Causes
This occurs because of resistance to aqueous flow between the iris and the anterior lens surface and is most likely to occur when the pupil is mid-dilated.  A pressure difference between the anterior and posterior chambers results in forward displacement of the iris-lens diaphragm, the trabecular meshwork becomes obstructed by peripheral iris and aqueous outflow is impeded. The result is a rise in intraocular pressure (IOP). The mechanism was first reported in the British Journal of Ophthalmology by Lowe in 1970.

Symptoms
These develop rapidly causing a painful eye, blurred vision, haloes, nausea and vomiting. The eye is red, the cornea cloudy and the pupil fixed and mid-dilated. The IOP may be between 60 and 80 mmHg (normal IOP less than 21 mmHg)

Treatment
Initial treatment requires Yag Laser Iridotomy. Often this cannot be done initially because of cornea oedema and the patient has to be treated medically first with intravenous Diamox or Mannitol. A recently re-described option for intial management is corneal indentation (this can be done with a glass rod, cotton applicator or gonio lens). This has been reported to reduce IOP by up to 45 mmHg, which may help to rapidly relieve pain and clear the cornea allowing Yag laser iridotomy to more easily completed.

Iridotomy should eliminate pupil block but does not necessarily open up the angle, particularly in the presence of plateau iris. Up to 50% of Chinese patients have persistently raised IOP following Yag Laser Iridotomy. This may be caused by i) a persistent anteriorly positioned ciliary body ii) direct trabecular damage and iii) peripheral anterior synechiae iv) the crystalline lens may push the peripheral iris anteriorly especially if cataractous.

Some evidence suggests that cataract extraction is more effective in preventing IOP rise than iridotomy after acute primary angle closure (Lam et al. Ophthalmology July 2008).