Postpartum endometritis

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©2024 UpToDate®

Postpartum endometritis
Author: Katherine T Chen, MD, MPH
Section Editor: Vincenzo Berghella, MD
Deputy Editor: Vanessa A Barss, MD, FACOG

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2024. | This topic last updated: Feb 20, 2024.

INTRODUCTION

Postpartum (puerperal) endometritis refers to a postpartum infection of the decidua (ie,

pregnancy endometrium) that can affect all layers of the uterus. It is a common cause of
postpartum fever and uterine tenderness and 10- to 30-fold more common after cesarean
than vaginal birth. Most infections are mild and resolve with antibiotic therapy; however, in
a minority of patients, the infection extends into the peritoneal cavity potentially resulting
in peritonitis, intraabdominal abscess, or sepsis. Rare patients develop necrotizing
myometritis, necrotizing fasciitis of the abdominal wall, septic pelvic thrombophlebitis, or
toxic shock syndrome.

Endometritis after a vaginal or cesarean birth will be discussed here. Endometritis in

patients who have had a pregnancy termination or spontaneous pregnancy loss and those
who have not been recently pregnant is reviewed separately. (See "Overview of pregnancy
termination", section on 'Infection/retained products of conception' and "Retained
products of conception in the first half of pregnancy", section on 'Medically stable patients
with endometritis' and "Endometritis unrelated to pregnancy".)

MICROBIOLOGY

Postpartum endometritis is typically a polymicrobial infection involving a mixture of two to

three aerobes and anaerobes from the lower genital tract. Microbiology is similar to that of
chorioamnionitis [1]. In a study of 55 antibiotic-naive patients with well-defined

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postpartum endometritis who had endometrial cultures obtained with a triple-lumen

catheter (to reduce the risk of contamination from organisms on the cervix), 51 (93
percent) had an endometrial isolate and seven (13 percent) had a blood isolate [2].
Bacterial findings included:
● At least one facultative or one anaerobic bacterial species – 42 of 51 (82 percent).
● Genital mycoplasmas – 39 of 51 (76 percent).
● A polymicrobial infection consisting of at least two facultative bacteria, anaerobic
bacteria, or both – 35 of 51 (69 percent).
● A combination of at least two bacteria and genital mycoplasmas – 26 of 51 (51
percent).
● Bacteremia in 38 percent of those with endometrial cultures positive for bacteria and
in none of those with negative bacterial endometrial cultures.

Aerobes include groups A and B streptococci, Staphylococcus, Klebsiella, Proteus,

Enterobacter, Enterococcus, and Escherichia coli. Anaerobes include Peptostreptococcus,
Peptococcus, Bacteroides, Fusobacterium, Prevotella, and Clostridium [3,4]. In patients
infected with HIV, the microbiology can be broader and include other less likely pathogens,
such as herpes simplex virus and cytomegalovirus [5].

Rare, but potentially lethal, causes of endometritis include Clostridium sordellii [6-9],
Clostridium perfringens [10], and streptococcal or staphylococcal toxic shock syndrome
[11-13]. (See 'Endometritis with toxic shock syndrome' below.)

RISK FACTORS

● Cesarean birth – Cesarean birth is the dominant risk factor for development of
postpartum endometritis, especially when performed after the onset of labor [14-16].
Among patients who receive antibiotic prophylaxis, which has become standard
practice, the frequency of postpartum endometritis is approximately 7.0 percent for
cesareans performed after the onset of labor and 1.5 percent for those that are
scheduled (by comparison, the frequencies in the absence of antibiotic prophylaxis
are approximately 18.4 and 3.9 percent, respectively) [17].

The frequency of postpartum endometritis after a vaginal birth is much lower than
after a cesarean birth, ranging from 0.2 to 2.0 percent [15,18,19]. Because of the low
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rate, antibiotic prophylaxis is not standard practice for patients in labor expecting to
give birth vaginally.
● Other – Other risk factors for postpartum endometritis include [19-32]:

• Chorioamnionitis
• Prolonged labor
• Prolonged rupture of membranes
• Multiple cervical examinations
• Internal fetal or uterine monitoring
• Large amount of meconium in amniotic fluid
• Manual removal of the placenta
• Low socioeconomic status
• Maternal diabetes mellitus or severe anemia
• Preterm or postterm birth
• Operative vaginal birth
• Obesity
• HIV infection
• Colonization with group B Streptococcus (see "Group B streptococcal infection in
pregnant individuals", section on 'Endometritis')
• Nasal carriage of Staphylococcus aureus
• Heavy vaginal colonization by E. coli

PATHOGENESIS

During labor and birth, the endogenous cervicovaginal flora migrate into the uterine
cavity, thereby contaminating its normally sterile contents [31,33]. The development of
infection versus colonization is thought to be related to a complex interaction among local
factors (eg, presence of devitalized or otherwise damaged tissue, foreign bodies), host
defense mechanisms, the size of the bacterial inoculum, and the virulence of the bacteria
involved [1].

The role of mycoplasmas in the pathogenesis of endometritis is unclear. Mycoplasmas are

often isolated from the endometrial cavity; however, antibiotic therapy is not usually
required for clinical cure in patients who have Ureaplasma urealyticum only, without
additional organisms, which suggests no pathogenic role [34-36].

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It is likely that several of the risk factors discussed above facilitate the development of
infection. For example, the size of the inoculum is influenced by the length of time in labor,
the duration of ruptured membranes, and the number of vaginal examinations and
invasive procedures. The potential for infection is enhanced 10- to 30-fold in cesarean
compared with vaginal births because of the presence of foreign bodies (eg, suture
material), myometrial injury and necrosis at the suture line, and formation of hematomas
and seromas [3].

CLINICAL FINDINGS

Signs and symptoms — In most patients with postpartum endometritis, the key clinical
findings are:
● Fever
● Uterine tenderness
● Tachycardia that parallels the rise in temperature
● Midline lower abdominal pain

The uterus may be slightly soft (subinvoluted), which can lead to excessive uterine
bleeding. Additional findings observed in some patients include malodorous purulent
lochia, headache, chills, malaise, and/or anorexia.

The time of onset of signs and symptoms depends on several factors, including whether
intrauterine infection developed antepartum, intrapartum, or postpartum and the
bacterium or bacteria causing the infection [30]. For example, group A Streptococcus
infection should be suspected in patients with an early-onset postpartum infection and
high fever. (See "Pregnancy-related group A streptococcal infection".)

Alarm findings (sepsis) — In febrile postpartum patients, the following criteria should
raise suspicion of severe infection/sepsis, based on expert opinion:
● Fever ≥103°F (39.4°C) or
● Fever ≥102°F (38.9°C) plus one or more of the following:

• Heart rate ≥110 beats/minute, sustained for at least 30 minutes

• Respiratory rate ≥20 respirations/minute, sustained for at least 30 minutes
• Manual white blood cell (WBC) differential showing ≥10 percent bands
• Blood pressure ≤90/60 mmHg, sustained for at least 30 minutes (in the setting of
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infection, septic shock can be diagnosed if mean arterial pressure is <65 mmHg
after 30 mL/kg fluid load)

An elevated lactic acid concentration (>2 mmol/L) is also a marker for serious infection.
(See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation,
diagnosis, and prognosis" and "Evaluation and management of suspected sepsis and
septic shock in adults".)

Note: In severely ill postpartum patients (eg, those with tachycardia, tachypnea,
hypotension out of proportion to the clinical scenario, oliguria, change in mental status),
sepsis should still be considered even if they are afebrile. In a study of maternal deaths in
Michigan, 3 of the 11 postpartum patients who died of sepsis had no fever during their
hospitalization [37].

Identification of patients at risk for sepsis — Medical society guidelines emphasize that
early identification of infected patients who may go on to develop sepsis is important to
decrease sepsis-associated mortality.
● The California Maternal Quality Care Collaborative (CMQCC) created a toolkit for
improving diagnosis and treatment of maternal sepsis, which is available online.
● The UK Obstetric Surveillance System (UKOSS) sepsis screening tool is also available
online.
● The two most commonly used scores to identify patients with sepsis in the intensive
care unit (ICU) are the Quick Sequential (Sepsis-related) Organ Failure Assessment
(qSOFA) score (calculator 1) and the National Early Warning Score (NEWS) score, but
their utility compared with clinical judgment in non-ICU patients has not been
established, and they have not been evaluated in patients with postpartum
endometritis. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical
presentation, diagnosis, and prognosis", section on 'Identification of early sepsis
(qSOFA, NEWS)'.)
● The FAST-M complex intervention (Fluids, Antibiotics, Source identification and
control, Transfer to an appropriate level of care, and ongoing Monitoring of mother
and neonate) was designed to improve the recognition and management of maternal
sepsis in low-resource settings [38,39]. Its effectiveness has not been assessed.
● In 2023, the Alliance for Innovation on Maternal Health created a "Sepsis in Obstetric
Care" patient safety bundle to provide guidance for health care teams to develop

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coordinated, multidisciplinary care for pregnant and postpartum people by

preventing infection and recognizing and treating infection early to prevent
progression to sepsis [40].

Laboratory
● White blood cell count and differential – The WBC count is elevated (15,000 to
30,000 cells/microL), but this can be a normal finding postpartum secondary to the
physiologic leukocytosis of pregnancy and the effects of labor [41,42]. Mean WBC
counts in laboring patients range from 10,000 to 16,000 cells/microL, with an upper
level as high as 29,000 cells/microL. A left shift (bandemia) and a rising, rather than
falling, neutrophil count postpartum are suggestive of an infectious process. (See
"Maternal adaptations to pregnancy: Hematologic changes", section on 'White blood
cells'.)
● Bacteremia – Bacteremia has been reported in 5 to 20 percent of patients [43];
however, in clinical practice most patients do not have microbiologic studies of blood,
endometrium, or cervix for laboratory confirmation of the infectious etiology of
endometritis. (See 'Role of blood and endometrial cultures' below.)

Imaging — There are no characteristic sonographic findings associated with postpartum

endometritis [44]. Imaging findings are nonspecific and overlap with expected postpartum
changes (nonspecific uterine enlargement, endometrial fluid, and/or gas). (See "Overview
of the postpartum period: Normal physiology and routine maternal care", section on
'Findings on ultrasound'.)

Computed tomography shows similar findings as ultrasound [45,46].

Histopathology — The endometrium is edematous and hyperemic, with marked

inflammatory infiltrates (primarily neutrophils) of the endometrial glands: ≥5 neutrophils
per 400 high-power fields in the superficial endometrium and ≥1 plasma cells per 120
high-power fields in the endometrial stroma. The inflammatory process may extend into
the myometrium and parametrium, and there may be areas of necrosis and thrombosis.

DIAGNOSTIC EVALUATION

The diagnostic evaluation of postpartum patients with fever and/or pain includes:
● History/physical examination to determine the possible source of the signs and

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symptoms. (See 'Differential diagnosis' below.)

● Complete blood count with differential.
● Urine culture.

In patients with suspected sepsis, additional assessments are performed to evaluate for
end organ injury, such as prothrombin time, activated partial thromboplastin time,
metabolic panel (should include creatinine, bilirubin), venous lactic acid, pulse oximetry,
urine output, and mental status [47].

Role of blood and endometrial cultures — In uncomplicated infections, it is not

important to establish the microbiologic cause since empiric treatment with broad
spectrum antibiotics is usually effective.
● Blood cultures – There is no consensus on whether blood cultures should be
obtained routinely during the initial evaluation. Although bacteremia occurs in 3
percent of all peripartum febrile patients and 5 to 20 percent of peripartum patients
with suspected sepsis [43,48], blood cultures are costly, the initial choice of antibiotic
therapy has to be made before the results are available, and the results usually do
not lead to a change in the initial empiric antibiotic regimen [49]. For these reasons,
we do not obtain blood cultures routinely in patients with endometritis. However,
blood cultures can be useful in guiding the duration of antibiotic therapy and the
choice of antimicrobial treatment in patients who have alarm findings (see 'Alarm
findings (sepsis)' above), are immunocompromised, are septic, or fail to respond to
empiric antibiotic therapy within 24 to 48 hours. (See "Detection of bacteremia: Blood
cultures and other diagnostic tests", section on 'Indications for blood cultures'.)

Interestingly, only a single organism may be identified in the blood culture despite
polymicrobial endometrial infection.
● Endometrial cultures – Endometrial cultures are not performed because of the
difficulty in obtaining an uncontaminated specimen through the cervix. Furthermore,
they yield results too late for clinical use and rarely changing treatment.

DIAGNOSIS

Diagnostic criteria for postpartum endometritis — Postpartum endometritis is

primarily a clinical diagnosis based on characteristic signs and symptoms and presence of

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risk factors. In the United States, the diagnosis is made in a patient with at least two of the
following signs or symptoms; small variations in the criteria are common worldwide [50]:
● Fever (≥100.4°F [38°C])
● Pain or tenderness (uterine or abdominal) with no other recognized cause
● Purulent drainage from the uterus

The presence of tachycardia and/or leukocytosis supports the diagnosis, but these findings
are nonspecific. Fever is a key sign because variable degrees of midline abdominal pain,
uterine tenderness, and leukocytosis are common after cesarean, and to a lesser extent
after vaginal birth, in the absence of infection. Some degree of malodorous yellow-red
lochia is also normal after any birth. Imaging is not helpful for making the diagnosis, but it
can be helpful to exclude other diagnoses (eg, retained products of conception, infected
hematoma, uterine abscess).

Endometritis with toxic shock syndrome — Although rare, Clostridium, Streptococcus,

and Staphylococcus infections can lead to endometritis with toxic shock syndrome and
other life-threatening complications (eg, necrotizing myometritis, necrotizing fasciitis). This
rare diagnosis is made in the following settings:
● Group A Streptococcus (GAS; eg, Streptococcus pyogenes) infection should be
suspected in patients with early-onset infection (within the first 48 hours postpartum)
and high fever (>101.3°F [38.5°C]). The diagnosis of streptococcal toxic shock
syndrome is established based on isolation of GAS from a normally sterile site (eg,
blood, cerebrospinal fluid, joint fluid, pleural fluid, pericardial fluid, peritoneal fluid,
tissue biopsy, or surgical wound) and clinical criteria: Hypotension plus involvement
of at least two other organ systems (eg, renal impairment [elevated creatinine],
abnormal liver function tests, coagulopathy, acute respiratory distress syndrome, soft
tissue necrosis, erythematous macular rash which may desquamate). An influenza-
like syndrome characterized by fever, chills, myalgia, nausea, vomiting,
and diarrhea occurs in approximately 20 percent of patients. Although pain is often
severe with GAS, the uterus may be boggy and nontender in patients with necrotizing
myometritis due to diminished innervation [51,52].

A detailed description of invasive GAS and toxic shock syndrome can be found
separately. (See "Invasive group A streptococcal infection and toxic shock syndrome:
Epidemiology, clinical manifestations, and diagnosis" and "Invasive group A
streptococcal infection and toxic shock syndrome: Treatment and prevention" and
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"Pregnancy-related group A streptococcal infection", section on 'Clinical

manifestations'.)
● Staphylococcal toxic shock syndrome is characterized by high fever >102°F (38.9°C),
hypotension, diffuse erythroderma, desquamation (unless the patient dies before
desquamation can occur), and involvement of at least three organ systems. Onset
may be early (within 24 hours of birth) and difficult to distinguish from GAS toxic
shock syndrome in the absence of laboratory confirmation ( table 1). Postpartum
methicillin-resistant S. aureus toxic shock syndrome has been reported, but is rare
[53]. (See "Staphylococcal toxic shock syndrome".)
● C. sordellii has been associated with a distinctive, lethal toxic shock-like syndrome. In
one report, affected patients were less than one week postpartum when they had
sudden onset of clinical shock: progressive, refractory hypotension was associated
with massive and generalized tissue edema, hemoconcentration, a marked
leukemoid reaction (total neutrophil count 66,000 to 93,600/mm3), absence of rash or
fever, limited or no myonecrosis, and a rapidly lethal course. (See "Toxic shock
syndrome due to Paeniclostridium sordellii" and "Clostridial myonecrosis".)
● C. perfringens should be considered in patients who rapidly become gravely ill with
evidence of intravascular hemolysis, which may be severe. It can cause clostridial
myonecrosis (gas gangrene), a life-threatening muscle infection that can be identified
by radiographic imaging. (See "Clostridial myonecrosis".)

C. sordellii and C. perfringens have also been found in patients with necrotizing
endomyometritis and fatal and nonfatal toxic shock after spontaneous or medical abortion
[10].

Differential diagnosis — In patients with postpartum fever but no or minimal uterine

tenderness or purulent vaginal discharge, other sources of postpartum fever should be
considered. Any disorder associated with fever, such as appendicitis or viral syndrome, can
present with fever in the postpartum period. Many of these disorders can be diagnosed or
excluded by history and physical examination alone; in the remainder, laboratory and/or
imaging studies will clarify the diagnosis. Some common causes of fever in postpartum
patients include:
● Surgical site infection (eg, abdominal wall incision, episiotomy incision, perineal
lacerations) is typically evident on physical examination of the surgical site (eg, local
erythema, edema, and/or tenderness). (See "Complications of abdominal surgical
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incisions" and "Approach to episiotomy".)

● Mastitis or breast abscess is usually evident on physical examination of the breast
(eg, local erythema, edema, and/or tenderness) and typically occurs later in the
postpartum course (the first three months of breastfeeding).

Breast engorgement (fullness and firmness accompanied by pain and tenderness)

may lead to a low-grade fever 24 to 72 hours postpartum. (See "Lactational mastitis"
and "Primary breast abscess".)
● Pyelonephritis is characterized by fever (>100.4°F [38°C]), chills, flank pain,
costovertebral angle tenderness, and possibly lower urinary tract symptoms. Pyuria
and/or a positive urine culture supports the diagnosis. (See "Acute complicated
urinary tract infection (including pyelonephritis) in adults and adolescents".)
● Aspiration pneumonia presents with fever, dyspnea, and possibly hypoxemia. Lung
auscultation may reveal diffuse crackles, and a chest radiograph will show infiltrates.
It primarily occurs in postpartum patients with compromise in the usual defenses
that protect the lower airways, such as those with a recent history of a difficult or
failed intubation. (See "Aspiration pneumonia in adults".)
● Unexplained fever with significant back pain after a neuraxial anesthetic, especially
when accompanied by neurologic symptoms, may be due to infection or
inflammation of the spinal cord. Consultation with the anesthesia and neurology
services is indicated. (See "Serious neurologic complications of neuraxial anesthesia
procedures in obstetric patients".)
● Pseudomembranous colitis due to Clostridioides difficile is a rare, but potentially
serious, cause of postpartum fever. It should be considered in postpartum patients
who have low-grade fever, abdominal and gastrointestinal symptoms, and recent
antibiotic exposure [54]. (See "Clostridioides difficile infection in adults: Clinical
manifestations and diagnosis".)

TREATMENT

Overview — Our approach to treatment of most patients is summarized in the algorithm

( algorithm 1) and discussed below. Prompt administration of appropriate antibiotics is
critical in septic patients [37]. (See 'Patients with sepsis' below.)

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Treatment is indicated for relief of symptoms and to prevent sequelae, such as peritonitis,
salpingitis, oophoritis, phlegmon or abscess, and septic pelvic thrombophlebitis. Treatment
is the same, regardless of mode of birth. Broad spectrum parenteral antibiotics that
include coverage for beta-lactamase-producing anaerobes are typically recommended,
given the microbiology of these infections (see 'Microbiology' above). Oral antibiotics are
an option for mild endometritis diagnosed after the patient has been discharged,
especially those post vaginal birth. (See 'Management of late-onset cases' below.)

Preferred initial regimen (no GBS colonization) — The following intravenous (IV)
regimen is for patients with normal renal function and results in resolution of infection in
90 to 97 percent of cases [55-65]:
● Clindamycin 900 mg every eight hours plus
● Gentamicin 5 mg/kg every 24 hours (preferred) or 1.5 mg/kg every eight hours
(without a loading dose)

Extended interval gentamicin dosing (5 mg/kg every 24 hours) is preferred because it more
convenient and cost-effective and as efficacious and safe as thrice daily dosing (1.5 mg/kg
IV every eight hours) for patients with normal renal function (risk of treatment failure with
once versus thrice daily dosing: risk ratio [RR] 0.70, 95% CI 0.49-1.00 [64]). Gentamicin
levels do not need to be monitored in patients receiving a dose every 24 hours who have
normal renal function and an expected short duration of therapy (≤72 hours or three
doses), which is common in this population. (See "Dosing and administration of parenteral
aminoglycosides", section on 'Extended-interval dosing and monitoring'.)

This choice of antibiotics is supported by a 2015 meta-analysis including 40 randomized

trials through 2003 that concluded the combination of clindamycin plus an aminoglycoside
is appropriate for the treatment of endometritis and that a regimen with activity against
Bacteroides fragilis and other penicillin-resistant anaerobic bacteria is better than one
without (eg, risk of treatment failure with clindamycin plus an aminoglycoside versus
cephalosporins alone: 10.2 versus 14.8 percent, RR 0.69, 95% CI 0.49-0.99) [64]. However,
cephalosporins (eg, cefotetan, cefoxitin, ceftizoxime, cefotaxime, cefuroxime) alone have
been proposed for treatment of chorioamnionitis and can be considered for treatment of
endometritis [66].

Two concerns regarding use of clindamycin are:

● Increasing resistance of group B Streptococcus (GBS) isolates. (See 'Preferred initial

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regimen (GBS colonization present or unknown)' below.)

● Increasing resistance among anaerobic bacteria [67-69], with widely varying rates of
resistance among different geographic regions and institutions. In geographic
regions or institutions where B. fragilis has significant clindamycin resistance,
ampicillin-sulbactam (3 g IV every six hours) is a reasonable alternative to gentamicin
plus clindamycin [70]. Metronidazole (500 mg IV every eight hours) is an alternative to
clindamycin [71] and provides good activity against most anaerobes; however,
metronidazole is avoided in breastfeeding individuals when similarly effective drugs
with better safety profiles are available.

Preferred initial regimen (GBS colonization present or unknown) — For those patients
who are known to be colonized with GBS as a result of universal screening, ampicillin
should be included in the regimen because clindamycin resistance in GBS isolates ranges
from 13 to 43 percent [72-77]. We suggest:
● Ampicillin 2 g IV every six hours plus
● Clindamycin 900 mg every eight hours plus
● Gentamicin 5 mg/kg every 24 hours (preferred) or 1.5 mg/kg every eight hours
(without a loading dose)

or
● Ampicillin-sulbactam 3 g IV every six hours

Vancomycin can be used instead of ampicillin in patients with immunoglobulin E (IgE)-

mediated, immediate allergic reactions, including anaphylaxis. (See "Choice of antibiotics
in penicillin-allergic hospitalized patients".)

As discussed above, metronidazole (500 mg IV every eight hours) is an alternative to

clindamycin [71] and provides good activity against most anaerobes; however,
metronidazole is avoided in breastfeeding individuals when similarly effective drugs with
better safety profiles are available. Cefoxitin (2 g IV every six hours) also provides good
anaerobic coverage. Alternatives for critically ill patients include piperacillin/tazobactam
(3.375 g IV every six hours infused over three hours), meropenem (1 g IV every eight hours
infused over three hours), or ertapenem (1 g IV every 24 hours) [78].

Patients with sepsis — Gentamicin, ampicillin, plus clindamycin or metronidazole is

preferred for patients with sepsis (life-threatening organ dysfunction caused by a
dysregulated host response to infection [79]). The CMQCC suggests administration of both
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ampicillin-sulbactam and gentamicin as an acceptable alternative [47]. For patients with

sepsis and penicillin allergy who are able to take a cephalosporin, the Society for Maternal-
Fetal Medicine suggests cefotaxime or ceftriaxone plus metronidazole [80].

Duration of therapy — A response to the initial antibiotic regimen should be evident

within 24 to 48 hours. IV treatment is typically continued until the patient is clinically
improved (no fundal tenderness) and afebrile for 24 to 48 hours.

Oral antibiotic therapy after successful parenteral treatment is unnecessary as it did not
improve outcome in randomized trials [64].

As discussed above, we do not obtain blood cultures routinely. If blood cultures were
obtained and bacteremia is present as indicated by a positive blood culture, consultation
with an infectious disease specialist is advised since a longer course of therapy may be
indicated, depending on the organism.

Options when intravenous therapy is not possible — In resource-limited countries

where IV lines are not available, a systematic review concluded that the following five
antibiotic regimens would provide >85 percent cure rates of early postpartum endometritis
and were compatible with breastfeeding [81]:
● Clindamycin 600 mg orally every six hours plus gentamicin 4.5 mg/kg intramuscularly
every 24 hours or
● Amoxicillin-clavulanic acid 875 mg orally every 12 hours or
● Cefotetan 2 g intramuscularly every eight hours or
● Meropenem or imipenem with cilastatin 500 mg intramuscularly every eight hours or
● Amoxicillin 500 mg plus metronidazole 500 mg orally every eight hours

The review did not provide guidance on duration of therapy since available data were too
limited to provide an evidence-based recommendation. If an oral antibiotic regimen is
administered, we suggest a 14 day course. If an intramuscular antibiotic regimen is used,
we suggest 48 to 72 hours of intramuscular therapy and then switching to an oral
antibiotic to complete a seven-day course.

Persistent postpartum fever — Most patients respond favorably to the initial antibiotic
regimen within 24 to 48 hours. If the patient has not improved by this time or has
deteriorated, then the antibiotic regimen is modified and an evaluation for other sources
of infection is indicated, as follows:

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● Approximately 20 percent of treatment failures are due to organisms, such as
enterococci, that are resistant to cephalosporins or clindamycin plus gentamicin. In
the absence of information from blood cultures, the addition of ampicillin 2 g IV every
six hours to the clindamycin plus gentamicin regimen, as well as a repeat physical
examination to exclude another source of fever, can be an effective approach if the
patient was not already on ampicillin [82,83].

Alternatively, the initial antibiotics can be discontinued, and ampicillin-sulbactam (eg,

Unasyn) can be initiated if the patient was not already on ampicillin [84-87]. This
regimen is at least as effective as clindamycin plus gentamicin and is used as first-line
therapy in some hospitals.

If blood cultures were performed, antibiotic treatment decisions are based on drug
sensitivity results for any organisms identified. (See "Treatment of enterococcal
infections".)
● If adding ampicillin or changing to ampicillin-sulbactam does not result in clinical
improvement within 24 hours of the change in antibiotic regimen, then physical
examination, complete blood count with differential, blood and urine cultures, and
pelvic imaging (eg, ultrasound, computed tomography [CT]) to evaluate for other
etiologies of signs and symptoms are performed. Sources of persistent fever include
an infected hematoma, pelvic cellulitis or abscess, surgical site infection, septic pelvic
thrombophlebitis, ovarian vein thrombosis, and myometrial necrosis. The possibility
of a nonpelvic source of fever, such as pneumonia or pyelonephritis, should also be
reconsidered. (See 'Differential diagnosis' above.)

The goals of the physical examination are to look for non-uterine sources of infection
and worsening pelvic findings (eg, new mass, increasing pain). Targeted imaging
studies may be useful to further evaluate suspicious clinical findings or fever
refractory to antibiotic therapy (clindamycin, gentamicin, and ampicillin or ampicillin-
sulbactam). Sonography is useful for visualizing pelvic abscesses and fluid collections
(eg, infected hematoma), but insensitive for the diagnosis of septic pelvic
thrombophlebitis or ovarian vein thrombosis where CT or magnetic resonance
imaging (MRI) is more helpful. Diagnosis and treatment are discussed in more detail
separately. (See "Septic pelvic thrombophlebitis" and "Complications of abdominal
surgical incisions".)

Knowledge of the characteristics of the normal postpartum uterus is useful when the
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postpartum uterus is imaged during evaluation of postpartum complications since

fluid, debris, and gas can be normal findings. (See "Overview of the postpartum
period: Normal physiology and routine maternal care", section on 'Findings on
ultrasound'.)
● In patients receiving a thrice daily gentamicin regimen (1.5 mg/kg every eight hours)
instead of 5 mg/kg every 24 hours, drug levels should be obtained as they may not be
in the therapeutic range, thus necessitating a change in dose. (See "Dosing and
administration of parenteral aminoglycosides", section on 'Gentamicin and
tobramycin dosing in adults'.)
● Retained products of conception after birth (almost always vaginal birth) can cause
acute or chronic endometritis related to microbial infection of the necrotic products
of conception (eg, fetal membranes, placental fragments) as well as the
endometrium. Ultrasound may demonstrate the retained tissue [88]. Diagnosis and
treatment are discussed in detail separately. (See "Retained products of conception in
the first half of pregnancy".)

Curettage to remove the necrotic material may be necessary to resolve the infection.
It is important to not curette the endometrium too vigorously as this can lead to
uterine perforation, adhesion formation, and subsequent infertility (ie, Asherman
syndrome) [89]. For this reason, suction curettage is preferable to sharp curettage.
(See "Intrauterine adhesions: Clinical manifestation and diagnosis".)
● The possibility of drug fever should be considered in the absence of any positive
findings on physical examination or imaging studies and a pulse rate that does not
vary significantly and does not parallel the patient's temperature. Drug fever can be
defined as "a disorder characterized by fever coinciding with the administration of the
drug and disappearing after the discontinuation of the drug, when no other cause for
the fever is evident after a careful physical examination and laboratory investigation."
(See "Drug fever".)

Management of relapse — For patients who present with recurrent signs/symptoms of

endometritis after having been treated for endometritis on initial hospitalization, the
details of the therapy and relevant laboratory/imaging results from initial hospitalization
should be reviewed, if available.
● If prior cultures were performed, then we target antibiotic therapy to cover the
organisms that were identified.
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● If no organism was identified, then we restart the same regimen that was
administered during the initial hospitalization.
● If the regimen used during the initial hospitalization is not known, then we start
clindamycin, gentamicin, and ampicillin at the doses described above. (See 'Preferred
initial regimen (GBS colonization present or unknown)' above.)

Other sources of infection and causes of fever should be considered, with appropriate
intervention. (See 'Persistent postpartum fever' above.)

Management of late-onset cases — Most cases of endometritis develop within the first
week after birth, but 15 percent present between one and six weeks postpartum [90,91].
Delayed presentation is more common after vaginal than cesarean birth, and it may
present as late postpartum hemorrhage [92,93]. (See "Secondary (late) postpartum
hemorrhage".)

Most patients with late postpartum endometritis have mild clinical signs and symptoms
[90]. Parenteral, inpatient treatment is probably unnecessary, although the optimum route
of drug administration has not been evaluated in comparative trials.

For broad spectrum oral therapy, we use:

● Amoxicillin-clavulanate 875 mg orally twice a day for seven days.

In penicillin-allergic patients, we use:

● Clindamycin 600 mg orally every six hours for seven days.

Breastfeeding is not a contraindication to administering these drugs.

OUTCOME

Most infections are mild and cured with antibiotic therapy [64].

Surgical site infection is a common associated condition when antibiotic therapy is

unsuccessful in resolving fever after cesarean birth and often requires drainage. Wound
infection affects 11 percent of patients. Severe complications, which occur in up to 4
percent of patients, include extension of infection to the peritoneal cavity resulting in
peritonitis, intraabdominal abscess, or sepsis [64]. Necrotizing myometritis, necrotizing
fasciitis of the abdominal wall, septic pelvic thrombophlebitis, and toxic shock syndrome
are rare complications. Hysterectomy and/or aggressive wound debridement may be

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Postpartum endometritis

necessary to treat severe infection. (See "Septic pelvic thrombophlebitis" and "Necrotizing
soft tissue infections" and "Toxic shock syndrome due to Paeniclostridium sordellii" and
"Staphylococcal toxic shock syndrome" and "Invasive group A streptococcal infection and
toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis" and "Invasive
group A streptococcal infection and toxic shock syndrome: Treatment and prevention".)

In gynecologic patients with endometritis, secondary infertility appears to be uncommon

with timely diagnosis and appropriate treatment, but data from patients with postpartum
endometritis are not available [94]. A severe infection may lead to exosalpingitis, whereas
endosalpingitis is unusual [30].

PREVENTION

At cesarean birth
● Role of antibiotic prophylaxis – Antibiotic prophylaxis within 60 minutes prior to
making the skin incision is routinely recommended as it significantly reduces the
incidence of postcesarean endometritis, for both planned and intrapartum
procedures. The optimum regimen is discussed in detail separately. (See "Cesarean
birth: Preoperative planning and patient preparation", section on 'Antibiotic
prophylaxis'.)

Vaginal preparation with an antiseptic solution (eg, 10% povidone-iodine, 4%

chlorhexidine gluconate) immediately before cesarean birth also reduces the
incidence of postcesarean endometritis. These data are discussed in detail separately
[95]. (See "Cesarean birth: Preoperative planning and patient preparation", section on
'Vaginal preparation'.)

Intrauterine antibiotic irrigation just before closure of hysterotomy incision may be as

effective as preoperative intravenous (IV) infusion, probably because the drug is
absorbed into the systemic circulation [96,97]. Nevertheless, irrigation has fallen out
of favor because it does not appear to offer any advantage over IV therapy and may
have disadvantages, such as variable absorption.
● Role of placental delivery method – For patients undergoing cesarean birth, a
meta-analysis of randomized trials found that manual removal of the placenta
increased the risk of postpartum endometritis compared with spontaneous placental
removal with cord traction (18.4 versus 11.3 percent; RR 1.64, 95% CI 1.42-1.90) [98].
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Postpartum endometritis

At vaginal birth
● Role of antibiotic prophylaxis – In high-income countries, patients undergoing
vaginal birth are not routinely given antibiotic prophylaxis, given their low rate of
postpartum endometritis (0.2 to 2.0 percent) [15,18,19]. By comparison, a large
randomized trial conducted in seven low- and middle-income countries (Bangladesh,
Democratic Republic of Congo, Guatemala, India, Kenya, Pakistan, Zambia) found
that prophylaxis at planned vaginal birth reduced the risk of the composite outcome
"postpartum maternal sepsis or death" [99], suggesting this intervention should be
considered in clinical settings that are similar to those in the trial. These data and
results of a similar trial that showed a reduction in maternal sepsis that was not
statistically significant are reviewed separately. (See "Labor and delivery:
Management of the normal first stage", section on 'Medication management'.)

Prophylactic antibiotics are sometimes given postpartum to patients who have a

vacuum- or forceps-assisted vaginal birth (especially when an episiotomy is
performed) and to patients who have a third- or fourth-degree perineal laceration.
(See "Assisted (operative) vaginal birth", section on 'Antibiotics' and "Repair of
perineal lacerations associated with childbirth", section on 'Antibiotics'.)
● Role of placental delivery method – Spontaneous rather than manual delivery of
the placenta is routine at vaginal birth, but manual extraction is sometimes
necessary. No randomized trials have evaluated use of prophylactic antibiotics in
patients who undergo manual removal of placenta [100]. Use of prophylactic
antibiotics in this setting varies. (See "Retained placenta after vaginal birth", section
on 'Perform manual extraction'.)

Antepartum antibiotic prophylaxis ineffective — In a systematic review of randomized

trials of antibiotic prophylaxis during the second and third trimester to reduce adverse
pregnancy outcomes and morbidity, the intervention did not clearly reduce the risk for
postpartum endometritis in unselected patients (risk ratio 0.51, 95% CI 0.24-1.08, two trials
with a total of 431 participants) [101]. The quality of the trials was limited, in part, because
a high (20 to 40 percent) proportion of patients were lost to follow-up.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

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Postpartum endometritis

regions around the world are provided separately. (See "Society guideline links:
Postpartum infection".)

SUMMARY AND RECOMMENDATIONS

● Overview – Endometritis is a common cause of postpartum febrile morbidity. The

infection is polymicrobial, usually involving a mixture of two to three aerobes and
anaerobes from the lower genital tract. Most infections are mild and cured with
antibiotic therapy. Cesarean birth, particularly when performed after the onset of
labor, is the dominant risk factor. (See 'Microbiology' above and 'Outcome' above and
'Risk factors' above.)
● Clinical findings

• History and physical – The key clinical findings present in most patients are:
- Fever
- Uterine tenderness
- Tachycardia that parallels the rise in temperature
- Midline lower abdominal pain

The uterus may be slightly soft and subinvoluted, which can lead to excessive
uterine bleeding. Additional findings observed in some patients include
malodorous purulent lochia, headache, chills, malaise, and/or anorexia. (See 'Signs
and symptoms' above.)

• Severe infection/sepsis – Findings suggestive of severe infection or sepsis

include fever ≥103°F (39.4°C) or fever ≥102°F (38.9°C) plus tachycardia, tachypnea,
hypotension, and/or bandemia. (See 'Alarm findings (sepsis)' above.)

• Laboratory – Laboratory studies are of limited value: a rising neutrophil count

associated with elevated numbers of bands is suggestive of infection, and an
elevated lactic acid concentration is a marker for serious infection. (See
'Laboratory' above.)

Endometrial cultures are not obtained at diagnosis since they are usually not
needed to guide therapy. Blood cultures are obtained in selected patients. (See
'Role of blood and endometrial cultures' above.)

Blood cultures are obtained selectively as they can be useful in guiding the choice
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Postpartum endometritis

of antimicrobial treatment in patients who have alarm findings, are

immunocompromised, are septic, or fail to respond to empiric antibiotic therapy
within 24 to 48 hours.
● Diagnosis – In the United States, the diagnosis is made in a patient with at least two
of the following signs or symptoms; small variations in the criteria are common
worldwide (see 'Diagnosis' above):
- Fever (≥100.4°F [38.0°C])
- Pain or tenderness (uterine or abdominal) with no other recognized cause
- Purulent drainage from uterus
● Treatment — Our approach is summarized in the algorithm ( algorithm 1).
Treatment of postpartum endometritis is indicated for relief of symptoms and
prevention of sequelae.

• Antibiotic choice and dose – Given the microbiology of these infections, we

recommend broad spectrum antibiotics with coverage of beta-lactamase-
producing anaerobes (Grade 1B).
- In patients without group B Streptococcus (GBS) colonization, we suggest
clindamycin (900 mg intravenously [IV] every eight hours) plus gentamicin (5
mg/kg every 24 hours [preferred] or 1.5 mg/kg every eight hours) (Grade 2B).
- In areas with significant clindamycin resistance in Bacteroides fragilis or if the
patient is colonized with GBS, adding ampicillin (2 g IV every six hours) to this
regimen or using ampicillin-sulbactam (3 g IV every six hours) is preferred.
(See 'Preferred initial regimen (no GBS colonization)' above and 'Preferred
initial regimen (GBS colonization present or unknown)' above.)

Duration of therapy – Antibiotics are administered until the patient is clinically

improved and afebrile for 24 to 48 hours. In the absence of bacteremia, we
recommend not prescribing oral antibiotic therapy after successful parenteral
treatment (Grade 1A). (See 'Duration of therapy' above.)

• Response to therapy and management of nonresponders – Signs and

symptoms should improve within 24 to 48 hours of initiating adequate antibiotic
therapy.

If the patient has not improved by this time, then the addition of ampicillin (or
vancomycin in penicillin-allergic patients) to the regimen can improve the
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Postpartum endometritis

response rate if the patient was not already on ampicillin; physical examination
should be performed to exclude another source of fever. Alternatively, the initial
antibiotics can be discontinued, and ampicillin-sulbactam can be initiated if the
patient was not already on ampicillin.

If adding ampicillin or changing to ampicillin-sulbactam does not result in clinical

improvement within 24 hours of the change in antibiotic regimen, then physical
examination, complete blood count with differential, blood and urine cultures, and
pelvic imaging to evaluate for other etiologies of the signs and symptoms are
performed. (See 'Persistent postpartum fever' above.)
● Prevention

• Before cesarean birth – For patients undergoing cesarean birth, we recommend

antibiotic prophylaxis prior to skin incision and spontaneous, rather than manual,
placental extraction to minimize the risk of postpartum endometritis (Grade 1A).
(See 'Prevention' above.)

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