SECOND VISIT COMPETENCIES - MODEL ANSWERS...

Pre-Registration Optometrist Learning Resource

Page 1 Second Visit Competencies Model Answers 2010/11 24/05/2010

SECOND VISIT COMPETENCIES - MODEL ANSWERS 2010/11 Competency group 1: Communication and Professional conduct 1.2 The ability to elicit significant symptoms. 1.3 The ability to elicit relevant family history. 1.4 The ability to elicit issues pertaining to the patients general health, medication, work, sports, lifestyle and special needs. 1.5 The ability to impart to patients an explanation of their physiological or pathological eye condition. 1.6 An ability to understand a patients fears, anxieties and concerns about their visual welfare, the eye examination and its outcome. 1.7 The ability to discuss with a patient the importance of systemic disease and its ocular impact, its treatment and the possible ocular side effects of medication 2.2 The ability to create and to keep clear, accurate and contemporaneous patient records. 2.3 The ability to interpret and respond appropriately to existing records. 6.1 The ability to interpret and investigate the presenting symptoms of the patient. Write a list of the history and symptoms questions you would normally ask in your Routine eye examination? You should normally have information on the patients age and gender and it may be appropriate to also note their race and take into account any increased risk of ocular problems associated with these factors. Your questioning strategy is a personal issue but should as a minimum cover the following areas: Reason for visit e.g. Why have you come to see me? or What is the reason for

your visit today? Often this will answer several of the other questions you might have asked and should indicate any additional questions you might need to ask.

When was your last eye examination? Existing spectacle correction, how old is it and any problems associated with it. Visual performance Present ocular history, i.e. headaches, pain, diplopia etc. Previous ocular history e.g. squint operations, patching, previous ophthalmological

assessments etc. General health Medication Family Ocular History Family General Health Occupation Driver Hobbies VDU user Contact lens wearer follow up questions as necessary



Remember it is better to ask open-ended questions e.g. has anyone in your family had any eye problems? as well as closed questions e.g. has anyone in the family had diabetes? A useful final question is something along the lines of is there anything else you want to tell me? Further reading on this subject might include Elliotts Clinical procedures in Primary Eye Care and Routine eye examination by Bill Harvey and Andy Franklin in the eye essentials series How would you expand your questioning strategy if the patient complained of: 1. Headaches Follow up questions might include: Where do you get the headaches? When do you get the headaches? Is it associated with anything specific? e.g. reading How long does the headache last? How severe is it? Is it throbbing, sharp or dull? Does anything make the headaches go away? Have you had any tests or diagnoses regarding the headaches? Are there any other symptoms associated with the headaches? e.g. nausea, loss of vision, visual field loss 2. Double vision

Follow up questions might include: Is it in both eyes or just one? When do you get the double vision? Is it associated with anything specific? e.g. reading How long does it last? How severe is it? Is the double vision horizontal or vertical Does anything make the double vision go away? Have you had any tests or diagnoses regarding the double vision? Are there any other symptoms associated with the double vision? e.g. headaches

3. Pain

Follow up questions might include: Where do you get the pain? When do you get the pain? Is it associated with anything specific? e.g. reading How long does it last? How severe is it? Is it throbbing, sharp or dull? Does anything make the pain go away? Have you had any tests or diagnoses regarding the pain? Are there any other symptoms associated with the pain? e.g. loss of vision



How would you explain the following eye conditions to a patient? You need to pitch your explanation in language that each patient will understand, this may mean altering your explanation to take account of the level of understanding of the specific patient you are dealing with. These are some suggestions. Myopia (Short-sightedness) Short sight occurs when light is focused in front of the retina causing distance vision to become blurred. Near vision, however, is usually clear. Short sight normally develops in childhood or adolescence and is often first noticed at school. Glasses may need to be worn all the time or just for driving, watching TV or sports. Short sight means your near vision is clear without glasses and your distance is blurred.

Short sightedness is the inability to see distant objects as clearly as near objects.

Short sightedness is where the light rays from distant objects are focused in front of the retina instead of on it, so that distant objects are not seen clearly.

Often called short sightedness, myopia causes distant objects to appear blurred. The eyeball is too long for the normal focusing power of the eye.

Myopia occurs when the cornea is too steep and/or the eye is too long, causing light to be focused in front of the retina, which results in blurred vision.

Also known as short sightedness, myopia is a refractive error caused by an eyeball that is too long to focus light on the retina or a cornea which is too steeply curved. In these cases light focuses instead in front of the retina.

A focusing defect in which the eye is overpowered. Light rays coming from a distant object are brought to focus before reaching the retina. Requires a minus lens correction to "weaken" the eye optically and permit clear distance vision.

Commonly known as short sightedness. Myopia is a refractive error in which the light rays focus in front of the retina, producing blurry distance vision but clearer up close vision. It is now believed that myopia is partly hereditary; youre more likely to become myopic if your parents are myopic.

Also known as short sight. A refractive error of the eye in which light is brought to a focus in front of the retina, causing distance vision to be blurred (corrected using negative lenses). Uncorrected myopia may cause problems with distance vision, for example not seeing road signs clearly when driving.



Hypermetropia (Long-sightedness)

Long sight occurs when light is focused behind the retina rather than on it, and the eye has to make a compensating effort to re-focus. This can cause discomfort, headaches or problems with near vision. Glasses may need to be worn all the time or just for close work, such as reading, writing or computer use. In older people, as re-focusing becomes more difficult, distance vision may also become blurred. Long sightedness means your distance vision is clear without glasses and your near vision is blurred.

Long sightedness; a condition in which light rays are focused behind the retina so that distant objects are seen more clearly than near ones.

Long sightedness is the inability to see near objects as clearly as distant objects, and the need for accommodation to see distant objects clearly.

Long sightedness is a refractive error, a focusing defect in which an eye is underpowered; light rays coming from a distant object strike the retina before coming to sharp focus, blurring vision. Long sighted people expend focusing effort to see clearly in the distance, and close-up vision is blurred because it takes even more focusing effort. It can be corrected with additional optical power, which may be supplied by a plus lens (spectacle or contact) or by excessive use of the eye's own focusing ability (accommodation).

Often called long sightedness, hyperopia is when the eyeball is too short for the normal focusing power of the eye. Depending on severity, it can cause blurred vision, eye fatigue and sometimes amblyopia or crossed eyes.

Also called long sightedness, this is a condition in which the length of the eye is too short, causing light rays to focus behind the retina rather than on it, resulting in blurred near vision. Additional symptoms include eyestrain and squinting.

Also known as long sightedness, hyperopia is a refractive error caused by an eyeball that is too short to focus light on the retina. Light strikes the retina before it can come to a sharp focus.

Astigmatism Astigmatism occurs when the curvature of the cornea or lens is not perfectly round. It is sometimes described as the eye being shaped like a rugby ball rather than a football. Most people have a small amount of astigmatism, which may not need correcting. If vision is blurred or headaches occur, glasses may help if worn all the time or just for specific tasks.



Astigmatism is where the front focussing part of the eye (the cornea) is shaped like a barrel, one curve being steeper than the other. It causes the image of a cross to be blurred in one direction more than the other and needs a special lens shaped like a barrel to cancel it out. Astigmatism is a refractive error, an optical defect in which refractive power is not uniform in all directions (meridians). Light rays entering the eye are bent unequally by different meridians, which prevents formation of a sharp image focus on the retina. Slight uncorrected astigmatism may not cause symptoms, but a large amount may result in significant blurring and headache.

Astigmatism means that the cornea is not spherical, or round, but rather has a different curvature at different points on the cornea. Think of an eye being shaped like a rugby ball, with the greatest, or steepest, amount of corneal curvature across the laces and the lesser, or flatter, corneal curvature across the end-to-end portion of the football. A normal eye is shaped like a football.

Astigmatism blurs vision at all distances because the optical parts of the eye (cornea and lens) do not focus light onto the retina clearly. This condition is quite common, and results from an unequal curve of the cornea when comparing the horizontal and vertical planes. For descriptive purposes, imagine half of a tennis ball, squeezed at the top and bottom; the ball is now curved unequally. In the eye, this results in inaccurate focus on the retina.

Condition in which the cornea's curvature is asymmetrical (the eye is shaped like a rugby ball, barrel or egg instead of a football); light rays are focused at two points on the retina rather than one, this can result in blurred vision.

Astigmatism is where instead of the front surface of the eye being round it is more oblong. This prevents the light being focused in the right way and leads to blurring. Astigmatism can be secondary to the shape of the cornea or the lens, and is usually correctable with spectacle or contact lenses.

Astigmatism is a condition when the Cornea, (sometimes the lens) curves differently in different directions (a slice through a rugby ball). This causes objects (light) to bend differently to focus on the retina. The image is thus blurred, ghosted, or blurred unless corrected by contact lenses or spectacles.

Presbyopia Presbyopia is where due to normal age related changes the lens inside the eye becomes less flexible and you lose the ability to focus as easily at near. It is why most people need reading glasses as they move past their 40s. Presbyopia is the inability to maintain a clear image (focus) as objects are moved closer.



Presbyopia is the loss of focusing ability that occurs naturally with age. In younger people, the lens is very flexible and the eye has a wide range of focus from far distance to close up. As you get older, the lens slowly loses its flexibility leading to a gradual decline in ability to focus on near objects. Presbyopia is not a disease but a normal and expected change which sooner or later affects everyone, whether you already wear glasses or contact lenses or not. Around the age of 40-45, you will begin to notice that you are holding the newspaper further away or need more light to read small print. There is no advantage in delaying using reading glasses, or changing to bifocals or varifocals. They will not make the eyes lazy.

Presbyopia is the loss of the ability to focus the eyes on near objects that occurs naturally with age, as a result of loss of elasticity of the lens of the eyes.

Presbyopia is the gradual loss of the eye's ability to change focus from distance to near, it occurs in almost everyone after the age of 40.

Presbyopia is a refractive condition in which there is a diminished power of accommodation arising from loss of elasticity of the crystalline lens, as occurs with aging. It usually becomes significant after age 45.

Presbyopia is the inability of the eye lens to focus incoming light, resulting in blurred vision at a reading distance and eyestrain.

Presbyopia is a condition in which the normal changes in the shape of the lens that occur when looking from a far away object to a near one (or vice-versa) are limited. Normally, the iris (the muscle around the lens) causes the lens to change shape as one looks at objects at varying distances. This phenomenon (called accommodation) allows the eye to focus at different lengths. When accommodation is impaired, the eye is unable to adjust sufficiently to nearby objects.

Presbyopia is the gradual loss of the ability to focus clearly for near vision.

Presbyopia is caused by decreased elasticity of the lens due to age which moves the near point of vision farther from the eye, making it difficult to focus on near objects.

Presbyopia is part of the normal process of aging. As a person becomes older, one begins to lose the flexibility of the lens of the eye which limits the ability of the eye to change its point of focus from distance to near.

ARMD

The macula is a tiny area of the retina that allows clear central vision such as that needed to read or drive. A deterioration of the macula is known as age-related macular degeneration (ARMD). Age-related macular degeneration (AMD) occurs when the delicate cells of the macula the small, central part of the retina responsible for the centre of our field of vision - become damaged and stop working.



Some additional information you may or may not want to pass on to your patient: There are two types of AMD: the dry form and the more severe wet form. Dry AMD is the more common, develops gradually over time and usually causes only mild loss of vision. The wet form accounts for only 10-15% of all AMD but the risk of sight loss is much greater. Because macular degeneration is an age-related process it usually involves both eyes, although they may not be affected at the same time. Children and young people can also suffer from an inherited form of macular degeneration called macular dystrophy. AMD is not painful and never leads to total blindness because it is only the central vision that is affected. This means that almost everyone with AMD will have enough side (or peripheral) vision to get around and keep their independence. In the early stages of AMD, central vision may be blurred or distorted and things may look an unusual size or shape. This may happen quickly or develop over several months, although if only one eye is affected it may not be noticed. People with AMD may become sensitive to light or find it harder to distinguish colours. The macula enables people to see fine detail so those with the advanced condition will often notice a blank patch or dark spot in the centre of their sight. This makes activities like reading, writing and recognising faces very difficult. The cause of AMD is unknown but several factors appear to increase the risk. These include smoking, a high-fat diet and excessive sun exposure. Risk also increases with advancing age and may be more common in those with a family history of AMD. The incidence is higher among women and those with light skin or eye colour. There is currently no treatment for dry AMD but the wet form can be treated in several ways. Various forms of laser treatment may be used to halt or slow the progression of abnormal blood vessels and prevent further sight loss. These are simple procedures that can be carried out on an outpatient basis. Drugs are also becoming available for treating wet AMD, whether in the early or late stages. Trials are also taking place for new types of drugs and for combination therapies using drugs and laser treatment. There is evidence that improving your diet by eating fresh fruits and dark green, leafy vegetables may delay or reduce the severity of AMD. Some studies show that taking nutritional supplements may be effective in slowing the progression of AMD although they do not prevent its initial development nor improve vision already lost (AMD Alliance). Cataract A cataract is a clouding of part of the eye called the lens. Vision becomes blurred or dim because light cannot pass through the clouded lens to the back of the eye.



Some additional information you may or may not want to pass on to your patient: Cataracts can form at any age, but most often are a natural consequence of getting older. They develop slowly and are painless. In younger people they can result from an injury, taking certain medication, long-standing inflammation, or illnesses such as diabetes. Early cataracts often make you more short-sighted, which in the early stages can be compensated for by altering the prescription of your glasses. Tinted lenses or shielding your eyes from the sun may also help. However, the benefit is usually only short-lived as the cataract continues to progress and the symptoms increase. At this stage the most effective treatment for cataracts is a simple operation to remove the cloudy lens. I can advise you when you need to be referred to your GP or hospital. Cataract surgery is one of the most common surgical procedures and in most cases can be carried out under local anaesthetic on a day-case basis, without an overnight stay in hospital. Diets or drugs have not been shown to slow or stop the development of cataracts. Glaucoma Glaucoma is the name for a group of eye conditions in which the optic nerve (the nerve at the back of the eye) is damaged, often in association with raised pressure within the eye. This leads to a reduction in the field of vision and in the ability to see clearly. In most cases glaucoma sufferers will experience no symptoms until significant damage has occurred. People aged 40 and over are at greater risk from glaucoma and there is an increasing risk with every decade of life. Those with a family history of glaucoma in close relatives, or in certain ethnic groups (e.g. African-Caribbean people) are considered to have a greater than average risk. People who diabetic or very short- sighted are also more prone to glaucoma.

Glaucoma is a group of eye diseases characterized by pressure that is too high for the optic nerve (the nerve that sends the signal of images created by the eye to the brain) to withstand. Damage to the optic nerve from glaucoma results in loss of peripheral and then central vision. Glaucoma may be treated with medications or surgery to try to stop further damage to the optic nerve and further loss of vision.

Glaucoma is an eye disease in which the normal fluid pressure inside the eyes slowly rises, leading to vision loss or even blindness.

Glaucoma is a disease characterized by elevated intraocular pressure, which causes optic nerve damage and subsequent peripheral vision loss. Most people have no initial symptoms of chronic (open-angle) glaucoma, but you can develop peripheral vision loss, headaches, blurred vision, difficulty adapting to darkness and halos around lights. Other forms of glaucoma (e.g., closed-angle glaucoma) may have additional symptoms such as eye pain, a pupil that doesn't respond to light, redness, nausea and a bulging eye.



Glaucoma is the name for a group of eye conditions in which the optic nerve is damaged at the point where it leaves the eye. The main cause of this damage is raised pressure inside the eye.

Glaucoma is an eye disease caused by impaired drainage of aqueous humour which results in increased intra ocular pressure. Finally the peripheral nerve fibres of the retina gradually die resulting in blindness of central vision to total blindness. Treatment may be medical (eye drops) or surgical. The condition may be acute (angle closure) or the more common open angle glaucoma.

Squint

Strabismus (sometimes called cross eyed) is a disorder of the eyes involving a lack of coordination between the muscles of the eyes. Essentially, the eyes do not point in the same direction. This prevents bringing the gaze of each to the same point in space, preventing proper binocular vision, which may adversely affect depth perception.

A squint is a condition in which the two eyes do not point in the same direction when the patient is looking at a distant object.

A squint is a constant or occasional eye turn, which may be seen in one eye or alternate between eyes. If the turn persists during childhood, then the affected eye may become lazy. Treatment to improve vision in the lazy eye involves patching the good eye. Treatment is most effective if started before school age.

A squint (also known as a strabismus) is a condition that arises because of an incorrect balance of the muscles that move the eye, faulty nerve signals to the eye muscles and focusing faults (usually long sight). If these are out of balance, the eye may turn in (converge), turn out (diverge) or sometimes turn up or down, preventing the eyes from working properly together. Some additional information you may or may not want to pass on to your patient: Squint can occur at any age. A baby can be born with a squint or develop one soon after birth. Around 5 - 8% of children are affected by a squint or a squint-related condition, which means one or two in every group of 30 children. Many children with squints have poor vision in the affected eye. If treatment is needed, the sooner it is started the better the results. Treatment varies accordingly to the type of squint. An operation is not always needed. The main forms of treatment are: Spectacles - to correct any sight problems, especially long sight. Occlusion - patching the good eye to encourage the weaker eye to be used. This is usually done under the supervision of an orthoptist. Eye drops - certain types of squint can be treated with the use of special eye drops. Surgery - this is used with congenital squints, together with other forms of treatment in older children, if needed. Surgery can be performed as early as a few months of age.



How would you discuss with a patient the ocular impact and treatment of the following systemic diseases? You may want use all or only some of the information below to inform your patient: Diabetes Eye problems are among the most significant complications of diabetes, which is the most common cause of blindness in people of working age. Diabetes affects the eye in a number of ways. The most damaging condition occurs when the fine network of blood vessels in the retina the light-sensitive inner lining of the back of the eye leak fluid. This is known as diabetic retinopathy. Cataracts also develop earlier and progress more rapidly in diabetics than in other people. Untreated diabetes may also make cause frequent or noticeable changes to your eyesight. Serious eye problems are less likely if the diabetes is well controlled or in its early stages. Most sight loss from diabetic eye disease can be prevented if detected early and treated.

Your optometrist has an important role to play in detecting the disease and in monitoring your eyes once diagnosed. Checking the appearance of the retina with an ophthalmoscope, a special torch for looking into the eyes, is the most commonly used test for diabetic eye problems. Photographs of the retina may also be used to detect and monitor any abnormalities. If diabetes is suspected, we can refer you to a GP or hospital for medical advice. If diabetes is diagnosed, your eyes will need to be examined regularly for signs of eye problems. You may be referred to a hospital eye clinic or be referred back to your optometrist for regular monitoring. Even though your vision may be good, changes can be taking place to your retina that need treatment. Remember, however, that if your vision is getting worse, this does not necessarily mean you have diabetic retinopathy. It may simply be a problem that can be corrected by glasses. Most sight-threatening diabetic problems can be prevented by laser treatment if it is carried out early enough. It is important to realise, however, that laser treatment aims to save the sight you have - not to make it better. The laser, a beam of high intensity light, can be focused with extreme precision to seal the blood vessels that are leaking fluid into the retina. If new blood vessels grow, more extensive laser treatment may be needed. Diabetics are entitled to a free eye examination provided by the NHS.



Hypertension

Patients with high blood pressure (hypertension) can also develop eye problems. These could include a stroke affecting the vision, temporary loss of vision (amaurosis fugax) or drying of the eye caused when the nerve controlling the upper lid muscle is damaged.

You can help reduce your blood pressure by reducing your energy intake, avoiding excess alcohol consumption (above 20 units/week BP rises linearly with intake). Reducing your salt intake (individual sensitivity to NaCl is highly variable. A realistic goal is around 100mmol/day i.e. no added NaCl and avoidance of salted foods), taking regular exercise (a workload sufficient to cause sweating 3x20mins/week). Other things that can help to reduce cardiovascular risk (without a direct effect on BP) are stopping smoking, reducing dietary fat content (and % saturated fat) and increasing fresh fruit and vegetables (folate deficiency may elevate plasma homocysteine).

These modifications can reduce blood pressure by 11/8 mmHg and either eliminate the need to start drug therapy or reduce need for high dose/multiple drug therapy.

Drug Treatments include:

Beta-blockers Thiazide Diuretics Angiotensin Converting Enzyme Inhibitors (ACEI) Calcium Channel Blockers Alpha-blockers Anti-Hypertensive Agents Vasodilators

N.B Cardiovascular disease affects not only the major arteries in the systemic circulation--retinal vascular disease can be a manifestation of generalised atherosclerosis or a result of embolic disease originating from the cardiovascular system.

Central retinal artery occlusion may occur secondary to emboli from the carotid artery, or from the heart.

Hypertension is a major risk factor for central retinal vein occlusion.

Atherosclerosis, hypertension and diabetes are all thought to be possible risk factors for non-arteritic ischaemic optic neuropathy (sudden, painless visual loss not associated with temporal arteritis).

Some effects of cardiovascular disease may be directly related, such as a cortical stroke affecting the visual pathway, or amaurosis fugax, indicating compromise of the anterior cerebral circulation, or problems may arise indirectly, such as corneal exposure secondary to a seventh nerve palsy affecting the obicularis oculi muscle (which aids lid closure).

http://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper4.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper5.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper6.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper7.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper8.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper9.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper10.htmlhttp://www-clinpharm.medschl.cam.ac.uk/pages/teaching/topics/hyper/hyper11.html



Stroke

A Stroke is a type of cardiovascular disease. It affects the arteries leading to and within the brain. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts. When that happens, part of the brain cannot get the blood (and oxygen) it needs, so it starts to die.

Stroke can be caused either by a clot obstructing the flow of blood to the brain or by a blood vessel rupturing and preventing blood flow to the brain.

The brain is an extremely complex organ that controls various body functions. If a stroke occurs and blood flow can't reach the region that controls a particular body function, that part of the body won't work as it should. A stroke is the popular term used for a cerebrovascular accident (CVA) which is an interruption of the blood supply to, or haemorrhage into, a part of the brain resulting in impaired function of the brain and nervous system. The part of the brain deprived of a blood supply will be damaged and the resulting impairment of body function will remain. The features of a stroke depend upon the site of damage to the brain. The most common site of brain damage results in hemiplegia (weakness or paralysis of part or all of one side of the body), hemianaesthesia (loss of sensation of part or all of one side of the body), and hemianopia (loss of vision to one or other side). Strokes affecting the right side of the body are commonly associated with dysphasia (difficulty with expressing and understanding language), and strokes affecting the left side are associated with perceptual problems (lack of awareness of the affected part of the body).Stroke affecting a part of the brain called the brain stem may produce vertigo (a disturbance of balance with sensations of movement or rotation), difficulty with speech, chewing and swallowing, weakness of the face, difficulty in controlling movements of the eyes, ataxia (unsteadiness and incoordination of movement) and nystagmus (fine rapid movements of the eyes). Stroke affecting the cerebellum causes, in the acute phase, in-coordination, decreased muscle tone, and some loss of limb power. Dysarthria (difficulty with articulating speech), nystagmus, ataxia and disorders of gait, are possible long term effects. Unless the stroke is so severe as to cause death within a few days a degree of recovery from the initial level of disability can be expected. One third will eventually make full recovery, one third will remain disabled to some extent, and the remaining third will remain severely disabled and dependent. Most of the recovery takes place within the first six months; no improvement of functional significance can be expected after one year. Recovery and the effectiveness of rehabilitation depend upon many factors including the size and site of the brain damage, the presence or absence of other disabling conditions (dementia, cardiac disease, lung disease, arthritis, mental illness, depression and blindness), motivation and the age of the disabled person.



Some affected individuals are prone to series of repeated episodes which resolve within 24 hours (called transient ischaemic episodes) which may cause temporary paralysis, repeated episodes of unconsciousness or altered awareness, and difficulties with speech or other special senses.

Treatment

Because their mechanisms are different, the treatments for the types of stroke are different:

Ischemic stroke is treated by removing obstruction and restoring blood flow to the brain.

In hemorrhagic stroke, doctors introduce an obstruction to prevent rupture and bleeding of aneurysms and arteriovenous malformations.

Ischemic Stroke

Acute Treatment

Clot-busters, e.g. tPA The most promising treatment for ischemic stroke is the clot-busting drug tPA, which must be administered within a three-hour window from the onset of symptoms to work best. Generally, only 3 to 5 percent of those who suffer a stroke reach the hospital in time to be considered for this treatment.

Preventative Treatment

Anticoagulants/Antiplatelets

Antiplatelet agents such as aspirin, and anticoagulants such as warfarin interfere with the blood's ability to clot and can play an important role in preventing stroke. Carotid Endarterectomy

Carotid endarterectomy is a procedure in which blood vessel blockage is surgically removed from the carotid artery. Angioplasty/Stents Doctors sometimes use balloon angioplasty and implantable steel screens called stents to treat cardiovascular disease in which mechanical devices are used to remedy fatty build up clogging the vessel.

Haemorrhagic Stroke

Surgical Intervention

For haemorrhagic stroke, surgical treatment is often recommended to either place a metal clip at the base, called the neck, of the aneurysm or to remove the abnormal vessels comprising an Arteriovenous Malformation (AVM). Endovascular Procedures, e.g., "coils" Endovascular procedures are less invasive and involve the use of a catheter introduced through a major artery in the leg or arm, guided to the aneurysm or AVM where it deposits a mechanical agent, such as a coil, to prevent rupture.

http://www.strokeassociation.org/presenter.jhtml?identifier=2532#Ischemic_Stroke#Ischemic_Strokehttp://www.strokeassociation.org/presenter.jhtml?identifier=2532#Hemorrhagic_Stroke#Hemorrhagic_Stroke



Identify the potential problems with this record?

Date of Exam Optometrist Patient Charles Brown

Age 27

CURRENT RX CONDITION Good, 2 years old

VISION

SPH CYL AXIS PRISM BASE VA

CONTACT LENS USER Y/N TYPE NA

R 6/9

-1.00 +0.50 180 6/6

REASON FOR VISIT Wants new glasses

L 6/6

-0.75 6/6

DATE OF LAST EXAM/LAST RX 2 years

ADD

NEAR VA N4.5

DISTANCE/NEAR/BIF/VARIF Distance

SYMPTOMS No problems

OMB

DIST H Ortho

NEAR H Ortho

NPC 6cm

V ortho

V ortho

IOP R L TIME MEAN OF READINGS

EXTERNAL R L LIDS/LASHES CORNEA A/C LENS

FIELDS R L

STEREO COLOUR

AMSLER

INTERNAL MEDIA

DISCS:CUP MARGIN

COLOUR VESSELS A/V3:4 MAC Reflex NAD PERIP

PD DIST 64mm

NEAR 58mm

ACCOMM R L BIN MOTILITY NAD

PUPILS D 4 C 4 N 4 NO RAPD

RETINOSCOPY R -1.00/+0.50 x 180 L -0.75

SUBJ SPH CYL AXIS VA PRISM BASE

BIN ADD

BIN VA ADD NEAR VA

R

-1.00 +0.50 180 6/6 6/6

N4.5

L

-0.75 6/6 N4.5

SPH

CYL AXIS PRISM

BASE OMB DIST H NEAR H NPC

RX R L

-1.00

+0.50 180 V V

-0.75

-0.25

180

ADVICE RE PRESCRIPTION New glasses

ADVICE TO PATIENT NEAR ADD INTER ADD

BACK VERTEX WD 12mm



Date of Exam No date Optometrist Not

signed or initialled Patient Charles Brown

Age 27 No Date of birth

CURRENT RX CONDITION Good, 2 years old

VISION

SPH CYL AXIS PRISM BASE VA

CONTACT LENS USER Y/N TYPE NA

R 6/9

-1.00 +0.50 180 6/6

REASON FOR VISIT Wants new glasses

L 6/6

-0.75 6/6

DATE OF LAST EXAM/LAST RX 2 years

ADD

NEAR VA N4.5

DISTANCE/NEAR/BIF/VARIF Distance

SYMPTOMS No problems Not enough detail, No mention of GH, FOH POH, etc.

OMB

DIST H Ortho

NEAR H Ortho

NPC 6cm

V ortho

V ortho

IOP R L TIME MEAN OF READINGS

EXTERNAL R L LIDS/LASHES CORNEA A/C LENS

FIELDS R L

STEREO COLOUR

AMSLER

INTERNAL MEDIA

DISCS:CUP MARGIN

COLOUR VESSELS A/V3:4 MAC Reflex NAD PERIP

PD DIST 64mm

NEAR 58mm

ACCOMM R L BIN MOTILITY NAD

PUPILS D 4 C 4 N 4 NO RAPD

RETINOSCOPY R -1.00/+0.50 x 180 L -0.75

SUBJ SPH CYL AXIS VA PRISM BASE

BIN ADD

BIN VA ADD NEAR VA

R

-1.00 +0.50 180 6/6 6/6

N4.5

L

-0.75 6/6 N4.5

SPH

CYL AXIS PRISM

BASE OMB DIST H NEAR H NPC

RX R L

-1.00

+0.50 180 V V

-0.75

-0.25

180

ADVICE RE PRESCRIPTION New glasses

ADVICE TO PATIENT NEAR ADD INTER ADD

BACK VERTEX WD 12mm

Theres insufficient information here, a tick or NAD is not acceptable (No Abnormality Detected often thought to stand for Not Actually Done!) theres no discrimination between left and right. There is no information in the advice to patient box, the minimum required would be the suggested next examination interval.

The right eye is written in plus cylinder form, the left in minus cylinder form. You should always be consistent and write both cylinders in the same power format.



Your patient mentions that they are taking medication X, what additional questions would you ask?

What the medication is for How long they have been taking it What is the concentration of the drug How frequently they are using it i.e. once a day, four times a day etc. Any problems associated with the medication i.e. side effects When they last saw their doctor i.e. should they still be using this drug

Your patient tells you that they enjoy reading, DIY and going to the cinema, what additional questions could you ask? Hopefully you have already asked the patient whether they have a reading correction and whether it is still adequate. It would be useful to ask if they use spectacles for the cinema and what kind of DIY (Do It Yourself) they enjoy and whether they wear protective spectacles and if so are they prescription safety spectacles. N.B. To achieve these competencies you must be able to demonstrate to your Assessor that you can get information from a patient in a structured and logical manner; that you can review and interpret existing patient records; that you can take into consideration significant symptoms, history and other relevant information reported by your patient; that you can arrange appropriate investigations and follow-up for symptomatic patients where necessary; that you can adapt your consultation style to meet the needs of different patients (e.g. age, level of understanding); that you can record findings in a format that is appropriate, legible and understandable; that you can explain to your patients the nature and consequences of physiological and pathological eye conditions in a clear, and understandable manner and that you can discuss the implications of specific systemic diseases and medications with ocular manifestations. You will need to provide patient records demonstrating that you have seen a patient presenting with headache and/or blurred vision; at least one patient with symptomatic cataract, patients with systemic disease e.g. cardiovascular, diabetes, a patient with a family history of glaucoma and at least one patient taking systemic medication with known possible ocular adverse reactions.



Competency group 2: Assessment of Visual function/Binocular Vision anomalies 3.1 The ability to refract a range of patients with common optometric problems by appropriate objective and subjective means. 6.8 The ability to identify abnormal colour vision and to appreciate its significance. 8.1 The ability to assess binocular status using objective and subjective tests. 8.4 The ability to manage an adult patient with heterotropia What tests and procedures would you use in your routine examination of a presbyopic patient? NOTE: There is no right and wrong answer to this but be prepared to justify the inclusion and omission of tests and procedures in your assessment and remember if you include a test you must be able to answer the following questions- 1. Why am I doing this test? 2. Can I do this test competently? 3. What do I do with the results of this test? If you take a measurement and dont know what to do with it, why do the test in the first place? For the assessments your patient will have "lost" their spectacles and supplementary tests (e.g. central fields, slit lamp etc.) are not required but it may be appropriate to suggest them as part of your advice and recommendations. A suggested routine would include: History & Symptoms (reason for visit, LEE (Last eye examination), OH (ocular

health), FOH (Family ocular history), GH (general health), FGH (Family general health), occupation/ hobbies, VDU (Visual Display unit may be called DSE (Display screen equipment) on some forms) user, Contact lens wearer, driver etc.)

Visions (DV & NV) monocularly and binocularly Unaided Cover test at 6m and near Ocular motility Convergence Pupil reactions Confrontation field testing N.B. this is no longer required in the final Routine exam External eye exam Internal eye exam Direct Ophthalmoscopy in the final exam Retinoscopy Monocular distance subjective to establish VA Binocular balancing and binocular visual acuity where appropriate Distance oculo-motor assessment (6m) Near add determination, acuities, working distance and range Near oculo-motor assessment Any other relevant tests (mention central fields, tonometry etc. with presbyopic

patients) Determination of correction needed and Advice and recommendations



Remember to measure monocular PDs before setting up the trial frame and make sure the patient is comfortable. Measuring and noting the back vertex distance would be sensible with prescriptions over +/- 4.00 dioptres. Completing the refraction before ophthalmoscopy is acceptable but in the assessments it might be sensible to complete ophthalmoscopy before the refraction. This is in order to avoid rushing ophthalmoscopy if you are running out of time at the end of the exam.

Remember to write down everything you do and see, you can not be failed for writing too much, you can be failed for failing to record things you observed or did (remember if it isnt written down, legally you havent done it!!) this is something the examiners may mark you on in the assessments. N.B. Do not assume that your routine patient will be routine. In the stage 2 work based assessment you may have a patient with an unusual fundal appearance, binocular vision abnormalities etc. in which case your advice and recommendations may include referral or the need for further investigation.

How should you conclude an eye examination? It may be appropriate at the end of your routine eye examination to carry out supplementary tests e.g. further assessment of binocular function. Certainly in the assessments it is unlikely you will have time to do slit lamp biomicroscopy or visual field assessment,, you should make clear at the end what additional tests you would carry out. At the end of the examination you must discuss your findings. What is the cause (if known) of the chief complaint and any secondary complaints? Give a full explanation of the diagnoses, in terminology which is appropriate to the patients perceived knowledge. This generally includes an explanation of the patients refractive error. Reassure the patient if no cause is found. Discuss possible treatment options and whether referral is necessary, discuss the type and use of correction if applicable, advise of any possible problems with treatment (adaptation to cylindrical changes, anisometropia etc.). Explain the likely prognosis of the patients condition(s), (progression of myopia etc.), finally indicate when you would like to see the patient again. If a new patient has no retinoscopy reflex, what simple measures might give you a useful means of determining your starting point for subjective refraction? Simple measures, which may be helpful for establishing a starting point, include: - History & symptoms: listen to the patients description of blur at different distances, if

they see clearly at near but not distance they are probably myopic A history of previous cataract surgery several years ago, might suggest aphakia Recording unaided near vision at appropriate working distance. (e.g. a - 6.OODS

myope reads N5 unaided at about 13cm). Correlating the unaided distance vision with refractive error -0.25DS = one line

acuity (e.g. in a young patient who is 6/36 unaided - expect Rx to be about -2.OODS).

Keratometer or stenopaic slit for astigmatism.



What tests might you use to check the spherical lens power during your monocular subjective refraction? Flip lenses The duochrome test The plus one blur test How do they work? Flip lenses use +/-0.25 lenses to find the most positive lens that gives maximum

contrast (clearest vision). The duochrome test relies on the fact that green light is refracted at a greater angle

than red light and will therefore form an image in front of that formed by red light. As the duochrome test consists of black targets on red and green backgrounds the two sets of targets are focused in different planes. If the green targets are seen more clearly than the red, the eye is underplussed and if the red is clearer, the eye is overplussed. The eye is usually left slightly overplussed, on the red.

The plus one blur test works on the assumption that visual acuity drops by one line

for each +0.25DS over plussed. The vision should drop to 6/18 (from 6/6) if the prescription is not underplussed.

Why is it better to perform the Duochrome test in lower room illumination? As the test uses chromatic aberration, reducing the room illumination will improve the performance, as the amount of aberration will be greater with a larger pupil. What clues might you have that a young myope was over-minused during a subjective refraction? 1. Higher Rx than would be predicted from unaided Vision 2. +1.00 would not blur back by 4 lines 3. Duochrome on Green 4. Problems reading Give examples of errors in retinoscopy technique that could result in inaccurate retinoscopy findings? What would their effect be? How are they corrected? 1. Off axis retinoscopy - inaccurate cylinder and axis. Use right eye for right side, left

for left side. 2. Inadequate control of accommodation - fluctuating reflex, particularly in a young

hypermetrope. You could try over-plussing the opposite eye while working (check quickly for an against reflex in the other eye before starting), using near retinoscopy/Mohindra technique or if required a cycloplegic refraction.



3. Incorrect working distance - this results in a consistent over or under correction of

errors compared with the subjective findings. Make sure you work at a known working distance and have calculated the correct working distance lens.

4. Poor end-point discrimination - this results in small unpredictable over or under

corrections. You can check you are at the neutral point by increasing and decreasing the working distance, once you think you are at the neutral point, look for an against and with reflex respectively. Adjust the retinoscope vergence when approaching the end point to increase sensitivity.

5. Retinoscopic collar up - complete reversal of retinoscopic reflexes (with for against etc.). Check your collar is down.

6. Holding the lenses away from the spectacle plane - resulting in over or under

correction of errors compared with the subjective findings.

7. Not concentrating on the movement in the centre of the pupil only, in patients with large pupils - resulting in over or under correction of errors compared with the subjective findings.

8. Blocking the patients view of the distance chart - stimulating accommodation What tests could you use to check the binocular function post refraction? Cover test (with/without prism bar) Maddox rod and wing Mallett unit (distance and near) Ask the patient if they have diplopia What are the advantages of binocular refraction? Patients usually view the world binocularly. Better control over, and greater relaxation of, accommodation, than traditional

monocular procedures Quicker than monocular refraction Occluder in monocular refraction manifests latent nystagmus What patients might benefit from a binocular refraction? Hypermetropic anisometropes Latent hypermetropes Pseudomyopes Antimetropes Unilateral amblyopics Patients with unequal acuities Patients with latent nystagmus Cyclophorics



What techniques are available for binocular refraction? Fogging - The modified Humphriss immediate contrast technique - the whole

refraction is performed under binocular conditions by first fogging the non-tested eye, reducing the VA by three or four lines, compared with the tested eye, with a +0.75/+1.00 (rather than occluding).

Septum - physically blocks or obstructs part of the target for each eye (Turville) Polarisation techniques - Analyzer and polarised target have the same axis of

polarisation, allowing the right eye to view the right half of the target, but blocking the left half of the target from view.

What is the purpose of binocular balancing? After finding the monocular prescription, binocular balancing checks the dynamic accommodative relationship between the two eyes. Youre trying to find the maximum plus or minimum negative, balancing the spherical component of the refraction for the two eyes (i.e. balancing accommodation, not acuities), while still keeping the best acuities. Be careful not to reduce the acuities especially of the dominant eye to avoid any intolerance. Accommodation may be equalised but not necessarily minimised following binocular balancing. Which patients might not need to be binocularly balanced? Little or no accommodation e.g. 70+, Patients with strabismus, Inter eye acuity difference (>1 lines), Marked ocular dominance, Reduced acuities, around 6/18 or less, Aphakes/Pseudophakes, Uniocular patients etc. What factors are you assessing in your examination of ocular motility? That both eyes move smoothly and follow your target. That there is corresponding lid movement accompanying the vertical eye

movements. That there is no under action or over action of the movement of one eye in any

direction of gaze. Patients are asked if they experience any diplopia (sensory adaptations in incomitant deviations may suppress this). A diplopic image due to a paretic muscle is displaced in the same direction as the rotation which contraction of that muscle normally produces. The eye that sees the outermost of the diplopic images in a cardinal position of gaze is therefore the eye with the paretic muscle. Patients should also be asked if they experience pain on extreme gaze as this may also indicate difficulties with ocular movement.



Using a simple diagram show the direction in which the extra-ocular muscles have their main action, and list their innervating nerves. RSR RIO LIO LSR RLR RMR LMR LLR

R L RIR RSO LSO LIR IIIrd SR; MR; IR; IO IVth SO VIth LR What are the muscle sequelae in a palsy? 1. The primary muscle palsy shows as the greatest underaction. 2. Overaction of the contralateral synergist. 3. Contracture of the ipsilateral antagonist, which shows as an overaction. 4. Secondary inhibition of the contralateral antagonist, which shows as an underaction. 1 & 2 occur at the onset of the palsy. 3 & 4 take a few months to develop.



Complete the table below to compare the three main types of accommodative esotropia Fully

Accommodative Esotropia

Partially Accommodative Esotropia

Convergence Excess Esotropia

Cover test without Rx distance Rx near

Esotropia D & N

Esotropia D & N (increases on accommodation)

Esotropia D > N (may be straight for D)

Cover test with Rx distance Rx near

Straight D & N

Esotropia decreases but still present D & N

Straight for D Esotropia for N

AC/A ratio

Normal

Normal

High

Amblyopia Y/N

No

Yes

No

Refractive error

Hyperopic

Hyperopic

Mostly Hyperopic

ARC

No

Possibly

No

Stereopsis

Good

None

Good

Constancy of Deviation

Present on accommodation

Constant

Squint for near

Management

Fully correct refractive error

Regular review Refer?

Fully correct refractive error

refer for surgery

Bifocals? Refer? Miotics?

What is Panums fusional area? In normal binocular vision, the fovea of one eye corresponds with a small area centred on the fovea of the other eye, this is Panums fusional area. What is fixation disparity? Fixation disparity is a small deviation from bifoveal fixation, which does not exceed Panum's fusional areas.



What is the associated phoria? The amount of prism required to precisely

place the image on corresponding points is known as the associated phoria and can be measured with the Mallett unit. The American Sheedy disparometer can be used to measure the size of the fixation disparity rather than the prism neutralisation point.

What justification is there for checking the associated phoria in a routine examination? Optometrists often use this measurement to help decide if a phoria is decompensated, although fixation disparity can be found in a well compensated phoria also. Indeed, there is one school of thought that fixation disparity is a normal finding in the presence of heterophoria representing a fresh innervational stimulus to decaying fusional vergence. In isolation, the associated phoria, as measured on the Mallett Unit is a meaningless figure. However, if other signs of decompensated phoria are found e.g. as poor fusional recovery movements on cover test, and reduced fusional reserves. The Mallett Unit can be used to assess progress in exercises or the relief in fusional stress which a change in prescription, such as increased plus for near in the case of decompensating near esophoria, might bring about. It is also a useful guide as to how much relieving prism is appropriate, particularly in vertical deviations which do not lend themselves to treatment with exercises.

How does heterophoria differ from fixation disparity? Fixation disparity is a physiological variant of normal binocular

vision,

Heterophoria is described monocularly when the eyes are dissociated

(during the cover test or Maddox rod or wing).

What is eccentric fixation? A monocular condition in which fixation is with a point on the retina other than the fovea. What is amblyopia? There are a variety of definitions, which include - Visual acuity worse than 6/9, which is not due to uncorrected refractive errors, ophthalmoscopically detectable anomalies of the fundus or pathology of the visual pathway or a visual loss resulting from an impediment or disturbance to the normal development of vision. What is the incidence of amblyopia in the general population? Between 2 and 3%.



How would you classify amblyopia? ORGANIC AMBLYOPIA 1) Retinal eye disease 2) nutritional 3) toxic 4) idiopathic or congenital FUNCTIONAL AMBLYOPIA 1) Stimulus (or visual) deprivation 2) strabismic 3) anisometropic 4) refractive 5) psychogenic (hysterical) List methods of amblyopia therapy in rough order of possible success. Full correction of refractive error, use cycloplegia, Occlusion (total, partial, full/part time), Partial occlusion usually an hour a day. Few recommend total occlusion these day Optical penalisation, blur back the better eye to a line or more than the worse eye Drug penalisation, (as an optometrist is this a diagnostic or therapeutic use of a

drug?), CAM visual stimulator, (questionable effectiveness, the original clinical work was

flawed) Pleoptic treatment, (questionable effectiveness), After-image transfer method, (questionable effectiveness). Do you consider it appropriate to treat amblyopia in private practice? Some practitioners might ask instead when do you consider it appropriate to treat amblyopia in private practice? As long as you can justify your answer you will be OK. Remember to be safe to practice you have to be sure that the patient has no underlying pathological cause for their amblyopia before beginning treatment. If in any doubt refer for ophthalmological opinion! You could argue that it is appropriate to attempt to treat discharged anisometropic amblyopes of between 7 and about 12 years of age, in private optometric practice, where patient motivation and co-operation are good. Or older patients where occlusion therapy has not been tried previously. Remember that this will require regular follow up and the GOS may not be prepared to pay for this!



What would you do with patients you considered inappropriate for practice treatment? Strabismic and refractive amblyopes up to about 6 years: - Refer for orthoptic

treatment through the hospital eye department. (You could argue that it is better for a child to be looked after by the same local optometrist with the appropriate equipment and skills, then travelling miles to wait in large hospital department).

Strabismic amblyopes older than about 6 years (and anisometropic amblyopes with

poor motivation) - Leave if you feel very brave, refer for Ophthalmological opinion and possible orthoptic treatment through hospital eye department if you are sensible.

Anisometropic amblyopes older than 12-14 you could try for a short period and

abandon if no useful improvement or not treat at all only refer if they have not been assessed by an ophthalmologist.

Amblyopia due to active organic cause: - Refer. Sudden unexplained strabismus or inconcomitant deviations:- Refer to

Ophthalmologist Poor motivation and co-operation: - Refer on but explain the problem to the GP.

What is microtropia? A small heterotropia (less than 6

), which may be difficult or impossible to detect by cover test.

What are its clinical characteristics? Small angle less than 6 The deviation may not show on cover test (because it is a fully adapted strabismus)

Anisometropia, there is usually a difference of more than 1.5 D. Amblyopia, usually the acuity is only reduced one or two lines to 6/9 or 6/12 Eccentric fixation, theres a suppression scotoma in the foveal area of the amblyopic

eye. The angle of eccentric fixation is the same as that of the angle of strabismus, thus theres no movement on cover test as the image in binocular vision falls on the eccentrically fixating retinal area.

Abnormal correspondence, HARC is present in microtropia i.e. the strabismus is fully adapted.

Peripheral fusion, the eyes in microtropia seem to be held in the nearly straight position of the small angle by the fusional impulses provided by the peripheral vision.

Monofixational syndrome, in many cases the angle of deviation may increase on the alternating cover test or even if one eye is covered for slightly longer time than normal during the cover test.

Stereopsis, a low grade of stereopsis may be present.



Evans suggests the following algorithm to assist in the diagnosis of microtropia

All the following characteristics must be present Angle less than 10Amblyopic eye with morphoscopic acuity of at least one

Eccentric fixation

line worse than the dominant eye

HARC

And three of the following characteristics must be present Angle less than 6Anisometropia over 1.5D

Microtropia with identity: angle of anomaly = angle of eccentric fixation, so no movement when dominant eye is covered Monofixational Motor fusion: pseudo-fusional reserves can be measured

syndrome: apparent phoria movement on cover test

Stereopsis of 100 or more Four prism dioptre test shows positive response

What is the four prism dioptre test? A 4

base out prism is placed before one eye. The typical response is a small initial vergence movement followed by a conjugate saccade (version movement) and then a symmetric vergence movement. In microtropia, if the prism is placed before the strabismic eye, the image will fall within the suppression area and there will be no movement of either eye. If the prism is placed before the other eye then both eyes will make the initial version movement but the microtropic eye will fail to make the subsequent vergence movement.

What treatment would you consider for microtropia? Treatment is not indicated since this is an asymptomatic, fully adapted squint of good cosmetic appearance, and microtropias do not respond readily to treatment. Younger children are sometimes treated either refractively or with occlusion but the results rarely justify the effort. Of course, anisometropic amblyopias respond readily to refractive correction, provided they are well motivated to wear the spectacles. If the microtropia has broken down into a larger deviation, or if monofixational heterophoria is decompensated and giving symptoms, treatment may be appropriate to restore full adaptation or compensation. What is abnormal retinal correspondence? ARC is a binocular condition in which the fovea of the fixating eye has a common visual direction with a non-foveal area of the deviating eye.



What are the commonest causes of neurological strabismus and the most likely nerve to be affected for each cause? Neurogenic lesions account for the majority of palsies, the sixth (abducens), fourth (trochlear) and third (oculomotor) being affected in that order of frequency.

Congenital:

- Most are isolated defects, sometimes familial of unknown cause (developmental defects), may be multiple or bilateral although usually asymmetrical. (Especially IV & VI) - Birth trauma (Especially VI) - Hydrocephalus or cerebral palsy

Acquired:

Trauma (III, IV & VI affected; VI most frequent ) Metabolic disorders - Diabetes (Especially VI & III) Vascular - Hypertension (VI), Aneurysm (Especially III ), CVA (III, IV & VI ) Space occupying lesions - Tumours (Especially VI ) Inflammation - Demyelinating disease, meningitis, encephalitis (Especially VI, IV ), HZO (Especially VI & III). How does this differ for different age groups? Nerve

Childhood

> 55 years

< 55years

Third

Trauma (including birth injuries)

Intracranial aneurysm (especially posterior communicating artery) Trauma

Small blood vessel disease (especially hypertension and diabetes)

Fourth

Trauma

Trauma

Trauma

Sixth

Idiopathic, isolated, benign (? viral infection) Raised intracranial pressure Trauma (including birth injuries)

Multiple sclerosis Space-occupying lesions Trauma

Small blood vessel disease Space-occupying lesions



How would you differentiate between a superior rectus and contralateral superior oblique palsies? Comparison of the amount of vertical deviation in extreme positions of gaze, using

the alternating cover test. The deviation would increase on dextro-depression in a left superior oblique palsy but increase on dextro-elevation in a right superior rectus palsy.

Inspection of the outer fields of the Hess chart Fixation preference, the majority of patients fixate with the unaffected eye Extorsion of the globe, more likely with an underaction of the superior oblique Comparison of the near and distance vertical deviation. Hypertropia increasing at

near suggests a superior oblique palsy Compensatory head posture, the chin should be elevated in a superior rectus palsy

and depressed in a superior oblique palsy. Bielschowsky head tilt, a positive result indicates a superior oblique palsy What is the Bielschowsky head tilt test? This aids in the differentiation of vertical and oblique muscle palsies. e.g. patient with a left fourth nerve palsy, on tilting the head to the left shoulder the vertical deviation becomes more obvious. This is because when the head is tilted to the left shoulder, the left eye has to intort in order to maintain fixation. This cannot happen because the left superior oblique, which is the primary intortor of the eye, is weak. In its place, the left superior rectus, which is the secondary intortor, comes into play. Because the superior rectus is a much more effective elevator than intorter, the eye shoots up. These findings are absent when the head is tilted to the right shoulder. Patients with bilateral superior oblique palsies will demonstrate a right hyperdeviation with the head tilted to the right shoulder and a left hyperdeviation with the head tilted to the left shoulder. What does this head tilt show? R

R L This head tilt to the left shows an increase of left hypertropia this implicates the left superior oblique. If there had been an increase of left hypertropia when tilting the head to the right this would implicate the left inferior rectus.



How would you differentiate between a unilateral neurogenic and mechanical paralytic strabismus?

Neurogenic

Mechanical

Deviation Deviation in the primary position can be marked

Little deviation in the primary position

Diplopia The separation of the images remains the same in different gaze positions (except for III nerve palsy) e.g. homonymous, right image above left

Diplopia may reverse e.g. between up-gaze and down-gaze

Head posture Head tilt in vertical muscle palsies

Vertical deviations are compensated by a chin elevation or depression (head tilt is rare)

Ocular movements

Movement often greater on duction than on version. Movement ceases gradually in the direction of limitation. Movement is most limited in the position of main action of the affected muscle.

Duction and version movements are equally limited. movement ceasing when the mechanical factor intervenes

Hess chart The field of the affected eye will be smaller but there is proportional spacing between the inner and outer fields. both fields are displaced according to the deviation

The outer field of the chart will be very close to the inner field in the direction of maximum limitation of movement. The field of the affected eye may be very narrow, either horizontally or vertically. Typically the field is limited in for example up-gaze rather than dextro-elevation (Browns syndrome excepted). There is no contracture of the ipsilateral antagonists.

Globe retraction None The globe often retracts when turned in the direction opposite to the site of the mechanical lesion

Pain on movement

None Found in acquired lesions and in some cases of Browns syndrome

Forced duction test

Full passive movement unless secondary muscle contracture has occurred over a long period

Limited passive movement, generally in the direction opposite to the site of the lesion, sometimes in the same direction, or in both directions

Intraocular pressure

Unchanged in different directions of gaze

Raised when looking away from the site of the mechanical lesion (a difference > 5mmHg between two opposite directions of gaze is significant)



What is the incidence of genetic colour defects? Male Female

Deutranomalous 5% 0.40% Anomalous Trichromatism:

Protanamalous 1% 0.02% Tritanamalous Unknown

Deutranopic 1% 0.02% Dichromatism:

Protanopic 1% 0.02% Tritanapic 0.001% 0.001%

Cone Unknown Monochromatism:

Rod 0.003% 0.003% What advice would you give to a seven year old boy and his parents with a congenital red green colour defect? All hereditary colour defectives should be reassured about their condition: that they are not colour blind, that it is not a disease and that the condition will always remain but will not get worse. If the family have been unaware of the condition you can use this as a demonstration of how little it has impaired development. However advice should be given about career limitations e.g. The forces, chemistry, photography, the paint and textiles industries and electronics. It would also be sensible to suggest that the parents should inform school of potential problems with colour discrimination. How would you differentiate between an acquired and congenital colour defect?

Acquired

Congenital

Monocular or unequal Equal in both eyes Recent onset, changing Long-standing, constant Equal incidence male and female

Predominantly male

Aware Unaware Other symptoms None Commonly Blue yellow Usually Red green

Most important thing to remember is to do the colour vision tests monocularly and look for a difference between the two eyes.



What is the significance of an acquired colour defect?

Acquired defects of colour vision are seen predominantly in acquired disorders e.g. patients with cataract, glaucoma or macular and optic nerve disease, and may complicate inherited retinal dystrophies particularly those causing abnormal cone function. Patients therefore need to be referred for further ophthalmological assessment with varying degrees of urgency to detect the underlying cause.

N.B. To achieve these competencies you need to demonstrate to your Assessor that you can accurately determine your patients spherical, astigmatic and presbyopic refractive errors; that you can assess your patients ocular motor balance using a range of objective and subjective tests; that you can manage heterotropia appropriately taking into consideration your patients age and clinical findings; that you can assess your patients colour vision using suitable tests under appropriate conditions and recognise any colour vision abnormality and that you can explain the implications of colour vision defects with respect to vocational and lifestyle requirements to your patients. You will need to provide patient records demonstrating that you have seen and managed at least one adult patient with heterotropia and at least one patient with a colour vision defect.



Competency group 3: Methods of Ocular examination 5.2 The ability to assess the external eye and adnexa. 5.3 The ability to assess the tear film. 5.5 The ability to use a slit lamp. 5.6 The ability to use diagnostic drugs to aid ocular examination. 5.7 The ability to examine fundi using direct and indirect techniques. 5.9 The ability to investigate visual fields and to analyse and interpret the results 5.11 The ability to make an assessment of the fundus in the presence of media opacities. 5.13 The ability to assess visual fields of patients with reduced visual acuity. What changes to legislation have occurred affecting the use of Pharmacy only (P) drugs by optometrists? Optometrists can now supply a range of P (Pharmacy Only) medicines to their patients outside the previous emergency only situation. What, in relation to ophthalmic drugs, are Level 1 exemptions? Exemptions to allow optometrists to use specific prescription-only medicines (POMs), are provided for in the Prescription Only Medicine (Human Use Order) 1997 SI No 1830 (the POM Order) and the Medicines (Sale or Supply) (Miscellaneous Provisions) Regulations 1980 SI No 1923. Two new exemption levels for optometrists, Level 1 and Level 2, have been established. Access to the Level 1 exemption list continues to be via entry-level registration and there is no requirement for further training. Level 1 represents an update of the exemptions list which had not been amended since 1978. As a result, several drugs on the original list are no longer commercially available and these have been removed. All medicines on the Level 1 list (with the exception of topical anaesthetics) can be sold or supplied by the optometrist directly to the patient in an emergency, or can be routinely supplied from the pharmacist, against an order signed by the optometrist (Signed Order). What prescription-only medicines (POMs) ophthalmic drugs are available to Level 1 prescribers? Anti-muscarinics: Cyclopentolate hydrochloride,

Tropicamide

Local anaesthetics: Lidocaine (lignocaine) hydrochloride Oxybuprocaine hydrochloride Proxymetacaine hydrochloride Tetracaine (amethocaine) hydrochloride

Anti-bacterial preparations: Chloramphenicol

Fusidic acid



Which diagnostic drugs are no longer available to level 1 prescribers? Atropine and Pilocarpine Under what circumstances would you consider a mydriatic fundus examination necessary? i) When there is difficulty in obtaining an adequate view of the posterior fundus due

to media opacities or miotic pupil. ii) For the differential diagnosis of any media or fundus abnormalities. iii) Where stereoscopic view of the fundus and/or media is preferred. Using Slit lamp

(Volk lens), Indirect ophthalmoscopy etc. iv) To get a better view in suspected retinal detachment and intra-ocular tumour

investigation. v) In the routine examination of the diabetic patient vi) In any patient having macular oedema and similar diseases, which are difficult to

spot with direct ophthalmoscopy through an undilated pupil. vii) For fundal, lens or vitreous photography. viii) Most young children especially at their first visit (although mydriasis may well be a

bonus following cycloplegic refraction) ix) -7.00 myopes for detachment/degeneration, or myopes >-7.00 for degeneration/

detachment (= -7.00 detach and >-7.00 degenerate more) x) After trauma, or unexplained symptoms

Inducing Closed Angle Glaucoma is always a concern when dilating a patients pupil, what steps would you take if the IOP subsequently rose by 2mmHg, 4mmHg and 9 mmHg? A rise of 2mmHg - nothing, as this is a normal and expected rise. A rise of 4mmHg - retain the patient and recheck every 30 minutes until the pressure

falls. If suspicious, have a look at the angle with a gonioscopic lens. Consider referral via GP to an Ophthalmologist, who might check the IOP during dilation, see if the patient is a topical steroid responder or occasionally even carry out a provocative water-drinking test.

A rise of 9mmHg - very worrying, especially after only 30 minutes. Phone the casualty officer/eye emergency informing them of the situation with a view to urgent referral and inform the GP.



What are the signs and symptoms of closed angle glaucoma (CAG) and what steps would you take to ensure appropriate treatment? The patient may experience sudden onset of violent eye/head pain and nausea. The pupil is usually mid-dilated, fixed, and irregular due to sector infarction. Vision will deteriorate The cornea will eventually become hazy due to oedema. Send or take the patient immediately to Eye Department or casualty. Consider asking the GP to provide systemic acetazolamide and topical dorzolamine (Diamox and Trusopt). Instil a regular miotic if hours away from help however pilocarpine even 4% often has little effect with an acute glaucoma attack and is no longer available to Level 1 prescribers. What are the indications for using a topical anaesthetic in practice? 1. Contact applanation/indentation tonometry 2. Gonioscopy 3. Removal of foreign bodies 4. Schirmer II where the reflex tear secretion is measured by irritating the

unanaesthetised nasal mucosa. 5. Moulding technique for fitting scleral contact lenses 6. Possibly initial fitting of RGP contact lenses (suggested to provide better assessment

by some practitioners) What are the topical anaesthetics that are available to the optometrist? Amethocaine hydrochloride 0.5%/1% Lignocaine hydrochloride 4% Oxybuprocaine hydrochloride 0.4% Proxymetacaine hydrochloride 0.5% Which is the most comfortable for the patient? Proxymetacaine hydrochloride 0.5% Which is the most uncomfortable for the patient? Amethocaine hydrochloride 0.5%/1%



How do topical anaesthetics work? Local anaesthetics prevent both the generation and conduction of nerve impulses. Suggestions as to how this works include: - i) Preventing the large, transient increase in nerve cell membrane permeability to Na+

ions. ii) Increasing the pressure of the lipid layer of the cell membrane causing closure of the

lipid pores through which ions move. iii) Successful competition with acetylcholine for receptor protein on sensory nerve

fibres (the topical anaesthetics available to Optometrists have similarity to ACH in structure).

iv) Successful competition with Ca2+ for a receptor site controlling membrane

permeability to Na. What are the potential side effects? i) Removal of the protective blink reflex (from dust, grit etc.) will reduce the ability to

sense the presence of a foreign body the patient should be kept in the practice until the blink reflex returns, usually within 20 minutes.

ii) Repeated instillations may lead to desquamation of the corneal epithelium (1:1000

chance), because normal functioning of the nerves is needed for their survival, an effect aggravated by the absence of reflex blinking and the reduction of tear secretions. This can greatly enhance the absorption of subsequent topical drugs.

iii) Allergic response - particularly the ester linked compounds (amethocaine,

oxybuprocaine, and proxymetacaine) - rather then the amide-linked lignocaine. Under what circumstances can you supply them to a Patient? Absolutely none. Why is this? A small subsection of the POM list allows only optometric use rather than supply. To prevent such products as topical anaesthetics from being supplied to the patient for analgesia. What is the theoretical interaction between ester-linked anaesthetics and sulphacetamide? Metabolites of the ester-linked anaesthetics are structurally similar enough to para-amino-benzoic acid (PABA) to be used by bacteria in the production of nucleic acids and thus DNA, exactly the process which sulphacetamide is designed to block.



What ophthalmic staining agents are available to the optometrist, in what forms and what are they used for? Rose bengal is available in 1% minims it stains devitalised corneal and conjunctival epithelial cells a visible red colour, crossing the cell membrane of dead cells only. It is especially useful for diagnosing Keratoconjunctivitis Sicca, staining the exposed triangular areas in the interpalpebral conjunctiva; dendritic ulcers, where it stains the ulcer processes and does not diffuse into the surrounding tissue; exposed areas (e.g. exophthalmos), etc. Care should be taken if local anaesthetic solutions have been used previously as a false positive result may result. It also irritates more than fluorescein and the staining is relatively persistent. Alcian blue is available as 1% eyedrops, it is a complex compound containing copper and stains mucous deposits but not damaged cells. It may be used for differentiating mucous deposits from diseased cells, unlike Rose bengal which will stain mucous deposits and diseased cells. It can produce a prolonged discolouration of stromal tissue (several months) and is uncomfortable. Fluorescein is not a stain. It is a pH indicator (fluorescing in alkaline conditions) and only appears to stain by entering damaged cells or the spaces between them. It is available in 2% minims, 1% or 2% multi-dose dropper bottles, on a paper strip in the form of a dried 20% solution, as 0.25% with 4% Lignocaine combined in minim form and in high molecular weight form also in dropper bottles. Its use in multi-dose forms is rare as they use phenyl mercuric nitrate as the preservative and provide an excellent medium in which to grow Pseudomonas aeruginosa. Fluorescein is used in the detection of foreign bodies, the detection of corneal damage, contact lens fitting, contact applanation tonometry, to demonstrate lacrimal patency and can also be used as an injection for fundus flourescein angiography How would you set up a slit lamp before use? Clean the forehead rest and replace the chin rest paper between each patient! N.B.

This is assessed in the final exam and by your assessor and is something many candidates forget under the pressure of examination as is washing their hands in between patients!

Focus each eyepiece, using a focusing rod or the patients closed upper lid, use parallax to check you are focused. N.B. make sure you understand parallax, assessors can ask you about it

Adjust the Pd Ensure the eyepieces and the illumination system are coupled using the focussing

rod! Ensure you are familiar with the controls Make sure you and the patient are comfortable and that the patients eyes are level

with the marker bar



When would you perform a slit lamp examination during a routine eye examination? Hopefully you would use the slit lamp biomicroscope as part of your routine on every patient. The slit lamp biomicroscope is used to examine the anterior segment and adnexa and should be used to assess patients, presenting with red, watery, dry and painful eyes. It should be used for the differential diagnosis of eyelid disease (Styes (hordeolum), Blepharitis, Meibomian Cysts, and ingrowing eyelashes) and of conjunctival inflammation. It can be used to examine patients with keratitis, anterior uveitis, glaucoma, foreign bodies, ocular trauma and lacrimal disorders. A Slit lamp examination should be carried out on all: i) Contact Lens wearers - careful slit lamp is required to check for contact lens

complications e.g. corneal staining / neovascularisation, and to assess the fit and condition of the contact lens.

ii) Patients who need dilating - Van Herricks technique is used to estimate anterior chamber depth,

iii) Patients who have lens opacities, iris pigmentation or irregular margins, iv) Patients with unexplained reduced VA, v) Patients with IOP over 40mmHg - due to the possibility of oedema. Describe the van Herick angle assessment technique

SECOND VISIT COMPETENCIES - MODEL ANSWERS...

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