AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Chorioamnionitis
Pelvic inflammatory disease
Salpingitis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab 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

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

Drug Category: Antibiotics

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

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• 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].

Article Last Updated: Mar 6, 2008