The patient is a 51 year-old stay-at-home mother who presented to the ED with severe R brow, R cheek and R eye pain/pressure that started 2-3 hrs prior. She also noticed blurry vision from that eye and rainbow-colored halos around lights around the same time. Accompanying symptoms include acute nausea. She has vomited twice since feeling the eye pain. Denies prior episodes. Denies flashes, floaters or diplopia. There is mild redness in the R eye.
Past Ocular History:
Hx myopia OU
No prior eye surgeries, trauma, amblyopia or strabismus
Past Medical History:
Degenerative disc disease – lower back
Past Family Ocular History:
Father: chronic angle closure glaucoma
No FHx of macular degeneration or other blinding diseases.
30 pack year smoking history
Drinks alcohol on occasion
No illicit drug use
Vicodin prn (uses few days/month for back pain)
Denies recent illnesses, new medications, CNS, lungs, GI, skin, joint problems except for above.
Visual Acuity (cc):
OD: 62 mmHg
OS: 11 mmHg
OD pupil mid dilated, sluggish to respond to light. OS pupil round and reactive to light
No obvious APD
Confrontational Visual Fields:
Full to finger counting OU
Normal, both sides
Lids and Lashes
Mild diffused injected conjunctiva OD, Normal OS
Hazy cornea OD, Normal OS
Shallow anterior chamber 360 OD – hazy view, Deep and quiet OS
Mid dilated iris OD, Normal OS
Trace nuclear sclerosis OU
Dilated Fundus Examination:
Dilation not performed, examination through undilated pupil showed hazy view, CDR 0.5 with sharp optic disc margins; flat macula
Dilation not performed, examination through undilated pupil showed clear media, CDR 0.4 with sharp optic disc margins; flat macula
Gonioscopy: Performed with Abraham 4 mirrored lens, shallow angle and no view of the angle structures 360 degrees OD, shallow angle with view of the trabecular meshwork 360 degrees OS without synechiae, mild pigmentation 360 degrees OS
Suspected acute angle closure glaucoma R eye
Narrow angle L eye
The patient described is presenting with acute angle closure glaucoma due to shallow anterior chamber angles. Other causes of increase intraocular pressure include open angle glaucoma or other pathology of the trabecular meshwork (pigmentary dispersion, pseudoexfoliation, trauma, neovascularization, etc.) that obstructs aqueous outflow. Forward displacement of intraocular structures (posterior tumor, choroidal swelling, etc.) can also block the outflow of aqueous and increased the intraocular pressure.
Acute angle closure glaucoma occurs when there is a relatively sudden blockage of the trabecular meshwork causing elevation of the intraocular pressure. One possible mechanism is the anterior bulging of the peripheral iris, occluding the trabecular meshwork and trapping aqueous humor inside the eye. The reason for the sudden anterior bulging of the peripheral iris may be due to pupillary block (where the lens presses up against the iris trapping all the aqueous humor behind it). This results in increased fluid in the posterior chamber, creating a pressure gradient that subsequently pushes the iris anteriorly and causes it to block the angle. The intraocular fluid accumulates and rises significantly (normal intraocular pressure is between 8 and 21 mmHg). Pupillary block is greatest when the iris is in a mid-dilated state. Individuals with a naturally occurring narrow angle are at a higher risk for acute angle closure.
Acute angle closure typically presents with severe ocular pain, headache, blurred vision, halos around lights, nausea, and vomiting. Some of the apparent non-ocular manifestations (nausea/vomiting) could be misleading to the inexperienced physician. However, the prompt recognition and subsequent treatment of an acute angle closure crisis is paramount in the preservation of the patient’s vision. Typical eye exam findings, as in this patient, include mild conjunctival injection, hazy cornea, mid dilated pupil, shallow angle and elevated intraocular pressure.
Angle closure is best observed using a goniolens (or gonioscope) that allows the viewer to see into the angle of the eye. Even if the acute episode is diagnosed and treated quickly and appropriately there can still be optic nerve damage and resultant visual loss. Other possible changes include iris ischemia causing sloughing of iris pigment that can be noted in the anterior chamber and on the corneal endothelium. Iris damage may cause it to remain in a permanent dilated position. The intraocular pressure may also rise enough to cause retinal vascular occlusion and retinal ischemia. Anterior subcapsular lens opacities may also occur as a result of ischemia (this is termed glaukomflecken).
Treatment of acute angle closure glaucoma is either laser or surgical peripheral iridectomy (placing a hole in the peripheral iris). This procedure restores aqueous flow from the posterior to anterior chamber by creating an extra opening in the iris, relieving the pathologic pressure gradient. This ultimately allows the iris to regress and pull away from the trabecular meshwork and then normal aqueous humor drainage is restored. This procedure is often curative of the affected eye. A prophylactic peripheral iridectomy of the non-affected eye is necessary to prevent an episode from occurring in the fellow eye. Individuals with one episode of acute angle closure glaucoma have a highly likelihood of an attack on the fellow eye over the next 5-10 years. Even when the intraocular pressure has decreased, subsequent follow up is necessary to be sure that the angle remains open. IOP may decrease soon after the attack due to ciliary body ischemia and decreased aqueous humor production, and not because the angle has reopened.
Self-Assessment Questions click or tap answer area to view the correct response
A patient presents with a sudden increase of intraocular pressure to 55 mmHg in the L eye. Gonioscopic examination demonstrates a closed angle with trabecular meshwork obstruction. Which of the following is not a likely presenting symptom in this patient:
What is the mechanism of angle closure in an episode of acute angle closure glaucoma resulting from a pupillary block?
Glaucoma BCSC, American Academy of Ophthalmology, 2009.