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Ocular Manifestations of Systemic Diseases
Endocrine-Metabolic Diseases
Diabetes Mellitus
Lids: Recurrent styes, xanthelasma and blepharitis.
EOMs: Paralytic squint with diplopia (The commonest is the lateral
rectus)
Iris: May show Rubeosis irids (neovascularization of iris):Spontaneous
hyphema and neovascular glaucoma may occur.
Lens: Cataract (True diabetic cataract; below 30 years, Pre-senile cataract), Changes
in refraction (Hyperglycemia causes index myopia, Hypoglycemia causes index
hypermetropia).
Vitreous: Hemorrhage (PDR).
Retina: Diabetic retinopathy (NPDR, PDR).
Optic nerve: Retrobulbar neuritis, diabetic papillopathy.
Postoperative complications: Infection and delayed wound healing.
Thyroid Eye Disease
Retraction of the eyelids (highly specific) and eyelid lag on downward gaze (von
Graefe sign), lagophthalmus.
Unilateral or bilateral axial proptosis.
When EOM are involved, elevation and abduction are commonly restricted and
there is resistance on forced-duction testing.
Vitamin Deficiency
Vitamin A Deficiency: Xerosis, Keratomalacia, Nyctalopia.
Vitamin C deficiency: Scurvy (spontaneous hemorrhages in conjunctiva, retina and orbit,
lens opacities, delayed healing of wounds, diminished resistance to infection).
Vitamin D deficiency: rickets and osteomalacia. It may be related to Cataract, Myopia.
Vitamin K deficiency: leads to bleeding tendency. It leads to excessive bleeding during
operations and spontaneous hemorrhages.
Vitamin B Deficiency :as follow
Vitamin B Deficiency
• Vitamin B1 (thiamin) deficiency produces beri -beri, retrobulbar neuritis and
ophthamoplegia.
• Vitamin B 2 (riboflavin) deficiency produces angular stomatitis, glossitis
peripheral corneal neovascularization, macular degeneration, papilloedema.
• Vitamin B 12 (cyanocobolamine) deficiency produces pernicious anaemia .The
eye shows the changes of severe anaemia.
• Vitamin B 7 (nicotinic acid) deficiency produces pellagra. The eye shows
retrobulbar neuritis and muscle palsy (occur with pellagra lateral sclerosis).
Roth spots in pernicious anaemia
Bitot's spots
Blood Diseases
Anaemia
Pallor of conjunctiva.
Fundus shows: Pallor, dilated vessels, hemorrhages , papilloedema.
Lens opacities may occur.
Primary optic atrophy may occur.
Polycythemia
Dilated conjunctival vessels.
Fundus:dilated veins, CRVO may occur.
Leukemia
The ophthalmic manifestations of leukemia can be divided into:
•1ry or direct infiltration of neoplastic cells (leukemic infiltrates and white-centered retinal hemorrhages).
•2ry or indirect involvement from nonviable or dysplastic cells, or from chemotherapy, leading to hematologic
abnormalities (anemia, thrombocytopenia and hyper-viscosity).
Symptoms: blurred vision, floaters
Findings: cellular infiltration of vitreous; infiltrative lesions of retina, optic nerve, or uvea;
multiple hemorrhages, Roth spots, cotton wool spots (CWS); pseudohypopyon, spontaneous
hyphema, uveitic glaucoma, cataract
Optic nerve infiltration causes loss of vision and papilledema.
Orbital infiltration (rare) causes proptosis, lid swelling, ecchymosis. (1-2% of patients)
a. left proptosis with PL vision,
b. ON thickening on T1-weighted MRI scan of the orbit and brain,
c. ONH and retinal infiltrates, with combined central retinal vein and artery occlusions.
d. After further chemotherapy, vision did not improve due to severe optic neuropathy.
Connective Tissue Disorders
Systemic Lupus Erythematosus (SLE)
Inflammation in SLE is caused by the formation of autoantibodies and immune complexes, can cause inflammatory
responses and activate the complement system. Ocular involvement is moderately common.
Eyelid: irritating, erythematous scaly plaque, which can involve the lid margin and can be complicated by scarring
and madarosis.
keratoconjunctivitis sicca [2ry Sjögren’s syndrome (SS)]: is the most common ocular feature of SLE.
Orbital involvement (rare): myositis.
Cornea: superficial punctate keratitis and may be 2ry to SS.
Episcleritis and scleritis.
Retinopathy: 3 types of direct retinal damage by lupus: microangiopathy, severe vaso-occlusion and vasculitis.
Neuro-ophthalmic manifestations (not common): optic neuritis, myasthenia gravis, visual field defects and optic
disc oedema.
Rheumatoid arthritis (RA)
RA is an inflammatory arthritis associated with a variety of extra articular manifestations
Dry Eye Syndrome is the most common ophthalmic manifestation; women are 9 times more
commonly affected than men.
Scleritis and Episcleritis are the 2nd most common ocular manifestation of RA.
Peripheral ulcerative keratitis (PUK): often accompanied with surrounding scleritis.
Presence of PUK or necrotizing scleritis in patients with rheumatoid arthritis indicates severe systemic
disease necessitating immunosuppressive therapy.
Metabolic and drug-induced
keratopathies
Vortex Keratopathy (cornea verticillata): occurs due to deposition of complex
lipids in the basal epithelial layer (amiodorone, chloroquine, and
chlorpromazine)
Kayser–Fleischer ring: deposition of copper at the level of Descemet’s
membrane in the peripheral cornea ( Wilson’s disease (hepatolenticular
degeneration))
Wilson’s Disease
(Hepatolenticular
Degeneration) (AR)
Increased copper levels due to deficiency in
ceruloplasmin
Copper deposition in:
Basal ganglia: spasticity, dysarthria, tremor,
ataxia
Liver: cirrhosis
Eye: Kayser-Fleischer ring (copper
deposition in peripheral Descemet’s),
sunflower cataract.
Treatment: oral tetrathiomolybdate
(penicillamine), followed by oral zinc
maintenance.
Cystinosis: lysosomal storage disorder characterized by
widespread tissue deposition of cystine crystals. Systemic
treatment is with cysteamine, which can be given in eye
drop form to reverse corneal crystal formation.
Corneal Stromal Clouding in Mucopolysaccharidoses:
lysosomal storage diseases due to deficiency of enzymes
needed for degradation of glycosaminoglycans leading to
altered metabolite deposition; excessive dermatan and
keratin sulphate deposition in the cornea.
Systemic Medication Side Effects
In Ophthalmology
Cataract Steroids, phenothiazines, ibuprofen, long-acting miotics
Retina
Edema: Chloramphenicol, indomethacin, tamoxifen.
Hemorrhage: Anticoagulants, ethambutol.
Vascular damage: Oral contraceptives, oxygen, aminoglycosides,
interferon.
Pigmentary degeneration: Phenothiazines, indomethacin, nalidixic
acid, ethambutol, chloroquine, hydroxychloroquine
Optic
Nerve
Neuropathy: Ethambutol, isoniazid, sulfonamides, digitalis,
streptomycin, busulfan, vincristine, chloramphenicol, disulfiram.
Papilledema: Steroids, vitamin A, tetracycline, amiodarone, nalidixic
acid, isotretinoin.
A 21-year-old female on hydroxychloroquine therapy for SLE presenting with advanced
toxicity, with preserved central vision (20/20) but with paracentral scotoma.
Color fundus photograph of the right eye showing bull’s-eye maculopathy with parafoveal
retinal pigment atrophy.
Spectral-domain optical coherence tomography showing parafoveal outer retinal and retinal
pigment epithelium atrophy with central sparing “flying saucer sign.”
Thioridazine retinopathy Interferon retinopathy
Thanks

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7. ocular, Systemic disease.pptx

  • 1. Ocular Manifestations of Systemic Diseases
  • 3. Diabetes Mellitus Lids: Recurrent styes, xanthelasma and blepharitis. EOMs: Paralytic squint with diplopia (The commonest is the lateral rectus) Iris: May show Rubeosis irids (neovascularization of iris):Spontaneous hyphema and neovascular glaucoma may occur.
  • 4.
  • 5. Lens: Cataract (True diabetic cataract; below 30 years, Pre-senile cataract), Changes in refraction (Hyperglycemia causes index myopia, Hypoglycemia causes index hypermetropia). Vitreous: Hemorrhage (PDR).
  • 6. Retina: Diabetic retinopathy (NPDR, PDR). Optic nerve: Retrobulbar neuritis, diabetic papillopathy. Postoperative complications: Infection and delayed wound healing.
  • 7. Thyroid Eye Disease Retraction of the eyelids (highly specific) and eyelid lag on downward gaze (von Graefe sign), lagophthalmus. Unilateral or bilateral axial proptosis. When EOM are involved, elevation and abduction are commonly restricted and there is resistance on forced-duction testing.
  • 9. Vitamin A Deficiency: Xerosis, Keratomalacia, Nyctalopia. Vitamin C deficiency: Scurvy (spontaneous hemorrhages in conjunctiva, retina and orbit, lens opacities, delayed healing of wounds, diminished resistance to infection). Vitamin D deficiency: rickets and osteomalacia. It may be related to Cataract, Myopia. Vitamin K deficiency: leads to bleeding tendency. It leads to excessive bleeding during operations and spontaneous hemorrhages. Vitamin B Deficiency :as follow
  • 10. Vitamin B Deficiency • Vitamin B1 (thiamin) deficiency produces beri -beri, retrobulbar neuritis and ophthamoplegia. • Vitamin B 2 (riboflavin) deficiency produces angular stomatitis, glossitis peripheral corneal neovascularization, macular degeneration, papilloedema. • Vitamin B 12 (cyanocobolamine) deficiency produces pernicious anaemia .The eye shows the changes of severe anaemia. • Vitamin B 7 (nicotinic acid) deficiency produces pellagra. The eye shows retrobulbar neuritis and muscle palsy (occur with pellagra lateral sclerosis).
  • 11. Roth spots in pernicious anaemia Bitot's spots
  • 13. Anaemia Pallor of conjunctiva. Fundus shows: Pallor, dilated vessels, hemorrhages , papilloedema. Lens opacities may occur. Primary optic atrophy may occur. Polycythemia Dilated conjunctival vessels. Fundus:dilated veins, CRVO may occur.
  • 14. Leukemia The ophthalmic manifestations of leukemia can be divided into: •1ry or direct infiltration of neoplastic cells (leukemic infiltrates and white-centered retinal hemorrhages). •2ry or indirect involvement from nonviable or dysplastic cells, or from chemotherapy, leading to hematologic abnormalities (anemia, thrombocytopenia and hyper-viscosity). Symptoms: blurred vision, floaters Findings: cellular infiltration of vitreous; infiltrative lesions of retina, optic nerve, or uvea; multiple hemorrhages, Roth spots, cotton wool spots (CWS); pseudohypopyon, spontaneous hyphema, uveitic glaucoma, cataract Optic nerve infiltration causes loss of vision and papilledema. Orbital infiltration (rare) causes proptosis, lid swelling, ecchymosis. (1-2% of patients)
  • 15. a. left proptosis with PL vision, b. ON thickening on T1-weighted MRI scan of the orbit and brain, c. ONH and retinal infiltrates, with combined central retinal vein and artery occlusions. d. After further chemotherapy, vision did not improve due to severe optic neuropathy.
  • 17. Systemic Lupus Erythematosus (SLE) Inflammation in SLE is caused by the formation of autoantibodies and immune complexes, can cause inflammatory responses and activate the complement system. Ocular involvement is moderately common. Eyelid: irritating, erythematous scaly plaque, which can involve the lid margin and can be complicated by scarring and madarosis. keratoconjunctivitis sicca [2ry Sjögren’s syndrome (SS)]: is the most common ocular feature of SLE. Orbital involvement (rare): myositis. Cornea: superficial punctate keratitis and may be 2ry to SS. Episcleritis and scleritis. Retinopathy: 3 types of direct retinal damage by lupus: microangiopathy, severe vaso-occlusion and vasculitis. Neuro-ophthalmic manifestations (not common): optic neuritis, myasthenia gravis, visual field defects and optic disc oedema.
  • 18. Rheumatoid arthritis (RA) RA is an inflammatory arthritis associated with a variety of extra articular manifestations Dry Eye Syndrome is the most common ophthalmic manifestation; women are 9 times more commonly affected than men. Scleritis and Episcleritis are the 2nd most common ocular manifestation of RA. Peripheral ulcerative keratitis (PUK): often accompanied with surrounding scleritis. Presence of PUK or necrotizing scleritis in patients with rheumatoid arthritis indicates severe systemic disease necessitating immunosuppressive therapy.
  • 20. Vortex Keratopathy (cornea verticillata): occurs due to deposition of complex lipids in the basal epithelial layer (amiodorone, chloroquine, and chlorpromazine) Kayser–Fleischer ring: deposition of copper at the level of Descemet’s membrane in the peripheral cornea ( Wilson’s disease (hepatolenticular degeneration))
  • 21. Wilson’s Disease (Hepatolenticular Degeneration) (AR) Increased copper levels due to deficiency in ceruloplasmin Copper deposition in: Basal ganglia: spasticity, dysarthria, tremor, ataxia Liver: cirrhosis Eye: Kayser-Fleischer ring (copper deposition in peripheral Descemet’s), sunflower cataract. Treatment: oral tetrathiomolybdate (penicillamine), followed by oral zinc maintenance.
  • 22. Cystinosis: lysosomal storage disorder characterized by widespread tissue deposition of cystine crystals. Systemic treatment is with cysteamine, which can be given in eye drop form to reverse corneal crystal formation. Corneal Stromal Clouding in Mucopolysaccharidoses: lysosomal storage diseases due to deficiency of enzymes needed for degradation of glycosaminoglycans leading to altered metabolite deposition; excessive dermatan and keratin sulphate deposition in the cornea.
  • 23. Systemic Medication Side Effects In Ophthalmology
  • 24. Cataract Steroids, phenothiazines, ibuprofen, long-acting miotics Retina Edema: Chloramphenicol, indomethacin, tamoxifen. Hemorrhage: Anticoagulants, ethambutol. Vascular damage: Oral contraceptives, oxygen, aminoglycosides, interferon. Pigmentary degeneration: Phenothiazines, indomethacin, nalidixic acid, ethambutol, chloroquine, hydroxychloroquine Optic Nerve Neuropathy: Ethambutol, isoniazid, sulfonamides, digitalis, streptomycin, busulfan, vincristine, chloramphenicol, disulfiram. Papilledema: Steroids, vitamin A, tetracycline, amiodarone, nalidixic acid, isotretinoin.
  • 25. A 21-year-old female on hydroxychloroquine therapy for SLE presenting with advanced toxicity, with preserved central vision (20/20) but with paracentral scotoma. Color fundus photograph of the right eye showing bull’s-eye maculopathy with parafoveal retinal pigment atrophy. Spectral-domain optical coherence tomography showing parafoveal outer retinal and retinal pigment epithelium atrophy with central sparing “flying saucer sign.”