Short bowel syndrome

Rhabdomyolysis caused by the metabolic disturbances seen in chronic short bowel syndrome has not been reported in the English literature to our knowledge. Presented is a case of hypokalemic-induced rhabdomyolysis associated with short bowel syndrome.

A 48-year-old man was presented to the emergency department with complaints of severe generalized weakness and pain. He had a history of acute aortic dissection with resultant ischemic bowel, necessitating partial resection of the small bowel, ileostomy, and colostomy. He developed chronic diarrhea because of the short bowel syndrome and required parenteral nutrition. This was complicated by multiple episodes of central venous catheter bloodstream infections. For 2 years he demonstrated poor tolerance of oral nutrition; 7 weeks before presentation, he underwent surgical ileocolic anastomosis, with discontinuation of parenteral nutrition. Subsequently, he reported pain and weakness of the extremities, poor appetite, and a weight loss of 14 kg. He denied any fevers, chills, seizures, trauma, vomiting, nausea, contacts with ill individuals, and recent travel, and also denied abuse of diuretics, laxatives, alcohol, or illicit drugs. His medications included metoprolol and codeine, with no recent change in his doses.

Physical examination was remarkable for temperature 35.8, pulse 111, respiration 22, and blood pressure 159/86; the patient was a cachectic appearing male. Mucosal membranes were dry, and there was no jugular venous distention. Neuromuscular examination revealed tenderness to palpation at the proximal muscle groups of upper and lower extremities. There was demonstrable weakness of the same muscle groups. Sensation, reflex, and cranial nerve test results were normal.

Laboratory data are summarized in Table I.

An electrocardiogram (EKG) revealed sinus rhythm and left ventricular hypertrophy with new ST segment changes and U waves.

The patient was diagnosed with rhabdomyolysis secondary to hypokalemia. He received IV hydration and potassium replacement totaling 710 mmol. The patient did well and on the day of discharge reported resolution of his symptoms. Follow-up laboratory results are shown in Table I. A repeated EKG result was normal.

Nontraumatic rhabdomyolysis associated with hypokalemia may be a relatively common occurrence1 and has been documented in several settings.2-4 The mechanism of hypokalemic-induced rhabdomyolysis may relate to the impairment of the physiologic vasodilatory effects mediated by the local release of potassium by skeletal muscle cells.5

No other obvious cause for rhabdomyolysis in this patient was identified. The presence of short bowel syndrome in this case was a predisposing factor to the development of severe hypokalemia and subsequent rhabdomyolysis.

REFERENCES

1. Singhal PC, Abramovici M, Venkatesan J, et al: Hypokalemia and rhabdomyolysis. Mineral Electrolyte Metab 17:335-339, 1991

2. Lucatello A, Sturani A, Di Nardo A, et al: Acute renal failure in rhabdomyolysis associated with hypokalemia. Nephron 67:115-116, 1994

3. Prat G, Petrognani R, Diatta B, et al: Hypokalemia causing rhabdomyolysis and precordialgia. Intensive Care Med 27:1096, 2001

4. Cervello A, Alfaro A, Chumillas MJ: Hypokalemic myopathy induced by Giardia lamblia. N Engl J Med 329:210-211, 1993

5. Rose, BD, ed. Hypokalemia. IN Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed. McGraw-Hill, New York, NY, 2001, pp 859-860

Jason M. Guardino, DO, MS; John K. Hix, MD; and Douglas Seidner, MD

From the Cleveland Clinic Foundation, Cleveland, Ohio

Received for publication, February 28, 2003.

Accepted for publication, March 26, 2003.

Correspondence: Dr. Jason M. Guardino, Desk E13, Internal Medicine, 9500 Euclid Avenue, Cleveland, OH 44195. Electronic mail may be sent to guardij@ccf.org.

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