Postpartum toxic shock syndrome associated with multiple splenic infarcts

Over the next 24 hours, she developed abdominal pain and sweats, and appeared flushed. On Day 3, her temperature was 37.6°C, and she developed nausea and diarrhoea. Empirical treatment was begun with intravenous ampicillin and metronidazole. She developed hypotension (blood pressure, 90/60 mmHg) and an erythematous rash of the legs and diffuse erythema of the trunk, anterior thighs and face. Relevant results of laboratory investigations are summarised in Box 1.

On Day 4, a vaginal swab was taken, and antibiotic therapy changed to ticarcillin–clavulanate and clindamycin on the basis of presumed toxic shock syndrome. The next day, the patient developed oedema of the hands and feet, a sore throat and sore ankles. Group A streptococcus grew from the vaginal swab. Blood cultures showed no growth, but the samples had been taken after antibiotic therapy was begun.

Over the next few days, the patient’s condition improved, but on Day 9 again deteriorated, with recurrence of low-grade fever and the development of sharp, retrosternal chest pain. Computed tomography (CT) of the chest with a pulmonary angiogram revealed a small right lower-lobe opacity, suggestive of a pulmonary infarct. The CT scan also revealed multiple splenic infarcts (Box 2). Screening for thrombophilia gave normal results. She was treated initially with intravenous heparin, followed by oral warfarin for 3 months. Her clinical recovery was slow but complete.

This patient had probable toxic shock syndrome caused by group A streptococcus.1 She had the non-specific features of toxic shock syndrome2 (fever, nausea, diarrhoea, rash, abnormal hepatic and renal function) and disproportionate abdominal pain as the initial symptom. The only criterion lacking for “definite” toxic shock syndrome was the isolation of group A streptococcus from a normally sterile site (it was isolated only from the vagina). Puerperal toxic shock syndrome caused by group A streptococcus is well reported,1,2 with mortality of 25%–50%.2

The patient’s clinical course was complicated by multiple splenic infarcts and a possible pulmonary infarct, thought to have developed in situ with no identifiable prothrombotic diathesis. Splenic infarction is not common and is usually associated with a haematological or rheumatological disorder.3,4 Spontaneous splenic infarcts have been associated with infections, but there is only one report of these infarcts in association with toxic shock syndrome, in that case caused by Staphylococcus aureus.5 The infarcts have been postulated to be caused by circulating endotoxin.5

2 Computed tomography of the abdomen

Scan shows one of multiple splenic infarcts — in the lateral third of the spleen.