Medical, Laser, and Surgical Management of Inadvertent CyclodialysisCleft With Hypotony | Congenital Defects | JAMA Ophthalmology | JAMA Network
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Clinicopathologic Reports, Case Reports, and Small Case Series
March 2004

Medical, Laser, and Surgical Management of Inadvertent CyclodialysisCleft With Hypotony

Author Affiliations


Arch Ophthalmol. 2004;122(3):396-398. doi:10.1001/archopht.122.3.399

Cyclodialysis cleft is the result of separation of the meridonal ciliarymuscle fibers from the scleral spur,1 therebyproviding a new drainage pathway of aqueous humor into the suprachoroidalspace. Cyclodialysis has been used as a surgical option for aphakic glaucoma2 but more often occurs inadvertently during anteriorsegment surgery or because of blunt ocular trauma. The new drainage channelincreases uveoscleral outflow and may result in chronic ocular hypotony. Choroidaleffusion, cystoid macular edema, optic nerve edema, engorgement and stasisof retinal veins, retinal folds, shallow anterior chamber, and cataract arerecognized complications of chronic ocular hypotony.

Medical management of inadvertent cyclodialysis cleft is a trial oftopical 1% atropine sulfate for 6 to 8 weeks. Topical or systemic corticosteroidtherapy is not indicated. If medical management is ineffective, noninvasivemethods of cleft closure, such as argon laser photocoagulation to the cleft,should be attempted. Should conservative therapy fail, then surgical closureof the cleft is the final option.

We describe 7 patients who had an inadvertent cyclodialysis cleft thatoccurred following uneventful extracapsular cataract extraction with posteriorchamber intraocular lens implantation in 5 patients, blunt trauma in 1 patient,and trabeculotomy in 1 patient (Table 1). Their ocular hypotony was successfully treated with topical 1%atropine in 4 patients, argon laser photocoagulation in 2 patients, and surgicalclosure in 1 pediatric patient.

Summary of Patient Data for Cyclodialysis Cleft
Summary of Patient Data for Cyclodialysis Cleft

Report of Cases

Case 1

A 52-year-old man underwent uneventful extracapsular cataract extractionwith posterior chamber lens insertion in his right eye in April 1990. Postoperatively,he developed a 20% hyphema that cleared spontaneously within several days;however, he developed ocular hypotony of 4.0 to 6.0 mm Hg in the operatedon eye with reports of metamorphopsia. He was referred to us in consultationwhen the hypotony failed to resolve after 18 months and his visual acuitydecreased from 20/20 immediately postoperatively to 20/50. The patient wasseen at the Pennsylvania State University Milton S. Hershey Medical Center,Hershey, for the first time in November 1991. Medications included dexamethasoneeye drops and aspirin.

On ophthalmic examination, his visual acuity was 20/100 OD and 20/20OS. Central Amsler grid distortion was noted in the right eye and intraocularpressure (IOP) was 2.0 mm Hg OD and 9.0 mm Hg OS. Anterior chambers were deep,equal, and quiet in both eyes. The corneoscleral wound had healed nicely andno inadvertent filtration bleb was observed. The posterior capsule was opacifiedand there were posterior synechiae to the implant at the 5-o'clock position.The implant was well centered. Gonioscopy revealed a cyclodialysis cleft atthe 11- through 1-o'clock positions with a peripheral anterior synechia bridgingthe cleft at the center. Funduscopic examination of the right eye revealeda hyperemic and swollen optic nerve head. Retinal veins were tortuous andslightly distended. There were prominent chorioretinal folds as well as choroidalthickening extending into the macular area in that eye. Findings from theexamination of the left eye were unremarkable.

The patient's condition was diagnosed as inadvertent cyclodialysis cleftfollowing cataract extraction. The treatment regimen of corticosteroid eyedrops was discontinued and 1% atropine, 3 times daily, was ordered in an attemptto close the cleft. Over the next 6 weeks, the IOP increased to only 5 mmHg and the cleft remained patent.

Argon laser treatment was then applied deep within the cleft to boththe ciliary muscle and scleral side (100 applications, 100-µm spot size,0.1-second duration, and 1.0- to 1.5-W power). After no subsequent rise inIOP was observed, a second argon laser treatment was applied 1 week afterthe initial treatment (160 applications, 100-µm spot size, and 1.0-to 1.5-W power). Treatment with topical 1% atropine was continued.

Four days later, the patient was seen in the emergency department reportingsevere headache, nausea, and pain in the right eye. Visual acuity was 20/60OD and 20/20 OS with moderate (2+) conjunctival hyperemia in the right eyeand trace corneal epithelial edema. Intraocular pressure was 46.0 mm Hg OD.Combined treatment with 0.5% timolol hemihydrate, acetazolamide, 250 mg/dorally, and glycerin was initiated. Within 2 hours, the IOP was reduced to24.0 mm Hg. Atropine therapy was discontinued; combined treatment with a topicalcorticosteroid and 0.5% timolol hemihydrate was prescribed. The patient returnedto his referring physician for continued monitoring of his condition.

Case 2

A 72-year-old woman was referred to the retina service for evaluationof chorioretinal folds of the left eye. The patient had undergone uneventfulextracapsular cataract extraction with posterior chamber intraocular lensimplantation. Her uncorrected visual acuity was 20/30 OS 8 weeks after theoperation. Intraocular pressure was not recorded. Three months postoperatively,her visual acuity dropped to 20/50 OS. Intraocular pressure was 16.0 mm HgOD and 0.0 to 1.0 mm Hg OS. The anterior chamber was deep with mild flare(1+) and no cells. The implant was decentered. Fundus examination showed noabnormality and intravenous fluoroscein angiography demonstrated patchy choroidalfilling. She was treated with 80 mg/d of oral prednisone for uveitis and possiblemacular edema. One month later, the patient's visual acuity was unchanged.The anterior chamber was quiet but the IOP remained 0.0 mm Hg OS. She wasthen referred to the glaucoma service for further evaluation and treatment4 months after her initial surgery.

On our examination, her visual acuity was 20/40 OD and 20/200 OS. HerIOP was 19.0 mm Hg OD and 1.0 mm Hg OS. On gonioscopy, no peripheral anteriorsynechia, angle recession, or filtration cleft was noted. No filtration blebwas visible on slitlamp examination. Fundus examination revealed optic discedema extending into the peripapillary retina. No choroidal or retinal foldswere visible. With the impression of possible anterior segment ischemia, theleft eye was treated with dexamethasone sodium phosphate (Decadron) eyedropsevery 2 hours.

Several weeks later, she was reexamined. Visual acuity was 20/100 OSand her IOP was 5.0 mm Hg OS. Careful gonioscopy at this time showed a small,less than 1 clock hour, cyclodialysis cleft between the 12- and 1-o'clockpositions. The anterior chamber was deep and quiet. Therapy with 1% atropineeyedrops 3 times daily was begun.

Three weeks after atropine therapy was initiated, her visual acuitywas 20/70 OS and IOP was 17.0 mm Hg OS. At her final visit, 6 weeks later,visual acuity was 20/25 OS and IOP was 14 mm Hg OS. The cyclodialysis cleftwas closed. Atropine therapy was tapered over a 3-week period.

Case 3

A 9-year-old boy was hit in his left eye with a BB 1 week before hewas referred to our glaucoma service for evaluation and treatment of hypotony.Immediately following trauma, he developed a 10% hyphema for which he washospitalized. The hyphema resolved uneventfully, but his IOP remained between2.0 and 4.0 mm Hg OS. Computed tomography of the left orbit showed no abnormalityfor an intraocular or intraorbital foreign body. He was treated with prednisolonephosphate eyedrops, 1 drop 4 times daily, without effect.

When we examined the patient, he reported photophobia. His visual acuitywas 20/15 OD and 20/200 OS. There was a myopic shift of −9.50 dioptersin his left eye and with correction, visual acuity improved to 20/50 OS. Anisocoriawas present, with an irregular, dilated left pupil. No relative afferent pupillarydefect was present. The anterior chamber in the left eye was slightly shallow.There was no evidence of anterior chamber inflammation. Intraocular pressurewas 12.0 mm Hg OD and 3.0 mm Hg OS. An iridodialysis was present from the8:30- through 10-o'clock positions in the left eye. Gonioscopy demonstrateda wide open angle in the right eye and a narrow angle in the left eye witha cyclodialysis cleft from the 10- through 1-o'clock positions. The rightfundus was normal; however, optic disc edema and minimal macular edema werenoted in the left eye. No choroidal or retinal folds were present.

Topical corticosteroid therapy was discontinued and 1% atropine eyedrops,3 times daily, were ordered. One week later, when examined by his referringophthalmologist, his visual acuity improved to 20/20 OS and his IOP was 22.0mm Hg OS. When reexamined 3 months after the trauma, his visual acuity was20/20 OS and his IOP was 18.0 mm Hg OS without receiving any medication. Thecyclodialysis cleft was closed.

Case 4

A 72-year-old man underwent uneventful extracapsular cataract extractionwith phacoemulsification and posterior chamber intraocular lens implantationin his left eye by his referring ophthalmologist on January 10, 1992. Immediatelyfollowing the procedure, he was found to have ocular hypotony with an IOPof 0.0 to 2.0 mm Hg OS and gradual decline in his visual acuity. Combinedtreatment with a topical corticosteroid every 2 hours, cyclopentolate hydrochloride,and dexamethasone sodium phosphate ointment was started. He was ultimatelyreferred to us 5 months postoperatively, when medical management was not alleviatinghis hypotony and decreased visual acuity.

When he was examined in consultation, his visual acuity was 20/30 ODand 20/200 pinholing to 20/60 OS. The eyes were without inflammation and theleft anterior chamber was slightly shallow. The implant was in place. Gonioscopyrevealed a small 1 clock hour cyclodialysis cleft superiorly. His IOP was22.0 mm Hg OD and 0.0 to 2.0 mm Hg OS. Fundus examination showed choroidalthickening and mild macular edema of the left eye.

Treatment with 1% atropine eyedrops, 3 times daily, were prescribed.When his condition was evaluated in 1 month, the clinical picture was unchanged.Atropine therapy was continued. When the patient was again seen 7 weeks later,his visual acuity was 20/40 OS and his IOP was 10.0 mm Hg OS. The macularedema was decreased. The patient returned to the referring ophthalmologistwith instructions to taper the atropine therapy.

Case 5

A 4½-month-old girl was referred to the pediatric ophthalmologyservice for bilateral congenital glaucoma in June 1993. She took no medications.Ocular history included an intermittent esotropia. During evaluation of hercondition, she was found to be in good general health.

She fixed and followed well with the right eye and poorly with her lefteye. Her pupils were dilated medically at the time. She was orthophoric withmotor testing and had full motility. Epiphora was observed in both eyes. Horizontalcorneal diameters were 12.0 mm OD and 3.0 mm OS. The left cornea appearedhazy on slitlamp examination; no Haab striae were noted. Intraocular pressuremeasured using a handheld electronic tonometer (Tono-Pen XL; Mentor Corp,Santa Barbara, Calif) was 19.0 mm Hg OD and 27.0 mm Hg OS. Funduscopic examinationrevealed a cup-disc ratio of 0.7 OD and 0.8 OS with normal vessels, macula,and periphery.

The patient underwent bilateral uncomplicated trabeculotomy 2 weeksapart. Postoperatively she was receiving a combination of polymyxin B sulfate–trimethoprimsulfate and 1% prednisolone phosphate eyedrops in both cases. Fundus examination1 week postoperatively showed shallow choroidal detachments in the right eye.On subsequent follow-up visits, the right eye was found to be soft and hypotonousto palpation. On funduscopic examination 2½ months later, hypotonymaculopathy and optic disc edema were present and the eye remained soft topalpation. Treatment with 1% atropine ointment, 3 times daily, was begun fora presumed cyclodialysis cleft. The patient was scheduled for examinationunder anesthesia.

Examination under anesthesia then revealed a shallow anterior chamberon the right side. The IOP was 0.0 mm Hg OD and 11 mm Hg OS. Funduscopic examinationof the right eye showed prominent optic disc swelling. Gonioscopy of the righteye was performed and revealed a cyclodialysis cleft extending for about 2clock hours in the superior nasal quadrant between the 10:30- and 12-o'clockpositions.

A 4 × 6-mm, partial-thickness, limbus-based scleral flap was createdsuperiorly. A scleral incision was created 2.5 mm posterior to the limbuswithin the scleral flap. Incision was carefully continued deep to the scleraat the center of the scleral bed; fluid was found in the suprachoroidal space,most prominently in the superior nasal quadrant. Several 10-0 nylon sutureswere used to close the cyclodialysis cleft in the superior nasal quadrant.The sutures were passed through the sclera, then through the ciliary body,then back to the sclera. On postoperative day 1, IOP taken with the handheldelectronic tonometer was 11.0 mm Hg OS and optic disc edema was reduced. Thepatient's condition was maintained on a combination therapy of 0.5 % atropineointment, 2 times daily, polymyxin B–trimethoprim, and 1% prednisoloneacetate. Atropine therapy was slowly tapered over months. Visual acuity 4years later was 10/16 OU and IOP was normal at 8.0 mm Hg OU.

Case 6

A 55-year-old woman underwent uneventful extracapsular cataract extractionwith phacoemulsification and placement of a posterior chamber intraocularlens in the left eye on March 7, 1995. On the first postoperative day, shereported a mild headache. Visual acuity was 20/200 OS pinholing to 20/80 OS.The wound was secure and intact with a deep anterior chamber and a moderate(2+) cellular reaction. Intraocular pressure was 6 mm Hg. Combined therapywas started with polymyxin B–trimethoprim and 1% prednisolone phosphateeyedrops.

On evaluation 2 days later, her visual acuity was unchanged. There wasa negative Seidel sign. There was no filtration bleb noted. The cornea wasmildly edematous and guttata were observed. The IOP was 4.0 mm Hg. On gonioscopy,a small cyclodialysis cleft was noted superiorly. Funduscopic examinationshowed no evidence of retinal detachment or hypotonous maculopathy. One percentatropine, 2 times daily, was added to her treatment regimen.

Five days later, she was doing very well. Her visual acuity was 20/200pinholing to 20/40 OS. The eye was quiet with a secure wound. Intraocularpressure was 14.0 mm Hg OS and the cyclodialysis cleft was closed on gonioscopy.Atropine therapy was tapered over 2 weeks. One month after surgery, her visualacuity was 20/40 OS. Intraocular pressure was 13.0 mm Hg bilaterally. Thewound was well healed. The posterior chamber intraocular lens was well positioned.Funduscopic examination revealed no abnormality. The patient underwent YAG-lasercapsulotomy at her 3-month postoperative visit. The patient's visual acuitywas 20/20 OS following that procedure.

Case 7

A 52-year-old man was referred to the retina service at our institutionin January 2002 because of decreased vision in the left eye. This patienthad a history of blunt trauma to the left eye in August 1999. He developeda traumatic cataract that was successfully removed by extracapsular cataractextraction in January 2000. There were no surgical or postoperative complications.Postoperatively, visual acuity was 20/25 OS, but gradually his visual acuitydecreased. He also had persistent anterior chamber reaction. He was treatedwith 1 drop of 2% cyclopentolate, every other day, and 1% prednisolone acetateeyedrops, 4 times daily, by his primary ophthalmologist. He was noted to havesome posterior retinal changes and was referred for retinal evaluation.

On presentation, the patient reported painless, persistent, decreasedvision. Visual acuity was 20/20 OD and 20/80 pinholing to 20/50 OS. He hada trace afferent pupillary defect in the left eye. Slitlamp examination ofthe eyelids, conjunctiva, and cornea were unremarkable. Anterior chamberswere deep and quiet. Intraocular pressure was 16.0 mm Hg OD and 6.0 mm HgOS. Funduscopic examination revealed chorioretinal folds through the maculaand optic disc swelling of the left eye.

The patient was referred that day to the glaucoma service where gonioscopyrevealed a superior cyclodialysis cleft encompassing 2 to 3 clock hours inthe left eye. Because the patient had been receiving cyclopentolate for almost1 year, the decision was made to use an argon laser to close the cleft. Hewas discharged from clinic receiving 1% atropine, 4 times daily, to the lefteye while awaiting argon laser treatment.

No changes were noted in 3 to 4 weeks, so he underwent argon laser treatment.The patient received 95 spots of 1500-mW power, 100-µm spot size, for0.1-second duration to the cyclodialysis cleft. Four days afterward, the patientwas examined and was found to have an IOP of 8 to 9 mm Hg by applanation;the cyclodialysis cleft remained open. He underwent a second argon laser treatmentof 1500 mW, 50-µm spot size, 0.1-second duration, and 45 spots to thecyclodialysis cleft.

Two days following his last argon laser treatment, the patient was seenin the emergency department reporting pain and blurred vision in the lefteye. His visual acuity was hand motions OS. He exhibited moderately severe(3+) conjunctival hyperemia, microcystic corneal edema, and hazy view of theposterior segment in the left eye. Intraocular pressure was 53.0 mm Hg OS.No view of angle was seen with gonioscopy. Intraocular pressure was reducedby using a combination therapy of glycerin, acetazolamide, timolol maleate–dorzolamidehydrochloride, and brimonidine tartrate. The patient's IOP was lowered to31.0 mm Hg over a few hours and he experienced improved visual acuity of 20/300OS and decreased corneal edema.

The next day, the IOP was 14.0 mm Hg. The patient continued the instillationof 1% atropine, 4 times daily, in the left eye. Four days later, the patientwas noted to have decreased hypotony maculopathy. At his last visit, 2 monthsafter argon laser treatment, visual acuity was 20/50 OS, IOP was 13.0 mm Hg,optic nerve edema was resolved, and chorioretinal folds had disappeared. Hewas sent back to the referring physician with instructions to taper the atropinetherapy.


A cyclodialysis cleft, resulting from the disruption of the meridionalciliary muscle insertion into the scleral spur, may result in ciliochoroidaldetachment and ocular hypotony.3-5 In1900, Fuchs6 reported separation of theciliary body and choroid following cataract extraction noted in pathologicanalysis. His observations suggested that there was a direct communicationbetween the anterior chamber and suprachoroidal space. Based on the observation,Heine7 described a new operation for aphakicglaucoma, which he termed, "cyclodialysis procedure." In 1932, Elschnig8 reported on the pathologic findings in an eye 14years after the cyclodialysis procedure was performed. He noted a direct communicationbetween the anterior chamber and suprachoroidal space accompanied by a choroidaldetachment.

Whether performed as a treatment for aphakic glaucoma, inadvertentlyproduced following surgery on the anterior segment of the eye, or resultingfrom blunt trauma to the eye, persistent hypotony due to cyclodialysis isan uncommon but significant complication. An analysis of complications ina large series of cyclodialysis procedures revealed that hypotony was presentin 24 (9%) of 291 cases.9 The magnitudeof the hypotony is not proportional to the size of the cyclodialysis cleft.9 The mechanism of this hypotony is presumed to beinternal filtration, decreased aqueous production, or both.10 Chandlerand Maumenee11 believe that there is a generalizeddetachment of the ciliary body in postcyclodialysis hypotony.

Hypotony may result in choroidal effusion, retinal thickening and folding,optic disc edema, macular edema, cataract, and shallow anterior chamber. Reducedvisual acuity may be due to cataract; however, the major cause of visual lossis because of transudation of protein-rich fluid from the posterior bloodvessels into the subretinal space in the posterior pole. Loss of vision causedby macular edema may become permanent if the condition is undetected and untreated.

It is speculative as to why and how patients develop cyclodialysis cleft.Unrecognized trauma to the angle and adjacent structures at the time of lensimplantation may be the cause of inadvertent cyclodialysis. The most commoncause of hypotony after cataract extraction is a leaking wound. Ocular hypotonyitself is the most frequent cause of ciliochoroidal detachment following cataractextraction. Therefore, in all cases, prior to considering cyclodialysis cleft,a wound leak should be ruled out. Other causes for persistent hypotony suchas retinal detachment, chronic inflammation, and anterior segment ischemiaalso should be excluded. Nevertheless, inadvertent cyclodialysis cleft resultingfrom extracapsular cataract extraction is a significant cause of persistentocular hypotony following such procedures.

A careful gonioscopic examination of the anterior chamber angle is thekey element in the diagnosis of iatrogenic or traumatic cyclodialysis cleft.Sometimes it is difficult to see the cleft itself, as it is often small andobscured by a narrowed anterior chamber angle. A shallow chamber generallyis caused by diffuse choroidal effusion that leads to forward displacementof the lens iris diaphragm. It has been suggested that anterior chamber deepeningby the injection of a viscoelastic agent into the anterior chamber may facilitatevisualization of the cleft.12 Sometimesimmersion B-scan ultrasound may be helpful in the diagnosis of the small cyclodialysiscleft.13 Diagnosis of cyclodialysis cleftusing conventional ultrasonography with a microconvex ultrasound probe of9-MHz frequency has been described.14 Morerecently, high-resolution ultrasound biomicroscopy has been used to providedetailed information about the extent and location of a cyclodialysis cleft.15,16

Once the diagnosis of cyclodialysis is made, medical treatment consistingof topical 1% atropine, 2 to 3 times daily, should be attempted for up to6 weeks. Miotics and corticosteroids should be avoided. A cyclodialysis cleftthat results in ocular hypotony unaccompanied by significant ocular structuralor functional abnormalities probably does not require treatment.

Since 1990, we have diagnosed cyclodialysis cleft in 7 patients: 1 eye(14.3%) following blunt ocular trauma, 5 eyes (71.4%) following extracapsularcataract extraction, and 1 eye (14.3%) after trabeculotomy. In 2 patients,ocular hypotony had been present 1 to 2 weeks prior to the diagnosis, in 3patients within 3 to 5 months, and in 2 patients more than 1 year. Four (57.1%)of 7 eyes responded to medical therapy alone and the hypotony was reversedwithin 1 week after initiation of 1% atropine therapy. Two (28.6%) of 7 eyeshad successful closure of the cleft with argon laser photocoagulation directedto the cyclodialysis cleft. One (14.3%) of 7 eyes (1 pediatric patient) requiredsurgical closure of the cleft, as she was unable to cooperate at the slitlampfor attempts at argon laser closure of the cleft.

Argon laser therapy for cyclodialysis induced ocular hypotony was usedfor the first time by Joondeph.17 The hypotonywas reversed following 2 sessions of argon laser treatment. He suggested apower of 400 to 800 mW, 200-µm spot size, and 0.1- to 0.2-second duration.Multiple other investigators have described success with argon laser treatment.3,18,19 The mechanismby which laser treatment causes reversal of hypotony is unknown. Harbin18 assumes that swelling of the choroid followinglaser treatment closes the cleft and blocks aqueous flow into the suprachoroidalspace, or, perhaps, the iritis that is caused by the treatment plays a rolein altering the aqueous humor composition, thereby obstructing drainage.

Other methods of laser photocoagulation of cyclodialysis clefts havebeen successful. Alward et al20 used a modifiedendophotocoagulator probe as an external source to treat the eye of a 7-year-oldboy with a traumatic hypotonous cyclodialysis cleft after he failed to respondto medical treatment. In this technique, the endophotocoagulator is adaptedfor use with the Swan-Jacobs goniolens to more directly focus treatment toa cleft that is particularly difficult to visualize. Caronia et al21 accomplished diagnosis and treatment of cyclodialysiscleft by directly imaging and treating the cleft with an endoscopic laser,with the need for a goniolens. Brooks et al22 describeclosure of a persistent cyclodialysis cleft in 3 patients using transcleralYAG laser photocoagulation with 6-J power, 20 applications, 2 to 3 mm behindthe limbus in the area of the suspected cleft. Krohn23 reportedusing external transconjunctival cryotherapy at the presumed location of acyclodialysis cleft to obtain successful cleft closure in a hypotonous eyefollowing trabeculotomy ab externo.

If laser photocoagulation or noninvasive methods of cleft closure fail,a number of surgical interventions such as direct cyclopexy, ciliochoroidaldiathermy, anterior scleral buckling, or vitreoretinal procedures may be performed.In direct cyclopexy, the detached ciliary body is sutured to the sclera nearthe opening of the cleft under direct visualization.24,25 Asimilar result can be obtained by suturing the iris base into the circumferentiallimbal stab incisions under a partial-thickness scleral flap.26 In1971, Maumenee and Stark1 proposed the applicationof penetrating diathermy in the area surrounding the cleft following drainageof suprachoroidal fluid. They treated 6 patients with persistent hypotonydue to cyclodialysis cleft—3 patients following intracapsular cataractextraction, 1 patient after surgical peripheral iridectomy, and 2 patientsfollowing intentional cyclodialysis procedure. In some complicated cases,anterior scleral bucking with cryotherapy or diathermy has been successful.27

Helbig and Foerster28 described managementof hypotonous cyclodialysis with pars plana vitrectomy, gas tamponade, andcryotherapy. Most recently, Hoerauf et al29 describedsuccessful treatment of a traumatic cyclodialysis cleft of a severe and chronicnature with vitrectomy, cryotherapy, and gas endotamponade with the principleof direct mechanical apposition of the detached ciliary muscle to the scleralspur by the gas bubble and scar induction by cryotherapy. It is our beliefthat these kind of invasive procedures should be reserved for those casesthat do not respond to medical treatment, laser treatment, or direct cyclopexy.

When the cyclodialysis cleft is closed, whether with 1% atropine therapy,argon laser treatment, or invasive surgery, there may be a period of acuteocular hypertension in the 2 weeks following the closure. This hypertensionis caused by collapse of the aqueous drainage channels during the prolongedhypotony period and inability to reestablish drainage once the IOP is restored.13 The onset of this hypertensive episode tends tobe delayed for several days following laser treatment; however, early pressurerise is common after surgical correction.30 Medicaltreatment with β-blockers, carbonic anhydrase inhibitors, and hyperosmoticagents is indicated during the hypertensive stage. Miotics are contraindicated,as they could lead to opening of the cleft.

Remarkable visual recovery often occurs when the hypotony is reversed,even after several years' duration.30,31 Delgadoet al31 recently described a patient whohad a 7-year history of hypotony prior to argon laser photocoagulation andgained improvement in visual acuity from 20/200 to 20/30 following cleft closure.Similarly, retinal choroidal changes and optic disc edema usually respondto normalization of IOP.

The clinician must suspect the presence of cyclodialysis cleft in anypatient exhibiting persistent ocular hypotony following surgical or nonsurgicalocular trauma. Treatment options are variable and with proper recognitionand therapy, most of these patients may have restoration of ocular functionand vision.

The authors have no relevant financial interest in this article.

Corresponding author and reprints: Ali Aminlari, MD, Penn State University,Milton S. Hershey Medical Center, Department of Ophthalmology, PO Box 850,Hershey, PA 17033 (e-mail:

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