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Diabetes Insipidus Case Study

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Summary: Adrian Headley, a 23-year-old male, is transferred to UCLA’s Intensive Care Unit after a motor vehicle accident; x-rays revealed both femoral and basilar fractures, and the patient is experiencing severe thirst coupled with an increased urinary output of 7-9 liters per day.

Question: What is the pathophysiology of neurogenic and nephrogenic diabetes insipidus?


Diabetes Insipidus (DI) occurs due to a deficiency in the production, or recognition of arginine vasopressin (AVP). Often times, it is characterized by a large output of dilute urine (polyuria) and extreme thirst (polydipsia), and can occur acutely as a result of head trauma, or chronically due to hereditary causes.1,2 Additionally, it can be further classified
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In patients with neurogenic DI, damaged osmoreceptors cannot facilitate dehydration-induced AVP release, but preserve the ability to trigger extreme thirst. The lack of AVP secretion by the pituitary can result in decreased water reabsorption, and increased excretion of dilute urine. Additionally, a basilar skull fracture is a risk factor for post-traumatic hypopituitarism and could be the reason for Mr. Headley’s acute onset of diabetes …show more content…
In Mr. Headley’s case, the desmopressin led to an increase in urine osmolality from 105mOsm/Kg (end of dehydration test value) to 625 mOsm/Kg. According to Camelia G. Garofeanu et. al, an increase in urine osmolality of greater than 150mOsm/Kg suggests that Mr. Headley’s symptoms are likely due to central diabetes insipidus.4 This is because desmopressin is a synthetic analog to vasopressin, and can thus act on receptors present in the distal tubule. An increase in urine osmolality means the polyuria is more likely due to decreased AVP production, rather than receptor insensitivity. Perhaps, Mr. Headley’s basilar fracture diminished the osmoreceptor’s functionality, thus leading to a decrease in the production of AVP, and subsequently, polyuria.1,5 Additionally, desmopressin may be helpful in the treatment of Mr. Headley’s neurogenic diabetes

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