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The Intraocular Changes of Anterior Segment Necrosis

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Eye (1991) 5, 214-221 The Intraocular Changes of Anterior Segment Necrosis ROSWELL R. PFISTER Birmingham, Alabama Summary Anterior segment necrosis is an acute or chronic process occasioned by embar­ rassment of the blood supply of the anterior segment of the eye. In the acute form this vascular obstruction leads to severe corneal oedema, necrosis of anterior uvea, hypo­ tony and cataract formation. Depression of aqueous humour formation accounts for severe reduction of glucose levels in corneal stroma and aqueous humour lasting for two days after cautery of the long posterior ciliary arteries (LPCA) in rabbits. Lac­ tate levels are initially significantly elevated but return to normal after one week. Stromal hydration was elevated for one week but then returned to normal. Corneal epithelial glycogen was diminished at one and two days after surgery but then returned to normal. Although unproven, oxygen deprivation probably plays a major role in endothelial ischaemia and therefore corneal oedema. It is concluded that the abnormalities seen in anterior segment necrosis stem from changes in aqueous meta­ bolic components resulting from severely reduced aqueous turnover. Hyperbaric oxygen and intracameral metabolite substitution are unproven treatments but merit further experimental study. Anterior segment necrosis (ASN) occurs as a buckling surgery is performed in patients chronic or acute process wherein the vascular manifesting haemoglobin Sc. 4,5 Strabismol­ supply of the anterior portion of the eye is ogists responding to a questionnaire reported compromised. Ischaemic ocular syndromes a total of 30 cases of ASN for a calculated inci­ such as pulseless disease and the aortic arch dence of one in 1,333 strabismus operations.6 syndrome represent a chronic ischaemia ASN is more common after the Hummel­ which is characterised by iris neovascularisa­ scheim transplantation operation in older tion and atrophy, pupillary dilation and cor­ individuals. 7,8,9,10 neal oedema with uveitis.1,2 The acute form Histopathological evidence of ASN has occasionally occurs after surgical procedures been verified in two studies. Iris and ciliary in which there is extensive disinsertion of the body necrosis were demonstrated in 21 of 150 rectus muscles and/or obstruction of the long eyes enucleated following trans scleral diath­ posterior ciliary arteries. 3 ermy, scleral resection, or polyethylene tubes In retinal detachment surgery, when three for retinal detachment.11 A more recent study muscles are disinserted, especially the medial showed ASN present in 8.2% of 49 eyes rectus, ASN is more likely to develop. These obtained from 43 patients who previously chances increase when the long posterior cili­ underwent retinal detachment surgery. 12 ary arteries are cauterised or when scleral The clinical presentation of ASN is domi- From: Eye Research Laboratories, Brookwood Medical Center, Birmingham, Alabama. Correspondence to: Roswell R, Pfister M.D., Suite 211,2008 Brookwood Medical Center Drive, Birmingham, AL35209, THE INTRAOCULAR CHANGES OF ANTERIOR SEGMENT NECROSIS 215 nated by changes evident in the cornea and the suprachoroidal space to the ciliary body. anterior uvea. Wrinkling of Descemets mem­ The contribution each system makes to the brane and anterior uveitis with keratic pre­ anterior segment of the human eye is 40% cipitates herald the early picture of ASN. anterior ciliary and 60% LPCA. In the rabbit Later, massive corneal stromal oedema may the anterior ciliary system makes a very minor be evident, followed by peripheral stromal contribution to this system.13 infiltratesand hypotony. Figure lea) shows the internal blood column in the normal rabbit eye and its inter­ Anterior Segment Circulatory ruption after LPCA cautery. (Fig l(b» In the Considerations rabbit eye transection of the four rectus Anterior segment necrosis (ASN) is predi­ muscles and perilimbal cautery has no effect cated on a failure of vascular perfusion of the on the corneal clarity. 14 There is a slight fall in anterior segment of the eye. Loss of the vas­ corneal epithelial glycogen but no effect on cular supply to the ciliary body and iris results aqueous humour glucose, corneal hydration, in partial necrosis of these tissues to a degree or corneal aerobic glycolysis. depending on the severity of the vascular deprivation. A decrease in the blood supply Experimental Anterior Segment Necrosis interferes with the active and passive trans­ Anterior segment necrosis has been induced port of ions and nutritional substances into in a number of animal models. Multiple disin­ the aqueous humour by the non-pigmented sertions of the rectus muscles in monkeyss or epithelium of the ciliary body. This depri­ injury to the ciliary arteries around the optic vation robs the cornea and crystalline lens of nerve of rabbits has led to ASN.15 Simple cut­ substances vital to their health. ting of the long posterior ciliary arteries in In the human, the vascular supply of the rabbits caused no change in aqueous glucose, anterior segment of the eye is dependent on corneal transparency, or calcium uptake by two sources. The anterior ciliary arteries issue the cornea. 14,16 The most effective technique from the terminal arteries of the rectus in rabbits was diathermy to both long pos­ muscles, perforating the sclera to join the terior ciliary arteries resulting in extensive iris greater arterial circle in the ciliary body at the and ciliary body changes. 17 root of the iris. The long posterior ciliary In the experiments described here, a per­ arteries branch (LPCA) from the ophthalmic itomy is performed in the anaesthetised rabbit artery deep in the orbit and progress and the medial and lateral rectus muscles are anteriorly on the medial and lateral portions tenotomised. A radiodiathermy unit (MIRA) of the globe, intrasclerally. Additional is used to place a continuous row of three or branches given off by the LPCA in its intra­ four transscleral cautery points along the scleral course penetrate sclera and travel in course of the arteries from behind the equator Fig la. Fig lb. Fig. 1. Interior view of long posterior ciliary artery (a) in the normal and (b) after immediately after LPCA cautery. Note loss of blood column in b. 216 ROSWELL R. PFISTER to a position ahead of the rectus insertions. blush at the junction of normal and atrophic Conjunctiva is then pulled back to the limbus. iris, expanding extensively over the ensuing one to two weeks. [4 General Anterior Segment Abnormalities The intraocular changes in experimentally Lens produced ASN in rabbit eyes has been pre­ Anterior subcapsular vacuoles appeared one viously documented in our laboratory.18 The day after diathermy. Water clefts between results noted here represent some citations cortical lamellar fibres developed by seven from that study, subsequent new and unpub­ days. Lens opacities progressed to a mature lished data, and additional studies gleaned cataract at six weeks. from the literature. Intraocular Pressure After LPCA cautery in the rabbit, ocular Clinical Findings hypotony of less than five mm Hg persisted for Anterior chamber six weeks, though the intraocular pressure Cells and flare appeared in the aqueous was higher after six weeks than in the first humour immediately after cautery, reaching week. These results were confirmed by the maximum at seven days and disappearing Guerry who showed that after LPCA cautery after three weeks. The anterior chamber rabbit eyes show hyptony for weeks,21 some became shallow two to seven days later from giving rise to phthisis bulbi.22 The squirrel posterior corneal swelling. At three to six monkey. with a ciliary circulation similar to weeks the cornea had returned to near normal humans, showed a depression of the lOP to thickness but cataract formation had swelled about 50% after five days and for the sub­ the lens sufficiently to maintain a narrow sequent 24 days.23 (Fig. 2) Although the sur­ anterior chamber. gery diminishes the volume of blood delivered Ciliary body and Iris to the ciliary body, additional hypotensive Immediately after diathermy the pupil effect might be gained by damage to the long became dilated and vertically oval with col­ posterior ciliary nerves coursing in the same lapse of the iris vasculature. After one day, sheath. Proof for this is secured from chemical the iris appeared pale, ultimately reducing to sympathectomy experiments in which a 35% a velamentous frill with minimal circulation reduction in the lOP was noted.24 It is likely after three weeks. Mild hyphaema was that both mechanisms are operative to reduce occasionally present. Anderson has demon­ lOP in the experimental model. strated rubeosis iridis beginning as a pink Chemical Findings Aqueous glucose-Aqueous glucose was 15 I. 7 " n"'22 " ""'10 0 6 .of ,;: h �"E 10 E � - , :. 514 ,i .! 'r�ll I.. :. 3 I] " iI 5 I ; I 8 • 2 c n-l0 "-10 � , I ;!; 1 n=lO � I In'lO -�.- -1 ·"-- , ,'i ]flrfl 1,1! --�- • o+-��+-������������ Normal 0 1 �2 .. T 5 6 7 21 42 -I -4 -2 0 2 • • • 10 12 '4 ,I la 20 22 24 DAYS TIME (DAYS) Fig. 2. Effect of cautery of both LPCA on the Fig. 3. Severe aqueous glucose depression after intraocular pressure in the squirrel monkey. (with induced anterior segment necrosis lasted for two days permission from Levy et ai, Invest Ophthalmol Vis Sci but level was normal at 4, 7 and 42 days (averages ± 1974, 13: 468-71.) SE). THE INTRAOCULAR CHANGES OF ANTERIOR SEGMENT NECROSIS 217 Stromal lactate-Figure 6 shows the large 6 increase in lactate concentration after three "-10 hours (P<O.OOl) and normal lactate from 15 6' 5 n-21 no. hours to four days. Thereafter, at seven, 21 i: "alO nag and 42 days, lactate levels were below normal. 4 �• Electrolytes, pH and osmolarity-Prelimi­ � 3 � i nary analyses of these components of aqueous � III i I humour do not shed more light on the disturb­ 2 I 5 �O I ances.
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