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An Unusual Case of Heroin Induced Central Diabetes Insipidus
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A3354 - An Unusual Case of Heroin Induced Central Diabetes Insipidus
Author Block: H. Iftikhar1, C. Zhang1, J. Hehar1, G. Nair2; 1Internal Medicine, Beaumont Health System, Royal Oak, MI, United States, 2Pulmonary Division, Beaumont Health System, Royal Oak, MI, United States.
Introduction Heroin, a recreational drug usually activates the opioid receptors in the “reward centers of the brain” - nucleus accumbens, ventral tegmental area and cerebral cortex to cause excessive release of dopamine. Chronic use of opioids has been implicated to interfere with hypothalamic-pituitary (HP) axis. We report a peculiar case of central diabetes insipidus related with acute heroin overdose. Case A 28-year-old male with history of polysubstance abuse was admitted to ICU with acute respiratory failure related with heroin overdose. He was found unresponsive at home. The initial vitals revealed blood pressure of 48/20 mmHg and oxygen saturation of 48%. He received naloxone and was intubated. He was resuscitated with fluids and started on norepinephrine with reversal of shock. His urine drug analysis was positive for cannabinoids and opiates. On the second day of hospitalization, he was noted to have excessive urine output of more than 2100 milliliters over 2 hours. The serum sodium was elevated to 149 millimoles per liter (mmol/L) and serum osmolality 300 mOsmol/kg, but low urine osmolality 46 mOsmol/kg. Serum random cortisol level was low at 0.8 mcg/dL, raising the possibility of adrenal insufficiency from hypoxia. An MRI of brain was normal. He was started on Desmopressin 0.25 mcg Q12H and Dexamethasone 1 mg IV every 8 hours. Patient’s urine osmolality improved to 551 mOsmol/kg and hypernatremia resolved. A subsequent Adrenocorticotrophic (ACTH) stimulation test showed less than 0.5mcg/dL cortisol as baseline, 8.5mcg/dL at 30 minutes and 12.2 mcg at 60 minutes. Without hypoxic brain injury, mass lesions and no previous history of pituitary dysfunction, the cause of central diabetes insipidus (CDI) and derangement of hypothalamus-pituitary-adrenal axis was attributed to acute heroin inhalation. He was extubated tenth day of hospitalization. A repeat ACTH stimulation test returned normal and he was tapered off steroids and desmopressin. Discussion CDI in the absence of pituitary ischemia is extremely uncommon. Pituitary gland has both mu and kappa opioid receptors. Heroin is rapidly hydrolyzed to 6-monoacetylmorphine and morphine, and affects the HP axis through mu receptors. Our patient developed both CDI and secondary adrenal insufficiency related to acute heroin inhalation. Our case illustrates the need for high clinical vigilance in detecting adverse physiological effects of heroin on the HP axis.
Author Block: H. Iftikhar1, C. Zhang1, J. Hehar1, G. Nair2; 1Internal Medicine, Beaumont Health System, Royal Oak, MI, United States, 2Pulmonary Division, Beaumont Health System, Royal Oak, MI, United States.
Introduction Heroin, a recreational drug usually activates the opioid receptors in the “reward centers of the brain” - nucleus accumbens, ventral tegmental area and cerebral cortex to cause excessive release of dopamine. Chronic use of opioids has been implicated to interfere with hypothalamic-pituitary (HP) axis. We report a peculiar case of central diabetes insipidus related with acute heroin overdose. Case A 28-year-old male with history of polysubstance abuse was admitted to ICU with acute respiratory failure related with heroin overdose. He was found unresponsive at home. The initial vitals revealed blood pressure of 48/20 mmHg and oxygen saturation of 48%. He received naloxone and was intubated. He was resuscitated with fluids and started on norepinephrine with reversal of shock. His urine drug analysis was positive for cannabinoids and opiates. On the second day of hospitalization, he was noted to have excessive urine output of more than 2100 milliliters over 2 hours. The serum sodium was elevated to 149 millimoles per liter (mmol/L) and serum osmolality 300 mOsmol/kg, but low urine osmolality 46 mOsmol/kg. Serum random cortisol level was low at 0.8 mcg/dL, raising the possibility of adrenal insufficiency from hypoxia. An MRI of brain was normal. He was started on Desmopressin 0.25 mcg Q12H and Dexamethasone 1 mg IV every 8 hours. Patient’s urine osmolality improved to 551 mOsmol/kg and hypernatremia resolved. A subsequent Adrenocorticotrophic (ACTH) stimulation test showed less than 0.5mcg/dL cortisol as baseline, 8.5mcg/dL at 30 minutes and 12.2 mcg at 60 minutes. Without hypoxic brain injury, mass lesions and no previous history of pituitary dysfunction, the cause of central diabetes insipidus (CDI) and derangement of hypothalamus-pituitary-adrenal axis was attributed to acute heroin inhalation. He was extubated tenth day of hospitalization. A repeat ACTH stimulation test returned normal and he was tapered off steroids and desmopressin. Discussion CDI in the absence of pituitary ischemia is extremely uncommon. Pituitary gland has both mu and kappa opioid receptors. Heroin is rapidly hydrolyzed to 6-monoacetylmorphine and morphine, and affects the HP axis through mu receptors. Our patient developed both CDI and secondary adrenal insufficiency related to acute heroin inhalation. Our case illustrates the need for high clinical vigilance in detecting adverse physiological effects of heroin on the HP axis.
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