Commotio Retinae and RPE Contusion
First described by Berlin in 1873,1,2 commotio retinae is a self-limited whitening of the neuroretinal tissue secondary to direct blunt trauma. The lesion can appear over the site of the trauma (direct) or on the contralateral side of the globe (indirect) due to shock waves that traverse from the site of impact.1,2 When clinically significant, the affected area is on the macula or close to it.1,3 However, the peripheral retina can also be affected,1 with the temporal and inferotemporal quadrants most commonly affected in children.1 This injury is usually associated with fractures of the orbital rim.1
Current studies of electronic microscopy and optical coherence tomography (OCT) have helped elucidate parts of the pathophysiological mechanism involved in commotio retinae.4 Evidence has shown that there is a disorganization of the photoreceptor cell layer, and disruption of the photoreceptors' outer segments along with cellular edema of Müller cells and ganglion cells' axons.1–3,5–7 Occasionally the trauma is severe enough that retinal pigment epithelial cells are also affected (RPE contusion).8 As they heal, many can be lost and lose their pigment granules with consequent loss of the photoreceptor cells that can lead to permanent visual loss.8 Inflammation plays a very small role in this pathology.4,6
Commotio retinae after closed-globe injury is a fairly frequent occurrence. Clinical symptoms can include a transient decrease in visual acuity, which typically resolves within a few weeks, although there are some reports of persistent visual scotomas.5,9 If the peripheral retina is involved, it can be asymptomatic or can present with a slightly restricted visual field. On dilated exam, there is a pale white appearance to the affected retina.6,9 Fluorescein angiography might show no abnormality, however near-infrared autofluorescence imaging can prove useful in detecting areas of clinical and subclinical trauma.6,10 Spectral domain OCT shows a brighter signal (hyper-reflective) from the photoreceptor cell layer.2,3,5,10 Recent studies using ultra high-definition OCT have shown a backscatter signal from the outer segment layer along with darkening of the union of inner and outer segments and retinal pigment epithelium hyper-reflectivity.2,3,5
Anti-inflammatory medication is not indicated except for topical corticosteroids if the commotio retinae is associated with traumatic iritis.9 Prognosis is usually good with at least partial visual recovery.9 This recovery can be dampened if the RPE is severely affected.9
Traumatic Macular Hole
Traumatic macular hole (TMH) is a full-thickness defect of the neurosensory retina at or near the center of the anatomic fovea secondary to an external force to the eye by means of a projectile, blunt trauma, electrical shock, expansile shock wave, or laser burns.11–16 It was first described by Knapp and Noyes almost simultaneously in the late 1800s.11,12,15,17 Both reported clinical cases of TMH after blunt trauma in young adolescents. Due to its relative rare occurrence, there are limited data regarding its exact incidence in the pediatric population. However, data from published series and the United States Eye Injury Registry (USEIR) have estimated that TMHs represent between 1% and 10% of the total annual incidence of macular holes. TMH is reported to occur in 1.4% of closed globe injuries and in 0.15% of open globe injuries, of which about 1% occurs in the pediatric population.11,15,18
Conversely to idiopathic macular hole (IMH), the population at risk tends to be young males (mean age about 15 years), usually involving high-velocity blunt trauma by some sort of sports ball19 and typically associated with other forms of traumatic retinal pathology such as commotio retinae, choroidal rupture, vitreous, retinal or subretinal hemorrhages, sclopetaria, retinal breaks, and macular retinal pigment epithelium (RPE) changes.14,19 Accidental laser burns and lightning injury have also been identified recently as another cause of TMH.
The pathophysiology of TMH in children is yet to be elucidated. Several theories have been proposed to explain its sudden appearance including violent retinal stretching due to traumatic ocular deformity, transmission of impact force to the macula resulting in its rupture or contusion necrosis, and cystoid degeneration and retinal dehiscence due to sudden posterior vitreous detachment.12–14 However, the most accepted theory is based on the fact that children have a stronger adhesion of the posterior hyaloid to the internal limiting membrane (ILM) that can remain even after the trauma.12,14,18,19 The violent compression of the globe induces an outward expansion of the equator. This results in the flattening of the posterior sclera.11,14 The change in the structure of the posterior pole produces a horizontal force that can split the layers of the retina.13,14 In addition, the sudden retraction of the posterior pole to its original position produces a trampoline-like movement that enhances the anterior-posterior vitreous traction over a relatively thin macula.13–15 The variable vector forces acting over the macula result in a more irregular and almost always elliptical macular hole.13–15
Clinically, central vision loss is a hallmark of TMH; it can range from 20/80 to 20/400 at the moment of presentation.11,13,14 The degree of visual dysfunction and recovery will depend on various factors, including its association with other traumatic pathology like photoreceptor damage or RPE damage.14 Fundus exploration reveals a full-thickness, sharply defined retinal defect that tends to be more eccentric and elliptical, with irregular edges, than the idiopathic form;15 it measures 100 to 500 µm.11,14 Small, yellow deposits located at the level of the RPE along with a cuff of subretinal fluid might also be observed.11,14 The presence of an operculum, epiretinal membrane, and posterior vitreous detachment (PVD) are rarely seen.11,19
Fluorescein angiography (FA) can show leakage of dye acutely after the trauma. FA also shows a central hyperfluorescent window defect corresponding to the base of the macular hole, which can be enhanced by RPE atrophy and pigment clumping.11,14 The surrounding cuff of subretinal fluid is mildly hypofluorescent along with the yellow deposits at the base of the hole. OCT findings confirm the diagnosis of TMH. Studies have found that TMH tend to have a thinner average retinal thickness and a larger basal diameter and basal area than IMH.15
Treatment of TMH in children remains controversial and the available information is limited.13,15,19,20 Spontaneous resolution without surgical intervention and good visual recovery, although unpredictable, has been reported in numerous case reports and series.12,13,20 Clinical characteristics that seem to be related to spontaneous resolution of the TMH are young age, small defects (100–200 µm), failure of the posterior hyaloid to detach, and absence of epiretinal membrane.12,13,20 The time for spontaneous closure of a TMH can range from 1 week to 6 months, although 55% of reported resolution happens between the 3rd and 4th month of follow-up.12,15 Therefore, some authors have suggested that a period of observation in children might be advised.13,20 Nevertheless, the decision to observe a pediatric patient with TMH should be taken with caution, especially in children of few months of life to 8 years of age, known to be vulnerable to deprivational amblyopia.18 In these cases, surgery could be recommended earlier. Alternatively, if the affected eye suffered previously from profound amblyopia, surgical intervention might not be indicated.18 Furthermore, patients who have an associated choroidal rupture through the fovea are also poor surgical candidates.
When needed, pars plana vitrectomy with ILM peeling and gas tamponade, assisted with vital dyes such as trypan blue or brilliant blue, is the technique of choice.13,15,17 The composition and firm retinal attachment of the pediatric posterior hyaloid to the internal limiting membrane poses a unique challenge for the retina surgeon; and vitreous delamination (vitreoschisis) can occur frequently during its mechanical separation.12,17,18 Iatrogenic retinal breaks, inner retinal damage, retinoschisis, visual field defects and vitreous hemorrhages can easily occur, increasing the risk of proliferative vitreoretinopathy.15,18 Surgical adjuvant therapy aimed at improving the closure rate and easing the mechanical separation of the posterior hyaloid in children — such as plasmin-assisted vitrectomy, transforming growth factor beta 2, and autologous platelet concentrate — has been used in the past without proving any definitive advantage over the standard surgical technique.15,18–20 Ocriplasmin (microplasmin/Jetrea; ThromboGenics, Iselin, NJ) is a recombinant truncated version of plasmin that is currently being assessed in a phase II trial for its use in pediatric vitreoretinopathies.15
As mentioned above, gas tamponade is recommended over silicon oil; however, adequate positioning might be hampered by the patient's age, associated injuries, or physical state. In those cases, silicon-oil tamponade is recommended with the understanding that a second surgery for silicon removal will be necessary.15,18
Anatomical results are usually good, but functional outcomes can be modest. TMH associated with choroidal fractures can be the exception where the fibrosis associated with rupture precludes hole closure. The formation of a posterior subcapsular cataract, RPE damage, and possible loss of foveal tissue are some factors that might be related to the modest visual recovery seen in these patients.18
First described by Von Graefe in 1854,21 choroidal rupture (CR) is an uncommon but serious complication of closed-globe trauma. Referring to the traumatic break of the choroid, Bruch's membrane, and RPE, CR occurs secondary to the sudden change in the globe geometry triggered by a forceful compression without penetration by an external mechanical force. It occurs in 5%–8% of all closed-globe injuries,22,23 although the prevalence tends to be higher among male children; and it frequently involves outdoor games or organized sports.22,24,25
The rapid compression of the globe creates a perpendicular and centripetal expansile force. The magnitude and direction of the vector force exerts extreme stress on Bruch's membrane, which is less elastic and has less tensile strength than the sclera, leading to fracture.26 CR can be secondary to direct trauma if the rupture occurs over the site of the trauma. In these cases, the ruptures tend to be more anterior and parallel to the ora serrata.21,27 Although rupture secondary to transmission of force from the impact site to the contralateral side of the globe (countercoup, indirect trauma) tends to be located on the posterior pole temporal to the optic nerve, more than 60% of cases involve the macula.27 Most of the patients have single ruptures, but 25% might have multiple CR.27
In cases in which CR affects the macula, decreased vision can be severe and usually has poor prognosis. This is especially true if there are additional associated lesions such as subretinal and intraretinal hemorrhages, vitreous hemorrhages, lesion to inner layers of the retina, pigment dispersion, choroidal hemorrhages, or late choroidal neovascularization (CNV).23,27 Other clinical signs can include variable types of visual field defects such as isolated scotomas (which might not coincide with the location of the CR), nasal steps, central or centrocecal defects, enlargement of the blind spot, or generalized constriction.21 On fundus examination, the CR will present as a curvilinear, crescent-shaped reddish/yellowish line.21 Usually it is concentric to the optic nerve and is widest at the center and tapered at the ends. In time, the rupture will evolve into a white streak with pigmented margins due to RPE hyperplasia.21
Fluorescein angiography (FA) usually shows early hypofluorescence due to filling failure secondary to the disruption of the choroidal flow, with hyperfluorescence of the rupture margins due to leakage of the dye into the scar tissue (staining).21 If there is an associated CNV, FA will show leakage of dye that increases in size and intensity through all study phases along with hypofluorescence due to blockage if there are any subretinal hemorrhages. Indocyanine green angiography shows hypofluorescence at the rupture site through all the study's phases. Near infrared autofluorescence imaging will show hypoautofluorescence due to RPE loss.21
About 5%–10% of all CR will develop secondary CNV,26 of which more than 80% will appear during the first year after trauma. Ruptures closer to the avascular fovea or larger than 4000 µm are more prone to CNV.26 In children, results from histopathological studies of CNV secondary to CR have shown absence of deposits in the basal membrane (in contrast to those observed in adults) and fibrovascular tissue composed of multiple layers of RPE cells and collagen.28
There is no general consensus about how to manage this complication.29 Therapeutic options are basically aimed to managing associated CNV.26 These include observation, photocoagulation of extrafoveal CNV, photodynamic therapy, surgical removal, and antiangiogenic drugs.26,29,30 Unlike CNV secondary to age-related macular degeneration, a single dose of intravitreal antiangiogenic drugs induces fast and stable inactivation up to a year after injection.29 Nevertheless, the safety of intravitreal antiangiogenic drugs in the pediatric population has not been established.29,30
Traumatic vitreous hemorrhage (TVH) is the extravasation of blood into the vitreous gel or to one of the several potential spaces formed within and around it. TVH is due to the forceful disruption of blood vessels, either in the posterior pole or the anterior chamber, that happens after an external mechanical force is applied to the eye.31–34 It is not a primary diagnosis, but a condition that occurs as consequence of a coincidental traumatic pathology (choroidal rupture, retinal tear/detachment, macular hole, optic nerve injury, etc.); these are often the main determinant of the anatomical and functional outcome.32,35
TVH from all sorts of traumatic insults (blunt, penetrating, surgical trauma, birth trauma, abusive head trauma, etc.), despite being uncommon, accounts for the majority of vitreous hemorrhages (VH) in children and adolescents, ranging from 54.3 to 82.5% of all causes of VH;31,35,36 though the incidence in neonates is smaller (0.039%).37,38 Among all traumatic causes, nonpenetrating (blunt) trauma accounts for the majority of TVH, being responsible for 29.6 to 64% of such cases. It has a predominance of male patients aged 3 to 18 years (mean about 7 to 8 years).31,36,37
The clinical presentation of TVH in younger patients is different from that in adults. For instance, younger children lack the ability to verbalize, resulting in difficulties in expressing their symptoms or eliciting a detailed history about the trauma and its source.35 Therefore, a good proportion of these patients will not have their TVH noted until they fail a vision screening or until a comprehensive ophthalmological examination is done. In addition, poor patient cooperation can render simple exploratory maneuvers such as assessing visual acuity or intraocular pressure very challenging.
The most common presenting symptom is decreased vision.37 Depending on the density of the hemorrhage and associated pathology, it can vary widely from 20/200 or better to hand motion or even light perception.36 Moreover, the association of blunt trauma and VH along with worse visual acuity at presentation, younger ages (3 years or less), dense VH, and the presence of cataract or aphakia are considered risk factors for poor visual outcomes after trauma.36 In patients younger than 3 years of age, visual acuity assessment is less reliable, therefore special attention must be placed on indirect cues about vision loss such as an inability to recognize their mother or a recent loss of interest in their surroundings.31 Other, less common, presentations in children include pain, abnormal pupillary reflex, strabismus, nystagmus, and floaters.35 During physical exploration, do not exert unnecessary pressure on the globe because ruptured globe is always a possibility in children with TVH, even if a traumatic etiology is not apparent or the history detailed by the caretaker does not point to a severe trauma.37 B-scan ultrasonography is useful to establish the presence of TVH and will show low-intensity echoes in the vitreous cavity, which can be widespread depending on the hemorrhage density. TVH after closed-globe injury is associated with a slow clearance rate of about 1% per day and low spontaneous clearing.32
Abusive head trauma is responsible for about 8.6% of all TVH.38,39 A high level of suspicion must be maintained, especially in cases of bilateral VH in very young patients (< 1 year).31,38,39 These patients might have previous history of two or more hospital admissions, an incongruent history regarding the mechanism and severity of trauma, a delay in seeking help of more than a week and, at the time of diagnosis, the patient might exhibit clinical or radiological evidence of prior injuries.38,39 A more detailed description regarding abusive head trauma can be found below.
There is no general consensus regarding the best treatment and treatment timing for TVH in the pediatric population. Each case should be evaluated individually because there are many factors that might influence the therapeutic approach.37 In patients presenting with a less dense TVH or without visual axis obstruction (which would allow a better assessment of the posterior fundus), surgical treatment could probably be delayed longer.37 Nevertheless, the length of the observation time will also be determined by the existence of comorbid conditions which might require a more urgent treatment.32,27 For example: retinal detachment, which is known to be related to higher rates of proliferative vitreoretinopathy and poorer visual outcomes when associated with TVH in children.32 Furthermore, unlike in adults, the plasticity of the visual system in patients aged 10 years or less can lead to deprivation amblyopia if the TVH prevents visual stimulation for enough time. Therefore, a more aggressive approach is indicated in these younger patients.35,36
Even though the appropriate surgical technique will depend on several factors, most retina surgeons tends to favor small-gauge (23-, 25-, 27-gauge) transconjunctival sutureless pars plana vitrectomy for clearing TVH due to its reliability, safety, and low rate of postoperative complications in children.40
Traumatic Retinal Detachment
Ocular trauma and related complications are the principal causes for monocular blindness in the pediatric population.41–43 The incidence and severity are higher among males by a factor of 4:1 with respect to females of the same age group.42,44–46 The incidence of the traumatic separation of the neuroretina from the RPE is about 0.8%.47 In the pediatric population, the incidence is even lower, ranging from 2.5 to 2.9 per 100,000 among children aged 10 to 19 years.44,46,47 Traumatic retinal detachment (RD) in children represents 3% to 6% of all causes of retinal detachment.46,48,49 The most common type of RD after trauma is rhegmatogenous. In this age group, patients usually present with the worst visual acuity and the detachment has a longer evolution with a higher incidence of macular involvement and proliferative vitreoretinopathy (PVR).28,47 Retinal dialysis is the most common type of predisposing lesion, responsible for more than half of the traumatic RD. Retinal tears are the second-most common predisposing lesion, responsible for about 20% of the traumatic RD.42
Traumatic RD after closed-globe trauma (as in other forms of trauma) is due to an abrupt deformation of the globe geometry by an external mechanical force (projectiles, airbags, free fall, etc.).50 The creation of holes and tears is secondary to the strong adhesions between the peripheral retina to the vitreous base and vitreous cortex.47 It is imperative to keep a high level of suspicion for globe rupture in all patients with history of closed-globe trauma and a retinal detachment, especially in very young children who cannot verbalize complaints. A comprehensive ophthalmological examination, including dilated fundus examination, is recommended for such cases, including examination under anesthesia if needed.41 It is important to perform scleral depression with caution because a ruptured globe is always a possibility in children, especially if there is a concomitant vitreous hemorrhage.37
Clinical symptoms can include visual field defects, floaters, loss of red reflex, and decreased vision. In the case of unclear media, B-scan ultrasonography can help establish the diagnosis.41,44
Surgical repair is indicated as soon as the patient's circumstances allow it. Using scleral buckles is controversial in very young children and requires clear media, anterior breaks, and no PVR.42,44 Due to the complexity of most cases, pars plana vitrectomy with tamponade agents as the primary surgical technique is preferred.28,47,48 In addition, almost 40% of the cases will need relaxing retinotomies to reattach the retina.42,44,46,48 The anatomical outcome is relatively high (62%–79%) although functional outcome is poor.28,45,48,51 Factors related to poor prognosis include younger age (less than 8 years), worse visual acuity at presentation, large and posterior retinal tears, extensive detachments, the association with congenital anomalies, and the presence of PVR (grade C or higher).42,44,47,49
Even after aggressive treatment, amblyopia is a potential cause for poor visual outcomes and only 17% of the cases will achieve best corrected visual acuity of count-fingers or better.43,47,48
Nonaccidental Trauma (Shaken-Baby Syndrome)
More than 1,400 children a year are diagnosed with shaken-baby syndrome or nonaccidental trauma (NAT)52 and up to 6% of cases are initially recognized by an ophthalmologist.53,54 The most common age group affected is infants less than 12 months old, and it is rare to have a child older than 5 with this diagnosis.53,55 NAT affects about 14–40 per 100,000 infants younger than 12 months. NAT is also associated with a mortality rate up to 23%. Because of the significant and serious impact on the child's vision and health, it is an important diagnosis that must not be missed.
The increased recognition of this syndrome has led to increased efforts focused on protecting these frustrated parents from harming their infants. NAT is typically associated with first-time parents.52,55 Male gender and the psychologic state of parents are the only risk factors with significant association to increased incidence of NAT. There has been no proven association between NAT and race, socioeconomic status, or ethnicity.52,55 The most effective way proven to reduce the incidence of NAT has been education for new parents by a medical professional.5,6 There has been a national effort to raise the awareness of NAT in the hopes of reducing the prevalence of this preventable injury.
NAT is a clinical diagnosis that can be extremely difficult to recognize or prove. NAT is the triad of subdural hematoma, subarachnoid hemorrhage, and retinal hemorrhage. The mechanism of trauma in NAT is hypothesized to be acceleration/deceleration forces exerted on the infant's skull. An infant's head is, on average, 10%–15% of its body weight.53,54 This disproportionate ratio of weight allows shearing forces to accumulate with shaking that can tear through the fragile vasculature of the skull and retina, leading to the hemorrhagic injuries that define NAT. Retinal hemorrhage seen in NAT is typically multilayered (pre-, intra-, and subretinal), can often be too numerous to count, and can extend all the way to the ora serrata.58 About 53%–85% of infants with NAT will present with retinal hemorrhages.55,58 Significant intracranial or retinal hemorrhage in the pediatric population should raise providers' suspicion of child abuse and should lead to further investigation.
Physicians should have NAT in mind when presented with a rapid change in mental status in an infant with or without a history of relatively minor trauma from the parents. Lethargy, irritability, seizures, vomiting, apnea, hyper-or hypotonia, and poor feeding are some of the concerning symptoms that should raise suspicion for intracranial bleeds.52,54 NAT is often associated with few or no signs of external trauma, which complicates recognition of this condition for the provider. NAT can sometimes be associated with paravertebral rib fractures, and with humeral or femoral fractures (any long bone can be involved) depending on the position of the adult's grip on the child. Ocular signs associated with NAT are seen in the periorbital region (lid edema, ecchymosis, orbital fractures), anterior segment (hyphema, iris prolapse, corneal lacerations, cataracts), and posterior segment (vitreous hemorrhage, retinal detachment, perimacular folds, optic nerve avulsion). Dilated fundus exam will often also reveal macular retinoschisis. β-amyloid precursor protein (β-APP) is a protein recognized on immunohistochemical stain that has been found to correlate with axonal injury such as is seen in NAT.8 The combination of β-APP and brain magnetic resonance imaging (MRI) has increased the accuracy with which providers can identify brain injury and bleeding leading to more accurate diagnoses of NAT.54,59
Treatment of NAT is directed at the increased intracranial pressure (ICP) due to cerebral edema and possible hemorrhage. Hematoma evacuation surgery and Burr hole craniotomy are some common procedures to relieve the increased ICP emergently. ICP monitoring is a critical aspect of management of NAT to avoid further cerebral injury. Physicians should admit the child to the hospital and notify police and child protective services (CPS) whenever there is suspicion of child abuse.
It is important to consider a broad differential diagnosis because of the serious implications of making a diagnosis of NAT. Vitamin D deficiency can lead to long-bone fractures. Subdural hemorrhage can be the result of accidental trauma, birth trauma, metabolic disease, autoimmune disorders, coagulopathy, or anemia. Terson syndrome is the association of vitreous hemorrhage and subarachnoid hemorrhage that can be difficult to distinguish from NAT.
Fifteen percent of infants with NAT suffer permanent cortical blindness and 30%–40% will have significant visual impairment. About 30%–50% have permanent paralysis or mental retardation. Some studies have indicated that nonreactive pupils and midline shift on imaging are indicators of higher risk of mortality. Ventilatory requirements have an association with poorer prognosis of visual function.53 NAT is a serious condition that requires vigilance by physicians to ensure rapid and accurate diagnosis and treatment.
- Blanch RJ, Good PA, Shah P, Bishop JR, Logan A, Scott RA. Visual outcomes after blunt ocular trauma. Ophthalmology. Aug 2013;120(8):1588-1591.
- Bradley JL, Shah SP, Manjunath V, Fujimoto JG, Duker JS, Reichel E. Ultra-high-resolution optical coherence tomographic findings in commotio retinae. Archives of Ophthalmology. Jan 2011;129(1):107-108.
- Oladiwura D, Lim LT, Ah-Kee EY, Scott JA. Macular optical coherence tomography findings following blunt ocular trauma. Clinical Ophthalmology. 2014;8:989-992.
- Mansour AM, Green WR, Hogge C. Histopathology of commotio retinae. Retina. 1992;12(1):24-28.
- El Matri L, Chebil A, Kort F, Bouraoui R, Largueche L, Mghaieth F. Optical Coherence Tomographic Findings in Berlin's Edema. Journal of Ophthalmic & Vision Research. Apr 2010;5(2):127-129.
- Andrew NH, Slattery JA, Gilhotra JS. Infrared reflectance as a diagnostic adjunct for subclinical commotio retinae. Indian Journal of Ophthalmology. Aug 2014;62(8):879-880.
- Sipperley JO, Quigley HA, Gass DM. Traumatic retinopathy in primates. The explanation of commotio retinae. Archives of Ophthalmology. Dec 1978;96(12):2267-2273.
- Friberg TR. Traumatic retinal pigment epithelial edema. American Journal of Ophthalmology. Jul 1979;88(1):18-21.
- Ahn SJ, Woo SJ, Kim KE, Jo DH, Ahn J, Park KH. Optical coherence tomography morphologic grading of macular commotio retinae and its association with anatomic and visual outcomes. American Journal of Ophthalmology. Nov 2013;156(5):994-1001 e1001.
- Mustafa MS, McBain VA, Scott CM. Autofluorescence imaging - a useful adjunct in imaging macular trauma. Clinical Ophthalmology. 2010;4:1497-1498.
- Gill MK, Lou PL. Traumatic macular holes. International ophthalmology clinics. Summer 2002;42(3):97-106.
- Sartori Jde F, Stefanini F, Moraes NS. Spontaneous closure of pediatric traumatic macular hole: case report and spectral-domain OCT follow-up. Arquivos brasileiros de oftalmologia. Jul-Aug 2012;75(4):286-288.
- Azevedo S, Ferreira N, Meireles A. Management of pediatric traumatic macular holes - case report. Case reports in ophthalmology. May 2013;4(2):20-27.
- Johnson RN, McDonald HR, Lewis H, et al. Traumatic macular hole: observations, pathogenesis, and results of vitrectomy surgery. Ophthalmology. May 2001;108(5):853-857.
- Miller JB, Yonekawa Y, Eliott D, Vavvas DG. A review of traumatic macular hole: diagnosis and treatment. International ophthalmology clinics. Fall 2013;53(4):59-67.
- Youssri AI, Young LH. Closed-globe contusion injuries of the posterior segment. International ophthalmology clinics. Summer 2002;42(3):79-86.
- Tsui I, Campolattaro BN, Lopez R. Progression of traumatic lamellar macular hole to full-thickness macular hole and retinal detachment in a 3-year-old child. Retinal cases & brief reports. Winter 2010;4(1):25-27.
- Margherio AR, Margherio RR, Hartzer M, Trese MT, Williams GA, Ferrone PJ. Plasmin enzyme-assisted vitrectomy in traumatic pediatric macular holes. Ophthalmology. Sep 1998;105(9):1617-1620.
- Wu WC, Drenser KA, Trese MT, Williams GA, Capone A. Pediatric traumatic macular hole: results of autologous plasmin enzyme-assisted vitrectomy. American journal of ophthalmology. Nov 2007;144(5):668-672.
- Wachtlin J, Jandeck C, Potthofer S, Kellner U, Foerster MH. Long-term results following pars plana vitrectomy with platelet concentrate in pediatric patients with traumatic macular hole. American journal of ophthalmology. Jul 2003;136(1):197-199.
- Patel MM, Chee YE, Eliott D. Choroidal rupture: a review. International ophthalmology clinics. Fall 2013;53(4):69-78.
- Estafanous MF, Seeley M, Traboulsi EI. Choroidal rupture associated with forceps delivery. American journal of ophthalmology. Jun 2000;129(6):819-820.
- Glazer LC, Han DP, Gottlieb MS. Choroidal rupture and optic atrophy. The British journal of ophthalmology. Jan 1993;77(1):33-35.
- Hargrave S, Weakley D, Wilson C. Complications of ocular paintball injuries in children. Journal of pediatric ophthalmology and strabismus. Nov-Dec 2000;37(6):338-343.
- Misra A, Cohen VM, Burton RL. Severe ocular trauma in a young girl with a paintball pellet. The Journal of pediatrics. Dec 2005;147(6):868.
- Ament CS, Zacks DN, Lane AM, et al. Predictors of visual outcome and choroidal neovascular membrane formation after traumatic choroidal rupture. Archives of ophthalmology. Jul 2006;124(7):957-966.
- Wood CM, Richardson J. Indirect choroidal ruptures: aetiological factors, patterns of ocular damage, and final visual outcome. The British journal of ophthalmology. Apr 1990;74(4):208-211.
- Abri A, Binder S, Pavelka M, Tittl M, Neumuller J. Choroidal neovascularization in a child with traumatic choroidal rupture: clinical and ultrastructural findings. Clinical & experimental ophthalmology. Jul 2006;34(5):460-463.
- Piermarocchi S, Benetti E, Fracasso G. Intravitreal bevacizumab for posttraumatic choroidal neovascularization in a child. Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus / American Association for Pediatric Ophthalmology and Strabismus. Jun 2011;15(3):314-316.
- Prasad A, Patel CC, Puklin JE. Intravitreal bevacizumab in the treatment of choroidal neovascularization from a traumatic choroidal rupture in a 9-year-old child. Retinal cases & brief reports. Spring 2009;3(2):125-127.
- Sudhalkar A, Chhablani J, Jalali S, Mathai A, Pathengay A. Spontaneous vitreous hemorrhage in children. American journal of ophthalmology. Dec 2013;156(6):1267-1271 e1262.
- Yeung L, Chen TL, Kuo YH, et al. Severe vitreous hemorrhage associated with closed-globe injury. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie. Jan 2006;244(1):52-57.
- Simon J, Sood S, Yoon MK, et al. Vitrectomy for dense vitreous hemorrhage in infancy. Journal of pediatric ophthalmology and strabismus. Jan-Feb 2005;42(1):18-22.
- Yan H, Ahmed AS, Han J, Cui J, Yu J. A vitreous hemorrhage animal model in rabbits using force percussion injury. Current eye research. Sep 2009;34(9):717-726.
- Spirn MJ, Lynn MJ, Hubbard GB, 3rd. Vitreous hemorrhage in children. Ophthalmology. May 2006;113(5):848-852.
- AlHarkan DH, Kahtani ES, Gikandi PW, Abu El-Asrar AM. Vitreous hemorrhage in pediatric age group. Journal of ophthalmology. 2014;2014:497083.
- Rishi P, Rishi E, Gupta A, Swaminathan M, Chhablani J. Vitreous hemorrhage in children and adolescents in India. Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus / American Association for Pediatric Ophthalmology and Strabismus. Feb 2013;17(1):64-69.
- Hinds T, Shalaby-Rana E, Jackson AM, Khademian Z. Aspects of abuse: abusive head trauma. Current problems in pediatric and adolescent health care. Mar 2015;45(3):71-79.
- Naik-Mathuria B, Akinkuotu A, Wesson D. Role of the surgeon in non-accidental trauma. Pediatric surgery international. Jul 2015;31(7):605-610.
- Singh R, Kumari N, Katoch D, Sanghi G, Gupta A, Dogra MR. Outcome of 23-gauge pars plana vitrectomy for pediatric vitreoretinal conditions. Journal of pediatric ophthalmology and strabismus. Jan-Feb 2014;51(1):27-31.
- Soliman MM, Macky TA. Pediatric rhegmatogenous retinal detachment. International ophthalmology clinics. Winter 2011;51(1):147-171.
- Sheard RM, Mireskandari K, Ezra E, Sullivan PM. Vitreoretinal surgery after childhood ocular trauma. Eye. Jun 2007;21(6):793-798.
- Gonzales CR, Singh S, Yu F, Kreiger AE, Gupta A, Schwartz SD. Pediatric rhegmatogenous retinal detachment: clinical features and surgical outcomes. Retina. Jun 2008;28(6):847-852.
- Soheilian M, Ramezani A, Malihi M, et al. Clinical features and surgical outcomes of pediatric rhegmatogenous retinal detachment. Retina. Apr 2009;29(4):545-551.
- Da Pozzo S, Pensiero S, Perissutti P. Ocular injuries by elastic cords in children. Pediatrics. Nov 2000;106(5):E65.
- Rahimi M, Bagheri M, Nowroozzadeh MH. Characteristics and outcomes of pediatric retinal detachment surgery at a tertiary referral center. Journal of ophthalmic & vision research. Apr 2014;9(2):210-214.
- Sarrazin L, Averbukh E, Halpert M, Hemo I, Rumelt S. Traumatic pediatric retinal detachment: a comparison between open and closed globe injuries. American journal of ophthalmology. Jun 2004;137(6):1042-1049.
- Fivgas GD, Capone A, Jr. Pediatric rhegmatogenous retinal detachment. Retina. 2001;21(2):101-106.
- Weinberg DV, Lyon AT, Greenwald MJ, Mets MB. Rhegmatogenous retinal detachments in children: risk factors and surgical outcomes. Ophthalmology. Sep 2003;110(9):1708-1713.
- Eliott D, Hauch A, Kim RW, Fawzi A. Retinal dialysis and detachment in a child after airbag deployment. Journal of AAPOS: the official publication of the American Association for Pediatric Ophthalmology and Strabismus/American Association for Pediatric Ophthalmology and Strabismus. Apr 2011;15(2):203-204.
- Kocaoglan H, Unlu N, Acar MA, Sargin M, Aslan BS, Duman S. The efficacy of conventional rhegmatogenous retinal detachment surgery in the pediatric population. Journal of pediatric ophthalmology and strabismus. Jan-Feb 2003;40(1):4-5.
- American Academy of Pediatrics: Committee on Child Abuse and Neglect (July 2001). Shaken baby syndrome: rotational cranial injuries-technical report. Pediatrics. 108 (1):206–10.
- Levin, Alex, Randell Alexander, Gil Binenbaum, Brian Forbes, and Carole Jenny. "Abusive Head Trauma/Shaken Baby Syndrome." American Academy of Ophthalmology. American Academy of Ophthalmology, 1 Mar. 2015. Web. 9 July 2015.
- Mian M, Shah J, Dalpiaz A, et al. Shaken baby syndrome: a review. Fetal Pediatr Pathol. 2015;34(3):169-75.
- Kivlin J, Simons K, Lazoritz S, Ruttum M. Shaken baby syndrome. Ophthalmology. 2000; 107(7): 1245-1254.
- Altman RL, Canter J, Patrick PA, et al. Parent education by maternity nurses and prevention of abusive head trauma. Pediatrics 2011;128(5):e1164–e1172.
- Bechtel K, Le K, Martin KD, et al. Impact of an educational intervention on caregivers' beliefs about infant crying and knowledge of shaken baby syndrome. Acad Pediatr 2011;11(6):481–486.
- Togioka BM, Arnold MA, Bathurst MA, et al. Retinal hemorrhages and shaken baby syndrome: an evidence-based review. J Emerg Med 2009;37(1):98–106.
- Geddes JF, Vowles GH, Hackshaw AK, et al. Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants. Brain 2001;124(Pt 7):1299–1306.