Abstract

Background: Cerebral air embolism (CAE) is a rare but potentially fatal complication of upper gastrointestinal endoscopy (UGIE). It often presents with sudden neurological deterioration and can be misdiagnosed due to non-specific clinical features and misleading early imaging findings. Prompt diagnosis and intervention are crucial for improving outcomes.
Case Presentation: A 56-year-old male with hypertension, type 2 diabetes, and advanced Parkinsonism underwent a routine UGIE for evaluation of gastrointestinal symptoms. During the procedure, he developed sudden altered mental status, tachycardia (HR 130/min), desaturation (SpO₂ 86%), and hypotension (BP 90/60 mmHg). Neurological examination revealed left hemiparesis and severe dysarthria.
An acute ischemic stroke was suspected, and MRI brain with MRA (images a-f) was performed after stabilization which revealed an acute infarct with diffusion restriction in the right middle cerebral artery (MCA) and MCA–posterior cerebral artery (PCA) watershed territories, with DWI-FLAIR mismatch. SWI sequences (image g,h) showed blooming artifacts in the frontotemporal sulci and venous sinuses. However, MRA was normal, which was unusual given the size and extent of infarction. This prompted further evaluation with a non-contrast CT brain (images i-l), which revealed multiple air emboli in the small vessels of the cortical sulci, explaining the blooming seen on SWI. A diagnosis of cerebral air embolism during UGIE was made.
The patient was managed with 100% oxygen via a non-rebreather mask and supportive care including intravenous fluids and vasopressors for hemodynamic stabilization. Although hyperbaric oxygen therapy (HBOT) was recommended, the family declined due to the patient's age and comorbidities. A 2D echocardiogram was performed to rule out intracardiac shunt, which was normal. The patient had one episode of seizure, managed with antiseizure medications. Repeat imaging 48 hours later showed an evolved infarct in the same distribution, with no edema or mass effect, and resolution of the intracranial air.
Despite supportive measures, the patient remained neurologically unchanged and subsequently developed aspiration pneumonia and sepsis. His condition deteriorated progressively, and he expired after seven days.
Conclusion: This case highlights the importance of considering cerebral air embolism as a differential diagnosis in patients presenting with acute neurological and cardiopulmonary compromise during or after UGIE. Early MRI may not always detect air embolism directly, and CT brain is often required for confirmation. Notably, intracranial air may completely resolve on follow-up imaging, making early diagnosis crucial. Preventive measures during endoscopic procedures, high clinical suspicion, and immediate supportive interventions can improve outcomes in such cases.
Keywords: Cerebral air embolism, upper GI endoscopy, acute stroke, air embolism diagnosis, CT brain, hyperbaric oxygen therapy