PUERPERAL SEPSIS

(Why are mothers dying?)

Dr.Zainab Shamsuddin
Hospital Kuala Lumpur

PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

Mary Wollstonecraft an early and

talented feminist, published The Rights
of Woman in 1790. Delivered of her
second child on 30 August 1797, and
required to have the placenta brought
away in pieces by Dr Poignaud, manmidwife to the Westminster lying-in
Hospital.
After 4 days of illness, Mary developed
shaking chills, a feature of childbed
fever, and her condition deteriorated
steadily. There was no effective
treatment available, and she died 12
days after delivery.
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The child, named Mary after

her mother, at the age of 16
eloped with the poet Shelley,
and 3 years later gave
evidence of her inherited
genius with the publication of
her
classic,
Frankenstein
(Kaiser 1976).
Kaiser I H 1976 The Obstetric death of
Mary Wollstonecraft. American Journal of
Obstetric and Gynecology 125:1-2

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For several hundreds of years, infection after

childbirth has been one of the chief hazards to the
parturient woman, and one of the prime causes of
maternal death.
Ever present in sporadic nature, there have been
major epidemics of puerperal sepsis which left
scarcely any survivors. (eg. Paris 1664, Lombardy
1772, was a year in which not one woman survived
childbirth).
(Graham H (pseud) 1950 Eternal Eve. Heinemann, London).

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The epidemic nature of the disease in the 18th and 19th

centuries was a direct result of the establishment of lyingin hospitals, with consequent overcrowding and more
significantly, the attendance on labouring women by
medical men-the so-called man-midwives.

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DEFINITIONS

Puerperal Pyrexia
Temperature of 38 C on any occasion in the first 14
days after delivery or miscarriage

Causes

Urinary tract infection

Genital tract infection
Breast infection
Deep vein thrombosis
Respiratory infection
Others

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DEFINITIONS-cont.
Puerperal sepsis refers to infection of the genital tract after
delivery. The term is synonymous with the older
expressions of puerperal fever and childbed fever.
(Although infection of the abdominal wound following
Caesarean section is more correctly termed a wound
infection, such cases are commonly regarded as variants of
puerperal sepsis).

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THE INCIDENCE OF PUERPERAL SEPSIS

Because of the difficulty in defining the condition, the
incidence as reported from different centres is variable, and
range from 1% to 8%
(Gibbs R S, Weinstein A J 1976 puerperal infection in the antibiotic era. American Journal of
Obstetric and Gynecology 124:769-785).

Holbrook, in a questionnaire-based survey of 19 650 mothers

in 1991, found an incidence of reported postpartum infections
of 4% in all women who had delivered. However the reply
rate to the questionnaire was only 36%, and of the infections
reported, only 7.6% were located in the genital tract.
(Holbrook K F, Nottebart V F, Hameed S R, Platt R 1991 Automated postdischarge
surveillance for postpartum and neonatal nosocomial infections.American Journal of
Medicine 91:125S-130S)

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Most studies will seriously underestimate the incidence

of puerperal morbidity. Still, there is no doubt that the
disease is less common, and less severe than it used to
be 40-50 years ago, and studies of puerperal sepsis
have been sparse in recent years.

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PATHOGENESIS

The placenta site is equivalent to an open wound immediately

after parturition. There are almost always lacerations of greater
or lesser magnitude in the epithelium of the vagina, cervix and
lower uterine segment.
Iatrogenic injuries, such as Caesarean section or episiotomy
incisions, provide additional breaches in the integrity of the
genital tract, and local diminution in the normal defense
mechanisms. Blood clots and retained necrotic portions of
placenta or membranes also provide an ideal culture medium
for the microorganisms which inhabit the female genital tract,
but which do not normally cause disease.

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The flora is mixed, with both aerobic and anaerobic bacteria

present, including numerous species which are potentially
pathogenic, such as group B haemolytic streptococci,
Bacteroides species, Staphylococcus aureus, Mycoplasma
hominis and Escherichia coli (Hurley 1987).
Hurley R 1987 Microbiology. In:Philipp E, Barnes J, Newton M (eds) Scientific foundations
of obstetric and gynecology, 3rd (international) edn.Heinemann, London.

The initial site of infection may be anywhere in the genital

tract, from perineum to Fallopian tubes, but the uterus is
involved in almost all cases.

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METHODS OF SPREAD
Puerperal sepsis is generally an ascending infection,
proceeding along the lumen of the genital tract. The
placental site is almost always involved and the
extraplacental decidua also offers very little resistance to
the spread of infection, being at this time very thin,
traumatized and infiltrated with blood.
Translumenal spread may extend beyond the uterus, into
and through the Fallopian tube, and thence to the pelvic
peritoneum where abscess formation may occur. A
generalized peritonitis may ensue. The full thickness of
the uterine wall, from decidua to peritoneum, is almost
always involved.
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Infection of local lacerations in the vagina and cervix

may spread along tissue planes. Extensions into the
myometrium and parametrium may results in pelvic
cellulitis, also known as parametritis.
Abscess formation and peritonitis may be a sequel to
extrauterine spread
(Barnes J, Bender S 1955 The abnormal puerperium. In:Holland Sir E(ed)British
obstetric and gynecological practice: obstetrics.Heinamann,London,pp 821-850).

Blood-borne spread from the primary site of may

account for septicaemia or for septic thrombophlebitis.
Spread is along venous channels, from the placental site
vessels, to the ovarian veins, the uterine and iliac
vessels, and ultimately the inferior vena cava.
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Maternal deaths from genital tract sepsis, rates per

million maternities; United Kingdom 1985-99
Triennium

Early
pregnancy
(n)

Puerperal
(n)

After
surgical
procedure
(n)

Before or
during
labour
(n)

Total
(n)

Rate per
million
maternities

1985 87

4.0

1988 90

17

7.2

1991 93

15

6.5

1994 96

2b

11

17

7.3

1997 99

2+2
Late

18

8.4

Includes deaths following miscarriage, ectopic and other causes; b in

1994 96 these deaths were included in Chapter 6 early pregnancy
deaths

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Maternal deaths from genital tract sepsis, rates per

100,000 livebirths; Malaysia1997-2000
Year

Total no. of
maternal
deaths

Total death
from
Puerperal
sepsis

Mode of
delivery

Accoucher

1997

158

1.9

2 SVD

DR 1

1998

182

4.9

7 SVD

DR 3

1999

168

1.2

2 SVD

2000

146

4.1

5 SVD

TOTAL

654

20

3.1

16 SVD

DR 1

Report on the confidential enquiries into Maternal Deaths in Malaysia

1997-2000

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SEVERITY OF INFECTION
AND DEGREE OF SPREAD

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Pathogen-related factors
a) The specific microorganism involved

b) The virulence of the specific microorganism

c) Bacterial resistance to antibiotics
d) The magnitude of the inoculum

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Host-related factors
a) General health
b) Immune status
c) Risk Factors related to the pregnancy
i. Route of delivery
ii. Duration of labour
iii.Invasive examinations in labour
iv.Rupture of the membranes and preterm labour

v. Prenatal bacterial colonization of the genital tract

vi.Other determinants
PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

THE MICROBIOLOGY OF ESTABLISHED PUERPERAL SEPSIS

1. Aerobic bacteria
a.Gram positive
Beta-haemolytic Streptococcus, Group B,D and A Staphylococcus epidermidis,
rarely St.aureus
b.Gram negative
Escherichia coli
Enterobacteriaceae including Klebsiella pneumoniae, Enterobacter,
Proteus mirabilis, Citrobacter, Pseudomonas aeruginosa
Haemophilus influenzae
c.Gram variable
Gardnerella vaginalis
2. Anaerobic bacteria
Peptostreptococcus sp.
Peptococcus sp.
Bacteroides bivius, B.fragilis, B.disiens
Clostridiumramosum, rarely Cl.perfringens
Fusobacterium
3. Unclassified
Mycoplasma hominis
Chlamydia trachomatis

MICROBIOLOGY
The most common organism responsible for serious and lifethreatening obstetric infections is the beta-haemolytic Streptococcus
pyogenes (Lancefield Group A). The Lancefield Groups C and G
streptococcus may also cause serious clinical syndromes but are
less common.

The Lancefield Group B streptococcus can be found in normal

vaginal flora and is most commonly associated with neonatal
septicaemia and meningitis, particularly in premature infants.
Serious maternal infections may also occur with this organism.

All these micro-organisms may be described as beta haemolytic

streptococci in laboratory reports but it should be good practice to
ensure that the Lancefield grouping is also reported.

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CLINICAL FEATURES
1. Head, neck and spine
2. Breasts
3. Heart and lungs
4. Abdomen
The abdomen must be generally examined, noting the presence of
free fluid, enlargement of liver and spleen, and any abnormal
masses. Particular note must be taken of uterine size and
tenderness, renal angle tenderness and the presence or absence
of signs of peritonitis. The presence or absence of bowel sounds
should be recorded.

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5.Pelvis
A pelvic examination must be performed in all cases. The lochia
should be checked for colour, consistency and unpleasant odour.
The external genitalia must be inspected, and infected lacerations
sought in the lower tract.
Bimanual palpation of the uterus and parametrial tissues must be
done. The size of the uterus and the degree of tenderness should
be noted. The pouch of Douglas must be carefully examined as
this is a common site for abscess formation.
6. Limbs

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MANAGEMENT
-is complex, and best undertaken in an ICU.
-aspects that will require therapy include :
a) Fluid balance

b) Respiratory support
c) Circulatory support
d) Renal failure

e) Infection control
f) Corticosteroids
PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

THE MANAGEMENT OF PUERPERAL SEPSIS

a) Epidemiological considerations
b) General care

c) Local therapy
d) Antibiotics

Antibiotic therapy is the mainstay of treatment for puerperal sepsis,

and has revolutionized the outcome of this formerly dreaded disease.
There are probably as many regimens of therapy as there are
maternity unit and there is not much to choose between them in terms
of results. It can be predicted with confidence that each newly
developed antibiotic agent will be put up in trial cases of puerperal
morbidity against one of the older effective formulations. The
principles of antibiotic therapy for puerperal sepsis remain inviolate
however , and they include the following :
PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

1. The disease is polymicrobial in origin , and treatment must

therefore cover Gram-positive and negative, aerobic and anaerobic
microorganism
2. Multiple-agent therapy is acceptable and perhaps to be preferred.
3. Parenteral, preferably intravenous administration is advisable in
the first instance. The change to oral administration may be made
when the patient is recovering, intestinal ileus is no longer present
and
there is certainty concerning gastrointestinal absorption
capacity. The antibiotic agent should therefore be capable of
administration by both parenteral and oral routes (although
Dinsmoor ) et al (1991) found that there was no difference between
patients followed up with oral therapy compared to those given
placebo after successful intravenous treatment of postpartum
endometritis).
(Dinsmoor M J, Newton E R,Gibbs R S 1991 A randomized, double-blind, placebo-controlled trial of oral antibiotic
therapy following intravenous antibiotic therapy for postpartum endometritis.Obstetric and Gynecology 77:60-62)

4. The common pathogens in a particular geographical area should

be known, and their probable susceptability to the planned therapy
borne in mind.
e)

Surgery

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CASE ILLUSTRATIONS
FROM CEMD

Remediable factors were identified:

Failure to appreciate severity
Inadequate,inappropriate or delayed therapy
Failure to diagnose
Failure of adherence to protocol

Case 1 (Failure to appreciate severity)

38 year old grandmultip

Had C-Section for big baby
Complicated by PPH
Given ampicillin and metronidazole
Discharged on D5
Re-admitted 6 days later with septicaemia

Case 2 (Failure to diagnose)

25 year old G4P2A1

Uncomplicated home delivery
Fever on D2
Consulted GP on D4 symptomatic
treatment
Went to government clinic on D6
symptomatic treatment
Admitted on D8 with septicaemia

PREVENTION OF PUERPERAL SEPSIS

a) Basic principles
b) The case of emergency Caesarean section
i. Technical aspects of the operation

ii. Antiseptic washes and douches

iii.Prophylactic antibiotics

PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

RECOMMENDATIONS
The onset of life-threatening sepsis at any stage of
pregnancy can be insidious and all doctors and
midwives must be aware of the symptoms and signs and
be prepared to institute immediate treatment to avoid
serious consequences.

A patient with prolonged rupture of the membranes who

develops a fever and/or tachycardia should be carefully
assessed by senior staff.

PERSIDANGAN KEMATIAN IBU KEBANGSAAN ,PULAU PINANG 30-31 OKT.2007

 In patient with spontaneous rupture of the membranes

and not in labour, vaginal assessments should be
avoided or kept to a minimum and undertaken with
appropriately aseptic precautions.

There is clear evidence from controlled trials showing the

benefits of prophylactic antibiotics for emergency
caesarean section. (The CEMD Report confirms that that
this policy is still not universally employed).

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 In the seriously ill obstetric patient where sepsis may be

implicated, it is advised that intravenous antibiotic
treatment be commenced immediately.

Bacteriological specimens, including blood culture, must

be obtained prior to commencing such treatment but the
results of the cultures will not be available.

The most appropriate antibiotic treatment based on the

organism identified in this Report, would be recently
introduced penicillin derivative piperacillin / tazobactam
in combination with the aminoglycoside, netilmicin.

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 When

infection develops and the patient is

systematically ill, urgent and repeated bacteriological
specimens, including blood cultures, must be obtained.
Advice from a microbiologist must be sought at an early
stage to assist with the use of appropriate antibiotic
therapy.

There is some evidence in this Report of a failure to use

the most appropriate antibiotics as recommended in
hospital protocols.

In severe cases of sepsis, doctors should be prepared,

without delay, to give parenteral antibiotics before the
diagnosis is confirmed.

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THANK YOU

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