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From Mechanical to Chemical: A Case of Diabetes Insipidus Induced by Concussive Brain Injury

young female doctor examines x-ray

Diabetes insipidus is a rare disorder of water-electrolyte balance characterized by either absolute (central) or functional (nephrogenic) deficiency of vasopressin or antidiuretic hormone.1 Central diabetes insipidus is a recognized complication of traumatic brain injury; however, those patients are much sicker and have other symptoms from the trauma as well.2 We present a case of complete central diabetes insipidus induced by a minor concussion where headache and polyuria were the only presenting complaints.

Case Report

A 34-year-old previously healthy man presented with a headache and generalized weakness 12 hours after sustaining a concussion to his head in an amateur boxing game. He reported transient unconsciousness after the clout but returned to his normal state without any residual deficits. He was evaluated at an outside hospital shortly after the injury and was discharged after normal work-up including computed tomography of the brain without contrast. The patient’s headache, however, got worse with time and he returned to the hospital. Physical examination showed moderate distress but no objective abnormality. The patient continued to have frontal headaches and myalgias and was admitted for observation. Soon he was found to have polyuria, with urine output of 850 mL/h. Lab work-up showed a serum osmolality of 288 mOsm/kg and urine osmolality of 160 mOsm/kg, with the urine-specific gravity of 1.002. Diabetes insipidus was suspected and water deprivation test was performed. The patient’s body weight, serum, and urine osmolality and urine output were measured periodically. His serum osmolality and sodium increased to 291 mOsm/kg and 141 mmol/L, respectively, while he maintained a urine output of 800 mL/h (10 L in 12 hours), with an average urine osmolality of 165 mOsm/Kg despite free water restriction. At that point, deamino-8-D-arginine vasopressin (a synthetic analogue of antidiuretic hormone) was administered. Following that, his urine osmolality increased to 630 mOsm/Kg and the serum osmolality decreased to 289 mOsm/Kg. The urine output normalized (Table). He was diagnosed with complete central diabetes insipidus (given >50% increase in urine osmolality following desmopressin) and was discharged home the next day on deamino-8-D-arginine vasopressin.

Discussion

Diabetes insipidus is an uncommon complication of a minor concussive brain injury. There are several reported cases of central diabetes insipidus following traumatic brain injury, but, in those patients, the extent of the head injury was more severe and resulted in other neurological deficits. A young population, especially those participating in contact sports, can develop this complication from a concussion. Early identification and intervention can prevent life-threatening complications. Given the paucity of this condition, it can be missed easily by the clinicians. In this case, for example, the patient was initially discharged home after an unremarkable neurological examination and normal computed tomography scan of the head. A high level of clinical suspicion, therefore, is required to recognize this complication. All patients with a concussion should be carefully monitored, even if the initial work-up is normal.3 In the majority of cases, the condition is transient and the patients recover completely within 6 months.2

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-Muhammad Hassaan Shahid, MBBS, Ashish Verma, MBBS, Laura Youngblood, MD

This article originally appeared in the July issue  of The American Journal of Medicine.

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