Case reports
© The Intensive Care Society 2012
Gout presenting as severe sepsis and septic shock M Cheung, JF Bion, R Kerry
This is a case of a 49-year-old patient presenting with signs consistent with sepsis, which proved to be secondary to acute gout. Keywords: sepsis; gout; surviving sepsis campaign; systemic inflammatory response syndrome; hyperuricaemia
49-year-old male presented to the medical admissions unit with a three-week history of general malaise, dizziness and malaena. His background history consisted of morbid obesity, type 2 diabetes treated with insulin, chronic renal impairment, dilated cardiomyopathy for which he was taking warfarin, and gout. On examination, he was morbidly obese with a BMI of 40.1, drowsy (GCS 8/15), pyrexial (38°C), tachycardic (140 bpm) and hypotensive (BP 80/63 mm Hg). His chest was clear and heart sounds normal, abdomen non-tender with bowel sounds present, and there was no evidence of a skin rash. Oxygen saturation was 94% on air. The ECG showed sinus tachycardia with left ventricular strain. The chest X-ray was normal. Initial management included fluid resuscitation, blood cultures and antimicrobials (intravenous tazocin and metronidazole). Abnormal laboratory tests included the following: Hb 4.5 g/dL, INR 1.6, WCC 10.2 × 109/L, CRP 30 mg/L, urea 7.8 mmol/L, Cr 23,072 µmol/L. The initial differential diagnosis was acute upper gastrointenstinal (GI) bleed complicating warfarin therapy, intraabdominal sepsis, and acute-on-chronic renal injury. Abdominal radiograph revealed dilated bowel loops. A CT of the abdomen and pelvis excluded mechanical obstruction either of bowel or urinary tract. A CT of the head excluded gross intracranial pathology as the cause of the reduced GCS. Upper gastro-intestinal endoscopy was deferred because the patient was considered too unstable. Sigmoidoscopy was normal. Transthoracic echocardiography demonstrated normal left ventricular contractility and chamber dimensions, and no vegetations could be identified. Refractory hypotension was therefore attributed to sepsis rather than cardiogenic shock. Over the next hours, the patient’s oxygen saturation dropped to 75% while on 60% oxygen via a facemask. He was hypoxaemic with a PaO2 of 7.3 kPa, increasingly pyrexial (40°C) and remained confused and hypotensive. That evening he was referred to intensive care for respiratory and cardiovascular support. Non-invasive ventilation was ineffective. He became anuric. He was intubated and mechanically ventilated. Vasopressors and continuous veno-
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venous haemofiltration (CVVH) were started, together with nasogastric feeding and a proton pump inhibitor. On detailed review, it was noted that his left first and second metocarpal-phalangeal (MCP) joints were swollen and inflamed. Septic arthritis was considered. Antimicrobial treatment was broadened and a joint aspiration performed. Pus cells but no organisms were identified on microscopy. The joint was then surgically opened, and caseous material washed out. Over the next few days, he remained intermittently pyrexial. Serial blood cultures were negative. On day five a tracheostomy was performed to facilitate weaning from mechanical ventilation, and hydrocortisone 50mg qds prescribed because of continued vasopressor dependence. On review the following day, he complained of pain in all joints. On clinical examination it was noted that caseous material was still being extruded from the first MCP joint, and that he had an ulcerated lesion discharging the same material over the right elbow (Figure 1). Uric acid crystals were reported in the original joint fluid. Serum uric acid levels were 32,119 µmol/L (normal values 175-415 µmol/L). After rheumatology review, colchicine 500 mg BD was prescribed via the nasogastric feeding tube. Over the next two days, he made an excellent recovery. C-reactive protein levels fell to 9.3 mg/L from 30 mg/L, he weaned rapidly from ventilatory support, and his pain was better controlled. The pyrexia settled and antibiotics were stopped. CVVH was discontinued. Hydrocortisone was converted to a reducing oral prednisolone regimen. On ICU day 10, the tracheostomy was removed and allopurinol started. Renal function continued to improve. He was discharged to the ward on ICU day 10. Warfarin was restarted uneventfully. Post-discharge he mobilised successfully, becoming independent of assistance by hospital day 15. He was discharged home on day 17.
Discussion Severe sepsis is a systemic inflammatory response attributable to infection and accompanied by organ failures, resulting in high mortality. The initial response to the systemic inflammatory response syndrome (SIRS) is therefore 57
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Case reports
Figure 1a Right elbow of patient.
Figure 1b Right elbow of patient.
appropriately focused on early identification, treatment and source control. Non-infective causes of SIRS are diverse, and the diseases that present in this way often cross specialist boundaries. Infective and non-infective causes of SIRS may co-exist, for example pancreatic necrosis precipitating abscess formation, or treated pneumonia becoming persistent acute lung injury. Co-existing non-microbial causes of SIRS need to be considered in any patient with persisting inflammation without a clear cause, as exemplified by this patient whose condition improved rapidly once we started treatment for acute gout. We were unable to identify a specific source of infection either as a precipitant or as a cause for persisting SIRS in our patient, and while concurrent infection remains a possibility, severe acute gout was the main cause for this presentation of severe inflammation accompanied by organ failures. We base this on the clinical history, the severe inflammatory polyarthritis with synovial fluid crystal formation, severe hyperuricaemia, gouty tophi, and the response to steroids and colchicine. Impaired renal function contributed to impaired urate clearance; there was no evidence of urinary tract obstruction, and renal function improved in conjunction with treatment of gout. The profound anaemia was caused by the upper GI bleed complicated by warfarin therapy. There is one other case report of acute gout presenting as sepsis when a 65-year-old man presented with culture-negative sepsis/SIRS. By using ACTH the authors were able to control the inflammatory cascade caused by the polyarticular inflammatory disorder.2
Learning points With all acutely ill patients it is important to re-visit the current and previous clinical history, and to repeat a thorough physical examination in order to identify concurrent chronic disease and optimise acute and long-term treatment. Failure to respond to treatment should stimulate reconsideration of the diagnosis and further investigations for alternative causes of sepsis, including non-microbial causes of SIRS. Gout should be considered part of the differential diagnosis in patients presenting with severe sepsis and joint inflammation.
References 1. Dellinger RP, Levy MM, Carlet JM et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008;36:296-327. 2. Nicholls DW, Rajapakse CN. Systemic inflammatory response syndrome (SIRS) from acute polyarticular gout. N Z Med J 1999;112:434-45.
Mary Cheung Core Trainee year 1, Anaesthetics
[email protected] Julian Bion Professor of Intensive Care Medicine
[email protected] Robbie Kerry Specialist Registrar, Anaesthetics and Intensive Care Medicine
[email protected] Queen Elizabeth Hospital, Birmingham
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