Central Retinal Vein Occlusion
Central retinal vein occlusion (CRVO), or branch retinal vein occlusion (BRVO), is the most common vascular disorder of the retina after diabetic retinopathy.
It develops when a thrombus obstructs venous drainage from the retina, causing blood stasis, increased venous pressure and leakage of fluid into the retinal tissue.
Clinically, it presents with a sudden or gradual reduction in vision, mainly as a result of macular oedema affecting the area responsible for sharp central vision.
Characteristic ophthalmoscopic findings include flame-shaped haemorrhages across all four retinal quadrants, optic disc oedema and dilated retinal veins. Risk factors include hypertension, diabetes mellitus, hyperlipidaemia, glaucoma and obesity.
Characteristics
Unlike arterial occlusion, which causes immediate ischaemic necrosis, venous occlusion produces a different pathophysiological process. Extensive blood stasis and the resulting oedema lead to chronic hypoxia, which develops more gradually but may be equally damaging.
At the same time, macular oedema compresses the photoreceptors and disrupts their delicate functional architecture.
Another important complication is ischaemia-driven neovascularisation. In severe CRVO, chronic retinal hypoxia stimulates the pathological growth of new blood vessels. These vessels are structurally immature and prone to leakage, potentially resulting in vitreous haemorrhage or neovascular glaucoma.
Preventing these complications by reducing retinal ischaemia is therefore a critical therapeutic objective.
Clinical Studies
Clinical studies and case series evaluating the use of hyperbaric oxygen therapy in retinal vein occlusion have reported reductions in macular oedema, improvements in visual acuity and a decrease in the extent of retinal ischaemia.
Its effects are multifactorial. Increased oxygenation compensates for hypoxia caused by venous stasis, while the vasoconstriction induced by hyperbaric oxygen therapy in healthy vessels reduces intraocular oedema.
Early reduction of ischaemia may be particularly relevant to the prevention of pathological neovascularisation, one of the most serious complications. By reducing the hypoxic stimulus for VEGF-mediated neovascularisation, hyperbaric oxygen therapy may lower the risk of these complications.
The Role of Hyperbaric Oxygen Therapy
In retinal vein occlusion, hyperbaric oxygen therapy may be used as an adjunctive intervention alongside contemporary ophthalmological treatment, including intravitreal anti-VEGF injections, laser photocoagulation and management of the underlying cause.
The aim is to compensate for the persistent ischaemia caused by venous stasis, which cannot always be addressed adequately through other measures.
Increasing oxygen tension within the vitreous humour allows oxygen to reach the retina from its inner surface, providing an alternative means of supporting retinal tissue despite impaired venous drainage.
At the same time, reducing ischaemia may suppress pathological VEGF-mediated signalling and complement the effects of intravitreal anti-VEGF treatment.
A typical treatment course consists of 15 to 20 sessions during the acute phase and may be extended according to the ophthalmological response, in close collaboration with the ophthalmologist.