CLOSED MICROSURGERY IN TRAUMA

Australian Journal of Ophthalmology 1984; 12: 383-390

CLOSED MICROSURGERY IN TRAUMA

DAVID MCLEOD, FRCS Surgical Vitreoretinal Unit. Moorfields Eye Hospital, London

Abstract Blunt and penetrating injuries to the eye provide ophthalmologists with a wide range of surgical challenges. The reconstruction and visual rehabilitation of traumatized eyes are described with particular emphasis on the role of closed microsurgical techniques in the posterior segment.

Key words: Blunt, penetrating eye injuries, closed microsurgical techniques.

Any discussion of closed microsurgical management of the traumatized eye is fraught with difficulty owing to: (i) the infinite variety of ways in which the eye can be traumatized; (ii) the differing degrees of damage sustained; (iii) the broad spectrum of injury-responses; and (iv) (to a limited extent) the differing underlying susceptibility of eyes to damage according to pre- existing pathology.

This problem is reflected in the published articles on the results of treatment for posterior segment trauma which, as a whole, are of only limited value to the individual surgeon who has to decide upon, and carry out, the most appropriate treatment for his individual patient. Although attempts have been made to use standardized and reproducible models of trauma in animals’** to help clarify matters, the experimental models sometimes bear relatively little relation to the problems seen clinically (except after severe trauma and in paediatric injuries). Many of the conclusions derived from clinical experience are based on dubious statistics and uncritical reflection, and we are often left to muse upon oft-repeated anecdotal reports of

individual bizarre foreign bodies and heroic deeds of surgery from which comprehensive trauma stratagems are only slowly emerging.

The dominating issue of trauma-induced retinal detachment is of concern not only to the vitreoretinal surgeon, but also to his anterior segment counterpart whose efforts in this area are prone to be overshadowed or ruined by posterior segment complications. The following discussion will leave aside consideration of severe injuries with expulsive suprachoroidal haemorrhage, gross retinal incarceration and massive posterior pole injury (e.g. from double perforat- ing missiles) which are frequently associated with no light perception from the outset.

MECHANISMS OF TRAUMATIC DETACHMENT A number of general principles govern this subject. 1. The great majority of trauma-induced retinal detachments have a rhegmatogenous component. True, we do from time to time see “pure traction” detachments, such as a macular pucker or detachment of retina surrounding a foreign-

Reprint requests: Dr David McLeod, Surgical Vitreoretinal Unit, Moorfields Eye Hospital, London ECIV 2PD.

CLOSED MICROSURGERY IN TRAUMA 383

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Figure I : Breaks from ocular contusion. ( I ) Vitreous base avulsion superonasally; bucket-handle and early flapping over of giant break. (2) Giant retinal dialysis superonasally. (3) Flapped-over 180" giant tear. (4) Radial slit-tear and oral disinsertion/dialysis. (Arrows indicated the sites of persistent major vitreoretinal

attachment.)

Figure 2: Histological section of bucket-handle removed at vitrectomy: peripheral retina, ora serrata

(arrow) and posterior pars plana.

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body impact-site and drawn forwards by transgel fibrosis. Occasionally, the retina detaches because of subretinal bleeding and may spontaneously reattach. Nevertheless, it is important to assume, until proved otherwise, that a retinal break is present in a traumatic detachment (as is usually indicated by the bullous configuration of the detachment either ophthal- mqscopically or on ultrasound examination), and to recognize that the identification and closure of the break is crucial to the patient’s management. Similarly, in those patients with opaque media but a flat retina at presentation, rhegmatogenous retinal detachment is the pre- dominant risk. 2. The retinal breaks causing retinal detachment are seldom located at the immediate site of the retinal perforation or foreign-body impaction; the associated repair-response generally seals any retinal disruption and this is frequently the only part of the retina which is not subsequently detached. Local breaks are commoner with blunt injuries, however, and are less frequently self-sealing. 3. The majority of traumatic breaks are located in the vitreous base region; that is, anterior to the ora serrata, at the ora or at the posterior border of the vitreous base. This holds true both for blunt and for penetrating injuries. The types of break have been admirably described by the Boston whose findings are no less important in eyes full of blood than in traumatized eyes with clear media. 4. Extensive epiretinal membrane proliferation and contraction is mainly seen in eyes with retinal breaks, whether the eye contains associated haemorrhage, lens-vitreous admixture or not. Such proliferations should generally be regarded as a complication of tear formation and rhegmatogenous detachment, rather than a primary injury response. 5 . Contusion breaks (Figure 1) generally occur at the moment of impact, and comprise: (i) oral disinsertion/dialysis; (ii) giant break formation at the posterior border of the vitreous base; (iii) vitreous base avulsion (“bucket handle”) (Figure 2); (iv) posterior slit-tears.


Other tears following blunt trauma occur some time after the injury. Within a few days, macular hole formation may occur in an area of posterior commotio retinae and breaks secondary to contusion-necrosis may develop in areas of direct focal injury. Other delayed tears follow posterior vitreous detachment related to the aphakic state, secondary to haemorrhage-induced o r inflammation-induced syneresis, or following the blunt injury itself (boxing injuries). A variety of types of tear can be produced-flap tears and giant tears.

The least severe disturbance of the vitreous base region-oral disinsertion, with opening of multiple individual oral bays is a frequent cause of traumatic detachment, but the offending breaks may be very difficult to recognize. Such cases are sometimes misdiagnosed as “hyper- tensive uveitis” with associated “serous retinal detachment”. The history of trauma, and the frequent association of pigment cells in the vitreous gel, should alert one to the correct diagnosis, which is traumatic retinal detachment following disinsertion with secondary uveitis causing high intraocular pressure owing to concomitant damage to the anterior chamber angle. Alternatively, in eyes with associated vitreous haemorrhage, these essentially rhegmatogenous detachments may be mistaken for “traction detachments”. 6. Although retinal disruption from penetrating trauma is frequently self-sealing, a notable exception is break formation at the impact-site of a foreign body which ricochets off the retina. Other breaks appear to arise subsequent to perforation (Figure 3) owing to incarceration of basal gel in a retinal or pre-oral wound.4 The typical disinsertions and dialyses develop most frequently at the ora serrata adjacent to the perforation site (or, in the case of severe vitreous loss and incarceration, opposite the perforation site), and tend to be slowly progressive whether due to: (a) gradual absorption of associated suprachoroidal haemorrhage and restoration of the normal oral contour (the retina being left “high and dry”); or (b) fibroblast proliferation and contraction within the basal gel from uveal or episcleral cells growing into the vitreous.

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Figure 3: Breaks from penetrating injuries. (1) Oral dialysis and break at the anterior border of the vitreous base in the same quadrant as the penetrating injury. (2) Oral dialysis opposite the site of the penetrating injury. (3) Flapped- over giant break after posterior vitreous detachment subsequent to penetrating injury. (4) Flap-tear near site of vitreo-

retinal incarceration. (Arrows indicate the directions of vitreoretinal traction.)

Small flap tears near retinal incarceration scars may cause highly elevated detachment of the distorted retina. Other tears, including giant tears, may be delayed in their formation until the time of posterior vitreous detachment, and retinal detachment may thus occur long after the original injury. IN TRAUMATIZED EYES

In summary, traumatic retinal breaks may occur either at the time of injury or after a

variable delay; they are frequently unpredictable, sometimes self-sealing, and give rise to considerable difficulty in decision-making about microsurgery of traumatized eyes.

ROLE OF CLOSED MICROSURGERY

The objectives of vitrectomy in trauma are as follows,


First, to establish a clear visual axis free of cataract, lens subluxation or lens-vitreous admixture, and persistent vitreous haemorrhage. The surgery is dominated by the need to exclude established retinal breaks, to avoid any intraoperative retinal damage and to guard against later detachment induced by the inevitable vitreous incarceration in pars plana entry sites.5 Where doubt exists regarding the integrity of the ora serrata, a gentle anteriorly- located encirclement of the globe is frequently indicated, together with post-oral cryopexy even up to 360” (provided the surgeon feels that the risk of cryo-induced proliferation is less than the risk of later detachment from unrecognized oral breaks).

Second, to allow identification of the site of retinal tear formation and so permit accurate scleral buckling. Wide anteriorly placed circum- ferentially orientated explants are necessary for most breaks in the vitreous base region, since it is generally impossible to remove all traction in this area by vitrectomy. The exception is giant tears at the posterior border of the vitreous base superiorly, only the extremities of which may require buckling.

Third, to assist in the management of retinal breaks which are difficult to close, for example, oral breaks with severe vitreoretinal traction from vitreous incarceration, posterior retinal breaks and giant retinal breaks (tears and dialyses). The use of vitrectomy and silicone oil exchange in the initial manipulation and subsequent tamponade of traumatic giant breaks (Figure 4) has proved very successful in our hands (Leaver et al, in preparation). Vitrectomy, internal subretinal fluid drainage, cryopexy or endophotocoagulation, and temporary intraocular tamponade using air or an air/SF6 gas mixture, allows post-equatorial breaks to be closed without resort to scleral buckling.

Fourth, to treat “static” traction, for example, epimacular membrane peeling for macular pucker (Figure 5 ) , removal of transgel traction bands and dissection of epiretinal membranes in massive preretinal retraction. In severe cases of massive preretinal retraction, vitrectomy and silicone oil exchange prior to membrane peeling


facilitate the epiretinal dissection and provide long term internal tamponade of associated breaks.

Vitrectomy techniques are, of course, also employed in the management of trauma-induced glaucoma (whether phacolytic or erythroclastic), in endophthalmitis, and as a means of removal of intraocular foreign bodies, but these are outside the scope of this discussion.

FACTORS INFLUENCING THE TIMING AND INDICATIONS FOR VITRECTOMY IN TRAUMA Considerable controversy surrounds the “optimal” timing of closed microsurgery for trauma. Two camps appear to have been established: those advocating very early vitrectomy,6 and others suggesting that surgery should be delayed until 7 to 14 days after injury. There is, however, no such thing as a broad “optimal” time for vitreous surgery in traumatized eyes. Each case must be considered on its merits bearing in mind the following problems. I. Visualization. Time is a great healer, and anterior chamber bleeding or corneal oedema often clear remarkably quickly. Temporary keratoprosthesis, Healon injection into the anterior chamber or liquid silicone injection may aid visualization and allow surgery where other factors determine the need for early intervention. 2. Bleeding tendency. Contusion-induced congestion of the globe may result in torrential intraocular bleeding if surgery is performed very early after injury, as has been found clinically and also experimentally.’ 3. Suprachoroidal haemorrhage. Blood in the suprachoroidal space initially clots, and several days are necessary for fibrinolysis to occur so allowing surgical evacuation of the suprachoroidal space, safe surgical access to the vitreous cavity via the pars plana (Figure 6) and efficient closure and sealing of breaks. 4. Posterior vitreous detachment. There is a considerable practical advantage in awaiting posterior vitreous detachment before carrying out closed microsurgery of the posterior segment; however, it must be recognized that delayed

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Figure 4: Traumatic giant retinal tear. Left: Photograph of posterior pole with superior retina flapped over the disc and macula. Right: Postoperative photograph after vitrectomy, manipulation of the break and fluid/silicone oil

exchange; reflex from silicone interface.

retinal breaks may be induced, or already estab- break. Retinal break formation may be suspected lished breaks “activated”, by the vitreous by concomitant signs, such as pigment in the detachment. vitreous gel (though this is not necessarily of 5 . Suspected retinal break formation. In eyes retinal pigment epithelial origin), and signs of with opaque media, ultrasound is of limited significant vitreous incarceration, such as “orien- value in determining the presence of a retinal tation” of the retrolental gel towards a perfora-

Figure 5: Traumatic macular pucker. Left: Preoperative appearance (left eye). Right: Fundal appearance after epimacular membrane peeling.


Figure 6: Horizontal B-scan ultrasound sections. (a) Suprachoroidal haemorrhage (arrow). (b) Suprachoroidal haemorrhage and giant tear (arrow). (c) Purse-string retinal detachment (arrow) and mobile vitreous haemorrhage (eye deviated left). (d) Retracted vitreous interface, retinal detachment (arrow) and subretinal haemorrhage (eye deviated right).

CLOSED MICROSURGERY I N TRAUMA 389

tion site. Surgery is performed if the risk of retinal detachment behind an unresolved haemorrhage appears to outweigh the potential morbidity from surgical complications.

6. Intraocular inflammation. A primary role of haemorrhage or lens-vitreous admixture in determining epiretinal membrane formation has perhaps been- overemphasized in the past. Nevertheless, an important “adjuvant” role of inflammation in stimulating retinal detachment is indicated by experimental studies,’.* whether by stimulating growth factors or by providing a scaffold for fibrous proliferation. It must be appreciated, however, that removal of potential gel “scaffolding” may be difficult or dangerous in the vitreous base region (especially if the eye is phakic), and epiretinal membranes may progress postoperatively despite thorough vitrectomy . 7. Established retinal detachment. Once the detachment is recognized clinically or ultra- sonically, surgery should be performed as soon as practical. Many traumatic detachments involve the oral retina and pars plana, and give rise to a characteristic B-scan appearance with water-bath coupling;* such information is useful in planning the location of entry sites for vitrectomy (Figure 6).

Other factors may also be important in the timing of surgery: for example, the presence of glaucoma, endophthalmitis, cyclitic membrane formation, and the risk of amblyopia or fusional/diplopia problems.

ACKNOWLEDGEMENTS I am grateful to Miss Heather Lucas for secretarial assistance, and to Messrs T. Tarrant and K. Sehmi for the illustrations.

References 1 . Cleary PE, Ryan SJ. Method of production and the

natural history of experimental posterior penetrating eye injury in rhesus monkey. Am J Ophthalmol 1979; 88: 212-220.

2. Gregor Z, Ryan SJ. Combined posterior contusion and penetrating injury in the pig eye. I . A natural history study. Br J Ophthalmol 1982; 66: 793-798.

3 . Cox MS, Schepens CL, Freeman HM. Retinal detachment due to ocular contusion. Arch Ophthalmol 1966; 76:

4. Cox MS, Freeman HM. Retinal detachment due to ocular penetration. I . Clinical characteristics and surgical results. Arch Ophthalmol 1978; 96: 1354-1361.

5. Gregor Z, Ryan SJ. Pars plana vitrectomy entry sites. Trans Ophthalmol SOC UK 1982; 102: 461-467.

6. Coleman DJ. Early vitrectomy in the management of the severely traumatised eye. Am J Ophthalmol 1982; 93:

7. Gregor 2, Ryan SJ. Combined posterior contusion and penetrating injury in the pig eye. 111. A controlled treatment trial of vitrectomy. Br J Ophthalmol 1983; 67:

8. Restori M, McLeod D. Ultrasonic examination of the traumatised eye. Trans Ophthalmol SOC UK 1978; 98:

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