Glaucoma

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eMedicine Specialties > Emergency Medicine > Ophthalmology

Glaucoma, Acute Angle­Closure
Ayim K Darkeh, MD, Staff Physician, Clinical Assistant Instructor, Department of Emergency Medicine, State University of New York Downstate Medical Center Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn Updated: Oct 3, 2007

Introduction
Background
Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased intraocular pressure (IOP) and decreased visual acuity. Acute angle-closure glaucoma (AACG) is an ocular emergency and receives distinction due to its acute presentation, need for immediate treatment, and well-established anatomic pathology. Rapid diagnosis, immediate intervention, and referral can have profound effects on patient outcome and morbidity. The acute angle closure literature has been plagued by the lack of a uniform definition and specific diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the various forms of angle closure disease. Primary angle closure, primary angleclosure glaucoma, acute angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, acute angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP >21 mm Hg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, and shallower chamber in the presence of occlusion. Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, lens opacities,

excessive trabecular pigmentation deposits). The term glaucoma is added if glaucomatous optic neuropathy is present.

Pathophysiology
AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle. Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, and a shorter axial eye length. Of the many predisposing anatomical variations, a narrow angle and a thin, floppy iris have the most devastating consequences. In AACG, the eye's natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. This term articulates the obstruction and blockage of aqueous flow from the posterior chamber to the anterior chamber. When pupillary block occurs in conjunction with a floppy thin iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage thus increasing IOP. Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP. Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or

vitreous pressure. This can be seen in pan-retinal photocoagulation, scleral buckles, and uveitis.

Frequency
United States

AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity.

Mortality/Morbidity
Outcome after AACG is dependent on duration from onset to treatment, underlying ocular disease, and ethnicity. The degree of IOP elevation has been shown to have less impact on future visual acuity. Studies report that as many as two thirds of individuals with AACG had no visual field loss. However, Asians appear to be more refractory to the initial medical management, and, even after definitive treatment, they experience a progressive increase in IOP and deterioration in visual acuity.

Race
AACG occurs in 1 of 1000 Caucasians, about 1 in 100 Asians, and as many as 2-4 of 100 Eskimos.

Sex
AACG predominately affects females because of their shallower anterior chamber.

Age
Elderly patients in their sixth and seventh decades of life are at greatest risk.

Clinical
History
Classically, patients are elderly, suffer from hyperopia, and have no h history of glaucoma. Most commonly, they present with periorbital pain and visual deficits. The pain is boring in nature and associated with an ipsilateral

h headache. Patients note blurry vision and describe the phenomenon of, "seeing h halos around objects." Careful investigation may elucidate a precipitating factor (ie, dim light, a anticholinergic, sympathomimetic medications). In a large percentage of patients, extraocular symptoms and systemic m manifestations are the chief complaint. Patients present with headache and may receive medications for m migraines or an evaluation for a subarachnoid hemorrhage. Several case reports discuss patients presenting with vomiting and abdominal pain that were misdiagnosed with gastroenteritis. P Physical The emergency department evaluation of the eye includes visual acuity, the external eye, visual fields, a funduscopic examination, pupils, ocular motility, and IOP. All of which tend to be affected in A AACG. Patients complain of blurred vision, and testing reveals the ability only to detect hand movements. They are unable to identify numbers a and letters on distance charts or near cards. Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea obscures the funduscopic e examination. Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed. C Causes Shallower anterior chambers; anteriorly situated lens; shorter axial eye length; a thin, floppy iris; and a narrow angle lead to a higher p propensity for development of AACG. Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants), dim light, and rapid correction of hyperglycemia.

Differential Diagnoses

Acute Orbital Compartment Syndrome Conjunctivitis Corneal Abrasion Corneal Laceration Corneal Ulceration and Ulcerative Keratitis Endophthalmitis

Other Problems to Be Considered
Anterior uveitisGlaucoma, malignantGlaucoma, neovascularPlateau iris syndrome

Workup
L Laboratory Studies

The diagnosis of AACG is predicated upon the clinical presentation of painful vision loss and a physical examination revealing a fixed mid-dilated pupil. No definitive laboratory or imaging studies are available. However, tonometry must be performed and must demonstrate increased IOP.

Treatment
Prehospital Care
The patient should be brought to the hospital in an expeditious manner to have IOP reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any cosmetic benefit.

Emergency Department Care
The treatment of AACG consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta-blocker, and a topical steroid. Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg PO. A dose of a topical beta-blocker (ie, carteolol, timolol) will

also aid in lowering IOP. Studies have not conclusively demonstrated the superior neuronal or visual field protectiveness of one beta-blocker over another. Both beta-blockers and acetazolamide are thought to decrease aqueous humor production and enhance opening of the angle. An alphaagonist can be added for a further decrease in IOP. Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids. Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting which can drastically increase IOP beyond its already elevated level. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that while supine, the lens falls away from the iris decreasing pupillary block. After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, adjunct drops, and considering the need for further intervention such as osmotic agents and immediate iridotomy. Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block. Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent.

No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP.1 If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol. Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should not be administered in cardiovascular and renal patients. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP.1 Repeat doses may be necessary if no effect is seen and if tolerated by the patient. Laser peripheral iridotomy (LPI) performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. While LPI is the current definitive treatment, there is evidence to suggest that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG. In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy. Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.The choice of which therapy to use will be made by an ophthalmologist who will evaluate all patients via gonioscopy with complete inspection of the angle. At institutions where an ophthalmologist is immediately available on staff, initial treatment should be performed in conjunction with the specialist. If there is a delayed interval between the initial presentation and definitive ophthalmologic care, the emergency department physician should begin treatment as described above. After an appropriate reduction in IOP, immediate ophthalmologic evaluation must be ensured. If the IOP is unchanged or increased from the time of treatment, further treatment should be discontinued and the attack most likely will terminate

only with LPI. Ocular massage through a closed eyelid may be preformed while waiting for ophthalmology if no other treatment reduces IOP.

C Consultations Ophthalmologic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmologic emergency.

Medication
The goal in treatment of AACG is to reduce IOP. Medical management is the first step. A prompt reduction in IOP using topical and systemic medication decreases the duration of elevated IOP and the potential for visual field loss. IOP reduction is accomplished via suppression of aqueous humor production, eliminating pupillary block, and reversing inflammation. As with any medical intervention, intimate knowledge of the drugs, their indications, contraindications, and potential side effects can aid the physician in providing the best treatment and a favorable outcome.

Carbonic anhydrase inhibitors
These are first-line agents that should be used immediately during the initial intervention. They reduce bicarbonate production in the ciliary epithelium and therefore decrease aqueous formation.

Acetazolamide (Diamox)

Reduces rate of aqueous humor formation by direct inhibition of enzyme carbonic anhydrase (CA) on secretory ciliary epithelium, causing, in turn, a reduction in IOP. More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated. IV administration of this medication may be used for rapid relief of increased IOP. A beneficial effect occurs when used with miotics or mydriatics.

Dosing
Adult

500 mg IV stat, followed by 500 mg PO
Pediatric

5-10 mg/kg/dose IV/IM, then 0-15 mg/kg/d PO divided q6-8h
Interactions

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
Contraindications

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose level in some diabetic patients

Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Dosing
Adult

50-100 mg PO bid/tid
Pediatric

Not established

Interactions

May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alter excretion of other drugs by alkalinizing urine
Contraindications

Documented hypersensitivity; renal impairment
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur

Beta-adrenergic blockers
These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.

Timolol (Timoptic, Timoptic XE)

Reduces elevated and normal IOP by reducing aqueous humor production or possibly the outflow.
Dosing
Adult

1 gtt of 0.25% or 0.5% solution in affected eye(s) bid; if IOP is maintained at satisfactory levels, reduce dosage to 1 gtt qd in affected eye(s)
Pediatric

Not established

Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Contraindications

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, mental changes (especially in the elderly persons)

Carteolol (Ocupress)

Nonselective beta-adrenergic receptor. Blocks beta1- and beta2receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation.
Dosing
Adult

1 gtt in affected eye(s) bid
Pediatric

Not established
Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Contraindications

Documented hypersensitivity; congestive heart failure; asthma; cardiac conduction defects; breastfeeding
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Levobetaxolol (Betaxon)

Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
Dosing
Adult

1 gtt in affected eye(s) bid
Pediatric

Not established
Interactions

May have additive systemic effects if patient is already on systemic betablockers
Contraindications

Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and thirddegree AV block; overt cardiac failure; cardiogenic shock

Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and may increase outflow of aqueous humor. Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If IOP not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously.
Dosing
Adult

0.5% solution: 1-2 gtt in affected eye(s) qd0.25% solution: 1-2 gtt in affected eye(s) bidSevere or uncontrolled glaucoma: 0.5% solution bid; closely monitor patient>1 gtt (0.5% levobunolol) bid not shown to be more effective; if IOP not at satisfactory level on this regimen, concomitant therapy can be instituted; do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously
Pediatric

Not established
Interactions

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Contraindications

Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and thirddegree AV block; overt cardiac failure; cardiogenic shock
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Alpha-adrenergic agonists
These agents are used as adjunct agents to further decrease IOP secondary to their affect on aqueous humor production.

Apraclonidine (Iopidine)

Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is relatively selective alphaadrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.
Dosing
Adult

1 gtt of 0.5% or 1% in affected eye(s) tid
Pediatric

Not established

Interactions

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAO inhibitors
Contraindications

Documented hypersensitivity; patients on MAO inhibitors or have taken them in the past 14 d
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy

Brimonidine (Alphagan, Alphagan-P)

Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow.
Dosing
Adult

1 gtt in affected eye tid
Pediatric

Not established
Interactions

Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants such as barbiturates, opiates, and sedatives may potentiate effects of brimonidine

Contraindications

Documented hypersensitivity; patients receiving MAO inhibitor therapy
Precautions
Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions

May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy

Corticosteroids
These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.

Prednisolone (AK-Pred, Econopred)

Used in treatment of acute inflammations following eye surgery or other insults to the eye.In cases of bacterial infections, concomitant use of antiinfective agents is mandatory. If signs and symptoms do not improve after 2 d, reevaluate the patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.
Dosing
Adult

Solution: 1-2 gtt of solution into conjunctival sac up to q1h during day and q2h at night prnWhen a favorable response observed, reduce dosage to 1 gtt q4h; further reduction in dosage to 1 gtt tid/qid may suffice to control symptomsSusp: Shake well before using; 1-2 gtt into conjunctival sac bid/qid; during initial 24-48 h, dosing frequency may be increased prn
Pediatric

Not established

Interactions

Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids
Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin lesions
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis

Ophthalmic agents, miotic
These agents pull the peripheral iris tissue away from the trabecular meshwork helping to eliminate obstructed aqueous humor flow. They are ineffective during the initial period due to the ischemic paralysis of the iris. Miotics should be used after the immediate management and initial reduction of IOP.

Pilocarpine (Pilagan, Pilocar, Pilostat)

Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields is present. May be used alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.Frequency of instillation and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths.
Dosing
Adult

Solution: 1-2 gtt tid/qidGel: Apply 0.5-inch ribbon in the lower conjunctival sac of affected eye(s) hsIf another glaucoma medication being used hs, use gtt at least 5 min before gel
Pediatric

Not established
Interactions

May be ineffective when used concomitantly with nonsteroidal antiinflammatory agents
Contraindications

Documented hypersensitivity; acute inflammatory disease of anterior chamber
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension

Hyperosmotics
Hyperosmotic agents increase serum osmolarity and cause a fluid shift from the eye into the vascular space. The subsequent osmotic diuresis reduces IOP.

Glycerin (Osmoglyn)

Used in glaucoma to interrupt acute attacks. Reduces IOP through its diuretic effects. Adds to tonicity of blood until metabolized and eliminated by kidneys. Maximal reduction of IOP occurs 1 h after glycerin administration. The effect lasts approximately 5 h.

Dosing
Adult

1-2 g/kg PO and repeat q5h prn; alternatively, 1 mL/kg PO as a 50% solution in juice
Pediatric

Administer as in adults
Interactions

None reported
Contraindications

Documented hypersensitivity; frank or impending acute pulmonary edema, anuria, severe dehydration, and severe cardiac decompensation
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Administer orally, never parenterally; for oral use only; avoid in acute urinary retention in preoperative period; continued use may result in weight gain; caution in hypervolemia, diabetes, severely dehydrated individuals, confused mental states, congestive heart disease, and cardiac, renal, or hepatic disease

Isosorbide (Ismotic)

In the eyes, creates an osmotic gradient between plasma and ocular fluids. Induces diuresis by elevating osmolarity of glomerular filtrate, thereby hindering tubular reabsorption of water. May be used to interrupt an acute attack of glaucoma. Use when less risk of nausea and vomiting, compared with other oral hyperosmotic agents, is needed.
Dosing

Adult

1.5 g/kg PO initially, followed by 1-3 g/kg PO bid/qid prn
Pediatric

Not established
Interactions

None reported
Contraindications

Documented hypersensitivity; anuria, severe dehydration, frank or impending acute pulmonary edema, and severe cardiac decompensation
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Use repetitive doses with caution, particularly in patients with diseases associated with salt retention

Mannitol (Osmitrol)

Reduces elevated IOP when pressure cannot be lowered by other means.Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.
Dosing
Adult

1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

Not established
Interactions

May decrease serum lithium levels
Contraindications

Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
Precautions
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Follow-up
F Further Inpatient Care A low threshold for admission should be used with AACG patients. Patients who received osmotic agents may require electrolyte and volume status monitoring. Immediate ophthalmologic follow up must be scheduled and, at certain institutions, admission will help to facilitate this. F Further Outpatient Care Patients will remain on oral acetazolamide, pilocarpine, and betablockers or alpha-agonists until definitive treatment. After LPI, 33% will require topical medication to maintain lower IOP.

D Deterrence/Prevention Fellow eye surgery C Complications P Permanent decrease in visual acuity R Repeat episode M Malignant glaucoma F Fellow eye attack Central retinal artery or vein occlusion P Prognosis Several studies evaluated patients after treatment for AACG and demonstrated favorable outcomes. With adequate treatment, most patients recover their lost vision. In Caucasians, IOP was controlled with LPI alone in 65-76%. Asians more often have medically refractory initial attacks and require medications after LPI. They also have higher rates of visual field loss and subsequent increases in IOP. It has been hypothesized that the initial attack is often more severe in Asians resulting in greater trabecular damage. Another possibility is the formation of peripheral synechiae (adhesions) causing a creeping angle reclosure. P Patient Education For excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see eMedicine's patient education articles Acute Angle-Closure Glaucoma, Glaucoma FAQs, Glaucoma Overview, and Understanding Glaucoma Medications.

Miscellaneous
Medicolegal Pitfalls
To reduce the risk of lawsuits, emergency physicians should make the diagnosis and obtain an ophthalmologic consult as soon as possible.

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