Self-Assessment Questions Unusual Findings in a Patient Taking Warfarin
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Postgrad Med J 1999;75:299–312 © The Fellowship of Postgraduate Medicine, 1999 Self-assessment questions Postgrad Med J: first published as 10.1136/pgmj.75.883.299 on 1 May 1999. Downloaded from Unusual findings in a patient taking warfarin R J Morgan, J B Bristol A 60-year-old man was admitted with a 48-hour history of left-sided abdominal pain. He was receiving anticoagulation therapy with warfarin for a prosthetic aortic valve. His INR on admis- sion was 4.1. Initial full blood count, urine microscopy and plain abdominal radiographs were normal. He underwent an abdominal computed tomography (CT) scan (figure 1). Within 24 hours the patient developed ecchymoses in the peri-umbilical region, both flanks, and down the left lower limb from the thigh to the lateral aspect of the foot (figure 2). Figure 1 Abdominal CT scan http://pmj.bmj.com/ on September 29, 2021 by guest. Protected copyright. Department of Surgery, Cheltenham General Hospital, Sandford Road, Cheltenham GL53 7AN, UK R J Morgan Figure 2 Cutaneous haemorrhagic discoloration of J B Bristol (A) the peri-umbilical region, and (B) the flank and lower limb, involving the foot Correspondence to Mr RJ Morgan, Specialist Registrar, Department of General Surgery, Level 7, Derriford Hospital, Questions Plymouth PL6 8DH, Devon, UK 1 What is the abnormality (arrowed) shown on the abdominal CT scan (figure 1)? Accepted 9 October 1998 2 Who first described these appearances? 300 Self-assessment questions Answers of splenic rupture.4 Retroperitoneal hae- Postgrad Med J: first published as 10.1136/pgmj.75.883.299 on 1 May 1999. Downloaded from matoma is an unusual cause of cutaneous QUESTION 1 haemorrhagic discolouration. Spontaneous The CT scan shows a left-sided retroperitoneal retroperitoneal haematoma has been described haematoma. in anticoagulated patients,5 although it is a rare occurrence when the INR is within the QUESTION 2 therapeutic range. Discolouration of the foot Cullen’s sign1 was originally described as peri- caused by retroperitoneal haematoma (or any umbilical ecchymoses in ruptured extra- other form of intra-abdominal haemorrhage) uterine pregnancy, but has come to be consid- has not been previously reported. ered a sign of acute haemorrhagic pancreatitis. Our patient was managed conservatively and Grey-Turner described haemorrhagic discol- re-established on warfarin at a lower dose. He ouration of the flanks in acute pancreatitis2 and was discharged home after 7 days with an INR Fox described discolouration of the thigh due of 2.8. to extraperitoneal haemorrhage.3 Final diagnosis Discussion Retroperitoneal haematoma. These appearances can be caused by a number of other conditions besides acute pancreatitis; Keywords: retroperitoneal haematoma; Cullen’s sign; for example, Cullen’s sign can occur as a result warfarin 1 Cullen TS. A new sign in ruptured extrauterine pregnancy. 5 Abad-Santos F, Carcas AJ, Capitan CF, Frias J. Retroperito- Am J Obstet Gynecol 1918;78:457–60. neal haematoma in a patient treated with acenocoumarol, 2 Grey-Turner G. Local discoloration of the abdominal wall phenytoin and paroxetine. Clin Lab Haematol 1995;17:195– as a sign of acute pancreatitis. Br J Surg 1919;7:394–5. 7. 3 Fox JA. A diagnostic sign of extraperitoneal haemorrhage. Br J Surg 1966;53:193–5. 4 Chung MA, Oung C, Szilagyi A. Cullen’s sign: it doesn’t always mean hemorrhagic pancreatitis. Am J Gastroenterol 1992;87:1026–8. http://pmj.bmj.com/ on September 29, 2021 by guest. Protected copyright. Self-assessment questions 301 Postgrad Med J: first published as 10.1136/pgmj.75.883.299 on 1 May 1999. Downloaded from New weakness in a critically ill patient John J Craig, Meenakshi Mirakhur, Bharat B Sawhney, Victor H Patterson A 24-year-old woman was admitted to her local hospital with an infective exacerbation of asthma. Apart from asthma, which had resulted in several previous uncomplicated admissions to hospital, she was otherwise well. She had no history of any neuromuscular problems and neurological examination on admission was unremarkable. She was treated with intravenous hydrocortisone (200 mg 6 hourly), aminophylline and augmentin and nebulized salbutamol and ipratropium bromide, but became increasingly wheezy and distressed and required mechanical ventilation. Arterial blood gas analysis on 60% oxygen prior to ventilation revealed the pH to be 7.09, and the partial pressures of O2 and CO2 to be 19 and 10.5 kPa, respectively. Other investigations were unremarkable, apart from a peripheral leucocytosis of 14 × 109/l. In the intensive care unit, mus- cle relaxation was achieved with intravenous suxamethonium, atracurium and a continuous infu- sion of vecuronium, and sedation with intravenous midazolam, propofol and alfentanil. Initial treatments were continued, but the dose of hydrocortisone was increased to 200 mg every 2 hours and intravenous cefotaxime and metronidazole were introduced. On day 3 the patient was transferred to the regional intensive care unit because of deteriorat- ing renal function. This resolved spontaneously without the need for dialysis, the maximum serum urea and creatinine levels being 24 mmol/l and 137 µmol/l, respectively. On one occasion when renal function was recovering serum potassium was 2.4 mmol/l; all other electrolytes including serum phosphate, calcium and magnesium were unremarkable. On day 11 airway obstruction was not evident on examination. On day 12 muscle relaxants, which had been administered from admission to the intensive care unit, and sedation were stopped. Mechanical ventilation was required for a further 8 days, however, because of severe generalised weakness. Examination on day 14 revealed the patient to be alert and obeying com- mands. A partial left sixth nerve palsy, mild facial weakness and flaccid tone in the limbs were noted. Power in the limbs was graded as a flicker of movement proximally and grade 2–3 distally. All deep tendon reflexes were absent. Sensory examination was normal. The patient was Department of Neurology, Ward 21, transferred to the neurology department on day 22 being able to maintain adequate ventilation Royal Victoria although she was still profoundly weak. Hospital, Belfast, http://pmj.bmj.com/ BT12 6BA, N Ireland Questions J J Craig M Mirakhur 1 What are the most probable causes of this patient’s new weakness resulting in diYculty weaning B B Sawhney V H Patterson from the ventilator? 2 What investigations should be performed to confirm the diagnosis? Accepted 2 November 1998 3 What is the prognosis for recovery? on September 29, 2021 by guest. Protected copyright. 302 Self-assessment questions Answers Although myasthenia gravis often presents Postgrad Med J: first published as 10.1136/pgmj.75.883.299 on 1 May 1999. Downloaded from with weakness, the extreme nature of the weak- QUESTION 1 ness in our patient was not typical of this con- The decreased tone, areflexia and preserved dition. In addition, the minimal involvement of mental state in this patient with severe the extra-ocular muscles and absent reflexes weakness suggest a neuromuscular disorder. A (which are typically normal in myasthenia central disorder, of either the brain or spinal gravis) made this diagnosis unlikely. cord, causing acute severe weakness can be dif- Prolonged blockade at the neuromuscular ficult to exclude in patients in the intensive care junction from the long-term administration of setting because of diYculties with communica- muscle relaxants, typically results in flaccid tion. A central disorder was felt to be unlikely paralysis, which may be very severe, and in our patient, however, as upper motor neuron areflexia.2 It usually occurs in the context of signs were never detected at any stage. Likewise impaired hepatic or renal function and has a spinal cord lesion as the sole cause of the mostly been described in cases where vecuro- patient’s weakness was excluded because she nium has been administered; two of these pre- had cranial nerve signs. Where the possibility of cipitants were present in our case. No choliner- a spinal lesion exists, however, the spinal cord gic features (miosis, sweating, bradycardia) should be imaged by magnetic resonance scan- were present, making inadvertent organophos- ning. The principal neuromuscular diseases phate exposure unlikely. causing new generalised weakness in critically Clinically, it is impossible to exclude either ill patients are shown in box 1. acute necrotizing myopathy or critical illness Of the neuropathies, critical illness polyneu- myopathy as the cause of this patient’s ropathy may be the most common cause of weakness. Both may result in flaccid weakness weakness in critically ill patients. This condi- with areflexia and little or no sensory distur- tion is thought to result from inadequate bance in critically ill patients exposed to perfusion of the peripheral nerves.1 It is usually neuromuscular blocking agents or high-dose associated with encephalopathy and multi- corticosteroids. organ failure and often results in more severe 1 distal than proximal weakness, all of which QUESTION 2 were in contrast to the findings in our patient. The minimum investigations necessary to Guillain-Barre syndrome (of which acute diVerentiate between the various causes of inflammatory demyelinating polyradiculoneu- weakness in the critically ill patient, once ropathy and acute motor axonal neuropathy are simple biochemical abnormalities have been two variants) results in flaccid weakness with or excluded, are shown in box 2. without prominent sensory symptoms and typi- The creatinine kinase