Vitreous Traction Research Articles

Intraoperative optical coherence tomography assisted analysis of pars Plana vitrectomy for retinal detachment in morning glory syndrome: a case report

BackgroundThe pathogenesis of non-rhegmatogenous retinal detachment (non-RRD) associated with morning glory syndrome (MGS) is not established, as well as best surgical approach to treat RD. Our purpose was to analyse intraoperative optical coherence tomography data (iOCT) in all steps of pars plana vitrectomy (PPV) for non-RRD in MGS, in order to follow pathophysiological aspects of the disease and to understand the tissues behaviour during surgical workflow.Case presentationIntraoperative spectral domain optical coherent tomography (iSD-OCT) assisted PPV using Rescan 700 (Carl Zeiss Meditech, Jena, Germany) with epiretinal membrane (ERM) and internal retinal membrane (ILM) peeling, and air endotamponade was performed on the only eye of a 21 years old female with non-RRD associated with MGS. BCVA, pre-, intra- and postoperative OCT were performed along with standard ocular examination. iOCT video and snapshots were analysed intra- and postoperatively using post-processing approach using graphic software. The progression of non-RRD resulted in best corrected visual acuity (BCVA) decrease from 0.8 to 0.2. Triamcinolone enhanced iOCT imaging revealed strong vitreous traction and adhesion above the macula and optic disc. Internal limiting membrane was peeled under iOCT control to prevent the peeling of inner layers of the retinal schisis. No retinal break was detected, and only air endotamponade was performed. The retina reattached during first 4 weeks of follow-up with gradual resolution of intraretinal- and subretinal fluid, and remained stable in 12 months. BCVA improved to 0.8.ConclusionBased on iSD-OCT findings we assume that non-RRD in this case of MGS is caused primarily by the vitreous traction with further possible formation of the retinal breaks. Retinal reattachment reached only with air endotamponade strongly advocates the tractional component of non-RRD and retinal schisis assotiated with MGS. Early PPV for central non-RRD and retinal schisis with the use of iOCT can be performed in more safe and controlled manner and has to be considered to reduce the risk of retinal break formation and to prevent the central vision loss.

CLINICAL FEATURES OF AFFECTED AND UNDETACHED FELLOW EYES IN PATIENTS WITH FEVR-ASSOCIATED RHEGMATOGENOUS RETINAL DETACHMENT.

To report the clinical characteristics of the affected and fellow eyes in patients with familial exudative vitreoretinopathy-associated rhegmatogenous retinal detachment (FEVR-RRD). This was a retrospective observational case series. The affected and fellow eyes were given complete examinations. The age, sex, clinical features of the affected eyes, and varied abnormalities of the fellow eyes were analyzed. Forty-three patients with FEVR-RRD were included. The average age was 21.8 ± 10.9 years, and the males (19.9 ± 9.6) were younger than the females (28.1 ± 1.2). Retinal round holes were noted in 32 (71.1%) eyes. In addition, horseshoe retinal tears and giant retinal tears were present in 10 (22.2%) eyes and 3 (6.7%) eyes. Subretinal fibrosis was seen in 20 (44.4%) eyes, and choroidal detachment was shown in 6 (13.3%) of the eyes. A high prevalence of abnormalities was noted in the undetached fellow eyes in the peripheral retina, including vascular leakage in fundus fluorescein angiography (75.6%), lattice degeneration (53.7%), and vitreous traction (51.2%). Male patients with FEVR-RRD experience an earlier onset than females in our series. Retinal tears, even giant tears, could be responsible for FEVR-RRD. The fellow eyes of FEVR-RRD patients were characterized by predetachment changes, which need both lifelong monitoring and timely vision-saving intervention.

Retinitis Pigmentosa and Other Dystrophies.

Retinitis pigmentosa (RP) is a heterogeneous group of inherited retinal degenerations characterized by progressive degeneration of rod and cone cells that affects predominantly peripheral visual fields. Macular edema may cause additional central visual acuity decrease. Cystoid macular edema (CME) is one of the few treatable causes of visual loss in RP. The prevalence of CME in RP has been found to be between 10 and 20% on fluorescein angiography-based studies, and as high as 49% on reports based on optical coherence tomography. Macular edema can manifest at any stage of the disease and may be unilateral or bilateral. It can be found in any genetic form, but is more often associated with RP caused by CRB1 mutations. The origin of macular edema in RP patients still remains poorly understood. Some mechanisms have been suggested, including antiretinal antibodies (retinal, carbonic anhydrase, and enolase antibodies), vitreous traction, retinal pigment epithelium dysfunction, and Müller cell edema. There is no gold standard therapeutic strategy. Drug therapy is the primary treatment. Systemic carbonic anhydrase inhibitors, such as oral acetazolamide or topical dorzolamide, are still the mainstays of initial therapy. If CME is refractory to acetazolamide, intravitreal corticosteroid injections may be a therapeutic option. However, antivascular endothelium growth factor injections have limited effect and should be avoided. Vitrectomy has also been evaluated, but its exact role remains to be determined. The benefits of these therapies are variable among patients. The establishment of therapeutic approaches is limited by our poor understanding of the pathophysiology of CME in patients with RP. Autoimmune retinopathies (AIRs) are a group of rare diseases characterized by acute or subacute progressive vision loss and are thought to be mediated by autoantibodies specific to retinal antigens. The AIRs encompass paraneoplastic syndromes, such as cancer-associated retinopathy and melanoma-associated retinopathy, and a larger group of AIRs that have similar clinical and immunological findings but without underlying malignancy. These diseases may also be complicated by macular edema. RP is one of the most common forms of inherited retinal degeneration. It displays extensive clinical and genetic variations and leads to progressive blindness with variable onset.

Formation of an Intraretinal Fluid Barrier in Cavitary Optic Disc Maculopathy

Cavitary optic disc maculopathy develops when fluctuating pressure gradients along anomalous communications in the optic nerve head induce migration of fluid into the adjacent retinal tissue. We sought to determine whether carefully titrated laser photocoagulation combined with vitrectomy and gas tamponade can safely create an effective intraretinal barrier to fluid egress from the optic disc cavitation. Retrospective interventional case series. We retrospectively evaluated medical records and imaging studies of 22 consecutive patients with cavitary disc maculopathy evaluated by a single surgeon between 1991 and 2014. Patients requiring surgery underwent carefully titrated juxtapapillary laser photocoagulation followed immediately by vitrectomy and gas tamponade. Main outcome measures were change in visual acuity, macular fluid resolution, and recurrence of maculopathy. Eleven patients (11 eyes) had undergone vitreous surgery and were included in the study. No preoperative evidence for vitreous traction on the optic disc or macula was seen in any eye. Nine patients underwent a single surgery and 2 patients required additional procedures to resolve the macular fluid. Mean length of follow-up after the last surgery was 48.2months (range, 4-143months). All 11 patients (100%) had complete resolution of macular fluid, with an average time to resolution of 8.5months (range, 1-18months). Only 1 of 11 patients (9%) had recurrence of macular fluid (14months postoperatively). The average preoperative visual acuity of 20/125 (logMAR 0.81, standard deviation [SD]=0.36) improved by nearly 4 lines to an average final visual acuity of 20/57 (logMAR 0.45, SD= 0.37) (P=.0072). A possible laser-induced central scotoma was suspected in only 1 patient who had undergone extensive prior laser treatments. An effective intraretinal barrier to fluid migration from cavitary optic disc anomalies can be safely achieved in most patients with carefully titrated juxtapapillary laser photocoagulation combined with vitrectomy and gas tamponade. Once achieved, the barrier facilitates resolution of macular fluid and long-term avoidance of recurrent maculopathy.

Signs and symptoms of uveitis

SummaryUveitis can be a sight‐threatening disease. Inflammation of uveal tract can be divided into: anterior, intermediate, posterior, and panuveitis. Blurred vision, ocular pain, photophobia and floaters are some of the symptoms complained by those who are affected by uveitis. The onset of uveitis can be either acute or insidious, bilateral rather than unilateral. Posterior uveitis is usually associated with vitritis. Anterior chamber cells and flare should be graded according to standardized uveitis nomenclature (SUN) working group. Binocular indirect ophthalmoscopy (BIO) score is used to evaluate the severity of vitritis. Vitreous changes may comprehend: vitreous hemorrhage, vitreous strands, and vitreous traction. A further classification of posterior uveitis depends on the primary site of inflammation, which can identify: retinitis, choroiditis, retinochoroiditis, and chorioretinitis. Posterior pole uveal involvement can be: focal, multifocal, and placoid. Retinal vasculitis can be present. Uveitis might be complicated by anterior and posterior synechiae, which can lead to uveitic glaucoma, cystoid macular oedema, retinal and choroidal neovascularizations, and retinal ischemia.

The vitreopapillary interface in healthy and glaucoma – the VPI study

PurposeDuring posterior vitreous detachment (PVD) the posterior hyaloid remains, for a certain period, attached to the posterior pole. At the macula, the vitreomacular interface and its associated disease has been studied extensively. The opposite is true for the vitreopapillary interface, especially in glaucoma patients. As glaucoma affects the shape and cupping of the optic nerve head, this study aims to investigate the possible influence of vitreous traction on the disc.MethodsThe VPI study (NCT02290795) is a cross‐sectional prospective study including healthy subjects and glaucoma patients. A subset of the glaucoma patients was followed‐up longitudinally to assess the impact of filtering surgery on the VPI. All glaucoma patients underwent a comprehensive ophthalmological investigation, automated visual field test, confocal scanner and OCT scan. Healthy subjects filled in a questionnaire on gender, age, medical history, medication use and had also had an OCT‐scan to determine PVD status.ResultsIn total, 258 healthy subjects and 349 glaucoma patients were included rendering data on 1214 eyes. Glaucoma patients were significantly older than their healthy counterparts (66.5 ± 12.8 vs. 60.1 ± 14.8, p < 0.001). Split up per PVD stage, the age did not differ in PVD stage 0, but for every following PVD stage, glaucoma patients were significantly older (54.2 ± 11.7 vs. 50.1 ± 14.4 (p = 0.071); 61.1 ± 10.4 vs. 54.7 ± 14.0 (p < 0.001); 72.5 ± 8.9 vs. 67.7 ± 5.9 (p < 0.001); 73.7 ± 9.9 vs. 71.4 ± 9.3 (p = 0.014) for PVD stage 0;1;3;4 respectively).ConclusionsThe process of PVD formation lasts significantly longer in glaucoma patients.

Surgery for Diabetic Eye Complications.

New modalities for the treatment of diabetic eye complications have emerged in the past decade. Nevertheless, many severe diabetic retinopathy complications can only be treated with vitreoretinal surgery. Technological advances in pars plana vitrectomy have expanded the gamut of pathologies that can be successfully treated with surgery. The most common pathologies managed surgically include vitreous opacities and traction retinal detachment. The indications, surgical objectives, adjunctive pharmacotherapy, microincisional surgical techniques, and outcomes of diabetic vitrectomy for proliferative diabetic retinopathy and diabetic tractional retinal detachment will be discussed. With the availability of new microincisional vitrectomy technology, wide angle microscope viewing systems, and pharmacologic agents, vitrectomy can improve visual acuity and achieve long-term anatomic stability in eyes with severe complications from proliferative diabetic retinopathy.

Wide-field fundus fluorescein angiogram assisted photocoagulation on familial exudative vitreoretinopathy

Objective To observe the application value and therapeutic efficacy of wide-field digital pediatric retinal imaging system (Retcam Ⅲ) fundus fluorescein angiograms (FFA) assisted photocoagulation on familial exudative vitreoretinopathy (FEVR). Methods The study included 46 eyes of 34 patients with staging 2 FEVR. All patients received color fundus photography and FFA under general anesthesia. The blood vessel reliability of color fundus photography and FFA was comparatively determined. Binocular indirect ophthalmoscope laser photocoagulation was applied to peripheral retina with abnormal leakage as indicated by FFA, the wavelength was 532nm, the duration was 0.25 s and the energy was 200 - 280 mW. After laser photocoagulation, fundus imaging and FFA was repeated. Further laser photocoagulation was immediately added to areas with vessel leakage but missing the photocoagulation. After treatment, the mean follow-up duration was 14.4 months. The follow up focused on neovascularization, exudative lesions, vitreous traction and merging of photocoagulation spots within 3 months, and on fibrosis membrane resulting in macular traction, tractional retinal detachment, vitreous hemorrhage or Coats disease-like retinal exudates after 3 months. Results It was hard to identify the blood vessels based on the color fundus images and some avascular zone maybe missed. Neovascularization can't be determined by shape of the blood vessels. On the other hand, those new blood vessels can be easily recognized by FFA as leakage sites at the boundary of avascular zone. The surgeon could quickly and accurately locate the FEVR area guided by the color fundus images and FFA from same angle under binocular indirect ophthalmoscope. During the treatment, there was no retinal FEVR area missed laser photocoagulation for all patients. There was no neovascularization, exudative lesions, vitreous traction within 3 months, and no fibrosis membrane, tractional retinal detachment, vitreous hemorrhage or Coats disease-like retinal exudates after 3 months. There were no ocular and systemic complications during and after the FFA and laser photocoagulation. Conclusion Wide-field Retcam Ⅲ FFA can help retinal specialists to identify abnormal neovascularization, locate the lesion area, and thus increase the success rate of laser photocoagulation, reduce the ocular and systemic complications for FEVR. Key words: Retinal diseases/congenital; Retinal diseases/diagnosis; Fluorescein angiography; Retinal diseases/therapy; Laser coagulation

Prevalence, characteristics, and pathogenesis of paravascular inner retinal defects associated with epiretinal membranes.

To investigate the prevalence, detailed characteristics, and pathogenesis of paravascular inner retinal defects (PIRDs) in eyes with epiretinal membranes (ERMs). In this prospective observational case series, we included 81 eyes of 81 patients with idiopathic ERMs, without high myopia. The retinal structure surrounding the PIRDs was assessed using sequential thin sectioning of optical coherence tomography. The PIRDs were classified into three grades. Typical defects of the inner retinal tissue were defined as grade 3. Inner retinal cleavages with openings to the vitreous cavity and no apparent defect of the inner retinal tissue were defined as grade 2. Inner retinal cleavages or cystoid spaces with no connection to the vitreous cavity were defined as grade 1. Of 81 eyes with ERMs, 31 (38.3%) had PIRDs along the temporal arcade vessels (grade 1 in six eyes, grade 2 in four eyes, and grade 3 in 21 eyes). PIRDs were frequently accompanied by broad defects of the inner retinal tissue (grade 3). Although some ERMs directly adhered to the edge of a PIRD or the retinal vessels, PIRDs were often located outside the area of adhesion to the ERM. In some OCT sections, vitreous traction on the inner retina seemed to contribute to the progression of PIRDs. Visual field abnormalities corresponded to the location of the PIRDs in 44.4% of eyes with grade 3 PIRDs. Deviation of retinal vessels due to the traction of the ERMs may contribute to the pathogenesis of PIRDs. PIRDs often cause visual field abnormalities corresponding to the location of the defect.

Iatrogenic retinal breaks in ultrahigh-speed 25-gauge vitrectomy: a prospective study of elective cases

Background/AimsTo evaluate the incidence of intraoperative retinal breaks in the ultrahigh-speed (UHS) 25-gauge vitrectomy system in elective vitreous-retina surgery cases.MethodsA prospective series of 1676 eyes of 1306 consecutive patients. All...

Photopsia and a temporal visual field defect

A 30-year-old woman presented with intermittent photopsia, a temporal visual field defect below the horizontal in her left eye, and flu-like symptoms. Slit-lamp and fundus examinations were unremarkable. Humphrey 30-2 threshold perimetry and 120-point screening visual field demonstrated blind spot enlargement of the left eye and a normal field in the right eye. Fundus autofluorescence, optical coherence tomography of the macula, full-field electroretinogram, electrooculogram, and multifocal electroretinogram were normal. Swept-source optical coherence tomography scan of the left optic nerve showed an intact outer retina, a remarkably thinned nerve fiber layer nasally, and peripapillary vitreous traction. Goldmann kinetic perimetry revealed a sector-shaped dense defect breaking out from the blind spot to the temporal periphery just below the horizontal in the left eye. The patient had nasal hypoplasia of the optic nerve and peripapillary vitreous traction.

Immunopathogenic Background of Pars Planitis.

Pars planitis is defined as an intermediate uveitis of unknown background of systemic disease with characteristic formations such as vitreous snowballs, snowbanks and changes in peripheral retina. The incidence of pars planitis varies 2.4–15.4 % of the uveitis patients. The pathogenesis of the disease is to be determined in future. Clinical and histopathological findings suggest an autoimmune etiology, most likely as a reaction to endogenous antigen of unknown source, with T cells predominant in both vitreous and pars plana infiltrations. T cells subsets play an important role as a memory-effector peripheral cell. Snowbanks are formed as an effect of post inflammatory glial proliferation of fibrous astrocytes. There is also a genetic predisposition for pars planitis by human leukocyte antigen and several other genes. A coexistence of multiple sclerosis and optic neuritis has been described in numerous studies. Epiretinal membrane, cataract, cystoid macular edema, retinal detachment, retinal vasculitis, neovascularization, vitreous peripheral traction, peripheral hole formation, vitreous hemorrhage, disc edema are common complications observed in pars planitis. There is a need to expand the knowledge of the pathogenic and immunologic background of the pars planitis to create an accurate pharmacological treatment.

Optic nerve head hemorrhage and vitreous traction

PurposeDuring posterior vitreous detachment (PVD) the posterior hyaloid remains, for a certain period, attached to the optic disc. It can exert traction with development of optic nerve head hemorrhages (ONHH). ONHH are known to be associated with glaucomatous progression and retinal nerve fiber layer (RNFL) defects. Therefore this study aims at investigating the relationship between PVD formation and ONHH in open angle glaucoma patients.MethodsPatients presenting with an ONHH, from November 2014 on, were included. They underwent a comprehensive ophthalmological investigation, automated visual field test, confocal scanner (HRT III), OCT (HRT‐Spectralis) scan and stereographic photos of the optic nerve head. This study is part of a larger, clinicaltrial.gov (NCT02290795) registered, study investigating vitreopapillary traction (VPT).ResultsEighteen eyes of 18 patients (11 normal tension, 6 primary open angle and 1 secondary open angle glaucoma) were included. Seven out of 18 (38.9%) eyes had concomitant VPT and 7 had a complete PVD. Seven ONHH were located infero‐, 5 supero‐ and 6 temporal. In the non‐VPT subgroup 5 out of 11 (45.5%) eyes showed matching retinal nerve fiber layer defects, with 2 out of 7 (28.6%) in the VPT subgroup.ConclusionsVPT could be a confounding factor in glaucoma assessment and ONHH development.

Diabetic maculopathy

SummaryVitreoretinal macular interface plays an important role in the formation and progression of diabetic macular edema. Main vitreoretinal diseases as epiretinal membrane, vitreous traction and macular holes may occur in this condition. They are due to abnormal mechanical and biochemical interactions between posterior hyaloid and retinal surface. OCT has changed our understanding of the contribution of vitreoretinal interface disorders on the course of macular edema. Tractional elements contribution seems to be more obvious compared to untractional elements as epiretinal membranes. The management of vitreoretinal retinal disorders associated to diabetic macular edema will be discussed. Specific surgical approach will be detailled and compared to same conditions occuring in non diabetic patients.

Signs and symptoms of uveitis

SummaryInflammation of uveal tract can be divided into: anterior, intermediate, posterior, and panuveitis. Uveitis can be a sight‐threatening disease. The commonest ocular symptoms are: blurred vision, ocular pain, photophobia and floaters, depending on the type of uveitis. The onset of uveitis can be either acute or insidious, involving one or both eyes. Posterior uveitis is usually associated with vitritis. Anterior chamber cells and flare should be graded according to standardized uveitis nomenclature (SUN) working group. Binocular indirect ophthalmoscopy (BIO) score is used to grade vitreous involvement. Vitreous changes may comprehend: vitreous hemorrhage, vitreous strands, and vitreous traction. A further classification of posterior uveitis depends on the primary site of inflammation, which can identify: retinitis, choroiditis, retinochoroiditis, and chorioretinitis. Posterior pole uveal involvement can be: focal, multifocal, and placoid. Retinal vasculitis can be associated with several sub‐types of posterior uveitis. Uveitis can present several complications such as, anterior and posterior synechiae, which can lead to uveitic glaucoma, cystoid macular oedema, retinal and choroidal neovascularizations, and retinal ischemia.

Venous occlusions

SummaryThe retinovitreal interface may be altered during retinal vein occlusions, either through vitreal traction participating to macular edema or the development of an epiretinal membrane. Surgical treatment of these may reduce macular thickness, although the severity of the underlying retinal damage may impair visual results. Epiretinal membrane peeling may also be useful to prevent multirecidivant macular edema. An emerging concern is surgical damage to the nerve fiber layer. Beside these well‐known entities, the role of a normal inner limiting membrane in the maintenance of macular edema is debated.

Resolution of postoperative macular hole with topical nepafenac: a case report

PurposeMacular hole (MH) is a rare complication of cataract extraction. Various etiologies are discussed but it seems that the combination of vitreous traction and pseudophakic macular edema are the causes most likely involved in its pathogenesis. Pars plana vitrectomy (PPV) and internal limiting membrane peeling is the gold standard treatment option for patients with postoperative MH. Medical treatment has not been very effective in resolving this pathology. We present a case of post‐surgical MH treated with topical Nepafenac.MethodsInterventional case report showing the role of topical Nepafenac as a therapeutic tool in post‐surgical MH.ResultsAn 81‐year‐old female with a history of uncomplicated cataract surgery in RE. Four weeks after surgery there was a progressive visual deterioration with a best corrected visual acuity (BCVA): 0.05. SD‐OCT revealed a full‐thickness MH. Nepafenac 0.1 mg/ml, 3 times a day, was administered for 8 weeks in RE. Four months later, an improvement of her visual acuity (BCVA: 0.4) and a recovery of the retinal structure were observed. No recidive has been observed in a follow‐up of 1 year.ConclusionsWe propose the therapeutic use of topical NSAIDs as a possible alternative to surgery for macular holes whose etiology is related to inflammatory processes.

Retinal Cavernous Hemangioma

An asymptomatic 14-year-old boy was incidentally found to have a “bunch-of-grapes”−like retinal lesion, consistent with a retinal cavernous hemangioma. Although typically sporadic and unilateral, these lesions can be familial and associated with cutaneous, hepatic, or intracranial hemangiomas. Vitreous hemorrhage may result from epiretinal membrane contraction and vitreous traction. Fundus photograph showing the retinal cavernous haemangioma (Fig A). Near-infrared spectroscopy (Fig B) and spectral-domain optical coherence tomography (Fig C) demonstrating the epiretinal membrane and vitreous traction.

Abnormal traction of the vitreous detected by swept-source optical coherence tomography is related to the maculopathy associated with optic disc pits.

Maculopathy associated with optic disc pits (ODP), which sometimes causes severe visual loss, usually appears in late childhood or early adulthood. However, it has long been unclear how the disease begins to develop at these ages. We evaluated the relationship between vitreous structure and maculopathy associated with ODP. Six patients (seven eyes) with ODP were diagnosed between July 1990 and May 2013. Fundus photographs and swept-source optical coherence tomography (SS-OCT) images were evaluated retrospectively, and the vitreous at the vitreoretinal interface was visualized by reconstructing three-dimensional SS-OCT images. Vitrectomy was performed in the eyes with maculopathy. Among the six patients, five had ODP in one eye each and one patient had bilateral ODP. The pits were mainly located in the temporal quadrant, and maculopathy, including retinoschisis and retinal detachment, was detected in five eyes associated only with the temporal pits. A flat retinal detachment was observed in four eyes and identified within the vascular arcade except in one eye. A posterior precortical vitreous pocket (PPVP) was observed in all eyes except in one eye without maculopathy. Reconstructing images from SS-OCT showed the vitreoretinal interface abnormalities around the optic disc and the macular area in all eyes, which was completely different from the vitreoretinal interface in the normal pediatric eye. Vitrectomy was performed in four eyes with retinal detachment to resect the abnormal vitreous traction. Posterior vitreous detachment was created in two eyes. Retinal reattachment was achieved in three eyes, and subretinal fluid receded in one eye. The visual acuity improved in all four eyes. Abnormal traction of the vitreous due to an abnormality of the vitreoretinal interface, which may be strengthened by the development of a PPVP, generates the maculopathy associated with ODP.

Circumferential macular folds associated with reduced macular hemorrhages in non-accidental trauma: implications for the theory of vitreous traction

References Results Methods Conclusion Discussion The direct intraocular mechanisms and forces required to create retinal hemorrhages in non-accidental head injury remain a matter of controversy and conjecture. The predominant theory implicates vitreous traction on retinal vessels; however, retinal hemorrhages occur in other settings without history of rapid acceleration-deceleration injury, such as in healthy newborns. Circumferential macular folds are seen almost exclusively in severe non-accidental trauma. We sought to document the pattern of retinal hemorrhages relative to macular folds to determine if the altered vitreoretinal interface may influence the formation of retinal hemorrhages.