Ординатура / Офтальмология / Английские материалы / Pediatric Ophthalmology Current Thought and A Practical Guide_Wilson, Saunders, Trivedi_2008

include increased age, proximity of rupture to the fovea, and length of rupture. Peripherally located choroidal ruptures are less likely to be associated with neovascular membrane formation, but are more likely to be associated with retinal detachments [4]. Treatment options for choroidal neovascular membranes associated with traumatic choroidal rupture include: observation, submacular surgery, photocoagulation, and photodynamic therapy. Visual outcomes vary, but most patients with choroidal rupture do not obtain visual acuity of 20/40 or better. On the whole, visual outcomes tend to be better in children, who are also less likely than adults to develop choroidal neovascular membranes [1, 44].

Moulineaux, France) is first threaded into the puncta and then through the distal end of the torn canaliculus. The proximal end of the torn canaliculus is then located by direct visualization in the medial canthal area. The procedure can often be facilitated by using an operating microscope. After placing the stent into the proximal end of the canaliculus, the distal and proximal ends of the canaliculus are sutured together.

Last, the lid laceration is sutured closed. The stent should be left in place for several months to ensure patency of the lacrimal system.

31.11Traumatic Chorioretinal Rupture (Sclopetaria)

Traumatic chorioretinal rupture (sclopetaria) is a fullthickness rupture of the retina and choroid that occurs when the shock wave from a high-velocity missile, such as a BB pellet traveling in close proximity to the globe, causes rapid deformation of the globe rupturing the choroid and retina but sparing the sclera [33].

Treatment is unnecessary because the intact posterior hyaloid over the chorioretinal rupture prevents acute retinal detachment, and subsequently the choroid and retina become firmly adherent to the sclera by the proliferation of fibrous tissue. Associated retinal detachment is usually due to simultaneously occurring peripheral retinal tears.

Fig. 31.8  Red-free photograph taken several weeks after blunt trauma reveals resolving retinal hemorrhage and multiple choroidal ruptures (arrows). The ruptures are concentric with the optic nerve and located temporal to the optic nerve and through the macula

31.12 Canalicular Laceration

Canalicular lacerations are usually the result of indirect trauma to the eyelids. In children, they frequently arise from the lower eyelid being stretched and then avulsing in the region of the canaliculus which is generally the weakest point of the lower eyelid [63]. Dog bites are a common cause of canalicular lacerations in children (Fig. 31.9) [52]. The canaliculus should be repaired soon after the injury. A stent (we prefer the Mini Monika; Fayette & Bernard, Issy-Les-

Fig. 31.9  Avulsion of the lower eyelid resulting in a tear of the inferior canaliculus in a 9-year-old girl following a dog bite

31.13 Orbital Fracture

Orbital fractures in children frequently result from sports injuries, physical assault, or motor vehicle accidents and are more common in boys [23]. They most frequently involve the orbital floor (67%) followed by combined orbital floor and medial wall fractures (14%), isolated medial wall fractures (8%), and orbital roof fractures (6%). Orbital roof fractures are more common in younger children because they have a higher cranium-to-face ratio rendering the skull more vulnerable to injury and because incomplete pneumatization of the frontal sinuses results in less even distribution of force. Signs and symptoms of orbital fractures vary. Some patients can be asymptomatic, but most patients will have some degree of bruising and swelling. Other signs and symptoms include diplopia, enophthalmos, hypoglobus, and hypoesthesia in the distribution of the infraorbital nerve.

Children, because they have flexible and more elastic facial bones are particularly susceptible to “trapdoor” fractures which occur when an elliptical segment of the bony orbit is displaced, while still remaining attached on one side. Muscle entrapment can occur (Fig. 31.10) and is frequently associated with nausea and vomiting as well as a marked motility restriction despite a relatively quiet looking eye (“white-eyed

Fig. 31.10  This “trapdoor” type fracture of the orbital floor occurred in a child following blunt injury. Note inferior rectus muscle entrapment (arrow), which is likely to result in ischemia and permanent muscle damage if not repaired expeditiously

blowout fracture”) [5]. Expeditious repair is often recommended to prevent tissue ischemia and necrosis and bradycardia [51].

31.13.1 Surgical Management

Management of orbital fractures in children includes CT to identify fractures and a complete ophthalmic examination to rule out associated ocular injuries.

Patients with orbital roof fractures should also be evaluated for possible intracranial injury. Indication for surgical intervention is controversial. A conservative approach is to perform surgery within 2 weeks in patients with symptomatic diplopia and positive forced ductions, CT evidence of muscle entrapment, enophthalmos of 3 mm or more, or large defects

(>50%) of the orbital floor [26]. More urgent repair may be indicated in cases of “trapdoor” fractures or globe herniation into the maxillary sinus.

31.14Traumatic Retrobulbar Hemorrhage

Orbital or facial trauma can result in retrobulbar hemorrhage which, if left untreated, can cause permanent visual impairment and even blindness. Patients generally present with decreased visual acuity, pain, proptosis, increased intraocular pressure, and limited ocular motility. Other signs include a hard, tense eye, optic disc pallor, afferent pupillary defect, pulsating central retinal artery and, less commonly, a cherry red spot from central retinal artery occlusion. Visual loss is thought to result from an orbital compartment syndrome leading to ischemic or direct injury to the optic nerve [61]. Associated displaced orbital fractures can be protective since blood can drain into the paranasal sinuses, thereby avoiding an orbital compartment syndrome. Permanent visual loss can occur 90–120 minutes after hemorrhage, so treatment includes both medical and surgical intervention. CT or ultrasound can be useful to confirm the diagnosis, but should not delay treatment if unavailable. Lateral canthotomy and cantholysis can be effective in producing urgent decompression, but surgical

evacuation of the hematoma is sometimes necessary. Medical treatment includes topical intraocular pressure lowering drops, and intravenous corticosteroids to reduce inflammation and stabilize cell membranes.

Diuretics may also shrink the vitreous and reduce intraocular pressure.

31.15 Traumatic Optic Neuropathy

Traumatic optic neuropathy results from either direct or indirect trauma to the optic nerve. The most common site of injury is in the optic canal where the nerve is tethered and confined to a narrow boney space. Injury can also occur in the orbit or intracranial space. The optic nerve may be compressed by boney fragments or a hematoma or have its vascular supply disrupted. In most cases, it results in a retrobulbar optic neuropathy with a normal-appearing optic nerve initially. It is not until weeks later that pallor of the optic nerve may become visible. The swinging flashlight test to check for a relative afferent papillary defect is the most helpful clinical sign for detecting a traumatic optic neuropathy in a child. The condition is usually unilateral and a child may not notice the unilateral loss of vision immediately. Traumatic optic neuropathy is most commonly caused by motor vehicle accidents, falls, and sports-related injuries [19].

High-resolution CT of the orbit is helpful in evaluating fractures in the optic canal, although CT underestimates the true incidence of these fractures.

31.15.1 Treatment

The treatment of traumatic optic neuropathy is largely based on retrospective series. An attempt was made to perform a randomized clinical trial of traumatic optic neuropathy (International Optic Nerve Trauma Study), but it was changed to an observational study due to low recruitment [32]. High doses of intravenous corticosteroids have been shown to be effective in the treatment of acute spinal cord injuries [7], but their efficacy in patients with traumatic optic neuropathy has not been established. It remains unclear whether intravenous steroids in fact improve visual outcome. Nor is it clear how soon after optic nerve

injury steroids need to be administered. Others have recommended decompression of the optic canal, particularly when a boney fragment is compressing the optic nerve. Decompression can be performed through an anterior approach along the medial orbital wall, a transnasal endoscopic approach, or intracranially [20, 66]. In a large series from Taiwan, Yang et al. [66] reported that the initial visual acuity was the most important factor in predicting the visual outcome. Nonetheless, many children with traumatic optic neuropathy who initially had no light perception vision have recovered vision.

31.16 In Utero Trauma

Mid-trimester amniocentesis rarely results in traumatic injury to the eye. Injuries are usually due to the amniocentesis needle penetrating the cornea or the sclera. In one report, a scleral opening plugged by uveal tissue was noted in the eye of a newborn with a retinal detachment who had undergone amniocentesis during the 17th week of pregnancy [2]. Corneal scars with peaked pupils have also been reported following amniocentesis [36]. The use of high-resolution realtime ultrasonography and smaller bore needles have reduced the incidence of ocular injuries following amniocentesis.

31.17 Birth Injuries

Ocular injuries may occur at the time of delivery particularly when forceps are used. The injuries may include eyelid lacerations, hyphemas, tears in Descemet’s membrane, retinal hemorrhages, and choroidal ruptures (Fig. 31.11) [24]. Tears in Descemet’s membranes after forceps deliveries are generally oriented vertically and may be single or multiple. These eyes frequently present with marked corneal edema, hyphema, and ecchymoses of the eyelids. While the corneal edema usually resolves in a few days, high astigmatic refractive errors often develop. If left untreated, these eyes often develop dense anisometropic amblyopia. Favorable visual results have been reported when the refractive errors have been treated from infancy with gas-permeable contact lenses [30].

Take Home Pearls

•The greater magnification that can be achieved with an operating microscope can be helpful in visualizing the proximal end of a torn canaliculus.

•Leaving a viscoelastic agent in the anterior chamber may temporarily seal a complex corneoscleral laceration that might otherwise continue to leak regardless of the number

of sutures used to close the wound.

•Intraocular lenses can safely be implanted in the capsular bag or sulcus of most eyes with traumatic cataracts even if the posterior capsule is damaged at the time of the injury.

•Ultrasonography may be used to evaluate the status of the retina and to identify intraocular foreign bodies in open globes with a low risk of extruding intraocular contents.

Fig. 31.11  Ocular forceps injury in a newborn (top) associated with corneal edema (bottom), a hyphema, and a high astigmatic refractive error

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5-fluorouracil  237, 356, 365, 367

A

Aarskog syndrome  8 abduction deficiency  94

ablepharon-macrostomia syndrome  305 abrasion  454, 472

AC/A  17, 106, 143

––high  107

––low  106

acute retinal necrosis (ARN) syndrome  421, 442 acyclovir  442, 444

adenovirus  454

adipose tissue adherence syndrome  237 adjustable IOL  335

adrenaline  332

after-cataract  337. see also posterior capsule opacification, visual axis opacification, VAO

aggressive posterior ROP  378 Ahmed glaucoma device  368 Aicardi syndrome  301, 303

airbag injury  476 Alagille syndrome  293

American Society for Testing and Materials (ASTM)  18

Amicar  428 aminoaciduria  320 aminocaproic acid  428, 472 aminocaproic acid gel  429

––psoriatic  433, 435

––reactive  433

––rheumatoid  435 artificial tear  455 Aspirin  472

asthenopia  99, 100, 114, 169, 171 astigmatism  5, 9, 16, 330, 450 astrocytic  405

astrocytic hamartoma  414 athlete  18

atopic  452, 455

axial length  7, 314, 321, 335, 338, 350, 352, 366, 413

azelastine  455 azithromycin  433, 454 Azopt  361

B

baclofen  9 Baerveldt  368 “bag-in-the-lens”  335

Bagolini glasses  122, 124 Bagolini glasses test  135 balloon catheter dilation  279

Bangerter filter  40 Bangerter foil  42

Barkan membrane  294, 351 basal cell carcinoma  269

base-down prism induced-tropia fixation test  315 base-out prism  91, 94

basic exodeviation  98 Batten disease  392 Behçet disease  420, 421 Behçet skin testing  424 Bell phenomenon  258 Bergmeister papilla  289 Berlin edema  477

Best disease  393 beta blocker  361 bevacizumab  383

Bielschowsky head tilt test  208 Bielschowsky phenomenon  157 bifocal  11, 17, 43, 90

bilateral aphakia  42

bilateral lateral rectus recession  99 bilateral retinoblastoma  411

bilateral uncorrected refractive error  64

chronic conjunctivitis  455 cimetidine  452

clarithromycin  436 clear lens extraction  38 cleft lip  262

click syndrome  201 clobetasol propeniate  267 CO2 laser  450

Coats disease  347, 395, 405, 411, 413 coccidioidomycosis  424

Cockayne syndrome  304 Cogan-Reese syndrome  295 cold compress  236, 455

coloboma  34, 49, 262, 270, 288, 290, 291, 292, 297, 300, 301, 353, 398, 399, 405

colobomata  17 color vision  468

comitant esotropia  86, 91 commotio retinae  477 computed tomography  80

congenital anterior lens opacity  321

congenital fibrosis of the extraocular muscles  206 congenital iris ectropion syndrome  347 congenital ocular motor apraxia (COMA)  75 congenital ptosis  256

congenital stationary night blindness  74 congenital superior oblique palsies  165 congenital X-linked retinoschisis  390 conjunctiva  451

conjunctival biopsy  425 conjunctivitis  453, 455

––acute  453

––allergic  455

––chronic  455 consecutive esotropia  92 consecutive exotropia  100 contact dermatitis  271

contact lens  5, 14, 16, 18, 42, 90, 250, 319, 337, 338, 469, 476

––bandage  25

––disposable  27

––extended-wear 18

––rigid  16

––rigid gas-permeable  337

––scleral  250

––Silsoft  336

––soft  14, 16

Contact Lenses and Myopia Progression (CLAMP)  16

contiguous gene syndrome  296 contrast sensitivity  34, 383, 468 convergence  90, 98

convergence insufficiency  98 corneal abrasion  454, 472 corneal dystrophy  298 cornea plana  8, 297 Cornelia de Lange  8

Correction of Myopia Evaluation Trial (COMET)  15

cortical visual impairment (CVI)  58, 63, 74, 75,

dellen  237

dendritic epithelial keratitis  442 dermatitis  452

119, 122, 123, 124, 125, 126, 128, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 142, 147, 150, 158, 169, 173, 180, 183, 194, 202, 214, 228, 427, 437, 480

––paradoxical 134, 135

––torsional  150, 171

––vertical  129 diplopia-free zone  132

dissociated deviation  146, 154 dissociated exotropia  108

dissociated horizontal deviation (DHD)  108 dissociated vertical deviation (DVD)  87, 170 distichiasis  263

Distometer  13 divergence  98

divergence insufficiency  94 doll’s head reflex  76

dominant eye  101, 126, 130, 131, 132, 133, 134, 136, 138

dorzolamide  361 double elevator palsy  203 double Maddox rod  122 double vision  124

Down syndrome  43, 305, 317, 347 doxycyline  270

D-penicillamine  383

Duane classification  98

Duane retraction syndrome  193, 229 Duane syndrome  142, 146, 468 DuraSite  454

DVD  88, 153–163, 171 dye  332

dynamic retinoscopy  9, 89