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Endometritis
Endometritis
Endometritis
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Endometritis
Other namesPostpartum endometritis, endomyometritis
Micrograph showing a chronic endometritis with the characteristic plasma cells. Scattered neutrophils are also present. H&E stain.
SpecialtyGynaecology, obstetrics
SymptomsFever, lower abdominal pain, abnormal vaginal bleeding, discharge[1]
TypesAcute, chronic[2]
CausesInfectious[2]
Risk factorsAbortion, menstruation, childbirth, placement of an IUD, douching[3][2]
TreatmentAntibiotics[1]
PrognosisGood with treatment[4]
Frequency2% (following vaginal delivery),
10% (following scheduled C-section)[5]

Endometritis is inflammation of the inner lining of the uterus (endometrium).[6] Signs and symptoms may include fever, lower abdominal pain, and abnormal vaginal bleeding or discharge.[1][4] It is the most common cause of infection after childbirth.[7][1] It is also part of spectrum of diseases that make up pelvic inflammatory disease.[8]

Endometritis is divided into acute and chronic forms.[2] The acute form is usually from an infection that passes through the cervix as a result of an abortion, during menstruation, following childbirth, or as a result of douching or placement of an IUD.[2][3] Risk factors for endometritis following delivery include Caesarean section and prolonged rupture of membranes.[1] Chronic endometritis is more common after menopause.[2] The diagnosis may be confirmed by endometrial biopsy.[3] Ultrasound may be useful to verify that there is no retained tissue within the uterus.[4]

Treatment is usually with antibiotics.[1] Recommendations for treatment of endometritis following delivery includes clindamycin with gentamicin.[9] Testing for and treating gonorrhea and chlamydia in those at risk is also recommended.[10] Chronic disease may be treated with doxycycline.[10] Outcomes with treatment are generally good.[4]

Rates of endometritis are about 2% following vaginal delivery, 10% following scheduled C-section, and 30% with rupture of membranes before C-section if preventive antibiotics are not used.[5] The term "endomyometritis" may be used when inflammation of the endometrium and the myometrium is present.[11] The condition is also relatively common in other animals such as cows.[12]

Signs and symptoms

[edit]

The primary clinical manifestations of endometritis include fever and uterine pain with tenderness upon palpation. When the physician moves the uterus during examination, patients typically experience increased discomfort. Post-delivery vaginal discharge (lochia) sometimes presents with an unpleasant smell, though this is not always observed. Fevers in affected patients commonly fall between 38°C and 40°C (100.4°F to 104°F), with most cases trending toward the lower end of this range. Symptom onset typically occurs 2-3 days following childbirth, although when fever appears within hours after delivery alongside low blood pressure, it strongly suggests an infection with β-hemolytic streptococci.[13]

More complicated and uncommon presentations may involve significant fever, general unwellness, sensitivity in the abdominal region, slowed intestinal activity, reduced blood pressure, and sepsis. It should also be noted that as many as 10% of uncomplicated postpartum endometritis cases will feature clinically insignificant bacteremia. Thus, positive blood cultures do not necessarily indicate systemic infection.[13]

The abdominal discomfort is typically concentrated in the lower middle abdomen. Blood tests commonly reveal an elevated white blood cell count, though it's important to note that such elevations can occur normally during labor and the early postpartum period without indicating infection.[13]

Types

[edit]

Acute endometritis

[edit]

There is very uncertain evidence supporting the use of prophylactic antibiotics to prevent endometritis after manual removal of the placenta in vaginal birth.[14] Histologically, neutrophilic infiltration of the endometrial tissue is present during acute endometritis. The clinical presentation is typically high fever and purulent vaginal discharge. Menstruation after acute endometritis is excessive and, in uncomplicated cases, can resolve after 2 weeks of clindamycin and gentamicin IV antibiotic treatment.

In certain populations, it has been associated with Mycoplasma genitalium and pelvic inflammatory disease.[15][16]

Chronic endometritis

[edit]

Chronic endometritis is characterized by the presence of plasma cells in the stroma. Lymphocytes, eosinophils, and even lymphoid follicles may be seen, but in the absence of plasma cells, are not enough to warrant a histologic diagnosis. It may be seen in up to 10% of all endometrial biopsies performed for irregular bleeding. The most common organisms are Chlamydia trachomatis (chlamydia), Neisseria gonorrhoeae (gonorrhea), Streptococcus agalactiae (Group B Streptococcus), Mycoplasma hominis, tuberculosis, and various viruses. Most of these agents are capable of causing chronic pelvic inflammatory disease (PID). Patients with chronic endometritis may have an underlying cancer of the cervix or endometrium (although an infectious cause is more common). Antibiotic therapy is curative in most cases (depending on the underlying cause), with fairly rapid alleviation of symptoms after only 2 to 3 days. Women with chronic endometritis are also at a higher risk of pregnancy loss, and treatment for this improves future pregnancy outcomes.[17][18]

Chronic granulomatous endometritis is usually caused by tuberculosis. The granulomas are small, sparse, and without caseation. The granulomas take up to 2 weeks to develop, and since the endometrium is shed every 4 weeks, the granulomas are poorly formed.

In human medicine, pyometra (also a veterinary condition of significance) is regarded as a form of chronic endometritis seen in elderly women, causing stenosis of the cervical os and accumulation of discharges and infection. Symptom in chronic endometritis is blood-stained discharge, but in pyometra, the patient complains of lower abdominal pain.

Pyometra

[edit]
Main article: Pyometra

Pyometra describes an accumulation of pus in the uterine cavity.[19] For pyometra to develop, there must be both an infection and a blockage of the cervix. Signs and symptoms include lower abdominal pain (suprapubic), rigors, fever, and the discharge of pus on introduction of a sound into the uterus. Pyometra is treated with antibiotics, according to culture and sensitivity.[20]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Endometritis

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from Grokipedia
Endometritis is an infectious of the , the inner lining of the , that can lead to severe complications if not promptly diagnosed and treated. It is classified into acute and chronic forms, with acute endometritis typically presenting with symptoms such as fever, , and abnormal uterine discharge within 30 days of onset, often linked to bacterial ascension from the lower genital tract. Chronic endometritis, by contrast, involves persistent low-grade lasting over 30 days, frequently or manifesting as , and is characterized histologically by infiltration in the endometrial stroma. Postpartum endometritis, a common subtype of acute endometritis, affects 1-3% of women after and up to 20 times more frequently after cesarean section, primarily due to polymicrobial infections involving . The primary etiology involves bacterial pathogens, including sexually transmitted infections like and for acute non-postpartum cases, while postpartum and chronic forms often stem from endogenous organisms such as group B streptococci, , and anaerobes. Risk factors include young age (<25 years), cesarean delivery, prolonged labor, intrauterine devices, and prior , which can facilitate microbial ascent. In chronic cases, particularly in regions with high prevalence, may play a role. Diagnosis of acute endometritis relies on clinical criteria like fever and uterine tenderness, supported by laboratory tests such as endometrial biopsy or if needed, whereas chronic endometritis requires histopathological confirmation via detection (e.g., using CD138 staining) or hysteroscopic findings of micropolyps. Treatment generally involves broad-spectrum antibiotics; for acute and postpartum cases, regimens like clindamycin plus gentamicin or ampicillin-sulbactam are recommended, often administered intravenously for severe presentations, while chronic endometritis responds to prolonged oral or other antibiotics tailored to identified pathogens. Untreated endometritis can progress to complications including , , , and , with chronic forms implicated in up to 30% of recurrent loss cases and reduced in vitro fertilization success rates (e.g., clinical rates improving from 33% to 65% post-treatment). Preventive measures, such as prophylactic antibiotics during cesarean sections per ACOG guidelines, have significantly reduced postpartum incidence.

Overview

Definition

Endometritis is an of the , the innermost lining of the , typically resulting from an infectious process but occasionally arising from non-infectious causes. This condition specifically targets the mucosal layer that lines the , distinguishing it from broader uterine inflammations. The consists of two main layers: a basal layer that remains intact and regenerates the functional layer, and a thicker functional layer that undergoes cyclic changes. Under the influence of and progesterone, it proliferates during the to create a receptive environment for implantation; if does not occur, it sheds during . During , the transforms into the to nourish the developing . Its anatomical position and vascularity make it particularly susceptible to following events that disrupt its integrity, such as postpartum placental separation, which exposes the raw endometrial surface to ascending bacteria, or uterine instrumentation like or placement, which can introduce pathogens or cause mechanical irritation. Endometritis differs from cervicitis, an confined to the cervix, and salpingitis, which affects the fallopian tubes, as it is localized to the uterine lining without necessarily involving adjacent structures. It frequently forms part of the (PID) spectrum, where lower genital tract infections ascend to involve the endometrium, and is a key component of occurring after delivery. Rare non-infectious variants may stem from for pelvic malignancies, leading to ischemic and inflammatory changes, or autoimmune processes that trigger chronic endometrial inflammation. The term "endometritis" derives from Greek roots—"endo" (within), "metra" (), and "itis" ()—reflecting its historical recognition as a uterine-specific inflammatory disorder since the .

Epidemiology

Endometritis predominantly manifests in the , affecting 1-3% of vaginal deliveries worldwide. The pooled global incidence of postpartum endometritis is approximately 1.4% (95% CI 0.9-1.9%), though rates vary by delivery mode and setting. Following scheduled cesarean sections, incidence rises to about 7%, while emergency cesareans—often involving prolonged —can reach up to 30%. In low- and middle-income countries, postpartum endometritis affects 1-7% of deliveries, with higher rates attributed to suboptimal , limited access to sterile procedures, and inadequate postpartum monitoring. For instance, puerperal infections, including endometritis, contribute disproportionately to maternal morbidity in these regions, where overall postpartum pyrexia rates range from 5-7%. Demographic patterns reveal elevated risks among multiparous women, particularly for chronic forms ( 1.8 compared to nulliparous), as well as those with a history of sexually transmitted infections or residing in areas with restricted obstetric care. In high-income countries, the incidence remains low, sustained by routine prophylaxis during cesarean deliveries, which has reduced rates from historical highs of 50-90% without intervention to 15-20%. Emerging trends indicate a potential rise in chronic endometritis cases, linked to increasing (IUD) utilization, with reported incidences up to 30% among IUD users compared to non-users.

Causes and risk factors

Causes

Endometritis is predominantly caused by polymicrobial bacterial infections originating from the lower genital tract. Common pathogens include aerobic bacteria such as group B , , and , as well as anaerobic species like and . These organisms typically ascend into the endometrial cavity, leading to acute , particularly in postpartum cases where the infection rate is 1-3% following . In the , the primary route of involves the breakdown of the endometrial barrier during placental separation, which exposes the uterine lining to and facilitates bacterial invasion. Similar ascending pathways occur after procedures such as (D&C), , or (IUD) insertion, where instrumentation disrupts cervical mucus barriers and introduces pathogens directly into the uterus. Sexually transmitted infections, including and , can also contribute via this route, though they are less common in isolation. In regions with high prevalence, chronic endometritis may be caused by . Non-infectious causes of endometritis are rare and include chemical irritation from substances like talc particles, which can migrate to the endometrium and provoke a foreign body inflammatory response. While chronic forms are primarily infectious, some cases show associations with autoimmune markers such as mononuclear cell infiltration.

Risk factors

Endometritis is associated with several obstetric risk factors that increase the likelihood of postpartum infection. Cesarean delivery, particularly emergency procedures, elevates the risk 5 to 20 times compared to vaginal delivery, with even higher susceptibility if performed after rupture of membranes. Prolonged labor exceeding 24 hours and prolonged rupture of membranes greater than 18 hours further heighten vulnerability by allowing ascending bacterial contamination. Additionally, multiple vaginal examinations during labor and operative vaginal deliveries introduce potential pathogens, contributing to the inflammatory process. Procedural interventions also predispose individuals to endometritis. Post-abortion procedures carry an elevated risk due to the open cervical os and retained tissue, which facilitate bacterial ascension. (IUD) insertion without adequate antibiotic prophylaxis is a notable factor, as it can promote chronic infection in the endometrial lining. Similarly, endometrial or performed without prophylactic measures increases susceptibility, particularly in patients with preexisting endometrial abnormalities. Patient-specific factors play a significant role in non-modifiable and modifiable risks. Preexisting sexually transmitted infections, such as or , substantially increase the odds of acute endometritis by providing a reservoir for pathogens. Conditions like , , and (including ) impair immune responses, exacerbating infection risk in both postpartum and non-obstetric contexts. Low , often linked to poorer and limited access to care, correlates with higher incidence, as seen in studies of maternal outcomes. Recent studies from 2023 to 2024 highlight the growing challenge of antibiotic resistance in hospital settings, which elevates risks for recurrent endometritis cases. Multidrug-resistant pathogens, such as extended-spectrum beta-lactamase-producing and , have shown resistance rates exceeding 30% to first-line therapies like fluoroquinolones, leading to treatment failures and persistent infections. Cross-sectional data indicate a significant rise in among chronic endometritis isolates from 2020 to 2024, with hospital-acquired strains contributing to up to 56% resistance to nitroimidazoles and , complicating management in recurrent scenarios.

Pathophysiology

Acute inflammation

Acute endometritis involves a swift inflammatory response primarily driven by the infiltration of neutrophils into the endometrial stroma, which occurs rapidly following bacterial ascension from the lower genital tract. This neutrophil-dominated process leads to significant and hyperemia in the endometrial tissue, typically manifesting within 24 to 48 hours of onset. The recruited neutrophils release pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which amplify the local inflammatory cascade and contribute to systemic effects such as fever while promoting the formation of purulent within the endometrial cavity. These cytokines facilitate further immune cell recruitment and changes, exacerbating tissue swelling and discharge. Common postpartum triggers, such as cesarean delivery or , often initiate this process by compromising cervical barriers. In severe cases, the acute can breach the endometrial-myometrial interface, allowing extension into the and potentially resulting in myometritis, which impairs uterine contractility and prolongs recovery. Histologically, acute endometritis is distinguished by dense aggregates of polymorphonuclear leukocytes (neutrophils) within the endometrial glands and stroma, often accompanied by focal areas of and microabscess formation. These features differentiate it from normal postpartum endometrial changes, which exhibit transient leukocytic infiltration without or persistent bacterial involvement.

Chronic inflammation

Chronic endometritis involves sustained immune activation characterized by the infiltration of plasma cells and lymphocytes into the endometrial stroma, reflecting a persistent mononuclear inflammatory response. This infiltration disrupts normal endometrial architecture and is frequently linked to intracellular pathogens, such as , which can evade acute immune clearance and promote chronic persistence. The ongoing impairs endometrial repair processes, leading to excessive through mechanisms like elevated transforming growth factor beta 1 (TGF-β1) expression and reduced matrix metalloproteinase 9 (MMP-9) activity, which hinder remodeling. Additionally, defects arise, potentially through reduced MMP-9 activity, compromising vascular development essential for tissue regeneration and resulting in disrupted implantation sites that affect attachment. This pathology is strongly associated with , as the chronic milieu alters endometrial receptivity by the presence of CD138+ plasma cells, which correlate with reduced implantation success and lower rates. Chronic endometritis may progress from unresolved acute or develop de novo, often in the context of sexually transmitted infections like those detailed in analyses; histological typically requires the presence of ≥5 CD138+ plasma cells per , though diagnostic criteria vary.

Clinical features

Symptoms

Patients with acute endometritis, particularly in the , commonly report lower abdominal or that is often crampy and may worsen with movement. In non-postpartum acute endometritis, symptoms may also include and . This pain is frequently accompanied by abnormal , which in postpartum cases presents as foul-smelling, purulent . Fever and chills are hallmark symptoms, typically exceeding 38°C and onset occurring 2-3 days after delivery, along with general malaise. Additional complaints may include and increased . In chronic endometritis, symptoms are often subtle or absent, but when present, patients may describe irregular menstrual bleeding, pelvic discomfort, or complaints related to . or spotting can also occur, contributing to vague pelvic sensations. These manifestations may prompt evaluation for reproductive issues rather than overt .

Physical examination findings

During of patients with endometritis, often reveal fever, typically exceeding 38°C (100.4°F), and , which are indicative of the systemic inflammatory response. If complicated by , and rebound tenderness may accompany lower abdominal tenderness due to peritoneal irritation. Bimanual commonly elicits uterine tenderness on , with the possibly enlarged or showing subinvolution, particularly in postpartum cases where it fails to return to pre-pregnancy size. is frequently observed, suggesting potential extension to (PID). Speculum examination of the typically discloses purulent or foul-smelling cervical discharge. These findings align with patient-reported but are distinguished by their objective elicitation during the exam.

Diagnosis

History and physical exam

The of endometritis begins with a detailed clinical and , which are essential for raising suspicion and guiding further evaluation. Key historical elements include recent obstetric events such as vaginal or cesarean delivery, , or intrauterine procedures like , as these are primary risk factors for postpartum or post-procedure endometritis. Symptom onset typically occurs within 24 to 48 hours postpartum for early-onset cases, though late-onset presentations up to six weeks may arise from ascending genital tract infections. A sexual is crucial, particularly to identify risk factors for sexually transmitted infections (STIs) such as Chlamydia trachomatis or Neisseria gonorrhoeae, which can contribute to pelvic inflammatory disease-related endometritis. Patients may report symptoms like lower abdominal pain, which warrants integration with to differentiate from other causes. Physical examination complements the history by assessing and pelvic findings to build clinical suspicion. Fever (oral temperature ≥38°C within 10 days postpartum or ≥38.7°C within 24 hours) combined with uterine or lower abdominal tenderness on is a hallmark finding, often accompanied by foul-smelling or purulent . and may also be present, particularly in acute cases, while adnexal tenderness suggests extension to . The integration of these elements—such as fever plus uterine tenderness—establishes a high index of suspicion for endometritis, with clinical criteria including at least one of abnormal discharge, , or delayed uterine involution alongside fever. In the differential diagnosis, history and exam findings help distinguish endometritis from urinary tract infections (e.g., via absence of dysuria predominance), appendicitis (e.g., right lower quadrant localization without obstetric history), or ovarian torsion (e.g., acute unilateral pain without fever or discharge). Post-2023 guidelines emphasize rapid history-taking and physical assessment in emergency settings for postpartum patients with fever or to facilitate early recognition and prevention, recommending urgent escalation if vital sign abnormalities like or altered mental status are noted. This approach aligns with maternal protocols, prioritizing prompt evaluation to mitigate progression to systemic infection.

Diagnostic tests

Diagnosis of endometritis often begins with laboratory tests to support clinical suspicion from history and physical examination. In acute cases, leukocytosis with white blood cell counts typically ranging from 15,000 to 30,000 cells/μL is common, though normal counts may occur in mild infections. C-reactive protein levels are elevated, serving as a nonspecific marker of inflammation. Blood cultures are recommended if sepsis is suspected, yielding positive results in 10-30% of cases, while endocervical cultures or nucleic acid amplification tests detect sexually transmitted pathogens like Chlamydia trachomatis and Neisseria gonorrhoeae. For chronic endometritis, endometrial cultures identify common bacteria such as Escherichia coli and streptococci, though results guide etiology in select cases. Imaging modalities provide supportive evidence but are not definitive. Transvaginal is the first-line imaging for postpartum endometritis, revealing a thickened, heterogeneous , intracavitary fluid, or gas bubbles indicating . In chronic cases, may show a thin with hyperechoic foci suggestive of or . is useful in complex or refractory presentations to detect subtle endometrial changes or rule out complications like abscesses. Invasive procedures confirm the diagnosis, particularly for chronic endometritis. Endometrial biopsy remains the gold standard, with histopathological examination identifying stromal plasma cells (≥1 per 10 high-power fields) via hematoxylin-eosin staining or CD138 immunohistochemistry. Hysteroscopy allows direct visualization, showing characteristic features such as micropolyps (1-2 mm protrusions), stromal edema, or focal hyperemia in the follicular phase. Polymerase chain reaction (PCR) on endometrial samples detects pathogens in culture-negative cases. Recent advances include multiplex real-time PCR panels targeting multiple pathogens (e.g., 11 common and sexually transmitted infections), offering rapid etiology identification in refractory chronic endometritis with higher sensitivity than traditional cultures.

Treatment

Acute endometritis

The treatment of acute endometritis primarily involves empirical intravenous to address the polymicrobial nature of the infection, typically involving aerobic and anaerobic from the genital tract. The first-line regimen consists of intravenous clindamycin (900 mg every 8 hours) combined with gentamicin (5 mg/kg once daily or 1.5 mg/kg every 8 hours), providing broad coverage against common pathogens such as group B , , and species. This combination has been established as the criterion standard due to its efficacy in resolving symptoms in approximately 90% of cases. Intravenous therapy is continued until the patient is afebrile and clinically improved for 24 to 48 hours, after which a transition to oral antibiotics is appropriate for completing the course. A common oral regimen is amoxicillin-clavulanate (875 mg twice daily) for an additional 7 to 10 days, ensuring total treatment duration aligns with clinical resolution while minimizing unnecessary exposure to reduce . Recent updates in guidelines emphasize shorter overall courses, typically totaling 14 days, to balance efficacy with resistance prevention, particularly in postpartum cases. Supportive care is essential alongside antibiotics and includes intravenous hydration to maintain , nonsteroidal drugs (NSAIDs) such as ibuprofen for pain and fever management, and close monitoring for clinical response within 48 to 72 hours. Hospitalization is recommended for patients with severe symptoms (e.g., high fever, hemodynamic instability), comorbidities (e.g., or ), or recent cesarean delivery, allowing for intravenous administration and observation. Antibiotic selection should be adjusted based on culture results if available; for instance, if (MRSA) is suspected or confirmed, (15 to 20 mg/kg every 8 to 12 hours, adjusted for renal function) may be added or substituted. Lack of improvement within 48 to 72 hours warrants reevaluation for alternative diagnoses or resistant organisms, potentially involving or specialist consultation.

Chronic endometritis

The primary treatment for chronic endometritis involves prolonged courses of oral antibiotics to target persistent bacterial infections, often guided by endometrial results or empirically selected based on common pathogens. As of , there is no standardized treatment protocol for chronic endometritis; therapy is often empirical or guided by cultures. at 100 mg twice daily for 14-21 days is a first-line option due to its broad coverage against intracellular bacteria like . Alternative regimens include combinations such as (500 mg twice daily) with a like or (500 mg twice daily), particularly for polymicrobial cases. Following antibiotic therapy, a repeat endometrial is essential to confirm resolution, as infiltration must be absent to verify cure. In cases of persistent chronic endometritis despite initial antibiotics, adjunctive therapies may be employed to address structural abnormalities or promote endometrial healing. Hysteroscopic resection of polyps or fibrotic tissue can eliminate focal reservoirs, achieving resolution in many patients without further antibiotics. Hormonal , such as progestins (e.g., dydrogesterone 10 mg daily for 10-14 days post-resection), supports endometrial repair by modulating and restoring cyclic changes. Treatment of chronic endometritis is particularly emphasized in the context of , where it is addressed prior to fertilization (IVF) to optimize outcomes. Antibiotic regimens achieve resolution rates exceeding 70%, which correlates with improved implantation and live birth rates in subsequent IVF cycles, as untreated cases show significantly lower success. For instance, women with resolved chronic endometritis post-treatment exhibit implantation rates approaching those of unaffected individuals. Challenges in managing chronic endometritis include emerging antibiotic resistance among common pathogens such as and . A 2020–2024 reported 75.8% resistance to tetracyclines like , with peaks at 97.4% in 2023 and 2024, emphasizing the need for susceptibility testing and antimicrobial stewardship to guide alternatives.

Complications

Pyometra

represents a severe complication of endometritis, defined as the accumulation of purulent material within the resulting from obstructed drainage. This condition arises when bacterial infection leads to formation, but cervical obstruction—commonly due to following or the presence of an (IUD)—prevents expulsion, causing progressive distension of the and potential rupture if pressure builds unchecked. The underlying bacterial infection from endometritis facilitates the purulent accumulation in this obstructed setting. is particularly prevalent in postmenopausal women, where atrophic changes exacerbate cervical narrowing. Clinically, it manifests as acute lower , systemic signs of including fever and hemodynamic instability, and notably scant owing to the blockage. Although is a rare of endometritis, with an overall incidence of 0.01–0.5% among gynecologic admissions, untreated cases carry substantial mortality risk, reaching up to 25–40% in instances of rupture and . A 2023 case report highlighted successful ultrasound-guided drainage as a minimally invasive approach in high-risk patients, underscoring its role in averting surgical escalation. Management demands prompt intervention to avert life-threatening progression, beginning with urgent uterine drainage via or catheter insertion to evacuate the and relieve pressure. Concurrent broad-spectrum intravenous antibiotics, such as piperacillin-tazobactam, target the polymicrobial , with culture-guided adjustments as needed. In recurrent or when is suspected, definitive is often recommended to prevent further episodes.

Systemic infections

Untreated or severe endometritis can progress to systemic infection through bacteremia, where from the endometrial source enter the bloodstream, triggering a (SIRS) characterized by fever, , and . This dysregulated host response may evolve into , defined as life-threatening , with early detection aided by the quick Sequential Organ Failure Assessment (qSOFA) score, which identifies high-risk patients via criteria such as ≥22 breaths/min, altered mentation, and systolic ≤100 mmHg.30246-7/fulltext) Additional systemic complications include pelvic abscess formation, from bacterial spread to the , and septic pelvic , where leads to pelvic vein thrombosis and persistent fever despite antibiotics. In extreme cases, endometritis-related carries risks of (DIC), marked by widespread clotting and bleeding, or (ARDS), involving severe lung inflammation and . Management of these systemic infections integrates broad-spectrum intravenous antibiotics targeting common pathogens like group B Streptococcus and , alongside source control measures such as drainage of any associated collections and (ICU) support for hemodynamic stabilization and organ failure. Mortality rates for postpartum arising from endometritis range from 5% to 20%, influenced by timely intervention and patient factors.00327-7/fulltext) Recent 2024 World Health Organization data highlight rising among sepsis-causing bacteria in maternal infections, complicating treatment efficacy and increasing the risk of adverse outcomes.

Prevention and prognosis

Prevention strategies

Prevention of endometritis focuses on reducing risk factors in obstetric and gynecological settings through targeted interventions. prophylaxis is a , particularly for cesarean deliveries, where a single preoperative dose of has been shown to reduce the incidence of endometritis by approximately 60-70% compared to no prophylaxis. This approach is recommended universally for cesarean sections, with administration ideally within before incision to optimize efficacy. For high-risk cases, such as those with chorioamnionitis or , extended regimens may be employed, incorporating broader-spectrum agents to further mitigate risk. Hygiene protocols play a critical role in minimizing ascending infections during labor and procedures. Strict aseptic techniques, including the use of sterile gloves and instruments, are essential for vaginal deliveries, operative procedures, and to prevent bacterial introduction into the . Limiting the number of vaginal examinations during labor—ideally to no more than four in the active phase—reduces the opportunity for ascension, particularly in the presence of ruptured membranes. In cases of suspected IUD-related infection, prompt removal of the device, typically within 48-72 hours if symptoms persist despite initial antibiotics, is advised to halt progression to endometritis. Screening for sexually transmitted infections (STIs) prior to or invasive procedures is vital, as untreated and are major contributors to endometritis. Routine testing and treatment of STIs in at-risk populations, including preconception counseling, significantly lower postpartum rates. Similarly, universal screening for (GBS) at 36-37 weeks of , followed by intrapartum prophylaxis for positive cases, has reduced the incidence of maternal endometritis alongside neonatal early-onset disease. Recent guidelines emphasize adjunctive therapies for specific scenarios. In 2024, the Society for Maternal-Fetal Medicine, endorsed by the American College of Obstetricians and Gynecologists (ACOG), recommended as an alternative to erythromycin in the regimen for expectant management of preterm (PPROM). Additionally, evidence from trials such as the C/SOAP study (2016) for cesarean deliveries and the A-PLUS trial (2023) for vaginal deliveries in labor indicates that adjunctive single-dose reduces endometritis rates by approximately 35-50%. As of 2025, these findings support broader consideration of in high-risk labors, though specific endorsements for single-dose use in prolonged ROM are pending further guideline updates.

Prognosis

The prognosis of acute endometritis is excellent with prompt therapy, achieving resolution in nearly 90% of cases within 48 to 72 hours and full recovery typically within one week. Recurrence is rare when underlying risk factors, such as postpartum complications or intrauterine devices, are addressed following treatment. In chronic endometritis, regimens yield cure rates of 70-80% after one to three courses, though persistent cases may require additional interventions. Untreated chronic endometritis is associated with impaired endometrial receptivity and reduced fertilization (IVF) success rates ( 1.97 for lower live birth rate compared to non-affected patients), and is found in approximately 10-30% of women with or recurrent implantation failure; post-treatment, live birth rates improve to levels comparable to non-affected patients (typically 50-65%). effects in chronic forms are further explored in sections on chronic . Overall, mortality from endometritis is low at less than 2% in treated cases but rises to 5-17% with treatment delays, particularly in postpartum settings. Long-term scarring, including pelvic adhesions, is possible if infection persists, potentially leading to chronic or tubal . improves in younger patients due to better endometrial regenerative capacity and lower burden. Recent meta-analyses indicate no sustained increase in risk following resolution of endometritis.

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