Case Study 1 - CC: Acute R Eye Pain

HPI:
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:
Started wearing reading glasses at age 42; now wears progressive bifocals with hyperopic correction for distance
No prior eye surgeries, trauma, amblyopia or strabismus

Ocular Medications:
None

Past Medical History:
Degenerative disc disease – lower back

Surgical History:
None

Past Family Ocular History:
Father: chronic angle closure glaucoma
No FHx of macular degeneration or other blinding diseases.

Social History:
30 pack year smoking history
Drinks alcohol on occasion
No illicit drug use

Medications:
Multivitamins
Vicodin prn (uses few days/month for back pain)

Allergies:
None

ROS:
Denies recent illnesses, new medications, CNS, lungs, GI, skin, joint problems except for above.

Ocular Exam

Visual Acuity (cc):
OD: 20/70
OS: 20/20

IOP (tonoapplantation):
OD: 62 mmHg
OS: 11 mmHg

Pupils:
OD pupil mid dilated, sluggish to respond to light. OS pupil round and reactive to light
No obvious APD

Extraocular Movements:
Full OU
No nystagmus

Confrontational Visual Fields:
Full to finger counting OU

External:
Normal, both sides

Slit Lamp:

Diagnosis
Suspected acute angle closure glaucoma R eye
Narrow angle L eye

Discussion

Differential Diagnosis:
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.

Definition:
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.

Examination:
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 gonioscopic contact lens 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. Another possible change includes iris ischemia which can cause sloughing of iris pigment. Pigment can be noted in the anterior chamber and on the corneal endothelium. Iris damage may cause the pupil to remain in a 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:
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 high likelihood of an attack in 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.

1.    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:
   1. Nausea/vomiting
   2. Diplopia
   3. Ocular pain
   4. Headache
   5. Halos around lights
2. What is the mechanism of angle closure in an episode of acute angle closure glaucoma resulting from a pupillary block?
   1. The apposition of the pupil border against the lens obstructs aqueous humor flow through the pupil and creates a pressure gradient with increased pressure behind the iris. This moves the iris forward with subsequent apposition of the peripheral iris with the trabecular meshwork.
   2. Decreased drainage by the trabecular meshwork causes increased pressure in the anterior chamber and pushes the iris against the lens.
   3. A portion of vitreous humor moves anteriorly and around the lens, blocking the trabecular meshwork.
   4. Increased aqueous humor drainage through the trabecular meshwork causes a decreased pressure in the anterior chamber, causing a pressure gradient that presses the iris forward and blocks the angle.

References/Resources:
Glaucoma BCSC, American Academy of Ophthalmology, 2009.

1. 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:

b. Diplopia

Most patients would have some ocular pain, periorbital headache, and maybe nausea with an acute increase in intraocular pressure to that degree. Corneal swelling would cause halos around light. Diplopia is a binocular condition and would not necessarily affect the patient in this case. 

2. What is the mechanism of angle closure in an episode of acute angle closure glaucoma resulting from a pupillary block?

a. The apposition of the pupil border against the lens obstructs aqueous humor flow through the pupil and creates a pressure gradient with increased pressure behind the iris. This moves the iris forward with subsequent apposition of the peripheral iris with the trabecular meshwork.