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Cerebral Air Embolism From Upper Endoscopy: A Fatal Case With No Improvement After Hyperbaric Oxygen Therapy FREE TO VIEW

Ji Hyun Rhee, MD; Amol Patil, MD
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University of Nebraska Medical Center, Omaha, NE

Chest. 2014;146(4_MeetingAbstracts):267A. doi:10.1378/chest.1989857
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SESSION TITLE: Critical Care Case Report Posters III

SESSION TYPE: Affiliate Case Report Poster

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Air embolism is an uncommon but potentially catastrophic event that occurs when air enters the vasculature. Most cases occur during invasive procedures but rarely in endoscopy(EGD). Here, we report a fatal case of cerebral air embolism(CAE) following EGD that failed to respond to hyperbaric oxygen therapy(HBOT).

CASE PRESENTATION: A 71yo male with chronic dysphagia presented to the ED complaining of a piece of meat stuck in his throat. Physical exam, vital signs and labs were unremarkable. An esophagogram confirmed a food bolus; EGD with esophageal dilatation under conscious sedation showed esophagitis and the food bolus was advanced into the stomach. Shortly thereafter, he became bradycardic(43bmp), hypotensive(82/47), hypoxic(62% on NRB) and unresponsive. EGD was immediately withdrawn and intubation performed. With IV fluids and manual ventilation, HR, BP and oxygenation improved. CXR revealed no acute cardiopulmonary abnormalities. However, CTH showed multiple cerebral air emboli [Fig1]. The patient was transferred to our facility and received HBOT for 5 hours. A bubble study showed no evidence of intracardiac shunt. HBOT was continued with minimal neurologic improvement. CTH 2 days post-event revealed resolved air pockets and significant cerebral edema. Despite aggressive measures to minimize further edema, patient remained unresponsive. CTH 6 days post-event showed increased swelling in the right with a new 5mm midline shift [Fig2]. Due to his poor prognosis, family chose comfort cares; he died the following day.

DISCUSSION: In this patient, air inflation during esophageal dilatation with inflammation and venous engorgement (esophagitis) likely led to air entry through an interruption in the mucosal barrier. Acute cardiopulmonary compromise with subsequent unresponsiveness suggests that air went through the right heart and lungs into the cerebral arterial system. No right-to-left shunt was seen on bubble study, suggesting insufficient pulmonary capillary filtration (due to the large volume/rate of air) as the potential cause for this patient's CAE. After 5 days of continued coma despite HBOT and poor prognosis, care was withdrawan at the family's wishes and the patient passed away.

CONCLUSIONS: Early diagnosis is crucial for successful treatment. CAE should be considered a potential complication of EGD and acted upon immediately. Supportive care including high FiO2, left lateral decubitus/Trendelenburg positioning and prompt HBOT may help.

Reference #1: AE complicating gastrointestinal endoscopy, PMID:23951390

DISCLOSURE: The following authors have nothing to disclose: Ji Hyun Rhee, Amol Patil

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