CASE of AMD

PATIENT PROFILE:
Patient is MQ 62/F, domestic worker, Roman Catholic, widowed from Manila who came in
with a chief complaint of blurring of vision, OD.
History of Present Illness:
1 year PTC, patient noted slowly progressive blurring of vision (characterized as difficulty
focusing especially distant objects) occasionally associated with tearing. Not associated with
flashes/floaters, photophobia, visual field cuts, and eye pain.
6 months PTC, patient consulted an optical shop and was prescribed with reading glasses
which improved her near-vision.
In the interim, blurring of vision, OD, worsened, associated with occasional holocranial
headache, dizziness, and tearing, OD.
Persistence of symptoms prompted consult at SOJR.
Review of Systems:
(-) Fever
(-) Weight loss
(+) Insomnia
(-) Cough
(-) Colds
(-) Difficulty of breathing
(-) Orthopnea

(+) Abdominal pain (RLQ)

(+) Constipation
(+) Nocturia (3x/night)
(+) Polydipsia
(+) Numbness
(-) Joint pains
(-)Edema

Past Medical History

(+) Previous trauma: 1988 Vehicular crash, confined for 1 week
(-) Hypertension
(?) DM (never been checked)
(-) allergy
(-) Bronchial asthma
Family Medical History
(+) Hypertension
(?) DM
(+) heart disease - mother
(+) blurring of vision (unrecalled cause) grandmother
OB-GYN History
G7P7(7007) all delivered via NSVD without fetomaternal complications
s/p ligation last 1984
Menopause at 50 yo
Personal Social history
Finished high school
Currently works as a househelp
Nonsmoker
PHYSICAL EXAM
Vital signs

BP: 120/90
PR: 73
O2S: 99%
RR: 16

Nonalcoholic beverage drinker

Denies illiit drug use

HEENT

Anicteric sclerae, pink palpebral conjunctivae

(5-point eye exam to follow)
Equal chest expansion, Clear breath sounds
Adynamic precordium, distinct heart sounds,
Flabby, soft abdomen
Full equal pulses, pink nail beds, (-) edema

Chest
CVS
Abdomen
Extremties
5-point eye exam
Visual Acuity
OD
OS
Gross Eye Exam

sc
20/50 +1
20/20 -2

ph
NIPH
20/20

Extraocular
movements

Digital
Tonometry

OD
OS
Fundoscopy
OD
OS
Other ocular tests
Indirect
OD
Ophthalmoscop
y
OS
Amsler Grid

OD
OS

Soft
Soft
(+) ROR, AVR 2:3, Clear media, vessels seen
(+) ROR, AVR 2:3, Clear media, vessels seen
(+) ROR, AVR 2:3, Clear media, CDR 0.4, (+) Drusen,with
hypopigmented areas on the retina (RPE changes)
(+) ROR, AVR 2:3, Clear media, CDR 0.4 (-)
hemorrhages/exudates
(-) distortion (-) scotoma
(-) distortion (-) scotoma

DIFFERENTIAL DIAGNOSES
1. Age-Related Macular
Degeneration
2. Diabetic Retinopathy

3. Senile Cataract
4. Hypertensive Retinopathy

Diagnostic Tests

Most likely
History: Blurring of vision,
age, gender
PE: Presence of drusen and
RPE changes on IO
History: blurring of vision,
unknown history of DM,
polydipsia and nocturia on
ROS,
History: Blurring of vision,
age
History: Blurring of vision

Least likely

(-) microaneurysms (and

exudates)on IO
(-) photophobia
Grossly clear lenses
No documented hypertensive
episodes
(-) narrowing of vessels

Fluorescein angiography can be used to visualize the vascularization of the retina.

This may exhibit neovascularization, microaneurysms and narrowing or ischemia of
retinal vessels.
FBS may be taken to confirm the presence of diabetes
HbA1c may be taken to check glucose control for the past 3 months.

Primary working impression:

AGE-RELATED MACULAR DEGENERATION (non-exudative), OD
DISCUSSION: Age Related Macular Degeneration, OD
Background
Age-related macular degeneration (AMD) is the leading cause of loss of vision and
visual disability in most Caucasians aged >60 years especially in Europe and North America
characterized with clinical findings of drusen and retinal pigment epithelium (RPE) changes
which are not caused by a secondary disorder. Later stages may manifest with visual
impairments.
Drusen are extracellular deposits which are thought to be by-products derived from
immune-mediated and metabolic processes in the RPE. These are located between the RPE
and Bruch membrane. Though the exact pathophysiology of the appearance of drusen is not
yet defined, it is usually associated with increase in age.
AMD is caused by multiple interactions between genetic and environmental factors. Risk
factors are as follows:
Age
Hypertension
and
other
cardiovascular risk factors
Caucasian race
Obesity
Family
history
(mutation
of
Others: history of cataract surgery,
chromosome 1q32)
blue iris color, high sunlight
Smoking
exposure, female sex

1.

Classification
AMD can be classified in two ways

First classification categorizes the presence of abnormal neovascularization

Dry (non-exudative) AMD
most common form (>90%); clinically manifests as geographic atrophy (GA) in
advanced stages
2. Wet (exudative) AMD
much less common and is associated with a more aggressive course causing sight
loss; clinically manifests as choroidal neovascularization (CNV) and pigment
epithelial detachment

Second classifies AMD according to extent of visual impairment (The International

Age-Related Maculopathy Epidemiological Study Group)
1. Early AMD characterized by medium-large drusen, RPE hyperpigmentation and/or
hypopigmentation
2. Advanced AMD with GA and CNV

The course of this disease begins in the Bruchs membrane and RPE later
resulting in sprouting of vessels in the choriocapillaris. At the appearance of CNV,
there is note of sudden worsening of vision (central vision). At the end-stage disease,
these will result in fibrovascular or atrophic macular scar causing permanent damage
in central vision.

AMD progression: from early AMD to late AMD

Clinical Presentation
Patients can complain of distortion, blurring or a scotoma in their central
vision, in either one or both eyes. Late AMD may present with visual hallucinations.

On fundoscopy, AMD encompasses the following findings:

drusen, hyperplasia of the retinal pigment epithelium (RPE), geographic atrophy and
choroidal neovascularization (CNV). Patients with drusen and mild RPE changes may still
have normal vision. Areas of central distortion or scotoma may be detected on Amsler grid.
1-2 drusen are said to have low risk in progression to advanced AMD. Fluorescein
angiography is especially helpful for patients with wet AMD in assessing the suitability of
some treatment modalities. It may also show a window defect due to unmasking background
of choroidal fluorsence. Other diagnostic tests that may be used is an Optical coherence

tomography which shows the cross-sectional image of the retina, RPE and choroid. This may
determine the presence of pigment epithelial detachments.

OUR PATIENT came in with chief complaint of slow progressive blurring of vision of
the right eye. Her risk factors for AMD are her age, female gender and previous
sunlight exposure. On her indirect ophthalmoscopy, there was note of drusen and
RPE changes with no note of neovascularization and hemorrhages and exudates. This
puts her in the category of dry AMD. As discussed earlier, dry AMD with 1-2 drusen
does not usually progress into more serious stages.

Treatment

For non-exudative AMD, monitoring of possible disease progression is needed

by regular follow-ups with the ophthalmologist or provision of low vision aids.
Prophylactic treatment may be given such as antioxidant supplementation and
avoidance of the modifiable risk factors.
There are some interventions that may help in the improvement of vision (e.g.
miniature intraocular telescope and laser photocoagulation); however, these are
high-risk procedures and are still experimental.

Reference:
SIM of Ophthalmalogy 2012
Kanski Clinical Ophthalmology, 7th ed