Pre-Registration FAQs: Ocular Disease & Investigative Techniques

At this time of the year, pre-registration trainees are once again completing their Assessments.

Following the popular Ask the Examiner threads in the past, we have compiled all of the questions and answers as FAQs and regrouped them all according to subject.

Our contributors have included Bill Harvey, Peter ChapmanJoy Myint, Dr Christine Astin, Prof David Henson, Henri Obstfeld, Catherine Viner, Miss Parul Desai, Simon Frackiewicz, Phyllis Northcott and Jane Macnaughton, to name but a few.

Please note that answers given are the opinion of each contributing individual and must be taken in context. You are still encouraged to liaise primarily with your supervisor and to read a book or two! (Terms & Conditions at base of post).

Q: Can you tell me what equipment I need for the NonEEA ODA station exam?

A: For the ODA Station exam you will need to take along with you your ophthalmoscope for fundus examination, and the equipment you would normally use to do cover test and motility on a patient with a BV anomaly.
At one station you will be expected to perform indirect Ophthalmoscopy on a patient using a Volk lens (patient and slit lamp are obviously provided ). If you have your own Volk that you are used to, you can take it along, otherwise there will be one at the station there for you to use.
The College Guidance states: ‘You may bring your own Volk lens for the station requiring the use of a binocular indirect examination technique but it must be fitted with an ultra violet filter.’ Volk lenses with ultra violet filters will be provided if you do not have your own.
Don’t forget to always take spare batteries or charged handles. You can’t leave the room to find spares.

Q:  I was asked to state the risk factors of Glaucoma in my second assessment which I stated with ease. However, I was totally thrown when asked to state why Afro- Caribbeans were more likely to develop Glaucoma. I have not been successful in finding out the answer to this question and I would appreciate any suggestions?

A: RE: Glaucoma Q. To be fair the reasons why Afro-Caribbean’s are more susceptible is a controversial subject. Some will say it is genetic (so family history is relevant) some say it is related to levels of pigment, some say that the disc is more susceptible to damage. There are other theories but none of them are definitive.

Q: How do I test visual fields on a low vision patient? I know that on HFA, the fixation target can be changed to 4 lights to allow eccentric fixation and on the newer Hensons the fixation target can also be changed, but is there any more info that I can add to the above?

A:  RE: Low Vision Fields. Consider peripheral fields with a confrontation stick, Amsler, Goldmann perimetry, and Bjerrum screen.

Q:  Non arteritic ION: how does it normally present and how does it differ to arteritic? I know arteritic associated with Giant Cell Arteritis (GCA) requires emergency referral, but how does the presentation & treatment differ?

A:  Both arteritic and non-arteritic present as a shutdown of supply of blood to the optic nerve head resulting in a sudden reported loss of vision. This loss is rarely total but is a sudden altitudinal loss affecting central vision. Both require emergency referral.

The arteritic is due to inflammatory cells and, importantly, the risk to the other eye is much greater (some say as much as a 45% chance of loss in the next week!). It is related to a systemic vasculitis, such as GCA or others, and so the patient is often symptomatic relating to the systemic problem. They require a biopsy and a sedimentation test (ESR) to establish the inflammatory load and site of inflammation and intensive steroid intervention is needed.

Non-arteritic AION is best thought of in the same way as an CRAO  calcific emboli blocking blood flow. It is therefore similarly an emergency. The threat to the other eye is less but significant while these patients have a serious risk of embolic damage to the brain (stroke), heart and lung, all potentially fatal.  Medical intervention is cardiovascular assessment to decide on the source of atheroma sloughing off the calcium (often the heart) and vessel treatments including surgery.

Q: I have been revising Complicated PVD and retinal detachments and both present with the same signs i.e Shaeffer’s sign, Weiss ring, flashes, floaters; so are they the same? Retinal Detachment is when the retina splits from RPE, and a Posterior Vitreous Detachment is when the vitreous splits from retina. So why are there signs the same? Can one occur without the other?

A: The clue here is the term ‘complicated’ as it implies a PVD resulting in retinal damage. The presence of Shaeffer’s sign is indicative of RPE damage and therefore treated as an emergency.  A PVD may occur without retinal damage and often does (nearly all myopes eventually show one) but there is unlikely to be Shaeffer’s nor persistence of the flashing. These you can monitor yourself as long as you take good notes and advise patient to report immediately any recurrence of symtoms. If in doubt refer according to the telephone advice from casualty.

Q: If my patient has attended with flashes and floaters, my management would be to check pupils, pressures, VAs, and perform a dilated-fundus exam and a slit lamp examination.  Assuming all this is normal and no tears are present, should I still refer for scleral indentation to be done by the HES in case of a peripheral tear?  Or is it ‘safe’ enough to advise the patient if any curtain over vision occurs to go straight to emergency?

A: Tricky one this as always and related to a discretionary interpretation of risk factors and symptoms.  With high myopes or any persistence of symptoms I would be minded to play safe at Pre-reg level and offer a referral to clinic via GP for a full peripheral retinal check.  Only if you are certain that the PVD is without retinal compromise (and the value of Shaeffer’s cannot be underestimated) might the latter option be suitable.

Q: Pre-retinal haemorrhages which can occur in diabetes: what is there exact location, how do they disappear, and how long do they take to disappear?

A:  Pre-retinal and sometimes under inner limiting membrane with a characteristic flat top or vitreal and spreading.  Reabsorption may take weeks depending on extent and loss of vision is directly related to obscuration of the macula

Q: Regarding iop measurement techniques: I believe the contact method uses the concept that the amount of force needed to flatten a specific amount of the cornea, is proportional to the IOP, whereas I don’t completely understand how the non contact method works?

A: Non Contact tonometry: you may need to go through some old uni notes here.

There are two basic methods.  One method is measuring the time it takes to flatten the cornea, the piston pressure remains constant.  The other is an increasing piston pressure cutting off at the point where the cornea is flattened.
A light beam is directed on to the cornea and is reflected back into a receiver at the point when the cornea is flattened. This will tell the machine when to cut off the puff from the piston.

Q:  Visual Fields: Why does macular sparing occur following a lesion to the visual cortex?  If I saw this field plot on a px at what urgency would I refer?

A: Macular sparing: this is all to do with the degree of cortical representation.  Proportionally, a greater area of cortex is given over to the macula.  So if a cortical lesion occurs (e.g. stroke) it would take a lot of damage before macular function is significantly affected or at least shows up on a central 30 degrees VF plot.

Macular sparing is not a ‘field plot’  it’s a lack of it.  Like all VF plots, think about the underlying cause, the length of time the lesion has existed and base your referral criteria upon that.  However, remember that a significant amount of nerve fibre damage must occur before a VF plot occurs, so something significant is likely to be the underlying cause (tumour, vascular accident etc).

Q:  Is the cherry red spot at macula in a artery occlusion due to the thin retina overlying the choroid at the macula?

A: Yes, the macula is nourished by unaffected choriocapillaris in this case.

Q:  If a patient told me he had high blood pressure and was on Beta-blockers, and upon Ophthalmoscopy I notice CWS and haems, what degree of urgency do I refer him and to whom? Is a referral to the GP sufficient for better control of his meds? Or do I refer to the ophthalmologist?

A:  If asked this question you need to have more detail.  Location of the haems for example  this will have a bearing upon the degree of urgency of your referral;  i.e. if the macula is involved. Ideally this many needs to been seen by both practitioners but the most important thing here is to get his BP under control.

Q: What’s the difference between Herpes Simplex and Herpes Zoster? Herpes Simplex lays dormant in trigeminal nerve and when activated causes dendritic ulcer? What cause the activation? How does this differ to herpes zoster?

A:  May I recommend you back to a basic ophthalmology text book for this one as this is purely and academic question. This text book is highly recommended and this web site also.

Q: In how much detail for my assessments would I need to know about refractive surgery?  For example if  the px’s history says he wants to have laser surgery, what do I do?  Do I need to be able to explain the procedure? Where do I tell him to go?

A:  I would say that detailed knowledge of refractive surgery procedures is not high upon you study list.  Be aware of its existence, basic knowledge but more importantly you need to know be able to recognise it and know what you would do if you come across complications.  Referral on for Refractive surgery really isn’t a tall priority and not within your remit.  It certainly won’t hold a pass/fail criteria unless you see complications.

Q: Before ophthalmoscopy in the routine exam / assessment would it be ok to use alcohol gel to disinfect my hands or must I wash them in a sink? Is it best to check with the examiner?

A:  Wash your hands before the exam. That is enough. No need to disrupt the beginning of the exam with a sharp exit to the sink or otherwise. If however you sneeze into them in the middle of the exam then you should ask to leave to room to wash again! If you use gel in your room, then that is also ok.

Q: How soon would I need to refer an acquired Horner’s Syndrome?

A: Acquired Horner’s  needs urgent investigation to work the position of the sympathetic nervous system defect.  For example, it could be caused by an internal carotid artery dissection.

Q: How soon would I need to refer an acquired nystagmus?

A: I would refer acquired nystagmus fairly promptly to a neuro-ophthalmologist.

Q: What causes ectopia fovea?

A:  Ectopia fovea is an unusual position of the fovea in relation to the optic nerve. It is associated with retinal pathology such as chorioretinitis, fribrous bands or colobomas.

Follow this link to a research paper: http://www.ncbi.nlm.nih.gov/pubmed/1594198

Q: In myasthenia gravis I understand patients need anitcholinesterases, so why are they given atropine which is an antimuscarinic?

A: Atropine is only used intravenously during the diagnostic phase of the edroponium test. This has potentially life threatening side effects in a small number of cases and by giving atropine the muscarinic side effects are minimalised.

Q:  Visual Fields:  Just wondering if you could help me with age-norm thresholds for field testing.  In Henson’s book on visual fields it says sensitivity reduces with age by 0.6dB per decade, but no starting value.  Besides this, I have been unable to find any other info about what constitutes a normal threshold for each decade. On Humphreys total and pattern deviation plots compare to age norms but I need to know for the other types of plots.

A:  There are a couple of points here that you need to be aware of:

1) dB scales are scales of attenuation not of intensity. 32dB on one instrument is not necessarily the same as 32dB on another instrument. Each instrument has a base line intensity, in the Humphrey it is 10,000 apostilbs and in the Henson it is 1000cd/m2. The dB value can be considered as a filter strength placed in front of the light source, the higher the value the deeper the filter and the dimmer the light. There are also other factors that effect the dB value, e.g. the background luminance. If the background is bright then the dB values will be lower.

2) The other point that you need to be aware of is that the sensitivity is not constant across the visual field but decreases with eccentricity. So you cannot talk about a fixed value for age without specifying location. In the Henson perimeters every location has a specific value that is stored within its memory. In addition the rate of loss with age is not consistent for all locations and while the average value might be 0.6-0.8 dB/decade it will be higher in the periphery. The Henson has a specific rate for each location that it uses when calculating normative values for a particular age.
I hope this helps, like everything else in perimetry things tend to be more complex than they might at first appear.

Q:  Always puzzled me: on a parallelepiped you increase the beam width from an optic section so the 3 sections of the beam become 2 sections.  If looking at the cornea, the anterior section is the epithelium but what is the posterior section of the beam – endothelium (where does the stroma go?) or epi/stroma/endo section with just magnified epithelium as first section of beam? I know this point isn’t majorly important, but I just wondered if anyone had a definitive answer?

A: In the optic section the three distinct layers are easily visible because you have a 2-dimensional slice through the cornea. By widening the beam you have introduced a three dimensional block view, or parallelepiped. The front or anterior surface is, as you say, the tears film/epithelial interface. The stroma is still there in your view, highlighted in green, and you are seeing it as the space between the two interfaces. The posterior face is that of the endothelium.

Q:  Just something that’s bothering me! On the AOP list of referrals, CSR is down as an Urgent (ie 1-14 days) referral.  Can anyone explain why this is, when it is a self-limiting condition, which ophthalmologists will only consider treating if persistent for 4months?  Is it just to confirm diagnosis? Otherwise wouldn’t routine referral be more appropriate?

A:  CSR can be suspected clinically from history and examination, but cannot be confirmed without further investigation.  Referral is indicated to,
(a) establish or confirm clinical diagnosis by diagnostic tests – FFA ( fundus fluorescein angiography), and  (b) to rule out any other causes of RPE leaks e.g. CNV, inflammatory disorders, tumours etc. Treatment is not always indicated, but that is not the purpose of the referral.

Q:  I was wondering in colour vision testing with Ishihara, how many plates can you get wrong before the colour vision is classed as abnormal?

A: For the 38 plate edition, 13 or less correct answers constitutes a fail, with 17 or more out of the 21 being a pass. 14 – 16 correct answers means the test is inconclusive and retesting by another method should occur.
Remember, there are the abbreviated and concise versions and these will have different pass/fail criteria.

The answers given are the opinion of the individual examiner or tutor. We make every effort to ensure that the information that appears on the site is correct and up to date.  However, we are not responsible for any errors or omissions or for the results obtained from the use of such information.