SEIZING THE DAY: A CASE OF POST-ICTAL NEUROGENIC PULMONARY EDEMA

Abstract

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Neurogenic pulmonary edema may present due to complex hemodynamic disturbances secondary to a central nervous system insult. It occurs rarely after generalized tonic-clonic seizures. We present a case of a young patient with recurrent generalized tonic-clonic seizures complicated by bilateral pulmonary edema requiring mechanical ventilation. CASE PRESENTATION: A 29-year-old African American man with a history of seizure disorder, cannabis use, and anxiety presented to the emergency department for decreased responsiveness after a seizure episode with a duration of 90 seconds. He had his first seizure 5 months ago and a concussion with loss of consciousness 2 months prior. He was not taking any anti-epileptic medications. On arrival, the patient had a respiratory rate of 41/min and was intubated for acute hypoxemic respiratory failure. Arterial blood gas prior to intubation showed a pH of 7.16, pCO2 of 41.5 mmHg, pO2 of 74.5 mmHg, and HCO3 of 14.4 mmol/L with a lactate of 5.84 mmol/L on FiO2 100%. Physical exam was remarkable for frothy blood in the mouth and chest auscultation revealed diffuse crackles bilaterally. Approximately 300 cc of pink frothy fluid was suctioned from the endotracheal tube. Chest x-ray (CXR) revealed bilateral pulmonary edema (Figure 1) and computed tomography (CT) chest showed dense central bilateral ground glass infiltrates with minimal sparing of periphery (Figure 2). CT head and electroencephalogram were unremarkable. Transthoracic echocardiogram estimated an ejection fraction of 50-55%. Bronchoscopy showed clearing pink secretions throughout the tracheobronchial tree. Seven days later, he was extubated and eventually discharged. DISCUSSION: The majority of neurogenic pulmonary edema is secondary to intracranial hemorrhage and less than two percent are caused by seizures. Other causes include spinal cord injury, stroke, and intracranial trauma. Post-ictal pulmonary edema can present within minutes to hours after a seizure resolving within days (1,2). Pathophysiology is hypothesized to be due to an intense hyperadrenergic state causing pulmonary and systemic vasoconstriction leading to increased capillary hydrostatic pressure and permeability (2). Postictal laryngospasm with deep inspiratory effort against a closed glottis increases negative intrathoracic pressure is another possible mechanism. This causes hydrostatic fluid shifts which further worsen the pulmonary edema (3). Treatment is supportive and centered on managing the underlying neurological disorder. CONCLUSIONS: Post-ictal pulmonary edema is an uncommon cause of neurogenic pulmonary edema. It is important to recognize this as a potential contributor to acute hypoxemic respiratory failure in patients with epilepsy and other central nervous system disorders. Reference #1: Izumida H, Homma K, Sasaki J, Hori S. Pulmonary edema following tonic–clonic seizure. Acute Med Surg. 2016 Dec 9;4(2):221-222. Reference #2: Romero Osorio OM, Abaunza Camacho JF, Sandoval Briceño D, Lasalvia P, Narino Gonzalez D. Postictal neurogenic pulmonary edema: Case report and brief literature review. Epilepsy Behav Case Rep. 2017 Sep 28;9:49-50. Reference #3: Kennedy JD, Hardin KA, Parikh P, Li CS, Seyal M. Pulmonary edema following generalized tonic clonic seizures is directly associated with seizure duration. Seizure. 2015 Apr;27:19-24. DISCLOSURES: No relevant relationships by Sarah Jaroudi, source=Web Response No relevant relationships by David Sotello Aviles, source=Web Response No relevant relationships by Victor Test, source=Web Response