Avastin Eye Injection: Key Actions and Benefits

Avastin (bevacizumab) was originally developed for cancer treatment but is now widely used in ophthalmology to manage abnormal blood vessel growth in the eye. It targets vascular endothelial growth factor (VEGF), a protein responsible for excessive blood vessel formation that can lead to vision-threatening complications.

This injection is commonly prescribed for conditions like age-related macular degeneration (AMD) and diabetic retinopathy, helping slow disease progression and preserve vision. Understanding its mechanism, treated conditions, and administration process can help patients make informed decisions about their eye care.

Molecular Structure And Anti-VEGF Action

Bevacizumab, the active component of Avastin, is a recombinant humanized monoclonal antibody that binds specifically to VEGF. Structurally, it is an immunoglobulin G1 (IgG1) antibody with two heavy and two light chains, forming a Y-shape that enables high-affinity binding to VEGF-A, the most active isoform. This prevents VEGF-A from interacting with its receptors, VEGFR-1 and VEGFR-2, which promote angiogenesis and vascular permeability. Blocking this pathway reduces pathological neovascularization and vascular leakage, key contributors to vision loss in retinal diseases.

Under normal conditions, VEGF maintains vascular homeostasis, but in disease states, its overexpression leads to fragile, leaky blood vessels. In the retina, this results in macular edema and hemorrhages, impairing vision. Clinical studies show that intravitreal bevacizumab significantly decreases central retinal thickness, as measured by optical coherence tomography (OCT), and improves best-corrected visual acuity (BCVA) in patients with neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME).

Bevacizumab has a prolonged intraocular half-life of approximately 5 to 10 days, allowing sustained VEGF inhibition and reducing injection frequency compared to some other anti-VEGF agents. However, as Avastin was originally developed for systemic oncology, its large molecular weight (approximately 149 kDa) limits rapid diffusion through retinal layers. Despite this, trials such as the CATT (Comparison of Age-Related Macular Degeneration Treatments Trials) study confirm its therapeutic effects are comparable to FDA-approved ophthalmic anti-VEGF agents like ranibizumab.

Ocular Conditions Associated With VEGF

VEGF plays a central role in retinal and choroidal diseases characterized by abnormal blood vessel growth and increased vascular permeability. One of the most studied conditions linked to VEGF dysregulation is neovascular age-related macular degeneration (nAMD). In this disorder, excessive VEGF promotes choroidal neovascular membranes (CNVs) beneath the retinal pigment epithelium, leading to exudation, hemorrhage, and photoreceptor damage. Without treatment, these vessels cause irreversible central vision loss. Clinical trials, including the CATT study, show that anti-VEGF therapy, including bevacizumab, reduces CNV activity and improves visual acuity.

Diabetic retinopathy (DR) results from chronic hyperglycemia-induced microvascular damage. As retinal ischemia progresses, VEGF levels rise in response to hypoxia, promoting fragile new blood vessels in proliferative diabetic retinopathy (PDR). These vessels are prone to rupture, leading to vitreous hemorrhage and sudden vision loss. VEGF also increases vascular permeability, worsening diabetic macular edema (DME), a major cause of vision impairment in diabetes. Randomized controlled trials, such as the DRCR.net Protocol T study, confirm that anti-VEGF agents reduce macular thickness and improve vision in DME.

Retinal vein occlusion (RVO), including central (CRVO) and branch (BRVO) subtypes, is another condition associated with VEGF elevation. Venous obstruction increases capillary pressure, causing fluid leakage and retinal ischemia. In response, VEGF levels rise, worsening macular edema and promoting complications like neovascular glaucoma. Studies, including the CRUISE and BRAVO trials, show that intravitreal anti-VEGF injections improve retinal thickness and visual acuity in RVO patients, making VEGF inhibition a key treatment approach.

Administration And Preparation

Avastin must be repackaged into smaller doses for ophthalmic use, as it was originally formulated for intravenous oncology treatment. Compounding pharmacies prepare these doses under strict aseptic conditions to prevent contamination. Each 1.25 mg/0.05 mL dose is stored in a sterile syringe under refrigeration to maintain stability.

Before administration, patients undergo an ophthalmic examination to assess disease severity. The procedure is performed in an outpatient setting under sterile conditions to minimize the risk of endophthalmitis, a rare but serious complication. The eye is anesthetized with topical or subconjunctival anesthetic drops, followed by the application of povidone-iodine to disinfect the area. A lid speculum keeps the eye open, and the injection is delivered through the pars plana, 3.0 to 4.0 mm posterior to the limbus, depending on whether the patient is phakic or pseudophakic. This placement ensures drug delivery into the vitreous cavity while avoiding damage to the lens or retina.

After the injection, intraocular pressure is briefly monitored, as transient elevations can occur. Patients are advised to report symptoms such as persistent pain, vision changes, or increased floaters, which could indicate complications like retinal detachment or intraocular inflammation. While most tolerate the procedure well, some may experience mild irritation or subconjunctival hemorrhage, both of which typically resolve without intervention. Treatment plans vary based on disease response, with some patients requiring monthly injections, while others transition to a pro re nata (PRN) or treat-and-extend regimen to optimize outcomes while minimizing injection burden.