Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

Careful history taking and examination to identify glaucoma, aphakia, pseudophakia, severe myopia, recent intraocular surgery and suprachoroidal hemorrhage in the fellow eye are critical.12,13 Intraocular pressure needs to be adequately controlled before surgery. Softening the eye with carbonic anhydrase inhibitors or intravenous osmotic agents can be considered if necessary. Preoperative ocular compression, however, can lead to rupture of a weakened artery or may contribute to choroidal hyperemia and should be avoided.

Hypertension and tachycardia are significant risk factors for the development of suprachoroidal hemorrhage and need to be well controlled during the surgery. Preoperative phenylephrine should be used with caution due to its potential exacerbation of systemic hypertension. Since general anesthesia may increase the risk of suprachoroidal hemorrhage, its choice should be evaluated critically.

Post-operatively, Valsalva-like maneuvers must be carefully avoided. Stool softeners and careful instructions regarding limits to activity can be helpful. Inflammation should be controlled vigorously to avoid serous fluid accumulation in the suprachoroidal space and postoperative hypotony particularly in glaucoma filtration procedures should be avoided as they both pose significant risks for development of suprachoroidal hemorrhage.

Diagnosis and Management

Occurrence of suprachoroidal hemorrhage during surgery should be recognized im-

Suprachoroidal Hemorrhage

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mediately and acted upon expeditiously to improve chances of a favorable outcome. Early signs include a sudden increase in intraocular pressure, firm globe, shallowing of the anterior chamber with forward displacement of the lens-iris diaphragm and loss of a red reflex. Immediate tamponade with closure of all surgical wounds or direct digital pressure should be performed, to avoid catastrophic expulsion of intraocular tissue. If intraocular contents are extruded, they need to be reposited as soon as possible. Posterior sclerotomies may be performed to soften the eye and enable replacement of intraocular tissues. The long-term effects of posterior sclerotomies are somewhat controversial. Verhoeff recommended emergency posterior sclerotomies as treatment for suprachoroidal hemorrhage.2 However, Lakhanpal showed in a rabbit experimental model that posterior sclerotomies can be detrimental in an acute setting with extension of the hemorrhage into the retina and vitreous cavity.6

Other intraoperative maneuvers include reformation of the anterior chamber to prevent vitreous entrapment into surgical wounds, removal of the lid speculum to reduce direct pressure on the eye, intravenous osmotic agents and lowering of blood pressure.

Postoperative suprachoroidal hemorrhage typically presents after uncomplicated glaucoma filtration procedures.15 The patient experiences sudden visual loss and severe ocular pain. Nausea, vomiting and headache may accompany it. On examination there may be shallowing of the anterior chamber with vitreous prolapse in aphakic or pseudophakic eyes, loss of red reflex and dark, dome-shaped

choroidal mounds (Figure 1). The immediate management includes lowering of the intraocular pressure, control of inflammation and pain management with cycloplegics and analgesics.16 Aspirin and nonsteroidal antiinflammatory agents should be avoided.

In patients where media haziness prevents visualization of the suprachoroidal hemorrhage, ultrasonographic examination is extremely valuable. On B-scan examination, suprachoroidal hemorrhage presents as dome-shaped choroidal swellings which is partial or completely filled with fluid of

moderate internal reflectivity. These swelling may be so elevated in severe cases that they appear to kiss, threatening retinal apposition (Figure 2). A-scan tracings reveal a double-peaked, steeply rising spike that is characteristic of choroidal detachment, with low reflective spikes in the suprachoroidal space, suggesting hemorrhage.

Ultrasonography is an important means of determining the degree of hemorrhage in any choroidal detachment as well as a tool for gauging the progress and liquefaction of the clot, once the definitive diagnosis of

suprachoroidal hemorrhage has been made. Fresh clots appear ultrasonographically as highly reflective masses with irregular shape and structure. As the clots liquefy, they become less reflective. Liquefaction time of these hemorrhages has been reported at between 7 to 14 days.17 Decisions regarding timing of surgical intervention are often aided by ultrasound findings, but should not be dictated by them, While complete liquefaction of the clotted hemorrhage can facilitate attempts at evacuation and reduce complications by mini-

mizing the need for probing and excessive manipulation other factors such as degree of pain, extent of vision loss, condition of the eye, and other patient factors need to be considered as well. Early intervention in attempt to remove even part of the hemorrhage in the hope of maximizing the chances for visual recovery may be a reasonable consideration in monocular patients; realizing that an additional procedure may be needed several days later.

Secondary Surgical

Management

Before the decision to operate is made, it is important to determine whether expulsive or delayed suprachoroidal hemorrhage has occurred, as the long-term prognosis for each differs. Some authors have proposed early surgical drainage. Major indications for earlier intervention include central retinal apposition, retinal detachment, breakthrough vitreous hemorrhage, vitreous incarceration in surgical wounds, increased IOP and intractable pain.18 Rhegmatogenous retinal detachments are the major indication for surgical intervention. Serous retinal detachments can be observed closely for evidence of progression since they typically resolve spontaneously. Central retinal apposition is a relative indication for earlier surgical drainage. Some authors have recommended longterm intraocular tamponade with gas or silicone oil.18 Poorer visual outcome is associated with increased complexity of the suprachoroidal hemorrhage. Retinal incarceration in the wound is especially associated with a poor prognosis.19

Surgical intervention can involve one of two options:

1.External drainage of the suprachoroidal hemorrhage.

2.External drainage procedure combined with a vitreoretinal surgery to remove vitreous hemorrhage or retained lens material, to relieve vitreoretinal traction or to reestablish normal posterior segment anatomy.

Optimal timing of the drainage intervention is critical for a favorable outcome. Mean clot lysis time is 7 to 14 days. Draining a suprachoroidal hemorrhage that is still mostly clotted is usually unsuccessful and can lead to further damage. It is therefore generally recommended that drainage procedures be carried out 1 to 2 weeks after the development of suprachoroidal hemorrhage, however, earlier attempts may be considered in particular cases. Clot lysis is best confirmed by ultrasonography.

Drainage sclerotomies are created equatorially in the quadrants of the hemorrhage. It is important to peel back the conjunctiva wherever possible, identify and tag the rectus muscles with sutures. This enables placement of the sclerotomies sufficiently posteriorly to facilitate adequate drainage. The IOP should be supported using an anterior chamber maintainer during the procedure. This enables the drainage of lysed blood through the sclerotomy without allowing the eye to become soft (Figure 3). A cyclodialysis spatula can be used to assist in draining the hemorrhage, but care must be exercised to probe along the inner surface of the sclera in order to avoid damaging the overlying retina in areas of shallow elevation. Continuous air-infusion can also be useful to maintain the IOP during the procedure, especially in aphakic eyes. A careful inspection for evidence of vitreous incarceration or vitreoretinal traction should also be undertaken at the time of the procedure.

If vitreoretinal surgery is planned with the drainageprocedure,thesequenceofmaneuvers is crucial to prevent complications.

It is imperative to begin drainage of the hemorrhage first as the anatomy is usually distorted in these eyes which could lead to misplacement of a posterior infusion cannula into the suprachoroidal space instead of the vitreous cavity. A 6 mm infusion cannula is particularly helpful to avoid such a complication. Perfluorocarbon liquid can be used to internally assist pushing posteriorly trapped blood from beneath the macula toward the more anteriorly located exit sclerotomies. After the bulk of the choroidal hemorrhage has been drained and a more normal anterior anatomy has been established, the three-port

vitrectomy can be performed. Retinal detachments can then be addressed. Long-term internal tamponade with intraocular gas or silicone oil is often required.

Prognosis

Expulsive choroidal hemorrhages generally have a poor visual prognosis and secondary surgical intervention may not be helpful for all patients. Second procedures should be based on clear indications for intervention. In delayed suprachoroidal hemorrhage, secondary drainage should

generally be planned when clot lysis is nearly complete and may be combined with vitreoretinal procedures to obtain the most favorable outcome. Prognosis appears to depend upon the extent of ischemia, which may relate to whether the vessel which initiates the hemorrhagic event is arterial or venous, the degree of anatomic disorganization which resulted from the event, and the extent of toxicity produced by the blood on the overlying photoreceptors. Careful but decisive intervention can offer an opportunity for some visual recovery in even the most severe cases.

References

1.Pfingst AO: Expulsive choroidal hemorrhage complicating cataract surgery. South Med J 29:323,1936.

2.Verhoeff FH: Scleral puncture for expulsive choroidal hemorrhage following sclerotomy: scleral puncture for post-operative separation of the choroid. Ophthalmic Res 24:55-59,1915.

3.Beyer CF, Peyman GA, Hill JM: Expulsive choroidal hemorrage in rabbits: A histopathological study. Arch Ophthalmol 107:1648-53,1989.

4.Manschot WA. The pathology of expulsive hemorrhage. Am J Ophthalmol 40:15-24,1955.

5.Zauberman H: Expulsive choroidal hemorrhage: an experimental study. Br J Ophthalmol 66:43-45,1982.

6.Lakhanpal V. Experimental and clinical observations on massive suprachoroidal hemorrhage. Trans Am Ophthalmol Soc 91:545-652, 1993.

7.Wolter JR, Garfinkel RA: Ciliochoroidal effusion as a precursor of suprachoroidal hemorrhage: a pathologic study. Ophthalmic Surg 19:344-349, 1988.

8.Mafee MF, Linder B, Peyman GA, et al: Choroidal hematoma and effusion: evaluation with MR imaging. Radiology 168:781-786,1988.

9.Campbell JK: Expulsive choroidal hemorrhage and effusion: a reappraisal. Ann Ophthalmol 12:332342,1980.

10.Speaker MG, Guerriero PN, Met JA, et al: A case-control study of risk factors for intraoperative suprachoroidal hemorrhage. Ophthalmology 98:202-210,1991.

11.Pollack AL, McDonald RH, Everett AI, et al. Massive suprachoroidal hemorrhage during pars plana vitrectomy associated with Valsalva maneuver. Am J Ophthalmol 132:383-7,2001.

12.Ling R, Kamalarajah S, James C, et al. Suprachoroidal hemorrhage complicating cataract surgery in the UK: a case control study of risk factors. Br J Ophthalmol 88:474-7, 2004.

13.Chu TG, Green RL. Suprachoroidal hemorrhage. Survey of Ophthalmol 43:471-86, 1999.

14.The Fluorouracil Filtering Surgery Study Group. Risk factors for suprachoroidal hemorrhage after filtering surgery. Am J Ophthalmol 113:501-7,1992.

15.Tuli SS, WuDunn D, Ciulla TA, et al. Delayed suprachoroidal hemorrhage after glaucoma filtration procedures. Ophthalmology 108:1808-11, 2001.

16.Healey PR, Herndon L, Smiddy W. Management of suprachoroidal hemorrhage. J Glaucoma 16:577-9, 2007.

17.Wirotsko WJ, Han DP, Mieler WF, et al. Suprachoroidalhemorrhage.Outcomeofsurgicalmanagement according to hemorrhage severity. Ophthalmology 105:2271-5,1998.

18.Meier P, Wiedemann P. Massive suprachoroidal hemorrhage: secondary treatment and outcome. Graefe’s Arch Clin Exp Ophthalmol 238:28-32,2000.

19.Mei H, Xing Y, Yang A, et al. Suprachoroidal hemorrhage during pars plana vitrectomy in traumatized eyes. Retina 29:473-6, 2009.

Introduction

Non penetrating trauma is the most common of ocular injuries(1). Although in most cases there is no treatment that can avoid posterior pole damage, early diagnosis and prompt treatment may prevent severe visual loss.

Non perforating trauma of the globe can result in a great variety of alterations in the posterior pole. These can include: preretinal, intraretinal and subretinal hemorrhages, suprachoroidal hemorrhage, Berlin’s edema, cystoid macular edema with subsequent formation of a macular hole, retinal pigment epithelium (RPE) hematomas and choroidal ruptures(2). Structural modifications can spare visual function or can cause up to total vision loss. Probably, Berlin’s edema represents

the more frequent alteration detected in non penetrating ocular trauma. Nevertheless, hemorrhages are not infrequent and most of them are associated with choroidal rupture(3). Since subretinal and suprachoroidal hemorrhage are two different clinical entities, they will be dealt with separately in this chapter.

TRAUMATIC SUBRETINAL HEMORRHAGE

There are many causes of the accumulation of blood in the subretinal space. Bleeding can come from either retinal or choroidal vessels. Examples of bleeding from retinal vessels include rupture of an arterial macroaneurism with bleeding under the neurosensory retinal space, or a Valsalva hemorrhagic retinopathy(4,5,6).Subretinal hemorrhages, however,

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usually come from the choroidal vessels. As examples, we can mention the subretinal neovascularization associated to age-related macular degeneration (ARMD), or to the Presumed Ocular Histoplasmosis Syndrome, and the choroidal ruptures of myopia. Likewise, complications in retinal surgery can cause choroidal bleeding when subretinal fluid drainage is made. Blunt ocular trauma as well as penetrating, can also cause choroidal bleeding, with accumulation of blood in the subretinal space.

Blood in this space results in photoreceptor damage that can compromise visual function permanently. In humans it can cause a permanent decrease in visual acuity. Bennett et al(7) analyzed various etiologies related to macular subretinal hemorrhage retrospectively. He showed that the etiology plays an important role in final visual acuity. Those patients with ARMD had an average final visual acuity of 20/1700, while visual acuity after hemorrhages secondary to traumatic choroidal ruptures averaged 20/35.

Because of these findings, recent interest has arisen to develop surgical techniques that allow the evacuation of massive subretinal hemorrhages, to avoid possible visual acuity impairment and sometimes achieve improvement. In this chapter we focus on the mechanisms that cause choroidal and retina damage secondary to trauma and the presence of blood in the subretinal space and the surgical possibilities to achieve its evacuation.

Origin of Subretinal Blood

in Trauma

Blunt, non penetrating trauma of the eye can present multiple manifestations in the posterior segment. Almaca et al(8) reviewed the records of 445 patients and found that that 9.4% presented with Berlin’s edema, 8.1% showed choroidal ruptures, and 3.6% had macular hemorrhages.

Hemorrhages in the posterior pole can be observed clinically in different levels. Most are intraretinal, being round and small when located in the external layers of the retina or in a flame-shaped form when found in the nerve fiber layer. These hemorrhages can also be preretinal.

Severe blunt trauma can also cause sub pigment epithelial, subretinal, intrachoroidal, and suprachoroidal (between the choroid and sclera) hemorrhages (Figure 1). In 1968, Gitter et al(9) reported the case of a patient with blunt trauma to the eye, who presented with a localized hemorrhage under the retinal pigment epithelium. The hemorrhage was caused by a choroidal rupture, detected after blood reabsorption.

In order to understand the origin of post-traumatic hemorrhages it is necessary to analyze the possible causes of these injures in different pathologies. In cases of subretinal hemorrhage associated with choroidal neovascularization secondary to ARMD, it has

Figure 1: Fundus photograph showing subretinal hemorrhage after blunt trauma to the eye.

been reported that blood can come from arterial vessels located in disciform scars. These vessels can have continuity with choroidal arteries. El Baba et al(10) speculated that blood or serum can leak from neovascular tissue and produce an RPE detachment. This could produce pressure over the entering artery and the vein coming from the fibrovascular scar causing necrosis and rupture of vessel walls, allowing the passage of blood to the subretinal space.

In general, it is considered that subretinal blood located in the macula secondary to trauma comes from vessels of the choriocapillaris and choroid. The bleeding mechanism can be due to rupture of vessels, with or without choroidal rupture. Gass(11) has demonstrated that a great variety of pathologies associated

with Bruch’s membrane disruption in the macular area can set the scenery of choriocapillaris or choroidal neovascular bleeding, producing hemorrhagic detachments. In these cases the firm adherence of the RPE at the margins of the hemorrhage acts as a barrier confining the detachment and giving it a dome-like shape.

Histopathology of

Choroidal Damage

manifests usually as choroidal ruptures, while damage to the RPE manifests as contusion (Figure 2).

In RPE contusion, cellular edema can provoke a serous retinal detachment. In a case reported by Friberg(12), a creamy color of the RPE was reported 48 hours after trauma. Angiography showed progressive staining of the RPE. Although the pigment epithelium appeared opaque, there was no hypofluorescence. After five months, transmission defects were detected but there was no staining of the RPE.

According to the study by Blight et al,(13) there is intracellular edema of the RPE due to rupture of the internal membranes. This damage also provokes defects in the external segments of the photoreceptors. The cellular edema can show resolution at three weeks and the zonula occludens appears intact in