From the Departments of Medicine—Neurology (Drs. Akhtar and Mozaffar), Gastroenterology (Dr. Jafri), and Pathology (Dr. Mozaffar), the Aga Khan University Medical College, Karachi, Pakistan.
Address correspondence and reprint requests to Dr. Tahseen Mozaffar, University of California at Irvine, Department of Neurology, Neurodiagnostic Lab, UCIMC, Bldg 22C, Rt. 13, 101 The City Drive South, Orange, CA 92868; e-mail: mozaffar{at}uci.edu
Cerebrovascular events during endoscopy are uncommon. Air embolismshould be considered in the differential diagnosis of any stroke,particularly if it develops during or after an endoscopic procedure.We report this unusual complication in a woman who had a cerebralartery air embolism during an esophagogastroscopy procedure.
An 80-year-old woman presented with a history of progressivedysphagia, initially for solid foods and later for liquids,and severe weight loss during the previous 6 months. She wastaking enalapril for hypertension. Initial investigations revealedthe presence of a malignant stricture in the esophagus. Sheunderwent an elective fiberoptic endoscopy under conscious sedation,which confirmed a malignant stricture at the esophagogastricjunction, along with a small esophagotracheal fistula. Multiplesmall biopsies were performed, confirming the presence of esophagealcarcinoma. Her level of consciousness deteriorated immediatelyfollowing the procedure. She became unresponsive, but remainedhemodynamically stable. Examination revealed a left hemiparesisinvolving the face, arm, and leg, with flexion of the rightupper limb in response to pain. An emergent unenhanced CT scanof the head revealed parenchymal air in the right hemisphere( figure). Right-sided sulci were effaced, which was suggestiveof an acute right middle cerebral artery infarct. Cerebral airembolism was diagnosed. She was treated conservatively with100% oxygen therapy. A transthoracic echocardiogram with bubblecontrast showed no evidence of a right-to-left intracardiacshunt. She was discharged from the hospital in a vegetativestate 2 weeks after admission.
Figure. Unenhanced CT scan of head shows right hemispheric swelling and effacement of gyri on that side. Free parenchymal air is seen in the subfrontal region.
Cerebral air embolism may occur with barotrauma1 and duringneurosurgical procedures,2 especially when performed in a sittingposition. This also has been reported as a complication of cardiaccatheterization, as well as in other diagnostic andtherapeuticprocedures.3 A few cases have been reported in the absence ofintracardiac defects. Penetrating duodenal ulcers may form fistulaswith colon, pancreatic or bile duct, or aorta. Other cases havebeen reported with duodenocaval fistulas after trauma and localradiation.4
Because of unique hepatic venous drainage, systemic air embolismis uncommon with gastrointestinal endoscopy procedures. Venousair embolism occurs only when the liver is bypassed, e.g., withportosystemic shunts in portal hypertension. Arterial air embolismis even more rare because of capillary filtration in the lungs.In certain circumstances, this filter is bypassed through aright-to-left intracardiac shunt.5 However, in our patient,such a shunt was not found. A small tracheoesophageal fistulaaround the stricture was seen. There have been reports of afatal cerebral arterial gas embolism caused by a large venousgas embolism, though no intracardiac defects or shunt mechanismscould be demonstrated.3 An alternative mechanism for paradoxicair embolism—intrapulmonary shunts as well as transcapillaryroute with large air emboli—has been proposed.6 This probablybest explains the mechanism in our patient.
The neurologic manifestations are myriad and include alteredconsciousness, seizures, and focal deficit. CT scanning is valuablein detecting this if performed early, as IV air is rapidly absorbedand delays would result in a failure of diagnosis. CNS dysfunctionresults from mechanical obstruction of arterioles, leading tocerebral ischemia and the thrombotic-inflammatory response ofair-injured epithelium. This results in a transient declineof cerebral blood flow and neural function. Treatment shouldbe started as soon as there is a strong clinical suspicion forthe diagnosis, including the removal of the air source, 100%oxygen by face mask, and hyperbaric oxygen. The aim of thistreatment is to rapidly reduce the volume of air embolus. Recentexperimental data suggest that agents with antithrombotic andanti-inflammatory properties may be of potential benefit whengiven prophylactically in subjects at risk for cerebral airembolism.5,6
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Received June 6, 2000.
Accepted in final form August 24, 2000.
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