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A 41-year-old woman came to the Emergency Department in January, 1998. She had awoken that morning in severe pain and had taken ibuprofen without improvement. The previous day, she had walked 4 miles. Examination showed a temperature of 36·9°C, pulse 86 beats per min, and blood pressure 118/56 mm Hg. She weighed 72 kg and her height was 158 cm. She had diffuse muscle tenderness in her thighs and biceps. No neurological deficits were noted. She was diagnosed as having musculoskeletal pain and given a prescription for paracetamol with codeine. 2 days later, she returned to the Emergency Department complaining of continued muscle pain, now accompanied by symmetrical muscle weakness. Examination again showed diffuse muscle tenderness in her arms and legs, with normal muscle tone and symmetrical, proximal, and distal muscle weakness (power 4/5). Laboratory investigations showed a sodium of 141 mmol/L, potassium of 1·1 mmol/L, chloride of 98 mmol/L, bicarbonate of 33 mmol/L, blood urea nitrogen of 3·9 mmol/L, creatinine of 106 �mol/L, and a glucose of 5·8 mmol/L. Her haemoglobin was 11·9 g/dL (mean corpuscular volume 77·0 fL), albumin 3·5 g/dL, calcium 1·9 mmol/L, magnesium 0·57 mmol/L, and phosphate 0·94 mmol/L. She had high concentrations of lactate dehydrogenase (748 U/L), aspartate aminotransferase (244 U/L), and creatine kinase (CK; 13 182 U/L). Her urine was positive for myoglobin. She was admitted to hospital with a diagnosis of rhabdomyolysis and hypokalaemia. She was treated with intravenous hydration and electrolyte replacement. Her CK peaked at 21 072 U/L. Her creatinine remained normal. Further investigation of her hypokalaemia included urine chemistry (random urine potassium 3·8 m m o l / L ; normal 10–160 mmol/L), a negative screen for diuretics, and normal corticotropin and renin concentrations.

We discovered from the patient’s husband that her diet consisted mostly of cheese sandwiches. She did not eat any fruits, vegetables, or meat products. No history of purging was discovered. A psychiatric consultation was arranged, but no definitive evidence for a primary eating disorder (anorexia or bulimia nervosa) was found. She received nutritional advice and was discharged. She came back to the Emergency Depratment in August, 1998, with a 1-day history of weakness. Her potassium was 1·1 mmol/L with a normal CK. An electrocardiogram showed first-degree atrioventricular block and probable TU wave fusion (figure). A h i s t o r y

of purging and laxative abuse was obtained. After medical treatment she was transferred to the psychiatric service for management of her bulimia nervosa. She was last seen in January, 1999. She had maintained more normal eating pattterns and a normal serum potassium, but had not attended for psychiatric follow-up.

Rhabdomyolysis is associated with both traumatic, (crush syndrome)1 and non-traumatic causes. Rhabdomyolisis secondary to hypokalaemia is a well- described non-traumatic cause2 and has been associated with several medical conditions including use of diuretics, eating liquorice, coeliac disease, infectious diarrhoea, anorexia nervosa/bulimia, and abuse of laxatives. Rhabdomyolysis can be a life-threatening disorder, with acute renal failure being one of the most serious complications.3 Although this patient did not develop renal failure, that consequence has been associated with rhabdomyolysis secondary to laxative abuse and induced hypokalaemia.4 The primary mechanism of rhabdomyolysis secondary to hypokalaemia appears to be that potassium is released from normal contracting muscle cells resulting in a vasodilatory response of the surrounding arterioles.5

Failure of this potassium-mediated arteriolar dilation may lead to muscle ischaemia. This case demonstrates the need to include hypokalaemia in a differential diagnosis of rhabdomyolysis, and the importance of screening for eating disorders in patients with hypokalaemia associated with a low urinary potassium. Other clues in the initial presentation suggesting an underlying eating disorder include the hint of excessive exercise, her very restricted eating patterns, and the laboratory abnormalities that point to malnutrition (eg, microcytic anaemia and low calcium, magnesium, potassium, and phosphate concentrations).

R e f e r e n c e s 1 Bywater EGL, Beall D. Crush injuries with impairment of renal

function. BMJ 1941; i: 4 2 7 – 3 2 . 2 Singhal PC, Abramovici M, Venkatesan J, Mattana J. Hypokalemia

and rhabdomyolysis. Miner Electrolyte Metab 1991; 17: 3 3 5 – 3 9 . 3 Zager RA. Rhabdomyolysis and myohemoglobinuric acute renal

failure. Kidney Int 1996; 49: 3 1 4 – 2 6 . 4 Copeland PM. Renal failure associated with laxative abuse.

Psychother Psychosom 1994; 62: 2 0 0 – 0 2 . 5 Knochel PL, Schlein EM. On the mechanism of rhabdomyolysis in

potassium depletion. J Clin Invest 1972; 51: 1 7 5 0 – 5 8 .

Muscle pain after exerc i s e

Craig Nielsen, Peter Mazzone

1062 THE LANCET • Vol 353 • March 27, 1999

Case report

Lancet 1999; 353: 1062 Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA (C Nielsen MD, P Mazzone MD)

Correspondence to: Dr Craig Nielsen

Patient’s electrocardiogram