MATA TENANG DENGAN

VISUS MENURUN MENDADAK

R HANDOKO PRATOMO
RSUD ARIFIN ACHMAD / SMF MATA FK - UNRI
KASUS EMERGENSI
 KLASIFIKASI

Acute visual loss

Unilateral Bilateral

ISCHEMIC
RETINAL
VITREO- OPTIC Hemorrhagic OR OTHER
ARTERIAL AION TOXIC
RETINAL NEURITIS AMD CORTICAL
OCCLUSIONS
DAMAGE
RIWAYAT KEJADIAN
 SEKETIKA

 BEBERAPA MENIT

 SAAT BERAKTIFITAS

 SAAT BANGUN TIDUR

 DIAWALI DENGAN GEJALA MATA LAINNYA

 ADANYA PENYAKIT SISTEMIK YANG MENYERTAINYA

BUTA MENDADAK UNILATERAL

RETINAL VASCULAR
OCCLUSION
 RETINAL VASCULAR OCCLUSION

 Retinal vascular occlusions are serious diseases and

significant causes of blindness that include arterial
and venous obstructions.
 The hallmark of clinical presentation in the retinal
occlusive disease is painless loss of vision, which
can be asymptomatic, gradual with only mildly
reduced visual acuity, or sudden and reduced to
counting fingers depending on the extent of the
irrigation area of the affected vesse
RETINAL ARTERY OCCLUSION

 A condition where the retinal artery is

occluded by an embolus
 Symptom: sudden visual loss without pain
 Two types :
 Central (CRAO) - occlusion behind the lamina
cribrosa
 Branch (BRAO) - occlusion in front of lamina
cribrosa
RETINAL ARTERY OCCLUSION

Causes :
 Arteriosclerosis
 Hypertension
 Carotid arterial disease
 Diabetes mellitus
 Valvular heart disease
 Others: oral contraception, trauma,
coagulopathy, toxoplasmosis, etc.
Symptoms and signs:
 Sudden blurred vision (HM - LP)
 Calm anterior segment
 Funduscopy
 ‘cherry-red spot’ (greyish pale retina except at
the fovea)
 small arteries, uneven caliber

 small veins, segmental

CENTRAL RETINAL ARTERY
OCCULSION
CENTRAL RETINAL ARTERY
OCCULSION

Therapy:
 The aim of treatment is to quickly recover
the arterial circulation by lowering the IOP :
 paracentesis (AH aspirated 0.15 - 0.2 cc)
 Acetazolamide (Diamox) 500 mg. i.v.
 digital massage of eyeball
 inhalation of 95% O2 - 5% CO2 mixture

 Look for cause  consult Internal Medicine

Branch RAO
 If macula not involved, vision relatively stable
 Retina pale only at the involved area
 A/v changes only at the occluded branch
Complications:
 Papil atrophy
 NVI + NVG
Prognosis:
 Poor. Visual recovery only if : 1. Occlusion overcome
within 1-2 hours after onset, 2. Occlusion temporary
(spasm), 3. Cilioretinal artery present
BRANCH RETINAL ARTERY OCCLUSION
RETINAL VENOUS OCCLUSION

 Similar to RAO, painless sudden loss of

vision as presenting symptom
 Two types:
 central (CRVO)
 occlusion behind lamina cribrosa
 branch (BRVO)
 occlusion in front of lamina cribrosa
 RVO 4-5 times more often than RAO
 Causes :
 hypertension & arteriosclerosis (60%)
 Common adventitial sheath at a-v crossing.
Sclerosis --> vein compressed --> slowed flow -->
thrombus --> occlusion
 open angle glaucoma (40-70%)
 hyperviscosity (polycythemia, hyperli-pidemia,
leukemia, etc)
 thromblophlebitis
 etc.
 Symptoms and signs :
 sudden loss of vision
 calm anterior segment
 funduscopy :
 dilated and tortuous vein
 edema, hemorrhage, soft exudate

 Complication :
 NVG
 30-35% of CRVO, 1-3 months after onset
 Branch RVO :
 NVG seldom
 nasal branch --> no visual disturbance
 Prognosis :
 without NVG --> edema, hemorrhage, exudate slowly
absorbed
 Therapy :
 medical therapy of no benefit
 laser photocoagulation
 look for cause --> consult Internal Medicine
RETINAL DETACHMENT

 RD  FIRST RECOGNIZED 1700s  SAINT-Yves

 1851  Helmoltz  Clinical Diagnosis

 1920  Jules Gonin  Repair of Retinal Detachment

= ablatio retina
separatio retinae

A condition where the sensoric retinal

layer seperates from the retinal pigment
epithelium layer (RPE)
 US : 6% RETINAL BREAKS
  MOST ASYMTOMATIC BENIGN ATROPIC HOLE
 INCIDENCE 1/10.000 OR 1 /300 OVER A LIFETIME
 IDIOPATHIC RD APP 12,5%/ 100.000 OR 28.000 CASE /YR

HIGHER PREV.
 HIGH MYOPIA (>6 D)
POST CATARACT OPERATION WITHOUT IOL
CATARACT SURGERY COMPLICATION
 INTERNATIONAL

 MORBIDITY
 15% WHEN FOUND RD IN ONE EYE DEVELOP DETACHMENT
IN THE OTHER EYE
NO RACE AND SEX DIFF INCIDENCE
AGE
40-70 YR
ANATOMY OF RETINA
THE LAYERS OF THE RETINA
1. Pigment epithelium layer
2. Layer of rods and cones
3. External limiting membrane
4. Outer nuclear layer
5. Outer plexiform layer
6. Inner nuclear layer
7. Inner plexiform layer
8. Ganglion cell layer
9. Nerve fibre layer
10.Internal limiting membrane
Classification based on pathogenesis :

 Rhegmatogenous RD
 Break/tear in the retina (degnration/trauma)

 fluid from the vitreous cavity enters sub-retina  retina

detached

 Nonrhegmatogenous RD
Process behind retina (tumor/inflammation)  subretinal fluid
retina detached

 Tractional RD
Fibrosis in vitreus (bleeding/inflammation)
 retinal traction  retina detached
Subjective symptoms
 Photopsia, floaters
 due to retinal traction, vitreous bleeding
 Dark shadow/curtain
 starts peripherally
 Reduced Vision
 macular involvement or vitreous bleeding
 Metamorphopsia
 macular involvement (detached)
 Objective signs
 Low IOP

 Relatively quiet anterior segment

 Funduscopy
 Detached retina greyish in color, elevated
towards the vitreous cavity, vessels also elevated,
surface often multi-lobulated
 The history should include inquiries into the following:
 History of trauma

 Previous ophthalmologic surgery

 Previous eye conditions (eg, uveitis and vitreous

hemorrhage)

 Duration of visual symptoms and visual loss

 Physical examination should include the following:
 Checking of visual acuity
 External examination for signs of trauma and
checking of the visual field
 Assessment of pupil reaction
 Measurement of intraocular pressure in both eyes
 Slit-lamp biomicroscopy
 Examination of the vitreous for signs of pigment or
tobacco dust
 Examination of the dilated fundus with
ophthalmoscopy (preferably indirect)
 Migraine with or without aura
 Posterior uveitis
 Posterior vitreous detachment
 Retinal Artery Occlusion
 Retinal artery occlusion
 Retinal vein occlusion
 Vitreous Hemorrhage
 Vitreous syneresis
CLINICAL EXAMINATION

INDIRECT
OPHTHALMOSCOPY
CLINICAL EXAMINATION

DIRECT
OPHTHALMOSCOPY
CLINICAL EXAMINATION

DIRECT

INDIRECT
SPECIFIC EXAMINATIONS
 ULTRASONOGRAPHY
 B-scan ultrasonography (US) is very useful in the diagnosis of
RD in eyes with opaque media, particularly severe vitreous
haemorrhage that precludes visualization of the fundus.
RETINAL BREAK

Retinal tears.
 (A) Complete U-shaped;  (B)  linear; (C)  Lshaped; (D)  operculated; 
(E) dialysis 
FUNDUS DRAWING

(B) colour
coding for
documenti
ng retinal
pathology
LATTICE DEGENERATION
Clinical features of
lattice
degeneration. 

(A) Small island of
lattice with an
arborizing network
of white lines; 

(B) lattice associated
with ‘snowflakes’; 

(C) lattice associated
with RPE changes; 

(D) small holes within

lattice seen on
scleral
indentation  
LATTICE DEGENERATION
 Complications of lattice
degeneration. 

(A) Atypical radial lattice

without breaks;

 (B) two U-tears, the

larger one of which
shows a small patch
of lattice on its flap
and is surrounded by
a small puddle of
subretinal fluid;

 (C) linear tear along the

posterior margin of
lattice;

(D) multiple small holes

within islands of
lattice  
SNAILTRACK DEGENERATION

 Islands of snailtrack
degeneration, some of
which contain holes 
RETINAL DETACHMENT
RETINAL DETACHMENT
RETINAL DETACHMENT

Exudative retinal
detachment
caused by a
choroidal
melanoma 
 RETINAL DETACHMENT
 Therapy
 Rhegmatogenous
Surgery
(Retinal repositioning)
 Tractional

 Nonrhegmatogenous towards primary d.

 Surgical objectives
 close the tear
 remove subretinal fluid

 remove vitreous traction

SCLERAL BUCKLING
PNEUMATIC RETINOPEXY

Indications

RD with superior
breaks
VITRECTOMY
Introduction

 Optic neuritis

 Atypical optic neuritis

 Treatment of optic neuritis

 Optic neuritis and MS

Optic Neuritis: Epidemiology
 Incidence: 1-5 per 100 000 per year

 Highest incidence in
 Caucasians
 Countries with high latitudes: genetics?
 Springtime
 Ages 20-49
 Women
 Optic Neuritis

 Sub-acute, monocular visual loss

 Painful extraocular movements

 RAPD

 Dyschromatopsia

 Decreased contrast

sensitivity
 VF deficits
Fundus Signs of Optic Neuritis
Investigations
Based on ONTT results for “typical” optic neuritis

 Demyelination is the most common cause

 No need for laboratory investigation

 i.e. ESR, ANA

 Need to do MRI of the brain

 Assess MS risk
Atypical Optic Neuritis

 Atypical symptoms
 Unusual tempo of onset
 Absence of pain
 Co-morbidity

 Atypical signs
 Progressive decline in vision > 2/52
 Severe/hemorrhagic disc edema
 Uveitis: vitritis, retinitis, choroiditis
 Persistent ON sheath enhancement on MRI
Fundus Photos: Atypical ON
Corticosteroid Dependent Optic Neuritis

 Another atypical optic neuritis

 Response to steroids

 Vision falls with taper

 Requires investigation
Atypical Optic Neuritis: Work-up

 Laboratory investigations
 CBC, ESR, ANA, MHA-ATP, ACE
 Lyme, Baronella, TB skin test

 CXR

 Consider LP

 Make sure MRI images optic nerve/orbits

Visual Fields
 Central scotomas

 Paracentral scotomas

 Altitudinal defects
Neuroimaging

 MRI
 FLAIR sequencing
 Gadolinium enhancement

 Optic nerve sheath enhancement with gad

 Periventricular white matter lesions on FLAIR

MRI: Nerve Sheath Enhancement

MRI: White Matter Lesions
The Optic Neuritis Treatment Trial
(ONTT)

 Objective: to evaluate the role of corticosteroids

in the treatment of unilateral optic neuritis

 Inclusion criteria: unilateral optic neuritis

The ONTT: Methods

 Randomization to one of 3 groups

1. IV steroids: 250 mg methylprednisolone qid x
3 days, oral prednisone (1mg/kg) x 11 days

2. Oral steroids: prednisone 1mg/kg/day x 14

days

3. Oral placebo: 14 days

ONTT: Results
 IV steroids
 More rapid recovery but
same endpoint
 Protective v. placebo at 2
years, not 3

 Oral prednisone
 Higher rate of new ON
attacks at 1 year
 Highest rate of relapse at 5
years
The ONTT and Oral Prednisone
 Routing vs. Dose?
 Probably dose: Greater CD4 than CD8 effect
Prognosis
 Natural history: worsening over days to weeks followed by
spontaneous recovery
 79% of patients begin to recover by 3/52
 93% of patients show improvement by 5/52

 Ongoing clinical improvement to 1 year

 VEP latency improves to 2 years

Prognosis
 Severity of initial visual loss is related to final visual outcome

 Most recover well

 74% ≥ 20/20
 92% ≥ 20/40
Visual Sequelae
 Optic nerve head pallor will develop

 VF deficits may persist

 Uhtoff’s phenomenon

 Pulfrich phenomenon
Optic Neuritis Recurrence
From the ONTT

 35% of patients experienced recurrence in the

previously affected eye or an attack in the fellow eye
at 10 years

 Recurrence rate was double in those with CDMS

 Recurrence rate highest in the oral steroid group

Sub-clinical Optic Neuritis
 Not all optic neuritis attacks are clinically evident

 Sisto et al 2005
 VEP abnormalities in 54.4% of CD-MS patients
asymptomatic for visual impairment
 Vidovic et al 2005
 70% of visually asymptomatic MS patients had GVF
defects consistent with optic neuritis
Optic Neuritis and MS

 Clinical diagnosis
 2 demyelinating attacks separated in time
and space
 Sequential optic neuritis in one eye than the
other meets the criteria
 Discrete attacks in the same eye meets the
criteria
 Radiologic: Mac Donald Criteria
Optic Neuritis and MS

 Lessell et al. 1988: 58% of optic neuritis at 15

years in initially isolated cases

 38-50% of all CDMS develops optic neuritis at

some point
Radiologic Predictors of MS
10 year ONTT data

 White matter lesions on MRI

 Risk is 22% if no baseline brain lesions

 Risk is 56% if ≥ 1 baseline lesion
 Risk increases with increasing lesions
Clinical Predictors of MS
ONTT 10 year data

 Low risk if no MRI lesions and

 Male gender
 Optic disc swelling

 No CDMS in subset with above and one of

 No pain
 Severe disc edema
 Peripapillary hemorrhages
 Retinal exudates
Managing Optic Neuritis and MS
 Positive MRI
 Consider immunomodulatory therapy ie
interferon or glatiramer acetate

 Patients should be seen by neurology

CHAMPS Study

 Effect of Interferon B 1a treatment in patients

with optic neuritis and MRI changes compatible
with MS
 Significantly less CDMS
 Less progression of MRI lesions
Conclusions

 Patients must be investigated for demyelination

 Remember the atypical optic neuritis

Anterior ischemic optic neuropathy
(AION)

 Most common over 50 years

 Painless monocular over hours to days

 Visual acuity

 Visual field

 APD
AION

 Arteritic AION is associated with giant cell

arteries (GCA)
 Nonarteritic AION
AAION

 Is less frequent 5-10%

 Older patients (mean 70yr)

 Inflammatory and thrombotic occlusion post.

Cilliary artery
 Systemic symptoms
Systemic Findings of GCA

 Are usually present

 Headache, temporal and scalp tenderness
 Jaw claudication
 Malaise, anorexia, weight loss, fever, joint &
muscle pain
 Ear pain
AAION

 Sever visual loss

 Pale edema

 Cotton wool spot

 F.A. delayed choroidal filling

 Normal cup.
Treating AAION

 Immediate therapy is critical

 Temporal artery biopsy may delayed treat

 IV prednisolone 1 g/day for 3-5 days

 Then oral prednisolone 100 mg/day tapered 3-

12 month or more
Major Goals of Therapy

 Prevent contralateral visual loss

 Fellow eye involved 95% days or weeks

 Affected eye improve somewhat

 Avoid systemic vascular complication

 Risk of recurrence is 7% so tapering must be

slow and careful
Nonarteritic Anterior ISchemic Optic
Neuropathy (NAION)

 More common 90-95% of AION

 In younger age groups (mean age 60yr)

 Related to optic disc microcirculation

 On awakening, noctural systemic Hypotension

 Systemic symptoms are absent

NAION

 V.A. > 20/200 in over 60% of cases

 Palor is less common

 Optic disk in other eye is small and small or

absent cup.
 5 yr risk of other eye is 14.7% (psued-foster
kennedy syd)
Risk Factors of NAION
 Crowding of disk (disk at risk)

 Systemic hypertension

 Diabetes (young)

 Smoking, hyperlipidemia

 Hyperhomocysteinemia, platelet polymorphism, sleep

apnea
 Phosphodiestrase inhibitors (sildenafil or viagra) ??
Hypotensive effect
Differential Diagnosis of NAION

 Optic neuritis

 Infiltrative optic neuropathies

 Anterior orbital lesion

 Diabetic papillopathy
 NAION Optic neurtis
<40 >50 Age
92%+ Unusual pain
APD+ APD+ Pupil
Central Altitudinal VF
Edema 33% Edema 100% Optic disk
hyperemic pale
Unusual Common Retinal
hemorrhage
No delayed Delayed disk F.A.
filling
enhancement No optic nereve MRI
enhancement
Treatment of NAION
 Untreated case remain stable but recovery of 3 lines
31% after 2 years
 Recurrence unusual 6.4%

 No proven therapy surgery no benefit

 No proven prophylaxis

 Asprin reducing incidence of fellow eye is unclear

 summary
60 yr Mean 70 yr Age
F=M F>M Sex
None Headache … Symptoms
>20/200 60% <20/200 60% VA
Small cup Normal cup pale Fundus
Hyperemic edema edema
Mean 20-40mm/hr Mean 70mm/hr ESR
Normal Elevated C.R.P.
31% improved Rarely improved Natural history
12-19% fellow eye 54-95% fellow
eye
None proven Systemic steroids treatment
TERIMA KASIH