- •Contents
- •Contributors
- •Preface
- •Glossary
- •2. Synthesising the evidence
- •3. Evidence in practice
- •4. Allergic conjunctivitis
- •6. Viral conjunctivitis
- •7. Screening older people for impaired vision
- •8. Congenital and infantile cataract
- •9. Congenital glaucoma
- •13. Infantile esotropia
- •14. Accommodative esotropia
- •15. Childhood exotropia
- •17. Entropion and ectropion
- •18. Thyroid eye disease
- •19. Lacrimal obstruction
- •20. Trachoma
- •21. Corneal abrasion and recurrent erosion
- •22. Herpes simplex keratitis
- •23. Suppurative keratitis
- •24. Ocular toxoplasmosis
- •25. Onchocerciasis
- •27. Cytomegalovirus retinitis in patients with AIDS
- •28. Anterior uveitis
- •29. Primary open angle glaucoma and ocular hypertension
- •30. Acute and chronic angle closure glaucoma
- •31. Modification of wound healing in glaucoma drainage surgery
- •32. Cataract surgical techniques
- •33. Intraocular lens implant biocompatibility
- •34. Multifocal and monofocal intraocular lenses
- •35. Perioperative management of cataract surgery
- •36. Age-related macular degeneration
- •37. Treatment of lattice degeneration and asymptomatic retinal breaks to prevent rhegmatogenous retinal detachment
- •38. Surgery for proliferative vitreoretinopathy
- •39. Rhegmatogenous retinal detachment
- •40. Surgical management of full-thickness macular hole
- •41. Retinal vein occlusion
- •42. Medical interventions for diabetic retinopathy
- •43. Photocoagulation for sight threatening diabetic retinopathy
- •44. Vitrectomy for diabetic retinopathy
- •45. Optic neuritis
- •47. Idiopathic intracranial hypertension
- •48. Toxic and nutritional optic neuropathies
- •49. Traumatic optic neuropathy
- •50. Ocular adnexal and orbital tumours
- •51. Uveal melanoma
- •52. Retinoblastoma
- •Index
21 Corneal abrasion and recurrent erosion
David F Anderson
Background
Definitions
Corneal abrasion comprises a defect in the corneal epithelial surface with or without breach of Bowman’s layer and implies that no substantial loss of stromal tissue has occurred. If, subsequently, microtrauma, insufficient to separate a healthy epithelium from the basement membrane, results in a corneal epithelial defect, the diagnosis of recurrent corneal erosion (RCE) is made.
Incidence
The incidence of hospital presentation of traumatic corneal abrasion (TCA) has been recorded in 11–12·9% of new presentations to eye accident and emergency units.1 Some 36% of patients at initial hospital presentation with RCE had a history of trauma and epithelial microcysts, 23% were patients with anterior basement membrane dystrophy alone and 7% had anterior basement membrane dystrophy and a history of trauma.2
Aetiology
Recurrent corneal erosion syndrome arises when abnormal adhesion between basal corneal epithelial cells and their basement membrane allows microtrauma at the ocular surface to cause detachment of the regenerating epithelial sheets. Corneal abrasion and RCE are associated with superficial corneal trauma, anterior basement membrane dystrophy (ABMD) or a combination of both.2 Traumatic cases may lead to RCE in otherwise normal eyes or in those with an underlying defect of the epithelial basement membrane or its deposition.2
Natural history
Studies have measured healing times in one of two ways: either the time to closure of the epithelial defect in days or the rate of healing over a defined period of time (usually 24 hours). Those studies that measured time to defect closure for the largest defects (those larger than 4/mm2) from TCA
reported a maximal healing time of 4·2 ± 0·5 days (mean ± SD) independent of treatment employed. Patients presenting with RCE were more likely to have suffered trauma than ABMD or ABMD and a history of trauma2 and lesions of the lower half of the cornea were more frequent than those in the upper half (P <0·0001).2 In the three studies evaluated2,4,5 all patients received treatment or patient numbers were too small to determine the recurrence rate without treatment.
Question
Does padding the eye make a difference to the rate of healing of the epithelial defect in TCA?
The evidence
Padding the eye is based upon the assumption that preventing upper eyelid excursion over regenerating corneal epithelium during blinking allows the formation of adhesion complexes to proceed in the absence of shearing forces and accelerates epithelial healing.
Five prospective RCTs investigated the time to closure of the epithelial defect, or rate of healing of an epithelial defect, over a 24-hour period secondary to a TCA1,3,6–8
(Table 21.1).
Kaiser et al.3 randomised the largest series of 223 patients (22 exclusions) with TCA secondary to direct corneal trauma (n = 120) or removal of superficial corneal foreign body (n = 81, 40% of total) to receive antibiotic ointment and cycloplegia with (Group I) or without (Group II) pressure pad. Follow up was daily. There was no statistical difference on presentation between the two groups in patient age and gender, time to presentation or abrasion size. In both aetiology groups of TCA larger abrasions (larger than 4/mm2 in area) took longer to heal than smaller abrasions, but those patients who were not padded demonstrated significantly faster healing (P <0·05). Thirteen per cent of patients in the padded group had removed their pad by 24-hour follow up, and all patients on the no pad group completed treatment (analysis performed on an
129
Significance
|
|
Results |
|
Principaloutcome |
measure |
|
Exclusion |
criteria |
|
Inclusion |
criteria |
|
Antibiotic/ |
cycoplegia |
characteristics |
Intervention/ |
groups |
outcomesand |
No. |
randomised |
Trial |
|
|
Table21.1 |
|
Authors |
0·005 |
|
notstated |
|
notstated |
0·04 |
notstated |
0·05 |
|
0·01 |
|
notstated |
|
0·05 |
0·05 |
0·02 |
|
<P |
|
=P |
|
=P |
=P |
=P |
<P |
|
<P |
|
=P |
|
<P |
<P |
=P |
|
Lowerrecurrence |
ingroupI |
Nosignificant |
difference |
Nosignificant difference |
FasteringroupII |
Nosignificant difference |
FasteringroupII |
forforeignbody |
andTCA Lesspainin |
groupII |
Pre-andpost- |
treatmentscores lowerIngroupI |
LessingroupII |
FasteringroupII |
FasteringroupII |
at24hours |
● |
|
● |
|
● |
● |
● |
● |
|
● |
|
● |
|
● |
● |
● |
|
RCE |
recurrence |
rate |
Visualacuity |
Refraction |
Closureof |
epithelial defect Pain |
Rateof |
healing |
Painat24 |
hours |
Painat24 |
hours |
Painat24 |
hours Closureof defect |
Closureof |
defect |
● |
|
|
● |
● |
● |
● |
● |
|
● |
|
● |
|
● |
● |
● |
|
Cornealdystrophy |
|
|
RCE |
>3/12of |
symptoms |
Yes/No |
|
|
IPTK+manual |
debridement |
IIManual debridement |
● |
|
● |
56 |
|
|
Öhmanand |
Fagerholm, |
1998 |
|
|
5 |
Foreignbody |
|
1stepisodeof |
TCA |
Yes/Yes |
|
IPad |
IINopad |
● |
● |
44 |
|
al., |
|
et |
1993 |
Kirkpatrick |
|
|
8 |
Cornealdystrophy |
|
|
TCA |
Foreignbody |
|
Yes/Yes |
|
|
IPad |
IINopad |
|
● |
● |
|
223 |
|
|
al., |
|
|
et |
3 |
|
Kaiser |
||
1995 |
– |
|
TCA |
|
Yes/No |
|
IPad |
IINopad |
● |
● |
50 |
|
al., |
|
et |
|
Patterson |
9 |
1996 |
–
2 >4/mm
Yes/Yes TCA
IPad |
IIBCL |
● |
● |
28
.,al
etAcheson 7 1987
– |
|
TCA |
Foreignbody |
Yes/Yes |
|
IPad |
IINopad |
● |
● |
74 |
|
al., |
|
et |
|
Campanile |
7 |
1997 |
=Pnotstated |
=Pnotstated |
=Pnotstated |
Nodifference |
Nodifference |
Nodifference |
● |
● |
● |
Closureof |
defect Pain |
Insomnia |
● |
● |
● |
Foreignbody |
|
|
|
2 |
|
TCA |
RCE>1/mm |
|
Yes/Yes |
|
|
IPad |
IINopad |
|
● |
● |
|
48 |
|
|
al., |
|
|
et |
|
|
Arbour |
6 |
|
1997 |
|
=P0·04 |
=P0·0003 |
=P0·001 |
=P0·001 |
=P0·005 |
Lowestingroups |
IIandIII |
Fastestingroups |
IIandIII |
Lowestingroups IIandIII |
● |
|
● |
|
● |
Recurrence |
|
Healingrate |
|
Symptoms |
● |
|
● |
|
● |
–
RCE
NA |
|
|
ILubricants |
IIOral |
tetracycline |
● |
● |
|
30
.al
etRoss - 4 Hope 1994
(Continued)
Significance
|
|
Results |
|
Principaloutcome |
measure |
|
Exclusion |
criteria |
|
Inclusion |
criteria |
|
Antibiotic/ |
cycoplegia |
|
Intervention/ |
groups |
(Continued) |
No. |
randomised |
Table21.1 |
|
Authors |
<P0·002 |
=P0·002 |
|
LowestingroupI |
LowestingroupI |
|
● |
● |
|
|
2hours |
treatment |
Pain |
Pain |
after |
● |
● |
|
RCE Cornealdystrophy Previouscorneal disease |
Pain<30%of |
visualanalogue scale |
|
|
TCA |
|
TCA |
|
|
|
Yes/No |
|
Yes/Yes |
|
IIIOral |
tetracycline+ topical prednisolone |
IDiclofenac 0·1% |
IIPlacebo |
IDiclofenac 0·1% |
IIPlacebo |
● |
|
● |
● |
● |
● |
40 |
|
49 |
|
al., |
|
|
|
et |
1997 |
Szucsetal., |
2000 |
Jayamanne |
|||
|
10 |
|
11 |
PTK, phototherapeutic keratectomy; RCE, recurrent corneal enosion; TCA, traumatic corneal abrasion
Evidence-based Ophthalmology
intention to treat basis), exhibiting better compliance with the treatment.
To measure precisely the rate of closure of the epithelial defect following corneal erosion, Arbour et al.6 studied the digitised images of slit lamp photographs of healing erosions taken daily and analysed using image analysis software. Two groups of patients were compared: group I underwent double eye patching (n = 25), whilst group II were not patched (n = 22). All patients were treated with topical cycloplegia and antibiotic and were prescribed oral analgesia. To avoid pathology arising at the level of Bowman’s layer, cases of foreign body removal were specifically excluded. No statistically significant difference was found between groups for the rate of closure of epithelial defect measured either by reduction in total area with time, or reduction over time of the radius of the largest circle included in the defect (linear speed of re-epithelialisation). The trial had 92% power to detect a 6-hour delay of epithelial closure between the two groups and 95% power to detect a 12-hour delay. The authors concluded that patching a corneal erosion did not significantly accelerate re-epithelialisation.
Campanile et al.7 compared the rate of healing of TCA in patients who were padded compared with those who were not. Of 74 patients who met the inclusion criteria, 64 were evaluated. The abrasion was measured at the slit lamp and transposed to a calibrated grid sheet from which the area was calculated. All patients were treated with topical antibiotic and cycloplegia. There was no statistical difference in the mean size of the abrasion before treatment but at 24-hour follow up the defects were significantly smaller (P = 0·028) in the non-patched group. All epithelial defects were completely closed by 72 hours.
Forty-four patients with a first episode of TCA were randomised by Kirkpatrick et al.8 into two groups treated by chloramphenicol ointment and cycloplegia with (group I) or without (group II) a double eye pad and bandage. Closure of the epithelial defect was significantly faster in group II (P = 0·04). By the end of the 24-hour follow up period, however, 49% of eye bandages were no longer in place, 29% were reported as having fallen off whilst the patient was asleep and 20% had been removed due to discomfort. The number of patients failing to attend follow up was similar between groups although follow up varied from two to seven months.
The effectiveness of a bandage soft contact lens (BCL) in the primary treatment of TCA of large surface area (>4/mm2) was investigated by Acheson et al. in 1987.1 Patients with abrasions from all causes were randomised to two treatment groups: occlusive pad and bandage (group I) or standard size BCL (group II). Both groups were treated with topical antibiotic and cycloplegics. Time to epithelial healing was measured by daily follow up and was significantly faster in
group II (P <0·05). All epithelial defects had closed by four days.
Comment
These studies concluded that padding the eye either made no difference to the rate of healing or that treatment with topical antibiotic and cycloplegia alone or BCL led to statistically faster healing of the defect. Potential sources of bias in these studies included compliance, size of defect and use of topical medication. Compliance tended to be higher in the no-pad groups and the number of non-compliant patients, i.e. those who removed the pad early, were particularly high in Kirkpatrick et al.’s study.8 Although in the BCL treatment arm of Acheson et al.’s study1 only one patient failed to re-attend for six days, the loss to follow up of a patient with a TCA and a BCL in situ might be of particular concern in view of the risk of infectious keratitis.
Those studies that examined larger defects3,6,7 reported that these defects took longer to heal but found no delay in healing rate in those patients who were not padded. Although padding the eye would have resulted in those patients being unable to instil topical medication that might have had an effect on healing rate, all patients in the studies reported were treated with topical antibiotic and cycloplegia at presentation and seen 24 hours later.
Evidence suggests that padding may decrease corneal oxygenation and tear clearance rate, increase the epithelial exposure time to infective and toxic products and increase corneal temperature, all of which would favour bacterial growth. Padding the eye also precludes binocular vision, which may lead to secondary morbidity.
Question
Which treatment modalities are the most effective in reducing the pain and discomfort of TCA?
The evidence
Symptoms of TCA were assessed by seven RCTs examining the effects of pad compared with no pad (n = 4),3,6,8,9 pad compared with BCL (n = 1)1 and treatment with topical diclofenac 0·1% compared with placebo (n = 2).10,11 In Kaiser et al.’s study of 223 patients (22 exclusions) with TCA secondary to direct corneal trauma or removal of superficial corneal foreign body, patients in the no-pad treatment arms reported significantly less pain at 24 hours (P <0·01) as well as a greater difference in pain score at 24-hour follow up compared with presentation (P <0·05) for both aetiologies.3 Patients were questioned about their level of pain, which was then assessed on a scale of 0 to 10.
132
Corneal abrasion and recurrent erosion
Although patients were allowed oral analgesia, the use of these was not monitored by the investigators.
The use of prescribed oral analgesia was recorded by Arbour et al.6 and pain was measured using a visual analogue scale (VAS; uncalibrated 100 mm line) in their study of 48 patients with symptoms from TCA or RCE randomised to undergo pad or no pad following topical antibiotic and cycloplegia. This study also recorded insomnia quantified as a difference between the number of hours actually versus usually slept. No statistical difference between groups was noted for mean or maximal pain score, hours of insomnia or use of prescribed analgesia.
Pain measured at 24-hour follow up compared with pain at presentation was selected as the main outcome measure in 33 patients randomised by Patterson et al.9 to treatment with topical antibiotic with (group I) or without (group II) a pressure pad. The change in mean pain score at 24-hour follow up was not significantly different between the padded and non-padded groups although absolute pain scores measured on a VAS were higher preand posttreatment in the non-padded group, suggesting possible selection bias. Patient selection was not consecutive and with the sample size and difference in starting pain scores the power of the study to detect a real difference between groups may have been limited.
Kirkpatrick et al.’s8 study of the outcomes of patients treated for TCA by chloramphenicol ointment and cycloplegia with or without a double eye pad and bandage showed no statistically significant difference between the two groups for difference in pain scores. The pain score was a secondary outcome measure of the trial and was measured using a VAS. As before, the relatively high rate of noncompliance with treatment in the padded group may well have masked any true treatment effect.
Acheson et al.1 investigated the pain experienced by patients with TCA of large surface area (>4/mm2). Patients were treated with topical antibiotic and cycloplegics and randomised to receive an occlusive pad and bandage (group I) or standard size BCL (group II). Pain as assessed by VAS was recorded as a percentage of that experienced at presentation and was significantly less at follow up in group II (P <0·05).
Jayamanne et al.10 explored the effectiveness of topical diclofenac 0·1% compared with placebo on pain arising from TCA. Forty patients were randomised to receive topical diclofenac 0·1% (n = 20) (group I) or normal saline (placebo) (n = 20) four times daily (group II). No specific instructions regarding the use of oral analgesics were given, no cycloplegics or eye pads were used and all patients were followed up on a daily basis until re-epithelialisation was complete. Pain was assessed in three ways: using a VAS comprising an uncalibrated 100 mm-long horizontal line, using a categorical quantitative pain scale, for example, mild,
moderate, severe and using a categorical qualitative pain scale, for example, foreign body-like, headache-like. At time of presentation there was no statistically significant
difference in pain, but by day one the VAS and categorical pain scores were significantly lower in group I (P <0·002,
P <0·02, respectively) using distribution-free analysis (Wilcoxon rank sum test).
The safety and efficacy of diclofenac sodium 0·1% in the treatment of TCA was also assessed by Szucs et al.11 Fortynine patients were treated with topical antibiotic and cycloplegia and topical diclofenac 0·1% four times daily (group I) or control four times daily (Group II) for 24 to 36 hours, and no eye pad was used. Pain was measured by VAS comprising a calibrated 100 mm-long horizontal line, but the size of the abrasion was not measured. The primary outcome measure was improvement of pain two hours after first treatment, which was assessed by structured telephone call promoting the patient to mark the VAS in their possession and record any rescue oral analgesia they had been prescribed. The two-hour pain score was significantly better in group I, 3·1 (95% CI 2·3–4·0, P = 0·002) compared with group II, 1·0 (95% CI 0·1–2·0, P = 0·002). Twenty per cent (95% CI 4–36%) of patients in group I took oral analgesia compared with 42% (95% CI 22–62%) of controls, although this difference did not achieve statistical significance.
Comment
The use of an eye pad did not significantly reduce pain or insomnia due to TCA,3,6,8,9 in fact in the largest study, patients reported greater pain when padded.3 The use of a BCL for large TCA1 was associated with significantly less pain compared with using an eye pad. Treatment with topical diclofenac 0·1% led to significantly less pain reported when compared with placebo.10,11
Question
Does excimer laser treatment influence the rate of recurrence of RCE?
The evidence
Öhman et al.5 randomised 56 patients with RCE to undergo excimer laser phototherapeutic keratectomy (PTK) ablation following manual epithelial debridement (group I) or epithelial debridement alone (group II). A Summit
ExciMed was used to perform a 6·5 mm central maximal diameter ablation of 5 m unless the debridement area was large or eccentric when additional zones were treated. Patients were followed up for 12 months. Trauma was an associated condition in 46% of cases of both groups. The
133
Evidence-based Ophthalmology
Table 21.2 Performance and quality of trials
|
|
Performance |
Attrition bias: |
|
Placebo |
Intention to treat |
|
Author/s |
bias: masked? |
follow up |
CI quoted |
controlled |
analysis |
|
|
|
|
|
|
|
Öhman and |
Non-masked |
Not stated |
No |
No |
No |
|
Fargerholm, 19985 |
|
|
|
|
|
|
Kirkpatrick et al., |
Non-masked |
16 % did not |
No |
No |
No |
|
19938 |
|
complete, similar |
|
|
|
|
|
|
|
between groups |
|
|
|
Kaiser et al., |
Non-masked |
13 % of padded |
Standard deviation |
No |
No |
|
19953 |
|
patients removed |
|
|
|
|
|
|
|
pad |
|
|
|
Patterson et al., |
Non-masked |
34 % did not |
No |
No |
No |
|
19969 |
Non-consecutive |
complete, similar |
|
|
|
|
|
|
|
between groups |
|
|
|
Acheson et al., |
Non-masked |
7 % in BCL and |
Standard deviation |
No |
Yes |
|
19871 |
|
21 % in pad group |
and standard |
|
|
|
|
|
|
did not complete |
error of mean |
|
|
Campanile et al., |
Masked |
9·4 % removed pad, |
No |
No |
No |
|
19977 |
|
9·0 % DNC in no |
|
|
|
|
|
|
|
pad group |
|
|
|
Arbour et al., |
Non-masked |
2 % (1 patient) did |
Mean + standard |
No |
No |
|
19976 |
|
not complete: group |
deviation |
|
|
|
|
|
|
not stated |
95 % power to |
|
|
|
|
|
|
detect 12-hr |
|
|
|
|
|
|
difference |
|
|
Hope-Ross et al., |
Non-masked |
3·3 % (1 patient) |
No |
No |
Yes |
|
19974 |
|
discontinued |
|
|
|
|
|
|
|
tetracycline |
|
|
|
Jayamanne et al., |
Masked |
All completed |
No |
Yes |
N/A |
|
199710 |
|
|
|
|
|
|
Szucs et al., 200011 Masked |
All completed |
Yes |
Yes |
N/A |
||
BCL, bandage soft contact lens; RCE, recurrent corneal erosion; TCA, traumatic corneal abrasion; DNC, did not complete
RCE recurrence rate was significantly lower in group I (P <0·005). There was no statistical difference between
groups for any other outcome measure. No patients treated by PTK who experienced RCE (7%) required retreatment.
Comment
Five studies investigated the rate of healing and seven outcomes of different treatments on the pain experienced by patients with TCA and RCE. Only one study of padding compared with no pad was single-masked (investigator), indicating that performance bias might have been an influencing factor in comparing outcomes within the populations studied (Table 21.2). Of the three studies
examining the effects of pharmacological intervention, two of topical diclofenac 0·1% and one of oral tetracycline, only the topical diclofenac 0·1% studies were double-masked.
No study showed that padding the eye following a TCA arising from primary trauma or from removal of a corneal foreign body accelerated healing or reduced pain. Three RCTs found that healing was significantly faster in the nopad group and three that pain at follow up was significantly lower in the no-pad group. This evidence would suggest that the primary management of TCA should not include padding the eye in addition to topical antibiotics and cycloplegics. Interestingly, when the effect of upper lid excursion was eliminated by the use of a BCL, both pain and healing at 24 hours was significantly faster and
134
Corneal abrasion and recurrent erosion
compliance with wearing the lens better than wearing a pad. Those RCTs that examined the effect of topical diclofenac 0·1% both concluded that the pain associated with TCA was significantly lower both two hours11 and 24 and 48 hours after presentation.10 Only one study recorded the use of rescue oral analgesia,9 which might have been a significant factor in pain modulation in the other trials.
Accurate measurement of healing rate (by grid drawing7 or computer image analysis software6) is important since in all studies the maximal time to closure of the defect was five days, with the majority closed by 48 hours. The natural history of TCA is of particular relevance to healthcare economists when more expensive treatments such as fitting a BCL are advocated.
Implications for practice
No trial suggested that application of a pressure pad, or pad and bandage, quickened epithelial healing or reduced the pain or discomfort of TCA. Treatment by topical cycloplegia and antibiotic alone led to healing rates that were at least as fast or significantly faster and levels of pain at follow up that were equivalent or significantly lower than additional padding. Use of a BCL was associated with significantly less pain and faster epithelial healing from large (>4/mm2) abrasions compared to padding, whilst patients treated with topical diclofenac 0·1% reported significantly less pain both two and 24 hours after TCA.
A significantly lower recurrence rate for RCE was observed in patients treated by excimer laser in addition to manual epithelial debridement, with more than 90% of patients recurrence-free for 12 months following treatment. The use of oral tetracycline for three months was also associated with a lower recurrence rate of RCE and faster epithelial closure. This effect was observed whether or not patients were treated with topical prednisolone 0·5% for seven days.
Implications for research
Further work is clearly needed to determine the true natural history of RCE and to determine if treatments other that excimer laser may reduce recurrence rates below that obtained with topical lubricant treatment alone. Specifically, a trial comparing BCL and topical medication to topical medication alone is needed in TCA.
References
1.Acheson JF, Joseph J, Spalton DJ. Use of soft contact lenses in an eye casualty department for the primary treatment of traumatic corneal abrasions. Br J Ophthalmol 1987;71:285–9.
2.Hykin PG, Foss AE, Pavesio C, Dart JKG. The natural history and management of recurrent corneal erosion: A prospective randomised trial. Eye 1994;8:35–40.
3.Kaiser PK, the corneal abrasion patching study group. A comparison of pressure patching versus no patching for corneal abrasions due to trauma or foreign body removal. Ophthalmology 1995;102:1936–42.
4.Hope-Ross MW, Chell PB, Kervick GN, McDonnell PJ, Jones HS. Oral tetracycline in the treatment of recurrent corneal erosions. Eye 1994;8:384–8.
5.Öhman L, Fagerholm P. The influence of excimer laser ablation on recurrent corneal erosions: A prospective randomized study. Cornea 1998;17:349–52.
6.Arbour JD, Brunette I, Boisjoly HM, Shi ZH, Dumas J, Guertin MC. Should we patch corneal erosions? Arch Ophthalmol 1997;115: 313–17.
7.Campanile TM, St Clair DA, Benaim M. The evaluation of eye
patching in the treatment of traumatic corneal epithelial defects. J Emerg Med 1997;15:769–74.
8.Kirkpatrick JNP, Hoh HB, Cook SD. No eye pad for corneal abrasion. Eye 1993;7:468–71.
9.Patterson J, Fetzer D, Krall J, Wright E, Heller M. Eye patch treatment for the pain of corneal abrasion. Southern Med J 1996;89:227–9.
10.Jayamanne DGR, Fitt AWD, Andrews RM, Mitchell KW, Griffiths PG. The effectiveness of topical diclofenac in relieving discomfort following traumatic corneal abrasions. Eye 1997;11:79–83.
11.Szucs PA, Nashed AH, Allegra JR, Eskin B. Safety and efficacy of diclofenac ophthalmic solution in the treatment of corneal abrasions. Ann Emerg Med 2000;35:131–7.
135
