HYPERGLYCEMIC CRISIS FUNCTIONING AS HYPEROSMOTIC RESCUE IN A PATIENT WITH ISCHEMIC CEREBELLAR STROKE

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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Cerebral injury is a rare complication of hyperglycemic crisis, typically occurring within 3-12 hours of treatment initiation. It is presumed to be a result of aggressive fluid resuscitation and rapid serum osmolality changes following initiation of insulin therapy. Incidence is less than 1% in children with only limited cases reported in adults. We report a rare case of hyperglycemic hyperosmolar state (HHS) secondary to acute pancreatitis and methamphetamine abuse in a patient with concomitant ischemic cerebellar infarct who rapidly deteriorated following corrective therapy. We propose a potential pathophysiological explanation of her presentation, highlighting the challenges in management. CASE PRESENTATION: A 54-year-old female with poorly controlled type-2 diabetes mellitus (DM) noncompliant with insulin therapy, hypertension, and methamphetamine abuse presented with acute encephalopathy and gastrointestinal distress. She was hypertensive and tachycardic on arrival in no respiratory distress. Labs were significant for profound hyperglycemia with blood glucose of 912 mg/dL, bicarbonate 19.5 mmol/L, anion gap 24 mmol/L, beta-hydroxybutyrate of 0.98 mmol/L, lactate 9.2 mmol/L, lipase 2462 U/L, and balanced electrolytes. Toxicology screen was positive for methamphetamine. ABG on room air showed normal range pH. CT head revealed a 2.6 cm region of hypoattenuation in the inferior cerebellum suggestive of acute ischemic infarct. She was given IV fluid followed by insulin infusion and admitted to the ICU. Shortly after, she became rapidly hypoxemic with bradypnea requiring rapid sequence intubation, followed by sudden bradycardia and ultimately fatal PEA arrest. DISCUSSION: To our knowledge, there has never been a reported case of concomitant HHS and acute cerebral ischemia in adults. Although MRI was unable to be performed, we suspect our patient suffered rapid intracranial pressure elevation as evidenced by development of Cushing triad. Patients with ischemic cerebellar infarcts are at high risk for reactive cerebral edema. Glucose is a natural osmotic agent, increasing serum tonicity, and may have provided an ironic therapeutic benefit. Rapid correction of her hyperosmolar state with insulin therapy in conjunction with aggressive fluid resuscitation, likely precipitated sudden intracellular fluid influx and subsequent herniation. Post-stroke hyperglycemia is a common physiological occurrence and may have served as a potential hyperosmotic rescue measure in our patient. CONCLUSIONS: Cerebral edema is a rare but potentially fatal complication of hyperglycemic crisis therapy. Risk is significantly elevated in those with acute ischemic infarcts and careful correction of glucose and electrolytes should be attempted. Reference #1: Varela D, Held N, Linas S. Overview of Cerebral Edema During Correction of Hyperglycemic Crises. Am J Case Rep. 2018;19:562-566. DISCLOSURES: No relevant relationships by Helen Li Mitchell, source=Web Response No relevant relationships by Sushant Soni, source=Web Response No relevant relationships by Shawnt Tosonian, source=Web Response No relevant relationships by Nathaniel Wise, source=Web Response No relevant relationships by Tommy Zaharakis, source=Web Response