![]() Oral acetazolamide should be given as the immediate release tabs and not the extended release version. Additionally, oral carbonic anhydride inhibitors, such as 1,000mg oral acetazolamide, are given as long as the patient does not have kidney disease or a sulfa allergy. Topical drops are given every five minutes for 30 minutes and the pressure is rechecked in one hour. Therapeutic agents used for acute angle attacks include topical beta blockers, alpha-2 agonists, carbonic anhydrase inhibitors and prostaglandin analogs-even though their onset of action may be delayed. The cornea can be cleared using glycerin, a topical hyperosmotic, to perform gonioscopy or a laser peripheiral ididotomy. Anterior segment optical coherence tomography (AS-OCT) can also be useful in identifying angle structures and showing angle closure, especially if the cornea is cloudy from edema. Other possible causes of secondary angle closure should also be explored, such as neovascular or inflammatory glaucoma. In this scenario, a laser peripheral iridotomy is contraindicated and filtration surgery or goniosynechialysis should be considered. However, if no deeper structures are seen, then peripheral anterior synechiae are present and the angle is closed. This may help to break the angle closure attack. On compression of the cornea with a flange-less gonioscopy lens, the iris should indent, exposing at least the posterior trabecular meshwork, implying appositional angle closure. The corneal wedge technique, using an optic section to find the end of Descemet’s membrane, can be helpful in determining your location within the angle. On slit lamp examination, the anterior chamber will be shallow and only anterior trabecular meshwork or Schwalbe’s line will be visible on gonioscopy. DiagnosisĬompression gonioscopy is key to properly diagnosing an acute angle closure. If the IOP remains elevated long enough, glaucomatous optic neuropathy may occur, resulting in primary angle closure glaucoma. Glaucomflecken is a result of lens epithelial cell necrosis from the elevated IOP. Glaucomflecken, whitish opacities on the anterior lens capsule, may also be present. Residual iris atrophy is common after acute angle closure attacks. Iris pigment cells may be liberated into the anterior chamber and coat the endothelium and anterior lens capsule. As the IOP increases to above 40mm Hg, the iris sphincter muscle becomes ischemic and can no longer constrict the pupil. First, the greatest amount of iris/lens contact occurs when the pupil is mid-dilated-this is why angle closure attacks commonly occur hours after patients are dilated as the drops start to wear off and the pupil begins to return to normal size. The mid-dilated pupil occurs in acute angle closure for two reasons. This semi-narrow angle patient is a candidate for the laser peripheral iridotomy. Slit lamp exam findings include conjunctival hyperemia, microcystic and stromal corneal edema, a shallow anterior chamber with cells and flare, iris bombé and a classic mid-dilated pupil. Patients with an acute angle closure attack will experience blurry vision with halos around lights, nausea, vomiting, headaches and severe eye pain. 1 Prolonged exposure to dim illumination or topical medications, such as tropicamide 1.0% or vasoconstrictors such as tetrahydrozoline 0.05% (found in Visine eye drops) may cause at-risk patients to develop an acute angle closure attack. Primary angle closure is more common in people of Asian or Inuit decent and usually occurs in female patients with hyperopia, shorter axial length and a thickened crystalline lens. Primary angle closure can occur by non-pupil block mechanisms as well, such as angle crowding from a thickened peripheral iris stroma, or plateau iris syndrome. This can occur acutely, causing an angle closure attack, or proper aqueous flow may be restored spontaneously, resulting in a subacute/intermittent or chronic disease course. As the iris continues to touch the trabecular meshwork, it can form peripheral anterior synechiae. As the peripheral iris bows forward, it makes contact with the trabecular meshwork and blocks the outflow of aqueous from the eye, leading to an elevated IOP. 1-3 Primary angle closure most commonly occurs when aqueous flow from the posterior to anterior chamber is blocked at the pupil by contact between the iris and the lens, leading to an increased intraocular pressure (IOP) in the posterior chamber and a forward bowing of the peripheral iris (known as iris bombé). If left untreated, primary angle closure glaucoma-a major cause of blindness worldwide-can occur and prompt intervention will be needed to preserve vision. ![]() A cute primary angle closure is an ocular emergency where hours can make the difference in a patient’s final visual outcome.
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