Transient central diabetes insipidus following ischemic stroke
A 35 years old male, presented with sudden onset left hemiparesis. Over the next 24 h, he developed generalized tonic-clonic seizure and progressive obtundation of sensorium. There was no history of preceding transient ischemic attack, headache, fever, trauma, hypertension or diabetes mellitus. On examination, he was normotensive, stuporous and pupils were equal in size and reaction. He had left sided hemiparesis and extensor plantar reflex bilaterally. Computerised tomography (CT) scan of the brain revealed bilateral frontal, temporopareital and occipital ischemic infarcts with hemorrhagic transformation. Magnetic resonance imaging (MRI) of brain confirmed these findings. [] MR Arteriography (MRA) and venography (MRV) did not show any evidence of vascular thrombosis.\nHe was managed with anti-cerebral edema measures (Mannitol), statins, antiplatelets and supportive care. Over the next two days, he developed worsening level of consciousness due to increasing mass effect. As a life saving measure, decompressive craniectomy with expansile duroplasty was done. Subsequently, he developed increasing urine output (volume 6900 ml, 5525 ml, 5500 ml in 24 h) with corresponding fluid intake of 3000-4000 ml over the next three days and serum sodium levels increased from 136 mMol/l to 145 mMol/l (N 135-144 mMol/l). Urinary spot sodium was 243 mMol/l. Plasma osmolality (calculated) was 294 mOsm/kg (285-295 mOsm/Kg).\nIn view of his neurological status, he was subjected to a limited water deprivation test. Over three hours of absolute water deprivation, all IV and oral fluids were withheld with a close watch over his BP and Urine output. During the test, he passed 775 ml of urine and developed hypotension (BP 90/60 mmHg), due to which the test was aborted and serum and urine samples were taken for osmolality. At the termination of test, he had serum sodium 145 mMol/l, calculated plasma osmolality of 305 mOsm/kg with corresponding Urine osmolality of 357 mOsm/kg (expected >600 mOsm/kg) which confirmed DI. He was started on Desmopressin nasal spray at a dose of 10mcg twice a day. Over the next two days, his daily urine output had reduced to 2 to 3 litres, commensurate with fluid intake. Urine osmolality increased to 685 mOsm/kg with normalization of sodium levels and plasma osmolality. After 5 days of starting Desmopressin, his urine output decreased to 1050 ml and serum sodium levels decreased to 131 mMol/l, when dose of desmopressin was reduced to 10 mcg once a day and subsequently withdrawn in view of persistent hyponatremia. Following withdrawal of desmopressin, he continued to have normal urine output and serum sodium levels. Urine osmolality was 762 mOsm/kg. He regained full consciousness, but had persistent aphasia, facial paresis and bilateral limb weakness (L > R) with bilateral extensor plantars. Other hormone evaluation including thyroid, cortisol, gonadotropins and testosterone were normal. MRI brain did not show any pituitary haemorrhage or necrosis. Posterior pituitary hyperintense (bright spot) was normally seen [].