A 33-year-old previously well G7P7 woman was admitted to Middlemore Hospital with postpartum endometritis 3 weeks after a normal vaginal delivery. She complained of increasing abdominal pain, vaginal discharge, diarrhea, and fever that started 3 days postdelivery. Outpatient therapy had failed. On admission to the gynecologic service, she was alert and responsive but had clinical signs consistent with systemic inflammatory response syndrome. She was febrile at 39.5°C, respiratory rate was 32 breaths/min, pulse was 100 beats/min, and white blood cell count was 5.5 × 109/L. The blood pressure was 100/65 mm Hg. Her hemoglobin was 107 g/L, and platelet count was 292 × 109/L. Her abdomen was tender, and there was a brown foul-smelling vaginal discharge. Over the next 24 hours, she developed increasing respiratory distress and septic shock. An ultrasound was consistent with retained products of conception. Chest x-ray (CXR) showed extensive nodular and infiltrative opacities which was interpreted as adult respiratory distress syndrome. Arterial blood gas obtained with oxygen was pH 7.16; Paco2, 6.0 kPa; Po2, 11.7 kPa; and oxygen saturation, 94%.
The patient was admitted to the intensive care unit for mechanical ventilation and inotropic support. Empirical antibiotics were started, and dilatation and curettage were performed. The gross findings at dilatation and curettage were consistent with infected retained products of conception. She developed multiorgan failure and oliguric renal failure and returned to the operating theater the following day because of worsening sepsis. At laparotomy, microabscesses were seen scattered throughout the omentum and pelvis. Pus was noted in the right fallopian tube. She underwent abdominal hysterectomy, right salpingectomy, and abdominal washout.
Results from histopathologic examination of the uterine curettings, hysterectomy, and right salpingectomy specimens were available on day 4. There was extensive necrotizing granulomatous inflammation containing acid-fast bacilli (AFB) in all the specimens. Conventional antituberculous treatment was started on day 4 with 3 drugs (isoniazid, rifampicin, and pyrazinamide) given local resistance pattern. Because of concerns about poor oral absorption, intravenous ciprofloxacin and amikacin were added. Antimicrobial treatment was continued with clindamycin. A short synacthen test was consistent with normal adrenal function. An echocardiogram showed hyperdynamic left ventricular function consistent with sepsis, impaired right ventricular function, and importantly no pericardial effusion. Despite antituberculous therapy, mechanical ventilation, and maximal use of inotropic support, her condition worsened into established oliguric renal failure. She died on day 14 of multiorgan failure.
Routine aerobic and anaerobic bacterial cultures were negative and included 7 sets of blood cultures, vaginal cultures, sputum, and bronchoalveolar lavage samples and specimens from peritoneal fluid, the right fallopian tube, and uterine tissue. A chlamydia polymerase chain reaction from peritoneal fluid was negative. Antibody test for HIV-1 and -2 was negative. An initial midstream urine on the day of admission had 300 × 106/L white blood cells and 130 × 106/L red cells, and Escherichia coli was recovered from the culture. A feces specimen on the day of admission grew Plesiomonas shigelloides. Mycobacterium tuberculosis, which was fully susceptible, was isolated on day 15 from uterine curettings, sputum, and bronchoalveolar lavage.
An autopsy was not done. The baby was evaluated at the time of the mother's illness and was clinically well and gaining weight appropriately. After gastric aspirates and early morning urines, she began isoniazid prophylaxis.
This woman presented with an acute fulminant illness that led to multiorgan failure and death in 14 days. The initial clinical findings were consistent with postpartum endometritis with septic shock, and her rapid deterioration was suggestive of Gram-negative sepsis. An initial urine culture at the time of admission was positive for E. coli, and a feces culture was positive for Plesiomonas shigelloides. Subsequent urines were negative. Although it is possible that these organisms caused her septic shock, they were not recovered from her blood or from other sterile site specimens. The crucial result was the demonstration of AFB in necrotizing granulomatous inflammation on histologic examination of the gynecologic organs.
Disseminated tuberculosis (TB) leading to multiorgan failure and septic shock has been reported in both non-HIV-infected as well as HIV-infected individuals. A search of the literature from 1966 to 2002 was conducted with MEDLINE computerized database. The terms "sepsis," "septic shock," "sepsis syndrome," and "multiorgan failure" were combined together with "Mycobacterium tuberculosis," "tuberculosis," and "military tuberculosis." This revealed 34 citations. A separate search was done combining the terms "Mycobacterium tuberculosis," "tuberculosis," and "military tuberculosis" with "endometritis." This revealed 8 citations. To date, there have been 15 case reports in the English literature1-10 of TB associated with septic shock. Four were HIV-negative patients, and 1 had an unknown HIV status. The case presented here is in a patient without HIV.
Table 1 shows a summary of 5 case reports2,6-9 of septic shock caused by disseminated TB in HIV-negative patients. The age range was from 37 to 69 years. All 5 cases had septic shock requiring mechanical ventilation and inotropic support. Three patients received antituberculous treatment. Only one patient survived. Three of the patients had a possible underlying immune deficiency including history of treated cancer of the tonsil, alcohol abuse, and autoimmune hemolytic anemia. None of the cases had concomitant infection that may have contributed to septic shock. Four of the 5 patients had disseminated TB. Diagnosis was made from sputum and bronchial washings in 2 patients and from postmortem tissue biopsy in 3 patients.
Extrapulmonary TB affecting the endometrium is probably not uncommon in areas of high prevalence. In 1 prevalence study from Darjeeling, TB was noted in the endometrium of 11.8% of 800 women who presented for dilatation and curettage.11
Our patient was 3 weeks postpartum when she presented. Pregnancy has been variously reported to improve, worsen, or to have no effect on natural history of TB. Studies done in the 1950s suggested that the postpartum period was associated with increased rates of relapse.12 However, recent data show that pregnancy does not appear to increase the chance of TB developing postpartum in either HIV-positive or HIV-negative women.13,14
TB can present as an acute fulminant illness in non-HIV-infected patients closely resembling Gram-negative sepsis. It is possible that lipoarabinomannan which may resemble Gram-negative bacterial lipopolysaccharide or another mycobacterial cell wall component can initiate the systemic inflammatory response syndrome.1,8
In summary, we have presented a patient with postpartum endometritis and septic shock caused by M. tuberculosis. Although it is rare, TB should be considered in patients who present with abnormal CXR and septic shock of uncertain etiology.
1. Ahuja SS, Ahuja SK, Phelps K, et al. Hemodynamic confirmation of septic shock in disseminated tuberculosis. Crit Care Med
2. Angoulvant D, Mohammedi I, Duperret S, et al. Septic shock caused by Mycobacterium tuberculosis
in a non-HIV patient. Intensive Care Med
3. Clark T, Burman W, Cohn D, et al. Septic shock from Mycobacterium tuberculosis
after therapy for Pneumocystis carinii
. Arch Intern Med
4. Gachot B, Wolff M, Clair B, et al. Severe tuberculosis in patients with human immunodeficiency virus infection. Intensive Care Med
. 1990; 16:491-493.
5. George S, Papa L, Sheils L, et al. Septic shock due to disseminated tuberculosis. CID
6. Lim K, Chong K. Multiple organ failure and septic shock in disseminated tuberculosis. Singap Med J
7. Pene F, Papo T, Brudy-Gulphe L, et al. Septic shock and thrombotic microangiopathy due to Mycobacterium tuberculosis in a nonimmunocompromised patient. Arch Intern Med
8. Schroder J, Siemann M, Vogel I, et al. Sepsis syndrome induced by tuberculous perforation of the eosophagus. Infection
9. Siemann M, Rabenhorst G, Bramann A, et al. A case of cryptic miliary tuberculosis mimicking cholecystitis with sepsis. Infection
10. Vadillo M, Corbella X, Carratala J. AIDS presenting as septic shock caused by Mycobacterium tuberculosis
. Scand J Infect Dis
11. Roy A, Mukherjee S, Bhattacharya S, et al. Tuberculous endometritis in hills of Darjeeling: a clinicopathological and bacteriological study. Indian J Pathol Microbiol
12. Fidelma B, Rigby M. Tuberculosis and pregnancy: update on an old nemesis. Infect Med
13. Espinal M, Reingold A, Lavandera M. Effect of pregnancy on the risk of developing active tuberculosis. J Infect Dis
14. Ormerod P. Tuberculosis in pregnancy and the puerperium. Thorax