What is the mechanism by which hyperbaric oxygen therapy (HBOT) works for treating optic infarct?

Mechanism of Hyperbaric Oxygen Therapy for Optic Infarct

Hyperbaric oxygen therapy (HBOT) works for optic infarct by dramatically increasing dissolved oxygen in plasma (up to 100% oxygen at 1.5-3.0 atmospheres absolute), which allows oxygen to reach ischemic retinal and optic nerve tissue through diffusion, bypassing the occluded arterial circulation until vascular recanalization can occur. 1, 2

Core Physiological Mechanisms

Oxygen Delivery Bypass

• HBOT increases plasma oxygen concentration to supraphysiologic levels, creating a pressure gradient that drives oxygen diffusion directly into hypoxic tissue independent of hemoglobin-mediated delivery. 1, 3
• At 2-3 atmospheres absolute pressure with 100% oxygen, dissolved oxygen in blood increases approximately 15-20 fold compared to breathing room air at sea level, achieving tissue oxygen tensions that can sustain cellular metabolism even when arterial blood flow is compromised 2, 3
• This mechanism is particularly relevant for retinal tissue, which has extremely high metabolic oxygen demands and minimal tolerance for ischemia (retinal ganglion cells begin irreversible damage within 90-100 minutes of complete ischemia) 2

Tissue Salvage Window

• The therapeutic rationale is to bridge the critical period until spontaneous or therapeutic recanalization occurs, preventing irreversible neuronal death in the penumbra of ischemic tissue 2, 4
• Oxygen diffusion from the choroidal circulation can reach the outer retinal layers, and increased dissolved oxygen in retinal vessels can supply inner retinal layers through diffusion when forward flow is blocked 2

Additional Beneficial Effects

Cellular and Vascular Benefits

• HBOT improves leukocyte function, which may reduce inflammatory damage in the acute ischemic period 5, 3
• The therapy promotes angiogenesis and may enhance antibiotic activity, though these effects are more relevant for infectious or chronic wound conditions 5, 3
• Hyperoxia may reduce tissue edema by decreasing capillary permeability and improving cellular energy metabolism 3

Evidence-Based Context and Limitations

Condition-Specific Efficacy

• HBOT has established efficacy for central retinal artery occlusion (CRAO) and branch retinal artery occlusion (BRAO), where direct arterial obstruction creates the hypoxic conditions that HBOT can address. 2, 4
• A retrospective study of BRAO patients showed final visual acuity of 0.69 ± 0.29 in HBO-treated patients versus 0.32 ± 0.23 in controls (p = 0.0009), demonstrating significant benefit 4

Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION) - Critical Caveat

• For NAION, a prospective study using 100% oxygen at 2.0 atmospheres showed no significant improvement in visual acuity or visual field compared to untreated controls, regardless of treatment timing. 6
• This lack of efficacy may reflect the different pathophysiology of NAION (watershed infarction of the optic nerve head with multifactorial microvascular insufficiency) versus embolic arterial occlusion 6

Posterior Ischemic Optic Neuropathy (PION)

• Case reports suggest potential benefit for perioperative PION when combined with systemic steroids, with one patient showing marked vision improvement immediately after the first HBOT session 7
• However, the evidence base consists only of case reports without controlled data 7

Clinical Application Algorithm

When HBOT Works Best

• Embolic or thrombotic retinal artery occlusions (CRAO, BRAO) where discrete vascular obstruction creates acute, reversible hypoxia 2, 4
• Treatment must be initiated emergently—start normobaric oxygen at the highest FiO2 possible immediately while arranging transfer to a hyperbaric facility 2
• The time window from symptom onset to HBOT initiation is critical, as retinal tissue tolerance for ischemia is measured in hours, not days 2, 4

When HBOT Does Not Work

• NAION shows no benefit from HBOT, even when initiated within 9 days of symptom onset 6
• Routine ischemic stroke (the American Heart Association/American Stroke Association gives HBOT a Class III: No Benefit recommendation for routine acute ischemic stroke) 1

Monitoring Requirements

• Visual acuity alone is inadequate—automated perimetry evaluating the central 30 degrees of visual field must be performed at appropriate intervals before, during, and after therapy 2