Ocular Manifestations of Systemic Diseases

Dalman

Dysthyroid Orbitopathy

• autoimmune disorder usually associated with Graves' disease

• 10-25% euthyroid• extra-ocular muscles are the target of the

autoimmune attack restrictive ophthalmoplegia and proptosis

• Cardinal Signs– upper eyelid retraction and lag, conjunctival

injection and chemosis, and periorbital edema.

Dysthyroid Orbitopathy

• Pathophysiology– antibody-mediated reaction against the TSH

receptor with orbital fibroblast modulation of T-cell lymphocytes

Dysthyroid Orbitopathy

• Pathophysiology

T- cells Thyroid cells inflammation

cytokines mucopolysaccharides

Orbital fibroblast

EOM edema

Hyperosmotic shift

Dysthyroid Orbitopathy

• Pathophysiology

Preadipocyte fibroblasts adipocytes

Inc. orbital volume Inc. fat proptosis

edema Tissue damage and fibrosis

lagophthalmos

EO motility restriction

Dysthyroid Orbitopathy

Dysthyroid Orbitopathy

Dysthyroid Orbitopathy

Dysthyroid Orbitopathy

• Management– self-limited (over 1 year)– No immediate cure available

Dysthyroid Orbitopathy

• Management– Orbital radiation

• moderate-to-severe inflammatory symptoms, diplopia, and visual loss in patients with TAO

– Optic nerve compression• High-dose steroids (proceed to surgery if unresponsive)

– Surgical• Orbital decompression• Strabismus surgery• Lid lengthening • Blepharoplasty

Occular Changes in Hypertension

• Damage to the retina caused by high blood pressure

• 3 manifestations– Hypertensive retinopathy– Hypertensive optic neuropathy– Hypertensive choroidopathy

Occular Changes in Hypertension

• Pathophysiology– Retinal microvasculature

Inc BPHyperoxic &

hypercapneic stress

Bifurcation angles and retinal arteriolar diameters show Dec

vascular reactivity

Disadvantageous branching geometry in retinal vasculature

Occular Changes in Hypertension

• Pathophysiology– Dynamics of ocular blood flow

Inc BP

Hypertensive arterial changes

Breakdown of autoregulation

Inc resistance to optic nerve head

blood flow

Occular Changes in Hypertension

• Pathophysiology– Different manifestations because• Acute HTN disrupts blood-retinal barriers• Retinal and optic nerve head vascular beds have

autoregulation (choroidal has none)• Choroidal vessels has no blood-ocular barrier• Retinal vessels (no autonomic nerve supply)• Choroidal vessels (richly supplied by both sympathetic

and parasympathetic nerves)

Hypertensive Retinopathy

• Represents target-organ damage

Grade II

Grade III

Grade IV

Hypertensive Retinopathy

• Clinical features– Vasoconstriction – Fundus• focal and generalised arteriolar narrowing,

microaneurysms, intraretinal hemorrhages, cotton-wool spots, hard exudates, optic disc swelling• 2o to arteriolosclerosis arteriovenous nipping• Flame-shaped hemorrhages (abnormal vascular

permeability)• Macular star (lipid deposition around the fovea)• Disc swelling (minimal microvascular change)

• Cotton-wool spots

Hypertensive Retinopathy

• Clinical features– Vasoconstriction – Fundus• Untreated hypertension hemorrhagic detachment of

retina and vitreous hemorrhage

Hypertensive Retinopathy

• Clinical features– Vasoconstriction – Fundus– Secondary arteriosclerosis• Bonnet’s sign - banking of the venule distal to the

crossing• Gunn’s sign - nipping of the blood column• Salus’ sign - displacement of the venule at right angles

to the arteriole

Hypertensive Retinopathy

• Gunn’s sign and Bonnet’s sign

Hypertensive Retinopathy

• Focal arterial narrowing of the retina

Hypertensive Optic Neuropathy

• Papilloedema or bilateral disc swelling– Grade IV hypertensive retinopathy– Poor prognostic sign– Other causes like space-occupying lesions and

benign intracranial HTN should be excluded– Theories on the pathophysiology• Ischemia and raised ICP as a part of hypertensive

retinopathy/enchephalopathy

Hypertensive Optic Neuropathy

• Usually resolve following control of BP, but some might develop disc pallor

• Longstanding uncontrolled HTN retinal nerve fiber loss

Hypertensive Choroidopathy

• Less well recognized than retinopathy• Commonly described features:– Choroidal vascular sclerosis– Elschnig spots – focal areas of degenerative retinal

pigment epithelium– Siegrist’s streaks – linear pigment epithelial

changes• poor prognosis

Hypertensive Choroidopathy

• Elschnig spots

Management

• Control hypertension• Grade I and II– Non-urgent referral

• Grade III– More urgent referral to the GP

• Grade IV– Patient is in medical crisis. Patient needs

immediate referral to a hospital eye casualty department