AGE-RELATED

MACULAR DEGENERATION
Fatima
Contents
 Case presentation
 What is AMD?
 Risk Factors
 Atrophic AMD
 Clinical Features
 Diagnosis
 Treatment
 Exudative AMD
 Clinical Features
 Diagnosis
 Treatment
 Discussion
 References
Case Presentation ♂
 77 year old gentleman
 Known case of hypertension, BPH, presbyopia and dementia
 Presenting complaint: Burning sensation in both eyes
 HOPC: The patient started experiencing the symptoms 2 months back. The burning was occasionally
accompanied with watery discharge and redness.
 The patient had essentially come to Dr. Jeeva’s clinic to seek a second opinion after being diagnosed
with cataract. He also complained of a metallic taste in his mouth ever since he started using
Flurobioptal eye drops and Multipack Forte, which he later discontinued after 1 month of use.
 Examination and Investigations:
 Visual Acuity: 20/70 (R) 20/60 (L)
 IOP : 12 mm Hg (B/L)
 Lens: Nuclear sclerosis
 Slit lamp: Positive findings indicative of cataract and ARMD
 B scan: Normal

A provisional diagnosis of Macular Degeneration (R>L), B/L Cataract and dry eyes was made. The
patient was advised to start off by getting an OCT done to determine if the degeneration is still
active. Furthermore, he was also advised to get biometry done to establish a plan for cataract
surgery. Moreover, the patient was counseled about preventing his eyes from getting dry and about
compliance regarding vitamin supplementation.
 What is AMD?
Age-related Macular Degeneration (AMD) is a degenerative disease of the retina. As the name
suggests, if primarily affects the macula resulting in loss of central vision. Patients usually present
with gradual or acute onset vision loss and metamorphasia. It can include either one or both eyes.

It can be classified into 2 categories for clinical purposes:

 Atrophic AMD

 Exudative AMD

Patients with late AMD or even moderate vision loss due to non-advanced AMD in one eye, have
about a 50% chance of developing advanced AMD in the other eye within 5 years.
Risk Factors
 Age > 50 years
 Caucasians
 Positive family history
 Hypertension
 Obesity
 Smoking
 Excessive Aspirin use
 Excessive exposure to sunlight
 Cardiovascular diseases
 Chronic Myeloproliferative diseases
 Alcoholism
 Cataract surgery
Atrophic AMD
Atrophic AMD also known as dry/non-neovascular AMD is the most common form. It
comprises almost 90% of all AMD cases.
The exact pathogenesis of Dry AMD is unknown but there is some evidence that
abnormalities in components of Bruch's membrane may be important.
Symptoms consist of gradual impairment of vision over months or years. Both eyes are
usually affected, but often asymmetrically.

Dry AMD or nonneovascular AMD is characterized by :

 nodular, hard drusen (localized deposits of extracellular material), with sharp edges
 diffuse soft drusen
 RPE hyperplasia and hyperpigmentation.
 Geographic atrophy (GA) is the advanced stage of dry AMD,

The risk for progression to wet or neovascular AMD increases with increasing number and
size of drusen and the presence of RPE pigmentary abnormalities.
 The bright yellow drusen are coalescing, and a large
Small, bright yellow drusen are visible area of atrophy is seen in the macula (arrow)
 Exudative AMD
It is also called wet or neovascular ARMD. It is responsible for only 10% cases of ARMD but is associated with
comparatively rapidly progressive marked loss of vision and legal blindness.
The pathogenesis of Wet AMD is better understood than Dry AMD. Choroidal neovascularization is controlled
by a dynamic balance between membrane-bound and diffusible substances with properties that either
promote or inhibit blood vessel development. VEGF is implicated in intraocular neovascularization associated
with age-related macular degeneration.

Wet AMD or neovascular AMD is characterized by :

Drusens with retinal pigment epithelial detachment (PED) seen as sharply circumscribed dome-shaped
elevation.
 Choroidal neovascularization (CNV) proliferating in sub-RPE spac is seen as greyish green or pinkish yellow
raised lesion.
Haemorrhagic pigment epithelial detachment (PED). It appears as dark elevated mount.
Haemorrhagic detachment of neurosensory retina which assumes diffuse outline and a lighter red colour
around and adjacent to the PED.
 Disciform sub-retinal scarring in the macular region may result from gradual organization of blood with
further fibrovascular ingrowth.
A large area of subretinal hemorrhage is Areas of blood vessel leakage are present, with a
present. large disciform scar (arrow).
 Diagnosis
 Clinical diagnosis is made from the typical signs described, which are best elucidated
on examination of the macula by slit-lamp biomicroscopy.
 Fundus fluorescein angiography and indocyanine green angiography help in detecting
choroidal neovascularization (CNV) in relation to foveal avascular zone. CNV may be
classical or occult.
 Optical coherence tomography (OCT) reveals subretinal fluid, intraretinal thickening,
choroidal neovascularization and haemorrhages in exudative ARMD

OCT showing nodules associated with the RPE OCT- outer retinal tubulations
Treatment
 Treatment of non-exudative ARMD:
 Dietary supplements and antioxidants.
 Amsler grid used regularly allows the patients to detect new or progressive
metamorphopsia prompting them to seek ophthalmic advice.
 Refraction with increased near add may be helpful in early cases.
 Low vision aid may be needed in advanced cases of geographical atrophy.
 Treatment modalities available for exudative ARMD :
 Intravitreal anti-VEGF therapy has become the treatment of first choice for all CNV
lesions.
 Photodynamic therapy (PDT) is the treatment of choice after anti-VEGF injections for
subfoveal and juxtafoveal classic CNVM.
 Transpupillary thermotherapy (TTT) with a diode laser may be considered for subfoveal
occult CNVM.
 Double frequency and YAG 532 nm photocoagulation may be used for extrafoveal
choroidal neovascular membrane (CNVM) treatment.
 Submacular surgery to remove CNVM and macular translocation surgery.
 Discussion
AMD is a very diverse and interesting pathology, that I had the fortune of seeing in Dr.
Jeeva’s clinic. After reading into this case and realizing that there is no effective
treatment course for Dry AMD, it shows that there is so much more room for exploration in
the field of ophthalmology. It is cases like these, although simple yet intriguing that tend
to keep students such as me involved in the clinic. A good example of this is how I returned
to clinic after a couple of hours to inquire if the patient had come back to get their OCT
done that day, only so I could figure out what was going on.
It is also interesting to note that my interest in following up with the patient was further
enhanced when I witness Dr. Jeeva’a counselling skills. Not only was he professional but
even more than that he was compassionate when communicating the next steps of the plan
to the patient. He explained to the patient their priority in a very crisp but calm manner,
something that is hard to appreciate in most clinics.
Furthermore, it is clinics and cases such as these that encourage me to go back, learn and
then come next time with even more enthusiasm. Not only is this way of learning
interesting, it is also much more effective in terms of grasping concepts and retention of
facts.
References

 N Engl J Med. 2004 Jul 22;351(4):320-2. Age-related macular degeneration

and the extracellular matrix. Johnson LV1, Anderson DH.
 https://
www.uptodate.com/contents/age-related-macular-degeneration-clinical-pres
entation-etiology-and-diagnosis#H3
 A K Khurana comprehensive Opthalmogology (2015)
 Endocr Rev. 2004 Aug;25(4):581-611. Vascular endothelial growth factor:
basic science and clinical progress Ferrara N1.
 Kanski’s clinical ophthalmology- A systematic approach (8th Edition)