Acute Closed Angle Glaucoma

Authors
Babak Khazaeni1; Leila Khazaeni2.

Affiliations
1
 Desert Regional Medical Center
2
 Loma Linda University

Last Update: September 15, 2020.

Introduction
Glaucoma is a set of ocular disorders often defined by increased intraocular pressures leading to
optic neuropathy and vision loss if untreated.[1] Glaucoma has traditionally been classified as
open-angle or closed-angle and as primary or secondary. The angle refers to the angle between
the iris and the cornea in the anterior chamber, which can become structurally obstructed. By
definition, primary glaucomas are not associated with known ocular or systemic disorders and
usually affect both eyes. Secondary glaucomas are associated with ocular or systemic disorders
and are often unilateral. Acute angle-closure glaucoma is a subset of primary angle-closure
glaucoma.
The commonly accepted range for intraocular pressure is 10-22 mmHg. Three factors that affect
the intraocular pressure are the rate of production of aqueous humor by the ciliary body, the
resistance to aqueous outflow through the trabecular meshwork and Schlemm’s canal, and the
episcleral venous pressure. The normal flow of aqueous humor starts in the ciliary body, goes
through the pupil and out through the trabecular meshwork and Schlemm's canal in the angle of
the anterior chamber. In acute angle-closure glaucoma, intraocular pressure increases rapidly due
to outflow obstruction of the aqueous humor. There are several factors leading to the obstruction
in acute angle-closure glaucoma, but the major predisposing factor is the structural anatomy of
the anterior chamber leading to a shallower angle.[2][3]

Etiology
Blockage to the flow of aqueous humor occurs due to a number of predisposing anatomic
variations. These variations include a shallower anterior chamber, lens size, anterior location of
the iris-lens diaphragm, and a narrow entrance to the anterior chamber angle. The shallower
anterior chamber angle leads to a large area of the iris and lens being in contact with each other
slowing the flow of aqueous humor from the posterior chamber to the anterior chamber. This, in
turn, leads to a pressure difference between the chambers called a pupillary block.[4] 
The pupillary block causes bowing of the iris which narrows the angle of the anterior chamber
further. This cycle will perpetuate increasing intraocular pressures leading to the clinical
presentation of acute angle-closure glaucoma.
Epidemiology
There are a number of risk factors for acute angle-closure glaucoma which include age, gender,
race and family history.[5]
 Age: The average age at presentation is 60 and prevalence increases thereafter. This is
felt to be due to the increasing size of the lens with age.
 Gender: There is a 4:1 ratio of the incidence of angle-closure glaucoma in women versus
men.
 Race: Angle-closure glaucoma is more common in Southeast Asians, Chinese, and
Eskimos. It is uncommon in black populations. In whites, acute angle-closure glaucoma
accounts for 6% of all glaucoma diagnoses.[6]
 Family history: Ocular anatomic features are inherited. 

Pathophysiology
An acute attack of angle-closure glaucoma is precipitated by pupillary dilatation leading to
increasing iris and lens contact increasing the pupillary block.[7] The increasing pupillary block
leads to bulging of the iris acutely closing the angle between the iris and cornea thus obstructing
the aqueous humor outflow tract. The intraocular pressure rises acutely leading to
symptomology.

History and Physical

Acute angle-closure glaucoma presents as a sudden onset of severe unilateral eye pain or a
headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and
vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with
marked conjunctival injection (most prominent at the limbus). Intraocular pressure will be
elevated and can be as high as 60 to 80 mm Hg in an acute attack. A mild amount of aqueous
flare and cells may be seen. The optic nerve may also be swollen during an acute attack.[8][9]

Evaluation
Measuring of an elevated intraocular pressure is diagnostic. There is no need for any imaging
studies. A basic metabolic panel should be checked if osmotic agents are used in the treatment
regime. A gonioscopic examination by an ophthalmologist to verify angle-closure makes the
definitive diagnosis. Gonioscopy of the unaffected eye will reveal a narrow occludable angle
given the anatomic predisposing factors to acute angle-closure glaucoma (See other issues for
further discussion). Glaucomflecken (grey-white opacities on the anterior lens capsule) may be
visible if previous attacks of angle-closure glaucoma have occurred.[10]

Treatment / Management
The medical treatment for acute angle-closure glaucoma aims to decrease the intraocular
pressure by blocking the production of aqueous humor, increasing the outflow of aqueous
humor, and reducing the volume of the aqueous humor.[11][12]
Initial medical therapy includes a combination of the following medications:
 Intravenous acetazolamide 500 mg to block the production of aqueous humor.
 Intravenous mannitol 1 to 2 grams/kg can be given (if there is no contraindication) to
rapidly reduce the volume of aqueous humor.
 Topical Beta-Blocker (Timolol 0.5%) one drop to block the production of aqueous
humor.
 Topical Alpha 2-Agonist (Apraclonidine 1%) one drop to block the production of
aqueous humor.
 Topical Pilocarpine 1% to 2% one drop every 15 minutes for two doses once intraocular
pressure is below 40 mm Hg to increase the outflow of aqueous humor. This is not
effective at higher pressures due to pressure-induced ischemic paralysis of the iris.
Intraocular pressure needs to be checked every hour.
Definitive treatment is peripheral iridectomy after the acute episode subsides. Laser iridectomy is
the treatment of choice. Surgical iridectomy is indicated when laser iridectomy can not be
accomplished. Iridectomy relieves the pupillary block as the pressure between the posterior and
anterior chamber approaches zero by allowing the flow of aqueous humor through a different
route. Iridectomy should be as peripheral as possible and covered by the eyelid to avoid
monocular diplopia through this second hole in the pupil.[13]

Differential Diagnosis
 Allergic conjunctivitis
 Bacterial conjunctivitis (Pink Eye)
 Viral conjunctivitis 
 Drug-induced glaucoma
 Malignant glaucoma
 Neovascular glaucoma
 Phacomorphic glaucoma
 Senile cataract (Age-Related Cataract)
 Lens subluxation[14]
 Migraine headache[15]
 Cluster headache
 Suprachoroidal hemorrhage
Prognosis
The prognosis depends on early detection and prompt treatment of acute closed-angle glaucoma.
A study conducted on 116 cases of acute angle-closure glaucoma concluded that the delay in
presentation and the time taken to end the acute episode was the most important factor in
determining the final outcome of these patients. High intraocular pressure was less effective in
determining the long-term prognosis of this condition.[16]

Complications
If acute closed-angle glaucoma is not detected and treated in its initial stages, it can lead to
temporary loss of vision or blindness. There is a loss of peripheral vision, followed by a loss of
central vision. In patients with peripheral patent iridotomy, there can be a significant increase in
IOP, with a flat anterior chamber. This condition is called malignant glaucoma. This condition is
difficult to treat and progressively leads to blindness.[17]

Deterrence and Patient Education

Patients with a history of acute angle-closure glaucoma should avoid dim light. Pupils dilate in
response to dim light, further narrowing the iridocorneal angle. Patients with hypermetropia are
at an increased risk of developing angle-closure glaucoma.

Pearls and Other Issues

An untreated fellow eye has a 40% to 80% chance of developing an acute attack of angle-closure
glaucoma over 5-10 years as it shares the same anatomic predisposing factors of the first eye.
[18] Hence peripheral iridectomy should be performed in the fellow eye as well as the affected
eye.
The gender and ethnicity predisposing factors to acute angle-closure glaucoma hint at a genetic
predisposition to the disease in certain populations. Recent large-scale studies have shown a clear
association to several genes and genetic loci with primary open-angle glaucoma, but evidence for
acute angle-closure glaucoma is sparse. So far, only one study has shown a genetic locus on
Chromosome 11 that can cause acute angle-closure glaucoma. Studies have been conducted on
possible therapeutic targets in patients with early-onset glaucoma based on molecular and
cellular events caused by MYOC, OPTN, and TBK1 mutations.[19]

Enhancing Healthcare Team Outcomes

Acute angle-closure glaucoma is best managed by an interprofessional team that also includes an
ophthalmology nurse and the pharmacist. After managing the emergency with eye drops, the
patient should be scheduled for an iridectomy. Clinicians need to be aware that the other eye is
also at risk for acute angle-closure glaucoma and prophylactic surgery is recommended.
The outcomes for patients with acute angle-closure glaucoma are good after treatment, however,
delay in treatment can lead to damage to the optic nerve and vision loss.
Case 1 A 77 year old woman was referred to the acute general medicine department by her general
practitioner following a general deterioration in her condition. Her past medical history included
Parkinson’s disease, recent weight loss, and 2 days of vomiting. On referral, her medications were
sodium picosulphate 10 ml once daily, and thrice daily doses of betahistine 8 mg, bromocriptine 5 mg,
domperidone 10 mg, levodopa 125 mg, and orphenadrine 50 mg. Family and personal history was
inconclusive. On clinical examination, she was drowsy but oriented. All vital signs were normal. Systemic
examination was within normal limits. Haematological and biochemical investigations, ECG, and chest x
ray were normal. Malnutrition, malignancy, or chest infection was suspected as the likely causes of her
condition. Swollen lids and conjunctival injection were also noted. The systemic problem was thought to
be with parkinsonism related generalised deterioration and cachexia, worsened by gastrointestinal
upset and its treatment. Chloramphenicol eye ointment was started for the eyes. After 6 days, the
patient was referred to the ophthalmologists with a persistent red eye. Ophthalmic examination showed
conjunctival injection and a semi-dilated, fixed pupil in both eyes. Fundus examination showed
glaucomatous optic disc changes. Intraocular pressure (IOP) was 50 mm Hg in the right eye and 38 mm
Hg in the left, suggesting acute angle closure glaucoma (AACG). She was given intravenous
acetazolamide 500 mg immediately, sustained release acetazolamide capsules 250 mg twice daily;
ocusert pilocarpine twice daily, levobunolol eyedrops twice daily, latanoprost eyedrops nightly, and
prednisolone acetate ophthalmic suspension 1% (Pred Forte) eyedrops four times daily in both eyes.
After 1 day, she was more comfortable, and IOP dropped to 25 mm Hg in the right eye, and 10 mm Hg in
the left. YAG laser peripheral iridotomies were made in both eyes. Subsequently, the IOP was 22 mm Hg
in the right eye and 25 mm Hg in the left.

Case 2

A 71 year old Indian woman was referred to the physicians by her general practitioner for sudden onset,
right sided temporal headache, vomiting, and a red, sore right eye. The vision was poor from
longstanding cataract and had not worsened. There had been similar "minor" episodes previously. On
examination, there was scalp tenderness, and the right eye was red with advanced cataract. Erythrocyte
sedimentation rate was 24 mm. A diagnosis of temporal arteritis was made. She was started on
prednisolone tablets 60 mg once daily and referred to the ophthalmologists for temporal artery biopsy.
On ophthalmic examination, her vision was light perception in te right eye and 6/12 in the left. The right
eye showed circum corneal congestion, corneal oedema, a shallow anterior chamber, semi-dilated fixed
pupil, mature cataract, and IOP of 52 mmHg. The left eye showed a shallow anterior chamber and a
pressure of 16 mmHg. A diagnosis of acute (?phacomorphic) glaucoma right eye was made. The patient
was treated as for case 1. IOP dropped to 8 mm Hg in 2 hours. Bilateral YAG laser peripheral iridotomies
were performed. Subsequently she underwent cataract surgery with intra cular lens implantation
separately for both eyes, and improved to 6/18 with correction in the right eye and 6/12 in the left.

Case 3

An 84 year old female with past medical history of Alzheimer’s disease presented following a fall at
home. She sustained a lacerated wound temporal to the left eye, which was sutured. There was no loss
of consciousness or head injury. Five days later, she developed increasing drowsiness with lucid interval,
new and progressive headache and increasing confusion. Examination revealed left periocular bruising,
mild subconjunctival haemorrhage and a red eye. The pupil was dilated and fixed. She was not oriented
in time and space. There was no focal neurological deficit. A CT scan excluded subdural or intracranial
bleed and showed fractures of the anterior and lateral walls of the left maxilla and displacement of the
zygomatic arch. A fracture of the optic canal was suspected and the patient thus referred to the
ophthalmologists. On ophthalmic review, vision in the left eye was down to detection of hand
movements. There was ecchymosis, chemosis, severe corneal oedema with pigment deposit, avery
shallow anterior chamber, a semi-dilated and fixed pupil, and some lenticular opacity in the left eye.
Right eye vision and examination was normal except for a shallow anterior chamber. IOP was 24 mmHg
in the right eye and 55 mmHg in the left. Gonioscopy revealed a narrow angle. An ophthalmic diagnosis
of angle closure glaucoma in the left eye was thus made. The patient was treated as for case 1. After 2
hours, the pressure was 35 mmHg, the headache had subsided, and the cornea had cleared. The lens
was swollen. YAG peripheral iridotomies were performed the following day. Ten days later, the patient
underwent complicated cataract extraction with anterior vitrectomy and anterior chamber intraocular
lens implantation. Three months later, vision was 6/60 and pressure 16 mmHg in the left eye, and the
optic disc was pale and cupped.