Cerebral Infarction from Arterial Air Emboli: Advanced Pathophysiology, Imaging Diagnosis, and Evidence-Based Management

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Keywords: Cerebral air embolism, arterial air emboli, cerebral infarction, cerebral air embolism CT, cerebral air embolism MRI, hyperbaric oxygen therapy, paradoxical embolism, patent foramen ovale, brain infarction imaging, neuroradiology

Introduction

Cerebral infarction from arterial air emboli, also known as cerebral air embolism (CAE), represents a rare but devastating neurological emergency that can lead to severe ischemic brain injury, seizures, coma, and death. Despite its rarity, CAE has gained increasing recognition due to the widespread use of invasive vascular procedures, hemodialysis, central venous catheterization, cardiothoracic surgery, and neurointerventional techniques. The growing complexity of modern medicine has paradoxically increased the incidence of iatrogenic arterial air embolism, making early diagnosis and management essential for neurologists, radiologists, intensivists, and emergency physicians.

From a pathophysiological perspective, arterial air emboli cause mechanical vascular obstruction, endothelial injury, neuroinflammation, platelet activation, and secondary microthrombosis, ultimately producing multifocal ischemic infarctions. Clinically, patients often present with abrupt neurological deterioration, seizures, altered consciousness, and focal neurological deficits, frequently mimicking acute ischemic stroke syndromes.

In this comprehensive expert-level review, we explore the pathophysiology, epidemiology, clinical presentation, imaging features, differential diagnosis, treatment, and prognosis of cerebral infarction from arterial air emboli, based on the most authoritative contemporary literature and radiological case data.

Pathophysiology of Cerebral Infarction from Arterial Air Emboli

The pathophysiology of cerebral air embolism is multifactorial and involves both mechanical and biological injury mechanisms. Air entering the arterial circulation leads to:

  1. Direct vascular obstruction of cerebral arterioles and capillaries

  2. Endothelial cell damage and blood–brain barrier disruption

  3. Platelet aggregation and fibrin activation

  4. Complement activation and the inflammatory cascade

  5. Secondary in-situ thrombosis

Unlike thrombotic emboli, air bubbles are highly deformable and dynamic, allowing them to migrate distally into microvascular territories. This explains the characteristic multifocal cortical and subcortical infarct distribution seen in CAE.

In cases of paradoxical air embolism, air enters the arterial circulation through right-to-left shunts such as patent foramen ovale (PFO) or atrial septal defects, bypassing pulmonary filtration. Hemodialysis patients are particularly vulnerable due to high-flow vascular access and venous air exposure.

Epidemiology

Cerebral air embolism is rare but likely underdiagnosed. Epidemiological studies show:

  • Predominantly iatrogenic origin (>80%)

  • Common triggers:

    • Central venous catheter manipulation

    • Hemodialysis catheter use

    • Cardiothoracic surgery

    • Neurosurgery

    • Endovascular procedures

    • Laparoscopic surgery

Patients with PFO, pulmonary arteriovenous malformations, or cardiac septal defects have an increased risk of arterial air embolization.

Clinical Presentation

The clinical spectrum of cerebral infarction from arterial air emboli is broad and includes:

  • Sudden unresponsiveness

  • Generalized tonic-clonic seizures

  • Acute encephalopathy

  • Focal neurological deficits

  • Visual disturbances

  • Hemiparesis

  • Aphasia

Systemic manifestations may include:

  • Hypoxia

  • Tachypnea

  • Cardiac arrhythmias

  • Chest pain

  • Right heart strain

Imaging Features

Figure 1. Axial Non-Contrast CT

Scattered foci of intracranial air within cortical sulci, associated with encephalomalacia in the left basal ganglia and corona radiata, mild ventricular prominence, and postsurgical changes from decompressive hemicraniectomy. These findings are diagnostic of cerebral air embolism in the acute clinical context.


Figure 2. Brain MRI (FLAIR and DWI)

Multifocal cortical and subcortical diffusion restriction involving frontal, parietal, occipital, and temporal lobes and right deep gray nuclei, consistent with multifocal ischemic infarctions due to arterial air emboli.


Figure 3. Neck CTA Sagittal

Normal cervical arterial anatomy without stenosis, dissection, or vasculitis.


Figure 4. Head CTA Sagittal

Normal intracranial arterial anatomy with no large vessel occlusion.


Figure 5. Head CTA Axial

No evidence of arterial occlusion, supporting embolic microvascular pathology rather than macrovascular disease.

Differential Diagnosis

  • Multifocal ischemic infarction

  • CNS vasculitis

  • Meningitis/encephalitis

  • Metastatic disease

  • Status epilepticus-related gyriform diffusion changes

  • Hypoxic-ischemic encephalopathy

Diagnosis

Diagnosis of cerebral infarction from arterial air emboli is based on:

  1. Clinical context (procedural exposure)

  2. CT evidence of intracranial air

  3. Multifocal ischemic lesions on MRI

  4. Exclusion of vascular occlusion on CTA/MRA

  5. Cardiac evaluation for PFO

Treatment

Evidence-based management includes:

  • Immediate cessation of the air source

  • 100% high-flow oxygen

  • Left lateral decubitus + Trendelenburg positioning

  • Hyperbaric oxygen therapy (HBOT)

  • Cerebral edema control

  • Seizure management

  • Anti-inflammatory therapy

HBOT remains the gold standard therapy due to bubble volume reduction, oxygen diffusion enhancement, and ischemia mitigation.

Prognosis

Prognosis depends on:

  • Speed of diagnosis

  • Volume of air embolism

  • Time to hyperbaric therapy

  • Extent of infarction

  • Patient comorbidities

Early treatment correlates with favorable neurological outcomes.

Quiz

Question 1. Most prominent CT finding in cerebral air embolism?

A. Encephalomalacia only
B. Ventricular enlargement
C. Scattered intracranial air
D. Postsurgical skull changes

Answer: C. Explanation: Air is the acute pathological finding.

Question 2. Which is NOT a valid diagnosis?

A. Multifocal ischemic infarction
B. Vasculitis
C. Meningitis
D. Metastatic disease

Answer: D. Explanation: Imaging pattern and acute presentation exclude metastasis.

Question 3. Best treatment for neurological deficits in cerebral air embolism?

A. Reverse Trendelenburg
B. IV CO₂ injection
C. Hyperbaric oxygen therapy
D. Antibiotics

Answer: C. Explanation: HBOT is definitive therapy.

References

[1] S. B. Jeon et al., “Clinicoradiological characteristics of cerebral air embolism,” Cerebrovasc. Dis., vol. 23, pp. 459–462, 2007.
[2] S. R. Kang et al., “Cerebral air embolism: Pathophysiology and MRI findings,” Investig. Magn. Reson. Imaging, vol. 23, no. 1, pp. 70–74, 2019.
[3] K. Malhotra et al., “Gyriform infarction in cerebral air embolism,” Ann. Indian Acad. Neurol., vol. 20, no. 3, pp. 313–315, 2017.
[4] M. Muth and E. Shank, “Gas embolism,” N. Engl. J. Med., vol. 342, pp. 476–482, 2000.
[5] J. Blanc et al., “Iatrogenic cerebral air embolism,” Stroke, vol. 36, pp. e50–e54, 2005.
[6] A. van Hulst et al., “Treatment of cerebral air embolism,” Crit. Care Med., vol. 31, pp. 155–160, 2003.
[7] E. Moon, “Hyperbaric oxygen therapy for air embolism,” Undersea Hyperb. Med., vol. 41, pp. 27–33, 2014.

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