Glaucoma

L Jay Katz
Anand V. Mantravadi


BASICS


DESCRIPTION


• Diverse mechanistic grouping of posttraumatic disorders that results in decreased aqueous outflow, elevated intraocular pressure (IOP), and subsequent optic neuropathy


• Early posttraumatic period mechanisms:


– Hyphema


– Angle recession


– Inflammation


– Lens subluxation


• Late posttraumatic period mechanisms:


– Angle recession


– Direct penetrating injury to angle structures


EPIDEMIOLOGY


Incidence


• Angle recession occurs in up to 75% of bluntly injured eyes.


– Incidence is almost 100% in cases with traumatic hyphema


– 10% of patients with angle recession >180° develop chronic glaucoma even many years after the trauma.


Prevalence


• 2.4 million eye injuries occur annually in the.


– Males are 3 times more likely to sustain eye trauma than females


RISK FACTORS


• In children and young adults, the most common cause is playground accidents.


• In ages 30+, the leading causes are sporting accidents, assaults, and motor vehicle accidents (airbag deployment).


GENERAL PREVENTION


• Appropriate protective eyewear and headgear


• Public safety measures to prevent injuries


PATHOPHYSIOLOGY


Non-penetrating blunt trauma


• A blunt force initiates an anterior-to-posterior axial compression and subsequent equatorial expansion.


• Shearing forces exceed the elasticity of the anterior chamber structures


Hyphema results from rupture of iris and ciliary body vessels.


Angle recession occurs when the ciliary body tears between the circular and longitudinal muscles.


Lens subluxation can occur with disruption of zonular fibers. Forward rotation of the lens, protrusion of vitreous through ruptured zonules, or total dislocation of the lens into the anterior chamber may result in pupillary block and iris bombe.


– The trabecular meshwork itself may be torn; subsequent scar tissue may obstruct outflow.


– Inflammation levels vary based on injury severity.


Acutely, ciliary body swelling and inflammatory debris can contribute to pressure spikes.


Chronic inflammation may result in synechiae formation and chronic angle-closure glaucoma.


Penetrating Injuries


• Usually, in the acute setting, penetration of the globe is associated with hypotony, but it can cause direct damage to outflow channels. This may result in a chronic glaucoma after the initial injury is addressed.


ETIOLOGY


Traumatic glaucoma is most commonly caused by a blunt compression injury to the globe.


COMMONLY ASSOCIATED CONDITIONS


• Unilateral cataract


• Traumatic mydriasis


• Iridodialysis


• Cyclodialysis


DIAGNOSIS


HISTORY


The inciting injury may not be recalled or may seem deceptively inconsequential.


PHYSICAL EXAM


• In the acute trauma setting, gonioscopy is difficult and sometimes impossible. The following may be seen:


– Hyphema


– Iridodialysis


– Iris sphincter tears


– Lens subluxation


– Corneal edema


• Remote to the trauma, gonioscopy can demonstrate angle abnormalities such as recession and/or peripheral anterior synechiae. The following may also be noted:


– Unilateral elevated IOP


– Unilateral cataract ± phacodonesis


DIAGNOSTIC TESTS & INTERPRETATION


Lab


Initial lab tests

In cases of hyphema where sickle cell trait or disease is a possibility, hemoglobin electrophoresis should be performed.


Follow-up & special considerations

• Hyphema in sickle cell disease or trait requires special considerations:


– Avoid carbonic anhydrase inhibitors


– Avoid epinephrine


– Poor prognosis if IOP uncontrolled >24 h


It is reasonable to hospitalize these patients for treatment and close observation.


If IOP is uncontrolled within the first 24 h, early surgical intervention is recommended.


Imaging


• Ultrasound biomicroscopy provides high-resolution imaging of the anterior chamber structures and can elucidate angle recession, iridodialysis, cyclodialysis, and zonular dehiscence.


• All patients with penetrating injury should receive a CT scan to rule out a retained foreign body.


• CT scanning may also be required to evaluate for comorbidities (orbital fractures).


Diagnostic Procedures/Other


• Traumatic glaucoma is a clinical diagnosis.


• Gonioscopy will elucidate damage to angle structures.


• Pachymetry is useful for determining the accuracy of IOP measurements.


Pathological Findings


• Angle recession has a characteristic tear between the longitudinal and circular muscles of the ciliary body.


• Abnormal corneal endothelial cell proliferation may occur in angle recession and, in some cases, has been noted to cover the meshwork with a hyaline membrane.


DIFFERENTIAL DIAGNOSIS


• Uveitis–glaucoma–hyphema syndrome


• ICE syndrome


• C-C fistula


TREATMENT


MEDICATION


First Line


• For Elevated IOP:


– Topical aqueous suppressants


– β-Blockers, α2-agonists, carbonic anhydrase inhibitors


– Prostaglandins


– Should be avoided in the acute setting when inflammation is present


– Likely helpful in chronic angle recession glaucoma


– Miotics should be avoided in traumatic glaucoma.


• For Hyphema:


– Topical cycloplegia


– Topical steroids


• For Pupillary Block from anterior lens dislocation:


– Dilation of the pupil while the patient is supine may allow the lens to fall back.


– Cataract extraction is the definitive treatment.


Second Line


• Systemic carbonic anhydrase inhydrase inhibitors


– Acetazolamide


– Diamox 125–250 mg p.o. q.i.d


– Diamox Sequels 500 mg p.o. b.i.d


– 500 mg i.v.


– Do not exceed 1 g in a 24-h period.


– Contraindicated in severe renal disease, hepatic disease, severe pulmonary obstruction, and adrenocortical insufficiency


– Methazolamide 50–100 mg p.o. b.i.d


Contraindicated in renal insufficiency


• Systemic hyperosmotic


– Mannitol 1.5—2 g/kg i.v. over a 30-min period


20% solution (7.5–10 mL/kg)


15% solution (10–13 mL/kg)


Do not exceed 500 mL in a 24-h period.


Contraindicated in anuria, progressive renal failure, CHF, severe dehydration, or intracranial bleeding


ADDITIONAL TREATMENT


Issues for Referral


• In cases of uncertain diagnosis, consultation with a glaucoma specialist is recommended.


• Referrals to the appropriate specialists may be necessary depending on the extent of the trauma and the structures involved.


SURGERY/OTHER PROCEDURES


• Surgical intervention is indicated when the maximally tolerated medical treatment has failed and the elevated IOP threatens the optic nerve.


• Surgery is also indicated when there is associated corneal blood staining.


Surgical Procedures in the acute setting:


– Anterior chamber wash-out


– Filtration surgery with anterior chamber wash-out


– In cases of papillary block from lens subluxation–-cataract extraction


Surgical Procedures in the late posttraumatic period:


– Laser trabeculoplasty has shown disappointing long-term success rates (<25% at 36 months


– Filtration surgery such as trabeculectomy or tube placement is more prone to fistula fibrosis in patients with history of trauma; use of an anti-metabolite is important to enhance the chances of long-term success.


ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


• Normotensive eyes with angle recession >180° require routine reexamination at least once a year indefinitely.


• Eyes with elevated pressure following trauma should be seen every 4–6 weeks in the 1st year following the trauma.


• The decision to treat eyes with elevated pressure is based on the overall clinical picture, taking into account the following factors:


– Severity of elevated IOP


– Optic nerve appearance


– Visual field findings


PATIENT EDUCATION


Patients should be advised of the importance of follow-up monitoring.


PROGNOSIS


Is variable and dependent on the success of maintaining a normotensive IOP and adequate patient monitoring


COMPLICATIONS


• Vision loss


• Traumatic cataract


• Loss of eye


ADDITIONAL READING


• Bazzaz S, Katz LJ, Myers JS. Post-traumatic glaucoma. In: Shaarawy TM, Sherwood MB, Hitchings RA, et al, eds: Glaucoma: Medical diagnosis and therapy, Vol. 1, Philadelphia: Saunders/Elsevier Limited, 2009:31–439.


• Canavan YM, Archer DF. Anterior segment consequences of blunt ocular injury. Br J Ophthalmology 1982;66:549–555.


• Kaufman JH, Tolpin DW. Glaucoma after traumatic angle recession: A ten-year prospective study. Am J Ophthalmology 1974;79:648–654.


• Macewan CJ. Eye injuries: A prospective survey of 5671 cases. Br J Ophthalmol 1989;73:888–894.


• Manners T, Salmon JF, Barron A, et al. Trabeculectomy with mitomycin C in the treatment of post-traumatic angle recession glaucoma. Br J Ophthalmol 2001;85:159–163.


• Melamed S, Ashkenazi I, Gutman I, et al. Nd:YAG laser trabeculopuncture in angle-recession glaucoma. Ophthalmic Surg 1992;23:31–35.


• Sihota R, Kumar S, Gupta V, et al. Early predictors of traumatic glaucoma after closed globe injury: Trabecular pigmentation, widened angle recess, and higher baseline intraocular pressure. Arch Ophthalmol 2008;126:921–926.


• Sullivan BR. Glaucoma, angle recession, eMedicine. Apr 29 2010. emedicine.medscape.com/article/1204999-overview


• Wolff SM, Zimmerman LE. Chronic secondary glaucoma. Association with retrodisplacement of iris root and deepening of the anterior chamber angle secondary to contusion. Am J Ophthalmol 1962;84:547–563.


CODES


ICD9


364.41 Hyphema of iris and ciliary body


364.77 Recession of chamber angle of eye


365.65 Glaucoma associated with ocular trauma


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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Glaucoma
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