eMedicine Specialties > Emergency Medicine > Ophthalmology

Glaucoma, Acute Angle-Closure

Author: Ayim K Darkeh, MD, Staff Physician, Clinical Assistant Instructor, Department of Emergency Medicine, State University of New York Downstate Medical Center
Coauthor(s): Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn
Contributor Information and Disclosures

Updated: Oct 3, 2007

Introduction

Background

Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased intraocular pressure (IOP) and decreased visual acuity. Acute angle-closure glaucoma (AACG) is an ocular emergency and receives distinction due to its acute presentation, need for immediate treatment, and well-established anatomic pathology. Rapid diagnosis, immediate intervention, and referral can have profound effects on patient outcome and morbidity.

The acute angle closure literature has been plagued by the lack of a uniform definition and specific diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the various forms of angle closure disease. Primary angle closure, primary angle-closure glaucoma, acute angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, acute angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP >21 mm Hg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, and shallower chamber in the presence of occlusion.

Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, lens opacities, excessive trabecular pigmentation deposits). The term glaucoma is added if glaucomatous optic neuropathy is present.

Pathophysiology

AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle.

Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, and a shorter axial eye length. Of the many predisposing anatomical variations, a narrow angle and a thin, floppy iris have the most devastating consequences.

In AACG, the eye's natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. This term articulates the obstruction and blockage of aqueous flow from the posterior chamber to the anterior chamber. When pupillary block occurs in conjunction with a floppy thin iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage thus increasing IOP.

Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP.

Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can be seen in pan-retinal photocoagulation, scleral buckles, and uveitis.

Frequency

United States

AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity.

Mortality/Morbidity

Outcome after AACG is dependent on duration from onset to treatment, underlying ocular disease, and ethnicity. The degree of IOP elevation has been shown to have less impact on future visual acuity. Studies report that as many as two thirds of individuals with AACG had no visual field loss. However, Asians appear to be more refractory to the initial medical management, and, even after definitive treatment, they experience a progressive increase in IOP and deterioration in visual acuity.

Race

AACG occurs in 1 of 1000 Caucasians, about 1 in 100 Asians, and as many as 2-4 of 100 Eskimos.

Sex

AACG predominately affects females because of their shallower anterior chamber.

Age

Elderly patients in their sixth and seventh decades of life are at greatest risk.

Clinical

History

Classically, patients are elderly, suffer from hyperopia, and have no history of glaucoma.

• Most commonly, they present with periorbital pain and visual deficits. The pain is boring in nature and associated with an ipsilateral headache.
• Patients note blurry vision and describe the phenomenon of, "seeing halos around objects."
• Careful investigation may elucidate a precipitating factor (ie, dim light, anticholinergic, sympathomimetic medications).
• In a large percentage of patients, extraocular symptoms and systemic manifestations are the chief complaint.
  • Patients present with headache and may receive medications for migraines or an evaluation for a subarachnoid hemorrhage.
  • Several case reports discuss patients presenting with vomiting and abdominal pain that were misdiagnosed with gastroenteritis.

Physical

• The emergency department evaluation of the eye includes visual acuity, the external eye, visual fields, a funduscopic examination, pupils, ocular motility, and IOP. All of which tend to be affected in AACG.
• Patients complain of blurred vision, and testing reveals the ability only to detect hand movements. They are unable to identify numbers and letters on distance charts or near cards.
• Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea obscures the funduscopic examination.
• Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed.

Causes

• Shallower anterior chambers; anteriorly situated lens; shorter axial eye length; a thin, floppy iris; and a narrow angle lead to a higher propensity for development of AACG.
• Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants), dim light, and rapid correction of hyperglycemia.

• Search for CME/CE on This Topic »

• Glaucoma, Drug-Induced (Ophthalmology)
• Glaucoma, Angle Closure, Acute (Ophthalmology)
• Glaucoma, Complications and Management of Glaucoma Filtering (Ophthalmology)
• Glaucoma, Primary Open Angle (Ophthalmology)

• Glaucoma Center
• Acute Angle-Closure Glaucoma Causes
• Acute Angle-Closure Glaucoma Treatment
• Acute Angle-Closure Glaucoma Overview
• Acute Angle-Closure Glaucoma Symptoms
• Understanding Glaucoma Medications
• Glaucoma Overview
• Glaucoma FAQs

• ARVO 2009: Trabeculectomy May Be More Effective Than Medical Therapy in Reducing Intraocular Pressure in Glaucoma Patients
• Current Glaucoma Care Is Cost-Effective
• Gold Shunt Controls Pressure With Glaucoma

• Common Ophthalmic Emergencies
• Which Quality of Life Score is Best for Glaucoma Patients and Why?
• Highlights in Glaucoma From the 2008 World Ophthalmology Congress

• Glaucoma Resource Center
• Pediatric Ophthalmology Resource Center