CHOROID

Two important trauma-related conditions involve the posterior uvea: choroidal rupture and SCH. The universally used term choroidal rupture is inaccurate because in

addition to the rupture of Bruch’s membrane, there is associated injury to the adjacent choriocapillaris and a break in the overlying RPE. It may lead to legal blindness if the fovea is involved. In SCH,a blood accumulates external to the choroid; the diagnosis may be difficult initially because of the presence of associated tissue injuries. SCH may develop/rebleed intraoperatively and result in the expulsion of intraocular contents with total blindness. Choroidal rupture is rather common1 in contused eyes; SCH is less frequently recognized than its true incidence.

CHOROIDAL RUPTURE

Etiology and Diagnosis

Choroidal ruptures have been classified2,3 as:

•direct, occurring at the site of impact, most commonly anteriorly and parallel with the limbus; or

•indirect, occurring away from the site of impact, usually in the posterior pole concentric to the optic disk or through the fovea (Fig. 22–1).

Choroidal rupture must always be ruled out in contused eyes; the lower (indirect) incidence figureb

aAlso called ECH (see ref. 33); although the latter term suggests loss of intraocular contents, SCH and ECH are not clearly distinguished in the literature. SCH is the term used throughout this chapter.

bIn the HEIR, the incidence of choroidal rupture is 10% among contused eyes and 1% among ruptured eyes (V. Mester and F. Kuhn, 1999).

FIGURE 22–1 Fundus photograph showing a choroidal rupture through the center of the fovea.

in rupture injuries is probably due to the diffusion of the expansile forces and to the eyewall defect acting as a vent to release the force of the impact. The choroidal rupture in contusion trauma is probably caused by a rapid shortening of the globe’s anteroposterior diameter and its expansion in the frontal plane. The relatively rigid sclera and the relatively distensible choriocapillaris and sensory retina are more resistant and thus less likely to rupture than Bruch’s membrane. The crescent shape of indirect choroidal ruptures may be secondary to a “tethering” effect of the optic nerve.4

The diagnosis of an indirect choroidal rupture is easily made with the IBO; if obscured by overlying subretinal and/or vitreous hemorrhage,4–7 the rupture

remains invisible until the blood resolves, also limiting the usefulness of FA in earlier detection.5–8 ICG imaging appears more helpful.7,9,10 Studies of associated visual field defects have been inconsistent, but usually there is no direct correlation between the perimetry findings and the location of the rupture.8

PEARL... Early identification of a transfoveal choroidal rupture assists the clinician in providing the patient with a more realistic prediction regarding the visual outcome.

Prognosis

The injured eye’s vision can vary with time: it may be initially poor due to overlying hemorrhage but improve as the hemorrhage resolves. A more realistic prognostic indicator is the location of the rupture in relation to the fovea4,11; in patients with:

•subfoveal rupture, the vision tends to remain poor;

•extrafoveal rupture, the vision may remain excellent until and unless CNV develops;

•contusion maculopathy, the visual potential is limited (Fig. 22–2).

The development of CNV is a late (even 37 years after injury16) cause of vision loss12–16 (Fig. 22–3). CNV presumably occurs from choroidal capillaries growing through the breaks in Bruch’s membrane. Ruptures closer to the fovea and with greater length may have an increased risk of subsequently developing CNV.11

Treatment

•There is no treatment for the rupture itself, although surgery may be indicated for the subretinal or vitre-

FIGURE 22–2 Choroidal rupture temporal to the fovea with associated traumatic macular hole.

ous hemorrhages (see Chapter 23). The CNV commonly regresses spontaneously2 or may not progress, for which the relatively healthy RPE surrounding the lesions may be responsible.16,c Photocoagulation, even though shown to prevent the recurrence of CNV in association with choroidal rupture,12,13 should therefore be used with caution.

PEARL... CNV associated with choroidal rupture, usually responding

poorly to laser photocoagulation, often involutes

spontaneously, leaving a relatively small scotoma.

c Normal RPE cells have been shown to inhibit angiogenesis.17

•Extrafoveal CNVs may be photocoagulated.

•Subfoveal and juxtafoveal lesions are usually observed, although successful surgical removal of subfoveal choroidal neovascular membranes in eyes with previously good vision has been reported.18 Surgical results may nevertheless be limited by a high recurrence rate.

Photodynamic therapy may eventually become a treatment option; however, to date, there is no datum or even anecdotal clinical report regarding this treatment.

SCHd

Anatomy and Pathophysiology

The suprachoroidal space is a potential one between the choroid and the sclera, containing only approximately 10 L of fluid.19 The choroid is attached to the sclera at the edge of the optic nerve, at the scleral spur, and at the ampullae of the vortex veins. The arterial supply of the choroid comes mainly through the short posterior ciliary arteries20 (Fig. 22–4); the long posterior ciliary arteries, passing within the

d Much of what is presented here is based on nontraumatic SCH; the literature on injury-related SCH is limited.

CHAPTER 22 CHOROID • 199

suprachoroidal space, contribute by forming anastamoses with the short posterior ciliary arteries.

Many hypotheses have been proposed for SCH development.21–24 It is probably caused by the rupture of a short/long posterior ciliary artery, rapidly filling the suprachoroidal space with blood.

•SCH in open globe injuries may be related to direct trauma to the vessels.

•Contusion may cause SCH via vessel rupture due to shearing forces (anteroposterior shortening and equatorial expansion of the globe).

•SCHs can be precipitated by hypotony, presumed to lead initially to choroidal effusion with subsequent expansion of the suprachoroidal space, causing stretching and rupture of the ciliary arteries and potential expulsion of intraocular contents through the wound.23

Etiology, Epidemiology, and Risk Factors

SCH may occur intraoperatively20–22,24–27 with tissue extrusion (expulsive SCH, Fig. 22–5), postoperatively (delayed SCH), or even spontaneously.28–31

PEARL... The incidence of SCH in trauma is not known but appears to be greatly underreported. Analyzing the pathological specimens of a series of 28 NLP eyes that underwent enucleation due to rupture, an incidence of 100% was found even though clinically

not a single eye was described to have SCH.33

FIGURE 22–4 Drawing of dissected globe. Choroidal arteries that enter the suprachoroidal space by piercing the sclera surrounding the optic nerve can be seen radiating from the optic nerve (left). Two vortex veins are at the top and bottom. (From Tasman W, Jaeger EA, ed. Duane’s Foundations of Clinical Ophthalmology. Philadelphia: Lippincott Williams & Wilkins, 1999:8, by permission from Lippincott Williams & Wilkins.)

FIGURE 22–5 Clinical appearance of an intraoperative expulsive SCH (cataract extraction).

Late and poor prognostic signs include:

•tissue extrusion; and

•appearance of fresh blood.

Multiple risk factors for the development of nontraumatic SCH have been reported,21,22,24–26,32,33 some of which may also play a role in the development of traumatic SCH (see Table 22–1). Few prophylactic measures to reduce the risk of SCH related to trauma are available (see Table 22–2).

PEARL... The surgeon must keep in mind that in eyes undergoing wound closure or secondary reconstruction following

trauma, SCH may develop or rebleed with removal of the blood’s tamponading effect when the eye is (re)opened. It is therefore crucial always to keep in mind that the time during which the eye is underpressurized (i.e., the wound is open) must be minimized.

PEARL... The most critical aspects in the management of an intraoperative

SCH are early recognition and instantaneous

restoration of the IOP.

To repressurize the eye immediately in case of an SCH (ECH), the surgeon has the following options:

•surgically close all wounds;

•reappose the wound lips by applying direct digital pressure; or

•use specialized tools (e.g., Byrne lens,33 Fig. 22–6) if the wound is anterior and especially if it is large.

Recognition and Management

Acute SCH

Common early signs of an intraoperative SCH include:

•shallowing of the AC;

•hardening of the globe (IOP elevation is likely to occur if tissue is being extruded);

•loss of the red reflex; and

•forward displacement of intraocular tissues/lens.

FIGURE 22–6 The Byrne lens, placed between the eyelids to maintain pressure on the globe while sutures are placed to close the surgical wound after an expulsive SCH.

PEARL... Repositioning of prolapsed tissues in case of major intraocular bleeding is not a priority; tissue incarcerations may be

best addressed secondarily.

Simultaneous drainage34 is usually not advocated because of:

•poor initial drainage secondary to rapid clotting of the suprachoroidal blood;

•high incidence of reaccumulation of the hemorrhage;

•the threat of massive rebleeding if infusion is not (appropriately) used to maintain the IOP; and

•a lack of statistically significant improvement experimentally in the size or duration of the SCH.22

Delayed SCH

It is more common in patients with previous glaucoma filtering surgery, postoperative hypotony, or following Valsalva maneuvers, and is less severe than acute SCHs. Although expulsion of intraocular contents is rare, retinal apposition may occur. Delayed SCH may mimic the signs/symptoms of a retrobulbar hemorrhage35 and usually causes severe ocular pain and loss of vision. The IOP may be elevated or low; in the latter case, it is crucial to restore the IOP as soon as possible.

Secondary Management

Systemic corticosteroids are thought to improve the prognosis.33 A crucial question is whether drainage

CHAPTER 22 CHOROID • 201

and/or vitrectomy should be performed. The two most important monitoring tools are the IBO and

ultrasound21,22,32,36:

•A-scan shows clotted blood as a choroidal spike and a scleral spike with an intervening area of middle to low internal reflectivity; with liquefaction, the internal reflectivity becomes lower;

•B-scan shows clotted blood as a solid mass (Fig. 22–7); with liquefaction, the clot size decreases within a greater amount of fluid. Dynamic echography shows the movement of smaller clots within the liquefied blood.

PEARL... Echography is helpful in determining the extent and consistency of SCH and, in patients with opaque media,

identifying the presence of associated retinal detachment. It also assists in decision making (e.g., the need for, and timing of, secondary reconstruction).

Drainage indications include:

•uncontrollable paine; and

•elevated IOP not adequately controlled with medical management.

e Believed to be secondary to stretching of the ciliary nerves within the suprachoroidal space.

Although time allows the clot to liquefy and the SCH may resorb spontaneously, vitrectomy offers an opportunity to drain the SCH even if it otherwise would not have been considered necessary. Ideally, however, drainage is not performed if the clot has not liquefied; this usually occurs in 7–14 days.

Early drainage may be unnecessary and:

•requires more skill; and

•has an increased risk.

If the clot is not liquefied, a surgeon experienced in vitreoretinal surgery may attempt “transscleral mechanical thrombectomy.”33

Surgical steps of draining the suprachoroidal blood include the following.

•Determine the incision(s) site (IBO, ultrasonography).

•Introduce BSS infusion in the AC (if vitrectomy is also performed, an alternative is through the pars plana, using the 6-mm cannula; this infusion cannot be turned on until the cannula’s tip becomes visible,37 see Fig. 22–8); vitreous substitutes include:

BSS38–40;

viscoelastics;

air (may interfere with visualization)41;

silicone oil42; and

PFCL.43

•Create an axial posterior drainage sclerotomy.

•Apply gentle pressure (e.g., cotton-tipped applicator) or use careful manipulation (e.g., cyclodialysis spatula underneath the sclera) to release the blood. If the wound is too small, an L- or T-shaped incision is preferred.33 The IOP must be monitored.

PEARL... Even if the SCH involves all quadrants, one or two sclerotomies may be sufficient to drain most of the liquefied blood.

Conversely, even vigorous efforts rarely allow complete removal of the SCH.

Vitreoretinal Surgery is usually performed in the presence of:

•incarceration of the vitreous and/or retina in the surgical wound;

•persistent vitreous hemorrhage;

•retinal detachment; and

•crystalline lens fragments in the vitreous (see Chapter 21).

C O N T R O V E R S Y

Permanent adhesion is not inevitable between the apposed retinal surfaces,44,45 representing a relative indication for surgical intervention.f

SURGICAL TECHNIQUE Vitrectomy is performed depending on the eye’s specific condition (see Chapter 23). General comments include the following:

•Be careful before turning on the infusion (see earlier).

•The sclerotomies are not prepared or should be plugged until at least some of the SCH has been drained.

•Carefully monitor the IOP, never allowing the eye to become hypotonous.

•The PFCL “sinks” posteriorly and helps to push the remaining SCH through the drainage sclerotomy, which may be placed more anteriorly than usual.

•The peripheral retina may be displaced anteriorly and adheres to the iris; that is, it appears attached when in fact it is not. In such cases, one must either:

start through limbal incisions and break the iridoretinal adhesions; or

anticipate the need for a large peripheral retinectomy.

Outcomes and Prognosis

The prognosis of SCH is guarded, determined by:

•whether the initial wound closure was timely44;

•the presence and nature of associated conditions (e.g., central choroidal apposition, vitreous or retinal incarceration, retinal detachment, APD, duration of central retinal apposition46); and

•the effectiveness of the secondary reconstruction.

The visual outcome is increasingly poor as the category/complexity of SCH increases.47 Immediate retinal detachment is a poor prognostic indicator.48

f Most vitreoretinal surgeons consider it a fairly strong argument for intervention.

CHAPTER 22 CHOROID • 203

P I T F A L L

Intraoperative drainage helps in repositing expulsed intraocular contents but may cause reaccumulation of the SCH, worsening the visual prognosis. Successful drainage of SCH does not ensure a good outcome; the risk remains for the development of retinal detachment, EMP, CME, and persistent hypotony despite otherwise successful management. Irregular reticular pigmentary changes in the mid/peripheral retina (reactive changes to subretinal blood) are common. Many eyes have poor vision for no discernible reason.

SUMMARY

Choroidal rupture in the posterior pole occurs in up to 10% of contused eyes. Poor initial visual acuity is due to a rupture underneath the fovea or to overlying subretinal/vitreous hemorrhage. Late decrease in vision is typically caused by a serosanguineous macular detachment because of CNV development. CNV may spontaneously regress or be photocoagulated or surgically removed, although the visual prognosis is guarded. Choroidal rupture, on the other hand, should not be regarded as a contraindication to surgery for other trauma-related conditions such as a macular hole.

SCH is a dreaded complication because of the potential for expulsion of intraocular contents and/or central retinal apposition. Intraoperative management includes immediate closure of the wound(s). Drainage during the primary management is rarely advocated. Postoperatively, the IOP, inflammation, and pain must be controlled. Indications for drainage/surgery include uncontrollable IOP and pain and certain posterior segment conditions (e.g., central retinal apposition, vitreous hemorrhage, vitreous/retinal incarceration, retinal detachment, retained lens fragments). The secondary reconstruction is ideally delayed for 1 to 2 weeks to allow clot liquefaction, determined by echography. The outcome is usually poor, although it varies with the complexity of the associated clinical findings. Immediate wound closure and meticulous reconstructive surgery, with drainage of the SCH if necessary, may improve the prognosis.

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