Hypokalemic Periodic Paralysis Developed in a Patient with Neurogenic Diabetes Insipidus

Hypokalemic periodic paralysis one of the channelopathy disorders with low serum potassium level, clinically presenting as acute onset extremity weakness. In most cases, the cause of the hypokalemia is familial, but rarely hypokalemic periodic paralysis occurs secondary to other diseases including endocrinopathies, renal disorders, gastrointestinal loss. We report a patient with no known underlying diseases, who were diagnosed with sporadic hypokalemic periodic paralysis accompanied by neurogenic diabetes insipidus.

Central Diabetes Insipidus in a Preterm Neonate Unresponsive to Intranasal Desmopressin

Central or neurogenic diabetes insipidus (DI) is uncommon in the pediatric age group and rarely occurs in neonates. It should be suspected in any neonate presenting with excessive urine output and hypernatremia that persists despite increased fluid administration. Diabetes insipidus may be secondary to asphyxia, intraventricular hemorrhage, infection, and structural abnormalities or may be idiopathic or genetic. Diagnosis includes a careful history, laboratory testing, and magnetic resonance imaging. Management of neonatal DI involves a careful balance between fluid intake and pharmacologic treatment. In this article we report a case of an extremely low birth weight infant presenting with central DI possibly caused by abnormality of the pituitary gland. Persistent hypernatremia was the initial presentation. Increased fluids were given initially but were only partially helpful. Eventually subcutaneous desmopressin (DDAVP) was required. The infant was unresponsive to intranasal DDAVP and required subcutaneous DDAVP upon discharge.

Central Neurogenic Diabetes Insipidus, Syndrome of Inappropriate Secretion of Antidiuretic Hormone, and Cerebral Salt-Wasting Syndrome in Traumatic Brain Injury

Central neurogenic diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome are secondary events that affect patients with traumatic brain injury. All 3 syndromes affect both sodium and water balance; however, they have differences in pathophysiology, diagnosis, and treatment. Differentiating between hypernatremia (central neurogenic diabetes insipidus) and the 2 hyponatremia syndromes (syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome) is critical for preventing worsening neurological outcomes in patients with head injuries.