Masquerading Abdominal Pain
Anne Messman, M.D.


Case: A 64-year old white female presents to the Emergency Department with a chief complaint of diffuse abdominal pain for the past 6 hours. She also complains of some nausea, vomiting, and a headache that began just before the abdominal pain started. Her past medical history is significant for hypermetropy (long-sightedness) that is corrected with glasses. She has no history of migraines and does not get headaches often. This is not “the worst headache ever” but she is in some distress due to the pain. Her abdominal pain is poorly localized, and on physical exam she has some mild diffuse tenderness to palpation. The remainder of your focused physical exam is unremarkable. Concerned about her abdominal pain, you order a CBC, electrolytes, BUN, creatinine, liver function tests, amylase, lipase, total/direct/indirect bilirubin, and urinalysis, all of which return within normal limits. At this point you are considering an abdominal CT. You go into the patient’s room to tell her you will be ordering the CT, and she remarks that her headache is worsening and her vision is somewhat blurry. You did not notice this before, but it seems that the conjunctiva of her left eye is somewhat injected and her left pupil seems slightly dilated. You begin to suspect that something else is going on with this patient completely unrelated to her abdominal pain. What is on your differential diagnosis? What should you order next?

Article: When a patient presents with abdominal pain, it is easy to get caught-up looking for an abdominal cause for their pain, even if they are also complaining of non-abdominal symptoms. Although acute angle closure glaucoma (AACG) is a relatively rare entity, it is a diagnosis that must not be missed in the ED and should always be somewhere on the differential of a patient complaining of abdominal pain, nausea and vomiting, or headache. If missed, this disease can lead to optic nerve atrophy and permanent loss of vision within hours. In an ideal world, all patients would read the textbook and present with an acutely red and painful eye, blurred vision with halos around light, with onset of symptoms after emerging from a dark environment like a movie theater. Unfortunately, this is often not the case and the patient’s main complaints may lead the emergency physician down the path of an abdominal work-up or migraine treatment.

In about 90% of cases, AACG results from pupillary block in which pupillary dilation causes apposition of the lens and the iris, resulting in obstruction of aqueous outflow from the eye. Normal intraocular pressure is 10 to 21 mmHg, however when aqueous outflow is obstructed, pressure will increase beyond this normal range, often (but not always) causing pain and loss or change in vision. AACG is more common in far-sighted patients, who already have a shallow anterior chamber angle. It is also more common in patients over the age of forty, and occurs more in women. Other associated symptoms include frontal headache, nausea, vomiting, and abdominal pain. Rarely, AACG may present as painless loss of vision, confounding diagnosis yet again. In approximately 50% of cases, the patient will report similar episodes in the past, frequently with onset of symptoms at night due to pupillary constriction, and resolution of symptoms with sleep.

If you suspect or want to evaluate for AACG remember, as is often the case, that your history and physical exam are extremely important. Patients may not offer that their vision has changed in conjunction with their headache or abdominal pain, so always ask. Make sure that you have an accurate medication list, as there have been case reports of AACG due to tricyclic antidepressants, anticholinergics, selective serotonin reuptake inhibitors, intranasal phenylephrine, topiramate, and nebulized albuterol. During your physical exam, look at the eye carefully. There may be circumcorneal conjunctival injection, a steamy cornea, or a mid-dilated (4-6 mm) and fixed pupil; but you won’t know if you don’t look. You can also have the patient’s visual acuity tested; patients with AACG often have impaired visual acuity. The affected globe may also feel tender and firm compared with the non-affected globe owing to the increase in intraocular pressure. Tonometry should obviously be performed; pressures greater than 70 mmHg can be seen in AACG, and pressure greater than 40-50 mmHg can cause rapid visual loss; any pressure outside of the normal range (i.e. greater than 21 mmHg) should raise suspicion.

Once the diagnosis of AACG is made, treatment should be initiated immediately in order to have the best chance of preserving vision. Ophthalmology should be consulted emergently. Treatment in the emergency department is aimed at decreasing intraocular pressure. This can be accomplished via suppression of aqueous humor production; typical agents used include topical beta-blockers, alpha-adrenergic agonists (ex. apraclonidine) and oral or intravenous carbonic anhydrase inhibitors. The decision to use intravenous versus oral carbonic anhydrase inhibitors will depend on the patient’s degree of nausea and/or vomiting. Intravenous mannitol should be used as an adjunct to decrease the intraocular pressure unless contraindications exist; contraindications include severe dehydration, active intracranial bleeding, pulmonary edema, and well-established anuria due to severe renal disease. Once the intraocular pressure is reduced below 40 mmHg, it is important to prevent recurrence of the angle closure. Pilocarpine 1% or 2% should be used topically after pressure reduction in order to make the pupil miotic, thereby reducing the chance of recurrence.

A summary of the treatment of acute angle closure glaucoma follows:
1. Identify mid-dilated, nonreactive pupil with increased intraocular pressure.
2. Topical beta-blocker (Timoptic 0.5%), one drop.
3. Topical alpha-agonist (Iopidine 0.1%), one drop.
4. Topical steroid (Pred Forte 1%), one drop every 15 minutes for four doses, then hourly.
5. Carbonic anhydrase inhibitor (acetazolamide) 500 mg IV or PO.
6. Mannitol 1-2g/kg IV.
7. Recheck intraocular pressure hourly.
8. Topical pilocarpine 1% to 2%, one drop four times daily once intraocular pressure is below 40 mmHg.
9. Consult ophthalmology.

Acute angle closure glaucoma is a condition that we will all probably encounter at some point during our careers. Although non-ocular symptoms may be the patient’s main complaints, acute angle closure glaucoma should always come to mind in the patient with abdominal pain and/or headache. Asking the patient about ocular symptoms and doing a quick exam of the patient’s eyes takes very little time, and may save the patient’s vision. It is our job to remember this the next time we encounter a patient who may potentially have acute angle closure glaucoma.

References:

1. Dargin JM, Lowenstein RA. “The Painful Eye.” Emergency Medicine Clinics of North America 26.1 (2008): 199-216.
2. Dayan M, Turner B, McGhee C. “Lesson of the Week: Acute angle closure glaucoma masquerading as systemic illness.” British Medical Journal 313 (1996): 413-415.
3. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 6th edition. New York: McGraw-Hill, 2004.
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Posted: Sunday, April 12, 2009