HYPOKALEMIA INDUCED RHABDOMYOLYSIS IN THE SETTING OF SPASTICITY: A CASE REPORT.

Case Diagnosis: Hypokalemia induced rhabdomyolysis. Case Description: A 56-year-old male with history significant for transverse myelitis resulting in spastic paraplegia of the lower extremities, and managed with a baclofen pump, presented to the emergency department with a four day history of progressive quadriparesis. Prior level of function included a four-wheeled walker for home mobility and independence of all activities of daily living. Intravenous corticosteroids were initiated due to concern for recurrence of transverse myelitis. Magnetic resonance imaging (MRI), lumbar puncture, and imaging of the baclofen pump were all normal. Laboratory analysis revealed creatine phosphokinase (CPK) was 13821 and serum potassium equal to 1.8. Clinical presentation was consistent with hypokalemia-induced rhabdomyolysis and nephrology consulted. Hypokalemia was multifactorial (laxative use, relative fasting, and vomiting prior to symptom onset) and concurrent spasticity a likely contributor. Potassium was repleted intravenously and stabilized at 3.6. At discharge the patient required moderate to maximum assistance with transfers and toileting and was a candidate for acute inpatient rehabilitation, but elected to discharge with home health. Discussions: Rhabdomyolysis is a pathologic condition of skeletal muscle in which toxic intracellular components are released into the blood stream. These include CPK, alanine aminotransferase, aspartate aminotransferase, myoglobin, and potassium. Local potassium levels impact capillary vascular tension. Low levels of serum potassium lead to capillary vasoconstriction, reduced blood flow to skeletal muscle, relative ischemia, eventual cell death, and lysis. To our knowledge, there have been no reports that address the role of spasticity in development of rhabdomyolysis. By definition, spasticity is velocity-dependent increase in stretch reflexes (muscle tone). It is possible that sustained muscle tone due to spasticity and resulting metabolic demand increases the risk of rhabdomyolysis in the setting of an already ischemic environment resulting from severe hypokalemia. Conclusions: Hypokalemia-induced rhabdomyolysis should be considered as a potential cause of acute weakness in patients with spasticity. [ABSTRACT FROM AUTHOR]