The management of an open globe injury in the pediatric patient is of utmost importance. Delay in taking these patients to the operative suite can result in significant visual sequelae. Open globe injury is a full thickness mechanical injury to the cornea and/or sclera. The injury can be classified as a rupture or a laceration of the globe. A laceration of the globe can be further subcategorized into penetrating or perforating injury.

In a 17-year review of open globe injury in the Canadian pediatric population, open globe injuries were three times as prevalent in males than females [9]. Around half of those included in the review were under the age of five.

An open globe injury should be suspected when low intraocular pressure, hemorrhagic chemosis, shallow anterior chamber, and peaked pupil are found during the ocular examination [10]. If an open globe injury is obvious, intraocular pressure measurements and dilation should be avoided.

Pediatric open globe injuries can result in specific late complications from surgical repair (secondary glaucoma, secondary strabismus, leukoma cornea and phthisis bulbi) that can produce significant visual consequences [11]. Lee et al. [12] reviewed 62 patients with open globe injury under the age of 16 and found that best visual outcomes occurred in those with only corneal injury. Poor prognostic indicators in open globe injury included location of injury, extent of injury, initial presentation of hyphema, vitreous hemorrhage, retinal detachment, central corneal wound, and endophthalmitis [13]. Low visual acuity at initial presentation in addition to subsequent number of surgeries also carries a guarded visual prognosis [14]. Risks of endophthalmitis increased with delayed repair of these penetrating injuries, thus surgical repair in a timely manner is critical [15].

Corneal abrasions are the most common eye injury in children presenting to the emergency department [16]. A corneal abrasion is a corneal epithelial defect related to trauma. They are usually caused by blunt trauma to the eye, foreign body, or contact lens use. In a study of random newborn subjects from 1 to 12 weeks of age, corneal abrasions were present in 49% of patients [17].

Symptoms include increased tearing, foreign body sensation, sharp pain, and photophobia. Preverbal patients with corneal abrasion may have unexplained inconsolable crying. Rubbing the eye may also be a sign of abrasion in the pediatric patient.

In patients wearing contact lenses, lenses should be removed prior to examination. Following topical anesthesia of proparicaine, topical fluorescein should be applied to the eye. Using a Wood’s lamp or Cobalt-blue light under the slit lamp, the epithelial defect will appear yellow-green (Fig. 13.2).

If vertical linear abrasions are observed, the examiner should be suspicious of retained foreign body in the superior palpebral conjunctiva. Eversion of the upper eyelid can be accomplished with aid of a cotton tip applicator, and a foreign body can be removed with a sterile cotton swab which has been soaked in proparicaine, a lens loop, a forceps, or a 30-gauge needle. Special care must be taken when using a needle.

Pharmacologic therapy in noncontact lens wearing pediatric patients can be erythromycin, bacitracin or polymyxin B/bacitracin, or topical antibiotic drops such as polymyxcin B/trimethoprim or ofloxacin [18]. Antipseudomonal coverage is necessary in contact lens wearers. These abrasions should be treated with a topical fluoroquinolone antibiotic. Topical steroids should be avoided in these patients due to potential delay in wound healing.

Oral acetaminophen can be used for pain relief. Patching is not necessary for a majority of corneal abrasions. However, for a larger corneal abrasion, do not be afraid to use a pressure patch. In a non-compliant child, a patch can prevent rubbing and promote healing. Evidence for NSAID use for treatment of pain from corneal abrasions is currently lacking. If topical NSAIDs are prescribed, patients should have close follow-up.

Secondary complications of corneal abrasion include corneal ulceration, secondary bacterial infection, corneal scarring, uveitis, and iritis. Recurrent corneal erosions can occur following the initial abrasion due to improper healing of the original epithelial defect.

Resolution often occurs with the above treatments within 1–5 days. Contact lens wearers and those with history of ocular herpes simplex should have particularly close follow-up.

Blunt trauma to the eye can cause rupture of the vascular supply of the iris and ciliary body resulting in blood in the anterior chamber or a hyphema (see Fig. 13.3). Up to 70% of hyphemas occur in children [19]. Lasting effects of pediatric traumatic hyphema are serious and therefore proper diagnosis and management are of utmost importance in the pediatric patient. A careful examination and identification of associated orbital and ocular injuries is necessary. The most common ocular lesions associated with pediatric traumatic hyphema are corneal abrasions [20].

Patients often present with history of blunt trauma, vision loss, and eye pain. Anisocoria can be present due to a torn iris sphincter muscle in the traumatized eye. Hyphemas are classified by amount of blood in the anterior chamber. A grade I hyphema occurs when there is pooled, layered blood, occupying less than one-third of the anterior chamber; whereas an 8-ball hyphema, or total hyphema, is a grade IV hyphema. Plasmin activates the fibrinolytic system that will break down the clot and allow for filtration of the material through the trabecular meshwork. In a prospective case series of 35 children treated as outpatients for traumatic hyphema, Rocha et al. found that visual prognosis is correlated with the grade of hyphema and posterior segment involvement in the trauma. A microhyphema is defined as red blood cells in the anterior chamber of the eye without layering of blood.

Rebleeding, corneal blood staining, secondary glaucoma and ischemic optic neuropathy are all possible secondary complications of hyphema. Risk of rebleeding, or secondary hemorrhage is increased in the African-American pediatric population [21]. Those patients who are of African-American decent should have a sickle cell screen laboratory analysis at the time of presentation to help rule out sickle cell disease. Patients with sickle cell hemoglobinopathy, who present with hyphema, should be monitored very closely. Mechanical obstruction of the trabecular meshwork from sickled cells can result in increased intraocular pressure. Carbonic anhydrase inhibitors have been shown to increase sickling of cells. In a study of 40 children from the United States with hyphema, sickle cell hemoglobinopathy was associated with increased intraocular pressure but not rebleeding [21].

Treatments for hyphema are often debated, but the general consensus is that topical steroid and topical cycloplegics should be given. Children’s dosing of acetaminophen can be given to patients for pain control. Strict bed rest should be encouraged. The head of the bed can be elevated to layer out the hyphema and precipitate clot absorption. Blood thinning agents should not be given. Evidence for use of antifibrinolytic agents including transexamic acid and aminocaproic acid for prevention of rebleeding in pediatric patients is currently lacking [22]. Children should be instructed to limit activity and wear eye shields, protecting them from further injury that may result in rebleed. Otherwise, rebleeding tends to occur posttrauma at day 4 or 5, when the clot contracts.

In hyphemas presenting without trauma, important underlying pathology should always be entertained. Non-accidental trauma should always be in the differential. Causes of spontaneous hyphema in the pediatric population include retinoblastoma, medulloepithelioma, juvenile xanthogranuloma, leukemia, melanoma, and other causes of rubiosis.

With blunt trauma to the eye, damage to the iris and ciliary body can occur resulting in anterior chamber inflammation, termed traumatic iridocyclitis. Traumatic iritis accounts for 20% of all iritis [23]. Necrotic blood products released from damage of the structures result in inflammation in the anterior chamber. Traumatic iridocyclitis can present with eye pain, redness, photophobia, and frequently miosis. Conjunctiva may also be injected. Diagnosis is made on slit lamp biomicroscopy with white blood cells present in the anterior chamber of the eye. Inflammatory mediators cause leak of proteinaceous material in the anterior chamber resulting in flare. No clinical trials exist for treatment of traumatic iridocyclitis [24]. Treatment involves topical steroids and topical cycloplegica. If severe, traumatic iridocyclitis can lead to posterior synechiae, keratic precipitates of the cornea, corneal edema and increased IOP potentially causing glaucoma and cystoid macular edema. Topical steroids are usually slowly tapered to prevent rebound iritis. Prognosis with proper treatment is excellent.

Pediatric traumatic cataract is a major cause of monocular blindness in children and accounts for a majority of pediatric cataract extraction surgical cases [25]. Without proper removal of a cataract, loss of binocular vision along with amblyopia, low vision, strabismus, or even blindness may ensue [26]. Cataract formation can be accompanied by other ocular morbidity resulting in further detriment to visual potential. A retrospective review of 25 children with unilateral cataracts showed that a majority of injuries were caused by paintball and BB gun injuries [27]. Injury from pencils and pens followed this as the second most common mode of injury. Modes of traumatic cataract vary depending on geographical location. In rural India, the most common cause of pediatric cataract was a wooden stick associated injury followed by a sharp thorn injury [28].

Poor visual outcome was seen by a greater majority of patients who were younger (5.25 years) than older (7.5 years). Penetrating injuries resulting in pediatric cataract were more often associated with penetrating injuries compared to blunt trauma [29].

Intervention in these cases involves cataract extraction. Surgical complications are usually minor [30]. However, posterior capsular opacification occurs in roughly 90% of patients, and a YAG capsulotomy procedure is required in the majority of cases. An IOL is placed in pediatric patients with a lens power that should take into account their eventual myopic shift. The main goal of cataract extraction and lens placement is to create a clear axis for proper visual development.

Lens dislocation can also occur with trauma. It may be associated with other types of ocular injury mentioned in this chapter. Underlying ocular and systemic conditions should be considered when minor trauma causes lens dislocation. These include simple ectopia lentis, ectopia lentis et pupillae, aniridia, Marfan Syndrome, Homocystinuria, Sulfite Oxidase Deficiency, and Weill–Marchesani syndrome. Lensectomy and vitrectomy are standard treatment for traumatic ectopia lentis. Over 90% of these surgical interventions result in vision or 20/40 or better [31].

Traumatic retinal detachments in the pediatric population likely occur as a result of secondary indirect impact from globe deformation [32]. They tend to form in adolescent years due to the protective support of well-formed vitreous earlier in life. Several factors can predispose patients to traumatic rhegmatogenous retinal detachments (RRDs), including inherited syndromes (Stickler syndrome, Wagner syndrome, Marfan syndrome, Knobloch syndrome), prior surgery and past trauma. Myopia is also a risk factor [33]. Most detachments are rhegmatogenous. In a German review of 259 patients under 20 years of age with retinal detachment, 72% were male [34]. 52% of the patient’s had disorders predisposing to retinal detachments such as myopia. In a review of RRDs in the pediatric population, Wenick and Baranano found that roughly 40% of RRDs were related to trauma.

With longstanding RRDs, proliferative vitreoretinopathy can ensue and lead to tractional retinal detachments. With communication often lacking in the pediatric patient, children are less likely to report symptoms of retinal detachment. Those who present with macula-on retinal detachments have a better visual prognosis than those who present with macula-off detachments [32].

Trauma is the most common cause of vitreous hemorrhage in children. In a review of 261 pediatric eyes from India with vitreous hemorrhage, trauma was the cause of vitreous hemorrhage in 69% of eyes with blunt trauma, accounting for the majority of these cases [37]. These data are supported by other reviews [38].

Younger patients may present with strabismus and/or nystagmus, while older patients will present with decreased visual acuity. Similar to the mechanism of a macular hole, blunt force in the anterior–posterior direction can cause the equatorial region of the eye to bulge and create traction on the retina. Traction on retinal vessels can cause rupture of the vessels resulting in vitreous hemorrhage. Evaluation with ultrasonography is key in identifying integrity of structures posterior to the blood.