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Postpartum endometritis

Postpartum endometritis
Author:
Katherine T Chen, MD, MPH
Section Editor:
Vincenzo Berghella, MD
Deputy Editor:
Vanessa A Barss, MD, FACOG
Literature review current through: Aug 2021. | This topic last updated: Jul 12, 2021.

INTRODUCTION — Postpartum endometritis refers to infection of the decidua (ie, pregnancy endometrium). It is a common cause of postpartum fever and uterine tenderness and is 10- to 30-fold more common after cesarean than vaginal delivery. Most infections are mild and resolve with antibiotic therapy; however, in a minority of patients, the infection extends into the peritoneal cavity 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 delivery will be discussed here. Endometritis after a spontaneous or induced early pregnancy loss, or in patients who have not been recently pregnant, is reviewed separately. (See "Overview of pregnancy termination", section on 'Infection/retained products of conception' 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 genital tract. In a study of 55 antibiotic-naive women with well-defined puerperal endometritis who had endometrial cultures obtained with a triple-lumen catheter (to reduce the risk of contamination from organisms on the cervix), 51 had an endometrial isolate and 7 had a blood isolate [1]:

At least one facultative or one anaerobic species of bacteria – 42/51 (82 percent).

Genital mycoplasmas – 39/51 (76 percent).

A polymicrobial infection consisting of at least two facultative bacteria, anaerobic bacteria, or both – 35/51 (69 percent).

A combination of at least two bacteria and genital mycoplasmas – 26/51 (51 percent).

Bacteremia was present in 38 percent of those with endometrial cultures positive for bacteria and 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 [2]. In HIV-infected women, the microbiology can be broader and include other less likely pathogens, such as herpes simplex virus and cytomegalovirus [3].

Rare, but potentially lethal, causes of endometritis include Clostridium sordellii [4-7], Clostridium perfringens [8], and streptococcal or staphylococcal toxic shock syndrome [9-11]. (See 'Endometritis with toxic shock syndrome' below.)

RISK FACTORS — Cesarean delivery is the dominant risk factor for development of postpartum endometritis, especially when performed after the onset of labor [12-14]. Among women 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 (without antibiotic prophylaxis, the frequencies are approximately 18 and 4 percent, respectively) [15]. Antibiotic prophylaxis is not standard practice for laboring women expecting to deliver vaginally; the frequency of postpartum endometritis in these women ranges from 0.2 to 2.0 percent [13,16,17].

Patients with bacterial vaginosis (BV) who undergo cesarean delivery appear to be at particularly high risk for postpartum endometritis [18,19]. In a multivariable analysis of factors independently related to postpartum endometritis in women delivered by cesarean, BV was associated with a nearly sixfold increase in risk (odds ratio 5.8, 95% CI 3.0-10.9) after adjusting for duration of labor, duration of membrane rupture, and maternal age [19]. The propensity for upper genital tract infection in women with BV may be related to higher vaginal concentrations of certain anaerobic and facultative bacteria observed in this disorder. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Epidemiology' and "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Consequences of infection'.)

Other risk factors for postpartum endometritis include [17,20-32]:

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 delivery

Obesity

HIV infection

Colonization with group B Streptococcus (see "Group B streptococcal infection in pregnant women", section on 'Endometritis')

Nasal carriage of Staphylococcus aureus

Heavy vaginal colonization by E. coli

PATHOGENESIS — During labor and delivery, 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 [34]. Although mycoplasmas are often isolated from the endometrial cavity, antibiotic therapy is not usually required for clinical cure in women who have Ureaplasma urealyticum only, without additional organisms [35-37]; thus, the role of mycoplasmas in the pathogenesis of endometritis is unclear.

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 deliveries 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 [2].

CLINICAL FINDINGS

Signs and symptoms — The key clinical findings present in most women with postpartum endometritis 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 women 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 infection and high fever. (See 'Endometritis with toxic shock syndrome' below.)

Alarm findings — The following findings are one academic teaching hospital's criteria for suspecting severe infection/sepsis in febrile postpartum patients, 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

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".)

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 mothers who died of sepsis had no fever during the hospitalization [38].

To decrease sepsis-associated mortality, societal guidelines emphasize early identification of infected patients who may go on to develop sepsis. The two most commonly used scores to identify these patients 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 patients outside of the intensive care unit 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 [39,40]. Its effectiveness has not been assessed.

Laboratory — The WBC count is elevated (15,000 to 30,000 cells/microL), but this can be a normal finding in postpartum women 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 occurs in 5 to 20 percent of patients [43]; however, 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 symptoms. (See 'Differential diagnosis' below.)

Complete blood count with differential.

Urine culture.

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 5 to 20 percent of patients [43], 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 [47]. For these reasons, we do not obtain blood cultures routinely in women with endometritis. However, blood cultures can be useful in guiding the choice of antimicrobial treatment in patients who have alarm findings (see 'Alarm findings' 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 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 while 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 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 [48]:

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 delivery, and to a lesser extent after vaginal delivery, in the absence of infection. Some degree of malodorous yellow-red lochia is also normal after any delivery. 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]). High fever with hypotension and tachycardia plus involvement of at least two other organ systems (eg, renal, liver, or pulmonary insufficiency; coagulopathy; soft tissue necrosis; erythematous macular rash with desquamation) suggests toxic shock syndrome. 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 [49,50]. For patients that meet the above clinical criteria, 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) confirms the diagnosis.

A detailed description of invasive GAS and toxic shock syndrome can be found separately. (See "Pregnancy-related group A streptococcal infection", section on 'Postpartum' 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".)

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 delivery) and difficult to distinguish from GAS toxic shock in the absence of laboratory confirmation (table 1). Postpartum methicillin-resistant S. aureus toxic shock syndrome has been reported but is rare [51]. (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 Clostridium 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 [8].

Differential diagnosis — In women 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, cesarean delivery 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 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 also lead to a low-grade fever in women 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".)

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 women who have low-grade fever, abdominal and gastrointestinal symptoms, and recent antibiotic exposure [52]. (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)

TREATMENT

Overview — Treatment is indicated for relief of symptoms and to prevent sequelae, such as peritonitis, salpingitis, oophoritis, phlegmon or abscess, and septic pelvic thrombophlebitis. Prompt administration of appropriate antibiotics is critical in septic patients [38]. Treatment is the same, regardless of mode of delivery. Our approach is summarized in the algorithm (algorithm 1) and discussed below.

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 patients have been discharged, especially those post vaginal birth. (See 'Late-onset postpartum endometritis' 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 [53-62]:

Clindamycin 900 mg every 8 hours plus

Gentamicin 5 mg/kg every 24 hours (preferred) or 1.5 mg/kg every 8 hours (without a loading dose)

Extended interval dosing of gentamicin (5 mg/kg every 24 hours) is more convenient and cost-effective and as efficacious and safe as thrice daily dosing (1.5 mg/kg IV every 8 hours) for patients with normal renal function and, thus, is preferred (risk of treatment failure with once versus thrice daily dosing: risk ratio [RR] 0.70, 95% CI 0.49-1.00 [62]). Gentamicin levels do not need to be monitored in patients receiving a gentamicin 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 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: 10.2 versus 14.8 percent, RR 0.69, 95% CI 0.49-0.99) [62].

One concern with this regimen is increasing resistance to clindamycin among anaerobic bacteria [63-65], 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 [66].

Another concern regarding this regimen is increasing resistance of group B Streptococcus (GBS) isolates to clindamycin. (See 'Preferred initial regimen (GBS colonization)' below.)

Preferred initial regimen (GBS colonization) — Resistance to clindamycin in GBS isolates ranges from 13 to 43 percent [67-72]. For those patients who are known to be colonized with GBS as a result of universal screening, we suggest:

Clindamycin 900 mg every 8 hours plus

Gentamicin 5 mg/kg every 24 hours (preferred) or 1.5 mg/kg every 8 hours (without a loading dose) plus

Ampicillin 2 g IV every 6 hours

or

Ampicillin-sulbactam 3 g IV every 6 hours

Other intravenous drug options — Drug treatments reported to be equivalent to clindamycin plus gentamicin include ampicillin-sulbactam, cefotetan, cefoxitin, ceftizoxime, and piperacillin with or without tazobactam [1,73-76]. These drugs, particularly ampicillin-sulbactam, are used as the initial antibiotic choice in some hospitals. However, the trials supporting use of these drugs have been small; thus, they may not have been able to achieve statistically significant differences in efficacy.

The combination of gentamicin, ampicillin, and metronidazole is another option that provides good activity against most anaerobes; however, metronidazole is avoided in breastfeeding women when similarly effective drugs with better safety profiles are available.

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 [62].

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 [77]:

Clindamycin 600 mg orally every 6 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 8 hours or

Meropenem or imipenem with cilastatin 500 mg intramuscularly every 8 hours or

Amoxicillin 500 mg plus metronidazole 500 mg orally every 8 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 — As discussed above, 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:

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 gentamycin 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 [78,79]. Alternatively, the initial antibiotics can be discontinued, and ampicillin-sulbactam (eg, Unasyn) can be initiated if the patient was not already on ampicillin [73,80-82]. This regimen is at least as effective as clindamycin plus gentamicin and is used as first-line therapy in some hospitals. 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".)

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, gentamycin, 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 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), 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 delivery (almost always vaginal delivery) 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 [83]. 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) [84]. 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".)

Relapse of endometritis — 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.

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)' above.)

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

Late-onset postpartum endometritis — Most cases of endometritis develop within the first week after delivery, but 15 percent present between one and six weeks postpartum [85,86]. Delayed presentation is more common after vaginal than cesarean delivery, and it may present as late postpartum hemorrhage [87,88]. (See "Secondary (late) postpartum hemorrhage".)

Most women with late postpartum endometritis have mild clinical signs and symptoms [85]. Parenteral, inpatient treatment is probably unnecessary, although the optimum route of drug delivery 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.

We do not consider these drugs contraindicated in breastfeeding mothers.

OUTCOME — Most infections are mild and cured with antibiotic therapy [62].

Surgical site infection is a common associated condition when antibiotic therapy is unsuccessful in resolving fever after cesarean delivery 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 [62]. 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 necessary to treat severe infection. (See "Septic pelvic thrombophlebitis" and "Necrotizing soft tissue infections" and "Toxic shock syndrome due to Clostridium 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".)

Although there are no data from women with postpartum endometritis, secondary infertility appears to be uncommon with timely diagnosis of endometritis and appropriate treatment in gynecologic patients [89]. A severe infection may result in exosalpingitis, but endosalpingitis is unusual [30].

PREVENTION

At cesarean delivery

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 delivery 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, povidone-iodine, chlorhexidine) immediately before cesarean delivery also reduces the incidence of postcesarean endometritis. These data are discussed in detail separately [90]. (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 [91,92]. 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 women undergoing cesarean delivery, four randomized trials with a total of over 2000 subjects reported that spontaneous delivery of the placenta resulted in a significant reduction in postpartum endometritis compared with manual removal [93-96].

At vaginal delivery

Role of antibiotic prophylaxis – Women undergoing vaginal delivery are not routinely given antibiotic prophylaxis given their low rate of postpartum endometritis (0.2 to 2.0 percent) [13,16,17]. There are few data from randomized trials regarding the efficacy of antibiotic prophylaxis to prevent endometritis in women at high risk.

A trial that randomly assigned women who underwent an operative vaginal delivery to postpartum antibiotics or placebo reported a similar rate of endometritis (1 percent) in both groups [97].

A double-blind trial that randomly assigned 424 HIV-infected pregnant patients anticipating vaginal delivery to receive either a single dose of cefoxitin (2 g) or placebo intrapartum reported a 53 percent reduction in risk of postpartum endometritis in the cefoxitin group (95% CI 0.24-0.90) [98]. The overall rate of sepsis was similar for both groups (40/211 women [19 percent] in the placebo group and 36/213 women [17 percent] in the cefoxitin group).

Role of placental delivery method – Spontaneous rather than manual delivery of the placenta is routine at vaginal delivery, but manual extraction is sometimes necessary. No randomized trials have evaluated use of prophylactic antibiotics in women who undergo manual removal of placenta [99]. Use of prophylactic antibiotics in this setting varies. (See "Retained placenta after vaginal birth", section on 'Perform manual extraction'.)

Women with bacterial vaginosis — Women with symptomatic bacterial vaginosis (BV) late in pregnancy are treated for symptom relief; treatment also reduces the risk of postpartum endometritis [100]. Asymptomatic pregnant patients are not screened for BV as there are no data that this is cost-effective. The major focus of BV screening has been to reduce the risk for preterm birth. The United States Preventive Services Task Force recommends against screening for BV in pregnant patients who are not at increased risk for preterm delivery and concluded that evidence is insufficient to assess the balance of benefits and harms of screening in pregnant patients who are at increased risk for preterm delivery [101]. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Consequences of infection' and "Bacterial vaginosis: Treatment".)

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 significantly reduce the risk for postpartum endometritis in unselected women (risk ratio 0.51, 95% CI 0.24-1.08, two trials with a total of 431 participants) [102]. 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 regions around the world are provided separately. (See "Society guideline links: Postpartum infection".)

SUMMARY AND RECOMMENDATIONS

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 delivery is the dominant risk factor. (See 'Microbiology' above and 'Outcome' above and 'Risk factors' above.)

Clinical manifestations and diagnosis

The key clinical findings present in most women 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 women include malodorous purulent lochia, headache, chills, malaise, and/or anorexia. (See 'Clinical findings' above.)

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' above.)

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

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

Treatment — Our approach is summarized in the algorithm (algorithm 1).

Treatment of postpartum endometritis is indicated for relief of symptoms and prevention of sequelae. 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 8 hours) plus gentamicin (5 mg/kg every 24 hours [preferred] or 1.5 mg/kg every 8 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)' above.)

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.)

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 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

For patients undergoing cesarean delivery, 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.)

The risk of postpartum endometritis may be reduced by treating women with symptomatic bacterial vaginosis (BV) late in pregnancy. We do not routinely screen asymptomatic women for BV to reduce the risk of postpartum endometritis as there are no data that this is a cost-effective approach. (See 'Prevention' above.)

REFERENCES

  1. Rosene K, Eschenbach DA, Tompkins LS, et al. Polymicrobial early postpartum endometritis with facultative and anaerobic bacteria, genital mycoplasmas, and Chlamydia trachomatis: treatment with piperacillin or cefoxitin. J Infect Dis 1986; 153:1028.
  2. Maharaj D. Puerperal pyrexia: a review. Part I. Obstet Gynecol Surv 2007; 62:393.
  3. Giraldo-Isaza MA, Jaspan D, Cohen AW. Postpartum endometritis caused by herpes and cytomegaloviruses. Obstet Gynecol 2011; 117:466.
  4. Hollier LM, Scott LL, Murphree SS, Wendel GD Jr. Postpartum endometritis caused by herpes simplex virus. Obstet Gynecol 1997; 89:836.
  5. Rørbye C, Petersen IS, Nilas L. Postpartum Clostridium sordellii infection associated with fatal toxic shock syndrome. Acta Obstet Gynecol Scand 2000; 79:1134.
  6. Bitti A, Mastrantonio P, Spigaglia P, et al. A fatal postpartum Clostridium sordellii associated toxic shock syndrome. J Clin Pathol 1997; 50:259.
  7. Aldape MJ, Bryant AE, Stevens DL. Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment. Clin Infect Dis 2006; 43:1436.
  8. Cohen AL, Bhatnagar J, Reagan S, et al. Toxic shock associated with Clostridium sordellii and Clostridium perfringens after medical and spontaneous abortion. Obstet Gynecol 2007; 110:1027.
  9. Jorup-Rönström C, Hofling M, Lundberg C, Holm S. Streptococcal toxic shock syndrome in a postpartum woman. Case report and review of the literature. Infection 1996; 24:164.
  10. Gibney RT, Moore A, Muldowney FP. Toxic-shock syndrome associated with post-partum staphylococcal endometritis. Ir Med J 1983; 76:90.
  11. Gibbs RS, Blanco JD. Streptococcal infections in pregnancy. A study of 48 bacteremias. Am J Obstet Gynecol 1981; 140:405.
  12. Gibbs RS. Infection after cesarean section. Clin Obstet Gynecol 1985; 28:697.
  13. Burrows LJ, Meyn LA, Weber AM. Maternal morbidity associated with vaginal versus cesarean delivery. Obstet Gynecol 2004; 103:907.
  14. Declercq E, Barger M, Cabral HJ, et al. Maternal outcomes associated with planned primary cesarean births compared with planned vaginal births. Obstet Gynecol 2007; 109:669.
  15. Smaill FM, Grivell RM. Antibiotic prophylaxis versus no prophylaxis for preventing infection after cesarean section. Cochrane Database Syst Rev 2014; :CD007482.
  16. Fernandez H, Gagnepain A, Bourget P, et al. Antibiotic prophylaxis against postpartum endometritis after vaginal delivery: a prospective randomized comparison between Amox-CA (Augmentin) and abstention. Eur J Obstet Gynecol Reprod Biol 1993; 50:169.
  17. Chaim W, Bashiri A, Bar-David J, et al. Prevalence and clinical significance of postpartum endometritis and wound infection. Infect Dis Obstet Gynecol 2000; 8:77.
  18. Soper DE. Bacterial vaginosis and postoperative infections. Am J Obstet Gynecol 1993; 169:467.
  19. Watts DH, Krohn MA, Hillier SL, Eschenbach DA. Bacterial vaginosis as a risk factor for post-cesarean endometritis. Obstet Gynecol 1990; 75:52.
  20. D'Angelo LJ, Sokol RJ. Time-related peripartum determinants of postpartum morbidity. Obstet Gynecol 1980; 55:319.
  21. Bobitt JR, Ledger WJ. Amniotic fluid analysis. Its role in maternal neonatal infection. Obstet Gynecol 1978; 51:56.
  22. Diamond MP, Entman SS, Salyer SL, et al. Increased risk of endometritis and wound infection after cesarean section in insulin-dependent diabetic women. Am J Obstet Gynecol 1986; 155:297.
  23. Jazayeri A, Jazayeri MK, Sahinler M, Sincich T. Is meconium passage a risk factor for maternal infection in term pregnancies? Obstet Gynecol 2002; 99:548.
  24. Tran SH, Caughey AB, Musci TJ. Meconium-stained amniotic fluid is associated with puerperal infections. Am J Obstet Gynecol 2003; 189:746.
  25. Wilkinson C, Enkin MW. Manual removal of placenta at caesarean section. Cochrane Database Syst Rev 2000; :CD000130.
  26. Ely JW, Rijhsinghani A, Bowdler NC, Dawson JD. The association between manual removal of the placenta and postpartum endometritis following vaginal delivery. Obstet Gynecol 1995; 86:1002.
  27. Caughey AB, Musci TJ. Complications of term pregnancies beyond 37 weeks of gestation. Obstet Gynecol 2004; 103:57.
  28. Louis J, Buhari MA, Allen D, et al. Postpartum morbidity associated with advanced HIV disease. Infect Dis Obstet Gynecol 2006; 2006:79512.
  29. Björklund K, Mutyaba T, Nabunya E, Mirembe F. Incidence of postcesarean infections in relation to HIV status in a setting with limited resources. Acta Obstet Gynecol Scand 2005; 84:967.
  30. Faro S. Postpartum endometritis. Clin Perinatol 2005; 32:803.
  31. Newton ER, Prihoda TJ, Gibbs RS. A clinical and microbiologic analysis of risk factors for puerperal endometritis. Obstet Gynecol 1990; 75:402.
  32. Jacobsson B, Pernevi P, Chidekel L, Jörgen Platz-Christensen J. Bacterial vaginosis in early pregnancy may predispose for preterm birth and postpartum endometritis. Acta Obstet Gynecol Scand 2002; 81:1006.
  33. Spore WW, Moskal PA, Nakamura RM, Mishell DR Jr. Bacteriology of postpartum oviducts and endometrium. Am J Obstet Gynecol 1970; 107:572.
  34. Casey BM, Cox SM. Chorioamnionitis and endometritis. Infect Dis Clin North Am 1997; 11:203.
  35. Watts DH, Eschenbach DA, Kenny GE. Early postpartum endometritis: the role of bacteria, genital mycoplasmas, and Chlamydia trachomatis. Obstet Gynecol 1989; 73:52.
  36. Harrison HR. Prospective studies of Mycoplasma hominis infection in pregnancy. Sex Transm Dis 1983; 10:311.
  37. Patai K, Szilágyi G, Hubay M, et al. Severe endometritis caused by genital mycoplasmas after Caesarean section. J Med Microbiol 2005; 54:1249.
  38. Bauer ME, Lorenz RP, Bauer ST, et al. Maternal Deaths Due to Sepsis in the State of Michigan, 1999-2006. Obstet Gynecol 2015; 126:747.
  39. Lissauer D, Cheshire J, Dunlop C, et al. Development of the FAST-M maternal sepsis bundle for use in low-resource settings: a modified Delphi process. BJOG 2020; 127:416.
  40. Cheshire J, Jones L, Munthali L, et al. The FAST-M complex intervention for the detection and management of maternal sepsis in low-resource settings: a multi-site evaluation. BJOG 2021; 128:1324.
  41. Acker DB, Johnson MP, Sachs BP, Friedman EA. The leukocyte count in labor. Am J Obstet Gynecol 1985; 153:737.
  42. Hartmann KE, Barrett KE, Reid VC, et al. Clinical usefulness of white blood cell count after cesarean delivery. Obstet Gynecol 2000; 96:295.
  43. Kankuri E, Kurki T, Carlson P, Hiilesmaa V. Incidence, treatment and outcome of peripartum sepsis. Acta Obstet Gynecol Scand 2003; 82:730.
  44. Mulic-Lutvica A, Axelsson O. Postpartum ultrasound in women with postpartum endometritis, after cesarean section and after manual evacuation of the placenta. Acta Obstet Gynecol Scand 2007; 86:210.
  45. Gui B, Corvino M, Grimaldi PP, et al. Multidetector CT appearance of the pelvis after vaginal delivery: normal appearances and abnormal acute findings. Diagn Interv Radiol 2019; 25:210.
  46. Laifer-Narin SL, Kwak E, Kim H, et al. Multimodality imaging of the postpartum or posttermination uterus: evaluation using ultrasound, computed tomography, and magnetic resonance imaging. Curr Probl Diagn Radiol 2014; 43:374.
  47. Locksmith GJ, Duff P. Assessment of the value of routine blood cultures in the evaluation and treatment of patients with chorioamnionitis. Infect Dis Obstet Gynecol 1994; 2:111.
  48. Centers for Disease Control. National Healthcare Safety Network (NHSN) Patient Safety Component Manual https://www.cdc.gov/nhsn/PDFs/pscManual/pcsManual_current.pdf (Accessed on August 24, 2020).
  49. Lurie S, Vaknine H, Izakson A, et al. Group A Streptococcus causing a life-threatening postpartum necrotizing myometritis: a case report. J Obstet Gynaecol Res 2008; 34:645.
  50. de Moya MA, del Carmen MG, Allain RM, et al. Case records of the Massachusetts General Hospital. Case 33-2009. A 35-year-old woman with fever, abdominal pain, and hypotension after cesarean section. N Engl J Med 2009; 361:1689.
  51. Deguchi Y, Horiuchi Y, Shojima K, et al. Postpartum Methicillin-Resistant Staphylococcus aureus Toxic Shock Syndrome Caused by a Perineal Infection. Case Rep Obstet Gynecol 2018; 2018:2670179.
  52. Ghai S, Ghai V, Sunderji S. Fulminant postcesarean Clostridium difficile pseudomembranous colitis. Obstet Gynecol 2007; 109:541.
  53. diZerega G, Yonekura L, Roy S, et al. A comparison of clindamycin-gentamicin and penicillin-gentamicin in the treatment of post-cesarean section endomyometritis. Am J Obstet Gynecol 1979; 134:238.
  54. Faro S, Phillips LE, Baker JL, et al. Comparative efficacy and safety of mezlocillin, cefoxitin, and clindamycin plus gentamicin in postpartum endometritis. Obstet Gynecol 1987; 69:760.
  55. Alvarez RD, Kilgore LC, Huddleston JF. A comparison of mezlocillin versus clindamycin/gentamicin for the treatment of postcesarean endomyometritis. Am J Obstet Gynecol 1988; 158:425.
  56. Faro S, Martens M, Hammill H, et al. Ticarcillin/clavulanic acid versus clindamycin and gentamicin in the treatment of post-cesarean endometritis following antibiotic prophylaxis. Obstet Gynecol 1989; 73:808.
  57. Gibbs RS, Blanco JD, Castaneda YS, St Clair PJ. A double-blind, randomized comparison of clindamycin-gentamicin versus cefamandole for treatment of post-cesarean section endomyometritis. Am J Obstet Gynecol 1982; 144:261.
  58. Gibbs RS, Blanco JD, Duff P, et al. A double-blind, randomized comparison of moxalactam versus clindamycin-gentamicin in treatment of endomyometritis after cesarean section delivery. Am J Obstet Gynecol 1983; 146:769.
  59. Gilstrap LC 3rd, Maier RC, Gibbs RS, et al. Piperacillin versus clindamycin plus gentamicin for pelvic infections. Obstet Gynecol 1984; 64:762.
  60. Herman G, Cohen AW, Talbot GH, et al. Cefoxitin versus clindamycin and gentamicin in the treatment of postcesarean section infections. Obstet Gynecol 1986; 67:371.
  61. Sweet RL, Roy S, Faro S, et al. Piperacillin and tazobactam versus clindamycin and gentamicin in the treatment of hospitalized women with pelvic infection. The Piperacillin/tazobactam Study Group. Obstet Gynecol 1994; 83:280.
  62. Mackeen AD, Packard RE, Ota E, Speer L. Antibiotic regimens for postpartum endometritis. Cochrane Database Syst Rev 2015; :CD001067.
  63. Hecht DW. Prevalence of antibiotic resistance in anaerobic bacteria: worrisome developments. Clin Infect Dis 2004; 39:92.
  64. Jamal W, Shahin M, Rotimi VO. Surveillance and trends of antimicrobial resistance among clinical isolates of anaerobes in Kuwait hospitals from 2002 to 2007. Anaerobe 2010; 16:1.
  65. Goldstein EJ, Citron DM. Activity of a novel carbapenem, doripenem, against anaerobic pathogens. Diagn Microbiol Infect Dis 2009; 63:447.
  66. McGregor JA, Crombleholme WR, Newton E, et al. Randomized comparison of ampicillin-sulbactam to cefoxitin and doxycycline or clindamycin and gentamicin in the treatment of pelvic inflammatory disease or endometritis. Obstet Gynecol 1994; 83:998.
  67. Phares CR, Lynfield R, Farley MM, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005. JAMA 2008; 299:2056.
  68. Borchardt SM, DeBusscher JH, Tallman PA, et al. Frequency of antimicrobial resistance among invasive and colonizing Group B streptococcal isolates. BMC Infect Dis 2006; 6:57.
  69. Castor ML, Whitney CG, Como-Sabetti K, et al. Antibiotic resistance patterns in invasive group B streptococcal isolates. Infect Dis Obstet Gynecol 2008; 2008:727505.
  70. DiPersio LP, DiPersio JR. High rates of erythromycin and clindamycin resistance among OBGYN isolates of group B Streptococcus. Diagn Microbiol Infect Dis 2006; 54:79.
  71. Back EE, O'Grady EJ, Back JD. High rates of perinatal group B Streptococcus clindamycin and erythromycin resistance in an upstate New York hospital. Antimicrob Agents Chemother 2012; 56:739.
  72. Francois Watkins LK, McGee L, Schrag SJ, et al. Epidemiology of Invasive Group B Streptococcal Infections Among Nonpregnant Adults in the United States, 2008-2016. JAMA Intern Med 2019; 179:479.
  73. Stovall TG, Thorpe EM Jr, Ling FW. Treatment of post-cesarean section endometritis with ampicillin and sulbactam or clindamycin and gentamicin. J Reprod Med 1993; 38:843.
  74. MacGregor RR, Graziani AL, Samuels P. Randomized, double-blind study of cefotetan and cefoxitin in post-cesarean section endometritis. Am J Obstet Gynecol 1992; 167:139.
  75. Soper DE, Brockwell NJ, Dalton HP. The importance of wound infection in antibiotic failures in the therapy of postpartum endometritis. Surg Gynecol Obstet 1992; 174:265.
  76. Figueroa-Damian R, Villagrana-Zesati R, San Martín-Herrasti JM, Arredondo-Garcia JL. [Comparison of the therapeutic efficacy of the piperacillin/tazobactame combination vs. ampicillin and gentamycin in in the management of post-cesarean endometritis]. Ginecol Obstet Mex 1996; 64:214.
  77. Meaney-Delman D, Bartlett LA, Gravett MG, Jamieson DJ. Oral and intramuscular treatment options for early postpartum endometritis in low-resource settings: a systematic review. Obstet Gynecol 2015; 125:789.
  78. Walmer D, Walmer KR, Gibbs RS. Enterococci in post-cesarean endometritis. Obstet Gynecol 1988; 71:159.
  79. Brumfield CG, Hauth JC, Andrews WW. Puerperal infection after cesarean delivery: evaluation of a standardized protocol. Am J Obstet Gynecol 2000; 182:1147.
  80. Gall S, Koukol DH. Ampicillin/sulbactam vs. clindamycin/gentamicin in the treatment of postpartum endometritis. J Reprod Med 1996; 41:575.
  81. Rijhsinghani A, Savopoulos SE, Walters JK, et al. Ampicillin/sulbactam versus ampicillin alone for cesarean section prophylaxis: a randomized double-blind trial. Am J Perinatol 1995; 12:322.
  82. Resnik E, Harger JH, Kuller JA. Early postpartum endometritis. Randomized comparison of ampicillin/sulbactam vs. ampicillin, gentamicin and clindamycin. J Reprod Med 1994; 39:467.
  83. Zuckerman J, Levine D, McNicholas MM, et al. Imaging of pelvic postpartum complications. AJR Am J Roentgenol 1997; 168:663.
  84. Klein SM, García CR. Asherman's syndrome: a critique and current review. Fertil Steril 1973; 24:722.
  85. Hoyme UB, Kiviat N, Eschenbach DA. Microbiology and treatment of late postpartum endometritis. Obstet Gynecol 1986; 68:226.
  86. Gibbs RS, Rodgers PJ, Castaneda YS, Ramzy I. Endometritis following vaginal delivery. Obstet Gynecol 1980; 56:555.
  87. Khong TY, Khong TK. Delayed postpartum hemorrhage: a morphologic study of causes and their relation to other pregnancy disorders. Obstet Gynecol 1993; 82:17.
  88. Atterbury JL, Groome LJ, Baker SL, et al. Hospital readmission for postpartum endometritis. J Matern Fetal Med 1998; 7:250.
  89. Haggerty CL, Ness RB, Amortegui A, et al. Endometritis does not predict reproductive morbidity after pelvic inflammatory disease. Am J Obstet Gynecol 2003; 188:141.
  90. Haas DM, Morgan S, Contreras K, Kimball S. Vaginal preparation with antiseptic solution before cesarean section for preventing postoperative infections. Cochrane Database Syst Rev 2020; 4:CD007892.
  91. Elliott JP, Flaherty JF. Comparison of lavage or intravenous antibiotics at cesarean section. Obstet Gynecol 1986; 67:29.
  92. Berkeley AS, Hirsch JC, Freedman KS, Ledger WJ. Cefotaxime for cesarean section prophylaxis in labor. Intravenous administration vs. lavage. J Reprod Med 1990; 35:214.
  93. Atkinson MW, Owen J, Wren A, Hauth JC. The effect of manual removal of the placenta on post-cesarean endometritis. Obstet Gynecol 1996; 87:99.
  94. Lasley DS, Eblen A, Yancey MK, Duff P. The effect of placental removal method on the incidence of postcesarean infections. Am J Obstet Gynecol 1997; 176:1250.
  95. Dehbashi S, Honarvar M, Fardi FH. Manual removal or spontaneous placental delivery and postcesarean endometritis and bleeding. Int J Gynaecol Obstet 2004; 86:12.
  96. Baksu A, Kalan A, Ozkan A, et al. The effect of placental removal method and site of uterine repair on postcesarean endometritis and operative blood loss. Acta Obstet Gynecol Scand 2005; 84:266.
  97. Knight M, Chiocchia V, Partlett C, et al. Prophylactic antibiotics in the prevention of infection after operative vaginal delivery (ANODE): a multicentre randomised controlled trial. Lancet 2019; 393:2395.
  98. Sebitloane HM, Moodley J, Esterhuizen TM. Prophylactic antibiotics for the prevention of postpartum infectious morbidity in women infected with human immunodeficiency virus: a randomized controlled trial. Am J Obstet Gynecol 2008; 198:189.e1.
  99. Chongsomchai C, Lumbiganon P, Laopaiboon M. Prophylactic antibiotics for manual removal of retained placenta in vaginal birth. Cochrane Database Syst Rev 2006; :CD004904.
  100. Miller JM, Binnicker MJ, Campbell S, et al. A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology. Clin Infect Dis 2018; 67:e1.
  101. US Preventive Services Task Force, Owens DK, Davidson KW, et al. Screening for Bacterial Vaginosis in Pregnant Persons to Prevent Preterm Delivery: US Preventive Services Task Force Recommendation Statement. JAMA 2020; 323:1286.
  102. Thinkhamrop J, Hofmeyr GJ, Adetoro O, et al. Antibiotic prophylaxis during the second and third trimester to reduce adverse pregnancy outcomes and morbidity. Cochrane Database Syst Rev 2015; :CD002250.
Topic 5488 Version 63.0

References

1 : Polymicrobial early postpartum endometritis with facultative and anaerobic bacteria, genital mycoplasmas, and Chlamydia trachomatis: treatment with piperacillin or cefoxitin.

2 : Puerperal pyrexia: a review. Part I.

3 : Postpartum endometritis caused by herpes and cytomegaloviruses.

4 : Postpartum endometritis caused by herpes simplex virus.

5 : Postpartum Clostridium sordellii infection associated with fatal toxic shock syndrome.

6 : A fatal postpartum Clostridium sordellii associated toxic shock syndrome.

7 : Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment.

8 : Toxic shock associated with Clostridium sordellii and Clostridium perfringens after medical and spontaneous abortion.

9 : Streptococcal toxic shock syndrome in a postpartum woman. Case report and review of the literature.

10 : Toxic-shock syndrome associated with post-partum staphylococcal endometritis.

11 : Streptococcal infections in pregnancy. A study of 48 bacteremias.

12 : Infection after cesarean section.

13 : Maternal morbidity associated with vaginal versus cesarean delivery.

14 : Maternal outcomes associated with planned primary cesarean births compared with planned vaginal births.

15 : Antibiotic prophylaxis versus no prophylaxis for preventing infection after cesarean section.

16 : Antibiotic prophylaxis against postpartum endometritis after vaginal delivery: a prospective randomized comparison between Amox-CA (Augmentin) and abstention.

17 : Prevalence and clinical significance of postpartum endometritis and wound infection.

18 : Bacterial vaginosis and postoperative infections.

19 : Bacterial vaginosis as a risk factor for post-cesarean endometritis.

20 : Time-related peripartum determinants of postpartum morbidity.

21 : Amniotic fluid analysis. Its role in maternal neonatal infection.

22 : Increased risk of endometritis and wound infection after cesarean section in insulin-dependent diabetic women.

23 : Is meconium passage a risk factor for maternal infection in term pregnancies?

24 : Meconium-stained amniotic fluid is associated with puerperal infections.

25 : Manual removal of placenta at caesarean section.

26 : The association between manual removal of the placenta and postpartum endometritis following vaginal delivery.

27 : Complications of term pregnancies beyond 37 weeks of gestation.

28 : Postpartum morbidity associated with advanced HIV disease.

29 : Incidence of postcesarean infections in relation to HIV status in a setting with limited resources.

30 : Postpartum endometritis.

31 : A clinical and microbiologic analysis of risk factors for puerperal endometritis.

32 : Bacterial vaginosis in early pregnancy may predispose for preterm birth and postpartum endometritis.

33 : Bacteriology of postpartum oviducts and endometrium.

34 : Chorioamnionitis and endometritis.

35 : Early postpartum endometritis: the role of bacteria, genital mycoplasmas, and Chlamydia trachomatis.

36 : Prospective studies of Mycoplasma hominis infection in pregnancy.

37 : Severe endometritis caused by genital mycoplasmas after Caesarean section.

38 : Maternal Deaths Due to Sepsis in the State of Michigan, 1999-2006.

39 : Development of the FAST-M maternal sepsis bundle for use in low-resource settings: a modified Delphi process.

40 : The FAST-M complex intervention for the detection and management of maternal sepsis in low-resource settings: a multi-site evaluation.

41 : The leukocyte count in labor.

42 : Clinical usefulness of white blood cell count after cesarean delivery.

43 : Incidence, treatment and outcome of peripartum sepsis.

44 : Postpartum ultrasound in women with postpartum endometritis, after cesarean section and after manual evacuation of the placenta.

45 : Multidetector CT appearance of the pelvis after vaginal delivery: normal appearances and abnormal acute findings.

46 : Multimodality imaging of the postpartum or posttermination uterus: evaluation using ultrasound, computed tomography, and magnetic resonance imaging.

47 : Assessment of the value of routine blood cultures in the evaluation and treatment of patients with chorioamnionitis.

48 : Assessment of the value of routine blood cultures in the evaluation and treatment of patients with chorioamnionitis.

49 : Group A Streptococcus causing a life-threatening postpartum necrotizing myometritis: a case report.

50 : Case records of the Massachusetts General Hospital. Case 33-2009. A 35-year-old woman with fever, abdominal pain, and hypotension after cesarean section.

51 : Postpartum Methicillin-Resistant Staphylococcus aureus Toxic Shock Syndrome Caused by a Perineal Infection.

52 : Fulminant postcesarean Clostridium difficile pseudomembranous colitis.

53 : A comparison of clindamycin-gentamicin and penicillin-gentamicin in the treatment of post-cesarean section endomyometritis.

54 : Comparative efficacy and safety of mezlocillin, cefoxitin, and clindamycin plus gentamicin in postpartum endometritis.

55 : A comparison of mezlocillin versus clindamycin/gentamicin for the treatment of postcesarean endomyometritis.

56 : Ticarcillin/clavulanic acid versus clindamycin and gentamicin in the treatment of post-cesarean endometritis following antibiotic prophylaxis.

57 : A double-blind, randomized comparison of clindamycin-gentamicin versus cefamandole for treatment of post-cesarean section endomyometritis.

58 : A double-blind, randomized comparison of moxalactam versus clindamycin-gentamicin in treatment of endomyometritis after cesarean section delivery.

59 : Piperacillin versus clindamycin plus gentamicin for pelvic infections.

60 : Cefoxitin versus clindamycin and gentamicin in the treatment of postcesarean section infections.

61 : Piperacillin and tazobactam versus clindamycin and gentamicin in the treatment of hospitalized women with pelvic infection. The Piperacillin/tazobactam Study Group.

62 : Antibiotic regimens for postpartum endometritis.

63 : Prevalence of antibiotic resistance in anaerobic bacteria: worrisome developments.

64 : Surveillance and trends of antimicrobial resistance among clinical isolates of anaerobes in Kuwait hospitals from 2002 to 2007.

65 : Activity of a novel carbapenem, doripenem, against anaerobic pathogens.

66 : Randomized comparison of ampicillin-sulbactam to cefoxitin and doxycycline or clindamycin and gentamicin in the treatment of pelvic inflammatory disease or endometritis.

67 : Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005.

68 : Frequency of antimicrobial resistance among invasive and colonizing Group B streptococcal isolates.

69 : Antibiotic resistance patterns in invasive group B streptococcal isolates.

70 : High rates of erythromycin and clindamycin resistance among OBGYN isolates of group B Streptococcus.

71 : High rates of perinatal group B Streptococcus clindamycin and erythromycin resistance in an upstate New York hospital.

72 : Epidemiology of Invasive Group B Streptococcal Infections Among Nonpregnant Adults in the United States, 2008-2016.

73 : Treatment of post-cesarean section endometritis with ampicillin and sulbactam or clindamycin and gentamicin.

74 : Randomized, double-blind study of cefotetan and cefoxitin in post-cesarean section endometritis.

75 : The importance of wound infection in antibiotic failures in the therapy of postpartum endometritis.

76 : [Comparison of the therapeutic efficacy of the piperacillin/tazobactame combination vs. ampicillin and gentamycin in in the management of post-cesarean endometritis].

77 : Oral and intramuscular treatment options for early postpartum endometritis in low-resource settings: a systematic review.

78 : Enterococci in post-cesarean endometritis.

79 : Puerperal infection after cesarean delivery: evaluation of a standardized protocol.

80 : Ampicillin/sulbactam vs. clindamycin/gentamicin in the treatment of postpartum endometritis.

81 : Ampicillin/sulbactam versus ampicillin alone for cesarean section prophylaxis: a randomized double-blind trial.

82 : Early postpartum endometritis. Randomized comparison of ampicillin/sulbactam vs. ampicillin, gentamicin and clindamycin.

83 : Imaging of pelvic postpartum complications.

84 : Asherman's syndrome: a critique and current review.

85 : Microbiology and treatment of late postpartum endometritis.

86 : Endometritis following vaginal delivery.

87 : Delayed postpartum hemorrhage: a morphologic study of causes and their relation to other pregnancy disorders.

88 : Hospital readmission for postpartum endometritis.

89 : Endometritis does not predict reproductive morbidity after pelvic inflammatory disease.

90 : Vaginal preparation with antiseptic solution before cesarean section for preventing postoperative infections.

91 : Comparison of lavage or intravenous antibiotics at cesarean section.

92 : Cefotaxime for cesarean section prophylaxis in labor. Intravenous administration vs. lavage.

93 : The effect of manual removal of the placenta on post-cesarean endometritis.

94 : The effect of placental removal method on the incidence of postcesarean infections.

95 : Manual removal or spontaneous placental delivery and postcesarean endometritis and bleeding.

96 : The effect of placental removal method and site of uterine repair on postcesarean endometritis and operative blood loss.

97 : Prophylactic antibiotics in the prevention of infection after operative vaginal delivery (ANODE): a multicentre randomised controlled trial.

98 : Prophylactic antibiotics for the prevention of postpartum infectious morbidity in women infected with human immunodeficiency virus: a randomized controlled trial.

99 : Prophylactic antibiotics for manual removal of retained placenta in vaginal birth.

100 : A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology.

101 : Screening for Bacterial Vaginosis in Pregnant Persons to Prevent Preterm Delivery: US Preventive Services Task Force Recommendation Statement.

102 : Antibiotic prophylaxis during the second and third trimester to reduce adverse pregnancy outcomes and morbidity.