Arterial cerebral gas embolism following insertion of PEG tube

A 67-year-old male patient with no previous neurological symptoms returned to ward after insertion of percutaneous endoscopic gastrostomy (PEG) tube. Upon arrival, he presented with left-sided hemiparesis, involuntary twitches of the right upper and left lower extremity, and decreased consciousness.

After symptom onset, a non-contrast CT imaging (NCCT) of the brain and CT angiography (CTA) of the cerebral arteries was performed. CTA showed no filling defect of the major cerebral arteries. NCCT revealed no evidence of infarction; however, several small round hypodense foci were noted in the cortex of right frontal and parietal lobes. Findings were suggestive of air entrapment in the regional distal cerebral arteries.

On the following day, after administering 100% oxygen, a follow-up NCCT was performed. The previously identified hypodensities were no longer visible. Although there were no definitive signs of cerebral infarction, the white matter in the affected region was slightly hypodense compared to the contralateral hemisphere and imaging the day before, there has been slight sulcal effacement.

Two days after symptoms onset, a follow-up MRI was performed. It revealed cortical oedema of the right frontal and parietal lobes with adjacent hyperintense white matter signal on FLAIR sequences. This, in conjunction with diffusion restriction of the affected cortex, strongly indicated the presence of cerebral infarction.

Cerebral Gas Embolism (CGE) occurs when air or gas bubbles enter the circulation, leading to a wide range of symptoms from mild discomfort to rapid death [1]. These bubbles can obstruct small vessels, causing neurological and/or cardio-respiratory manifestations [2]. Presentation is varied, but includes motor weakness, loss of vision, confusion, seizures, and decreased consciousness [3]. CGE can be venous or arterial, with various origins such as diving accidents, barotrauma during mechanical ventilation, intravascular equipment manipulation, and peri-operative procedures, including neurosurgical, vascular, cardiac, thoracic, orthopaedic, and laparoscopic surgery. It is important to always suspect CGE in peri-operative stroke [4].

Cerebral Arterial Gas Embolism (CAGE) is a dangerous variant where gas bubbles preferentially enter the cerebral arterial circulation, causing sudden neurological signs. In Cerebral Venous Gas Embolism (CVGE), the gas bubbles must first bypass the pulmonary circulation; thus, a right-to-left shunt (most commonly in the form of a patent foramen ovale) is necessary for the bubbles to reach the cerebral arterial system [5]. Thus making CAGE even more dangerous.

In cerebral vessels, gas bubbles cause mechanical obstruction of blood flow, damage the endothelium, activate the coagulation cascade, and induce platelet and leukocyte activation. This leads to impaired microcirculation, vasospasm, ischemic injury, damage to the blood-brain barrier, cerebral oedema, and raised intracranial pressure [6].

Radiographically, the presence of gas in cerebral vascular system can exhibit different stroke distribution patterns, with extensive cerebral infarction, frequently occurring in a watershed distribution. In the acute setting, CT is the preferred modality to detect gas in the cerebral vessels. The use of lung windows may help in detection [7]. It is important to note that gas is swiftly absorbed and may not be visible if imaging is delayed. MRI is primarily employed to assess the complications, notably infarction, rather than directly detecting the presence of gas [8].

Immediate treatment is essential. CGE management involves identifying and eliminating the source, providing life support, and administering oxygen. Studies indicate hyperbaric oxygen therapy to be beneficial when administered promptly [9]; however, the feasibility and benefit should be assessed on a case-by-case basis. Time is critical in addressing this potentially life-threatening condition.

In our case the exact mechanism of air intrusion into the bloodstream has not been identified.

Written informed patient consent for publication has been obtained.