ANATOMICAL CLASSIFICATION
Retinal thrombosis can be classified in various types with different natural evolution, prognosis and treatment depending on the blood vessels it affects.
- Central Retinal Vein Occlusion (CRVO)
- Branch Retinal Vein Occlusion
- Superior or inferior Hemicentral Retinal Occlusion, behaves as a central retinal vein occlusion
PHYSIOPATHOLOGY AND RISK FACTORS
There are ocular risk factors whether they are anatomical due to the proximity of the artery and the central vein of the retina, location and narrowing of the vessels in the cribiform plate or due to open angle glaucoma present in 40% of patients with CRVO (or they develop it).
And risk factors at a systemic level such as uncontrolled arterial hypertension, diabetes, hyperlipidaemia, blood hyperviscosity and thrombophilia amongst which one must highlight antiphospholipid antibodies (anticardiolipin and lupus anticoagulant), hyperhomocysteinemia (in many cases due to a genetic mutation in the MTFHR gene) and natural anticoagulant system (Factor V Leiden, protein C, protein S and antithrombin).
It is the responsibility of the ophthalmologist to study the main systemic risk factors, interpret the results and refer the patient to the appropriate specialist. As a rule, medical management of the risk factors should be done within the first two months following diagnosis.
On occasions, it is impossible to find an underlying cause.
CLINICAL SYMPTOMS
Symptoms: sudden loss of visual field that can be severe in CRVO and moderate in branch retinal vein occlusions, painless and more pronounced in the ischemic forms with a loss of visual field associated, often irreversible. Macular oedema is the most common cause of visual loss.
Signs: vascular tortuosity, venous dilation, superficial retinal haemorrhages in the well-defined area that affects the thrombosis, macular oedema and in some cases cottony exudates, arteriolar narrowing and lipid exudate. In the chronic stage of the disease, the apparition of a macular epiretinal membrane and the alteration of the retinal pigment epithelium are common.
COMPLEMENTARY TESTS
- Fluorescein Angiography (FA): determines the extent of the ischemia, if any and the macular oedema confirms the apparition of neovessels, if any, in the ischemia. It may have a certain prognosis value.
- Optical coherence Tomography (OCT): provides information regarding the macular oedema through the analysis of the thickness of the retina and the study of its different layers.
- Visual field: provides information regarding the degree of ischemia and visual prognosis.
TREATMENT
Associated ischemic diseases should always be treated when present.
A difference should be made between ischemic and non-ischemic forms as well as between Central Vein Occlusion and Branch Vein Occlusion.
CRVO and ischemic branch retinal vein occlusion:
Monthly regular follow-up checks to detect iris or angle neovascularisation. When the first signs of iris or angle neovascularisation appear laser photocoagulation of the retinal ischemic areas must be performed The presence of neovessels in the retina must be treated with laser photocoagulation to avoid the neovascularisation of the anterior segment.
CRVO and non-ischemic branch retinal vein occlusion:
- Regular checks during at least three years to detect conversion to ischemic.
- Reasonable good prognosis if it does not evolve to ischemic.
Treatment of macular oedema:
Monthly intravitreal injections of anti-angiogenic drugs (Ranibizumab and Aflibercept) while the macular oedema is present, sometimes these can be persistent.
Sustained release intravitreal implants of Dexamethasone. Implants of Fluocinolone every six months depending on the recurrence of the oedema.
Sometimes, in cases of branch vein thrombosis instead of central vein thrombosis, if visual acuity is good and the macular oedema is moderate, it can be treated with NSAIDs and high doses of topical corticoids associated to Acetazolamide, accompanied by monthly check-ups to monitor progression and response to the aforementioned treatment.