Spleen and gone? An interesting case of fever in a young man.

نویسندگان

  • Christopher Myles Rowe
  • Caroline Spillane
  • Dario Winterton
  • Laura-Beth Pilkington
چکیده

To cite: Rowe CM, Spillane C, Winterton D, et al. BMJ Case Rep Published online: [please include Day Month Year] doi:10.1136/bcr-2016216196 DESCRIPTION A 38-year-old man attended accident and emergency department (A and E) reporting of a 2-week history of fever and rigors, vomiting and left flank pain. The patient had a medical history of hypertension and obesity, but denied being diabetic and had not recently travelled. Later history taking did not reveal any abdominal trauma. Abdominal examination elicited pain in the left upper quadrant, but no palpable mass. Cardiovascular examination revealed the patient to be peripherally warm and tachycardic, with a flash capillary refill, but normotensive. The patient was febrile at 39.0°C. All other examinations were normal. Admission blood tests demonstrated a white cell count of 40.0×10/L, and C reactive protein of 155 mg/L. Liver function tests, and urea and electrolytes were normal. Urine dip was negative and admission chest X-ray was normal. An ultrasound of the abdomen was undertaken, which revealed a heterogenic encapsulated mass in the superior aspect of the spleen, containing echogenic clumps, with the appearance of an organising abscess. A subsequent abdominal CT showed a welldefined large splenic abscess (figure 1A–C) with mildly thick fluid content, tiny calcifications along the upper medial contour and loculated gas. A percutaneous drain was placed, from which puss drained; culture and sensitivities grew Escherichia coli. The patient was discharged with antibiotics and the drain in situ; however, 3 days later, he re-presented to A and E describing the recurrence of fever and rigors. Clinical examination revealed diffuse upper abdominal pain, a heart rate of 130 bpm, blood pressure of 85/40 mm Hg, and an arterial blood gas revealing metabolic acidosis and lactic acidaemia—all indicative of sepsis. A repeat abdominal CT revealed recurrence of the splenic abscess. After fluid resuscitation, the patient attended surgery for a splenectomy and, postoperatively, the intensive care unit (ICU) for vasopressor support and escalated antibiotic therapy. A transthoracic echocardiogram undertaken on the ICU was normal. During both attendances, clinical and radiological investigations did not reveal an obvious source for the splenic abscess. The most common causes of splenic abscesses are haematogenous spread from distant infections, including endocarditis, or contiguous spread from infections of the adjacent/local anatomy. Trauma is a predisposing factor. The most common causative pathogens are aerobes, including the Gram-positive organisms Streptococcus viridans, Enterococcus sp. and Staphylococcus aureus, and the Gram-negative pathogens E. coli and Klebsiella pneumonia. Up to half of the cases are polymicrobial. Less common causative pathogens can include anaerobes, Mycobacterium tuberculosis and fungal infections.

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عنوان ژورنال:
  • BMJ case reports

دوره 2016  شماره 

صفحات  -

تاریخ انتشار 2016