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A 66 year old Trinidadian Asian woman was admitted with a two day history of fever, nausea, and vomiting. Type 2 diabetes had been diagnosed 17 years before and she had extensive microvascular and macrovascular complications. Glycaemic control had been consistently poor (HbA1 readings 13–16%), and she had needed insulin treatment over the preceding two years. She was hypertensive and had a typical diabetic dyslipidaemia. She had retinopathy for which she had received bilateral photocoagulation treatment. She had presumed diabetic nephropathy with proteinuria (previously quantified at 3 g/day) and impaired renal function (serum creatinine 140–160 μmol/l). She had a peripheral neuropathy. She had cerebrovascular disease, having previously suffered a transient ischaemic attack, and had been shown to have bilateral carotid stenoses. She had absent foot pulses, so she also had peripheral vascular disease.
On examination she was febrile but had no abdominal signs. Initial chest x ray was normal. White blood cell count was 12.6 × 109/l, alanine transaminase 172 IU/l, bilirubin 38 μmol/l, alkaline phosphatase 257 IU/l, and albumin 29 g/l. Clotting profile and platelet count were normal. Liver imaging showed a solitary lesion (fig 1) from which pus was aspirated, and also gallstones. Aspiration of the hepatic lesion was complicated by haemorrhage, requiring resuscitation and laparotomy to achieve haemostasis. The period of hypotension resulted in acute oliguric renal failure for which the patient required haemodialysis before spontaneous recovery of renal function. Culture of both liver aspirate and blood grew Klebsiella pneumoniae, and intravenous antibiotics were given according to sensitivities.
The patient developed progressive dyspnoea, persistent fever, and bilateral pleural effusions on chest x ray. Computed tomography of the chest showed numerous small areas of consolidation throughout both lung fields (fig 2). Despite continued treatment with appropriate antibiotics, she suffered several respiratory arrests, from which she was successfully resuscitated. Fluid balance was complicated by limited cardiac reserve (demonstrated by echocardiography) as well as by impaired renal function.
With continued antibiotic treatment, she made a slow recovery. Despite clinical improvement, she developed an acute left sided pyramidal weakness. Computed tomography of the brain showed an area of low attenuation in the right parietal region (fig 3). Her neurological signs improved over the ensuing few weeks. Her respiratory function improved, and repeated imaging showed resolution of both hepatic and lung lesions. She subsequently left hospital, fully mobile and independent, and has remained well since discharge.
- How does this woman's diabetes relate to her current infective illness?
- What was the probable source of her Klebsiella pneumoniae septicaemia?
- What was the cause of her left pyramidal deficit?
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