Vitreous Block (Malignant Glaucoma, Aqueous Misdirection)

From EyeWiki
(Redirected from Aqueous Misdirection)


All content on Eyewiki is protected by copyright law and the Terms of Service. This content may not be reproduced, copied, or put into any artificial intelligence program, including large language and generative AI models, without permission from the Academy.

Article initiated by:
Manishi Desai, MD, Meenakshi Chaku, MD, Melissa Mei Yiu Wong, MD
All contributors:
Monica K. Ertel, MD, PhD, Ahmad A. Aref, MD, MBA, Dr John Davis Akkara (MBBS, MS, FAEH, FMRF, FAICO), Manishi Desai, MD, Leonard K. Seibold, MD, Srishti Khullar, Harry Quigley
Assigned editor:
Leonard K. Seibold, MD
Review:
Assigned status Update Pending
 by Leonard K. Seibold, MD on May 12, 2023.


Vitreous Block (Malignant Glaucoma, Aqueous Misdirection)
ICD-10
H40.8


Summary

Vitreous block, also referred to as malignant glaucoma and aqueous misdirection, is a form of secondary angle closure glaucoma characterized by elevated intraocular pressure (IOP) and flat central and peripheral anterior chamber, despite the presence of a peripheral iridotomy. There is agreement that it involves abnormal behavior of the vitreous humor, with increasing evidence that the inciting factors include lowering of IOP during surgery, smaller eye size, and choroidal expansion. While medical therapy with cycloplegics and YAG laser treatment to visible vitreous are used, definitive vitrectomy to produce a unicameral eye is most effective.

Disease Description

The term “malignant” was first applied to the immediate post-operative course in eyes with elevation of IOP and axial flattening of the anterior chamber by von Graefe.[1] It was recognized as a rare complication in eyes with acute angle closure glaucoma unresponsive to iridectomy. In 1950, Chandler[2] reported that this uncommon condition was more frequent in smaller eyes, but could occur during or after a variety of surgical procedures for glaucoma. Shaffer noted that the vitreous was involved in the process, advocating incisions of vitreous with needle or knife. This was confirmed by observations of Simmons[3] , who noted that while ciliary processes were sometimes in contact with the lens, complete closure of the space between ciliary body and lens did not occur. It was recognized that bilateral or sequential occurrence in the two eyes was an inherent tendency. Shaffer and Hoskins proposed that the force moving the iris and lens forward to flatten the anterior chamber was due to “misdirected aqueous”, and this term has persisted in both naming the condition[4] and in consideration of its pathogenesis. Surgical vitrectomy to eliminate vitreous block has become the standard of care and its definitive treatment.[5] Since multiple terms are used to describe overlapping entities within the same clinical spectrum, Table 1 summarises the nomenclature and its practical clinical meaning.

Table 1. Nomenclature and practical meaning

Term Practical meaning
Malignant glaucoma Historical term; still commonly used clinically, but potentially misleading because the condition is not malignant in the oncologic sense.
Aqueous misdirection Commonly used term emphasising posterior diversion or trapping of aqueous, with anterior displacement of the lens-iris or IOL-iris diaphragm.
Ciliary block glaucoma An older term emphasising the relationship between ciliary processes, lens equator, zonules, and anterior hyaloid.
Vitreous block Term emphasising resistance to forward fluid movement through the anterior vitreous/anterior hyaloid region, causing a pressure-compartment problem.
Fluid misdirection syndrome A broader umbrella term that can include acute intraoperative and chronic postoperative forms.
Infusion misdirection syndrome Intraoperative variant precipitated or worsened by pressurised irrigation/infusion during anterior segment surgery.
Acute intraoperative fluid misdirection Sudden shallow anterior chamber, iris prolapse, raised posterior pressure, and rock-hard globe during cataract or anterior segment surgery.

Epidemiology

Vitreous block has been reported throughout the world, with an incidence intraoperatively, postoperatively, or rarely without preceding surgery. Reported incidence varies from approximately 0.6 to 4 %, depending on the population studied, surgical context, and diagnostic criteria used.[6][7] The condition most commonly develops unilaterally, but the fellow eye is often involved at a later time or after surgery on the second eye.  It is more common in females, which may coincide with its greater prevalence in angle closure.[8] It has been reported in both phakic, aphakic and pseudophakic eyes.[9].Pseudophakic aqueous misdirection may occur shortly after cataract surgery or be delayed for several years; in one recent series, onset ranged from 1 day to 2920 days after cataract surgery.[10][11] Miotic eye drops are known to precipitate the condition.[12]  It has been reported after many ocular surgical procedures and in a variety of ocular conditions. Risk factors for vitreous block are summarised in Table 2.

Table 2. Risk Factors

Risk factor Clinical relevance
Short axial length Crowded anterior segment and reduced reserve during surgery.
Hyperopia Often associated with smaller ocular dimensions and narrow angles.
Shallow anterior chamber Predisposes to angle crowding and chamber instability.
Primary angle closure / narrow angles Classic anatomic predisposition.
Plateau iris configuration Anteriorly positioned ciliary body may worsen crowding.
Nanophthalmos / microphthalmos Very high-risk anatomy; also associated with uveal effusion risk.
Thick crystalline lens / intumescent cataract Lens-related anterior segment crowding and higher intraoperative pressure shifts.
Prior vitreous block / malignant glaucoma Strong warning sign for recurrence and fellow-eye risk.
Fellow-eye history Important for preoperative planning and counselling.
Prior trabeculectomy or glaucoma drainage device Classical association with postoperative aqueous misdirection.
Miotic use May worsen anterior rotation/crowding and should generally be avoided in suspected cases.
Excessive infusion pressure May precipitate or aggravate acute intraoperative infusion/fluid misdirection.

Etiology and Proposed Mechanisms

The precise underlying mechanism of aqueous misdirection is unknown. Generally, it is understood to result from diversion of aqueous or intraocular fluid into the posterior segment with forward displacement of the lens-iris or intraocular lens-iris diaphragm. This diversion of fluid results from an abnormal relationship between the ciliary body processes, lens, anterior hyaloid face and vitreous body. Several mechanisms have been proposed, including choroidal expansion, anterior rotation of the ciliary body, reduced hydraulic conductivity of the vitreous gel, and impaired forward movement of fluid from the vitreous cavity to the posterior and anterior chambers for the pathogenesis of aqueous misdirection have been proposed (i.e. from pressure differential between the anterior and posterior chambers) [13]. Regardless of the initiating cause, a self-perpetuating cycle may develop in which posterior segment pressure rises, the fluid build-up cannot decompress or exit to balance anterior chamber pressure, resulting in forward movement of the lens-iris diaphragm.

Pathophysiology

The final common pathway in vitreous block is anterior displacement of the lens–iris diaphragm or intraocular lens–iris diaphragm, resulting in uniform shallowing of the central and peripheral anterior chamber and secondary angle closure. Unlike pupillary block, this process persists despite a patent iridotomy because the principal resistance to forward fluid movement lies posterior to the iris, at the level of the anterior hyaloid, vitreous body, zonules, ciliary body, lens, or intraocular lens complex[14].

Several clinical observations support the role of the vitreous and anterior hyaloid interface. Iridectomy or iridotomy alone usually does not reverse the condition, whereas disruption of the anterior hyaloid face or vitrectomy may break the acute cycle. Surgical success is greatest when a communication is created between the anterior chamber, posterior chamber, and vitreous cavity, such as by irido-zonulo-hyaloidectomy or pars plana vitrectomy with irido-zonulectomy[8].

Choroidal expansion hypothesis

Choroidal expansion has been proposed as an important initiating or amplifying event. In susceptible eyes, especially short eyes and with primary angle closure, even a relatively small increase in choroidal volume can increase posterior segment pressure and promote forward movement of the lens–iris diaphragm. The choroid occupies about 2% of the internal volume of the normal eye and over 4% of smaller eyes (prone to angle closure) due to thicker choroid and smaller overall volume. Based on the known pressure—volume relationship of the living eye, even a tripling of the normal choroid thickness of ~300 µm would increase IOP to over 60 mm Hg.[15] Yoga head-standing doubles IOP[16] and the Valsalva effect of trumpet playing increases IOP to 40 mm Hg with only a 20% increase in choroidal thickness measured by ultrasonic biomicroscopy.[17] These increases in the posterior 2/3 of the eye would increase aqueous outflow from the posterior and anterior chambers as a response to the pressure differential.

This may explain why vitreous block is more common in eyes with crowded anterior segments and why it may occur after intraocular surgery, when sudden anterior segment decompression can create a posterior-to-anterior pressure gradient.[18]

Choroidal volume could increase by an increase in either its intravascular or extravascular spaces. Intravascular choroidal expansion would be very short term (e.g. Valsalva, tight necktie) and not sufficiently sustained to cause vitreous block. It is thus more likely that abnormal permeability of the choriocapillaries or larger vessels allows large proteins into its extravascular stroma. Angle closure eyes have greater propensity for choroidal expansion,[19] likely contributing to their propensity to vitreous block. The pressure difference from posterior to anterior eye induced by anterior segment surgical incisions potentiates choroidal expansion intra-operatively.

Once expansion of the choroidal stroma by serous fluid occurs, its exit through the sclera is slow, since the normal osmotic pressure to return fluid to the veins is gone. Fluid within the vitreous chamber must pass into the posterior chamber through the Berger's space. Vitreous that is compressed in this space blocks further fluid movement forward. Thus, sustained higher pressure in the vitreous cavity allows vitreous block in susceptible eyes.

Optical coherence tomography studies have provided support for the choroidal component of this mechanism. Increased choroidal thickness has been reported in eyes with malignant glaucoma. Choroidal vascularity index changes have been described in malignant glaucoma after trabeculectomy for primary angle closure glaucoma[20][21].

Vitreous Hydraulic Resistance

The older term “aqueous misdirection” implies simple posterior diversion of aqueous through or behind the vitreous. However, experimental studies suggest that simple misdirection of aqueous alone is unlikely to fully explain the condition. Epstein and colleagues found that factors other than, or in addition to, posterior diversion of aqueous must be involved, and proposed that reduced permeability or altered hydraulic conductivity of the vitreous may contribute to the syndrome[22][23]. If fluid from the vitreous cavity moves to replace the departing aqueous, the anterior chamber would remain formed and IOP would return to normal. This compensation to reduce IOP fails in eyes with vitreous block. Studies of normal vitreous humor show its ability to transmit water across the gel is finite and decreases when the pressure differential across it is higher.[23] Studies in post mortem human eyes found that “differences in composition or structure can have an important influence on the permeability of the vitreous body”.[22] This suggests that eyes with vitreous block have either a low water conductivity or a greater tendency to compress under pressure,[24] leading to a vicious cycle that carries the vitreous, lens and iris forward until the anterior chamber completely empties.[18]

Shaffer recognized that aqueous misdirection behind or through the vitreous required a one-way valve mechanism,[25] but no evidence has been presented to support this mechanism. Epstein concluded from experiments with human eyes that “there must be factors other than, or in addition to, diversion of aqueous humor through the vitreous body to explain this condition. It seems in malignant glaucoma that the permeability of the vitreous humor must be less than normal”.[22]Thus, the terms aqueous misdirection and ciliary block are not compatible with present evidence and a recent review confirms vitreous block[14]  as an appropriate designation for the condition.

Clinical Features

The clinical features of this condition include the following:

1) The vitreous appears relatively opaque and either disruption of the gel or its removal can break the acute cycle[24].

2) Elimination of pupil block by iridectomy is not effective.

3) The iris and lens are so far anteriorly that the chamber is typically emptied of aqueous humor, leading to high IOP.

4) Expansion (thickening) of the choroid is now recognized as a feature identified by optical coherence tomography[20][21] in both acutely involved and fellow eyes, compared to eyes with angle closure disease or open angles.

Surgical implication

The pathophysiology explains why cycloplegia, aqueous suppression, and hyperosmotic therapy may temporarily improve the condition, but may not be definitive in persistent cases. Cycloplegia moves the lens–iris diaphragm posteriorly and may widen the ciliary body–lens/IOL space; aqueous suppressants and hyperosmotic agents reduce fluid production and posterior segment volume. Definitive treatment often requires disruption of the anterior hyaloid–zonular barrier and removal of obstructing anterior vitreous to create a unicameral eye[26]. Intraoperative fluid or infusion misdirection can be understood as an acute form of the same pressure-compartment disorder. Pressurized irrigation during cataract or anterior segment surgery may aggravate posterior fluid displacement in a susceptible eye, producing sudden anterior chamber shallowing, iris prolapse, raised posterior pressure, and a firm globe. This clinical presentation is described as “Acute Intraoperative Fluid Misdirection.”

Acute Intraoperative Fluid Misdirection During Cataract Surgery

Acute intraoperative fluid misdirection syndrome (AIFMS) is an uncommon but important intraoperative presentation of the vitreous block spectrum during cataract surgery. It is characterized by sudden shallowing of the anterior chamber, marked elevation of intraocular pressure, globe hardening, iris prolapse, and ina[27]bility to maintain the surgical space, in the absence of suprachoroidal hemorrhage, choroidal effusion, wound leak, or external globe compression. The proposed mechanism involves misdirection of irrigating fluid through the zonules into the retrolenticular space, including Berger’s space, with forward displacement of the lens–iris or intraocular lens–iris diaphragm[28][29][30]. Intraoperative warning signs of acute fluid misdirection are summarised in Table 3.

Table 3. Intraoperative warning signs of acute intraoperative fluid misdirection

Sign Interpretation
Sudden uniform shallowing of the anterior chamber Suggests forward displacement of the lens-iris or IOL-iris diaphragm.
Iris prolapse through the incision Indicates raised posterior pressure and loss of chamber stability.
Firm or rock-hard globe Suggests acute intraocular pressure rise.
Anterior chamber cannot be maintained despite OVD Ongoing posterior pressure or misdirection should be suspected.
Worsening during irrigation/infusion Supports infusion-related misdirection.
No wound leak but progressive chamber shallowing Points away from hypotony/wound leak and toward posterior pressure mechanism.
Patent PI but persistent shallow AC Pupillary block is less likely; true misdirection may persist.
Poor red reflex or severe pain Red flag warranting urgent ruling out of suprachoroidal hemorrhage or expulsive event.

Diagnosis

The diagnosis is clinical and should be considered when there is uniform shallowing or flattening of both the central and peripheral anterior chamber with elevated, or occasionally normal, intraocular pressure. [13]A patent iridotomy or iridectomy helps exclude pupillary block.

  • The involved eye usually shows marked anterior chamber asymmetry compared with the fellow eye. The anterior chamber of the affected eye is flat or nearly so, often with lens to corneal contact.
  • Ocular pain and decreased visual acuity result from IOP elevation and forward lens movement.
  • A history of vitreous block in the first eye is important, since occurrence in the second eye is likely.
  • The condition is more likely in those with angle closure disease, but can occur in any eye.
  • Wound leak should be ruled out.
  • B-scan ultrasound examination or posterior OCT images often show thickening of the choroid, though this can be only 3 times normal thickness without clear separation of choroid from sclera.
  • Imaging modalities and diagnostic adjuncts for this condition are highlighted in Table 4.


Table 4 . Imaging and diagnostic adjuncts

Modality Utility
Slit-lamp examination and gonioscopy Documents central/peripheral AC shallowing, angle closure, wound status, and pupillary block features.
Ultrasound biomicroscopy (UBM) Evaluates ciliary body rotation, supraciliary effusion, plateau iris, anterior hyaloid region, and IOL/ciliary body relationship.
Anterior segment OCT Assesses AC depth, angle anatomy, iris configuration, and anterior chamber response to therapy.
B-scan Ultrasound Rules out suprachoroidal hemorrhage or choroidal effusion when fundus view is poor.
Posterior segment OCT / EDI-OCT Assesses choroidal thickening and posterior segment complications.
OCT Macula after surgery/vitrectomy Useful for cystoid macular edema surveillance and postoperative visual recovery assessment.
Biometry Axial length and ACD help identify high-risk short/crowded eyes before surgery.

Differential diagnosis

Vitreous block should be differnertiated from other causes of a shallow or flat anterior chamber because the management and urgency differ substantially. The key differentials and their distinguishing features are summarised in Table 5.

Table 5. Key differentiating features of vitreous block and common causes of shallow anterior chamber

Feature Vitreous block / aqueous misdirection Pupillary block Suprachoroidal hemorrhage Choroidal effusion / detachment Wound leak / overfiltration Positive vitreous pressure
Typical setting After glaucoma surgery, cataract surgery, laser procedures; may occur intraoperatively or spontaneously Narrow angles, blocked/absent PI, postoperative inflammation Intraoperative or early postoperative period, especially after intraocular surgery Postoperative hypotony, nanophthalmos, inflammation, uveal effusion Early postoperative period after filtering surgery or leaking cataract wound During surgery; tight speculum, squeezing, Valsalva, obesity, retrobulbar pressure
Anterior chamber depth Uniform shallowing of central and peripheral AC Peripheral AC shallow with iris bombe; central AC may be relatively deeper Sudden severe AC shallowing or collapse Shallow AC, often with visible choroidal elevation Shallow or flat AC Shallowing tendency during surgery
IOP Usually high; may occasionally be normal High Usually very high, tense painful eye Often low, but may be normal/high in some cases Usually low/soft eye Variable; globe may feel firm due to posterior pressure
Pain Variable; due to high IOP/corneal-lens touch Ocular pain/headache common Severe sudden pain, often dramatic Mild to moderate discomfort Usually mild unless hypotony severe Usually absent unless patient squeezing/anesthesia inadequate
Iridotomy / iridectomy effect Does not resolve condition if true vitreous block Relieves pupillary block if patent and adequate No therapeutic effect No therapeutic effect No therapeutic effect No therapeutic effect
Iris configuration Iris-lens/IOL diaphragm displaced forward; no classic iris bombe Iris bombe typical AC collapse; may have tissue prolapse in severe cases Forward rotation may occur with ciliochoroidal effusion Iris may be apposed forward due to hypotony Iris may prolapse due to posterior pressure
Fundus clue May show choroidal thickening; no large hemorrhagic choroidal detachment Usually no choroidal detachment Dark hemorrhagic choroidal elevation, loss of red reflex Serous choroidal elevation/detachment Hypotony signs; choroidal folds/detachment possible Usually no true choroidal pathology
B-scan ultrasound May show choroidal thickening without frank detachment Usually unremarkable posteriorly Hemorrhagic choroidal detachment Serous choroidal detachment/effusion May show hypotony-related choroidal detachment Usually normal
Response to cycloplegia Often helpful; pulls lens-iris diaphragm posteriorly May not be definitive unless block relieved Not definitive May help if ciliary body rotation present Not primary treatment Variable
Effect of miotics May worsen condition May worsen angle crowding; not preferred acutely No benefit No benefit No benefit No benefit
Main immediate management Aqueous suppression, cycloplegia, hyperosmotics; laser/surgical hyaloid disruption or vitrectomy if persistent Patent PI/iridectomy + IOP control Close wounds urgently, raise IOP, urgent retina help Treat underlying hypotony/inflammation; cycloplegia/steroids; drainage rarely Seal wound, manage hypotony/overfiltration Remove external pressure, deepen anesthesia, reduce squeezing/Valsalva
Key differentiating point Flat/shallow central and peripheral AC despite patent PI Improves after adequate PI Sudden painful event with hemorrhagic choroidal detachment Choroidal detachment/effusion on exam or B-scan, often low IOP Soft eye with leak/overfiltration Intraoperative external/posterior pressure without true misdirection

The most useful bedside distinction is that vitreous block produces uniform shallowing of both the central and peripheral anterior chamber and persists despite a patent iridotomy, whereas pupillary block improves after iridotomy. Suprachoroidal hemorrhage must be excluded urgently in any sudden painful intraoperative or postoperative anterior chamber collapse.

Management

Medical Management

Maximum IOP-lowering should be delivered topically (without pilocarpine) and with acetazolamide orally.

  • Cycloplegic drops are recommended[31] to widen the ciliary body ring of space to the lens, allowing more fluid transfer from vitreous to posterior chamber.
  • Osmotic agent intravenously or orally decrease fluid from the choroid and vitreous, especially as part of intraoperative management.
  • Anti-inflammatory eye drops may be given.
  • Oral pain relief by narcotic may be needed.
  • If IOP is not relieved nor the chamber reformed within days, surgery should be planned.
  • If the acute condition resolves medically, long-term cycloplegia is continued.

Laser Management

  • If an iridotomy is not present nor clearly patent, it should be made, though the flat anterior chamber makes this difficult.
  • YAG laser delivery to disrupt the vitreous gel has occasionally aborted vitreous block.[32] The energy is placed ideally in the zonular area through an existing iridectomy, or posterior to the lens or IOL-capsule area. While the vitreous may be compressed anteriorly, YAG treatment often cannot produce a channel adequate to allow freer fluid passage.
  • Slit lamp delivery of diode (“argon”) laser to ciliary processes was reported[33] to alleviate vitreous block prior to the development of YAG lasers. It is uncomfortable and not preferred to YAG laser.

Surgical Management

Surgical therapy is frequently necessary to definitively manage aqueous misdirection. In a retrospective review of 26 eyes from 24 patients with aqueous misdirection from a single center, all but one case required surgery eventually within 3 months of presentation.[34] If the patient is refractory to both medical and laser management of aqueous misdirection, surgery is necessary to disrupt the anterior vitreous face or remove vitreous, thereby increasing aqueous flow to the anterior chamber.

  • Surgical vitrectomy is often needed when medical and laser treatments fail.[34]
  • Either a pars plana[35] or anterior vitrectomy[36] approach may be used.
  • It is critical to remove vitreous from the space between the ciliary body and lens/IOL, most often by performing irido-zonulo-hyaloidectomy (IZH), resulting in a “unicameral” eye. Persistent or recurrent pseudophakic aqueous misdirection often requires pars plana vitrectomy combined with irido-zonulectomy or hyaloido-zonulo-iridectomy to create a communication between the anterior chamber, posterior chamber, and vitreous cavity[37].
  • The anterior approach for IZH is favored in the phakic eye and lens extraction may be necessary[38].
  • When surgery is planned on the fellow eye of a person with vitreous block in the first eye, vitrectomy should be planned or available.[39]
  • With long-standing vitreous block or advanced pre-existing glaucoma, permanent angle closure may be present, necessitating either combined or subsequent glaucoma surgery. Tube shunt placed in the pars plana has been advocated in this situation.[40]
  • In acute intraoperative setting, simple maneouver of main port posterior lip depression has also been described to reverse the direction of fluid misdirection by creating a negative pressure differential between anterior and posterior chamber[29].
  • Management approach in cases presenting with vitreous block is highlighted in Table 6 .

Table 6 : Stepwise management algorithm of Vitreous block/ Aqueous misdirection

SUSPECT

Vitreous block

→ EXCLUDE

Dangerous mimics

→ START

Medical Therapy

→ REASSESS

AC + IOP

Shallow/flat central + peripheral AC

High or normal IOP

Patent PI / no wound leak

Suprachoroidal hemorrhage

Choroidal effusion

Pupillary block

Wound leak / overfiltration

Cycloplegic + aqueous suppressants

± Acetazolamide

± Hyperosmotic agent

Topical steroid

Is AC deepening?

Is IOP controlled?

Is cornea/lens safe?

If stable / improving If persistent / recurrent
Continue cycloplegia

Taper IOP therapy as appropriate

Close follow-up

OR Laser if suitable:

Nd:YAG capsulo-hyaloidotomy/ anterior hyaloidotomy

→ Surgery if needed:

IZHV / anterior vitrectomy

or PPV + irido-zonulectomy

Clinical Pearls

  • Vitreous block is a diagnosis of exclusion.
  • The hallmark is uniform shallowing of both central and peripheral anterior chamber.
  • IOP is usually high but may occasionally be normal.
  • A patent PI excludes pupillary block but does not treat true vitreous block.
  • Cycloplegics help whereas miotics may worsen the condition.
  • During cataract surgery, suspect acute fluid misdirection when there is sudden AC shallowing, iris prolapse, raised posterior pressure, and a firm or rock-hard globe.
  • Always rule out suprachoroidal hemorrhage in a sudden intraoperative shallow chamber.
  • Definitive treatment requires communication between anterior chamber, posterior chamber, and vitreous cavity.
  • Core vitrectomy alone may be inadequate if the anterior hyaloid-zonular barrier remains intact.

References

  1. ↑ von Graefe A. Beitrage zur pathologie und therapie des glaucoms. Arch Fur Ophthalmol. 1869:15;108-252.
  2. ↑ Chandler PA. Malignant glaucoma. Trans Am Ophthalmol Soc. 1950;48:128-143.
  3. ↑ Simmons RJ. Malignant glaucoma. Br J Ophthalmol. 1972;56(3):263-272.
  4. ↑ 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. 1987; 105(6):770-773.
  5. ↑ Lynch MG, Brown RH, Michels RG, Pollack IP, Stark WJ. Surgical vitrectomy for pseudophakic malignant glaucoma. Am J Ophthalmol. 1986;102(2):149-153.
  6. ↑ Chandler PA, Simmons RJ, Grant WM. Malignant glaucoma. Medical and surgical treatment. Am J Ophthalmol. 1968;66(3):495-502.
  7. ↑ Lowe RF. Malignant glaucoma related to primary angle closure glaucoma. Aust J Ophthalmol. 1979;7:11.
  8. ↑ 8.0 8.1 Debrouwere V, Stalmans P, Van Calster J, Spileers W, Zeyen T, Stalmans I. Outcomes of different management options for malignant glaucoma: a retrospective study. Graefes Arch Clin Exp Ophthalmol. 2012 Jan;250(1):131-141.
  9. ↑ Saunders PP, Douglas GR, Feldman F, Stein RM. Bilateral malignant glaucoma. Can J Ophthalmol. 1992 Feb;27(1):19-21.
  10. ↑ Lincke, JB., Häner, N., Schawkat, M. et al. Treatment of pseudophakic aqueous misdirection syndrome. Sci Rep 15, 1415 (2025). https://doi.org/10.1038/s41598-024-83659-y
  11. ↑ Schwartz AL, Anderson DR. Malignant glaucoma in an eye with no antecedent operation or miotics. Arch Ophthalmol. 1975;93(5):379-381.
  12. ↑ Pecora JL. Malignant glaucoma worsened by miotics in a postoperative angle-closure glaucoma patient. Ann Ophthalmol. 1979;11(9):1412-1414.
  13. ↑ 13.0 13.1 Greenfield, D.S., et al., Aqueous misdirection after glaucoma drainage device implantation. Ophthalmology, 1999. 106(5): p. 1035-40.
  14. ↑ 14.0 14.1 Kaplowitz K, Yung E, Flynn R, Tsai JC. Current concepts in the treatment of vitreous block, also known as aqueous misdirection. Surv Ophthalmol. 2015 May-Jun;60(3):229-41. doi: 10.1016/j.survophthal.2014.12.004. Epub 2014 Dec 27. PMID: 25639795.
  15. ↑ Silver DM., Geyer O. Pressure-volume relation for the living human eye. Curr Eye Res. 2000; 20:115–120.
  16. ↑ Baskaran M, Raman K, Ramani KK, Roy J, Vijaya L, Badrinath SS. Intraocular pressure changes and ocular biometry during Sirsasana (headstand posture) in yoga practitioners. Ophthalmology. 2006 Aug;113(8):1327-1332.
  17. ↑ Schuman JS, Massicotte EC, Connolly S, Hertzmark E, Mukherji B, Kunen MZ. Increased intraocular pressure and visual field defects in high resistance wind instrument players. Ophthalmology. 2000;107(1):127-133.
  18. ↑ 18.0 18.1 Quigley HA, Friedman DS, Congdon NG. Possible mechanisms of primary angle-closure and malignant glaucoma. J Glaucoma. 2003;12(2):167-180.
  19. ↑ Arora KS, Jefferys JL, Maul EA, Quigley HA. Choroidal thickness change after water drinking is greater in angle closure than in open angle eyes, Invest Ophthalmol Vis Sci. 2012;53(10):6393-6402.
  20. ↑ 20.0 20.1 Chen X, Guo X, Hu X, Xiao H, Liu X. Is Thicker Choroid a Risk Factor for Malignant Glaucoma? Ophthalmic Res. 2018;60:161–168.
  21. ↑ 21.0 21.1 Zuo C, Wang D, Guo X, et al. Associations Between the Choroidal Vascularity Index and Malignant Glaucoma After Trabeculectomy for Primary Angle Closure Glaucoma. Front Med (Lausanne). 2021;Dec 8;8:747720.
  22. ↑ 22.0 22.1 22.2 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. 1979 Dec;88(6):1078-1086.
  23. ↑ 23.0 23.1 Fatt I. Hydraulic flow conductivity of the vitreous gel. Invest Ophthalmol Vis Sci 1977;16:565–568.
  24. ↑ 24.0 24.1 Quigley HA. Malignant glaucoma and fluid flow rate. Am J Ophthalmol. 1980;89(6):879-880.
  25. ↑ Shaffer RN, Hoskins HD. Ciliary block (malignant) glaucoma. Ophthalmology. 1978;85(3):215-21.
  26. ↑ AlQahtani RD, Al Owaifeer AD, AlShahwan S, et al. Outcomes of Medical and Surgical Management in Aqueous Misdirection Syndrome. Clin Ophthalmol, 2023. 17:797-806.
  27. ↑ Lau OC, Montfort JM, Sim BW, Lim CH, Chen TS, Ruan CW, Agar A, Francis IC. Acute intraoperative rock-hard eye syndrome and its management. J Cataract Refract Surg. 2014 May;40(5):799-804. doi: 10.1016/j.jcrs.2013.10.038. Epub 2014 Mar 27. PMID: 24684967.
  28. ↑ Kawasaki S, Suzuki T, Yamaguchi M, Tasaka Y, Shiraishi A, Uno T, Sadamoto M, Minami N, Naganobu K, Ohashi Y. Disruption of the posterior chamber-anterior hyaloid membrane barrier during phacoemulsification and aspiration as revealed by contrast-enhanced magnetic resonance imaging. Arch Ophthalmol. 2009 Apr;127(4):465-70. doi: 10.1001/archophthalmol.2008.594. PMID: 19365026.
  29. ↑ 29.0 29.1 Ambiya, Vikas; Khullar, Srishti*; Kapoor, Gaurav; Sharma, Vijay Kumar. Main port posterior lip depression versus intravenous mannitol to rescue acute intraoperative fluid misdirection syndrome. Taiwan Journal of Ophthalmology ():10.4103/tjo.TJO-D-25-00115, January 29, 2026. | DOI: 10.4103/tjo.TJO-D-25-00115
  30. ↑ Anisimova NS, Arbisser LB, Shilova NF, Melnik MA, Belodedova AV, Knyazer B, Malyugin BE. Anterior vitreous detachment: risk factor for intraoperative complications during phacoemulsification. J Cataract Refract Surg. 2020 Jan;46(1):55-62. doi: 10.1016/j.jcrs.2019.08.005. PMID: 32050233.
  31. ↑ Simmons RJ. Malignant glaucoma. Br J Ophthalmol. 1972;56(3):263-272.
  32. ↑ Epstein DL, Steinert RF, Puliafito CA. Neodymium-YAG laser therapy to the anterior hyaloid in aphakic malignant (ciliovitreal block) glaucoma. Am J Ophthalmol. 1984;98(2):137-143.
  33. ↑ Herschler J. Laser shrinkage of the ciliary processes. A treatment for malignant (ciliary block) glaucoma. Ophthalmology. 1980;87(11):1155-1159.
  34. ↑ 34.0 34.1 AlQahtani RD, Al Owaifeer AD, AlShahwan S, et al. Outcomes of Medical and Surgical Management in Aqueous Misdirection Syndrome. Clin Ophthalmol, 2023. 17:797-806.
  35. ↑ Koerner FH. Anterior pars plana vitrectomy in ciliary and iris block glaucoma. Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1980;214(2):119-127.
  36. ↑ Lois N, Wong D, Groenewald C. New surgical approach in the management of pseudophakic malignant glaucoma. Ophthalmology. 2001;108(4):780-783.
  37. ↑ Lincke, JB., Häner, N., Schawkat, M. et al. Treatment of pseudophakic aqueous misdirection syndrome. Sci Rep 15, 1415 (2025). https://doi.org/10.1038/s41598-024-83659-y
  38. ↑ Dikshit S, Tuluva S, Senthil S. Acute intraoperative fluid misdirection managed with anterior approach irido-zonulo-hyaloido-vitrectomy. Indian J Ophthalmol. 2024 Nov 1;72(11):1630-1634. doi: 10.4103/IJO.IJO_16_24. Epub 2024 Oct 26. PMID: 39462923; PMCID: PMC11668203.
  39. ↑ Chaudhry NA, Flynn HW, Murray TG, Nicholson D, Palmberg PF. Pars plana vitrectomy during cataract surgery for prevention of aqueous misdirection in high-risk fellow eyes. Am J Ophthalmol. 2000;129(3):387-388.
  40. ↑ Azuara-Blanco A, Katz LJ, Gandham SB, Spaeth GL. Pars plana tube insertion of aqueous shunt with vitrectomy in malignant glaucoma. Arch Ophthalmol. 1998 Jun;116(6):808-810.
Retrieved from "https://eyewiki.org/w/index.php?title=Vitreous_Block_(Malignant_Glaucoma,_Aqueous_Misdirection)&oldid=128133"
The Academy uses cookies to analyze performance and provide relevant personalized content to users of our website.
Learn more
Powered by MediaWiki
Powered by Canasta
Powered by Semantic MediaWiki