4- Ophthalmology (Gradual deterioration of vision) 2/2 Flashcards
Diabetic retinopathy
Background
- Where the retina is damaged by prolonged exposure to high blood sugar levels – hyperglycaemia – causing progressive deterioration in the health of the retina
Pathophysiology of diabetic retinopathy
there are dilated tortuous capillaries in the retina
o These can shunt between the arterial and venous vessels in the retina
- Neovascularization -> growth factor releases in the retina causing development of new blood vessels
- Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells
- Increased vascular permeability leads to leakage from blood vessels -> blot haemorrhage and formation of hard exudates
o Hard exudates are yellow/white deposits of lipids in the retina - Damage of blood vessel walls leads to microaneurysms and venous beading
o Microaneurysms -> weakness in the wall causes small bulges
o Venous beading is where the walls of the veins are no longer straight and parallel and look more like a string of beads - Damage to nerve fibres in the retina cause fluffy white patches to form on the retina -> cotton wool spots
- Intraretinal microvascular abnormalities (IMRA) is where - Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells
- Increased vascular permeability leads to leakage from blood vessels -> blot haemorrhage and formation of hard exudates
o Hard exudates are yellow/white deposits of lipids in the retina - Damage of blood vessel walls leads to microaneurysms and venous beading
o Microaneurysms -> weakness in the wall causes small bulges
o Venous beading is where the walls of the veins are no longer straight and parallel and look more like a string of beads - Damage to nerve fibres in the retina cause fluffy white patches to form on the retina -> cotton wool spots
- Intraretinal microvascular abnormalities (IMRA) is where
classification of diabetic retinopathy
Non-proliferative
- no neovascularisation
- can develop into proliferative retinopathy
Proliferative
- vascularisation -> new development of blood vessels
Diabetic maculopathy
Non-proliferative Diabetic Retinopathy
- Mild: microaneurysms
- Moderate: microaneurysms, blot haemorhages, hard exudates, cotton wool spots and venous beading
- Severe: blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrates, intraretinal microvascular abnormality (IMRA) in any quadrant
Proliferative Diabetic Retinopathy
- Neovascularisation
- Vitreous haemorrhage
Diabetic Maculopathy
- Macular oedema
- Ischaemic maculopathy
The macula is the part of the eye that helps to provide us with our central vision. Diabetic maculopathy is when the macula sustains some form of damage. One such cause of macular damage is from diabetic macular oedema whereby blood vessels near to the macula leak fluid or protein onto the macula.
If the leakages cause the retina to harden and exudates (deposits of fat from the blood) become significantly large and close to the fovea, then the condition is termed as Clinically Significant Macular Oedema (CSMO).
key findings on fundoscopy for diabetic retinopathy
- cotton wool spots
- dot to blot haemorrhage
- hard exudates
- neovascularisation
- microaneurysms
key findings on fundoscopy for diabetic retinopathy
- cotton wool spots
- dot to blot haemorrhage
- hard exudates
- neovascularisation
- microaneurysms
Management of diabetic retinopathy
- Laser photocoagulation
- Anti-VEGF medications such as ranibizumab and bevacizumab
- Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
Complications of Diabetic Retinopathy
- Retinal detachment
- Vitreous haemorrhage (bleeding in to the vitreous humour)
- Rebeosis iridis (new blood vessel formation in the iris)
- Optic neuropathy
- Cataracts
Hypertensive retinopathy
Background
- Damage to small vessels in the retina relating systemic hypertension
Cause
- Chronic hypertension
- Malignant hypertension (can develop quickly)
pathophysiology of hypertensive retinopathy
Initially, there is arterial narrowing (visible as copper wiring). This is followed by vascular leakage and subsequent arteriosclerosis, which is graded 1-4. It has a characteristic appearance on fundoscopy (described below). Rarely, choroidal changes may occur, usually in the context of an acute hypertensive crisis (accelerated hypertension) in a young adult
There are a number of signs that occur within the retina in response to the effects of hypertension in these vessels.
- Silver wiring or copper wiring is where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
- Arteriovenous nipping is where the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.
- **Cotton wool spots **are caused by ischaemia and infarction in the retina causing damage to nerve fibres.
- Hard exudates are caused by damaged vessels leaking lipids into the retina.
- Retinal haemorrhages are caused by damaged vessels rupturing and releasing blood into the retina.
- Papilloedema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
classification of hypertensive retinopathy
Keith-Wagener Classification
* Stage 1: Mild narrowing of the arterioles
* Stage 2: Focal constriction of blood vessels and AV nicking
* Stage 3: Cotton-wool patches, exudates and haemorrhages
* Stage 4: Papilledema
fundoscopy findigns hypertensive retinopathy
- cotton wool spots
- retinal hemaorrhage
- papilloedema
- copper/silver wiring
- hard exudates
- arteriovenous nipping
Management of hypertensive retinopathy
Management is focused on controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
Thyroid eye disease
Background
- Autoimmune condition resulting in inflammation and swelling of the extraocular muscles, fatty tissue and connective tissue within the orbit -> problem is with the cone and not the actual eye -> compression of the nerves
- Most commonly occurs in patients with Graves disease
o But can present in euthyroid or hypothyroid patients
o In most patients eye disease and thyroid issues evolve within 1.5 years of each other - Most common cause of unilateral and bilateral exophthalmos in adults
Pathophysiology of thyroid eye disease
- Autoimmune
- Closely correlating with Graves disease, patients with TED have been found to have elevated antibodies against TSH receptors, which are expressed in orbital fat and connective tissue
- Causes enlargement and fibrosis of extraocular muscles, which can compress the optic nerve causing blinding
- Studies have also attributed increased fibroblast activity as well as accumulation of collagen and hyaluronic acid to the enlargement and fibrosis of the extraocular muscles
Causes/ risk factors of TED
- Graves disease
- Hashimotos thyroiditis
- Female
- 30-50 yo
- Although men have more serious disease
- Previous radioiodine therapy
**- Smoking – SINGLE LARGEST MODIFIABLE RISK FACTOR **
Differentials of TED
- CN palsy
- Dysthyroid optic neuropathy (DON)
presentation of TED
Eye symptoms
- Excessive watering
- Gritty sensation
- Photophobia
- Eye pain
- Sensation of pressure
Vision symptoms:
Problems with extraocular muscles
- Double vision- LR and MR compression – diplopia
Problems with optic nerve:
- If swelling of muscles and fat press on the optic nerve- compressive optic neuropathy
- Reduced visual acuity
- Colour vision
- Contrast sensitivity
Systemic signs
- Pretibial myxoedema
- Goitre
- Acropachy (soft tissue swelling of hands and clubbing of fingers)
- Depression
TED signs
- Eyelid retraction (Dalrymple’s sign)
- Temporal flare
- Proptosis
- Lid lag (Von Graefe’s sign) -> on downgaze
- Lid oedema
- Diplopia due to restriction of extraocular muscles, most commonly inferior rectus
- Glabellar furrows (search)
- Incomplete eyelid closure
- Lagophtalmos- failure of lids to close
- Strabismus -> due to problems with inferior rectus and medial rectus
Examination for TED
- Always measure proptosis and assess optic disc (exopthalmometer)
- Visual acuity
- Colour vision (ishihara)
- Afferent pupillary defect
- Ocular health
- Upper lid retraction (Dalrymple sign- where you can see the inferior and superior limbus (sclera)
- Orthoptic assessment
Radiological findings of TED
- Straightening/ stretching of optic nerve (usually S shaped)
- Belly of muscle swollen and tendon spared- > pathognominc for TED
Bloods for TED
- Thyroid function tests (raised T3/T4 and low TSH levels)
o May be normal - Antibody testing – TSH receptor antibodies, thyroid-stimulating antibodies and TSH-binding inhibitor immunoglobulins and thyroid peroxidase antibodies
Management of TED
Need input from both ophthalmology and endocrine
- Aim: euthyroidism
- Smoking cessation– reduces risk of exacerbation
- Symptoms control e.g. due to corneal exposure
o Artificial tears and tapes - Steroids in severe cases can reduce inflammation and swelling
o IV methylprednisolone - Severe cases
o Surgery: surgical orbital decompression and lid surgery if significant corneal exposure and progressing proptosis
management of hyperthyroidism
Hyperthyroidisms
- Block and replace with carbimazole and levothyroxine
Complications of TED
- Loss of sight secondary to compressive optic neuropathy
- Corneal damage due to eyelid not closing e.g. superficial punctate keratitis
- Globe subluxation: eye ‘popping out’
- Gaze abnormalities
- Raised intraocular pressure leading to glaucoma
Compressive optic neuropathy and TED
Due to enlarged muscles and fat
Presentation
- Reduced visual acuity
- Colour vision
- Contrast sensitivity
Management
SIGHT THREATENING
- Urgent IV methylprednisolone
Compressive optic neuropathy and TED
Due to enlarged muscles and fat
Presentation
- Reduced visual acuity
- Colour vision
- Contrast sensitivity
Management
SIGHT THREATENING
- Urgent IV methylprednisolone
