A 50-year-old Asian female presents to the emergency department (ED) with severe nausea, vomiting, right eye pain, and blurry vision. She reports the symptoms began only a few hours earlier. She has no significant past medical history. On gross examination, her visual acuity is OD 20/200, her right eye is injected, and her right pupil is larger than her left. There does NOT appear to be a relative afferent pupillary defect (RAPD).
Question 19.2.1 With regard to this patient's presentation, which of the following would NOT be considered in the differential diagnosis?
A) Trauma secondary to blunt injury from a softball
B) Central retinal artery occlusion
C) Contact lens associated bacterial keratitis
D) Acute angle closure glaucoma
Answer 19.2.1 The correct answer is "B." Among these choices, only central retinal artery occlusion would be painless and also associated with a RAPD (from diffuse retinal ischemia). All of the others will present with pain and WITHOUT a RAPD. "A," blunt injuries, may result in decreased vision secondary to corneal abrasions or edema, intraocular inflammation, hyphema, or retinal injuries. Injury can also cause injection and a traumatic mydriasis (dilation of the pupil). Direct and consensual pupillary reflexes would be normal (no RAPD) unless there was an associated traumatic optic neuropathy or significant retinal damage. "D," acute angle closure glaucoma, would cause diffuse injection with a mid-dilated pupil and no RAPD. "E," anterior uveitis, would also cause injection—but often only ciliary flush—and no RAPD. There is often asymmetry of the pupils in chronic anterior uveitis secondary to central posterior synechiae (adhesions between the iris and lens).
Question 19.2.2 Which of the following is required in order to diagnose acute angle closure glaucoma?
C) Fluorescein and appropriate UV light
Answer 19.2.2 The correct answer is "B." The most important examination technique used to diagnose acute glaucoma is intraocular pressure measurement. This could be achieved by Tonopen, Goldmann applanation tonometry at the slit lamp, Schiotz tonometer (anyone remember this antique?), assessed via digital palpation, etc. "A" is incorrect. A slit lamp is useful for diagnosing structural problems, iritis, etc. "C," fluorescein, is used to diagnose corneal injuries (de-epithelized cornea will take up fluorescein). "D," a Snellen eye chart, is used to determine visual acuity but is not necessary for diagnosing glaucoma. It is always a good idea to check vision in each eye in every patient with eye complaints; think of checking visual acuity as taking "vital signs" for the eye (see Fig. 19-3).
FIGURE 19-3. Acute angle closure glaucoma. Note the injection, hazy corneal reflex, and mid-dilated pupil.
Question 19.2.3 Which of the following is NOT a risk factor for acute angle closure glaucoma?
A) Hyperopia (farsightedness)
D) Pharmacologic dilation
Answer 19.2.3 The correct answer is "C." Associated risk factors for acute angle closure glaucoma are hyperopia, Asian ancestry, female gender, and older age. Patients with hyperopia have smaller eyes and more shallow anterior chambers. Females and people of Asian descent also tend to have smaller eyes. As people age, cataracts may develop, become thicker, and crowd the anterior chamber, increasing the likelihood of developing pupillary block leading to glaucoma.
Pharmacologic dilation may result in an attack of acute angle closure glaucoma. But where better a place for it to show up than in your office or the ED? Neovascularization of the eye (such as from diabetes or retinal hypoxia) can lead to "neovascular glaucoma" from neovascularization of the iris and angle. Hyphema can cause glaucoma from clot obstructing the outflow of aqueous humor.
Question 19.2.4 Which of the following is NOT a presentation of acute closed-angle glaucoma?
D) Limitation of extraocular motion
Answer 19.2.4 The correct answer is "D." Patients with acute closed-angle glaucoma can present with all of the above findings except for the limitation of extraocular motion. Severe eye pain and blurred vision are commonly noted due to corneal edema and clouding secondary to the increased intraocular pressure.
You call your local ophthalmologist or optometrist to see this patient with suspected acute angle glaucoma. She is going to be delayed because of traffic—it's Iowa, so she's likely stuck behind a big tractor … we don't have "rush hour," only "rush minute."
Question 19.2.5 Which of the following drugs is NOT appropriate to use as a temporizing measure?
A) Topical carbonic anhydrase inhibitors
D) Topical atropine drops
E) Topical prostaglandin analog drops
Answer 19.2.5 The correct answer is "D." Atropine is contraindicated in acute glaucoma since it will dilate the eye, exacerbating the problem. Topical β-blockers ("B") and topical ("A") or oral carbonic anhydrase inhibitors (e.g., acetazolamide) reduce aqueous production and thereby reduce intraocular pressure. In addition to the medications noted above, a topical α-adrenergic agonist (e.g., brimonidine, apraclonidine) also lowers eye pressure by selectively affecting the α-2 receptors and decreasing aqueous production. Topical glycerin ("C") is used to clear the corneal edema. Prostaglandin analogs ("E", e.g., latanoprost, etc.) increase aqueous outflow, thereby also decreasing intraocular pressure. It is generally third line after iridotomy for acute closed-angle glaucoma.
In general, eye drops that dilate the eye have a red cap on them, so if you are in a panic and you've forgotten all the good advice from this awesome book, a good rule of thumb is to use any eye drop WITHOUT a red cap. See Table 19-1 for details on glaucoma medications.
TABLE 19-1DRUGS USED FOR ACUTE GLAUCOMA AND HOW THEY WORK ||Download (.pdf) TABLE 19-1 DRUGS USED FOR ACUTE GLAUCOMA AND HOW THEY WORK
|Drug ||Mechanism of Action |
|Topical β-blockers (e.g., timolol) ||Decreases aqueous humor production |
|Topical α-adrenergic agonists (e.g., brimonidine) ||Decreases aqueous humor production |
|prostaglandin analogs (e.g., latanoprost, bimatoprost, travoprost) ||Increases aqueous humor outflow through uveoscleral channels |
|Topical carbonic anhydrase inhibitors (e.g., dorzolamide, brinzolamide) ||Decreases aqueous humor production |
|Oral carbonic anhydrase inhibitor (e.g., acetazolamide) ||Diuretic and, more importantly, decreases the production of aqueous humor |
|mannitol (rarely use now for acute glaucoma, mostly OR cases only) ||Osmotic diuretic draws aqueous humor from the eye |
Did you notice that pilocarpine, the classic agent for treating acute glaucoma, is absent from the list? Turns out it doesn't work all that well unless the intraocular pressure is already less than 40 mm Hg.
An ophthalmologist makes it to the hospital and recommends surgery.
Question 19.2.6 What is the definitive treatment of choice for acute angle closure glaucoma?
A) Laser peripheral iridotomy
B) Tapping of the anterior chamber to lower intraocular pressure
C) Aqueous suppressant therapy
E) Chiropractic manipulation of the iris
Answer 19.2.6 The correct answer is "A." The treatment goal is to allow the free flow of aqueous so that it does not accumulate behind the iris to push it forward to obstruct the trabecular meshwork. A laser peripheral iridotomy creates a small hole in the peripheral iris that allows aqueous flow to improve and thereby decreases intraocular pressure. As long as this hole remains patent, the patient is no longer at risk for an attack of angle closure glaucoma, and it is unusual for the hole to close unless there is a history of intraocular inflammation. "B," tapping the anterior chamber, can be used before laser therapy in order to clear the cornea so that visualization is better for the procedure. However, it is adjunctive and not a treatment of choice. Also, topical glycerin works well and can accomplish the same goal without being invasive. "C," aqueous suppressant therapy, is discussed in the previous question. "D," a surgical iridectomy, is performed for patients who are unable to sit still for the laser procedure (i.e., children, intellectually disabled). As to "E" … nothing against chiropractors, but this might not be the right time.
Question 19.2.7 Which is FALSE regarding closed- and open-angle glaucoma?
A) The main difference is that the drainage angle (trabecular meshwork) is closed in angle closure glaucoma and open in open-angle glaucoma
B) Scopolamine and other agents with anticholinergic properties are contraindicated in open-angle glaucoma but not in closed angle
C) Acute angle closure glaucoma usually occurs in hyperopic individuals while myopia is associated with open-angle glaucoma
D) The majority of people diagnosed with glaucoma have primary open-angle glaucoma
Answer 19.2.7 The correct answer (and false statement) is "B." Scopolamine and agents with anticholinergic properties, which would cause dilation of the pupil, are actually contraindicated in those with closed-angle glaucoma (and those with narrow angles who may not yet have obstructed). Once peripheral iridotomy is performed, anticholinergics are no longer an issue since the patient is no longer at risk. All of the rest of the statements are correct.
Question 19.2.8 Which of the following does NOT increase a patient's risk for primary open-angle glaucoma?
C) Elevated intraocular pressure (>21 mm Hg)
Answer 19.2.8 The correct answer is "B." Patients of African heritage are much more likely to develop open-angle glaucoma than are Caucasians and are also more likely to suffer vision loss from glaucoma. Family history, high intraocular pressures, and thin corneas are all risk factors for the development of open-angle glaucoma. High intraocular pressures lead to optic nerve damage. Minor risk factors include diabetes and myopia (nearsightedness). All patients should be screened for glaucoma as part of their routine eye examination. This is usually done by assessing intraocular pressure, examining the optic nerve and corneal thickness, and performing any ancillary diagnostic tests such as peripheral visual field analysis.
Question 19.2.9 Which of the following is typical of early open-angle glaucoma?
B) Peripheral vision loss
Answer 10.2.9 The correct answer is "C." Most people with early open-angle glaucoma are asymptomatic. This is why screening is important. A significant number of the approximately one million axons of the optic nerve may be damaged before this manifests itself as visual field loss. Examination of the optic nerve for abnormalities is the best way to diagnose early glaucoma. Later symptoms involve loss of peripheral or central vision.
Question 19.2.10 Which of the following is necessary to diagnose a patient with open-angle glaucoma?
A) Optic nerve head cupping or irregularity with corresponding visual field loss
C) Elevated intraocular pressure
D) Narrow but open drainage angle
Answer 19.2.10 The correct answer is "A." Cupping of the optic nerve head is caused by thinning of the neural rim secondary to damage from high intraocular pressure. There should be a corresponding visual field defect consistent with the appearance of optic nerve cupping to diagnose a patient with glaucoma. In open-angle glaucoma, the mechanism of injury to the optic nerve is thought to be direct mechanical compression. Note that elevated intraocular pressure is not diagnostic of open-angle glaucoma. Glaucoma describes the changes to the optic nerve that are often secondary to ocular hypertension. Elevated intraocular pressure by itself is considered a risk factor for glaucoma. When not accompanied by cupping or visual field loss, it is considered ocular hypertension. Patients with ocular hypertension still need to be monitored and treated to prevent the development of open-angle glaucoma. Conversely, some patients with glaucoma never develop high intraocular pressure indicating that glaucoma may, in fact, be due to optic nerve damage arising from a variety of etiologies, the most common being elevated intraocular pressure. Thinner corneas ("B") increase the risk of glaucoma but are not required for diagnosis. "D" is incorrect. The drainage angle must be widely open—thus the name "open-angle glaucoma."
Question 19.2.11 Which of the following statements regarding glaucoma is true?
A) If treated early enough, normalizing the intraocular pressure can reverse the process of glaucoma and restore sight
B) The funduscopic examination in patients with glaucoma will generally show small retinal hemorrhages in addition to optic nerve cupping
C) Papilledema is seen with glaucoma as a result of increased pressure on the optic nerve
D) There are no identified genetic markers that correlate to development of glaucoma
Answer 19.2.11 The correct answer is "E." So, wrong, wrong, wrong … and wrong. Once there is visual loss, it cannot be restored ("A"). Optic nerve hemorrhages, and not retinal hemorrhages, are seen in glaucoma ("B"). Retinal hemorrhages are typically seen with diabetic or hypertensive retinopathies. Papilledema results from increased intracranial—not intraocular—pressure ("C"). There are multiple genes that have been identified that contribute to the development of glaucoma ("D"). See Figure 19-4 for images of normal-appearing optic nerves, and compare these with Figure 19-5, which shows optic nerve findings in patients with glaucoma.
FIGURE 19-4. Normal optic nerve.
FIGURE 19-5. Glaucomatous optic nerve. Observe the cupping of the optic nerve head. The cup (central depression, seen as the bright part of the disc) of the optic nerve, which represents the axons diving down into the optic nerve, is larger compared with normal. A cup >50% of the disc width is indicative of glaucoma. Cupping represents damage to the optic nerve and fewer axons are present.
Objectives: Did you learn to…
Recognize the signs and symptoms of acute angle closure glaucoma?
Identify risk factors associated with acute angle closure glaucoma?
Describe the pathology and basis for treatment for glaucoma?
Differentiate between angle closure and open-angle glaucoma?
Describe optic nerve findings in glaucoma?