Ocular surface and anterior segment inflammation: management options for UK optometrists part 6: course code: C-15087 O/AS/SP/IP.
In this final article of this series, the management of a range of fairly common mild-to-moderate inflammatory conditions of the anterior segment is discussed. Many of these conditions, such as complex cases of blepharitis, blepharoconjunctivitis, limbal and peripheral corneal infiltrates, non-perforating abrasions, and foreign bodies, can present to and be managed by an optometrist, especially those with additional supply (AS) therapeutic qualifications. Pharmacological options range from artiicial tears and lubricants to topical analgesics and the therapeutic use of cycloplegics; the latter are more likely to be utilised by optometrists trained to independent prescriber (IP) level, as highlighted later.
Aetiology of ocular surface and anterior segment inflammation
The sub-epithelial connective tissue (parenchyma) usually contains inflammatory cells, including additional white blood cells (eg, macrophages) that have initially non-specifically migrated from the dilated capillaries into the conjunctival tissue in response to the inflammatory stimulus, followed later by specifically recruited white blood cells (eg, polymorphonuclear leucocytes--PMNs) that migrate to the region where the foreign antigens are located. (1,2) These cell types, especially the former, along with mast cells, can release inflammatory mediators from granules in the cells. These non-specific mediators include histamine and certain prostaglandins. As inflammation develops, the natural cell complement of the conjunctiva and peripheral cornea becomes affected and, in turn, these cells also provide a source of further inflammatory mediators mostly of the prostaglandin type (see later).
When a generalised inflammatory response of the anterior segment develops, a patient is likely to report some type of ocular discomfort, including foreign body sensation, which can progress to a dulled pain feeling that may also be associated with a progressive development of photophobia. In rare cases far more substantial pain can develop, especially as associated with eye movement, because of the generally inflamed tissue, which includes the extraocular muscles and their connective tissue sheaths.
Part of the general discomfort is caused by general or localised vasodilatation and tissue oedema that accompanies the inflammation. For the most part, in the majority of cases of anterior segment inflammation, the tissue oedema is superficial and associated with blood vessels close to the conjunctival surface, whether this is at bulbar, palpebral or fornical regions, or a combination of these. This can often result in the patient wanting to rub their eyes and actually worsening any redness and puffiness of the conjunctiva and lid margins. Overall, these responses are all inflammatory in nature, but can be associated with bacteria or carry the risk of being infected.
The redness can, however, be more localised to a certain region of the ocular surface (bulbar or palpebral conjunctiva) and this forms the basis (in part) of a differential diagnosis for the various conditions. Vasodilatation of the more superficial vasculature across the bulbar conjunctiva should be self-evident (especially if assessed by slit-lamp biomicroscopy), but any concern that deeper lying blood vessels have been affected (ie, as in scleritis) could be checked with a simple 'blanching' test, ie, instil phenylephrine 2.5% eye drops and assess the extent of clearing of the hyperaemia.
Conditions such as contact lens associated papillary conjunctivitis (CLPC) are well defined by the terminology, ie, the inflammation is clearly associated with papillae, which are located across the tarsal surface and associated with localised regions of thickening (hyperplasia) of the conjunctival epithelium. The progression of the inflammation and thus the increase in the grade of CLPC3 could therefore be localised to the hyperplastic regions, and while this has not been well-documented in systematic studies, it is likely associated with increased risk of discrete focal 'staining' with sodium fluorescein (NaFl) across the tarsal plate. In related conditions such as vernal keratoconjunctivitis (VKC) or atopic keratoconjunctivitis patients with conjunctival or corneal conditions, the hyperplasia is so substantial that the 'hardened' focal regions of the palpebral surface are sufficient to essentially cause mechanical damage to the corneal epithelium and a central or more peripheral 'shield' ulcer can develop. (4-6)
[FIGURE 1 OMITTED]
Accompanying the CLPC can be an aggregation of white blood cells under and/or within the palpebral conjunctiva (whereas the normal, non-inflamed palpebral conjunctiva and parenchyma should contain few, if any, white blood cells). Illustrated in Figure 1 is a high magnification electron micrograph from a rabbit with mild follicular conjunctivitis, (1) where a presumed PMN (white arrow) and macrophages (black arrows) are found in abundance. A likely consequence of the presence of these inflammatory cells is an alteration of the goblet cells and their secretions of mucous. As a result, in some cases of 'follicular' conjunctivitis, and more especially in VKC, it is entirely possible that a thick 'mucoid' discharge may line the furrows or groves between papillae and follicles, and also be present at the lower fornix.
Such aggregates of white blood cells may also invade the superficial epithelium of the limbus and even the peripheral cornea, having migrated from the peri-limbal vascular arcade. As with the conjunctival epithelium (Figure. 1), the corneal epithelium cells will become increasingly disorganised by the presence of extra cells (ie, the invading macrophages and even PMNs). This has a very important consequence since a cluster of white blood cells will distort the superficial (squamous) cell layers and the immediately underlying intermediate (wing) cells, so progressively disrupting the tight junctions between superficial epithelial cells. In early stages of an inflammatory response affecting the limbus and/or peripheral cornea, the surface may not be 'broken', ie, the white blood cell infiltrates are under the surface. However, at some stage, the surface may be breached as in some cases of limbitis associated with reaction to contact lens care solutions, in contact lens associated peripheral 'ulcers' (CLPU) (OT, November 12 2010), or a range of other inflammatory conditions affecting the limbus. (4-6)
The focal inflammation may also be a reaction to microorganisms and/or their metabolic products, eg, to bacterial toxins (see later), or in later stages of epidemic keratoconjunctivitis (EKC) associated with adenoviral infections. The infiltrates, usually more easily seen in the peripheral cornea, have a circular shape reflecting aggregation around a focal site where the stimulus for white blood cell migration is located (Figure 2). In conditions such as VKC, the aggregates can become sufficiently dense to be evident as raised limbal nodules.
Any infiltrate cluster can result in a compromise of the surface barrier and the net result is discrete regions of NaFl 'staining' (Figure 2). Whenever there is a break in the surface, no matter how small, there will be continued migration of white blood cells to that location (see later). In management of these inflammations, the goal is both to reduce the aggregation of white blood cells and promote their removal, and to regain the integrity of the ocular surface barriers especially across the cornea.
There are several relevant College of Optometrists Clinical Management Guidelines (CMGs) that should be consulted, namely 'CL-associated papillary conjunctivitis', 'Keratitis--CL-associated infiltrative', and 'Keratitis--marginal', 'Ocular Rosacea', 'Episcleritis', 'Corneal abrasion' and 'Recurrent corneal epithelial erosion syndrome'.
Pharmacology of anti-inflammatory drugs and options for optometrists
Anti-inflammatory drug treatment, for the types of conditions outlined above, are mainly directed towards controlling the inflammatory response, but also promoting wound healing. In general terms, macrophages underpin the initial inflammatory response and then are largely responsible for removing (by phagocytosis) those secondarily recruited PMN leukocytes so as to end the inflammatory reaction. The latter is especially important in cases of recurrent corneal erosion syndrome (see later) where the failure to completely re-heal the epithelial surface drives a recurrent cycle of recruitment of inflammatory cells that re-disrupt the epithelial barrier.
The prostaglandins that drive the inflammatory response are derived from cell membrane phospholipids, both externally and internally. A sequence of enzyme-mediated reactions results in the release of a pro-inflammatory precursor molecule, a 'lipid autoacid' called arachidonic acid (a type of unsaturated fatty acid), with a cell membrane-associated phospholipase A2 enzyme being a notable activity. This enzyme activity is indirectly regulated by natural immune modulators such as glucocorticosteroids and can be inhibited by exogeneous cortisosteroids used as anti-inflammatory drugs. (7,8) The mechanism of inhibition, by drugs such as hydrocortisone and prednisolone, is complex; both are used as eye drops. It involves both that the corticosteroid binds to the affected cells and be translocated to the cell nucleus, and that there is an elaboration of an intracellular peptide messenger called lipocortin-1. If the inflammatory response is not blocked at this level by exogenous corticosteroids, then continuing activity of phospholipase A2 results in more and more arachidonic acid being produced to start an inflammatory cascade involving cycloxygenase COX-1 and COX-2 enzymes. (8,9) In normal tissues, there will always be some COX-1 activity to convert arachidonic acid into pro-inflammatory prostaglandins, but this conversion is augmented by an inducible COX-2 (ie, higher levels of enzyme produced in chronically inflamed tissues) that will produce the same or other pro-inflammatory prostaglandins. All of these cyclooxygenase activities can be inhibited by aspirin-like drugs, the Non-Steroidal-Anti-Inflammatory Drugs (NSAIDs). The NSAID most relevant to management of anterior segment inflammation is diclofenac eye drops.
[FIGURE 2 OMITTED]
In more recent years, increasing attention is being given to other natural pro-inflammatory biochemical pathways and anti-inflammatory mechanisms involving 'protective lipid mediators'. (2) There are three aspects of these that deserve consideration for future therapeutic options. The first of these is the enzyme lipoxygenase (specifically LOX-15) that is present in the epithelia, and generates both an anti-inflammatory and 'pro-inflammatory resolving' prostaglandin-like molecules such as lipoxin A4. The lipoxin pathway is considered important in inflammation and epithelial resurfacing control. Other unsaturated fatty acid-type products from this pathway such as 12(S)- and 15(S)-HETE have been shown in animal models to be substantially elevated following continuous wear of contact lenses, associated with development of inflammatory cornea oedema and corneal neovascularisation. (10) A set of other lipoxin pathway-related molecules are peptides such as the resolvins, which have been reported in animal studies to reduce the severity of experimentally-induced ocular surface inflammation. (11) The resolvins are derived more from another polyunsaturated fatty acid (PUFA) which has received considerable attention in relation to inflammation of the ocular surface and the Meibomian glands, namely the omega-3 compound docosahexaenoic acid (DHA). (2,12)
Contact lens wear-related papillary conjunctivitis and related conditions
As noted in the previous article (OT, November 12 2010), the ideal management of CLPC involves discontinuation of contact lens wear followed by a four-times-daily (QDS) regimen of a mast cell stabilizer such as sodium cromoglicate. (13-16) The logic of such a treatment might be questioned since sodium cromoglicate is not considered to have any constitutive anti-inflammatory activity; the removal of the stimulus to inflammation should help and better results might be obtained with other mast cell stabilisers/anti-eosinophil drugs such as lodoxamide or nedocromil sodium (both available to AS optometrists). The treatment, whilst the patient has stopped lens wear, should be continued until the eyelid inner surface is quiet and any 'staining' of papillae is reversed. (13,14) Depending on severity, most resolution should take two to four weeks, after which the dosing could be reduced to TDS or BDS for a further two to three weeks to ensure complete resolution. (14,16)
This approach should work for mild to moderate CLPC, but more severe cases of GPC (with notable conjunctival hyperplasia) may require a short period topical corticosteroid treatment. This would require referral to an IP optometrist (preferably one specialising in conta ct lenses) or an ophthalmologist. The topical corticosteroid therapy should reduce conjunctival vessel leakiness within a few hours, (17) reduce PMN leukocyte recruitment and migration into the conjunctiva (extravasation), (18,19) and reduce any further elaboration and secretion of other inflammatory mediators by the leukocytes. (20) A short term topical ocular corticosteroid regimen (eg, prednisolone 0.5% or 1% gtt, QDS, for two to three weeks) may be beneficial in substantial cases of GPC, as opposed to CLPC, associated with soft lens wear. (21) By current perspectives, regular lens replacement, improved lens hygiene and patient education are considered the mainstay of preventing CLPC/GPC from developing in the first place, (22) but a short course of topical ocular corticosteroids can be used simply to manage discomfort, photophobia and also improve appearance by reducing conjunctival hypaeremia. (23)
Long-term and/or extended wear of contact lenses may result in marginal keratitis, which is a mild-to-moderate inflammatory response that is often refractory to management. While the tarsal plate may not show an exaggerated reaction, such inflammatory reactions now likely include a hardening of the palpebral conjunctival infiltrates. Corneal infiltrates and even larger deep stromal infiltrates, as opposed to small and localized peri-limbal infiltrates, can also develop. (3 16,24,25) Such conditions are less likely to be acute in presentation but progressive. A further extension of such reactions may be the development of neovascularization or deeper infiltrates (in the palpebral conjunctiva, corneal epithelium or stroma) both of which are the clear signs of an extended recruitment of inflammatory cells in response to persistent irritation. It is likely that any patient with such infiltrates will show low grade corneal and bulbar conjunctival staining with NaFl. The presence of just a mild inflammation, as might be expected in many cases of contact lens wear-associated superior epithelial arcuate lesions (SEALs), can likely be managed without corticosteroids (ie, discontinue lens wear). The more substantial cases are likely accompanied by notable peri-limbal reaction, the presence of neovascularisation, peri-limbal or peripheral corneal infiltrates with an accompanying anterior chamber reaction. For these, along with stopping contact lens wear for several weeks, an aggressive but carefully monitored treatment with topical ocular corticosteroids may well be needed. (16,24)
Similarly cautious use of topical ocular corticosteroids might also be appropriate to help manage the initial gross inflammatory response in contact lens associated acute red eye (CLARE), concurrently with intensive antibiotic coverage. Some might argue that it is best to discontinue lens wear and let the eye quieten down on its own, but the presence of tissue oedema and substantial peripheral infiltrates may need the judicious use of strong anti-inflammatory drugs such as corticosteroids. Patience is required in monitoring such patients to decide on the most appropriate intervention.
[FIGURE 3 OMITTED]
A case can be made that substantial signs of inflammation need to verified and carefully documented before corticosteroid use is justified. The efficacy of the topical corticosteroid therapy should be assessed with the expectation of reduced symptoms and biomicroscopy performed to confirm the reduction of oedema, quieting of the vasculature, reduction in infiltrates and anterior chamber reaction. (26) The infiltrates should be examined (and graded) to check for resolution. (27) For contact lens wearers, it can be noted that the removal of the offending contact lens in itself should reduce most of the exogenous inflammatory stimulus and so the steroid therapy is really to arrest the further development of inflammatory cell recruitment and to promote recovery. Contact lens wear might be reconsidered after a suitable abstention (eg, a few weeks after cessation of corticosteroid therapy).
Overall, the same principles for use and follow-up of corticosteroids would apply for cases of non-specific keratitis associated with limbal inflammation in the absence of contact lens wear, ie, more substantial cases of limbitis or superficial (punctuate) limbal keratitis including those associated with VKC, (4,5) or atopic keratoconjunctivitis. (6)
Marginal keratitis in the absence of contact lens wear
As noted earlier, non-infectious inflammatory conditions such as VKC can be associated with marginal keratitis and can even progress to substantial corneal epithelial problems such as non-infectious (shield) ulceration. There is another cause of marginal keratitis that has an association with infection-causing bacteria but is not necessarily infected. Such a condition used to be referred to as a 'sterile inflammation', now recognised to be a rather special inflammatory response to toxins secreted by bacteria eg, from certain strains of Staphylococcus aureus, S. epidermidis or the Propionibacterium acnes associated with rosacea and related conditions. (28,29) These spread from the eyelid margins via the tear film to the edge of the cornea, and can result in additional marginal infiltration and even ulceration of the superficial corneal epithelium at the limbus, (30-33) which will likely show as punctuate localised staining with NaFl. This is more likely to occur when there is a hypersensitivity to the toxins, and would be a limbitis or superior limbic keratoconjunctivitis (SLK) with an indirect infectious aetiology. Such toxins can also be a cause of peripheral infiltrates in a contact lens wearer that may be mistaken for peripheral infectious ulcers. They can progress, if not managed carefully, to the development of severe corneal ulceration.
That the condition is largely inflammatory in nature can be established by the nature of the signs that can include notable 'angular' blepharitis (Figure 3) associated with both a limbal inflammatory reaction and peripheral corneal infiltrates. If the signs indicate infection (ie, the presence of some mucopurulent discharge as opposed to simply excessive lacrimation), then antibiotic treatment would be appropriate, eg, with chloramphenicol or even fusidic acid viscous eye drops. (32,34) Good eyelid margin hygiene should also reduce the recurrence of the condition, but recurrent and stubborn inflammatory episodes may also need topical corticosteroid treatment (eg, prednisolone 0.5% QDS for a few days) to generally quieten the eye, reduce lacrimation and photophobia as well as reduce further development of corneal infiltrates (27,30,35) As an inflammatory condition, some limbitis cases may respond to topical mast cell stabilizers (eg, regular use of sodium cromoglicate over one month). (31) Adjunct measures could also include the use of dark sunglasses, as well as the as-needed use of artificial tears to promote comfort.
Other conditions where marginal infiltrates can occur include sequelae following adenoviral infections. In some cases it may prove difficult to distinguish between infiltrates being associated with bacterial toxins or a similar immune-mediated response to the virus in epidemic keratoconjunctivitis (EKC), ie, the former could also be spread from one eye to the other and even between individuals if peri-ocular and facial hygiene were poor. Notwithstanding, if substantial infiltrates are seen to be developing then judicious use of topical corticosteroids is again appropriate.
[FIGURE 4 OMITTED]
Non-perforating foreign body injury and trauma to the anterior eye
Abrasions or other forms of non-penetrating foreign body injury to the cornea or conjunctiva will likely elicit initial pain followed by considerable discomfort associated with an inflammatory response. In contact lens wearers, this could be caused by grit under the lens or a fingernail during lens insertion or removal. As recognised many years ago, as long as there is an open "wound" (ie, an epithelial defect), macrophage and then leukocyte recruitment is likely to continue. (36) The sooner a superficial wound resurfaces, the faster the secondary recovery stage of the inflammation (see later).
In A&E as well as in optometric practice, coverage with an antibiotic will likely be considered appropriate, eg, chloramphenicol eye ointment or fusidic acid viscous eye drops. (37) Substantial eyelid patching is no longer recommended. (38,39) Patients need to be instructed to continue the antibiotic coverage for a few days, whether this be QDS for chloramphenicol or BDS for fusidic acid. In many cases, however, infection is not apparent nor does it develop but the antibiotic coverage is a sensible precautionary measure.
Since the abrasion can be rather painful, systemic analgesics are often required. Lesser presentations can often be managed with the patient's preferred systemic analgesic but there is only limited data from organised trials as to whether an oral NSAID (eg, ibuprofen 400 mg, TDS) is sufficient or whether patients would be better managed with an NSAID-narcotic combination (eg, paracetamol 500 mg with codeine or dihydrocodeine 7 to 8 mg QDS); these options are available as P Medicines in the UK, for use by adults (not children less than 12 years of age).
AS and IP-trained optometrists can also access the same topical NSAID-analgesic preparation as used in some A&E departments, namely diclofenac sodium eye drops. This is available in unit-dose form as PoM Voltarol Ophtha. The successful use of eye drops containing an NSAID in the management of corneal abrasions has been reported in organised trails, with the key effect being improved patient comfort through reduced blepharospasm from the analgesic activity (Figure 4). (40,41) This surface analgesia is different from surface anaesthesia, ie, the patients are still able to sense a foreign body (or similar) and feel if anything touches their eye. A single use of a topical ocular anaesthetic may well be a necessity to allow a patient's eye to be opened and examined after an abrasion or foreign body injury, but is not to be used as a means of controlling pain in the longer term. (9,43) While (sadly) this is still sometimes done (either by a health care professional prescribing the eye drops, or self-initiated by a patient after 'stealing' a bottle of the 'magic' eye drops from the attending health care professional), the selfuse of a topical anaesthetic can result in such devastating corneal problems that a transplant is needed.
Thus there is an important distinction between surface analgesia and anaesthesia which can be assessed by measuring the mechanical (touch) sensitivity of the cornea with the nylon filament of a Cochet-Bonnet aesthesiometer, (44) the longer the filament length (in mm) that can be detected, the greater the sensitivity. Similar results would be expected if a dry Q-tip or wisp of soft tissue paper were touched to the eye. As shown in Figure 4, even repeated use (four drops repeated at five min intervals) of diclofenac 0.1% eye drops would not be expected to reduce touch sensitivity by more than 25% in a normal eye, while a single drop of topical anaesthetic should essentially remove corneal touch sensitivity within five min or less. (45)
The usually recommended use of diclofenac for corneal abrasions would likely be to instil two or more drops prior to the antibiotic, with the patient being supplied with a few more single dose units (eg, one or two packs of 5) to repeat the treatment over the next two to three days on a QDS basis. It would likely be better to recommend such regular use to ensure good antibiotic coverage, rather than reducing to BDS (as might be acceptable for adequate analgesia). Even much longer-term use of topical ocular NSAIDs (eg, as a routine post-operative treatment for several weeks after cataract surgery) has not been reported to produce much more surface analgesia to that shown in Figure 4.
The main issues in following-up management of abrasions, especially of the cornea, are to consider how well the wound is healing (with appropriate NaFl staining assessments). Many mechanical wounds should show good signs of healing within 24 hours and if this does not occur then the eye should be considered at risk for recurrent episodes of un-healing and re-healing, a condition now usually referred to as recurrent corneal epithelial erosion syndrome. A series of deep and centrally located abrasions from a paper edge cut are show n in Figure 5. The abrasion may also be geographic (ie, covering a large area).
Some will advocate routine short-term management of substantial abrasions with a large diameter 'bandage' soft contact lens, (46,47) although such patients need to monitored carefully for lens adhesion or other complications. (48) The bandage lens can be of the daily disposable type so avoiding any issues in lens care and disinfection. (49) Bandage (soft contact) lenses have been used concurrently with an NSAID such as diclofenac (preferably in its unit-dose preservative-free form, PoM Voltarol Ophtha), (50,51) and may also be used with antibiotics (eg, Minims chloramphenicol) on a BDS basis. (52) Either of such treatments need to be carefully monitored by regular follow-up.
The logic behind use of a bandage lens, with or without adjunct medications that could even include topical corticosteroid therapies, (53,54) is to promote re-adherence of the lifted edges of the epithelium and so facilitate spreading of dividing epithelial cells across the abraded region. The use of a bandage lens may, in itself, reduce the dull discomfort (pain) of the abrasion so making additional topical analgesia unnecessary (although systemic analgesics may still be wanted). Eyelid movement across lifted edges of an abrasion may exacerbate this and/or the non-wetting surface of the lesion may adhere to the overlying palpebral conjunctiva (which is likely to be inflamed due to the response to the abrasion). The latter may result in well-known characteristic symptoms that should alert the patient (as well as the optometrist) that recurrent erosion is a problem; the symptoms typically involve sudden-onset 'sharp' pain in the affected eye on waking or even during sleep as the movement of the lids detaches the epithelium. (55) Other symptoms will include tearing, photophobia and blurred vision as the eye responds to the re-wounding of the corneal (or conjunctival) surface. Once recurrent erosion episodes have started, it may take many weeks, months or even years to resolve. (48)
[FIGURE 5 OMITTED]
Current opinion on the mainstay of management of recurrent erosion syndromes is to keep the eye well lubricated, day and night.56 This involves use of preservative-free simple artificial tears (as needed) and application of a preservative-free bland ointment (eg, P Lacrilube or P Simple Eye Ointment) prior to retiring to bed for as long as it takes such that a re-current episode does not occur. Patients should be reviewed regularly (eg, once a month) to assess the condition of the corneal epithelium and the epithelial interface with the corneal stroma for any signs of disturbance, breaks or inflammation. This inflammation could extend to the corneal endothelium (eg, as pseudoguttata) or even be evident in the anterior chamber as flare and even cells as the blood-ocular barrier is compromised by ongoing development of inflammation.
[FIGURE 6 OMITTED]
Therapeutic use of mydriatic/cycloplegics
Over many years of largely ad-hoc and anecdotal evidence, it has become customary to provide a special sort of palliative therapy for cases of corneal abrasions and foreign bodies. This has involved the use of a mydriatic/ cycloplegic. Its use could also be considered in the immediate aftermath of a recurrent erosion episode. It is a controversial issue with different arguments being presented as to whether it serves to reduce reactive miosis (ie, relieve pupil spasm that can occur with substantial release of prostaglandins into the anterior chamber following activation of the innate immune response) and/or ciliary (body) spasm, or whether the use of the cycloplegia serves to reduce ongoing cell-mediated inflammation by beneficial reduction of blood flow in the uveal and iris vasculature. In either case, anecdotal accounts indicate that photophobia could be reduced as well if there really was an inflammatory response. An equally important issue is more one of preventing sequelae from substantial intraocular inflammation and whether the immediate use of a cycloplegic/mydriatic will reduce the risk of iris adhesions to the crystalline lens that could ultimately develop into posterior synechiae.
Traditional cycloplegics included atropine (eg, 0.5% or 1% eye drops used BDS, or 1% ointment applied prior to pressure patching) and homatropine (2% or 5% administered at least BDS). Both would be expected to exert extended 'therapeutic' effects on the iris and ciliary body (along with similarly prolonged effects on vision due to substantial mydriasis and cycloplegia) and both of these are available to AS optometrists. However, the non-therapeutically trained optometrist can only access the shorter-acting cyclopentolate for this purpose and so the frequency of instillation may need to be increased to TDS, or even QDS in substantial abrasions and/or those with darkly pigmented irides, for example.
Other inflammations of the anterior segment
There are numerous other commonly occurring inflammatory conditions of the anterior segment that may present to optometrists. These include cases of chronic allergic conjunctivitis unresponsive to routine treatments (OT, November 12 2010), advanced presentations of VKC (again unresponsive to mast cell stabilizer treatments), ocular rosacea, episcleritis (of various aetiologies) and, of course, intraocular inflammations of the anterior segment associated with the iris and anterior uvea. It will sometimes be a dilemma to assess the cause of such problems (Figure 6) and there is likely no substitute for seeing such conditions on a regular basis to establish a diagnosis and be able to manage them on a long-term basis. For any patient with recurrent or chronic inflammatory conditions of the anterior segment, two other issues also need to be considered; namely whether their condition is the result of an allergic reaction to ocular or peri-ocular pharmaceuticals or products (eg, follicular conjunctivitis), and whether this is the result of an interaction with other (systemic) medications (including those for any other form of allergic condition), which will need to be carefully reviewed.
As noted earlier, any 'red eye' with an inflammatory aetiology (including episcleritis) will likely respond in the short term to being kept adequately lubricated (to offset the effects of persistent lacrimation) and some comfort be realized with the judicious use of a topical ocular decongestant (eg, naphazoline eye drops). Anti-allergy drops (eg, mast cell stabilizers) might also have been tried in cases where allergy is a factor. All of these conditions can however progress to the stage where routine use of topical ocular corticosteroids is needed and sometimes on a chronic basis. (7,57) Such therapeutic options are available to IP optometrists where safe and effective management of these conditions can be realised.
A range of fairly common mild-to-moderate inflammatory conditions of the anterior segment can present to optometrists. Many of these conditions can be managed by optometrists, especially those with AS and IP qualifications, and can include more complex cases of blepharitis and blepharoconjunctivitis, limbal and peripheral corneal infiltrates and non-perforating abrasions and foreign bodies. Pharmacological options range from artificial tears and ocular lubricants, to mast cell stabilisers, topical analgesics (NSAIDs) and the therapeutic uses of cycloplegic drugs such as cyclopentolate.
About the Author
Professor Doughty has been teaching ocular pharmacology, as well as many aspects of ocular physiology and eye disease, for over 25 years and authored books on the subject. He has held the post of research professor at Glasgow-Caledonian University, Department of Vision Sciences, since 1995.
See www.optometry.co.uk and search 'references'
Course code: C-15087 O/AS/SP/IP
1. For anterior segment inflammation, the phenylephrine test:
(a) should indicate if pupil dilation is excessive
(b) should provide an indication of how deep any dilated vessels are
(c) will only work if dilute (0.125%) solutions are used
(d) should be carried out for every patient presenting with a red eye
2. In limbal or peripheral corneal infiltrates, the ocular surface:
(a) can be breached as white blood cells emigrate through the epithelia
(b) will rarely stain with fluorescein because the leukocytes stop this occurring
(c) will only be affected if neovascularization is also present
(d) is unlikely to show any signs of vasodilation
3. Which of the following drugs acts as an indirect inhibitor of phospholipase A2 enzyme?
(a) sodium cromoglicate
4. Which of the following daily doses of lodoxamide eye drops would be commonly recommended to treat grade 2 CLPC?
(a) As needed with or without contact lens wear
(b) BDS whilst continuing contact lens wear
(c) QDS after discontinuing lens wear
(d) QDS whilst continuing lens wear
5. Toxins associated with development of marginal keratitis come from which organisms?
(a) Staphylococcus aureus
(b) Staphylococcus epidermidis
(c) Propionibacterium acnes
(d) Any of the above
6. For stubborn and recurrent cases of marginal blepharitis, which of the following treatments can be considered?
(a) prednisolone 0.5% eye drops QDS for a few days
(b) artificial tears as needed for comfort
(c) sodium cromoglicate eye drops for a month
(d) all of the above
7. The following therapeutic drugs are available to additional supply optometrists EXCEPT:
(a) nedocromil sodium
(b) prednisolone phosphate
(c) diclofenac sodium
8. Which of the following statements about superficial limbal keratitis is TRUE?
(a) It can result from inflammatory reactions to contact lens care solutions
(b) It can be seen in some chronic cases of vernal keratoconjunctivitis
(c) It can be observed in some patients with atopic skin conditions
(d) All of the above
9. Which of the following would be a suitable narcotic analgesic for optometric use in cases of corneal foreign body injuries?
10. Which of the following statements about pharmacologically-induced topical ocular analgesia is TRUE?
(a) It would reduce corneal sensitivity to touch by up to 25%
(b) It would remove a patient's ability to sense further contact or abrasion from a foreign body
(c) It would promote eyelid closure as a protective (relaxing) mechanism
(d) It would produce equivalent effects to repeated use of oxybuprocaine or proxymetacaine
11. Which of the following would be a routinely recommended dose for diclofenac after a corneal abrasion?
(a) QDS for 2 days with or without antibiotic coverage
(b) A single use of the eye drop once only, followed by chloramphenicol for 1 day
(c) As needed over the following 2 to 3 weeks
(d) Every hour for the first day, then reduce gradually
12. Which of the following statements is about the use of cyclopentolate 1% following a non-penetrating foreign body injury to the eye is TRUE?
(a) Only a single drop is usually used because it is a strong cycloplegic
(b) Dosing may need to be rather frequent (QDS) to obtained the desired effect
(c) The drug may induce an unwanted ciliary spasm
(d) Its effects would be routinely expected to be at least as good as using atropine
PLEASE NOTE There is only one correct answer. All CET is now FREE. Enter online. Please complete online by midnight on January 12 2011--You will be unable to submit exams after this date--answers to the module will be published on www.optometry.co.uk
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|Title Annotation:||CET: CONTINUING EDUCATION & TRAINING|
|Author:||Doughty, Professor Michael J.|
|Date:||Dec 10, 2010|
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