Review

OPEN

New Concept and Management for Sepsis in

Pregnancy and the Puerperium
Shang-Rong Fan1,2,∗, Ping Liu1, Shao-Mei Yan1, Lei Huang3, Xiao-Ping Liu4

Abstract
Sepsis, which is life-threatening organ dysfunction resulting from a dysregulated host response to infection, remains a major cause
for the admission of pregnant women to the intensive care unit and is one of the leading causes of maternal morbidity and mortality.
The obstetric causes include uterine infection, septic abortion, and wound infection. The non-obstetric causes include pyelonephritis
and pneumonia. Maternal sepsis may also be from obstetrical critical illness, such as obstetric severe hemorrhage, obstetric (amniotic
fluid/pulmonary) embolism, acute fatty liver of pregnancy, and congestive heart failure, cardiopulmonary arrest, and major trauma.
The most commonly reported pathogens in maternal sepsis include Escherichia coli, Streptococcus, Staphylococcus, and other
gram-negative bacteria. Maternal sepsis may cause intrauterine infection, which results in (1) preterm premature rupture of
Downloaded from http://journals.lww.com/mfm by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 06/15/2021

membranes or preterm labor or birth, (2) cerebral white matter damage or cerebral palsy or neurodevelopmental delay, (3) stillbirth, (4)
early- or late-onset sepsis, and (5) perinatal death. The “Hour-1 bundle” should be initiated within the first hour of the recognition of
sepsis. The use of early, appropriate antibiotics is crucial in the management of maternal sepsis. Fetal status should be monitored.
Appropriate and early source control should be provided. The decision for delivery is often quite complex and should be individualized
to each patient’s clinical scenario while taking into consideration the suspected source of infection, maternal status, fetal well-being,
and gestational age. Extracorporeal membrane oxygenation has been increasingly used in refractory sepsis during pregnancy and
the puerperium.
Keywords: Sepsis; Pregnancy; Puerperium; Maternal; Fetal; Morbidity; Mortality; Maternal near-miss

Introduction increased risk of sepsis compared to the antenatal period.3

Maternal sepsis is a life-threatening condition with organ
dysfunction resulting from infection during pregnancy,
childbirth, post-abortion, or in the postpartum period.1
The World Health Organization estimated that the global
prevalence of maternal sepsis is 4.4% among live births,
with an incidence of 9–49 per 100 000 deliveries in high-
income countries depending on the definition used and
population studied.1 The incidence of pregnancy-associat-
ed severe sepsis in the USA has increased by 236% over the
past decade, rising from 11 hospitalizations per 100 000
annual total estimated pregnancies in 2001–2002 to 26 in
2009–2010.2 Prospective studies in the UK have suggested
that labor and the puerperium may have a 2- to 3-fold
1
Department of Obstetrics and Gynecology, Peking University
Shenzhen Hospital, Shenzhen 518036, China; 2 Shenzhen Key
Laboratory on Technology for Early Diagnosis of Major Gynecological
Diseases, Shenzhen 518036, China; 3 Department of Critical Care
Medicine, Peking University Shenzhen Hospital, Shenzhen 518036,
China; 4 Department of Laboratory Science, Peking University
Shenzhen Hospital, Shenzhen 518036, China.
∗
Corresponding author: Prof. Shang-Rong Fan, Department of
Obstetrics and Gynecology, Peking University Shenzhen Hospital,
Shenzhen 518036, China. E-mail: fanshangrong@163.com
Copyright © 2020 The Chinese Medical Association, published by
Wolters Kluwer Health, Inc.
This is an open access article distributed under the terms of the
Creative Commons Attribution-Non Commercial-No Derivatives License
4.0 (CCBY-NC-ND), where it is permissible to download and share the
work provided it is properly cited. The work cannot be changed in any
way or used commercially without permission from the journal.
Maternal-Fetal Medicine (2020) 2:4
Received: 17 March 2020
http://dx.doi.org/10.1097/FM9.0000000000000058
Several studies from developed countries have shown that
the rate of maternal sepsis has been increasing in the last
decade, with high mortality rates.2–6
Maternal sepsis is the main cause of maternal death and
a major contributor to severe maternal morbidity
worldwide,5,7–24 accounting for 11% of maternal deaths
worldwide and is the third most common direct cause of
maternal death.20 Maternal sepsis is currently the third or
fourth leading cause of maternal mortality in the USA,
accounting for 13% of all maternal deaths with a cause-
specific maternal mortality ratio of 2.2 deaths per 100 000
live births5,6 In low- and middle-income countries, rates of
fatality after puerperal infection can be as high as 50%.1
Under new sepsis definitions,25 some representative
reports gave ranges on the mortality of sepsis in the
general population of 25%–30%. The mortality range for
septic shock was 40%–70%.26
Failure to recognize sepsis early is a significant cause of
preventable morbidity, resulting in delayed treatment and
escalated care, which are critical if lives are to be saved.27
There are only a few evidence-based and pregnancy-
specific guidelines for healthcare providers regarding how
to best treat, prevent and recognize the early warning signs
of peripartum sepsis.20,21 In this review, we aim to discuss
the new definitions regarding sepsis and recommended
diagnosis and management strategies of sepsis adapted to
pregnant and postpartum women.
Pathophysiology
The pathophysiology core issue is a multifaceted host
response to an infecting pathogen that may be significantly
amplified by endogenous factors. The “sepsis 1” and

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“sepsis 2” focused solely on inflammatory excess. Sepsis is

now recognized to involve early activation of both pro-
and anti-inflammatory responses, along with major
modifications in nonimmunologic pathways such as
cardiovascular, neuronal, autonomic, hormonal, bioen-
ergetic, metabolic, and coagulation, all of which have
prognostic significance. Patients with sepsis can have
clinical presentations in various systems, including
respiratory, cardiovascular, hepatic and gastrointestinal,
renal, hematological, endocrinological, and central ner-
vous systems.25 Maternal sepsis may cause intra-amniotic
infection, which results in (1) premature rupture of
membranes or preterm labor or birth; (2) cerebral white
matter damage or cerebral palsy or neurodevelopmental
delay; (3) stillbirth; (4) early- or late-onset sepsis; (5)
perinatal death.28–31Figure 1 shows the pathophysiology
and manifestation of sepsis. Figure 2 shows the micro-
scopic findings in the placenta of one 26 weeks pregnant
woman with septic shock and stillbirth caused by Listeria
monocytogenes infection.

Causes, risk factors, and microorganisms

Causes and risk factors
Changes in maternal immune responses occur during
pregnancy to protect the unborn fetus from rejection.
These changes may predispose pregnant patients to the
development of infections. Sepsis may be due to obstetric
or non-obstetric causes.32 The obstetric causes include
uterine infection, such as chorioamnionitis and endomyo-
metritis, septic abortion, and wound infection. Sepsis may
follow invasive procedures such as amniocentesis, chori-
onic villus sampling, cervical cerclage, or percutaneous
umbilical blood sampling. In a French study, the most
common source of bacteremia was chorioamnionitis
(47%).33 The non-obstetric causes of sepsis include
pyelonephritis and pneumonia.32
Maternal sepsis may also be from obstetrical critical
illness, such as obstetric severe hemorrhage,34 obstetric
(amniotic fluid/pulmonary) embolism, acute fatty liver of
pregnancy (AFLP),35 and congestive heart failure, cardio-
pulmonary arrest, major trauma, and 2019 coronavirus
disease infection.36–38 In an Indonesian study, 12 of 18
patients with AFLP died due to maternal sepsis, and AFLP Figure 1. Causes and major related organ system changes in patients
was the common direct cause of maternal death.39–41 with sepsis. Maternal sepsis can result from chorioamnionitis, endomyo-
metritis, pyelonephritis, or pneumonia, which cause multiple organ
Risk factors correlated with the development of sepsis dysfunction or failure such as respiratory, cardiovascular, hepatic and
during pregnancy are as follows. Obstetric-related risk gastrointestinal, renal, hematological, endocrinological, and central
factors: group A streptococcal infection in close contacts/ nervous system dysfunction or failure and adverse perinatal outcomes.
family members; a history of group B streptococcal
infection; the induction of labor; invasive procedures
such as amniocentesis and cervical cerclage, prolonged
rupture of membranes; instrumented or cesarean deliv- Microorganisms
ery; a lack of prenatal care; mastitis; preeclampsia;
postpartum hemorrhage; retained products of concep- The most commonly reported pathogens in maternal sepsis
tion; the use of antibiotics within 2 weeks of birth, include Escherichia coli, Streptococcus, Staphylococcus,
including prophylaxis for cesarean sections; and wound and other gram-negative bacteria.49–51Streptococcus type
hematoma. Patient-related risk factors: anemia; chronic A, although currently infrequent, may cause maternal
hypertension; diabetes mellitus; decreased function of the sepsis following abortion or labor and cause shock, with a
spleen; group A streptococcal infection in patients with mortality of 30%–60%.52–55 Group A streptococcal
close contact with individuals with a history of pelvic infections are invasive, and toxin production allows the
infection; immunosuppression; obesity; poverty; and organism to spread across tissue planes and cause necrosis
poor nutrition.42–48 while evading containment and abscess formation by the

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Figure 2. Microscopic findings in the placenta of one 26 weeks of gestation pregnant woman with septic shock and stillbirth caused by Listeria
monocytogenes infection. A The villi are distended and contain numerous acute inflammatory cells (acute villitis). B The villus was destroyed by the
inflammation, and fibrinogen (placental villous fibrinoid necrosis). C Umbilical phlebitis shows amniotropic migration of fetal neutrophils into the muscle
layer of the umbilical vein. D Umbilical arteritis is a stage 2 fetal inflammatory response. (HE staining, 100). HE: hematoxylin and eosin.

maternal immune system.53–57 Maternal sepsis caused by
Candida has been reported. Maternal Candida sepsis
could cause chorioamnionitis, stillborn birth, abortion,
preterm birth, and congenital Candida infection in
newborns.58–61 The reported rare microorganisms in
maternal sepsis include Clostridium innocuum, Clostridi-
um novyi, Plasmodium vivax, and Chlamydia psittaco-
sis.28,62–64Figure 3 shows the organisms isolated from
maternal blood cultures in sepsis during pregnancy and the
puerperium.3,33,49,51,65–72
Screening and diagnosis
To recognize maternal sepsis early, many early warning
scores have been developed. Bauer et al. studied screening
tools for sepsis in pregnant women.51 The sensitivity and
specificity of sepsis screening tools with the highest to lowest
sensitivity were systemic inflammatory response syndrome,
maternal early warning, and quick sequential organ failure
assessment (qSOFA) criteria, and the highest to lowest
specificity were qSOFA, maternal early warning, and
systemic inflammatory response syndrome. Foeller and
Gibbs proposed an obstetrically modified qSOFA.46
Currently, there are no ideal screening tools for sepsis in
pregnancy. Table 1 shows the common screening tools for
sepsis in pregnancy.25,46,73–76 The diagnosis of sepsis is
based on a sequential organ failure assessment (SOFA) score
of ≥2 with a suspicion of infection. In individuals with no
baseline disease, the initial SOFA score should be zero. The
higher SOFA score, the probability of mortality is more
increased. The present definition of sepsis emphasizes signs
of organ dysfunction rather than signs of infection. The
main diagnosis procedures include blood cultures and
cultures from any suspected source of infection, additional
laboratory tests, and imaging to confirm the suspected
anatomic site of infection.25,32Table 2 shows the SOFA
score criteria.77
The differential diagnoses include hypovolemic or
hemorrhagic shock, pulmonary embolism, myocardial
infarction, acute pancreatitis, diabetic ketoacidosis, pri-
mary adrenal insufficiency, and transfusion reaction.45
Management
The management includes initial respiratory and haemo-
dynamic stabilization, the initiation of empiric antimicro-
bial treatment with broad-spectrum agent therapy within
the first hour of diagnosis, source control within the first
12 hours if possible, and the prevention of complications
and sequelae.
The elements of the 2018 bundle, intended to be initiated
within the first hour, include blood cultures before anti-
biotics, lactate measurement, the administration of broad-
spectrum antibiotics, the administration of a 30 mL/kg
crystalloid fluid bolus in cases of hypotension or high serum
lactate levels of at least 4 mmol/L, and the administration of

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Figure 3. Organisms isolated from maternal blood cultures in sepsis during pregnancy and the puerperium. aIncluding: Clostridium perfringens 35 strains
and Clostridium sp. 5 strains. bIncluding: Klebsiella pneumoniae 31 strains and Klebsiella oxytoca 2 strains. cIncluding: Acinetobacter baumannii 19
strains, Acinetobacter Lwoffii 5 strains and Acinetobacter junii 1 strain. dIncluding: Enterobacter cloacae 17 strains and Enterobacter Species 3 strains.
e
Including: Bacteroides fragilis 5 strains, Bacteroides capillosus 1 strain, Bacteroides melaminogenicus 1 strain and Bacteroides sp. 13 strains. fIncluding:
Pseudomonas aeruginosa 5 strains, Pseudomonas fluorescens 2 strains, Pseudomonas alcaligenes 1 strains and Pseudomonas sp. 4 strains. gIncluding:
Morganella morganii 6 strains, Haemophilus influenzae 5 strains, Citrobacter freundii 3 strains, Citrobacter sp. 1 strain, Meningococcus 3 strains,
Moraxella sp.2 strains, Raoultella ornithinolytica 2 strains, Brucella sp.1 strain, Flavimonas oryzihabitans 1 strain, Fusobacterium necrophorum1 strain,
Gardnerella vaginalis 1 strain, Salmonella Enteritidis 1 strain, Veillonella sp. 1 strain and Other gram-negative bacteria 19 strains. hIncluding: Streptococcus
agalactiae 122 strains, Group A streptococcus 58 strains, b haemolytic streptococcus Lancefield group A 35 strains, Streptococcus pyogenes 23 strains,
Streptococcus Miller 9 strains, Streptococcus unspecified 8 strains, haemolytic streptococcus Lancefield group B 5 strains, Group C streptococcus 3
strains, Group G streptococcus 2 strains, Streptococcus salivarius 2 strains, Streptococcus oralis 1 strain, Streptococcus Gallolyticus 1 strain,
Streptococcus pyogenes (A) 1 strain, b haemolytic streptococcus Lancefield group C 1 strain, b haemolytic streptococcus Lancefield group D 1 strain and
Streptococcus sp. 23 strains. iIncluding: Staphylococcus aureus 123 strains, Staphylococcus epidermidis 11 strains, coagulase negative staphylococci 4
strains, Staphylococcus Saprophyticus 2 strains, Staphylococcus lugdunensis 1 strain and Staphylococcal sp. 35 strains. jIncluding: Enterococcus
faecalis 21 strains and Enterococcus spp. 17 strains. kIncluding: Tuberculosis 6 strains, Actinobacter 1 strain and other gram-positive bacteria sp.32
strains. lIncluding: human immunodeficiency virus 12 strains, H1N1 3 strains, Varicella 2 strains and Toxoplasma gondii 3 strains and Candida 1 strain.

vasopressors to maintain a mean arterial pressure of at least Antibiotics

65 mm Hg.78–80Figure 4 shows the main management of
sepsis during pregnancy and the puerperium.32 The early and appropriate use of antibiotics is crucial in the
management of maternal sepsis.81 Mortality is increased
by 7.6% with each hour delay in appropriate antibiotic
administration in the general population.82 The spectrum
might need to be broad, covering both gram-positive and
Table 1 gram-negative pathogens. Antibiotic coverage for mater-
Definitions of SIRS, qSOFA, and omqSOFA criteria. nal sepsis should be aimed at covering the most common
bacteria: E. coli, Staphylococcus, Streptococcus, and other
Tool Definition
gram-negative bacteria. Viral and fungal cover should be
SIRS ≥2 of the following: considered, if suspected. Combination therapy is preferred
(1) Temperature >38°C or <36°C; over monotherapy.
(2) HR >90 bpm Most often, a broad-spectrum carbapenem (eg, mer-
(3) RR >20 breaths/min or PaCO2 <32 mm Hg; openem, imipenem/cilastatin, or doripenem) or extended-
(4) WBC <4  109/L or >12  109/L range penicillin/b-lactamase inhibitor combination (eg,
qSOFA ≥2 of the following: piperacillin/tazobactam or ticarcillin/clavulanate) is used.
(1) RR ≥22 breaths/min; Several third- or higher-generation cephalosporins can
(2) SBP: 100 mm Hg; also be used, especially as part of a multidrug regimen.79
(3) Altered mentation The surviving sepsis campaign strongly recommends
omqSOFA ≥2 of the following: antibiotic stewardship in the de-escalation of antibiotics
(1) RR ≥25 breaths/min; tailored to specific microorganisms to prevent drug
(2) SBP 90 mm Hg; resistance. Optimal antibiotic duration remains conten-
(3) Altered mentation tious, and few prospective randomized controlled trials
HR: Heart rate; omqSOFA: Obstetrically modified quick sequential organ failure assessment; qSOFA:
have been performed. The surviving sepsis campaign
Quick sequential organ failure assessment; RR: Respiratory rate; SBP: Systolic blood pressure; SIRS: guidelines suggest 7–10 days.79 Procalcitonin levels can be
Systemic inflammatory response syndrome; WBC: White blood cell. used as a biomarker for the initiation, de-escalation, and

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Table 2
∗
Sequential (sepsis-related) organ failure assessment score.
Score
Organ system variables 0 1 2 3 4
Respiration
PaO2/FiO2, mm Hg (kPa) ≥400 (≥53.3) 300–<400 (40–<53.3) 200–<300 (26.7–<40) 100–<200 (13.3–< <100 (<13.3) with
26.7) with respiratory respiratory support
support
Coagulation
Platelets  103/mL ≥150 100–<150 50–<100 20–<50 <20
Liver
Bilirubin, mg/dL (mmol/L) <1.2 (<20) 1.2–1.9 (20–32) 2.0–5.9 (33–101) 6.0–11.9 (102–204) > 12.0 (>204)
Cardiovascular
MAP ≥70 mm Hg MAP <70 mm Hg Dopamine <5 or any dose Dopamine 5.1–15 or Dopamine >15 or
of dobutamine† epinephrine 0.1 or Epinephrine >0.1 or
norepinephrine 0.1† Norepinephrine >0.1†
Central nervous system
Glasgow coma scale score‡ 15 13–14 10-12 6–9 <6
Renal
Creatinine, mg/dL (mmol/L) <1.2 (<110) 1.2–1.9 (110–170) 2.0–3.4 (171–299) 3.5–4.9 (300–440) >5.0 (>440)
Urine output, mL/dL – – – 200–<500 <200
Sequential organ failure assessment (SOFA) score of ≥2 with a suspicion of infection. In individuals with no baseline disease, the initial SOFA score should be zero. The higher SOFA score, the probability of
mortality is more increased.
FiO2: Fraction of inspired oxygen; MAP: Mean arterial pressure; PaO2: Partial pressure of oxygen; –: Not applicable.
∗
Adapted from Vincent et al.77
†
Catecholamine doses are given as mg/kg/min for at least 1 hour.
‡
Glasgow Coma scale scores range from 3 to 15; higher score indicates better neurological function.

discontinuation of antimicrobial therapy.79,83–85 Schuetz 6-hour delay in achieving source control.32,75,79 If surgical
et al. found that the inability to decrease procalcitonin by intervention for source control, including cesarean section,
more than 80% is a significant independent predictor of is required, the decision about regional or general
mortality.86 When suspected, invasive group A streptococ- anesthesia should be made on a case-by-case basis. When
cal infections should be treated emergently with aggressive sepsis is diagnosed in the antepartum period, one
fluid resuscitation, antibiotic administration (penicillin and prospective case-control study of a national database in
clindamycin), and source control that may be extensive and the UK from 2011 to 2012 found the median gestational
may involve hysterectomy. Table 3 proposes broad- age to be 35 weeks (interquartile range 27–40 weeks) and
spectrum empiric antibiotic coverages in sepsis during the median diagnosis-to-delivery interval was 0 day
pregnancy and the puerperium.32,44,75,79,87–92 (interquartile range 0–36 days).49 Hysterectomy were
performed on 5.4% of severe sepsis cases.93
Source control
Extracorporeal membrane oxygenation (ECMO)
Once a source of sepsis is identified, source control is a
priority and may involve abscess drainage or the delivery As a treatment for respiratory failure in patients in the
of the fetus if the uterus is found to be the source of the intensive care unit, ECMO has been used increasingly during
infection. There is a direct increase in mortality with each pregnancy and the puerperium.94–96 Based on published

Figure 4. Management of sepsis during pregnancy and the puerperium. DVT: Deep venous thrombosis; FHR: Fetal heart rate; PCT: Procalcitonin.

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Table 3
Proposed broad-spectrum empiric antibiotic coverage in sepsis during pregnancy and the puerperium.
Source infection Recommended antibiotics
Community-acquired pneumonia Cefotaxime, ceftriaxone, ertapenem, or ampicillin plus azithromycin, clarithromycin, or erythromycin
Hospital-acquired pneumonia Patients at low-risk of mortality may be treated with piperacillin-tazobactam, meropenem, imipenem, or cefepime;
Patients at high risk of mortality may need double coverage for pseudomonas (beta-lactam plus an aminoglycoside
or a quinolone) and MRSA coverage with vancomycin or linezolid
∗
Chorioamnionitis Ampicillin plus gentamicin plus anaerobic coverage with clindamycin or metronidazole if cesarean delivery required
∗
Endomyometritis Ampicillin, gentamicin, and metronidazole (or clindamycin)
Alternatively may use cefotaxime or ceftriaxone plus metronidazole
∗
Urinary tract infections Gentamicin with ampicillin alternatively, may use monotherapy with a carbapenem or piperacillin-tazobactam
Abdominal infections Ceftriaxone, cefotaxime, ceftazidime, or cefepime plus metronidazole;
Complicated cases may require monotherapy with a carbapenem or piperacillin-tazobactam
Skin and soft tissues (necrotizing) Vancomycin + piperacillin-tazobactam or
Clostridium perfringens are present, use penicillin G plus clindamycin
Source not apparent
Community-acquired sepsis At low-risk of mortality: amoxicillin/clavulanic acid or cefotaxime + metronidazole or cefuroxime + gentamicin +
metronidazole
If the patient is allergic to penicillin and cephalosporins:
Severe hypersensitivity: clindamycin + gentamicin
Mild-moderate hypersensitivity: cefazolin + gentamicin + metronidazole
Severe hypersensitivity: ciprofloxacin + vancomycin
If there are risk factors for MRSA: add teicoplanin or linezolid or vancomycin
At risk of multidrug-resistant Gram-negative organisms: add meropenem
At risk of GAS sepsis: add clindamycin + consider normal immunoglobulin
Hospital-acquired sepsis Piperacillin/tazobactam + consider gentamicin if local epidemiology suggests Gram-negative aminoglycoside
∗
susceptibility
∗
Cefuroxime + gentamicin + metronidazole
At risk of MRSA sepsis add vancomycin
At risk of multidrug-resistant gram-negative organisms: meropenem
At risk of GAS sepsis: add clindamycin + consider normal immunoglobulin
If the patient is allergic to penicillin and cephalosporins; severe hypersensitivity: ciprofloxacin + vancomycin
GAS: Group A streptococcal; MRSA: Methicillin-resistant Staphylococcus aureus.
∗
Aminoglycoside including gentamicin was less used in China.

reports, overall maternal and fetal survival rate on ECMO
were 80% and 70%, respectively.97 ECMO may be a choice
for the treatment of refractory sepsis.
Fetal considerations
It is imperative to stabilize the mother first, and the fetal
status will also improve. The decision of whether to deliver
the fetus or to continue the pregnancy is influenced by a
number of factors, including the patient’s condition, the
gestational age of the foetus, the fetal condition, the
presence of chorioamnionitis and the stage of labor. In the
setting of antenatal sepsis, there should be frequent
assessment of fetal status after viability. Efforts should
be aimed at treating maternal sepsis and prolonging
pregnancies that are far from term if the source of infection
is outside the uterus. If the source of sepsis is from the
uterus, delivery of the fetus is required. If delivery is
imminent, then betamethasone should be administered if
gestational age is less than 34 weeks. A previable fetus
(<23 to 24 weeks, depending on institutional practice)
may not need fetal monitoring.32
Gaps and future directions
Seacrist et al.98 studied quality improvement opportunities
identified through a review of cases of maternal death from
sepsis and found several key deficiencies in the care of
women who died from sepsis. Quality improvement
opportunities were identified in the readiness, recognition,
response, and reporting domains of the 4R framework.
The single most common theme in their findings was
women’s lack of recognition of the signs and symptoms of
sepsis or of the risk for sepsis during the initial birth
hospitalization or postpartum period. Health-care facili-
ties and providers need to reduce barriers for women who
seek care, recognize early symptoms, and respond with
appropriate treatment. Many cases of maternal sepsis give
rise to litigation. The reasons for the litigations include
failure to recognize sepsis; failure to instigate appropriate
investigation; delayed treatment; incomplete treatment;
failure to consider urgent delivery; failure to isolate the
source of infection; failure to involve senior clinicians at an
early stage; failure to utilize a multidisciplinary team,
including anesthetists, intensivists, microbiologists, and
infectious disease specialists, at an early stage; delay in
recognizing failed treatment and instigating additional or
alternative antimicrobials; and failure to transfer to the
critical care setting.
It is important from both a clinical and research
viewpoint to remain up to date and understand the
change in terminology of sepsis. Further research into risk
factors for maternal sepsis is required to reduce the
incidence and to facilitate early identification and treat-

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ments. Interventions such as ECMO have gained increas-
ing support and require more studies to assess their role in
the management of maternal sepsis.
Conclusions and recommendations
Sepsis remains a major cause for the admission of pregnant
women to the intensive care unit and is a leading cause of
maternal morbidity and mortality. The causes of maternal
sepsis include obstetric and non-obstetric causes. Maternal
sepsis may also be from obstetrical critical illness. The
most commonly reported pathogens in maternal sepsis
include E. coli, Streptococcus, Staphylococcus, and other
gram-negative bacteria. The management of sepsis during
pregnancy should follow the same basic principles as that
in the nonpregnant population, including early recogni-
tion, fluid therapy, timely broad-spectrum antibiotics, and
source control.
Acknowledgment
Figure 1 was drawn by Shengmenart.
Funding
This research was supported by the Shenzhen Science and
Technology Innovation Commission (JCYJ201802281
62311024).
Conflicts of Interest
None.
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Edited By Dan-Dan Shi