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Symptoms

May be very mild early in course. Moderate pain, red eye, and photophobia may develop. Classically follows incisional (e.g., cataract, glaucoma, retinal) or laser surgery in eyes with small anterior segments (e.g., hyperopia, nanophthalmos) or with primary angle closure glaucoma. May occur spontaneously or be induced by miotics.

Signs

Critical

Diffusely shallow or flat anterior chamber and increased IOP in the presence of a patent PI and in the absence of both a choroidal detachment and iris bombé. IOP may not be significantly elevated, especially early in the presentation.

Differential Diagnosis

Etiology

Believed to result from anterior rotation of the ciliary body with posterior misdirection of the aqueous; aqueous then accumulates in the vitreous resulting in forward displacement of the ciliary processes, crystalline lens, intraocular implant, or the anterior vitreous face, causing secondary angle closure. Newer theories point toward choroidal expansion, reduced conductivity of fluid through vitreous, and reduced trans-scleral fluid movement as factors in development.

Work Up

Workup
  1. History: Previous eye surgery?
  2. Slit lamp examination: Determine if a patent PI or iris bombé is present. Pupillary block is unlikely in the presence of a patent PI unless it is plugged, bound down, or plateau iris syndrome is present.
  3. Gonioscopy and IOP measurement.
  4. Dilated retinal examination unless phakic angle closure is likely.
  5. Perform B-scan US to rule out choroidal detachment and suprachoroidal hemorrhage.
  6. Seidel test to detect postoperative wound leak if clinically indicated.

Treatment

  1. If an iridectomy is not present or an existing PI is not clearly patent, pupillary block cannot be ruled out, and a PI should be performed. See 9.4, ACUTE ANGLE CLOSURE GLAUCOMA. If signs of aqueous misdirection are still present with a patent PI, attempt medical therapy to control IOP and return aqueous flow to the normal pathway.
  2. Atropine 1% and phenylephrine 2.5% q.i.d. topically. Miotics can worsen condition and are contraindicated.
  3. Systemic CAI (e.g., acetazolamide 500 mg i.v. or two 250-mg tablets p.o.).
  4. Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.).
  5. Topical α2 agonist (e.g., apraclonidine 1.0% or brimonidine 0.1% to 0.2% b.i.d.).
  6. If needed, hyperosmotic agent (e.g., mannitol 20% 1 to 2 g/kg i.v. over 45 minutes).

If the attack is broken (anterior chamber deepens and IOP normalizes), continue atropine 1% daily, indefinitely. At a later date, perform PI in the contralateral eye if the angle is occludable.

If steps 1 through 6 are unsuccessful, consider one or more of the following surgical interventions to disrupt the anterior hyaloid face in an attempt to restore the normal anatomic flow of aqueous. Ultimately, the goal is to create a unicameral eye:

  • YAG laser disruption of the anterior hyaloid face and posterior capsule if aphakic or pseudophakic. If phakic, may attempt through a preexisting large PI.
  • Pars plana vitrectomy combined with irido-zonulo-hyaloidectomy: Performing vitrectomy with localized excision of iris, lens capsule, zonules, and anterior hyaloid face plus reformation of the anterior chamber has been shown to be helpful.
  • Lensectomy with disruption of the anterior hyaloid or vitrectomy.
  • Argon laser of the ciliary processes.
NOTE:

An undetected anterior choroidal detachment may be present. Therefore, a sclerotomy to drain a choroidal detachment may be considered before vitrectomy.

Follow Up

Variable, depending on the therapeutic modality used. PI is usually performed in an occludable contralateral eye within a week after treatment of the involved eye.