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Puerperal fever

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Postpartum fever
From American Family Physician, 8/1/95 by Ghassan Hamadeh

Puerperal fever was first described by Hippocrates; however, it was not described as a virulent epidemic until the mid-17th century.(1) Today, epidemics are rare, but the disease has not disappeared. Puerperal febrile morbidity is defined as an oral temperature of 38.0[degrees]C (100.4[degrees]F) or higher on any two of the first 10 days postpartum, or a single oral temperature of 38.7[degrees]C (101.6[degrees]F) in the first 24 hours.(2)

Postpartum fever is a complication in 2 to 4 percent of vaginal deliveries and in 29 to 95 percent of cesarean deliveries.(3) The rate of endometritis is at least 10 times higher in patients who have a cesarean delivery, compared with patients who have a vaginal delivery. The clinician who practices obstetrics should be aware of current antibiotic choices for treatment of postpartum fever and the modalities available to evaluate patients whose febrile episode does not resolve.(4) This article reviews the causes of postpartum fever and associated risk factors and delineates an approach to this common obstetric complication.

Risk Factors for Postpartum Fever

Risk factors for each of the described postpartum febrile complications are listed in Table 1. (3)(5)(6)(7)(8)(9) It is important to note that if invasive procedures are performed on a patient in labor who has other risk factors, a higher risk exists for a febrile complication. This is particularly true in the case of endometritis, in which the risk for a febrile complication increases from less than 4 percent in an uncomplicated vaginal delivery to as much as 85 percent in an indigent patient with membranes ruptured for more than six hours and multiple pelvic examinations followed by a cesarean section.(3)

TABLE 1 Risk Factors for Postpartum Fever

Derived from references 3,5-9.

Causes of Postpartum Fever

The most common avenue of puerperal fever is the genitourinary tract, including the uterus, vagina, episiotomy site or bladder, or their associated vascular structures. These organs may become infected during delivery or be subject to hematomas and phlebitis, which contribute to the febrile morbidity. The causes of postpartum fever are listed in Table 2.(3)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16) The mode of delivery is the most significant factor affecting febrile morbidity, with a higher incidence of infections (in particular, endometritis and urinary tract infection) occurring after cesarean section. Therefore, antibiotic prophylaxis before cesarean section is becoming a routine practice. However, the latter topic is beyond the scope of this article.

TABLE 2 Causes of Postpartum Fever

ENDOMETRITIS

Endometritis is the most common cause of infectious morbidity in the puerperium (Table 2). Fever, uterine tenderness, foulsmelling lochia and malaise suggest the diagnosis. Fever may occur early or late in the course of the illness.(17)(18) When fever occurs in the first 24 to 48 hours of delivery, Streptococcus agalactiae infection should be suspected. A later onset of fever suggests a mixed infection containing aerobic organisms, facultative and obligate aerobes. Fever originating more than seven days after delivery suggests the presence of Chlamydia trachomatis. In both early- and late-onset endometritis, anaerobes play a significant role. If these infections are not treated aggressively, the organisms may act synergistically to form complex abscesses or necrotizing infections.

Laboratory studies, including a complete blood count and endometrial culture obtained with a flexible endometrial catheter (Pipelle), aid in formulating a diagnosis of endometritis.(19) Blood cultures should be performed if sepsis is suspected. However, the physiologic mobilization of polymorphonuclear white blood cells and the difficulty in obtaining an endometrial culture without contamination limit the value of these particular diagnostic modalities.(20) The diagnosis is therefore made clinically, particularly when risk factors are prominent (Table 1). Treatment is initiated on the assumption that a polymicrobial infection with two or three organisms exists.(19) Coverage for anaerobic bacteria is important.

Antibiotic prophylaxis in a high-risk patient is common practice. However, this practice only reduces the risk of endometritis by 50 percent.(21) It has been postulated that early endometritis is related to contamination of the endometrial cavity with vaginal organisms introduced during labor and delivery. Late-onset endometritis is more likely secondary to the ascent of organisms along mucosal surfaces and subsequent establishment of a subclinical infection. The latter situation may explain the failure of prophylactic antibiotics to completely prevent endometritis.(21)

PELVIC ABSCESS

Pelvic abscess should be suspected in the patient with persistent spiking fever despite antibiotic coverage.(22) An ultrasound examination or computed tomographic (CT) scan is very helpful in making the diagnosis.(4) Ultrasound may confirm an abscess when fluid and gas collections are associated with shaggy walls and fluid in the cul-de-sac. The treatment of choice is surgical drainage.

URINARY TRACT INFECTION

Bacteriuria in the postpartum period is often asymptomatic, with only 21 percent of culture-positive women reporting symptoms.(5) Of all risk factors, urethral catheterization contributes most to the incidence of nosocomial urinary tract infections. Suprapubic urine culture is the diagnostic gold standard; however, when risk factors (Table 1) are associated with a positive midstream urine culture, the diagnosis is highly probable.(5) Failure to treat a urinary tract infection in the postpartum period results in persistence of the bacteriuria in about 30 percent of cases. A three-day course of antibiotics is usually enough to eradicate the infection in uncomplicated cases.(5) A 10-day course is preferable in patients with suspected early pyelonephritis.

THROMBOPHLEBITIS

The risk of thrombosis increases during pregnancy secondary to the prevalent hypercoagulable state. These changes worsen around the puerperium, particularly after cesarean section.(6)(7) Classic symptoms of deep venous thrombosis include unilateral leg pain, tenderness and swelling; however, the first sign may often be a pulmonary embolus. When thrombophlebitis is recognized early, the risk of pulmonary embolism can be greatly reduced with appropriate anticoagulant therapy.(7)

Septic pelvic thrombophlebitis is more common after cesarean section(23) than after vaginal delivery. The mechanism of action involves the presence of a hypercoagulable state and ascent of infection from the myometrium to pelvic and ovarian veins.(24) The diagnosis is suspected when a patient responds poorly to antibiotic treatment of endometritis and a mass is palpable on pelvic examination. The diagnosis is confirmed by CT of the pelvis or magnetic resonance imaging.(4) When diagnostic imaging is negative but the diagnosis is highly suspected, a trial of anticoagulation therapy with heparin may suggest the diagnosis.

MASTITIS

Breast engorgement is common in the first few days postpartum. It is associated with a low-grade fever, often less than 38.4[degrees]C (101.1[degrees]F).(25) Mastitis, however, occurs two to three weeks postpartum and is associated with cellulitis over the breast area and a temperature of 39[degrees]C (102.2[degrees]F) or higher.(8) Mastitis should be distinguished from late engorgement caused by milk stasis,(14) which can cause inflammation of the breast but is not associated with high fever or cracked nipples, and does not require antibiotic therapy. Staphylococcus aureus is the most common causative agent in patients with mastitis. Therapy includes local care and continuation of breast-feeding. Antistaphylococcal antibiotics are used, especially if risk factors are present (Table 1).

WOUND AND EPISIOTOMY INFECTIONS

Infections of abdominal incisions following cesarean section are more common than infections of episiotomy incisions (Table 2). Post-cesarean wound infections are usually detected between day 3 and day 7, postoperatively. Swelling, edema, erythema and tenderness of the wound are present. Later, drainage of purulent material is noted.(9)

Treatment consists of local care: the wound is opened, cleaned and debrided. When the infection occurs within the first 48 hours after delivery, it is usually due to group A Streptococcus or, occasionally, Clostridium perfringens, and requires prompt treatment with debridement and intravenous antibiotics. In wound infections following cesarean section, the integrity of the fascia must be checked, and any defects must be repaired to prevent possible evisceration.

Necrotic fasciitis must be considered whenever infection of the fascia is suspected. This is a rare, life-threatening infection that usually is caused by group A beta-hemolytic streptococci, Staphylococcus aureus and anaerobic streptococci, although other organisms may be involved. It is more common in persons with preexisting tissue susceptibility, such as persons with diabetes and those with vascular insufficiency disorders. Mortality rates in these patients are generally quoted as 30 to 60 percent.(26)

The diagnosis of necrotic fasciitis can be made if the patient has a high fever resistant to antibiotics, with associated systemic toxicity and a hard, "wooden" feel to the infected area. The infected area may quite often have anesthestic areas. Treatment requires surgical excision of the involved fascia and other necrotic tissue, plus antibiotic treatment covering both aerobic and anaerobic bacteria.

Although episiotomy infections are infrequent, they do occur and may be associated with significant complications and even death.(16) An infection of the episiotomy site should be suspected in patients with significant perineal pain, hip pain or erythema and swelling beyond the episiotomy site. Pelvic examination may detect the presence of hematomas or abscesses. If no abscess or extension is suspected, Sitz baths are usually sufficient treatment. If an abscess is suspected, CT scanning may be necessary to see if the abscess is located in the retroperitoneal or gluteal muscle areas. Treatment consists of exploration of the episiotomy, drainage and debridement. The wound is then allowed to heal secondarily.

RESPIRATORY TRACT INFECTIONS

Atelectasis occurs in the first 72 hours postoperatively. It presents with a low-grade fever and bibasilar rales. The use of an incentive spirometer and early ambulation are sufficient to halt progression. If left untreated, it may progress to pneumonia.

MISCELLANEOUS CAUSES

As with any patient with fever, the possibility of other causes, such as viral infection, connective tissue disease, malignancy, human immunodeficiency virus infection or subacute bacterial endocarditis, should be considered if the course of illness is atypical or the patient is unresponsive to standard therapy.

Treatment Options for Postpartum Fever

Figure 1 demonstrates an algorithmic approach to the management of the patient with postpartum fever. A single temperature elevation less than 38.4[degrees]C (101[degrees]F) in the first 24 hours does not require investigation.(2) An elevation of this extent is usually transient. Physical examination and temperature charting are sufficient.

[ILLUSTRATION OMITTED]

Higher temperatures or the recording of more than one temperature elevation above 38.4[degrees]C (101.1[degrees]F) requires a work-up, including a complete physical examination, with particular attention to the pelvic area.(19) If no obvious source of infection is identified, the patient is assumed to have endometritis and is treated with broad-spectrum antibiotics. As mentioned earlier, an average of two to three different bacterial agents are isolated in cases of endometritis, with Bacteroides and other anaerobes being the most common agents. For this reason, clindamycin (Cleocin) is recommended in most treatment regimens.(11)(27) The usual recommendation is to start treatment with clindamycin and gentamicin (Garamycin). This combination covers anaerobes, group B Streptococcus and gramnegative organisms.

After initiation of treatment, the patient is observed for 48 to 72 hours. If no response has occurred, despite adequate doses of antibiotics, or no source of the fever is identified, a third antibiotic is added. Usually, ampicillin is added to provide better synergistic coverage for enterococci.(11) The triple antibiotic regimen is tried for up to 72 hours. If the patient fails to defervesce, an ultrasound examination or CT scan of the pelvis is performed to search for abscesses or thrombophlebitis.(4) If no abscess or thrombophlebitis is discovered, a trial of heparin is warranted.(22) If the latter fails, surgical exploration is necessary.

A common mistake in the treatment of postpartum endometritis is underdosing of the antibiotic. Most antibiotics used to treat postpartum endometritis (e.g., penicillin, cephalosporins, aminoglycosides) are eliminated through the kidneys. Renal clearance and the blood and extracellular volume increase during pregnancy. This physiologic change allows the drugs to clear faster during pregnancy and the postpartum period. The pregnant patient has a much larger volume of distribution of the drug and theoretically may need larger doses to achieve therapeutic concentrations. Higher doses should be considered if an adequate response is not achieved at lower levels. Patients should receive parenteral antibiotics rather than oral therapy, because of the greater cure rates with the former.

The choice of antibiotics can be changed if there is a concern about toxicity. Extended-spectrum cephalosporins or imipenem-cilastatin (Primaxin) or ampicillin-sulbactam (Unasyn) are frequently used; however, the clindamycin/gentamicin regimen remains the "gold standard" of treatment when endometritis is suspected.(11) Table 3(11)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37) lists antibiotics preferred for commonly identified agents in puerperal infections.

[TABULAR DATA OMITTED]

Figure 1 is derived from data in references 10 and 25.

REFERENCES

(1.)Seligman SA. The lesser pestilence: non-epidemic puerperal fever. Med Hist 1991; 35:89-102.

(2.)Filker R, Monif GR. The significance of temperature during the first 24 hours postpartum. Obstet Gynecol 1979; 53:358-61.

(3.)Gibbs RS. Clinical risk factors for puerperal infection. Obstet Gynecol 1980; 55(5 Suppl):178S-84S.

(4.)Lev-Toaff AS, Baka JJ, Toaff ME, Friedman AC, Radecki PD, Caroline DF. Diagnostic imaging in puerperal febrile morbidity. Obstet Gynecol 1991; 78:50-5.

(5.)Stray-Pdersen B, Blakstad M, Bergan T. Bacteriuria in the puerperium. Risk factors, screening procedures, and treatment programs. Am J Obstet Gynecol 1990; 162:792-7.

(6.)Bonnar J. Venous thromboembolism and pregnancy. Clin Obstet Gynecol 1981; 8:455-73.

(7.)Villasanta U. Thromboembolic disease in pregnancy. Am J Obstet Gynecol 1965; 93:142-51.

(8.)Niebyl JR, Spence MR, Parmley TH. Sporadic (nonepidemic) puerperal mastitis. J Reprod Med 1978; 20:97-100.

(9.)Mead PB. Managing infected abdominal wounds. Contemp Ob Gyn 1979; 14:69-75.

(10.)Sweet RL, Ledger WJ. Puerperal infectious morbidity: a two-year review. Am J Obstet Gynecol 1973; 117:1093-100.

(11.)Yonekura ML. Treatment of postcesarean endomyometritis. Clin Obstet Gynecol 1988; 31:488-500.

(12.)Calman RM, Gibson J. Pyrexia in the puerperium. Lancet 1953; 2:649-52.

(13.)Guldholt I, Espersen T. Maternal febrile morbidity after cesarean section. Acta Obstet Gynecol Scand 1987; 66:675-9.

(14.)Thomsen AC, Espersen T, Maigaard S. Course and treatment of milk stasis, noninfectious inflammation of the breast, and infectious mastitis in nursing women. Am J Obstet Gynecol 1984; 149:492-5.

(15.)Gibbs RS, Blanco JD, St. Clair PJ. A case-control study of wound abscess after cesarean delivery. Obstet Gynecol 1983; 62:498-501.

(16.)Thacker SB, Banta HD. Benefits and risks of episiotomy: an interpretative review of the English language literature, 1860-1980. Obstet Gynecol Surv 1983; 38:322-38.

(17.)Watts DH, Eschenbach DA, Kenny GE. Early postpartum endometritis: the role of bacteria, genital mycoplasmas, and Chlamydia trachomatis. Obstet Gynecol 1989; 73:52-60.

(18.)Hoyme UB, Kiviat N, Eschenbach DA. Microbiology and treatment of late postpartum endometritis. Obstet Gynecol 1986; 68:226-32.

(19.)Mead PB. Postpartum endometritis. Contemp Ob Gyn 1990; 35:29-34.

(20.)Eschenbach DA, Rosene K, Tompkins LS, Watkins H, Gravett MG. Endometrial cultures obtained by a triple-lumen method from afebrile and febrile postpartum women. J Infect Dis 1986; 153:1038-45.

(21.)Gonik B, Shannon RL, Shawar R, Costner M, Seibel M. Why patients fail antibiotic prophylaxis at cesarean delivery: histologic evidence for incipient infection. Obstet Gynecol 1992; 79:179-84.

(22.)Gibbs RS. Severe infections in pregnancy. Med Clin North Am 1989; 73:713-21.

(23.)Duff P, Gibbs RS. Pelvic vein thrombophlebitis: diagnostic dilemma and therapeutic challenge. Obstet Gynecol Surv 1983; 38:365-73.

(24.)Dunnihoo DR, Gallaspy JW, Wise RB, Otterson WN. Postpartum ovarian vein thrombophlebitis: a review. Obstet Gynecol Surv 1991; 46:415-27.

(25.)Almeida OD Jr, Kitay DZ. Lactation suppression and puerperal fever. Am J Obstet Gynecol 1986:154:940-1.

(26.)Thompson CD, Brekken AL, Kutteh. Necrotizing fasciitis: a review of management guidelines in a large obstetrics and gynecology teaching hospital. Infect Dis Ob Gyn 1993; 1:16-22.

(27.)Soper DE. Clindamycin. Obstet Gynecol Clin North Am 1992; 19:483-96.

(28.)Chow AW, Marshall JR, Guze LB. Anaerobic infections of the female genital tract: prospects and perspectives. Obstet Gynecol Surv 1975; 30:477-94.

(29.)Ledger WJ, Norman M, Gee C, Lewis W. Bacteremia on an obstetric-gynecologic service. Am J Obstet Gynecol 1975; 121:205-12.

(30.)Rosene K, Eschenbach DA, Tompkins LS, Kenny GE, Watkins H. Polymicrobial early postpartum endometritis with facultative and anaerobic bacteria, genital mycoplasmas, and Chlamydia trachomatis: treatment with piperacillin or cefoxitin. J Infect Dis 1986; 153:1028-37.

(31.)Brook I. Cefoxitin in the prevention and treatment of infections. Hosp Pract [Off Ed] 1990; 25(Suppl 4):46-56.

(32.)McGregor JA, Gordon SF, Krotec J, Poindexter AN. Results of a randomized, multicenter, comparative trial of a single dose of cefotetan versus multiple doses of cefoxitin as prophylaxis in cesarean section. Am J Obstet Gynecol 1988; 158(3 Pt 2):701-6.

(33.)Martens M, Faro S, Hammill H, Maccato M. Treatment of postpartum endometritis. Hosp Pract [Off Ed] 1990; 25(Suppl 4):13-9.

(34.)Ismail MA, Moawad AH, Poon E, Henderson C. Role of Chlamydia trachomatis in postpartum endometritis. J Reprod Med 1987; 32:280-4.

(35.)Faro S, Hammill HA, Maccato M, Martens M. Ticarcillin/clavulanate for treatment of postpartum endometritis. Rev Infect Dis 1991; 13(Suppl 9):S758-62.

(36.)Zambrano D. Clindamycin in the treatment of obstetric and gynecologic infections: a review. Clin Ther 1991; 13:58-80.

(37.)Ruiz-Moreno JA, Garcia-Rojas JM, Lozada-Leon JD. Prevention of postcesarean infectious morbidity with a single dose of intravenous metronidazole. Int J Gynaecol Obstet 1991; 34:217-20.

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