eMedicine Specialties > Pediatrics: Surgery > Gynecology

Endometritis

Latha Chandran, MD, MPH, Associate Professor of Pediatrics, Associate Dean for Academic Affairs, Director, Division of General Pediatrics, State University of New York at Stony Brook School of Medicine
Joseph A Puccio, MD, FAAP, Director, Division of Adolescent Medicine, Stony Brook University Hospital; Assistant Professor, Department of Pediatrics, Stony Brook University School of Medicine

Updated: Mar 6, 2008

Introduction

Background

Endometritis is inflammation of the endometrial lining of the uterus. Endometritis can be divided into pregnancy-related endometritis and endometritis unrelated to pregnancy. When the condition is unrelated to pregnancy, it is referred to as pelvic inflammatory disease (PID). Endometritis is often associated with inflammation of the fallopian tubes (salpingitis), ovaries (oophoritis), and pelvic peritoneum (pelvic peritonitis). This article focuses on pregnancy-related endometritis. In addition to the endometrium, inflammation may involve the myometrium and, occasionally, the parametrium.

Pathophysiology

Inflammation of the endometrium usually results from an ascending infection from the lower genital tract. Differentiating the normal physiologic leucocyte infiltration from an inflammatory process such as endometritis is sometimes difficult. However, most cases of endometritis have a substantially increased number of B lymphocytes compared with less than 1% in normal endometrial samples. Endometritis is often difficult to clinically diagnose. Pathologically, the process involves infiltration of normal architecture with neutrophils, plasma cells, and lymphocytes.

The following factors increase the risk for endometritis in general:

• Presence of an intrauterine device: The vaginal part of the device may serve as a track for the organisms to ascend into the uterus.
• Absence of the normal cervical mucus plug
• Presence of menstrual fluid in the uterus
• Associated cervicitis secondary to gonorrhea or chlamydia
• Associated bacterial vaginosis^1,2
• Uterine instrumentation (eg, abortion, dilatation, curettage)
• Postpartum and postabortal states: These patients are particularly vulnerable because of the open nature of the cervical os, presence of large amounts of blood and debris, and instrumentation risks.
• Frequent douching
• Unprotected sexual activity
• Multiple sexual partners
• Cervical ectopy
• Cesarean delivery: Women with cesarean deliveries before 28 weeks' gestation appear to be especially high risk.
• Administration of multiple courses of corticosteroids to women at risk for premature delivery

During the postpartum period, risk factors include duration of labor, time of rupture of membranes prior to delivery, severely meconium-stained amniotic fluid, cesarean delivery, number of vaginal examinations during labor, manual placental removal,³ and postpartum anemia.

Frequency

United States

Postpartum endometritis occurs in fewer than 3% of vaginal deliveries and in 38.4% of emergency cesarean deliveries.

Mortality/Morbidity

Endometritis is associated with increased maternal mortality due to septic shock. However, mortality is rare in the United States because of aggressive antimicrobial management. The association between endometritis and reproductive morbidity was evaluated in the PID Evaluation and Clinical Health (PEACH) study.⁴ Endometritis was not found to be associated with increased risk of infertility or chronic pelvic pain.

Clinical

History

A pediatrician is most likely to witness pregnancy-related endometritis following a terminated pregnancy.

• In postpartum cases, patients present with fever, chills, lower abdominal pain, and foul-smelling lochia. Often, a history of prolonged rupture of membranes and prolonged labor is present. History of meconium-stained amniotic fluid⁵ or manual removal of placenta is more likely in patients with endometritis.
• Patients with pelvic inflammatory disease (PID) present with history of lower abdominal pain, vaginal discharge, dyspareunia, dysuria, fever, and other systemic signs. However, PID caused by chlamydia tends to be indolent, with no significant constitutional symptoms.

Physical

• Uterine tenderness is the hallmark of the disease. Adnexal tenderness may be elicited if associated salpingitis is present.
• Lochia may be foul smelling.
• An oral temperature of 38°C or higher within the first 10 days postpartum or 38.7°C within the first 24 hours postpartum is required to make the diagnosis.
• In severe cases, the patient may appear septic. Laboratory criteria are not reliable in patients with endometritis. Because of the physiologic changes associated with pregnancy, the presence of an elevated leukocyte count or neutrophil count does not indicate endometritis. Therefore, clinical findings are more reliable than laboratory findings in diagnosing postpartum endometritis.
• For PID, the minimum diagnostic criteria are lower abdominal tenderness, cervical motion tenderness, or adnexal tenderness.

Causes

• The etiology is polymicrobial; a mixture of aerobic and anaerobic organisms is usually found.
• Gram-positive cocci include Streptococcus agalactiae, Streptococcus viridans, Streptococcus faecalis, Staphylococcus aureus, and Staphylococcus epidermidis.
• Some severe cases have been associated with group A streptococcus.
• Gram-negative organisms include Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Enterobacter aerogenes, Gardnerella vaginalis, and Neisseria gonorrhae.
• Chlamydia trachomatis and mycoplasmas such as Ureaplasma urealyticum may also be etiological agents.
• Anaerobes include Bacteroides bivius (most common), Peptococcus species, Peptostreptococcus species, and species of Bacteroides and Fusobacterium.

Differential Diagnoses

Urinary Tract Infection

Other Problems to Be Considered

Chorioamnionitis
Pelvic inflammatory disease
Salpingitis

Workup

Laboratory Studies

• CBC count reveals leukocytosis with a left shift. However in the postpartum period, this finding may be physiological and, therefore, unreliable as a diagnostic tool.
• Gram stain or wet mount of the vaginal discharge may be useful in ruling out endometritis. If no pus cells are observed in the gram stain, the negative predictive value for endometritis is 95%.
• Anemia is a risk factor for the development of endometritis.
• The role of endocervical cultures is controversial. They are not generally helpful in management.
• Urine cultures help rule out urinary tract infection.

Histologic Findings

Pathologically, endometritis is defined as 5 or more neutrophils per 400 high-power fields in the superficial endometrium and one or more plasma cells per 120 high-power fields in the endometrial stroma.

Treatment

Medical Care

• Prophylactic antibiotics significantly decrease the incidence of postpartum endometritis and are indicated for cesarean deliveries, especially if the risk factors for endometritis, such as prolonged labor and manual removal of placenta, occur.^6,7 A Cochrane database systematic review concluded that the use of vaginal chlorhexidine douching during labor does not prevent endometritis.⁸
• The criterion standard of treatment, once endometritis is diagnosed, is intravenous gentamicin and clindamycin administered every 8 hours. Some studies have shown that daily dosing as opposed to 8-hour dosing has similar therapeutic results.^9,10 Recently, a trend toward the use of broad-spectrum monotherapy has emerged. These agents are generally efficacious in 80-90% of patients. Cephalosporins, extended-spectrum penicillins, and fluoroquinolones are used as monotherapy. In addition, cefoxitin concomitant with doxycycline and/or metronidazole may be used in doses used in treating pelvic inflammatory disease (PID).
• Treat patients with the same regimen for at least 48-72 hours to determine clinical efficacy. If the patient is improving, continue parenteral therapy until the patient is afebrile for 24-36 hours. At-home treatment with oral antibiotics is generally unnecessary, and patients have poor compliance.
• In teenagers, postabortion endometritis may be caused by organisms that cause PID and initial treatment regimen usually includes intravenous cefoxitin and doxycycline.
• If the patient does not improve in the expected 48- to 72-hour period, reevaluate for complications such as abscess. Reevaluation dictates further medical management.

Medication

A combination of gentamicin and clindamycin is considered the criterion standard against which other antibiotic trials are compared. Postabortion endometritis in teenagers is treated with broad-spectrum coverage for aerobes and anaerobes using intravenous cefoxitin and oral doxycycline.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Use lean body mass when calculating the dose. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution.

Dosing

Adult

3 mg/kg/d IV divided q8h
Obtain trough serum level 30 min before 4th dose; may draw a peak level 30 min after 30-min infusion

Pediatric

<5 years: 2.5 mg/kg/dose IV q8h
>5 years: 1.5-2.5 mg/kg/dose IV q8h or 6-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults

Interactions

Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index; caution in renal failure (adjust dose and/or interval), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Clindamycin (Cleocin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

600-1200 mg/d IV/IM divided tid/qid

Pediatric

20-40 mg/kg/d IV divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use caution in patients with history of colitis or atopic dermatitis; decrease doses in renal insufficiency

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.

Dosing

Adult

1-2 g IV q6-8h

Pediatric

80-160 mg/kg/d IV divided q4-6h

Interactions

Probenecid may increase effects of cefoxitin; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients with renal insufficiency

Doxycycline (Bio-Tab, Doxy, Vibramycin, Vibra-Tabs)

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.

Dosing

Adult

100 mg doxycycline IV q12h and 2 g cefoxitin IV qid; continue treatment for at least 4 d and for at least 48 h after patient improves; follow by PO doxycycline (100 mg) bid for 10-14 d

Pediatric

<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO/IV qd or divided bid; not to exceed 200 mg/d

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (ie, <8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Follow-up

Further Inpatient Care

• Patients with endometritis need inpatient care until clinical improvement occurs. Fever, foul-smelling vaginal discharge, and uterine tenderness should be fully resolved.
• In adolescents, the risk of future infertility and pregnancy complications is increased. Therefore, a more conservative therapeutic approach is recommended.

Further Outpatient Care

• Once the patient has completed inpatient therapy, an oral cephalosporin or clindamycin may be continued for a total of 10-14 days. However, several studies, including a recent systematic review, suggest that follow-up oral antibiotic therapy may not be necessary.¹¹
• Pregnancy prevention and sexually transmitted disease (STD) prevention counseling should be provided to avoid future episodes.¹²

Deterrence/Prevention

• Aseptic techniques of medical termination of pregnancy can avoid episodes of postabortal endometritis.

Complications

• Salpingitis, oophoritis, localized peritonitis, and tuboovarian abscesses may result from spread of infection from the endometrium to the tubes, ovaries, and the peritoneal cavity. Salpingitis subsequently leads to tubal dysmotility and adhesions that result in infertility, higher incidence of ectopic pregnancy, and chronic pelvic pain.
• In the recent PEACH study, patients who were adequately treated for endometritis were found to have no increased risk of future pregnancy-related complications, chronic pelvic pain, or infertility.⁴

Prognosis

• Prognosis is fair. Delay in initiation of antibiotic therapy can result in systemic toxicity.

Patient Education

• For excellent patient education resources, visit eMedicine's Pregnancy and Reproduction Center, Women's Health Center, and Sexually Transmitted Diseases Center. Also, see eMedicine's patient education articles Pelvic Inflammatory Disease and Endometriosis.

Miscellaneous

Special Concerns

• In the adolescent population who undergo termination of pregnancy, subsequent endometritis with associated salpingitis poses a significant risk of infertility. Therefore, earlier and more aggressive antibiotic therapy is warranted in this group.

References

1. Haggerty CL, Hillier SL, Bass DC, et al. Bacterial vaginosis and anaerobic bacteria are associated with endometritis. Clin Infect Dis. Oct 1 2004;39(7):990-5. [Medline].

2. Jacobsson B, Pernevi P, Chidekel L, et al. Bacterial vaginosis in early pregnancy may predispose for preterm birth and postpartum endometritis. Acta Obstet Gynecol Scand. Nov 2002;81(11):1006-10. [Medline].

3. Dehbashi S, Honarvar M, Fardi FH. Manual removal or spontaneous placental delivery and postcesarean endometritis and bleeding. Int J Gynaecol Obstet. Jul 2004;86(1):12-5. [Medline].

4. Ness RB, Soper DE, Holley RL, et al. Douching and endometritis: results from the PID evaluation and clinical health (PEACH) study. Sex Transm Dis. 2001;28(4):240-5. [Medline].

5. Tran SH, Caughey AB, Musci TJ. Meconium-stained amniotic fluid is associated with puerperal infections. Am J Obstet Gynecol. Sep 2003;189(3):746-50. [Medline].

6. Donowitz LG, Norris SM. The efficacy of antibiotic prophylaxis in the prevention of post-cesarean section endometritis. Infect Control. May 1985;6(5):189-93. [Medline].

7. French L. Prevention and treatment of postpartum endometritis. Curr Womens Health Rep. Aug 2003;3(4):274-9. [Medline].

8. Lumbiganon P, Thinkhamrop J, Thinkhamrop B, Tolosa JE. Vaginal chlorhexidine during labour for preventing maternal and neonatal infections. Cochrane Database Sys Rev. 2004;Oct 18 (4):[Medline].

9. Livingston JC, Llata E, Rinehart E, et al. Gentamicin and clindamycin therapy in postpartum endometritis: the efficacy of daily dosing versus dosing every 8 hours. Am J Obstet Gynecol. Jan 2003;188(1):149-52. [Medline].

10. Sifakis S, Angelakis E, Makrigiannakis A, et al. Chemoprophylactic and bactericidal efficacy of 80mg gentamicin in a single and once daily dosing. Arch Gynecol Obstet. 2004;Dec 17:[Medline].

11. French LM, Smaill FM. Antibiotic regimens for endometritis after delivery. Cochrane Database Syst Rev. 2004;(4):CD001067. [Medline].

12. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines 2002. MMWR Recomm Rep. May 10 2002;51(RR-6):1-78. [Medline].

13. Akalin HE. The role of beta-lactam/beta-lactamase inhibitors in the management of mixed infections. Int J Antimicrob Agents. Aug 1999;12 Suppl 1:S15-20; discussion S26-7. [Medline].

14. Casey BM, Cox SM. Chorioamnionitis and endometritis. Infect Dis Clin North Am. Mar 1997;11(1):203-22. [Medline].

15. Disep B, Innes BA, Cochrane HR, et al. Immunohistochemical characterization of endometrial leucocytes in endometritis. Histopathology. Dec 2004;45(6):625-32. [Medline].

16. Duff P. Antibiotic selection in obstetric patients. Infect Dis Clin North Am. Mar 1997;11(1):1-12. [Medline].

17. Ehrenkranz NJ, Blackwelder WC, Pfaff SJ, et al. Infections complicating low-risk cesarean sections in community hospitals: efficacy of antimicrobial prophylaxis. Am J Obstet Gynecol. Feb 1990;162(2):337-43. [Medline].

18. Haggerty CL, Ness RB, Amortegui A, et al. Endometritis does not predict reproductive morbidity after pelvic inflammatory disease. Am J Obstet Gynecol. 2003;188(1):141-8. [Medline].

19. Hawrylyshyn PA, Bernstein P, Papsin FR. Risk factors associated with infection following cesarean section. Am J Obstet Gynecol. Feb 1 1981;139(3):294-8. [Medline].

20. Newton ER, Prihoda TJ, Gibbs RS. A clinical and microbiologic analysis of risk factors for puerperal endometritis. Obstet Gynecol. Mar 1990;75(3 Pt 1):402-6. [Medline].

21. NIH. Effect of corticosteroids for fetal maturation on perinatal outcomes. JAMA. Feb 1 1995;273(5):413-8. [Medline].

22. Partlow DB Jr, Chauhan SP, Justice L, et al. Diagnosis of post partum infections:clinical criteria are better than laboratory parameter. J Miss State Med Assoc. 2004;45(3):67-70. [Medline].

23. Ross JD. What is endometritis and does it require treatment?. Sex Transm Infect. Aug 2004;80(4):252-3. [Medline].

24. Stefonek KR, Maerz LL, Nielsen MP, et al. Group A streptococcal puerperal sepsis preceded by positive surveillance cultures. Obstet Gynecol. Nov 2001;98(5 Pt 1):846-8. [Medline].

Keywords

pelvic inflammatory disease, endometritis, PID, pregnancy-related endometritis, endometrium, fallopian tubes, salpingitis, ovaries, oophoritis, pelvic peritoneum, pelvic peritonitis, cervicitis, bacterial vaginosis, cesarean delivery, postpartum anemia, cervical ectopy, Streptococcus agalactiae, Streptococcus viridans, Streptococcus faecalis, Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Enterobacter aerogenes, Gardnerella vaginalis, Neisseria gonorrhae, Chlamydia trachomatis, Ureaplasma urealyticum, Bacteroides bivius, Peptococcus, Peptostreptococcus, Bacteroides, Fusobacterium

Contributor Information and Disclosures

Author

Latha Chandran, MD, MPH, Associate Professor of Pediatrics, Associate Dean for Academic Affairs, Director, Division of General Pediatrics, State University of New York at Stony Brook School of Medicine
Latha Chandran, MD, MPH is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph A Puccio, MD, FAAP, Director, Division of Adolescent Medicine, Stony Brook University Hospital; Assistant Professor, Department of Pediatrics, Stony Brook University School of Medicine
Joseph A Puccio, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics and Society for Adolescent Medicine
Disclosure: Nothing to disclose.

Medical Editor

Elizabeth Alderman, MD, Director of Fellowship Training Program, Director, Adolescent Ambulatory Service, Clinical Professor, Department of Pediatrics, Division of Adolescent Medicine, Albert Einstein College of Medicine and Montefiore Medical Center
Elizabeth Alderman, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, North American Society for Pediatric and Adolescent Gynecology, and Society for Adolescent Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Wayne Wolfram, MD, MPH, Clinical Associate Professor, Departments of Pediatrics, Children's Hospital and University of Cincinnati
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Maureen Strafford, MD, Arnold P Gold Foundation Associate Professor, Departments of Anesthesiology and Pediatrics, Tufts University and Tufts-New England Medical Center
Maureen Strafford, MD is a member of the following medical societies: American Medical Women's Association, American Pain Society, American Society of Anesthesiologists, International Anesthesia Research Society, Society for Education in Anesthesia, Society for Pediatric Anesthesia, and Society of Cardiovascular Anesthesiologists
Disclosure: Nothing to disclose.

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