From the Guidelines
Acute angle closure glaucoma (AACG) is primarily caused by pupillary block, which leads to an anterior bowing of the iris and crowding of the angle in predisposed eyes.
Pathophysiology of AACG
The pathophysiology of AACG involves the following key mechanisms:
- Pupillary block: The pressure in the posterior chamber is higher than in the anterior chamber due to impairment of aqueous humor flow from the posterior chamber at the pupil, causing an anterior bowing of the iris that crowds the angle in predisposed eyes 1.
- Anatomical features: Certain anatomical features can increase the pressure disparity between the two chambers, such as pupil dilation and the crystalline lens size, shape, position, and thickening with age, which then results in iris apposition to the anterior chamber angle structures 1.
- Iris configuration: The relative position and thickness of the ciliary body, the location of the iris insertion into the ciliary body, and the volume of the iris also contribute to the pathogenesis of AACG 1.
Clinical Presentation
The clinical signs and symptoms of AACG include:
- Pressure-induced corneal edema: Experienced as blurred vision and occasionally as halos around lights 1.
- Mid-dilated pupil: A characteristic sign of AACG 1.
- Vascular congestion: Conjunctival and episcleral injection 1.
- Eye pain: A common symptom of AACG 1.
- Headache and nausea/vomiting: Systemic symptoms that can occur in AACG 1.
Diagnosis and Treatment
Diagnosis of AACG is typically made using dark-room dynamic gonioscopy to verify improvement in angle configuration following treatment 1. Ultrasound biomicroscopy (UBM) and anterior segment optical coherence tomography (AS-OCT) can also aid in the diagnosis of angle closure 1. Treatment of AACG involves medical therapy to lower the intraocular pressure (IOP) acutely and relieve symptoms, followed by laser iridotomy or iridectomy 1.
From the Research
Pathophysiology of Acute Angle Closure Glaucoma (AACG)
The pathophysiology of AACG involves the obstruction of aqueous humor outflow, leading to a sudden and marked rise in intraocular pressure (IOP) 2, 3, 4, 5, 6. Several mechanisms have been suggested, including:
- Pupil-block, where the iris is pushed forward, blocking the drainage angle 3
- Anterior nonpupil-block, including plateau iris and peripheral iris crowding 3
- Lens-related mechanisms, where the lens is anteriorly positioned or thickened 3, 5
- Retrolenticular mechanisms, where the space behind the lens is crowded 3
- Anterior displacement of the lens-iris diaphragm due to mass effect, uveal effusion, or weakened zonules 5
Risk Factors
Several risk factors have been identified, including:
- Female gender 3, 5
- Increasing age 3, 5
- Inuit or East Asian ethnicity 3
- Shallow anterior chamber depth 3, 5
- Short axial length 3
- Genetic factors 3
- Family history 5
- Plateau iris configuration 5
- Thick lens 5
- Anteriorly positioned lens 5
- Intraocular tumor (rarely) 5
Triggering Factors
Several medications and substances can trigger AACG, including: