Multiple splenic infarcts associated with toxic shock syndrome

INTRODUCTION Toxic shock syndrome (TSS) is characterized by high fever, hypotension, vomiting, diarrhea, myalgia, nonfocal neurologic abnormalities, conjunctival hyperemia, strawberry tongue, and scarlatiniform erythroderma with subsequent desquamation on the hands and feet (1). A strong correlation has been found between TSS and the recovery of Staphylococcus aureus from vaginal or cervical cultures of affected patients (2,3). TSS occurs most commonly in menstruating females of childbearing age, particularly in adolescents who use hyperabsorbent tampons regularly (2,3). The remainder of TSS cases occur in prepubertal children and in adults of both sexes, and are associated with focal or surgical wound infections, postpartum infections, burns, nasal packing, or various methods of barrier contraception (2,3). We describe a 15-year-old female who developed multiple splenic infarcts secondary to TSS. To our knowledge, the association of TSS and splenic infarcts has never before been reported. CASE A previously well 15-year-old female presented with a 4-day history of high fever, anorexia, nausea, headache, sore throat, listlessness, and myalgia. Twenty-four hours prior to admission, she developed a rash on her palms that subsequently spread to her trunk and legs, as well as a constant left upper quadrant abdominal pain associated with pain in the left shoulder. She had just completed her menstrual period and had used 3 to 4 tampons per day. On examination, her temperature was 39.6°C, heart rate 90 beats per minute, respiratory rate 16 breaths per minute, and blood pressure 90/50 mmHg. The conjunctiva, tympanic membranes, and pharynx were hyperemic. The tongue was erythematous with prominent papillae and small white plaques. There were palpable lymph nodes in the anterior cervical and axillary areas. A fine erythematous macular rash was noted on the trunk and extremities. The left upper quadrant of the abdomen and left flank were tender. The spleen tip was palpable 3 cm below the left costal margin and was tender. Laboratory investigation revealed a hemoglobin of 122 gm/L, white blood cell count (WBC) of 20.0 × 109/L with 54% neutrophils, 44% bands, 1% lymphocytes, and 1% monocytes, platelet count 180 × 109/L, erythrocyte sedimentation rate 22 mm/hr, serum total bilirubin 70 μmol/L, direct bilirubin 60 μmol/L, lactic dehydrogenase (LDH) 274 U/L, and alanine amino transaminase (ALT) 60 U/L. Urinalysis revealed 10 to 20 red blood cells and 15 to 25 WBC/high power field (HPF). Monospot test was negative. Urine cultures grew β-lactamase producing S. aureus with a colony count of 100,000/mL, but blood cultures were negative. Throat swab culture was negative. Abdominal ultrasound and computer tomographic (CT) scan revealed splenomegaly and multiple areas of hypodensity, the largest of which measured 7 cm in diameter, within the spleen. These radiologic findings were consistent with multiple splenic infarcts. The renal anatomy was normal. The patient was started on penicillin G, 2 million units intravenously (IV) q6h, and cloxacillin 1.25 g IV q6h. The patient developed a grade I-II/VI systolic ejection murmur in the evening. She had no previous history of a cardiac murmur or rheumatic fever, nor did she have any stigmata of bacterial endocarditis on physical examination. Nevertheless, because of concerns regarding possible bacterial endocarditis, as well as her splenic findings, she was transferred to the Intensive Care Unit of the Alberta Children’s Hospital, and we were consulted at this point. On admission to the Alberta Children’s Hospital, her antibiotics were changed to cloxacillin 1.5 g IV q6h and gentamicin 70 mg IV q8h. Echocardiogram revealed a very small pericardial effusion, but the cardiac anatomy was normal and no vegetations on the valves were seen. Electrocardiogram and chest radiograph were both normal. Repeat CT scans of the abdomen reconfirmed the presence of the splenic infarcts with mild resolution. Vaginal culture grew S. aureus, but repeat blood and urine cultures were negative. Prothrombin time and activated partial thromboplastin time were normal. Her serum was positive for TSS toxin-1. After admission to the Alberta Children’s Hospital, she developed a marked pruritic desquamation on the palms and soles. Her fever subsided the following day, and the gentamicin was discontinued. Five days after her admission to hospital, she no longer had any abdominal pain or tenderness. By the 10th day, her cardiac murmur had resolved, and the consensus was that the murmur was functional. She was treated with a 4-week course of IV antibiotic. A follow-up CT scan of the abdomen done 2 months later revealed no hepatosplenomegaly and continued resolution of the splenic lesions, the largest of which then measured only 2 cm in diameter. Ultrasound of the spleen done 12 months later showed complete resolution of the spleen lesions. DISCUSSION Our patient represents a moderately severe case of TSS. The unique finding in this patient was the presence of multiple splenic infarcts. Intestinal infarct, however, has been reported in children with endotoxic shock (4), and cerebral infarct in a 38-year-old male with TSS (5). To our knowledge, splenic infarct has never been described before in association with TSS. We believe that the most likely pathogenesis for this finding is that the infarcts are secondary to the effects of circulating toxin. TSS toxin-1 induces production of interleukin-1 and tumor necrosis factor, resulting in fever, hypotension, and multisystem involvement (2). However, it is also possible that she had endocarditis and subsequently developed septic emboli causing splenic infarcts. We do not think that this is a likely possibility for several reasons. While the patient did develop a transient cardiac murmur, this is most likely secondary to a hyperdynamic state. Furthermore, she had no stigmata of endocarditis; blood cultures were all negative, and the echocardiogram was unremarkable. Finally, she had no history of an underlying condition, such as congenital, rheumatic, or degenerative cardiac disease, previous endocarditis, or cardiac surgery, which would have predisposed her to developing endocarditis. CONCLUSIONS Splenic infarction is a seldom encountered clinical entity. The usual clinical presentation is sudden onset of left upper quadrant abdominal pain, anorexia, and vomiting. Examination often shows a rigid abdomen with rebound tenderness simulating an acute surgical abdomen. Causes of splenic infarction include bacterial endocarditis, sickle cell anemia, leukemia, wandering spleen, pancreatitis, systemic lupus erythematosus, and diabetes mellitus (6,7). We would like to add TSS as a potential cause of splenic infarction. The association of splenic infarcts with TSS may be more than coincidental. With the report of this case, we hope that more case reports will be forthcoming.

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