Acute Closed-Angle Glaucoma

Pathophysiology (as I understand it)

  • The cause of acute closed angle glaucoma is a block of the  flow of aqueous humor between the anterior and posterior chambers caused by the movement of the lens to be anterior to the insertion of the iris at the ciliary body to sit against the cornea.  The reason for this to occur is largely unknown, although genetic, dietary, PMHx and RHx have all been thought to have an effect.  (NB the use of steroid drops are an independent risk factor).
  • This causes a raise in intraocular pressure and neuronal injury (although the two seem to be disproportionate in glaucoma).  The risk of blindness in patients presenting with ACAG is high, so is an ophthalmological emergency.
  • It is more commonly seen in hypermetropic (long-sighted i.e. small eye; has needed reading glasses from an early age) patients; as a post-surgical complication of general anaesthetic or with the use of nebulised drugs (e.g. β-adrenergics antagonists; anticholinergics).

Risk factors

  • More common in females (4:1); and Eastern Asians
  • Hypermetropia (long sightedness)
  • Age (angle of the anterior chamber becomes shallower as the lens thickens with age)
  • Eye surgery
  • Drugs e.g. anticholinergics; adrenergics

Presentation

  • Acute onset severe eye pain- usually unilateral; may be severe as to cause nausea and vomiting.
  • Other systemic features may be present, e.g. headache
  • Preceding the pain, there may be visual disturbances (blurring, haloes).  This is due to an oedematous cornea
  • Photophobia- light may worsen the pain
  • Patients may have had similar episodes in the past that was relieved by sleeping (pupil constriction)
  • On Examination
    • The eye is often inflamed and tender; limbal and conjunctival injection (ciliary flush)
    • The cornea may be hazy and the pupil (semi-)dilated and fixed (may also be vertically eliptical).  Vision can be impaired because of this.
    • On gentle palpation, the globe may be relatively hard.
    • The anterior chamber may appear shallow, with the iris being closer to the cornea.  There may also be flare or cells
    • The optic disc is oedematous and hyperaemic
    • If you can measure intra-ocular pressure, it will be high
  • NB If the attack has resolved, the eye may appear completely normal.

Management

  • Referral to a specialist is crucial to preserve sight.
  • Measure IOP (normally between 10-20mmHg- in PACG it can be >40mmHg)
  • IV or oral acetazolamide (Diamox 500mg- CA inhibitor)- the loss of bicarbonate production halts the movement of sodium into the anterior chamber which, in turn, inhibits aqueous humor production
  • Topical pilocarpine 2-4% (pupil constrictor)- stretches and opens the trabecular meshwork through which humor can drain
  • Surgical/laser iridectomy will permanently open the iridocorneal angle but carries invasive risks.
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3 thoughts on “Acute Closed-Angle Glaucoma”

  1. In regard to the cause of acute closed angle glaucoma, I think the explanation of the mechanism is incorrect. Just from reading about (mainly the Oxford Handbook) I have understood that in fact there is a blockage of the drainage of aqueous (from the anterior chamber).

    The aqueous is drained via the canal of Schlemm, which get blocked resulting in an increase in pressure (as would be expected).

    I appreciate I may be wrong, but this is just something I came across as I was looking through these notes and thought it would be good to comment. Hope this helps, not confuses!

    1. You might be right- but my understanding was that this was the case in primary open angle glaucoma (but not in acute angle closure glaucoma- which instead results from blockage of flow from the posterior to anterior chambers by the above mechanism).

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