Continually Updated Clinical Reference
 
 
  All Sources     eMedicine     Medscape     Drug Reference     MEDLINE
 
eMedicine - Glaucoma, Malignant : Article by

Quick Find
Authors & Editors
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
Miscellaneous
Multimedia
References

Related Articles
Choroidal Detachment

Pupillary Block, Aphakic

Pupillary Block, Pseudophakic




Patient Education
Glaucoma Center

Glaucoma FAQs

Understanding Glaucoma Medications


AUTHOR AND EDITOR INFORMATION

Section 1 of 11 Click here to go to the next section in this topic  

Author: Mauricio E Pons, MD, Associate in Private Practice, Charles A Garcia, MD, PA

Mauricio E Pons is a member of the following medical societies: American Academy of Ophthalmology and Association for Research in Vision and Ophthalmology

Coauthor(s): Bret A Hughes, MD, Assistant Professor, Department of Ophthalmology, Kresge Eye Institute, Wayne State University

Editors: Neil T Choplin, MD, Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences; Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles; Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc; Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri; Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Author and Editor Disclosure

Synonyms and related keywords: malignant glaucoma, ciliary block glaucoma, aqueous misdirection syndrome, ciliovitreolenticular block, ciliolenticular glaucoma, ciliolenticular block glaucoma, ciliovitreal block glaucoma, direct lens block angle-closure glaucoma, blindness, vision loss

INTRODUCTION

Section 2 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Background

In 1869, von Graefe first used the term malignant glaucoma to describe an entity characterized by elevated intraocular pressure (IOP) with a shallow or flat anterior chamber in the presence of a patent peripheral iridectomy. In its classic form, malignant glaucoma is rare but one of the most serious complications of glaucoma filtration surgery in patients with narrow-angle or angle-closure glaucoma.

The term malignant glaucoma refers to a sustained ongoing process that is difficult to treat and characteristically progresses to blindness. It is sometimes unresponsive and occasionally worsened with conventional management. 

Many different terms, including ciliovitreal block and aqueous misdirection syndrome, have been proposed based on diverse unproven pathophysiological and anatomical mechanisms. In the international literature, a common term used to describe a flat anterior chamber is "athalamia."1 However, it seems appropriate to continue using well-established nomenclature.

Pathophysiology

A blockage of the normal aqueous flow at the level of the ciliary body, lens, and anterior vitreous face is believed to cause malignant glaucoma. Posterior misdirection of aqueous humor into the vitreous cavity occurs producing a continuous expansion of the vitreous cavity and increased posterior segment pressure. This accumulation of aqueous fluid in the vitreous cavity causes anterior displacement of the lens-iris diaphragm in phakic and pseudophakic eyes or forward displacement of the anterior hyaloid in aphakic patients. The resulting shallow or flat chamber is believed to exacerbate the condition because of the decreased access of aqueous to the trabecular meshwork. The IOP is often markedly increased but may be normal.

Epstein et al proposed that forward displacement of the vitreous into apposition with the posterior ciliary body caused a decrease in available hyaloid surface, increasing the resistance to flow from the vitreous body.2 Small hyperopic eyes are at higher risk for malignant glaucoma.

Malignant glaucoma has been described following: cataract surgery with or without intraocular implant (aphakic or pseudophakic malignant glaucoma), implantation of a large posterior chamber intraocular lens, cessation of topical cycloplegic therapy, induction of miotic therapy, laser iridotomy, laser capsulotomy, Nd:YAG cyclophotocoagulation, laser sclerotomy, Molteno implantation, Baerveldt glaucoma drainage device implantation, viscoelastic use, intravitreal injection of triamcinolone acetonide, Aspergillus flavus intraocular infection, and acute hydrops in Down syndrome. Malignant glaucoma has also been described spontaneously in an eye with no antecedent of surgery or miotics. A pseudomalignant glaucoma syndrome has been reported after pars plana vitrectomy.

Frequency

United States

Malignant glaucoma has been reported to occur in 0.6-4% of eyes following filtration surgery for angle-closure glaucoma. Trope et al reported that 71% of 14 patients with malignant glaucoma had chronic angle-closure glaucoma.3 Malignant glaucoma also can be a rare complication of extracapsular cataract extraction with posterior chamber intraocular lens implantation.

International

In Germany, Duy and Wollensak reported 2 cases of ciliary block in 9000 patients following cataract extraction.4 However, both patients had previous filtration procedures with temporary shallowing of the anterior chamber postoperatively.

Mortality/Morbidity

Malignant glaucoma remains a difficult clinical problem that results in irreversible blindness if not promptly treated. The surgeon should be aware preoperatively of eyes at risk and observe them closely postoperatively. Early recognition is the most important step to prevent irreversible vision loss.

Age

Trope et al reported that the average age of patients with malignant glaucoma was 70 years.3


CLINICAL

Section 3 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

History

Typically, patients with narrow-angle or acute or chronic angle-closure glaucoma, who recently underwent filtration surgery, present shortly after surgery; however, it can develop months later or even in the absence of surgery.

  • Patients may present with pain and discomfort, increasing redness, blurring, or decreased visual acuity.
  • Pain may be severe enough to cause nausea and induce vomiting, similar to an attack of acute angle-closure glaucoma.
  • Precipitating factors are suture lysis, initiation of miotic therapy, or discontinuation of cycloplegics.
  • Shallowing of the anterior chamber due to wound leak must be ruled out by performing a Seidel test during slit lamp examination.

Physical

  • In malignant glaucoma, slit lamp examination reveals anterior displacement of the lens-iris diaphragm in phakic patients and the anterior hyaloid face in aphakic patients, shallowing of the central and peripheral anterior chamber, and elevated intraocular pressure with a patent iridectomy present.
  • Optically clear spaces can be observed within the vitreous cavity and have been interpreted as pockets of fluid.
  • With the Goldman lens, a completely closed angle can be observed. Choroidal detachments or suprachoroidal hemorrhage should be ruled out using the goniolens mirrors and indirect ophthalmoscopy. The retina should be evaluated for vascular occlusions, and the vitreous should be evaluated for possible hemorrhages. B-mode ultrasound can be extremely useful if direct visualization is not possible.
  • Malignant glaucoma is not caused by pupillary block where laser iridotomy can relieve the flow obstruction. In malignant glaucoma, a patent iridectomy must be demonstrated. If not, a new laser iridotomy must be performed.
  • Ultrasound biomicroscopy has demonstrated anterior rotation of the ciliary body with apposition to the ciliary process in contact with the lens equator and anterior displacement of the ciliary body and lens, causing iridocorneal touch and appositional angle closure in these patients.

Causes

The exact mechanism that leads to malignant glaucoma is not clearly understood. Movement of aqueous humor from the posterior chamber into the vitreous instead of draining to the anterior chamber may be the cause.

  • Malignant glaucoma may occur within hours to days or years after surgery. Most commonly, it is seen after trabeculectomy or surgical iridectomy. This condition may be noted after the cessation of cycloplegic drops or the initiation of miotic therapy after surgery for angle-closure glaucoma.
  • The fellow eye is predisposed strongly to develop malignant glaucoma.
  • In 1954, Shaffer proposed that misdirection of aqueous humor into the vitreous body or around it was the pathogenic mechanism.5
  • In 1972, Levene suggested that malignant glaucoma results from forward movement of the lens with direct closure of the angle intensified by surgery, and it represents a more severe form of angle-closure glaucoma.6 The tone of the ciliary body muscle and the tension of the zonules could explain the anterior movement of the lens.
  • Epstein et al hypothesized that a sustained expansion in total vitreous volume moves available peripheral anterior hyaloid into apposition with the posterior ciliary body increasing the resistance for anterior fluid transfer and causing forward displacement of the lens-iris diaphragm and shallowing of the anterior chamber.2
  • In 1980, Quigley incorporated data from Fatt into this theory and proposed that dehydrated and compressed vitreous with a decreased fluid conductivity establishes a vicious circle of elevated pressure and anterior chamber shallowing.7, 8


DIFFERENTIALS

Section 4 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Choroidal Detachment
Pupillary Block, Aphakic
Pupillary Block, Pseudophakic

Other Problems to be Considered

Suprachoroidal hemorrhage
Overfiltration
Wound leak
Occult annular ciliary body detachment


WORKUP

Section 5 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Imaging Studies

  • A-mode ultrasound is used to measure axial length.
  • B-mode ultrasound can discover occult choroidal effusions or hemorrhages or vitreous hemorrhage.
  • Ultrasound biomicroscopy (UBM) is used to obtain cross-sectional images of the anterior segment, cornea, iris, lens, and ciliary body at 50 µm resolution with a tissue penetration of 5 mm.

Procedures

  • Bleb or wound leaks should be identified and treated first.
  • Because of its simplicity, a new laser iridotomy should be performed if suspicion of pupillary block exists.


TREATMENT

Section 6 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Medical Care

The first line of treatment should be medical. The goal is to decrease aqueous humor production, shrink the vitreous body, and move the iris-lens diaphragm backward. Treatment consists of the following:

  • Cycloplegic agents, including tropicamide, cyclopentolate, and topical atropine, paralyze the sphincter muscle of the ciliary body, increasing zonular tension with flattening and posterior movement of the lens and deepening the anterior chamber.
  • Topical phenylephrine is used to tighten the zonules by stimulating the longitudinal muscle of the ciliary body.
  • Topical beta-blockers, alpha-adrenergic agonists, and topical and oral carbonic anhydrase inhibitors are effective in decreasing aqueous humor production and lowering intraocular pressure, presumably decreasing aqueous misdirection.
  • Osmotic agents used to decrease vitreous volume include oral glycerol or isosorbide, or intravenous mannitol. Hyperosmotic agents are very effective in lowering intraocular pressure and have an onset of action in minutes reaching its maximum peak at 60 minutes. They should be used with caution due to possible metabolic disorders and intravascular volume overload; they are contraindicated in patients with renal or heart failure.
  • Medical treatment works in approximately one half of patients. Medical management should be continued unless intraocular pressure is higher than acceptable, given the state of the optic nerve. Also, flat anterior chamber with lens-corneal touch and increased intraocular pressure is an indication to proceed with surgical therapy. Once the condition resolves, medications can be withdrawn gradually. The condition may recur when therapy is decreased. Atropine may be required indefinitely to prevent recurrences.
  • Bimatoprost, travoprost, and latanoprost are effective new medications for lowering intraocular pressure in patients with glaucoma and ocular hypertension. Prostaglandin analogues reduce intraocular pressure by increasing uveoscleral aqueous outflow; however, their role in the treatment of malignant glaucoma is not clearly defined.

Surgical Care

  • Argon laser can be used through a peripheral iridectomy to diminish the volume of ciliary processes and, therefore, ciliolenticular block. In 1980, Herschler reported that transpupillary laser shrinkage of ciliary processes in aphakic patients was successful in reversing the posterior secretion of aqueous humor and restoring anterior chamber depth.9
  • YAG laser can break the anterior hyaloid to allow free movement of fluid from the vitreous cavity to the anterior chamber. Hyaloidotomy is preferably performed in the peripheral hyaloid through a large peripheral iridectomy to avoid lens injury in phakic patients and to prevent lens capsule or retained cortical material to obstruct the fluid path in pseudophakic patients. Clear media is required to perform laser treatment for optimal focusing.
  • If medical or laser treatment fails or if lens-corneal touch occurs, surgery should be considered.  
    • Pars plana vitrectomy, with or without lensectomy, disrupts the impermeable anterior vitreous face and reduces the vitreous volume. The goal is to create a direct communication between the vitreous cavity and the anterior chamber. In phakic eyes, anterior vitreous is difficult to remove without damaging the lens; therefore, treatment is less likely to succeed.
    • Byrnes et al reviewed the medical records of 21 patients with pars plana vitrectomy surgery for malignant glaucoma.10 Vitrectomy was unsuccessful in alleviating glaucoma in 6 eyes, 5 of them were phakic. Zacharia and Abboud reported a case of malignant glaucoma after pars plana vitrectomy in which the hyaloid face was left intact.11
    • Because pseudophakic patients often have retained cortex in the peripheral capsule, core vitrectomy, anterior hyaloidectomy, and removal of peripheral cortical elements are necessary to create a fluid path from the posterior segment to the anterior chamber. Lynch et al proposed such a method to surgically treat malignant glaucoma in pseudophakic patients.12 A pars plana approach is advised. A core vitrectomy and peripheral anterior hyaloidectomy are performed. A small area of lens zonules and capsule is excised. This is accomplished using low suction with a high-cutting frequency. Visualization through a previous iridectomy reduces complications and risk to the lens optic and haptics. When visualization is poor in spite of the presence of a peripheral iridectomy, the probe tip can be used to gently push against the posterior capsule and lens optic. The haptics can be identified because they distort the iris anteriorly.


MEDICATION

Section 7 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Beta-adrenergic receptor blocking agents

The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous humor production.

Drug NameTimolol (Timoptic)
DescriptionFirst-line treatment. Precise mechanism by which timolol decreases IOP is not well established, although it is thought to be through reduction of aqueous formation.
Adult Dose1 gtt of 0.25% or 0.5% in affected eye bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; bronchial asthma or history of bronchial asthma; COPD; sinus bradycardia; second- or third-degree atrioventricular block; overt cardiac failure; cardiogenic shock
InteractionsOccasionally, mydriasis results from concomitant therapy with epinephrine; potential additive effects on patients receiving oral beta-adrenergic blocking agents; possible atrioventricular conduction disturbances, left ventricular failure, and hypotension with concomitant use of calcium antagonists; avoid coadministration in patients with impaired cardiac function; possible additive effects, hypotension, and marked bradycardia, vertigo, syncope, or postural hypotension with concomitant use of catecholamine-depleting drugs
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in patients with cerebrovascular insufficiency; in myasthenic syndromes, may potentiate muscle weakness; patients with an anaphylactic reaction may be unresponsive to usual dose of epinephrine

Drug NameBetaxolol (Betoptic)
DescriptionCardioselective beta1-adrenergic receptor blocking agent with minimal effect on pulmonary and cardiovascular parameters. Precise mechanism by which betaxolol decreases IOP is thought to be through reduction of aqueous formation.
Adult Dose1 gtt of 0.25% in affected eye(s) bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; sinus bradycardia greater than first-degree; atrioventricular block; cardiogenic shock; overt cardiac failure
InteractionsPotential additive effects on patients receiving oral beta-adrenergic blocking agents; possible additive effects, hypotension, and marked bradycardia with concomitant use of catecholamine-depleting drugs; caution in patients using adrenergic-psychotropic drugs concomitantly
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMay be absorbed systemically; death due to bronchospasm in patients with asthma and death in association with cardiac failure have been reported; may mask signs and symptoms of acute hypoglycemia and certain clinical signs of hyperthyroidism; abrupt withdrawal might precipitate a thyroid storm in patients suspected of developing thyrotoxicosis; in myasthenic syndromes, may potentiate muscle weakness; may need to be withdrawn gradually prior to general anesthesia because of reduced ability of the heart to respond to sympathetic reflex stimuli; patients with an anaphylactic reaction may be unresponsive to usual dose of epinephrine

Drug NameCarteolol hydrochloride (Cartrol, Ocupress)
DescriptionNonselective beta-adrenergic receptor blocking with intrinsic sympathomimetic activity. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation.
Adult Dose1 gtt of 1% in affected eye(s) bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; bronchial asthma or history of bronchial asthma; COPD; sinus bradycardia; overt cardiac failure; cardiogenic shock; second- or third-degree atrioventricular block
InteractionsPossible additive effects, hypotension, and marked bradycardia, vertigo, syncope, or postural hypotension with concomitant use of catecholamine-depleting drugs; use of 2 or more beta-adrenergic receptor blocking agents not recommended
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsPatients with anaphylactic reaction may be unresponsive to usual dose of epinephrine; caution in diabetes mellitus, thyrotoxicosis, and cerebrovascular or pulmonary insufficiency

Drug NameLevobunolol hydrochloride (Betagan, AKBeta)
DescriptionNoncardioselective beta-adrenergic receptor blocking agent. Precise mechanism by which levobunolol decreases IOP is thought to be through reduction of aqueous formation.
Adult Dose1 gtt of 0.25% or 0.5% in affected eye(s) qd/bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; bronchial asthma or history of bronchial asthma; COPD; sinus bradycardia; overt cardiac failure; cardiogenic shock; second- or third-degree atrioventricular block
InteractionsOccasionally, mydriasis results from concomitant therapy with epinephrine; possible additive effects of hypotension, bradycardia, vertigo, syncope, or postural hypotension with concomitant use of catecholamine-depleting drugs or systemic beta-adrenergic blocking agents; possible atrioventricular conduction disturbances, left ventricular failure, and hypotension with concomitant use of calcium antagonists; avoid coadministration in patients with impaired cardiac function; use of 2 or more beta-adrenergic receptor blocking agents not recommended
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in cerebrovascular or pulmonary insufficiency

Drug NameMetipranolol (OptiPranolol)
DescriptionNonselective beta-adrenergic receptor blocking agent. Precise mechanism by which metipranolol decreases IOP is thought to be through reduction of aqueous formation.
Adult Dose1 gtt 0.3% in affected eye(s) bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; bronchial asthma or history of bronchial asthma; COPD; sinus bradycardia; second- or third-degree atrioventricular block; overt cardiac failure; cardiogenic shock
InteractionsPossible additive effects, hypotension, and marked bradycardia, vertigo, syncope, or postural hypotension with concomitant use of catecholamine-depleting drugs; possible atrioventricular conduction disturbances, left ventricular failure, and hypotension with concomitant use of calcium antagonists; avoid coadministration in patients with impaired cardiac function and concomitant administration with adrenergic psychotropic drugs; potential additive effects on patients receiving oral beta-adrenergic blocking agents; use of 2 or more beta-adrenergic receptor blocking agents not recommended
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in cerebrovascular, cardiac, or pulmonary insufficiency

Drug Category: Alpha2-adrenergic receptor agonists

May decrease IOP by reducing aqueous humor production.

Drug NameApraclonidine HCl (Iopidine)
DescriptionReduces elevated, as well as normal, IOP whether accompanied by glaucoma or not. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. It has minimal cardiovascular effects. Generally used in short-term therapy.
Adult Dose1 gtt of 0.5% or 1% in affected eye(s) tid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; patients on MAOIs or have taken them in the past 14 d
InteractionsMonitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in coronary insufficiency, chronic renal failure, recent myocardial infarction, cerebrovascular disease, Raynaud disease, thromboangiitis obliterans, and patients with depression

Drug Category: Oral carbonic anhydrase inhibitors

By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Drug NameAcetazolamide (Diamox)
DescriptionInhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP.
Adult Dose125-250 mg PO q4-6h
Acute situations: 250-500 mg IV initially, then 125-250 mg IV q4-6h; not to exceed 1 g/d
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; history of metabolic or ketoacidosis; hepatic insufficiency; severe COPD; kidney stones; sulfa allergy; blood dyscrasias; possibility of teratogenicity during first trimester of pregnancy
InteractionsCoadministration with high-dose salicylate therapy may increase toxicity; can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsRarely, aplastic anemia has been reported; patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients

Drug Category: Hyperosmotic agents

Lower IOP by creating an osmotic gradient between ocular fluids and plasma. They are not for long-term use.

Drug NameMannitol (Resectisol, Osmitrol)
DescriptionLowers IOP by increasing the osmotic gradient between blood and ocular fluids, resulting in loss of water from the vitreous.
Adult DoseMannitol 20%: 0.25-0.5 g/kg IV
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; pulmonary edema; severe dehydration; cardiac decompensation; anuria
InteractionsUse caution with drugs that may compromise renal or cardiovascular status
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsAvoid long-term use, dehydration, electrolyte imbalance, or congestive heart failure; must be used with caution in patients with hypervolemia, confused mental status, prostatic hypertrophy, and cardiac, renal, or hepatic disease

Drug NameGlycerol (Osmoglyn, Ophthalgan)
DescriptionLowers IOP by increasing the osmotic gradient between blood and ocular fluids, resulting in loss of water from the vitreous.
Adult DoseGlycerol 50%: 1-1.5 g/kg PO bid/qid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; pulmonary edema, severe dehydration, cardiac decompensation, and anuria; in patients with diabetes, may acutely elevate blood glucose levels
InteractionsUse with caution with drugs that may compromise renal or cardiovascular status
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsAvoid long-term use, dehydration, electrolyte imbalance, or congestive heart failure; must be used with caution in patients with hypervolemia, confused mental status, prostatic hypertrophy, and cardiac, renal, or hepatic disease


FOLLOW-UP

Section 8 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Deterrence/Prevention

  • Trabeculectomy surgery modification, including releasable sutures, the use of viscoelastics during the surgery, and the postoperative use of atropine, has been proposed to prevent malignant glaucoma.
  • The fellow eye is at increased risk of developing malignant glaucoma postoperatively. Hyperopic eyes and eyes with short axial length also are at increased risk. Prophylactic iridotomy is recommended if support for occludable angle exists, preferably with avoidance of the use of miotics.

Prognosis

  • The prognosis depends on the length and the severity of the attack. In patients with relatively healthy optic nerves, the prognosis can be good if the attack is abated and intraocular pressure is controlled.

Patient Education


MISCELLANEOUS

Section 9 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Medical/Legal Pitfalls

  • Patients undergoing glaucoma surgery should be informed of the risk of malignant glaucoma.


MULTIMEDIA

Section 10 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic  

Media file 1:  Phakic malignant glaucoma.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Image

Media file 2:  A 70-year-old man with a history of nanophthalmos underwent cataract extraction. Subsequently, he developed malignant glaucoma.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo


REFERENCES

Section 11 of 11 Click here to go to the previous section in this topic Click here to go to the top of this page

  1. Gnad HD. Athalamia as a late complication after keratoplasty on aphakic eyes. Br J Ophthalmol. Jul 1980;64(7):528-30. [Medline].
  2. Epstein DL, Hashimoto JM, Anderson PJ, Grant WM. Experimental perfusions through the anterior and vitreous chambers with possible relationships to malignant glaucoma. Am J Ophthalmol. Dec 1979;88(6):1078-86. [Medline].
  3. Trope GE, Pavlin CJ, Bau A, Baumal CR, Foster FS. Malignant glaucoma. Clinical and ultrasound biomicroscopic features. Ophthalmology. Jun 1994;101(6):1030-5. [Medline].
  4. Duy TP, Wollensak J. Ciliary block (malignant) glaucoma following posterior chamber lens implantation. Ophthalmic Surg. Oct 1987;18(10):741-4. [Medline].
  5. Shaffer RN. The role of vitreous detachment in aphakic and malignant glaucoma. Trans Am Acad Ophthalmol Otol. 1954;58:217.
  6. Levene R. A new concept of malignant glaucoma. Arch Ophthalmol. May 1972;87(5):497-506. [Medline].
  7. Quigley HA. Malignant glaucoma and fluid flow rate. Am J Ophthalmol. Jun 1980;89(6):879-80. [Medline].
  8. Fatt I. Hydraulic flow conductivity of the vitreous gel. Invest Ophthalmol Vis Sci. Jun 1977;16(6):565-8. [Medline].
  9. Herschler J. Laser shrinkage of the ciliary processes. A treatment for malignant (ciliary block) glaucoma. Ophthalmology. Nov 1980;87(11):1155-9. [Medline].
  10. Byrnes GA, Leen MM, Wong TP, Benson WE. Vitrectomy for ciliary block (malignant) glaucoma. Ophthalmology. Sep 1995;102(9):1308-11. [Medline].
  11. Zacharia PT, Abboud EB. Recalcitrant malignant glaucoma following pars plana vitrectomy, scleral buckle, and extracapsular cataract extraction with posterior chamber intraocular lens implantation. Ophthalmic Surg Lasers. Apr 1998;29(4):323-7. [Medline].
  12. Lynch MG, Brown RH, Michels RG, Pollack IP, Stark WJ. Surgical vitrectomy for pseudophakic malignant glaucoma. Am J Ophthalmol. Aug 15 1986;102(2):149-53. [Medline].
  13. Arya SK, Sonika, Kochhar S, Kumar S, Kang M, Sood S. Malignant glaucoma as a complication of Nd:YAG laser posterior capsulotomy. Ophthalmic Surg Lasers Imaging. May-Jun 2004;35(3):248-50. [Medline].
  14. Azuara-Blanco A, Dua HS. Malignant glaucoma after diode laser cyclophotocoagulation. Am J Ophthalmol. Apr 1999;127(4):467-9. [Medline].
  15. Azuara-Blanco A, Katz LJ, Gandham SB, Spaeth GL. Pars plana tube insertion of aqueous shunt with vitrectomy in malignant glaucoma. Arch Ophthalmol. Jun 1998;116(6):808-10. [Medline].
  16. Berger RR, Kenyeres AM, Powell DA. Suspected ciliary block associated with Viscoat use. J Cataract Refract Surg. Apr 1999;25(4):594-6. [Medline].
  17. Brown RH, Lynch MG, Tearse JE, Nunn RD. Neodymium-YAG vitreous surgery for phakic and pseudophakic malignant glaucoma. Arch Ophthalmol. Oct 1986;104(10):1464-6. [Medline].
  18. Cashwell LF, Martin TJ. Malignant glaucoma after laser iridotomy. Ophthalmology. May 1992;99(5):651-8; discussion 658-9. [Medline].
  19. Cekic O, Batman C. Pars plana vitrectomy in the treatment of phakic and pseudophakic malignant glaucoma. Arch Ophthalmol. Jan 1998;116(1):118. [Medline].
  20. Chandler PA, Simmons RJ, Grant WM. Malignant glaucoma. Medical and surgical treatment. Am J Ophthalmol. Sep 1968;66(3):495-502. [Medline].
  21. Dugel PU, Heuer DK, Thach AB, Baerveldt G, Lee PP, Lloyd MA, et al. Annular peripheral choroidal detachment simulating aqueous misdirection after glaucoma surgery. Ophthalmology. Mar 1997;104(3):439-44. [Medline].
  22. Epstein DL, Steinert RF, Puliafito CA. Neodymium-YAG laser therapy to the anterior hyaloid in aphakic malignant (ciliovitreal block) glaucoma. Am J Ophthalmol. Aug 15 1984;98(2):137-43. [Medline].
  23. Greenfield DS, Tello C, Budenz DL, Liebmann JM, Ritch R. Aqueous misdirection after glaucoma drainage device implantation. Ophthalmology. May 1999;106(5):1035-40. [Medline].
  24. Harbour JW, Rubsamen PE, Palmberg P. Pars plana vitrectomy in the management of phakic and pseudophakic malignant glaucoma. Arch Ophthalmol. Sep 1996;114(9):1073-8. [Medline].
  25. Hardten DR, Brown JD. Malignant glaucoma after Nd:YAG cyclophotocoagulation. Am J Ophthalmol. Feb 15 1991;111(2):245-7. [Medline].
  26. Heatley CJ, Lim KS, Siriwardena D, Barton K. Malignant glaucoma as a complication of intravitreal triamcinolone acetonide. Acta Ophthalmol Scand. Oct 2006;84(5):712-3. [Medline].
  27. Jain V, Maiti A, Shome D, Borse N, Natarajan S. Aspergillus-induced malignant glaucoma. Cornea. Jul 2007;26(6):762-3. [Medline].
  28. Johnson DH. Options in the management of malignant glaucoma. Arch Ophthalmol. Jun 1998;116(6):799-800. [Medline].
  29. Levene RZ. Current concepts of malignant glaucoma. Ophthalmic Surg. Aug 1986;17(8):515-8, 520. [Medline].
  30. Liebmann JM, Weinreb RN, Ritch R. Angle-closure glaucoma associated with occult annular ciliary body detachment. Arch Ophthalmol. Jun 1998;116(6):731-5. [Medline].
  31. Little BC. Treatment of aphakic malignant glaucoma using Nd:YAG laser posterior capsulotomy. Br J Ophthalmol. Jun 1994;78(6):499-501. [Medline].
  32. Luntz MH, Rosenblatt M. Malignant glaucoma. Surv Ophthalmol. Sep-Oct 1987;32(2):73-93. [Medline].
  33. Margo CE, Hamed LM. Diagnostic Problems in Clinical Ophthalmology. Saunders; 1993:293.
  34. Massicotte EC, Schuman JS. A malignant glaucoma-like syndrome following pars plana vitrectomy. Ophthalmology. Jul 1999;106(7):1375-9. [Medline].
  35. Mastropasqua L, Ciancaglini M, Carpineto P, Lobefalo L, Gallenga PE. Aqueous misdirection syndrome: a complication of neodymium: YAG posterior capsulotomy. J Cataract Refract Surg. Sep 1994;20(5):563-5. [Medline].
  36. McClellan KA, Billson FA. Spontaneous onset of ciliary block glaucoma in acute hydrops in Down's syndrome. Aust N Z J Ophthalmol. Nov 1988;16(4):325-7. [Medline].
  37. Melamed S, Cahane M, Gutman I, Blumenthal M. Postoperative complications after Molteno implant surgery. Am J Ophthalmol. Mar 15 1991;111(3):319-22. [Medline].
  38. Park M, Unigame K, Kiryu J, Kondo T. Management of a patient with pseudophakic malignant glaucoma; role of ultrasound biomicroscopy. Br J Ophthalmol. Jul 1996;80(7):676-7. [Medline].
  39. Pecora JL. Malignant glaucoma worsened by miotics in a postoperative angle-closure glaucoma patient. Ann Ophthalmol. Sep 1979;11(9):1412-4. [Medline].
  40. Reed JE, Thomas JV, Lytle RA, Simmons RJ. Malignant glaucoma induced by an intraocular lens. Ophthalmic Surg. Mar 1990;21(3):177-80. [Medline].
  41. Robinson A, Prialnic M, Deutsch D, Savir H. The onset of malignant glaucoma after prophylactic laser iridotomy. Am J Ophthalmol. Jul 15 1990;110(1):95-6. [Medline].
  42. Ruben S, Tsai J, Hitchings RA. Malignant glaucoma and its management. Br J Ophthalmol. Feb 1997;81(2):163-7. [Medline].
  43. Schwartz AL, Anderson DR. Malignant glaucoma" in an eye with no antecedent operation or miotics. Arch Ophthalmol. May 1975;93(5):379-81. [Medline].
  44. Tello C, Chi T, Shepps G, Liebmann J, Ritch R. Ultrasound biomicroscopy in pseudophakic malignant glaucoma. Ophthalmology. Sep 1993;100(9):1330-4. [Medline].
  45. Tomey KF, Senft SH, Antonios SR, Shammas IV, Shihab ZM, Traverso CE. Aqueous misdirection and flat chamber after posterior chamber implants with and without trabeculectomy. Arch Ophthalmol. Jun 1987;105(6):770-3. [Medline].
  46. Tsai JC, Barton KA, Miller MH, Khaw PT, Hitchings RA. Surgical results in malignant glaucoma refractory to medical or laser therapy. Eye. 1997;11 (Pt 5):677-81. [Medline].

Glaucoma, Malignant excerpt

Article Last Updated: Feb 29, 2008