Acute hypokalemic
paralysis is characterized by
muscle weakness or
paralysis secondary to low serum
potassium levels.
Neurogenic diabetes insipidus (DI) is a condition where the patient excretes large volume of dilute urine due to low levels of
antidiuretic hormone. Here, we describe a patient with neurogenic DI who developed hypokalemic
paralysis without a prior history of periodic
paralysis. A 30-year-old right-handed Hispanic male was admitted for refractory
seizures and acute DI after developing a dental
abscess. He had a history of
pituitary adenoma resection at the age of 13 with subsequent pan-
hypopituitarism and was noncompliant with hormonal supplementation. On hospital day 3, he developed sudden onset of
quadriplegia with motor strength of 0 of 5 in the upper extremities bilaterally and 1 of 5 in both lower extremities with absent deep tendon reflexes. His routine laboratory studies revealed severe
hypokalemia of 1.6 mEq/dL. Nerve Conduction Study (NCS) revealed absent compound motor action potentials (CMAPs) with normal sensory potentials. Electromyography (EMG) did not reveal any abnormal insertional or spontaneous activity. He regained full strength within 36 hours following aggressive correction of the
hypokalemia. Repeat NCS showed return of CMAPs in all nerves tested and EMG revealed normal motor units and normal recruitment without myotonic discharges. In patients with central DI with
polyuria,
hypokalemia can result in sudden
paralysis. Hypokalemic
paralysis remains an important differential in an acute case of
paralysis and early recognition and appropriate management is key.