Glaucoma

• Glaucoma is a progressive optic neuropathy as a result of increased IOP.
• There are numerous causes of glaucoma. For the purpose of the EP, glaucoma can be classified into primary vs. secondary and angle closure vs. open angle disease.
• Primary vs. secondary: Is the disease idiopathic or is there an underlying secondary cause such as trauma, recent eye surgery, hyphema, inflammation, diabetes etc?
• Angle closure vs. open angle: angle closure glaucoma occurs in far-sighted persons with an abnormally shallow anterior chamber or flat iris who are predisposed to blockage of aqueous humor flow from the posterior to anterior chamber. The outflow tract is normal in patients with open angle disease.
• The primary concern of the EP is acute angle closure glaucoma which can lead to rapid vision loss. Open angle disease is slowly progressive and patients remain asymptomatic until late in the course. The majority of glaucoma is open-angle.
• The treatment for glaucoma is generally the same no matter what the cause. Secondary glaucoma also requires attention to the underlying disorder.

Primary Acute Angle Closure Glaucoma

• Etiology: In predisposed patients, pupil dilation obstructs aqueous humor flow and causes acute symptom development. Causes include pharmacological dilation, stress and recent attendance in an area with dim lighting. It is important to obtain medication history-is the patient taking any anticholinergic or sympathomimetic agents?
• Presentation: Glaucoma symptoms include sudden onset of blurred vision, light halos, photophobia, the red eye pain, nausea, vomiting and headache.
• Examination: Patients have a mid-range fixed pupil(s), marked conjunctival injection and corneal clouding secondary to edema. On SLE, the AC is shallow. IOP is increased.
• Treatment: Prompt initiation of therapy is necessary as permanent vision loss may occur within a period of hours. The goal of treatment is to increase aqueous humor flow, decrease production and decrease volume. Obviously, those patients with higher pressures and more pronounced vision loss mandate more aggressive treatment. Decreased aqueous humor production:
• Carbonic anhydrase inhibitors such as acetazolamide, brinzolamide and dorzolamide. Acetazolamide is given IV or by mouth at a dose of 500 mg. The other two agents are topical and used for maintenance therapy. Avoid in patients with sulfa allergy.
• Topical �-blockers: The most commonly used agent in the ED is 0.25% or 0.5% timolol with one drop applied to the affected eye. Use with caution in patients who have diabetes, pulmonary disease and heart failure.
• Decrease volume of aqueous humor: Achieved with mannitol or glycerol. Glycerol is p.o. and often poorly tolerated. Dose of mannitol is 1-2 g/kg IV over 30 min.
• Increased aqueous humor flow: The most commonly used agent in the ED is topical pilocarpine 2% with one drop applied to both the affected and unaffected eyes.
  The dose is repeated every 15 min in the affected eye until the pupil constricts.

Chemical Injuries
Etiology Exposure to any number of possible agents including acids, bases, detergents, pepper spray and super glue.

• Alkali
• Sources include lime, ammonia, cement, plaster and some household cleaners.
• Alkalis cause extensive tissue destruction via liquefaction necrosis and rapidly penetrate to a depth sufficient to cause severe damage to deep ocular structures.
• Acids
• Sources include hydrofluoric acid (glass cleaning agents and rust removers) and car batteries.
• Acids cause coagulation necrosis which tends to limit the depth of penetration.
• Super glue (cyanoacrylate adhesive): Exposure seals the eyelids shut. Corneal abrasions occur as a result of hardened glue rubbing against the epithelium.

Presentation

• Depends upon the duration of exposure and the pH and concentration of the offending agent. Glaucoma signs and symptoms range from mild conjunctival injection, chemosis, pain and photophobia to severe burns with complete corneal opacification, corneal perforation, and vision loss. Patients may also have burns of surrounding periorbital tissue.

Examination

• The entire eye needs to be examined and the lid margins completely everted. Any particulate matter and necrotic tissue should be gently removed with a Q-tip in order to minimize continued chemical exposure.
• Fluoroscein staining: corneal defects are common. However, if all of the corneal epithelium has been denuded, there will be minimal or no fluoroscein uptake.
• IOP: Sometimes elevated. Assess with tonopen or tonometer.
• pH: Easily measured with litmus paper placed in the fornix. Check pH both before and several times after treatment.

Treatment

• Irrigation
• No matter what the offending chemical, immediate irrigation is mandatory. If it is possible to direct prehospital care, instruct patients to begin irrigation with tap water as soon as possible after exposure.
• In the ED, patients should receive topical tetracaine and then irrigation with normal saline or lactated ringers via a Morgan lens. Irrigation is continued until a neutral pH is achieved. When checking pH after irrigation, wait 10-15 min in order to avoid measuring the pH of the irrigating solution. Note that normal pH can vary slightly between individuals and the measured pH does not necessarily reflect the pH of the AC and deeper structures.
• In general, all significant exposures will require irrigation with at least 2 L of fluid.
  With strong acids and bases, irrigation is continued over a period of hours.

Hydrofluoric acid (HF):
Treatment for ocular HF exposure is the same as for other ocular chemical injuries. While calcium gluconate is used for skin exposures, topical ocular therapy with this agent is not yet standard of care.

Super glue (cyanoacrylate adhesive):
Patients should be referred to ophthalmology. Do not attempt to pry the eyelids open or dissolve glue with other substances.

• Topical cycloplegics, eye patching and parenteral analgesics are helpful for the patient with severe photophobia and pain.
• Increased IOP requires treatment with appropriate agents: �-blockers, pilocarpine, etc.
• Patients should be given either antibiotic solution or ointment.
• Never attempt to neutralize acids or bases. This will cause a heat-producing reaction and further tissue damage.
• Ophthalmologic consultation is warranted for all significant exposures.
• Complications: perforation, glaucoma, cataracts, retinopathy, adhesions and neovascularization of the cornea.