ABSTRACT
Rhabdomyolysis is caused by the breakdown and necrosis of muscle tissue and the release of intracellular content into the blood stream. There are multiple and diverse causes of rhabdomyolysis but central to the pathophysiology is the destruction of the sarcolemmal membrane and release of intracellular components into the systemic circulation. The clinical presentation may vary, ranging from an asymptomatic increase in serum levels of enzymes released from damaged muscles to worrisome conditions such as volume depletion, metabolic and electrolyte abnormalities, and acute kidney injury (AKI). The diagnosis is confirmed when the serum creatine kinase (CK) level is > 1000 U/L or at least 5x the upper limit of normal. Other important tests to request include serum myoglobin, urinalysis (to check for myoglobinuria), and a full metabolic panel including serum creatinine and electrolytes. Prompt recognition of rhabdomyolysis is important in order to allow for timely and appropriate treatment. A McMahon score, calculated on admission, of 6 or greater is predictive of AKI requiring renal replacement therapy. Treatment of the underlying cause of the muscle insult is the first component of rhabdomyolysis management. Early and aggressive fluid replacement using crystalloid solution is the cornerstone for preventing and treating AKI due to rhabdomyolysis. Electrolyte imbalances must be treated with standard medical management. There is, however, no established benefit of using mannitol or giving bicarbonate infusion. In general, the prognosis of rhabdomyolysis is excellent when treated early and aggressively.
Subject(s)
Rhabdomyolysis , Combined Modality Therapy , Diagnosis, Differential , Humans , Prognosis , Rhabdomyolysis/diagnosis , Rhabdomyolysis/epidemiology , Rhabdomyolysis/etiology , Rhabdomyolysis/therapy , United States/epidemiologyABSTRACT
Among the serious complications associated with radioiodine therapy (RAI) for thyroid cancer, cerebral edema is uncommon and has been reported previously in cases of swelling of brain metastases. This case is of a patient with papillary thyroid carcinoma who complained of nausea and vomiting after RAI and was then found unconscious the next day. Laboratory results showed electrolyte imbalances including hyponatremia and cranial imaging only revealed cerebral edema, and she regained consciousness after sodium correction. The etiology of the cerebral edema here is likely multifactorial - due to hyponatremia from hypothyroidism, aggravated by vomiting, copious water intake and a low sodium diet.
