Csa 2014 Fall Tuesday

2014 Fall Anesthesia Seminar
Preeclampsia Update:
2014-15
Mark Zakowski, M.D.
Chief Obstetrical Anesthesiology
Cedars-Sinai Medical Center
Los Angeles CA 90048
Associate Prof, Adjunct
Drew University, Los Angeles
Disclosures
No relevant financial relationship with any
commercial interest.
Member, CMQCC Task Force Preeclampsia
Passionate about Maternal and Baby well
being
Quantum Birthing, LLC
Learning Objectives
Recognize preeclampsia in the peripartum period.
Understand assessments of patients for
preeclampsia and preeclampsia related
complications.
Implement current guidelines and practices for
preeclampsia therapies.
Understand the role of communication in
prevention, recognition and treatment of
preeclampsia related maternal and neonatal
complications.
OUTLINE
Preeclampsia
Recognition
Current treatment protocols 2014-15
Communication keys to success
Bonus
Hypertensive Disorders of Pregnancy
6-10% of pregnancies worldwide

Preeclampsia increased 25%/20yr USA
50,000+ maternal deaths/yr worldwide
50-100x more near miss
Major cause of prematurity, infant mortality
Long term sequelae Maternal and Offspring
Less than optimal care contributes
Communication large part of that
-ACOG Task Force HTN Preg rev 5-2014
Age-adjusted incidence per 1,000 deliveries for women with gestational hypertension (b
0.0024; P < 0.0001) or preeclampsia (b = 0.0009; P = 0.009) for 2-year periods, 19872004
Wallis A B et al. Am J Hypertens 2008;21:521-526

2008 by the American Journal of Hypertension, Ltd.
CA-PAMR: Chance to Alter Outcome

Grouped Cause of Death; 2002-2004 (N=145)
Grouped Cause of Death
Chance to Alter Outcome

Strong / Some
Good (%) (%)
None
(%)
Total
N (%)
Obstetric hemorrhage
69
25
16 (11)
Deep vein thrombosis/

pulmonary embolism
53
40
15 (10)
Sepsis/infection
50
40
10
10 (7)
Preeclampsia/eclampsia
50
50
25 (17)
Cardiomyopathy and other

cardiovascular causes
25
61
14
28 (19)
Cerebral vascular accident
22
78
9 (6)
Amniotic fluid embolism
87
13
15 (10)
All other causes of death
46
46
26 (18)
Total (%)
40
48
12
145
Preventability Maternal Death

Cause
% of deaths
Preventable %
Cardiomyopathy
21
22
Hemorrhage
14
93
Preeclampsia spectrum
10
60
CVA
Chronic Medical problem
89
AFE
Infection
43
Pulm Embolism
17
CV condition
40
North Carolina maternal deaths, n=108, 1995-1999

-Berg Obstet Gynecol 2005:106:1228-34
Preeclampsia: an Evolving Disease

Starts 1st trimester
abnormal placental implantation
Altered remodeling spiral arteries
2nd trimester
Angiogenic imbalance
3rd trimester
Endothelial dysfunction
Maternal effects widespread
Clinical symptoms
Preeclampsia: an Evolving Disease

Early onset (<34 weeks GA)
Placental origin
Late Onset (>34 weeks GA)

Maternal Origin
Increased Maternal CV risk later

Unmasking disease vs. altering the course
Offspring have altered health.
Risk Factors Preeclampsia
Prior preeclampsia (OR 7) or family Hx (OR 2-4)

Primiparity
IVF
Diabetes type I OR type II
Maternal age >40
Obesity
Chronic HTN or renal disease
Multiple Gestation
Lupus
-ACOG 2013 Task Force HTN Pregnancy
Placental Implantation Normal

Anaerobic
Placenta releases PlGF, VEGF grows
into endometrium
Invades and dilates spiral arteries to
increase blood flow
Low resistance high flow
Increases oxygen delivery for
development
Placenta Preeclampsia
Incorrect growth placenta/invasion
endometrium
Spiral arteries maintain smooth muscle and
thickness
Smaller diameter => higher blood flow
velocity
Relatively under-perfused = less oxygen
delivery
Higher oxidative stress
Antiangiogenic sFlt-1 binds to VEGF, PlGF
Genetic Causes Preeclampsia

STOX1 overexpression
Modulates trophoblast proliferation and
migration
Placental preeclampsia
ACVR2A
Maternal preeclampsia
-Biochimica et Biophysica Acta 2012:1960-9
Hum Genet 2007:120:607-12
Early Onset Preeclampsia (<34

weeks)
Higher maternal mortality
Higher recurrence rate
More placental pathology
Higher rate remote postpartum medical
problems
Higher remote risk maternal CV disease
Higher remote risk maternal Diabetes
-Hypertension 2013:61:932-42
ONE SUGGESTED PATHOPHYSIOLOGIC MODEL
-Hypertension 2013:61:932-42
ONE SUGGESTED PATHOPHYSIOLOGIC MODEL
-Biochimica et Biophysica Acta 2012:1960-9
Late Onset Preeclampsia
Maternal (late onset) preeclampsia

IUGR absent
Less severe generally
Fewer long term consequences
Late Onset Preeclampsia

>34 weeks gestation, 80% of all
preeclampsia
Maternal causes
Maternal Risk factors
Maternal Risk Factor
OR Increased Preeclampsia
Diabetes Type I or II
3.5
Multiple Gestation
BMI increased
2.5
Maternal Age >40
Cardiovascular disease
3.8
-Hum Genet 2007:120:607-612
OUTLINE
Preeclampsia
Recognition
Preeclampsia Definitions - OLD

Preeclampsia (mild)
HTN >140/90 mmHg
Proteinuria >0.3 g/24hr
Severe Preeclampsia
BP >160/110 mmHg
Proteinuria >5 g/24hr
HELLP syndrome
CNS symptoms
-ACOG Practice Bulletin 33, 2002
Preeclampsia Definitions - NEW

Preeclampsia without severe features (new term)
BP >140/90
Proteinuria >300 mg/24hr OR dipstick 1+ OR
protein/creatinine ratio >0.3
Absence of proteinuria with any:
Platelets <100k
Creatinine >1.1
LFT elevation
CNS symptoms
-ACOG Task Force HTN Pregnancy Nov 2013
Preeclampsia Definitions NEW

Severe Preeclampsia = ANY ONE of:
BP >160/110 must TREAT within 1hr
Platelets <100k
LFT elevation
Creatinine >1.1
Pulmonary edema
CNS symptoms
-ACOG Task Force HTN Pregnancy Nov 2013
Post-Partum Preeclampsia
Occurs up to 6 weeks postpartum
De novo increase of BP
First diagnosis post-partum
Physiology:
BP rises again 3-6 days postpartum
BP usually decreases 1-2 days postpartum
-CMQCC Preeclampsia Toolkit 5-2014
Preeclampsia Foundation
Preeclampsia Overview
Classification
Preeclampsia
Chronic Hypertension
Chronic Hypertension with Superimposed
Preeclampsia
Gestational HTN
-Druzin, CMQCC/ACOG/Stanford
Classification HTN Pregnancy

Pre-Pregnancy
Chronic hypertension
After 20 weeks
Preeclampsia/eclampsia
Chronic hypertension with superimposed

preeclampsia
50% chronic HTN develop superimposed Preecl.
After 20 weeks
Gestational hypertension HTN and no other sx.
Often evolve into something more
-Druzin, CMQCC/ACOG/Stanford
Forecast: Preeclampsia
HTN alone
OR
Proteinuria alone
40% develop classic preeclampsia
-. Obstet Gynecol. 2008;112(2 PART 1): 359-372.
Preeclampsia Update 2014-15

Why the big secret? People are smart, they can
handle it. -Agent J(Will Smith)
A person is smart. People are dumb, panicky,
dangerous animals and you know it. Fifteen
hundred years ago everybody knew the Earth was
the center of the universe. Five hundred years
ago, everybody knew the Earth was flat, and
fifteen minutes ago, you knew that humans were
alone on this planet...
Imagine what you'll know tomorrow

Agent K(Tommy Lee Jones)
-Men in Black 1997
Preeclampsia Blood Tests

Angiogenic:
Placental Growth Factor (PlGF)
Vascular Endothelial Growth Factor (VEGF)
Anti-angiogenic factors:
Soluble fms-like tyrosine kinase-1 (sFLT-1)
Soluble Endoglin (sENG)
Endothelial dysfunction:
Endocan
Placenta
Placental protein 13
Predicting Preeclampsia
Uterine artery Dopper velocimetry
Early onset Preeclampsia, OR 5-20
Angiogenesis
sFlt-1 rises 4-5 weeks prior to clinical sx
Early onset preeclampsia
PlGF starts to decreases 9-11weeks,

accelerates 5 weeks prior to clinical sx
Placental protein-13 low 1st trimester
Early onset preeclampsia
Predicting Preeclampsia
PlGF/Endoglin ratio mid-trimester
Sensitivity 100% specificity 98% early onset PE
Multivariable algorithm
Uterine pulsatility, MAP, pregnancy-associated
plasma protein A, PlGF, BMI, nulliparity, prior PE
93% predictive, OR 16 early onset PE
NEJM 2004:350:672-83
Hypertension 2009:53:812-8
OUTLINE
Preeclampsia
Recognition
Pitfalls and Protocols:

Preventing Maternal Death
Delayed response to triggers
Maternal mortality Preeclampsia
92% delayed recognition and treatment
Calif Pregnancy Assoc Mortality Review 2002-5
Written criteria to observe change or

deterioration
Joint Commission Sentinel Event Alert #44:
Preventing Maternal Death 2010
-Calif Pregnancy Assoc Mortality Review 2002-5
Maternal Early Obstetric Warning

System (MEOWS)
1 point/Yellow Trigger
2 Points/Red Trigger
SBP
150-160 or 90-100
>160 or <90
DBP
90-100
>100
HR
100-120 or 40-50
>120 or <40
Oxygen Saturation%
<95%
Temp oC
35-36
<35 or >38
Neurologic
response to voice
(motor block >2 hrs PACU)
unresponsive
(motor block >3 PACU)
Call physician to evaluate patient for 2 points or more
-NHS U.K., CMQCC, et al.
The Joint Commission

2010 Sentinel Alert #44, Preventing
Maternal Death
All centers have process for
RECOGNITION and RESPONSE to
patients deteriorating condition with
WRITTEN CRITERIA describing EARLY
WARNING SIGNS for when to seek
assistance
-CMQCC Preeclampsia Toolkit revised 5-2014
Fluid Restriction Guideline

Generally fluid restricted
Oliguria <30 ml/hr x2 hr
Fluid bolus 250-500 ml crystalloid NS/LR
After 1 L and considered hypovolemic:
Albumin
Must use pulse oximetry
Furosemide if suspect pulmonary edema
Consider cardiac dysfunction

ECHO, BNP

-ACOG Task Force HTN Pregnancy 2013
Post-Partum Preeclampsia
Occurs up to 6 weeks postpartum
BP rises again 3-6 days postpartum
Only 1/3 women who had Sx postpartum
sought care
Follow-up BP within 7 days - NEW
Patient education - NEW
www.preeclampsia.org
-CMQCC Preeclampsia Toolkit 5-2014
Timing of Delivery Preeclampsia

<37 weeks GA - 1.5% Preeclampsia
<34 weeks GA 0.3% Preeclampsia
Deliver by Vaginal or Cesarean:
>37 weeks preeclampsia
>34 weeks Severe Preeclampsia
<34 weeks GA wait unless unstable [NEW]

Deliver for Eclampsia, HELLP, Pulm Edema,
Coagulopathy, BP not controlled, Clinical Sx
persist (HA, Vision, RUQ pain)

Preeclampsia
Treat BP >160/105-110 within 1 hr
Seizure first line Rx Magnesium
Cocaine/Amphetamine + BP Rx >
resistant hypotension
40% new onset HTN or proteinuria ->
Preeclampsia
Early onset preeclampsia often more
severe
Cause of U.S. Maternal Mortality

CDC Review of 14 years of coded data: 1979-1992
4024 maternal deaths
790 (19.6%) from preeclampsia
90%
of CVA were
from
hemorrhage
MacKay AP, Berg CJ, Atrash HK. Obstetrics and Gynecology 2001;97:533-538
Preeclampsia Mortality Rates

in California and UK
Cause of Death among
Preeclampsia Cases
CA-PAMR (2002-04)
Rate/100,000
Live Births
UK CMACE (2003-05)
Rate/100,000
Live Births
Stroke
1.0
.47
Pulmonary/Respiratory
.06
.00
Hepatic
.25
.19
OVERALL
1.6
.66
The overall mortality rate for

preeclampsia in California
is greater than 2 times that of the UK,
largely due to differences in deaths
caused by stroke.
Acute HTN Rx 2014

Timely Rx <1 hr of BP>160/105-110 - NEW
preferably <30 min of confirm 2nd BP by 15 min
Systolic important
First Line Rx one of:

Labetalol 20 mg IV
Hydralazine 5-10 mg IV
PO Nifedipine 10 mg
NO to SL Nifedipine 10 mg
Acute HTN Rx 2014

Timely RX <1 h of BP>160/105-110 - NEW
preferably <30 min of confirm 2nd BP by 15 min
Second Line RX one of:

Labetalol 40 mg IV, 80 mv IV in ten min
Max dose 300 mg
Hydralazine 5-10 mg IV, repeated every 15-20

min
Nifedipine 10 mg oral
Nitropusside must have A-line
Consult anesthesiologist
Magnesium
Prevention or TREATMENT of seizures in Severe
preeclampsia
4-6 g load/20 min
Recurrent seizure - 2 g/5min additional
Infused at 1-2 g/h
NEW: Continue Intra-op cesarean!
Preeclampsia without severe features (formerly

mild)
SOGC (Canada), WHO yes to magnesium,
ACOG not needed, OB may choose to use
Eclampsia
Maternal mortality 0.3-1%
Morbidity serious pulmonary edema,
renal failure, stroke, arrest
Long term effects
White matter brain lesions 36%
Cognitive failures 50%+
Depression and Anxiety
-AJOG 2014:211:37:e1-9
Visual changes
ACOG Task Force HTN Preg 2013
Obstet Gynecol 2012:119:959-66
Eclampsia
-AJOG 2014:211:37:e1-9
Another NEW rule?

NSAIDs OLD the best!
New- may be bad!
NSAIDs may increase BP
Suggest using other analgesics if patient
has HTN beyond day 1 postpartum
Politics: Narcotic Rx overdoses pressure
to use less Oxycodone, hydrocodone
-ACOG Task Force HTN Preg rev 5-2014
OUTLINE
Preeclampsia
Recognition
Preeclampsia Overview
Obstetric Management
BP control (acute for >160/105-110)
Seizure prophylaxis
Delivery NSVD or Cesarean
34 weeks if Severe Preeclampsia
37 weeks if not Severe Preeclampsia
Post Partum follow-up BPs
-Druzin, CMQCC, ACOG, Stanford
Communication
Triggers
Maternal agitation, confusion
Severe headache
Shortness of breath
Prolonged motor block after regional
anesthesia
Oliguria <0.5 ml/kg/hr for 2 hours
-NY Times 2006
Teamwork
Escalation people, equipment, place
Alert physician or qualified clinician
BEDSIDE evaluation (phone misses key
clues)
Local protocols
Multi-disciplinary team work
Proper communication (e.g. SBAR)
Team trainings/simulations
Communications
Communication failure - top 3 leading causes
of maternal and newborn sentinel events TJC
Communication, teamwork, shared decision
making fundamental
Preeclampsia #2 maternal death CA-PAMR 2002-3
Clinician factors 78%
Facility/system issues 57%
Preeclampsia deaths 48% good chance to
change outcome
Delays Diagnosis, Treatment, Denial severity
-CA-PAMR 2011, 2002-3 Maternal Death Review
Communication Skills
Briefings
Debriefings
Language- Concerned, Uncomfortable,
Safety issue
SBARRR situation, background,
assessment, recommendation, reasoning,
ratification
Closed Loop communication read back
Call outs confirm phase of process

Communication
Signs and Symptoms of Preeclampsia
Antepartum
Office consult?
Upon L&D admission
Postpartum
Up to 6 weeks post delivery Emergency Dept.
Severe BP >160/105-110 mmHg

Repeat 5 min, but must treat within 1 hr first BP
Reduce risk stroke, ICH
Communication
Preeclampsia lifetime disease
CV risk equal to smoking, hyperlipidemia
Death
Diabetes
Preop History
Children of Preeclamptic mothers
Higher BP
Fetal programming
OUTLINE
Preeclampsia
Recognition
Bonus
20
years from birth
40
-Skjaerven BMJ 2012;345:bmj.e7677
Preeclampsia: Maternal Health

Long-Term Effects
Disease in future
OR
HTN
Dose effect severity, #
Early onset > Late onset PreE
3-4
CV Disease
dose effect, risks
End Stage Renal Disease
3-5
Hypothyroidism
1.8
Diabetes
-Chen Cardiovasc Res 2014:101:579-86
Preeclampsia: Childrens Health

Long-Term Effects
Children 9-12 years old
Control
Gestational
HTN
Preeclampsia
BMI
17.6
18.1
17.9
.001
SBP
104
106
107
.001
DBP
60
61
62
.001
Also effects biomarkers HDL relative IL-6, CRP small but statistically significant
-Eur Heart J 2012:33:335-45
Risk Factors CV Disease

Risk Factor
OR Coronary Artery Dis
95% Confidence Interval
Smoking
2.1
1.5-2.9
HTN
2.1
1.4-3
LDL >4.1 mmol/L
1.7
1.2-2.4
Preeclampsia
2.2
1.9-2.5
Preeclampsia as bad as smoking and chronic HTN !!!
PMH h/o Preeclampsia = pertinent information
-Heart Lung Circ 2014:23:203-12
Posterior Reversible Encephalopathy

Syndrome (PRES)
MRI diagnosis bilateral vasogenic edema
posterior cerebral circulation white matter
Occipital and posterior parietal lobes
Sx: HTN, seizure, altered mental status, HA,
vision
Pathophysiology: endothelial dysfunction,
cerebral autoregulation dysfunction, leaky
Up to 6 weeks postpartum
MRI Posterior Reversible Encephalopathy Syndrome (PRES)
Posterior Reversible Encephalopathy

Syndrome (PRES)
Treatment same as preeclampsia/eclampsia
Antihypertensive medication
ED also likes IV Nicardipine
Anti-seizure medication
Magnesium
Patient Education Materials
This and many other

patient education
materials can be
ordered from
www.preeclampsia.org/
market-place
Upcoming Events
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January 12-16, 2015 | Wailea Maui, Hawaii
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CSA Spring Anesthesia Seminar
April 16-19, 2015| San Francisco, California
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November 2-6, 2015| Kauai, Hawaii
Grand Hyatt Resort and Spa
Visit www.csahq.org/CMEevents for more information.
New Modes of Mechanical

Ventilatory Support:
What every Anesthesia Provider
Should Know
Michael A. Gropper, MD, PhD
Professor and Interim Chair
Department of Anesthesia and
Perioperative Care
UCSF
Disclosures
I have received research support
from:
NIH
The Gordon and Betty Moore
Foundation
Learning Objectives
At the conclusion of the activity participants
should be able to:
Define barotrauma, volutrauma,
atelectrauma, biotrauma and their relevance
to mechanical ventilation.
Discuss the relationship between tidal volume
and acute lung injury.
Describe factors associated with tidal volume
reduction and improved patient outcomes.
1st Published Scientific Paper on

Positive Pressure Ventilation
"But that life may ... be restored to the
animal, an opening must be attempted
in the trunk of the trachea, in which a
tube of reed or cane should be put; you
will then blow into this, so that the lung
may rise again and the animal take in
air. ... And as I do this, and take care
that the lung is inflated in intervals, the
motion of the heart and arteries does

not stop..."
Andreas Wesele Vesalius, 1543
Early Mechanical Ventilation
New Modes of Mechanical

Ventilatory Support
Ventilator Associated Lung Injury

Protective Mechanical Ventilation
Prone Mechanical Ventilation
High Frequency Ventilation
Post-extubation CPAP
Ventilator Associated Lung Injury
Barotrauma
Volutrauma
Atelectrauma
Biotrauma
Barotrauma
Parenchymal injury resulting from
high intrapulmonary air pressures
Most studies estimate that
barotrauma occurs when plateau
pressures exceed 35 cmH2O
Barotrauma in ALI/ARDS
High Airway Pressure Increases Pulmonary

Vascular Permeability
.6
Permeability
Kf,c
(ml/min/cmH20/10
0g)
.4
.2
0
0
20
40
Peak Airway Pressure (cmH2O)
70
Parker et al, JAP, 1984
Volutrauma
Direct injury to the lung parenchyma
from overdistention
Results from regional variability in lung
compliance
Significant overdistention may occur in
normal areas of lung
Peri-Vascular Hemorrhage
Is it the Pressure or the Volume?

Dreyfuss et al, Am Rev. Respir. Dis. 137:11591164.
Lung Water
HiP-HiV LoP-HiV HiP-LoV
Protein Permeability
HiP-HiV LoP-HiV HiP-LoV
Atelectrauma
Injury to alveoli resulting from the cyclic
collapse and opening of atelectatic
alveoli.
Very high shear forces can be created
at the air-liquid interface with alveolar
collapse
Exacerbated by surfactant depletion
Collapsed
alveolus
Atelectrauma
Inflated alveolus
Cytokine release
Cytokine release
Biotrauma
Lung and distant organ injury
resulting from the release of
inflammatory mediators into the
airspaces and into the systemic
circulation.
Mediators may originate from the
lung, or from other organs
Is perpetuated by mechanical
ventilation
Physiologic Changes with VILI
NEJM 369;22, 2013
Ventilator Induced Lung Injury

Lung injury
Mechanical ventilation
Alveolar collapse
Regional
overdistention
Neutrophil activation
inflammation
Edema formation
Surfactant inactivation
Worsening lung injury
Are you using protective

mechanical ventilation in
patients with acute lung
injury?
Sepsis-induced ARDS
23
CT in Early ARDS
Normal
Lung
Pleural
effusion
Consolidation in dependent lung

zones
Pressure-volume relationship
appropriate
Vt
excessive
Vt
protective
Vt
Pflex
Paw
Respiratory failure and mechanical

ventilation
Respiratory failure is the leading cause
for admission to the ICU.
Approximately 45% of our patients are
mechanically ventilated.
Strong evidence suggests that patients
with acute lung injury and acute
respiratory distress syndrome should be
managed with a protective ventilation
strategy.
Respiratory failure and mechanical

ventilation
Definitions:
ALI:
ARDS:
Acute onset
bilateral infiltrates on CXR
PaO2/FiO2<300 mmHg
No evidence of LA hypertension
Same as above, except
PaO2/FiO2<200 mmHg
Berlin Definition of ARDS
JAMA, June 20, 2012Vol 307, No. 23
ARDSnet Trial: Ventilator

Procedures
All Patients
Mode: Volume-Assist Control
Rate: Set rate < 35; adjust for pH goal
= 7.30-7.45 (if possible)
I:E:
1:1 - 1:3
Weaning by Pressure Support when
PEEP/FiO2 < 8/.40
PaO2 / FiO2
Ventilator-Free Days
Mortality Prior to Hospital

Discharge
P=0.0054
6 ml/kg
12 ml/kg
ARDS Protocol @ UCSF
Multicenter, double-blind, parallel-group trial of 400 pts with major abd

surgery
Control group had 10-12 ml/kg tidal volume, no PEEP or recruitment
maneuvers
Intervention was 6-8 ml/kg tidal volume, PEEP 6-8 cnH2O, recruitment
maneuver of 30 cmH2O for 30 seconds every 30 minutes
Primary outcome was a composite of major pulmonary and extrapulmonary
complications within 7 days after surgery: (atelectasis, pneumonia,
ALI/ARDS, need for ventilation, sepsis, death)
Futier et al, NEJM 2013
Intraoperative Procedures
Variable
Control
(N = 200)
Lung Protection
(N = 200)
P Value
Tidal volume (ml)
719 + 128
406 + 76
<0.001
Tidal volume (ml/kg)
11.1 + 1
6.4 + 1
<0.001
PEEP (cmH2O)
<0.001
# Recruitments
<0.001
Peak Pressure (cmH2O)
20.1 + 4.9
18.9 + 3.6
0.04
Plateau Pressure
(cmH2O)
16.1 + 4.3
15.2 + 3.0
0.02
Compliance ml/cmH2O
45.1 + 12.9
55.2 + 26.7
<0.001
FiO2
0.47 + 7.6
0.46 + 7.3
0.27
Fluids (liters)
2.0 crystalloid
0.5 colloid
1.5 crystalloid
0.5 colloid
0.47
0.97
(at end of surgery)
Variable
Control
(N=200)
Lung
protection
(N=200)
Primary
composite
outcome (30d)
58(29.0)
25(12.5)
0.45(0.28-0.73)
<0.001
Pulmonary
complication
42(21.0)
10(5.0)
0.23(0.11-0.49)
<0.001
Atelectasis
34(17.0)
13(*6.5)
0.37(0.19-0.73)
0.004
Pneumonia
16(8.0)
3(1.5)
0.19(0.05-0.66)
0.009
Need for
ventilation
7(3.5) IV
29(14.5)NIV
2(1.0) IV
9(4.5) NIV
0.40(0.08-1.97)
0.29(0.13-0.65
0.26
0.002
29(14.5)
13(6.5)
0.48(0.25-0.93)
0.03
30d mortality
7(3.5)
6(3.0)
1.13(0.36-3.61)
0.83
Hospital LOS
13
11
-2.45(-4.17 to -0.72)
0.006
ICU LOS
-1.21(-4.98 to 7.40)
0.69
Sepsis
Adjusted relative risk
P Value
Probability of Composite Event

(pneumonia, ventilation, sepsis, death)
Managing Severe Hypoxemia
Recruitment Maneuvers
Hypothesis:
Sustained lung inflation to recruit
atelectatic alveoli
Usually done with CPAP at 15-20
cmH2O
May be accompanied by hypotension,
especially in volume depleted patients
Canine Oleic Acid Injury

Maximum Inspiratory Capacity [%]
100
80
IC = 100%
60
IC = 93%
IC = 81%
40
IC = 59%
20
IC = 22%
0
IC = 0%
Best PEEP ?
10
20
30
40
After Gattinoni L, Pelosi

P, Marini JJ et al, with
permission: Ref
AJRCCM, 2001:164.
50
60
Recruitment Maneuver
Before recruitment
After recruitment
Recruitment
Prospective trial of 68 pts with ALI/ARDS

Whole body CT at different lung volumes
Measured percentage of potentially
recruitable lung.
CT Measurement of Recruitable Lung
Gattinoni et al, NEJM 2006
Mortality as Function of Recruitable Volume
Gattinoni et al, NEJM 2006
What about PEEP?

Pro: Anesthesia and surgery cause
atelectasis, leading to hypoxemia. May
contribute to overdistention and lung
injury
Con: PEEP increases intrathoracic
pressure, which decreases venous
return, and may contribute to
hypotension
Randomized, controlled trial at 30 centers in

Europe, Americas
900 Patients at risk for postoperative pulmonary
complications
Tidal volume set at 8 ml/kg
Randomized to either high PEEP (12 cmH2O) with
recruitment maneuvers or to low PEEP (< 2 cmH2O)
without recruitment maneuvers
Measure composite pulmonary outcomes
High PEEP plus RMs vs Low PEEP and no RM
Lancet, 2014
High PEEP plus RMs vs Low PEEP and no RM
Lancet, 2014
Probability of Postoperative Pulmonary

Complications by Day 5
Lancet, 2014
Multicenter, double-blind trial of 340 patients with early-onset,

severe ARDS
Randomized to cisatracurium or placebo
All other management identical
Primary outcome was 90-day mortality
N Engl J Med 2010;363:1107-16.
N Engl J Med 2010;363:1107-16.
Cisatracurium
(N=177)
Placebo
(N=162)
RR with
Cisatracurium
(95% CI)
P Value
42%
52%
57%
54%
63%
67%
0.71(0.51-1.00)
0.76(0.56-1.02)
0.78(0.59-1.03)
0.05
0.06
0.08
Vent Free Days

(D1-D90)
53.1+35.8
44.6+37.5
0.03
Days without any

organ failure
15.8 + 9.9
12.2 + 11.1
0.01
9 (5.1 [2.7-9.4])
19 (11.7 [7.6-17.6])
0.43 (0.20-0.93)
0.03
7 (4.0 [2.0-8.0])
19 (11.7 [7.6-17.6])
0.34 (0.15-0.78)
0.01
72/112
(64.3 [55.1-72.6])
61/89
(68.5 [58.3-77.3])
Outcome
Mortality
28D
ICU
Hospital
Barotrauma
N(%[RR})
Pneumothorax
N(%[RR})
Days without ICUacquired paresis

N(%[RR})
0.51
N Engl J Med 2010;363:1107-16.
Prone Positioning
Prone Positioning
Hypothesis:
Dependent atelectasis causes V/Q
mismatching and shunt
Improves weight distribution of
edematous lung and heart, allowing
improved lung expansion
Last year I recommended against using
it
Prone Positioning
Supine
Prone
Prone Positioning: Meta-analysis
Abroug et al, Crit Care. 2011
PROSEVA Trial
PROSEVA: Protocol
474 pts randomized
Dose of proning:
Within 55 minutes of
randomization
PP daily duration of
17 + 3 hours
All patients
ventilated with lung
protective strategy
Criteria for cessation

of PP:
P/F > 150

PEEP < 10
FiO2 < 0.6
All criteria persist at
least 4 hours in
supine position
Guerin et al, NEJM 2013
Survival
Guerin
et al,
NEJM
2013
Prone Positioning: Recommendation

PROSEVA more effective than previous
studies
More complications than expected in
supine group (13% incidence cardiac
arrest)
Highly experienced centers: no adverse
events with proning
Watch video at NEJM.org
Most patients received NMBs

Guerin et al, NEJM 2013

Rationale:
Low tidal volumes protect the lung from
ventilator associated lung injury
Maximize mean airway pressure,
prevent atelectasis
Limit peak pressures

Refers to rates > 100 breaths/min in adult and >
300 breaths/min in neonates
Jet ventilation
exhalation is passive
set frequency, jet volume, entrainment volume
inspiratory time, and baseline pressure
Oscillatory ventilation
piston or microprocessor gas controllers
bias flow through circuit determines Paw
set oscillator frequency, displacement, I:E times,
bias flow

Ventilator Type
Frequency
Breaths/min
Inspiration
Expiration
CV
2 - 40
Active
Passive
HFPPV
60 - 100
Active
Passive
HFJV
100 - 200
Active
Passive
HFO
200 - 2400
Active
Active
Gas Transport During HFV

1.
2.
3.
4.
Bulk flow
Taylor dispersion
Pendeluft
Assymetric velocity
profiles
5. Cardiogenic mixing
6. Molecular Diffusion
High Frequency Jet Ventilation
High Frequency Oscillation

Original design was
a home stereo
speaker
Oscillator creates
inspiratory and
expiratory flow
Changing inspiratory
bias flow adjusts
mean airway
pressure
Multicenter, randomized, controlled trial

548 patients 39 ICUs in 5 countries
Ferguson et al, NEJM. 2013
OSCILLATE Trial
HFOV
(N=275)
Control
N=273
Relative Risk
(95%CI)
P Value
Death in
hospital
129 (47%)
96 (35%)
1.33 (1.091.64)
0.005
Death in ICU
123 (45%)
84 (31%)
1.45 (1.171.81)
0.001
Barotrauma
46/256 (18%)
34/259 (13%)
1.37 (0.912.06)
0.13
Refractory
hypoxemia
19 (7%)
38 (14%)
0.50 (0.290.84)
0.007
9 (3%)
8 (3%)
1.12 (0.442.85)
0.82
ICU LOS (D)
15
14
0.93
0.93
Hosp LOS (D)
30
25
0.74
0.74
Outcome
Refractory
acidosis
Multicenter, randomized, controlled trial comparing

HFOV to usual ventilator care
800 Patients randomized in 29 hospitals
Young et al, NEJM. 2013
OSCAR Trial
OSCAR vs OSCILLATE
Different oscillators
Different algorithms for adjustment:
Mean airway pressure in oscillator arm:
OSCILLATE: 31 + 2.6 cmH2O
OSCAR: : 27 + 6.2 cmH2O
Different ventilation in control groups

Control mortality:
35% in OSCILLATE
41% in OSCAR
Wavering on Oscillation?
Taken together, no benefit, potential
harm with HFOV in ARDS
Negative effects may be due to:
Ventilator-associated lung injury
? Higher vasopressor, fluid, sedatives
Control arm not ARDSnet protocol
Other strategies for severe

hypoxemia
Airway pressure release ventilation

(APRV)
Time-triggered, pressure-limited, and
time-cycled mode
high continuous positive airway
pressure (P high) is delivered for a long
duration (T high) and then falls to a
lower pressure (P low) for a shorter
duration (T low)
allows spontaneous breathing (with or
without PS) during both the inflation and
deflation phases
Gonza l ez et al. Intensive Care Med (2010) 36:817827
Airway Pressure Release Ventilation
Airway pressure release ventilation

(APRV)
Potential benefits:
improved alveolar recruitment and oxygenation

Some observational studies show decreased
peak airway pressure, improved alveolar
recruitment, increased ventilation of the
dependent lung zones and improved
oxygenation
No mortality benefit
Potential risks: In severe obstructive

disease, could lead to hyperinflation and
barotrauma
Biphasic Ventilation
Similar to APRV, except that T low
is longer during biphasic ventilation,
allowing more spontaneous breaths
to occur at P low
AKA Bi-Vent, BiLevel, BiPhasic,
and DuoPAP ventilation.
Biphasic Ventilation
Post-Extubation CPAP
Randomized, unblinded
study of postop laparotomy
patinents with hypoxemia
209 patients in 15 hospitals
Randomized to oxygen vs
CPAP
Primary outcome was
reintubation
Post-extubation CPAP
1322 Patients enrolled
230 met postop criteria
209 randomized
104 assigned to oxygen by

facemask
105 assigned to oxygen + CPAP
2 unable to tolerate
4 unable to tolerate
104 included in analysis
105 included in analysis

Squadrone et al, JAMA 2004.
Reintubation Rate
10
Intubation
%
0
0
20
60
100
140
Time (hours)
Postextubation CPAP: Secondary Outcomes

Outcome
Control
(104)
CPAP
(105)
Relative
Risk
P Value
ICU LOS
(d)
2.6
1.4
.09
Hosp LOS
(d)
17
15
.10
Pneumoni
a #(%)
10(10)
2(2)
0.19
0.02
Infection
#(%)
11(10)
3(3)
0.27
.03
Sepsis
#(%)
9(9)
2(2)
0.22
.03
Deaths
#(%)
3(3)
0(0)
.12
Meta analysis of 9 clinical trials.
Annals Surgery, 2008.
CPAP and Postop Complications
Conclusions
Ventilator associated lung injury is
multifactorial
6 ml/kg IBW tidal volume should be
used in the ICU and OR for all high-risk
patients, even those without lung injury
Consider early use of NMBs in patients
with ARDS
In a recent trial, prone positioning has
been shown to reduce mortality
Conclusions (cont)
HFOV may improve oxygenation, but
has not shown mortality benefit
APRV and Bilevel ventilation may
improve oxygenation, but have no other
proven benefit.
Post-extubation CPAP in the PACU can
prevent reintubation in high risk patients
Upcoming Events
Fairmont Kea Lani
Perioperative Management of
Neurovascular Procedures
Keith J Ruskin, MD
Professor of Anesthesiology and
Neurosurgery
Yale University School of Medicine
Disclosures
Consultant: Masimo Corporation
Learning Objectives
Explain the pathophysiology of intracranial
aneurysms and arteriovenous
malformations.
Discuss the unique challenges of working
in the interventional radiology suite.
Manage critical events that occur during
neurointerventional procedures, including
hemorrhage and vascular occlusion.
Neurovascular Surgery
Intracranial aneurysms
Arteriovenous malformations
Stroke
Endovascular vs open management
Intraoperative management
Vasospasm, cerebral protection
Intracranial Aneurysm
3% US population: Unruptured aneurysm

Case control study
Reasons for imaging (unruptured)
Atherosclerotic disease (23%)
Positive family history (18%)
Headache (8%)
Preventive screening (3%)
Other (46%)
Aneurysm Risk Factors
Current smoking
Hypertension
Family history of stroke other than
subarachnoid hemorrhage
Reduced risk:
Regular physical exercise
Hypercholesterolemia
Vlak MH et al. Stroke. 2013 Apr;44(4):984-7.
Risk Factors (Rupture)
Smoking
History of migraine
Decreased risk factors:
Hypertension
Hypercholesterolemia
Heart disease
Why?
Vlak MH et al. Stroke. 2013 May;44(5):1256-9.
Subarachnoid Hemorrhage
Incidence: 8-10 per 100,000 people

Most common at 55-60 years
75% of SAH: Ruptured cerebral aneurysm

20% idiopathic origin
Subarachnoid Hemorrhage
Risk of rupture: 1 - 2% annually

16,000 patients per year in US
30-day mortality: 45%
Priebe HJ. Br J Anaesth 2007 Jul; 99(1):102-18.
Cardiac Involvement
ECG changes in 50 - 100%
ST depressions, T wave inversions
Dysrhythmias
Ventricular ectopy
Sinus bradycardia, tachycardia
Atrial fibrillation
? Hypothalamic injury
Jain: AJNR Am J Neuroradiol. 2004 Jan;25(1):126-9.
Fluid, Electrolyte Balance
30% SAH patients hypovolemic

Increases risk of vasospasm
Impairs perfusion
Electrolyte disturbances
Hyponatremia (30%)
Hypokalemia
Hypocalcemia
Salt wasting, SIADH
Autoregulation
Impairment correlates with clinical grade

Decreased CBF, CMRO2
PaCO2 response preserved post-bleed
Endovascular or Craniotomy
Randomized controlled trial

2143 patients with ruptured aneurysm
42 institutions (UK and Europe)
Primary outcomes:
Death, dependence at 1 year
Secondary outcomes:
Rebleeding, seizures
ISAT Trial: Results
Death: 7.4% Absolute risk reduction
Early survival advantage maintained 7 years
Rebleed rate: 0.2%

Fewer seizures (relative risk 0.52)
Molyneux AJ. Lancet. 2005 Sep 3-9;366(9488):809-17.
Arteriovenous Malformations
Incidence 0.05% in autopsy series
Occur predominantly in males
Congenital abnormality
20%- 60% Seizures
25% Headache, bruit
Peak diagnosis: 10 - 30 years

Yearly mortality: 1.5%
Mortality from hemorrhage: 10 15%
AVMs: Physiology
Mass of thin-walled vessels, no capillaries

Low pressure, high flow A-V shunt
60 mmHg proximal to AVM
Distal autoregulation impaired

Resistance arterioles maximally dilated
Normal pressure breakthrough bleeding
Dural A-V fistulas
Outside pia, involve dura

Direct: Well-defined AV shunt, few feeders
Indirect (sinus): Small arterial feeders drain
into dural sinus
Can cause a steal phenomenon
AVMs: Management
Endovascular procedure
Stereotactic radiotherapy
Vascular occlusion with glue

Gamma knife
Surgical excision
Combined procedure
Acute Ischemic Stroke
Intravenous rtPA:
Persistent neurologic deficits, < 3 hours
Not suggestive of subarachnoid hemorrhage
Intra-Arterial rtPA:
Major stroke, < 6 hour duration
MCA occlusion
IV thrombolysis contraindicated
Meyers PM. Circulation 2009;119(16):223549.
Preop Evaluation
History, physical examination

Hemorrhage severity
Neurologic examination
Laboratory values
Electrolytes, coagulation studies
Radiologic examination
CT, angiography
Hunt and Hess Grading

Grade 0
Unruptured aneurysm
Grade 1
Asymptomatic, minimal
headache
Moderate to severe
headache, rigidity
Drowsiness, confusion,
mild focal deficit
Stupor, hemiparesis
Grade 2
Grade 3
Grade 4
Grade 5
Coma, decerebrate
rigidity
Anesthetic Management
Hemodynamic stability
Brain relaxation (if open procedure)
Cerebral protection?
Rapid emergence
Premedication
Continue Ca++ antagonists (nimodipine),

anticonvulsants
H2 antagonists (e.g., ranitidine)
Sedatives?
Decrease anxiety, catecholamines
May mask changes in mental status
Monitoring
Routine monitors
Intra-arterial catheter
Anticoagulation (ACT or aPTT)
If endovascular treatment planned
Consider EP monitoring if temporary

occlusion planned
Anesthetic Management
Induction
Hemodynamic stability
Patient may be hypovolemic
Maintenance
Volatile anesthetics increase ICP
N2O increases ICP, CMRO2
Narcotic, low-dose potent volatile agents
Emergence
Endovascular Anesthesia
Remote location
Limited equipment, supplies, assistance
Patient access
Intravenous, intra-arterial catheters
Secure airway, extension tubes on circuit
Radiation safety
Catastrophic events
Blood Pressure (Aneurysm)
Establish normal range

Fighting with medication
Ca++ antagonists
Nitroglycerine to prevent vasospasm
Autoregulation:
Describes a population, not an individual
Consider MAP lower limit 70 mmHg
Patel PM. In: Miller RD, et al, eds. Millers anesthesia. New York: Churchill Livingstone;
2010. pp. 30539.
Transmural Pressure
Gradient
TMPG = MAP ICP

Same formula for CPP: TMPG = CPP!
Maintain adequate CPP, avoid spikes
Antihypertensives: Labetalol, nicardipine
Blood Pressure (AVM)
Impaired distal autoregulation

Hypotension may cause ischemia
During resection:
Increased PO2, pH; decreased PCO2

Charbel FT. Neurol Med Chir (Tokyo) 1998; 38(Suppl):1716.
After resection:
Resistance arterioles: Impaired
vasoconstriction
Normal perfusion pressure breakthrough
Spetzler RF: Clin Neurosurg. 1978;25:651-72.
Management Strategy
(Stroke)
General anesthesia or MAC?
No clear data; depends upon patient status

SNACC. J Neurosurg Anesthesiol. 2014 Apr;26(2):95-108.
Maintain cerebral perfusion pressure:

Within 10-20% of admission BP
Less than 185/105 mmHg
Avoid hyperglycemia
Tarlov N. Neurology. 2012 Sep 25;79(13 Suppl 1):S182-91.
Intracranial Catastrophe
Intracranial Catastrophe
Communicate with team, call for help

Secure the airway
Hemorrhage:
Reverse anticoagulation
Low normal MAP
Occlusion
Hypertension guided by exam, imaging
Catastrophe (Contd)
Head up 15 if possible
Adjust PaCO2 as appropriate
Consider
Mannitol 0.5 g/kg
EEG burst suppression
Passive cooling to 33 to 34
Ventriculostomy
Anticonvulsants
Intraoperative Rupture
High morbidity and mortality

Prevention: Manage transmural pressure
Incidence: 11% if previously ruptured
Maintain normovolemia
Temporary occlusion of blood supply
Consider transient hypotension
Cerebral Relaxation
Timing important
Prevent abrupt transmural pressure changes
Moderate hypocapnia (25 - 30 mmHg)?

Mannitol (0.25 - 1.0 g / kg)
CSF drainage
Lumbar drain, ventricular catheter
Hypocapnia
102 mechanically ventilated SAH patients

92%: ETCO2 below 35 mmHg
Mean duration: 4 days
68% while breathing spontaneously
Hypocapnia correlated with poor outcome,

symptomatic vasospasm
Solaiman O. J Neurosurg Anesthesiol. 2013 Jul;25(3):25461.
Hypothermia
No benefit from mild hypothermia

Todd et al: N Engl J Med. 2005 Jan 13;352(2):135-45.
Fever worsens neurologic outcome

Todd et al: Neurosurgery. 2009 May;64(5):897-908
For giant aneurysms, consider:

Profound hypothermia
Circulatory arrest
Brain Protection
Ischemia during temporary occlusion

Classical brain protection:
Hypothermia
Barbiturates
IHAST temporary occlusion subgroup

Hypothermia, protective drugs
Thiopental, etomidate
No effect on outcome
Hindman BJ et al. Anesthesiology. 2010 Jan;112(1):86-101.
Cerebral Vasospasm
30%-70% incidence after SAH

3-12 days post-bleed
Diagnosis:
Clinical symptoms
Angiography
Etiology unclear
Prevention and Treatment
Nimodipine
Class 1, level A
Prevents 1 poor outcome / 13 patients
Prevent hypotension, maintain euvolemia

Positive fluid balance?
Triple-H therapy?
Cerebral angioplasty
Lazaridis C. Neurosurg Clin N Am. 2010 Apr;21(2):353-64.
Triple-H Therapy
Hypertension, hypervolemia, hemodilution

Increase in pressure, decrease in viscosity
improves CBF in spastic vessels
SBP 160-200 mmHg after clipping
CVP 8-12 mmHg, PCWP 15-18 mmHg
Hematocrit 30%-35%
Triple-H Therapy
No current standard approach
Consensus for symptomatic vasospasm
Indications, contraindications, methods

Hypertension, hypervolemia
No endpoints to guide therapy

Meyer R. Neurocrit Care. 2011 Feb;14(1):24-36.
Conclusions
Skilled anesthesiologist
Pathophysiology of neurovascular disease
Skilled surgeon / proceduralist

Rapid, atraumatic procedure
Rapid control of intraoperative bleeding
Attention to details (BP control)

Postoperative management
Upcoming Events
Fairmont Kea Lani
Management of Traumatic
Brain Injury
Keith J Ruskin, MD
Professor of Anesthesiology and
Neurosurgery
Yale University School of Medicine
Disclosures
Consultant, Masimo Corporation
Learning Objectives
Discuss the pathophysiology of TBI.
Explain how to manage the airway and
ventilate patients who have a TBI.
Discuss fluid management in the braininjured patient.
Common: 1.7 million / year (US)

Poor outcome when severe
Leading cause of death < 45 years old
50% of survivors: moderate or severe disability
Thornhill S: BMJ. 2000 Jun 17;320(7250):1631-5.
Early cognitive deficits common

Complete recovery: 6 months 1 year
Possible association: psychiatric illness, suicide
Carroll LJ. Arch Phys Med Rehabil. 2014 Mar;95(3 Suppl):S152-73.
Death rate increased for 7 years after event

McMillan TM Brain. 2007 Oct;130(Pt 10):2520-7.
Axonal injury
Shearing, compressive forces
Physical destruction, loss of homeostasis
Swelling, hypoperfusion, neurotoxic events
Ischemic injury
Decreased glucose use, lactate accumulation
Ca2+ influx causes depolarization
Excitotoxicity
Algattas H. Int J Mol Sci. 2013 Dec 30;15(1):309-41.
Messengers, immune cells enter brain

Neutrophilic infiltration
Astrocytosis
Cytokines
Edema
Proposed therapy:
Hyperosmolar agents
Decompressive craniectomy
Hormones (progesterone)
Algattas H. Int J Mol Sci. 2013 Dec 30;15(1):309-41.
Small proportion of TBI patients

Two broad groups:
Early deaths: Severe extracranial injuries, traumatic
shock
Late deaths: Older patients with less severe
extracranial injuries, lower incidence of
hypotension on arrival
Anticoagulation therapy in both groups

Davis DP. J Trauma. 2007 Feb;62(2):277-81.
Maintain cerebral perfusion, oxygenation

Avoid iatrogenic injury
Avoid hypo- and hypercapnia
Avoid hyperglycemia
No clear evidence, practice based on guidelines
Usually responds to medical therapy

Medically untreatable in 10-15% of patients
Sustained ICP > 20 mmHg: 100% mortality
Reduces cerebral perfusion pressure
May cause herniation
Early intubation may improve outcome in some

patients, but may harm others
Time from injury to intubation does not affect
mortality
Indications for endotracheal intubation:
Glasgow Coma Score < 8
Inability to maintain airway
Impending respiratory failure
No clear evidence for prehospital intubation
187,709 adults; 16,078 cervical spine injury

Risk factors:
Older age
Skull, facial fractures
Spine fracture, dislocation
Upper limb injury
Thoracic injury
Hypotension
Axial CT required (plain films unreliable)

Fuji T. J Emerg Trauma Shock. 2013 Oct;6(4):252-8.
Hypercapnia increases brain volume

Hypocapnia may worsen injury:
Causes cerebral ischemia
Increases zero-flow pressure
Maintain normocapnia
Maintain SpO2 > 90% - 95%
Hypotension associated with poor outcome

Avoid hypotension
Systolic pressure > 120 mmHg
MAP > 90 mmHg
Theoretical concern about cerebral edema after

massive resuscitation
No evidence of exacerbation in clinical practice
BTF: Treat increased ICP with mannitol

May decrease mortality
Guide treatment with intracranial pressure
Hypertonic saline may be more effective
Wakil A. Cochrane Database Syst Rev. 2013 Aug 5;8:CD001049.
Prospective cohort study

Adult TBI patients, sustained ICP > 30 mmHg
14.6% hypertonic saline, 40 ml bolus dose
11 patients, 56 doses of HS, 3 survivors
Mean ICP decreased: 40 mmHg to 33 mmHg
Eskandari R. J Neurosurg. 2013 Aug;119(2):338-46.
Improves cerebral venous outflow

Decreases CBV, capillary leak
CSF moves to spinal subarachnoid space
May decrease CPP in hypotensive patients
Reduces intracranial volume

Enhanced clearance of edema
Role unclear in severe head injury
Propensity score: decompressive craniectomy

2602 patients matched criteria
450 patients received DC
No difference in mortality
No difference in neurologic outcome
Nirula R. J Trauma Acute Care Surg. 2014 Apr;76(4):944-55.
Retrospective review
Patients with GCS < 8, no evidence of shock
Normalized for age, sex, injury severity, GCS,
hemodynamics
28 day mortality increased if Hgb > 10 g/dL
Each unit increased multiorgan dysfunction
score by 0.45
Elterman J et al. J Trauma Acute Care Surg. 2013 Jul;75(1):8-14.
Anemia is a risk factor for secondary brain injury

Increased risk when combined with hypoxia
Treating anemia improves oxygenation

No level I evidence for RBC transfusion trigger
Large trials needed
LeRoux P. Curr Opin Crit Care. 2013 Apr;19(2):83-91.
Hyperglycemia worsens outcome

Hyperglycemia, glucose variability increases
mortality, prolongs length of stay
Jacka MJ: Can J Neurol Sci. 2009 Jul;36(4):436-42.
Perioperative hyperglycemia
200 nondiabetic patients with TBI
20%: intraoperative glucose > 180 mg/dL
Routine glucose monitoring
Bhattacharjee S. J Neurosurg Anesthesiol. 2014 Mar 13.
Titrate to burst suppression, isoelectricity

Reduce CMRO2
Extensive support
Hypotension in 25% of patients
Continuous hemodynamic monitoring
Intubation, mechanical ventilation
Hypotension offsets decreased ICP

No evidence for improved outcome
Roberts I. Cochrane Database Syst Rev. 2012 Dec 12;12:CD000033.
Seizures common after traumatic brain injury

4-25% within one week
Negative effects:
Increased cerebral metabolic rate, ICP
Enhanced neurotransmitter release
Multiple risk factors:

GCS < 10
Cortical contusions, depressed skull fracture
Hematoma, penetrating head wound
Temkin NR. N Engl J Med. 1990 Aug 23;323(8):497-502.
Phenytoin, carbamazepine reduce early seizures

No effect on mortality, long-term seizure risk
US guidelines recommend seizure prophylaxis
European guidelines do not discuss seizures
Levetiracetam: Binds synaptic vesicle
glycoprotein 2A; probably inhibits Ca2+
May improve neurobehavioral outcome
Benge JF. Front Neurol. 2013 Dec 2;4:195.
Improves outcome in animal models of TBI

Systematic review: 20 trials, 1885 patients
Significant reduction in mortality, poor outcome
No evidence for association with pneumonia
Conclusions:
Majority of studies poor quality
Need high-quality randomized controlled trials
Crossley S. Crit Care. 2014 Apr 17;18(2):R75.
Nimodipine (Ca2+ channel antagonist)

Demonstrated benefit after aneurysmal
subarachnoid hemorrhage
No significant effect after TBI
Magnesium
Ca2+ antagonist, NMDA antagonist
No demonstrated benefit
Trial stopped: increased mortality
Affects multiple parts of injury cascade

Limits vasogenic, cytotoxic edema
May reduce free radical formation
Upregulates antioxidant enzymes
Decreases inflammation
Modulates cytokine release
Limits neuronal apoptosis

May promote central, peripheral remyelination
100 adults, TBI, GCS 4-12

Intravenous progesterone vs placebo
Blinded observers
Neurologic events, 30-day outcome
Progesterone group:
Lower 30-day mortality
More likely to have moderate to good outcome
Wright DW. Ann Emerg Med. 2007 Apr:49(4):391-402.
Rat model of permanent MCA occlusion

Intraperitoneal progesterone
Brains examined 22 days after stroke
8, 16 mg/kg attenuated infarct volume
Functional outcomes improved
Movement
Grip
Spatial navigation
Improves outcome
Wali B. Brain. 2014 Feb;137(Pt 2):486-502
Maintain cerebral perfusion, oxygenation

Avoid iatrogenic injury
Avoid hypo- and hypercapnia
Avoid hyperglycemia
No clear evidence, practice based on guidelines
Progesterone: Promising new agent
Upcoming Events
Fairmont Kea Lani

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2014 Fall Anesthesia Seminar

Hypertensive Disorders of Pregnancy

6-10% of pregnancies worldwide

Wallis A B et al. Am J Hypertens 2008;21:521-526

CA-PAMR: Chance to Alter Outcome

Chance to Alter Outcome

Deep vein thrombosis/

Cardiomyopathy and other

Cerebral vascular accident

Amniotic fluid embolism

All other causes of death

Preventability Maternal Death

Chronic Medical problem

North Carolina maternal deaths, n=108, 1995-1999

Preeclampsia: an Evolving Disease

Preeclampsia: an Evolving Disease

Late Onset (>34 weeks GA)

Increased Maternal CV risk later

Risk Factors Preeclampsia

Prior preeclampsia (OR 7) or family Hx (OR 2-4)

Placental Implantation Normal

Genetic Causes Preeclampsia

Early Onset Preeclampsia (<34

ONE SUGGESTED PATHOPHYSIOLOGIC MODEL

ONE SUGGESTED PATHOPHYSIOLOGIC MODEL

-Biochimica et Biophysica Acta 2012:1960-9

Late Onset Preeclampsia

Maternal (late onset) preeclampsia

Late Onset Preeclampsia

Maternal Age >40

-Hum Genet 2007:120:607-612

Preeclampsia Definitions - OLD

Preeclampsia Definitions - NEW

Preeclampsia Definitions NEW

Classification HTN Pregnancy

Chronic hypertension with superimposed

-. Obstet Gynecol. 2008;112(2 PART 1): 359-372.

Preeclampsia Update 2014-15

Imagine what you'll know tomorrow

Preeclampsia Blood Tests

PlGF starts to decreases 9-11weeks,

Communication keys to success

Pitfalls and Protocols:

Written criteria to observe change or

Maternal Early Obstetric Warning

Call physician to evaluate patient for 2 points or more

-NHS U.K., CMQCC, et al.

The Joint Commission

-CMQCC Preeclampsia Toolkit revised 5-2014

-CMQCC Preeclampsia Toolkit revised 5-2014

Fluid Restriction Guideline

Consider cardiac dysfunction

-CMQCC Preeclampsia Toolkit revised 5-2014

Timing of Delivery Preeclampsia

<34 weeks GA wait unless unstable [NEW]

-CMQCC Preeclampsia Toolkit revised 5-2014

Cause of U.S. Maternal Mortality

Preeclampsia Mortality Rates

The overall mortality rate for

Acute HTN Rx 2014

First Line Rx one of:

Acute HTN Rx 2014

Second Line RX one of:

Hydralazine 5-10 mg IV, repeated every 15-20