Endocrine Abstracts

Nontraumatic rhabdomyolysis is mostly caused by drugs, alcohol consumption or compression of muscles. Severe hyperosmolarity rarely can cause rhabdomyolysis. Our case has santral diabetes insipidus that has admitted with the clinical picture of rhabdomyolysis.

Case: Twenty-six-years old male has admitted to our clinic with the complaint of weakness, nausea, vomitting, polydipsia, polyuria, difficulty in walking and tendency to sleep. Neurologic examination was normal. In laboratory glucose: 166 mg/dl, Na: 168 mEq/l, Urea: 19 mg/dl, Cr: 1.6 mg/dl, K: 2.8 mEq/l, CK: 2916 IU/l, plasma osmalality 348 mosmol/l, and urine density 1005 were. Serum CK level have increased progressively up to 15 000 IU/l during the follow up. We have thought that rhabdomyolysis might have been due to hyperosmolality caused by high Na and low K levels. We have administered hypotonic fluids and followed the urine output and fluid intake of the patient. His general condition was not well enough to tolerate fluid restriction test and he had severe polyuria that is why we have directly made the desmopressin administration test. Plasma osmolality was 348 mosmol/l before desmopressin administration and it regressed to 330 mosmol/l thereafter. Urine osmolality has increased to 330 mosmol/l from 77 mosmol/l after desmopressin administration. Amount of urine per hour has decreased significantly after desmopressin. Consequently the patient has been diagnosed to have central DI. In pituitary MRI a lesion was detected at the level of hypothalamus in right anterolateral neighborhood of 3rd ventricule and 14×18×11 in size. It was interpreted as low grade glial lesion. Desmopressin was started po 0.1 mg three times daily and clinical picture has improved thereafter. Serum Na, K and CK levels have returned to normal values after the treatment.

Conclusion: Rhabdomyolysis is a rare but very important complication of hyperosmolality due to DI. CK levels should be monitor strictly in hyperosmolar states.