Primary angle-closure is the synechial or appositional closure of the anterior chamber angle secondary to multiple mechanisms resulting in raised intraocular pressure and structural changes in the eyes.
Iridotrabecular contact is the hallmark of primary angle-closure  and the most commonly identified sign which indicates that treatment is required.
It is defined by at least 180 degrees of iridotrabecular contact together with an elevated intraocular pressure or peripheral anterior synechiae or btoh
Primary angle-closure glaucoma is the presence of glaucomatous optic neuropathy.


Primary Angle-Closure versus Secondary Angle-Closure

  • Primary angle-closure can occur w/ no identifiable cause (idiopathic)
  • If the cause of angle closure can be identified, then it is said to be secondary

Primary Angle-Closure Glaucoma (PACG)

  • PAC in the presence of glaucomatous optic neuropathy
  • Patients may be asymptomatic presenting for routine eye care, or may present w/ sudden onset of symptoms & signs of acute angle closure attacks
    • Symptoms may include intermittent or episodic blurring of vision, eye pain, eye redness, frontal headache, glare & halos or colored rings around lights, poor light or dark adaptation, difficulty tracking fast-moving objects, nausea, vomiting
  • PACG causes 3x more blindness than primary open-angle glaucoma (POAG)

Primary Angle-Closure Suspect (PACS)

  • Characterized by ≥2 quadrants of iridotrabecular contact (ITC), w/ normal intraocular pressure (IOP), absence of peripheral anterior synechiae (PAS) & w/o evidence of glaucomatous optic neuropathy

Acute Angle-Closure Crisis

  • Rapid increase of IOP due to sudden obstruction of the chamber angle
  • May lead to pressure-induced corneal edema (manifested as blurred vision & at times, multicolored halos around lights), mid-dilated pupil, vascular congestion, eye pain, &/or headache
  • Elevated IOP can be accompanied by nausea & vomiting
  • May be self-limited & resolve spontaneously or may occur repeatedly
  • May result to permanent loss of vision if left untreated & may affect the other eye


Clinical Subtypes

Acute Angle-Closure Glaucoma (AACG)

  • Sudden & severe elevation of the intraocular pressure (IOP) that does not resolve spontaneously, resulting from total closure of the iridocorneal angle
  • Often brought about by sudden dilation of pupils from darkness, medications or sympathetic arousal
  • Symptoms include blurring of vision, ocular pain, frontal headache on the affected side, “halos” around lights, occasional nausea & vomiting, occasional palpitations & abdominal cramps
  • Signs:
    • IOP is rapidly & severely elevated (>21 mmHg, usually 50-80 mmHg) & does not resolve spontaneously
    • Decreased visual acuity
    • Corneal epithelial edema & ciliary injection
    • Peripheral anterior chamber is shallow w/ steep iris configuration & peripheral iridocorneal contact
    • Pupil is mid-dilated & nonreactive or w/ reduced reactivity
    • Fundoscopy reveals disc edema, w/ venous congestion & splinter hemorrhages
    • 360 degrees ITC on gonioscopy
    • Optic disc on fundoscopy may show either edema w/ splinter hemorrhages & venous congestion, or glaucomatous excavation
    • Bradycardia or arrhythmia

Chronic Angle-Closure Glaucoma (CACG)

  • Characterized by permanent synechial closure of the chamber angle confirmed by indentation gonioscopy
  • Eye discomfort, visual disturbances & transient “halos” may be experienced
  • Signs:
    • Elevated IOP (>21 mmHg, depending on degree of ITC)
    • Peripheral anterior synechiae of varying degrees
    • Optic nerve head damage pattern consistent w/ glaucoma
    • Visual field defects

Intermittent Angle-Closure Glaucoma (IACG)

  • Sometimes referred to as Subacute Angle-Closure Glaucoma
  • Similar to AACG but w/ symptoms occurring in intermittent milder attacks; symptoms are spontaneously relieved after ≥ 1 hour
  • Signs:
    • May resemble AACG but in a milder form
    • May vary according to degree of ITC of chamber angle
    • Atrophy of optic disc rim w/ afferent pupillary defect may be seen


Past Ophthalmic History

  • Use of topical or systemic medications that may precipitate angle narrowing (eg sulfonamides, Topiramate, phenothiazines, anticholinergic drugs, tricyclic antidepressants, steroids)
  • Trauma, previous eye treatment or laser surgery
  • Allergies & adverse effects of drugs

Past Medical History

  • Exclude past history of systemic conditions that may mimic glaucoma but are not progressive (eg hemodynamic crises like postpartum hemorrhage, blood transfusions, severe trauma, anterior ischemic optic neuropathy that may cause optic pallor and cupping, or intracranial diseases)
  • Systemic diseases [eg asthma, chronic obstructive pulmonary disease (COPD), cardiac arrhythmias, hypotension/hypertension, diabetes, thyroid eye disease, pituitary tumors, previous head injury, cerebrovascular accidents, dementia, arthritis]
  • Inquire regarding all medications taken including drug allergy
  • Factors that will affect life expectancy

Family History

  • Type & course of disease in the family

Socioeconomic Factors

  • Consider patient’s compliance & financial capacity
  • Effects of glaucoma in the patient’s life, work, & family

Physical Examination

Ophthalmological Examination

Refractive Status

  • Hyperopic eyes, especially in older patients, have narrower anterior chamber angles & are at higher risk of primary angle-closure (PAC)
    • Approximate the refractive status by measuring the eyeglass power to determine the possibility of hyperopia or refracting the other eye 
  • Retinoscopy to assess the actual refractive status


  • Examine the size, shape, reactivity of the pupil & presence of relative afferent pupillary defect
    • Pupil may be asymmetric or oval in the affected eye during or after an acute attack
    • Pupil may be poorly reactive or mid-dilated during an acute attack; tonic following an attack
    • Afferent pupillary defect may be present in chronic angle closure or in an asymmetric optic nerve damage

Slit-lamp Biomicroscopy

  • In acute cases, look for conjunctival hyperemia, corneal swelling w/ or w/o microcytic edema
  • In recent attacks, check for anterior chamber inflammation, iris abnormalities (eg diffuse or focal atrophy, posterior synechiae, abnormal pupillary function, irregular pupil shape, & a mid-dilated pupil)
  • Other manifestations:
    • Central & peripheral anterior chamber depth narrowing
    • Lens changes such as cataract and glaukomflecken (patchy, localized, anterior subcapsular lens opacities)
    • Corneal endothelial cell loss

Intraocular Pressure (IOP) Measurement

  • Normal IOP is 10-21 mmHg & tends to increase w/ age
  • Use a contact applanation method, typically Goldmann tonometry, to determine the IOP
  • Perform IOP measurement prior to gonioscopy
  • Measure central corneal thickness after the acute attack has resolved

Provocative Tests

  • Provide little additional information since they cannot exclude the possibility of angle closure even if the tests are negative
  • May trigger an acute angle-closure attack

Pupil Dilation

  • May not be advisable in patients w/ iridotrabecular contact (ITC)
    • However, an attempt should be made to evaluate the fundus & optic nerve head using direct ophthalmoscope or indirect ophthalmoscopy at the slit-lamp biomicroscope w/ a 90-diopter lens
  • Not also recommended in PAC & primary angle-closure suspect (PACS) patients who are not having an acute attack until an iridotomy has been performed
    • Dilation can precipitate acute attacks
  • Evaluation of the optic nerve head, retinal nerve fiber layer, & visual fields may be done after an adequate treatment of an acute attack


Anterior Segment Imaging

  • Examples are ultrasound biomicroscopy & anterior segment optical coherence tomography
  • Useful in elucidating plateau iris
  • Used only in cases which are most difficult to interpret because of its limited availability & costs


  • Standard technique for identifying iridotrabecular contact (ITC)
  • Evaluates the angle anatomy, appositional closure, presence of peripheral anterior synechiae (PAS)
  • Should be done in a dark room w/ a bright, short, & thinnest beam that does not pass through the pupil to avoid inducing pupillary constriction, which can widen the angle
  • Visualization of the angle may be impaired due to corneal edema in cases of acute angle-closure glaucoma
    • Topical glycerin can be used to clear the cornea to have a better view
  • Serial gonioscopy may also be a preferred therapy if w/o signs of chronic angle damage & glaucomatous optic neuropathy


  • No single screening test is sufficient to determine patients w/ & w/o glaucoma
  • It has been estimated that half of glaucoma cases worldwide is caused by primary angle-closure (PAC)
    • Optic nerve damage occurs in approximately 75% of patients w/ primary angle-closure glaucoma (PACG) in Asia
  • Opportunistic glaucoma screening relies on detection of glaucoma in patients who present for other reasons
    • Involves comprehensive ophthalmologic examination among patients >35 years old who seek ophthalmic attention for any reason
  • Universal glaucoma screening is a strategy wherein health care professionals seek out patients in the general population
    • Not feasible in developing countries since there is not enough infrastructure available (eg availability of expertise, time, instrumentation required to confirm diagnosis among patients w/ positive results)
  • For non-ophthalmologic professionals, screening consists of a comprehensive assessment for risk factors,intraocular pressure (IOP) measurement & optic disc examination
    • If slit-lamp examination is available, assess limbal anterior chamber depth (ACD)
  • Screening in an ophthalmologist’s clinic consists of a comprehensive clinical examination which includes slit-lamp examination, IOP measurement, dilated optic disc examination & gonioscopy
    • Optic disc examination & perimetry will only detect PAC in the presence of a damaged optic disc or visual field (VF)
    • Tonometry will only detect PAC if IOP is elevated
  • Currently, periodic routine comprehensive eye examination is the optimal method for screening glaucoma
    • Opportunistic screening is recommended in the absence of an ideal screening method
  • Diagnosis is based on history & comprehensive ophthalmological examination
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