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Acute Angle-Closure Glaucoma

The Royal College of Ophthalmologists (RCO) Management of Angle Closure Glaucoma Guideline Jun 2022.

NICE CKS Glaucoma Last Revised: Feb 2023.

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma, often referred to as acute glaucoma, is an ophthalmic emergency caused by sudden obstruction of aqueous humour outflow, leading to a rapid rise in intraocular pressure.

This updated UKMLA guide to acute angle-closure glaucoma is based on RCOphth guidance and NICE CKS, which covers causes, risk factors, symptoms, diagnosis, and management.

Terms and Definitions

Term / condition Definition / description
Glaucoma A group of eye diseases that cause progressive optic neuropathy, characterised by visual field defects and optic disc changes

Commonly associated with raised IOP (but NOT always)

Ocular hypertension Elevated IOP (> 21 mmHg) but with no signs of glaucoma (i.e. no optic neuropathy / no visual field defect)
Normal tension glaucoma Presence of optic neuropathy (characterised by visual field defects and optic disc changes), but with normal IOP
Angle-closure glaucoma (narrow-angle glaucoma) Glaucoma secondary to narrowing/closure of the iridocorneal angle → impaired aqueous humour drainage → ↑ IOP

Most often presents acutely

Open-angle glaucoma Glaucoma secondary to trabecular meshwork dysfunction, despite an open (normal) iridocorneal angle

Often associated with ↑ IOP

Most often presents chronically

Raised IOP ≠ glaucoma.

Optic nerve neuropathy is needed for it to be glaucoma, indicated by optic disc changes and visual-field defects.

Relevant Anatomy and Physiology

Intra-ocular pressure (IOP)

  • IOP helps maintain the shape of the globe
  • IOP is mainly determined by the balance between aqueous humour production and aqueous humour drainage

Aqueous humour pathway:

  1. Produced by the ciliary body (the enzyme carbonic anhydrase plays an important role)
  2. Flows from the posterior chamber, through the pupil, into the anterior chamber
  3. Drained out of the eye via the iridocorneal angletrabecular meshwork → Schlemm’s canal
    • A small % is drained via the uveoscleral pathway (via the venous circulation of the iris, ciliary body, choroid, and sclera)

Control of aqueous humour secretion:

  • Stimulated by beta-2 receptors
  • Decreased by alpha-2 receptors

Causes

Angle-closure glaucoma is most commonly primary (PACG):

  • Due to the narrowing of the irido-corneal angle
  • Most commonly due to contact/apposition of the peripheral iris and trabecular meshwork (irido-trabecular contact)
  • As a result, aqueous humour production continues, but aqueous humour drainage reduces (production > drainage → raised IOP)

Secondary causes (uncommon):

  • Lens dislocation / subluxation
  • Anterior uveitis (posterior synechiae can block aqueous humour drainage via the pupil, and inflammation can also alter the aqueous drainage)
  • Anterior segment neovascularisation (e.g. from retinal vein occlusion)

Risk Factors

Risk factors for PACG:

  • Advancing age (as the lens size increases with age → narrowing the iridocorneal angle)
  • Females (as they tend to have shallower anterior chambers)
  • Asian (prevalence is highest in China)
  • Hypermetropia (long-sighted) (long-sighted eyes usually have a shorter axial length, resulting in a shallower anterior chamber and narrower iridocorneal angle)
  • Family history

Hypermetropia (long-sighted) → shorter eye axis → associated with angle-closure glaucoma

Myopia (short-sighted) → longer eye axis → associated with open-angle glaucoma

Raised IOP is a major risk factor for primary open-angle glaucoma.

However, in primary angle-closure glaucoma, the key risk factors are anatomical features that narrow the iridocorneal angle; this narrowing then reduces aqueous humour outflow and causes raised IOP. Therefore, in angle-closure glaucoma, raised IOP is better understood as a consequence of angle closure rather than the primary predisposing risk factor.

Diagnosis

Clinical Features

Angle-closure glaucoma often presents as an acute, painful red eye, with associated:

  • Headache
  • Nausea and vomiting
  • Blurred vision + seeing halos around light

Possible examination findings:

  • Red, tender, hard eye
  • Hazy oedematous cornea
  • Semi-dilated / mid-dilated, poorly reactive pupil (classically vertically oval shape)

A history of the following also makes acute angle-closure glaucoma more likely

  • Previous episodes of eye pain, blurred vision, headaches, nausea and seeing halos around light (indicate intermittent angle closure episodes that self-resolved)
  • Presence of a precipitating factor (any cause of mydriasis), such as:
    • Dark room (e.g. watching television)
    • Semi-prone position (e.g. reading)
    • Use of anticholinergic (e.g. TCA) or adrenergic (e.g. phenylephrine) medications
    • Stress or emotional arousal

Angle-closure glaucoma can also be non-acute:

  • Intermittent: causes less severe symptoms that often spontaneously resolve, typically on lying supine and closing the eyes, or after sleeping
  • Chronic PACG: typically asymptomatic until severe visual field defects affect vision

~10% of the UK blindness registrations are due to glaucoma.

Globally, glaucoma is the leading cause of irreversible blindness, and the 2nd most common cause of blindness (after cataracts)

Investigation and Diagnosis

Acute angle-closure glaucoma is an ophthalmological emergency → admit to ophthalmology immediately for assessment and treatment.

Diagnostic work-up for suspected acute primary angle-closure glaucoma (in secondary care):

Investigation / test Interpretation / description
 Slit lamp examination Definitive investigation: gonioscopy
  • To demonstrate objective narrowing of the iridocorneal angle
  • Specifically, irido-trabecular contact

Measure the anterior chamber depth

  • Depth would be reduced in angle-closure glaucoma
  • The main purpose is to check for marked asymmetry in central anterior chamber depth (between the patient’s 2 eyes), which indicates a possible secondary cause
IOP measurement Methods:
  • Goldmann applanation tonometry (done during a slit lamp exam)
  • Handheld tonometry (useful if slit lamp access is limited, e.g. in A&E)

Finding in acute-closure glaucoma: ↑ (>21 mmHg)

Anterior segment OCT can be used as a supplementary test alongside gonioscopy. Importantly, it does NOT replace the need for gonioscopy.

It can image and measure the iridocorneal angle, therefore it can be used as a triage test in community or primary care settings to exclude the need for gonioscopy.

To diagnose acute primary angle-closure glaucoma, ALL the following must be met:

  • Presence of angle-closure (demonstrated on gonioscopy)
  • IOP
  • Secondary causes excluded (by measuring the anterior chamber depth)

Management

This section covers acute primary angle-closure glaucoma, rather than other forms of angle-closure glaucoma.

This is the most important type to recognise in exams at a non-specialist level, as it is an ophthalmic emergency requiring urgent assessment and treatment.

Primary Care Management

If acute angle-closure glaucoma is suspected → refer immediately to be admitted under ophthalmology

If immediate admission is not possible → start emergency treatment in primary care:

  • Lie patient flat with face up, do NOT support the head with a pillow
  • Pharmacological management
    • Analgesia and antiemetic as needed
    • IOP-lowering agents:
      • Pilocarpine eye drops
      • Acetazolamide oral 500 mg

Secondary Care Management

Initial stat medications (to be given once the diagnosis is confirmed):

  • Dorzolamide 2% + timolol 0.5% combined eye drops
  • Apraclonidine 0.5% eye drops
  • Pilocarpine 2% (defer if IOP >40 mmHg – withhold until IOP is <40 mmHg)
  • IV acetazolamide 250 mg (if IOP >40 mmHg)

Further management:

1st line definitive management Laser peripheral iridotomy 
  • To be performed ASAP once the stat medications achieve initial IOP control and the cornea is clear enough to proceed
  • The procedure should be performed on both eyes (as the contralateral eye is at very high risk)
  • After the iridotomy, give steroid eye drops at least hourly for 24 hours, then QDS for 1 week

If laser iridotomy is not technically possible, consider a surgical iridectomy

Other interventions If the initial stat medications failed to reduce IOP / relieve symptoms / cornea remains too oedematous to perform laser peripheral iridotomy, consider:
  • Laser Iridoplasty
  • Cycloablation

If the patient has a concurrent cataract with acute primary angle-closure glaucoma:

  • Emergency treatment is still required first to lower IOP and control the acute attack
  • Once the eye is stabilised, offer early phacoemulsification (typically 1-4 weeks after the initial acute presentation)

Do not perform the following:

  • Emergency trabeculectomy
  • Limbal paracentesis

References

Related Articles

Chronic Open Angle Glaucoma

Red Eye Referral

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