Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma
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Clinical Diagnosis and Management of Ocular Trauma |
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gently examined to evaluate the extent of damage. |
shelved wounds, the placement of sutures should be |
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If the globe appears unstable, sutures are first applied |
equidistant with respect to internal aspect of the wound |
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prior to exploration of the wound. |
and tied without undue tension to optimize tissue |
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apposition. On the other hand, wounds with |
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Most Corneal Lacerations |
macerated or edematous edges require longer sutures |
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Most corneal lacerations require suture placement. |
for security. |
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Prompt, secure wound closure is especially important in |
Suture Bites through the Visual Axis |
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children who are at greater risk of inadvertently rubbing |
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the eye with consequent reopening of a tissue adhesive |
Suture bites through the visual axis should be avoided. |
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or contact lens supported wound. Large corneal |
If suture needs to be taken through the visual axis, |
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laceration, sclera laceration, corneoscleral laceration, |
a number of techniques can be used to minimize |
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displaced wound, wounds with tissue incarceration such |
scarring. Sutures near to visual axis should be shorter, |
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as iris or lens or vitreous incarceration should be taken |
superficial and relatively loose as against the peripheral |
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up for primary wound repair at the earliest possible. |
sutures which should be longer, deeper and tighter. |
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So, also the visual axis can be straddled by sutures |
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Small Corneal Laceration with Reasonably |
placed at each side of, but not directly through the |
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Formed Anterior Chamber |
axis itself. More importantly, No Touch Technique |
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Suture the corneal wound directly with 10-0 nylon |
is employed wherein the globe is stabilized away from |
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the site of corneal wound and sutures are directly |
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suture, need not enter into anterior chamber. |
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passed through the corneal wound without holding |
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Less Stable Wound with Shallow or Flat Anterior |
the corneal wound edges which will prevent tissue |
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damage in visual axis thereby preventing scarring at |
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Chamber |
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visual axis. |
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Wound cleaning with normal saline, formation of |
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anterior chamber with help of viscoelastic. Viscoelastic |
Number of Suturing Techniques |
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can be injected through side port made with help of |
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Number of suturing techniques has been discussed and |
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MVR blade, but in cases of collapsed globe it might be |
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difficult to make the side port and form the chamber |
described in the literature. In cases with straight |
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with viscoelastic and hence in such cases viscoelastic can |
lacerations, a running shoestring closure may minimize |
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be injected directly through the corneal wound and |
astigmatism and scarring, however at times the wound |
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chamber can be completely or partly formed. The |
integrity may not be achieved as perfectly as it could |
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eventual aim in corneal laceration repair is definitive |
have been with interrupted sutures. If a running suture |
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placement of corneal sutures to make the wound |
is used, the bites should be placed perpendicular and |
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watertight, minimize scarring, and reconstruct the native |
equidistant to a best fit imaginary line through the |
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nonastigmatic corneal contour. One can start by taking |
wound, irrespective of laceration itself. However, while |
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superficial temporary sutures in order to approximate |
using an interrupted suture technique for curvilinear |
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the wound edges and subsequently those sutures can |
or irregular lacerations, all sutures should be placed |
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be replaced with definite deep sutures at end of surgery. |
perpendicular to the wound to avoid transverse shifting |
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of the wound margins. |
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Monofilament 10-0 Nylon Suture Material |
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Monofilament 10-0 nylon suture material on a fine spatulated design microsurgical needle is used for corneal suturing. Some surgeons even prefer use of 11-0 nylon sutures especially for wounds involving visual axis. A number of strategies for corneal suturing are available. The simplest involves progressively halving the wound with simple interrupted sutures. These definitve corneal sutures should be approximated 1.5 mm long, approximately 90% deep in the stroma, and of equal depth on both sides of the wound. Shallow sutures will cause internal wound gape; sutures that are asymmetric or of unequal depth will result in wound override. On the contrary, full thickness sutures can act as conduit for microbial invasion. In
Corneoscleral Laceration
In cases with corneoscleral laceration, first, a suture is applied to the limbus, and the wound is tightly secured. This suture helps to anatomically approximate the wound. After the first suture is applied, an iris prolapse or a vitreous prolapse is treated. In the presence of an iris prolapsed depending on the viability of iris tissue it is either repositioned or absiccised. In the presence of a vitreous prolapse, a vitrectomy is performed with cellulose sponges or an automated vitrector. During the vitrectomy, traction on the vitreous should be avoided. Any vitreous in the anterior segment may be removed using a vitrectomy machine. After the corneal wound is repaired, the scleral wound
Primary Globe Repair |
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is explored. This exploration is achieved by performing a limbal peritomy at the site of the limbal wound. The sclera wound is secured with help of interrupted or continuous 7-0 vicryl suture or 8-0 vicryl suture. Segments of scleral laceration are explored and repaired. This method helps to stabilize the eye and to prevent uveal or vitreous prolapse.
Scleral Laceration
Scleral laceration should be repaired as far posteriorly as possible; far posterior scleral ruptures may be left unsutured. While repairing scleral lacerations, care must be taken to not exert pressure on the globe. In the presence of uveal prolapse, the prolapsed tissue is reposited. The preferred method of sclera wound closure over prolapsed uveal tissue is a zippering technique wherein the sclera wound is closed from anterior end, i.e. limbal end with interrupted sutures placed successively proceeding posteriorly. One should never do excision of the prolapsed uveal tissue unless it is necrotic because it causes excessive bleeding. Vitreous prolapse is managed by performing a vitrectomy with cellulose sponges and scissors or by using an automated vitrector. At every step, care should be taken to prevent iatrogenic damage. The sutures are placed closely together and tied to achieve a watertight closure. The conjunctiva is sutured using 8- 0 or 9-0 Vicryl.
Posterior Scleral Laceration
Scleral laceration without corneal involvement may occur in a variety of settings. Posterior sclera dehiscence or occult sclera dehiscence can be suspected based on history and mode of ocular trauma, poor visual acuity, conjunctival chemosis, deep or shallow anterior chamber, low intraocular pressure, hyphema and/or subconjunctival pigmentation. Lacerations extending beyond equator of the globe can be left unsutured if attempting suturing is causing more trauma to the globe, this sclera perforations will be taken care by delayed secondary healing.
Patch and a Shield
A patch and a shield are applied to the eye. Postoperatively, patients should be carefully monitored for signs of infection. Pain, photophobia, redness, tearing, or a deterioration of vision should alert the physician to look for signs of endophthalmitis. Conjunctival injection, chemosis, corneal edema, and elevated intraocular pressure may be present but are not diagnostic of infection. A more than expected anterior chamber reaction and cells in the vitreous are most suggestive of endophthalmitis.
Fig. 33.1: Corneal laceration operated elsewhere
Fig. 33.2: Corneal laceration repaired under topical anesthesia
Fig. 33.3: Corneal laceration repaired with hypopyon
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Clinical Diagnosis and Management of Ocular Trauma |
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Fig. 33.4: Corneal laceration with eye lash in wound |
Fig. 33.7: Corneal wound revision done |
Fig. 33.5: Corneal laceration with infection of |
Fig. 33.8: Open globe injury repaired |
wound edges |
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Fig. 33.6: Corneal laceration with traumatic cataract |
Fig. 33.9: Open globe injury with iris prolapse |
Primary Globe Repair |
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wound should be carefully explored and should be addressed by doing atraumatic sclera laceration repair.
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Bibliography |
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1. |
Beatty RF, Beatty RL. The repair of corneal and sclera |
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lacerations. Semin Ophthalmol 1994;9(3):165-76. |
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2. |
Coumhaire-Poutchinian Y. Management of the repair of |
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scleral and corneal injuries. Bull Soc Belge Ophtalmol |
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1996;260:81-88. (Article in Ffrench) |
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3. |
Drews RC. Sodium Hyaluronate (Healon) in the repair |
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of perforating injuries to the eye. Ophthalmic surg |
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1986;17:23-29. |
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4. |
Eisner G: Eye surgery: an introduction to operative |
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technique, New York, 1980 Springer-Verlag. |
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Fig. 33.10: Post-corneal tear repaired with SFIOL |
5. |
Hamill BM. Corneal and Scleral trauma. Ophthalmol Clin |
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N Am 15(2002):185-94. |
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Summary |
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6. |
Hersh PS, Shingleton BJ, Kenyon KR. Management of |
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corneoscleral lacerations. Eye Trauma. 1991. Mosby's |
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Corneal and sclera wounds commonly present to the |
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Publications 143-58. |
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7. |
Lamkin JC, Azar DT. Simultaneous corneal laceration |
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emergency clinic and management of this cases should |
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repair, cataract removal and posterior chamber intraocular |
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be prioritize to optimize visual potential in traumatized |
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lens implantation. Am J Ophthalmolo. 1992 Jun 15; |
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eyes. Management of corneal and sclera laceration |
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113(6):626-31. |
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requires careful evaluation and planning prior to closure. |
8. |
Lin DT, Webster RG Jr, Abbott RL. Repair of corneal |
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The globe must be closed so that it is watertight with |
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lacerations and perforations. Int Ophthalmol Clinics. |
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the original anatomy restored and the original function |
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1988 Spring 28(1):69-75. |
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9. |
Rowsey JJ, Hays JC, Refractive reconstruction for acute |
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can be as approximated as possible. Closure of the |
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eye injuries, Ophthalmic Surg 1984;15:569-74. |
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cornea and sclera is different from the typical skin |
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10. |
Russel SR, Olsen KR, Folk JC. predictors of sclera rupture |
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technique of halving the wound. Corneal wound is |
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and the role of vitrectomy in severe blunt ocular trauma. |
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closed based on the principles explained whereas sclera |
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Am J Ophthalmol 1984;102:547-50. |
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Iatrogenic Ocular Trauma
and its Complications
Management
C H A P T E R
34Management of Iatrogenic
Inflammation of the Eye
NR Biswas, GK Das, Viney Gupta (India)
Introduction
For the treatment of any type of inflammation including iatrogenic, both the steroids and non-steroidal anti-inflammatory drugs may be used.
The corticosteroids are essential drugs in ophthalmological diseases. It is a boon to the patients when it is used with proper indications. It is a two-edged sword, and can cause serious complications and side effects if it is used unwisely. Are we using corticosteroids judiciously? This question must always be kept in mind and answered before instituting this therapy. Before planning the corticosteroid therapy, we must keep in mind its ocular hazards. In clinical practice corticosteroids are often used as shotgun therapy or as a placebo when all is not going well. This practice must be discouraged.
to their use. In experimental studies the available 0.1 percent dexamethasone further diluted as 1:10 or 1:20 dilution had no virus or fungal replications enhancing effect when instilled 10 times a day, while 1:5 dilution or undiluted available dexamethasone drops (0.1%) enhanced virus and fungal growth. Moreover, adequately diluted corticosteroid does not increase the risk of enhancing the collagenase effect.
c.Corticosteroid therapy in vernal conjunctivitis and allergic disorders: The use of corticosteroids locally has a beneficial effect in vernal conjunctivitis. But prolonged use is attended by unwanted side effects like cataracts, glaucoma and secondary keratoconus.
d.Use of corticosteroids in alkali burns of cornea and conjunctiva: The use of corticosteroids in alkali burns is obligatory and seems beneficial.
Topical Application
The route of administration of corticosteroids depends primarily on the site of involvement. Topical therapy is effective in anterior segment diseases, including disorders of lids, conjunctiva, cornea, iris and ciliary body. Ease of application, relatively low cost, and absence of systemic complications strongly favor local routes whenever they are effective.
The course of posterior segment disease (chorioretinitis, optic neuritis, and posterior scleritis) is not appreciably affected by topical corticosteroids and requires systemic therapy.
a.Are diluted corticosteroid drops effective in controlling intraocular inflammation?
It was demonstrated that diluted corticosteroids have therapeutic anti-inflammatory effect in strengths of 0.01 and 0.005 percent.
b.Corticosteroids in infective corneal diseases:
Local installation of corticosteroids in frank suppurative conditions are generally considered as contraindications
e.Use of corticosteroids in pseudophakic bullous keratopathy (PBK): The effects of 5% hypertonic sodium chloride drop and deturgescent drops, prepared by mixing betamethasone eye drops (0.1%) 1 ml; glycerin, 1 ml and artificial tear drops 8 ml, achieving 10% glycerin and 1:0 betamethasone eye drops (0.1%), were compared in a controlled clinical trial in 50 cases of PBK. These were instilled 10 times a day. The deturgescent drops were significantly superior in subjective as well as objective parameters like discomfort, foreign body sensation, corneal clarity and improvement in vision, etc. as compared to 5% hypertonic saline.
f.Ocular hypertensive effect of corticosteroids:
Surgical trauma causes inflammation which demands the use of corticosteroids to prevent the trabecular meshwork, corneal endothelium and other inner structures of the eye from damage by inflammatory response as well as its debris. But, ocular hypertension inducing effects restrict their wide usage. In this regard, 1:10 or 1:20 diluted steroid did not have any ocular hypertensive effect.
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Clinical Diagnosis and Management of Ocular Trauma |
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The use of 1:10 or 1:20 dexamethasone (0.1%) |
Indications |
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for specified periods is safe to be used in glaucoma |
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In general, corticosteroid therapy may be helpful for |
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patients after intraocular surgery or when there is an |
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associate uveitis, as there should be negligible risk of |
all allergic ocular diseases, for most non-pyogenic |
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producing hypertension. |
inflammations (episcleritis, scleritis, uveitis, interstitial |
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keratitis, optic neuritis and the like), and for the |
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Systemic Therapy |
reduction of immunologic responses. |
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Prednisone has become a corticosteroid of choice because it is inexpensive, short acting, and relatively free from sodium retention. It may be used in divided doses, a single daily dose, or a single alternate day dose.
Single daily dose: For long-term low-dosage maintenance (as for chronic uveitis), a single, morning, daily dose of prednisone may be optimal.
Alternate day therapy: The undesirable side effects of systemic corticosteroid therapy can be substantially reduced by using alternate day therapy rather than divided dosage. Briefly stated, the entire total dose of corticosteroid that would have been given during a 2-day period is administered as a single dose every other morning.
Repository Injection
The ophthalmologist who wishes to administer corticosteroids by “subconjunctival” injection should consider use of the repository form of methyl-prednosolone acetate (Depo-Medrol). Thus suspension form of prednisolone provides a constant source of corticosteroid that lasts for 2 to 4 weeks.
Intravitreal Injection
Intravitreal 0.1 ml (Dose 50 mg/ml) is injected to prevent proliferation of fibroblast. It seems helpful to combat proliferative vitreoretinopathy.
Controlled Release Vehicles
Ocusert devices delivering 10 mg of hydrocortisone acetate/hr were used to treat allergic conjunctivitis.
Pulse Therapy
Slow intravenous infusion of 100 mg Prednisolone daily for consecutive three days shows good response in Harada’s disease. If needed, repeat dose can be given after 14 days.
USE IN OCULAR SURGERY
1.Cataract
2.Corneal graft rejection
3.Glaucoma surgery
4.Retinal detachment
5.Vitreous surgery
6.Strabismus
7.Intraocular foreign body.
Contraindications and
Complications
SYSTEMIC COMPLICATIONS
•Peptic ulceration
•Osteoporosis
•Femoral head ischemia necrosis
•Pseudotumor cerebri
•Exophthalmos.
LOCAL CONTRAINDICATIONAND
COMPLICATIONS
•Superinfection
•Activation of tuberculosis
•Uveitis
•Glaucoma
•Corticosteroid mydriasis
•Corticosteroid induced cataract.
The severe scleritis associated with rheumatoid arthritis, an example of immunological disorder does respond to corticosteroid treatment but the patient may suffer structural loss of sclera upto more severe scleromalacia as a result of treatment.
Sympathetic ophthalmia is a classic example of a disease responsive to corticosteroid therapy, but requires prolonged therapy.
Non-specific iridocyclitis and chorio-retinitis, as well as herpetic keratitis do seem to benefit from corticosteroid therapy.
Posterior ocular effects require systemic administration or retrobulbar injection.
Management of Iatrogenic Inflammation of the Eye |
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Responsive Diseases |
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TOXOPLASMOSIS |
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BOECK’S SARCOID UVEITIS |
It can be treated with high corticosteroid doses (upto |
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100 mg prednisone per day for a prolonged period |
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The response of Boeck’s sarcoid uveitis to |
with specific antitoxoplasmic therapy). |
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corticosteroid therapy may be very gratifying. Topical |
OTHER INDICATIONS |
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use of corticosteroids and mydriatics is often |
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insufficient to arrest the disease. Addition of systemic |
Corticosteroid is found to be useful in cysticercosis. |
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corticosteroid therapy has frequently given prompt |
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subjective relief, followed within a few weeks by |
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considerable objective improvement. Upto 200 mg |
Use of Nonsteroidal Anti- |
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daily was used and produced a consistently favorable |
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inflammatory Drugs in |
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symptomatic effect. |
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ORBITAL MYOSITIS |
Inflammation |
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In the treatment of ocular inflammation, the appeal |
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Acute inflammation of one or more extraocular muscles |
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of nonsteroidal anti-inflammatory drugs (NSAIDs) |
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may be a sequel to upper respiratory infections. These |
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hinges on the complications associated with the more |
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painful restrictions of movement may respond |
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established therapy for ocular inflammation, i.e. |
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promptly to corticosteroid therapy. |
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corticosteroids. Although an overlap exists between |
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OCULAR PEMPHIGOID |
the mechanisms of action of both, the use of NSAIDs |
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may be safer than the use of corticosteroids, as the |
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Although pemphigoid is characteristically a slowly |
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latter may produce adverse effects such as glaucoma, |
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progressive chronic subepithelial scarring process, |
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opportunistic infections, and posterior subcapsular |
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episodes of acute inflammation may occur. These |
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cataracts. In sharp contrast, topical NSAIDs are known |
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typically are nonresponsive to topical corticosteroid |
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to cause only minor adverse effects such as burning, |
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therapy. Systemic corticosteroids in dosage of 60 to |
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stinging and hyperemia of the conjunctiva. |
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100 mg/day have caused remission of the disease. |
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HERPES ZOSTER |
OCULAR INFLAMMATION |
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A simple definition of ocular inflammation would be |
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In a small series of 11 patients with herpes zoster, very |
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inflammation of any part of the eye. Intraocular |
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favorable results were reported from the systemic |
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inflammation can be subdivided into inflammation of |
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administration of cortisone or ACTH. |
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the anterior and posterior segments of the eye. The |
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NEOPLASMS |
cardinal signs of ocular inflammation are hyperemia, |
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increased vascular permeability, oedema, and cellular |
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Hemangiomas, intracranial plasmacytoma, medullo- |
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(leukocytes, mast cell, platelets, etc.) infiltration into |
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blastoma, ewings tumors respond well to corticosteroid |
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ocular fluids and tissues. In experimental anterior |
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therapy. |
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uveitis, miosis and a rise in intraocular pressure which |
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TOLOSA-HUNT SYNDROME |
is usually due to the breakdown of the blood-aqueous |
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barrier with subsequent release of protein and fibrin |
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Recurrent unilateral, painful, acute ophthalmoplegia |
into the aqueous humor, but not of cellular infiltration, |
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responds dramatically to corticosteroid therapy within |
is observed. Inflammation after paracentesis usually |
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2 to 3 days. A daily dosage of 60 mg prednisone was |
disappears within 2-3 hrs. |
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used. |
To understand the history of NSAID use in |
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ANTERIOR SEGMENT ISCHEMIA |
ophthalmology, one must appreciate the relevance of |
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prostaglandins in the eye. In 1971, Vane and Smith |
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Prednisolone 1% was used four times daily, with |
established the connection between the clinical effect |
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gradual clearing of the corneal edema and anterior |
of acetylsalicylate and inhibition of prostaglandin |
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chamber cellular reaction. |
systesis1,2. It is now well-known that aspirin and other |
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PSEUDOTUMOR CEREBRI |
NSAIDs produce their clinical efficacy by inhibiting |
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cyclooxygenase and thus inhibiting prostaglandin |
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Dexamethasone 0.5 mg is prescribed three doses daily |
synthesis (Fig. 34.1). Specific drugs belonging to each |
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for 3 weeks. |
class are listed in Tables 34.1 and 34.2. |
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226 |
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Clinical Diagnosis and Management of Ocular Trauma |
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TABLE 34.1: Systemic nonsteroidal anti-inflammatory agents |
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Drug |
Drug name |
How supplied |
Typical adult daily dose |
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(mg) |
(mg) |
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Salicylates |
Aspirin |
325-925 |
650 |
q4th |
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Diflunisal |
250, 500 |
250-500 bid |
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Fenamates |
Mefenamate |
250 |
250 |
qid |
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Meclofenamate |
50, 100 |
50-100 qid |
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Indoles |
Indomethacin |
25, 50, 75 |
25-50 tid-qid, |
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(slow release) |
75 bid |
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Sulindac |
150, 200 |
150-200 bid |
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Tolmetin |
200, 400, 600 |
400 |
tid |
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Phenylacetic acids |
Diclofenac |
35, 50, 75 |
35-75 bid |
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Pheynylalkanoic acids |
Fenoprofen |
200, 300, 600 |
300-600 tid |
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Ketoprofen |
25, 50, 75 |
75 tid, - 50 qid |
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Piroxicam |
10, 20 |
10 bid, 20 daily |
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Flurbiprofen |
50, 100 |
100 |
tid |
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Ketorolac |
10 |
10 qid |
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Naproxen |
250, 375, 500 |
250-500 bid |
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275-550 |
275-550 bid |
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200, 300, 400 |
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Ibuprofen |
600, 800 |
400-800 tid |
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Pyrazolones |
Phenylbutazone |
100 |
100 |
tid-qid |
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Oxyphenylbutazone |
100 |
100 |
tid-qid |
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Para-aminophenols |
Acetaminophen |
80, 325, 500, 650 |
650 |
q4th |
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Fig. 34.1: Mechanism by which nonsteroidal antiinflammatory drugs produce their clinical effect
MECHANISM OF ACTION
NSAIDs act mainly as anti-inflammatory agents by inhibiting cyclooxygense and lipo-oxygenase enzymes which lead to inhibition of products like prostaglandins, thromboxane and leukotrienes which induce inflammation. Ocular actions of prostaglandins include
TABLE 34.2: Topical nonsteroidal anti-inflammatory agents
Name |
Strength |
Typical doses |
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Flurbiprofen |
0.03% solution |
1 drop every 30 minutes |
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for 2 hrs |
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Preoperatively (Total |
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dose: 4 drops) |
Suprofen |
1.0% |
solution |
2 drops at 1.2 and 3hours |
|
|
|
preoperatively or every |
|
|
|
4 hours while awake |
|
|
|
on the day of surgery. |
Diclofenac |
0.1% |
solution |
qid |
Ketorolac |
0.5% |
solution |
tid |
Indomethacin 0.5%-1.0% |
qid |
||
|
suspension |
|
|
an increase in vascular permeability, breakdown of the blood-aqueous barrier and induction of miosis.
Cystoid Macular Edema (CME)
Topical NSAIDs are effective in preventing postsurgical angiographic CME when topical or subtenon’s corticosteroid injections are given concurrently. Only one study (involving 50 patients) has demonstrated similar effect with a topical NSAID in the absence of concurrent corticosteroid therapy.4 Several studies have demonstrated that prophylactic treatment with a topical NSAID has a beneficial effect on visual function. In one study, this effect was shown even in the absence
