Western Visayas Medical Center

West Visayas State University – College of Medicine

CASE REPORT

Submitted by:
Lennon D. Ponta-oy
Clinical Clerk
Rotation: September 16-30, 2018
 HEALTH HISTORY

I) GENERAL DATA

Patient’s name: G. L.
Age: 63 y/o
Address: Brgy. Tabuc, Suba, Jaro, Iloilo City
Sex: Male
Nationality: Filipino
Civil Status: Single

II) CHIEF COMPLAINT

Loss of vision

III) HISTORY OF PRESENT ILLNESS

1 year prior to consult, patient experienced gradual loss of vision on his right eye. He also
complained of seeing light and shadows with associated occasional pain and tearing. However,
no consult was done.
2 days prior to consult, patient had sudden vision loss on his right eye. No tearing, pain,
and itchiness. Persistence prompted consult.

III) PAST MEDICAL HISTORY

Patient was previously diagnosed with liver cirrhosis last 2013. Patient has no diabetes
and not hypertensive. No other illnesses were noted. Patient had history of accident resulting to
fracture in the temporal area however date cannot be recalled. No food and drug allergies.

IV) FAMILY HISTORY

Patient’s mother and other relative in the maternal side were noted to have cataract.
Patient’s siblings were noted to have diabetes.

V) PERSONAL-SOCIAL HISTORY
Patient previously works as a construction worker and farmer. He is a 48 pack year
smoker. He is also a chronic alcoholic beverage drinker, claiming to drink at least 1 “lapad” of
Tanduay everyday.

PHYSICAL EXAMINATION

I) GENERAL SURVEY
The patient was alert, coherent, cooperative and responsive during the physical
examination. Well kempt and groomed. Not in cardiopulmonary distress.

II) VITAL SIGNS

Normal Values Results Interpretation

Blood Pressure 90-120 / 60-80 130/90 (right Slightly Hypertensive
mmHg arm)
Respiratory Rate 12 – 20 18 breaths/min Eupnic
breaths/min
 Pulse Rate 60-100 bpm 80 bpm Normal
Temperature 36.5-37.5 °C 36.7 °C (axilla) Normothermic
(Axillary)

III) INTEGUMENTARY:
Skin is brown, smooth, with good turgor and warm to touch. Hair is equally distributed,
black with gray to white strands at the roots; dandruff noted. Nails slightly clean with pale to pinkish
undertones. Capillary refill time less than 2 seconds. No clubbing or nail changes.

III) OPHTHALMOLOGIC EXAMINATION:

Right eye: Anicteric sclera, pinkish conjunctiva, haziness noted in lens, 2-3 mm briskly
reactive to light, visual acuity at hand movements, able to move in 6 cardinal positions of gaze,
negative red-orange reflex, and intraocular pressure at 10 mmHg.
Left eye: Anicteric sclera, pinkish conjunctiva, haziness noted in lens, RAPD noted, visual
acuity at no light perception, able to move in 6 cardinal positions of gaze, positive red-orange
reflex, cherry red spot noted, intraocular pressure at 10 mmHg.

V) HEAD, EARS, NOSE, THROAT:

Head: Normocephalic, symmetrical facial movements, no gross deformities. Able to move
jaw from one side to the other side.
Ears: Ear shape and size symmetrical to both sides. Canal walls without nodules or
lesions, no discharges. Ears are soft and pliable. No lumps, lesions or nodules in
the area around ears. Internal examination showed that tympanic membrane is
intact, pearly and translucent with no bulging or retraction.
Nose: Septum midline. Nasal passages patent. No flaring. No discharges.
Throat and Mouth: Lips were pink and slightly dry to moist. No perioral lesions noted.
Oral mucosa was pink, free of lesions, and moist. Uvula was midline. Palate is intact
and highly arched. Mallampati Class I. No redness or exudated noted on tonsils.
Dental caries noted on lower molars. Tongue was pink, symmetrical, and midline;
moves freely with no fasciculation.

VI) NECK:
Midline trachea, no nuchal rigidity, no lumps, no masses. Able to flex, extend, rotate and
lateral bend. Thyroid glands not enlarged. No thyroid bruit noted. JVP at 2 cm.

VI) CHEST AND LUNGS:

Anterior: symmetrical chest expansion, no masses or any gross deformities, no
adventitious breath sounds noted.
Posterior: symmetrical, no masses or gross deformities, crackles noted on bilateral lower
lungs fields, more prominent on the left, upon inspiration

VII) CARDIOVASCULAR:
Adynamic precordium. PMI at 5th ICS MCL. No heaves, lifts or thrills. Regular rhythm. No
murmurs and other abnormal heart sounds. Oxygen saturation at 97%.

VIII) ABDOMEN:
Flat abdomen. No tenderness. Generalized tympany over 4 quadrants. Normoactive
bowel sounds on four quadrants. No scars, striae, masses noted. No bruit.

XI) GENITALIA:
Not assessed.
XII) ANUS AND RECTUM:
Not assessed.

XIII) EXTREMITIES, TRUNK AND SPINE:

Pulses in the popliteal, posterior tibial, and dorsalis pedis arteries on both left and right
lower extremities at Grade +1; radial arteries on both left and right wrist at Grade 2+. No
crepitation and masses noted when palpating the elbow, knees, clavicles and hips. Lymph nodes
not tender and palpable. Muscle strength on bilateral upper and lower extremities is 5/5. Spine at
midline. No sacral dimpling, pigmented spots, hairy patches, ulcers, lumps or masses.

NEUROLOGIC EXAMINATION

I) CRANIAL NERVES EXAMINATION

Cranial Patient’s response

Nerves
I Able to smell.
II Visual Acuity, OD: hand movements
Visual Acuity, OS: No light perception
II, III OD: Direct and consensual pupillary reflexes present, 2-3 mm briskly
reactive to light
OS: Positive RAPD
IV,V,VI Eyes move in a smooth, coordinated motion in all 6 cardinal fields of
gaze.
V Temporal and masseter muscles contract bilaterally. Able to clench teeth
without difficulty. Eyelids blink bilaterally. Correctly identifies dull stimuli
(paper clip) and light touch (wisp of cotton).
VII Symmetrical facial expressions when smiling, raising eyebrows, puffing
cheeks and closing eyes. Taste not assessed but patient mentioned no
recent change in taste perception.
VIII Rinne and Weber tests not done. Negative Romberg’s test. Able to hear
when called.
IX
Can swallow without difficulty. Gag reflex not assessed.
X
XI Able to shrug shoulders and turn head from side to side against
resistance.
XII No deviations and fasciculations; symmetric tongue movement. Able to
move tongue from side to side.

II) MOTOR EXAMINATION

Parameter Results
Condition and Good muscle mass on both upper and lower extremities.
Movement of muscles Spontaneous movements. No fasciculations, tics or tremors noted.

Strength 5/5 on both upper and lower extremities.

 Gait and Stance Patient is able to ambulate alone and walk properly.
Coordination Patient is able to perform finger-to-nose and heel-to-shin test.

IV) SENSORY EXAMINATION

Parameter Results
Pain and Temperature Able to perceive both pain and temperature stimuli
on all dermatomal levels.
Position and Vibration Able to detect vibration on bony prominences.
Light Touch Able to perceive light touch on all dermatomal
levels.
Discriminative Sensation Able to discriminate sharp and dull sensation on
all dermatomal levels
a. Astereognosis Patient can identify object placed on both hands.
b. Agraphesthesia Patient is able to identify figure drawn on both
hands.

V) CEREBELLAR FUNCTION
Intact cerebellar function. Patient is able to perform finger-to-nose and heel-to-shin test.

VI) REFLEXES

Biceps 2+

Triceps 2+

Brachioradialis 2+

Patellar 2+

Achilles 2+

Babinski sign Negative

VI) MENINGEALS
Negative Brudzinki’s, Kernig’s and nuchal rigidity tests.

WORKING DIAGNOSIS:
Cataract OD, Central Retinal Artery Occlusion OS

I) EPIDEMIOLOGY
 Central retinal artery occlusion (CRAO) is an ocular emergency
 Incidence of CRAO is approximately 1 to 2 in 100,000 with mean age of 60-65 years.
 Usually affects adult patients with cardiovascular risk factors such as hypertension,
hyperlipidemia, and diabetes.
 CRAO is slightly more common in men than in women.
II) RISK FACTORS
• The major risk factors for CRAO can be divided into nonarteritic and arteritic.
• Nonarteritic. More than 90% of CRAOs are nonarteritic in origin. Ipsilateral carotid
artery atherosclerosis is the most common cause of retinal artery occlusion with a
prevalence as high as 70% reported among patients with CRAO or branch retinal artery
occlusion.
• Other causes of nonarteritic retinal artery occlusion include cardiogenic embolism,
hematological conditions (sickle cell disease, hypercoagulable states, leukemia,
lymphoma, etc.), and other vascular diseases, such as carotid artery dissection,
moyamoya disease, and Fabry disease.
• Arteritic. CRAO of arteritic etiology is mostly caused by giant cell arteritis, although
other vasculitic disorders such as Susac syndrome, systemic lupus erythematosus,
polyarteritis nodosa, and granulomatosis with polyangiitis have also been associated
with retinal artery occlusion.

III) ETIOLOGY
• Visual loss due to CRAO occurs once the inner two-thirds of the retina has lost its blood
supply.
• Retinal artery occlusion may be due to embolism or thrombosis.
• Emboli may come from any of the following: Atherosclerotic plaques, Endocarditis, Fat,
Atrial myxoma
• Thrombosis is a less common cause of retinal artery occlusion but can be seen with
systemic vasculitis such as SLE and giant cell arteritis, which is an important cause of
arterial occlusion that requires prompt diagnosis and treatment.

IV) CLINICAL MANIFESTATIONS

• The most common presenting complaint of central retinal artery occlusion (CRAO) is
acute, unilateral, persistent, painless vision loss in the range of counting fingers to light
perception in 90% of patients.
• Some patients with CRAO reveal a history of amaurosis fugax (transient vision loss
lasting seconds to minutes but that may last up to 2 hours), which may result from
transient CRAO.
• The clinician should inquire about the symptoms of temporal arteritis in older patients
(eg, headache, jaw claudication, scalp tenderness, proximal muscle and joint aches,
anorexia, weight loss, fever).
• Past medical history should include any medical problems that could predispose to
embolus formation (eg, atrial fibrillation, endocarditis, atherosclerotic disease,
hypercoagulable state).
• On examination, a relative afferent pupillary defect occurs regardless of the visual acuity
or macular sparing.
• Classic ophthalmoscopic signs: retinal edema (ischemic retinal whitening), cherry red
spot (due to underlying normal choroidal circulation), retinal arteriolar attenuation, and, in
the acute phase, segmentation of blood in retinal arterioles (also known as box-carring).
• A retinal embolus may be visible in up to 40% of patients. The embolic material can be a
shiny cholesterol plaque, gray-white platelet plaque, or white calcium plaque.

V) PROGNOSIS
• Most patients with CRAO continue to experience severe vision loss, in the counting
fingers to hand motion range.
 • As many as 10% of patients retain central vision because of the presence of a cilioretinal
artery. In this case, visual acuity improves to 20/50 or better in 80% of cases over a 2-
week period.
• The presence of a retinal embolus is associated with a 56% mortality rate over 9 years
compared to 27% in patients without arterial emboli.

V) MANAGEMENT
• There is no standard treatment for CRAO.
• Among the suggested treatments are noninvasive and more invasive treatments.
Some of the noninvasive treatments include ocular massage, hyperbaric oxygen (HBO)
therapy, carbogen inhalation therapy, intraocular pressure reduction (with systemic or
local agents), anticoagulation therapy, sublingual isosorbide therapy, and systemic
steroid therapy. The goal of each is to increase blood flow and blood oxygen content.
• Invasive procedures include anterior chamber paracentesis, laser embolectomy, pars
plana vitrectomy, and intraarterial thrombolysis. Most invasive procedures are aimed to
reduce intraocular pressure and lyse/dislodge the obstructive embolus, although none of
the treatments has enough supportive evidence to become the standard of care. Recent
publications demonstrated that intraarterial thrombolysis may be an alternative to
recover blood flow and vision after embolic CRAO.