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 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. In a study of 55 antibiotic-naive patients 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 seven had a blood isolate . Bacterial findings included:
●At least one facultative or one anaerobic species of bacteria – 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 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 . In HIV-infected patients, the microbiology can be broader and include other less likely pathogens, such as herpes simplex virus and cytomegalovirus .
Rare, but potentially lethal, causes of endometritis include Clostridium sordellii [4-7], Clostridium perfringens , and streptococcal or staphylococcal toxic shock syndrome [9-11]. (See 'Endometritis with toxic shock syndrome' below.)
●Cesarean birth – Cesarean birth is the dominant risk factor for development of postpartum endometritis, especially when performed after the onset of labor [12-14]. 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) . 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 [13,16,17]. Because of the low rate, antibiotic prophylaxis is not standard practice for patients in labor expecting to give birth vaginally.
●Other – Other risk factors for postpartum endometritis include [17-30]:
•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
•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 [29,31]. 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 .
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 [33-35].
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 .
Signs and symptoms — The key clinical findings present in most patients with postpartum endometritis are:
●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.
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 . For example, group A Streptococcus infection should be suspected in patients with an early-onset infection and high fever. (See "Pregnancy-related group A streptococcal infection".)
Alarm findings (sepsis) — The following findings are the criteria for suspecting severe infection/sepsis in febrile postpartum patients at one academic teaching hospital, 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 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".)
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 .
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 created a toolkit for improving diagnosis and treatment of maternal sepsis, which is available .
●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 [37,38]. Its effectiveness has not been assessed.
●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 [39,40]. 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 ; 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 . 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 [43,44].
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.
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 , 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 . For these reasons, we do not obtain blood cultures routinely in patients with endometritis. However, blood cultures can be useful in guiding 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.
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 :
●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 [47,48].
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 "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 . (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 .
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 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 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 patients who have low-grade fever, abdominal and gastrointestinal symptoms, and recent antibiotic exposure . (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)
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 . Treatment is the same, regardless of mode of birth. 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 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 [51-60]:
●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)
However, two concerns regarding use of clindamycin are:
●Increasing resistance among anaerobic bacteria to clindamycin [61-63], 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 .
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 8 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 ). 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 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) .
Preferred initial regimen (GBS colonization) — Resistance to clindamycin in GBS isolates ranges from 13 to 43 percent [65-70]. 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
●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 [1,71-74]. 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 or ceftriaxone and metronidazole is another option that provides good activity against most anaerobes; however, metronidazole is avoided in breastfeeding individuals 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 .
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 :
●Amoxicillin-clavulanic acid 875 mg orally every 12 hours or
●Cefotetan 2 g intramuscularly every 8 hours or
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:
●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 [76,77].
Alternatively, the initial antibiotics can be discontinued, and ampicillin-sulbactam (eg, Unasyn) can be initiated if the patient was not already on ampicillin [71,78-80]. 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 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 . 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) . 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.
●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.)
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 [83,84]. Delayed presentation is more common after vaginal than cesarean birth, and it may present as late postpartum hemorrhage [85,86]. (See "Secondary (late) postpartum hemorrhage".)
Most patients with late postpartum endometritis have mild clinical signs and symptoms . 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 .
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 . 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 patients with postpartum endometritis, secondary infertility appears to be uncommon with timely diagnosis of endometritis and appropriate treatment in gynecologic patients . A severe infection may result in exosalpingitis, but endosalpingitis is unusual .
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, povidone-iodine, 4% chlorhexidine gluconate) immediately before cesarean birth also reduces the incidence of postcesarean endometritis. These data are discussed in detail separately . (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 [89,90]. 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, four randomized trials with a total of over 2000 participants reported that spontaneous delivery of the placenta resulted in a significant reduction in postpartum endometritis compared with manual removal [91-94].
At vaginal birth
●Role of antibiotic prophylaxis – Patients undergoing vaginal birth 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 patients at high risk.
•A trial that randomly assigned patients who underwent an operative vaginal birth to postpartum antibiotics or placebo reported a similar rate of endometritis (1 percent) in both groups .
•A double-blind trial that randomly assigned 424 HIV-infected pregnant patients anticipating vaginal birth 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) . The overall rate of sepsis was similar for both groups (40 out of 211 patients [19 percent] in the placebo group and 36 out of 213 patients [17 percent] in the cefoxitin group).
●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 . 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) . 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
●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.)
•History and physical – The key clinical findings present in most patients are:
-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 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 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.)
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 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.)
•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.)