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Best Practice & Research Clinical Obstetrics and Gynaecology xxx (2013) 110

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Best Practice & Research Clinical


Obstetrics and Gynaecology
journal homepage: www.elsevier.com/locate/bpobgyn

12

Puerperal sepsis
N. Arulkumaran, MRCP *, M. Singer, MD
Bloomsbury Institute of Intensive Care Medicine, University College London, Cruciform Building,
Gower Street, London WC1E 6BT, UK

Keywords:
Infections during pregnancy are relatively prevalent, and the ma-
sepsis jority of cases are managed well in the community. Occasionally,
intensive care however, infections may be life-threatening. Sepsis may be
resuscitation associated with multiple organ dysfunction and a high mortality.
The treatment of sepsis is time critical and requires early uid
resuscitation and antibiotics. Early involvement of other specialties
and allied health-care professionals to provide a multidisciplinary
approach to patient care is important. Continuous monitoring of
maternal vital signs and provision of supportive care for multiple
organ dysfunction are best done within the intensive care unit.
Despite advances in patient care, the mortality rate associated with
maternal sepsis remains high. Health-care services in low-income
countries face particular problems that account for an increased
incidence of puerperal sepsis and maternal mortality. These
include lack of access to health care, septic abortions and a greater
incidence of human immunodeciency virus. The key to man-
agement of sepsis is early recognition, aggressive resuscitation,
antibiotic administration and source control.
2013 Elsevier Ltd. All rights reserved.

Introduction

Over ve million new cases per year of maternal sepsis occur globally with an estimated 62,000
maternal deaths resulting [1]. In high-income countries, the incidence of sepsis-related maternal
morbidity is reported to be 0.10.6 per 1000 deliveries and accounts for 2.1% of all maternal deaths.
However, in low-income countries, sepsis-related mortality rate is signicantly higher and accounts for
up to 11.6% of maternal deaths [2]. Although the incidence of maternal sepsis is relatively low compared

* Corresponding author. Tel.: 44 7876707350.


E-mail address: nish_arul@yahoo.com (N. Arulkumaran).

1521-6934/$ see front matter 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.bpobgyn.2013.07.004

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to other obstetric emergencies, the relative risk of mortality is signicant. The mortality rate associated
with maternal sepsis approaches 10% in developed countries [3,4]. There has been an increase in deaths
related to genital tract sepsis, despite a decline in the overall UK maternal mortality rate. This is related
primarily to community-acquired Group A streptococcal disease. Sepsis is now the most common
cause of direct maternal death in the UK, with an increase in the maternal mortality rate from 0.85
deaths per 100,000 maternities in 200305 to 1.13 deaths in 200608 [5]. A similar rise in the rates of
maternal sepsis has been described in a recent large study in Maryland, USA [6]. Maternal deaths
relating to sepsis are often associated with failure to recognise the severity of illness [5].
In low-income countries, the mortality related to puerperal sepsis is approximately 33% [7,8].
Deaths due to sepsis are 22.7-fold higher in Africa, Asia, Latin America and the Caribbean than in
developed countries [2]. The long-term morbidity associated with maternal sepsis is signicant and
includes chronic pelvic inammatory disease, chronic pelvic pain, bilateral tubal occlusion and infer-
tility. The impact on neonatal mortality is also signicant, with over one million infection-related
neonatal deaths every year [9].
Sepsis, as dened by the International Surviving Sepsis Campaign, is the presence of infection
(either suspected or proven) along with features of systemic inammation [10]. These features are
characterised by criteria dening the systemic inammatory response syndrome (SIRS) [11]. However,
many physiological changes associated with pregnancy, such as tachycardia and hypotension (Chapter
1), overlap with sepsis. Cut-off values for cardiorespiratory variables, including blood pressure and
respiratory rate, for the denition of sepsis may not be directly applicable in the parturient. Never-
theless, any physiological value more than two standard deviations from the expected should be
considered pathological. Sepsis-induced hypotension is dened as a systolic blood pressure (SBP)
<90 mmHg or mean arterial pressure (MAP) <70 mmHg or a SBP decrease >40 mmHg or more than
two standard deviations below normal for age in the absence of other causes of hypotension. Septic
shock is dened as sepsis-induced hypotension persisting despite adequate uid resuscitation. When
accompanied by signs of infection-induced hypotension, organ dysfunction or tissue hypoperfusion
(e.g., lactataemia or oliguria), severe sepsis is said to have occurred.
While the SIRS criteria are a sensitive but nonspecic criteria of generalised inammation, they are
an oversimplication of the physiological changes associated with sepsis. As such, criteria for the
systemic manifestations of infection have been elaborated further (Table 1). It must be emphasised that
these diagnostic criteria do not specically address maternal sepsis.

Table 1
Diagnostic criteria for sepsis [10].

Variable Infection (documented or suspected) and some of the following:


General Fever (>38.3  C) or hypothermia (core temperature <36  C)
Heart rate >90 beats/min
Tachypnea
Altered mental status
Signicant oedema or positive uid balance (>20 ml/kg over 24 hrs)
Hyperglycaemia (plasma glucose >7.7 mmol/L) in the absence of diabetes
Inammatory Leukocytosis (WBC count >12,000/ml)
Leukopenia (WBC <4000/mL)
Normal WBC count with greater than 10% immature forms
Plasma C-reactive protein >2 SD above the normal value
Plasma procalcitonin >2 SD above the normal value
Haemodynamic Arterial hypotension (SBP <90 mmHg, MAP <70 mmHg, or an SBP decrease >40 mmHg in adults
or more than 2 SD below normal for age
Organ Arterial hypoxaemia (PaO2/FIO2 < 300)
dysfunction Acute oliguria (urine output <0.5 mL/kg/hr for at least 2 hrs despite adequate uid resuscitation)
Creatinine rise >0.5 mg/dL or 44.2micromol/L
Coagulation abnormalities (INR >1.5 or aPTT >60 s)
Ileus (absent bowel sounds)
Thrombocytopenia (platelet count <100,000/mL)
Hyperbilirubinaemia (plasma total bilirubin > 4 mg/dl or 70 mmol/L)
Tissue Hyperlactaemia >1 mmol/L
hypoperfusion Decreased capillary rell or mottling

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Aetiology and presentation

Infectious complications in pregnancy may be divided into the following:

1. Pregnancy-related infection

The causes of maternal sepsis vary in relation to the stage of pregnancy [5]. Sepsis in early preg-
nancy may be associated with a miscarriage or follow a termination of pregnancy. In the second or third
trimester, pre-labour rupture of membranes (PROM) is associated with an increased risk of cho-
rioamnionitis. Perineal infections, endometritis, wound infections and mastitis should be considered in
the post-delivery period.

2. Non-pregnancy-related infection

Most women of childbearing age are healthy with no chronic co-morbidity. However, a small
proportion have predisposing factors, including human immunodeciency virus (HIV), co-morbid
illness (e.g., cystic brosis), or may be on medications (e.g., steroids or other immunosuppressants)
that may predispose to infection.

3. Nosocomial infection

Prolonged hospital stay, indwelling lines or catheters and overcrowding may predispose to
hospital-acquired infections.
Fever, diarrhoea, vomiting, abdominal pain, generalised maculopapular rash (staphylococcal or
streptococcal sepsis), offensive vaginal discharge and visible evidence of infection in caesarean wounds
are the common symptoms of puerperal sepsis [5].
In severe cases of puerperal pyrexia, group A beta-haemolytic streptococcus (Streptococcus pyo-
genes, GAS) should be suspected. This organism has been the leading infective cause of puerperal
deaths and has an attributable mortality greater than other invasive bacteria [12]. Streptococcal throat
infections are relatively common in the community, particularly among young children. Up to 30% of
the population are carriers of GAS and are easily able to transmit the bacteria via a droplet spread.
Precautions against hand to genital tract transmission should be taken, including hand washing before
and after using the lavatory and changing sanitary towels. This is particularly important when the
mother has had a recent close contact with someone with a sore throat or upper respiratory tract
infection [5]. GAS causes a wide spectrum of illness ranging from bacteraemia without a focus of
infection (46%) to endometritis (28%) and peritonitis (8%). Invasive GAS is associated with necrotising
fasciitis (3%) and toxic shock syndrome (3%) [13]. Though less common than other clinical manifes-
tations of GAS, invasive GAS is associated with a mortality of 3.514.3% [3,13] and is the leading cause of
sepsis-related deaths in the UK [5].
The single most important risk factor for post-partum infection is caesarean section [14]. Retained
products of conception may also become embedded, confounded by poor wound healing due to tissue
oedema, resulting in endometritis. Endometritis is most commonly associated with GAS infection,
though Staphylococcus, coliforms and anaerobes may also be implicated. Patients often present with
uterine tenderness, abdominal pain, purulent foul-smelling lochia and features of systemic infection.
Cervical and high vaginal swabs must be obtained for culture. The rate of endometritis is approximately
threefold higher in non-elective caesarean sections compared to elective sections (28.6% vs. 9.2%,
respectively). Similarly, the risk of major puerperal infection is threefold higher in a low-risk planned
caesarean delivery compared to a planned vaginal delivery at term [15]. The use of prophylactic an-
tibiotics prior to section is associated with a signicant reduction in the rates of post-partum fever,
wound infection and endometritis [16].
Ascending bacterial colonisation of the genital tract may result in uterine contractions and/or
membrane weakening that in turn results in pre-term pre-labour rupture of membranes (PPROM). This
may result in chorioamnionitis, which typically presents with abdominal tenderness and fever

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following PPROM. The use of prophylactic antibiotics is associated with prolongation of pregnancy,
fewer neonatal infections and a reduction in rates of chorioamnionitis [17]. There are concerns
regarding the use of co-amoxiclav and its association with a relative increase in the risk of neonatal
necrotising enterocolitis. It is therefore recommended that a 10-day course of erythromycin is
administered following PPROM. If group B streptococcus is isolated, penicillin should be administered
(or clindamycin to women who are allergic to penicillin) [18]. A long-term follow-up of children
demonstrates that the use of maternal antibiotics is not associated with adverse outcomes [17].
Prolonged use of antibiotics for PPROM may result in antibiotic resistance among commensal mi-
croorganisms, particularly group B streptococci [19]. The selective use of antibiotics in patients with
evidence of sub-clinical infection based on amniotic uid sampling has been argued. However, not all
centres may have the facilities to perform this, and there is no compelling evidence to start antibiotics
guided by amniocentesis [20].
Other risk factors for maternal sepsis include maternal anaemia, obesity, poor nutrition, induced
labour, prolonged labour (>12 hr) and frequent (>5) vaginal examination [21,22].

Management

The Surviving Sepsis Campaign recommends protocolised care bundles in the management of
severe sepsis and septic shock [10]. The protocolised care of patients with severe sepsis and septic
shock is associated with a signicant decrease in mortality [23]; however, it is unclear whether this is
directly related to the protocol per se or simply due to earlier recognition and intervention. The
management of the patient is divided into the initial resuscitation phase, antimicrobial therapy
(including obtaining blood cultures and source control) and subsequent supportive therapies. How-
ever, it must be emphasised that these management guidelines do not specically address maternal
sepsis. The emphasis of these guidelines should be on the institution of early aggressive treatment and
a multidisciplinary approach.

Resuscitation

The principle is to promptly restore adequate organ perfusion with uid resuscitation and, if needed,
drug support. One strategy currently being promoted is that of early goal-directed therapy (EGDT),
whereby a central venous oxygen saturation value >70% is targeted in addition to the standard cardio-
vascular markers such as blood pressure and urine output. This is based upon a single open, randomised
emergency room study performed in Detroit, where signicant mortality benet was seen when this
approach was applied in the rst 6 h after presentation [24]. Fluid loading and, in some cases, dobut-
amine and blood transfusion were given to reach the predened haemodynamic goals. The validity and
generalisability of this approach is currently being tested in three multicentre studies in Australasia, the
USA and the UK. As mentioned above, the applicability of EGDT to the pregnant patient is also uncertain.
A similar approach is likely to be less effective once organ dysfunction is established [25].
Tissue hypoxia may develop due to low blood ow and/or perfusion pressure. Fluid resuscitation
should be initiated promptly in patients with haemodynamic instability or evidence suggestive of tissue
hypoperfusion, such as an elevated lactate, to achieve an adequate oxygen delivery. Controversy rages as
to the best type of uid (colloid vs. crystalloid, type of colloid (e.g., albumin vs. gelatin vs. starch),
balanced vs. unbalanced solutions, the optimal lling target, etc.). The literature is not particularly clear
other than an excessive amount of starch-based solutions should be avoided as this has been associated
with increased rates of acute kidney injury and, in some cases, higher mortality rates [26].
Consensus guidelines, based on a limited-existent evidence base, recommend targeting a mean
arterial pressure of >65 mmHg [9]. Whether this applies to young, pregnant women who, in health, are
often completely asymptomatic at lower blood pressures is questionable. A reasonable compromise is
to achieve a blood pressure compatible with adequate organ perfusion, as manifested by normal
conscious level, good urine output, normal lactate level, etc. Foetal well-being also needs to be
conrmed. Early delivery, if appropriate, may be indicated.
In critically ill patients, lactate is used as a surrogate marker of inadequate tissue oxygenation.
Though this is not strictly accurate, a good relationship is nevertheless seen between the degree of

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hyperlactaemia and mortality [27,28]. Lactate has therefore been promoted as a target in the goal-
directed therapy for early sepsis. An EGDT guided by early lactate clearance (within the rst 6 h
after sepsis presentation) was associated with a reduction in 60-day mortality [29,30]. As serum lactate
does not change signicantly in pregnancy, this is likely to be a reasonable guide to resuscitation.
The assessment of adequate uid loading is more problematic in pregnant patients. The physio-
logical effects of pregnancy, especially in the third trimester, including alterations in circulating blood
volume, cardiac output, oxygen consumption, haemoglobin, vascular compliance, blood pressure and
venous compression, form the gravid uterus. In severe sepsis/septic shock, there is a decreased vascular
tone and decreased responsiveness to exogenous catecholamines, increased capillary leak and a high
incidence of myocardial depression. Thus, a critically ill pregnant patient warrants close haemody-
namic monitoring, preferably with a reliable measure of cardiac output, to titrate uid and drugs more
precisely. Arbitrary target values of central venous pressure (CVP), for example, recommended by the
Surviving Sepsis Campaign guidelines as 812 mmHg in non-ventilated patients and >12 mmHg in
mechanically ventilated patients, may not be applicable in the pregnant patient. A poor correlation
between CVP values and uid responsiveness is well recognised [31].
Fluid resuscitation should be titrated to achieve an adequate tissue perfusion. It is not possible to be
prescriptive about the precise amount of uid that should be administered. The volume of uid required
to achieve haemodynamic stability may vary signicantly between patients. However, if the patient
remains haemodynamically unstable or there is evidence of persistent organ hypoperfusion despite 20
30 ml kg1 of intravenous uid, a vasoactive therapy may be required. In such circumstances, haemo-
dynamic monitoring may be useful to assess the patients response (in stroke volume) to a uid challenge
(functional haemodynamic monitoring). A cumulative positive uid balance over days is associated with
a worse outcome in sepsis [32], and therefore over-zealous uid resuscitation should also be avoided.
Resuscitation should aim to achieve adequate global oxygen delivery. Oxygen delivery (DO2) depends
on the haemoglobin concentration (Hb), arterial oxygen saturation (SaO2) and cardiac output (CO):

DO2 ml=min COL=min  Hbg=dL  SaO2 %  1:34


The central venous saturation (ScvO2), measured in blood drawn from the internal jugular vein or
right atrium, reects the balance of oxygen supply and demand. With a normal arterial saturation (97
100%), the normal ScvO2 is 7075%. Values below this range suggest an ongoing tissue hypoperfusion;
however, levels may be normal or even elevated in established sepsis due to failure of cellular oxygen
utilisation (mitochondrial dysfunction) and, possibly, microvascular shunting. An elevated SvO2 is
associated with an increase in mortality [33].

Antimicrobial therapy and source control

Appropriate antibiotic therapy should also be initiated promptly for the treatment of sepsis, as it is
more likely to be effective when given early rather than late. Maternal sepsis is commonly associated
with polymicrobial infections, reecting colonisation of the genital tract [4,14]. There is considerable
uncertainty as to whether a single or a combination therapy is better, but empiric therapy should
certainly aim to cover the likely infecting organism. Appropriate samples should be taken for culture
(e.g., blood, mid-stream urine, high vaginal swab) before starting antibiotics, but these should not
unnecessarily delay the commencement of antibiotics. In cases of suspected or proven infection with
GAS, broad-spectrum antibiotics that have good tissue penetration should be administered promptly. A
combination of clindamycin and a piperacillin bactam offers a broad-spectrum cover with bactericidal
activity. The prevalence of resistant organisms, including methicillin-resistant Staphylococcal aureus
(MRSA) and resistant Gram-negative bacteria (extended spectrum beta-lactamases (ESBL)), is
increasing [5]. Following GAS, ESBL now accounts for the majority of sepsis-related maternal deaths in
the UK. Failure to respond to conventional antibiotic treatment should raise the suspicion of resistant
organisms. The choice of antibiotics will depend on local resistance patterns and the mothers own
previous microbiological pattern. Local microbiology expertise should be sought.
Source control refers to the denitive management of a focus of infection amenable to surgical
drainage or debridement. In the post-partum patient, this should include consideration of evacuation

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of retained products of conception that may have become infected, or laparotomy, if uterine or bowel
injury is a possibility. Spontaneous miscarriage may result in ascending infection and intrauterine
sepsis. In such circumstances, an abortion may be required to save the mothers life. Such procedures
should be undertaken promptly after haemodynamic stabilisation and commencing antibiotics.

Adjunctive therapy

This has been a highly disappointing area as multiple drugs and interventional strategies have been
tested and all have failed to show outcome benet in large randomised controlled trials. These range
from various immunomodulatory agents, either specic (such as monoclonal antibodies directed
against a pro-inammatory cytokine, such as tumour necrosis factor (TNF) or interleukin 1 (IL-1)),
semi-specic (such as activated protein C) or general (such as corticosteroids), to extracorporeal
techniques such as plasmapheresis (that non-specically removes evil humours) or polymyxin B
absorption columns (that bind and remove endotoxin). Intravenous immunoglobulin (IVIg) should be
considered in suspected streptococcal or staphylococcal severe infections that are resistant to antibi-
otic therapy [34]. IVIg exerts immunomodulatory effects and is able to bind to and neutralise endotoxin
[35] and has been used successfully in the peripartum period. However, large randomised controlled
trial data on the benets of IVIg in sepsis are lacking.
These repeated failures highlight the major complexities presented by sepsis where multiple
pathways are simultaneously affected and where marked uctuations occur over time. It is becoming
increasingly apparent that many of the biological and physiological alterations previously viewed as
pathological may actually be adaptive and protective and that our well-meaning but misguided at-
tempts to normalise or over-correct the perceived abnormality may actually be injurious. Likewise, the
host response to infection is highly variable both between individuals as well as over time. An
appropriately dosed intervention at one time point may thus cause harm when given earlier or later in
the disease process. Similarly, the assumption that sepsis simply represents a pro-inammatory state
has also been laid bare. Many patients, even on admission to intensive care, are in a state of immu-
nosuppression [36]. Thus, the addition of an immunosuppressive therapy may further compromise the
host response, increasing the risk of secondary infection and a poor outcome. Some small studies have
shown that immunostimulatory therapies may be benecial in the right patient subset [37]. A per-
sonalised medicine approach where patients can be individually targeted by relevant biomarkers to
receive appropriate therapies given at optimal dose and duration will lead to better patient selection
and, hopefully, improved outcomes.

General therapy

The patient is supported through their acute septic condition until the organs recover sufcient
function to cope independently. However, it is important to stress that most of the major outcome
benets in critically ill patients over the last few decades have been achieved by being less interven-
tional. Thus, there may be a requirement for ventilator and renal support and for vasoactive drugs to
maintain an adequate circulation, for nutrition and strict infection control, venous thromboprophylaxis,
etc. Yet excessive sedation, over-ventilation, excess feed, excess blood transfusion and excess cate-
cholamine administration, to name but some routine procedures, are all associated with worse out-
comes. A balance needs to be struck between keeping the patient alive and well perfused but not
overdoing the intervention. As a consequence, lower transfusion targets are tolerated (e.g., 79 g dl1)
[38] and hyperglycaemia [39,40] (though not excessively strict glucose control) avoided. Physiological
alterations in glucose tolerance and haemoglobin levels may complicate matters in the pregnant patient.

Global initiatives

Prevention and early diagnosis

In under-resourced countries, the prevention of puerperal infection is a priority. It is crucial to


ensure that health-care practices are tailored to low-resource situations for adaptation to the local

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setting. In developing countries, many women still deliver at home. Traditional birth attendants may
not be aware of the need for infection prevention measures. Organisational change at the national level
is required for the provision of good delivery by health professionals.
The increasing institutional delivery rates in under-resourced settings may contribute to the
occurrence of puerperal sepsis due to a strain on existing health-care resources and the delivery of
suboptimal care. Overcrowding and low staffpatient ratios are more likely to result in the trans-
mission of infectious diseases between patients, as infective organisms are often introduced when the
birth attendant conducts invasive procedures, such as vaginal examination. In addition to the provision
of adequately trained birthing staff and resource allocation, implementing infection prevention and
appropriate processing of instruments, gloves and other items may reduce the rates of puerperal sepsis
(Infection Prevention Guidelines for Healthcare Facilities with Limited Resources). [41] For instance, a
simple measure such as using chlorhexidine vaginal wipes prior to examination may reduce the risk of
developing sepsis. [42,43]

Septic abortions

Each year 42 million abortions are estimated to take place worldwide, almost half of which are
carried out unsafely. [44] Unsafe abortion accounts for 70,000 maternal deaths each year and causes a
further ve million women to suffer complications, including severe sepsis [45]. In 2003, more than
97% of all unsafe abortions took place in developing countries [44].
The proportion of all abortions that are unsafe has increased over the past few years. Restrictive
abortion laws are not associated with lower abortion rates, and maternal mortality due to complica-
tions of unsafe abortion is higher in regions with restricted abortion laws than in regions with no or
few restrictions on access to safe and legal abortion [46]. Global initiatives are therefore required to
make contraceptives and emergency contraception accessible, making abortion a safe procedure and
by providing postabortion contraception [47].

Early access to health care

The cornerstone of sepsis management is timely resuscitation, antibiotic administration and source
control [10]. Successful management of sepsis is thus dependent on time-critical interventions. The
overall maternal mortality rate is signicantly higher in under-resourced countries compared to
developed countries (3.3% vs. 14%, respectively) despite similar rates of ICU admission and the prole of
obstetric patients admitted to ICUs [48]. One of the key factors associated with poor outcomes in
developing countries is the lack of access to an ICU within 24 h of illness [49]. This is supported by higher
illness severity scores among patients admitted to ICUs from under-resourced countries [48]. It is likely
that the majority of maternal deaths in under-resourced countries do not receive any ICU services [50].

HIV and AIDS

An estimated 20 million women have HIV, and more than two million pregnancies occur in HIV-
positive women each year [51]. The maternal mortality ratio in HIV-infected women is approxi-
mately 10-fold higher than healthy women and is a particular problem in resource-poor settings,
where women have no access to anti-retroviral treatment [52]. In HIV-prevalent regions, HIV-related
illness is a relatively common cause of death compared to direct obstetric causes such as hypertension
and pregnancy-related sepsis [52,53]. Maternal deaths among HIV-positive women relate to non-
pregnancy-related infectious diseases, including AIDS, pneumonia, tuberculosis and meningitis. Suc-
cessful strategies to reduce mother-to-child transmission of HIV, appropriate care for pregnant women
and the prevention of new infections in the population are required.

Conclusion

Most women of childbearing age are healthy with no chronic co-morbidity. However, in a small
proportion of women, severe and sometimes life-threatening complications do occur. Due to

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physiological changes in pregnancy, early sepsis may be easily missed. A high index of suspicion must
be held particularly in the presence of risk factors. Early resuscitation and antibiotic administration
form the cornerstone of management. Prophylactic antibiotics should be considered in surgical de-
liveries, particularly with non-elective caesarean sections. There remains signicant discrepancy be-
tween the mortality rates in developed and resource-poor countries. Context-specic and culturally
appropriate strategies to decrease maternal mortality and morbidity need to be instituted at a national
and international level.

Practice points

1. Early recognition of sepsis and uid resuscitation.


2. Obtain cultures, administer antibiotics early and undertake source control where appropriate.
3. The use of prophylactic antibiotics prior to caesarean sections should be considered as it is
associated with a signicant reduction in the rates of post-partum fever, wound infections
and endometritis.
4. In HIV-positive patients presenting with sepsis, non-pregnancy-related infectious diseases,
including AIDS, pneumonia, tuberculosis and meningitis, should be considered.

Research agenda

1. Development for guidelines for sepsis management specic to the parturient.


2. The use of prophylactic antibiotics in preventing puerperal sepsis following PROM is less well
established.
3. Educating traditional birth attendants regarding infection prevention measures including
limiting vaginal examinations where possible and hand washing before and after examina-
tion of the patient.
4. Organisational change at the national level to implement simple cost-effective measures to
prevent sepsis, including chlorhexidine vaginal wipes prior to examination.
5. Promoting simple and cost-effective measures to prevent puerperal sepsis in resource-poor
countries.

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