Department of Ophthalmology
Case Studies

Case 1


Sudden onset of right eye pain, severe headache, blurred vision, nausea, and vomiting

 History
HPI:

A 51 year-old African American female presents with a sudden onset of right eye pain, severe headache, blurred vision, nausea, and vomiting.

The patient also reports seeing rainbow colored halos around lights. These symptoms began 2 hours ago without any inciting event. The patient was watching television when the symptoms began. There is no history of trauma, flashing lights, curtains, metamorphopsia or diplopia.

Past Ocular History:
Mild myopia
No surgeries, laser, injection or other treatment

Past Medical History:
Degenerative disc disease (low back)

Surgical History:
None

Past Family Ocular History:
Father: Chronic primary angle closure glaucoma
No history of macular degeneration, retinal detachment, blindness, or autoimmune disorders

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

Medications:
Daily Multivitamin
Vicodin prn (uses it about 1 day/month when back pain worsens)

Allergies: NKDA

 Exam

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

IOP:
OD: 62
OS: 11

Extraocular Movements: Intact

Pupils: Right pupil mildly dilated, sluggishly responsive to light. Left normal

Confrontational visual fields: Normal OU

Amsler Grid:
OD: Blurred throughout
OS: Normal

Slit Lamp:
Lids and Lashes: Normal OU
Conjunctiva/Sclera: Injected conjunctiva OD, Normal OS
Cornea: Normal OS, OD demonstrates corneal edema
Anterior Chamber – Shallow anterior chamber OD, normal depth OS,
Iris: Iris appears pushed forward OD, normal OS
Lens: Normal OU
Anterior Vitreous – Normal OU
Gonioscopy: Closed angle right eye, demonstrating iris bombe (bulging of the peripheral iris). Left eye demonstrates a narrow angle, but no apparent obstruction of the trabecular meshwork.

Dilated Fundus Examination:
OD: Hazy view through edematous cornea, CDR (cup to disc ratio) 0.3, no AV nicking, macula normal, periphery normal with no signs of retinal breaks or detachments.
OS: CDR0.3, no AV nicking, macula normal, periphery normal with no signs of retinal breaks or detachments.
 

 Discussion

Diagnosis:
Acute angle closure glaucoma

Discussion:
Normal Intraocular pressure in adults usually ranges between about 10 and 21. Acute angle closure glaucoma can cause pressures to rise very high, as seen in this patient. Angle closure is best observed using a goniolens (or gonioscope) that allows the viewer to see into the angle of the eye that cannot be done with a traditional slit lamp examination.

Acute angle closure glaucoma occurs when there is a relatively sudden blockage of the trabecular meshwork by the anterior bulging of the peripheral iris. This may occur initially with pupillary block (where the lens presses up against the iris, decreasing aqueous humor flow into the anterior chamber) resulting in increased intraocular pressure in the posterior chamber, creating a pressure gradient that subsequently presses the iris anteriorly and causes it to block the angle. Pupillary block is greatest when the iris is in a mid-dilated state. When the pupil dilates the iris bunches up on itself and makes pupillary block more likely. Individuals with a naturally occurring narrow angle are at a higher risk for acute angle closure.

As in this patient, 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. 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 iritic ischemia causing sloughing of iris pigment that can be noted in the anterior chamber and on the corneal endothelium. Permanent iris damage may cause the iris to remain in a permanent dilated position. The intraocular pressure also may rise enough to cause retinal vascular occlusion causing 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. Often times, a prophylactic peripheral iridectomy of the non-affected eye is necessary especially when it also has a chronic narrow angle. Individuals with one episode of acute angle closure glaucoma have a 40-80% chance of having another attack of the other 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 due to ciliary body ischemia and decreased aqueous humor production, and not because the angle has reopened.

 Questions
  1. A patient presents with a sudden increase of intraocular pressure to 55 in the left 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 lens obstructs aqueous humor flow through the pupil and creates a pressure gradient 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, blocks the pupil, creates a pressure gradient that subsequently results in the iris moving forward and blocks the angle.
    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:
George A Cioffi, MD, F. Jane Durcan, MD, Christopher A. Girkin, MD, Ronald L. Gross, MD
Peter A. Netland, MD, John R. Samples, MD, Thomas W. Samuelson, MD, Sara S. O’Connell, MD, Keith Barton, MD, Glaucoma BCSC, American Academy of Ophthalmology, 2009.


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For questions regarding the cases:

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Kimberly E. Stepien, MD Email

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Page Updated 11/04/2014
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