Ординатура / Офтальмология / Учебные материалы / Ocular Traumatology Springer

References

[1]Abu el-Asrar AM, al-Obeidan SA (1995) Pars plana vitrectomy in the management of ghost cell glaucoma. Int Ophthalmol 19: 121−124

[2]AnmarkrudN,BergaustB,BulieT,SandAB(1987)Argonlasertrabeculoplasty:5 years experience from a local eye department. Acta Ophthalmol (Suppl) 182: 34−36

[3]Beckman H, Fuller TA (1979) Carbon dioxide laser scleral dissection and filtering procedure for glaucoma. Am J Ophthalmol 88: 73−77

[4]Blanton FM (1964) Anterior chamber angle recession and secondary glaucoma. A study of the aftereffects of traumatic hyphemas. Arch Ophthalmol 72: 39−43

[5]Campbell DG (1981) Ghost cell glaucoma following trauma. Ophthalmology 88: 1151−1158

[6]Canavan YM, Archer DB (1982) Anterior segment consequences of blunt ocular injury. Br J Ophthalmol 66: 549−555

[7]Chandra M, Sharma V, Ghose S, Kashyap S, Pushker N (2003) Phthisis bulbi with a large protruding foreign body: a rare complication of penetrating injuries. Orbit 22: 145−149

[8]Chorich LJ, Derick RJ, Chambers RB, Cahill KV, Quartetti EJ, Fry JA, Bush CA (1998) Hemorrhagic ocular complications associated with the use of systemic thrombolytic agents. Ophthalmology 105: 428−431

[9]DeBry PW, Perkins TW, Heatley G, Kaufman P, Brumback LC (2002) Incidence of late-onset bleb-related complications following trabeculectomy with mitomycin. Arch Ophthalmol 120: 297−300

[10]Girkin CA, McGwin G Jr, Long C, Morris R, Kuhn F (2005) Glaucoma after ocular contusion: a cohort study of the United States Eye Injury Registry. J Glaucoma 14: 470−473

[11]Girkin CA, McGwin G Jr, Morris R, Kuhn F (2005) Glaucoma following penetrating ocular trauma: a cohort study of the United States Eye Injury Registry. Am J Ophthalmol 139: 100−105

[12]Goldsmith AJ (1963) Indications for surgery in glaucoma. Secondary glaucoma. Trans Ophthalmol Soc UK 83: 233−244

[13]Greenfield DS, Tello C, Budenz DL, Liebmann JM, Ritch R (1999) Aqueous misdirection after glaucoma drainage device implantation. Ophthalmology 106: 1035−1040

[14]Haymes SA, Leblanc RP, Nicolela MT, Chiasson LA, Chauhan BC (2007) Risk of falls and motor vehicle collisions in glaucoma. Invest Ophthalmol Vis Sci 48: 1149−1155

[15]Immonen IJ, Puska P, Raitta C (1994) Transscleral contact krypton laser cyclophotocoagulation for treatment of glaucoma. Ophthalmology 101: 876−882

462 Ferenc Kuhn

[16]Joussen AM, Walter P, Jonescu-Cuypers CP, Koizumi K, Poulaki V, Bartz-Schmidt KU, Krieglstein GK, Kirchhof B (2003) Retinectomy for treatment of intractable glaucoma: long term results. Br J Ophthalmol 87: 1094−1102

[17]Kim DD, Moster MR (1999) Transpupillary argon laser cyclophotocoagulation in the treatment of traumatic glaucoma. J Glaucoma 8: 340−341

[18]Kivela T, Puska P, Raitta C, Immonen I, Tarkkanen A (1995) Clinically successful contact transscleral krypton laser cyclophotocoagulation. Long-term histopathologic and immunohistochemical autopsy findings. Arch Ophthalmol 113: 1447−1453

[19]Kronfeld PC (1954) The fluid exchange in the successfully cyclodialyzed eye. Trans Am Ophthalmol Soc 52: 249−263

[20]Lerner SF (1997) Small incision trabeculectomy avoiding Tenon’s capsule. A new procedure for glaucoma surgery. Ophthalmology 104: 1237−1241

[21]Makley TA, Azar A (1978) Sympathetic ophthalmia. A long-term follow-up. Arch Ophthalmol 96: 257−262

[22]Melamed S, Ashkenazi I, Gutman I, Blumenthal M (1992) Nd:YAG laser trabeculopuncture in angle-recession glaucoma. Ophthalmic Surg 23: 31−35

[23]Mooney D (1973) Angle recession and secondary glaucoma. Br J Ophthalmol 57: 608−612

[24]Palimeris G, Moschos M, Chimonidou E, Velissaropoulos P (1976) Some observations on the use of cyclocryopexy in the treatment of various forms of glaucoma. Klin Monatsbl Augenheilkd 169: 439−441 [in German]

[25]Peyman GA, Peralta E, Ganiban GJ, Kraut R (1998) Endoresection of the iris and ciliary body in epithelial downgrowth. J Cataract Refract Surg 24: 130−133

[26]Raivio VE, Immonen IJ, Laatikainen LT, Puska PM (2001) Transscleral contact

krypton laser cyclophotocoagulation for treatment of posttraumatic glaucoma. J Glaucoma 10: 77−84

[27]Read J (1975) Traumatic. hyphema: surgical vs medical management. Ann Ophthalmol 7: 659−670

[28]Schlote T, Derse M, Zierhut M (2000) Transscleral diode laser cyclophotocoagulation for the treatment of refractory glaucoma secondary to inflammatory eye diseases. Br J Ophthalmol 84: 999−1003

[29]Sharma A, Sii F, Shah P, Kirkby GR (2006) Vitrectomy-phacoemulsification-vitrec- tomy for the management of aqueous misdirection syndromes in phakic eyes. Ophthalmology 113: 1968−1973

[30]Sihota R, Sood NN, Agarwal HC (1995) Traumatic glaucoma. Acta Ophthalmol Scand 73: 252−254

[31]Sivak-Callcott JA, O’Day DM, Gass JD, Tsai JC (2001) Evidence-based recommendations for the diagnosis and treatment of neovascular glaucoma. Ophthalmology 108: 1767−1776; quiz 1777, 1800

[32]Tesluk GC, Spaeth GL (1985) The occurrence of primary open-angle glaucoma in the fellow eye of patients with unilateral angle-cleavage glaucoma. Ophthalmology 92: 904−911

[33]Theelen T, Klevering BJ (2005) Malignant glaucoma following blunt trauma of the eye. Ophthalmologe 102: 77−81 [in German]

[34]Thomas M, Parrish R, Feuer W (1986) Rebleeding after traumatic hyphema. Arch Ophthalmol 104: 206−210

[35]Tonjum AM (1968) Intraocular pressure and facility of outflow late after ocular contusion. Acta Ophthalmol (Copenh) 46: 886−908

[36]Verma N (1996) Trabeculectomy and manual clot evacuation in traumatic hyphaema with corneal blood staining. Aust N Z J Ophthalmol 24: 33−38

[37]Viestenz A, Kuchle M, Naumann GO (2003) Block excision of epithelial ingrowth after cataract surgery: report on 15 patients. Klin Monatsbl Augenheilkd 220: 465−470 [in German]

[38]Vijaya L, Mukhesh BN, Shantha B, Ramalingam S, Sathi Devi AV (2000) Comparison of low-dose intraoperative mitomycin-C vs 5-fluorouracil in primary glaucoma surgery: a pilot study. Ophthalmic Surg Lasers 31: 24−30

[39]Walton W, Hagen S von, Grigorian R, Zarbin M (2002) Management of traumatic hyphema. Surv Ophthalmol 47: 297−334

[40]Wolff SM, Zimmerman LE (1962) Chronic secondary glaucoma. Associated with retrodisplacement of iris root and deepening of the anterior chamber angle secondary to contusion. Am J Ophthalmol 54: 547−563

[41]Zaidman GW, Wandel T (1988) Transscleral YAG laser photocoagulation for uncontrollable glaucoma in corneal patients. Cornea 7: 112−114

466 Ferenc Kuhn

2.19.3Treatment

Hypotony and phthisis are not diseases: they are the consequence of a certain intraocular pathology. It is this pathology that requires treatment (see below). If the underlying cause responsible for hypotony cannot be cured, silicone oil implantation remains the only hope for preventing phthisis. If the IOP is restored, the visual function can improve substantially [3].

2.19.4Specific Conditions Responsible for Hypotony

2.19.4.1Increased Aqueous Outflow

2.19.4.1.1Wound Leak

The wound is usually easy to find, although occasionally an occult rupture or exit wound (see Chap. 2.12) is responsible. If a corneal wound has spontaneously closed, the diagnosis may be difficult, but Seidel positivity (see Chap. 2.2) is a telling sign.

The treatment is straightforward: surgical wound closure.

2.19.4.1.2Ciliochoroidal Detachment

The pathomechanism of how the detachment and hypotony interrelate is not absolutely clear [2], but a vicious circle may be caused by the hypotony leading to inflammation, transudation, and decreased aqueous secretion with consequent hypotony. The suprauveal fluid may be a transudate or blood.

The treatment is primarily anti-inflammatory (topical cycloplegics and corticosteroids); paradoxically, CAIs may be given to speed up the absorption of the suprauveal fluid. Viscoelastics can be injected into the AC [1], the ciliary body reattached with sutures, or the suprauveal fluid drained (see Chap. 2.8).

2.19.4.1.3Retinal Detachment

The pathomechanism of increased fluid removal by the RPE is unknown. The treatment is reattachment of the retina (see Chap. 2.9).

468 Ferenc Kuhn

chapter or Chap. 2.8. The AC is shallow and the cornea may show foldings of Descemet’s membrane.

The treatment is injection of viscoelastics into the AC, repeatedly if necessary. It may take months for the ciliary body to recover.

2.19.4.2.3Ciliary Body Destruction

The etiology is the same as above, except that there is true and visible damage to the ciliary epithelium and processes. The ciliary processes are shortened, may have lost some of their pigment content, and can dramatically shrink with time (Fig. 2.19.1). The pathomechanism is probably vascular occlusion. Commonly there is a serious iris abnormality as well.

There is no treatment for the condition, although phthisis may be preventable (see below). Anterior PVR can also destroy the ciliary body if the scar is not removed in time (see Chap. 2.8).

2.19.5Consequence of Chronic Hypotony: Phthisis

The difference between an eye in “prephthisical” vs “phthisical” stage is that in the latter, tissue disruption is evident; the condition results from the cessation of aqueous production. If treatment of all known pathologies, including that of anterior PVR, has been exhausted and the eye starts to shrink, there are two options left besides eye removal (see below).

This is the clinician’s observation; there is no explanation for the phenomenon in the available literature.

Major iris damage is an indicator of ciliary body trauma (see Chap. 2.6). The term means “wasting away”.

Meticulous removal of membranes covering the ciliary body should be attempted even in late cases. The phthisis is not reversible but stoppable if the intervention was not too late – but this can be determined only after the attempted scar removal has failed, and should not serve as an excuse not to attempt scar removal.

Fig. 2.19.1  Intraoperative image of repair for ciliary body destruction. This 8-year-old boy had a rupture with vitreous hemorrhage. He underwent several surgeries and eventually the eye was given up on. He developed iris scarring into the wound; there was no pupil, the retina was detached, the visual acuity was light perception, and the axial length of the previously emmetropic eye was 21 mm. After a pupil was created, the ciliary body was debulked, the preand subretinal scars were removed, and silicone oil was implanted (restricted to the vitreous cavity). There was no anterior PVR. The most probable explanation for the partial destruction of the ciliary processes (arrow) is that the posterior lens capsule was not removed originally. Twelve months after surgery, the IOP is normal, the eye has stopped shrinking, the retina is attached, and the visual acuity has improved to 20/40

2.19.5.1Permanent Keratoprosthesis

Implanting such a device (see Chaps. 2.15, 3.1) may not only preserve the eye but actually improve function [4].

2.19.5.2Silicone Oil Fill

The purpose of silicone oil implantation is different here from that in all other indications, in which the surgeon’s aim is to achieve a 100% fill in the vitreous cavity without silicone oil prolapse into the AC.

470 Ferenc Kuhn

ZPearl

The goal of silicone oil implantation in the prevention or “treatment” of phthisis management is to achieve a “101%” fill: the entire globe, not only the vitreous cavity, is filled, and the IOP is set at a higher-than- normal value to mechanically prevent globe shrinkage.

The surgical steps are as follows:

•Perform a complete vitreous removal if this has not yet been done.

•Remove the lens in its entirety if the eye is still phakic. If the eye is pseudophakic, remove the IOL and the capsule.

•Perform a large inferior iridectomy.

•Do a fluid−air exchange.

•Be patient until the BSS is completely evacuated from the eye.

The cornea is expected to tolerate the silicone oil touch for many months, even years, but eventually it will gradually opacify. When zonular opacity appears, there is ample time to decide whether PK with an “oil change” is performed, or the blind, potentially painful, and cosmetically unappealing eye is removed (enucleation or evisceration). This decision is best made by the patient (see Chap. 1.4).

This is not truly treatment but rather a prophylaxis of further deterioration.

Based on the principle that fluids are incompressible.

The goal is to prevent any aqueous that may still be produced to access the cornea. The endothelium will survive longer if silicone is able to prevent “aqueous touch.”

Fig. 2.19.2  Silicone oil implantation for phthisis. a The typical silicone oil fill is intended to be 100% in the vitreous cavity and 0% in the AC. b If there is no aqueous production, the globe starts to shrink. This is stopped when the internal volume of the eye equals that of the silicone oil. c If the eye is completely filled with silicone oil (i.e., the vitreous cavity as well as the AC), globe shrinkage is prevented

DO:

•intervene early if the IOP is low after an injury

•restore normal ciliary body anatomy as soon as possible since this almost always restores normal aqueous production; anterior PVR is the most common preventable cause of enucleation due to phthisis

DON’T:

•give up on the eye even if shrinking of the globe has already started; although phthisis is irreversible, further shrinkage can be halted