy (44), patients with ascites or patients with large
intra-abdominal tumours), the spread of spinal anaesthetic solution is greater than
normal (4). Other CSF parameters such as pressure, protein content, chloride
concentration, pH and specific gravity, have no effect on spread (13, 15).
CONTROLLABLE FACTORS:
Solution, Density and Posture:
Hyperbaric local anaesthetic solutions spread preferentially to the dependant region if
position is maintained for at least 5 minutes after injection (3, 8, 15, 16, 17, 18, 19,
20, 21). In contrast, hypobaric solutions spread preferentially to the non-dependant
region. For example, if the patient is sitting then a hypobaric solution will spread
preferentially cephalad (Figure 30.1). Changes in position can alter spread of
analgesia for up to an hour after injection (47). (Chapter 30)
Volume, Dosage, Concentration and Temperature of Anaesthetic:
In general, the dermatomal level achieved is directly related to the volume of local
anaesthetic solution used (31, 32, 33). When using an isobaric solution, it is the
volume of the agent (rather than the posture of the patient) which is the most
important determinant of the extent of spread (41); In contrast, with hyper- and hypo-
baric solutions, posture becomes a more important factor. If volume is constant and
the dose (and, therefore, the concentration) of the anaesthetic solution is increased,
there is a marginal increase in spread (46). If the anaesthetic solution is warmed to
37 degrees C, spread is increased (48); another study does not support this
conclusion (49).
Technique of Injection:
Rapid injection of anaesthetic (0.5 to 1.0mI/sec) produces significantly greater spread
than a slower rate of injection (0.02 to 0.2ml/sec) (37). The direction of the bevel of
the needle is also a factor. Spread is greater in the direction of the bevel (37).
Barbotage has been found in one study to increase spread (50). Most other studies
have failed to demonstrate this effect (34, 38, 39).
CONCLUSION:
The most significant factors affecting spread of anaesthesia are patient height,
patient position and the baricity of the anaesthetic solution. Other factors are relevant
but are of much lesser significance.
1. Moore D.C. Reg Anesth, 1982; 7:20-25.
2. Gordh T. Reg Anesth. 1979; 4:3-8.
3. Bengtsson M. Acta Anaesthesiol Scand 1983; 27:278-283.
4. Green N.M. Anesth Analg 1985; 64:715-730.
5. Attygalle D. Anaesthesia 1985; 40:1006-1008.
7. McCulloch W Br J Anaesth 1986; 58:610-614.
8. Gray D.C. Anesthesiology 1980; 53:234.
9. Pitkanen M.T, Anesth Analg. 1987; 66:127-131.
10. Cameron A.E. Anaesthesia. 1981;36:318-322,
11. Pitkanen MT. Br J Anaesth. 1984; 56:279-284.
13. Kalso E. Br J Anaesth. 1982; 54:1179-1184.
15. Kruger D. Reg Anesth. 1983; 6:1-3.
16. Gielen M. Reg Anesth. 1984; 9:62-67.
17. Wildsmith J. Br J Anaesth. 1981; 53:273-279.
18. Brown D.T. Br J Anaesth. 1980; 52:589-595.
19. Chambers Br J Anaesth. 1981; 53:279-282
20. Moller IW. Br J Anaesth. 1984; 56:1191-1194.
21. Cummings G.C. Br J Anaesth. 1984; 56;573-79.
32. Axelsson K. Acta Anaestheslol Scand. 1982; 26:439-445.
33. Axelsson K. Br J Anaesth. 1984; 56:271-277.
34. Nightingale P.J. Anaesthesia. 1983; 38:7-9.
37. Neigh J.L. Anesth AnaIg. 1970; 49:912-920.
38. Pitkanen M. Acta Anaesthesiol Scand, 1985; 29:590-593.
39. Levin E. Anesth Analg. 1981; 60 ;810-813.
40. Huffnagle S.L Reg Anesth. 1994; 19:330-334.
41. Hartwell B.L. Reg Anesth. 1991;16:17-19.
42. Talvainen T. Br J Anaesth. 1990; 64:542-546
43. Nydahl P.A. Anesth Analg. 1991;73:780-786.
46. King H.K. Reg Anesth. 1995; 20:45-49.
47. Horlocker T.T. Anesth Analg. 1994; 773-777.
48. Callesen T. Anaesthesia. 1991; 46:17-19.
49. Kristoffersen E. Br J Anaesth. 1990; 65:504-507.
50. Janik R. Reg Anesth. 1989; 14:26-30.
Joanne Douglas
Local anaesthetics (LA) are basic drugs that bind to alpha1-acid glycoprotein and
cross the placenta by simple diffusion. At physiologic pH they are lipid soluble and
exist mainly in the unionised form, enhancing placental transfer. The amount
transferred depends on the concentration of unionised (free) drug on the maternal
and fetal sides of the placenta, which is turn is dependent on:
1. Maternal concentration:
Total dose of drug administered,
Route of administration,
Rate of absorption,
Metabolism, and
Excretion.
2. Characteristics of the drug:
pKb,
Protein binding (maternal, fetal).
3. Uteroplacental blood flow.
Maternal plasma concentration is largely influenced by the anaesthetic technique
including the use of adjuvants such as epinephrine to delay absorption.
Spinal anaesthesia requires a lower total dose of LA than does epidural anaesthesia,
resulting in less drug in the maternal circulation. Perineal infiltration and paracervical
block (Figure 46.2) often result in higher placental transfer due to rapid uptake of the
LA from these highly vascular tissues (1).
Bupivacaine is 96% protein bound, so less free drug is available for transfer than with
lidocaine (67% bound). The mean F/M ratio for bupivacaine is approximately 0.3 and
for lidocaine 0.5, confirming lidocaine's greater placental transfer. 2-Chloroprocaine is
rapidly metabolised by plasma cholinesterase and it was thought that placental
transfer was limited. However, transfer does occur (F/M = 0.92) but the levels of
unchanged 2-Chloroprocaine are low in the normal infant making it clinically
insignificant (2). Maternal and fetal pH and pKb of the LA (3) are of prime importance
in placental transfer as only the unionised (free) portion can cross the lipid
membrane. With fetal hypoxia and acidosis there is increased transfer as a greater
amount of LA is ionized in the fetus. (4) The local anaesthetic is thus "trapped" in the
fetus and cannot diffuse back to the maternal circulation. This may lead to LA toxicity
in the newborn (5).
Pharmacokinetic data relating to these local anaesthetics is shown in Table 77.1.
References:
1. Philipson EH et al. Am J Obstet Gynecol 1984;149:403
2. Kuhnert BR et al. Anesthesiology 1980;53:21
3. Brown WU et al. Anesthesiology 1975;42:698
4. Gaylard DG et al. Anesth Analg 1990;71:42
5. Morishima HO et al. Anesthesiology 1981;54:182
6. Moore DC. Anesth Analg 1981;60:833
John Doyle and Alan Sandler.
Inadvertent IV injection of Local Anaesthetics: What do I do?
INTRODUCTION
Inadvertent injection of local anaesthetics during regional anaesthesia can result in
potentially serious complications such as seizures or cardiovascular collapse. This
summary deals with the prevention, recognition and treatment of local anaesthetic
toxicity in the obstetrical and nonobstetrical settings. A number of practical points in
the use of local anaesthetics are also given (Table 36.1).
LOCAL ANAESTHETIC BLOOD LEVELS
To start with, one should understand the factors influencing local anaesthetic blood
levels (Table 36.2) and the recommended maximum doses of the various local
anaesthetic agents (Table 36.3). Four factors influence blood levels of local
anaesthetics:
1. drug dose,
2. drug type,
3. route of administration, and
4. site of administration.
Obviously, blood levels are proportional to the amount of drug given; thus, increasing
the drug dose to increase the degree of anaesthetic block also increases the risk of
local anaesthetic toxicity. The type of drug also influences blood levels in that some
drugs, such as prilocaine, are so rapidly metabolized (by plasma cholinesterase in
this instance) that high blood levels are relatively difficult to achieve (Chapter 91). Of
course, this rapid metabolism also means that the local anaesthetic block is of a
relatively short duration. Drugs injected intravenously achieve a high peak
concentration shortly after injection, while those injected into a peripheral
compartment (eg. infiltration into tissues) take a longer time to achieve a peak level
and this peak level is smaller than for the intravenous route. Finally, administration of
local anaesthetics in highly vascular areas increases the likelihood of encountering
high (sometimes toxic) drug levels.
BLOOD LEVELS AND ADMINISTRATION SITE
The following lists some sites of administration in approximate order of their
associated blood levels:
intercostal nerve blocks (highest level),
paracervical nerve blocks (Figure 46.2),
brachial plexus anaesthesia,
epidural anaesthesia.
Spinal anaesthesia, on the other hand, requires very little drug and is associated with
very low blood levels of anaesthetic.
Local Anaesthetic Toxicity (Chapter 89)
Local anaesthetic toxicity occurs in two main forms (Table 36.4):
1) toxicity to the central nervous system (CNS)
2) cardiovascular (CVS) toxicity.
CNS Toxicity
When blood levels of local anaesthetic become excessive, CNS toxicity may occur.
Classically, this is said to occur in 3 phases.
In the excitation phase the patient may complain of tinnitus, confusion, restlessness,
perioral tingling, metallic taste, lightheadedness, and/or a sense of impending doom.
This may be followed by a convulsive phase consisting of a grand mal clonic-tonic
seizure of variable duration.
The convulsions, if they occur, are later followed by CNS depression with drowsiness
or even unconsciousness. Respiratory depression and apnea may occur in extreme
cases (Table E.2).
Treatment centers around airway management and the abolition of seizures (Table
36.5). In obstetrical cases consideration should be given to immediate Cesarean
Section to save the baby (Chapter 12). An intravenous line should be established
prior to administering local anaesthesia. Seizures that do not terminate immediately
should be treated with intravenous diazepam 5 to 10 mg IV in adults (0.1 mg/kg in
children) or with sodium thiopental 50 to 150 mg IV (1 mg/kg in children). Although
many nonanaesthetists are uncomfortable using sodium thiopental, it can be
particularly useful when first line treatment (eg. diazepam) fails (Chapter 7).
Airway management is the second aspect of handling CNS toxicity from local
anaesthetics. If the seizures are not immediately abolished, or if CNS depression
results with diminished ability to protect the airway, then endotracheal intubation is
warranted. Apart from reversing the hypoxaemia, this will help protect the lung from
aspiration of gastric contents and will allow for positive pressure ventilation if
significant respiratory depression occurs.
CVS Toxicity
An even more dreaded form of toxicity to local anaesthetics is cardiovascular toxicity.
This is most frequently associated with bupivicaine overdose. In the initial phase
(excitation phase) hypertension and tachycardia may occur in conjunction with
convulsions. This is followed by a phase of cardiovascular depression with reduced
cardiac output and hypotension. Peripheral vasodilation also occurs, worsening the
hypotension (Chapter 57). This may lead to complete cardiovascular collapse with no
pulse, no blood pressure and no cardiac rhythm. Treatment (Chapter 13) is per the
American Heart Association (AHA) Advanced Cardiac Life Support (ACLS) protocol
with three exceptions:
1) bretylium is the preferred ventricular antiarrhythmic,
2) generous amounts of epinephrine should be used (2 or 3 times that in the ACLS
protocol), and
3) the resuscitation should be carried out for far longer than would be ordinarily
attempted because of the strong binding of the anaesthetic to cardiac and brainstem
tissue.
Overdose is more likely to result in cardiovascular collapse with bupivacaine than
with other agents (Table 36.6). For example, the dose needed for cardiovascular
collapse divided by the dose needed for convulsions is 3.7 for bupivacaine compared
with 7.1 for lidocaine. When bupivacaine toxicity occurs, it is more likely to result in
ventricular arrhythmias than with other agents. As indicated, these arrhythmias are
best treated with bretylium. Pregnant women appear to be more sensitive to
bupivicaine cardiac toxicity. Finally, this toxicity is enhanced by acidosis and
hypercarbia.
Hal Feldman
Local anesthetic agents are relatively safe when administered in proper dosages
(Table 36.3) at appropriate anatomical sites (Chapter 91). However, when excessive
dosages or incorrect site of administration occurs (Chapter 36), there is a potential
for severe toxic reactions. In general, the relative toxic potential of local anesthetics
parallels the agents' relative anesthetic potency (1). In others words, longer acting,
highly protein bound and lipid soluble agents appear to be more toxic than those of
lesser potency.
Several factors influence the acute systemic toxicity of local anesthetics:
1. Physico-chemical properties (2),
2. rate and route of administration of the drug (3, 4, 5),
3. blood gas and acid base balance (6, 7, 8, 9, 10, 11),
4. pre-existing medical conditions (12, 13, 14),
5. age (15, 16, 17, 18, 19), and
6. pregnancy (20, 21, 22).
Local anesthetics work by blocking impulse conduction along nerves. They have
similar action in other impulse conducting organs such as the brain and heart. The
primary target organ of local anesthetic toxicity is the central nervous system (CNS)
(2). Early signs of toxic reactions can often be detected by symptoms associated with
the CNS, such as changes in speech patterns and muscle twitching (23) (Table
36.4). More severe CNS toxicity may be displayed as seizures or coma (Table 36.6
and Table E.2).
The cardiovascular system (CVS) is generally more resistant to local anesthetic
toxicity than is the CNS (Table 57.3, Figure 57.1)(2). However, local anesthetics can
have profound effects upon the CVS. Relative potency for CVS toxicity again seems
to follow the relative anesthetic potency. More potent agents, such as bupivacaine
have been shown to be more cardiotoxic than less potent agents such as lidocaine.
There have been laboratory and clinical reports of sudden acute CVS toxicity
associated with clinically acceptable dosages, which included ventricular arrhythmias,
fibrillation and death. Difficult and prolonged resuscitation has also been reported
following intoxication (2) (Chapter 13).
The anesthetic technique should be designed to minimise the risk of accidental
over-dosage. A protocol, equipment and pharmacologic agents necessary for the
treatment of local anesthetic induced toxicity should be immediately available to the
physician (Table 36.5). Early aggressive treatment is essential and prolonged
resuscitation may be necessary (Chapter 13).
References:
1. Strichartz GK, Covino BG. Local anesthetics In: Anesthesia, Editor: Miller RD,
Churchill Livingstone, New York.
2. Feldman HS Toxicity of local anesthetic agents. In: Anesthetic Toxicity, eds. Rice
SA, Fish Y,J, Raven Press Ltd, New York 1994.
3. Scott DB. Evaluation of the toxicity of local anaesthetic agents in man. Br. J.
Anaesth. 1975; 47:56-61.
4. Arthur GR, Feldman HS, Covino BG. Comparative pharmacokinetics of
bupivacaine and ropivacaine, a new amide local anesthetic. Anesth. Analg. 1988;
67:1053-1058.
5. Munson ES, Paul WL, Embro WJ. Central nervous system toxicity of local
anesthetic mixtures in monkeys. Anesthesiology 1977; 46:179-183.
6. Englesson S, Grevsten S. The influence of acid-base changes on central nervous
system toxicity of local anesthetic agents II. Acta Anesth Scand 1974; 18:88-103.
7. deJong RH, Wagman TH, Prince DA. Effect of carbon dioxide on the cortical
seizure threshold to lidocaine. Exp. Neurol. 1967; 17:221-232.
8. Munson ES, Wagman IH. Acid-base changes during Lidocaine induced seizures in
Macaca mulatta. Arch Neurol 1969; 20:406-412.
9. Rosen MA, Thigpen IW, Shnider SM, Foutz SE, Levinson G, Koike M.
Bupivacaine-induced cardiotoxicity in hypoxic and acidotic sheep. Anesth. Analg.
1985; 1089-1096
10. Heavner E, Dryden CF, Sanghani V, Huemer G, Bessire A, Bagwell YM. Severe
hypoxia enhances central nervous system and cardiovascular toxicity of bupivacaine
in lightly anaesthetised pigs. Anesthesiology 1992; 77: 142-147.
11. Sage DJ, Feldman HS, Arthur GR, et al. Influence of lidocaine and bupivacaine
on isolated guinea pig atria in the presence of acidosis and hypoxia. Anesth Analg
1984; 63: 1-7.
12. Long JH, Oppenheimer MJ, Wester MR, Durant TM. The effect of intravenous
procaine on the heart. Anesthesiology 1949; 10; 406-415.
13. Gould DB, Aldrete JA. Bupivacaine cardiotoxicity in a patient with renal failure.
Acta Anaesth Scand 1983; 27:18-21
14. Gupta PK, Lichstein E, Chadda KD. Lidocaine-induced heart block in patients
with bundle branch block. Am. J. Cardiol. 1974; 33:487-492
15. Morishima HO, Pedersen H, Finster M, et al. Toxicity of lidocaine in adult,
newborn, and fetal sheep. Anesthesiology 1981; 55:57-61.
16. Badgwell JM, Heavner JE, Kytta J. Bupivacaine toxicity in young pigs is age
dependent and is affected by volatile anesthetics. Anesthesiology 1990; 73:297-303.
17. Liu PL, Covino BM, Feldman HS. Effect of age on local anesthetic central
nervous system toxicity in mice. Reg Anesth 1983; 8:57-60.
18. McIlvaine WB, Knox RF, Fennessey PV, Goldstein M. Continuous infusion of
bupivacaine via intrapleural catheter for analgesia after thoracotomy in children.
Anesthesiology 1988; 69:261-264.
19. McCloskey JJ, Haun SE, Deshpande JK. Bupivacaine toxicity secondary to
continuous caudal epidural infusion in children. Anesth. Analg. 1992; 75:287-290.
20. Morishima HO, Pedersen H, Finster M, et al. Bupivacaine toxicity in pregnant and
non-pregnant ewes. Anesthesiology 1985; 63: 134-139.
21. Santos AC, Arthur GR, Pedersen H, Morishima HO, Finster M, Covino BG,
Systemic toxicity of ropivacaine during ovine pregnancy. Anesthesiology 1991;
75:137-141.
22. Santos AC, Pedersen H, Harmon TW, et al. Does pregnancy alter the systemic
toxicity of local anesthetics? Anesthesiology 1989; 70:991-995.
23. Scott DB. Toxic effects of local anaesthetic agents on the central nervous
system. Br. J. Anaesth. 1986; 58:732-735.
Brendan Finucane
Hemodynamic effects of parenterally administered local anaesthetics:
Lidocaine is one of the few local anaesthetics approved for parenteral use. It is a very
effective anti-arrhythmic agent (Vaughan Williams Class 1B) (Table E.1). In patients
with normal cardiac outputs, it has negligible effects on hemodynamics when injected
intravenously in low dosage (<1.5 mg/kg) (1).
Accidental intravascular injection of local anaesthetics occurs occasionally in the
course of regional anaesthesia and can cause hemodynamic changes (Chapter 36).
The magnitude of these changes depends upon the potency of the local anaesthetic
injected and also upon a number of factors, such as:
1. site and speed of injection,
2. mass of local anaesthetic,
3. cardiac output,
4. Arterial PCO2,
5. acid-base status, and
6. patient-related factors (2).
Convulsant doses of lidocaine occur usually when plasma levels exceed 10 mcg/ml,
(Table E.2). Serious hemodynamic changes do not occur until plasma levels far
exceed these values (3). (Table 57.3) Supraconvulsant doses of lidocaine alter
cardiac conductivity, automaticity and contractility leading to cardiovascular collapse,
profound bradycardia and sinus arrest (2).
Bupivacaine, when injected intravascularly, causes serious cardiac arrhythmias
(Table 36.6). Parturients may be more susceptible to these cardiotoxic effects (4).
Ropivacaine is a new, long acting, amide local anaesthetic currently undergoing
clinical investigation (Chapter 4). Studies to date indicate that it is
pharmacodynamically similar to bupivacaine but is less cardiotoxic (5, 6).
Hemodynamic effects of epidurally administered local anaesthetics:
Hemodynamic changes induced by epidural injection of local anaesthetics depend
upon a number of factors including:
1. the extent of sympathetic blockade,
2. the site of blockade,
3. absorption of local anaesthetics,
4. the addition or absence of epinephrine, and
5. patient-related factors (7).
Obstetric patients are somewhat unique in their hemodynamic response to epidural
anaesthesia. The large uterine mass interferes with venous drainage from the lower
extremities causing engorgement of vertebral vessels in the epidural space.
Therefore, a given injection of local anaesthetics into the epidural space will spread
further and uptake of local anaesthetics into the circulation is more rapid. However,
when one compares hemodynamic changes induced by epidural anaesthesia in
pregnancy with those in the non-pregnant state the effects are far greater in
pregnancy (8).
In late pregnancy, the uterus is extremely vascular and is a huge repository for
venous blood. Furthermore, epidural anaesthesia impairs the homeostatic responses
which would normally occur during aortocaval compression by the enlarged uterus
(Figure 28.1) (Chapter 28). Finally, pooling of blood in the lower extremities,
enhanced by uterine contractions, may add to this impairment of venous return. The
key to the prevention of most of these problems is patient positioning (Figure 28.2)
and intravenous fluid loading. Vasopressors may also be necessary. Patients should
be nursed on the left side with slight elevation of the lower extremities.
Rapid uptake of epinephrine containing local anaesthetics adds further to
hemodynamic changes (Table 57.4).
References:
1. Covino BG Epidural Anesthesia and Analgesia. Grune & Stratton Inc. 1985
2. Covino BG. Local Anesthetics. Grune & Stratton. 1976
3. Liu PL. Anesth Analg 62:375,1983
4. Albright GA Cardiac arrest following regional anesthesia with etidocaine or
bupivacaine Anesthesiology 1979 51:4:285-287
5. Feldman HS. Anesth Analg 1989; 69:794
6. Scott DB Anesth Analg 1989;69:563
7. Bromage PR Epidural Anaesthesia. WB Saunders & Co Philadelphia. 1978
8. Assali NS J Clin Invest 1950;29:1354
David Gambling
Epidural PCA (often known as PCEA ) has been investigated as a means of
1. optimizing epidural analgesia during labor, using dilute combinations of local
anesthetic and lipid soluble opioids, and
2. improving postoperative pain relief following cesarean delivery.
PCEA in Labor.
Many studies have indicated that use of a background infusion for PCEA during labor
is not necessary for most women (1, 2, 3, 4, 5, 6, 7). Indeed, it has been
demonstrated that bolus-only PCEA is very effective without a background infusion
and is superior, in some aspects, to a continuous epidural infusion or intermittent
top-up injections. To date, only one study has suggested that a background infusion
would be beneficial with PCEA during labor because a reduced need for
supplemental analgesia was demonstrated (8). However, in the original study
comparing PCEA with or without a background infusion, Paech (Chapter 60) found
no benefit from the addition of a background infusion (9). Many clinicians start PCEA
without a background infusion because dose-sparing is associated with a reduction in
local anesthetic and opioid side-effects. A reasonable approach to dosing with PCEA
is to use 0.125% bupivacaine with 2mcg/ml fentanyl. Satisfactory analgesia can be
achieved using a 4 ml bolus dose and a lockout interval of 15 minutes.
Epidural PCA after cesarean birth.
The first study of PCEA following cesarean birth, by Parker and White, described it
as a safe, effective alternative to intravenous PCA with less opioid use and more
rapid recovery (10). In a follow-up study, the same investigators found that the
efficacy of PCEA was not improved by adding a background infusion (11). In fact, a
basal infusion of hydromorphone and dilute bupivacaine resulted in leg weakness
and a higher incidence of postoperative nausea and pruritus. The use of a 10 ml per
hour background infusion of buprenorphine and bupivacaine with PCEA probably
contributed to difficulty in ambulation in 43% of patients in another study of
post-cesarean analgesia (12). Other studies have confirmed that PCEA without a
background infusion can provide adequate analgesia after cesarean birth, using
either fentanyl (13) or meperidine (14).
In summary, most studies have indicated that a background infusion is not required
for PCEA. The addition of a background infusion introduces a form of drug delivery
that is physician-controlled (not patient-controlled). This defeats the purpose of the
PCA concept, which acknowledges that it is the patient who knows how much pain is
tolerable and conversely how much analgesia is adequate.
It was felt by some that a background infusion for night-time use would overcome the
problem of patients sleeping and being unable to keep up with dosing requirements.
This is not as big an issue in obstetrics because 1. during labor the parturient is often
woken regularly for vital signs and other evaluations, and 2. after cesarean delivery a
mother is often disturbed to feed her newborn or by routine vital sign measurements.
In both cases she will have ample opportunity to self-administer a PCA bolus as
required.
References:
1. Gambling DR, McMorland GH, Yu P, Laszlo C. Comparison of patient controlled
epidural analgesia and conventional intermittent "top-up" injections during labor.
Anesth Analg 1990; 70: 256-261.
2. Ferrante FM, Lu L, Jamison SB, Datta S. Patient-controlled epidural analgesia:
Demand dosing. Anesth Analg 1991; 73: 547-552.
3. Purdie J, Reid J, Thorburn J, Asbury AJ. Continuous extradural analgesia:
Comparison of midwife top-ups, continuous infusions and patient-controlled
administration. Br J Anaesth 1992; 68: 580-584.
4. Gambling DR, Huber CL Berkowitz J et al. Patient-controlled epidural analgesia in
labour: Varying bolus dose and lockout interval. Can J Anaesth 1993; 40: 211-217.
5. Paech ML Patient-controlled epidural analgesia during labor: Choice of solution. Int
J Obstet Anesth 1993; 2: 65-71.
6. Tan S, Reid J, Thorburn J. Extradural analgesia in labour: complications of three
techniques of administration. Br J Anaesth 1994; 73: 619-6
7. Curry PD, Pacsoo C, Heap DG. Patient-controlled epidural analgesia in obstetric
anaesthetic practice. Pain 1994; 57: 125-128.
8. Ferrante FM, Rosinia FA, Gordon C, Datta S. The role of continuous background
infusions in patient-controlled epidural analgesia for labor and delivery. Anesth Analg
1994; 79: 80-84.
9. Paech M. Patient-controlled epidural analgesia in labour - is a continuous infusion
of benefit? Anaesth Intens Care 1992; 20: 15-20.
10. Parker RK, White PF. Epidural patient-controlled analgesia: An alternative to
intravenous patient-controlled analgesia for pain relief after cesarean delivery. Anesth
Analg 1992; 75: 245-251.
11. Parker ILK, Sawaki Y, White PF. Epidural patient-controlled analgesia: Influence
of bupivacaine and hydromorphone basal infusion on pain control after cesarean
delivery. Anesth Analg 1992; 75: 740-746.
12. Cohen S; Amar D; Pantuck CB; Pantuck EJ; Goodman EJ; Widroff JS; Kanas
RJ; Brady JA Adverse effects of epidural 0.03% bupivacaine during analgesia after
cesarean section. Anesth Analg 1992; 75: 753-756
13. Yu P, Gambling DR A comparative study of patient-controlled epidural fentanyl
and single dose epidural morphine for post-cesarean section analgesia. Can J
Anaesth 1993; 40: 416-419.
14. Yarnell RW, Polis T, Reid GN et al Patient-controlled analgesia with epidural
meperidine after elective cesarean section. Reg Anesth 1992; 17: 329-333.
Stephen Gatt
Epidural blood patch (EBP) is used to treat refractory post-dural puncture headache
(PDPH). Alternatives to EBP are discussed in Chapter 85.
Who should be treated?
A mother has received a 'wet tap' epidural or subarachnoid injection, and who has a
headache which:
1. is sufficiently incapacitating as to interfere with her ability to care for her baby,
2. has the characteristics of a PDPH, and
3. has not been relieved by 2-3 days of conservative management (bed rest in the
supine position, hydration, caffeine or caffeine-containing drinks, oral simple
analgesics, non-steroidal anti-inflammatory agents),
and who also has:
4. no neurological symptoms* arising from the index lumbar puncture
5. no active neurological disease (13) (Chapter 96),
6. no infection Iocalised to the lumbar area or septicaemia,
7. no coagulopathy (13).
* (This requirement may be waived if the headache or nuchal pain is very severe and
associated with protracted vomiting or if there is evidence of auditory nerve (hearing
loss) or abducens nerve (diplopia preceded by headache) stretching (14) .)
Why use the technique?
EBP has an extremely high success rate of close to 100% when placed in the
epidural space at the same level as the initial needle puncture (1, 7, 8). The blood
patch works as a gelatinous glue which prevents CSF leakage and allows the dural
hole to heal (2). Blood may also be forced through the dural puncture forming a plug
(9). The immediate relief from PDPH may be due to an increase in CSF pressure.
When should EBP be used?
Preferably, 48-72hrs after the puncture which caused the PDPH (when success rate
is 91-100%) (1, 7, 8, 13). If performed at the time of inadvertent dural puncture, or
through an epidural catheter placed at this time, the success rate is dismal and is no
different to doing nothing at all (3). If EBP is attempted at <24hr the success rate is
reported to be as low as 29% but it may reduce the occurrence rate of PDPH (4, 10).
How should EBP be performed?
Prepare the patient by:
1. Explaining the technique, hazards and anticipated success rate.
2. Obtaining consent for the procedure (Chapter 55).
3. Pre-medicating if necessary.
4. Starting an intravenous infusion of crystalloid.
5. Positioning in the left lateral, fully-flexed position.
The EBP is, preferably, a two-operator technique.
Both operators should scrub, gown and glove as is standard in the particular
institution.
Operator 1.
1. Cleans and drapes the patient's back using a standard epidural kit and technique,
2. Identifies the site of original puncture and locates the epidural space using a
standard technique (Figure E.3).
Operator 2.
1. At the same time as operator 1 is prepping the back, the second operator cleans
and drapes the antecubital area of (usually) the left (downside) arm. A second
epidural/spinal kit and drapes containing a 20cc glass syringe with 22G sterile
straight or butterfly needle is ideal for the task.
2. Once the epidural space is located by operator 1, the second operator, using a
rigidly aseptic technique, performs a venepuncture, withdraws 22ml of blood,
removes the needle from the syringe, hands the syringe to the first operator (without
breaching the integrity of the sterile fields) and applies pressure and a sterile
dressing to the venepuncture site.
How should the blood should be injected?
1. Inject the blood slowly until either, the patient complains of tightness in the
buttocks, lower back or thighs (usually when 12 to 15ml are injected) (11) or, until 20
ml is injected.
2. Withdraw the needle, apply a sterile dressing and turn the patient to the supine
position.
3. Inject the residual blood through a fresh, sterile needle into a blood culture bottle
and send to bacteriology for culture and antibiotic sensitivity.
How should the patient be managed subsequently?
1. Place a pillow under the mother's knees.
2. Nurse her supine for four hours.
What advice should be given to the patient?
Advise her;
1. not to carry anything heavier than the baby for 2-3 weeks,
2. to squat rather than bend when picking items in a low position,
3. to avoid excessive straining,
- all of which can cause 'patch blow-out' with return of the PDPH.
4. To report pyrexia, back or radicular pain, return of PDPH or other untoward
symptoms immediately.
The patient can, in the majority of cases, expect almost instantaneous relief from the
PDPH. In some, the relief comes on gradually over a 24hr period. Following the EBP
some will experience mild backache for a few days (5). Less than 2% will also have
mild, transient paraesthesiae, neck pain or radicular pain (6, 12). The EBP should not
cause obliteration of the epidural space, infection, cauda equina syndrome or
adhesive arachnoiditis.
References:
1. Ostheimer GW: Headache in the Postpartum Period in Clinical Management of
Mother and Newborn (Eds. Marx GF), Springer-Verlag, New York, p.27-41, 1979.
2. DiGiovanni A J, Galbert MW, Wahle WM: Epidural Injection of Autologous Blood
for Postlumbar-puncture Headache. Anesth Analg 51:226-232, 1972.
3. Palahnuik R J, Cumming M: Prophylactic Blood Patch Does Not Prevent
Postlumbar Puncture Headache. Can Anaesth Soc J 26:132-133, 1979.
4. Looser EA, Hill GE, Bennett GM, et al: Time Versus Success Rate for Epidural
Blood Patch. Anesthesiol 49:147-148, 1978.
5. Abouleish E, de la Vega S, Blendinger L, et al: Long-term Follow-up Epidural
Blood Patch. Anesth Analg 54:459-463, 1975.
6. Ostheimer GW, Palahnuik RJ, Shnider SM. Epidural Blood Patch for Post-Lumbar
Puncture Headache. Anesthesiol 41:307-308, 1974.
7. Glass PM, Kennedy WF: Headache following Subarachnoid Puncture: Treatment
with Epidural Blood Patch. JAMA 219:203-204, 1972.
8. Crawford JS: Experience with Epidural Blood Patch. Anaes 35:513, 1980.
9.Rosenberg PH, Heavner JE: An In-Vitro Study of the Effect of Epidural Blood Patch
on Leakage through a Dural Puncture. Anesth Analg 64:501, 1985.
10. Colonna-Romano P, Shapiro BE: Unintentional Dural Puncture and Prophylactic
Epidural Blood Patch in Obstetrics. Anesth Analg 69:522, 1989.
11. Szeinfeld M, Ihmeidan IH, Moser MM, et al: Epidural Blood Patch: Evaluation of
the Volume and Spread of Blood Injected into the Epidural Space. Anesthesiol
64:820, 1986.
12. Carrie LES: Postdural Puncture Headache and Extradural Blood Patch. Anaes
71:179, 1993.
13. Ostheimer GW: Prophylactic Epidural Blood Patch. Reg Anes Oct-Dec, 17-19,
1979.
14. Hayman IR, Wood PM: Abducens Nerve Paralysis following Spinal Anaesthesia.
Ann Surg 115:864, 1942.
Stephen Gatt
Epidural blockade is achieved by the introduction of local anaesthetic solution into the
epidural space (outside the dura) to produce diminished or absent perception of pain
with a variable degree of (or no) motor paralysis. Uterine contractions continue, but
the parturient is not aware of them.
Attempts have been made to use this form of analgesia in obstetrics since the
beginning of this century, but continuous epidural anaesthesia was only introduced by
Curbello in 1949.
While the commonest indication for epidural block is the relief of labour pain, there
are many other reasons for placing 'an epidural'.
These indications include:
1. Maternal distress caused by painful uterine contractions not adequately relieved by
simpler forms of analgesia (pethidine (demerol), nitrous oxide);
2. Caesarean section. In many centres, the majority of Caesarean sections are
performed under epidural or combined spinal-epidural (CSE) anaesthesia (Figure
73.1);
3. Provision of anaesthesia for instrumental delivery;
4. Treatment of pregnancy-induced and -associated hypertension (PIH). Epidural
anaesthesia not only reduces the amount of sedation required but also lowers the
arterial blood pressure. Once the blood pressure is controlled, the likelihood of
eclampsia becomes more remote;
5. Provision of analgesia for repairs to birth canal tears, eg. episiotomy;
6. Breech delivery where the presence of an epidural in situ gives the obstetrician
increased flexibility to intervene expeditiously should the need suddenly arise, eg. to
apply forceps to the difficult-to-deliver aftercoming head (Figure 14.1);
7. Multiple delivery where anaesthesia (or, at least, superior analgesia) may be
required urgently to deliver the second (and subsequent) infants, eg. for version of
the second twin;
8. Cardiac disease or pulmonary hypertension where the epidural will attenuate the
increase in cardiac output, mean arterial pressure and cardiac work which occurs
during labour.
9. Restoration of coordinate uterine activity when the endocrine response to stress
and pain has induced abnormal uterine activity.
Natural Childbirth
Stephen Gatt
In 'Natural' or 'Prepared' childbirth the emphasis is on securing delivery without the
need for drugs using a combination of techniques which may include:
1. reduction of fear and anxiety by thorough education in the processes of
childbearing;
2. promotion of the concept that childbirth can be a drug-free, pleasurable experience
('psychoprophylaxis') (2, 7);
3. a variety of postures for labour, eg. leaning over a bean bag, intermittent
ambulation, rocking;
4. conditioning exercises to strengthen back and abdominal muscles and relax pelvic
joints;
5. a pleasurable, quiet and (sometimes) dimly-lit environment with soothing music (4);
6. psychological exercises and conditioned reflexes;
7. breathing control and mental exercises that focus on the breathing pattern;
8. hot packs, gentle massage and warm showers; and
9. a supportive partner who acts as a 'coach'.
Education and psychological preparation of women for labour often results in a
valuable reduction in the pain scores and the reaction to pain experienced by them
(6) (Figure 58.1). These parturients are less apprehensive and more cooperative (5).
The antenatal classes offer a good opportunity to educate mothers about the
alternative pharmacological and regional analgesia techniques available.
Only about 10-20% of women do not require some form of pain relief. Since many
mothers will not be able to carry on in labour without assistance and will require some
additional pain relief, it is most important that these parturients should not feel
frustration at having failed. In an obstetric unit where regional analgesia is available
but not actively promoted and where the bulk of these alternative techniques are
available to mothers in labour, experience has shown that the epidural rate over the
last twenty years has been stable at over 40% (Figure 64.1). Painless labour should
never be promised to any mother who undertakes to study and practise a method of
psychological preparation for labour (1).
References:
1. Gatt SP and Lacy L Analgesia and anaesthesia in obstetrics.
In: Handbook of Obstetrics and Gynaecology. (Leader L, Bennett M, Wong F, Eds)
4th ed. Chapter 8, Chapman and Hall Medical. In press, Mar 1996.
2. Brownridge P, Wood M. Soothing the pain of childbirth. Flinders Media, Flinders
Medical Centre. 1992
4. Chantigian R. Non-Pharmacological methods for pain relief in obstetrics. In: Clinics
in Anesthesiology - Obstetric analgesia and anesthesia. Ostheimer GW Editor. WB
Saunders, Philadelphia, 197-207 1986
5. Climie CR and Gatt SP. Analgesia and Anaesthesia in obstetric practice. In:
Handbook of obstetrics and gynaecology. (Wren BG, Lobo RA, Eds) 3rd ed. , ch 8,
Chapman and Hall medical pp 189-206. 1987
6. Melzack R, Taenzer P, et al Labour is still painful after prepared childbirth training.
Can Med Ass J 125:357-363 1981
7. Bonica J. Principles and practice of obstetric analgesia and anesthesia. Principles
and practice of obstetric analgesia and anesthesia. (Bonica J Ed) FA Davis
Philadelphia. pp 764-820 1967
Stephen Gatt
Complete relief of labour pain is not easily accomplished in all parturients because of
the large number of variables that need to be controlled. The severity and quality of
pain and its perception (Figure 58.1) depends on a combination of many factors
which include the:
1. severity and duration of pain and its associated hormonal stress response
(Chapter 33);
2. various methods of pain relief which are available to the patient;
3. quality and extent of coaching and education at antenatal classes (5);
4. personality of the mother and support persons;
5. cultural and ethnic background of the mother (1);
6. extent, nature and effectiveness of support offered to the mother by the partner
and her attendants; and
7. degree and duration of fear, anxiety, fatigue, dehydration and nausea associated
with the labour (1, 5).
The non-pharmacological methods of pain relief in labour include:
1. Prepared childbirth (Chapter 64);
2. Hypnosis;
3. Acupuncture;
4. Transcutaneous Electrical Nerve Stimulation (TENS)
Hypnosis:
Hypnosis is a state of altered consciousness in which, during a period of profound
concentration, acutely enhanced responsiveness to suggestions occurs. Reduced
awareness of the pain of labour is possible in this trance-like state. Unfortunately, the
technique is most successful when a great deal of individual rapport with a particular
hypnotist over many sessions has been established. Hypnosis requires considerable,
time-consuming antepartum coaching. 15% of patients cannot be hypnotised. Even in
those who can be hypnotised, the results have not been impressive.
Acupuncture:
Gate control and enkephalin-production theory have been applied to acupuncture but
do not fully explain how it relieves pain in labour. Why subcutaneous insertion (and
vibration, electrical stimulation or heating) of needles along 'energy pathways'
(meridians) or at points of high A-beta (gate-closing) fibre concentration relieves pain
is poorly understood. Acupuncture has not achieved widespread use because the
acupuncture points for vaginal delivery pain have not been established. The pain
relief obtained, without the additional use of significant doses of narcotics, is usually
poor and inconsistent. The acupuncture needles also limit the parturient's mobility.
Acupuncture is not suitable for rapid delivery (4).
Transcutaneous Electrical Nerve Stimulation (TENS):
Cutaneous application of electrical current can relieve pain. The mechanism by which
this is achieved may be similar to that pertaining to acupuncture, i.e. release of
endorphins or closure of the pain gate by A-beta stimulation. For relief of labour pain
TENS is of limited value with, at best, a 44% patient acceptance and satisfaction rate
(2). The electrodes over the dermatomes of T10 - L1 (1st stage stimulation) (9) and
over the sacrum (late 1st and 2nd stage) transmit a 40-150Hz stimulus of 1-40 mA
(1). TENS seems to be most useful when it is started in early labour and then mostly
to relieve pain in the early first stage (1).
References:
1. Gatt SP and Lacy L Analgesia and anaesthesia in obstetrics. In: Handbook of
Obstetrics and Gynaecology. (Leader L, Bennett M, Wong F, Eds) 4th ed. Chapter 8,
Chapman and Hall Medical. In press, Mar 1996
2. Brownridge P, Wood M. Soothing the pain of childbirth. Flinders Media, Flinders
Medical Centre. 1992
3. Lamaze F. Painless Childbirth - Psychoprophylactic methods. Pocket Book 1972
4. Chantigian R. Non-Pharmacological methods for pain relief in obstetrics. In: Clinics
in Anesthesiology - Obstetric analgesia and anesthesia. Ostheimer GW Editor. WB
Saunders, Philadelphia, 197-207 1986
In: Handbook of Obstetrics and Gynaecology. (Leader L, Bennett M, Wong F, Eds)
4th ed. Chapter 8, Chapman and Hall Medical. In press, Mar 1996.
5. Climie CR and Gatt SP. Analgesia and Anaesthesia in obstetric practice. In:
Handbook of obstetrics and gynaecology. (Wren BG, Lobo RA, Eds) 3rd ed. , ch 8,
Chapman and Hall medical pp 189-206. 1987
9. Augustinsson L, Bohlin P, Bundsen P. Pain Relief during delivery by
transcutaneous nerve stimulation. Pain 4:59-65, 1977
Stephen Gatt
Pharmacological Management of Severe Postpartum Haemorrhage (PPH) in the
presence of Regional Block for Post-delivery Analgesia.
In the early postpartum period, the unwary may attribute unexplained hypotension to
sympathetic block (from neuraxial blockade) rather than to bleeding. The important
causes of PPH are outlined in Table 74.1. Once a diagnosis of PPH has been made,
the patient must be rapidly assessed (Table 74.2) and volume replacement and other
resuscitative measures must be initiated in earnest (Table 74.3).
A number of drugs are available to limit the degree of bleeding. The most common
cause of PPH is uterine atony and the most important agents which can enhance
uterine contraction and increase uterine tone or reinitiate contractions are:
1. Oxytocin, eg. Synthetic oxytocin (Syntocinon) administered as a 5 to 10
International Units (IU) bolus slowly IVI followed by an infusion of 10 to 20 IU (some
recommend doses as high as 50 IU) syntocinon in 1000 mL 4% dextrose in 1/5N
Saline or an isotonic electrolyte solution at 250 mL/hr. Occasionally, the
vasodilatation produced by a bolus of syntocinon can produce profound hypotension
and reflex tachycardia (1, 2, 3, 4, 12).
2. Prostaglandin, eg. 15-methyl analogue of prostaglandin (PG) F2-alpha
(Prostinfenem) 0.25 mg IV in 500 ml 5% dextrose. PG E2-alpha (Prostin E2-alpha)
can be used by intrauterine irrigation, rectal suppositories or vaginal pessaries or gel.
PG F2-alpha (Prostin F2-alpha, 1 to 5 mg.) should be used intramyometrially
because of its extensive multisystem effects. Prostinfenem (250 to 500 mcg) can also
be used by this route. Systemic prostaglandins can cause pulmonary oedema,
hypotension or hypertension and should be avoided in those with hypertensive heart
disease or severe pre-eclampsia. Bronchospasm is also not uncommon so that its
use in asthmatics is contraindicated (5, 6, 7, 8, 9, 14).
3. Ergot, eg. Methylergobasin (Ergometrine) 1 to 2 mg. slowly IV or,
methylergonovine (Ergonovine) up to 0.2 mg. very slowly IVI or 0.2 to 0.3 mg. IMI.
Ergometrine (4 to 6 mg.) can also be injected directly into uterine muscle.
Ergometrine can produce peripheral vasoconstriction and further compromise organ
perfusion (eg. myocardial ischaemia can occur) (2, 3, 13).
More rarely, PPH is due to a coagulopathy. In selected cases the following
pharmacological agents may be useful: 1. Desmopressin acetate (DDAVP) in those
with a platelet function abnormality (10). 2. Epsilon aminocaproic acid (EACA,
Amicar) in those with disseminated intravascular coagulation.
References:
1. Rose J, Morris M, Meis P: Hemorrhage in Newborn Lambs: Effects on Arterial
Blood Pressure, ACTH, Cortisol and Vasopressin. Am J Physiol 240:585-590, 1981.
2. Pedron N, Mondragon H, Marcushamer B, et al: Estimates of Postpartum
Bleeding. Contraception 35:4:339-345, 1987.
3. Biehl D: The Anesthetic Management of Obstetrical Hemorrhage. Intl Anesthesiol
Clinics 28:1:52-57, 1986.
4. Prendiville W, Elbourne D, Chalmers I: The Effects of Routine Oxytocic
Administration in the Management of the Third Stage of Labour: An Overview of the
Evidence from Controlled Trials. Br J Obstet Gynaecol 95:3-16,1988.
5. Cruikshank S: Management of Postpartum and Pelvic Hemorrhage. Clin Obstet &
Gynecol 29:2:213-219, 1986.
6. Peyser R, Kupferminc M: Management of Severe Postpartum Hemorrhage by
Intrauterine Irrigation with Prostaglandin E2. Am J Ob Gyn 162:3:694-696, 1990.
7. Oleen M, Mariano J: Controlling Refractory Atonic Postpartum Hemorrhage with
Hemabate Sterile Solution. Am J Ob Gyn 162:1:205-208, 1990.
8. Granstrom L, Ekman G, Ulmsten U: Intravenous Infusion of 15
methyl-prostaglandin F2alpha (Prostinfenem) in Women with Heavy Post-partum
Hemorrhage. Acta Obstet Gynecol Scand 68:365-367, 1989.
9. Herbert N, Cefalo R: Management of Postpartum Hemorrhage. Clin Obstet
Gynecol 27:1:139-147, 1984.
10. Schindler M, Gatt S, Isert P, et al: Thrombocytopenia and Platelet Functional
Defects ln Pre-eclampsia: Implications for Regional Aneesthesia. Anaes & Int Care
18:2:169-174, 1990.
11. Beaudoin M, Gatt S: Disseminated Intravascular Coagulation In: Common
Problems in Obstetric Anesthesia (Eds. Datta S, Ostheimer G), Year Book Medical
Publications, Chicago, 21:348-361, 1986.
12. Hendricks CH, Brenner WE: Cardiovascular Effects of Oxytocic Drugs used
Postpartum. Am J Ob Gyn, 108:751-759,1970.
13. Browning DJ: Serious Side-effects of Ergometrine and its Use in Routine
Obstetric Practice. MJA 1:157-159, 19
14. Brenner WE: The Place of Prostaglandins in Modern Obstetrics. In: Risks in the
Practice of Modern Obstetrics (Editor: Aladjen E), Mosby, St Louis, p.211-244, 1975.
Stephen Gatt
In most instances, removing an epidural catheter should be easy. This should be
done (at least initially) in the lateral decubitus position (5). Sometimes, resistance is
encountered during removal of the catheter. This can be due to the catheter
becoming locked either in the vertebral spaces (in the posterior joints, the processes
or the arches) or in the ligamentum flavum (Figure E.2) or due to knotting, kinking or
curling of the catheter (1, 2, 3, 10, 11). Catheter knotting occurs very rarely (about
0.0015% of epidurals) (12).
When the catheter cannot be removed using minimal traction a number of
manoeuvres may facilitate removal of the catheter. These include:
1. maximal flexion of the back (and, more rarely, extension of the back) with the
patient in the lateral decubitus position,
2. rotation of the spine,
3. returning the patient to the position she was in at the time of insertion (eg. the
sitting position with legs extended),
4. allowing tissues to soften before another attempt is made,
5. placing the patient in the sitting position with the legs extended or the kneeling
position with hands down and back flexed,
6. filling the catheter with a rapid injection of saline to increase the turgor of the
catheter and to lubricate it,
7. placing the patient prone on a Wilson (Zimmer) convex or the "Sydney Harbour
Bridge" laminectomy frame,
8. complete relaxation using general anaesthesia with muscle relaxant, and 9.
surgical removal. (4, 5 , 6, 7, 8, 9.)
Undue force during tugging should not be used because this will cause the catheter
to stretch and tear. The tensile strength of most epidural catheters is about 1.7 Kg (8)
(Table 42.1). It may be preferable to measure the tension being applied during these
difficult extractions by using an electronic scale. Lengthening of the catheter is a sign
that further traction is not advisable (Chapter 42).
References:
1. Yoshada H, Yokoyama K. Difficult Removal of Epidural Catheter -Report of a
Case. Masui 27:314,1978.
2. Tio T, MacMurdo S, McKenzie R. Mishap with an Epidural Catheter.
Anesthesiology 50:260-262, 1979.
3. Browne R, Politi V. Knotting of an Epidural Catheter: a Case Report. Can Anaes
Soc J 26:142, 1979.
4. Sia-Kho E, Kudlak T. How to Dislodge a Severely Trapped Epidural Catheter.
Anesth Analg 74:929, 1992.
5. Blackshear R, Gravenstein N, Rodson E. Tension applied to Lumbar Epidural
Catheters during Removal is much Greater with Patient Sitting versus Lying.
Anesthesiology 75:A833, 1991.
6. Gadalla F. Removal of a Tenacious Epidural Catheter. Anesth Analg
75:1071-1072, 1992.
7. Pasquariello C, Betz R. A Case for the Removal of the Retained Intrathecal
Catheter. Anesth Analg 72:562, 1991.
8. Gravenstein N, Blackshear R, Wissler R. An approach to spinal or epidural
catheters that are difficult to remove. Anesthesiology 75:544, 1991.
9. Start R, Greenberg D, Herman N. Use of a Wilson Convex Frame in Removing
"Irretrievable" Epidural Catheters. Anesth Analg 75:305-6, 1992.
10. Saberski L, Schwartz J, Greenhouse B, et al. A Unique Complication of a Lumbar
Epidural Catheter. Anesthesiology 69:634-5, 1988.
11. Fibuch E, McNitt J, Cussen T. Knotting of the 'Teracath' after an Uneventful
Epidural Insertion for Cesarean Delivery. Anesthesiology 73:1293, 1990.
12. McGregor P. A Reply - Knotting. Anesthesiology 73:1293, 1990.
Stephen Gatt
General Properties of Ropivacaine:
Ropivacaine is a 'long acting' (1, 2) amido-amine local anaesthetic which, because it
has mild local vasoconstrictive properties, does not require the addition of adrenaline
(3, 4). At low concentration, it produces sensory analgesia without profound motor
blockade because of its diminished (dose-related) effect on motor fibres (A-fibres) (5,
6, 7) (Chapter 88).
Ropivacaine is enantiomerically homogeneous and is more than 99% pure S-(-)
enantiomer (unlike bupivacaine, which is a racemate). Its lipid solubility lies
somwhere between that of lignocaine and bupivacaine (8). It is highly plasma protein
binding (94%)(9). The duration of action and onset time (5) are similar to those of
bupivacaine. The drug has no affinity for histaminic, serotoninic, alpha- or
beta-adrenergic or muscarinic receptors. It is rapidly cleared from plasma and is
extensively metabolised by cytochrome P450 to PPX, 3'-OH Ropivacaine and 4'-OH
Ropivacaine (10). It has a greater margin of safety (higher therapeutic ratio) than
bupivacaine.
Advantages of Ropivacaine over Existing Local Anaesthetic Agents:
Reduced CNS Toxicity:
Local anaesthetics produce their effects by blocking excitable membranes (Chapter
53). Inadvertent intravascular injection or massive systemic absorption will, as the
blood level rises progressively, alter these membranes' functions (mainly in the CNS
and CVS) (Chapter 36). Convulsions are due to removal of inhibition of central neural
structures, probably by alterations to the GABA receptor complex (11). At higher
doses, blockage of the sodium channels produces the depressant effects (and the
cardiovascular toxicity) (11) (Chapter 95).
Ropivacaine produces less of the mild CNS effects (lightheadedness, tinnitus, tongue
numbness) (12) (Table E.2) and is less likely to cause convulsions than bupivacaine.
If convulsions occur, they are of shorter duration than those of bupivacaine (Table
36.4) and, provided that treatment starts immediately, resuscitation is almost always
effective (Table 36.5). This is not always the case with bupivacaine overdosage
(Chapter 12) .
Ropivacaine toxicity from overdosage does not seem to be worsened by pregnancy
(unlike bupivacaine) so that the convulsive dose is the same in the pregnant and the
non-pregnant female (13, 14).
Reduced CVS Toxicity:
At high dose, ropivacaine is less cardiodepressant than bupivacaine (15). For
example, bolus injection of twice the convulsive dose of ropivacaine (16) produces
fewer ventricular dysrhythmias and deaths than bupivacaine (Figure 57.1). As is the
case for treatment of convulsions, severe systemic toxicity produced by
administration of large doses of ropivacaine is easier to treat than that induced by
overdosage with bupivacaine.
Malignant ventricular dysrhythmias which are common following bupivacaine
intoxication are rare in ropivacaine overdosage. Indeed, the dysrhythmia dose
threshold is (approximately) bupivacaine 3.4: ropivacaine 1.7 : lignocaine 1.0
(Chapter 37).
Epidural adrenaline is unnecessary:
Ropivacaine at lower concentrations (unlike bupivacaine) seems to have a mild
vasoconstrictive effect. The addition of adrenaline to ropivacaine is not necessary
and does not seem to markedly reduce (3, 4) peak plasma levels (Table 113.4).
Effects on the Neonate:
While this is not as yet certain, neonates born to mothers receiving ropivacaine seem
to have a higher neurological and adaptive score (NACS) than those having epidural
bupivacaine (1, 5, 17, 18) (Table 35.2).
Clinical Use:
Clinical experience in using the drug is reported in Chapter 116.
References:
1. Gatt S. Ropivacaine and other Local Anaesthetics in the 20th Century and
Beyond. Proceedings of the Combined ANZCA/ASA Continuing Education Seminars,
New Drugs- New Techniques - New Challenges, in press, 1995.
2. Feldman H, Covino B. Comparative Motor-blocking Effects of Bupivacaine and
Ropivacaine, a New Amino Amide Local Anesthetic, in the rat and dog. Anesth &
Analg 67:1047,1988.
3. Arthur G, Feldman H, Covino B. Comparative Pharmacokinetics of Bupivacaine
and Ropivacaine, a New Amide Local Anesthetic. Anesth & Analg 67:1053, 1988.
4. Cederholm I, Evers H, Lofstrom J. Skin Blood Flow after Intradermal Injection of
Ropivacaine in Various Concentrations with and without Epinephrine Evaluated by
Laser Doppler Flowmetry. Reg Anesth 17:322,1992.
5. Gatt S, Crooke D, Anderson A, Lockley S. Pain Relief and Sensory and Motor
Block in Mothers receiving Epidural Ropivacaine 0.25% and Bupivacaine 0.25% for
Analgesia in Labour - a Double Blind, Parallel, Randomised Comparison of Efficacy.
Acta Anaesth Scand, in press, 1995.
6. Kopacz D, Emanuelsson B, Thompson G, Carpenter R, Stephenson C.
Pharmacokinetics of Ropivacaine and Bupivacaine for Bilateral Intercostal Blockade
in Healthy Male Volunteers. Anesthesiology 81:1139, 1994.
7. Zaric D, Axelson K, Philipson L, Nydahl P, Larsson P, Jansson J, Leissner P.
Blockade of the Abdominal Muscles Measured by EMG during Lumbar Epidural
Analgesia with Ropivacaine - a Double Blind Study. Acta Anaesth Scand 37,1993.
8. Rosenberg P, Kytta J, Alila A. Absorption of Bupivacaine, Etidocaine, Lignocaine
and Ropivacaine into n-Heptane, Rat Sciatic Nerve and Human Extradural and
Subdural Fat. BJA 58:310, 1986.
9. Lee A, Fagan D, Lamont M, Tucker G, Halldin M, Scott D. Disposition Kinetics of
Ropivacaine in Humans. Anesth & Analg 69:736, 1989.
10. Oda Y, Furuichi K, Tanaka K, Hiroi T, Imaoka S, Asada A, Fujimori M, Funae Y.
Metabolism of a New Local Anesthetic, Ropivacaine, by Human Hepatic Cytochrome
P450. Anesthesiology 82:214, 1995.
11. McCaughey W. Adverse Effects of Local Anaesthetics. Drug Safety 7:178, 1992.
12. Scott D, Lee A, Fagan D, Bowler G, Bloomfield P, Lundh R. Acute Toxiclty of
Ropivacaine Compared with that of Bupivacaine. Anesth & Analg 69:563, 1989.
13. Morishima H, Pedersen H, Finster M, Hiraoka H, Tsuji A, Feldman H, Arthur R,
Covino B. Bupivacaine Toxicity in Pregnant and Non-pregnant Ewes. Anesthesiology
63:134, 1985.
14. Santos A, Pedersen H, Moroshima H, Finster M, Arthur G. Pharmacokinetics of
Ropivacaine in Nonpregnant and Pregnant Ewes. Anesthesiology 69:A432, 1988.
19. Santos AC; Arthur GR; Pedersen H; Morishima HO; Finster M; Covino BG
Systemic toxicity of ropivacaine during ovine pregnancy. Anesthesiology 1991
Jul;75(1):137-41
15. Kerkkamp H, Gielen M. Cardiovascular Effects of Epidural Local Anaesthetics.
Comparison of 0.75% bupivacaine and 0.75% ropivacaine, both with adrenaline.
Anaesthesia 46:361-5, 1991.
16. Rutten A, Nancarrow C, Mather L, Illsley A, Runciman W, Upton R.
Hemodynamic and Central Nervous System Effects of Intravenous Bolus Doses of
Lidocaine, Bupivacaine and Ropivacaine in Sheep. Anesth & Analg 69:291,1989.
17. Gatt S, Crooke D, Lockley S, Anderson A, Armstrong P, Alley L. A Double Blind,
Randomised, Parallel Investigation into the Neurobehavioural Status and Outcome of
Infants Born Vaginally to Mothers Receiving Epidural Ropivacaine 0.25% and
Bupivacaine 0.25% for Analgesia in Labour. Anaes Int Care, in press, 1995.
18. Stienstra R, Jonker T, Bourdrez P, Kuijpers J, vanKleef J, Lundberg U.
Ropivacaine 0.25% versus Bupivacaine 0.25% for Continuous Epidural Analgesia in
Labor: a Double Blind Comparison. Anesth & Analg 80:285, 1995.
Stephen Gatt
The problem of how best to manage the broken spinal or epidural catheter, while
uncommon, remains an area of utmost concern to the practising obstetric
anaesthetist.
Causes:
There are a number of reasons why a catheter may tear. These include:
1. the use of undue force in removing a catheter which is trapped between the
vertebral spinous processes or is knotted in the epidural space (Chapter 75);
2. shearing of the catheter by the needle when attempts are made to withdraw the
catheter through the Tuohy needle;
3. nicking of the catheter by a barb on the bevel of the needle;
4. shredding of the catheter if the needle is advanced over the catheter after the
catheter has been placed ;
5. weakness of the catheter produced by imperfections in manufacture; or
6. damage to a catheter occurring after placement (eg. fraying by pinching between
two vertebral processes) (1, 3, 7, 8, 9).
Diagnosis:
Radio-opaque epidural catheters are easier to locate radiologically than
non-radio-opaque ones but, paradoxically, they have a lower tensile strength than
standard clear catheters (Chapter 42). It makes little sense to use a catheter which is
more liable to fracture on the grounds that the broken segment can be more easily
located after the incident! In fact, even a radio-opaque fragment may be impossible to
locate radiologically because the surrounding structures are radio-dense.
Another drawback of some radio-opaque catheters is the problem of diagnosing
inadvertent intravascular or dural puncture because it is more difficult to visualise
CSF or blood through an opaque catheter.
Ultrasonographic Iocalisation of torn catheters is singularly unrewarding but
xeroradiography, computerised tomography (CT) scanning or magnetic resonance
imaging (MRI) may prove more fruitful.
Successful Iocalisation of the catheter segment by medical imaging is no guarantee
that the task of finding the missing segment at subsequent surgery will be made any
easier.
Prevention:
1. The force required to remove a catheter should be minimal. If resistance is
encountered, a number of simple manoeuvres have been described to enable
removal of the catheter without stretching or tearing (Chapter 75).
2. Needles should be checked for barbs on the bevel and the catheter for
manufacturing defects before insertion.
3. No more than about 5cm of catheter should be advanced into the epidural space to
reduce the risk of kinking, curling up or knotting (2).
4. Catheters should never be withdrawn through the metal needle.
5. Catheters of high breaking strain (tensile strength) (Table 42.1) and of a sufficient
diameter (eg. 16 or 18G epidural) should be obtained from a reputable, reliable
manufacturer.
Management:
Epidural catheters are inert and should not produce a foreign body reaction. In most
cases, segments of catheter are best left alone because surgical removal can
produce more harm than good (5). Foreign bodies in the epidural space are not likely
to migrate (although this is not impossible).
There are three situations where a policy of non-interference and reassurance does
not apply:
1. where infection or symptoms supervene,
2. if the spinal catheter fragment is sitting partially intrathecally and is acting as a wick
which allows persistent CSF leakage (6), or
3. if the proximal end of the segment is known to be located very close to the skin
such that it can be retrieved simply through a superficial incision (7).
In the majority of situations the mother can be managed expectantly and reviewed
periodically to ensure that there is no discomfort, infection or radiculopathy.
Conclusion: The best intentions and the exercise of utmost care can still result in
tearing of the catheter. In only in a small proportion of cases is it prudent to attempt
to remove the offending retained portion of catheter.
References:
1. Moerman N, Porcelijn T, Deen L. A Broken Epidural Catheter. Reg Anesthesie
(Springer-Verlag) 3:17-18, 1980.
2. Dawkins M. An Analysis of the Complications of Extradural and Caudal Block.
Anaesthesia 24:554. 1969.
3. Tio T, Macmurdo S, McKenzie R. Mishap with an Epidural Catheter. Anesthesiolgy
50:3:260-262. 1979.
4. Herrera M, Hsia T, Becker T. Migration of Teflon Mesh from Abdominal Wall into
Large Bowel. NY State J Med 76:452. 1976.
5. DeVera H, Ries M. Complications of Continuous Spinal Microcatheters: Should
We Seek Their Removal if Sheared? Anesthesiol 74:794, 1991.
6. Pasquariello C, Betz R. A Case for the Removal of the Retained Intrathecal
Catheter. Anesth. Analg 72:562, 1991.
7. DeArmendi A, Ryan J, Chang H, et al. Retained Caudal Catheter in a Paediatric
Patient. Paed Anaes 2:325-327, 1992.
8. Chun L, Karp M. Unusual Complications from Placement of Catheters in the
Caudal Canal in Obstetrical Anesthesia. Anesthesiol 36:71-72, 1968.
9. Simpson P. Defective Epidural Cannulae. Anaes 36:72, 1981.
Uterine relaxation
Stephen Gatt
Uterine relaxation in the parturient with a major block in situ.
Indications for Uterine Relaxation:
Uterine relaxation may be required if there is:
1. an obstruction to an after-coming shoulders or head during assisted breech
delivery (Figure 14.1),
2. a placenta retained within the uterus which needs to be removed manually,
3. a uterine constriction ring which has to be relieved,
4. a transverse-lying second twin who needs to be operatively delivered, and
5. an inverted uterus that requires correction.
Techniques Available:
If adequate analgesia in the form of epidural or other major regional block
(subarachnoid, caudal, combined-spinal-epidural) is already present and uterine
relaxation is required, this can be achieved using:
1. minibolus intravenous nitroglycerine (GTN/NTG), (Chapter 52).
2. inhalational agent (eg. isoflurane, enflurane, halothane) (1),
3. beta-adrenergic agonists (salbutamol, ritodrine, terbutaline), or
4. amyl nitrate.
Precautions:
a.Hypovolaemia
1. The parturient must be euvolaemic before the GTN or the inhalational agent is
administered.
2. If there is significant blood loss or hypovolaemia this should be treated
aggressively with colloid or crystalloid as appropriate before uterine relaxation is
undertaken.
3. While hypotension is uncommon in euvolaemic patients, if it ensues, the blood
pressure fall should be treated aggressively with volume expansion and pressor
agent (eg. incremental doses of ephedrine 3mg/ml) as appropriate.
b. Loss of laryngeal protective reflexes
1.Inhalational agents must be titrated carefully to effect without rendering the mother
unconscious.
2. Care must be exercised where other agents (narcotics, tranquillisers, ketamine,
N20), which may obtund pharyngo-laryngeal reflexes, are already in use. In these
situations, manoeuvres aimed at securing the airway (eg. rapid sequence induction
and intubation) may need to take precedence over the uterine relaxation.
c. Heart Disease
In patients with severe valvular heart disease or cardiomyopathy the use of minibolus
GTN, tocolytic beta-agonist or inhalational agent may be deleterious and the
therapeutic benefit must be weighed against the potential risk (2).
d.Monitoring
1. Maternal systemic arterial pressure should be monitored frequently or
continuously.
2. Maternal electrocardiogram and/or Sa02 (oximetry) should be displayed
continuously when appropriate.
3. If the uterine relaxation is required antepartum, fetal heart rate monitoring may be
necessary.
References:
1. Marx G, Kim Y, Lin C, Halvey S, Schulman H. Postpartum Uterine Pressures
under Halothane or Enflurane Anesthesia. Obstet Gynecol 51:695, 1978.
2. Benedetti T. Maternal Complications of Parenteral Beta-sympathomimetic Therapy
for Premature Labor. Am J Ob Gyn 145:1-6, 1983.
Stephen Gatt
A Treatment Protocol for Uterine Relaxation in the Parturient who already has a
Regional Block:
In the patient who is already receiving analgesia in labour or who is having a
caesarean section under regional anaesthesia, uterine relaxation may be required for
a variety of reasons. Sometimes, the need may arise suddenly (eg. difficulty
encountered during delivery of an aftercoming head in assisted breech delivery).
Pharmacological agents which can render uterine muscle quiescent and, in higher
concentrations, paralysed and flaccid, include:
Inhalationed General Anaesthetics:
halothane (1, 2, 3, 4, 5, 6),
methoxyflurane (5),
enflurane (2, 5, 6),
isoflurane (2),
sevoflurane (8),
desflurane,
Nitrates:
(intravenous) nitroglycerine (GTN/NTG),
(inhaled) amyl nitrate,
Beta adrenergic agents:
(intravenous) ritodrine,
(intravenous) salbutamol,
(intravenous) terbutaline.
Indications for these regimens:
Situations where uterine relaxation may be necessary in the parturient with an
epidural block in the peridelivery period include:
1. manual removal of a retained placenta,
2. breech delivery: obstructed aftercoming head or shoulders,
3. multiple pregnancy: second twin in transverse-lie,
4. inadvertent oxytocic overdose prior to delivery,
5. uterine constriction ring,
6. inverted uterus, and
7. (some cases of) fetal distress.
My preferred technique for use in conjunction with regional analgesia is IV
nitroglycerine and I attempt to produce adequate uterine muscle relaxation without
the need for general anaesthesia.
Drug Dosage:
Presentation: Use the 50mgs in 10mls (5mg/ml) ampoule of glyceryl trinitrate.
Final dosage required for bolus injection: 50 micrograms/ml.
Dilution:
1. Dilute 1 ampoule (50mgs) in a 1000ml (1 Litre) bag of N/Saline or 5% Dextrose to
produce a solution of GTN 50 mcg/ml.
2. Withdraw 10mls into a 10cc syringe and label it: 'GTN 50mcg/ml'.
[Do not forget to discard the 1000ml bag containing the remaining GTN.]
Treatment:
1. Preload the patient with Hartmann's solution (compound sodium lactate) or colloid
as appropriate until the patient is euvolaemic.
2. Into a free-flowing IV, inject 1 ml (50mcg) of the diluted (50 mcg/ml) GTN solution.
3. Titrate the injection to effect at intervals of a minute or so, up to a maximum of 10
doses (500 mcg).
An alternative dosage regimen is contained in Table 14.7.
Management of Side Effects:
1. Hypotension is uncommon in euvolaemic patients and can be treated either with
increments of ephedrine 3mg intravenously and/or volume replacement.
2. The effect of this dose of GTN on uterine, cervical and vaginal muscle is very
transient, and any persisting loss of uterine muscle tone can be reversed with
oxytocics (syntocinon +/- ergometrine).
Monitoring:
1. Repeated blood pressure monitoring.
2. Continuous fetal heart monitoring and maternal ECG or oximetry (where
appropriate).
Contraindications:
1. Significant blood loss.
2. (Some cases of) valvular heart disease.
Effect:
With GTN, uterine relaxation should be achievable in 75 to 90 seconds and is
maintained for less than 10 minutes (without the need for general anaesthesia).
References:
1. Miller J, Stoelting V, Stander R, et al: In vitro and in vivo Responses of the Uterus
to Halothane Anesthesia, Anesth Analg 45:583-589, 1966.
2. Munson E, Embro W: Enflurane, Isoflurane and Halothane and Isolated Uterine
Muscle. Anesthesiol 46:1:11-14, 1977.
3. Naftalin N, McKay D, Phear W, et al: The Effects of Halothane on Pregnant and
Non-pregnant Human Myometrium. Anesthesiol 46:1:15-19, 1977.
4. Crawford JS: The Place of Halothane in Obstetrics. BJA 34:386-390, 1962.
5. Paull J, Ziccone S: Halothane, Enflurane, Methoxyflurane, and Isolated Human
Uterine Muscle. Anaesth Int Cr 8:4:397-401, 1980.
6. Marx G, Kim Y, Lin C, et al: Postpartum Uterine Pressures Under Halothane or
Enflurane Anesthesia. Obstet Gynecol 51:695, 1978.
7. Gatt S. Intravenous Nitroglycerine (GTN/NTG) for Utero-relaxation. Protocol 77,
Department of Anaesthesia & Acute Care, Royal Hospital for Women, August 1994.
8. Gambling D, Sharma S, White P, et al. Use of sevoflurane during elective
cesarean birth: A comparison with isoflurane and spinal anesthesia. Anesth Analg
81:90-95, 1995.
Lenore George
Peri-partum Cardiomyopathy (PPCM) is a relatively rare disease estimated to occur
in 1 in 3000- 4000 pregnancies (1). Criteria for diagnosis include:
1. Development of cardiac failure in the last trimester of pregnancy or within five
months of delivery,
2. absence of a determinable aetiology for the cardiac failure, and
3. absence of demonstrable heart disease prior to the last month of pregnancy (2).
The diagnosis therefore, is largely one of exclusion as the disease has no
pathognomic features (3, 4). The aetiology of PPCM remains poorly understood with
theories generally centred upon viral infection triggering autoimmune mechanisms in
susceptible individuals (1, 2, 4).
Considerations for regional anaesthesia in these patients are similar to those with
other causes of heart failure. With regard to anaesthesia for caesarean section,
general anaesthetic techniques involve either cardiodepressant drugs such as
thiopentone and the inhalational anaesthetic agents, or high dose narcotic
techniques, which, while they maintain haemodynamic stability, may necessitate
post-operative ventilation for both mother and infant. Further considerations with
narcotic techniques are the less well defined endpoint at induction of anaesthesia,
which may increase the risk of aspiration of gastric contents in this susceptible
population. The management of a failed intubation may also be complicated by the
longer acting nature of these drugs and the difficulty with mask ventilation that may
occur.
Epidural anaesthesia offers several advantages in addition to avoiding these
problems. Anaesthesia may be induced in a gradual and controlled manner and if a
pulmonary artery catheter is used to guide fluid and inotrope requirements, minimal
change in haemodynamic parameters can be achieved. Small bolus doses or an
incremental infusion of bupivacaine 0.5% with fentanyl 4-5 mcg/ml is suitable for
these purposes. In addition, major neuraxial blockade may actually improve
myocardial performance by reducing the afterload on the left ventricle without
impairing contractility, although not all authors agree (6).
References:
1. Veille JC. Periparturn Cardiomyopathy - A Review. Am J Obstet Gynecol 148;
805-818, 1984.
2. Demakis JG Rahimtoolas SH. Peripartum Cardiomyopathy. Circulation 44;
964-968, 1971.
3. Demakis JG. Rahimtoolas SH. Sutton GS et al Natural Course of Peripartum
Cardiomyopathy. Circulation 44; 1053-1061, 1971.
4. Julian DG, Szekely P. Peripartum Cardiomyopathy Progress in Cardiovasc.
Diseases 27; 223-240, 1985.
5. Sanderson JE, Olsen EGJ. Gatei D. Peripartum Heart Disease: An
Endomyocardial Biopsy Study. Br. Heart J. 56; 285-91, 1986.
6. Brown G, O'Leary M, Douglas I, Herkes R Perioperative Management of a Case of
Severe Peripartum Cardiomyopathy. Anaesth. Intens. Care 20; 80-83, 1992.
7. Hutchinson RC, Ross AW, Severe Peripartum Cardiomyopathy. Anaes. Int. Care.
20; 398 (correspondence) 1992.
8. Scott JR, Wagoner LE, Olsen S. Pregnancy in Heart Transplant Recipients.
Management and Outcome. Obstet & Gynecol. 82; 324-327, 1993.
9. Hughes R, Kapur P, Sutton GC, et al A case of fatal Peripartum Cardiomyopathy.
Br Heart Jn. 32; 272-276, 1970.
10. Homans DC. Current Concepts. Peripartum Cardiomyopathy NEJM 312;
1432-1437, 1985.
11. Wesley L, Cotton DB. Peripartum Cardiomyopathy: Current Concepts and Clinical
Management. Clinical Obstets Gynecol. 20; 54-67, 1989.
Mathieu Gielen
The incidence of post-dural puncture headache (PDPH) after the use of a standard
spinal needle (Quincke) is, firstly, dependent on the size of the needle. In young
female patients the mean incidence of PDPH, calculated from different studies, is
around 15% when using a 25G needle and around 5% when using a 26G needle.
Hurley et al reported a significant reduction in PDPH from 6.3% to 2.5% using a 27G
needle instead of a 26G one in obstetric patients (1). The incidence can be further
reduced by puncturing the dura parallel to the dural fibers and at a small angle (2, 3)
(Chapter 97).
New spinal needles with special tip design (all modifications of the original pencil
point Hart and Whitacre needle (4)) have lowered the incidence of post-dural
puncture headache (PDPH) to an acceptable level. Figure E.1. shows some of the
currently-available needle tip designs.
In 1987 Sprotte et al. introduced the 'atraumatic' spinal needle (a modified pencil
point needle) and reported that the incidence of PDPH could be reduced to less than
1% (5). Although more authors reported the very low incidence of PDPH using the
Sprotte needle, a higher failure rate was reported and related to the dimensions and
placement of the sideport of this needle (6). The modern Whitacre needles, with a
smaller sideport closer to the tip, are superior to the Sprotte needle and their use has
reduced the incidence of significant PDPH to less than 1% (7).
A modern Whitacre 25G needle is easy to handle, results in few failures and is highly
recommended in obstetric patients.
References:
1. Hurley RJ, Hertwig LM, Lambert DH. Incidence of PDPH in the obstetric patient:
25G Whitacre vs 26 and 27G Quincke tip needles. Regional Anesthesia 1992; 17:35
Supplement.
2. Gielen MJM. Postdural puncture headache (PDPH): a review. Regional Anesthesia
1989;14:101-106.
3. Gielen MJM. How to prevent postdural puncture headache. International Monitor
on Regional Anesthesia 1994;6;2-7.
4. Hart JR, Whitacre RG. Pencil-point needle in prevention of postspinal headache.
JAMA 1951;147:657-58.
5.Sprotte G, Schedel R, Pajunk H. An atraumatic needle for single shot regional
anaesthesia. Regional Anaesthesie 1987;10:104-108.
6. Crone LL, Vogel W. Failed spinal anaesthesia with the Sprotte needle.
7.Halpern S, Preston R. Postdural puncture headache and spinal needle design.
Meta-analyses. Anesthesiology 1994;81:1376-83.
Recent references on this topic include:
Krommendijk EJ, Verheijen R, van Dijk B, Spoelder EM, Gielen MJ, de Lange JJ.
The PENCAN 25-gauge needle: a new pencil-point needle for spinal anesthesia
tested in 1,193 patients. Reg Anesth Pain Med. 1999 Jan-Feb;24(1):43-50.
Genevieve Goulding
A continuing dilemma for obstetric anaesthetists is the difficulty in obtaining informed
consent for epidural analgesia from the labouring parturient. The patient, often very
distressed with pain and possibly under the influence of narcotic or other analgesia,
may not be receptive to detailed discussions of the technique and its attendant risks.
Obstetric patients often have unrealistic expectations of the birth experience - a
healthy baby, a healthy mother, a natural birth without intervention, complete control
and active participation are the anticipated outcomes. Anything less than this may be
perceived as a failure by them or the providers of their obstetric care. The patients'
knowledge of the analgesic techniques available to them as obtained by ante-natal
education varies greatly and may be influenced by educator bias, the womens' media
and the patients' own cultural and personal characteristics.
A recent (1) study of patients receiving epidurals during labour showed that patients
who attended antenatal epidural information classes had statistically significantly
better recall of epidural risk information than those who did not attend, although
overall recall of information was poor. The risks of the epidural had been outlined in a
short, but detailed, discussion prior to insertion of the block. The authors
recommended that:
1. women attend antenatal epidural information classes,
2. informed consent for epidural analgesia be obtained antenatally whenever
possible, and
3. details of the informed consent explanation be recorded in the patients notes.
The legal requirements for informed consent vary greatly between and within
countries. It would generally be agreed, however, that the notion of informed consent
implies that it is a doctor's duty of care to disclose the material risks inherent in a
procedure.
In Australian law (Rogers v Whitaker) a risk is defined as a material risk if
1. in the circumstances of the particular case, a reasonable person in the patient's
position, if warned of the risk, is likely to attach significance to it, or
2. the medical practitioner is aware that the particular patient, if warned of the risk, is
likely to attach significance to it.
It should be noted that the patient's signature on a consent form is not proof that the
duty of disclosure has been fulfilled.
Information regarding epidurals can be provided in a number of ways during the
antenatal period:
1. leaflets (2) in antenatal clinics and obstetricians' offices,
2. lectures at ante-natal classes, and
3. video presentations showing the practical aspects of the procedure.
The information should be available in a number of languages if required.
Staff who are capable of answering the pregnant woman's questions appropriately
and discussing the side-effects and risks of regional techniques should become
actively involved in this education process.
At the time of insertion of the block, the minimum information that should be recorded
on the epidural record is:
1. the nature of any antenatal epidural information received - brochure / video / class;
2. whether specific risks were mentioned or discussed;
3. clear documentation of the procedure and any difficulties or complications.
(A tick-box system can facilitate this)
Ideally, a post-delivery visit should be made by a departmental member prior to the
patient being discharged from hospital.
Suggestions for the content of a fact-sheet for epidural analgesia are outlined in
Chapter 56.
References:
1. Swan HB, Borshoff DC. Informed Consent - Recall of Risk Information Following
Epidural Analgesia in Labour. Anaesth Intens Care 1994; 22: 139-141
2. Pamphlet Planning Your Childbirth (Anesthesia & You series) American Society of
Anesthesiologists
Genevieve Goulding
The following points should be considered when designing a fact sheet to be given to
a woman contemplating regional analgesia for labour and delivery.
The following information should be covered in clear and simple language:
1. A brief description of the anatomy.
2. A simple explanation of what will happen:
- intravenous infusion
- posture during placement of block
- approximate duration of procedure
- approximate time until it starts to work
- need for fetal monitoring
3. An explanation of commonly used terms (catheter, test-dose, top-up)
4. Common 'benign' side-effects:
- shivering
- heaviness or tingling in the legs
- urinary retention
5. Common more serious side-effects:
- hypotension - the importance of avoiding aorto-caval compression (Chapter 28)
- back pain (1, 2) (Chapter 84)
6. Possible effects on the labour (Chapter 102):
- first stage (duration / contractions / fetus)
- second stage (duration / assisted delivery / episiotomy rate)
7. Possible technical difficulties:
- with the insertion
- unequal, patchy or failed blocks (Chapter 94)
8. Rare but potentially serious complications:
- dural tap and post dural puncture headache (Chapter 97)
- intravascular injection (Chapter 36)
- high block (Chapter 8)
- neurological damage (Chapter 112)
It is also worth mentioning that:
1. there may be other medical or therapeutic indications for epidural blockade apart
from the provision of analgesia. For example, regional anaesthesia may be required
for delivery of a second twin, or management of breech, forceps or occipito-posterior
vertex delivery, pre-eclampsia or other maternal diseases, induction of labour or
caesarean section. Post-delivery indications such as retained placenta or the suture
of tears can also be included;
2. there may be contraindications to an epidural ( sepsis, coagulopathy);
3. epidural analgesia and anaesthesia is a common procedure with a high margin of
safety and patient satisfaction. Epidurals are only inserted by specialist anaesthetists
or specialists-in-training.
Of course, any discussion of risk should be balanced by a mention of the benefits of
epidural analgesia for both the mother and fetus.
References:
1. Macarthur A, Macarthur C, Weeks S. Epidural Anaesthesia and Low Back Pain
after Delivery: a prospective cohort study. BMJ 1995; 311 : 1336 - 9
2. Macarthur A, Macarthur C, Weeks S. Is epidural anesthesia in labor associated
with chronic low back pain? A prospective cohort study. Anesth Analg. 1997
Nov;85(5):1066-70.
Genevieve Goulding
Ropivacaine was first used at the Royal Hospital for women (RHW) in 1992 as part of
a worldwide double-blind trial comparing bupivacaine 0.25% and ropivacaine 0.25%
for analgesia for labour and vaginal delivery.
In general, all participating centres found bupivacaine and ropivacaine to be equally
effective and without significant adverse neonatal or maternal effects. Time to onset
of pain relief, duration of analgesia between top-ups, pain scores, quality of
analgesia, extent and duration of sensory block and delivery outcome were similar
(Chapter 4).
In some centres, patients receiving ropivacaine were noted to have less motor block
however this difference was statistically significant only in the RHW group. Writer
(1)
performed a meta-analysis of data from all centres involved in the trial and reported
significant results for ropivacaine in terms of reduced motor block, lower instrumental
delivery rate and improved NACS scores.
Early comparative studies of bupivacaine and ropivacaine used10-15 ml volumes of a
0.25% solution for initiation of block, followed by either 10ml top-ups or a 6-12 ml/hr
continuous infusion for maintenance. However, by the time ropivacaine appeared on
the market in 1996, several aspects of its use had changed. Firstly, it was marketed
as a mg/ml rather than a % solution, secondly it was released as a 2mg/ml solution
(versus2.5mg/ml in initial studies. Finally and most importantly, there was a definite
trend towards using lower-strength solutions of bupivacaine (0.125% or even
0.0625%) in combination with a narcotic (fentanyl) for epidural labour analgesia. Also,
CSE (combined spinal epidural) analgesia was also emerging as a useful technique.
Using ropivacaine, therefore, was no longer a matter of simply switching from one
anaesthetic solution to the other while administering the same volume as before.
Moreover, many anaesthetists were satisfied with the quality of analgesia and patient
acceptance of these low-dose bupivacaine solutions and saw no reason to change
At the RHW in 1996, for routine labour analgesia, most anaesthetists were using
0.25% bupivacaine with 75-100 mcg fentanyl for initiation of block, followed by an
infusion of 0.125% with fentanyl 5mcg/ml. Having already witnessed the efficacy of
ropivacaine first hand, in particular its reduced motor block, most of our anaesthetists
switched to the new agent (2mg/ml) as soon as it became available. It is now used
routinely by eight of our nine specialists and all of our registrars.
Initially, ropivacaine used without fentanyl, but patients seemed to require more
frequent top-ups. We then began adding fentanyl, which improved the quality of the
analgesia. As there have been few reports in the literature on the use of low-dose
ropivacaine + fentanyl our current regimens have evolved by trial and error. Each
anaesthetist has his or her own preference for dosage and volume used. Some
examples of regimens currently in use are provided in tables below.
Drug Test Dose Loading Dose Infusion
Lignocaine 2% + adr 3 mls - -
Ropivacaine 2mg/ml - 12 mls 47 mls
Fentanyl - 50 mcgs 150 mcgs
(Infusion equivalent to ropivacaine 1.88mg + fentanyl 3 mcg/ml in 50 mls)
Fentanyl - - 200 mcgs
(Infusion equivalent to ropivacaine 1.87mg + fentanyl 3.3 mcg/ml in 60mls)
Fentanyl - 50 150 mcgs
Normal Saline - - 7 mls
(Infusion equivalent to ropivacaine 1.6 mg/ml + fentanyl 3 mcg/ml in 50 mls)
Note:
1) Commence infusion at 8ml/hr. Increase up to 12 ml/hr. Cease infusion when
preparing for delivery. Pump rate adjustments to be made by midwife.
2) 12.5 mls ropivacaine 2mg/ml is equivalent to 10mls bupivacaine 0.25% or 20mls
0.125% Larger volumes of ropivacaine are required than those you may be
accustomed to using with bupivacaine (up to 20 mls if lignocaine is not used for a test
dose).
3) Pain usually subsides within 3-4 contractions. Consider using a more potent agent
or subarachnoid injection of opioid/local anaesthetic (CSE) if patient in extreme pain.
4) The level of block should be assessed hourly by the midwife. Patients receiving
infusions may need to change sides every few hours to prevent unilateral block.
5) Breakthrough pain is invariably due to a low level of block on one side and usually
responds to a bolus via the infusion pump. Persistent low back pain or deep perineal
pain remain a challenge.
6) This agent is suitable for ventouse or low forceps delivery, but consider using a
more potent agent for mid-cavity forceps.
7) If the patient requires a caesarean section, discontinue the infusion. Check the
level of the block and add 10-12 mls of a more potent agent in increments.
8) Ropivacaine infusions have been used successfully for 1 year now at the Prince of
Wales Private Hospital, where midwives do top-ups and infusion syringe changes.
In summary, at the RHW we have found ropivacaine to be an excellent analgesic
agent for routine labour. In our experience it is as effective as bupivacaine and more
cost-effective. Its increased margin of safety with regard to cardiotoxicity is also
appealing.
We have been impressed by the agents motor-sparing effect a feature very well
received by patients and midwives. Patients are advised that although they cannot
ambulate, they can still move about in bed and should have sufficient motor power to
push effectively.
Anecdotally, in both our institutions we have recently observed a reduction to
approximately 30% in the instrumental delivery rate of patients receiving ropivacaine
epidurals (compared with up to 60% in the bupivacaine patients). Note that in his
meta-analysis of the original ropivacaine studies Writer
(1)
also reported a significant
reduction in instrumental delivery rate from 40% to 27%.
We are about to commence offering ambulatory epidurals to our patients. Two
regimens will be used, low-dose bupivacaine and low-dose ropivacaine, both in
combination with fentanyl.
Steven Halpern
Introduction:
Uterine artery resistance is increased by maternal hypertension (essential or
pregnancy induced), uterine contractions, uterine hypertonus and vasoconstrictors.
Uterine venous pressure is also raised by contractions because of increased
intramural pressure. Uterine artery pressure is reduced by such factors as maternal
systemic hypotension and aortic compression by the uterus (Chapter 28). Umbilical
artery blood flow is reduced by severe hypoxia, catecholamines and mechanical
factors (1).
The effect of epidural anaesthesia on uterine blood flow (UBF):
The changes in UBF secondary to epidural anaesthesia are due to several factors.
These include the drugs used and the effects produced as a result of the technique
itself. Clinically, the most important effect is a reduction in perfusion pressure.
Local anaesthetics:
Local anaesthetics in low concentrations have no effect on UBF (2, 3).
Vasoconstrictors:
Epinephrine has both alpha- and beta-adrenergic effects with the predominant effect
being determined by the dose. There is no clinically significant reduction in UBF when
the usual doses are administered. Transient reductions can be observed when
epinephrine is injected intravenously during a test dose. Both intravenous ephedrine
and phenylephrine can be used to treat hypotension. Neither will cause a reduction in
UBF (4).
Fentanyl:
Epidural fentanyl does not reduce UBF (5).
Epidural analgesia for labour and caesarean section:
Epidural analgesia for labour with or without epinephrine, does not usually reduce
UBF in normal or pre-eclamptic patients. Pre-eclamptic parturients who received
epidural analgesia had an increase in intervillous blood flow (6, 7, 8, 9, 12, 13, 17)
(Chapter 39).
Epidural anaesthesia for caesarean section without epinephrine does not cause any
alteration in UBF but there may be a reduction in flow when epinephrine is added (10,
11, 15, 16, 18). There is no change in umbilical blood flow (18).
References:
1. Pater JT. Uteroplacental circulation and respiratory gas exchange. In: Obstetrical
Anesthesia. Editors Shnider SM, Levinson G. 1987. Williams and Wilkins, Baltimore
pp 14-21.
2. Greiss FC, Still JG, Anderson SC. Effects of local anesthetic agents on the uterine
vasculatures and myometrium. Am J Obstet Gynecol 1976; 124:889-899.
3. Biehl D, Shnider SM, Levinson G, Calender K. The direct effects of circulating
lidocaine on uterine blood flow and foetal well-being in the pregnant ewe. Can
Anaesth Soc J 1977; 24:445-451.
4. Raminathan S, Grant GJ. Vasopressor therapy for hypotension due to epidural
anesthesia for cesarean section. Acta Anaesthesiol Scand 1988;32:559-565.
5. Craft JB Jr, Robichaux A, Kim HS, Thorpe DH, Mazel P, Woolf WA, Stolte A. The
maternal and fetal cardiovascular effects of epidural fentanyl in the sheep model. Am
J Obstet Gynecol 1984; 148:1098-1104.
6. Jouppila R, Jouppila P, Hollmen A, Kuikka J. Effect of segmental extradural
analgesia on placental blood flow during normal labour. Br. J. Anaesth 1978;
50:563-567.
7. Jouppila P, Jouppila R, Hollmen A, Koivula A. Lumbar epidural analgesia to
improve intervillous blood flow during labor in severe preeclampsia. Obstet Gynecol
1982; 59: 158-161.
8. Hollmen AI, Jouppila R, Jouppila P, Koivula A, Vierola H. Effect of extradural
analgesia using bupivacaine and 2-chloroprocaine on intervillous blood flow during
normal labour. Br J Anaesth 1982; 54:837-842.
9. Hollmen AI, Jouppila R, Albright GA, Jouppila P, Vierola H, Koivula A. Intervillous
blood flow during caesarean section with prophylactic ephedrine and epidural
anaesthesia. Acta Anaesthesiol Scand 1984; 28:396-400.
10. Skjolderbrand A, Eklund J, Lunell N-O, Nylund L, Sarby B, Thomstrom S. The
effect on uteroplacental blood flow of epidural anaesthesia containing adrenalin for
caesarean section. Acta Anaesthesiol Scand 1990; 34:85-89.
11. Skjoldenbrand A, Eklund J, Johansson H, et al. Uteroplacental blood flow
measured by placental scintigraphy during epidural anaesthesia for caesarean
section. Acta Anaesthsiol Scand 1990; 34:79-84.
12. Hughes AB, Devoe LD, Wakefield ML, Metheny WP. The effects of epidural
anesthesia on the Doppler velocimetry of umbilical and uterine arteries in normal term
labor. Obstet Gynecol 1990; 75:809-12.
13. Patton DE, Lee W, Miller J, Jones M. Maternal, uteroplacental and fetoplacental
hemodynamic and Doppler velocimetric changes during epidural anesthesia in
normal labor. Obstet. Gynecol 1991; 77:17-19.
14. Petrikovsky BM, Cohen M, Tancer L. Uterine and umbilical blood flow during
cesarean section under epidural anesthesia. Acta Obstet Gynecol Scand 1988;
67:737-740
15. Chestnut DH, Weiner CP, Herrig JE. Effects of intravenously administered
2-chloroprocaine upon uterine artery blood flow velocity in gravid guinea pigs.
16. Chestnut DH, Weiner CP, Martin JG, Herrig JE, Wang J. Effect of intravenous
epinephrine upon uterine artery blood flow velocities in the pregnant guinea pig.
17. Ramos-Santos E, Devoe LD, Wakefield ML, Sherline DM, Metheny WP. The
effects of epidural anesthesia on the Doppler velocimetry of umbilical and uterine
arteries in normal and hypertensive patients during active term labor. Obstet Gynecol
1991 ;77:20-26.
18. Halpern SH, Glanc P, Myhr T, Ryan ML, Fong K, Amankwah K, Ohlsson A. The
effect of epidural anaesthesia for caesarean section on uterine and umbilical blood
flow in normal and high risk pregnancies. Can J Anaesth 1994;41: 1057-1062.
Kazuo Hanaoka
Spinal or epidural anesthesia is widely used in obstetric anaesthesia. Sometimes, the
duration of spinal anesthesia alone is too short for the completion of surgery (Chapter
70). At other times, the intensity ("depth") of epidural anesthesia is insufficient to
perform the operation which is contemplated.
The combination of spinal with epidural anaesthesia has the potential to eliminate or
reduce these problems (Chapter 6). Hanaoka's needle is one such needle
combination designed for continuous spinal epidural anaesthesia (CSE) (Chapter 51).
These needles are disposable and consist of spinal and epidural components which
allow practically simultaneous spinal injection and epidural catheterisation (Figure
54.1).
The technique for the insertion of the needle is as follows (Chapter 62):
1. The disposable epidural needle (17G) is inserted into the epidural space using a
standard epidural anaesthesia technique.
2. The disposable spinal needle (26G) is now inserted through the epidural needle
and advanced until the tip of the spinal needle exits through the back-hole ("rear
eye") of the epidural needle and punctures the arachnoid membrane (Figure 54.2).
The spinal needle is 7 mm longer than the epidural needle (Chapter 59).
3. A subarachnoid dose of local anesthetic is injected through the spinal needle
(Chapter 61).
4. The spinal needle is removed.
5. The epidural catheter is advanced down the epidural needle.
5. The epidural needle is removed and the catheter is taped to the patient's skin.
The advantages of this technique are that:
1. The spinal component of the anaesthetic leads to the rapid onset of surgical
anaesthesia with good muscle relaxation.
2. Continuous epidural anesthesia is available when surgery is prolonged or the
height or depth of the spinal anesthetic is insufficient.
3. Local anaesthetic toxicity is less likely because smaller amounts of drug are
required.
Phil Harrington
Post-Dural Puncture Headaches (PDPH) have been recorded since the
commencement of spinal anaesthetics. Bier and his assistant, Hildebrandt, both
experienced this complication after undergoing experimental spinal anaesthesia
(using a needle developed by Heinrich Quincke) in 1898 . Bier published his results
in 1899 (1). Vandam and Dripps identified needle size as a factor in the incidence of
PDPH (2).
The headache may first be experienced several hours to days after the dural
puncture. It is usually bifrontal and occipital and is aggravated by the upright posture
and by straining. It is relieved by lying down (Chapter 85). It needs to be
differentiated from aseptic meningitis, infective meningitis, cortical vein thrombosis,
cerebral/epidural haematoma and tension/migraine headache.
The incidence of PDPH can be as high as 80% if puncture occurs with a 16G needle.
Series have been reported suggesting that the incidence of PDPH can be reduced to
almost 0% with the use of specially designed, non-cutting point, fine gauge needles.
However, most recent series report incidences of 1% - 3% even with these smaller
gauge needles.
The fact that not every patient has a headache after dural puncture, even with 16G
needles, would indicate that the degree of inter-patient variability and difference in
technique of insertion also have a profound effect on incidence.
The factors which have been identified in affecting the incidence of PDPH are the:
1. size of needle (3) - decreased incidence with smaller needles,
2. design of needle (Figure E.1) - decreased incidence with a non-cutting tip as
compared with a cutting tip (3),
3. relationship of bevel to the dural fibres - decreased incidence if needle bevel is
parallel to dural fibres (Chapter 63),
4. angle of puncture of the dura - less with acute angles,
5. age- most studies have shown a decreased incidence with increasing age,
6. gender - females (even after removing the bias introduced by obstetric
patients)have almost double the incidence of headache when compared with males
in the under 50yr age group,
7. use of Povidone-lodine skin-prep. One study showed that removal of the skin-prep
decreased the incidence of PDPH,
8. formation of a burr on the tip of a needle if the lamina is encountered before dural
puncture,
9. concentration of local anaesthetic solution - less with weaker solution,
10. choice of local anaesthetic agent - lignocaine > bupivacaine > tetracaine (4).
The meta-analyses performed by Halpern and Preston confirmed that there was a
reduction of PDPH when a small spinal needle was used, compared with a large
needle of the same type (p <0.05). In addition, PDPH was reduced with the use of
non-cutting spinal needles ( p < 0.05) (3).
The designers of spinal needles have sought to minimise the incidence of PDPH
while also improving speed of CSF flashback. For epidural needles the compromise
is between sufficient sharpness of the tip to permit easy insertion and a degree of
bluntness which will minimise the likelihood of dural puncture with a large needle
(Chapter 31).
The nomenclature of needle size derives from the "Standard Wire Gauge" used to
measure electrical wires. The commonly used sizes of spinal needles are 22G-27G.
However, spinal needles are available in a variety of sizes from 19G-30G. The
epidural needles in common use in obstetrics are 16G-18G.
The quest for a minimally damaging needle with optimal ease of insertion continues.
There are a variety of needle tips and sizes available today which have a low
incidence of PDPH and an acceptably low failure rate. These include the Whitacre,
Greene and Sprotte needles (Chapter 59).
References:
1. Bier A Dtsch Z Chir 51:361, 1899
2. Vandam L, Dripps R. JAMA 2:586-591, 1956
3.Halpern S, Preston R. Postdural puncture headache and spinal needle design.
Meta-analyses. Anesthesiology 81:1376-1383, 1994
4.Naulty JS et al Anesthesiology 72: 450-454, 1990
Patricia Harrison and Mark Lema.
Respiratory depression from Intrathecal and Epidural Opioids:
With the introduction of intrathecal and epidural opioids came the hope that, due to
binding with specific spinal cord receptors, pain relief would be produced without
adverse side effects (Chapter 60). However, respiratory depression although not
common, is a recognizable complication of this technique. It occurs as an "early" or
"late" phenomenon and depends to some extent, on the lipid solubility of the agent.
The spread of the lipid-soluble opioids, eg. fentanyl and sufentanil, has been thought
to be more limited than that of morphine(1) with a presumed lower risk of severe
respiratory depression. This has been recently questioned (2, 3) as the incidence of
0.6% is similar to that of morphine (4). The large epidural doses required for
analgesic effect are similar to intravenous doses for fentanyl and even higher for
sufentanil supporting the theory that early respiratory depression, if it occurs, is the
result of systemic absorption from the epidural veins with these agents. Following
intrathecal administration, respiratory depression within 15-30 minutes has been
reported with both fentanyl (5) and sufentanil (6).
Morphine crosses the dura slowly with peak CSF concentrations seen at 90-120
minutes after epidural administration. CSF morphine concentration remains high due
to prolonged elimination (7) and cephalad spread to the medullary respiratory center
is probably the cause of late respiratory depression. Intrathecal doses are markedly
reduced to avoid this complication which may also be precipitated if parenteral
opioids are given at this time. Dose-dependent depression of CO2 response curves
has also been demonstrated (9).
Respiratory depression and other systemic effects have been treated with a low dose
of naloxone such that epidural analgesia is not reversed. Other longer-acting
antagonists are currently being investigated. Results with agonist-antagonists, eg.
nalbuphine, are conflicting (9).
All patients who receive spinal opioids should be observed carefully for at least the
first 12 hours. This has been done successfully on surgical wards provided that
nursing staff are well trained and monitoring includes respiratory rate and degree of
sedation (10). Continuous pulse oximetry has been advocated but is not mandatory.
If these measures are implemented, respiratory depression is a rare event and
neuraxial narcotics are probably safer than parenteral opioids (where the frequency
of monitoring is traditionally lower) (11).
References:
1. Bromage PR, Camporesi E, Leslie J. Epidural narcotics in volunteers: Sensitivity to
pain and to carbon dioxide. Pain 9: 145-160, 1990
2. Colten SE, Lasaille T, Benhamou D, Levron JC Respiratory effects of epidural
sufentanil after cesarean section. Anesth Analg 74:677-82, 1992.
3. Brockway MS, Noble DW, Sharwood-Smith GH, McClure JH Profound respiratory
depression after extradural fentanyl. Br J Anaes 64:243-5, 1990,
4. Weightman WM Respiratory arrest during epidural infusion of bupivacaine and
fentanyl. Anaes Intensive Care 19:282-284, 1991,
5. Belzarena SD. Clinical effects of intrathecally administered fentanyl in patients
undergoing cesarean section. Anesth Analg 74:653-659, 1992.
6. Palmer CM Early respiratory depression following intrathecal fentanyl-morphine
combination. Anesthesiology 74:1153-1155, 1991.
7. Nordberg G, Hedner T, Mellstrand T et al Pharmacokinetics of epidural morphine
in man. Eur J Clin Pharm 26:233-237, 1984.
8. Rawal N, Wattwil M. Respiratory depression following epidural morphine: an
experimental and clinical study. Anesth Analg 63:8-14, 1984.
9. Etches RC, Sandler AN, Lawson SL A comparison of the analgesic and respiratory
effects of epidural nalbuphine or morphine in post thoracotomy patients.
10. Ready LB, Loper KA, Nessly M, Wild L. Postoperative epidural morphine is safe
on surgical wards. Anesthesiology 75:452-456, 1991.
11. Hughes SC. The safety of intraspinal narcotics in obstetric patients. Survey of
Anesthesia 33:261-264, 1989.
Samuel Hughes
The introduction of cocaine into clinical practice in 1884 brought a new era to
medicine - regional anesthesia. The early use of intrathecal cocaine, 10 mg, in 1900
ushered in the use of local anesthetics in obstetric anesthesia (1). While this practice
was apparently effective, the use of local anesthetics in obstetrics languished for a
number of years because of concerns regarding maternal and fetal safety, toxicity of
local anesthetics, and a poor understanding of pain pathways. 2-chloroprocaine
(2-CP), like cocaine, is an ester local anesthetic agent. It is a direct descendent of
procaine, the first synthetic local anesthetic that allowed the safe use of regional
anesthesia. The search for the ideal anesthetic led to the introduction of 2-CP in the
United States in 1952.
Structure and Metabolism
2-CP and tetracaine are the ester local anesthetics used routinely in clinical practice.
The ester linkage of the local anesthetic's aromatic ring and the alkyl chain-tertiary
amine sets them apart from the amide-linked agents like lidocaine. The ester linkage
allows these agents to be hydrolyzed by plasma pseudocholinesterase. This process
is more rapid than the hepatic microsomal metabolism of the amide local anesthetics
and thus, contributes to greater safety. In pregnancy, the activity of plasma
pseudocholinesterase is decreased by 40 to 50%, but this seems to have little clinical
effect on the metabolism of 2-CP (2). The half-life of 2-CP in maternal plasma is still
less than 60 seconds (3, 4). An unexpected intravenous injection would be rapidly
metabolized and, in fact, it seems difficult to achieve toxic levels with routine clinical
use of this drug (Chapter 36). This is a unique feature of 2-chloroprocaine which
makes it extremely safe.
Toxicity
Systemic toxicity of local anesthetics ranges from numbness of the tongue and light
headedness to convulsions and respiratory-cardiovascular arrest (Table 36.4). 2-CP
is perhaps the least toxic when considering (systemic) central nervous system (CNS)
toxicity (bupivacaine > lidocaine > 2-CP) (Table 36.6) (Table E.2) (5). While cardiac
toxicity is all too easily achieved with bupivacaine, it is not a problem with 2-CP.
However, the increased use of 2-CP in the mid 1970's and into the early 1980's led to
the discovery of a potentially unique neurotoxicity. In the clinical setting, prolonged or
permanent sensory and motor deficits resulted from unexpected, large subarachnoid
injections (6, 7). The recent concerns regarding the neurotoxicity of lidocaine suggest
that perhaps all local anesthetics can be toxic to some degree (8), although the
ester-linked agents are not more likely to be neurotoxic (9).
The preparation of 2-CP which was reported to cause toxicity was Nesacaine-CE
with a pH of approximately 2.7 to 4.0 which contained metabisulfite (2 mg/ml).
Interestingly, the original formula contained methylparaben which was removed in the
1960's. The proposal by Gissen et al. (10) suggested that the metabisulfite in 2-CP
generated sulfur dioxide (lipid soluble) which diffused into neural tissue and
generated intracellular sulfurous acid, profound local acidosis and, thus,
neurotoxicity. The metabisulfite has been removed from the formulation and the pH
raised slightly. The current product in common use (Nesacaine-MPF, Astra),
however, now contains ethylene diamine-tetra acetic acid (EDTA) to stabilize the
local anesthetic. This, potentially, could lead to new forms of complication or toxicity.
Backaches - the 'New Toxicity' (Chapter 84)
There have been numerous clinical reports of back pain following the epidural
administration of large volumes of 2-CP (12, 13) since the first report by Orkin and
Bogetz (11). It appears that when volumes greater than 25 to 30mls of epidural 2-CP
are used, intense back pain may result in some patients. This may require epidural
fentanyl, lidocaine or intravenous narcotics or, possibly, calcium chloride to treat the
pain. This does not seem to be a problem in the parturient. Thus, while there are
significant limits placed on the use of 2-CP in some clinical settings, it is not a serious
consideration in labor analgesia or anesthesia.
Obstetric Considerations
High doses of all local anesthetics will lead to a decreased uterine blood flow (UBF).
This has been confirmed in human uterine arteries in vitro and in the sheep model in
vivo (14, 15). In clinical doses there is no change in UBF with 2-CP (Figure 106.1a)
(Figure 106.1b) (15, 16). Umbilical cord blood flow, while challenging to measure, is
another indicator of the adequacy of the maternal-fetal placental unit. Noninvasive
Doppler imaging has been used to evaluate cord blood flow and demonstrated no
adverse effect of epidural local anesthetics. In parturients receiving epidural
analgesia with 2% 2-CP, Doppler measurements indicated a beneficial effect upon
umbilical artery vascular resistance (17). In addition, intervillous blood flow has been
shown to increase with both epidural bupivacaine and 2-CP during normal labor (18).
Finally, large doses of local anesthetics may increase uterine tone and contractility
which would decrease uteroplacental perfusion (Chapter 76). This could easily be
achieved with a paracervical block with 2-CP (Figure 46.2), for example, but in
clinical concentrations with regional anesthesia this is not a concern. Thus, 2-CP
should have no adverse effect on the maternal-fetal well-being in routine clinical
practice and, in fact, may actually lead to increased umbilical blood flow in some
patients.
Fetal and Newborn Effects
All local anesthetics cross the placenta and levels can be measured in the fetus and
newborn (Chapter 77). However, as drugs reach the fetus they undergo metabolism
and excretion. Historical concerns about the neurobehavioural response of newborn
infants after epidural lidocaine administration for labor analgesia led to a series of
extensive evaluations of the effects of local anesthetics on the newborn (19) (Chapter
25). While subtle changes can be detected with all commonly used local anesthetics,
there is no indication that these changes are significant with regards to a long-term
outcome (20, 21, 22, 23). It is clear that there are other perinatal factors that are far
more important than the choice of a local anesthetic. There has also been concern
about the effects of local anesthetics on fetal heart rate (FHR) changes. Alterations in
FHR beat-to-beat variability and a greater incidence of periodic decelerations have
been reported with all local anesthetics used for labor analgesia (Chapter 3) (Table
3.1). This does not appear to be the case when large doses of local anesthetics are
given for cesarean section to patients not in labor (24). Any FHR changes found
during labor are transient and seem to have no effect upon the condition of the
newborn and are likely to be due to other factors than the direct effect of a local
anesthetic.
With regards to possible teratogenicity of local anesthetics, this would appear to be a
theoretical risk as opposed to real clinical concern. On the other hand, as agents for
in vitro fertilization are evaluated, it has been suggested that all local anesthetics
adversely affect mice in vitro fertilization and embryo development in the order
chloroprocaine > lidocaine> bupivacaine (25). The relevance of this work to clinical
practice is yet to be determined. In summary, while all local anesthetics have been
extensively evaluated for fetal and newborn effects, it is my view that there is
probably no real difference in 2-CP versus lidocaine versus bupivacaine and that all
of these agents can be used safely for labor and delivery.
2-Chloroprocaine and Intraspinal Narcotics
It has been reported that the use of epidural 2-CP may interfere with the quality and
duration of pain relief produced by epidural morphine or fentanyl (26, 27). 2-CP or its
metabolite, chloroaminobenzoic acid, may act as a mu receptor antagonist. However,
this is difficult to demonstrate. It has been claimed that kappa receptors are not
antagonized by 2-chloroprocaine (28). However, the receptor specific antagonism
hypothesis has been challenged (29). I suspect that the chief problem is simply the
rapid fade of a block with 2-CP (a quality that is desirable in some situations) which
leads to a "window effect" before the onset of analgesia from epidural narcotics.
While this issue remains controversial and proof of narcotic receptor antagonism may
yet be established, close attention to the pain relief achieved with epidural narcotics
after the administration of epidural 2-CP will solve the issue from the clinical
viewpoint. The administration of small doses of intravenous fentanyl or morphine or
an additional epidural dose of fentanyl or sufentanil added to epidural morphine will
bring about adequate pain relief.
Use of 2-CP in Labor and Delivery
2-CP is an ideal drug in many ways. It has a rapid onset, high efficacy, rapid
metabolism, and short half-life in both mother and fetus. These features make it a
very appealing drug for epidural use. Our clinical group demonstrated the rapid onset
(2-3 min) of epidurally administered 3% 2-CP in patients for postpartum tubal ligation
with T4 level being achieved in 10 +/- 4min (Figure 106.2) (30) (Chapter 67). On the
other hand, the reality is that its use is limited because of the very short duration of
action. If 8 to 10ml of 2% 2-CP are given for labor analgesia, it is highly effective but
the duration of action is only 45 to 50 minutes and the offset is exceedingly rapid.
Thus, the drug must be topped-up promptly approximately every 45 minutes or the
patient will rapidly go from feeling very comfortable to exceedingly uncomfortable.
2-CP has been administered as a continuous infusion for labor (0.75%) (31), as well
as a continuous infusion for cesarean delivery (3.0%) (32). While this approach has
been satisfactory, others have suggested that a tachyphylaxis may well develop and,
thus, the continuous infusion technique is not commonly used. While labor epidurals
may be initiated with chloroprocaine to achieve pain relief rapidly, this is not
commonly done, both because of the short duration of action and the potential
interference with the later use of epidural narcotics or bupivacaine. 2-CP (3%) has
been shown to be very effective for cesarean section (32) and is popular in some
institutions because of its rapid onset and the rapid fade of the block. This latter
property may cut down on the recovery room stay.
The greatest use of 2-CP today may be either to "save" an inadequate epidural block
(Chapter 94) where it is felt that the catheter is in place but a high dose of an amide
local anesthetic has already been given, or to achieve a rapid onset of epidural
anesthesia when good conditions for surgery are urgently needed. In the
"chloroprocaine save" the addition of 10 to 20mls of 3% 2-CP may be adequate to
achieve analgesia in a block that was previously "patchy" and to avoid the toxicity
that would result from giving larger doses of an amide local anesthetic.
If an effective labor epidural is in place and a surgical delivery or cesarean section
must be urgently performed, the addition of 12 to 15mls (to as much as 25mls) of 3%
2-CP will provide rapid anesthesia within 10 minutes. The higher dose of 2-CP would
be required for a cesarean delivery while the lower dose will achieve adequate
analgesia for a forceps or a vacuum delivery. Thus, while 2-CP was initially very
popular as a routine drug for a cesarean section, it is now used most often in specific
situations which are, generally, urgent or clinically complicated.
While it is an excellent local anesthetic and clearly has a place in obstetric clinical
practice, its role today in obstetric anesthesia is limited. When using 2-CP the drug's
short comings must be considered, but it is a unique local anesthetic and, when used
appropriately, it is an excellent choice.
References:
1. Kreis O: Uber Medullarnarkose bei Gebarenden. Zentralbl Gynakol 24:724, 1900.
2. Shnider SM: Serum cholinesterase activity during pregnancy, labor and the
puerperium. Anesthesiology 26:335-339, 1965.
3. Kuhnert BR, Kuhnert PM, Prochaska AL, Gross TL: Plasma levels of
2-chloroprocaine in obstetric patients and their neonates after epidural anesthesia.
4. Kuhnert BR, Kuhnert PM, Philipson EH, et al: The half-life of 2-chloroprocaine.
Anesth Analg 65:273-278, 1986.
5. Covino BG, Vassallo HG: Local anesthetics: Mechanisms of Action and Clinical
Use. New York, Grune & Stratton, 1976, p 126.
6. Ravindran R, Bond VK, Tasch MD, et al: Prolonged neural blockade following
regional analgesia with 2-chloroprocaine. Anesth Analg 59:447-451, 1980.
7. Reisner LK, Hochman BN, Plumer MH: Persistent neurologic deficit and adhesive
arachnoiditis following intrathecal 2-chloroprocaine injection. Anesth Analg
59:452-454, 1980.
8. Fenerty J, Sonner J, Sakura S, Drasner K: Transient radicular pain following spinal
anesthesia: Review of the literaure and a report of a case involving 2% lidocaine.
International Journal of Obstetric Anesthesia (in press, 1996).
9. Kalichman MW, Moorhouse DF, Powell HC, Myers RR: Relative neural toxicity of
local anesthetics. J Neuropathol Exp Neurol 52:234-240, 1993.
10. Gissen AJ, Datta S, Lambert D: The chloroprocalne controversy. I. A hypothesis
to explain the neural complications of chloroprocalne epidural. Reg Anesth
9:124-134, 1984.
11. Orkin FK, Bogetz MS: Back pain following uncomplicated epidural anesthesia
with chloroprocaine. Anesthesiology 71 :A716, 1989.
12. Hynson JM, Sessler Dl, Glosten B: Back pain in volunteers after epidural
anesthesia with chloroprocaine. Anesth Analg 72:253-256, 1991.
13. Stevens RA, Bray JG, Chester WL, et al: Back pain after epidural anesthesia with
chloroprocaine in volunteers: preliminary report. Reg Anesth 16: 199-203, 1991.
14. Fishburne JI, Greiss FC, Hopkinson R, Rhyne AL: Responses of the gravid
uterine vasculature to arterial levels of local anesthetic agents. Am J Obstet Gynecol
33:753-761, 1979.
15. Wallis KL, Shnider SM, Hicks JS, Spivey HT: Epidural anesthesia in the
normotensive pregnant ewe: Effects of uterine blood flow and fetal acid-base status.
16. Chestnut DH, Weiner CP, Herrig JE: The effect of intravenously administered
2-chloroprocaine upon uterine artery blood flow velocity in gravid guinea pigs.
17. Marx GF, Patel S, Betman JA, et al: Umbilical blood flow velocity waveforms in
different maternal positions and with epidural analgesia. Obstet Gynecol 68:61-64,
1986.
18. Hollmen AI, Jouppila R, Jouppila P, et al: Effect of extradural analgesia using
bupivacaine and 2-chloroprocaine on intervillous blood flow during labour. Br J
Anaesth 54:837, 1982.
19. Scanlon JW, Brown WU, Weiss JB, Alper MH: Neurobehavioral response of
newborn infants after maternal epidural anesthesia. Anesthesiology 40: 121-128,
1974.
20. Abboud TK, Khoo SS, Miller F, et al: Maternal, fetal and neonatal responses after
epidural anesthesia with bupivacaine, 2-chloroprocaine or lidocaine. Anesth Analg
61:638-644, 1982.
21. Abboud TK, Afrassiabi A, Sarkis F, et al: Continuous infusion epidural analgesia
in parturients receiving bupivacaine, chloroprocaine or lidocaine: maternal, fetal, and
neonatal effects. Anesth Analg 63:421-428, 1984.
22.. Kileff ME, James FM, Dewan DM, Floyd HM: Neonatal neurobehavioral
responses after epidural anesthesia for cesarean section using lidocaine and
bupivacaine. Anesth Analg 63:413-417, 1984.
23. Kuhnert BR, Harrison MJ, Linn PL, Kuhnert PM: Effects of maternal epidural
anesthesia on neonatal behavior. Anesth Analg 63:301-308, 1984.
24. Loftus JR, Holbrook RH, Cohen SE: Fetal heart rate after epidural lidocaine and
bupivacaine for elective cesarean section. Anesthesiology 75:406-412, 1991.
25. Schnell VL, Sacco AG, Savoy-Moore RT, Ataya KM, Moghissi KS: Effects of
oocyte exposure to local anesthetics on in vitro fertilization and embryo development
in the mouse. Toxicology 6:323-327, 1992.
26. Kotelko DM, Thigpen JW, Shnider SM, et al: Postoperative epidural morphine
analgesia after various local anesthetics. Anesthesiology 59:A413, 1983.
27. Malinow AM, Mokriski BLK, Wakefield ML, et al: Choice of local anesthetic
affects post-cesarean epidural fentanyl analgesia. Reg Anesth 13: 141-145, 1988.
28. Camann WR, Hartigan PM, Gilbertson LI, et al: Chloroprocaine antagonism of
epidural opioid analgesia: a receptor-specific phenomenon? Anesthesiology
73:860-863, 1990.
29. Camann WR, Hurley RH, Gilbertson LI, Long ML, Datta S: Epidural nalbuphine
for analgesia following caesarean delivery: dose-response and effect of local
anaesthetic choice. Can J Anaesth 38:728-732, 1991.
30. Glosten B, Dailey PA, Preston PG, Shnider SM, Ross BK, Rosen MA, Hughes
SC: pH-adjusted 2-chloroprocaine for epidural anesthesia in patients undergoing
postpartum tubal ligation. Anesthesiology 68:948-950, 1988.
31. Abboud T, Abrasiabi A, Sarkis F, et al: Continuous infusion epidural analgesia in
parturients receiving bupivacaine, chloroprocaine or lidocaine: Maternal, fetal and
neonatal effects. Anesth Analg 63:421-428, 1984.
32. De Leon-Casasola OA, Syed N, Lema M J, Emrich L: Continuous
2-chloroprocaine infusion versus intermittent bolus injections of bupivacaine or
2-chloroprocaine for epidural anesthesia in cesarean delivery. Reg Anesth 16:
154-160, 1991.
33. Crosby E, Read D: Salvaging inadequate epidural anaesthetics: "The
chloroprocaine save." Can J Anaesth 38:136-137, 1991.
Peter Keast and Andy Pybus.
Reducing the Risk of Mendelson's Syndrome During Obstetric Anaesthesia.
The pulmonary acid-aspiration syndrome was first reported 50 years ago (1) in a
group of parturients undergoing general anaesthesia for vaginal delivery. The
description given by the author was so accurate and so complete that it rapidly
acquired the eponym 'Mendelson's syndrome'.
For the full picture to develop ("cyanosis and labored respiration ... with a pink froth
exuding from the respiratory passages"), aspiration must occur in the presence of a
'triad' of features, namely:
1. A stomach that contains gastric secretions at a 'low' pH (less than 2.5) or one that
contains particulate matter.
2. Vomiting or regurgitation.
3. Depression of the laryngeal reflexes.
An essential component of the syndrome is the development of a pulmonary 'burn' -
usually produced by the inhalation of gastric acid at a 'low' pH. As such, Mendelson's
syndrome is at one end of the spectrum of the pulmonary aspiration syndromes.
Aspiration of non-particulate, gastric contents at a 'high' pH (&gt6.0) does not
produce the same histological lesion as acid-aspiration (2) and is probably associated
with a lower mortality rate. Aspiration of 'high' pH, particulate matter also produces a
different histological picture from acid-aspiration, but may be associated with an
equally poor outcome. This may account, in part, for the wide variation (3 to 70%) (1)
in reported mortality rates from aspiration in association with anaesthesia.
Since the description of the syndrome, important therapeutic strategies intended to
minimise the risks of aspiration, have been evolved by anaesthetists. This has led to
a progressive reduction in the maternal death rate from aspiration syndromes such
that, in the United Kingdom, the first Report on Confidential Enquiries into Maternal
Deaths (1952) indicated that there were 32 deaths from aspiration and by 1988-90
this had fallen to zero.
The therapeutic strategies which have been adopted include:
1. Fasting of women in labour.
2. Measures which may increase gastric pH.
3. Measures which may reduce the volume of gastric secretions.
4. The use of regional rather than general anaesthesia.
And, if general anaesthesia is administered:
5. Pre-oxygenation and the application of cricoid pressure prior to intubation.
6. Protection of the airway by a cuffed endotracheal tube.
1. Fasting during labour.
There is a fundamental conflict between the needs of the parturient as perceived by
the patient or her midwife and the needs of the parturient as perceived by the
obstetric anaesthetist. As far as the latter is concerned, the safest strategy with
regarding to a feeding policy is to insist on fasting during labour, to meet all maternal
needs for hydration by the administration of intravenous fluids, and to limit oral intake
to the sucking of ice. It has been clearly demonstrated that both the intake of food (3)
and the drinking of dextrose-containing solutions (4) can significantly delay gastric
emptying (Chapter 26).
2. Measures which may increase gastric pH (Chapter 80).
Two techniques intended to raise the gastric pH before the administration of an
obstetric anaesthetic have gained widespread acceptance.
a. The administration of 30mls of 0.3Molar sodium citrate 15-20 minutes before
anaesthesia for caesarean section (CS) has been shown to raise gastric pH above
2.5 in about 90% of patients (5). This antacid is preferable to the particulate antacids
because the solution mixes more effectively with the gastric contents, and it has also
been suggested that particulate antacids themselves are capable of producing a
severe aspiration syndrome (6).
b. The administration of an H2 antagonist such as ranitidine is even more effective
than sodium citrate at raising gastric pH. If used prior to elective CS, two oral doses
of ranitidine (150mg) should be given, one the night before surgery and one on the
morning of surgery. For emergency CS, ranitidine 50mg can be given intravenously.
Sodium citrate should also be used. H2 antagonists may have the additional
advantage of reducing gastric volume. The combined use of ranitidine and sodium
citrate will raise gastric pH above 2.5 in the great majority of parturients (7).
3. Measures which may reduce the volume gastric secretions.
Metoclopramide has been used by some to promote gastric emptying during labour
(8). However, the effectiveness of this technique is debatable (9). Attempts to empty
the stomach by the use of a nasogastric tube or a pro-emetic drug are likewise
relatively ineffective and are also unacceptable to most patients. The effect of the
analgesic technique used in labour and its relationship to the volume of gastric
contents measured at subsequent CS has also been studied. Holdsworth (10) found
that the largest gastric aspirates were found in patients who had received pethidine
analgesia and the smallest aspirates in patients who had received either epidural
analgesia or no analgesia. Pethidine, rather than the 'emotional stress of labour', was
thought to cause the relative gastric stasis.
4. The use of regional rather than general anaesthesia.
Provided that no sedation is administered and that regional anaesthesia is
complication-free, the use of major regional blockade for CS virtually eliminates the
risk of aspiration. Nevertheless, it is still imperative to administer aspiration
prophylaxis to patients who are to undergo CS under regional anaesthesia.
5. The use of cricoid pressure.
If a general anaesthetic is administered, the use of cricoid pressure ('Sellick's
Manoeuvre') at induction (11) (in association with pre-oxygenation) is mandatory.
Properly applied pressure will withstand a 'head' of pressure of 100cms of water.
There may be a small risk of oesophageal rupture if pressure is applied in the
presence of active vomiting. Some authorities have advocated the release of the
applied pressure if vomiting occurs but others disagree.
6. Protection of the airway by a cuffed endotracheal tube.
If a general anaesthetic is administered, protection of the airway by a cuffed
endotracheal tube is also mandatory. However, it should be noted that modern
high-volume, low-pressure cuffs, inflated to 25cms H2O, do not afford complete
protection against aspiration.
References:
1. Mendelson CL The aspiration of stomach contents into the lungs during obstetric
anesthesia. Am J Obstet Gynecol 52:191 1946
2. Schwartz DJ, Wynne JW, Gibbs CP et al The pulmonary consequences of
aspiration of gastric contents at pH values greater than 2.5. Am Rev Respir Dis
121:119 1980
3.Lewis M, Crawford JS Can one risk fasting the obstetric patient for less than 4
hours? Br J Anaesth 59:312 1987
4.Hinder RA, Kelly KA Canine gastric emptying of solids and liquids. Am J Physiol
233:335 1977
5.Dewan DM, Floyd AM, Thistlewood JM et al Sodium citrate pretreatment in elective
cesarean section patients. Anesth Analg 64:34 1985
6.Gibbs CP, Schwartz DJ, Wynne JW et al Antacid pulmonary aspiration in the dog.
Anesthesiology 51:380 1979
7.Ormezzano X; Francois TP; Viaud JY; Bukowski JG; Bourgeonneau MC; Cottron
D; Ganansia MF; Gregoire FM; Grinand MR; Wessel PE Aspiration pneumonitis
prophylaxis in obstetric anaesthesia: comparison of effervescent cimetidine-sodium
citrate mixture and sodium citrate Br J Anaesth 1990 Apr;64(4):503-6
8. Howard FA, Sharp DS Effect of metoclopramide on gastric emptying during labour.
Br Med J 1:446 1973
9. Cohen SE, Jasson J, Talafre M-L Does metoclopramide decrease gastric volume
in cesarean section patients? Anesthesiology 61:604 1984
10.Holdsworth JD Relationship between stomach contents and analgesia in labour.
Br J Anaesth 50:1145 1978
11. Sellick BA Cricoid pressure to control regurgitation of stomach contents during
induction of anesthesia. Lancet 2:404 1961
Frank Lah
Abnormalities of the cardiotocograph following major regional blockade:
Cardiotocography is a method of intrapartum fetal surveillance which allows the
observer to correlate the frequency, duration and intensity of contractions with
variations in fetal heart rate.
The fetal heart rate has a short term (beat to beat) variability. This is the normal
irregularity of cardiac rate which results from the continuous interplay between the
sympathetic (cardioacceleration) and the parasympathetic (cardiodeceleration)
nervous systems.
The typical variability from the baseline is 6-10 beats per minute with values outside
this range being of clinical significance. This variability is seen even when there is no
stress or stimulation to the fetus. It is a reassuring feature which suggests that the
fetus has sufficient reserves to handle the stresses of labour.
Long term variability or periodic changes in the fetal heart rate are transient
accelerations or decelerations from the baseline. They usually occur in response to
stress, eg. uterine contractions, but can also occur with stimulation, eg. fetal
movement. They are classified as:
1. accelerations,
2. early decelerations,
3. late decelerations,
4. variable decelerations.
Each of these abnormal traces provides some indication of the mechanism of the
underlying insult (1).
The effects of regional anaesthesia on the cardiotocograph trace are summarised in
Table 3.1.
Stan Lee-Son
Where do Local Anesthetics Work?
Mechanism of Action
Local anesthetics (LA) block conduction along nerve pathways by inhibiting the
excitatory changes in axon membrane that sustain propagation of the nerve impulse.
During depolarization, the major excitatory process is the opening of sodium
channels to allow Na+ ions into the nerve. When this local ionic current fails to
depolarize a long enough patch of membrane to open enough sodium channels,
conduction along the nerve fails. (1)
Nodes of Ranvier
When the active Na+ currents at the node of Ranvier are exposed to a high
concentration of LA (sufficient to reduce the Na+ current to zero) only three
consecutive nodes of Ranvier of a single myelinated fiber need to be blocked to
prevent transmission of the impulse. In a peripheral nerve, however, the inhibition of
the Na+ channels at the node of Ranvier is seldom complete and fibers are capable
of an attenuated response at clinically realized intraneural LA concentrations. For
each sequential node of Ranvier along a nerve, the partial excitatory response is less
with a progressive decrement in the action potential. When the attenuated response
is too weak to depolarize the next node to threshhold, conduction fails. In order to
block conduction under clinical conditions the length of nerve exposed to LA must
exceed three nodes of Ranvier. (2)
Sodium Channel
Receptor sites for LA have been postulated within the sodium channel (3). It is
accessible to charged LA's only from the cytoplasmic side. Stereoselective inhibition
of neuronal sodium channels by LA's suggested the possibility of two sites of action.
(4, 5). The sodium channel is a large glycoprotein consisting of four repeating
domains, each containing 6 to 8 sequences of amino acids that probably form
alpha-helical structures spanning the nerve membrane. The receptor site for LA is on
the alpha subunit, probably near the ion-conducting pore. (6). Binding of the LA to the
receptor sites prevents the conformational changes of channel activation and, to
some degree, also results in occlusion of the ion conductance pathway. (1).
Pregnancy
During pregnancy there is an increase in functional blocking effect in vivo of a given
concentration of LA (6, 7). The neural uptake of lidocaine over time in pregnant and
non-pregnant rats appears to be the same (8, 9). Hence, the increased potency is
probably due to pharmacodynamic, rather than pharmacokinetic, factors.
Conclusion
Local anesthetics inhibit the excitatory changes which result in nerve conduction. LA
binds to a receptor on the sodium channel, inhibiting the channel's function so that no
sodium current is generated, thereby blocking nerve impulses.
References:
1. Butterworth JF, Strichartz GR Molecular Mechanisms of Local Anesthesia: a
review Anesthesiology 72:711-734 1990
2. Raymond SA, Steffensen SC, Gugino LD, Strichartz GR The role of length of
nerve exposed to local anesthetics in impulse blocking action Anesth Analg
68:563-70 1989.
3. Hille B. Ionic channels of excitable membranes. Sinuaer Associates Inc.
Sunderland, Massachusetts 01375. 1984
4. Lee-Son S, Wang GK, Concus A, Crill E, Strichartz GR Stereoselective inhibition
of neuronal sodium channels by local anesthetics; evidence for two sites of action
Anesthesiology 77:324-335 1992.
5. Zamponi GW, Sui X, Codding PW, French RJ Dual actions of procaineamide on
batrachotoxin-activated sodium channels: open channel block and prevention of
inactivation Biophysical Journal 65:2324-2334. 1993
6. Ragsdale DS, McPhee JC, Scheuer T and Catterall WA. Molecular Determinants
of State-dependent block of Na+ channels by Local Anesthetics Science
265:1724-1728, 1994.
7. Flanagan HL, Datta S, Lambert DH, Gissen AJ, Covino BG . Effect of pregnancy
on bupivacaine-induced conduction blockade in the isolated rabbit vagus nerve
Anesth Analg 66:123-126, 1987.
8. Butterworth JF, Walker FO, Lysak SZ Pregnancy increases median nerve
susceptibility to lidocaine Anesthesiology 72:962-965, 1990.
9. Popitz-Bergez F, Strichartz GR, Thalhammer JG . Differences in lidocaine uptake
in the sciatic nerve of the pregnant rat in vivo Regional Anesthesia 20:2S: 88 1995.
Henry Liberman
The effect of posture on the spread of epidurally or spinally administered local
anaesthetics
Epidural Route (Chapter 1):
The variables which are responsible for the spread of anaesthetics are:
1. volume,
2. mass of solution,
3. speed of injection,
4. age,
5. body weight,
6. height, and
7. position of patient (1, 2, 3, 4).
The evidence for an effect of posture on the spread of epidurally-administered local
anaesthetics is inconclusive and conflicting. Studies have shown a variable effect of
posture with regard to speed of onset, extent of spread and duration of anaesthesia
(5, 6, 7, 8).
Nishimura (8) found that posture had no significant effect on the extent of blockade
but Bromage (5) showed that there was a slight, but significant, difference in the
spread between the supine and the sitting positions.
It is probably fair to say that gravity does play a part in the distribution of anaesthetic
solutions with the sitting position favouring caudad spread and the Trendelenberg
position favouring cephalad spread. The magnitude of this difference in the extent of
blockade is not great.
Spinal Route (Chapter 98):
The spread of local anaesthetics in the subarachnoid space is dependent on:
1. gravity,
2. volume,
3. mass,
4. baricity,
5. speed of injection, and
6. size of needle (9, 10, 11).
Hyperbaric solutions (SG &gt1.009) will tend to spread caudad in patients in the
sitting position and cephalad in patients in the Trendelenberg position (Figure 30.1).
As a result of the intrinsic curves of the spine an injection made at L4 or lower with
the patient in the supine position will tend to spread caudad and that made at L3 or
higher will spread cephalad. Hypobaric solutions (SG < 1.003) will spread in the
opposite direction.
The distribution of isobaric solutions (SG between 1.003 and 1.009) is, in the main,
unaffected by gravity and, therefore, by patient posture.
References:
1. Bonica JJ. Principles & Practice of Obstetric Analgesia & Anesthesia. Williams &
Wilkins, 1995
2. Bromage PR. Epidural Analgesia. Philadelphia. WB Saunders, 1978: 131-148.
3. Whalley et al. The Effect of Posture on the Induction of Epidural Anesthesia for
Peripheral Vascular Surgery. Regional Anaesthesia 20(5): 407-411, 1995.
4. Hodgkinson R, Husain FJ. Obesity, Gravity and Spread of Epidural Anesthesia.
Anesth Analg 1981: 60: 421-424.
5. Bromage PR. Spread of Analgesic Solutions in the Epidural Space and their site of
action: A statistical study. Br J Anaesth 1962: 34: 161-178.
6. Apostolou GA, Zarmakoupis PK, Mastrokostopoulos GT. Spread of epidural
anesthesia and the lateral position. Anesth Analg 1981: 60: 584-586.
7. Park WY, et al. The sitting position and anesthetic spread in the epidural space.
Anesth Analg 1984: 63: 863-864.
8. Nishimura N, Kitahara T, Kusakabe T. The spread of lidocaine and I-131 solution
in the epidural space. Anesthesiology 1959: 20: 785-788.
9. Bonica JJ. Principles & Practice of Obstetric Analgesia & Anesthesia. Williams &
Wilkins, 1995
10.Patel M, et al. Posture and the spread of hyperbaric bupivacaine in parturients
using the combined spinal epidural technique. Canadian J of Anaesthesia:
40(10):943-946, 1993
11.King HK, Wooten DJ. Effects of drug dose, volume, and concentration on spinal
anesthesia with isobaric tetracaine. Regional Anesthesia 20(1): 45-9, 1995
Saywan Lim
"REGIONAL ANAESTHESIA WORLDWIDE: IS IT A VIABLE OPTION IN
OBSTETRICS?"
At all times, the main concern of every practising anaesthetist is the safety of the
patient under anaesthesia. In the field of Obstetric Anaesthesia, this concern must of
necessity extend to the newly-born baby.
From the early reports of maternal deaths in England and Wales from Obstetric
Anaesthesia, it became clear that potential hazards threaten the mother and child
whenever an anaesthetic needs to be administered. The ever present dangers of
vomiting or regurgitation resulting in pulmonary aspiration of acidic contents (Chapter
26), unexpectedly difficult intubation (Chapter 38), awareness and the possibility of
patients being attended to by less experienced personnel (especially after office
hours) have all been well documented (1).
The experiences of the worldwide educational programmes run by the World
Federation of Societies of Anaesthesiologists (WFSA) over the past forty years show
clearly that conditions of work vary markedly in different countries. Differing
educational and training standards and the availability, or lack of, supporting staff,
essential equipment and drugs contribute to varying standards of professional
practice and delivery of health care (Chapter 29). Irrespective of the different factors
which contribute to the complex system in which the anaesthetist does his/her work,
the bottom line remains the same - the safety of the patient (and the yet-to-be-born
baby) will dictate the technique of choice for any obstetric case in any part of the
world. Human life is just as valuable anywhere!!
Outcome studies have generally attributed the majority of anaesthetic incidents to
human error (2). The main factor minimizing an adverse outcome is a well-trained
anaesthetist who is alert and ever present at the patient's side and assisted in his/her
task by dependable monitoring equipment. Under these circumstances, the safest
anaesthetic technique to be employed by any anaesthetist is arguably the technique
he/she is most familiar with, be it a general or a regional.
Notwithstanding the complications that may arise with regional anaesthesia for the
obstetric patient (such as toxicity (Chapter 91), hypotension (Chapter 6), cardiac
arrhythmias and headache (Chapter 97)), and considering cost benefits and
satisfactory outcomes, it appears compelling to forego general anaesthesia (and its
associated 'high tech' costs) for the generally economical cost, simplicity of technique
and comparative safety of regional anesthesia as the first choice when attending on
an obstetric patient.
References:
1. Campling E A, Devlin H B, Lunn J N. The Report of the National Confidential
Enquiry into Perioperative Deaths HMSO UK, 1989.
2. Runciman W Symposium on AIMS Anaesth Intens Care, Vol 21, No 5, October
1993.
Judith Lynch
The following tables outline some of the determinants of the distant effects of
epidurally administered drugs:
1. Factors affecting plasma level of epidurally administered narcotics.
2. Achieved plasma levels of epidurally administered narcotics.
3. Side-effects of epidural narcotics.
4. Toxic levels of local anaesthetics.
5. Comparative CNS and CVS toxicity of local anaesthetics.
6. Factors affecting plasma level of epidurally administered local anaesthetics.
7. Fetal effects of epidurally administered drugs.
Marco Marcus and H Van Aken.
How do we Prevent the Development of Local Anaesthetic Toxicity?
The use of local anesthetics (LA) may be accompanied by systemic and Iocalised
adverse reactions, usually secondary to:
1. accidental intravascular injection (Chapter 36),
2. inadvertent intrathecal injection, or
3. administration of an excessive dose.
Intravenous injection of 20-25 mg of bupivacaine has been reported to induce fatal
cardiovascular collapse (Table 36.6) (1).
Factors which can diminish the incidence of toxic reactions are:
1. fractionation of the injected dose,
2. aspiration before injection,
3. selection of less toxic LAs (Chapter 60),
4. reduction in the concentration of LA, and
5. test-dosing before injection of the main dose.
The diagnosis of inadvertent intravascular placement of an epidural needle or
catheter can be made by using either air or a sympathomimetic amine as the 'marker'
agent. Unintended intrathecal placement can be diagnosed by the injection of an
appropriately small dose of a rapid onset LA.
Injection of 1 ml of air into an epidural catheter can be a highly specific and sensitive
marker of intravascular catheter Iocalisation (3), but the safety of the doppler test has
yet to be proven and, moreover, a precordial doppler and an extra person have to be
available (2).
Epinephrine, the catecholamine currently used in most test-doses, has several
disadvantages. This mixed alpha- and beta-adrenergic agent does not consistently
produce maternal tachycardia in laboring women. Cyclic maternal heart rate changes,
due to painful uterine contractions, occur normally in unanesthetised parturients. The
effect of epinephrine superimposed on these physiological changes in heart rate is
not always discernible. Moreover, a major adverse effect of systemic epinephrine is
its inhibition of uterine blood flow (UBF). This reduction of UBF has been
demonstrated in gravid ewes and lasts for 2-5 minutes (2).
Although the chronotropic response in term pregnant women is reduced, a test dose
containing 5 mcg of isoproterenol (isoprenaline) might be a safer and more effective
alternative (3). Isoproterenol produces a superior increase in maternal heart rate with
minor effects on uterine blood flow in the chronic maternal fetal sheep preparation
(4). In this animal model, incorporation of isoproterenol as a test dose does not
produce neurotoxicty (5, 6). These results suggest that isoproterenol may be safe for
use as an epidural test dose in pregnant women.
Questions still to be solved are:
1. Will the required amount of local anesthetics increase, if isoproterenol is used as
test-dose?
2. Is the relief of pain adequate when isoproterenol is used as an epidural test-dose?
3. What is the effect of isoproterenol on uterine blood flow?
Some contradictory results exist concerning the increased sensitivity, during
pregnancy, to the toxicity of local anesthetics. Santos et al. (7) compared the
systemic toxicity of ropivacaine (Chapter 4) and bupivacaine in non-pregnant and
pregnant ewes and concluded that..."The systemic toxicity of ropivacaine or
bupivacaine is not enhanced by gestation in sheep. This is in contrast to an earlier
study in which cardiotoxicity of bupivacaine was enhanced during ovine pregnancy."
(8).
A major concern in pregnancy is the trans-placental distribution of local anesthetics
(Chapter 77). Differences in the cord-to-maternal plasma drug concentration ratio
essentially reflect trans-placental differences in the extent of plasma binding (Chapter
50). When this ratio is high there should be a delay in the equilibration of drug in fetal
tissues. Conversely, similar umbilical artery and umbilical vein concentration ratios
observed for the various agents argue against large differences in their equilibration
rates in the fetus. Thus, the impact, if any, of plasma binding on the risks of fetal
toxicity is unclear (9).
The prevention of toxicity of local anesthetics (Chapter 89) in the mother and the
fetus is of utmost importance but, in this field, many questions remain to be
answered.
References:
1. Van Zundert A. Is there a need for chloroprocaine 3% and bupivacaine 0.75 %?
Acta Anesth Belg 1988;39;151.
2. Shnider SM, Levinson G, Ralston DH. Regional anesthesia for labor and delivery.
In: Anesthesia for obstetrics ed. Shnider SM, Levinson G; Williams & Wilkins pp
137-141
3. Leighton BL, Desimone CA, Norris MC, et al. Isoproterenol is an effective marker
of intravenous injection in laboring women. Anesthesiology 1989;71 ;206-209.
4. Marcus MAE, Vertommen JD, Van Aken H, et al. The hemodynamic effects of
different doses of isoproterenol in the pregnant ewe. Anesth Analg 1994;78,s267
5. Marcus MAE, Vertommen JD, Van Aken H, et al. Light microscopic
neuropathological observations after intrathecal bolus injections of isoproterenol.
Anesthesiology 1994;V81 ;A1175.
6. Marcus MAE, Bruyninckx F, Vertommen et al. Effects of epidural isoproterenol on
spinal somatosensory evoked potentials in the pregnant ewe and the non pregnant
ewe. Anesth Analg 1995;80;s295
7. Santos AL, Arthur R, Wlody D, et al. Comparative systemic toxicity of ropivacaine
and bupivacaine in non-pregnant and pregnant ewes. Anesthesiology
1995;82;734-740
8. Morishima HO, Pedersen H, Finster M, et al. Bupivacaine toxicity in pregnant and
non-pregnant ewes. Anesthesiology 1985 ;63;134-139.
9. Tucker GT. Safety in numbers. The role of pharmacokinetics in local anesthetic
toxicity: the 1993 ASRA lecture. Reg Anesth 1994;19(3);155-63.
Pamela Morgan
Choice of Vasopressor in the Management of Hypotension Following Combined
Spinal/Epidural, Spinal and Epidural Block for Obstetrics.
EPHEDRINE
Ephedrine remains one of the most extensively studied vasopressors used to treat
hypotension in the obstetric population. It has both direct and indirect mechanisms of
action, stimulating both alpha- and beta-receptors to increase cardiac output, heart
rate and systolic and diastolic blood pressure. Coronary, cerebral and muscle blood
flow are increased, while renal and splanchnic blood flow are decreased (1). Studies
have indicated that ephedrine returns uterine blood flow towards normal and reverses
the fetal acidosis, hypoxia and hypercarbia associated with hypotension (2, 3). The
prophylactic intramuscular administration of ephedrine before central neural blockade
is no longer advocated due to its variable absorption and potential for causing
hypertension (4, 5). Ephedrine may be used prophylactically or therapeutically as
intravenous boluses of 5-10 mg or as an infusion (0.01%) which can be titrated to
maintain blood pressure in the appropriate range. It appears that when ephedrine is
used as an infusion, the incidence of nausea is less than when it is given as a bolus
injection (6). The total dose of ephedrine required does not seem to differ significantly
whether given as a bolus or as an infusion (6). If the administration of a total dose of
50mgs of ephedrine administered in 5-10mg intravenous increments does not correct
the hypotension, phenylephrine should be substituted (7). Etilefrine, another
combined alpha- and beta-agonist, compares favourably with ephedrine. Metaraminol
restores maternal blood pressure but does not improve the fetal acidosis (2, 7, 8).
PHENYLEPHRINE
Early studies suggested that phenylephrine and methoxamine, both alpha-agonists,
would cause uterine vasoconstriction and were, therefore, best avoided in obstetrics
(9, 10). Recent work has suggested that phenylephrine can be just as effective as
ephedrine in the treatment of hypotension associated with either spinal or epidural
anaesthesia and produces no adverse fetal effects (11, 12). If tachycardia is
undesirable, phenylephrine may be better than ephedrine. Studies to date involving
phenylephrine have been on healthy women and caution has been suggested
regarding its concomitant use with ritodrine or magnesium sulphate (13, 14).
Phenylephrine may be given intravenously in 20-100 mcg increments (13, 14).
Other vasopressors have been used to treat hypotension secondary to obstetric
anaesthesia. Dopamine has been shown to decrease uterine blood flow in animals,
and has not been shown to have any benefit over ephedrine in humans (15, 16).
Angiotensin II has also been investigated and been found to have no clear
advantages (17).
Generally speaking, ephedrine appears to remain the vasopressor of choice to treat
hypotension in the obstetric population (Chapter 6). Phenylephrine may be used if a
total dose of 50 mg of ephedrine has failed to improve the blood pressure or if
tachycardia is deemed detrimental to the maternal situation. In healthy parturients,
phenylephrine 20-100 mcg may be an alternative mode of therapy for the
hypotension associated with regional anaesthesia.
References:
1. Weiner, N. Norepinephrine, epinephrine, and the sympathomimetic amines. In:
Gilman AG, Goodman LS, Rall TW, Murad F (Eds.). The Pharmacological Basis of
therapeutics. New York: Macmillan, 1985: 145-80.
2. James FM III, Greiss FC, Kemp RA. An evaluation of vasopressor therapy for
maternal hypotension during spinal anesthesia. Anesthesiology 1970: 33; 25-34.
3. Shnider SM, de Lorimier AA, Holl JW, Chapler FA, Morishima HO. Vasopressors
in obstetrics. I. correction of fetal acidosis with ephedrine during spinal hypotension.
Am J Obstet Gynecol 1968; 102:911-919.
4. McCrae AF, Wildsmith JAW. Prevention and treatment of hypotension during
central neural block. Br J Anaesth 1993; 70: 672-680.
5. Rolbin SH, Cole AFD, Hew EM, Pollard A, Virgint S. Prophylactic intramuscular
ephedrine before epidural anaesthesia for Caesarean section: efficacy and actions on
the foetus and newborn. Can Anaesth Soc J 1982; 29: 148-153.
6. Kang YG, Abouleish E, Caritis. Prophylactic intravenous ephedrine infusion during
spinal anesthesia for Cesarean section. Anesth Analg 1982; 61: 839-842.
7. Rout CC, Rocke DA. Prevention of hypotension following spinal anesthesia for
Cesarean section. Int Anesthesiol Clin 1994; 32: 117-135.
8. Shnider SM, deLorimier AA, Steffenson JL. Vasopressors in obstetrics. III. fetal
effects of metaraminol infusion during obstetric spinal hypotension. Am J Obstet
Gynecol 1970; 108: 1017-1022.
9. Ralston DH, Shnider SM, deLorimier AA. Effects of equipotent ephedrine,
metaraminol,mephenteramine and methoxamine on uterine blood flow in the
pregnant ewe. Anesthesiology 1974; 40: 354-370.
10. Greiss FC, Pick JR. The uterine vascular bed: adrenergic receptors. Obstetrics
and Gynecology 1964; 23:209-213.
11. Ramanthan S, Grant GJ. Vasopressor therapy for hypotension due to epidural
anesthesia for Cesarean section. Acta Anaesthesiol Scand 1988; 32: 559-565.
12. Moran DH, Perillo M, LaPorta RF, Bader AM, Datta S. Phenylephrine in the
prevention of hypotension following spinal anesthesia for Cesarean delivery. J Clin
Anesth 1991; 3: 301-305.
.13. Sipes SL, Chestnut DH, Vincent RD, DeBruyn CS, Bleuer SA, Chatterjee P.
Which vasopressor should be used to treat hypotension during magnesium sulfate
infusion and epidural anesthesia? Anesthesiology 1992; 77: 101-108.
14. McGrath JM, Chestnut DH, Vincent RD, et al. Ephedrine remains the
vasopressor of choice for treatment of hypotension during ritodrine infusion and
epidural anesthesia. Anesthesiology 1994; 80: 1073-1081.
15. Rolbin SH, Levinson G, Shnider SM, Biehl DR, Wright RG. Dopamine treatment
of spinal hypotension decreases uterine blood flow in the pregnant ewe.
Anesthesiology 1979; 51: 36-40.
16. Clark RB, Brunner JA. Dopamine for the treatment of spinal hypotension during
Cesarean section. Anesthesiology 1980; 53: 514-517.
17. Ramin SM, Ramin KD, Cox K, Magness RR, Shearer VE, Gant NF. Comparison
of prophylactic angiotensin II versus ephedrine infusion for prevention of maternal
hypotension during spinal anesthesia. Am J Obstet Gynecol 1994; 171: 734-739.
Anton Neilson
The story of local anaesthesia begins in 1884 when the naturally occurring alkaloid
cocaine was used by Carl Koller in his search for a topically effective anaesthetic for
eye surgery. Operating conditions were much superior to those provided by
contemporary general anaesthesia and surgeons were quick to appreciate the
advantages of local methods. Injections of cocaine, either by local infiltration or more
centrally, soon brought an appreciation of agent toxicity and unwanted effects. The
search for less toxic drugs followed and procaine was synthesised in 1905.
Numerous examples have followed; a major advance was the Swedish discovery of
the stable amide lignocaine in 1948 by Lofgren.
Some knowledge of the following topics is necessary to understand how local
anaesthetics produce their effects:
1. physiology of neural conduction,
2. differing neuron types,
3. anatomy of neural tissues,
4. physico-chemical properties, and
5. formulation of local anaesthetic drugs.
1. Physiology of Neural Conduction and Effects of Local Anaesthetics
Neural tissue is fundamentally excitable in an electrical sense and is capable of
responding in an ordered way to perturbations of the resting ionic gradients which
normally exist across the axon membrane. The so-called resting potential is about
70mV negative (inside relative to the outside) (1). The resting potential is generated
as a result of the activity of a sodium-potassium pump which continually pumps
sodium to the outside of the membrane in exchange for potassium which is pumped
in. As a result of this pump activity, marked concentration gradients for these two
cations are developed across the membrane. The respective extracellular and
intracellular concentrations of the ions are:
Na+ (Outside) 145 mMol/L
Na+ (Inside) 15 mMol/L
K+ (Outside) 5 mMol/L
K+ (Inside) 140 mMol/L
Membrane depolarisation is triggered by the sudden opening of sodium-specific
channels which is followed by a massive influx of Na+ passing down its concentration
gradient. This produces a transient rise in membrane potential to around 40mV
positive (inside relative to outside). As the intracellular potential rises, the voltage
change leads to a slower opening of potassium specific channels.
Repolarisation occurs as a result of closure of the sodium channels in the presence
of the continued efflux of potassium down its own concentration gradient through the
still-open potassium channel. As the intracellular potential falls back to the resting
level, the potassium channel closes and potassium conductance returns to the basal
state. These phenomena can be demonstrated in appropriate physiological
preparations (eg. giant squid axon) and are illustrated in Figure 53.1.
The depolarisation wave is propagated in neighbouring areas of the axon membrane
by the serial repetition of this sequence. This wave travelling along the axon
constitutes the transmitted impulse. If a nerve is myelinated, neural transmission by
the process of saltatory conduction occurs. This form of transmission involves
depolarisation only at the nodes of Ranvier and is much more rapid and energy
efficient than transmission in unmyelinated nerves.
Local anaesthetic agents occupy Na+ channels and inhibit the rapid passage of Na+
ions and the propagation of the wave. These events are complex and not fully
understood. Suffice to say that nerve block by local anaesthetics is not an 'all or
none' phenomenon and that the degree of impedance of neuronal traffic will depend
on numerous interrelated factors (Chapter 95).
2. Differing Neurone Types Axons differ widely in structure and function. The three
major classes of nerve fibres in decreasing diameter are:
1. 'A' fibres: myelinated somatic nerves,
2. 'B' fibres: myelinated preganglionic autonomic nerves, and
3. 'C' fibres: fine non-myelinated axons.
'A' fibres are further divided into alpha, beta, gamma and delta fibres, of decreasing
diameter.
Myelinated fibres propagate impulses more rapidly that non-myelinated and are more
resistant to blockade.
The degree of myelination, speed of conduction and size of the fibre determine the
sensitivity of the neurone to various local anaesthetic agents and to different
concentrations of the same drug (Chapter 4). The differing sensitivities of the
neurone types explain the phenomenon known as 'differential neural blockade' which
is responsible for 'sensory-motor split' (Chapter 88).
3. Anatomy of Neural Tissue
There is considerable variation in neural anatomy. For example, the sciatic nerve is
heavily invested with fibrous and connective tissue, epidural nerve roots considerably
less so, and nerve roots in the subarachnoid space hardly at all. It can be readily
appreciated that access to neuronal tissue by diffusion of local anaesthetic can vary
widely in different situations.
4. Physico-chemical Properties and Formulation of Local Anaesthetics
In pure form, weakly basic local anaesthetics are largely non-ionised and, therefore,
poorly water soluble. Formulation as HCI salts at a pH of 4.0 to 7.0 greatly increases
the ionised fraction which then equilibrates, in aqueous solution, with a small amount
of free base. Upon injection into the body, physiological buffers raise the pH so that
the non-ionised fraction increases.
It is as the lipophilic, non-ionised form that the drug diffuses across the axon
membrane. The acidic intracellular conditions drive the equilibrium back towards the
ionised fraction. It is in this form that the drug finally exerts its blocking action.
Summary
Local anaesthetics act at the axonal membrane to inhibit the transmission of impulses
along the nerve cell. The pharmaco-dynamics and -kinetics are complex and the
complete picture is not yet elucidated.
Reference:
1. deJong RH Clinical Physiology of Local Anesthetic Action. In: Cousins MJ,
Bridenbaugh PO (eds). Neural Blockade in Clinical Anesthesia and Management of
Pain, 2nd ed, JB Lippincott Co, Philadelphia,1988. p 21-44
Julius Neumark
Drug Interactions in the Obstetric Patient Receiving Major Regional Blockade:
A drug interaction is the (potentiating or antagonising) influence of one drug on the
effects or side effects of another drug. The interaction may be pharmacokinetic or
pharmacodynamic. For example, the increased duration of epidural block from
inhibition of the absorption of local anaesthetics (LA) produced by addition of
epinephrine is a pharmacokinetic interaction; the same increase obtained by the
addition of an opiate (due to the effect on the receptors in the spinal cord) is a
pharmacodynamic interaction.
Interactions:
1. Epinephrine: Maximum enhancement of a LA block by epinephrine is obtained by
the addition of a dose of 5 mcg/ml (its ceiling effect). In obstetrics, if epinephrine is
unintentionally injected intra-vascularly the main side effect is vasoconstriction of the
uterine arteries, which could be harmful for the fetus (5).
2. Opiates: Opioids added to LAs also exhibit a ceiling effect. For fentanyl this occurs
at 50 mcg epidurally and 10 mcg subarachnoidally (6) even though higher doses are
recommended. For sufentanil the corresponding ceiling doses are 25 mcg and 10
mcg respectively (3) and for morphine it is 0.1 mg subarachnoidally (7). These
amounts are safe for both mother and fetus (1, 2, 9). Morphine, a hydrophilic drug, in
a dose up to 3mg epidurally, as an additive to the LAs, is also safe as far as late
respiratory depression is concerned. This 3mg epidural dose is significantly lower
than the morphine ceiling effect dose.
3. Clonidine: The pharmacodynamic potentiation of LA effects can also be obtained
with clonidine, but its use in pregnancy is controversial because of its haemodynamic
side effects.
4. Bicarbonate: Since penetration of LAs is dependent upon their ionization, the
addition of bicarbonate (4) or CO2 (8) may shorten the onset and increase the
intensity of the block (a pharmacokinetic interaction). With bupivacaine, however, this
effect is limited because the drug precipitates at a specific pH.
5. H2 antagonists: Repeated intake of cimetidine (but not ranitidine) may enhance
bupivacaine toxicity by inhibiting bupivacaine metabolism (5).
6. Others: All drugs with high protein binding may increase toxicity of bupivacaine
(Table 36.6) and ropivacaine (Chapter 4) (a pharmacokinetic interaction). This is
especially so in the fetus where decreased protein binding produces higher serum
and tissue free drug levels (Chapter 77 and Chapter 50).
References:
1. Benlabed M et al Anesthesiology 1990 73:1110
2. Capogna G et al Reg Anesth 1989 14:S24.
3. Courtney MA et al Reg. Anesth 1992 17:274
4. DiFazio CA et al. Anesth Analg 1986 65:760
5. Janowski EC. Anesthesiology Clinics of North America 1990 8:1
6. Naulty JS. Anesthesiology 1985; 63:694
7. Schaer H et al Anaesthesist 1992 41:689
8. Sukhani R, Winnie AP. Anesth Analg 1987 66:739
9. Youngstrom P. Anesthesiology 1984 61 :A414
Geraldine O'Sullivan
Fasting During Labour - Its Effect on Outcomes following Regional
Anaesthesia/Analgesia
In the past few years, maternal mortality from acid pulmonary aspiration (Mendelson's
Syndrome) (1) has declined dramatically (Chapter 45). In the very first triennial
Report on Confidential Enquiries into Maternal Deaths (1952) there were 32 deaths
from Mendelson's Syndrome; in the 1967-69 Report there were 26 deaths; in the
latest Report (1988-90) there were no clearly defined deaths from this condition (2).
This remarkable success can probably be attributed, in part, to the introduction of
fasting regimens for parturients, the increasing use of regional anaesthesia for
Caesarean section (CS), the universal adoption of cricoid pressure (Sellick's
manoeuvre) (4) for CS under general anaesthesia and the introduction of the H2
antagonists into obstetric practice (Chapter 80). Perversely, this carefully audited
success is now being used by midwives and maternal pressure groups as an
example of the excessively dictatorial approach of obstetric anaesthetists in not
allowing mothers to eat or drink during labour. They argue that prolonged fasting
during labour has never been scientifically proven to influence pulmonary aspiration
and that since most maternal anaesthetic deaths are now caused by difficult / failed
intubation in the hands of inexperienced anaesthetists, it is illogical to continue to
make women fast during labour.
Moreover, the metabolic consequences of fasting (e.g. ketosis, changes in lactate,
insulin and Growth Hormone) might even be detrimental to the progress of labour. In
addition, maternal intravenous hydration using 5% and 10% dextrose solutions has
been shown to result in rebound neonatal hypoglycaemia. (3)
The safety of 'no feeding' policies during labour can never be disputed for those
mothers who ultimately require an urgent or emergency Caesarean section. The
effect of fasting or, indeed, feeding during labour on outcomes, both maternal and
fetal, has never been evaluated in women receiving regional analgesia. A study on
feeding during labour is currently in progress at St. Thomas' Hospital where
parameters being evaluated include maternal and fetal metabolic effects of feeding,
obstetric outcome, ultrasonic examination of the stomach (to measure residual
gastric content) and maternal satisfaction.
References:
1. Mendelson CL. The aspiration of stomach contents into the lungs during obstetric
anesthesia. Am J Obstet Gynecol 1946; 52:191
2. Report on the Confidential Enquiries into Maternal Deaths in England and Wales
London:HMSO (1952-54), (67-69) and (1988-90)
3. Kenepp W, Sheeley WC et al. Fetal and neonatal hazards of maternal hydration
with 5% dextrose before Caesarean section. Lancet 1982; i: 1150-1152
4. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during
induction of anaesthesia. Lancet 2:404, 1961
Michael Paech
Local Anaesthetic and Narcotic of Choice in Combined Spinal-Epidural for Labour
and Delivery.
Combined spinal-epidural analgesia (CSE) in labour is a new approach to pain relief
which uses an initial dose of subarachnoid opioid, usually with bupivacaine, to rapidly
achieve analgesia (Figure 61.1) (Chapter 62). This is followed by conventional
epidural therapy for maintenance, if required. There are, to date, no dose-response
and few comparative studies of subarachnoid analgesic solutions, so suggestions are
based on clinical experience and dose-response studies of subarachnoid opioid
alone during labour.
When used as sole agents in early labour, effective analgesic doses of subarachnoid
opioid which are associated with an acceptable incidence of nausea and pruritus lie
in the range of 3 to 10mcg sufentanil (1, 2, 3) and 15 to 25mcg fentanyl, although the
optimal doses may be 10mcg and 15mcg respectively (4, 5, 6). Sufentanil may be
superior to fentanyl (7), although it can also cause more pruritus (8). Pethidine
(meperidine) 10mg appears to be more effective than both, especially in late labour
(3), but has not been investigated as part of a CSE regimen (Figure 61.2). There
appears to be little merit in combining morphine with a lipophilic opioid, since side
effects and the risk of respiratory depression may be increased (9, 10).
Bupivacaine alone is unsatisfactory, since doses of 2.5 to 5.0mg do not reliably
produce good analgesia and the 5mg dose results in a high incidence of dense motor
block (11, 12) .
The combination of bupivacaine and opioid improves pain relief compared with either
drug alone (11), and seems the best approach (13, 14) (Figure 61.3). No
demonstrable neonatal effects have been shown and although significant falls in
blood pressure may occur in the first 30 minutes, thereafter, it is safe to ambulate and
most women are capable of doing so (13, 14, 15). The optimal combination has yet to
be determined, with some authors favouring as little as 1mg of bupivacaine with
opioid (14,16). Because of a synergistic analgesic effect, the optimal dose of opioid
may also be reduced in combination regimens.
The addition of adrenaline (epinephrine) by some investigators (14, 16) has not been
confirmed as beneficial in this setting, and may increase nausea without improving
analgesia (2). Studies of the influence of the volume of injectate on clinical response
show no difference when 10 mcg of subarachnoid sufentanil (with no local
anaesthetic) was administered in 1, 2 or 3ml of solute (17, 18).
References:
1. Naulty J Anesthesiology 1990;73:A964
2. Camann W Anesthesiology 1993;78:870
3. Honet J Anesth Analg 1992;75:734
4. Van Decar T Anesthesiology 1994;81:A1148
5. Van Decar T Anesth Analg 1995;80:S522
6. Hays R Anesthesiology 1994;81:A1149
7. Leicht C Anesth Analg 1991;72:
8. Arkoosh V Reg Anesth 1994;19:243
9. Caldwell L Reg Anesth 1994;19:2
10. Palmer C Anesthesiology 1991;74:1153
11. Campbell D Anesthesiology 1994:82:A1145
12. Stacey R Br J Anaesth 1993;71:499
13. Collis R Int J Obstet Anesth 1994;3:75
14. Joos S Int J Obstet Anesth 1995;4:155
15. Shennan A Br J Obstet Gyn 1995;102:192
16. Kartawiadi L Br J Anaesth 1995;74;A351
17. Isaacson W Anesthesiology 1994;81:A1154
18. Riley E Anesthesiology 1994;81:A1145
Michael Paech
Local Anaesthetic and Narcotic of Choice in Epidurals for Labour and Delivery.
Epidural analgesia in labour is best achieved using a combination of drugs. The
choice of solution, its strength and formulation should be based on consideration of
the specific indication (eg. pain relief in early or late labour; anaesthesia for
instrumental delivery) (Chapter 73), the woman's expectation and requirements
(Chapter 58), the epidural technique (Chapter 1) and the medical status of the mother
and her fetus.
The best local anaesthetic for pain relief is the long-acting amide, bupivacaine, which
is unlikely to give rise to cumulative local anaesthetic toxicity when used in the usual
therapeutic dose range (1), and is safe for the fetus and neonate. Lignocaine
(lidocaine) is suitable for establishing analgesia, or rapidly augmenting an epidural
anaesthetic for instrumental or Caesarean delivery (2). Ropivacaine, to be released
in 1996, appears to have very similar clinical sensory and motor characteristics to an
equivalent concentration of bupivacaine, when used as a sole agent (3, 4) (Chapter
4).
Because 0.125% bupivacaine with epinephrine is only effective in selected
populations (5, 6), I would recommend that initial pain relief be obtained using either
0.25% bupivacaine, or 0.125% with opioid (7). The latter has the advantage of being
both a test and therapeutic dose (8). If administered by intermittent bolus, the
addition of fentanyl to bupivacaine provides greater maternal satisfaction than
bupivacaine alone (9).
There are few controlled comparisons of epidural opioids during labour, so that the
choice often depends on local availability, cost and prescriber familiarity. Morphine is
unsuitable, due to its slow onset and high incidence of side effects. Fentanyl,
sufentanil, diamorphine and pethidine are popular and, when used appropriately,
appear safe for the healthy, term infant. Only fentanyl and sufentanil have been
evaluated extensively in this setting. The optimal concentration of intermittent bolus
bupivacaine with opioid is 0.125%, and the most suitable dose of opioid is fentanyl
50mcg (6, 10, 11), sufentanil 7.5 mcg (12), or pethidine 25mg (13). Fentanyl 100mcg
may be indicated in certain circumstances (14, 15).
For maintenance of pain relief by patient-controlled epidural analgesia (PCEA),
bupivacaine 0.0625 to 0.125% with either fentanyl or sufentanil allows the majority of
parturients to remain ambulant and produces less motor block than 0.25%
bupivacaine (16). PCEA is associated with an overall reduction in the amount of drug
used when compared with other techniques. Adrenaline significantly increases the
degree of motor block (17) (Figure 60.1). A recommended solution is 0.1%
bupivacaine with fentanyl 2 mcg/ml given as a 5ml incremental bolus on demand
(18). A continuous infusion technique using bupivacaine 0.125% at 10-15ml/hr is
effective. The addition of fentanyl allows the concentration of bupivacaine to be
reduced to 0.0625% whilst efficacy is retained and motor block diminished (19).
Success has also been reported a with combination of 0.01% bupivacaine, sufentanil
and epinephrine (20). When given by infusion at 7.5mls/hr, bupivacaine 0.125% with
diamorphine 0.0025% was more efficacious than bupivacaine 0.125% with fentanyl
0.0002%, but both combinations produced better analgesia than bupivacaine alone
(21). The addition of sufentanil 10mcg/hr is better than fentanyl 20mcg/h (20).
References:
1. Reynolds F Br J Anaesth 1973 45:1049
2. Price M Int J Obstet Anesth 1991;1:13
3. Stienstra R Anesth Analg 1995;80:285
4. McCrae A Br J Anaesth 1995;74:261
5. Bleyaert A Anesthesiology 1979;31:435
6. Yau G Anaesthesia 1990;45:1020
7. Russell R Int J Obstet Anesth 1993;2:78
8. Van Zundert A Anesthesiology 1988;69:998
9. Murphy J, Henderson K, Bowden MI, Lewis M, Cooper GM. Bupivacaine versus
bupivacaine plus fentanyl for epidural analgesia: effect on maternal satisfaction. Br
Med J 1991;302:564-7
10. Cohen S Anesthesiology 1987;67:403
11. Yau G Anaesth Intens Care 1990;18:532
12. Vertommen JD Anaesthesia 1994;49:678
13. Brownridge P Anaesth Intens Care 1992;17:15
14. Reynolds F Anaesthesia 1989;44:341
15. Celleno D Can J Anaesth 1988;35:375
16. Paech M Int J Obstet Anesth 1993;2:65
17. Lysak S Anesthesiology 1990;72:44
18. Paech M Int J Obstet Anesth 1996 5: in press
19. Russell R Int J Obstet Anesth 1995 4:82
20. Cohen S Anesth Analg 1992;74:S47
21. Enever G, Noble HA, Kolditz D, Valentine S, Thomas TA. Epidural infusion of
diamorphine with bupivacaine in labour. A comparison with fentanyl and bupivacaine.
Anaesthesia 1991;46:169- 73
John Paull
The Contribution of Regional Techniques to the Safe Conduct of Obstetric
Anaesthesia and Analgesia.
Most obstetric anaesthetists presuppose that regional analgesia has made a
contribution to the safe conduct of obstetric anaesthesia and analgesia and would
like to believe that efforts to increase the use of regional blockade has reduced the
risks of obstetric pain relief. Proving this is not easy.
Mortality in Obstetric Anaesthesia and Analgesia
Despite many deficiencies in data collection we know that maternal mortality is
declining. In the 1600's, one woman in every 44 died in childbirth. In the 1930's
maternal mortality was 670:100,000 births. In the 1980's it had fallen to 9.6: 100,000.
In the 1990's in Australia it is 6.7:100,000 births, a 100-fold reduction in 60 years.
Regrettably, the contribution of anaesthesia to the maternal death rate, as a
percentage, has risen. This is because, in most countries, total anaesthetic-related
maternal deaths have remained relatively constant whilst there has been a dramatic
fall in the numbers of maternal deaths due to the three great killers: sepsis,
haemorrhage and toxaemia.
Because of deficiencies in the denominator of national databases we are still unable
to say with confidence what numbers of pregnant women undergo general
anaesthesia and what numbers undergo regional anaesthesia in childbirth.
In national maternal mortality reports of the USA, Britain and Australia, it is apparent
that the number of maternal deaths from general anaesthesia-related causes
outnumber those from regional analgesia causes. However, because of the
denominator deficiencies we are still unable to say with certainty that regional
blockade is safer than general anaesthesia.
Morbidity in Obstetric Anaesthesia and Analgesia
Prospective collection of morbidity data has not been undertaken on a large enough
scale to enable one to reliably comment on the relative morbidities of general and
regional anaesthesia techniques.
The significance of morbidity depends on the point of view of the observer. The
mother as an observer may well have a different perspective of post-anaesthesia
morbidity when compared to the anaesthetist. The data are just not available to allow
us to form a conclusion about the safety of both techniques, either from the point of
view of the mother or the anaesthetist. Most anaesthetists would feel that permanent
morbidity associated with general anaesthesia is relatively rare. The incidence of
permanent neurological sequelae after epidural anaesthesia appears to be in the
range of 1:15,000 to 1:100,000 epidurals (1). It must be remembered that permanent
neurological sequelae have been reported in childbirth when regional blocks have not
been used.
Better collection of procedural, morbidity and mortality data in the age of the
microchip will allow us to provide an answer to our question. At present we don't
have the solution.
Timothy Pavy
Sensory-motor split: its implications for analgesia in labour and delivery.
The goal of modern epidural analgesia in labour is optimum sensory blockade without
motor blockade. Parturients ideally are aware of contractions and descent of the fetal
head, feel the urge to push and do so effectively, and feel the baby's expulsion - but
without pain at any stage. It is fortunate for parturients and epiduralists alike that
most of the pain of the first stage of labour is conducted along sympathetic nerves,
which enter the spinal cord from T10 to L1. These nerves are small-diameter,
unmyelinated C fibres, which are readily blocked with small volumes of dilute local
anaesthetic (LA). It is therefore theoretically possible to obtain complete relief from
this most severe and (for some) distressing pain without using the concentrated
solutions which lead to motor blockade. Motor block is considered undesirable
because of the possible increase in the need for assisted deliveries (1), loss of pelvic
floor tone (which may interfere with fetal head rotation) (2) and impaired ability to
ambulate. Russell (3) has described a method of assessing motor blockade in labour.
Attempts have been made to obtain analgesia without using LA, but the results of
intrathecal opioids alone are disappointing (4). Apart from inadequate pain relief,
there is a significant incidence of nausea, vomiting and pruritus. Data concerning
combined spinal-epidural techniques (using spinal analgesia for the initial dose) in
respect of labour outcome are awaited. As low-dose LA (e.g 0.125% bupivacaine
alone) is generally inadequate for epidural analgesia (5), the addition of adjuvants is
necessary. Fentanyl achieved initial popularity following work which demonstrated its
efficacy in improving perineal analgesia (6), while pethidine and the expensive
sufentanil have been used extensively in different parts of the world. More recently,
clonidine has been tried with good results, although sedation is significant (7).
Critics of epidural analgesia suggest that there is an increased rate of intervention,
particularly caesarean section (8), although evidence is conflicting. Chestnut's work
suggests that infusions of 0.125% bupivacaine beyond 8cm cervical dilatation in
primigravid women improve analgesia compared to placebo but at the expense of a
prolonged second stage and increased instrumental deliveries (9). Importantly,
caesarean rates are unchanged. Surprisingly, very low dose bupivacaine-fentanyl
infusions which are maintained until full dilatation do not reduce the rate of
intervention, even though motor block is reduced. Analgesia is, however,
considerably improved (10), indicating that the practice of withholding analgesia in
second stage is to be condemned. Active management, using oxytocin infusions,
reduces the instrumental delivery rate (11). "Catastrophe" modelling techniques
suggest that changes in epidural practice from high-dose to low-dose LA-opioid result
in fewer interventions, despite increased use of epidurals in labour (12).
Low-dose patient controlled epidural analgesia (PCEA) may improve the rate of
spontaneous vaginal deliveries (13). It certainly minimises drug consumption when
compared to infusions and intermittent bolus as techniques for maintaining analgesia
(14, 15) and may, by empowering the parturient, introduce an important factor in the
debate over how best to manage the second stage (pain from which involves the
larger pudendal nerve S2-S4 (Figure 21.1)): the woman's choice. The upright posture
for delivery is historically important, and maternal satisfaction is enhanced if mobility
in labour is possible (16). Excessive motor block makes both of these difficult. The
challenge for obstetric anesthesiologists is to produce consistently a degree of
sensory blockade that increases the likelihood of spontaneous delivery by minimising
motor blockade and maximising expulsive powers. Optimum analgesia may enable
parturients to push more effectively if they are neither distressed nor distracted by
pain.
References:
1. Thorburn J, Moir DD Extradural analgesia: the influence of volume and
concentration of bupivacaine on the mode of delivery, analgesic efficacy, and motor
block. Br.J. Anaesth. 1981; 53:933
2. Walton P Anaesthesia 1984, p 218
3. Russell R Int J Obstet Anesth 1992 p 230
4. Caldwell L Reg Anesth 1994 p 2
5. Yau G Anaesthesia 1990 p 1020
6. Reynolds F Anaesthesia 1989, p 341
7. O'Meara M BJA 1993; 71: p 651
8. Thorp J Am J Obstet Gynecol 1993, p 851
9. Chestnut D Anesthesiology 1987; 66: p 774
10. Chestnut D Anesthesiology 1990; 72; p 613
11. CarIi F Int J Obstet Anesth 1993, p 15
12. Naulty J Anesthesiology 1988 69: 3A, A660
13. Ferrante M Anesth Analg 1991; 73: p 547
14. Gambling D Can J Anaesth 1988, p 249
15. Gambling D Anesth Analg 1990; 70: p 256
16. Murphey J BMJ 1991, p 564.
Jackie Porter and Felicity Reynolds
Maternal Hypoxaemia Following Major Regional Blockade During Labour and
Delivery.
Episodes of hypoxaemia occur in healthy women during painful labour (1).
Hyperventilation during a contraction reduces maternal arterial PC02 and so reduces
ventilatory drive. Subsequent hypoventilation or apnoea between contractions may
cause maternal hypoxaemia (2). Systemic opioids increase the incidence of maternal
hypoxaemia whilst epidurals using local anaesthetic alone are associated with a
reduced incidence compared with pethidine (3), 'Entonox' (4) or no analgesia (5, 6).
Effective analgesia promotes more regular respiration and the need for systemic
opioids or 'Entonox' (nitrous oxide:oxygen 50:50 mixture) is avoided (Chapter 33).
The recent addition of opioids to epidurals reduces the dose of local anaesthetic used
and lessens the degree of motor block (Chapter 60, Chapter 88). However, epidural
infusions of bupivacaine with fentanyl increase the incidence of maternal hypoxaemia
during the second stage of labour compared with infusions of bupivacaine alone (6)
(Figure 87.1, Table 87.1). The reasons for this are unclear but hypoxaemia
associated with breath holding during pushing may be corrected more slowly between
pushes due to opioid-induced respiratory depression. (Chapter 90)
Effects on the fetus
Maternal hypoxaemic episodes may cause a reduction in fetal oxygenation (2) but
there is little evidence that the baby is adversely affected (3, 6) (Chapter 35).
However, a sub-set of 'at risk' babies may be more susceptible (eg. some cases of
preeclampsia, eclampsia, maternal respiratory or cardiac disease, intra-uterine
growth retardation or fetal distress) (Table 3.1) (Chapter 25). Pulse oximetry and/or
oxygen therapy may be of benefit in these cases.
Caesarean section
During regional blockade for caesarean section, the sensory block T4 - T5 required
to provide adequate anaesthesia is accompanied by paralysis of the abdominal
muscles and a number of intercostal muscles. Breathing becomes predominantly
diaphragmatic and is limited by the gravid uterus and the supine position. The
administration of oxygen to the mother before delivery has been recommended (7) to
maximise fetal oxygenation (Chapter 76). The ability to cough is also impaired (8) and
persists for some time post-operatively. Whilst this degree of motor block may not be
dangerous for most women, in those with respiratory or musculoskeletal disease it
may pose a clinically significant risk to ventilation. Epidural and intrathecal opioids,
given during surgery or for post-operative analgesia, also have the potential to cause
respiratory depression (9) and reduce maternal oxygenation (Chapter 99).
References:
1. Porter KB, Goldhamer R, Mankad A, Peevy K, Gaddy J, Spinnato JA. Evaluation
of arterial oxygen saturation in pregnant patients and their newborns. Obstetrics &
Gynecology 1988; 71:354-357.
2. Huch A, Huch R, Schneider H, Rooth G. Continuous transcutaneous monitoring of
fetal oxygen tension during labour. British Journal of Obstetrics and Gynaecology
1977; 84 (Supp. 1): 1-39.
3. Minnich ME, Brown M, Clark RB, Miller FC, Thompson DS. Oxygen desaturation in
women in labor. Journal of Reproductive Medicine 1990; 35:693-696.
4. Arfeen Z, Armstrong PJ, Whitfield A. The effects of Entonox and epidural
analgesia on arterial oxygen saturation of women in labour. Anaesthesia 1994;
49:32-34.
5. Curtis J, Shnider SM, Saitto C, Orezzi C, Volante I, Bertini L, Cosmi EV. The
effects of painful uterine contractions, position, and epidural anesthesia on maternal
transcutaneous oxygen tension (tcP02). Anesthesiology 1980; 53:S315.
6. Griffin RP, Reynolds F. Maternal hypoxaemia during labour and delivery: the
influence of analgesia and effect on neonatal outcome. Anaesthesia 1995;
50:151-156.
7. Ramanathan S, Gandhi S, Arismendy J, Chalon J, Turndorf H. Oxygen transfer
from mother to fetus during cesarean section under epidural anesthesia. Anesthesia
and Analgesia 1982; 61:576-581.
8. Kirby SA, Kendrick AH, Anderson M, Williams AB, Thomas TA. Dynamic
respiratory functions and expiratory mouth pressures in obese and non-obese
patients during sub-arachnoid (SAB) anaesthesia for caesarean section. International
Journal of Obstetric Anesthesia 1995; 4:260-261.
9. Gustafsson LL, Schildt B, Jacobsen K. Adverse effects of extradural and
intrathecal opiates: Report of a nationwide survey in Sweden. British Journal of
Anaesthesia 1982; 54:479-486.
Lloyd Redick
I. Unable to achieve adequate epidural placement:
Cause:
1. Anatomic variations (Chapter 105, Chapter 48).
2. Equipment (needle) inadequacy.
Management:
1. Switch to spinal anesthesia: continuous for labor; single shot for cesarean section.
2. Labor: Abandon epidural; use IV analgesics or other techniques (Chapter 65).
3. Cesarean section: switch to general anesthesia (Chapter 20).
II. Epidural placed but: No Anesthesia:
Cause:
1. Catheter not in epidural space, IV, out through a foramen.
Management:
1. Labor: Repeat epidural; consider switch to continuous spinal or combined
spinal-epidural (CSE) (Chapter 70).
2. Cesarean Section:
a. repeat epidural.
b. switch to spinal, CSE or general anesthesia.
III. Epidural placed but: One-sided analgesia:
Cause:
1. Patient position (Chapter 30).
2. Anatomic or functional division of epidural space (Chapter 32).
Management:
1. Labor:
a. turn patient to opposite side and supplement dose (1/3 to 1/2 initial dose).
b. pull epidural catheter back 0.5 to 1 cm and redose.
c. add narcotic to local anesthetic (Chapter 60).
d. repeat epidural.
2. Cesarean Section:
a. repeat epidural.
IV. Epidural placed but: 'patchy' anesthesia or missed segment:
Cause:
1. Air used for loss of resistance technique.
2. Scarring or deformation of epidural space (eg. kyphoscoliosis).
3. Anatomical variations of epidural space.
Management:
1. Labor:
a. turn patient to opposite side and supplement dose.
b. pull epidural catheter back 0.5 to 1 cm and redose.
c. add narcotic to local anesthetic.
d. repeat epidural.
2. Cesarean section:
a.repeat epidural.
c. ask surgeon to supplement with local infiltration if area small (Chapter 100).
d. supplement with IV or inhalational analgesia if discomfort mild.
V. Epidural placed, segmental level adequate, but block not intense enough:
Cause:
1. Insufficient time allowed for block to 'mature'.
2. Inadequate concentration of local anesthetic.
3. Loss of local anesthetic (volume) through intervertebral foramina.
4. Patient perception of adequacy of sensory block.
Management:
1. Labor:
a. allow more time for development of block.
b. add narcotic,
c. increase concentration of local anesthetic,
d. redose.
e. wait 3-5 minutes.
a. allow more time for development of block.
b. redose,
c. increase concentration of local anesthetic,
d. add narcotic,
e. wait 2-3 minutes.
f. supplement with IV/inhalation analgesics.
g. proceed to general anesthesia if necessary.
VI. Epidural placed, satisfactory intensity of block but inadequate segmental level:
(Chapter 8)
Cause:
1. Inadequate volume of local anesthetic.
2. Loss of local anesthetic volume out through intervertebral foramina (Chapter 1).
3. Insufficient time allowed for block to reach desired level.
Management:
1. Labor:
a. allow more time for development of height of block.
b. redose; consider using larger volume to achieve higher segmental spread.
a. allow more time for development of height of block.
b. add volume.
c. repeat epidural.
d. switch to spinal, CSE or general anesthesia.
VII. Previously working epidural, now appears not to be working:
Cause:
Epidural catheter has probably become displaced.
Management:
1. Labor:
a. examine catheter insertion site.
b. if catheter position appears satisfactory and intravascular migration has been
excluded, give a significant dose, ie. repeat of initial dose,
c. if no improvement in appropriate period of time, REPLACE!
a. examine catheter insertion site.
b. give significant dose,
c. if no response, consider replacement, spinal, CSE, or general anesthesia
depending on circumstances and time.
VIII. Other suggestions:
1. Patients with a long labor, 5 or more hours, may become mentally fatigued, even
with a well functioning epidural. Butorphanol 0.5mg IV may produce an improved
mental state.
2. Do not allow a block to recede; top up by the clock if not using a continuous
infusion.
3. Always allow adequate time for the selected local anesthetic to become effective.
4. If quality of analgesia for cesarean section is found to be inadequate after surgery
has commenced, the choices for action become limited, ie. a change to spinal, CSE
or repeat epidural is no longer an option.
Lloyd Redick
Management of Failure of Spinal (Subarachnoid) Anesthesia in Obstetrics.
I. Problem: Failure to Place:
Cause:
1. Anatomic location difficult to find.
2. Flexible, small spinal needle bends away from dural sac (Chapter 59).
3. Inadequate needle length, especially when using introducer (Chapter 105).
Prevention:
1. Use longer or stiffer (larger) spinal needle.
2. Sitting posture may be helpful for anatomic localisation of the space.
Management:
1. Switch to epidural anesthesia (stiffer needle).
2. Switch to general anesthesia.
3. Local infiltration or pudendal block if vaginal delivery planned.
II. Problem: Inadequate anesthesia: missed segment, "hot spot".
Cause:
1. "Scarring" about nerve rootlets,
2. Poor distribution of local anesthetic, etc.
Prevention:
?Not preventable.
Management:
1. Use larger dose of local anesthetic and/or add narcotic to spinal anesthetic.
2. Have surgeon inject local anesthetic in area.
3. IV or inhalational analgesic supplementation.
4. If 1, 2, or 3 not adequate, go to general anesthesia.
III. Problem: Inadequate anesthesia: not dense enough or not high enough.
Cause:
1. Inadequate dose (mg) of local anesthetic (Chapter 78).
2. Inadequate volume (mls) of local anesthetic.
3. Inadequate spread, especially with hyperbaric solution (Figure 30.1).
4. Injection of local anesthetic partially in and out of dural sac (multicompartment
block, Chapter 11).
5. Slow onset of block.
Prevention:
1. Use adequate dose of local anesthetic (bupivacaine 12 to 15mg; tetracaine 10 to
13mg; lidocaine 75 to 100mg).
2. Use adequate volume (1.5 to 3.5ml).
3. Advance spinal needle 1mm more after apparent puncture, rotate spinal needle
180-360 degrees to further assure tip and bevel within subarachnoid space (Figure
E.1).
4. Adding narcotic to local anesthetic may help, but should not be relied upon for
anesthesia (Chapter 61).
Management:
1. If incision not made and time allows, spinal may be repeated: use full dose.
2. If time since injection less than 12 minutes, upper level may be enhanced by
having patient cough, especially if isobaric solution has been used.
3. It is usually necessary to use some head down tilt to achieve an adequate level
with hyperbaric solutions (Chapter 30) (Figure 30.1).
4. If slow onset suspected, wait 3 minutes more if situation allows.
5. If incision made or emergency situation, supplement with IV and/or inhalation, or
go to general anesthesia (dependent on degree of inadequacy of block).
IV. Problem: Inadequate duration:
Cause:
1. Surgery lasting longer than duration of local anesthetic action: May be due to
surgical reasons, inadequate initial dose, or inappropriate choice of local anesthetic
agent.
Prevention:
1. Select local anesthetic to provide 1.5 times expected length of procedure.
2. Consider addition of epinephrine or phenylephrine to spinal solution (Chapter 5),
and/or
3. Consider addition of narcotic to spinal solution (may increase duration).
Management:
1. IV and/or inhalation supplementation if inadequacy mild.
2. General anesthesia if inadequacy moderate to severe and/or expected further
duration unpredictable.
Justin Reed and Michael Scarf.
The issue of whether to perform an epidural blood patch (EBP) on HIV patients has
raised some concern amongst anaesthetists (1, 2, 3, 4). This is despite the fact that
HIV penetration of the CNS occurs early in the disease (perhaps with the first
viraemic episodes). Possible reasons for this concern may include:
1. fear of enhancing the CNS spread of the virus,
2. masking of adverse neurological sequelae of EBP by coexistent neurological
complications of HIV.,
3. possible epidural infection in immuno-compromised patients, and
4. potential for HIV-associated coagulopathy to produce an epidural haematoma.
Only one study has looked at EBP's in this group of patients (1). It reviewed yearly
physical examinations and biannual neuropsychological testing in six HIV
seropositive males who had required an EBP for post-dural puncture headaches
(PDPH). The authors were unable to identify morbidity attributable to the EBP in
these patients who were followed for a period of six months to two years.
In another relevant study (6), Hughes et al reviewed the outcome of regional
analgesia in eighteen parturients infected with HIV. The patients were followed for a
period of 4-6 months post-partum. The authors found no neurologic or infectious
complications related to the anaesthetic management.
Finally, three single case histories of EBP's (1, 2, 3) in HIV patients have likewise
demonstrated no adverse sequelae. One of these patients was followed for a period
of nineteen months, while a second had received two blood patches over a period of
three years. The authors' own experience of EBP in an HIV positive patient concur
with the above findings.
Background
HIV penetration of the CNS occurs early in the disease (perhaps with the first
viraemic episode) and CNS complications are common (5). This explains why
relatively frequent diagnostic or therapeutic lumbar punctures are needed in this
group of patients.
Postulated mechanisms of spread include the central migration of systemically
infected macrophages. Subsequent CNS dysfunction may occur as a result of:
1. direct disruption of brain structure and function,
2. opportunistic infections,
3. growth of tumours, and
4. peripheral neuropathies.
Subtle brain dysfunction can be detected in asymptomatic HIV patients using
sophisticated neurophysiologic and neuropsychologic tests. Twenty five to thirty
percent of asymptomatic (CDC stage 2 and 3) patients show evidence of minor
cognitive/motor dysfunction, involving activities such as attention, memory and speed
processing.
More severe dysfunction (dementia) occurs rarely in CDC stages 2 and 3, but has an
incidence of 14% in CDC stage 4 infection.
Peripheral nervous system involvement also occurs in 15 - 20% of patients, resulting
in sensory neuropathies, myopathies and Guillain-Barre syndrome.
In summary, the safety of EBP's in HIV patients remains to be fully evaluated. The
patients' immuno-compromised status (with the possibility of occult infection and the
potential for coexistent neurological dysfunction) may pose some hazard. However,
evidence from the reports to date appears to demonstrate no associated morbidity.
Alternatives to EBP's (including conservative therapy and patching with saline or
colloid) or even the use of homologous (HIV negative) blood for EBP may be
considered.
References:
1. Tom DJ, Gulevich SJ, Shapiro HM, Heaton RK, Grant l. Epidural Blood Patch in
the HIV Patient. Anesthesiology. 76: 943-947. 1992.
2. Frame WA, Lichtmann MW. Blood Patch in the HIV - positive Patient.
Anesthesiology. 73:1297. 1990. Letter to the Editor.
3. Bevacqua BK, Slucky AV. Epidural Blood Patch in a Patient with HIV Infection.
Anesthesiology. 74: 952. 1991. Letter to the Editor.
4. Gibbons JJ. Post Dural Puncture Headache in the HIV - positive patient.
Anesthesiology. 74: 953. 1991. Letter to the Editor.
5. Shapiro HM, Grant I, Weinger M. AIDS and the Central Nervous System.
Anesthesiology. 80:187-200. 1994.
6. Hughes SC, Dalley PA, Landers D, Dattel BJ, Crombleholme WR. Parturients
Infected with Human Immunodeficiency Virus and Regional Anesthesia .
Anesthesiology. 81: 32-37. 1995.
Andrew Ross
"The Place of Intraoperative and Postoperative Intravenous Patient Controlled
Analgesia following Regional Anaesthesia for Caesarean Section"
Regional anaesthesia may require intraoperative narcotic supplementation, but
usually a single anaesthetist-administered dose suffices. Intraoperative Patient
Controlled Analgesia (PCA) during Caesarean Section (CS) does not seem
warranted because of the additional complexity of the technique and the need for
specialised apparatus.
Mainly on the basis of patient preference for control, rather than absolute quality of
analgesia, intravenous PCA (IV-PCA) has become the 'de facto' standard for post-CS
analgesia in many obstetric units (1) (Chapter 99). In general, those caring for the
mother have shown poor clinical judgment of both the degree of pain and the level of
sedation experienced by the patients following CS (2). The quality of analgesia
produced by IV-PCA is similar to that obtained following intramuscular narcotic
administration, but is inferior to analgesia obtained from intraspinal opioids. In some
series, maternal satisfaction has related more to the quality of analgesia than to the
patient's ability to control her pain (3).
Overall side effects of IV-PCA (especially nausea and vomiting), when compared to
epidural morphine, have been less in some (but not all) series (4). Sedation has been
less and ambulation earlier for IV-PCA when compared to conventional intravenous
infusion or intramuscular analgesia despite a greater total dose of drug (5).
Post-surgical recovery seems similar, whatever the analgesic modality used.
Pethidine has been the commonest narcotic used, though its metabolites will
accumulate in breast milk and lead to a reduced neonatal neurobehavioural score
(6). Larger bolus doses tend to produce greater patient satisfaction (4).
Morphine or fentanyl provide similar analgesia, and morphine may be less
troublesome, in achieving the desired analgesia (7). Whilst IV-PCA may seem to be
an inherently safer method of analgesic administration, there are no large number
series comparing safety of one method with another.
The overall benefits seem to be subjective rather than objective in the caesarean
section setting. The additional cost of the apparatus and delivery system is small
compared to the benefits experienced by the patient as a result of use of the
technique and to the savings in nursing time.
References:
1. Stoddart PA, Cooper A, Russell R, Reynolds F. A comparison of epidural
diamorphine with intravenous patient-controlled analgesia using the Baxter infusor
following caesarean section. Anaesthesia 1993;48: 1086-90.
2. Olden AJ, Jordan ET, Sakima NT, Grass JA. Patients' versus nurses'
assessments of pain and sedation after cesarean section. J Obstet Gynecol Neonatal
Nurs 1995;24:137-41.
3. Cohen SE, Subak LL, Brose WG, Halpern J. Analgesia after cesarean delivery:
patient evaluations and costs of five opioid techniques. Reg Anesth 1991; 16:141-9
4. Cade I, Ashley J. Towards optimal analgesia after caesarean section: comparison
of epidural and intravenous patient-controlled opioid analgesia. Anaesth Intensive
Care 1993;21:696-9.
5. Perez-Woods R, Grohar JC, Skaredoff M, Rock SG, Tse AM et al. Pain control
after cesarean birth. Efficacy of patient-controlled analgesia vs traditional therapy (IM
morphine). J Perinatol 1991 ;11:174-181.
6. Wittels B, Scott DT, Sinatra RS. Exogenous opioids in human breast milk and
acute neonatal neurobehaviour: a preliminary study. Anesthesiology 1990;73:864-9
7. Howell PR, Gambling DR, Pavy T, McMorland G, Douglas MJ. Patient-controlled
analgesia following cesarean section under general anesthesia: a comparison of
fentanyl with morphine. Can J Anaesth 1995;42:41-45.
Robin Russell
Backache is a common symptom in both the ante- and post-natal periods. Recently,
a possible association between long term backache and epidural analgesia in labour
has been highlighted in both the medical and lay press.
Short term backache is a common problem in the first week after delivery and should
not be confused with more chronic back problems. When questioned in the first few
days after delivery, up to 45% of women report tenderness at the site of epidural
needle insertion (1). A similar proportion of women in whom regional analgesia has
not been used suffer from generalised lower backache following labour (2).
Long term backache after childbirth and its association with epidural analgesia in
labour was highlighted in a retrospective study from the Birmingham Maternity
Hospital (3). Long term backache was reported by 23% of women and, in 14% this
had not been present before delivery. The incidence of new, long term backache was
18.9% in those who received epidural analgesia compared with 10.5% in those using
other methods of pain relief in labour. Epidural anaesthesia for elective caesarean
section did not produce an increased incidence of long term backache. It was,
therefore, suggested that 'stressed' positions in labour exacerbated by muscular
relaxation and the abolition of pain resulted in a postural backache. A second,
retrospective study also demonstrated the association between epidurals and long
term backache (4) (Figure 84.1). In most cases, backache was found to be postural,
not severe and, usually, resolving.
In both these retrospective studies, the incidence of antenatal backache was
significantly lower than that demonstrated in previous work conducted during
pregnancy, in which backache was reported by 50% of these women. The more
severe the antenatal backache, the longer it persisted after delivery. It would appear
that, when questioned retrospectively, many women forget that they suffered from
antenatal backache.
Recently performed prospective studies have failed to find an association between
pain relief and long term backache (Figure 84.2). Backache was no more frequent
after epidural or spinal analgesia compared with other forms of pain relief (5, 6, 7, 8)
There was no relationship between the incidence of backache and the degree of
motor block (7).
References:
1. Crawford JS. Some maternal complications of epidural analgesia for labour.
Anaesthesia 1985; 40: 1219-1225.
2. Grove LH. Backache, headache, and bladder dysfunction after delivery. Br J
Anaesth 1973; 45: 1147-1149.
3. MacArthur C, Lewis M, Knox EG, Crawford JS. Epidural anaesthesia and long
term backache after childbirth. BMJ 1990; 301: 9-12.
4. Russell R, Groves P, Taub N, O'Dowd J, Reynolds F. Assessing long term
backache after childbirth. BMJ 1993; 306: 1299-1302.
5. Breen TW, Ransil BJ, Groves PA, Oriol NE. Factors associated with back pain
after childbirth. Anesthesiology 1994; 81: 29-34.
6. Macarthur AJ, Macarthur C, Weeks S. Epidural anaesthesia and postpartum back
pain. Anesthesiology 1993; 79: A973.
7. Russell R, Reynolds F. Long term backache after childbirth and motor block with
epidural analgesia. Society of Obstetric Anesthesia and Perinatology 1995 Abstract
Book p 100.
8. Fernando R, Patel M, Gill P, Urquhart J, Morgan B. A prospective study of long
term backache after childbirth in primigravida -the effect of ambulatory epidural
analgesia during labour. Society of Obstetric Anesthesia and Perinatology 1995
Abstract Book p51.
Robin Russell
A number of drugs are being used to provide epidural analgesia for labour (Chapter
60). Traditional techniques using plain local anaesthetics are being modified by the
addition of opioids. More recently, the role of alpha-adrenergic agonists and
anticholinergics has been investigated (Chapter 5).
Local Anaesthetics:
Local anaesthetics act by producing a reversible blockade of sodium channels in
nervous tissue preventing the transmission of the electrical impulses (Chapter 95,
Chapter 53). The action is relatively non-selective producing a variable degree of
block of sensory, motor and autonomic pathways (Chapter 88).
Following epidural injection, local anaesthetics rapidly gain access to the
cerebrospinal fluid (CSF) with a peak concentrations recorded between 10 and 20
minutes. The most important route of entry is by diffusion at the dural cuff region,
where arachnoid granulations protrude into the epidural space (Figure 86.1). There
is, in addition, direct diffusion across the dura and direct uptake into blood vessels
supplying the cord. The onset of a local anaesthetic block is segmental reflecting the
rapid block of spinal nerve roots. By 30 minutes, access has also been gained to the
peripheral cord and spinal nerves in the paravertebral space, the latter resulting from
loss of local anaesthetic through intervertebral foramina (1).
With repeated injections of the more fat-soluble local anaesthetics such as
bupivacaine, the epidural fat acts as a reservoir for the drug and so systemic blood
levels do not rise providing appropriate doses are used. However, less lipid soluble
agents such as lignocaine do not tend to accumulate in the epidural fat and blood
levels may rise after multiple dosing.
Regression of epidural block is more circumferential unlike the segmental onset. This
is caused by the continued action of local anaesthetics in the peripheral regions of
the spinal cord.
Epidural opioids:
Epidural opioids have their major site of action on pre- and post-synaptic receptors in
the substantia gelatinosa of the dorsal horn producing selective block of nociceptive
pathways (2) (Figure 86.2). Following epidural injection, opioid drugs cross the dura
to enter the CSF at a rate which is dependent on physico-chemical properties such
as their molecular weight, pKa and relative oil-water solubility. There is also evidence
of diffusion at the dural cuff region and direct transport via the spinal cord blood
supply. The speed of uptake form the CSF into the cord substantia gelatinosa is
again related to lipid solubility.
Lipid soluble opioids such as fentanyl and sufentanil, cross the dura and penetrate
the cord quickly producing a rapid onset of action. The onset of analgesia
corresponds to a high CSF concentration which occurs before the blood level is
sufficiently high to be analgesic. More water-soluble opioids such as morphine, have
a slower onset of analgesia but a more prolonged duration of action.
Drug elimination by vascular uptake is also related to lipid solubility. Thus, despite
their rapid onset, the duration of action of fentanyl and sufentanil is short.
Nausea, vomiting, pruritus, urinary retention and respiratory depression may follow
the use of epidural opioids. Early respiratory depression may occur within an hour of
administration of larger doses of lipophilic epidural opioids. However, respiratory
depression may not arise until 12 hours after an epidural dose of morphine as slow
penetration of the spinal cord increases the potential for cephalad spread within the
CSF (3) (Chapter 90).
Alpha-adrenergic receptor agonists:
When injected into the epidural space, alpha-adrenergic receptor agonists adrenaline
and clonidine supplement analgesia produced by other drugs. The alpha-1 action of
adrenaline produces vasoconstriction of the epidural vessels and prolongs the action
of other agents by slowing vascular uptake. Stimulation of alpha-2 adrenergic
receptors present in the dorsal horn modifies the transmission of noxious sensory
information by mimicking the activation of descending noradrenergic pathways and
inhibiting neurotransmitter release (4). Clonidine, a more selective alpha-2 agonist
than adrenaline, has been used in combination with epidural opioids and local
anaesthetics to treat both labour (5) and post-caesarean section pain (6). There are,
however, concerns over sedation and cardiovascular depression associated with
larger doses of epidural clonidine, both of which are undesirable in labour (7).
Anticholinesterases:
Intrathecal administration of the anticholinesterase neostigmine has been
demonstrated to produce analgesia in animals. Interaction between cholinergic and
alpha-2 adrenergic systems have been investigated with spinal clonidine/neostigmine
combinations. By increasing spinal preganglionic sympathetic activity, neostigmine
counteracts hypotension and bradycardia produced by spinal clonidine. However,
due to its poor lipid solubility, it needs to be administered well before clonidine. The
more lipophilic physostigmine may prove to be a more suitable alternative.
References:
1. Bromage PR. Mechanisms of action of extradural analgesia. Br J Anaesth 1975;
47: 199-211.
2. Cousins MJ, Mather LE. Intrathecal and epidural administration of opioids.
Anesthesiology 1984; 61: 276-310.
3. Bromage PR, Camporesi EM, Durant PAC, Nielson CH. Rostral spread of epidural
morphine. Anesthesiol 1982; 56:431-436
4. Eisenach J, Detweiler D, Hood D. Hemodynamic and analgesic actions of
epidurally administered clonidine. Anesthesiology 1993; 78: 277-287.
5. O'Meara ME, Gin T. Comparison of 0.125% bupivacaine with 0.125% bupivacaine
and clonidine as extradural analgesia in the first stage of labour. Br J Anaesth 1993;
71: 651-656.
6. Eisenach JC, D'Angelo R, Taylor C, Hood DD. An isobolographic study of epidural
clonidine and fentanyl after cesarean section. Anesth Analg 1994; 79: 285-290.
7. MacDonald R. Extradural clonidine - the need for well designed controlled trials. Br
J Anaesth 1994; 72: 255-257.
David Sage
Aspirin, Heparin and Low Molecular Weight Heparinoids and Major Regional Blocks.
In the presence of normal haemostasis, the incidence of spinal haematoma and
paraplegia associated with epidural/spinal is extremely low and similar in incidence to
the spontaneous occurence of this complication. However, partial or complete
haemostatic failure from any cause or combination of causes produces a spectrum of
risk, negligible in the case of low dose aspirin, and very high (&gt1%) in fully
heparinised patients (1, 2, 3). In obstetrics, impairment of platelet or coagulation
system function is common in conditions such as pre-eclampsia or sepsis and care is
needed to exclude all such possibilities before assessing the risk of spinal
haematoma following neuraxial blockade (Chapter 72).
Aspirin:
The useful anti-thrombotic effects of aspirin are due to its inhibition of platelet
cyclooxygenase as well as other platelet and non-platelet pathways (4, 5). Although a
single 600mg aspirin dose increases bleeding time (initially by 50%) for the platelet
life span (one week) (6), this minor degree of haemostatic impairment is compatible
with safe epidural outcome. Support for this view is the absence of any reports of
aspirin induced spinal haematoma cases following epidural or spinal, and case series
of neuraxial blockade in the presence of aspirin without incident (7, 8). Measurement
of bleeding time is not recommended in view of the fact that no consistent
relationship exists between bleeding time and bleeding tendency (9).
Heparin:
High dose, unfractionated heparin.
Unfractionated heparin in high dose (1500 to 2500 IU/hr) significantly increases the
risk of clinically important haemorrhage (10) and is contraindicated prior to
epidural/spinal. Low dose, unfractionated heparin.
A single dose of unfractionated heparin (5000 IU) given subcutaneously does not
alter laboratory coagulation parameters but may increase wound haematoma rate.
Repeated doses can cause thrombocytopenia in a small proportion of patients after
several days. An exaggerated bleeding tendency can be expected when low dose
heparin occurs in the presence of liver failure or is used in combination with other
drugs acting on the coagulation system. Under normal circumstances, however, the
risk of spinal bleeding after epidural/spinal is acceptably low (11, 12) . Fractionated
heparins.
Fractionated (low molecular weight) heparins (LMWHs) were introduced in the
expectation that the incidence of bleeding complications would be reduced. However,
it is likely that the different LMWHs each have different specific modes of action.
This, together with variations in dose schedules, may explain the differing incidences
of bleeding complications and the sometimes paradoxical increase in bleeding when
compared to unfractionated heparin (13, 14). In any case, the difference is small and,
in combination with neuraxial blockade, LMWHs in low dose are associated with
minimal risk (15).
References:
1. Brem SS, Hafler DA, Van Uitert RL, Ruff RL, Reichert V: Spinal subarachnoid
hematoma a hazard of lumbar puncture resulting in reversible paraplegia. N Engl J
Med 1981;304:1020
2. Owens EL, Kasten GW, Hessel EA: Spinal subarachnoid hematoma after lumbar
puncture and heparinsation: a case report, review of the literature and discussion of
anesthetic implications. Anesth Analg 1986;65:1201-1207
3. Rao L, El-Etr AA: Anti-coagulation following placement of epidural and
subarachnoid catheters: an evaluation of neurological sequelae. Anesthesiology
1981; 55:618-620
4. Buchanan MR, Rischke JA, Hirsh J: Aspirin inhibits platelet function independent
of the acetylation of cyclooxygenase. Thromb Res 1982; 25:363-373
5. Loew D, Vinazzer A: Dose dependent influence of acetylsalicylic acid on platelet
functions and plasmatic coagulation factors. Haemostasis 1976:5:239-249
6. Harker LA, Slichter S J: The bleeding time as a screening test for evaluation of
platelet function. N Engl J Med 1972; 287:155-159
7. Benzon HT, Brunner EA, Vaisrub N: Bleeding time and nerve blocks after aspirin.
Reg Anaesth 1984; 9:86-89
8. Horlocker TT, Wedel DJ, Schroeder DR, Rose SH, Elliott BA, McGregor DG,
Wong GY: Preoperative antiplatelet therapy does not increase the risk of spinal
hematoma associated with regional anesthesia. Anesth Analg 1995; 80:303-309
9. Rodgers RPC, Levin J: A critical reappraisal of the bleeding time. Semin Thromb
Hemost 16:1-19, 1990
10. Green D, Lee MY, Ito VY, Cohn T, Press J, Filbrandt PR, VadenBerg WC,
Yarkony GM, Meyer PR: Fixed vs adjusted dose heparin in the prophylaxis of
thromboembolism in spinal cord injury. JAMA 1988; 260:1255-1258
11. Vandermeulen EP, Van Aken H, Vermylen J: Anticoagulants and spinal-epidural
anesthesia. Anesth Analg 1994; 79:1165-77
12. Wille-Jorgensen P, Jorgensen LN, Rasmussen LS: Lumbar regional anaesthesia
and prophylactic anticoagulant therapy - is the combination safe? Anaesthesia
1991:46:623-627
13. Kakkar VV, Cohen AT, Edwardson RA, Philips MJ, Coopere D J, Das SK. Low
molecular weight versus standard heparin for prevention of venous thromboembolism
after major abdominal surgery. Lancet 341;259-165, 1993
14. Bergqvist D, Lindblad B, Matzsch T: Low molecular weight heparin for
thromboprophylaxis and epidural/spinal anaesthesia is there a risk? Acta
Anaesthesiol Scand 36;605-709, 1992
15. Wolf H. Experience with regional anaesthesia in patients receiving low molecular
weight heparins. Sem Thromb Hemost 19 (suppl 1); 152-154, 1993
David Scott
Pathophysiological Effects of Major Neuraxial Block in the Patient with
Cardiovascular Disease.
Spinal anaesthesia in the form of either epidural or subarachnoid block, causes
inhibition of sensory, motor and autonomic fibre activity in the spinal segments
affected by the local anaesthetic.
From the point of view of the patient with cardiac disease, the effects on the
autonomic nervous system, both direct and reflex, are the most relevant. Vasomotor
activity influences both arteriolar tone as well as venomotor tone via small,
unmyelinated C-type fibres.
Preload is decreased by blood pooling in the dilated venous capacitance vessels,
including the splanchnic vessels. The extent of preload reduction will depend on the
existing resting venous tone, the volume status of the patient and the effectiveness of
compensatory vasoconstriction in the unblocked regions of the body. This may cause
a reduction in cardiac output and a fall in blood pressure which is aggravated by the
decrease in systemic vascular resistance (SVR) due to arteriolar dilation.
Baroreceptor responses which would normally act to preserve perfusion pressure are
limited by the amount of the vascular bed which will respond to vasoconstrictor
activity. If the autonomic block affects the upper thoracic segments, particularly T1 to
T4 levels, then reflex chronotropic responses will also be prevented, and a relative
increase in vagal tone to the heart results. This has implications for maintenance of
blood pressure and cardiac output as well as effects on the heart rhythm and
conducting system (Chapter 83). It is worth noting that the upper level of autonomic
block may be two or more segments higher than the measured sensory level.
Patients with heart disease are often taking medications which may obtund their
ability to compensate for the circulatory changes induced by spinal anaesthesia.
Beta-adrenergic blocking drugs in particular may prevent chronotropic responses to
hypotension, even if the level of block is below the thoracic segments, although Reiz
(1) and Stenseth (2) have found thoracic epidural anaesthesia to be safe in such
patients.
Vasodilators, including nitrates, may attentuate the compensatory cardiovascular
response to spinal anaesthesia, although in practice their impact is often negligible.
This is particularly true in the pregnant patient at term, where vasodilators are often
singularly ineffective.
References:
1. Reiz S, Haggmark S, Rydvall A, Ostman M. Beta-blockers and thoracic epidural
analgesia. Cardioprotective and synergistic effects. Acta Anaesthesiol Scand.
76S:54-61; 1982
2. Stenseth R, Berg EM, Bjella L, Christensen O, Levang OW, Gisvold SE. The
influence of thoracic epidural analgesia alone and in combination with general
anesthesia on cardiovascular function and myocardial metabolism in patients
receiving beta-adrenergic blockers. Anesth Analg 77:3; 463-468 1993
David Scott
Major Neuraxial Block (Subarachnoid and Epidural 'Spinals') in the Patient with
Specific Cardiovascular Diseases.
1. Hypertension
There are a number of potential problems associated with the hypertensive patient
having spinal anaesthesia. If left ventricular hypertrophy is present, then it is
important to maintain an adequate perfusion pressure in order to ensure adequate
myocardial perfusion.
Autoregulation limits in organs such as the brain and the kidney may have become
reset to higher levels and, thus, these organs will cope poorly with low perfusion
pressure. Also, hypertension is associated with cerebrovascular disease and, if
carotid artery stenosis is present, this mandates prompt and relatively aggressive
support of blood pressure.
In patients with controlled hypertension receiving thoracic epidural anaesthesia,
clinical experience suggests that risks are similar to the non-hypertensive population
(3). Patients with uncontrolled hypertension are also prone to a greater lability of
blood pressure (4) and may have a relative hypovolaemia (contracted circulating
blood volume) which can be unmasked by spinal blockade (Chapter 39).
2. Ischaemic Heart Disease
Spinal anaesthesia is not contraindicated in patients with coronary artery disease.
There is evidence that high thoracic epidural anaesthesia can improve the ratio of
endocardial to epicardial blood flow (5), and cardiac sympathetic blockade has been
used to ease intractable angina (6). Thoracic epidural anaesthesia may improve
myocardial energy balance, although a study in patients receiving epidural
anaesthesia during fentanyl-based coronary artery surgery showed no difference in
myocardial metabolism compared with controls (7). Wall motion abnormalities have
been shown to improve during epidural anaesthesia with a sensory block to the T9
level, provided preload reduction is maintained (8).
Spinal anaesthesia is capable of substantially modifying the stress response in many
types of infra-umbilical surgery. This may confer an advantage to spinal over general
anaesthesia with respect to the incidence of myocardial ischaemia, although data is
conflicting (9). For major abdominal and thoracic surgery, there has been no
consistently demonstrated benefit or disadvantage of spinal over general anaesthesia
(10, 11, 12).
There is no advantage to having the patient awake so that they can report the
occurrence of angina. Silent ischaemia is common, possibly more so if the cardiac
sympathetics are blocked. Appropriate ST-segment ECG monitoring is a more
sensitive method of detecting myocardial ischaemia than verbal reports of chest
discomfort.
It is possible, although not yet proven, that postoperative myocardial ischaemia and
infarction may be reduced due to the ability of intra- and post-operative epidural
analgesia to reduce the hypercoagulability seen in the postoperative period and the
lowered incidence of tachycardia resulting from better pain control. Large
prospective, properly-randomised studies need to be performed to clarify these
issues.
3. Valvular Disease
The reduction in preload associated with spinal anaesthesia can worsen the condition
of patients with severe mitral valve prolapse or hypertrophic subaortic stenosis (13)
(Chapter 111). The maintainence of adequate circulating fluid volume in these
patients is essential.
Patients with aortic stenosis have been safely managed with spinal anaesthesia but
in this situation the maintainence of arterial pressure is crucial and epidural
anaesthesia is often chosen so that the spread of the block can be titrated more
gradually. The avoidance of the myocardial depressant effects of many general
anaesthetic agents by the use of spinal anaesthesia is an advantage.
Spinal anaesthesia presents difficulties in women with mitral stenosis and the onset
of a tachycardia may result in cardiac decompensation and pulmonary oedema.
Metaraminol or phenylephrine are more appropriate vasopressors than ephedrine in
this population (Chapter 79) (Chapter 76).
In aortic and mitral valvular regurgitation, the afterload reduction theoretically helps to
reduce the regurgitant fraction, but preload and heart rate need to be maintained.
Clearly, patients receiving anticoagulant therapy associated with prosthetic valve
replacements must have coagulation normalised prior to spinal anaesthesia being
instituted (Chapter 72).
4. Cardiac Failure
A significant reduction in the incidence of cardiac failure after major abdominal
surgery in high-risk patients has been demonstrated with combined epidural and
general anaesthesia and postoperative epidural analgesia (14). Intraoperatively,
spinal anaesthesia alone might be expected to confer an advantage over a combined
technique due to the unloading of the heart and the avoidance of negatively inotropic
general anaesthetic agents. There is a risk, however, that intraoperative fluid
therapy, compensating for venous pooling, may result in postoperative fluid overload
once the sympathetic block has regressed. A careful balance of fluid and
vasopressor therapy is therefore necessary in patients with a history of heart failure.
5. Dysrhythmias
There are a number of reports in the literature noting aggravation of conduction
defects or cardiac arrest in association with spinal anaesthesia (15, 16, 17). These
have a common theme of relative vagal hyperactivity causing increased sinus or
atrio-ventricular nodal block in patients with spinally-induced blockade of cardiac
sympathetic fibres. Preoperative assessment to identify patients at risk, and
avoidance of hypovolaemia should help to limit the occurrence of these
brady-dysrhythmias.
Many vasopressors cause a reflex bradycardia (e.g. phenylephrine, metaraminol) and
in these patients, an agent with more beta-1 activity, such as ephedrine, is often
preferable. In the near-arrest situation, adrenaline is appropriate and should be given
early.
Conclusions
Spinal anaesthesia, using epidural or subarachnoid block, is appropriate and safe in
patients with many forms of cardiac disease. Although the benefits of spinal
anaesthesia over general anaesthesia with respect to cardiac morbidity reduction
remain unproven, there is no reason to believe that morbidity is increased provided
that there is a clear understanding of the haemodynamic effects and of the
requirement for appropriate and timely intervention. The advantages of spinal
anaesthesia techniques in other areas, including improved pain control and reduced
recovery time, can then be achieved.
References:
3. Sharrock NE, Mineo R, Urquhart B. Haemodynamic effects and outcome analysis
of hypotensive extradural anaesthesia in controlled hypertensive patients undergoing
total hip arthroplasty. BJA. 67:1: 17-25 1991
4. Dagnino J, Prys Roberts C. Studies of anaesthesia in relation to hypertension. VI:
Cardiovascular responses to extradural blockade of treated and untreated
hypertensive patients. BJA. 56:10:1065-1073 1984
5. Davis RF; DeBoer LWV; Maroko PR. Thoracic epidural anesthesia reduces
myocardial infarct size after coronary artery occlusion in dogs. ANESTH ANALG.
65/7 (711-717) 1986
6. Blomberg S, Curelaru I, Emanuelsson H et al: Thoracic epidural anaesthesia in
patients with unstable angina pectoris. Eur Heart J 10:437, 1989
7. Stenseth R; Berg EM; Bjella L; Christensen O; Levang OW; Gisvold SE. The
influence of thoracic epidural analgesia alone and in combination with general
anesthesia on cardiovascular function and myocardial metabolism in patients
receiving beta -adrenergic blockers. ANESTH ANALG. 77/3 (463-468) 1993
8. Baron JF, Coriat P, Mundler O et al: Left ventricular global and regional function
during lumbar epidural anesthesia in patients with and without angina pectoris.
Influence of volume loading. Anesthesiology 66:621, 1987.
9. Reiz S, Balfors E, Sorensen MB et al: Coronary haemodynamic effects of general
anaesthesia and surgery: modification by epidural analgesia in patients with
ischaemic heart disease. Reg Anesth 7(suppl 4):8, 1982.
10. Yeager MP, Glass DD, Neft RK et al: Epidural anesthesia and analgesia in
high-risk surgical patients. Anesthesiology 66:729, 1987.
11. Baron J-F, Bertrand M, Barr E et al: Combined epidural and general anesthesia
versus general anesthesia for abdominal aortic surgery. Anesthesiology 75:611, 1991
12. Scott NB, Kehlet H: Regional anaesthesia and surgical morbidity. Br J Surg
75:299, 1988.
13. Sato M; Hori M; Akiyama H; Kawamura M; Iwasaki Y; Suzuki M.
Echocardiographic observation of intraoperative circulatory collapse in a patient with
hypertrophic obstructive cardiomyopathy. JPN J ANESTHESIOL. 42/12 (1838-1843)
1993
14. Yeager MP, Glass DD, Neft RK et al: Epidural anesthesia and analgesia in
high-risk surgical patients. Anesthesiology 66:729, 1987.
15. Bernards CM; Hymas NJ. Progression of first degree heart block to high-grade
second degree block during spinal anaesthesia. CAN J ANAESTH. 39/2 (173-175)
1992
16. Underwood SM; Glynn CJ. Sick sinus syndrome manifest after spinal
anaesthesia. ANAESTHESIA. 43/4 (307-309) 1988
17. Caplan RA; Ward RJ; Posner K; Cheney FW. Unexpected cardiac arrest during
spinal anesthesia: A closed claims analysis of predisposing factors.
ANESTHESIOLOGY. 68/1 (5-11) 1988
Tom Torda
Analgesia following caesarean section under regional blockade.
Analgesia following caesarean section does not differ in basics from analgesia for a
lower abdominal operation in a young and, usually fit, individual. The positive attitude
of the patient, however, is of assistance in achieving good results and early mobility.
If spinal anaesthesia is used, it is my practice to use parenteral analgesia. My
preference is for opiate patient controlled analgesia (PCA) with oral NSAIDs to
control 'afterpains'. NSAIDs can cause uterine atony (and increase uterine bleeding)
and should only be used if no other contraindication exists (peptic ulcer, asthma,
renal disease, allergy). Ketorolac is an alternative, especially if opioids cause nausea
(1, 2) .
If epidural anaesthesia is used it should be continued for postoperative analgesia, a
method of pain relief equal or superior to others (3, 4, 5). Although some dispute this
(6, 7), the majority opinion favours a mixture of an opioid and bupivacaine(less than
or equal to 0.125 %) (8, 9, 10). It is important to use a loading dose followed by a
maintenance infusion or maintenance PCA to produce the best results (11). Effect
and vital signs need to be monitored regularly. The Prince Henry Hospital pain scale
(7) (Figure 99.1)provides an objective measure. A pain score of 0 or 1 should be
achieved using this scale.
The choice of opioid is also disputed, but all high intrinsic activity opioids are effective
(Figure 99.2). Morphine has the lowest ratio of epidural:systemic dose (Figure 99.3)
and the best quality of analgesia (11) but, also, the highest incidence of delayed
respiratory depression and the slowest onset. Fentanyl is widely used and alfentanil
is considered optimal by some (11).
Important adverse effects of these techniques include delayed respiratory
depression, urinary retention, hypotension, drowsiness, nausea, vomiting and itch.
References:
1. Merry AF et al. Br J Anaesth 69:92-4, 1992
2. Bonnet F and Vesinet C. Cahiers dAnesthesiologie 42:191-4, 1994.
3. Cohen SE and Woods WA. Anesthesiology 58:500-4, 1983.
4. Perriss BW et al., Br J Anaesth 64:355-7, 1990.
5. Salomaki TE et al., Anesthesiology 75:790-5, 1991.
6. Badner NH et al., Can Anesth Soc J 39:330-6,1992.
7. Torda TA et al., Br J Anaesth 74:35-40, 1995.
8. Millon D et al., Ann Fr dAnesth Reanim 2:273-9, 1983.
9. Gaffud MP et al., Anesthesiology 65:331-4, 1986.
10. Paech MJ et al., Anaesth Int Care 18:22-30, 1990.
11. Chrubasik J, Chrubasik S, Mather L, Postoperative Epidural Opioids, Springer,
Berlin, 1993.
Robert Turner
Spinal anaesthesia (Chapter 63) compared to other techniques of anaesthesia
(including epidural analgesia (Chapter 1), caudal analgesia (Chapter 22) and
combined subarachnoid-epidural analgesia (Chapter 62) ) for labour and delivery.
The use of subarachnoid local anaesthetic agents and narcotics for labour and
delivery varies between institutions and individual anaesthetists. While practices may
vary, the role of subarachnoid anaesthesia in comparison with other regional
techniques can be defined in terms of the relative advantages and disadvantages of
this method of anaesthesia.
Efficacy and application of blockade:
Local anaesthetics may be used intrathecally to accomplish sacral anaesthesia for
instrumental vaginal deliveries and for other obstetric procedures. Subarachnoid
blockade to a level above T7 may also be employed for cesarean section. Under
these circumstances, subarachnoid blockade provides reliable, dense surgical
anaesthesia.
Epidural anaesthesia is also suitable for both labour and delivery but, sometimes,
sacral segments may be difficult to block (with a lumbar epidural) and the blocks may
occasionally be patchy or asymmetrical (1).
In comparison to subarachnoid blockade, caudal blockade is only suitable for sacral
anaesthesia (Chapter 2).
Opiates may also be administered by the subarachnoid route and provide good
analgesia for labour but not for delivery (2). Furthermore, intrathecal opiates provide
superior analgesia when compared to opiates administered via the epidural route (3).
Side effects such as pruritus may be higher in patients receiving intrathecal opiates.
Speed of onset:
When compared to epidural or caudal anaesthesia, subarachnoid anaesthesia offers
a rapid onset of action which is often of benefit to the patient, anaesthetist and
surgeon. Unfortunately, an increased speed of onset of anaesthesia is only
purchased at the price of a greater degree of hypotension (4) .
Postdural puncture headache:
Postdural puncture headache may occur in up to 20% of patients when a 25-gauge
spinal needle is used (5) (Chapter 97). This miserable complication occurs more
frequently in young females and is responsible for the reluctance of many
anaesthetists to use this technique in the parturient. Except in cases of inadvertent
dural puncture with the needle, this problem is not seen with epidural or caudal
anaesthesia. The use of 26-gauge spinal needles has been shown to lower the
incidence of postdural puncture headache (6). The use of 29-gauge needles has
been associated with little risk of postdural puncture headache, even in young
patients (7). The low incidence of headache with these small needles increases the
acceptability of subarachnoid blockade in obstetric anaesthesia (Chapter 97).
Titratable level of blockade and continuous infusions:
The use of epidural catheters to provide a means by which the level of anaesthesia
can titrated, topped up, or continuously infused for labour and delivery has been well
established. The routine use of subarachnoid catheters for uncomplicated vaginal
delivery has not gained wide acceptance in obstetric anaesthesia for several
reasons. It has been stated that the large bore needles usually employed to introduce
catheters would be associated with a high incidence of postdural puncture headache
but this does not appear to occur in clinical practice (8). These catheters may
increase the risk of infection, although again, there is very little supporting evidence
for this concern. In an attempt to address these issues, microcatheters (32-gauge)
which can be passed through a standard 25 or 26-gauge spinal needle have been
used. Continuous spinal anaesthesia is obtained with negligible risk of local
anaesthetic toxicity to the mother and fetus. Significant problems have been reported
with these microcatheters and include cauda equina syndrome, kinking, difficulty in
threading and catheter fracture (9) (Chapter 42) (Chapter 104).
The more recent use of combined spinal epidural techniques allows for continuous
and titratable anaesthesia with the advantage of a rapid and dense subarachnoid
block. The potential disadvantages of an intrathecal catheter are avoided and, with a
small spinal needle, the risk of postdural puncture is minimal (Chapter 62)
Overall, because of its advantages spinal anaesthesia (especially with the use of
smaller spinal needles) continues to challenge the pre-eminent role of epidural
anaesthesia in obstetrics.
References:
1. Carrie LES. Extradural, spinal or combined block for obstetric surgical
anaesthesia. British Journal of Anaesthesia 1990 65:225-233
2. Scott PV, Bowen FE, Cartwright P, Rao BCM, Deeley D, Wotherspoon HG,
Sumrein IMA. Intrathecal morphine as a sole analgesic during labour. British Medical
Journal 1980 281:351-353
3. Camann WR, Denney RA, Holby ED, Datta S . A comparison of intrathecal,
epidural, and intravenous sufentanil for labor analgesia. Anesthesiology 1992 77
:884-887.
4. Parnass SM, Curran MJA, Becker GL. Incidence of hypotension associated with
epidural anesthesia using alkalinized and nonalkalinized lidocaine for cesarean
section. Anesthesia and Analgesia 1987 66:1148-1150.
5. Russell IF. Effect of posture during induction of spinal anaesthesia. British Journal
of Anaesthesia. 1987 59:347-353.
6. Barker P. Are obstetric spinal headaches avoidable? Anaesthesia and Intensive
Care. 1990 18:553-554.
7. Flaatten H, Rodt SA, Vamnes J, Rosland J, Wisborg T, Koller, ME. Postdural
puncture headache. A comparison between 26- and 29-gauge needles in young
patients. Anaesthesia. 1989 44:147-149.
8. Denny N, Masters R, Read J, Sihota M, Pearson D, Selander D. Postdural
puncture headache after continuous spinal anesthesia. Anesthesia and Analgesia
1987 66:791-794.
9. Hurley RJ, Lambert DH. Continuous spinal anesthesia with a microcatheter
technique. Anesthesia and Analgesia. 1990;70: 97-102.
Andre van Zundert
"Labor pain is among the most severe pain human beings experience and compares
in its intensity to severe cancer pain or pain from the amputation of a digit. Parity also
influences labour pain and primiparous woman experience more pain during early
labour, while multiparae have greater pain in the second stage. Although several
factors influence parturition pain and its severity varies widely, the occurrence of truly
painless labor is rare" (1) (Figure 58.1).
Labour pain is described as intolerable in about one third of women (2) (Chapter 64).
The nature of parturitional pain (incidence, intensity and quality) is extensively
described in a recent edited book (3).
Pain in the first stage of labour results from dilatation of the cervix and lower uterine
segment and from distension of the body of the uterus by uterine contractions and is
transmitted by afferent nerve fibers (accompanied by sympathetic fibers) of the 10th,
11th and 12th thoracic and 1st lumbar nerves. The descending head causes
pressure on the lumbosacral plexus responsible for pain felt in the back , thighs and
legs (Figure 46.1).
Pain in the second stage of labour results from distension of the birth canal and
perineum and is transmitted by the 2nd, 3rd and 4th sacral nerves (Figure 46.1).
The degree of discomfort is described in the following table (shortened and modified)
from Bonica (4) (Table 58.1).
References:
1. Writer WDR Physiology of Labor. In: Handbook of obstetric analgesia and
anesthesia. (Eds McMorland G, Marx F). WFSA p24 - 34, 1992
2. Melzack R. The myth of painless childbirth. Pain 1984;19:321-325.
3. Pain relief and anesthesia in obstetrics. Eds: van Zundert A, Ostheimer GW. 1995.
Churchill Livingstone, New York. p19-52
4. Bonica JJ. Obstetric analgesia and anesthesia. Springer-Verlag Berlin, Heidelberg,
New York 1972. p 31-33.
Arthur Vartis
By design, a combined spinal epidural anaesthetic (CSE) sets out to produce a
deliberate multicompartment block through a breached dural membrane. In the more
usual setting of conventional epidural anaesthesia, an inadvertent multicompartment
block constitutes a major, potentially serious, complication of the technique.
Since the lateral holes of the epidural catheter (inserted as part of a CSE
anaesthetic) may lie in close proximity to the dural puncture site, a bolus of local
anaesthetic or narcotic injected via the epidural catheter has the potential to leak
through the dural puncture hole into the subarachnoid space.
Collier (1) performed an epidurogram by injecting contrast into the epidural catheter
of three patients who had had a CSE anaesthetic. In one of these patients he
documented a spread of contrast from the epidural into the subarachnoid space.
The implications of an intrathecal leak arising from a bolus epidural injection give
cause for serious concern with anecdotal evidence supporting this in the literature
(2).
The incidence of leakage from the epidural into the subarachnoid space through the
dural puncture site is still not known. Contrast epidurography studies which look at
such leakage following the insertion of a catheter as part of a CSE anaesthetic using
Tuohy epidural and pencil-point spinal needles (in cases where there is no clinical
evidence of dural puncture by the Tuohy needle) are needed.
At the Royal Hospital for Women, a preliminary study of this potential problem is
being undertaken (3). To date, fifteen CSE women have received an injection of
10-13mls of the contrast iohexol 300mg/ml via the epidural catheter within three
hours of catheter insertion. The spread of contrast has been followed
fluoroscopically. No evidence of intrathecal leakage has been demonstrated.
Nevertheless, following a combined CSE anaesthetic, the fact that the dura has been
breached should be kept in mind. This is particularly so when bolus injections are
given via the epidural catheter soon after placement of the CSE.
References:
1. Collier C. Cardiorespiratory arrest following combined spinal epidural anaesthesia
(letter) Anaesthesia 49 (3):259, 1994.
2. Myint Y. Cardiorespiratory Arrest Following Combined Spinal Epidural Anaesthesia
for Caesarean Section Anaesthesia 48; 684-686, 1993.
3. Vartis A, Collier CB, Gatt SP. Potential intrathecal leakage of solutions injected
into the epidural space following combined spinal epidural anaesthesia.Anaesth
Intensive Care 1998 Jun;26(3):256-61
Nicola Volpe
The parturient with heart disease, whether congenital or acquired, represents a
challenge even for the experienced anaesthesiologist. The main goal in the
management of these patients is to prevent further derangement of cardiac function
during labour in a heart which is already stressed by the "physiological" changes of
pregnancy. This can be accomplished by effective anxiolysis, analgesia and
anaesthesia. Ultimately, the aim of any anaesthetic intervention is to ensure the
wellbeing of both the mother and the fetus.
Pregnancy induces an increase in cardiac output (30-40%), which reaches its
maximum by the end of the 10th week and which is maintained for the remainder of
the gestational period. The increase in cardiac output results from an increase in both
heart rate and stroke volume. There is a concomitant decrease in peripheral vascular
resistance (PVR), which reflects the hormonally-induced vasodilation seen in
pregnancy (1). Circulating blood volume increases by about 1 litre as a result of an
increase in plasma volume and, to a lesser extent, an increase in red cell mass.
Labour itself is associated with additional cardiovascular stresses. The pain of labour
can lead to a sustained increase in cardiac output of about 45 percent as compared
to the pre-labour value. The parturient can be exposed to wide variations in
ventricular preload. - During each uterine contraction preload increases as a result of
autotransfusion from the uterine vascular bed. Conversely, preload can be decreased
as a result of caval compression, haemorrhage (average blood loss during a vaginal
delivery is about 500mls and during caesarean section about 1000mls) or the
sympatholytic effects of neuraxial blockade (Chapter 82). The effects of the Valsalva
manoeuvre (which occurs during pushing) are complex. All of these physiological
changes have the potential to precipitate acute cardiac failure in patients whose
cardiac performance is already compromised.
Drugs used during obstetric analgesia or anaesthesia can affect cardiovascular
performance either directly or indirectly through the autonomic nervous system. If an
appropriate analgesic or anaesthetic technique is selected for a parturient, the
haemodynamic consequences of the chosen method can sometimes be used to the
advantage of the parturient with cardiovascular disease.
Accurate cardiovascular monitoring during labour and in the puerperium is essential
in the management of all parturients with heart disease. Monitoring of ECG, BP
(preferably invasive) and Sa02 is mandatory in patients with severe disease.
Parturients with Valvular Disease:
The general principles of regional blockade in a patient with valvular disease are
outlined in Chapter 108. Mitral Stenosis
This condition is usually the result of rheumatic heart disease. The main
haemodynamic features are pulmonary congestion and reduced left ventricular
diastolic filling. Epidural analgesia for labour has been successfully used in these
patients and has been shown to have little influence (and sometimes beneficial
effects) on the haemodynamic picture. Pulmonary artery pressure monitoring
(Swan-Ganz catheter) is strongly recommended by some authors (8) in patients with
moderate-to-severe mitral stenosis. Many authors recommend epidural block as the
technique of choice in providing anaesthesia for caesarean section in these patients
(2, 9, 10). Great care is needed in the administration of the block and its cephalad
spread should be restricted at T5 level.
Mitral Regurgitation
In these patients an increase in systemic vascular resistance should be prevented.
Epidural block is the technique of choice (3, 11, 12) for analgesia in labour as well as
for anaesthesia for caesarean delivery (3).
Aortic Stenosis.
The key to the anaesthetic management of these parturients is the maintenance of
both preload and afterload. - Coronary perfusion is crucially dependent on the
maintenance of diastolic pressure and time, and cardiac output is relatively fixed.
Analgesia for labour is best provided by parenteral narcotics as well as by inhalation
of nitrous oxide and oxygen. For the second stage of labour, pudendal nerve
blockade can be used. Good analgesia has also been provided by intrathecal
narcotics. General anaesthesia is the technique of choice for caesarean section.
Aortic Regurgitation
These patients tolerate the circulatory overload produced by pregnancy very well and
most techniques of analgesia and anaesthesia have been used successfully. A
decrease in left ventricular afterload (such as occurs with neuraxial blockade) can
lead to an improvement in cardiac function by reduction of the regurgitant fraction.
Anaesthesia and Analgesia in Patients with Congenital Heart Disease:
Tetralogy of Fallot (Figure E.4)
This condition is the most common cyanotic heart condition observed in pregnant
patients. Cyanosis is the result of a right-to-left shunt the degree of which is
determined by the amount of obstruction to right ventricular outflow. One of the
principal anaesthetic aims in managing these patients is to prevent an increase in this
shunt. As with Eisenmenger's syndrome, the ratio of systemic to pulmonary vascular
resistance is one determinant of the magnitude of the right-to-left shunt and the level
of cyanosis is also affected by changes in cardiac output (mixed venous oxygen
saturation effect).
All known techniques of analgesia and anaesthesia have been used with good
results but major regional blocks have to be used with caution due to the risk of a
severe decrease of systemic vascular resistance (2). For caesarean section both
light and deep levels of general anaesthesia have been advocated (3). Tachycardia
or infundibular spasm can be prevented by the administration of propranolol.
Eisenmenger Syndrome
These patients present with pulmonary hypertension with right-to-left or left-to-right
shunt at aortopulmonary, ventricular or atrial level. A decrease in the ratio of systemic
to pulmonary vascular resistance results in increasing cyanosis. In these patients
pregnancy and delivery are associated with a high mortality rate (4). Epidural
blockade using low concentrations of local anaesthetic has been used to produce
satisfactory analgesia in labour (5, 6). For caesarean section the anaesthetic
technique of choice is general anaesthesia using drugs that do not depress
cardiovascular function.
Coarctation of the Aorta.
The main cardiovascular consequence of coarctation is a chronically-increased left
ventricular afterload that causes hypertrophy of the left ventricle. Epidural blockade
as well as intrathecal morphine have both been successfully used to provide
analgesia in labour (7). General anaesthesia is preferred for caesarean section (3).
Patients with Cardiomyopathy:
On the basis of anatomical and functional features cardiomyopathies can be
classified as either dilated or hypertrophic. There is little information regarding the
anaesthetic management of patients with a cardiomyopathy in labour. In principle,
depression of myocardial function should be avoided in those patients with a dilated
cardiomyopathy, but mild afterload reduction may be of benefit. In those patients
suffering from a hypertrophic cardiomyopathy, preload should be well-maintained (to
avoid systolic cavity-obliteration) and beta-agonists (whether used for tocolysis or
cardiovascular reasons) should be avoided. Peri-partum cardiomyopathy is discussed
in Chapter 41.
References:
1. Walters WAW, McGregor WG. Cardiac Output at rest during pregnancy and
puerperium. Clin Sc 30:1, 1966
2. Ostheimer GU, Alper MH. Intrapartum anaesthetic management of pregnant
patient with heart disease. Clin Obstet Gynecol 18: 81, 1975
3. Mangano DT. Anesthesia for the pregnant cardiac patient. In: Anesthesia for
obstetrics. S Shnider & G. Levinson eds. 345-381, William and Wilkins, Baltimore
1986
4. Gleicher N, Midwall J, Hockberger D, et al. Eisenmenger's syndrome in pregnancy.
Obs Gynecol Surv 3:721, 1979
5. Crawford JS, Mills WG, Pentecost BL. A pregnant patient with Eisenmenger's
syndrome. Br J Anaesth 43:1091, 1971
6. Midwall J, Jarfin H, et al. Shunt flow and pulmonary haemodynamics during labour
and delivery in Eisenmenger syndrome. Anesth Analg 56: 543, 1977
7. Barnes CG. Medical Disorders in obstetric practice, 4 Edition, 72-79, Blackwell
Scientific, Oxford 1974
8. Clark SL, Phelan JP, et al. Labour and delivery in presence of mitral stenosis:
central haemodynamic observation. Am J Obstet Gynecol 152: 984, 1985
9. Moir DD, Willocks J. Epidural analgesia in British obstetrics. Br J Anaesth 40:129,
1968
10. Marx GF, Hodgkinson R. Special considerations in complications of pregnancy. In
Marx GF; Bassel GM eds, 297-334, Elsevier 1980
11. Crawford JS. Principles and practice of obstetric anaesthesia. Blackwell
Scientific, 1988
12. Ferguson JE, Wyner J, et al. Maternal Health complications. In Anaesthesia in
obstetrics, G. Albright et al. eds. Butterwoths 1986
Seiji Watanabe
Regional Anaesthesia in the Presence of a Coagulopathy
Hemorrhagic complications can occur after virtually all regional anesthetic
techniques. Bleeding into the spinal canal is perhaps the most serious of these
complications. A review of a large number of clinical reports shows that this can
happen in clinical circumstances in which subarachnoid (SAB) or epidural block
(EDB) is performed.
Spinal hematoma (SH) can even occur in a young, otherwise healthy patient, who is
not on any anticoagulant, has a normal coagulation profile, and receives SAB or EDB
after a clean, single puncture performed by an experienced anesthetist using a small
gauge needle (Chapter 59).
Tryba estimates the risk of SH to be 1:150,000 after EDB, and 1:220,000 after SAB.
However, for medico-legal reasons, the real incidence may be under-reported. SAB
is probably less traumatic than EDB. Spinal bleeding occurs in a significant number of
patients in whom central nerve block (CNB) has been performed using accepted
guidelines. The potential development of an SH in patients receiving CNB must
always be kept in mind whether or not an anticoagulant has been used (1). Following
surgery, a hypercoagulable state usually occurs. The etiology of this is uncertain but
the stress response appears to be an important initiator. EDB may prevent some of
the complications which flow from this state and may improve clinical outcome
(compared with inhalational anaesthesia alone). This has been confirmed
experimentally and clinically in vascular surgery (2). The beneficial effects of regional
anesthesia on coagulation in patients on anticoagulants have not been quantitated.
With regard to the effects of preoperative antiplatelet therapy on the risk of SH,
Horlocker reported results obtained from an extensive study using 924 patients who
underwent major orthopedic surgery (Chapter 34). Preoperative antiplatelet therapy
did not increase the incidence of minor hemorrhagic complications. However:
1. female gender,
2. increased age,
3. a history of excessive bruising/bleeding,
4. surgery to the hip,
5. a continuous catheter technique,
6. a large needle gauge,
7. multiple needle passes, and
8. difficult needle placement
were all significant risk factors.
'Bloody tap' is relatively common (3 to 4%) but it usually produces a clinically
insignificant collection of blood in the epidural space.
Preoperative antiplatelet therapy is not a significant risk factor for the development of
neurological dysfunction from SH in patients who undergo SAB or EDB while
receiving these medications (3).
Guidelines for safer CNB in a woman with impaired coagulation:
1. Perform CNB only if:
a. PT is less than 1.5 times the international normalized ratio,
b. APTT is less than 1.5 times control,
c. platelet is 80,000 or greater, and
d. bleeding time is < 10 min.
2. If a bloody tap occurs, postpone surgery for 24h if possible and place the patient
under strict neurologic surveillance;
3. Remove the CNB catheter when the coagulation profile has returned to normal.
Guidelines for safer CNB in a woman who is heparinised, or in whom heparinisation
is planned:
1. Heparin should be stopped 3-6hrs before CNB;
2. Withold CNB if clotting times remain abnormal;
3. If bleeding occurs during needle or catheter insertion in patients who are
heparinized later, close neurological observation is mandatory following delivery or
surgery;
4. Observe a minimum time interval of 60min between initiation of CNB and
subsequent heparinization.
5. Remove the CNB catheter as early as possible prior to reheparinisation.
Early Diagnosis of Spinal Haematoma Following CNB.
Should SH occur, the symptoms include a severe, radiating back pain which is
radicular in character and associated with sensory and motor deficit. The sensory
block, muscle weakness, and urinary retention outlast the expected duration of CNB.
Paraplegia develops over the ensuing 14.5+/-3.7hr. The time span between the
development of a SH causing neurological deficit and surgical decompression should
be less than 8hr.
References:
1. Vandermeulen EP et al. Anticoagulant and Spinal-Epidural Anesthesia. Anesth
Analg 1994;79:1165-77
2. Spencer L et al. Epidural anesthesia and analgesia their role in postoperative
outcome. Anesthesiology 82;6:1474-1506.
3. Horlocker TT, et al. Preoperative antiplatelet therapy does not increase the risk of
spinal hematoma associated with regional anesthesia. Anesth Analg 1995;80:303-9.
Leonie Watterson
The first report of "supine hypotension in late pregnancy" was published in 1953 (2).
This described hypotension which occurred in patients upon assuming the supine
position, and which resolved with lateral positioning.
The features of supine hypotensive syndrome were then elucidated. It occurs in:
1. late pregnancy,
2. the supine, and to a lesser extent, the sitting position, and
3. more frequently in those with varicose veins.
It is caused by compression of the inferior vena cava (IVC) by the gravid uterus with
a consequent reduction in venous return. Three to seven minutes are generally
required for significant hypotension to become manifest (2). Supine hypotension is
most severe in the latent stage of labour and is more severe in non-labouring patients
undergoing caesarean section than those who are labouring (6, 7). The magnitude of
IVC compression is reduced during contractions because the uterus rides away from
the IVC (2). Supine hypotension is cured by delivery.
Two compensatory mechanisms are available for attenuating the degree of
hypotension which occurs as a result of impairment of venous return. Firstly, there
may be a generalised increase in sympathetic tone and, secondly, the internal
vertebral venous plexus and the azygos vein can act as a collateral conduit for blood
returning from the lower part of the body (Figure 28.1).
It was subsequently recognised that aortic compression could be as important as
caval compression in the generation of decreased utero-placetal perfusion and fetal
distress.
During labour, aortic compression occurs almost exclusively during uterine
contractions. It occurs in up to 86% of parturients. It is less dependent upon posture
and less responsive to lateral tilt than IVC compression (4, 5). Compression of the
aorta occurs at the level of maximal lumbar lordosis (L4 - L5).
'Aortocaval compression' is a blanket term which describes compression of the
inferior vena cava and the aorta by the gravid uterus in women at term (1, 2, 3, 4).
On assuming the supine position, 46% of women at term develop brachial and
femoral hypotension; a further 31% develop femoral hypotension in the absence of
brachial hypotension (10). This has implications for both mother and fetus. Maternal
hypotension as measured by a reduction in brachial artery blood pressure, occurs as
a result of a diminution in venous return. It is most pronounced in hypovolaemic
states, either actual, as occurs with haemorrhage, or relative, as occurs following
sympathetic blockade. Acute fetal distress can be caused by: 1. hypoperfusion of the
uteroplacental unit secondary to maternal hypotension, or 2. occult aortic
compression (in the presence of a normal maternal brachial arterial blood pressure)
causing a reduction in iliac arterial flow (8) (Chapter 76).
The efficacy of left lateral displacement was demonstrated in 1972 (9). The full left or
right lateral position completely relieves aortocaval compression (Figure 28.2).
Elevating the mother's right hip 10-15cm completely relieves aortocaval compression
in 58% of term parturients (1, 5, 8).
Lateral displacement remains an important technique in the prevention of supine
hypotension and in the management of hypotension in all women during late
pregnancy.
References:
1. Leighton BL: Anaesthetic Complications:Intraoperative. in: Obstetric Anesthesia
Norris MC (ed), JB Lippincott Co. Philadelphia, 1993; p.616-618.
2. Howard BK, Goodson JH, Mengert WF. Supine hypotensive syndrome in late
pregnancy. Obstet Gynecol 1953; 1: 371.
3. Wright L. Postural hypotension in late pregnancy Br. Med. J. 1962; 1: 760.
4. Goodlin RC. Importance of the lateral position during labor. Obstet Gynecol 1971
37:698.
5. Kinsella SM, Whitwam JG, Spencer JAD. Aortic compression by the uterus:
Identification with the Finapres digital artery pressure instrument. Br. J. Obstet.
Gynaecol. 1990 97:700.
6. Clark RB, Thompson DS, Thompson CH. Prevention of spinal hypotension
associated with cesarean section. Anesthesiology 1976 45: 670.
7. Brizgys RV, Dailey PA, Schnider SM, Kotelko DM, Levinson G. The incidence and
neonatal effects of maternal hypotension during epidural anesthesia for cesarean
section Anesthesiology 1987 67:782.
Footnote:
Recent papers on this subject include those by:
Chen GY, Kuo CD, Yang MJ, Lo HM, Tsai YS. Return of autonomic nervous activity
after delivery: role of aortocaval compression. Br J Anaesth. 1999 Jun;82(6):932-4.
Yun EM, Marx GF, Santos AC: The effects of maternal position during induction of
combined spinal-epidural anesthesia for cesarean delivery. Anesth Analg 1998
Sep;87(3):614-8.
Leonie Watterson
Methods of assessing the sensory level of the block
The sensory level of the block reflects the extent of local anaesthetic blockade of
nerves subserving pain and temperature (A-delta and C nerve fibres) and sensation
to soft touch (Beta nerve fibres). The sensory level may be determined by mapping
out the distribution of loss of appreciation of pain to pinprick, cold sensation with ice
and paraesthesiae to soft touch (Chapter 8). These are compared to a standard
dermatome chart.
Methods of measurement of motor blockade
The degree of motor blockade is quantitated in a variety of ways including
dynamometry and the Bromage scoring method (1, 2). Dynamometry has been
shown to be more accurate than the Bromage method but the latter is simple and can
be performed at the bedside.
BROMAGE SCORE (3)
0: No motor block: full flexion of knee and foot.
1: Inability to raise extended leg. Just able to move knee.
2: Inability to flex knee. Able to move foot only.
3: Inability to flex ankle joint. Unable to move foot or knee.
The assessment of sympathetic blockade
The degree of sympathetic blockade is difficult to quantify. It may be assessed
indirectly from changes in maternal vital signs which result from the cardiovascular
effects of neuraxial blockade.
Sympathetic blockade below the level of the cardiac accelerator fibres (T1 - T4)
causes venodilatation, and to a lesser extent arterial vasodilatation, in the lower
extremities and abdominal viscera. This may manifest as hypotension the degree of
which will be influenced by the state of maternal hydration and the presence of
aortocaval compression (Chapter 57).
Sympathetic blockade above the level of the cardiac accelerator fibres (T1 - T4) will
cause a bradycardia. However, it should be noted that, even in the absence of a high
block, significant decreases in right atrial pressure (decreased venous return) can
also result in bradycardia which is mediated by intrinsic chronotropic stretch receptors
located in the right atrium and great veins. This effect can be prevented by
preservation of venous return. This can be achieved by prehydration, avoidance of
aortocaval compression (Chapter 28) and Trendelenberg or leg lift manoeuvres.
Blockade of the cardiac sympathetic supply above T4 may also result in hypotension
secondary to a loss of myocardial contractile force (4).
Hypotension secondary to sympathetic blockade should be anticipated with every
block. If the epidural is felt to be the cause of hypotension, therapy should be
targeted at the specific mechanism using volume replacement, venoconstrictors,
vagolytics, vasoconstrictors and inotropes as appropriate (Chapter 6). However, it is
imperative to exclude other possible causes of hypotension (Table 6.2).
Sympathetic blockade has also been detected indirectly by measuring increases in
skin temperature (5, 6). Over 50% of parturients will demonstrate a rise in foot
temperature of 3 degrees within 30 minutes of onset of lumbar sympathetic blockade
(Chapter 71). Temperature measurement in both feet is useful in detecting unilateral
sensory blocks early in the establishment of blockade. A change of posture can then
be effected to secure a reliable bilateral block (6) (Chapter 30).
References:
1. Lanz E, Theiss D, Kellner G, Zimmer M, Staudte HW. Assessment of motor
blockade during epidural anaesthesia. Anesth Analg 1983 62: 10: 889-893.
2. Van Zundert A, Vaes L, Soetens M, De Vel M, Maesen F. Measuring motor block
during lumbar epidural analgesia for vaginal delivery. Obstet Anesth Digest 1984;
4:31-34
3. Bromage PR. Epidural Analgesia. p144 Philadelphia WB Saunders 1978:
4. Cousins MJ. Physiologic effects of epidural blockade. In: Cousins MJ, Bridenbaugh
PO (eds). Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed,
JB Lippincott Co, Philadelphia,1988. pp 230-2.
5. Chamberlain DP, Chamberlain BDL. Changes in skin temperature of the trunk and
their relationship to sympathetic blockade during spinal anesthesia. Anesthesiology
1986 65: 139-143
6. Griffin RP, Reynolds F. The association between foot temperature and
asymmetrical epidural blockade. International Journal of Obstetric Anesthesia 1994 3:
132-136.
Leonie Watterson
Epidural analgesia has become an established technique in the management of
severe labour pain. Many feel that its use, however, has been implicated in
prolonging the duration of labour and in increasing the incidence of fetal malposition.
Both of these events have been associated with an increased instrumental delivery
rate as a result of fetal distress (Table 3.1) and maternal exhaustion or because
accepted limits for the duration of second stage have been exceeded. The
association between instrumental delivery and perinatal morbidity has been
responsible for a reluctance to employ epidurals in high risk deliveries (eg. twin
gestations and breech presentations) (Figure 14.1) (1, 2).
Several mechanisms have been proposed to explain the association of epidural
analgesia with instrumental delivery.
These mechanisms generally become manifest in the second stage of labour (from
full dilatation of the cervix to delivery) and include:
1. blockade of the motor units of sacral nerves resulting from local anaesthetic
agents administered during the first stage of labour. This effect may be cumulative
and persist into the second stage (3). The resulting weakness of pelvic floor muscles
reduces the effectiveness of maternal pushing and the involuntary bearing down
reflex;
2. blockade of sensory fibres disrupting the coordination between maternal pushing
and uterine contractions;
3. diminution of a neuro-endocrine reflex, in which distension of the vaginal wall
causes an augmented secretion of oxytocin from the posterior pituitary. Evidence to
support this includes an observed reduction in the force of uterine contractions and
oxytocin levels during second stage of labour during epidural analgesia (4, 5);
4. depression of uterine contractility by adrenaline-containing local anaesthetic
solutions by a direct effect similar to that of beta-agonist tocolytic agents used to
inhibit premature labour (6).
In contrast to the above, there is evidence to show that epidural analgesia may
accelerate an already prolonged and exhausting labour and reduce the need for
delivery by caesarean section for failure to progress. The provision of effective
analgesia reduces the inhibitory effect of endogenous maternal catecholamines on
uterine contractility, attenuates the maternal acidosis and permits the mother to
tolerate augmentation with oxytocin (7, 8, 9) (Chapter 33).
Evidence in the literature does not consistently support either view. Clarification of
the issue has been difficult for a number of reasons:
1. Whilst the collective experience is great, the techniques used to achieve epidural
analgesia over the last four decades have not been uniform. For example, the
techniques vary in choice of agent, drug concentration, administration during the
second stage and addition of an opioid. Over the same period of time, obstetric
practice has evolved. Prolongation of the second stage beyond 2 hours in the
absence of fetal distress is no longer an indication for forceps delivery (10). The
definition of 'forceps delivery' has been revised to distinguish between true mid-cavity
and low forceps (11). A tendency to avoid forceps delivery in favour of caesarean
section has lowered the rate of instrumental delivery independent of anaesthetic
practice (12). Finally, the inability to control for institutional or individual practice
persists.
2. Many of the studies to date have been criticised for bias because allocation to the
analgesic groups has been determined by maternal request for epidural analgesia
rather than true randomization (13). For example, a parturient with a minor degree of
cephalo-pelvic disproportion or occipito-posterior presentation is more likely to
experience severe pain and therefore more likely to request epidural analgesia. Such
patients are also more likely to require instrumental delivery. Two studies have
attempted to eliminate this bias, one by randomizing study groups (13), the other by
restricting the study group to those with occipito-anterior presentations (14). In both
of these studies, epidural analgesia was associated with an increased instrumental
delivery rate.
3. Early reports describing the association between instrumental delivery and poor
neonatal outcome failed to differentiate between the different instrumental techniques
used. It is now recognised that mid-cavity, rotational forceps deliveries are strongly
associated with increased perinatal mortality whereas there is no such association
with the use of low- and outlet-forceps, or Ventouse vacuum extraction.
Despite these difficulties, three firm conclusions can be drawn about the effects of
epidural analgesia on the progress of labour:
1. Overall, epidurals 'per se' are associated with an increased incidence of
instrumental deliveries but progressively more dilute concentrations of local
anaesthetic agents reduce this increased incidence. The dose-sparing effect of
opioid-local anaesthetic combinations further adds to this reduction.
2. Epidurals are associated with a prolongation of the second stage of labour. This is
not associated with neonatal morbidity in an properly managed labour.
3. Low (as opposed to high) concentration local anaesthetic solutions appear to
reduce the increased incidence of mid-cavity rotation forceps delivery.
The arguments for these conclusions are expanded below:
1. Progressively more dilute concentrations of local anaesthetic agents reduce the
increased incidence of instrumental deliveries observed with epidurals.
The increasing trend towards the use of bupivacaine in low concentrations reflects a
perception that in doing so there will be less motor block and that there will be
maximisation of its property of differential sensory blockade thus providing analgesia
without motor blockade, a lower instrumental delivery rate, and greater maternal
satisfaction (15). This has been borne out by the observation that 0.5% bupivacaine
is associated with high rates of malposition (3 times control rate) and forceps delivery
(5 times control rate) (16).
While a progressive reduction from a high concentration has been associated with a
reduction in instrumental deliveries (3, 17, 19), the experience with bupivacaine
0.25% (14, 20, 21, 22, 23, 24) and 0.125% (13) has not clearly demonstrated a
decreased instrumental delivery rate. In contrast, studies using very low
concentration solutions of both bupivacaine 0.0625% (25) and lignocaine 0.75% (26)
have shown that epidural analgesia may be continued throughout the second stage
without an increase in the instrumental delivery rate.
In the case of lignocaine 0.075%, this has been associated with less effective
analgesia (26). The addition of epidural opioids to local anaesthetic solutions appears
to improve the analgesic efficacy of low dose bupivacaine regimens which hitherto
had demonstrated a reduction in the forceps delivery rate, but which were limited by
high failure rates with respect to pain relief (25, 26, 27, 32). The combination of
bupivacaine 0.0625% with fentanyl 0.002% has been shown to decrease the higher
instrument rate which is observed when bupivacaine 0.125% is used alone whilst
maintaining the same quality of analgesia (27). This is consistent with the dose
sparing effect of opioids described in other series (33, 34, 35, 36, 37) (Figure 102.1)
(Chapter 60).
There is further support for the practice of minimizing motor blockade and preserving
involuntary expulsive efforts by reducing the amount of local anaesthetic which
reaches sacral segments of the spinal cord. This support is derived from studies
which demonstrate a reduced forceps rate as a result of practicing segmental
epidural blockade. This technique involves positioning the tip of the epidural catheter
near the T11 - T12 segments during the first stage of labour, thereby avoiding the
progressive effects of local anaesthesia on pelvic muscle tone. When full cervical
dilation has been achieved, it may be repositioned to include sacral segments during
second stage (7, 28, 29, 30).
Ropivacaine may be further able to reduce instrumental delivery rate.
The practice of discontinuing the epidural when the cervix is fully dilated is
widespread in labour wards. It should be appreciated that this will not reliably
eliminate the effects of first stage epidural analgesia. Several studies have described
persistent perineal anaesthesia after saline was blindly substituted for epidural
solution during second stage. The forceps rate is not reliably reduced. This may
reflect progressive motor weakness occurring during first stage (22). Moreover, the
percentage of women reporting inadequate analgesia is clearly increased ( 21, 22,
26, 31).
2. Epidurals are associated with a prolongation of the second stage of labour.
The effect of epidural analgesia on the duration of labour has been studied in many
series. As with the mode of delivery, results are inconsistent. In general, there
appears to be no clear effect on the duration of the first stage (8, 22). The second
stage is more consistently prolonged in both primiparous and multiparous women (8,
13, 39, 29, 40), but this prolongation appears to be less marked when dilute solutions
are used (17, 26, 22, 27).
Several authors have argued that a prolonged second stage is not associated with
fetal heart rate abnormalities, low Apgar scores (Table 35.1), or low umbilical cord
pHs, as long as electronic fetal heart rate monitoring is employed, and maternal
analgesia and hydration are maintained (13, 40, 41, 42). In addition, there is support
for observation of a latent period in early second stage to allow descent of the head
before pushing is commenced, as opposed to pushing from the time of cervical
dilatation. It has been argued that the instrumental delivery rate can be reduced by
the acceptance of a longer second stage (24, 40, 42, 43).
3. Low concentration local anaesthetic solutions appear to reduce the incidence of
mid-cavity rotation forceps delivery.
The increased perinatal mortality rate associated with instrumental delivery is largely
attributable to intracranial hemorrhage or birth asphyxia and is often associated with
the use of mid-cavity, rotational (eg. Kiellands) forceps (1, 2).
Premature infants are at particular risk as are term infants in the presence of
undiagnosed cephalo-pelvic disproportion. In contrast, morbidity associated with low
forceps or ventouse, vacuum extraction appears to be confined to facial bruising and
cephalohaematoma, respectively (44).
Low concentration local anaesthetic solutions can reduce the forceps delivery rate
(43). The equivocal results obtained for 0.25% bupivacaine are of interest: a high
incidence of mid-cavity forceps deliveries in some series (14, 20), low forceps or
vacuum extractions in others (21) or no observed increase in instrumental deliveries
in others still (22, 23, 24).
Similarly, 0.125% bupivacaine has not reliably demonstrated a non-increased
instrument rate (13, 17). However, a high incidence of mid-cavity forceps deliveries is
not apparent, with instrumental deliveries largely representing low forceps or vacuum
extractions.
A meta-analysis of the subject has been recently published by Halpern et al. (45).
References:
1. O'Driscoll K, Meagher D; Traumatic intracranial haemorrhage in firstborn infants
and delivery with obstetric forceps. British Journal of Obstetrics and Gynaecology,
88:6, June 1987. 577-579.
2. Chiswick ML, James DK; Kielland's forceps: association with neonatal morbidity
and mortality . British Medical Journal, 6th Jan, 1979. 7-9.
3.Thorburn J, Moir DD; Extradural analgesia: the influence of volume and
4.Bates RG, Helm CW; Uterine activity in the second stage of labour and the effect
of epidural analgesia. British Journal of Obstetrics and Gynaecology, Dec 1985, 92
1246-1250.
5.Matadial L, Cibils L; The effect of epidural analgesia on uterine activity and blood
pressure. Am. J. Obstet. Gynecol., July 1976, 125:6 846-854.
6.Lederman RP, Lederman E, Work B, McCann DS: Anxiety and epinephrine in
multiparous women in labour: Relationship to duration of labour and fetal heart
pattern. Am J. Obstet Gyaecol. Dec 15th, 1985 153:8 870-877.
7.Maltau JM, Andersen HT; Epidural anaesthesia as an alternative to caesarean
section in the treatment of prolonged, exhaustive labour. Acta Anaesth. Scand. 1975
19; 349-354.
8. Crawford JS; The second thousand epidural blocks in an obstetric hospital
practice. Brit. J. Anaesth. 1972; 44; 1277-1286.
9. Schnider SM, Abboud TK, Artal R, Henriksen EH, et al; Maternal catecholamines
decrease during labor after lumbar epidural anesthesia. Am. J. Obstet. Gynecol. Sep
1, 1983,147:1 13-15.
10. American College of Obstetrician and Gynecologists Committee Opinion:
Obstetric forceps #59 1988.
11. American College of Obstetricians and Gynecologists Committee Opinion:
Obstetric forceps, #59, 1988.
12.Lyons ER, Papsin FR; Caesarean section in the management of breech
presentation. Am. J. Obstet. Gynecol. Mar 1978, 130:5 558-561.
13.Chestnut DH, Vandewalker MD, Owen CL, Bates JN, Choi WW: The influence of
continuous epidural bupivacaine analgesia on the second stage of labour and method
of delivery in nulliparous women. Anesthesiology 1987 66: 774-780.
14. Kaminiski HM, Stall A, Aiman J; The effect of epidural analgesia on the frequency
of instrumental obstetric delivery. Obstet Gynecol May 87, 69:5 770-773
15.Morgan BM; Analgesia and satisfaction in childbirth the Queen Charlottes 1000
mother survey. The Lancet Oct 9,1982 808-810.
16. Hoult IJ, Maclennan AH, Carrie LES; Lumbar epidural analgesia in labour:
relation to fetal malposition and instrumental delivery. Br. Med. J. 1977; 1: 14-16.
17.Bleyaert A, Soetens M, Vaes L, Van Steenberge AL, Van der Donck A:
Bupivacaine 0.125%, in obstetric epidural analgesia: experience in three thousand
cases. Anesthesiology 1979, 51:435-438
18. Challen
19. Littlewood DG, Scott DB, Wilson J, Covino BG: Comparative anaesthetic
properties of various local anaesthetic agents in extradural block for labour. Br. J.
Anaesth. 1977; 49: 75.
20.Thorburn J, Moir DD; Extradural analgesia: the influence of volume and
concentration of bupivacaine on the mode of delivery, analgesic efficacy and motor
21. Johnsrud M, Dale PO, Lovland B; Benefits of continuous infusion epidural
analgesia throughout vaginal delivery. Acta Obstet Gynecol Scand 1988; 67:
355-358.
22.Phillips KC, Thomas TA; Second stage of labour with or without extradural
analgesia. Anaesthesia 1983; 38: 972-976.
23.Bailey PW; Epidural analgesia and forceps delivery: laying a bogey. Anaesthesia
1983; 38:282-285.
24. Goodfellow CF, Studd C; The reduction of forceps in primigravidae with epidural
analgesia - a controlled trial. British Journal of Clinical Practice 1979; 33: 287-288.
25. Sanchez-Pereles MC, Uribarn FJ, Gragera I; 0.0625% bupivacaine compared
with 0.125% bupivacaine continuously perfused epidurally during vaginal delivery.
Rev Esp Anesthesiol 1993; Jan-Feb 40:1 9-11
26.Chestnut DH, et al; Continuous infusion epidural analgesia with lidocaine: efficacy
and influence during the second stage of labor. Obstet Gynecol 1987; 69: 3 part 1
323-327.
27.Chestnut DH, et al; Continuous epidural infusion of 0.0625% bupivacaine -
0.002% fentanyl during the second stage of labor. Anesthesiology 1990; 72: 613-618.
28. Doughty A; Selective epidural analgesia and the forceps rate Br. J. Anaesth.
1969; 41: 1058-1062.
29.Matouskova A, Dottori L, Forssman L, Victorin L; An improved method of epidural
analgesia with reduced instrumental delivery rate Acta Obstet Gynec Scand 1975;
54: 231-235.
30. Joupilla R: Segmental epidural analgesia in labour- related to progress of labour,
foetal malposition and instrumental delivery Acta. Obstet. Gynecol 1979; 67: 85.
31.Chestnut DH, Owen CL, Bates JN, Ostman LG, Choi WW; Continuous infusion
epidural analgesia during labor: a randomized , double blind comparison of 0.065%
bupivacaine/ 0.002 % fentanyl versus 0.125% bupivacaine. Anesthesiology 1988; 68:
754-759.
32.Reynolds F, O'Sullivan G; Epidural fentanyl and perineal pain in labour. Anaesth.
Apr 89; 44:4: 341-344.
33.McGrady EM, Brownhill DK, Davis AG; Epidural diamorphine and bupivacaine in
labor. Anesthesia 1989; 44: 5 40-43.
34.Jones G, Paul DL, Elton RA et al; Comparison of bupivacaine and bupivacaine
with fentanyl in continuous extradural analgesia during labor. Br. J. Anaesth. 1989;
63:3 254 - 259.
35.Cooper RA, et al; Epidural analgesia for labor using a continuous infusion of
bupivacaine and alfentanil. Eur. J. Anesthesiol. 1993 10: 3 183-187.
36. Adamski D, Kruszyuski Z, Wiewoirowski K: Comparison of continous extradural
analgesia during labour using 0.25% bupivacaine or mixtures of 0.25% bupivacaine
and fentanyl. Ginekol Pol 1994; 65:7 394-399.
37. Dailland P, et al: Opioids for epidural analgesia: for or against? Can Anesthesiol
1994 42:2 275-285.
38.McCrae AF, Jozwiak H, McClure JH: Comparison of ropivacaine and bupivacaine
in extradural analgesia for the relief of pain in labour. Br. J. Anaesth. Mar 1995; 3:
261-265.
39.Abboud TK, Afraisiabi A, Sarkis F, et al; Continuous epidural analgesia in
parturients receiving bupivacaine, chloroprocaine, or lidocaine- maternal, fetal, and
neonatal effects. Anesth Analg 1984; 63:421.
40. Studd JWW, Crawford JS, Duignan NM, Rowbotham CJF, Hughes AO: The
effect of lumbar epidural on the rate of cervical dilatation and the outcome of labour
of spontaneous onset Br. J. Obstet. Gynecol 1980; 87: 1015-1021.
41. Cohen WR: Influence of the duration of second stage labor on perinatal outcome
and puerperal morbidity Obstet. Gynecol. 1977; 49:3 266-269.
42. Maresh M, Choong KH, Beard RW: Delayed pushing with lumbar epidural
analgesia in labour Br. J. Obstet. Gynecol. 1983; 90: 623-627.
43.Stoddart AP, Nicholson KE, Popham PA: Low dose bupivacaine - fentanyl
epidural infusion in labour and mode of delivery Anaesth. 1994; 49:12 1087-1090.
44. Danforth DN: Operative Delivery in Current Obstetric and Gynecologic Diagnosis
and Treatment 5th ed Lange California 1984. pp960-961
45.Halpern SH, Leighton BL, Ohlsson A, Barrett JF, Rice A. Effect of epidural vs
parenteral opioid analgesia on the progress of labor: a meta-analysis. JAMA. 1998
Dec 23-30;280(24):2105-10.
Leonie Watterson
Hypotension is the most common complication of regional blockade. A systolic blood
pressure of less than 100 mmHg, or a fall of greater than 30% should be considered
significant (1). Hypotension usually results from the physiologic effects of sympathetic
blockade on the cardiovascular system and will be exacerbated by aortocaval
compression (Figure 28.1) (Chapter 28) or reverse Trendelenberg positioning. It is
important to bear in mind the other possible causes of a low blood pressure in the
parturient who has a functioning epidural block (Table 6.2).
The incidence of hypotension can be markedly reduced by the employment of
preventative measures. A reduction from 79%-100% to 0-10% has been
demonstrated as a result of the use of the left lateral position, intravenous preloading,
and vasopressor therapy (2, 3).
The management of hypotension should be approached in three stages:
1. Commence supportive measures to stabilise maternal blood pressure: (Table 6.1)
Untreated hypotension will be poorly tolerated by the mother. Secondary
complications of organ hypoperfusion may result. These include loss of
consciousness with associated hypoventilation, regurgitation and cardiac
dysrhythmias. Acidosis may be severe. In shocked patients, hypotension may
become self-perpetuating. The fetus suffers the same risks. Supportive measures
should be instituted early regardless of the cause.
2. Consider possible causes of hypotension in the mother: (Table 6.2)
Sympathetic blockade is the most predictable cause of hypotension in a patient who
has recently had a form of neuraxial blockade established. Other causes are possible
and must be considered. After the delivery, the important causes of post-partum
haemorrhage should be borne in mind (Table 74.1).
3. Maintenance of the welfare of the fetus: (Table 6.3)
Uterine blood flow is poorly autoregulated and as such is strongly dependent upon
maternal mean arterial blood pressure. If hypotension occurs in the mother, her
cardiovascular reflexes will act to shunt blood away from non-vital organs (including
the uterus). This has the effect of restoring central blood pressure as a means of
preserving flow to the vital organs of brain and heart. Vasoconstriction will occur in
non-vital organs because their vasculature is richly endowed with alpha
adrenoreceptors. Uterine blood flow falls in direct proportion to the decrease in
maternal blood pressure. Hypotension that appears to be well tolerated by the mother
may be causing hypoxaemia and asphyxia in the fetus. It has been demonstrated that
infants of hypotensive mothers ( Mean Arterial Pressure < 70 mmHg) whilst achieving
normal Apgar scores (Table 35.1) had weak rooting and sucking reflexes for a period
of two days after birth (4).
References:
1. Norris M: Obstetric Anesthesia. Lippincott, 1993, p616
2. Kang YG, Abouleish E, Caritis S: Prophylactic intravenous ephedrine infusion
during spinal anesthesia for cesarean section. Anesth Analg 1982;61:839
3. Clark RB, Thompson CH: Prevention of spinal hypotension associated with
cesarean section . Anesthesiology, 1976;45:670
4. Hollmen AI, Joupilla R, Koivisto M: Neurologic activity of infants following
anesthesia for cesarean section. Anesthesiology 1978 248:350
Leonie Watterson
During labour, assessment of the level of the block is an important monitor of the
spread of local anaesthetic solution. A "high spinal" may occur as a result of
inadvertent subarachnoid or subdural spread of solution (Chapter 15), or excessively
high epidural spread. The former situations may result from epidural catheter
migration or catheter malposition and may occur with both intermittent dose or
infusion techniques. Conversely, the mechanisms of an apparently unsatisfactory
block may be better evaluated. For instance, inappropriate doses of local anaesthetic
versus malpositioned catheter. Ensuring that an appropriate sensory level has been
achieved is an important prelude to surgery for caesarean section.
The three neural modalities affected by neuraxial blockade (sensory, motor,
sympathetic) may be assessed individually (Chapter 10).
Methods of assessing the sensory level of the block include:
1. analgesia to pin prick,
2. loss of temperature sensation to ice, and
3. anaesthesia to soft touch.
Methods of measurement of motor blockade include:
1. the Bromage scoring method, (Table 8.1) and
2. dynamometry.
The degree of sympathetic blockade may be assessed by observing changes in:
1. haemodynamic status, and
2. temperature regulation.
Assessing the adequacy of the block for Caesarean section:
Perception of pain to pin prick, temperature change, or paraesthesiae (loss of
sensation to soft touch) are all methods used for determining the upper sensory level
of a neuraxial block.
A zone of differential blockade is observed between analgesia to pin prick and
paraesthesiae - the former typically several segments more cephalad. Temperature
perception extends one or two segments further cephalad than pin prick and reflects
sympathetic blockade (1). There is no constant relationship between the width of this
differential zone for any of these modalities (1, 2).
A recent study has concluded that the upper sensory level which is required for
satisfactory conditions during caesarean section can be defined accurately if a
standardised approach to the measurement of this level is used (3). In this study, an
upper level of anaesthesia to soft touch at or above the T5 dermatome was found to
be the most reliable index of a satisfactory block.
In contrast, levels of analgesia to pin prick which were subsequently associated with
pain during the operation, varied from T1-T9. Interestingly, 25% of patients who
experienced pain had a sensory level to pinprick of T3 or T4 which is commonly
recommended as the sensory level which will provide adequate conditions for
caesarean section. A level of anaesthesia to soft touch at or above the T5
dermatome was never associated with pain. This applied to both epidural and spinal
blockade. For levels of anaesthesia below T4, pain was more likely to occur with an
epidural than a spinal block ( 46% vs 22% ).
References:
1. Brull SJ, Greene NM. Zones of differential sensory block during extradural
anaesthesia Br. J. Anaesth 1991; 66: 651-55.
2. Rocco AG, Raymond SA, Murray E, Dhingra U, Freiberger D. Differential spread of
blockade of touch, cold, and pinprick during spinal anesthesia . Anesth Analg 1985;
64: 917-23.
3. Russell IF. Levels of anaesthesia and intraoperative pain at caesarean section
under regional block . International Journal of Obstetric Anesthesia. 1995; 4: 71-77.
4. Pedersen H, Santos AC, Steinberg ES, Schapiro HM, Harmon TW, Finster M.
Incidence of visceral pain during cesarean section: The effect of varying doses of
spinal bupivacaine Anesth Analg 1989; 69: 46-49.
5. Alahuhta S, Kangas - Saarela T, Hollmn AI, Edstr#m HH. Visceral pain during
cesarean section under spinal and epidural anaesthesia with bupivacaine Acta
Anaesthesiol Scand. 1990; 34: 95-98
Leonie Watterson
Whether caesarean section is performed under emergency or elective conditions, the
use of a regional anaesthetic technique should be considered.
The increased maternal mortality rate associated with general anaesthesia in
singleton pregnancies is now recognised (4, 5). This risk is theoretically further
increased in multiple pregnancies. The larger uterus encroaches to a greater degree
upon the functional residual capacity, increasing hypoxaemia in the supine position.
An unfavourable shift in the angle of the lower oesophageal sphincter increases the
likelihood of regurgitation of gastric contents. The resulting risk of aspiration
pneumonitis is compounded by a reduction in gastric pH induced by elevated gastrin
levels. There is an increased incidence of postoperative vomiting. General
anaesthesia has been associated with poorer outcome in the second twin (1, 7). All
of these factors support the avoidance of general anaesthesia (1, 2, 6).
Regional anaesthetic techniques include epidural and subarachnoid blockade. Some
authors avoid the latter on the basis of an increased incidence of hypotension (2, 11).
Aortocaval compression is more pronounced in multiple pregnancies. In addition
unpredictability in the spread of solution has been described. The increased
aortocaval compression causes shunting of venous return through the epidural
plexus thereby reducing the volume of CSF (Figure 28.1). For equivalent doses and
volumes of heavy solution, subarachnoid blockade will develop more rapidly and will
ascend an average of two spinal segments higher than in singleton pregnancies (8).
The unpredictability of response is a limitation of a single shot subarachnoid
technique. For this reason, it may be preferable to consider the use of titratable
techniques such as epidural and combined spinal-epidural blockade (Chapter 62).
Unfortunately, these may be technically more difficult to perform as a result of the
increased maternal body weight and accentuated lumbar lordosis which are observed
in multiple pregnancies (10). The slower onset of sympathetic blockade associated
with bupivacaine has led to its recommendation as the agent of choice (9). The
benefits of neuraxial opioids have not been specifically studied in this population.
Uterine hypotonia and blood loss are increased in multiple pregnancies which may
necessitate aggressive fluid replacement and oxytocic therapy (Chapter 74).
Rapid uterine relaxation may be required to expedite delivery of the infants who may
be malpresented (Chapter 24).
References:
1. Guttmacher AF, Schuyler GK; The fetus of multiple gestations. Obstet Gynecol,
1958 12:5 528 - 541.
2. James FM Anesthetic Considerations for Breech or Twin Delivery. Clinics in
Perinatology, 9:1 Feb, 1982 77 - 94.
3. Craft JB, Levinson G, Schnider SM Anaesthetic considerations in caesarean
section for quadruplets. Canad Anaesth. Soc. J., 25:3, May 1978. 236-239.
4. May AE The confidential enquiry into maternal deaths 1988-90 (editorial). Br. J.
Anaesth. Aug 1994; 73:2, 129-131.
5. Report on Confidential Enquires into Maternal Deaths in the United Kingdom 1988-
1990. London: HMSO, 1994.
6. Hartwell BL Fetal malpresentation and multiple births. in: "Obstetric Anesthesia"
Ed Norris MC. JB Lippincott Co. Philadelphia, 1993 p 696
7. Aaron JB, Halperin J Fetal survival in 376 twin deliveries. Am J Obstet. Gynecol.
1955 69:794
8. Jawan B, Lee JH, Chong ZK, Chang CS: Spread of spinal anaesthesia for
caesarean section in singleton and twin pregnancies Br.J. Anaesth. 1993; 70:
639-641.
9. James FM, Dewan DM, Floyd HM Chloroprocaine versus bupivacaine for lumbar
epidural analgesia for elective caesarean section Anesthesiology, 1980 52:488
10. Abouleish E: Caudal analgesia for quadruplet delivery Anesth Analg. Curr.
Res.1976; 55: 1 61-67
11. Malinov AM, Ostheimer GW Anesthesia for the high risk parturient. Obstet
Gynecol. 69:6, June 1987. pp 951 - 964.
Leonie Watterson
Twin gestations occur in 1% of pregnancies. The implications for anaesthesia
presented by twin and multiple gestation pregnancies will be in part determined by
the planned mode of delivery. As with other high risk pregnancies, including breech
presentation (Figure 14.1) (Chapter 47), some obstetricians advocate elective
caesarean section as a means of reducing the high perinatal mortality rate seen with
vaginal delivery (1).
The risks associated with twin pregnancy are well described (2). The perinatal
mortality rate for twins born by vaginal delivery is three to six times that for singleton
pregnancies (3).
The increased perinatal morbidity and mortality relates in part to a high incidence of
prematurity which affects over 50% of twins. The majority of these are between 32
and 38 weeks with approximately 10% below this age (1). Intracranial haemorrhage
is a significant complication of prematurity. This occurs as a result of compression
and traction on the soft cranial vault during its descent through the pelvis. It is a
particular hazard of midcavity forceps delivery or breech extraction (4, 5). Another
factor increasing perinatal morbidity is low birthweight, which, when corrected for
age, is reduced by an average of 650g (1). In addition, there is a high incidence of
malpresentation. The second twin presents breech in 41% of deliveries. The first twin
presents breech in 17% (2). More rarely, the twins may be locked.
The second twin is acknowledged to carry the highest perinatal risk as a result of
breech presentation and birth asphyxia. The latter may result from contraction or
partial separation of the placenta after delivery of the first twin or a longer period
during which the infant is subjected to the effects of aortocaval compression (Chapter
28). On the basis of this, it has become a general principle to minimise the second
stage of delivery of the second twin (1, 2, 6).
Similarly, with triplets and quadruplets, the likelihood of malpresentation in the later
fetuses increases, thus increasing the requirement for version and breech extraction
- both of which procedures are associated with a high incidence of morbidity and
mortality.
The likelihood of either instrumental or operative delivery in multiple pregnancies is
recognised to be higher in than in singletons (2). Forceps may be applied electively to
protect the premature head from a traumatic delivery. Following delivery of the first
twin, version may be attempted to convert the second to a more favourable
presentation. Pre-eclampsia (Chapter 40), placental abruption (Table E.3), vasa
praevia and cord prolapse occur more commonly. Uterine distension contributes to
the higher incidence of dysfunctional labour. Postpartum haemorrhage (Chapter 74)
secondary to uterine atony is two to three times that seen with singleton pregnancies
(7) (Table 74.1).
References:
1. Guttmacher AF, Schuyler GK The fetus of multiple gestations. Obstet Gynecol,
1958: 12:5 528 - 541.
2. James FM. Anesthetic Considerations for Breech or Twin Delivery. Clinics in
Perinatology, 9:1 Feb, 1982 pp77 - 94.
3. Malinov AM, Ostheimer GW Anesthesia for the high risk parturient . Obstet
Gynecol. 69:6, June 1987. pp951 - 964.
4. O'Driscoll K, Meagher D Traumatic intracranial haemorrhage in firstborn infants
and delivery with obstetric forceps . British Journal of Obsterics and Gynaecology,
88:6, June 1987. 577-579.
5. Chiswick ML, James DK Kiellands forceps: association with neonatal morbidity and
mortality . British Medical Journal, 6th Jan, 1979. 7-9.
6. Craft JB, Levinson G, Schnider SM Anaesthetic considerations in caesarean
section for quadruplets. Canad Anaesth. Soc. J., 25:3, May 1978. 236-239.
7. Little WA, Friedman EA The twin delivery: Factors influencing second twin
mortality - a review. Obstet. Gynecol. Surv. 1958 13:611
Leonie Watterson
The goals for delivery of twins include:
1. The provision of good analgesia which facilitates a non-precipitate, atraumatic
delivery.
2. The capacity to provide conditions for rapid delivery by caesarean section, forceps
delivery (perineal anaesthesia, pelvic floor relaxation) or version and extraction
(perineal anaesthesia, uterine relaxation) (Chapter 24).
3. A minimal duration of second stage for the second twin.
4. Avoidance of factors which may contribute to fetal distress or depression.
The use of epidural analgesia for delivery of twins has been controversial in the past.
Early studies examining its influence on the progress of labour in singleton
pregnancies suggested a prolonged second stage and an increase in mid-cavity
forceps deliveries. This led to a reluctance to employ it in twin pregnancies (1).
Studies specifically addressing the effect of epidural analgesia on the progress of
labour in multiple pregnancies have not supported this. Dysfunctional and prolonged
labour is well described in twin pregnancies, however, these do not appear to occur
more commonly in the presence of epidural analgesia. The duration of first stage
does not appear prolonged and the second stage may be shortened (1, 2, 3).
The incidence of instrumental deliveries is clearly increased in twin pregnancies, in
association with prematurity and malpresentation (4). Epidural analgesia does not
appear to increase the incidence of this (1). No studies to date have specifically
addressed the merit of low concentrations of local anaesthetic agents in multiple
pregnancy. Experience with singleton pregnancies on the progress of labour support
a reduction in motor block and instrumental delivery with concentrations of
bupivacaine of 0.125% or less (5, 6, 7). Progressive sparing of involuntary expulsive
reflexes may be less desirable in the delivery of twins, especially for premature and
breech infants (Figure 14.1). This implies a reduced role for very low concentration
solutions.
Continuous epidural analgesia would appear to achieve many of the goals outlined
for twin deliveries. It provides satisfactory analgesia throughout first and second
stages, and is readily modified to provide conditions for either caesarean section or
instrumental vaginal delivery. As with other regional techniques, it does not provide
uterine relaxation. Traditionally this necessitated general anaesthesia. More recently,
parenteral; or inhaled glyceryl trinitrate has been shown to achieve comparable
uterine relaxation and is associated with a low side effect profile by virtue of its short
duration of action (8) (Chapter 24). Other techniques available include epidural and
subarachnoid opioids, continuous or intermittent subarachnoid blockade, caudal, and
pudendal blockade (Chapter 70). Opioid analgesia provides acceptable analgesia for
first stage, however is often inadequate for second stage. It does not achieve the
perineal anaesthesia required for instrumental deliveries (9). Furthermore, the
considerations of prematurity and potential for hypoxaemia lend support to the
avoidance of depressant drugs in these infants. Subarachnoid blockade is limited by
the need to repeat the block if instrumental delivery is imminent, and continuous
infusions via a subarachnoid catheter are associated with a higher incidence of
central nervous system infection and nerve injury (10). Trauma to the fetus as a
result of passage of the needle through the sacral foramina is a described
complication of caudal anaesthesia (Figure 22.1). Pudendal anaesthesia does not
provide first stage analgesia and a failure rate of 50% has been reported with its use
(11). Whether regional analgesia is employed or not, the requirements for general
anaesthesia in the labour ward should be met in anticipation of this being required.
Communication between staff is important to ensure that the potential dangers of
anaesthetising for this procedure in this venue are well understood. Large bore
venous access should be established and blood bank facilities readily available. Staff
and facilities for resuscitation of the neonates should be prepared.
References:
1. Weekes ARL, Cheridjian VE, Mwanje DK 1977 Lumbar epidural analgesia in
labour in twin pregnancy. Br. Med. J.; ii: 730.
2. Jaschevatzky OE, Shalit A, Levy Y, Grunstein S Epidural analgesia during labour
in twin pregnancy . British Journal of Obstetrics and Gynecology. May 1977; 84,
327-331.
3. Schnider SM, Levinson G: Anesthesia for Obstetrics 3rd ed Williams and Wilkins,
Sydney 1993. p302.
4. Zuidema L Twin pregnancy. The management of labor . Clin Perinatol. 1988 Mar;
15:1, 87-91.
5. Sanchez Pereles MC, Uribarn FJ, Gragera I. 0.065% Bupivacaine compared with
0.125% Bupivacaine continuously perfused epidurally during vaginal delivery. Rev.
Esp. Anesthesiol. Banim. 93 40: 1 9-11
6. Stoddart AP, Nicholson KE, Popham PA. Low dose bupivacaine fentanyl infusions
in labor and the mode of delivery. Anaesth. 1994 49:12 1087-1090
7. Bleyaert A, Soetens M, Vaes L, Van Steenberge AL, Van der Donck A:
Bupivacaine, 0.125%, in obstetric epidural analgesia: experience in three thousand
cases . Anesthesiology 1979, 51:435-8
8. Mayer DC, Weeks S: Antepartum uterine relaxation with nitroglycerin at caesarean
delivery. Can. J. Anaesth. 1992; 39:2, 166-9.
9. Reynolds F, O'Sullivan G Epidural fentanyl and perineal pain in labour.
Anaesthesia 1989 44:4 341-344
10. Glosten B: Obstetric anesthesia risk: a review of recent literature . International
Journal of Obstetric Anesthesia 1994; 3: 7-12.
11. Scudamore JH, Yates MJ: Pudendal block - a misnomer? Lancet 1966; 1: 23
Paracervical Block
Leonie Watterson
Paracervical blockade may be used as a means of reducing pain during the first
stage of labour. Pain associated with uterine contraction and cervical stretching and
dilatation is transmitted from these structures on visceral afferents which accompany
sympathetic fibres. These pass sequentially through the uterine, cervical, inferior
hypogastric and superior hypogastric plexuses to the lumbar and lower thoracic
sympathetic chains. During early labour, the bulk of these enter the spinal cord at the
T11 - T12 segments. As pain becomes more severe, the two adjacent segments,
T10 and L1 become involved (1) (Figure 46.1).
The block is performed bilaterally with the patient in the lithotomy position. The
proximity of the broad ligaments just deep to the lateral fornices of the vagina is
exploited with the aim of interrupting pain transmission at the level of the uterine and
pelvic plexuses (2) (Figure 46.2). An 18.5 cm needle with a security tip (Iowa trumpet,
Kobak) is used to limit the injection to within 1.5 - 2 cm of the epithelium. The needle
is connected to a 20 ml Luer-Lok syringe. Measures to avoid intravascular injection
are vital. After careful aspiration non-adrenaline containing local anaesthetic solution
is infiltrated. The specific injection sites have been variously described: 3 and 9
oclock; 4 and 8 oclock; or alternatively all sites (2, 3). The distribution of
radio-opaque dyes observed in X-ray studies is similar (4). An interval of 15 minutes
should be observed between injections during which time signs of maternal (Table
36.4) and fetal toxicity should be excluded.
Paracervical blockade can be used to provide analgesia during the first stage of
labour when contraindications of epidural analgesia are present (Chapter 2). The
optimal time for institution of this block is the accelerated phase of the first stage
when the severity of pain increases. The presenting part is typically engaged. The
cervix is thin and effaced and has a tendency to be drawn up during uterine
contractions (2). Paracervical blockade does not provide analgesia of the perineum
during the second stage during which pain is transmitted primarily via the pudendal
nerves to the S2 - 4 spinal cord segments (Figure 21.1).
The technique has several limitations. The failure rate is reported to be as high as
18% (5). The proximity of uterine blood vessels in the vaginal fornices creates
maternal and fetal risks. Fetal bradycardia occurs in 10-50% of cases (6). This is
attributed to asphyxia which is believed to result from transient uterine artery
vasospasm due to high concentrations of local anaesthetic in the paracervical region.
The technique has a duration of action limited to 90 minutes with plain lignocaine.
The use of adrenaline or bupivacaine in an attempt to increase the duration of the
block should be avoided as both increase the incidence of fetal bradycardia (2, 3).
References:
1. Bonica JJ: Obstetric Analgesia and Anesthesia World Federation of Societies of
Anaesthesiologists Amsterdam 2nd ed. 1980.
2. Kobak AJ, Sadove MS: Combined paracervical and pudendal nerve blocks- a
simple form of transvaginal regional anesthesia Am. J. Obst. Gyn. 1961; 81:72
3. Marx G, Bassell G ed ; Obstetric Analgesia and Anesthesia Monographs in
Anaesthesiology , vol 7 Excerpta Medica New York, 1980 p233-235.
4. Spanos WJ, Steele JC: Obstet Gynecol 1959; 13: 129.
5. Pitkin PM, Goddard WB: Obstet. Gynecol. 1963;21: 737-744.
6. Cibils LA: Am. J. Obstet. Gynecol. 1976; 126: 202- 210
Leonie Watterson
Adequate preparation of the obstetric patient is vital in order to minimise the
complications of regional anaesthesia. This will be achieved by obtaining a history,
performing a physical examination, and, if indicated, performing preliminary
investigations.
Of particular relevance in the history is the presence of cardiac disease (Chapter 83),
pre-eclampsia (Chapter 39), coagulopathy, or any maternal condition which may
present a relative contraindication to neuraxial blockade. The presence of any of
these conditions may preclude the selection of the spinal and/or epidural route for
analgesia or anaesthesia.
Informed consent must be obtained (Chapter 55).
Fasting (Chapter 26) and acid-aspiration prophylaxis (Chapter 80) should be
observed in patients undergoing caesarean section.
The presence of a skilled assistant is essential (Document P14).
During the performance of the block and subsequently, careful attention to
positioning will increase the likelihood of a succesful block (Chapter 30).
Large bore intravenous access and adequate prehydration will be required to
minimise hypotension.
All equipment used for the insertion of an epidural must be sterile. The necessary
equipment for the performance of epidural and spinal blockade is outlined in Table
44.1 and Table 44.2.
Either reusable or disposable Tuohy needles and syringes may be used. Tuohy
needles feature blunt cutting tips whose ends are curved. This assists in identification
of the epidural space without dural puncture. The commonly used sizes for obstetric
analgesia are 16g and 18g. These needles accept 18 and 20 gauge catheters
respectively.
Epidural catheters are typically made from PVC. The tip features either three
helically-arranged lateral injection holes, or a single end hole (Figure 9.3). Three
holed designs have been criticised for their potential to result in a malpositioned
catheter such that individual holes may lie between different meningeal layers or in
an epidural vein. This can result in a multi-compartment block (Figure 11.1) (Chapter
11) or inadvertent intravascular injection of local anaesthetic (Chapter 36). Single
ended catheters have a higher incidence of false negative aspiration for blood and
missed segments (1, 2, 3, 4).
Appropriate monitoring should be instituted. This should include monitoring of:
1. The maternal circulation (pulse rate and blood pressure).
Hypotension may complicate neuraxial blockade despite careful attention to
prehydration (Chapter 6) and avoidance of aortocaval compression (Chapter 28). A
baseline pulse rate and blood pressure must be obtained before initiating the block.
Blood pressure should be measured at intervals of not more than 5 minutes during
establishment of the block and thereafter hourly whilst the block is being maintained.
During caesarean section the blood pressure should be measured at 5 minute
intervals. A qualified person should be responsible for hemodynamic monitoring.
Appropriate management of hypotension should be instituted early.
2. The level of the block.
The level of the block should be monitored as outlined in Chapter 8.
3. The fetus.
Methods of monitoring fetal wellbeing include:
a. Auscultation of heart rate with pinnards or doppler.
b. Graphical display of the cardiotocograph (Table 3.1).
c. The use of scalp electrodes.
d. Measurement of fetal scalp pH.
The fetus should be monitored whenever an epidural is being utilised. In
uncomplicated labours this is usually accomplished with a cardiotocograph. Scalp
electrodes are used when the cardiotocograph fails to generate a reliable trace or
when fetal distress is present. This requires a sufficiently dilated cervix. Scalp pH is
used to gain more information on fetal wellbeing when other signs of fetal distress are
present.
4. Bladder function.
Painless bladder distension as the result of neural blockade may contribute to
postpartum stress incontinence. This has been observed to occur in association with
concentrations of bupivacaine of 0.5% (5). The bladder should be emptied
intermittently.
References:
1. Beck H, Brassow F, Doehn M, et al: Epidural catheters of the multiorifice type:
dangers and complications. Acta Anaesthesiol Scand. 1986; 30: 549
2. Morrison LMM, Buchan AS: Comparison of complications associated with single
holed and multiholed extradural catheters. Br. J. Anaesth. 1990; 64:183.
3. Michael S, Richmond MN, Birks RJS: A comparison between open ended (single
holed) and closed ended ( three lateral holes ) epidural catheters. Complications and
quality of sensory blockade. Anaesthsia 1989; 44:578
4. Reynolds F; Epidural catheter migration during labour (letter). Anaesthesia
1988;43:69.
5. Thorburn J, Moir DD Extradural analgesia: the influence of volume and
Leonie Watterson
During the second stage of labour, pain largely results from distension of the lower
vagina, vulva and perineum. In addition, the musculature of the anterior compartment
of the pelvis must be negotiated by the descending presenting part. These structures
obtain most of their sensory and motor innervation from the second to fourth sacral
nerve roots via the pudendal nerve. Pudendal nerve blocks are of value in providing
analgesia for the second stage when contraindications to neuraxial blockade exist
and for the provision of pelvic floor relaxation when forceps delivery is required. They
may also be used to provide anaesthesia of the perineum in order to create or repair
an episiotomy. Pudendal nerve blocks have been utilized in the past as an alternative
to epidurals in assisted twin and breech deliveries (Figure 14.2). Increasing evidence
supporting the safety of epidurals in these situations has contributed to a diminished
use of pudendal nerve blocks (1).
The anatomy of the pudendal nerve (Figure 21.1) (2) should be considered when
performing the block. The block is performed with the patient in the lithotomy
position. Two approaches have been described: transvaginal and transcutaneous or
perineal. The basis of both approaches is to block the nerve before it gives off its
terminal branches. Its most reliable landmarks are exploited - the ischial spine in the
transvaginal, and the ischial tuberosity, in the perineal approach.
Transvaginal approach:
In the transvaginal approach, the ischial spine can be palpated either transvaginally
or per rectum. It is important to use a needle with a guide in order to limit the depth of
submucosal penetration ("Huber" security point ). When a left sided block is
performed, the ischial spine is palpated (Figure 21.2) with the index finger of the left
hand, the syringe is held in the right hand and the needle is guided between the index
and middle fingers of the left hand towards the ischial spine. The sacrospinous
ligament lies 1 cm medial and posterior to the spine. The needle is passed through
the ligament for a distance of 1 cm until a loss of resistance is appreciated. The tip
now lies in the area of the pudendal nerve. The pudendal vessels are closely
associated. After aspiration, 10 mls of local anaesthetic solution are injected. The
block is repeated on the other side.
Perineal approach:
The perineal approach is considered valuable when the engaged head makes
vaginal palpation difficult. The ischial tuberosity is located by palpation (Figure 21.2).
The needle is introduced slightly medial to this point, for a distance of 2.5 cm. The
nerve is usually encountered without eliciting paraesthesia. Up to 8 mls of solution is
infiltrated at this point. The needle is then withdrawn and directed into the deep and
superficial tissue of the vulva along its anterior margin in order to block the the
ilioinguinal and genitofemoral component (Figure 21.1). The block is repeated on the
other side.
The limitations of this block include:
- Failure to provide adequate analgesia. It has been reported that up to half of all
bilateral pudendal blocks are ineffective on one or both sides (1). A pudendal nerve
block will not abolish sensation to the anterior part of the perineum because this
region is supplied by branches of the ilioinguinal and genitofemoral nerves.
Subcutaneous infiltration anteriorly along the vulva is therefore described as a
component of this technique. Failure to wait sufficient time is a commonly cited
reason for failure of a pudendal block. Pudendal nerve blocks do not abolish the pain
of uterine contraction and cervical dilation which is transmitted via sympathetic nerve
fibres derived from spinal levels T10 - L2 (Figure 46.1). It does not cause relaxation
of the uterus.
- Intravascular injection with subsequent local anaesthetic toxicity is a risk imposed
by the close proximity of the pudendal vessels (Chapter 36).
- Fetal complications are uncommon. Exposure of the fetus to a high plasma level of
local anaesthetic is a possibility that should be considered. Delivery usually occurs
within a short period of time which may not allow for clearance of local anaesthetic
from fetus via the placenta. 1% lignocaine is the most commonly used agent. Peak
concentrations occur within 10 - 20 minutes. The maternal plasma concentrations
which occur after this block are much lower than after either epidural or paracervical
blocks.
This block has been reported to prolong the second stage of labour as a result of loss
of the bearing-down reflex. The addition of adrenaline may further prolong the second
stage of labour (3).
References:
1 Scudamore JH, Yates MJ: Pudendal block - a misnomer?
2 Ellis H and Feldman S ' Anatomy for Anaesthetists '
3 Norris MC Obstetric Anesthesia Norris MC (ed)
Leonie Watterson
Breech presentation is defined as the entrance of the fetal lower extremities or pelvis
into the maternal pelvic inlet. Three types are described:
Frank breech where the hips are flexed and the knees extended (Figure 14.1).
Complete breech, where the hips and knees are both flexed. Footling breech, where
one or both hips are not flexed and one or both feet are below the buttocks.
Breech presentation complicates 3% - 4% of pregnancies (1). The anaesthetic
management will vary with the mode of delivery which is planned. The increased
perinatal mortality which is observed with vaginal delivery has led to an increase in
elective caesarean section in this group (2). The hazards associated with vaginal
delivery are well recognized (3). There is a higher incidence of dysfunctional labour -
both first and second stages may be prolonged (1). Arrest of the after-coming head
either due to dystocia or containment by an incompletely dilated cervix is well
described, particularly within the context of premature pushing or small infants in
premature labour (4, 5). The head can be also be arrested by a contracting lower
uterine segment. Fetal asphyxia may then occur due to the resulting compression of
the umbilical cord within the pelvis. This risk increases with the duration of the
second stage. There is an increased risk of cord prolapse (1). The obstetrician is
faced with a high possibility of needing to perform an emergency operative or
assisted vaginal delivery (2). As with vertex presentations, forceps delivery is
associated with an increased incidence of intracranial hemorrhage(6, 7). This is a
particular problem for premature breech infants. Other risks include injury to the
spinal cord, peripheral nerves and intra-abdominal organs (1).
Analgesia for vaginal delivery:
The goals of anaesthetic management for vaginal delivery can be summarized as:
1. Adequate pain relief for the mother during first and second stage.
2. Perineal analgesia to facilitate regular examinations.
3. Prevention of a premature bearing-down reflex before full cervical dilatation.
4. A slow, controlled delivery over a relaxed perineum.
5. The ability to rapidly create conditions for delivery by caesarean section or forceps.
6. The ability to relax the uterus if required.
7. Consideration of the special requirements of a premature or acutely distressed
fetus.
Epidural analgesia for breech delivery:
The use of epidurals for breech deliveries has been the subject of controversy in the
past. Early reports which examined the effect of epidural analgesia on the progress of
labour in cephalic presentations suggested a prolongation of the second stage and
inhibition of the normal rotation of the presenting part during second stage. Both of
these effects increased the incidence of forceps deliveries (8, 9) (Figure 14.2). This
observation led to a widespread belief that epidural analgesia in breech vaginal
delivery would increase the incidence of fetal asphyxia and total breech extraction (4,
5). The latter involves complete extraction of the fetus with forceps. It carries a high
mortality for the fetus and a risk of uterine rupture or cervical trauma for the mother
(5). Studies specifically addressing this group have demonstrated that epidural
analgesia can be safely employed. The second stage of labour may be prolonged,
however there is no increase in the incidence of breech extraction, and the condition
of the fetus is either improved or unchanged (10, 11, 12). The sparing effect on
perineal muscle tone which has been achieved in cephalic presentations with very
low concentration local anaesthetic (eg 0.065% bupivacaine) and epidural opioids is
associated with an increased incidence of inadequate perineal analgesia (13, 14, 15).
It may also be associated with less reliable suppression of the bearing-down reflex. In
contrast, experience with 0.125% bupivacaine has demonstrated that titration of the
dose to achieve adequate perineal analgesia is also associated with reliable
suppression of the bearing-down reflex (16). Available data suggests that the goals
outlined above can be achieved with 0.125% bupivacaine with or without opioid (1,
16).
Spinal anaesthesia for breech delivery:
Spinal anaesthesia may provide excellent analgesia and perineal relaxation for
breech delivery (5) (Chapter 63). It is of particular benefit when these conditions are
required rapidly and epidural analgesia has not been established. The extent of
sensory and motor blockade can be controlled by exploiting concentration and
baricity (Chapter 30) (Figure 30.1). As with epidural analgesia, dense motor blockade
can be avoided by employing low concentration solutions (17). A major limitation is
that the conditions obtained are limited to the duration which is achieved from a
single dose unless a subarachnoid catheter is placed or the block is repeated. The
former approach has been associated with neurological complications (18).
The requirement for emergency intervention is higher in breech deliveries. Acute cord
prolapse and fetal distress (Table 3.1) will require emergency caesarean section in
the operating theatre. Assisted delivery of the after-coming head following
spontaneous delivery of the breech and total breech extraction are examples of
situations which may be managed in either the operating theatre or the delivery room.
The constraints of the chosen area, whether it be the operating theatre or the labour
room, should be clearly understood by obstetric, nursing and anaesthetic staff. If
delivery is planned in the labour room the requirements for general anaesthesia in the
labour ward should be met. The patient should be fasted and acid aspiration
prophylaxis be given, if an emergency delivery appears likely (Chapter 109). Finally,
staff and facilities for resuscitation of the neonate should be prepared.
It is important to stress, that if time permits, all of these situations can be managed
using a regional technique. The superior safety afforded is well described in the
literature (19). This lends support for the early placement of epidural catheters in this
group. If breech extraction or assisted breech delivery are required perineal
relaxation can be achieved with higher concentrations of local anaesthetic agent.
Uterine relaxation may be required (Chapter 24). This can be achieved in a number
of ways. Inhalational anaesthetic agents cause dose dependent uterine relaxation
which remains responsive to oxytocics in normal anaesthetic concentrations. This
effect may be lost at higher concentrations (20). This technique carries with it the
risks associated with general anaesthesia. Moreover, the long duration of action of
inhalational agents creates a risk of uterine atony and post-partum hemorrhage.
Large bore intravenous cannula should be established and blood bank services
readily available.
A technique of uterine relaxation which is compatible with regional anaesthesia is the
use of glyceryl trinitrate. When administered in intravenous boluses of 50 micrograms
it gives effective relaxation which is well tolerated by the mother. Prolonged uterine
atony is avoided because of its short half life (21). It has recently become available
as an intra-nasal preparation (22) (Chapter 52).
Anaesthesia for Caesarean Section:
Either an epidural or spinal technique may be employed. Extraction of the breech
through the lower uterine segment may be difficult and may require uterine relaxation.
References:,br> 1. James FM. Anesthetic Considerations for Breech or Twin Delivery
Clinics in Perinatology 1982; 9:1 77-94.
2. Lyons ER, Papsin FR. Cesarean section in the management of breech
presentation Am. J. Obstet. Gynecol. 1978;130:558-561.
3. De Crespigny LJC, Pepperell RJ. Perinatal mortality and morbidity in breech
presentation Obstet Gynecol 1979; 53:2 141-145.
4. Donnai ADG: Epidural analgesia, fetal monitoring and the condition of the baby at
birth with breech presentation Br. J. Obstet Gynecol 1975; 82: 360-365.
5. Moir D Obstetric Anaesthesia and Analgsia 2nd ed Balliere Tindall London, 1980;
pp252-277.
6. O'Driscoll K, Meagher D: Traumatic intracranial haemorrhage in firstborn infants
and delivery with obstetric forceps Br. J. Obstet Gynecol 1987; 88:6 577-579
7. Chiswick ML, James DK: Kiellands forceps: association with neonatal morbidity
and mortality British Medical Journal, 6th Jan,1979; 7-9
8. Hoult IJ, MacLennan AH, Carrie LES: Lumbar epidural analgesia in labour: relation
to foetal malposition and instrumental delivery. Br. Med J. 1977; 1: 14-16.
9. Kaminiski HM, Stafl A, Aiman J: The effect of epidural analgesia on the frequency
of instrumental obstetric delivery . Obstet Gynecol May 1987; 69:5 770-773
10. Confino E, Ismajovich B, Rudick V, David MP: Extradural analgesia in the
management of singleton breech delivery. Br. J. Anaesth 1985; 57: 892-895.
11. Breeson AJ, Kovacs GT, Pickles BG, Hill JG: Extradural analgesia- the preferred
method of analgesia for vaginal breech delivery. Br. J. Anaesth. 1978; 50:1227-1230.
12. Bowen-Simpkins P, Fergusson IL: Lumbar epidural block and the breech
presentation. Br. J. Anaesth. 1974; 46: 420-424.
13. Chestnut DH, et al: Continuous epidural infusion of 0.0625% bupivacaine -
0.002% fentanyl during the second stage of labor. Anesthesiology 1990; 72: 613-618.
14. Chestnut DH, et al: Continuous infusion epidural analgesia with lidocaine: efficacy
and influence during the second stage of labor. Obstet Gynecol 1987; 69: 3 part 1
323-327.
15. Reynolds F, O'Sullivan G: Epidural fentanyl and perineal pain in labour. Anaesth.
Apr 89; 44:4: 341-344.
16. Van Zundert A, Vaes L, Soetens M, De Vel M, et al: Are breech deliveries an
indication for lumbar epidural analgesia? Anesth Analg 1991; 72: 399-403.
17. Russell IF: Spinal anesthesia for cesarean delivery with dilute solutions of plain
bupivacaine: the relationship between infused volume and spread Reg Anesth 1991
16:3 130-136
18. Glosten B: Obstetric anesthesia risk: a review of recent literature. International
Journal of Obstetric Anesthesia 1994; 3: 7-12.
19. Report on Confidential Enquires into Maternal Deaths in the United Kingdom
1988- 1990. London: HMSO, 1994.
20. Schnider SM, Levinson G: Anesthesia for Obstetrics 3rd ed Williams and Wilkins,
Sydney 1993. p53-56.
21. Mayer DC, Weeks S: Antepartum uterine relaxation with nitroglycerin at
caesarean delivery . Can. J. Anaesth. 1992; 39:2, 166-169.
22. Redick LF, Livingston E: A new preparation of nitroglycerin for uterine relaxation
International Journal of Obstetric Anaesthesia 1995; 4:1 7-14
Subarachnoid space
Leonie Watterson
The subarachnoid space is the compartment within the spinal column which contains
the cerebrospinal fluid (CSF). CSF is produced in the ventricular system of the brain.
It communicates freely with the subarachnoid space via the foramina of Luschka and
Magendie near the brainstem. CSF entering the subarachnoid space circulates
caudad toward the lumbar cistern. Most of this is returned to the venous system via
arachnoid villi which are present on the dural sleeves of spinal nerves although a
small amount returns to the brain.
The subarachnoid space is bounded by the spinal meninges. These form a fluid filled
dural sac which surrounds the spinal cord. The pia mater is a delicate, vascular
membrane which closely invests the surface of the spinal cord. The subarachnoid
space lies between the pia mater and the arachnoid mater. The latter is a thin,
avascular membrane which adheres closely to the fibrous dura mater, creating
between them a potential space of small capacity, called the subdural space (Chapter
15). Inadvertent administration of local anaesthetic solution into this space can result
in a subdural block (Figure E.2). This is one of the mechanisms postulated for the
complication of epidural blockade referred to as a 'total spinal block'
The subarachnoid space extends from the basal cisterns surrounding the brainstem
superiorly, to its termination opposite the level of the second sacral vertebra (Figure
16.1). The meninges continue caudad from this point fused as the filum terminale
which anchors the spinal cord to its attachment on the coccyx.
The dimensions of the subarachnoid space are determined by the cross-sectional
shape of the spinal cord at each segmental level. The sac widens in the cervical and
lumbar regions which correspond to the enlargement of the spinal cord by nerves
subserving the limbs. Above the level of the first lumbar vertebra it exists as a ring
shaped recess. Here, the distance between the arachnoid mater and undivided spinal
cord is 2-3 mm. The caudal end of the spinal cord, the conus medullaris, usually lies
opposite the disc between the first and second lumbar vertebrae. Below this point the
subarachnoid space expands as a large lumbar cistern which contains the mobile
cauda equina. The diameter at this point approaches 9 mm (Figure 16.2).
The subarachnoid space is anatomically a single compartment which contains the
body of the spinal cord and CSF. The space is trabeculated by extensions of the pia
mater in several planes. Laterally these form the dentate ligament - a toothed
longitudinal membrane which anchors the spinal cord to the arachnoid and dura
mater. Anteriorly a pial extension runs along the length of the anterior median fissure
as the linea splendens. Posteriorly, in the mid-line, it extends from the posterior
median sulcus to the dura as the posterior subarachnoid septum.
Tony Wildsmith
Anaphylactic and histaminoid reactions following regional anaesthesia in the
parturient - A management plan:
Anaphylactic and histaminoid reactions are rare, but potentially fatal,
accompaniments of all anaesthetic techniques. True allergy to the modern,
amide-linked local anaesthetic agents is even rarer than to the other agents in the
anaesthetic armamentarium, but the possibility cannot be totally excluded.
Unfortunately, the classical concept of an antigen-antibody reaction producing
massive histamine release, typical features of hypotension, bronchospasm and
peripheral oedema, accompanied by measurable changes in plasma markers of the
reaction is not the only manifestation of "allergy". Reactions may occur without
previous drug exposure by activation of complement or by direct pharmacological
effect. The picture may be complicated further by the occurrence of "partial"
syndromes. An immunologically mediated reaction may not produce all the classic
symptoms and signs. The release of other mediators and/or the influence of
concurrent drug administration on the actions of histamine and these other mediators
may further modify the response. Yet another difficulty is that totally different
aetiologies, particularly anaesthetic misadventure, may lead to similar signs and
symptoms. Human nature being what it is, it may be easier to attribute "blame" to the
patient by diagnosing an immunological reaction!
Against this complicated background, the clinician must be constantly on the alert for
physiological changes in response to drug administration and seek to diagnose
rapidly the cause of a particular reaction. The range of alternative diagnoses is wide
and includes:
1. drug interactions,
2. adverse physiological response to anaesthetic depression or surgical stimulation,
3. complications (eg acid aspiration) of anaesthesia, and
4. vagal overactivity in the conscious patient.
A wide range of precipitants may produce a true immunological reaction, including
the active agent, the solvent or any preservative in the drug solutions administered.
Agents administered coincidentally, such as antibiotics, skin preparation solutions
and latex rubber should also be considered.
Rapid diagnosis needs to be accompanied by equally rapid response. There is
increasing evidence that immunologically based reactions must be treated with
adrenaline before any other agent. Fortunately, this drug will correct many (but not
all) of the adverse effects of other pathological states which produce a similar
physiological picture. The preferred method of administration is small (1ml)
incremental doses of adrenaline 1:10,000, titrated to effect. Subsequent management
will very much depend on the nature and severity of the reaction, but serial blood
samples should be taken for complement, immunoglobulin and other assays.
Prolonged intensive care may be necessary.
Once the acute event, is over it is necessary to try and establish the true cause of the
reaction so that definitive information may be given to the patient and incorporated in
the patient's records. This requires careful consideration of all possible causes of the
reaction and thoughtful analysis of blood results. In some circumstances, there may
only be circumstantial evidence that a particular agent was involved, but it may be
unnecessary to proceed further if alternative chemical entities can be used to achieve
the same effect in a subsequent procedure. However, in the case of local anaesthetic
drugs this is not possible and it is certainly appropriate to offer to the patient a
"challenge" testing exercise involving intradermal and subcutaneous injection of
progressively increasing doses of local anaesthetic to see what happens. There is
some risk, but true allergy to local anaesthetics is rare and subsequent patient
management can be very difficult if this diagnosis has been made without genuine
evidence. Finally, if a diagnosis is reached of aIlergy a report should be made
through the appropriate regulatory body.
Breech Presentation
Des Writer
Regional Anaesthesia for Breech Presentation.
Breech presentation is the commonest of the abnormal presentations (3-4 percent at
term) (1, 2, 3). The incidence exceeds 25 percent before 28 weeks' gestation. The
possible causal factors are outlined in Table 14.1.
Nomenclature:
Three types of breech presentation are described (Figure 14.1) :
(i) frank breech,
(ii) complete breech, and
(iii) incomplete [footling] breech.
Obstetric risks of breech presentation:
Perinatal mortality and neonatal morbidity are 3 to 10 times higher than for cephalic
presentation, but current data are imperfect. After excluding fetal congenital
anomalies, birthweight and gestational age are the most significant determinants of
outcome. Many obstetric complications are also more frequent than in the non-breech
delivery (Table 14.2).
Principles of obstetric management:
External cephalic version (ECV) performed close to term lowers the caesarean
section (CS) rate (4, 5) and is successful in 40 to 80 percent of non-laboring gravidae
(Table 14.3). Some obstetricians favour uterine tocolysis to facilitate ECV but this is
controversial. The administration of epidural analgesia for ECV may increase its
success rate (59% vs 24%) by lessening pain (6).
The choice of method of delivery (CS vs trial of vaginal delivery) is dependent on
fetal gestational age. For a term breech, obstetrical consensus supports vaginal
delivery of selected cases provided that management protocols are strictly adhered
to (Table 14.4) (7). If the management criteria cannot be satisfied, elective CS is
indicated. The obstetric manoeuvres used in breech delivery are outlined in Figure
14.2. For a preterm breech, the choice of CS is not controversial when the fetal
weight is < 1500gm. Studies confirm that the peri- and neo-natal mortality/morbidity
are reduced if these infants are delivered by CS. Some obstetricians advocate a trial
of labour after 32 weeks gestation when estimated fetal weight is > 1,500gm. The
survival of a preterm breech is mainly determined by the gestational age and infant
birthweight.
Vaginal breech delivery - Obstetric management:
There are three possible methods by which a vaginal delivery can be achieved:
1. spontaneous breech delivery - the infant is born with support of the trunk but
without traction or manipulation;
2. assisted breech delivery (preferred technique) - spontaneous delivery of the
breech up to the level of the umbilicus followed by obstetrician-assisted delivery of
the shoulders and aftercoming head (Figure14.2); and,
3. total breech extraction - the obstetrician extracts the entire body of the infant. This
method of delivery is unacceptable for a term singleton breech (2, 8).
Vaginal breech delivery - Anaesthetic management:
Epidural analgesia is the "gold standard" for breech vaginal delivery, but it presents
an anaesthetic challenge because:
1. the technique must obtund the involuntary urge to push which often occurs before
full dilatation;
2. it must give good analgesia yet allow effective 2nd stage pushing;
3. delivery of the shoulders and aftercoming head (especially forceps-assisted) may
require profound perineal anaesthesia and relaxation.
There are four approaches to the anaesthetic management of breech vaginal delivery
which are effective:
1. 'Two catheter' epidural.
This technique may be preferable and is described in Table 14.5.
2. Combined spinal-epidural (CSE).
CSE analgesia can also provide excellent conditions and is described in Table 14.6.
3. Single catheter epidural (Chapter 1).
If a single catheter technique is to be used, a dilute local anaesthetic plus opioid
solution (eg. bupivacaine 0.0625% with fentanyl 0.0004%) is used for the 1st stage.
Additional doses of epidural fentanyl can be used to obtund early pushing.
4. Subarachnoid analgesia (Chapter 63).
Some anaesthetists advise subarachnoid block alone in selected situations. Dilute
local anaesthetics (eg. lignocaine 1.5%) preserve the ability to push while providing
excellent sensory anaesthesia.
Anaesthetic 'standby' for general anaesthesia for breech delivery should now be
obsolete!
Caesarean section - Anaesthetic management:
Epidural or spinal anaesthesia are preferable and GA (which can cause neonatal
depression) is very rarely indicated.
Fetal head entrapment remains the obstetrician's greatest fear. It typically occurs with
premature vaginal breech delivery when the fetal buttocks and thighs pass through
an incompletely dilated cervix and the uterus then clamps tightly around the fetal
head. It can also occur during CS particularly if the uterine incision is too small.
Successful treatment requires immediate tocolysis (Table 14.7) (Chapter 52) (9).
Local anaesthetics are not tocolytic (Chapter 24); no advantage accrues from
extending the block.
References:
1. Writer WD. Breech presentation and multiple pregnancy: obstetric aspects and
anaesthetic management. Clinics in Anaesthesiology 1986 4:305-20.
2. Seeds JW. Malpresentations. In: Obstetrics: normal and problem pregnancies.
(Gabbe SG, Niebyl JR, Simpson JL, eds) Churchill Livingstone p.539-72. 2nd Edition
New York. (1991)
3. Mokriski BK. Abnormal presentation and multiple gestation. In: Obstetric
anesthesia: principles and practice. Chestnut DH, editor. St. Louis: Mosby-Year
Book, 1994:669-85.
4. Hanss, JW Jr. The efficacy of external cephalic vesion and its impact on the
breech experience. Am J Obstet Gynecol 1990 162: 1459-1464.
5. Gifford DS, Keeler E, Kahn KL. Reductions in cost and cesarean rate by routine
use of external cephalic version: a decision analysis. Obstet Gynecol 1995
85:930-936.
6. Carlan SJ, Dent JM, Huckaby T, et al. The effect of epidural anesthesia on safety
and success of extemal cephalic version at term. Anesth Analg 1994 79:525-528.
7. Society of Gynaecologists of Canada. The Canadian Consensus on Breech
Management at Term. Journal SOGC 1994 16:1839-1848.
8. Baskett TF. Essential management of obstetric emergencies. Essential
management of obstetric emergencies. 2nd Edition Bristol: Clinical Press, 1991
126-135.
9. Mayer DC, Weeks SK. Obstetric forum: antepartum uterine relaxation with
nitroglycerin at caesarean delivery. Can J Anaesth 1992 39: 166-169.
Breech Presentation
Caudal Analgesia
CSE: Technique
Epidural Technique
Extradural Space
Guidelines for anaesthetic practice in a delivery suite
Guidelines for Conduct of Epidural Analgesia
Natural Childbirth
Neonatal Outcome
Paracervical Block
Subarachnoid space
Subdural Space
Uterine relaxation
Dose (mgs) of agents in lateral position @ L2-3*
Height (cms) 150 157.5 165 172.5
(5ft) (5ft 3in) (5ft 6in) (5ft 9in)
Cesarean Section**
Lidocaine 50 60 70 80
Bupivacaine 8 9 10 11
Tetracaine 8 9 10 11
Post-partum TL***
Lidocaine 65 75 85 100
Bupivacaine 10 11 12.5 13.5
Tetracaine 10 11 12.5 13.5
* Add more local anesthetic in the sitting position or the use of L3-4 interspace (e.g.,
1.5 mg bupivacaine or equivalent for either situation).
** Add 0.2 mg morphine for intra- and postoperative analgesia, and 0.2 mg
epinephrine for intensifying and prolonging the block.
*** Add morphine only because it is a relatively short procedure. Morphine improves
the quality of the block and provides postoperative analgesia.
The Apgar Score:
SCORE 0 1 2
Heart Rate Absent Less than 100 More Than 100
Resp. Effort Absent Irregular Good
Reflex Irritability No response Grimace Cough / Sneeze
Muscle Tone Flaccid Good Tone Spontaneous flexion
Colour Blue / Pale Body pink / Limbs Blue Entirely Pink
Virginia Apgar graduated from Columbia University's College of Physicians and
Surgeons in 1933. She wanted to be a surgeon but was persuaded by Dr Alan
Whipple, chairman of Surgery, to enter anesthesia.
Her initial training was with nurse anesthetists at Columbia. She then spent six
months each with Ralph Waters at Madison, Wisconsin, and Ernest Rovenstine at
Bellevue Hospital, New York.
She returned to Columbia in 1938 as Director of the Division of Anesthesia, and
established a strong unit over 10 years. In 1949, Emmanuel Papper became
chairman of the department, and Dr Apgar moved into obstetric anesthesia.
The idea for her score was conceived over breakfast in the hospital cafeteria when a
medical student questioned her about methods for assessing the newborn. Apgar
promptly sat down and wrote her scoring method on the back of a notice which told
people what to do with their trays. It was first presented at a meeting in 1952, and
published in 1953. Virginia Apgar then went on to do further important research in
neonatal acid-base status, especially in terms of hypoxia and acidosis, and also on
the effects of maternal anesthesia on the neonate. She also introduced the anterior
approach to the stellate ganglion in 1948.
She is one of only two anesthesiologists to be honored on a U.S.stamp (the other
being Crawford Long).
Michael Cooper.
Tensile Strengths of epidural catheters
Nylon
Gauge 19 20 20
Manufacturer Pharmaseal Kendall Burron
Load to failure (kg) 3.66 +/-0.05 2.68+/-0.3 2.85+/-0.3
Elongation(%) 1120+/-260 580+/-120 380+/-150
Teflon
Manufacturer Deseret Deseret Kendall
Load to failure (kg) 2.05+/-0.1 1.17+/-0.1 1.91+/-0.1
Elongation(%) 270+/-50 350+/-70 400+/-40
Ounces of pull needed to extract catheters in the lateral decubitus and sitting
positions.
Forces required to break various spinal catheters.
The effect of the full lateral position on aorto-caval compression
The sources of variation in the duration of the second stage of labour and their
relative contribution to the total variability on the basis of multiple linear stepwise
regression in 964 parturients (Nullipara 473, Multipara 491). Total R2 = 0.233.
Reproduced with permission from Piper et al Am J Obstet Gynecol 1991;
165:976-979.
Classification of ante-partum haemorrhage:
Grade Severity of
coagulopathy
Proportion
of
Placenta
separated
Estimated
Blood Loss
Fetal
Distress
Hypotension
I Mild Less than
1/6
Less than
250mls
None None
II Moderate 1/6-1/2 250-1000mls Common Unlikely
III Severe More than
1/2
More than
1000mls
Common Common
Cimetidine
Ranitidine
The ligaments of the intervertebral space (L3-L4). The supraspinous ligament runs
between the tips of the spinous processes. In the elderly, the ligament may be heavily
calcified.
The interspinous ligament connects the spinous processes.
The ligamentum flava run between the inferior, anterior surfaces of the superior
lamina to the superior, posterior surfaces of the lamina below. The subarachnoid
space is separated from the ligamentum flava by the dural membrane. Note the
presence of the potential subdural space.
Technique for caudal injection:
The needle is inserted at an angle of 70-80 degrees to the skin and slowly
advanced until the bony resistance of the sacrum is detected. The needle is
withdrawn slightly, the entry angle reduced by about half, and then reinserted
to a depth of 2-3 cm, bearing in mind that the dural sac terminates at the S2
level.
Note the proximity of the fetal head.
Needle Tip Designs
Features of note are:
1. The presence of a cutting tip on the Quincke type needle.
2. The dimensions of the terminal hole.
- A large hole contributes to a rapid flashback.
- A long hole increases the possibility of injecting part of the intended sub-arachnoid
dose into the epidural space.
3. The original pencil point needle (HART) is illustrated. (Hart and Whitacre, JAMA
1951;147:657-58.)
CAUDAL/SPINAL INDICATIONS:
ROYAL WOMEN'S HOSPITAL MELBOURNE 1989-1995
YEAR SPINAL
PRIMIP
(%)
LABOUR
PAIN
% PLACENTAL REMOVAL %
FORCEPS
DELIVERY
% PERINEAL PAIN
1989 7

4 57 1 14 2 29 0
1990 8 63 6 75 2 25 0

1
1991 10 50 5 50 2 20 2 20 1
1992 72 64 16 22 31 43 18 25 4
1993 87 59 7 8 35 40 40 46 2
1994 136 67 10 15 22 32 37 54 0
1995 68 72 10 15 22 32 37 54 0

CAUDAL

1989 573 73 405 71 49 9 45 8 306
1990 469 74 356 76 42 9 30 6 261
1991 339 75 235 6 24 7 38 11 182
1992 156 75 101 65 8 5 10 6 92
1993 84 85 51 61 7 8 12 14 28
1994 29 72 17 59 1 3 3 10 14
1995 13 77 12 92 0

1 8 2

RECOMMENDED MAXIMUM DOSES OF LOCAL ANAESTHETICS
-Illustrated in the case of a 60Kg woman
Drug Dose Dose/Kg
AMIDES
Lidocaine with epi 420 (7mg/kg)
Lidocaine plain 300 (5mg/kg)
Bupivacaine with epi 180 (3mg/kg)
Bupivacaine plain 120 (2mg/kg)
Etidocaine 240 (4mg/kg)
Mepivacaine 420 (7mg/kg)
Prilocaine 720 (12mg/kg)
ESTERS
Cocaine 180 (3mg/kg)
Procaine 840 (14mg/kg)
Chloroprocaine 840 (14mg/kg)
Tetracaine 180 (3mg/kg)
Possible Effects of Major Regional Blockade on Cardiotocographic
Patterns.
Uterine Contractions Mechanism
Increased Frequency and
intensity
Analgesia decreases catechol amine levels
Decreased Frequency and
intensity
Decreased blood supply to uterus.
?Inhibition of motor nerve supply to uterus
?Direct effect of Local Anaesthetic on smooth
muscle.
Fetal heart rate:
beat to beat variability
Increase Acute fetal hypoxia due to placental
hypoperfusion
Decrease Direct effect of local anaesthetic agents.
Chronic hypoxia and acidosis from placental
hypoperfusion
Fetal heart rate:
Long term decelerations
Early Head compression from increased uterine tone.
Late Placental insufficiency worsened by placental
hypoperfusion
Variable Cord compression aggravated by
maternal hypotension and increased intensity
of uterine contractions.
Nerve supply to perineum
The nerve supply to the perineum originates from three main sources:
1. The Genito-femoral Nerve (L1,L2).
2. The pudendal nerve arises from the anterior rami of the second to fourth sacral
roots. These form a trunk before leaving the pelvis via the greater sciatic foramen. It
passes immediately behind the ischial spine and swings forward to enter the
perineum via the lesser sciatic foramen. The nerve passes through the ischiorectal
fossa where it gives off its terminal branches. The inferior rectal nerve innervates the
external anal sphincter and the perianal skin. The perineal nerve innervates the
sphincter urethrae and other muscles of the anterior compartment via a deep branch,
and the skin of the perineum poterior to the clitoris via its superficial branch. The
dorsal nerve of the clitoris supplies the skin surrounding this structure.
3. The perineal branch of the posterior femoral nerve.
The effect of posture on the spread of a hyperbaric spinal solution
Hyperbaric solutions (SG > 1.009) will tend to spread caudad in patients
in the sitting position and cephalad in patients in the Trendelenberg
position .
As a result of the intrinsic curves of the spine an injection made at L4 or
lower with the patient in the supine position will tend to spread caudad
and that made at L3 or higher will spread cephalad.
The effect of posture on the spread of a hyperbaric spinal solution
Hypobaric Solutions (SG < 1.003) spread in the opposite direction to
hyperbaric solutions.
The vertebral levels which correspond to important landmarks within the spinal canal.
In 3% of the population the cord ends at L1 or above.
In 94% of the population the cord ends at L1 or L2.
In 3% of the poulation the cord ends at L3.
Modified and re-drawn from:
'Lumbar Puncture and Spinal Analgesia'.
R. Macintosh. Blackwells Books, Oxford.
KEY FEATURES OF BUPIVACAINE TOXICITY
(i) More likely to result in cardiovascular collapse (CV collapse dose / dose for
convulsions = 3.7 for bupivacaine and 7.1 for lidocaine).
(ii) Ventricular arrhythmias are more likely to accompany cardiac toxicity (use
bretylium).
(iii) Pregnant women are more sensitive to cardiac toxicity from bupivacaine.
(iv) Resuscitation is usually lengthy.
(v) Toxicity is enhanced by acidosis and hypercarbia.
FACTORS INFLUENCING LOCAL ANAESTHETIC BLOOD LEVELS
(i) Drug dose: Blood levels are proportional to the amount given. Increasing the dose
also increases the extent of the block and increases the risk of local anesthetic
toxicity.
(ii) Drug type: Some drugs such as prilocaine are so rapidly metabolized (by plasma
cholinesterase in this instance) that high blood levels are harder to achieve.
(iii) Pattern of absorption (Pharmacokinetics): Drugs injected intravascularly achieve
a high peak level shortly after injection, while those injected into a peripheral
compartment (eg. infiltration into tissues) take a longer time to achieve a peak level.
(iv) Site of administration: Administration of local anesthetics in highly vascular areas
increases the likelihood of high drug levels.
NEUROTOXICITY OF LIGNOCAINE:
[mcg/ml] SYMPTOMS:
3 Lightheadness.
4 Tongue Numbness
6 Visual disturbances.
8 Generalised twitching.
12 Convulsions.
15 Profound Coma.
20 Respiratory Arrest.
25 CVS Depression
Diazepam
MANAGEMENT OF LOCAL ANESTHETIC TOXICITY
(a) Prevention (pretreatment with benzodiazepines when appropriate; aspirate before
injection)
(b) Early recognition (converse with patient)
(c) Prevention of progression (thiopental 50-75mg IV; diazepam 5-10 mg IV)
(d) Airway management (Oxygen; Ventilation; Intubation)
(e) Care of the fetus (Fetal monitoring; Immediate Cesarean section if CPR needed.)
A correctly positioned spinal-epidural needle ('Hanaokoa').
A combined spinal-epidural needle. (Becton Dickinson 'Durasafe'). The spinal needle
is of the Whitacre type.
Original Lee epidural catheter. Side hole 10 mm from the end.
Later catheter developments of the sixties and seventies.
The most commonly used types of epidural catheter in use today. The 'terminal eye'
variant and the 'three lateral eye' variant.
A modern 'three lateral eye' catheter. Note the proximity of the three eyes in
comparison to the original design.
Lateral view of L3-L4 Interspace.
The principles of the 'loss of resistance' technique for epidural localisation are shown
in this diagram.
The Tuohy needle is inserted into the interspinous ligament with the stylette in place.
Once in the ligament, the stylette is removed and the needle connected to a syringe
containing either air or saline. The needle is now advanced slowly through the
interspinous ligament into the ligamentum flavum using either a continuous or
intermittent movement. As the needle is advanced, pressure is applied to the plunger
of the syringe. While in the ligament, it is not possible to inject the air/saline. As soon
as the needle enters the epidural space, the air/saline can be freely injected. Recent
studies suggest that saline may be preferable to air as the loss-of-resistance
indicator.
Once the space has been localised, various methods can be used to initiate the block
and place an epidural catheter. Some operators prefer to inject a small amount of
saline (or local) before insertion of the catheter, while others thread the catheter first
and administer all solutions through the catheter. Both techniques have their merits.
Whichever technique is chosen, it is important not to thread more than ~3-4 cms of
catheter into the space.
Epidural Catheterisation
A close up view of the L3-L4 Interspace. After successful localisation of
the space with the Tuohy needle using a 'loss of resistance' technique,
the epidural catheter is slowly advanced a few centimetres into the
space.
After ensuring that neither blood nor spinal fluid can be aspirated
through the catheter, an appropriate amount of analgesic solution is
injected. The solution spreads through the space, enveloping the
subarachnoid space and the emerging nerve roots.
Review P14 - 1993
Guidelines for the Conduct of
Epidural Analgesia in Obstetrics
Preamble:
Epidural analgesia is a safe and effective method of pain relief in labour,
provided appropriate precautions are taken as follows:
1. Epidural puncture and/or cannulation of the epidural space should be carried
out only by persons with adequate training and experience in the technique.
2. Such persons must be:
2.1 readily available to supervise the subsequent management of the
epidural
2.2 competent to deal with the occasional life threatening and other
complications which may arise following the injection of agents into the
epidural or sub-arachnoid space.
3. An appropriately trained person must be present to assist the anaesthetist
whilst performing the epidural block.
4. Once epidural analgesia has been established, and the response of the
patient to the agent or agents has been assessed by the anaesthetist, further
doses to maintain analgesia may be administered by other suitably trained
medical or nursing staff, provided that:
4.1 The dose has been prescribed by the anaesthetist;
4.2 The anaesthetist delegating the "top-up" procedure is satisfied that the
person who will carry out the task is competent to do so and competent to
appropriately monitor the patient and her fetus;
4.3 The person carrying out these tasks is satisfied that he or she is
competent to do so;
4.4 Appropriate equipment and skilled staff are readily available to treat
complications and any adverse reactions; and
4.5 Written instructions and management guidelines are provided.
5. All patients undergoing epidural analgesia must be nursed in an area
4.5 Written instructions and management guidelines are provided.
5. All patients undergoing epidural analgesia must be nursed in an area
appropriately equipped with staff able to:
5.1 monitor both the patient and fetus;
5.2 detect the extent of the block and any adverse effects; and
5.3 judge the necessity for top-up doses.
6. A record must be made of the procedure, the clinical and other observations
and the instructions delegated to the attending staff.
7. All patients receiving epidural analgesia must have an intravenous infusion
commenced before the institution of the block and the infusion must be left in
situ for the duration of the block.
8. Satisfactory and safe epidural analgesia can be produced by continuous or
patient-controlled epidural infusion of local anaesthetic alone, opioid alone or
local anaesthetic-opioid mixtures. The same principles of management should
apply when epidural analgesia is administered by any of these methods.
9. When there is no further need for the epidural, the catheter should be
removed by the anaesthetist or other suitably trained medical or nursing staff.
10. At all times the ultimate responsibility for the management of epidural
analgesia remains that of the anaesthetist who performs the procedure or a
delegated suitably trained registered medical practitioner.
11. All patients having epidural analgesia in labour must be admitted under the
direct care and supervision of a registered medical practitioner.
February 1993
This document is copyright and cannot be reproduced in whole or in part
without prior permission.
The anaesthetic techniques used for caesarean section at the Royal Hospital for
Women, Sydney, Australia, 1994-1995.
823 caesarean sections were performed in the year.
Potential mal-positions of a multi-hole catheter.
Note the potential for drug entry into both the subdural and subarachnoid spaces .
CHARACTERISTICS OF LOCAL ANESTHETIC TOXICITY
(I) CNS toxicity:
a) Excitation Phase: tinnitus, confusion, restlessness, perioral numbness or tingling,
metallic taste, lightheadness, sense of dread and impending doom.
b) Convulsive Phase: grand-mal clonic-tonic seizure
c) Depression Phase: CNS depression with drowsiness and unconsciousness.
d) Repiratory depression and apnea.
(II) CVS Toxicity:
a) Excitation Phase: - hypertension, tachycardia (with convulsions)
b) Depression Phase:
(i) Negative inotropic effect with decreased blood pressure, cardiac output and stroke
volume.
(ii) Peripheral vasodilation with further hypotension.
c) Cardiovascular Collapse
Methods of assessing the impact of maternal drug administration on neonatal
condition.
* Apgar Score
* Blood chemistry / Acid Base Status
* EEG
* Maternal-to-fetal drug ratios
* Neonatal suckling behaviour
* Brazelton Neonatal Behavioural Assessment Score [NBAS]
* Breathing frequency
* Early Neonatal Neurobehavioural Scale [ENNS]
* Neurologic & Adaptive Capacity Score [NACS]
Bupivacaine
Robin Russell
Backache is a common symptom in both the ante- and post-natal periods. Recently,
a possible association between long term backache and epidural analgesia in labour
has been highlighted in both the medical and lay press.
Short term backache is a common problem in the first week after delivery and should
not be confused with more chronic back problems. When questioned in the first few
days after delivery, up to 45% of women report tenderness at the site of epidural
needle insertion (1). A similar proportion of women in whom regional analgesia has
not been used suffer from generalised lower backache following labour (2).
Long term backache after childbirth and its association with epidural analgesia in
labour was highlighted in a retrospective study from the Birmingham Maternity
Hospital (3). Long term backache was reported by 23% of women and, in 14% this
had not been present before delivery. The incidence of new, long term backache was
18.9% in those who received epidural analgesia compared with 10.5% in those using
other methods of pain relief in labour. Epidural anaesthesia for elective caesarean
section did not produce an increased incidence of long term backache. It was,
therefore, suggested that 'stressed' positions in labour exacerbated by muscular
relaxation and the abolition of pain resulted in a postural backache. A second,
retrospective study also demonstrated the association between epidurals and long
term backache (4) (Figure 84.1). In most cases, backache was found to be postural,
not severe and, usually, resolving.
In both these retrospective studies, the incidence of antenatal backache was
significantly lower than that demonstrated in previous work conducted during
pregnancy, in which backache was reported by 50% of these women. The more
severe the antenatal backache, the longer it persisted after delivery. It would appear
that, when questioned retrospectively, many women forget that they suffered from
antenatal backache.
Recently performed prospective studies have failed to find an association between
pain relief and long term backache (Figure 84.2). Backache was no more frequent
after epidural or spinal analgesia compared with other forms of pain relief (5, 6, 7, 8)
There was no relationship between the incidence of backache and the degree of
motor block (7).
References:
1. Crawford JS. Some maternal complications of epidural analgesia for labour.
Anaesthesia 1985; 40: 1219-1225.
2. Grove LH. Backache, headache, and bladder dysfunction after delivery. Br J
Anaesth 1973; 45: 1147-1149.
3. MacArthur C, Lewis M, Knox EG, Crawford JS. Epidural anaesthesia and long
term backache after childbirth. BMJ 1990; 301: 9-12.
4. Russell R, Groves P, Taub N, O'Dowd J, Reynolds F. Assessing long term
backache after childbirth. BMJ 1993; 306: 1299-1302.
5. Breen TW, Ransil BJ, Groves PA, Oriol NE. Factors associated with back pain
after childbirth. Anesthesiology 1994; 81: 29-34.
6. Macarthur AJ, Macarthur C, Weeks S. Epidural anaesthesia and postpartum back
pain. Anesthesiology 1993; 79: A973.
7. Russell R, Reynolds F. Long term backache after childbirth and motor block with
epidural analgesia. Society of Obstetric Anesthesia and Perinatology 1995 Abstract
Book p 100.
8. Fernando R, Patel M, Gill P, Urquhart J, Morgan B. A prospective study of long
term backache after childbirth in primigravida -the effect of ambulatory epidural
analgesia during labour. Society of Obstetric Anesthesia and Perinatology 1995
Abstract Book p51.
NYHA Classification of heart disease
I. Asymptomatic.
II. Slight limitation of physical activities; Comfortable at rest.
III. Marked limitation with less-than-ordinary activity, causing fatigue, palpitation,
dyspnoea or angina. Remains comfortable at rest.
IV. Symptoms at rest.
Tetralogy of Fallot
Tetralogy of Fallot. The components of the tetralogy are:
1. R. Ventricular Outlet Obstruction.
2. R. Ventricular Hypertrophy.
3. Ventricular Septal Defect.
4. Aorta over-riding the septal defect.
The amount of blood which enters the pulmonary circulation is
determined by the degree of fixed outlet obstruction, the tone of the
infundibular region and the pulmonary vascular resistance. If either of
the latter two increase, more blood is shunted through the VSD and the
patient becomes more cyanosed.
The degree of cyanosis will also increase if systemic cardiac output
(CO) decreases. A reduction in CO leads to a fall in mixed venous
oxygen saturation and a subsequent fall in arterial saturation even if
shunt fraction remains unchanged.
Relative Toxicity ratios of bupvacaine and lignocaine
AGENT CVS/CNS RATIO ANIMAL
BUPIVACAINE 2.7 SHEEP (PREGNANT)
3.7 SHEEP (NON-PREGNANT)
4.5 DOGS (AWAKE)
4.8 CATS (VENTILATED)
LIGNOCAINE 2.6 CATS (VENTILATED)
3.5 DOGS (AWAKE)
7.1 SHEEP (NON-PREGNANT)
Equipment for spinal anaesthesia should include:
Tray, drape, gown and gloves
Spinal needle
Syringes for skin infiltration
Syringe for local anaesthetic
25G needle for skin infiltration
19G needle or introducer for creation of skin defect
Gauze
Prepping forceps
Prepping solution
All equipment must be sterile.
A strict aseptic technique must be used.
The effect of the full lateral position on aorto-caval compression
The efficacy of left lateral displacement was demonstrated in 1972 . The full left or
right lateral position completely relieves aortocaval compression.
Elevating the mother's right hip 10-15cm completely relieves aortocaval compression
in 58% of term parturients.
Caval Compression
The principal site of venous obstruction in the supine hypotensive syndrome is at the
pelvic brim. In the majority of patients, the compensatory mechanisms are sufficient
to maintain arterial blood pressure.
When caval compression occurs, blood is diverted into the vertebral and azygos
system. This system constitutes a 'protected' conduit for blood returning from the
lower part of the body.
As the vertebral veins distend, so the volume of the subarachnoid and epidural space
is reduced. This reduction in the volume of the epidural space can enhance the
spread of recently-administered epidural solutions.
MODIFIED WHITE'S CLASSIFICATION OF DIABETES IN PREGNANCY
Gestational Diabetes Mellitus Non-insulin Requiring (GDMNI):
Abnormal carbohydrate tolerance during pregnancy only not requiring insulin.
Gestational Diabetes Mellitus Insulin Requiring (GDM):
Abnormal carbohydrate tolerance during pregnancy only requiring insulin
Class A: Abnormal carbohydrate tolerance in the nonpregnant state identified before
the present pregnancy that does not require insulin either before or during the
pregnancy.
Class B: Onset of insulin-requiring diabetes after 20 years of age, with duration of
less than 10 yr.
Class C: Onset of insulin-requiring diabetes between 10 and 20 years of age with
duration of less than 20yr, or duration 10-20 yr regardless of age of onset.
Class D: Onset of insulin-requiring diabetes before 10 years of age, or duration
greater than 20 yr regardless of age of onset, or insulin-requiring diabetes with
chronic hypertension, or insulin-requiring diabetes with benign retinopathy.
Class F: Insulin-requiring diabetes with diabetic nephropathy (proteinuria of greater
than 500 mg in a 24-hr urine collection).
Class R: Insulin-requiring diabetes with proliferative retinopathy.
Class T: Insulin-requiring diabetes with renal transplant.
Class H: Insulin-requiring diabetes with coronary artery disease.
The relationship between Fasting Blood Sugar and Haemoglobin A1C in pregnancy.
Acknowledgements:
Used with permission from O'Shaughnessy R, et al. Glycosylated hemoglobins and
diabetes mellitus in pregnancy. Am J Ob Gyn 1979; 135: 783-790.
The infant on the left has severe IUGR (470g) and the one on the right has
macrosomia (5,100g).
Used with permission from:
Landon MB:
Diabetes mellitus and other endocrine diseases. pp1100. In Gable SG, Niebyl JR,
Simpson JL (eds): Obstetrics: normal and problem pregnancies. New York, 1991.
Fetal/Maternal ratios of various local anaesthetics.
Local
Anaesthetic
pKb %Protein
Bound
F/M
Ratio
pH *
Lidocaine 7.9 64% 0.5 Plain ~ 6.3 + E ~
3.82
Bupivacaine 8.2 96% 0.2-0.4 Plain ~ 5.7 + E ~
3.8
Chloroprocaine 8.9 0.92 Plain ~ 3.0
* Moore DC, Anesth Analg 1981;60:833 + E = Commercial solution with epinephrine
Practical Points in using local anaesthetics:
1. Adding epinephrine (e.g, 1:200,000 to 1:100,000) can be particularly helpful in
increasing the duration of local anaesthetic effect and in reducing bleeding. There is,
however, a downside to using epinephrine. First, when absorbed systematically it can
cause hypertension, tachycardia and even arrhythmias, and this is obviously a
potential concern in hypertensive patients or patients with coronary artery disease.
Secondly, using epinephrine may disguise bleeding sites that later become apparent
once the epinephrine wears off. Thirdly, epinephrine can reduce uteroplacental blood
flow.
2. When using local anaesthesia in large amounts, always ensure that the patient
has an intravenous line in place in case of local anaesthetic toxicity. Drugs to treat
convulsions should be readily available (e.g, injectable diazepam) as well as
equipment and drugs for airway management.
3. Know the relationship between drug concentration in percent and concentration in
mg/ml. Remember that a 1% solution (1gm of solute in 100mls of solution) has a
concentration of 10mg/ml. In a 60 kg woman, for example, the maximum dose of
lidocaine without epinephrine is 5mg/kg = 300mg = 30 ml of 1% lidocaine **.
4. Poor anaesthesia is frequently obtained when local anaesthetics are injected into
infected or inflamed areas (e.g. Bartholin's abscess). This has to do with the fact that
although a normal tissue pH is around 7.4, it may drop to 5 or 6 with inflammation,
rendering most of the anaesthetic in the ionized form (which crosses cell membranes
poorly), thereby reducing its effectiveness.
** Editors note: The maximum recommended dose of plain lidocaine is variously
reported at between 3 and 5 mgs/kg.
Paracervical block entails the particular risks of:
Intravenous injection.
Intra-arterial injection.
Intra-fetal injection.
Note particularly the proximity of the presenting part. (In this case the fetal head.)
NEUROTOXICITY OF LIGNOCAINE:
[mcg/ml] SYMPTOMS:
3 Lightheadness.
4 Tongue Numbness
6 Visual disturbances.
8 Generalised twitching.
12 Convulsions.
15 Profound Coma.
20 Respiratory Arrest.
25 CVS Depression
Comparative CNS and CVS Toxicity
Drug Cumulative convulsive dose
(Mean +/- SEM)
Cumulative lethal dose
(Mean +/- SEM)
CV/CNS
Lidocaine 22.0 +/- 6.7 76.2 +/- 15.1 3.5
Etidocaine 8.0 +/- 2.2 40.4 +/- 6.0 5.1
Tetracaine 4.0 +/- 2.2 26.9 +/- 4.6 6.7
Bupivacaine 5.0 +/- 0 20.4 +/- 2.4 4.1
Liu PL:
Anesth Analg 62:375, 1983
Percent deaths after IV convulsive and supraconvulsive doses of various local
anaesthetic agents in the unanaesthetized dog. Pooled data is presented from a
single research laboratory.
The numbers on each cohort represent the sample size. Note that no animals were in
the etidocaine group at three times the convulsive dose.
Modified by the Editor from:
Feldman HS. The relative acute systemic toxicity of selected local anaesthetic
agents. Acta Universitatis Upsalliensis Comprehensive Summaries of Upsalla
Disertations from the faculty of medicine. No. 226 1989.
Vaughan-Williams classification of anti-arrhythmic drugs:
Ia Moderate depression of phase 0 and conduction slowing; prolongation of
repolarisation (eg quinidine )
Ib Minimal effect on phase 0 and on conduction properties; shortening of
repolarisation (eg lidocaine )
Ic Marked depression of phase 0 and conduction slowing; slight effect on
repolarisation (eg flecainide )
II Beta-adrenergic blockade (eg propranolol )
III Lengthening of repolarisation (eg amiodarone )
IV CaIcium channel blockade (eg verapamil )
Effect of thoracic lidocaine epidural on haemodynamic parameters of non-parturients.
T5 LIDOCAINE EPIDURAL
% CHANGE IN PARAMETER:
Parameter Plain + Epinephrine
MAP -9 -22
HR +7 +16
CO -5 +30
SVR -3 -40
Modified from Ward RJ JAMA, 99:191,1965
The three breech presentations:
In the frank breech, there is flexion of both hips, with extension of
both knees, and the presenting part fits snugly into the birth canal.
Seeds JW. Malpresentations. In: Gabbe SG, Niebyl JR, Simpson JL,
editors. Obstetrics: normal and problem pregnancies. 2nd ed. New
York: Churchill Livingstone, 1991:5 3 9 -72. With permission
Note the flexion of the hips and knees in the complete breech
presentation. Seeds JW. Malpresentations. In: Gabbe SG, Niebyl
JR, Simpson JL, editors. Obstetrics: normal and problem
pregnancies. 2nd ed. New York: Churchill Livingstone, 1991:5 3 9
-72. With permission
The incomplete (footling) breech shows some deflexion of the left hip
and knee, with the left foot presenting. Seeds JW. Malpresentations.
In: Gabbe SG, Niebyl JR, Simpson JL, editors. Obstetrics: normal
and problem pregnancies. 2nd ed. New York: Churchill Livingstone,
1991:5 3 9 -72. With permission
An evaluation of the severity of labour pain in comparison to other forms of pain using
the McGill Pain Questionnaire.
Note the effect of 'Prepared Childbirth Training' in reducing the intensity of pain
experienced by primiparae.
The Pain Rating Index is derived by ranking the values of 20 sets of pain-descriptive
words.
Data have been replotted by the editors from: Melzack R 1984. 'The Myth of Painless
Childbirth.'
The use of epidural analgesia in labour at the Royal Hospital for Women, Sydney,
Australia over the last 20 years.
Figures are expressed as a percentage of all labours.
Important Causes of Post-partum Haemorrhage:
Uterine Atony General Anaesthesia, Uterine
fibromyomata, grand multiparity,
polyhydramnios, multiple pregnancy.
Retained placenta/membranes. Placenta praevia, intervention in the third
stage.
Thrombocytopaenia/Coagulopathy Pre-eclampsia, amniotic fluid embolism, in
utero fetal death.
Birth Canal Trauma Precipitate labour, multiple pregnancy,
breech extraction.
Assessment of the patient with post-partum haemorrhage:
* Visually assess the degree of bleeding.
* Measure the pulse rate.
* Measure arterial pressure supine and sitting.
* Inspect the placenta for completeness.
* Inspect the genital tract for trauma.
* Assess uterine tone.
Resuscitation of the patient with post-partum haemorrhage:
* Administer oxygen by face mask.
* Elevate the patient's legs.
* Insert at least one 14G cannula.
* Infuse colloid / crystalloid.
* Administer appropriate oxytocic.
* Massage uterine fundus.
* Group and cross match blood.
* Administer blood once "allowable loss" exceeded.
* Use bimanual compression if appropriate.
* Suture lacerations.
* Consider aortic compression.
* Explore uterus manually if appropriate.
Ropivacaine
Factors which affect the plasma level of epidurally administered
local anaesthetics
Total dose * Risk of toxicity is increased with increasing dosage.
* Tachyphylaxis may require increased dosage and
result in cumulative toxicity (short acting drugs).
Rate of administration * Rapid rate of administration increases plasma levels
of lignocaine and etidocaine.
* Bolus administration results in higher plasma levels
than continuous infusion, particularly with lignocaine.
Epidural fat
deposition (drug
reservoir)
* Bupivacaine - high fat uptake; minimal plasma
increase with repeat bolus or infusion compared to
lignocaine or etidocaine (accumulation) .
Vertebral venous
plexus dynamics
* Rate of blood flow influences drug uptake.
Physiological
variables
* dependent on cardiac output & renal & hepatic
function
Adrenaline * Delays absorption of lignocaine and etidocaine
proportionately more than longer acting agents.
Sodium Bicarbonate * Increases rate of absorption of lignocaine and
bupivacaine
Plasma levels of local anaesthetic usually peak 15-20 mins after an
epidural bolus.
ANAESTHETIC MANAGEMENT OF FETAL HEAD ENTRAPMENT
INTRAVENOUS NITROGLYCERIN (GTN)
* GTN must be immediately available for all vaginal breech deliveries.
* Inject GTN 250-500mcg intravenously (IV) in divided doses.
* Monitor maternal blood pressure and heart rate.
* 40-60 seconds after the dose, maternal tachycardia (which signals the onset of
uterine relaxation) ensues.
* When maternal tachycardia occurs, advise the obstetrician of the onset of uterine
relaxation.
* Give an additional GTN 250mcg IV, if necessary.
* Continue to monitor blood pressure, and heart rate. (Rarely, phenylephrine 20 to 40
mcg IV, may be necessary to restore blood pressure but should not be administered
before delivery).
TERBUTALINE
* Inject terbutaline 250mcg subcutaneously.
* Monitor maternal blood pressure and heart rate.
* Avoid fluid overload (risk of pulmonary oedema).
GENERAL ANAESTHESIA (LEAST PREFERABLE OPTION)
* Rapid sequence induction.
* Tracheal intubation.
* Administer > 2 MAC volatile agent (preferably halothane).
* Monitor maternal vital signs appropriately.
Needle Tip Designs
Features of note are:
1. The presence of a cutting tip on the Quincke type needle.
2. The dimensions of the terminal hole.
- A large hole contributes to a rapid flashback.
- A long hole increases the possibility of injecting part of the intended sub-arachnoid
dose into the epidural space.
3. The original pencil point needle (HART) is illustrated. (Hart and Whitacre, JAMA
1951;147:657-58.)
Fentanyl
Effects of epidural anesthesia (Thick black bar) on uterine blood flow. All values
subsequent to each control value are given as mean percentage changes with
standard errors.
(Reprinted by permission from Wallis KL, et al. Anesthesiology 44:481, 1976.)
Effects of epidural anesthesia (Thick black bar) on mean blood pressure. All values
subsequent to each control value are given as mean percentage changes with
standard errors.
(Reprinted by permission from Wallis KL, et al. Anesthesiology 44:481, 1976.)
The rapid onset of 2-chloroprocaine is easily seen by the time to T4 level of 10 -+ 4
min. Values are expressed as mean + SD.
(Figure created from data published in tabular form in Glosten B, et al.
Anesthesiology 68:948,1988. and reproduced with permission).
Factors determining plasma level of an epidural opiate
Total dose Increases plasma levels and side effects
Lipid
solubility
Increasing lipid solubility increases vascular uptake rather than
rostral spread, eg. fentanyl/pethidine versus morphine. CSF (rather
than plasma) concentration parallels analgesia.
Opiate
receptor
affinity
High for lofentanil & sufentanil (less vascular absorption; shorter
duration of action)
Uptake Of Epidural Narcotics.
Drug CSF [ ] Plasma [ ]
Pethidine (50mg)
10 min 8mcg/ml 0.02mcg/ml
20 min 10 0.1
40 min 20 0.3
Morphine (0.02mg/kg)
10 min 3 mcg/ml 0.03mcg/ml
20 min 8 0.04
40 min 10 0.05
Fentanyl (80mcg)
10 min 0.9 nanogm/ml
20 min 0.6 nanogm/ml
Side-effects of epidural narcotics.
Nausea and
vomiting
Depends on plasma concentration of narcotic. Incidence 10-25%
with Fentanyl/Morphine/Pethidine
Pruritus Up to 50% with Morphine (only 5% severe). 15-35% with
Fentanyl/ Pethidine.
Respiratory
depression
Delayed onset with Morphine (up to 12 hours). May occur within
2-3 hours for Fentanyl/Pethidine. Less sedation with tolerance to
narcotics
Urinary
retention
Synergistic effect with local anaesthetics (10-40%)
Comparative toxicity of local anaesthetics:
Drug Plasma
Concentration
Signs
Lignocaine 5 mcg/ml Initial CNS symptoms
>12 mcg/ml Convulsions
>24 mcg/ml Cardiovascular collapse
Bupivacaine 2-4 mcg/ml Convulsions
>4 mcg/ml Ventricular arrhythmias Intractable ventricular
fibrillation
Etidocaine 2 mcg/ml Convulsions
Effects on the fetus of epidurally administered local anaesthetics and opiates:
Placental Transfer Of Drugs
(Narcotics and local anaesthetics)
Rapid equilibration across placenta (peak
levels 15 to 30 mins).
Free (non-ionised) fetal drug concentration
depends on plasma protein binding and fetal
acidosis.
Toxic Effects Loss of fetal heart rate variability (lignocaine).
Large doses cause central nervous system
and cardiovascular depression.
Neurobehavioural Assessment Correlates with neonatal peak local
anaesthetic plasma level.
Minimal depressant effect with bupivacaine.
Hypotonia & decreased motor reflexes with
1.5% lignocaine or mepivacaine.
Cocaine
Lidocaine
The change in trans-membrane potential and ionic conductance during the passage
of an action potential along the axonal membrane.
The rate of onset of spinal analgesia as measured by the time to the first painless
contraction following subarachnoid injection of bupivacaine 2.5 mg and fentanyl 25
mcg.
From: Collis R et al Int J Obstet Anesth 1994;3:75
Analgesia in the first stage of labour following subarachnoid injection of meperidine
10mg, fentanyl 10 mcg or sufentanil 5 mcg.
* P &lt0.05 for meperidine vs fentanyl and sufentanil.
Reproduced with permission from Honet J, Anesth Analg 1992;75:734.
Percentage of parturients with dense (grade 2 or 3) motor block following institution
of epidural anesthesia and for 5 hours subsequently in those receiving:
CEI: Continuous Epidural Infusion of plain bupivacaine.
PCEA-B: PCEA with plain bupivacaine.
PCEA-BF: PCEA with bupivacaine/fentanyl solution.
PCEA-BFE: PCEA with bupivacaine/Epinephrine/Fentanyl solution.
Each point represents the mean of 8-22 patients. Group PCEA-BFE differs from the
others by 2 way ANOVA. *P <0.05 cf 0 time point. Data from Lysak S et al.
Anesthesiology 1990:72 p 47 Figure 4.
Note the increase in motor block both with the increasing duration of epidural
analgesia and in association with the use of epinephrine-containing solutions.
Hypoxaemic episodes during the 2nd stage of labour in parturients receiving
different forms of pain relief.
NA = No Analgesia
PE = Pethidine + Entonox
EB = Epidural Bupivacaine
EBF = Epidural Bupivacaine + Fentanyl
Reproduced with permission of the editor of Anaesthesia and RP Griffin and F
Reynolds. Anaesthesia 1995; 50:151-156.
Incidence of oxygen desaturation below SpO2 94%: median (range): minutes per
hour, for different analgesic groups:
Stage NA PE EB EBF
Last hour of first stage 0.2
(0-11.4)
1.4
(0-16.4)*
0
(0-0.2)*
0
(0-12)
Second Stage 3.0
(0-10.8)**
0.9
(0-7.7)
0.1
(0.0-0.8)**
0.9
(0-40.3)**
*In the last hour of the first stage the incidence of desaturation was significantly lower
in the EB group when compared with the PE group (p < 0.001).
**In the second stage the incidence of SpO2 below 94% was significantly lower in the
EB group compared with the EBF group (p < 0.05) and the NA group (p < 0.05).
The incidence of backache at various stages of pregnancy in patients receiving
epidural analgesia compared with those receiving other analgesic techniques.
Reproduced using data from: Russell R et al. BMJ 1993; 306: 1299-1302.
The incidence of backache at various stages of pregnancy.
Reproduced using data from: Russell R, Reynolds F. Soc. Obst. Anesth. &
Perinatology 1995 p 100.
Local anaesthetic solution spreads laterally within the epidural space with major entry
in the 'dural cuff' region. Rapid entry into the CSF occurs via the arachnoid
granulations in this region.
Direct diffusion across the dura also occurs.
Modified with permission from: Figure 8.2 p 256 Cousins MJ and Bridenbough PO.
'Neural Blockade' 2nd edition. JB Lippincott. Philadelphia.
The spread an opiate within the epidural space.
A opioid is seen being injected through an epidural catheter. The drug spreads laterally through the epidural space and enters the
spinal canal particularly in the region of the nerve roots. It then spreads to exert its principal effects on pre- and post-synaptic
receptors in the substantia gelatinosa of the dorsal horn. This is in contrast to the effect of local anaesthetic solutions whose
effects are exerted primarily in the region of the emerging spinal nerves.
The Prince Henry Hospital pain score system:
The system classifies the degree of postoperative pain by response to deep breaths
and coughing.
The patient is positioned comfortably, and well supported in bed.
If she has no pain at rest, she is asked to take a deep breath. If that is painless, she
is requested to give a cough.
Comparison of the average duration of action of four opioids: morphine 6mg,
methadone 6mg, meperidine 60mg and fentanyl 60mcg.
All were administered in 10ml saline in a within-patient study following abdominal
surgery. The subjects did not find any of the drugs preferable to the others.
The ratio of the doses of drugs required for analgesia by epidural administration
compared to IV doses for some opioids. The lower the ratio (i.e. the smaller the
epidural requirement) the less likely is any major systemic drug effect contribution to
analgesia and also, the less likely are systemic adverse effects.
Delayed respiratory depression is due to CSF carriage of the drug to the brain stem
and is usually not related to systemic concentration.
(Modified after Chrubachik et al. Postoperative epidural opioids, Springer, Berlin,
1993)
Pain in the first stage of labour results from dilatation of the cervix and lower uterine
segment and from distension of the body of the uterus by uterine contractions and is
transmitted by afferent nerve fibers (accompanied by sympathetic fibers) of the 10th,
11th and 12th thoracic and 1st lumbar nerves. The descending head causes
pressure on the lumbosacral plexus responsible for pain felt in the back , thighs and
legs
Stage of Labour
Degree of discomfort
First stage (Latent Phase)
(Cervix < 3cms dilated)
Usually mild pain; Fear and anxiety may lead to moderate or severe pain
First Stage (Active Phase)
3 - 10 cms dilatation
Moderate uterine pain. May progress to severe pain.
Second Stage:
a) Early
b) Late.
Severe uterine pain.:
Moderate perineal pain.
Severe Perineal pain.
Third Stage:
Delivery of the placenta.
Minimal uterine pain
Fourth stage: Little or no pain.

POSSIBLE CAUSES OF MATERNAL HYPOTENSION
IN THE PRESENCE OF A NEURAXIAL BLOCK:
Haemorrhage
Aortocaval compression
Excessive sympathetic blockade
- high epidural
- unintended subdural block
- unintended subarachnoid block
Intravascular injection of local anaesthetic
Anaphylaxis
Embolism
Vasovagal episode
Cumulative proportion of patients continuing without a top-up after epidural
infusion of 0.08% bupivacaine at 15mls/hr, with or without fentanyl 2.5 mcg/ml.
B = Bupivacaine alone.
B+F = Bupivacaine + Fentanyl
Reproduced with permission from: Jones G et al Br. J. Anaesth. 1989; 63:3 254 -
9.
MANAGEMENT OF MATERNAL HYPOTENSION:
Stop obvious causative agents
Administer supplemental oxygen
Assume left lateral position, Trendelenberg, leg lift
Commence fluid resuscitation
Administer vasopressors
Consider the use of adrenaline
Consider additional monitoring
Treat a pulseless state as cardiac arrest
MAINTAINING THE WELFARE OF THE FETUS
Administer maternal oxygen
Nurse mother in lateral position
Commence fetal monitoring
Expedite delivery of the fetus
The Bromage Scoring Method
0: No motor block: full flexion of knee and foot.
1: Inability to raise extended leg. Just able to move knee.
2: Inability to flex knee. Able to move foot only.
3: Inability to flex ankle joint. Unable to move foot or knee.
Equipment for epidural analgesia should include:
- tray, drape, gown and gloves
- Tuohy needle
- epidural catheter
- loss of resistance syringe
- syringes for skin infiltration
- syringe for local anaesthetic
- 25 gauge needle for skin infiltration
- 19 gauge needle to create defect in skin
- gauze
- prepping forceps
- prepping solution
- clear adhesive covering
Obstetric manoeuvres for breech delivery:
Maternal expulsion delivers the frank breech from the lower birth canal, while
the contractile forces of the uterus maintain flexion of the fetal head.
Inappropriate traction on the breech at this point may lead to extension of the
fetal head, or entrapment of an arm behind the head (nuchal arm).
After spontaneous expulsion of the breech to the umbilicus, the obstetrician
delivers the extended legs. The fingers splint the thigh, while flexing and
abducting the hip.
Note the lateral rotation of the thighs on the hips, to deliver the legs. The
obstetrician must avoid the instinctive manoeuvre of hooking the thigh down,
thus bending the knee in the wrong direction.
Note the lateral rotation of the thighs on the hips, to deliver the legs. The
obstetrician must avoid the instinctive manoeuvre of hooking the thigh down,
thus bending the knee in the wrong direction.
Further maternal efforts deliver the fetal abdomen and the obstetrician gently
hooks down a loop of umbilical cord, to avoid occlusion of the circulation. At
this point in the delivery, the breech should hang downwards, while maternal
efforts expel the infant until the lower border of the scapula is visible below the
pubic arch. Gentle traction by the obstetrician ensures the back does not
rotate posteriorly. For delivery of the shoulders and arms, the obstetricians
thumbs overlie the sacrum with the fingers around the iliac crests, so that the
hands cradle the fetal pelvis.
If the fetal arms have not become extended, the obstetrician passes the index
and middle fingers over the shoulder, and sweeps the left arm medially across
the chest, thus delivering it.
If the fetal arms have extended, the obstetrician applies Lovset's manoeuvre.
Lateral flexion of the fetus is exaggerated to enable descent of the posterior
shoulder below the sacral promontory.
Lovset's manoeuvre. (Continued). The obstetrician then rotates the body with
the back uppermost, 180 degrees. (b) The posterior shoulder has been
rotated anteriorly, and lies beneath the symphysis. The obstetrician hooks the
arm downwards, then rotates the body back 180 degrees, to deliver the other
arm in the same manner.
Gentle elevation of the fetal trunk allows the obstetrician access to the fetal
airway. The obstetrician must avoid over-extension, because of the risk of
fetal cervical injury, with hyperextension of the fetal head.
Application of Piper's forceps to the fetal head, the preferred method of
delivering the head.
When Piper's forceps have been applied, the fetal trunk, wrapped in a 'breech
towel', is supported by one hand, while the other exerts gentle traction on the
forceps in the direction of the pelvic axis (arrow).
While an assistant supports the fetal trunk, avoiding hyperextension, the
obstetrician kneels, to facilitate application of the forceps, and subsequent
traction in the axis of the pelvis.
The Mauriceau-Smellie-Veit manoeuvre, although not as desirable as Piper's
forceps, can prove useful when events progress rapidly, and the obstetrician
has inadequate time to apply forceps. The fetal trunk lies astride the
obstetrician's forearm, and the obstetrician's middle finger, placed in the fetal
mouth, gently flexes the head. The upper hand on the fetal back enables
gentle downward and backward traction, while the middle finger of the upper
hand pushes upwards on the occiput, encouraging flexion of the head, to
avoid damage to the fetal cervical spine.
Images from:
Seeds JW. Malpresentations. In: Gabbe SG, Niebyl JR, Simpson JL, editors.
Obstetrics: normal and problem pregnancies. 2nd ed. New York: Churchill
Livingstone, 1991:5 3 9-72.
Baskett TF. Essential management of obstetric emergencies. 2nd ed. Bristol: Clinical
Press, 1991:126-3 5.
With permission.
The palpating finger is used to locate the ischial spine and sacrospinous
ligament per vaginam. The needle is inserted through the vaginal wall, is
directed towards the spine and then passed through the sacrospinous
ligament. As soon as the needle has passed through the ligament, a loss of
resistance is felt. At this point 10mls of local anaesthetic solution (eg 1%
Lignocaine with adrenaline) is injected after careful aspiration.
The perineal approach to pudendal nerve block. This approach is particularly
useful when the head is fully engaged.
The relationship between the spinal cord and nerve roots at three vertebral levels.
The subarachnoid space is shown in red .
Modified and re-drawn from:
'Lumbar Puncture and Spinal Analgesia'.
R. Macintosh. Blackwells Books, Oxford.
Possible aetiology of breech presentation at term.
MATERNAL
PREGNANCY-RELATED
multiparity
multiple pregnancy
polyhydramnios
placenta praevia
cornual-fundal placentation
NON-PREGNANCY RELATED
uterine anomalies
uterine/pelvic tumours (eg. fibroids)
pelvic abnormalities
FETAL
FETAL ANOMALIES/ABNORMALITIES
trisomy 13, 18 or 21
Potter's syndrome
fetal alcohol syndrome
hydrocephalus
anencephaly
SOME OBSTETRIC COMPLICATIONS OF BREECH PRESENTATION
COMPLICATION INCIDENCE
FETAL/NEONATAL
Intrapartum fetal death 16 times (x) non-breech
Intrapartum fetal asphyxia 3 to 8 x non-breech
Intrapartum fetal distress ~60% (of all breech presentations
Umbilical cord prolapse 2.5 % overall (18 x non-breech)
Birth trauma = < 13 x non-breech
Entrapment of aftercoming head ~9% (of babies > 2500 g)
Perinatal/neonatal mortality
(mainly intracranial hemorrhage)
3 to 5 x non-breech
MATERNAL
(Largely due to cesarean section) Variable
FACTORS FAVOURING SUCCESSFUL EXTERNAL CEPHALIC VERSION
* Obstetrician experience
* Non-obese patient
* Multiparity
* Presenting part not in the pelvis
* Normal, or slightly increased, amniotic fluid volume
* Fetal back not positioned anteriorly
* ? Tocolysis (controversial)
MANAGEMENT OF THE BREECH PRESENTATION AT TERM
* Only women with frank or complete breech (Figure 14.1) should undergo a trial of
labour.
* Trial of labour appropriate in both nullipara and multipara.
* If no other risk factors, maternal age should not preclude planned vaginal delivery.
* X-ray pelvimetry not a prerequisite for planned vaginal delivery.
* Trial of labour at term reasonable if (a) estimated fetal weight (on clinical or
ultrasound assessment) judged to be less than 4000gms and (b) no hyperextension
of fetal head.
* Presence of medical or obstetric complications should not preclude trial of labour
unless they may lead to mechanical difficulties at delivery.
* Breech presentation alone not a contraindication to induction of labour.
* Careful oxytocin augmentation of labour a reasonable practice if care is taken to
exclude feto-pelvic disproportion.
* No limit to duration of first stage labour if cervical dilatation progresses at least
0.5cm/hr (after reaching 3 cm dilatation).
* Caesarean section recommended if breech has not descended to the perineum in
second stage labor, after 2 hr of 2nd stage in the absence of active pushing, or if
vaginal delivery not imminent after 1hr of active pushing.
* Breech presentation, by itself, is not an indication for continuous fetal monitoring but
vaginal examination is essential immediately after spontaneous rupture of
membranes to exclude cord prolapse.
* Pain relief should be individualized. Breech presentation not an indication for, or
contraindication to, epidural anaesthesia.
* The indications for amniotomy are the same as for cephalic presentation.
* Assisted breech delivery is the method of choice, either with forceps to aftercoming
head, or Mauriceau-Smellie-Veit manoeuvre. Total breech extraction should not be
performed in the singleton breech.
Modified from: The Canadian Consensus on Breech Management at Term. Journal
SOGC 1994; 16:1839-48.
EPIDURAL ANALGESIA FOR TRIAL OF LABOUR:
THE 2-CATHETER TECHNIQUE
* Preload with Ringer's lactate, 500-1000ml.
* Place the patient in the left lateral position with legs fully flexed and back aligned
along the edge of the bed.
* Prepare the back with antiseptic (eg. povidone-iodine), and drape appropriately.
* Infiltrate (1% lignocaine) skin overlying a lower thoracic or upper lumbar interspace
eg. T12- L1, L1-2.
* Infiltrate deeper tissues at the same level.
* Using loss of resistance to air or saline, identify the epidural space (angulation of
lower thoracic vertebral spines may require a more cephalad approach).
* Inject 5-10 mL dilute bupivacaine (eg. 0.0625%).
* Thread the epidural catheter approximately 5 cm into the epidural space, and
confirm catheter placement in the epidural space. Tape the entry point of this upper
catheter.
* Infiltrate the skin over the lower lumbar L4-5, or L5-S1, interspace. After deep
infiltration, locate the epidural space by loss of resistance to air or saline.
* Gently rotate Tuohy needle such that bevel faces caudally. (Avoid inward
displacement of the Tuohy needle, which can 'core' the dura mater.)
* Inject 5ml 0.9% preservative-free saline, and insert the catheter approximately 5cm
into the epidural space.
* Tape the entry point of this lower catheter. Remove drapes. Then, tape both
catheters to the back, labelling each appropriately.
* Commence continuous infusion of dilute local anaesthetic plus opioid (eg.
bupivacaine 0.0625% + fentanyl 0.0004%) through the upper catheter at a rate of 6-8
ml/hr.
* If patient experiences premature urge to push, inject opioid (eg. fentanyl 100 mcg)
+/-dilute local anaesthetic (eg. bupivacaine 0.03125%, 5-10 mL) via the lower
catheter.
CSE ANALGESIA FOR VAGINAL BREECH DELIVERY.
(Technique appropriate in late 1st stage labour, especially in
multipara)
* Position the patient and prepare the back.
* Identify epidural space at L3-4, or L4-5, using a loss of resistance technique.
* Advance 24G, 120mm Sprotte needle through Tuohy needle, until resistance is
encountered at the needle tip.
* Gently advance the Sprotte needle until a dural 'pop' is felt.
* Support the Sprotte needle, while bracing the dorsum of the left hand against the
patient's back.
* Remove stilette gently to avoid displacement of Sprotte needle.
* Inject local anaesthetic mixture (bupivacaine 0.25%, 0.5 ml + fentanyl 25 mcg +
NaCI 0.9%, to 2 ml).
* Remove the Sprotte needle. Thread approximately 5cms of catheter into the
epidural space. Pre-injection of bupivacaine (0.03125%, 5ml) through the Tuohy
needle (after removing the Sprotte needle) will facilitate advancement of the epidural
catheter.
* After taping the epidural catheter to the back rotate the patient onto her right side,
to spread the local anaesthetic more evenly.
* Unless the patient proceeds rapidly to full dilatation and delivery commence a
continuous epidural infusion.

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