Age-related Macular Degeneration (AMD) is a progressive eye condition and a primary cause of vision loss among older adults. This disease specifically targets the macula, a small area in the center of the retina responsible for sharp, detailed central vision. While AMD does not typically lead to complete blindness, the loss of central vision significantly impacts daily life and independence. Understanding the distinction between the two main forms, Dry AMD and Wet AMD, is important because their underlying mechanisms, progression speed, and treatment approaches are vastly different.
Dry Age-Related Macular Degeneration: Pathology and Progression
Dry AMD, also known as atrophic AMD, accounts for approximately 80 to 90% of all AMD cases. The core pathology involves the slow deterioration of the light-sensing cells in the macula and the supporting retinal pigment epithelium (RPE).
The condition is characterized by the accumulation of yellowish deposits known as drusen beneath the retina. These drusen are composed of lipids, proteins, and cellular debris, building up between the RPE and the underlying Bruch’s membrane. As drusen increase, they disrupt RPE function, leading to cell thinning and death.
The advanced stage is termed geographic atrophy, where sharply defined areas of RPE and photoreceptor cell death lead to permanent patches of missing retina. The progression of Dry AMD is typically slow, often taking many years to advance to the late stage. Early stages may cause little noticeable vision change, though Dry AMD can eventually lead to significant vision impairment.
Wet Age-Related Macular Degeneration: Pathology and Progression
Wet AMD, or neovascular AMD, comprises only about 10 to 20% of cases, but it is responsible for up to 90% of severe AMD-related vision loss. This form is defined by the growth of abnormal and fragile blood vessels from the choroid, the layer of blood vessels beneath the retina, into the macular area. This process is known as choroidal neovascularization (CNV).
These newly formed vessels are highly permeable and leak blood and fluid beneath or into the retina. This leakage causes the macula to swell and lift, rapidly damaging the retinal tissue. The growth of these abnormal vessels is stimulated by an overproduction of a protein called Vascular Endothelial Growth Factor (VEGF).
The rapid leakage and swelling can lead to the formation of scar tissue in the macula, causing irreversible central vision loss if not addressed quickly. Wet AMD frequently develops in eyes that already have intermediate or advanced Dry AMD. This results in a much more aggressive disease course compared to the slow progression of the dry form.
Distinguishing Symptoms and Rate of Vision Loss
The primary difference between the two forms lies in the patient’s experience of vision changes and the speed at which they occur. Dry AMD typically presents with a slow, progressive blurring or haziness in the central field of vision. Patients may also notice that colors appear less vibrant, and they may have difficulty adapting to low-light environments.
In contrast, Wet AMD is characterized by a sudden and dramatic change in vision. A hallmark symptom is metamorphopsia, the distortion of straight lines, making them appear wavy or crooked. This distortion is a direct result of the retinal layers being warped by the leaking fluid.
Patients with Wet AMD may also experience a rapid onset of a dark or empty spot, known as a blind spot, directly in their central vision. Because of the potential for rapid damage, patients are often advised to monitor their vision using a simple grid test, called an Amsler grid. The rate of vision loss in Dry AMD is generally measured over years, while in Wet AMD, significant central vision can be lost within days or weeks without treatment.
Management and Treatment Protocols
The management strategies for Dry and Wet AMD differ due to their underlying pathologies. For Dry AMD, the primary intervention focuses on slowing the progression of the disease in intermediate and advanced stages. This is primarily achieved through the use of specific high-dose vitamin and mineral supplements.
These supplements are based on the Age-Related Eye Disease Study 2 (AREDS2) formula, which has been shown to reduce the risk of progression to advanced AMD by approximately 25% in certain patients. The AREDS2 formula includes antioxidants and minerals such as:
- Vitamins C and E
- Lutein
- Zeaxanthin
- Zinc
- Copper
For geographic atrophy, the advanced stage of Dry AMD, new treatments are emerging that aim to reduce inflammation and slow the rate of cell death.
The treatment for Wet AMD is significantly more aggressive, focusing on neutralizing abnormal blood vessel growth and leakage. The current standard of care is the use of anti-VEGF (anti-vascular endothelial growth factor) agents. These medications are administered directly into the eye via injection and work by blocking the VEGF protein that stimulates vessel growth. Common anti-VEGF drugs, such as Aflibercept, Ranibizumab, and Bevacizumab, can stabilize or improve vision by shrinking the abnormal vessels and allowing the fluid to be reabsorbed. Anti-VEGF injections require repeated administration, often every four to twelve weeks, to maintain the therapeutic effect and prevent recurrence of leakage.