Ophthalmology - Gradual visual disturbance Flashcards Preview

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Flashcards in Ophthalmology - Gradual visual disturbance Deck (71):
1

Outline some causes of gradual visual loss

Glaucoma
Refractive error
Cataracts
Retinal degeneration
Macular degeneration
Compressive lesions (i.e. on the optic nerve)

2

How should refractive errors be investigated?

The pinhole test is more useful for identifying refractive errors. If there is a refractive error, the vision will improve when the pinhole is used. A patient with thick glasses should wear them for the pinhole test. Once other causes of visual loss have been excluded, the patient can be sent to the optometrist for refraction and correction of refractive error.

3

How can corneal disease cause gradual visual loss?

Various disorders can cause gradual loss of the corneal endothelial cells and increasing oedema in the cornea (for example, Fuch's endothelial dystrophy). This leads to a gradual decrease in visual acuity that does NOT improve substantially with pinhole. If the damage is advanced the cornea may appear opaque. A corneal graft from a donor may be required.

4

What is a cataract? How can it be diagnosed and what other features should you look for?

This is probably the most common cause of gradual visual loss. It can be diagnosed through testing for the red reflex. The patient should be referred if the visual disturbance interferes with their lifestyle. If a patient with a cataract cannot project light or has an afferent pupillary defect, however, other diseases such as retinal detachment must be excluded.

5

How do patients with glaucoma present with gradual visual loss?

Unfortunately, the patient with primary open angle glaucoma may not complain of visual disturbance until late in the course of the disease. Hence, the need for screening. Primary open angle glaucoma should, however, be excluded in any patient with gradual visual loss. Establish whether there is a family history of glaucoma. The vision can be 6/6 so the visual field should be checked with a red pin. Also check for cupping of, or asymmetry between, the optic discs.

6

How does age related macular degeneration present?

This may occur gradually and is typified by loss of the central visual field. There are usually pigemented changes to the macula. The disease occurs in both eyes, but is asymmetrical, and it is more common in short sighted individuals. The gradual deterioration is not treatable, but if acute visual distortion develops this may indicate a leaking area under the retina (choroidal neovascularisation), which may respond to laser photocoaglation.

7

What is a macular hole?

A macular hole is a full thickness absence of neural tissue at the centre of the macula. Between 10% to 20% of full thickness macular holes (FTMH) will become bilateral. Patients usually present with painless loss of central vision or distortion of the central visual field, although early macular holes may be asymptomatic.

Patients with established FTMH can be treated with vitrectomy and instillation of intraocular gas (to provide retinal tamponade), which have a higher chance of closing the hole successfully.

8

What are the important clinical features of diabetic maculopathy?

Diabetic retinopathy occurs in both insulin dependent and non-insulin dependent diabetics and affects ALL age groups. The patient may or may not give a history of diabetes, although the longer the duration of diabetes the more likely the patient is to have retinopathy. Remember that although the patient may describe the onset of visual loss as gradual, sight threatening diabetic retinopathy may still be present.

Non proliferative diabetic retinopathy is typified by microaneurysms, dot haemorrhages, and hard yellow exudates with well defined edges. There may also be oedema of the macula, which is less easy to identify but can lead to a fall in visual acuity. Non proliferative diabetic retinopathy at the macula (diabetic maculopathy) is the major cause of blindness in type 2 diabetics, but it also occurs in younger type 1 patients. Some forms of diabetic maculopathy may be amenable to laser photocoagulation.

9

How is gradual visual disturbance managed?

The initial management of gradual visual loss depends on the cause. Refractive errors usually require no more than a pair of glasses. Cataracts can be removed an an artificial lens implanted. Glaucoma requires treatment to lower the IOP. In general, patients with unexplained visual loss should be referred.

10

What steps can be taken to maximise low vision?

Strong light from behind for reading
Magnifying aids
Large print books
Closed circuit television
Home aids - e.g. tactile markins for cookers

11

What is hereditary degeneration of the retina?

These conditions are relatively rare (for example, retinitis pigmentosa) but should be suspected if there is a family history of visual deterioration. Symptoms include night blindness and intolerance to light. Most types of retinal degeneration are not yet treatable, but some are associated with metabolic disorders that CAN be treated. These patients should be referred.

Patients with severe visual impairment may develop visual hallucinations and sleep disturbance. It is particularly important for these patients to have an opportunity to discuss their diagnosis and prognosis and to have genetic counselling.

12

"My vision has gradually become cloudy and dim, but there is no pain in my eye" - what differentials would you consider?

The main differentials are:
- cataracts
- age related macular degeneration (dry type)
- diabetic retinopathy
- primary open angle glaucoma

Gradual progressive loss of vision is a common complaint in the elderly. Although cataract is a common diagnosis, it is important to exclude coexisting conditions such as age related macular degeneration, diabetic retinopathy and glaucoma.

13

"My vision has gradually become cloudy and dim, but there is no pain in my eye" - what issues in the history support the diagnosis?

The gradual onset and progressive visual loss is typical of cataract and dry ARMD.

14

"My vision has gradually become cloudy and dim, but there is no pain in my eye" - what additional features in the history would you seek to support a particular diagnosis?

Is the deterioration in vision for distance, near or both? Cataracts affect BOTH near and distance vision, whereas ARMD and diabetic maculopathy may affect near vision to a greater extent than distance vision. Ask about a history of diabetes and hypertension. Does the patient smoke? Is there a family history of glaucoma?

15

"My vision has gradually become cloudy and dim, but there is no pain in my eye" - what clinical examination would you perform and why?

Measure the visual acuity. Examine the red reflex - this is reduced if there is nuclear sclerotic cataract. Intraocular pressure is measured. Ophthalmoscopy is performed looking for signs of ARMD and diabetic retinopathy, including retinal haemorrhages and hard exudates at the macula. Examine the optic disc closely. Note the colour, the contour of the disc margins and the cup:disc ratio. The cup:disc ratio is enlarged in primary open angle glaucoma.

16

"My vision has gradually become cloudy and dim, but there is no pain in my eye" - what investigations would be most helpful and why?

If diabetic maculopathy is detected, the patient may require fundus fluorscein angiography. Fluorescein angiography may also be helpful in excluding wet ARMD, which may coexist with the dry type. The blood pressure, blood sugar and lipid profile are measured. Visual fields analysis is performed if glaucoma is suspected.

17

Outline the treatment options for dry ARMD

Unfortunately, there is no effective treatment of dry ARMD. Although prophylactic laser treatment has been tried, there is little evidence that is has any benefit. The Age Related Eye Disease Study (AREDS) evaluated the effect of high doses of zinc and selected anti-oxidants (beta carotene and vitamins C and E) and found significant reduction in the risk of progression in patients with advanced ARMD (categories 3 and 4). Further studies have shown that omega 3 fatty acids did not affect the progression of advanced ARMD.

There may be benefits to substituting lutein/ zeaxanthin for beta carotene in the original AREDS formulation, especially for current or former smokers. Specific nutritional supplements are therefore indicated in advanced ARMD. The patient should also be advised to stop smoking. Arrangements for the provision of low visual aids and rehab should be made.

18

Outline the main treatment options for primary open angle glaucoma

Medical treatment: most cases can be managed with primary open-angle glaucoma is successfully treated with antiglaucoma eyedrops

Laser treatment: laser trabeculoplasty is sometimes used in the treatment of glaucoma (it is also performed in diabetic maculopathy, if there is clinically significant macular oedema)

Surgical treatment: glaucoma filtration surgery (trabeculectomy) or a glaucoma drainage device may become necessary if medical treatment is not tolerated or effective

19

"I have difficulty seeing at night" - what is the differential diagnosis?

Differential diagnosis includes:
- retinitis pigmentosa (RP)
- vitamin A deficiency
- primary open angle glaucoma
- cataracts
- degenerative myopia
- previous panretinal laser photocoagulation

20

"I have difficulty seeing at night" - what issues in the history support the diagnosis?

Night blindness (nyctalopia) is a feature of MANY diseases. Vitamin A is necessary for the conversion of light energy to an electrical signal in the rod outer segments. The rods function at low levels of illumination, so vitamin A deficiency results in night blindness. Difficulty with night vision may indicate an abnormality of rod function and is characteristic of retinitis pigmentosa. However, ANY cause of extensive peripheral retinal degeneration, including primary open angle glaucoma and degenerative myopia, results in peripheral visual field loss and poor night vision. Cataracts cause a general reduction in the amount of light entering the eye and can therefore produce similar symptoms.

21

"I have difficulty seeing at night" - what additional features in the history would you seek to support a particular diagnosis?

It is important to determine the onset of symptoms. Patients with RP often begin having difficulty with night vision in teenage years (e.g. they may report having had difficulty finding their way around a cinema or other dark environment). Does the patient have a hearing deficit? Usher's syndrome is a variation of RP that also impair's hearing. Ask about symptoms that may suggest constriction of the peripheral visual field, such as involvement in RTAs. Is the patient myopic? Does the patient wear spectacles or contact lenses? The incidence of myopia is increased in RP. Ask about a family history of RP, night blindness, glaucoma and cataracts. Enquire about any history of abdominal surgery involving small bowel resection and liver disease, which may cause malabsorption and hypovitaminosis.

22

"I have difficulty seeing at night" - what clinical examination would you perform and why?

Measure visual acuity and assess visual fields to confrontation. Examine the red reflex, which may be reduced in eyes with cataract. Posterior subcapsular cataract often occurs in patients with RP. Check the intra-ocular pressure. Dilated fundoscopy may show the classic appearance of RP with pigment proliferation and accumulation of pigment shaped as bone corpuscles ("bone spicules") in the midperipheral retina. There may be diffuse large areas of chorioretinal atrophy in degenerative myopia. Examine the optic disc carefully for optic atrophy and/or pathological optic disc cupping (enlarged cup: disc ratio). Look for retinal arteriolar attenuation and cystoid macular oedema seen as a dull or absent foveal light reflex, because this may occur in patients with RP.

23

"I have difficulty seeing at night" - what investigations would be most helpful and why?

In patients with RP or advanced glaucoma, visual field testing shows marked constriction of the peripheral field (tunnel vision). In RP, the electroretinogram is the most useful diagnostic test. It is reduced in amplitude or non-recordable and helps confirm the diagnosis. Cataracts are uncommon at such a young age and, if present, fasting blood sugar should be requested to exclude diabetes.

24

Outline the treatment options available for RP

In patients with RP, the eyes should be examined annually to determine the progression of the disease and to monitor for the development of cataract and glaucoma. Genetic counselling is mandatory. A complete family history and ophthalmological assessment of all family members will help to classify the disease as X chromosome linked, autosomal dominant or autosomal recessive. Many patients with RP are legally blind in middle age.

25

What compressive lesions can affect the optic pathways?

These are relatively rare, but should always be considered. Clues in the history and examination include headaches, focal neurological signs, or endocrinological abnormalities such as acromegaly. There should NOT be an afferent pupillary defect in most patients with cataract, macular degeneration or refractive error. Therefore, if an afferent defect is seen, suspect a compressive or other lesion of the optic pathways. Testing of the visual fields may show a bitemporal field defect due to a pituitary tumour. The optic discs should be checked for optic atrophy and papilloedema.

26

What drugs can cause gradual visual disturbance?

Several drugs may cause gradual visual loss. In particular, a history of excessive alcohol intake or smoking; methanol ingestion; or taking chloroquine, hydroxychloroquine, isoniazid, thioridazone, isotretanoin, tetracycline, or ethambutol should lead to suspicion of drug induced visual deterioration. Systemic, inhaled or topical corticosteroids may cause cataracts and glaucoma.

27

How is a patient registered as blind?

Blind or partially sighted registration is not essential but it helps patients to access financial benefits and specialist support and advice from local authorities.

The person should be referred to a consultant ophthalmologist who, with the patient's agreement, completes form BD8. The requirements for registration are:
1) Partially sighted - the patient must have vision of 6/60 or worse in both eyes. The vision can be better than 6/60 if the visual fields are markedly reduced, for example, a patient with 6/6 vision but severely restricted fields caused by POAG

2) Blind - the current statutory definition of blindness is "that a person should be so blind as to be unable to perform any work for which eyesight is essential". However, many registered blind people continue in their employment with appropriate resources. The guidelines for registration as blind are a visual acuity of 3/60 or worse in both eyes

28

What is ARMD?

Age related macular degeneration is the late stage of age related maculopathy and is the most common cause of blindess in developing countries. The condition is characterised by progressive, bilateral atrophic changes in the choriocapillaris, Bruch's membrane and the retinal pigment epithelium. The incidence of blinding ARMD increases sharply with age, and is present in about 15% of people aged over 85. ARMD can be divided clinically into dry (atrophic) and wet (exudative) forms.

29

What is dry (atrophic) ARMD?

This is the common form of ARMD; about 85% of ARMD is of this type. It is characterised by widespread atrophic changes in the macular area and is bilateral. Dry ARMD usually progresses slowly and with great variability and may result in severe visual impairment over five to ten years in some patients.

30

What is the definition of wet ARMD?

Wet ARMD is more aggressive and although only 15% of all ARMD cases are of this type, it accounts for 90% of severe visual loss in ARMD. The clinical course is much more rapid than dry ARMD and 75% of patients will have marked reduction in vision over about three years. The chance of second eye involvement in wet ARMD is very HIGH.

In wet ARMD the problems stems from an abnormal growth of new blood vessels (choroidal neovascularisation) that invade the retina from the choroid. These abnormal blood vessels leak fluids and are associated with bleeding in the macular region.

31

What risk factors are associated with ARMD?

The aetiology of ARMD is multifactorial and not completely understood. The main risk factor for development is age.

Others include:
- female sex
- smoking history
- positive family history
- hypertension
- raised cholesterol
- hypermetropia

32

What is the natural history and clinical presentation of ARMD?

Most patients with dry atrophic ARMD present with gradual loss of CENTRAL vision of both eyes, which affects their ability to read and recognise faces etc. Patients may notice mild distortion of their central vision (metamorphosia) but characteristically retain good peripheral fields.

In the wet form of ARMD, patients present more acutely with a sudden change in their central vision (usually in one eye initially). They often experience marked central distortion ("straight lines have a bend in the middle")

33

What signs can be found in dry ARMD?

The earliest detectable sign of dry ARMD is the appearance of drusen in the macular region of both eyes. Drusen are tiny pinpoint, discrete yellow deposits, which correspond pathologically to focal accumulations of abnormal hyaline material located specifically at the interface between the Bruch's membrane and the retinal pigment epithelium.

Later atrophic changes occur in the macula area, causing a diffuse, pale and mottled appearance. This appearance corresponds to to atrophy of the retinal pigment epithelium and choroid, with some areas of secondary RPE hyperplasia.

34

What are the signs of wet ARMD?

As in dry ARMD, there are drusen and atrophic changes at the macula, but the distinctive signs of wet ARMD relate to the abnormal growth of new blood vessels and leakage of serous fluid and blood in the macula region. Choroidal neovascularisation appears as a small, focal, pale pink yellow or grey green elevation at the macula. There may be associated exudation of serous fluid or blood in the subretinal or sub-RPE space.

35

How should cases of ARMD be investigated?

Fundus Fluorescein Angiography (FFA) is used to confirm the presence of an area of choroidal neovascularisation. at the macula. In both techniques, intravenous administration of a dye allows assessment of the retinal and choroidal circulations and highlights the area of macular pathology. There is a small risk of anaphylaxis due to the fluorescein.

On the basis of FFA, choroidal neovascularisation can be divided into classic (neovascularisation fully delineated) and occult (full extent of neovascularisation not visible). The classic form usually progresses faster than the occult form.

36

Outline the general management of ARMD

Most patients with ARMD will have a variable progression in the reduction of their central visual acuity. Ophthalmologists have a key role in demonstrating to the patient that their peripheral fields are intact. The patient can be offered visual rehabilitation and registration as partially sighted or blind. Dietary supplementation can help to reduce progression of ARMD in some patients. A balanced diet is important and this can be supplemented with additional vitamins.

37

Are there any specific treatments for wet ARMD?

Treatments specifically for wet ARMD aim to close off blood flow through the area of choroidal neovascularisation, to allow resolution of exudative changes at the macula and the restoration of central vision. The first stage is to determine whether the patient is in the subgroup for whom ablation of the choroidal neovascularisation is effective. Patients with severely fibrotic changes in the delicate tissues of the macula are less likely to regain visual function. Several different methods for ablation are available including laser photocoagulation and external beam radiation.

38

What is a cataract?

Cataract means loss of lens clarity (or any opacification of the lens). They are very common, and almost everyone over the age of 70 has some degree of lenticular opacity. Although most of these people remain asymptomatic and relatively few require surgery.

Congenital and infantile cataracts differ morphologically and aetiologically from age related opacity.

39

What is the aetiology of cataracts?

The majority of cataracts encountered clinically are caused by "normal" age related degenerative changes in the lens (senile cataract). The pathogenesis is unknown, but UV light may play a role. Cataract presenting in young or early middle aged individuals with no apparent cause should prompt further investigation as there are systemic diseases that are associated with cataract.

40

What systemic conditions can cause cataracts?

Diabetes
Corticosteroid therapy
Atopy
Galactoseamia
Hypocalcaemia
Dystrophic myotonica

41

What is the aetiology of congenital or infantile cataracts?

These are frequently an isolated finding. About a third are inherited in an autosomal dominant fashion, and another third are caused by birth trauma or infection during pregnancy. Rubella and toxoplasmosis are particularly important causes. These infections typically result in a variety of additional systemic abnormalities. Galactosaemia is the most common metabolic cause of congenital or infantile cataract. Wilson's disease, Lowe's syndrome and Fabry's disease are rare causes.

42

What is the morphology of cataracts?

Some morphological variants of cataracts are seen in particular aetiologies. For example, posterior subcapsular opacity is frequently associated with steroid related cataract, and the "oil-drop" appearance of galactosaemia. The appearance of congenital cataract varies, but tends to involve the nucleus, the earliest part of the lens to develop in utero.

Senile cataract takes the form of one or a combination of:
- NUCLEAR SCLEORISIS = gradually deepening diffuse brunescence
- SUBCAPSULAR = shallow opacification just beneath the capsule, more commonly posterior than anterior
- CORTICAL = discrete spoke like opacities of the cortex

43

How do patients with cataract present?

Symptoms are decreased vision, glare, monocular diplopia, and a change in refraction. Disturbance of vision is the usual symptom. Symptoms may vary with changes in ambient illumination, as the pupil constricts and dilates. If cataract is predominantly uniocular, it may go unnoticed until the other eye becomes affected.

44

How should suspected cases of cataract be clinically assessed?

Snellen visual acuity is always measured but correlates poorly with functional impairment. Since the prognosis for visual recovery after surgery depends especially on retinal health, dilated fundal examination is mandatory. If the retina cannot be seen, field or vision testing using a light of hand waving pupil test for RAPD and ultrasonic examination (to exclude retinal detachment or tumour) should be performed.

A cataract can be detected by examination of the red reflex after pupil dilation, using the direct ophthalmoscope.

45

What is an important part of cataract assessment in children?

In children and infants, cataract must be differentiated from other causes of leukoracia. This includes:
- toxocara granuloma
- retinoblastoma
- advanced retinopathy of prematurity
- retinal dysplasia
- Coats disease

46

What are the indications for cataract surgery?

Surgery to improve visual function depends on the degree of impairment and the visual needs of the individual.

Other indications include diabetic retinopathy, when cataract prevents adequate retinal examination or laser treatment, and lens induced glaucoma or uveitis.

47

What is the prognosis of cataract surgery?

80% of eyes achieve 6/12 vision or better following surgery. Failure to improve is usually due to pre-existing disease. Posterior capsule opacification after successful surgery will reduce vision but can be treated by laser capsulotomy.

48

Why is cataract surgery in children challenging?

Cataracts in children are a cause of ambylopia (reduction in vision despite an organically normal lens). Thus, removal of the opacity does not restore vision. Principal difficulties are correction of the aphakia and management of ambylopia. The eye may still be growing, so that lens implantation is controversial. Ambylopia is likely to limit visual improvement, especially in unilateral cataract.

49

What is ectopia lentis?

This means the partial or complete dislocation of the lens from its physiological position. It may be associated with glaucoma. Contact lenses may need to be worn to overcome refractive consequences of ectopia lentis. Refractive errors and secondary glaucoma are recognised complications. Lens removal may be necessary.

Unusually, the optic effects of partial dislocation are MORE disabling than complete dislocation.

50

What causes ectopia lentis?

Acquired causes:
Trauma
Hypermature cataractous lens
Anterior intraocular tumour
Syphilis

Inherited:
Marfan's
Homocystinuria

51

What is optic atrophy?

Optic atrophy is seen as a pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision (strictly speaking, optic atrophy is a descriptive term, it is the optic neuropathy that causes visual loss).

52

Name some acquired causes of optic atrophy

MS
Papilloedema
Raised intraocular pressure (e.g. glaucoma, tumour)
Retinal damage (e.g. choroiditis, retinitis pigmentosa)
Ischaemia
Toxins: methanol, quinine, arsenic, lead
Nutritional: vitamin B1, B2, B6 and B12 deficiency

53

Name some congenital causes of optic atrophy

Freidrich's ataxia
Mitochondrial disorders - e.g. Leber's optic atrophy
DIDMOAD - association of cranial diabetes insipidus, diabetes mellitus, optic atrophy and deafness

54

Painless, gradual, reduced peripheral visual field, possible RAPD, raised or normal intraocular pressure

Chronic open angle glaucoma

55

Painless, glare, abnormal red reflex

Cataract

56

Deteriorating central vision (difficulty reading, recognising faces) macular drusen

Age related macular degeneration (dry)

57

Diabetes mellitus, microaneurysms, dot and blot haemorrhages, exudates, cotton wool spots, vitreous haemorrhage

Diabetic retinopathy

58

Age >40, difficulty reading, decreased near vision, no other ocular signs

Presbyopia

59

Young adult, increasing difficulty in correcting poor vision with glasses/ frequently changing glasses prescription and astigmatism

Keratoconus

60

Medication history includes: hydroxychloriquine, steroids, sildenafil, chlorpromazine, tamoxifen, ethambutol, chronic alcohol excess

Toxic retinopathy/ optic neuropathy

61

Young adult, gradually progressive night vision deterioration, fundus - pigmented, bone speculae

Retinitis pigmentosa

62

Elderly patient, night time glare, altered red reflex

Age related cataract

63

Malnutrition, malabsorption (e.g. coeliac disease, cystic fibrosis, Crohn's)

Vitamin A deficiency (night blindness)

64

Refractive error and poor night vision

Myopia

65

Persistent flashing and curtain like field loss

Retinal detachment

66

Persistent floater (possibly ring shaped), no field loss

Posterior vitreous detachment

67

Floaters, decreased vision, possible associated systemic disorder e.g. MS, TB, syphilis, sarcoidosis

Intermediate/ posterior/ panuveitis

68

Transient zig zag arc like flashes, headache, transient neurological signs

Migraine

69

Sub acute onset of painful eye movements, RAPD, red desaturation and initial flashes (rarely)

Optic neuritis

70

Halos post ocular surgery

Corneal oedema

71

Halos, reduced visual acuity, foreign body sensation, loss of corneal epithelium, conjunctival redness

Keratitis

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