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Systemic disease and
the eyeDeric De Wit
Aldrin KhanProfessor Lightman
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Common systemic diseases
affecting the eye
Infectious
Toxoplasmosis
Toxocariasis
TBSyphilis
Leprosy
HIVCMV
Non-infectiousEndocrine – diabetes,thyroid
Connective tissue
disease – RA/SLE/Wegeners/PAN/Systemic sclerosis
Vasculitides (GCA)
Sarcoidosis
Behcet’s Disease Vogt Koyanagi Haradasyndrome
Phakomatoses
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DIABETIC RETINOPATHY
1. Adverse risk factors
2. Pathogenesis
5. Clinically significant macular oedema
6. Preproliferative diabetic retinopathy
3. Background diabetic retinopathy
4. Diabetic maculopathies• Focal• Diffuse• Ischaemic
7. Proliferative diabetic retinopathy
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Adverse Risk Factors
1. Long duration of diabetes
• Obesity
• Hyperlipidaemia
2. Poor metabolic control
3. Pregnancy
4. Hypertension
5. Renal disease
6. Other
• Smoking
•
Anaemia
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Location of lesions in backgrounddiabetic retinopathy
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Signs of background diabetic retinopathy
Microaneurysms usuallytemporal to fovea
Intraretinal dot andblot haemorrhages
Hard exudatesfrequently
arranged in clumps orrings
Retinal oedema seen as thickening on biomicroscopy
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Preproliferative diabetic retinopathy
Treatment - not required but watch for proliferative disease
• Cotton-wool spots
• Venous irregularities
• Dark blot haemorrhages
• Intraretinal microvascularabnormalities (IRMA)
Signs
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Proliferative diabetic retinopathy
• Flat or elevated
• Severity determined by comparing with area of disc
Neovascularization
Neovascularization of disc = NVD
• Affects 5-10% of diabetics• IDD at increased risk (60% after 30 years)
Neovascularization elsewhere = NVE
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• Spot size (200-500 m) dependson contact lens magnification
• Gentle intensity burn (0.10-0.05 sec)
• Follow-up 4 to 8 weeks
• Area covered by complete PRP• Initial treatment is 2000-3000 burns
Laser panretinal photocoagulation
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Retinal Vein Occlusion
Second most common cause of vascular-related visual loss.
Risk factors: hypertension, age, blood dyscrasias (OCP,HRT) and
vasculitis (Behcets,sarcoidosis,AIDS,SLE)
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Retinal Artery Occlusion
Risk factors: Carotid artery atherosclerosis (CRAO), carotid emboli
(BRAO), vasculitis (GCA,SLE,PAN), coagulopathy.
OCULAR EMERGENCY - Immediate referral to ophthalmologist
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1. Soft tissue involvement• Periorbital and lid swelling
• Conjunctival hyperaemia
• Chemosis
• Superior limbic keratoconjunctivitis
2. Eyelid retraction
3. Proptosis
4. Optic neuropathy
5. Restrictive myopathy
THYROID EYE DISEASE
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Soft tissue involvementPeriorbital and lid swelling
Chemosis
Conjunctival hyperaemia
Superior limbickeratoconjunctivitis
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Signs of eyelid retractionOccurs in about 50%
• Bilateral lid retraction
• No associated proptosis
• Bilateral lid retraction
• Bilateral proptosis
•
Lid lag in downgaze• Unilateral lid retraction
• Unilateral proptosis
P i
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Proptosis
Treatment options
• Systemic steroids
•
Radiotherapy• Surgical decompression
• Occurs in about 50%• Uninfluenced by treatment of hyperthyroidism
Axial and permanent in about 70% May be associated with choroidal folds
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Optic neuropathy• Occurs in about 5%• Early defective colour vision•
Usually normal disc appearance
Caused by optic nervecompression atorbital apex by enlarged recti
Often occurs in absence of significantproptosis
R i i h
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• Occurs in about 40%• Due to fibrotic contracture
Restrictive myopathy
Elevation defect - most common Abduction defect - less common
Depression defect - uncommon Adduction defect - rare
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SARCOIDOSIS
Idiopathic multisystem disorder
Characterised by non-caseating
granulomata
More common in women 20-50 yrs
More common in blacks and Asians
? Related to mycobacteria
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SARCOIDOSIS
Systemic InvolvementLung lesions – 95%
Thoracic lymph nodes
– 50%
Skin lesions – 30%
Eyes – 30%
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SARCOIDOSIS
Ocular InvolvementAnterior segmentlesions (30%)
Conjunctival granuloma
Lacrimal gland
involvement/dry eye Acute or chronic uveitis
KPs described as‘mutton fat’ because they
are large and greasy
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SARCOIDOSIS
Ocular InvolvementPosterior segmentlesions (20%) Patchy venous sheathing
Cellular infiltrate aroundvessels
Chorioretinalgranulonmas
Vasculitis includingocclusive causing:-
Neovascularisation
Infiltrate in vitreous(vitritis) including cellclumps (snowballs)
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SARCOIDOSIS
Ocular InvolvementSheathing of the
retinal veins
Fluoresceinangiography showing
leakage and staining
at sites of sheathing
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SARCOIDOSIS
Granuloma in Fundus
Retinal and pre-
retinal
Choroidal
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SARCOIDOSIS
Granuloma in FundusOptic nerve head
granuloma
Normal optic nervehead
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SARCOIDOSIS
Systemic SignsLupus pernio affecting
the nose – a chronic
progressive
cutaneous sarcoidthat most commonly
affects face and ears
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SARCOIDOSIS
Systemic signsFacial palsy
Salivary gland
enlargement
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SARCOIDOSIS
Systemic signsHilar adenopathy on
chest x-ray
Lung infiltrate
Erythema nodosum
Arthritis
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SARCOIDOSIS
Investigations (1)CXR – to detect
pulmonary signs
Bilateral hilar lymph-
adenopathy
Pulmonary mottling
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SARCOIDOSIS
Investigations (2)
Serum angiotensin-converting enzyme
(ACE) – elevated in active sarcoidosis
Mantoux test – caution in patients who
have had BCG vaccination. Test may be
negative
Lung function tests
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SARCOIDOSIS
Investigations (3)Gallium scan showing
increased uptake in
the lacrimal and
parotid glands andpulmonary regions in
a patient with active
sarcoidosis
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SARCOIDOSIS
Treatment
Systemic steroids may be necessary in
patients with posterior segment disease
where vision is threatened, especially if
optic nerve is involved
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PHACOMATOSES
1. Neurofibromatosis
2. Tuberous sclerosis (Bourneville disease)
3. von-Hippel-Lindau syndrome
4. Sturge-Weber syndrome
• Type I (NF-1) - von Recklinghausen disease
• Type II (NF-2) - bilateral acoustic neuromas
Neurofibromatosis type 1 (NF 1)
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Neurofibromatosis type-1 - (NF-1)
Appear during first year of life
Café-au-lait spots
• Most common phacomatosis
Increase in size and number throughoutchildhood
• Affects 1:4000 individuals
• Presents in childhood• Gene localized to chromosome 17q11
Fibroma molluscum in NF 1
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Fibroma molluscum in NF-1
• Appear at puberty
• Pedunculated, flabby nodules consisting of
neurofibromas or schwannomas
• Increase in numberthroughout life
• Frequently widely distributed
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Plexiform neurofibroma in NF-1
• May be associated withovergrowth of overlying skin
• Appear during childhood• Large and ill-defined
Skeletal defects in NF 1
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Skeletal defects in NF-1
• Mild head enlargement - uncommon• Other - scoliosis, short stature, thinning of
long bones
• Facial hemiatrophy
Orbital lesions in NF 1
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Orbital lesions in NF-1
Spheno-orbital encephaloceleOptic nerve glioma in about 15%
• Sagittal MRI scan of optic nerve gliomainvading hypothalamus
•
Glioma may be unilateral or bilateral
• Axial CT scan of congenital absence of left greater wing of sphenoid bone
•
Causes pulsating proptosis without bruit
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Eyelid neurofibromas in NF-1
Nodular Plexiform
May cause mechanical ptosis May be associated with glaucoma
Intraocular lesions in NF-1
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Intraocular lesions in NF-1Lisch nodules
Very common - eventually presentin 95% of cases
Congenital ectropion uveae
Uncommon - may be associatedwith glaucoma
Retinal astrocytomas
Rare - identical to those seen in
tuberous sclerosis
Choroidal naevi
Common - may be multifocal
and bilateral
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Ocular features of NF-2
Common - combined hamartomas of RPand retina
Very common -presenile cataract
Tuberous sclerosis (Bourneville disease)
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Tuberous sclerosis (Bourneville disease)
• Diffuse thickening overlumbar region
• Present in 40%
Shagreen patches
• Autosomal dominant• Triad - mental handicap, epilepsy, adenoma sebaceum
Adenoma sebaceum
• Around nose andcheeks
• Appear after age 1
and slowly enlarge
Ash leaf spots
• Hypopigmented skin patches
• In infants best detected usingultraviolet light (Wood’s lamp)
Systemic hamartomas in tuberous sclerosis
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Systemic hamartomas in tuberous sclerosisAstrocytic cerebral hamartomas
• Slow-growing periventricular tumours
• May cause hydrocephalus, epilepsy andmental retardation
• Usually asymptomatic andinnocuous
• Kidneys (angiomyolipoma), heart
(rhabdomyoma)
Visceral and subungual hamartomas
Retinal astroc tomas in t bero s scleritis
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Retinal astrocytomas in tuberous scleritis
Dense white tumour Mulberry-like tumour
Early
• Innocuous tumour present in 50% of patients• May be multiple and bilateral
Semitranslucent nodule White plaque
Advanced
Systemic features of v-H-L syndrome
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Systemic features of v H L syndromeAutosomal dominant
• Tumours - renalcarcinoma and
phaeochromocytoma
• Cysts - kidneys, liver,pancreas, epididymis,ovary and lungs
• Polycythaemia
CNS Haemangioblastoma
MRI of spinal cord tumour
Angiogram of cerebellartumour
Visceral tumours
Retinal capillary haemangioma
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Retinal capillary haemangiomain v-H-L syndrome
Round orange-red mass
Early
• Vision-threatening tumour present in 50% of patients• May be multiple and bilateral
Tiny lesion betweenarteriole and venuole
Small red nodule
Associated dilatation and
tortuosity of feeder vessels
Advanced
Systemic features of Sturge Weber syndrome
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Systemic features of Sturge-Weber syndrome
• Congenital, does not blanchewith pressure
• Associated with ipsilateralglaucoma in 30% of cases
Naevus flammeus
• CT scan showing leftparietal haemangioma
• Complications - mental handicap,epilepsy and hemiparesis
Meningeal haemangioma
Ocular features of Sturge-Weber syndrome
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Ocular features of Sturge Weber syndrome
Normal eye
Buphthalmos in 60% May be associated with
episcleral haemangioma
Affected eye
Diffuse choroidal haemangioma
Glaucoma
Peripheral corneal involvement in
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Peripheral corneal involvement inrheumatoid arthritis
• Chronic and asymptomatic
• Circumferential thinning with intactepithelium (‘contact lens cornea’)
• Acute and painful
• Circumferential ulceration andinfiltration
Treatment - systemic steroids and/or cytotoxic drugs
Without inflammation With inflammation
Peripheral corneal involvement in
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Peripheral corneal involvement inegener granulomatosis and polyarteritis nodo
Circumferential and centralulceration similar to Mooren ulcer
Unlike Mooren ulcer sclera may alsobecome involved
Treatment - systemic steroids and cyclophosphamide
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
(Temporal or Cranial Arteritis)Idiopathic vasculitis
Same disease spectrum as polymyalgia
rheumatica
Mainly women 65-80 years old
Medium and large arteries in head & neck
involved
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
PresentationHeadache
Scalp tenderness
Thickened temporal
arteriesJaw claudication
Acute visual loss
Weight loss, anorexia,
fever, night sweats,malaise & depression
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Ocular ComplicationsTransient monocular visual loss (amaurosisfugax)
Visual loss due to Central retinal artery
occlusion (CRAO) or
Anterior ischaemicoptic neuropathy
(AION)Visual field defects
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
ManagementESR if suspected
Start high dose steroids immediately to
prevent stroke or second eye involvement
Temporal artery biopsy within a week of
starting steroids
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Temporal Artery BiopsyArteries have skiplesions
ultrasound/Doppler mayhelp identify involved
areasIf positive, confirmsdiagnosis – helpful inmanagement of futuredisease
If negative, doesn’texclude diagnosis, butneed to think about analternative diagnosis
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
HistopathologyGranulomatous cell
infiltration
Giant cells
Disruption of internalelastic lamina
Proliferation of intima
Occlusion of lumen
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Treatment
Intravenous and oral steroids – prolonged
course of steroids often necessary
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Ocular manifestations of
HIV infection
I t d ti
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Introduction
AIDS is an infectious disease caused by the gradual
decrease in CD4+ T lymphocytes causing
subsequent opportunistic infections and neoplasia. It
is a blood borne and sexually transmitted infection
caused by the HIV (Human Immunodeficiency Virus) Approximately 36 million persons around the world
are infected. Up to 70% of patients infected with HIV
will develop some form of ocular involvement, ie:
direct infection by HIV,opportunistic infections andneoplasia.
HIV infection progresses though different phases
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Ophthalmic Manifestations of HIV Infection
AROUND THE EYE
Molluscum Contagiosum
Herpes Zoster
Ophthalmicus
Kaposi’s Sarcoma Conjunctival Squamous
Cell Carcinoma
Trichomegaly
FRONT OF THE EYE
Dry Eye
Anterior Uveitis
BACK OF THE EYE
Retinal Microvasculopathy
CMV Retinitis
Acute Retinal Necrosis
Progressive Outer RetinalNecrosis
Toxoplasmosis
Retinochoroiditis
Syphilis Retinitis
Candida albicansendophthalmitis
NEURO-OPHTHALMIC
M ll C t i
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Molluscum Contagiosum
Molluscum contagiosum is a
viral infection of the skin.
Affects up to 20% of
symptomatic HIV infected
patients.
Clinically appears like painless,
small, umbilicated nodules,
which produce a waxy
discharge when pressured.
Treatment consists on excisionof the lesion, curettage or
cryotherapy
Herpes Zoster Ophthalmicus
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Herpes Zoster Ophthalmicus
Due to the reactivation of a latent infection by Varicella
Zoster Virus in the dorsal root of trigeminal nerve
ganglion.
It manifests with a maculo-papulo-vesicular rash whichoften is preceded by pain. Usually involves the upper lid
and does not cross the midline
Treatment consists on oral Aciclovir 800mg 5 times
/day. In immunocompromised patients Aciclovir is givenintravenously for two weeks. Ocular manifestations
such as anterior uveitis, are treated with topical steroids
and mydriatics.
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Kaposi’s Sarcoma
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Kaposi s Sarcoma
Kaposi’s sarcoma is a vascular neoplasm which is almost
exclusively seen in patients with AIDS.
KS is the commonest anterior segment lesion seen in AIDS;
appears as a violaceous non-tender nodule on the eyelid or
conjunctiva.
Typically KS involves only the skin but when there is a
reduced CD4 count it can progress rapidly to other sites
such as the gastrointestinal tract and CNS
Treatment of ocular adnexal KS may be necessary for
cosmesis and to relieve functional difficulties. The mainstay
of treatment is radiotherapy. Other options include
cryotherapy or chemotherapy.
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Conjunctival Squamous Cell Carcinoma
Squamous cell carcinoma (SCC) is the third mostcommon neoplasm associated to HIV infection. This may
be due to an interaction between HIV, sunlight and
Human Papilloma Virus infection.
SCC appears as a pink, gelatinous growth, usually in theinterpalpebral area. Often an engorged blood vessel
feeding the tumour is seen. It may extend onto the
cornea, but deep invasion and metastasis are rare.
The treatment of choice is local excision and cryotherapybut the presence of orbital invasion is an indication of
exenteration
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T i h l
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Trichomegaly
Trichomegaly or hypertrichosis is an
exaggerated growth of
the eye lashes found in
the later stages of thedisease
The cause is not known
When symptomatic or for
cosmetic reasons theeyelashes can be
trimmed or plucked
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Dry EyeSicca syndrome is
frequent amongpatients with HIV
infection
Patients complain of
burning uncomfortablered eyes.
There are several
causes of dry eye in
HIV infection from
blepharitis to
destruction of the
lacrimal glands.
Treatment is with tear
supplements
Anterior Uveitis
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Anterior Uveitis
HIV related anterior uveitis can
be: Direct manifestation of the
human immunodeficiency
virus infection
autoimmnune in origin drug induced ie: rifabutin,
secondary to direct toxic
effect upon the non-
pigmented epithelium of the
ciliary body
Any of the different infections
associated with AIDS, ie:
Herpes Zoster Virus, Herpes
Simplex Virus,
Rifabutin induced anterior uveitis
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Rifabutin induced anterior uveitis
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Retinal microvasculitis
Retinal microvasculopathy occurs in more than half of thepatients with HIV
It is seen as transient cotton wool spots (CWS), intra-retinal
haemorrhages and microaneurysm, which occurs in 50-70% of
patients. It is usually asymptomatic.It has an unclear pathogenesis, but it is thought to be HIV
infection of retinal vascular cells.
In an otherwise healthy individual the presence of CWS, should
be differentiated from other forms of retinopathy, such asdiabetic or hypertensive retinopathy. Serological test for HIV will
confirm the diagnosis
Treatment is based in delaying the progression of the disease
associated with HIV
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Cotton Wool Spots
CMV Retinitis
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CMV Retinitis
Introduction
CMV Retinitis is the commonest intraocular ocular opportunistic infectionseen in patients with AIDS
Antibodies are found in almost 95% of adults, causing a trivial illness in
immunocompetent adults, however severe immunosuppression causes
viral reactivation and tissue invasive disease
Pathogenesis
Reactivation from extraocular sites leads to seeding in other sites such
as the retina
Epidemiology
The number of newly diagnosed cases of CMVR has decreased sincethe introduction of the HAART
Highly Active Antiretroviral Therapy
CMV Retinitis
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CMV Retinitis
Clinical manifestations
Patients may complain of minor visual symptoms such as floaters,flashing lights or mild blurred vision, or be totally asymptomatic.
It presents with a wide range of clinical appearances. From cotton wool
spots which may look like HIV Retinopathy to confluent areas of full
thickness retinal necrosis and vasculitis. CMVR can progress in a
“brushfire” pattern from the active edge of an active lesion. The retinalvessels in an affected area show attenuation, becoming ghost vessels
eventually.
Treatment
The treatment of CMVR in patients with AIDS requires the use of specific
antiviral agents, ganciclovir, foscarnet or cidovir in conjunction withHAART.
These treatments can be administered orally, intravenously or
intravitreally. Systemic treatment has the advantage of treating infection
elsewhere in the body as well as the other eye but has the
disadvantages of systemic side effects.
CMV Retinitis
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CMV Retinitis
Acute Retinal Necrosis
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Acute Retinal Necrosis
ARN is a confluent peripheral whitening of the retina withmarked vitritis and blood vessel closure. Optic neuritis
and retinal detachment are frequent complications.
ARN is usually due to Varicella-Zoster infection, but it can
also be caused by Herpes Simplex virus or
Cytomegalovirus.
Initially described in the immunocompetent, it has also
been described in the immunosuppressed.
The diagnosis is mainly clinical and is confirmed by PCR
assays on vitreous samples.
Patients are treated with high doses of intravenous
aciclovir or famciclovir, combined with laser treatment to
prevent retinal detachment.
Acute Retinal Necrosis
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Acute Retinal Necrosis
rogress ve u er e naNecrosis
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Necrosis
(Varicella-Zoster Retinitis)
PORN is a devastating viral retinitis caused by Varicella-Zoster virus, without vitritis or retinal vasculitis.
The retinitis can be located anywhere but it is common for the
lesions to coalesce and spread posteriorly in a rapid fashion.
The main symptom is rapid loss of vision.The retina showstypically a white lesion with no haemorrhages or exudates.
Treatment is often unsatisfactory and usually requires
combination of Ganciclovir and Aciclovir. The prognosis is very
poor and retinal detachment is common. Resolution may leavea white plaque with the appearance of “cracked mud”.
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Toxoplasma Retinochoroiditis
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Toxoplasma Retinochoroiditis
Toxoplasmosis retinochoroiditis is an uncommoninfection of the eye in AIDS. Ocular toxoplasmosis in HIV
positive patients is different in appearance from
immunocompetent patients. Unlike in immunocompetent
patients, HIV infected patients often have bilateral andmultifocal disease associated with anterior uveitis and
vitritis but unlike immunocompetent patients, in HIV
infected patients often have with no pigmented scars
adjacent to the areas of retinal necrosis. Toxoplasmosis
in immunocompromised patients is not self-limiting as it
is in imunocompetent patients.
Toxoplasma Retinochoroiditis
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Toxoplasma Retinochoroiditis
When testing patients for antibodies to toxoplasmosisboth IgG and IgM levels may be raised, but in
immunocompromised patients these tests may be
negative.
Treatment in immunocompromised patients consists inthe association of sulphadiazine or clindamycin,
pyrimethamine and folinic acid (triple therapy).
Long term maintenance treatment may be needed in
order to prevent relapses.Often associated with toxoplasma lesions in the Central
Nervous System.
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MRI T1 showing an uniformly
enhancing lesion in the
midbrain
One week later, the lesion
showing ring enhancement
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Immunocompetent Immunocompromised
Syphilis Retinitis
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Syphilis Retinitis
There is a strong association between syphilis andHIV infection.
It can manifest as a retinitis with dense vitritis,
retinal vasculitis, serous retinal detachment or
neuroretinitis, as well as other types of ocular involvement such as, conjunctivitis, anterior uveitis,
cranial nerve palsies and optic neuritis.
Treatment consists in high dose of intravenous
Penicillin for 2 weeks.
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Candida albicans
d hth l iti
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endophthalmitis
Infection with candida albicans is rare. Candida albicansis the commonest cause of fungal endophthalmitis
Affected patients usually have a history of drug abuse
or indwelling central lines
In the initial stages, floaters are the main symptom. Asthe condition progresses, whitish “puff -balls” and
vitreous strands develop. Later, similar infiltrates appear
in the choroid and retina
The treatment depends on the severity of the ocular involvement and systemic disease. The original foci
should be removed. The drugs of choice are
Amphotericine B and Fluconazol
Candida albicans
d hth l iti
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endophthalmitis
Glossary
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y
CD4: Director of the immune response. When activated it
releases cytokines which in turn will activate the immunesystem
Cotton Wool Spots: Light-coloured deposits in the retina
secondary to infarcts of the nerve fibre layer
HAART: Highly Active Antiretroviral TherapyImmunoblogulin: Protein in charge of fighting foreign
substances in our body. IgG is the commonest type of
immunoglobulin and IgM is the earliest class
of immunoglobulin.PCR: Polymerase Chain Reaction is a technique used to make
numerous copies of an specific portion of DNA
VDRL: Venereal Disease Research Laboratory. The test
becomes negative after successful treatment of the disease.
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