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|LETTER TO EDITOR
|Year : 2010 | Volume
| Issue : 5 | Page : 794-796
Left hemiparesis during esophagogastroduodenoscopy: A unique syndrome due to cerebral air embolism
Anuradha Kolluru1, Sule Salami1, Shyam S Moudgil2
1 Department of Internal Medicine, St. John Hospital and Medical Center, Detroit, MI, USA
2 Department of Neurology, St. John Hospital and Medical Center, Detroit, MI, USA
|Date of Acceptance||22-Jul-2010|
|Date of Web Publication||28-Oct-2010|
Department of Internal Medicine, St. John Hospital and Medical Center, Detroit, MI
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kolluru A, Salami S, Moudgil SS. Left hemiparesis during esophagogastroduodenoscopy: A unique syndrome due to cerebral air embolism. Neurol India 2010;58:794-6
Esophagogastroduodenoscopy (EGD) is a widely performed procedure for evaluating the upper gastrointestinal tract. It is relatively safe and without significant complications. Neurological adverse events are infrequent and mostly due to sedating medications used during the procedure. Ischemic stroke as a complication is extremely rare and results from cerebral air embolism. A literature review reveals only nine such cases associated with EGD [Table 1].
|Table 1 :Cases of cerebral air embolism during esophagogastroduodenoscopy |
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A 71-year-old man with history of stage IV squamous cell cancer of the left tonsil undergoing chemotherapy and radiotherapy had an elective EGD for evaluation of esophageal abnormalities seen on positron emission topography (PET) scan. EGD was performed under conscious sedation through a peripheral line. During the procedure, the patient was placed in the left lateral position, and an Olympus GIF-160 forward-viewing video-endoscope was used. A small ulcer was seen in the esophagus, and the biopsies were taken from the esophagus and stomach. A 1-cm arterio-venous malformation was seen in the bulb of the duodenum, which was ablated using a gold probe. Rest of the duodenum was normal. Immediately after the procedure, the patient was unable to move the left side. Examination revealed left hemiparesis, left lower facial weakness, decreased mentation and respiratory distress. Computerized tomography (CT) scan of the head revealed multiple air bubbles in the right middle cerebral artery territory [Figure 1]a. Radiographic imaging of the chest did not reveal mediastinal or subcutaneous air. He subsequently became more lethargic and developed tonic-clonic seizure and respiratory failure requiring ventilatory support. He was treated with 100% oxygen. Phenytoin was started for seizure prophylaxis. A follow-up CT scan of the head showed evolving ischemic infarct in the right frontoparietal lobe and resolution of intravascular air [Figure 1]b. Echocardiogram with bubble study failed to demonstrate a patent foramen ovale (PFO). He was extubated on day 4. Further hospital course was uneventful. He was subsequently transferred to an inpatient rehabilitation unit with residual left hemiparesis.
|Figure 1 :Computed tomography of the head (a) performed within 1 hour of symptom onset, showing multiple small hypodensities consistent with air emboli in the right frontoparietal region; and (b) a follow-up scan 24 hours later showing resolution of air and resultant ischemic infarction|
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Ischemic stroke during EGD is an uncommon event, and a cerebral air embolism originating from the venous circulation is the most common etiology. Air embolism during EGD is facilitated by disruption of the mucosa due to ulceration, biopsy, sphincterotomy or dilatation. , Air enters the venous system through disrupted mucosa due to a pressure gradient during insufflations.  Venous air then enters the arterial circulation via a right-to-left cardiac shunt, pulmonary arteriovenous fistulas or as a result of incomplete filtration by the pulmonary capillaries.  Right-to-left cardiac shunts occur with patent foramen ovale or atrial septal defects. Incomplete filtration or "overloading" of pulmonary filtering capabilities may occur if the venous air exceeds the capacity of the lung to filter microbubbles from the venous air. Embolism of pulmonary arterial system leads to hemodynamic compromise and respiratory failure, as is commonly seen in these patients. Air in the cerebral vasculature causes ischemia due to mechanical obstruction and vasospasm. In addition, there is endothelial injury leading to inflammatory reaction, altered vascular permeability, and cerebral edema.  The neurological manifestations are diverse and depend upon the affected brain region. The motor deficits are by far the commonest and earliest recognized manifestations. Sensory, visual or a global neurological dysfunction may be seen.
Since the first report of cerebral air embolism during EGD,  eight more cases have been described in the English literature. Clinical and radiological features as seen in these cases are appended in the [Table 1]. Left hemiparesis and impaired consciousness were the most common manifestations, followed by respiratory distress and seizures. Presence or absence of an intracardiac shunt did not seem to alter the clinical picture. The right hemisphere is predominantly affected because EGD is performed in the left lateral position, thus facilitating the entry of air into the right carotid system and leading to left hemibody dysfunction. All nine previously reported cases, as well as our case, had right hemispheric involvement.
The treatment involves supportive therapy with administration of high-flow oxygen, early ventilatory and pressor support in case of respiratory failure and hypotension. Seizures should be treated with benzodiazepines or one of the parenterally administered antiepileptics. Antiplatelet agents are recommended to prevent platelet aggregation. Hyperbaric oxygen is the treatment of choice and should be instituted at the earliest, where available. Outcome varies widely and depends upon multiple variables, the most important being the amount of intravascular air. Other factors include clinical setting and timeliness of the treatment.
| » References|| |
|1.||Bou-Samra G, Darby PJ, Christensen GD. Cerebral air embolism during endoscopy. Mo Med 1997;94:704-7. |
|2.||Raju GS, Bendixen BH, Khan J, Summers RW. Cerebrovascular accident during endoscopy: Consider cerebral air embolism, a rapidly reversible event with hyperbaric oxygen therapy. Gastroinest Endosc 1998;47:70-3. |
|3.||Green BT, Tendler DA. Cerebral air embolism during upper endoscopy: Case report and review. Gastroinest Endosc 2005;61:620-3. |
|4.||Mitchell S, Gorman D. The pathophysiology of cerebral arterial gas embolism. J Extra Corpor Technol 2002;34:18-23. |
|5.||Christl SU, Scheppach W, Peters U, Kirchner T. Cerebral air embolism after gastroduodenoscopy: Complication of a duodenocaval fistula. Gastroinest Endosc 1994;40:376-8. |
|6.||Akhtar N, Jafri W, Mozaffar T. Cerebral artery air embolism following an esophagogastroscopy: A case report. Neurology 2001;56:136-7. |
|7.||Demaerel P, Gevers A, Bruecker YD, Sunaert S, Wilms G. Stroke caused by cerebral air embolism during endoscopy. Gastroinest Endosc 2003;57:134-5. |
|8.||McAree BJ, Gilliland R, Campbell DM, Lucas JW, Dickey W. Cerebral Air Embolism complicating esophagogastroduodenoscopy (EGD). Endoscopy 2008;40:E191-2. |
|9.||Vinetti M, De Roock S, Hantson P. Massive Cerebral Air Embolism During Esophagogastroduodenoscopy. Clin Gastrol hepatol 2010;8:A20. |
|10.||Laan M, Totte E, van Hulst RA, van der Linde K, van der Kamp W and Pierie JE. Cerebral gas embolism due to upper gastrointestinal endoscopy. Eur J Gastrol Hepatol 2009;21:833-5. |