Download Systemic disease in ophtlhalmology

Systemic disease in
ophtlhalmology
MR NIYOUSHA. MD
HIV ocular manifestation
1 . HIV retinopathy
2- Opportunistic Infections
Ocular disease occurs in 50–75% of HIV-infected patients
The most common manifestation is HIV microvasculopathy, followed
by cytomegalovirus (CMV) retinitis, ocular toxoplasmosis, non-CMV
herpetic retinitis, herpes zoster ophthalmicus (HZO), and ocular
neoplasia
HIV microvasculopathy
Hypotheses regarding the pathogenesis of retinal microvasculopathy
include :
HIV-induced increase in plasma viscosity,
HIV-related immune complex deposition
The clinical spectrum of HIV retinopathy includes
infarct of the nerve fiber layer (often called cotton-wool spots),
retinal hemorrhages,
telangiectasia,
lack of capillary perfusion,
vascular occlusion
CMV
The most common AIDS-related opportunistic infection and remains an
important cause of visual morbidity.
CMV retinitis frequently occurs in AIDS patients with a CD4+ count <50
cells/uL and is the most common ocular opportunistic infection associated
with AIDS
Toxoplasmosis
Larger lesions
Bilateral more common
Lower inflammation
Multiple lesions
JIA
Pauci - articular
poly – articular
Still disease
JIA
Eye is usually quiet .
10 – 15 % chronic uveitis
periodic ocular examination is needed.
Risk factors
Female
Pauci articular
ANA +
RF
Treatment
Corticosteroids
Long lasting flair
Mydriatic
NSAIDs and Imunomedulatory Drugs
Marfan Disease
AD
Zonolysis
Lens Subluxation
Retinal detachment
The most important one to be differentiated from Marfan
syndrome is surely homocystinuria.
lens dislocation is usually
downward—atypical for Marfan syndrome
Marfan disease
Retinal detachment is the most serious ocular complication in Marfan syndrome.
The incidence lies between 8% and 25.6%
It is more common in the younger age, with an average age of 22 years.
Myastenia Gravis
Auto immune disorder
Female > male
3rd and 4th decade
Circulating Antibodies against Neuromuscular junction
Muscle weakness
Improvement with rest
Evening worse than morning
Myastenia Gravis
Ocular involvement in 90% of patients
60% ocular manifestation is first manifestation
Deteriorates by β Blocker , CCB, Aminoglycosides , Corticosteroids
Ocular manifestation
Ptosis
Unilateral and bilateral
Symmetric or nonsymmetric
Diplopia
Any kind of strabismus
Pupil involvement
Diagnosis
Tensilon test
Sleep test
Ice test
Circulating auto antibodies
Paraclinic
CT scan of chest and neck
Search for thymoma
Methanol Poisoning
Max serum level
30- 60 min
Max toxic effect
12 – 24 hr
20 cc can cause death
15 cc can cause blindness
Methanol Poisoning
Acidosis and vision loss
Vision loss and constricted visual field
Complete blindness
Methanol Poisoning
Pupil reaction is reduced
Ocular Muscles paresis and ptosis may happen
Metabolic injury to optic nerve and retina
Optic disk Hyperemia
Treatment
Gastric lavage
Acidosis treatment
Ethanol
Hemodialysis
So methanol level is not detectable
Vit B12 1000 mg daily
Acid folic 1mg daily
Corticosteroid 2mg/kg
Chloroquine
Central visual loss : Maculopathy
Depends on total dosage used
Hydroxychloroquine better tolerated
Chloroquine
Slit lamp examination
Macular pigmentary changes
Examination every 6 months
May be Non Reversible
May progress despite halting the drug
Bull eye maculopathy
Corticosteroids
Cataract
Glaucoma
Hepes simplex recurrences
Keratitis
Hypertension
Hypertension directly affects the retinal and choroidal circulations, causing hypertensive
retinopathy and choroidopathy.
Hypertension is associated with :
acceleration of diabetic retinopathy and
increases the risk of retinal vascular occlusion,
ischemic optic neuropathy,
retinal artery macroaneurysm
Because hypertension is frequently asymptomatic, the presenting signs or symptoms
may be visual
Hypertensive retinopathy is the most common ophthalmic manifestation of hypertension
with a reported prevalence of 2–14% in nondiabetic adults over age 40 years
Hypertensive retinopathy is associated with increased risks of stroke, cognitive
impairment, and cardiovascular death
Initially, retinal arteriolar constriction occurs as part of an autoregulatory mechanism.
With continued disease, breakdown of the inner blood-retinal barrier
occurs, with subsequent hemorrhages and exudates, followed by retinal edema
In advanced cases, optic nerve edema (hypertensive optic neuropathy) may ensue,
which is caused by ischemia leading to axonal edema