Cerebral Air Embolism Complicating Esophageal Dilation

Abstract

A 57-year old man with history of HIV (undetectable viral load) and compensated liver cirrhosis underwent an elective upper endoscopy for a yearlong history of mid-sternal solid food dysphagia. The EGD was performed under conscious sedation. He was found to have severe mid and distal esophagitis with white patches and a tight esophageal stricture at 34 cm through which an adult gastroscope was unable to pass. With help of a pediatric endoscope length of the stricture was determined to be 1 cm. A through-the-scope controlled radial expansion balloon (TTS-CRETM, Boston Scientific) was advanced through stricture with guidewire. Serial balloon dilations were performed (6-7-8mm) with post dilation oozing seen above the stricture site that resolved spontaneously. His post-procedure course was complicated by oxygen desaturation, tachycardia and hypotension. He failed to recover from propofol sedation and despite getting naloxone remained unresponsive to verbal or painful stimuli. Physical examination revealed non-reactive pupils, absent corneal and gag reflexes, flaccid muscle tone and positive Babinski sign bilaterally. He was immediately transferred to ICU for ventilator and vasopressor support. CT-head revealed multiple small foci of pneumocephalus overlying the vertex and bilateral frontal lobes without intravascular gas (Image 1). On CT-chest the esophagus had diffuse distal wall thickening with associated fat stranding but no evidence of esophageal rupture. A transthoracic echocardiogram did not reveal any intra-cardiac shunt. The patient underwent an MRI revealing diffuse cortical laminar necrosis and hypoxic-ischemic encephalopathy (Image 2), marked cerebellar edema with mass effect upon the midbrain and pons with early ascending trans-tentorial herniation (Image 3). Due to his hemodynamic instability he could not be transferred to another facility for hyperbaric oxygen therapy. His neurological status remained unchanged and the family decided to focus on his comfort along with withdrawal of life support. Only a handful cases have been reported of cerebral air embolism during esophageal dilation. Patients usually present with coma, seizures or upper motor neuron signs. Air is thought to enter the arterial vasculature during insufflation though the disrupted mucosa. Air embolism can also occur through venous system via arteriovenous shunts or pulmonary capillary bed. Air embolism results in ischemia, vascular endothelial damage, edema and platelet aggregation. Patients are mainly treated with hyperbaric oxygen or high-flow oxygen, left-lateral decubitus or Trendelenburg's position and supportive care. Morality is >90% for untreated patients but can be reduced to 7% with hyperbaric oxygen though survivors often have neurological deficits.Figure 1Figure 2Figure 3