CILIARY BODY

Normal functioning of the ciliary body has a pivotal role in the long-term health of the traumatized eye. Dysfunction of the ciliary body may result in

loss of the normal IOP.

PEARL... Frequently, the ultimate success or failure of the surgical or medical management of the traumatized eye rests on whether or not the eye can maintain a normal IOP.

Even after successful treatment of an open globe injury, which in many cases also includes repair of various corneal and AC pathologies as well as a complicated retinal detachment (see Chapter 25), it is not uncommon for eyes to become and remain hypotonous.

P I T F A L L

With the loss of IOP, phthisis invariably ensues, leading to a poor functional and cosmetic result.

PEARL... Occasionally, abnormally high IOP is the long-term consequence of trauma-associated inflammation, but the mechanisms of treating elevated IOP are better

developed (see Chapter 20).

This chapter discusses the causative mechanisms of hypotony along with management of the individual conditions.

DEFINITION

Hypotony has been defined statistically in the past as an IOP below 6.5 mm Hg,1 but harmful effects on the eye are only rarely noted before the IOP falls and remains below 4 mm Hg.2

PATHOPHYSIOLOGY

IOPs that chronically remain below 4 mm Hg can result in a prephthisical state with:

•anterior and posterior segment infolding; and

•marked limitation of vision.

The causes of hypotony in the traumatized eye are varied and sometimes difficult to determine. They are generally divided into two classes.

1.The first class is excessive filtration secondary to:

•wound leak;

•ciliochoroidal detachment;

•cyclodialysis cleft; or

•retinal detachment.

2.The second class is reduced aqueous production as a result of:

•intraocular inflammation;

•anterior PVR; or

•ciliary body ischemia and/or damage.

Dynamics of the Aqueous

Aqueous humor is produced by a combination of mechanisms in the pigmented and nonpigmented layers of the ciliary epithelium in the ciliary processes. In the human eye:

•aqueous is formed by the ciliary body at approximately 2.5 L min and

•1% of the aqueous is turned over every minute.3

There are four pathways for the aqueous to drain from the eye:

1.through the trabecular mesh;

2.uveoscleral outflow;

3.through the vitreous; and

4.through a wound.

Most of the aqueous passes out through the trabecular meshwork as a result of a pressure gradient since the IOP in Schlemm’s canal exceeds episcleral venous pressure.a This outflow is so pressure dependent that very little drainage occurs through Schlemm’s canal when the IOP is less than the episcleral venous pressure.

PEARL... When significant hypotony is present, the aqueous humor must leave

the eye by some route other than Schlemm’s

canal.

Of the other pathways of aqueous drainage, the most important is the uveoscleral outflow,5 leading from

•the AC through

•the intermuscular spaces of the ciliary muscle, into

•the suprachoroidal space and into

•the choroidal vessels or out through the sclera or emissarial channels.

The actual percentage of aqueous humor that exits via the uveoscleral route depends on the IOP. In humans with a normal IOP, approximately 10% of the aqueous passes along this route.

In addition to these two routes, aqueous may also escape either:

•posteriorly through the vitreous, across the retina and choroid; or

•in the presence of a full-thickness wound.

a The typical episcleral venous pressure is approximately 9 mm Hg.4

PEARL... The magnitude of hypotony depends on the rate of aqueous produc-

tion and the facility of extracanalicular outflow.

It is important to note that if no other parameter is altered, reduced aqueous humor production can account for hypotony only if it falls below 10% of its normal rate,6 which is uncommon.

PEARL... Generally, increased extracanalicular outflow and reduced aqueous

production coexist to produce hypotony.

CLINICAL CONDITIONS:

THE CAUSES OF HYPOTONY

Increased Filtration

Wound Leak

Wound leak is a common cause of hypotony after open globe injury, although it may occasionally be very difficult to recognize.

P I T F A L L

The only manifestation of a leaking wound may be a low and diffuse filtering bleb, which can be difficult to distinguish from postoperative chemosis.

Diagnosis Occasionally, subepithelial microcystic conjunctival changes may signal leakage through the scleral wound. However, in cases of:

•a posterior wound (e.g., the exit wound in a perforating injury; see Chapter 26); or

•an occult wound (see Chapters 13 and 15), there may be no anterior signs of aqueous loss.

In selected cases, if the view is unobstructed, the posterior wound can be directly visualized.

P I T F A L L

On occasion, a posterior rupture may behave in a trap-door fashion: open only upon application of slight pressure on the globe.

An anterior wound fistula may be detected using the Seidel test (see Chapters 9 and 14). Failure to detect a positive result on the Seidel test is commonly due to one of two factors:

•use of diluted fluorescein; or

•inadequate pressure on the globe while inspecting the suspected area.

PEARL... Use of a fluorescein-impreg- nated paper strip for the Seidel test is preferable to using a drop of fluorescein–topical anesthetic solution because in the latter case the concentration of fluorescein is often inadequate for detection of a subtle leak. Pressure on the globe is also important because the leak may be

only intermittent if the IOP is very low.

B-scan ultrasonography is occasionally useful in identifying discontinuities in the posterior sclera (Fig. 19–1). However, care must be taken to avoid excessive pressure on a globe with an open wound to prevent extrusion of further intraocular contents.

P I T F A L L

There is no definitive test for finding a posterior wound fistula; its existence must frequently be diagnosed by indirect clinical findings based on a high index of suspicion.

CHAPTER 19 CILIARY BODY • 159

Management In general, leaking wounds must be surgically repaired because they:

•have a very low rate of spontaneous closure;b and

•represent a significant risk for endophthalmitis, despite a formed AC.

Common exceptions to this “close the full-thick- ness traumatic wound” rule include:

•a small (e.g., typically less than 2 mm long), linear, sharp, clean wound, which may close spontaneously with medical management alone; or

•a wound too posterior for safe closure (see Chapter 15).

Conservative treatment includes use of:

•pressure patch;

•CAIs; and

•topical beta-blocker(s).

These measures reduce the aqueous flow, potentially allowing the fistula to close. Devices that also may be helpful are a bandage contact lensc or Simmons shell, which tamponade the leak.

PEARL... An inadvertent, small filtering bleb that develops after cataract surgery need not be repaired unless it is causing significant discomfort or visual impairment secondary to astigmatism or hypotony (Fig. 19–2). Closure of a scleral fistula often results in an initially marked IOP elevation until the trabecular

meshwork begins to function normally again.

Cyclodialysis

Pathophysiology Separation of the ciliary body from the scleral spur can be seen after:

•anterior segment surgery;

•ocular trauma (especially contusion); or as the intended goal of

•glaucoma surgery.d

Cyclodialysis creates free communication between the AC and the suprachoroidal space.8,e

FIGURE 19–1 B-scan echogram documenting an occult posterior scleral rupture with incarcerated retinal tissue and localized choroidal detachment.

bEven leaks occurring through the conjunctiva at the limbus may not close spontaneously.

cA contact lens increases the risk of infection.7

dThis surgery has been almost completely abandoned.

eIn experimentally induced cyclodialysis, uveoscleral outflow is markedly enhanced in monkeys9; in rabbits, fluorescein moves more readily into the supraciliary space.10

It has been argued that cyclodialysis also results in reduced aqueous production.11 However, aqueous flare is commonly present in eyes with an acute cyclodialysis, which prevents measurement of aqueous production. It has been found that eyes showing hypotony from chronic cyclodialysis but no aqueous flare have normal aqueous flow as measured by fluorophotometry.6

PEARL... Hypotony associated with a cyclodialysis is due to increased fluid egress.

If there is reduced aqueous production in an eye with acute cyclodialysis, it is the result of associated inflammation rather than the cyclodialysis itself.

PEARL... The presence of a cyclodialysis cleft should be suspected in any hypotonous eye that had recent surgery or

trauma (Fig. 19–3 A–C).

Cyclodialysis creates a rather unique clinical condition.

•If the cyclodialysis cleft suddenly closes, the IOP may rise to extreme levels.12 This is analogous to the rapid rise in pressure that occurs after closure of a wound leak.

•If the cleft is reopened with miotics, the IOP may again fall rapidly.13

PEARL... The size of the cyclodialysis cleft does not appear to correlate directly with the degree of hypotony.11,14 Even a small

cleft is capable of carrying the full amount of aqueous produced.

Diagnosis The cleft between the ciliary body and the scleral spur can be directly identified by gonioscopy. With profound hypotony, visualization of the cleft may be difficult because of corneal deformation during gonioscopy.

PEARL... A viscoelastic agent may be injected into the AC to facilitate the diagnosis; this can also aid in the treatment.15–18

Management More than one treatment modality may be necessary to close the cleft.

PEARL... The cleft may close spontaneously; observation prior to surgical

intervention should be considered.

•If the cleft can be visualized, argon laser photocoagulation can be applied directly in and around the cleft to induce an inflammatory response. This is typically adequate to allow closure of the cleft.15–18

A

C

•Typical argon laser settings are 100 m spot size, 0.1 to 0.2 second duration, and 0.5 to 1 watt of power, applied confluently to the cleft and the surrounding area.

•An IOP spike lasting several days is common after successful closure of the cleft.

Other techniques used to close the cyclodialysis cleft include:

•external diathermy;

•cryotherapy19,20;

•ciliary body suturing21,22; and

•external plumbage.23

Occasionally, additional measures are necessary to identify a cyclodialysis cleft:

•exploratory surgery;

•fluorescein-stained BSS; if injected into the AC, the fluorescein-stained fluid will rapidly exit from a supraciliary sclerostomy11; or

•ultrasound biomicroscopy, a noninvasive technique.24

Surgical closure of the cleft involves:

•localization of the cleft with a diagnostic goniolens;

CHAPTER 19 CILIARY BODY • 161

B

FIGURE 19–3 (A) Color photograph documenting the posterior segment manifestations of hypotony in an eye with a post-traumatic cyclodialysis cleft. Note the prominent chorioretinal folds. (B) Corresponding FA highlighting the chorioretinal folds. (C) B-scan echogram documenting diffuse thickening of the chorioretinal layer with an overlying posterior vitreous separation.

•marking the precise site on the sclera over the cleft;

•preparation of a partial-thickness scleral flap over the cleft, hinged at the limbus;

•passage of a 9-0 or 10-0 nylon suture deeply through the scleral bed to reattach the ciliary body;

•optional placement of cryotherapy or diathermy in the scleral bed to create an inflammatory response to secure the reattachment; and

•closure of the scleral flap.

Ciliochoroidal Detachment

Pathophysiology Ciliochoroidal detachment is commonly seen in the presence of hypotony. However, the relationship between the two is not fully understood.25 It was originally believed that suprachoroidal fluid was derived from aqueous humor, which was responsible for creating the ciliochoroidal detachment. However, electrophoretic protein analysis of suprachoroidal fluid suggests that the fluid originates from the choroidal vessels with molecular sieving across the capillary endothelium.26

Human eyes with a ciliochoroidal detachment have been shown to have stagnation of aqueous

flow, as estimated after systemic administration of fluorescein.11,f

PEARL... Uveoscleral outflow is enhanced as a result of the ciliochoroidal

detachment and attendant ciliary body edema.

In most eyes with ciliochoroidal detachment, aqueous flare is also present,28–30 and a breakdown of the blood–aqueous barrier may be responsible for the observed hyposecretion. Thus, the hyposecretion seen clinically in humans with ciliochoroidal detachment may be a result of the concurrent iridocyclitis and not the detachment of the ciliary body.

Most patients with ciliochoroidal detachment undergo spontaneous resorption of the suprachoroidal fluid. This may occur by absorption into choroidal vessels or by passage of fluid through the emissarial channels.29,30

P I T F A L L

Hypotony can induce a cycle: increasing transudation across the choroidal vessels and reducing the pressure drop across the sclera; the suprachoroidal fluid remains and contributes to continued hypotony.

f In a monkey model,27 injection of silicone oil into the suprachoroidal space, which created large choroidal detachments, did not lower the IOP. This strongly suggests that mechanical detachment of the ciliary body does not cause hyposecretion. However, injection of Ringer’s solution or autologous serum into the suprachoroidal space in the same model led to hypotony associated with a normal rate of aqueous humor flow.

Diagnosis In most cases the diagnosis of ciliochoroidal detachment can be made by:

•direct observation of the retina (Fig. 19–4A and B); or by

•B-scan echography of the posterior segment (Fig. 19–5).31

Small anterior choroidal detachments or very shallow localized ciliochoroidal detachments can occasionally be missed. Useful diagnostic modalities for the detection of very anterior ciliochoroidal detachments include:

•echographic biomicroscopy; or

•B-scan echography using an immersion mode.

Management Treatment of the ciliochoroidal detachment is based upon:

•maintenance of a normal anatomy; and

•breaking the vicious circle of hypotony–supra- choroidal fluid transudation–ciliary body inflamma- tion–aqueous hyposecretion–hypotony.

Nonsurgical treatment includes the use of:

•cycloplegics;

•topical corticosteroids; and

•CAIs (e.g., acetazolamide, which may also speed up the absorption of suprachoroidal fluid, although the mechanism is poorly understood32).

PEARL... Cycloplegics are useful in deepening the AC and preventing corneal

touch.

The maintenance of normal anatomy provided by cycloplegics is valuable even though they increase the uveoscleral outflow and may theoretically slightly worsen the degree of hypotony.

Topical corticosteroids are useful in decreasing ciliary body inflammation and normalizing aqueous

humor production. Occasionally, systemic corticosteroids are used if the eye is unusually inflammed. Increased fluid intake may also increase the production of aqueous humor.

Surgical drainage of the suprachoroidal fluid is indicated if:

• the AC is flat with corneal decompensation; or

•peripheral anterior synechiae are forming (Fig. 19–6).33

PEARL... Hypotony may improve after drainage of suprachoroidal fluid alone.11

To prevent recurrence of a flat AC:

•a viscoelastic agent may be injected into the AC34,35; or in more difficult/recurrent cases,

•suturing of the ciliary body to the sclera.36

Hypotony in uveal effusion syndrome may also be treated by injection of a viscoelastic agent into the AC.37

Retinal Detachment

Rhegmatogenous retinal detachment is most commonly associated with mild hypotony, although occasionally profound hypotony develops.38

PEARL... The level of hypotony is frequently related to the extent of the retinal detachment, even if not all detached eyes

become hypotonous (Fig. 19–7).

Pathophysiology The etiology of the hypotony is controversial. Hypotony could be due to:

•decreased aqueous production; or

•increased filtration.

The production of aqueous humor in retinal detachment has been assessed in several studies.

•It was suggested that the aqueous may be shunted posteriorly through the vitreous, through the retinal hole, and across the RPE/choroid.41,g

•In experimental rhegmatogenous retinal detachment, fluorescein-labeled dextran injected into the vitreous moved into the subretinal space, where it was sequestered for many months.42,43

•Presumably, the rate of fluid removal in the vitreous cavity by the RPE exceeds the rate of aqueous production.

•Iris retraction syndrome also offers clinical evidence: in an eye with retinal detachment and a secluded pupil, administration of CAIs can cause posterior iris retraction.

P I T F A L L

Occasionally, the IOP becomes very elevated after retinal detachment repair, presumably as a consequence of aqueous hypersecretion compensating for increased filtration while the retina was attached. This typically normalizes within a few days with the application of the usual medications reducing aqueous production.

•Aqueous flow was found to be reduced39 as well as normal.40

•Decreased aqueous production may be caused by concurrent iridocyclitis.

•In eyes with more profound hypotony, reduced aqueous humor production alone cannot explain the low IOP.

FIGURE 19–7 B-scan echogram documenting a retinal detachment with an underlying choroidal detachment in a patient who sustained an open globe injury.

The diagnosis and management of retinal detachment are discussed in Chapter 23.

Decreased Aqueous Production

Iridocyclitis

Pathophysiology Clinicians are familiar with mild hypotony that commonly accompanies acute anterior uveitis.44 In these cases, the flow of aqueous is reduced, and the blood–aqueous barrier is abnormal, as manifested by aqueous flare.39,45,46 These two observations may be interrelated because the transport processes of the ciliary epithelium do not function efficiently in the presence of abnormal permeability of the blood–aqueous barrier.47

If edema of the ciliary body exists, fluid would be expected to move more readily through the edematous tissue from the AC into the suprachoroidal space.48,h

gThis posterior filtration could cause the extremely viscous nature of cronic subretinal fluid: protein-rich fluid continues to enter the subretinal space from the vitreous while only water is pumped through the RPE, leaving the protein behind

h In experimentally induced iridocyclitis and an edematous ciliary body, uveoscleral outflow is markedly increased.45 In more profound cases of uveitis, ciliary body vasculitis may lead to vascular occlusion and reduced blood flow.49

Diagnosis The diagnosis of post-traumatic iridocyclitis causing hypotony is based upon the identification of intraocular inflammation. Cells and flare in the AC are the critical signs.

P I T F A L L

In the traumatized eye, recognizing inflammation in the AC is frequently not straightforward because corneal edema and intraocular pigment or hemorrhage may interfere with visualization.

The presence of keratic precipitates, ocular pain, and periocular vascular congestion may also be equivocal given the traumatized state of the eye. The diagnosis of iridocyclitis is frequently only presumed in a post-traumatic eye with hypotony.

Management The treatment of post-traumatic iridocyclitis is the same as that of iridocyclitis in the nontraumatized eye.

•Strong cycloplegics help reduce pain and relax the ciliary muscle. This helps break the inflammatory cycle of muscle spasm and inflammation.

•Topical corticosteroids (and occasionally systemic corticosteroids) directly reduce the amount of inflammation.

Anterior PVR

Pathophysiology The clinical findings of anterior PVR include:

•chronic hypotony after trauma or surgery (especially following lensectomy and concurrent vitrectomy);

•a fixed, widely dilated pupil; and

•a posteriorly displaced iris.50

PEARL... A posteriorly displaced iris indicates adhesions via a proliferative tissue between the posterior iris surface and the

ciliary processes, remnants of the zonules/lens and the anterior insertion of the vitreous base, and/or the presence of secondary membranes in the retroiridal space.

Additional findings include the following.

•Eyes with anterior PVR have a high incidence of hypotony compared with eyes with only posterior PVR.51

CHAPTER 19 CILIARY BODY • 165

•Frequently there is no evidence of suprachoroidal fluid or ciliochoroidal detachment; the hypotony must be secondary to another mechanism. Instead, there is an abnormal tissue covering and/or causing traction on the ciliary processes.

•Two basic patterns of fibrosis are recognized.51

In some eyes, there is a prominent, white, fibrotic ring of contracted tissue. It is slightly elevated from the ciliary body and causes traction on the ciliary processes via the remaining zonules. This tissue is thought to represent fibrosis and contracture of the remaining equatorial lens material and capsule. This causes decreased aqueous fluid production by detachment of the ciliary body and distortion of the normal architecture.i

In other eyes, there is a continuous sheet of fibrous-appearing material extending from the vitreous base to the posterior iris, completely covering the pars plicata ciliaris. The tissue originates from cellular invasion, and secretion and contraction of new collagen within the anterior cortical vitreous over the ciliary body. The membrane causes decreased aqueous production by physically obstructing outflow and distorting the anatomy of the ciliary body.

Diagnosis Clinical signs of anterior PVR include:

•dense anterior membranes;

•posterior synechiae; and

•posterior retraction of the iris.

PEARL... Anterior PVR as a cause of hypotony must always be considered in

severely traumatized eyes.

This area is exceptionally difficult to visualize with the IBO, especially in the presence of a retracted and poorly functional iris. Traditional B-scan ultrasound could be utilized in an immersion mode. Ultrasound biomicroscopy could potentially have great utility in these cases to allow detailed visualization of the ciliary body.

The diagnosis is best confirmed via direct visualization during vitrectomy. Scleral depression and use of a wide-angle system are especially helpful. The endoscope offers unparalled advantages in such eyes (see the Appendix).

i This may be one reason why removal of the posterior lens capsule may be preferred to keeping it for the sake of IOL implantation (see Chapter 21).

Management The mainstay of treatment for anterior PVR is pars plana vitrectomy with:

•radical vitreous base dissection; and

•careful removal of all fibrotic material from the ciliary body.

Hypotony may be reversed by:

•removal of the cyclitic membrane or epiciliary tissue, presumably as a result of canceling the tractional irritation on the ciliary epithelium52; and by

•releasing traction from a shrunken posterior cap- sule.53–56 This may allow reattachment of the ciliary body and a reduction in uveoscleral outflow.

Upon removal of the fibrotic ring, it is not uncommon for a posterior shift of the ciliary body to be observed. In these cases with a flatly adherent sheet of scar over the ciliary body, incision of the membrane frequently leads to extrusion of the ciliary processes through the opening, implying compression of the ciliary body by the scar. In one report of patients undergoing meticulous surgical dissection of anterior scar tissue for anterior PVR with hypotony, resolution of the hypotony occurred in 64% of eyes.51

Panoramic endoscopic systems provide adequate visualization not only for diagnostic purposes but also for the surgical removal of any scar tissue that may contribute to ciliary body dysfunction (see the Appendix).

In these eyes, ischemic necrosis of the ciliary body occurs and aqueous production falls to very low levels. The hypotony eventually proceeds to phthisis.

PEARL... Even with necrotic-appea- ring ciliary processes, aqueous produc-

tion may be sufficient to prevent phthisis development.51

Diagnosis The diagnosis of ciliary body ischemia is frequently a diagnosis of exclusion. It can be suspected at the time of pars plana vitrectomy when, upon direct inspection, the ciliary processes appear white. Scleral depression is typically employed to visualize the ciliary body under anesthesia. Endoscopic viewing systems allow visualization of the ciliary body without scleral depression (see the Appendix).

Management After it has been established that it is the ciliary body itself that is damaged and thus simply cannot produce enough aqueous to prevent hypotony, management options revolve around the prevention of fluid egress or artificial maintenance of globe volume.

When the ciliary body is only temporarily nonfunctional as a result of inflammation, repeated fluid–gas exchanges have been utilized to keep the eye inflated temporarily.56 This, however, is certainly not a long-term solution.

PEARL... Prevention of anterior PVR development is becoming a goal of lensectomy/vitrectomy procedures. Adequate removal of the peripheral vitreous (even in phakic eyes) and of the posterior capsule in selected cases (see Chapters 21 and 24) is crucial. The tremendous advantage of wide-angle viewing systems must again be emphasized in helping maneuvers

at the vitreous base.

Ciliary Body Ischemia/Necrosis

Pathophysiology In many severely injured eyes, blood flow to the ciliary body is compromised by damage to:

•the long posterior and anterior ciliary arteries; and

•the major arterial circle. This damage can arise from:

•the original trauma; or from

•subsequent interventions during:

wound repair;

scleral buckling; and/or

cryotherapy.

PEARL... In an eye with poor fluid turnover, clearance of the intraocular gas is much slower than usual (see the Appendix),

and long-acting gases may keep the eye inflated for months.

MANAGEMENT OF THE PHTHISICAL EYE

It is increasingly common for ophthalmologists treating patients with severe eye injuries to observe during follow-up eyes that have an attached retina but are gradually becoming phthisical because of ciliary body nonfunction or dysfunction (see Chapter 25).

Whereas in the past these eyes were eventually lost, usually enucleated for reasons of cosmesis and convenience, our armamentarium today has at least one useful weapon.

•Silicone oil has been employed successfully (see Chapter 18) in an attempt to maintain the IOP and mechanically prevent the eye from shrinking.57 This requires, however, that an adequate volume of silicone oil be infused into the eye (i.e., a complete fill; see Chapter 8) because there will be little contribution from aqueous production.

An additional option would be to reduce aqueous outflow by inducing scarring in the angle. Theoretically, argon laser photocoagulation to the ciliary body face in the angle could produce peripheral anterior synechiae and reduce uveoscleral outflow in eyes with hypotony.

SUMMARY

Hypotony after ocular trauma is a rather common occurrence and is frequently the major determinant

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