ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Postpartum endometritis

Postpartum endometritis
Literature review current through: Jan 2024.
This topic last updated: Aug 22, 2023.

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

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

MICROBIOLOGY — Postpartum endometritis is typically a polymicrobial infection involving a mixture of two to three aerobes and anaerobes from the lower genital tract. Microbiology is similar to that of chorioamnionitis [1]. In a study of 55 antibiotic-naive patients with well-defined postpartum endometritis who had endometrial cultures obtained with a triple-lumen catheter (to reduce the risk of contamination from organisms on the cervix), 51 (93 percent) had an endometrial isolate and seven (13 percent) had a blood isolate [2]. Bacterial findings included:

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

Genital mycoplasmas – 39 of 51 (76 percent).

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

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

Bacteremia in 38 percent of those with endometrial cultures positive for bacteria and in none of those with negative bacterial endometrial cultures.

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

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

RISK FACTORS

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

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

Other – Other risk factors for postpartum endometritis include [19-32]:

Chorioamnionitis

Prolonged labor

Prolonged rupture of membranes

Multiple cervical examinations

Internal fetal or uterine monitoring

Large amount of meconium in amniotic fluid

Manual removal of the placenta

Low socioeconomic status

Maternal diabetes mellitus or severe anemia

Preterm or postterm birth

Operative vaginal birth

Obesity

HIV infection

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

Nasal carriage of Staphylococcus aureus

Heavy vaginal colonization by E. coli

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

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

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

CLINICAL FINDINGS

Signs and symptoms — In most patients with postpartum endometritis, the key clinical findings are:

Fever

Uterine tenderness

Tachycardia that parallels the rise in temperature

Midline lower abdominal pain

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

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

Alarm findings (sepsis) — In febrile postpartum patients, the following criteria should raise suspicion of severe infection/sepsis, based on expert opinion:

Fever ≥103°F (39.4°C) or

Fever ≥102°F (38.9°C) plus one or more of the following:

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

Respiratory rate ≥20 respirations/minute, sustained for at least 30 minutes

Manual white blood cell (WBC) differential showing ≥10 percent bands

Blood pressure ≤90/60 mmHg, sustained for at least 30 minutes (in the setting of infection, septic shock can be diagnosed if mean arterial pressure is <65 mmHg after 30 mL/kg fluid load)

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

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

Identification of patients at risk for sepsis — Medical society guidelines emphasize that early identification of infected patients who may go on to develop sepsis is important to decrease sepsis-associated mortality.

The California Maternal Quality Care Collaborative (CMQCC) created a toolkit for improving diagnosis and treatment of maternal sepsis, which is available online.

The two most commonly used scores to identify patients with sepsis in the intensive care unit (ICU) are the Quick Sequential (Sepsis-related) Organ Failure Assessment (qSOFA) score (calculator 1) and the National Early Warning Score (NEWS) score, but their utility compared with clinical judgment in non-ICU patients has not been established, and they have not been evaluated in patients with postpartum endometritis. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Identification of early sepsis (qSOFA, NEWS)'.)

The FAST-M complex intervention (Fluids, Antibiotics, Source identification and control, Transfer to an appropriate level of care, and ongoing Monitoring of mother and neonate) was designed to improve the recognition and management of maternal sepsis in low-resource settings [38,39]. Its effectiveness has not been assessed.

In 2023, the Alliance for Innovation on Maternal Health created a "Sepsis in Obstetric Care" patient safety bundle to provide guidance for health care teams to develop coordinated, multidisciplinary care for pregnant and postpartum people by preventing infection and recognizing and treating infection early to prevent progression to sepsis [40].

Laboratory

White blood cell count and differential – The WBC count is elevated (15,000 to 30,000 cells/microL), but this can be a normal finding postpartum secondary to the physiologic leukocytosis of pregnancy and the effects of labor [41,42]. Mean WBC counts in laboring patients range from 10,000 to 16,000 cells/microL, with an upper level as high as 29,000 cells/microL. A left shift (bandemia) and a rising, rather than falling, neutrophil count postpartum are suggestive of an infectious process. (See "Maternal adaptations to pregnancy: Hematologic changes", section on 'White blood cells'.)

Bacteremia – Bacteremia has been reported in 5 to 20 percent of patients [43]; however, in clinical practice most patients do not have microbiologic studies of blood, endometrium, or cervix for laboratory confirmation of the infectious etiology of endometritis. (See 'Role of blood and endometrial cultures' below.)

Imaging — There are no characteristic sonographic findings associated with postpartum endometritis [44]. Imaging findings are nonspecific and overlap with expected postpartum changes (nonspecific uterine enlargement, endometrial fluid, and/or gas). (See "Overview of the postpartum period: Normal physiology and routine maternal care", section on 'Findings on ultrasound'.)

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

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

DIAGNOSTIC EVALUATION — The diagnostic evaluation of postpartum patients with fever and/or pain includes:

History/physical examination to determine the possible source of the signs and symptoms. (See 'Differential diagnosis' below.)

Complete blood count with differential.

Urine culture.

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

Role of blood and endometrial cultures — In uncomplicated infections, it is not important to establish the microbiologic cause since empiric treatment with broad spectrum antibiotics is usually effective.

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

Interestingly, only a single organism may be identified in the blood culture despite polymicrobial endometrial infection.

Endometrial cultures – Endometrial cultures are not performed because of the difficulty in obtaining an uncontaminated specimen through the cervix. Furthermore, they yield results too late for clinical use and rarely changing treatment.

DIAGNOSIS

Diagnostic criteria for postpartum endometritis — Postpartum endometritis is primarily a clinical diagnosis based on characteristic signs and symptoms and presence of risk factors. In the United States, the diagnosis is made in a patient with at least two of the following signs or symptoms; small variations in the criteria are common worldwide [50]:

Fever (≥100.4°F [38°C])

Pain or tenderness (uterine or abdominal) with no other recognized cause

Purulent drainage from the uterus

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

Endometritis with toxic shock syndrome — Although rare, Clostridium, Streptococcus, and Staphylococcus infections can lead to endometritis with toxic shock syndrome and other life-threatening complications (eg, necrotizing myometritis, necrotizing fasciitis). This rare diagnosis is made in the following settings:

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

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

Staphylococcal toxic shock syndrome is characterized by high fever >102°F (38.9°C), hypotension, diffuse erythroderma, desquamation (unless the patient dies before desquamation can occur), and involvement of at least three organ systems. Onset may be early (within 24 hours of birth) and difficult to distinguish from GAS toxic shock syndrome in the absence of laboratory confirmation (table 1). Postpartum methicillin-resistant S. aureus toxic shock syndrome has been reported, but is rare [53]. (See "Staphylococcal toxic shock syndrome".)

C. sordellii has been associated with a distinctive, lethal toxic shock-like syndrome. In one report, affected patients were less than one week postpartum when they had sudden onset of clinical shock: progressive, refractory hypotension was associated with massive and generalized tissue edema, hemoconcentration, a marked leukemoid reaction (total neutrophil count 66,000 to 93,600/mm3), absence of rash or fever, limited or no myonecrosis, and a rapidly lethal course. (See "Toxic shock syndrome due to Paeniclostridium sordellii" and "Clostridial myonecrosis".)

C. perfringens should be considered in patients who rapidly become gravely ill with evidence of intravascular hemolysis, which may be severe. It can cause clostridial myonecrosis (gas gangrene), a life-threatening muscle infection that can be identified by radiographic imaging. (See "Clostridial myonecrosis".)

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

Differential diagnosis — In patients with postpartum fever but no or minimal uterine tenderness or purulent vaginal discharge, other sources of postpartum fever should be considered. Any disorder associated with fever, such as appendicitis or viral syndrome, can present with fever in the postpartum period. Many of these disorders can be diagnosed or excluded by history and physical examination alone; in the remainder, laboratory and/or imaging studies will clarify the diagnosis. Some common causes of fever in postpartum patients include:

Surgical site infection (eg, abdominal wall incision, episiotomy incision, perineal lacerations) is typically evident on physical examination of the surgical site (eg, local erythema, edema, and/or tenderness). (See "Complications of abdominal surgical incisions" and "Approach to episiotomy".)

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

Breast engorgement (fullness and firmness accompanied by pain and tenderness) may lead to a low-grade fever 24 to 72 hours postpartum. (See "Lactational mastitis" and "Primary breast abscess".)

Pyelonephritis is characterized by fever (>100.4°F [38°C]), chills, flank pain, costovertebral angle tenderness, and possibly lower urinary tract symptoms. Pyuria and/or a positive urine culture supports the diagnosis. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)

Aspiration pneumonia presents with fever, dyspnea, and possibly hypoxemia. Lung auscultation may reveal diffuse crackles, and a chest radiograph will show infiltrates. It primarily occurs in postpartum patients with compromise in the usual defenses that protect the lower airways, such as those with a recent history of a difficult or failed intubation. (See "Aspiration pneumonia in adults".)

Unexplained fever with significant back pain after a neuraxial anesthetic, especially when accompanied by neurologic symptoms, may be due to infection or inflammation of the spinal cord. Consultation with the anesthesia and neurology services is indicated. (See "Serious neurologic complications of neuraxial anesthesia procedures in obstetric patients".)

Pseudomembranous colitis due to Clostridioides difficile is a rare, but potentially serious, cause of postpartum fever. It should be considered in postpartum patients who have low-grade fever, abdominal and gastrointestinal symptoms, and recent antibiotic exposure [54]. (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)

TREATMENT

Overview — Our approach to treatment of most patients is summarized in the algorithm (algorithm 1) and discussed below. Prompt administration of appropriate antibiotics is critical in septic patients [37]. (See 'Patients with sepsis' below.)

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

Preferred initial regimen (no GBS colonization) — The following intravenous (IV) regimen is for patients with normal renal function and results in resolution of infection in 90 to 97 percent of cases [55-65]:

Clindamycin 900 mg every eight hours plus

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

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

This choice of antibiotics is supported by a 2015 meta-analysis including 40 randomized trials through 2003 that concluded the combination of clindamycin plus an aminoglycoside is appropriate for the treatment of endometritis and that a regimen with activity against Bacteroides fragilis and other penicillin-resistant anaerobic bacteria is better than one without (eg, risk of treatment failure with clindamycin plus an aminoglycoside versus cephalosporins alone: 10.2 versus 14.8 percent, RR 0.69, 95% CI 0.49-0.99) [64]. However, cephalosporins (eg, cefotetan, cefoxitin, ceftizoxime, cefotaxime, cefuroxime) alone have been proposed for treatment of chorioamnionitis and can be considered for treatment of endometritis [66].

Two concerns regarding use of clindamycin are:

Increasing resistance of group B Streptococcus (GBS) isolates. (See 'Preferred initial regimen (GBS colonization present or unknown)' below.)

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

Preferred initial regimen (GBS colonization present or unknown) — For those patients who are known to be colonized with GBS as a result of universal screening, ampicillin should be included in the regimen because clindamycin resistance in GBS isolates ranges from 13 to 43 percent [72-77]. We suggest:

Ampicillin 2 g IV every six hours plus

Clindamycin 900 mg every eight hours plus

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

or

Ampicillin-sulbactam 3 g IV every six hours

Vancomycin can be used instead of ampicillin in patients with immunoglobulin E (IgE)-mediated, immediate allergic reactions, including anaphylaxis. (See "Choice of antibiotics in penicillin-allergic hospitalized patients".)

As discussed above, metronidazole (500 mg IV every eight hours) is an alternative to clindamycin [71] and provides good activity against most anaerobes; however, metronidazole is avoided in breastfeeding individuals when similarly effective drugs with better safety profiles are available. Cefoxitin (2 g IV every six hours) also provides good anaerobic coverage. Alternatives for critically ill patients include piperacillin/tazobactam (3.375 g IV every six hours infused over three hours), meropenem (1 g IV every eight hours infused over three hours), or ertapenem (1 g IV every 24 hours) [78].

Patients with sepsis — Gentamicin, ampicillin, plus clindamycin or metronidazole is preferred for patients with sepsis (life-threatening organ dysfunction caused by a dysregulated host response to infection [79]). The CMQCC suggests administration of both ampicillin-sulbactam and gentamicin as an acceptable alternative [47]. For patients with sepsis and penicillin allergy who are able to take a cephalosporin, the Society for Maternal-Fetal Medicine suggests cefotaxime or ceftriaxone plus metronidazole [80].

Duration of therapy — A response to the initial antibiotic regimen should be evident within 24 to 48 hours. IV treatment is typically continued until the patient is clinically improved (no fundal tenderness) and afebrile for 24 to 48 hours.

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

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

Options when intravenous therapy is not possible — In resource-limited countries where IV lines are not available, a systematic review concluded that the following five antibiotic regimens would provide >85 percent cure rates of early postpartum endometritis and were compatible with breastfeeding [81]:

Clindamycin 600 mg orally every six hours plus gentamicin 4.5 mg/kg intramuscularly every 24 hours or

Amoxicillin-clavulanic acid 875 mg orally every 12 hours or

Cefotetan 2 g intramuscularly every eight hours or

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

Amoxicillin 500 mg plus metronidazole 500 mg orally every eight hours

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

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

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

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

If blood cultures were performed, antibiotic treatment decisions are based on drug sensitivity results for any organisms identified. (See "Treatment of enterococcal infections".)

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

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

Knowledge of the characteristics of the normal postpartum uterus is useful when the postpartum uterus is imaged during evaluation of postpartum complications since fluid, debris, and gas can be normal findings. (See "Overview of the postpartum period: Normal physiology and routine maternal care", section on 'Findings on ultrasound'.)

In patients receiving a thrice daily gentamicin regimen (1.5 mg/kg every eight hours) instead of 5 mg/kg every 24 hours, drug levels should be obtained as they may not be in the therapeutic range, thus necessitating a change in dose. (See "Dosing and administration of parenteral aminoglycosides", section on 'Gentamicin and tobramycin dosing in adults'.)

Retained products of conception after birth (almost always vaginal birth) can cause acute or chronic endometritis related to microbial infection of the necrotic products of conception (eg, fetal membranes, placental fragments) as well as the endometrium. Ultrasound may demonstrate the retained tissue [88]. Diagnosis and treatment are discussed in detail separately. (See "Retained products of conception in the first half of pregnancy".)

Curettage to remove the necrotic material may be necessary to resolve the infection. It is important to not curette the endometrium too vigorously as this can lead to uterine perforation, adhesion formation, and subsequent infertility (ie, Asherman syndrome) [89]. For this reason, suction curettage is preferable to sharp curettage. (See "Intrauterine adhesions: Clinical manifestation and diagnosis".)

The possibility of drug fever should be considered in the absence of any positive findings on physical examination or imaging studies and a pulse rate that does not vary significantly and does not parallel the patient's temperature. Drug fever can be defined as "a disorder characterized by fever coinciding with the administration of the drug and disappearing after the discontinuation of the drug, when no other cause for the fever is evident after a careful physical examination and laboratory investigation." (See "Drug fever".)

Management of relapse — For patients who present with recurrent signs/symptoms of endometritis after having been treated for endometritis on initial hospitalization, the details of the therapy and relevant laboratory/imaging results from initial hospitalization should be reviewed, if available.

If prior cultures were performed, then we target antibiotic therapy to cover the organisms that were identified.

If no organism was identified, then we restart the same regimen that was administered during the initial hospitalization.

If the regimen used during the initial hospitalization is not known, then we start clindamycin, gentamicin, and ampicillin at the doses described above. (See 'Preferred initial regimen (GBS colonization present or unknown)' above.)

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

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

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

For broad spectrum oral therapy, we use:

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

In penicillin-allergic patients, we use:

Clindamycin 600 mg orally every six hours for seven days.

Breastfeeding is not a contraindication to administering these drugs.

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

Surgical site infection is a common associated condition when antibiotic therapy is unsuccessful in resolving fever after cesarean birth and often requires drainage. Wound infection affects 11 percent of patients. Severe complications, which occur in up to 4 percent of patients, include extension of infection to the peritoneal cavity resulting in peritonitis, intraabdominal abscess, or sepsis [64]. Necrotizing myometritis, necrotizing fasciitis of the abdominal wall, septic pelvic thrombophlebitis, and toxic shock syndrome are rare complications. Hysterectomy and/or aggressive wound debridement may be necessary to treat severe infection. (See "Septic pelvic thrombophlebitis" and "Necrotizing soft tissue infections" and "Toxic shock syndrome due to Paeniclostridium sordellii" and "Staphylococcal toxic shock syndrome" and "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis" and "Invasive group A streptococcal infection and toxic shock syndrome: Treatment and prevention".)

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

PREVENTION

At cesarean birth

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

Vaginal preparation with an antiseptic solution (eg, 10% povidone-iodine, 4% chlorhexidine gluconate) immediately before cesarean birth also reduces the incidence of postcesarean endometritis. These data are discussed in detail separately [95]. (See "Cesarean birth: Preoperative planning and patient preparation", section on 'Vaginal preparation'.)

Intrauterine antibiotic irrigation just before closure of hysterotomy incision may be as effective as preoperative intravenous (IV) infusion, probably because the drug is absorbed into the systemic circulation [96,97]. Nevertheless, irrigation has fallen out of favor because it does not appear to offer any advantage over IV therapy and may have disadvantages, such as variable absorption.

Role of placental delivery method – For patients undergoing cesarean birth, a meta-analysis of randomized trials found that manual removal of the placenta increased the risk of postpartum endometritis compared with spontaneous placental removal with cord traction (18.4 versus 11.3 percent; RR 1.64, 95% CI 1.42-1.90) [98].

At vaginal birth

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

Prophylactic antibiotics are sometimes given postpartum to patients who have a vacuum- or forceps-assisted vaginal birth (especially when an episiotomy is performed) and to patients who have a third- or fourth-degree perineal laceration. (See "Assisted (operative) vaginal birth", section on 'Antibiotics' and "Repair of perineal lacerations associated with childbirth", section on 'Antibiotics'.)

Role of placental delivery method – Spontaneous rather than manual delivery of the placenta is routine at vaginal birth, but manual extraction is sometimes necessary. No randomized trials have evaluated use of prophylactic antibiotics in patients who undergo manual removal of placenta [100]. Use of prophylactic antibiotics in this setting varies. (See "Retained placenta after vaginal birth", section on 'Perform manual extraction'.)

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

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Postpartum infection".)

SUMMARY AND RECOMMENDATIONS

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

Clinical findings

History and physical – The key clinical findings present in most patients are:

-Fever

-Uterine tenderness

-Tachycardia that parallels the rise in temperature

-Midline lower abdominal pain

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

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

Laboratory – Laboratory studies are of limited value: a rising neutrophil count associated with elevated numbers of bands is suggestive of infection, and an elevated lactic acid concentration is a marker for serious infection. (See 'Laboratory' above.)

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

Blood cultures are obtained selectively as they can be useful in guiding the choice of antimicrobial treatment in patients who have alarm findings, are immunocompromised, are septic, or fail to respond to empiric antibiotic therapy within 24 to 48 hours.

Diagnosis – In the United States, the diagnosis is made in a patient with at least two of the following signs or symptoms; small variations in the criteria are common worldwide (see 'Diagnosis' above):

-Fever (≥100.4°F [38.0°C])

-Pain or tenderness (uterine or abdominal) with no other recognized cause

-Purulent drainage from uterus

Treatment — Our approach is summarized in the algorithm (algorithm 1). Treatment of postpartum endometritis is indicated for relief of symptoms and prevention of sequelae.

Antibiotic choice and dose – Given the microbiology of these infections, we recommend broad spectrum antibiotics with coverage of beta-lactamase-producing anaerobes (Grade 1B).

-In patients without group B Streptococcus (GBS) colonization, we suggest clindamycin (900 mg intravenously [IV] every eight hours) plus gentamicin (5 mg/kg every 24 hours [preferred] or 1.5 mg/kg every eight hours) (Grade 2B).

-In areas with significant clindamycin resistance in Bacteroides fragilis or if the patient is colonized with GBS, adding ampicillin (2 g IV every six hours) to this regimen or using ampicillin-sulbactam (3 g IV every six hours) is preferred. (See 'Preferred initial regimen (no GBS colonization)' above and 'Preferred initial regimen (GBS colonization present or unknown)' above.)

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

Response to therapy and management of nonresponders – Signs and symptoms should improve within 24 to 48 hours of initiating adequate antibiotic therapy.

If the patient has not improved by this time, then the addition of ampicillin (or vancomycin in penicillin-allergic patients) to the regimen can improve the response rate if the patient was not already on ampicillin; physical examination should be performed to exclude another source of fever. Alternatively, the initial antibiotics can be discontinued, and ampicillin-sulbactam can be initiated if the patient was not already on ampicillin.

If adding ampicillin or changing to ampicillin-sulbactam does not result in clinical improvement within 24 hours of the change in antibiotic regimen, then physical examination, complete blood count with differential, blood and urine cultures, and pelvic imaging to evaluate for other etiologies of the signs and symptoms are performed. (See 'Persistent postpartum fever' above.)

Prevention

Before cesarean birth – For patients undergoing cesarean birth, we recommend antibiotic prophylaxis prior to skin incision and spontaneous, rather than manual, placental extraction to minimize the risk of postpartum endometritis (Grade 1A). (See 'Prevention' above.)

  1. Casey BM, Cox SM. Chorioamnionitis and endometritis. Infect Dis Clin North Am 1997; 11:203.
  2. 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.
  3. Maharaj D. Puerperal pyrexia: a review. Part I. Obstet Gynecol Surv 2007; 62:393.
  4. Singh N, Sethi A. Endometritis - Diagnosis,Treatment and its impact on fertility - A Scoping Review. JBRA Assist Reprod 2022; 26:538.
  5. Giraldo-Isaza MA, Jaspan D, Cohen AW. Postpartum endometritis caused by herpes and cytomegaloviruses. Obstet Gynecol 2011; 117:466.
  6. Hollier LM, Scott LL, Murphree SS, Wendel GD Jr. Postpartum endometritis caused by herpes simplex virus. Obstet Gynecol 1997; 89:836.
  7. Rørbye C, Petersen IS, Nilas L. Postpartum Clostridium sordellii infection associated with fatal toxic shock syndrome. Acta Obstet Gynecol Scand 2000; 79:1134.
  8. Bitti A, Mastrantonio P, Spigaglia P, et al. A fatal postpartum Clostridium sordellii associated toxic shock syndrome. J Clin Pathol 1997; 50:259.
  9. 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.
  10. 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.
  11. 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.
  12. Gibney RT, Moore A, Muldowney FP. Toxic-shock syndrome associated with post-partum staphylococcal endometritis. Ir Med J 1983; 76:90.
  13. Gibbs RS, Blanco JD. Streptococcal infections in pregnancy. A study of 48 bacteremias. Am J Obstet Gynecol 1981; 140:405.
  14. Gibbs RS. Infection after cesarean section. Clin Obstet Gynecol 1985; 28:697.
  15. Burrows LJ, Meyn LA, Weber AM. Maternal morbidity associated with vaginal versus cesarean delivery. Obstet Gynecol 2004; 103:907.
  16. 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.
  17. Smaill FM, Grivell RM. Antibiotic prophylaxis versus no prophylaxis for preventing infection after cesarean section. Cochrane Database Syst Rev 2014; :CD007482.
  18. 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.
  19. 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.
  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. Watts DH, Eschenbach DA, Kenny GE. Early postpartum endometritis: the role of bacteria, genital mycoplasmas, and Chlamydia trachomatis. Obstet Gynecol 1989; 73:52.
  35. Harrison HR. Prospective studies of Mycoplasma hominis infection in pregnancy. Sex Transm Dis 1983; 10:311.
  36. Patai K, Szilágyi G, Hubay M, et al. Severe endometritis caused by genital mycoplasmas after Caesarean section. J Med Microbiol 2005; 54:1249.
  37. 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.
  38. 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.
  39. 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.
  40. Bauer ME, Albright C, Prabhu M, et al. Alliance for Innovation on Maternal Health: Consensus Bundle on Sepsis in Obstetric Care. Obstet Gynecol 2023; 142:481.
  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. Improving Diagnosis and Treatment of Maternal Sepsis: A CMQCC Quality Improvement Toolkit. California Maternal Quality Care Collaborative (CMQCC). Available at: https://www.cmqcc.org/sites/default/files/Sepsis%20Toolkit_FINAL.2_Errata_7.1.22.pdf (Accessed on March 22, 2023).
  48. Wilkie GL, Prabhu M, Ona S, et al. Microbiology and Antibiotic Resistance in Peripartum Bacteremia. Obstet Gynecol 2019; 133:269.
  49. 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.
  50. 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).
  51. 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.
  52. 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.
  53. 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.
  54. Ghai S, Ghai V, Sunderji S. Fulminant postcesarean Clostridium difficile pseudomembranous colitis. Obstet Gynecol 2007; 109:541.
  55. 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.
  56. 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.
  57. 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.
  58. 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.
  59. 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.
  60. 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.
  61. Gilstrap LC 3rd, Maier RC, Gibbs RS, et al. Piperacillin versus clindamycin plus gentamicin for pelvic infections. Obstet Gynecol 1984; 64:762.
  62. 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.
  63. 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.
  64. Mackeen AD, Packard RE, Ota E, Speer L. Antibiotic regimens for postpartum endometritis. Cochrane Database Syst Rev 2015; :CD001067.
  65. WHO recommendations for prevention and treatment of maternal peripartum infections https://apps.who.int/iris/bitstream/handle/10665/186171/9789241549363_eng.pdf;jsessionid=8C9A4AEA4E583145D8F88A832AD081E7?sequence=1 (Accessed on March 22, 2023).
  66. Conde-Agudelo A, Romero R, Jung EJ, Garcia Sánchez ÁJ. Management of clinical chorioamnionitis: an evidence-based approach. Am J Obstet Gynecol 2020; 223:848.
  67. Hecht DW. Prevalence of antibiotic resistance in anaerobic bacteria: worrisome developments. Clin Infect Dis 2004; 39:92.
  68. 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.
  69. Goldstein EJ, Citron DM. Activity of a novel carbapenem, doripenem, against anaerobic pathogens. Diagn Microbiol Infect Dis 2009; 63:447.
  70. 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.
  71. Martens MG, Faro S, Hammill HA, et al. Sulbactam/ampicillin versus metronidazole/gentamicin in the treatment of post-cesarean section endometritis. Diagn Microbiol Infect Dis 1989; 12:189S.
  72. 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.
  73. 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.
  74. 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.
  75. 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.
  76. 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.
  77. 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.
  78. Pacheco LD, Saad AF, Saade GR. A Practical Approach to Antibiotic Use in Critically Ill Obstetric Patients. Obstet Gynecol 2021; 138:459.
  79. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315:801.
  80. Society for Maternal-Fetal Medicine (SMFM). Electronic address: [email protected], Plante LA, Pacheco LD, Louis JM. SMFM Consult Series #47: Sepsis during pregnancy and the puerperium. Am J Obstet Gynecol 2019; 220:B2.
  81. 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.
  82. Walmer D, Walmer KR, Gibbs RS. Enterococci in post-cesarean endometritis. Obstet Gynecol 1988; 71:159.
  83. Brumfield CG, Hauth JC, Andrews WW. Puerperal infection after cesarean delivery: evaluation of a standardized protocol. Am J Obstet Gynecol 2000; 182:1147.
  84. Gall S, Koukol DH. Ampicillin/sulbactam vs. clindamycin/gentamicin in the treatment of postpartum endometritis. J Reprod Med 1996; 41:575.
  85. 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.
  86. 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.
  87. 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.
  88. Zuckerman J, Levine D, McNicholas MM, et al. Imaging of pelvic postpartum complications. AJR Am J Roentgenol 1997; 168:663.
  89. Klein SM, García CR. Asherman's syndrome: a critique and current review. Fertil Steril 1973; 24:722.
  90. Hoyme UB, Kiviat N, Eschenbach DA. Microbiology and treatment of late postpartum endometritis. Obstet Gynecol 1986; 68:226.
  91. Gibbs RS, Rodgers PJ, Castaneda YS, Ramzy I. Endometritis following vaginal delivery. Obstet Gynecol 1980; 56:555.
  92. Khong TY, Khong TK. Delayed postpartum hemorrhage: a morphologic study of causes and their relation to other pregnancy disorders. Obstet Gynecol 1993; 82:17.
  93. Atterbury JL, Groome LJ, Baker SL, et al. Hospital readmission for postpartum endometritis. J Matern Fetal Med 1998; 7:250.
  94. 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.
  95. 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.
  96. Elliott JP, Flaherty JF. Comparison of lavage or intravenous antibiotics at cesarean section. Obstet Gynecol 1986; 67:29.
  97. 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.
  98. Anorlu RI, Maholwana B, Hofmeyr GJ. Methods of delivering the placenta at caesarean section. Cochrane Database Syst Rev 2008; :CD004737.
  99. Tita ATN, Carlo WA, McClure EM, et al. Azithromycin to Prevent Sepsis or Death in Women Planning a Vaginal Birth. N Engl J Med 2023; 388:1161.
  100. Chongsomchai C, Lumbiganon P, Laopaiboon M. Prophylactic antibiotics for manual removal of retained placenta in vaginal birth. Cochrane Database Syst Rev 2006; :CD004904.
  101. 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 75.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟