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Emergency And Acute Medicine - Glaucoma
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
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