- •Contents
- •Preface
- •Abbreviations
- •Introduction
- •Orbit and external eye
- •Extraocular muscles
- •Anterior segment
- •Posterior segment
- •Introduction
- •Ocular examination
- •The ‘red reflex’
- •Assessment of vision and visual acuity
- •Cover test for strabismus
- •Light reflex testing
- •Color vision testing
- •Assessment of stereoacuity
- •Ophthalmoscopy
- •Vision screening
- •Photoscreening
- •Autorefraction
- •Visual evoked potential
- •Strabismus
- •Comitant strabismus
- •Congenital esotropia
- •Accommodative esotropia
- •Congenital exotropia
- •Intermittent exotropia
- •Incomitant strabismus
- •Third cranial nerve palsy
- •Fourth nerve palsy
- •Sixth nerve palsy
- •Strabismus syndromes
- •Duane’s syndrome
- •Brown’s syndrome
- •Monocular elevation deficiency (MED)
- •Möbius syndrome
- •Introduction
- •Conjunctivitis
- •Bacterial conjunctivitis
- •Viral conjunctivitis
- •Herpes conjunctivitis
- •Giant papillary conjunctivitis
- •Allergic conjunctivitis
- •Vernal keratoconjunctivitis
- •Phlyctenular keratoconjunctivitis (phlyctenulosis)
- •Ophthalmia neonatorum
- •Introduction
- •Congenital corneal opacity
- •Embryology
- •Peters anomaly
- •Sclerocornea
- •Congenital dermoid
- •Birth trauma
- •Congenital hereditary endothelial dystrophy
- •Congenital hereditary stromal dystrophy
- •Posterior polymorphous membrane dystrophy
- •Metabolic diseases
- •Mucopolysaccharidosis
- •Hurler’s syndrome (MPS I-H)
- •Scheie’s syndrome (MPS I-S)
- •Hunter’s syndrome (MPS II)
- •Sly’s syndrome (MPS VII)
- •Mucolipidosis
- •Sialidosis (ML I)
- •I-Cell disease (ML II)
- •Pseudo-Hurler dystrophy (ML III)
- •Miscellaneous metabolic diseases
- •Fabry’s disease
- •Cystinosis
- •Tyrosinemia
- •Infectious diseases
- •Herpes simplex virus (HSV)
- •Congenital syphilis
- •Rubella
- •Introduction
- •Structural lens abnormalities
- •Aphakia
- •Spherophakia (microspherophakia)
- •Coloboma
- •Subluxation (ectopia lentis)
- •Lenticonus
- •Persistant fetal vasculature
- •Cataracts
- •Nuclear cataracts
- •Lamellar cataracts
- •Anterior polar cataracts
- •Posterior polar cataracts
- •Sutural cataracts
- •Anterior subcapsular cataracts
- •Posterior subcapsular cataracts
- •Cerulean (blue-dot) cataracts
- •Complete cataracts
- •Etiology of cataracts
- •Genetic and metabolic diseases
- •Trauma
- •Medication and toxicity
- •Maternal infection
- •Diagnosis of cataracts
- •Management/treatment of cataracts
- •Visual significance
- •Surgery
- •Aphakia
- •Pseudophakia
- •Amblyopia
- •Cataract prognosis
- •Introduction
- •Diagnosis of pediatric glaucoma
- •Ocular examination
- •Differential diagnosis of pediatric glaucoma
- •Primary infantile glaucoma
- •Juvenile open-angle glaucoma
- •Primary pediatric glaucoma associated with systemic disease
- •Lowe’s syndrome
- •Sturge–Weber syndrome
- •Neurofibromatosis
- •Axenfeld–Rieger syndrome
- •Aniridia
- •Peters anomaly
- •Secondary childhood glaucoma
- •Trauma
- •Neoplasia
- •Glaucoma following pediatric cataract surgery
- •Other causes of secondary glaucoma in children
- •Treatment of pediatric glaucoma
- •Drug treatment
- •Surgical management
- •Summary
- •Introduction
- •Coats’ disease
- •Leber’s congenital amaurosis
- •X-linked congenital stationary night blindness
- •Achromatopsia
- •Stargardt disease
- •Best’s disease
- •Persistent fetal vasculature
- •X-linked juvenile retinoschisis
- •Albinism
- •Retinal dystrophies with systemic disorders (ciliopathies)
- •Introduction
- •Common clinical features
- •Classification
- •Anterior uveitis
- •Juvenile idiopathic arthritis
- •Juvenile spondyloarthropathies
- •Sarcoidosis
- •Herpetic iridocyclitis
- •Intermediate uveitis
- •Posterior uveitis
- •Toxoplasmosis
- •Toxocariasis
- •Vogt–Koyanagi–Harada syndrome
- •Sympathetic ophthalmia
- •Masquerade syndromes
- •Retinoblastoma
- •Leukemia
- •Introduction
- •Optic nerve hypoplasia
- •Morning glory disc anomaly
- •Optic disc coloboma
- •Peripapillary staphyloma
- •Congenital tilted disc
- •Optic pit
- •Myelinated retinal nerve fibers
- •Papilledema
- •Pseudopapilledema
- •Optic disc drusen
- •Introduction
- •Dacryocele
- •Nasolacrimal duct obstruction
- •Lacrimal sac fistula
- •Decreased tear production
- •Dacryoadenitis
- •Introduction
- •Cryptophthalmos and ankyloblepharon
- •Coloboma of the eyelid
- •Blepharoptosis
- •Epicanthal folds and euryblepharon
- •Lagophthalmos
- •Lid retraction
- •Ectropion, entropion, and epiblepharon
- •Blepharospasm
- •Blepharitis
- •Hordeolum
- •Chalazion
- •Tumors of the eyelid
- •Preseptal and orbital cellulitis
- •Herpes simplex, molluscum contagiosum, and verruca vulgaris
- •Allergic conjunctivitis
- •Trauma
- •Summary
- •Introduction
- •Cystinosis
- •Marfan’s syndrome
- •Homocystinuria
- •Wilson’s disease
- •Fabry disease
- •Osteogenesis imperfecta
- •The mucopolysaccharidoses
- •Sickle cell disease
- •Albinism
- •Congenital rubella
- •Introduction
- •Genetics
- •Malignant potential
- •Formes frustes
- •Neurofibromatosis (von Recklinghausen’s syndrome)
- •Retinocerebellar hemangioblastomatosis (von Hippel–Lindau syndrome)
- •Racemose hemangiomatosis (Wyburn-Mason syndrome)
- •Encephalofacial cavernous hemangiomatosis (Sturge–Weber syndrome)
- •Oculoneurocutaneous cavernous hemangiomatosis
- •Organoid nevus syndrome
- •Introduction
- •Cortical visual impairment
- •Migraine headache
- •Spasmus nutans
- •Opsoclonus
- •Horner’s syndrome
- •Congenital ocular motor apraxia
- •Myasthenia gravis
- •Introduction
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Diagnostic approaches
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Therapeutic approaches
- •Eyelid and conjunctiva
- •Intraocular tumors
- •Orbital tumors
- •Eyelid tumors
- •Capillary hemangioma
- •Facial nevus flammeus
- •Kaposi’s sarcoma
- •Basal cell carcinoma
- •Melanocytic nevus
- •Neurofibroma
- •Neurilemoma (schwannoma)
- •Conjunctival tumors
- •Introduction
- •Choristomatous conjunctival tumors
- •Epithelial conjunctival tumors
- •Melanocytic conjunctival tumors
- •Vascular conjunctival tumors
- •Xanthomatous conjunctival tumors
- •Lymphoid/leukemic conjunctival tumors
- •Non-neoplastic lesions that simulate conjunctival tumors
- •Conclusions
- •Intraocular tumors
- •Retinoblastoma
- •Retinal capillary hemangioma
- •Retinal cavernous hemangioma
- •Retinal racemose hemangioma
- •Astrocytic hamartoma of the retina
- •Melanocytoma of the optic nerve
- •Intraocular medulloepithelioma
- •Choroidal hemangioma
- •Choroidal osteoma
- •Uveal nevus
- •Uveal melanoma
- •Congenital hypertrophy of retinal pigment epithelium
- •Leukemia
- •Orbital tumors
- •Dermoid cyst
- •Teratoma
- •Capillary hemangioma
- •Lymphangioma
- •Juvenile pilocytic astrocytoma
- •Rhabdomyosarcoma
- •Granulocytic sarcoma (‘chloroma’)
- •Lymphoma
- •Langerhan’s cell histiocytosis
- •Metastatic neuroblastoma
- •Introduction
- •Eyelid
- •Open globe
- •Ocular surface injury
- •Intraocular trauma
- •Iridodialysis
- •Cataract
- •Retina
- •Optic nerve injury
- •Orbital fracture
- •Other orbital injury
- •Child abuse
- •Shaking injury
- •Index
280 CHAPTER 19 Ocular trauma
Ocular surface injury
The conjunctiva is the thin, connective tissue that covers the sclera. A common injury to the pediatric eye is a subconjuctival hemorrhage (335). This is most often caused by blunt injury or Valsalva maneuver. Subconjunctival hemorrhages are usually painless and selflimiting, and require no treatment. The mechanism of injury is important to rule out additional complications, such as scleral laceration. A conjunctival laceration (336) may occur without involving the underlying sclera. Treatment of conjunctival laceration is dependent on its extent. Most lacerations will heal without surgical intervention, but extensive or complex lacerations may require suturing. Nonsurgical repair involves lubrication with antibiotic or antibiotic–steroid ophthalmic ointment until closure occurs.
The cornea is composed of five layers with the epithelium being the most superficial layer. When all or part of the epithelium is lost secondary to a trauma, it is called a corneal abrasion. Evaluation includes history, visual acuity, and inspection. The abrasion can readily be identified with the instillation of fluorescein and observation with blue light (337–339). Treatment involves analgesics and cycloplegic agent with frequent instillation of an antibiotic ophthalmic ointment. Patching of the eye was once considered standard practice but has not been shown to improve healing time or increase comfort. A corneal abrasion in a contact lens wearer should not be patched as this may increase the risk for Pseudomonas infection. The abrasion should be re-evaluated in 1–2 days to ensure healing and that no infection has occurred.
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336 |
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335 Subconjunctival hemorrhage.
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336 Conjunctival laceration.
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337 Corneal abrasion with fluorescein staining. |
338 Corneal abrasion with fluorescein staining. |
Ocular surface injury 281
Corneal foreign bodies are another source of pediatric ocular trauma, and may be organic or nonorganic (340). All corneal foreign bodies must be removed to minimize risk of infection, inflammation, and scarring. A superficial, peripheral foreign body may be removed in the office in a cooperative child. After removal, the treatment is the same as that of an abrasion. Deep or central foreign bodies may need to be removed in the controlled environment of the operating room to minimize corneal scarring. Metallic foreign bodies are more complicated because the iron in the foreign body often oxidizes and may cause rust to be deposited in the cornea. The rust must be removed to ensure proper healing. Therefore, it is best to have the metallic foreign body and rust removed by an ophthalmologist.
Chemical injuries to the ocular surface may be sight-threatening and should be considered an ophthalmic emergency. It is important to identify the substance to which the eye was exposed. Acidic chemicals tend to precipitate in the ocular tissues. Bases tend to coagulate the ocular tissues and will penetrate deeper into the eye. Upon arrival, the child with a chemical exposure should receive immediate irrigation with saline for 10 minutes. The pH of the ocular surface should then be checked and irrigation continued until neutrality. If significant exposure has occurred, the patient should be seen promptly by an ophthalmologist to initiate further treatment. The goal of treatment is to minimize vision-threatening sequelae such as conjunctival scarring, corneal scarring/opacification, glaucoma, cataract, vision loss, and phthisis (341).
339
339 Corneal abrasion with fluorescein staining.
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340 Corneal foreign body.
341
341 Early phthisis.
282 CHAPTER 19 Ocular trauma
Intraocular trauma
Traumatic iritis occurs after blunt trauma to the eye. The symptoms include eye pain, photophobia, tearing, and blurred vision. The symptoms usually present within 3 days of injury. Iritis is the presence of intraocular inflammation demonstrated by conjunctival injection and the presence of white cells in the anterior chamber. Traumatic iritis is treated with a cycloplegic agent to immobilize the iris, which in turn improves comfort. Many practitioners also recommend topical steroid treatment to reduce inflammation.
Hyphema can be caused by blunt or penetrating injury to the eye and represents a vision-threatening situation. Blunt force to the eye causes posterior displacement of the lens–iris diaphragm, which results in tearing of structures, including vessels, in the iris root. When these vessels tear, blood is released into the anterior chamber, causing a hyphema (342, 343). The IOP acts as a tamponade to stop the bleeding and allow the formation of fibrin clot. Symptoms of a hyphema include immediate decrease in vision and pain. Hyphema is diagnosed by observing blood in the anterior chamber. If a view of posterior structures is obscured, ultrasonography may be useful to rule out retinal detachment or intraocular foreign body. Treatment of hyphema involves efforts to minimize the vision-threatening sequelae such as rebleeding, glaucoma, and corneal blood staining (344). A shield is placed on the affected eye, and a cycloplegic agent is used to immobilize the iris. Additionally, topical steroids are used to minimize intraocular inflammation and antiemetics should be considered if the patient is experiencing nausea. All nonsteroidal anti-inflammatories and asprin must be avoided. Frequent visits are required to check IOP and for new bleeding. If IOP is elevated, topical and systemic pressure-lowering medications are used. If the pressure is not controlled by such measures then surgical intervention may be required to minimize the risk of permanent vision loss. Patients with sickle cell disease present an additional concern in managing hyphema. Because of the shape and relative rigidity of the red blood cells in these patients, their clearance through the normal outflow pathways can be limited. This creates a higher risk for developing increased IOP. Additionally,
the sickle cell patient’s optic nerve is more predisposed to damage from ischemia, and so these patients can sustain permanent vision loss at a lower IOP than expected.
Iridodialysis
Iridodialysis occurs secondary to blunt trauma when the iris root becomes disinserted from the sclera. Hyphema is often present and should be treated if present. If the iridodialysis is small and the patient is asymptomatic (345), then treatment may not be needed. If the iridodialysis is large, it may cover the pupil or form a secondary pupil which may cause monocular diplopia or reduced vision (346). If this occurs then surgical intervention may be required.
Iridodialysis 283
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343 |
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342 Small hyphema in the anterior chamber. |
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343 Hyphema in the anterior chamber. |
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344 |
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344 Corneal blood staining secondary to |
345 Asymptomatic iridodialysis. |
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hyphema. |
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346 |
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346 Large,symptomatic iridodialysis.
