Ocular Manifestations In AIDS

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Ocular Manifestationsin AIDS

ANUMEHA


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Infectious :Herpes zoster ophthalmicusherpes simplex keratitis,

fungal keratitis, bacterial keratitismolluscum contagiosum,cytomegalovirus retinitis,toxoplasmic retinochoroiditis,acute retinal necrosis,progressive outer retinal necrosis,HIV retinitis, syphilitic retinitis,Pneumocystis carinii choroiditis,fungal and bacterial endophthalmitis,fungal choroiditis,neuroophthalmic disorders, Kaposi's sarcoma andBurkitt's lymphoma


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Noninfectious :subconjunctival hemorrhageConjunctival microvasculopathy,keratoconjunctivitis sicca,

peripheral ulcerative keratitis,acute angle-closure glaucomaneuroophthalmic disorders

cotton-wool spots and retinalmicrovasculopathy


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HISTORY:begins with inoculation of the virus

directly into the blood stream, by exposureof broken skin or mucous membranes toHIV-contaminated fluids, or

by perinatal transmission from infectedmother to infant


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Molluscum contagiosumproduces pearly white, centrally umbilicated skin

papules 3 to 5 mm in diameter

follicular conjunctivitis or keratitis may be seen

In the patient with AIDS, lesions have a rapidonset, are more numerous, and are larger thanin normal hosts and tend to be more resistant tostandard therapies


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Lesions of molluscum contagiosum in a patient with AIDS


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CMV retinitis:

Varients of the disease: ( based on morphology)Stages

NON GRANULAR TYPE: (hemorrhagic type)More common.

The disease progresses along the retinal bloodvessels, causing confluent areas of retinal whitening,often associated with intraretinal hemorrhages and hardexudates --described as "pizza pie" or "cheese pizza"in appearance.

Brush fire stage: The lesions progress in abrushfire manner, led by an active border. The rate ofprogression is typically slow.


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GRANULAR TYPE : peripheral type of lesion

granular appearance with satellite lesions and lesshemorrhage. Behind the advancing border is necrotic retina with

mottled pigmentation from hyperplasia of the retinal

pigment epithelium (RPE).

Retinitis follows the nerve fiber layer. Retinitis produces wide areas of necrosis, scarring, and

atrophy __ it is full thickness geographical necrotizingretinitis


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Brush fire appearance


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GRANULAR TYPE


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The area of retinal involvement divided into threeconcentric zones

zone 1 includes all of the retinal area within 2 DD ofthe center of the macula or within 1 DD of the margin ofthe optic disc

Zone 2 extends from the borders of zone 1 to theampullae of the vortex veins, zone 3 is the retina peripheral to zone 2.

Zone 1 disease affects the macula, papillomacular bundle, or opticnerve and is therefore immediately vision threatening.


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The diagnosis of CMV retinitis is a clinical onesuggested by the presence of a white, necrotic,enlarging retinitis, with or without hemorrhage, inan immunocompromised patient

ganciclovir 2.5 to 5.0 mg/kg every 8 to 12 hours IV for 2 to 3weeks Foscarnet IV bolus injection of 20 mg/kg over 30 minutes,followed by a continuous infusion of 230 mg/kg/day

Cidofovir 5 mg/kg IV once a week , intravitreal : a single 20-mginjection prevents progression for a period of 55 to 64 daysinhibit progression but not curing, CMV retinitis.


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Toxoplasmic Retinitis

occurs during newly acquired primary infection orfrom dissemination to the retina from latent extraocular

sitesC/F

floaters, photophobia, and decreased vision.

O/E:granulomatous anterior uveitis with moderate to severe

vitritisFocal areas of necrotizing retinitis anywhere in the retina

,not located next to preexisting chorioretinal scars

Associated retinal hemorrhage or rhegmatogenousretinal detachment may occur


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Toxoplasmic retinitis in a patient with AIDS


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does not resolve spontaneously in the patient with AIDS,and treatment is required

Pyrimethamine (100 mg loading dose, followed by 25 to50 mg daily) plus a sulfonamide (4 to 6 g/day) is used.

clindamycin (300 mg four times per day)

Folinic acid may be administered to reduce the incidenceof pyrimethamine-induced bone marrow suppression.

Regression may be seen within 7 to 10 days, andcomplete inactivation of the retinitis takes 3 to 4 weeks


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Inactivation of the Toxoplasma lesion after T/t


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Progressive Outer Retinal Necrosis

involvement of the outer retinaminimal vitreal inflammationand poor response to IV acyclovir

Multifocal yellow, deep retinal lesions thatrapidly become confluentEarly involvement of the macula is common, and

optic nerve inflammation may be present.Varicella-zoster virus is thought to be the agent

responsible


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Progressive outer retinal necrosis with outer retinal opacificationand overlying retinal hemorrhage.


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The prognosis is poor, with blindnessresulting from either retinal detachment or

total retinal destruction

Therapies include acyclovir, ganciclovir,vidarabine, and foscarnet, success is quitelimited.

Retinal detachment occurs in 70% ofpatients, and prophylactic laser retinopexyis ineffective.


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P. carinii infection :diagnosed before death are rare

disseminated P. carinii with involvement of thechoroidClinically

multifocal, pale, 1- to 3-mm choroidal lesionswith minimal inflammationThe lesions are slowly progressive and do notappear to interfere with vision.patients have had previous episodes of PCP andare on aerosolized pentamidine prophylaxis.


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Kaposis sarcoma:

KS occurs in approximately 10% of patients with AIDS and 20% ofpatients have ophthalmic involvement

(proliferation of vascular channels lined by malignant-appearingendothelial cells surrounded by numerous spindle-shapedcells.Extravasation of erythrocytes is often present. The cell of originis likely lymphatic endothelium )

a multifocal, malignant sarcoma characterized by vascular tumors ofthe skin, oral mucosa, and internal organs

Conjunctival KS is more common in the inferior fornix,

With orbital involvement, proptosis, ptosis, eyelid edema, anddiplopia from ocular nerve palsies may occur.

Excision, chemotherapy, radiation therapy, and cryotherapy areused, but r not curative and recurrence is common


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NONINFECTIOUS OCULAR MANIFESTATIONS :

Cotton-wool spots :most common ophthalmic complication occurs inapprox half of patientsas white spots with feathered edges on thesurface and associated with small hemorrhages.distributed near the large vessels of theposterior retinal vascular arcade, near the optic

nervedisappear approximately 2 months later


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Neuroophthalmic disorders cranial nerve palsies visual-field defects and papilledema

These may result from infectious, vascular, orneoplastic lesions involving the brain, cranialnerves, or orbit.

Visual hallucinations may occur with cerebralcortical lesions.

Extraocular motility disorders may be an earlymanifestation of intracranial disease

Ocular Manifestations In AIDS

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