Cerebral artery air embolism following an esophagogastroscopy: A case report
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Cerebrovascular events during endoscopy are uncommon. Air embolism should 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 cerebral artery air embolism during an esophagogastroscopy procedure.
Case report.
An 80-year-old woman presented with a history of progressive dysphagia, initially for solid foods and later for liquids, and severe weight loss during the previous 6 months. She was taking enalapril for hypertension. Initial investigations revealed the presence of a malignant stricture in the esophagus. She underwent an elective fiberoptic endoscopy under conscious sedation, which confirmed a malignant stricture at the esophagogastric junction, along with a small esophagotracheal fistula. Multiple small biopsies were performed, confirming the presence of esophageal carcinoma. Her level of consciousness deteriorated immediately following the procedure. She became unresponsive, but remained hemodynamically stable. Examination revealed a left hemiparesis involving the face, arm, and leg, with flexion of the right upper limb in response to pain. An emergent unenhanced CT scan of the head revealed parenchymal air in the right hemisphere ( figure). Right-sided sulci were effaced, which was suggestive of an acute right middle cerebral artery infarct. Cerebral air embolism was diagnosed. She was treated conservatively with 100% oxygen therapy. A transthoracic echocardiogram with bubble contrast showed no evidence of a right-to-left intracardiac shunt. She was discharged from the hospital in a vegetative state 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.
Discussion.
Cerebral air embolism may occur with barotrauma1 and during neurosurgical procedures,2 especially when performed in a sitting position. This also has been reported as a complication of cardiac catheterization, as well as in other diagnostic andtherapeutic procedures.3 A few cases have been reported in the absence of intracardiac defects. Penetrating duodenal ulcers may form fistulas with colon, pancreatic or bile duct, or aorta. Other cases have been reported with duodenocaval fistulas after trauma and local radiation.4
Because of unique hepatic venous drainage, systemic air embolism is uncommon with gastrointestinal endoscopy procedures. Venous air embolism occurs only when the liver is bypassed, e.g., with portosystemic shunts in portal hypertension. Arterial air embolism is even more rare because of capillary filtration in the lungs. In certain circumstances, this filter is bypassed through a right-to-left intracardiac shunt.5 However, in our patient, such a shunt was not found. A small tracheoesophageal fistula around the stricture was seen. There have been reports of a fatal cerebral arterial gas embolism caused by a large venous gas embolism, though no intracardiac defects or shunt mechanisms could be demonstrated.3 An alternative mechanism for paradoxic air embolism—intrapulmonary shunts as well as transcapillary route with large air emboli—has been proposed.6 This probably best explains the mechanism in our patient.
The neurologic manifestations are myriad and include altered consciousness, seizures, and focal deficit. CT scanning is valuable in detecting this if performed early, as IV air is rapidly absorbed and delays would result in a failure of diagnosis. CNS dysfunction results from mechanical obstruction of arterioles, leading to cerebral ischemia and the thrombotic-inflammatory response of air-injured epithelium. This results in a transient decline of cerebral blood flow and neural function. Treatment should be started as soon as there is a strong clinical suspicion for the diagnosis, including the removal of the air source, 100% oxygen by face mask, and hyperbaric oxygen. The aim of this treatment is to rapidly reduce the volume of air embolus. Recent experimental data suggest that agents with antithrombotic and anti-inflammatory properties may be of potential benefit when given prophylactically in subjects at risk for cerebral air embolism.5,6⇓
- Received June 6, 2000.
- Accepted August 24, 2000.
References
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Tommasino C, Rissardi R, Baretta L. Cerebral ischemia after venous air embolism in absence of intracardiac defects. J Neurosurg Anesth . 1996; 1: 30–34.
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Ryu KH, Hindman BJ, Reasoner DK, Dexter F. Heparin reduces neurologic impairment after cerebral artery air embolism in rabbit. Stroke . 1996; 27: 303–309.
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