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.
Keywords hypokalemia, paralysis, diabetes insipidus
Case ReportA 30-year-old Hispanic male with a history of pituitary adenoma resection at the age of 13, with subsequent pan-hypopituitarism, epilepsy, and medication noncompliance was admitted with seizures and acute diabetes insipidus (DI). During the hospitalization, he remained seizure free on levetiracetam 1 g q12H and was treated with appropriate antibiotics for a dental abscess. He was initiated on a stress dose steroid taper, restarted on hormone replacement and desmopressin replacement therapy for DI.The patient's initial hospital stay was without complication until hospital day 3 when a dose of desmopressin acetate (DDAVP) was delayed, and he developed acute quadriplegia. Magnetic resonance imaging (MRI) brain and computed tomography (CT) brain did not reveal any acute abnormalities. Routine laboratory studies were notable for acute hypokalemia from 3.8 to 1.6 mEq/dL (Table 1), which he developed over 12 hours. His thyroid studies were suggestive of secondary hypothyroidism with low thyroid-stimulating hormone level, free T3, total T3 level, and normal free T4 level (Table 1).On examination, he was afebrile and in no apparent distress. He was fully oriented with intact cranial nerves. Muscle strength was 0 of 5 in the bilateral upper extremities, 0 of 5 in the proximal lower extremities, and 1 of 5 in the distal lower extremities. Sensory evaluation of la...