Ординатура / Офтальмология / Учебные материалы / Ocular Traumatology Springer

3.1.3.1.2 Additional Steps to be Taken

•Perform slit lamp examination, take the visual acuity and the IOP (oral acetazolamide treatment must be initiated if the IOP is elevated), measure the pH of the ocular surface, and grade the injury.

•If the injury is Grade I or II, topical therapy should be used: corticosteroids [17]; ascorbic acid [5, 16]; and antibiotics. Admission is not mandatory,12 but daily evaluations are recommended until the corneal epithelium is healed.

•If the injury is Grade III or IV,13 the irrigation must be continued, using phosphate-free solutions such as Isopto Max14 or Corti-biciron15 [17], and the patient should be admitted.

•All efforts are aimed at rescuing the limbal stem cells [19] by reducing the inflammation and scar formation (and by subsequent surgery, see below). Hourly16 drops of corticosteroids, ascorbic acid, and antibiotics, continued for up to 2 weeks, are employed.

•Superficial debridement should be done twice daily by rinsing the eye with ringer lactate solution.

•A round-tipped glass rod should be rolled across the upper and lower fornices to prevent adhesion development.

•If insufficient limbal regeneration is seen within the first 4 days, an amniotic graft should be placed to secure the corneal surface and improve healing.

•At least 2 days after the injury, the demarcation of necrotic areas is well appreciated. The necrotic tissue should be surgically removed; if the necrosis involves large areas of the limbus and conjunctiva, an initial tenonplasty is required [12]. Tenon’s capsule is bluntly dissected; its soft sheets are advanced up to the limbus (Fig. 3.1.3) and fixed to the

12This also depends on factors such health insurance system, the patient’s socioeconomic and hygienic situation, and financial circumstances.

13The prognosis is poor, mostly because of the damage to the limbal stem cells.

14Alcon Pharma GmbH, Freiburg, Germany

15S&K Pharma, Perl, Germany

16Ointment is used for nighttime.

494 Norbert Schrage and Ferenc Kuhn

sclera by full-thickness sutures (similar to that in scleral patching; see Chap. 2.3).

•In Grade IV burns, the primary goal of treatment is to prevent secondary damage such as glaucoma or ulceration with perforation.

Fig. 3.1.3  Prochaska− Marburg tenonplasty. The epibulbar tissues are liberated and advanced up to, and sutured to, the limbus. a Schematic drawing. b Intraoperative photograph

Once the acute phase is passed and the surface of the eye is stable, the patient can be discharged on topical corticosteroids, antiglaucoma medications, and antibiotics; these are used until the redness diminishes.

3.1.3.2Secondary Intervention

With the appearance of pale scars, ocular surface restoration becomes possible via a step-by-step approach.

3.1.3.2.1 Lid Reconstruction

Scars must be removed, normal lid position restored (anti-entropium or ectropium surgery), and the normal eyelash configuration restored (antidistichiasis or trichiasis surgery). If required, the lid skin must be reconstructed [10, 17].

!Pitfall

Ocular surface reconstruction is likely to fail if it has not been preceded by restoration of the normal lid anatomy.

3.1.3.2.2 Symblepharon Management

Although symblepharon development is more common after heat than after chemical injury, it does represent a significant problem, which needs to be addressed:

•In eyes without conjunctival shortening, incision and conjunctivoplasty are sufficient.

•In eyes with shortened fornices, the scars need to be removed and bucchal mucosa or amniotic membrane transplanted [11]. To prevent rolling up of the donor tissue, two silicone bands must be secured, sandwiching the lid: one over the graft internally and one over the skin externally.

3.1.3.2.3 Ocular Surface Restoration

The process of ocular surface restoration is as follows:

Fig. 3.1.4  Fjodorov keratoprosthesis. The device has a titan ring and a PMMA optic. A rigid retroprosthetic membrane has occurred, but a central hole still allows some vision

Fig. 3.1.5  ACTO Tex-KPRO keratoprosthesis. Implanted 8 months previously, this device allows 0.4 visual acuity; the retina is reattached under silicone oil, and the IOP is 15 mmHg

DO:

•consider irrigation the most important element of the treatment

•use any neutral fluid for irrigation and irrigate both the visible, easily accessible areas as well as the upper fornix, and remove all agent particles mechanically

•admit patients with Grade III or Grade V injuries

•administer topical corticosteroids and antibiotics long-term to prevent infection, and to reduce inflammation and scarring

•surgically reconstruct the severely damaged anterior segment

DON’T:

•delay irrigation to take a detailed history

•forgo the irrigation even if the injury is not fresh: it may still improve the final outcome

•neglect the IOP: if elevated, it can quickly make the prognosis much worse

•try to restore the ocular surface without first addressing lid and eyelash position abnormalities

Summary

A chemical injury is one of the very few conditions in which the prognosis may be determined literally by minutes: if the irrigation is delayed or done inappropriately, the damage can be irreversible.

References

[1]Dohlman CH, Doane MG (1994) Some factors influencing outcome after keratoprosthesis surgery. Cornea 13: 214−218

[2]Falcinelli G, Falsini B, Taloni M, Colliardo P, Falcinelli G (2005) Modified osteo- odonto-keratoprosthesis for treatment of corneal blindness: long-term anatomical and functional outcomes in 181 cases. Arch Ophthalmol 123: 1319−1329

[3]Gerard M, Merle H, Chiambaretta F, Rigal D, Schrage N (2002) An amphoteric rinse used in the emergency treatment of a serious ocular burn. Burns 28: 670−673

[4]Hall AH, Blomet J, Mathieu L (2002) Diphoterine for emergent eye/skin chemical splash decontamination: a review. Vet Hum Toxicol 44: 228−231

[5]Heckelen A, Hermel M, Kondring B, Schrage NF (2004) Ascorbic acid reversibly inhibits proliferation of retinal pigment epithelial cells. Acta Ophthalmol Scand 82: 564−568

[6]Ho W, Ying S, Chan H, Chow C (2001) Assault by burning: a reappraisal. Burns 27: 471−474

[7]Kompa S, Redbrake C, Langefeld S, Brenman K, Schrage N (2001) The Type II Aachen-Keratoprosthesis in humans: case report of the first prolonged application. Int J Artif Organs 24: 110−114

[8]Krause A, Tost M, Schlaffer G (1995) [Putschkowaskaja corneal protection]. Klin Monatsbl Augenheilkd 206: 161−164

[9]Kuckelkorn R, Kottek A, Schrage N, Reim M (1995) Poor prognosis of severe chemical and thermal eye burns: the need for adequate emergency care and primary prevention. Int Arch Occup Environ Health 67: 281−284

[10]Kuckelkorn R, Schrage N, Becker J, Reim M (1997) Tarsoconjunctival advancement: a modified surgical technique to correct cicatricial entropion and metaplasia of the marginal tarsus. Ophthalmic Surg Lasers 28: 156−161

[11]Kuckelkorn R, Schrage N, Redbrake C, Kottek A, Reim M (1996) Autologous transplantation of nasal mucosa after severe chemical and thermal eye burns. Acta Ophthalmol Scand 74: 442−448

[12]Kuckelkorn R, Schrage N, Reim M (1995) Treatment of severe eye burns by tenonplasty. Lancet 345: 657−658

[13]Merle H, Donnio A, Ayeboua L, Michel F, Thomas F, Ketterle J, Leonard C, Josset P, Gerard M (2005) Alkali ocular burns in Martinique (French West Indies) Evaluation of the use of an amphoteric solution as the rinsing product. Burns 31: 205−211

[14]Rama P, Bonini S, Lambiase A, Golisano O, Paterna P, Luca M de, Pellegrini G (2001) Autologous fibrin-cultured limbal stem cells permanently restore the corneal surface of patients with total limbal stem cell deficiency. Transplantation 72: 1478−1485

[15]Ray S, Khan BF, Dohlman CH, D'Amico DJ (2002) Management of vitreoretinal complications in eyes with permanent keratoprosthesis. Arch Ophthalmol 120: 559−566

[16]Reim M, Beil KH, Kammerer G, Krehwinkel S (1982) Influence of systemic ascorbic acid treatment on metabolite levels after regeneration of the corneal epithelium following mild alkali burns. Graefe's Arch Clin Exp Ophthalmol 218: 99−102

[17]Reim M, Kottek A, Schrage N (1997) The corneal surface and wound healing. Progr Ret Eye Res 16: 183−225

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[18]Reinhard T, Sundmacher R (1994) Lamellar horseshoe sclerokeratoplasty and thermoplasty in keratoconus with peripheral ectasia of the cornea. Klin Monatsbl Augenheilkd 205: 305−308 [in German]

[19]Tsai RJ, Tseng SC (1994) Human allograft limbal transplantation for corneal surface reconstruction. Cornea 13: 389−400

[20]Yao YF, Zhang B, Zhou P, Jiang JK (2002) Autologous limbal grafting combined with deep lamellar keratoplasty in unilateral eye with severe chemical or thermal burn at late stage. Ophthalmology 109: 2011−2017

  3.2  Electromagnetic Trauma

Yaniv Barkana, Michael Belkin, Ferenc Kuhn

3.2.1Introduction

Electromagnetic waves, both in the visible and invisible spectrum, are able to damage the eye. With the increasing availablity of intense light sources and interest in laser weapons, the significance of such trauma for individuals and society is expected to rise. In this chapter we describe the interaction of electromagnetic waves with the eye and the clinical course of consequent injuries. In the absence of effective treatment for most conditions, prevention is the best option against vision loss.

3.2.2Evaluation

In some cases, the patient himself seeks medical attention because of pain (e.g., welder’s photokeratitis; see Chap. 2.2). In other cases the source is more difficult to identify (e.g., light damage sustained during eye surgery). Reliable history may also be difficult to obtain in certain cases (e.g., self-in- flicted damage, children’s solar trauma, or if the patient was unaware of the exposure). The ophthalmoscope is the most important diagnostic tool.

3.2.3Specific Conditions

3.2.3.1Light-induced Damage (Photic Eye Injury)

Light, especially if powerful (direct viewing of the sun or an atomic bomb explosion, even if it is many miles away [4]) and concentrated, such as that

502 Yaniv Barkana, Michael Belkin, Ferenc Kuhn

coming from artificial sources, can cause permanent ocular damage [2]. The cornea and lens refract and focus the visible and near IR light onto the retina, which is thus uniquely vulnerable since its irradiance is 10,000 times higher than that of the cornea. The extent of the photic damage depends on the following:

•Wavelength of the radiation. Rapidly absorbed by organic tissues are photons of wavelengths shorter (UV) or longer (IR) than the visible spectrum. These do not reach the retina but may cause corneal injury.

•Duration and intensity of the exposure.

–Thermal damage occurs when heat is produced faster than it can be dissipated [15]. An increase of at least 10°C causes denaturation and coagulation of proteins with ensuing cell death, necrosis, and scarring .

–Mechanical damage occurs when the energy transfer is in the picoto nanosecond range: the tissue disintegrates into plasma [15] and a compressive pressure pulse (explosion) irradiates and disrupts the surrounding tissues.

–Photochemical damage occurs when the delivery of energy is slow and without significant heat build-up [8]. Single photons induce chemical reactions in the absorbing molecules, breaking bonds in nucleic acids and proteins.

•Tissue involvement and specific location of injury. This is the most important factor in determining the extent and importance of the sensory damage.

–A foveal lesion causes immediate and significant visual loss, even if subsequent improvement is possible.

–A parafoveal lesion’s initial effect may persist via the spreading of neural cell degeneration into the fovea.

e.g., ophthalmic instruments and laser systems.

This is the basis for argon laser photocoagulation of the retina. This is the basis for YAG laser photodisruption of the iris.

This is the basis for excimer laser use in the cornea.

Edema and inflammation, which can extend over several times the diameter of the original burn.