- •Foreword
- •Erratum
- •Preface
- •The Physical Examination of the Eye
- •The orbit
- •The external eye
- •The eyeball
- •The conjunctiva
- •Tenon’s capsule
- •The sclera and episclera
- •The cornea
- •The anterior chamber
- •The uvea
- •The iris
- •The ciliary body
- •The choroid
- •The lens
- •The retina
- •The vitreous
- •The extraocular muscles
- •The rectus muscles
- •The oblique muscles
- •Innervation of the eye
- •The optic nerve (II)
- •The oculomotor nerve (III)
- •The trochlear nerve (IV)
- •The trigeminal nerve (V)
- •The abducens nerve (VI)
- •The blood supply of the eye
- •Physical examination of the eye
- •Vision
- •External examination
- •Extraocular movements
- •Examination of the conjunctiva
- •Examination of the sclera and episclera
- •Examination of the uvea
- •Intraocular pressure
- •Examination of the cornea
- •Examination of the pupils
- •Examination of the anterior chamber
- •Ophthalmoscopy
- •Summary
- •References
- •Visual acuity testing
- •Slit lamp examination
- •Flourescein examination
- •Tonometry
- •Lid eversion
- •Foreign body removal
- •Contact lens removal
- •Eye irrigation
- •Paracentesis
- •Lateral canthotomy
- •Ocular ultrasonography
- •Summary
- •References
- •Conjunctivitis
- •Subconjunctival hemorrhage
- •Episcleritis
- •Scleritis
- •Uveitis
- •Acute angle-closure glaucoma
- •Summary
- •References
- •Conjunctivitis
- •Viral conjunctivitis
- •Bacterial conjunctivitis
- •Neonatal conjunctivitis
- •Episcleritis
- •Keratitis
- •Viral keratitis
- •Bacterial keratitis
- •Keratitis due to light exposure
- •Uveitis
- •Anterior uveitis
- •Intermediate uveitis
- •Posterior uveitis and retinitis
- •Hordeolum and chalazion
- •Dacryocystitis
- •Periorbital and orbital cellulitis
- •References
- •Acute Monocular Visual Loss
- •Temporal arteritis
- •Epidemiology
- •Etiology
- •Clinical features
- •Diagnosis and treatment
- •Optic neuritis
- •Epidemiology
- •Etiology
- •Clinical features and diagnosis
- •Treatment
- •Central retinal artery occlusion
- •Epidemiology
- •Etiology
- •Cardiogenic embolism
- •Other causes
- •Clinical features
- •Diagnosis and treatment
- •Central retinal vein occlusion
- •Epidemiology
- •Etiology
- •Clinical features
- •Diagnosis and treatment
- •Retinal detachment
- •Epidemiology
- •Etiology
- •Clinical features
- •Diagnosis and treatment
- •Retinal vasculitis
- •Epidemiology and etiology
- •Clinical characteristics
- •Diagnosis and treatment
- •Summary
- •References
- •Trauma to the Globe and Orbit
- •History and physical examination
- •Imaging techniques
- •CT scan
- •Ultrasound
- •Blunt trauma to the orbit
- •Periorbital tissues
- •Orbital fractures
- •Retrobulbar hemorrhage
- •Anterior chamber
- •Traumatic hyphema
- •Subconjunctival hemorrhage
- •Injury to the iris and ciliary body
- •Traumatic iridocyclitis (uveitis)
- •Traumatic mydriasis and miosis
- •Iridodialysis
- •Acute glaucoma
- •Injury to the lens
- •Subluxation and dislocation
- •Cataract formation
- •Globe injury
- •Globe rupture
- •Globe luxation
- •Posterior segment
- •Vitreous hemorrhage
- •Chorioretinal injury
- •Commotio retina
- •Penetrating ocular injury
- •Periorbital tissues
- •Conjunctival lacerations
- •Laceration of the eyelid
- •Globe injury
- •Corneoscleral laceration and puncture wounds
- •Intraocular foreign body
- •Orbital foreign body
- •Delayed complications
- •Endophthalmitis
- •Sympathetic ophthalmia
- •Burns
- •Acid and alkali exposure
- •Miscellaneous irritants, solvents, and detergents
- •Thermal burns
- •UV keratitis
- •Prevention
- •Acknowledgment
- •References
- •Chemical burns
- •Pathophysiology
- •Alkali injury
- •Acid injury
- •Cyanoacrylate exposure
- •Treatment
- •Thermal injuries
- •Radiation injuries
- •Treatment
- •Biologic exposures
- •Treatment
- •Disposition
- •References
- •Neuro-Ophthalmology
- •Neuroanatomy and neuro-ophthalmologic examination
- •The visual pathway
- •The cranial nerves
- •Neuro-ophthalmologic examination
- •Visual acuity
- •Funduscopic examination
- •Testing ocular motility
- •Pupillary disorders
- •Pupil size and reactivity
- •Anisocoria
- •Horner syndrome
- •Tonic (Adie) pupil
- •Pharmacotherapy and pupils
- •Traumatic optic neuropathy
- •Optic neuritis
- •Oculomotor nerve palsy
- •Extraocular movement disorders
- •Cranial nerve palsies and binocular diplopia
- •Cranial nerve III
- •Cranial nerve IV
- •Cranial nerve VI
- •Nystagmus
- •Peripheral nystagmus
- •Central nystagmus
- •Myasthenia gravis
- •Multiple sclerosis
- •Stroke syndromes and gaze palsies
- •Stroke syndromes and the visual system
- •Anterior cerebral artery
- •Internal carotid artery
- •Middle cerebral artery
- •Posterior cerebral artery
- •Basilar artery
- •Vertebal arteries
- •Gaze palsies/conjugate gaze deviation
- •Hemispheric lesions
- •Midbrain lesions
- •Pontine lesions
- •Summary
- •References
- •Visual development
- •The eye examination in a child
- •Examination of the newborn and young infant
- •Older infants and preverbal children
- •Verbal children
- •Conjunctivitis
- •Ophthalmia neonatorum (neonatal conjunctivitis)
- •Childhood conjunctivitis
- •Orbital and periorbital cellulitis
- •Lacrimal system infections
- •Congenital
- •Nasal lacrimal duct obstruction
- •Congenital cataracts
- •Congenital glaucoma
- •Misalignment
- •Oncology
- •References
- •The Painful Eye
- •Acute angle closure glaucoma
- •Scleritis
- •Anterior uveitis (iritis)
- •HLA-B27-associated uveitis
- •Other noninfectious etiologies
- •Infectious etiologies
- •Treatment of anterior uveitis
- •Optic neuritis
- •Keratitis
- •Noninfectious keratitis
- •Ulcerative keratitis
- •Infectious keratitis
- •Bacterial
- •Viral
- •Fungal
- •Amoebic
- •Corneal abrasion
- •References
- •Acquired syphilis
- •Varicella-zoster virus infection
- •Lyme disease
- •Reiter’s syndrome
- •Infectious endocarditis
- •Kawasaki’s disease
- •Temporal arteritis
- •Hypertension
- •Diabetes
- •Summary
- •References
- •Emergency ophthalmology consultation caveats
- •Emergency diagnoses requiring emergency ophthalmology consultation
- •Trauma
- •Endophthalmitis
- •Acute angle closure glaucoma
- •Severe uveitis
- •Corneal ulceration
- •Acute visual loss
- •Optic neuritis
- •Central retinal artery occlusion
- •Retinal detachment
- •Orbital cellulitis
- •References
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plasminogen to plasmin and therefore delays clot dissolution and theoretically decreases the risk of rebleeding. Studies have shown that topical ACA is as e ective as systemic ACA and avoids the side e ects typically associated with administration such as nausea, vomiting, and hypotension [1]. These agents should be avoided in pregnant patients, patients who have renal or hepatic dysfunction, or those at risk for thromboembolic disease. Intracameral tissue plasminogen activator currently is under investigation and is reserved for large clots of prolonged duration or malignant elevation of intraocular pressure. In addition, elevated intraocular pressure (O 24 mm Hg) can be treated with topical beta-blockers and carbonic anhydrase inhibitors such as acetazolomide. Acetazolomide lowers pH, causing increased sickling, and should be avoided in pediatric patients or those who have sickle cell trait or anemia. Methazolomide is the preferred agent in this situation [21]. Mannitol may be administered for severely elevated intraocular pressure (O 35 mm Hg). Nonsteroidal anti-inflammatory medications and aspirin should be avoided because of the increased risk of rebleeding. Surgery usually is reserved for delayed complications such as corneal staining and persistently elevated intraocular pressures but often is performed early in patients who have sickle cell anemia or trait.
Subconjunctival hemorrhage
Subconjunctival hemorrhage is caused by the rupture of small subconjunctival blood vessels. Although patients may report a prior sneezing or coughing episode or a Valsalva maneuver, some patients may have no recollection of the preceding events. Patients often seek care because of the dramatic appearance. On examination a painless, smooth, bright-red area is noted over the bulbar conjunctiva and is sharply demarcated at the limbus. Visual acuity should be normal. If there is preceding blunt or penetrating trauma, underlying scleral penetration should be considered. Pain on extraocular movements and bloody chemosis also should prompt suspicion for injury to the globe. Subconjunctival hemorrhage should always be distinguished from chemosis: a hemorrhage is flat and smooth, whereas chemosis presents as erythema with edema, and the area is raised. Bilateral or recurrent subconjunctival hemorrhage may require a work-up for bleeding diathesis. Treatment of subconjunctival hemorrhage consists of reassurance and local cold compresses for 24 hours. Subconjunctival hemorrhages heal spontaneously in 2 to 4 weeks.
Injury to the iris and ciliary body
Traumatic iridocyclitis (uveitis)
Blunt injury to the globe may contuse and inflame the iris and ciliary body, resulting in ciliary spasm. Patients may complain of photophobia, blurred vision, and eye pain. Examination reveals conjunctival injection, specifically ciliary flush, cells, and flare in the anterior chamber and a small,
TRAUMA TO THE GLOBE AND ORBIT |
107 |
poorly dilating pupil. Cells and flare are best seen in the slit lamp with high magnification and very bright light. This condition is self limited; symptomatic treatment consists of paralyzing the iris and ciliary body with long-act- ing cycloplegic agents such as homatropine 5% for a period of 7 to 10 days. If there is no improvement after 5 to 7 days, prednisolone acetate 1% may be used to decrease inflammation in consultation with an ophthalmologist. Topical steroids should be withheld in patients who have a corneal epithelial defect. Resolution typically occurs within 1 week.
Traumatic mydriasis and miosis
Blunt injury to the orbit may damage the iris sphincter. Bruising and irritation of the sphincter leads to constriction of the pupil (miosis). Small tears to the sphincter muscle may result in dilatation or mydriasis. In the setting of significant head trauma and altered mental status, one must rule out a cranial nerve palsy and brain herniation. Treatment is supportive, and the condition often resolves spontaneously.
Iridodialysis
Traumatic iridodialysis is a tearing of the iris root from the ciliary body leading to formation of a ‘‘secondary pupil’’ (Fig. 6). This injury may also cause a hyphema. Large tears can be a cause of monocular diplopia. Urgent ophthalmologic consultation is warranted when iridodialysis causes a hyphema or decreased visual acuity. Surgical repair may be indicated for persistent monocular diplopia.
Acute glaucoma
Acute glaucoma can occur following trauma. The underlying pathophysiology is narrowing of the anterior chamber or disruption of outflow of
Fig. 6. Iridodialysis. (Courtesy of D. Wagner, MD, Washington, DC.)
