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 60% ocular manifestation is first manifestation 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