CENTRAL DIABETES INSIPIDUS IN THE SETTING OF ANOXIC BRAIN INJURY

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Central diabetes insipidus (CDI) presents with polyuria, increased thirst, hypernatremia, and the inability to concentrate urine due to low antidiuretic hormone (ADH). The most common causes of CDI are craniopharyngioma, Langerhans cell histiocytosis, trauma, sarcoidosis, metastases, and brain malformations. There are many case reports of CDI induced by traumatic brain injury, however few reports of CDI in the setting of anoxic brain injury. CASE PRESENTATION: A 35-year-old female with past medical history of polysubstance abuse and prior cardiac arrest presented after resuscitation from an out of hospital cardiac arrest. The patient was unresponsive for an unknown length of time. She was intubated in the emergency room and given naloxone without response. On exam she had absent brain stem reflexes with Glasgow coma scale of 3 and was hypotensive.Urine drug screen was positive for cannabinoids, cocaine, opiates, and phencyclidine. Bloodwork was significant for WBC 13,100 uL, creatinine 1.8 mg/dl, BUN 12 mg/dl, Glucose 463, sodium 136 mM, bicarbonate 15 mM, and lactate 16.8 mM. COVID-19 antigen and Influenza B were positive. Head CT showed diffuse loss of grey-white mater differentiation and diffuse sulcal effacement, consistent with global anoxia.She received 0.9% NaCl, broad-spectrum antibiotics, oseltamivir, insulin drip, sodium bicarbonate, and norepinephrine. 24 hours after admission, urine output increased from 1.3 to 7.8 liters/day and Serum sodium increased from 144 to 161 mM. She was started on 5% dextrose in water, however sodium continued to rise to 171 mM. Urine output was 290 ml/hour. Urine sodium was 21 mM and urine osmolality was 99 mOsm/kg, which suggests predominantly free water diuresis. The patient was given 2 L of 0.9% NaCl, the rate of D5W was increased, and 1 mcg of desmopressin was given parenterally. Following desmopressin administration, urine output reduced to 80 ml/hour, urine osmolality increased to 588 mOsm/kg, and sodium trended down to 144 mM.The diagnosis of CDI is supported by the favorable response to therapy. All sedation was held during hospitalization, however the patient remained unresponsive for 5 days and was terminally extubated. DISCUSSION: The exact mechanism behind development of CDI post-cardiac arrest is unknown, however theorized to be due to edema or injury to the hypothalamus. The hypothalamus is generally resistant to hypoxia, however extremely prolonged hypoxia and hypercapnia will cause extensive destruction via neuronal damage. There are few reported cases of CDI post-cardiac arrest. Our patient had significant response to desmopressin administration but had very poor neurologic response. As per our observation and prior reports, the development of CDI post-cardiac arrest is a poor prognostic indicator. CONCLUSIONS: Here we highlight the importance of diagnosing CDI in cardiac arrest patients to prevent further damage to the brain. REFERENCE #1: Koubar, S, Younes, E. Transient Central Diabetes Insipidus and Marked Hypernatremia following Cardiorespiratory Arrest. Hindawi, Case Reports in Nephrology (2017). https://doi.org/10.1155/2017/1574625 REFERENCE #2: Arisaka, O, Arisaka, M, Ikebe, A et al. Central diabetes insipidus in hypoxic brain damage. Child's Nerv Syst 8, 81–82 (1992). https://doi.org/10.1007/BF00298445 DISCLOSURES: No relevant relationships by ahmad alkhatatneh, source=Web Response No relevant relationships by Sharath Bellary, source=Web Response No relevant relationships by Nilam Bhavsar, source=Web Response No relevant relationships by Gowthami Sai Jagirdhar, source=Web Response