Protracted hypocalcemia following post-thyroidectomy lumbar rhabdomyolysis secondary to evolving hypoparathyroidism

Rhabdomyolysis is characterized by skeletal muscle breakdown. It is a potential cause of serious electrolyte and metabolic disturbances, acute kidney insufficiency, and death. Recently, rhabdomyolysis has been increasingly recognized following certain surgical procedures. We discuss the case of a morbidly obese 51-year-old woman who developed postoperative rhabdomyolysis of the lumbar muscles following a prolonged thyroidectomy for a large goiter. We discuss how her morbid obesity, the supine surgical position, the duration of surgery (including prolonged exposure to anesthetic agents), and postoperative immobility contributed to the development of rhabdomyolysis. Immediately after surgery, the patient developed hypocalcemia, which was likely due to rhabdomyolysis since her serum parathyroid hormone level was normal. Later, however, persistent hypocalcemia despite resolution of the rhabdomyolysis raised a suspicion of iatrogenic hypoparathyroidism, which was confirmed by a suppressed parathyroid hormone level several days after surgery. In post-thyroidectomy patients with risk factors for rhabdomyolysis, maintaining a high degree of clinical suspicion and measuring serum creatine kinase and parathyroid hormone levels can allow for an accurate interpretation of hypocalcemia.