P047: RUPTURED CEREBELLAR ARTERIOVENOUS MALFORMATION INCITING NEUROGENIC PULMONARY EDEMA IN A 22-YEAR-OLD MALE
Michael D Collins, DO, MS; Aaron Hacker, DO; Imani Thornton, MD
HCA Florida Westside Anesthesiology Program
Introduction: Neurogenic pulmonary edema (NPE) is the sudden onset of pulmonary congestion and life-threatening respiratory failure following neurological events such as traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), seizures, and increased intracranial pressure (ICP) of any etiology. The administration of naloxone, often used to reverse opioid-induced respiratory depression, has emerged as a potential trigger for this disorder. NPE requires rapid identification and intervention to prevent patient morbidity and mortality. Currently, treatment of NPE involves management of the underlying neurological insult and its pulmonary sequelae. Typically, this is achieved with surgical interventions to reverse the insult, and pharmacologic and ventilatory strategies to manage edema.
We report a case of a 22-year-old male who presented to the ED after being found unresponsive at home after taking an unknown medication for a severe headache. Due to his complicated presentation of unresponsiveness, agonal breathing, and bilateral miosis with unclear etiology, he was suspected to have overdosed and was administered intranasal naloxone (2 mg). After a repeat dose of IV naloxone, the patient rapidly deteriorated, developing distributive shock requiring vasopressor support and acute hypoxic respiratory failure necessitating mechanical ventilation. Upon further investigation, imaging revealed a right cerebellar hemorrhage with associated arteriovenous malformation (AVM) and mass effect along with a finding of extensive pulmonary edema.
Neurosurgery placed an external ventricular drain, and embolization was planned. In the operating room, the patient was placed in the prone position and immediately became difficult to ventilate with a significant amount of frothy, pink fluid exuding from the endotracheal tube. His oxygen saturation dropped to as low as 62% and he was quickly returned to a supine position. The anesthesia team then performed a bronchoscopy which confirmed severe pulmonary edema. Due to hemodynamic instability and the high probability of mortality with prone positioning for a prolonged period, the decision was made to abort the procedure in favor of ICU medical management for intracranial hypertension as well as continuing the external ventricular drain. The patient developed acute renal failure and heart failure secondary to distributive shock and was started on IV Lasix with minimal improvement in urine output. After he was weaned from sedation, the patient remained unresponsive to stimuli. A nuclear medicine brain flow study was completed and revealed no intracerebral blood flow consistent with brain death. The patient was pronounced deceased 3 days status-post AVM rupture.
Discussion: NPE arises from the dysregulation of sympathetic nervous system activity, leading to increased pulmonary vascular permeability and subsequent alveolar flooding. The surge in catecholamine release and sympathetic outflow triggers a series of hemodynamic changes, including elevated systemic and pulmonary pressures and capillary leakage. Naloxone administration can trigger a similar response, exacerbating pulmonary edema even in opioid-naïve patients.
Management of NPE requires ventilatory support, fluid balance control, and neurological stabilization. While surgery is the definitive treatment for ICP control, patients must first be hemodynamically stabilized. Recognizing NPE early is crucial to optimizing patient outcomes. Further research is needed to assess risk factors and refine treatment strategies for NPE compounded with Naloxone use.