S006: OBSTETRIC CEREBRAL AIR EMBOLISM AFTER EPIDURAL ANESTHESIA: DIAGNOSTIC CONSIDERATIONS
Ritu Channagiri, BS; Elena Garcia, BS; Zeena Shather, Student; Melanie Altizer, MD
Florida Atlantic University
Cerebral air embolism (CAE) occurs when air enters the cerebral circulation either arterial or venous leading to vascular occlusion, ischemia, or intracranial hypertension. Arterial emboli typically cause infarction through obstruction of cerebral arteries, while venous emboli may result in venous infarction, cerebral edema, and raised intracranial pressure [1,2].
During epidural anesthesia, the loss-of-resistance to air (LORA) technique is commonly used to identify the epidural space. Use of air increases the risk of dural puncture and intracranial air entry compared to saline [3]. Some studies have found higher rates of unblocked segments and accidental dural puncture when using air rather than saline for the loss-of-resistance technique while others report no significant risk elevation for using air. Air may accumulate in subarachnoid, subdural, subgaleal, or intraventricular compartments after dural breach [2,3].
A 40-year-old G3P2002 at 38 weeks and 3 days gestation with two prior uncomplicated vaginal deliveries, presented to the emergency department with contractions and vaginal bleeding. She was 70% effaced, 5 cm dilated, and –3 station.
The patient received epidural anesthesia using the LORA technique. She developed a 10-minute episode of fetal bradycardia and maternal hypotension. Ephedrine was administered, resulting in improved blood pressure and partial recovery of the fetal heart rate. The patient became somnolent and complained of dyspnea. Pitocin infusion was discontinued, and an emergent low transverse cesarean section was performed. The delivery was otherwise tolerated without intraoperative complications.
A post operative non-contrast head CT demonstrated cerebral air embolism. The patient was placed in the Trendelenburg position and admitted to the intensive care unit for hourly neurological monitoring. Levetiracetam 500 mg bid was initiated for seizure prophylaxis. She subsequently underwent two hyperbaric oxygen therapy sessions. Repeat CT showed near-complete resolution of intracranial air, with a small residual punctate focus in the ventricles expected to resolve spontaneously. The patient remained neurologically intact, with no evidence of residual gas embolism.
The recommended approach is to maintain supine position with immediate initiation of high flow oxygen [2]. Supplemental oxygen increases arterial oxygen while lowering nitrogen partial pressure, promoting diffusion of nitrogen out of intravascular air bubbles. This process reduces bubble volume and accelerates resorption [2].
Hyperbaric oxygen therapy (HBOT) is the definitive treatment for CAE, it reduces air bubble size through gas compression and enhances oxygen delivery to ischemic tissue. Observational studies demonstrate significantly improved outcomes when HBOT is initiated early, ideally within six hours of symptom onset [6]. Access to hyperbaric facilities remains limited, especially in non-urban settings, potentially delaying treatment.
Multiple obstetric case reports and reviews link LORA with pneumocephalus after inadvertent dural puncture, showing that these events are rare [4]. A Cochrane-style review found low-quality evidence of no clear difference between air and saline for identifying the epidural space or reducing complications overall [5].
Unfortunately since CT has relatively low sensitivity for detecting small volumes of intracranial air and MRI may only show nonspecific multifocal diffusion restriction depending on ischemic damage it further adds to the difficulty in confident diagnosis and early treatment of CAE. [1,2]