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Purpose: To characterize the classification, incidence, diagnosis and prognosis of traumatic choroidal injuries., Methods: Subjects were selected from the database of the Eye Injury Vitrectomy Study (EIVS) and were examined for occurrences of different categories of choroidal injuries. Standard photographs were collected. Anatomical and visual outcomes were assessed in patients with greater than 1 year of follow-up. Eyes that had no light perception (NLP) and/or phthisis bulbi were defined as having had unfavourable outcomes. The percentage of eyes with an unfavourable outcome was analysed for different types of choroidal injuries., Results: Nine categories of choroidal injuries with distinctive features were identified in the EIVS database. The incidence and the percentage of eyes with an unfavourable outcome in each injury category were as follows: suprachoroidal effusion, 21.2% (7.2%); suprachoroidal haemorrhage, 12.8% (11.2%); massive suprachoroidal haemorrhage, 4.0% (64.9%); choroidal avulsion, 4.2% (92.2%); traumatic chorioretinal rupture, 1.8% (13.3%); choroidal rupture, 4.8% (6.8%); choroidal loss, 1.6% (79.3%); choroidal hole, 1.1% (5.3%); and choroidal damage at the wound site, 39.2% (17.7%)., Conclusions: Ocular trauma can cause a variety of choroidal injuries that have distinctive features, some of which are associated with a high frequency of unfavourable prognoses., (© 2020 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.)

Background: As an increasing age-related eye disease, age-related macular degeneration (AMD) is becoming a common cause of irreversible visual loss in elder population. The mechanism of AMD remains uncertain and covers a complex risk factors. Choroidal vascularity index (CVI) is a sensitive parameter obtained by enhanced depth imaging of optical coherence tomography which allows the choroid in more detail and accurate assessment in the pathogenesis of AMD. The objective of this current study is to evaluate choroidal structural alternations measured by CVI in AMD., Methods: We will review 4 English databases (PubMed, Embase, Cochrane Library, and Web of Science) from their inception until present to select eligible articles. English-language and case-control studies will be accepted. The data extraction content and quantitative analysis will be performed systematically by 2 independent authors. The primary outcome is the alternation of CVI in AMD. The secondary outcomes consist of choroidal thickness (CT), luminal area (LA), stromal area (SA), and total choroidal area (TCA). Subgroup analysis, sensitivity analysis, and publication bias will be performed to check the robustness of the pooled outcome data., Results: Changes of quantitative parameters such as CVI will be obtained in patients with AMD., Conclusion: This study will elucidate alternations of choroidal vascular and stromal component in AMD and provide robust evidence on the pathophysiology of AMD., Registration Number: INPLASY.

Background: So far only single cases with short follow-up have been reported on the use of intravitreal anti-VEGF for traumatic choroidal neovascularizations (CNV). This paper reports a large case series of patients with CNV secondary to choroidal rupture after ocular trauma receiving intravitreal anti-VEGF (vascular endothelial growth factor) injections., Methods: Fifty-four patients with unilateral choroidal rupture after ocular trauma diagnosed between 2000 and 2016 were retrospectively evaluated. Eleven patients with CNV secondary to choroidal rupture were identified. Five eyes with traumatic secondary CNV were treated with anti-VEGF and were systematically analysed. The other 4 patients with inactive CNV underwent watchful observation., Results: Four men and one woman with a mean age of 29 years (SD 12.4; range 19-45) had intravitreal anti-VEGF therapy for traumatic CNV. Another 4 patients with a mean age of 37 years (SD 6.6; range 31-46) presented with inactive CNV and did not receive specific treatment. In all 9 cases the mean interval between the ocular trauma and the diagnosis of CNV was 5.7 months (SD 4.75; range 2-12). In the treatment group per eye 4.2 injections (SD 3.2; range 1-8) were given on average. Four eyes were treated with bevacizumab and one eye with ranibizumab. Regression of CNV was noted in all eyes. In 4 eyes visual acuity (VA) improved, one eye kept stable visual acuity., Conclusions: Here, we present the up to now largest case series of traumatic CNV membranes treated with anti-VEGF injections with a mean follow-up period of 5 years. Intravitreal anti-VEGF therapy seems to be safe and effective for secondary CNV after choroidal rupture. Compared to exudative age-related macular degeneration fewer injections are needed to control the disease., Trial Registration: Retrospective registration with local ethics committee on 21 March 2019. Trial registration number is 19-1368-104.

Purpose: The aim of this study was to investigate wound healing in the retinal pigment epithelium (RPE) after traumatic indirect choroidal rupture using fundus autofluorescence (FAF) and spectral-domain optical coherence tomography (SD-OCT)., Methods: A total of 14 eyes of 14 patients with traumatic indirect choroidal rupture were included. Baseline and last follow-up FAF images were compared to evaluate the extent of RPE healing after choroidal rupture, and associated morphologic characteristics were examined by SD-OCT., Results: The size of the RPE lesion was reduced in five eyes. The change occurred in the fovea in four eyes and in the macula in three eyes. The change was noted in both the fovea and the macula in two eyes; in these cases, the changes were more prominent in the fovea than in the macula. Extra-macular lesions and lesions with deep choroidal involvement did not show any reduction in size. Choroidal neovascularization (CNV) developed in seven eyes. There was no extra-macular CNV., Conclusion: Retinal pigment epithelium (RPE) wound healing after traumatic choroidal rupture is affected by location and extent of the lesion., (© 2016 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.)

Purpose: To investigate whether intravitreal ranibizumab injections administered to a child alter systemic plasma levels of total and free VEGF 165., Methods: A 9-year-old child sustained a choroidal rupture from blunt trauma. He subsequently developed a secondary choroidal neovascular membrane, which was treated with five ranibizumab injections over a period of 8 months. Peripheral venous blood samples were taken at each visit over a period of 12 months and plasma was extracted. Plasma VEGF 165 levels were determined using enzyme-linked immunosorbent assay and were assayed both pre- and post-immunodepletion to remove complexed VEGF., Results: Plasma VEGF 165 levels proved labile following intravitreal injection of ranibizumab. Levels increased by 30% above baseline following the first intravitreal ranibizumab injection, but then returned to baseline despite two subsequent injections. There was then a rebound increase of 67% in total plasma VEGF levels following a further injection, which remained above baseline for 12 weeks despite two further intravitreal ranibizumab injections. Baseline levels were re-attained 26 weeks after the final injection., Conclusions: These results suggest intravitreal ranibizumab injections can cause significant, multiphasic changes in systemic VEGF levels. This may be of particular clinical significance in children as VEGF is known to be vital in the development of major organs, in addition to its role in the maintenance of normal organ function in adults.

Purpose: To comprehend the mechanism of focal chorioretinal damage by analysis of the pressure distribution and dynamic pressure induced by infused air during fluid-air exchange., Methods: A precise simulation featuring a model eye and a fluid circuit was designed to analyze fluid-air exchange. The pressure distribution, flow velocity, and dynamic pressure induced by infusion of air into an air-filled eye were analyzed using an approach based on fluid dynamics. The size of the port and the infusion pressure were varied during simulated iterations. We simulated infusion of an air-filled eye with balanced salt solution (BSS) to better understand the mechanism of chorioretinal damage induced by infused air., Results: Infused air was projected straight toward a point on the retina contralateral to the infusion port (the "vulnerable point"). The highest pressure was evident at the vulnerable point, and the lowest pressure was recorded on most retinal areas. Simulations using greater infusion pressure and a port of larger size were associated with elevations in dynamic pressure and the pressure gradient. The pressure gradients were 2.8 and 5.1 mm Hg, respectively, when infusion pressures of 30 and 50 mm Hg were delivered through a 20-gauge port. The pressure gradient associated with BSS infusion was greater than that created by air, but lasted for only a moment., Conclusions: Our simulation explains the mechanism of focal chorioretinal damage in numerical terms. Infused air induces a prolonged increase in focal pressure on the vulnerable point, and this may be responsible for visual field defects arising after fluid-air exchange., (Copyright 2014 The Association for Research in Vision and Ophthalmology, Inc.)

After wounding, multiple cell types interact to form a fibrovascular scar; the formation and cellular origins of these scars are incompletely understood. We used a laser-injury wound model of choroidal neovascularization in the eye to determine the spatiotemporal cellular events that lead to formation of a fibrovascular scar. After laser injury, F4/80(+) myeloid cells infiltrate the wound site and induce smooth muscle actin (SMA) expression in adjacent retinal pigment epithelial cells, with subsequent formation of a SMA(+)NG2(+) myofibroblastic scaffold, into which endothelial cells then infiltrate to form a fibrovascular lesion. Cells of the fibrovascular scaffold express the proangiogenic factor IL-1β strongly, whereas retinal pigment epithelial cells are the main source of VEGF-A. Subsequent choroidal neovascularization is limited to the area demarcated by this myofibroblastic scaffold and occurs independently of epithelial- or myeloid-derived VEGF-A. The SMA(+)NG2(+) myofibroblastic cells, F4/80(+) macrophages, and adjacent epithelial cells actively proliferate in the early phase of the wound healing response. Cell-lineage tracing experiments suggest that the SMA(+)NG2(+) myofibroblastic scaffold originates from choroidal pericyte-like cells. Targeted ablation of macrophages inhibits the formation of this fibrovascular scaffold, and expression analysis reveals that these macrophages are Arg1(+)YM1(+)F4/80(+) alternatively activated M2-like macrophages, which do not require IL-4/STAT6 or IL-10 signaling for their activation. Thus, macrophages are essential for the early wound healing response and the formation of a fibrovascular scar., (Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Blunt ocular trauma from a child's plastic foam-covered toy baseball bat caused traumatic optic neuropathy and choroidal rupture in a 9-year-old child. The examination revealed a visual acuity of 6/60, a relative afferent pupillary defect, optic nerve swelling, commotio retinae and retinal haemorrhages. There was no orbital fracture or intraorbital haematoma on CT scanning. Optical coherence tomography showed macular oedema and disruption of the retinal pigment epithelium and Bruch's membrane. The child was admitted for intravenous methylprednisolone and discharged on topical steroid treatment. At 1 month follow-up, visual acuity had improved to 6/12. Optic nerve swelling had resolved and the fundus had two crescent-shaped choroidal rupture scars. Choroidal rupture and optic neuropathy can be secondary to indirect trauma, and even when the mechanism of injury is with a piece of equipment designated as suitable for children, serious ocular injury can occur.

The role of apoptosis in the formation and regression of neovascularization is largely hypothesized, although the detailed mechanism remains unclear. Inflammatory cells and endothelial cells both participate and interact during neovascularization. During the early stage, these cells may migrate into an angiogenic site and form a pro-angiogenic microenvironment. Some angiogenic vessels appear to regress, whereas some vessels mature and remain. The control mechanisms of these processes, however, remain unknown. Previously, we reported that the prevention of mitochondrial apoptosis contributed to cellular survival via the prevention of the release of proapoptotic factors, such as apoptosis-inducing factor (AIF) and cytochrome c. In this study, we investigated the regulatory role of cellular apoptosis in angiogenesis using two models of ocular neovascularization: laser injury choroidal neovascularization and VEGF-induced corneal neovascularization in AIF-deficient mice. Averting apoptosis in AIF-deficient mice decreased apoptosis of leukocytes and endothelial cells compared to wild-type mice and resulted in the persistence of these cells at angiogenic sites in vitro and in vivo. Consequently, AIF deficiency expanded neovascularization and diminished vessel regression in these two models. We also observed that peritoneal macrophages from AIF-deficient mice showed anti-apoptotic survival compared to wild-type mice under conditions of starvation. Our data suggest that AIF-related apoptosis plays an important role in neovascularization and that mitochondria-regulated apoptosis could offer a new target for the treatment of pathological angiogenesis., (Copyright © 2012 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

AMD is the most common disease leading to acquired blindness in developed countries. CNV is the foremost cause of AMD and is thought to be induced by regional inflammation as a result of age-related conformational changes of the chorioretinal interface. Here, we show that IL-27, a member of the IL-6/IL-12 cytokine family, has an angiostatic effect and regulates the development of laser-induced experimental CNV in mice. In this model, IL-27 expression increased in the damaged choroid and peaked at the 24 h-time-point. IL-27 neutralization, induced by inoculating an antagonistic antibody into the vitreous cavity, enhanced VEGF production and the extent of CNV. By contrast, the administration of rIL-27 reduced VEGF production and the extent of CNV. Mice deficient in the EBI3, which lack IL-27, also showed more CNV than C57BL/6 mice, and this was reduced by IL-27 supplementation. We additionally investigated the effect of IL-27 on the function of macrophages, which play a critical role in CNV. IL-27 did not affect macrophage migration but inhibited its VEGF production. IL-27 therefore appears to regulate CNV and is a promising candidate target for treating sight-threatening diseases caused by ocular neovascularization.

Purpose: To report fundus autofluorescence and optical coherence tomography (OCT) findings in patients with blunt ocular trauma., Methods: Six eyes of six consecutive patients with blunt ocular trauma were evaluated in an observational case series using colour fundus photography, the Heidelberg Retina Angiograph 2 (HRA2) system for fundus autofluorescence (FAF) and OCT (Stratus OCT)., Results: Three patients presented with secondary retinal pigment epitheliopathy that was identified as a reduced FAF plaque with interposed increased FAF granular smaller lesions. These findings were not as evident in fundus examination and colour photography in two patients. Visual field in one patient showed a decreased area of sensitivity that correlated to the reduced/increased autofluorescent lesion. The other three patients had subretinal haemorrhage and choroidal rupture, which appeared with a reduced FAF with an increased FAF rim after resolution. OCT demonstrated a choriocapillaris/ retinal pigment epithelium (RPE) complex disruption and its resolution over time in all patients with choroidal rupture., Conclusion: Damaged RPE area was more evident and better delineated by FAF imaging compared with fundus examination and fundus photography alone. Autofluorescence imaging might be a useful exam to show the length and severity of post-traumatic retinal lesions and it may add relevant information in the global evaluation of blunt ocular trauma complications. Moreover, OCT added valuable information to the diagnosis and progression of choroidal rupture. Further studies to determine the predictive value of FAF in ocular blunt trauma are warranted., (© 2009 The Authors. Journal compilation © 2009 Acta Ophthalmol.)

Purpose: To study the in vivo response of mononuclear phagocytes (i.e., dendritic cells [DCs] and macrophages [MPhis]) in the posterior eye segment after laser-induced injury, and to gain a better understanding of the role of these cells in inflammatory eye disease., Methods: CX(3)CR1(GFP/+) knockin mice were used, in which DCs, MPhis, and microglia cells (microGCs) are constitutively fluorescent. These reporter mice were examined by a confocal scanning laser ophthalmoscope (cSLO) after argon laser coagulation. cSLO was complemented by fluorescence microscopy of retinal flatmounts and eye cryosections, to study cell morphology and location, and by multicolor flow cytometry, to determine the number and identity of the fluorescent cells., Results: The retina of healthy reporter mice featured abundant fluorescent microGCs. After laser injury to the fundus, these cells accumulated and migrated laterally toward injury after 60 minutes. Distinctly shaped fluorescent cells accumulated within laser spots and were identified by flow cytometry and immunofluorescence microscopy as DCs and MPhis in the retina and choroid. The DCs rapidly disappeared from the retina, whereas the MPhis stayed longer. Choroidal infiltrates were detectable even 35 days after laser injury, in particular in larger spots resulting from higher laser intensity. In addition, nonfluorescent granulocytes were detected in the choroid., Conclusions: The synergistic use of ophthalmoscopy, flow cytometry, and immunofluorescence microscopy allows detailed dissection of the in vivo response of mononuclear phagocytes to laser injury of the fundus. The number of microGCs increased in the retina. DCs and MPhis were present in the retina and choroid infiltrate. MPhis and granulocytes persisted in the choroid infiltrate longer than previously thought.

We report a case of a choroidal neovascular membrane (CNVM) following ocular penetration during peribulbar anesthesia in a 55-year-old male patient. A combination of photodynamic therapy with intravitreal bevacizumab led to resolution of the persistent CNVM.

We report two cases of significantly large choroidal holes following penetrating trauma that led to suprachoroidal migration of internal tamponading agents during repair of retinal detachments with proliferative vitreoretinopathy secondary to penetrating trauma. In the first case, choroidal hole was a direct result of the injury and was identified immediately after vitreoretinal surgery which was done for traumatic retinal detachment with hemorrhagic choroidal detachment. In the second case, the hole occurred over a period of several months after the repair of traumatic retinal detachment with silicone oil tamponade. This was attributed to progressive fibrosis exerting traction on the bare choroid/retinal pigment epithelium. Choroidal hole significant enough to cause suprachoroidal migration of internal tamponading agents is a very rare complication seen in eyes with posttraumatic retinal detachment with proliferative vitreoretinopathy.

The authors present a patient with posttraumatic choroidal neovascular membrane (CNVM) treated with PDT resulting in regression of the CNVM.

Air-bags have received widespread support as an effective means of enhancing automotive safety, and they are becoming more common as standard automobile equipment on many cars. Although air-bag induced ocular injuries are rare, they present a serious concern because of the possibility of permanent damage or visual impairment. To date, most reports have investigated ocular injury from high velocity motor vehicle accidents and reports of ocular injury from low speed motor vehicle accidents have been rare. We describe a patient who sustained severe ocular injury, including periorbital fracture, hyphema, vitreous hemorrhage, and choroidal rupture of the macular area, due to an inflated air-bag in a low speed motor vehicle accident.

Purpose: This investigation retrospectively examined ocular injuries associated with air bag deployment to gain a better appreciation of potential risk factors in motor vehicle accidents. National statistics regarding the efficacy of air bags were reviewed., Methods: Review of the literature from 1991 to 1998 identified 44 articles describing 97 patients with air-bag-induced ocular injuries. Variables extracted from each case were age, sex, height, position in the car, eye wear, vehicle impact speed, visual acuity, and specific ocular injuries., Results: Corneal abrasions occurred in 49% of occupants, hyphemas in 43%, vitreous or retinal hemorrhages in 25%, and retinal tears or detachments in 15%. The globe was ruptured in 10 patients. Patients involved in higher-speed accidents (over 30 mph) sustained a greater percentage of vitreous or retinal hemorrhages and traumatic cataracts, while those at slower speeds were more prone to retinal tears or detachments. In a subset of 14 patients with serious ocular injuries, the impact speed of 11 patients was recorded at 30 mph or less. Slower speed may be a risk factor for some ocular injuries. Occupant height was not a significant factor. National statistics confirm that air bags reduce fatalities in motor vehicle accidents. However, children sitting in the front seat without a seat belt and infants in passenger-side rear-facing car seats are at risk for fatal injury., Conclusion: Air bags combined with seat belts are an effective means of reducing injury and death in adults during motor vehicle accidents. However, this study has documented a wide variety of ocular injuries associated with air bag deployment. It is hoped that researchers can develop modifications that continue to save lives while minimizing additional harm.

Purpose: To investigate the indocyanine green (ICG) angiographic findings of healed traumatic choroidal ruptures., Methods: Three eyes of two patients with choroidal ruptures underwent both fluorescein angiography and ICG angiography with a digital high-resolution system., Results: Fundus examination showed healed choroidal ruptures in all three eyes. Two of the eyes had old macular scars and one eye had a recent choroidal neovascular membrane with serous detachment of the macula. On fluorescein angiography, the choroidal ruptures showed hypofluorescence at very early stages followed by late hyperfluorescence. On ICG angiography, the choroidal ruptures were hypofluorescent in early, mid and late phases. ICG angiography provided a clear delineation of the choroidal ruptures. In all eyes, the lesion was better defined on the ICG angiogram than on the fluorescein angiogram., Conclusions: ICG angiography can be helpful in the clinical evaluation of choroidal ruptures and can be used together with fluorescein angiography for the diagnosis and follow-up of choroidal ruptures.

A case of uniocular visual loss secondary to trauma sustained during a competitive karate bout is reported.

Indirect choroidal ruptures result from blunt ocular trauma and have a pathognomonic fundal appearance. We analysed a group of 30 patients with indirect choroidal ruptures with specific reference to the circumstances of the injury, the pattern of ocular damage, the cause of any visual loss, and the final visual outcome. Using this analysis we deduce a pathogenetic explanation for the characteristic fundus signs in patients with indirect choroidal ruptures. The majority of cases were young males injured during sport or by an assault, a minority were injured at work. Diffuse nonfocal impact injuries due to punches were associated with ruptures concentric with and adjacent to the optic disc. Focal impact injuries, due to projectiles, showed more extensive ocular damage. Seventeen of 30 patients regained 6/12 vision after injury. Injuries due to projectiles and temporally situated ruptures were associated with a poorer visual outcome than others. Macular damage was the commonest cause of visual loss, principally due to pigmentary maculopathy, traumatic inner retinal damage, and choroidal neovascular membranes rather than direct focal damage by the rupture.

Chorioretinal neovascular membranes are a recognised but rare cause of late visual loss in eyes suffering contusional injuries. A series of eight cases is presented all with indirect choroidal ruptures involving the perifoveal region. Two main patterns of 'at risk' rupture were noted: a temporally situated rupture passing almost directly through the fovea, and a rupture which curves inferior or superior to the optic disc stopping just short of the fovea. In six of eight cases there was only a partial thickness rupture of the choroid. These neovascular membranes may present at any time after the original injury, either early (within six months of the injury), which could be related to persistence of the normal reparative neovascular response, or late (at least one year after the injury), which are more likely to have resulted from a secondary breakdown of the outer blood-retina barrier.

The retinas of six pigmented rabbits (12 eyes) were irradiated with a cw-Nd:YAG laser using two different pulse forms, in conjunction with a constant pulse duration of 200 msec and a retinal focus diameter of 200 microns. The first pulse form (a) was characterized by an initial transient, lasting 15-20 msec, with a peak power twice that of the ensuing plateau phase of 180-185 msec. The second pulse form (b) was almost rectangular in shape. Although the average energies (and powers) for each pulse form were identical, almost 20% of this entity was delivered within the first 20 msec for the first pulse form. Impact lesions were examined at the biomicroscopic, light, and electron microscopic levels, and the characteristic morphologic features described for the cw-mode in general. Comparison of the effects produced using each pulse form revealed a number of differences. At low pulse energies (less than 150 mJ) the rectangular pulse form produced a photocoagulation reaction within the outer sensory retina, but when using the pulse form with the initial transient, this effect was superimposed by a degree of mechanical disruption. Ruptures produced within the elastic component of Bruch's membrane first appeared at lower pulse energies (ie, at 75 mJ, as opposed to 150 mJ for the rectangular pulse form) and were more frequent, and choroidal macrohemorrhaging (observed at pulse energies greater than or equal to 200 mJ) occurred only, when this latter pulse form was employed. Each of these phenomena may be attributed to the higher power and energy densities attained during the initial transient, which has disruptive properties. In order to avoid the risk of severe bleeding, these irradiation parameters should be maintained below approximately 6.4 X 10(3) W/cm2 and approximately 0.13 X 10(3) J/cm2.

After chorioretinal biopsy in dogs, obtained without vitreous loss, accessory glial cells and fibroblasts filled the defect between cortical vitreous and bare sclera. The proliferating glial cells laid down a new basement membrane which was complete both on the internal and external aspects of the defect. After biopsy complicated by vitreous loss, however, cellular proliferation failed to re-establish complete internal and external limiting membranes, and new formed fibroblastic tissue extended into the vitreous. To our knowledge, this is the first report to describe effective regeneration of the internal limiting membrane of the retina in any species. These findings suggest that when vitreous loss can be avoided, healed chorioretinal biopsies are unlikely to lead to delayed pathological complications.

A series of comparative exposures to both argon and krypton lasers have been made at 3 locations in a human retina--the fovea, the macula, and intraretinal vessels. In the fovea argon irradiations resulted in damage to both the inner and outer retinal layers as a result of absorption within the pigment epithelium and the macular pigment, while krypton exposures damaged the outer retina and the choroid. In the macula both systems resulted in damage to the outer retina, and again sufficient krypton radiation passed into the choroid to induce blood vessel occlusion, haemorrhage, and oedema. When intraretinal vessels were irradiated, only with argon was sufficient energy absorbed within the vessels to damage them or their surroundings in the inner retina. The implications of these findings are discussed in relation to the therapeutic uses of lasers.

Retinal fluorescein angiographic and visual field studies were performed on 10 patients who had developed indireect choroidal tears, these procedures being repeated at intervals until the retinal disturbances stabilised. Fluorographic investigations revealed that a transient breakdown of the choroidoretinal barrier to fluorescein dye could be detected in cases investigated within 4 days of injury, and also that the late complication of neovascularisation, producing a serous maculopathy, may resolve and good central vision be retained without recourse to photocoagulation therapy. Patients who had visual field examinations performed within a few days of trauma were noted to have dense central scotomata, but some recovery occurred in most cases, although to a variable degree. Field defects away from fixation corresponded to an extent with areas of post-traumatic pigmentary retinopathy, but in some portions of retina with normal background appearances sensitivity was also noted to be reduced. Scotomata corresponding specifically to choroidal tears or nerve fibre bundle defects were not recorded. Improvement of visual acuity may be expected, except in cases where a choroidal tear has involved the fovea or progressive choroidal neovascularisation led to permanent macular damage.

Acute laser injury to the tapetum of the feline retina produces thrombosis of the choriocapillaris. Early changes are characterized by the appearance of platelet-fibrin thrombi within capillary loops and disruption of endothelial integrity. By 4 days, thrombi have disappeared, and the endothelium shows regenerative changes. No endothelial cell mitotic activity is seen. The endothelial cytoplasm becomes plump, and there is a loss of the fenestrations adjacent to Bruch's membrane. By 10-20 days, the capillary structure shows gradual restoration. At 30 days, endothelial cell fenestrae are clearly evident adjacent to Bruch's membrane. The reparative process in this model appears to evolve as a result of thrombolysis and endothelial cell activation.