Systemic disease and the eye
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Systemic Disease and the Eye. Dr Sancy Low. Background. Patients of all ages and medical history can present with eye problems Symptoms are often associated with systemic disease

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  • Patients of all ages and medical history can present with eye problems

  • Symptoms are often associated with systemic disease

  • Cardiovascular, endocrine, rheumatoid, connective tissue disease, inherited eye disease and HIV are prominent examples

Topics covered in this lecture
Topics covered in this lecture

  • Diabetic Retinopathy

  • Hypertensive Retinopathy

  • Thyroid Eye Disease

  • Inherited Eye Disease

  • HIV and AIDS

Diabetic retinopathy dr1
Diabetic Retinopathy (DR)

  • Microvascular disease of the retinal microcirculation

  • Commonest cause of blindness under 65y

  • Symptom less until loss of vision :

    • Gradual = Central (macula) area of retina involved by oedema, exudates or haemorrhage (maculopathy)

    • Sudden = vitreous haemorrhage from new blood vessels (proliferative DR)



  • Glycosylation of proteins (capillary basement membranes)

  • Loss of endothelial supporting cells (pericytes)

  • Microaneurysms (hallmark of disease) = leakage

  • Capillary closure = ischaemia

Type 2 diabetes


Background diabetic retinopathy


Type 1 diabetes


Background diabetic retinopathy

Pre-proliferative diabetic retinopathy


Vitreous haemorhage

Tractional retinal detachment

Background dr
Background DR


  • Microaneurysms / haemorrhages (‘dots and blots’)

  • Exudates

    Treatment:- Observe



Background DR changes but in the macula area


  • Argon Green laser (induces thermal burn)

  • Either focal or grid laser photocoagulation

Pre proliferative dr
Pre-proliferative DR


  • Cotton wool spots

  • Extensive haemorrhages

  • Venous beading

  • Intraretinal microvascular abnormalities (IRMA)

Pre proliferative dr1
Pre-proliferative DR


Close observation

Proliferative dr new vessel formation
Proliferative DR: new vessel formation

Treatment: Argon laser panretinal photocoagulation (PRP)

Panretinal photocoagulation
Panretinal photocoagulation

3 days post treatment

Old burns

Laser burns destroy retina in prp
Laser burns: Destroy retina in PRP

End stage disease fibrosis retinal traction and eventual detachment
End Stage Disease: fibrosis, retinal traction and eventual detachment

End stage disease retinal detachment
End Stage Disease: retinal detachment

Prevention of dr
Prevention of DR

  • Progressive disease

    • Type I DM: 25% affected by 10y

    • Type II DM: 50% affected by 10y

  • Regular eye tests: Optician, GP, Diabetic team, Ophthalmologists

  • BM control (DCCT)

  • BP control (UKPDS)

  • Stop smoking

Hypertensive retinopathy1
Hypertensive retinopathy

  • Has been graded 1 to 4 (but not satisfactory!)

    • Grade 1: arteriolar narrowing and vein concealment

    • Grade 2: severe arteriolar attenuation and venous deflections at crossings (AV nipping)

    • Grade 3: arteriolar copper wiring, haemorrhages, CWS and hard exudates

    • Grade 4: all of the above plus silver wiring and optic disc swelling


  • Systemic hypertension

    • Early signs difficult to tell from ageing changes

  • Malignant hypertension

    • Accelerated severe hypertension causing encephalopathy and papilloedema (sign of raised intracranial pressure)

Note black areas of non perfusion on ffa fundus fluorescein angiogram
Note black areas of non-perfusion on FFA (fundus fluorescein angiogram)

Malignant hypertension papilloedema ischaemia infarction and macular star
Malignant hypertension - papilloedema, ischaemia, infarction and macular star


  • Treat the hypertension!

  • Watch out for other complications such as central retinal artery and central retinal vein occlusions (acute visual loss lecture)

Thyroid eye disease aka grave s ophthalmopathy
Thyroid Eye Disease (aka Grave’s Ophthalmopathy)

  • Associated with thyrotoxicosis (but patient can be clinically and biochemically euthryoid)

  • Organ specific IgG mediated disease

  • Infiltration of muscles and fat surrounding eye

  • Unilateral or bilateral

  • Two stages:

    • Acute inflammatory (risk of sight loss); lasts approx 12-18 months

    • Chronic fibrotic


Conjunctival chemosis (oedema)

Eyelid retraction (worse on downgaze)

Diplopia (usually upgaze +/- lateral gaze)


Corneal exposure (corneal ulcers if severe)

Compressive optic neuropathy: decreased V/A, RAPD, field loss, reduced colour vision


Ted symptoms
TED symptoms

  • Nil

  • Grittiness

  • Redness

  • Eyelid swelling

  • Diplopia

  • Cosmetic appearance “bulgy eyes”

  • Visual loss

American thyroid association classification
American Thyroid Association Classification

  • NOSPECS – 6 stages

    • (0) No signs or symptoms

    • (1) Only ocular irritation (dryness, FB)

    • (2) Soft tissue involvement (oedema)

    • (3) Proptosis

    • (4) EOM (extraocular muscle) involvement

    • (5) Corneal involvement

    • (6) Sight loss

Investigation ct orbit proptosis and eom infiltration medial inferior rectus most commonly involved
Investigation: CT orbit Proptosis and EOM infiltration(medial & inferior rectus most commonly involved)


  • Manage thyroid dysfunction

  • Ocular lubricants alone (in mild cases)

  • Acute optic nerve compression & corneal exposure

    • Systemic corticosteroids

    • Radiotherapy

    • Surgical orbital decompression

  • Chronic phase

    • Diplopia: Squint surgery, Prisms, Botulinum toxin

    • Cosmetic: Orbital decompression; lid surgery eg blepharoplasty, lid lowering etc

Inherited eye disease e g retinitis pigmentosa
Inherited eye diseasee.g. Retinitis Pigmentosa

Inherited eye disease
Inherited eye disease

  • Genetic eye disease accounts for 20% of blind registration in young adults

  • 40-50% of blindness in children is inherited

  • Retinitis Pigmentosa is the commonest inherited retinal dystrophy

  • Affects 1:5000 of the population

  • It is a heterogeneous condition which primarily affects the retinal rods and later retinal cones

Retinitis pigmentosa
Retinitis Pigmentosa

  • Bone-spicule pigmentation around blood vessels

  • Pale waxy appearance or the peri-papillary retina


  • RP can be inherited in all forms: AR, XL, AD, and mitochondrial or simplex (where there is no other known family history)

  • Patients usually present with night blindness but can progress to tunnel vision and total blindness (as rods then cones are affected)

  • Syndromic forms of RP exist e.g. Usher syndrome = night blindness and deafness (usually recessive)

Photoreceptor loss
Photoreceptor loss

  • Progressive disease

  • Loss of rods first

  • Cone loss eventually

  • Night blindness first then peripheral field loss, tunnel vision and eventual blindness


  • Symptoms are usually present before ophthalmoscopic signs

  • Electroretinography (ERG): contact lens probe and measurement of electrical potential of the photoreceptors

  • Visual field analysis

  • Good family history, examine relatives

Treatment research
Treatment/ Research

  • Currently no treatment for RP

  • Low visual aids and blind registration

  • Anti-oxidants (Vitamins A+E have been tried but majority or RP patients not responsive)

  • Genetic mapping and linkage studies

  • E.g. Peripherin gene – current research to find gene therapy

Hiv and aids1

  • AIDS is a multisystem disorder of opportunistic infections caused by HIV.

  • Ocular manifestations:

    • Keratitis sicca

    • Common infections: HSV/ HZO/ VZV/ CMV

    • Rarer: Candida choroiditis, Retinal toxoplasmosis

    • Neoplasms: Karposi’s sarcoma, Non-Hodgkin’s lymphoma

Herpes simplex keratitis see red eye lecture
Herpes Simplex Keratitis: see red eye lecture

Herpes zoster ophthalmicus ophthalmic division of trigeminal nerve
Herpes Zoster Ophthalmicus: Ophthalmic division of trigeminal nerve

Cmv retinitis
CMV retinitis

  • Commonest – Occurs in 25% of AIDS patients

  • “Pizza fundus” with overlying vitritis

  • Related to high viral load or low CD4+ count

  • <50 cells/mm3 at greatest risk

Symptoms of cmv retinitis
Symptoms of CMV retinitis

  • May be minimal

  • Floaters and flashing lights

  • Visual field loss

  • Central visual loss (V/A)

  • Signs: progressive necrotising retinitis, retinal haemorrhage and intraretinal necrosis, hazy vitreous

Cmv retinitis treatment
CMV retinitis treatment

  • 14 day induction course: iv ganciclovir or foscarnet

  • May require lifelong treatment

  • 80-100% respond to initial therapy but 50% recur within 3 months

  • May require intravitreal injections or implants


  • Related to ocular disease or treatment

  • Blindness from retinal detachment

  • Optic nerve head involvement

  • Ganciclovir causes neutropenia

  • Foscarnet causes renal toxicity

  • Co-existence of other infections (low CD4)

Other systemic diseases
Other systemic diseases

  • Remember dry eyes associated with Rheumatoid Arthritis (Sjogren’s syndrome or keratoconjunctivitis sicca)

  • Remember acute anterior uveitis associated with the seronegative arthritides (50% of patients are HLA-B27 positive and there is an association with ankylosing spondylitis)

Further reading
Further reading

  • There are many other interesting associations of eye disease and general medicine - read up more in good ophthalmology textbooks (see section in the library)

    • Murray, Fielder: Pocket book of Ophthalmology (concise, short notes)

    • Batterbury: Churchill Livinstone colour guide to ophthalmology (good general text)

    • Kanski: Clinical ophthalmology (reference)