Blunt or perforating trauma can injure intact vessels directly and is the leading cause of vitreous hemorrhage in people younger than The blood is not an extension of the subarachnoid hemorrhage.
Rather the sudden increase in intracranial pressure can cause retinal venules to rupture. Blood from an adjacent source. Pathology adjacent to the vitreous can also cause vitreous hemorrhage. Hemorrhage from retinal macroaneurysms, tumors and choroidal neovascularization can all extend through the internal limiting membrane into the vitreous.
Early or mild hemorrhage may be described as floaters, cobwebs, haze, shadows or a red hue. More significant hemorrhage limits visual acuity and visual fields or can cause scotomas. Patients often say vision is worse in the morning as blood has settled to the back of the eye, covering the macula. Patients should be questioned regarding a history of trauma, ocular surgery, diabetes, sickle cell anemia, leukemia, carotid artery disease and high myopia.
Complete examination consists of indirect ophthalmoscopy with scleral depression, gonioscopy to evaluate neovascularization of the angle, IOP and B-scan ultrasonography if complete view of the posterior pole is obscured by blood. Dilated examination of the contralateral eye can help provide clues to the etiology of the vitreous hemorrhage, such as proliferative diabetic retinopathy. The presence of vitreous hemorrhage is not hard to detect. In nondispersed hemorrhage, a view to the retina may be possible and the location and source of the vitreous hemorrhage may be determined.
Vitreous hemorrhage present in the subhyaloid space is also known as preretinal hemorrhage. Such a hemorrhage is often boat-shaped as it is trapped in the potential space between the posterior hyaloid and the internal limiting membrane, and settles out like a hyphema. Dispersed vitreous hemorrhage into the body of vitreous has no defined border and can range from a few small distinct red blood cells to total obscuration of the posterior pole.
The blood is typically cleared from within the vitreous hemorrhage at a rate of approximately 1 percent per day. Blood outside the formed vitreous resolves more quickly. Vitreous hemorrhage is cleared more quickly in syneretic and vitrectomized eyes, and more slowly in younger eyes with well-formed vitreous. The natural history of vitreous hemorrhage depends on the underlying etiology with the worst prognoses for diabetics and AMD patients.
With the exception of proliferative vitreoretinopathy, complications of vitreous hemorrhage typically occur if blood has been present for more than one year. Hemosiderosis bulbi is a serious complication thought to be caused by iron toxicity as hemoglobin is broken down. Since hemolysis occurs slowly, the iron-binding capacity of proteins in the vitreous usually outpaces the slow rate of hemolysis, thereby avoiding hemosiderosis bulbi. Proliferative vitreoretinopathy.
After vitreous hemorrhage, proliferative vitreoretinopathy can occur. It is thought that macrophages and chemotactic factors induce fibrovascular proliferation, which can lead to scarring and subsequent retinal detachment. Ghost cell glaucoma. Ghost cells are spherical, rigid, khaki-colored red blood cells filled with denatured hemoglobin present in long-standing vitreous hemorrhage.
If these cells gain access to the anterior chamber, their shape and rigidity can block the trabecular meshwork, resulting in ghost cell glaucoma. Hemolytic glaucoma. A short period of cautious observation for vitreous clearing may be reasonable. For example, occasionally a retinal tear associated with vitreous hemorrhage can be seen with a bright indirect ophthalmoscope, but adequate uptake of laser spots to the posterior margin of the break cannot be achieved.
Red laser may be tried in such cases as it has better penetration. Cryotherapy can be considered in these cases, but the dual risk of cryotherapy and vitreous hemorrhage [7] potentially leading to proliferative vitreoretinopathy should be considered compared to the risk of pars plana vitrectomy with endolaser.
If the retina cannot be adequately visualized in degrees and the etiology of the vitreous hemorrhage is unknown, prompt pars plana vitrectomy is indicated. Again, a short period of cautious observation for vitreous clearing may be reasonable. For example, in a case of a superior retinal tear with dense vitreous hemorrhage, adequate treatment of the superior retinal tear may be achieved.
However, undetected inferior retinal breaks may be present. Therefore, if the view is not clearing briskly, pars plana vitrectomy is indicated. Neovascularization of the iris or angle in the setting of new dense vitreous hemorrhage would prompt earlier surgical intervention. Diabetics frequently present with vitreous hemorrhage, and in general the same principles apply as outlined above. Of note, new vitreous hemorrhage in diabetics cannot always be assumed to be secondary to diabetic retinopathy if there is an inadequate view; diabetics are susceptible to retinal tears and detachments like the general population.
The severity of the fellow eye may give a clue as to the etiology of the vitreous hemorrhage, but asymmetric levels of retinopathy are relatively common. In any case, diabetic patients with proliferative diabetic retinopathy, new vitreous hemorrhage prohibiting adequate panretinal photocoagulation, and no history of panretinal photocoagulation benefit from pars plana vitrectomy with intra-operative panretinal photocoagulation or intravitreal anti-vascular endothelial growth factor anti-VEGF injection.
In this scenario, if the vitreous hemorrhage does not clear in about one month, many surgeons will perform pars plana vitrectomy. However, in the case of an established patient with known proliferative diabetic retinopathy and known panretinal photocoagulation, a new or recurrent vitreous hemorrhage is far more likely to be secondary to diabetes than a retinal tear. Longer periods of observation 3 to 6 months before considering pars plana vitrectomy may be reasonable in these situations.
As always, individual situations, patient wishes, and surgeon judgment are paramount. Patients are instructed to minimize strenuous activity, as an increase in blood pressure may disrupt the newly formed clot and cause new active bleeding. Patients are also instructed to keep their head of bed elevated to allow settling of the blood, improving their vision and permitting more complete fundoscopic examination.
Bilateral patching and bedrest may facilitate settling of blood. However, the patches must be removed immediately before examination or treatment, as normal eye movements quickly disperse the hemorrhage again.
For this reason and its inconvenience to patients, bilateral patching is infrequently attempted. Neovascularization from proliferative retinopathy, associated with diabetes or otherwise, is often treated with panretinal photocoagulation if the view is adequate.
This will cause regression of neovascularization and help reduce the risk of further hemorrhage. Intravitreal injection of anti-VEGF agents may be used to cause regression of neovascularization in proliferative retinopathies, particularly if there is no view to perform panretinal photocoagulation [8].
Bhavsar et al [9]. Additionally, there is anecdotal evidence that anti-VEGF injection may worsen tractional retinal detachment as neovascular membranes contract, so the the potential risks and benefits should be considered in this setting. Recently, the initial results from Protocol AB from the Diabetic Retinopathy Clinical Research Retina Network evaluated patients with vitreous hemorrhage from proliferative diabetic retinopathy initially treated with aflibercept vs.
At 24 weeks, there was no statistically difference in the primary outcome of mean visual acuity letter score between the vitrectomy and aflibercept cohorts, although the vitrectomy group showed a faster visual recovery. Many surgeons use pre-operative anti-VEGF agents 1 to 7 days before pars plana vitrectomy for vitreous hemorrhage in diabetics, as regression of neovascular membranes reduces intra- and post-operative bleeding and dissection of tissue may become easier.
Several small studies support this belief [8] [12] [13] [14] , although other small studies refute it [15] [16]. There is concern, however, that these patients frequently fail their pre-anesthesia testing and that their surgery may be cancelled after the anti-VEGF agent has been given, potentially exacerbating tractional retinal detachment. For this reason, many surgeons wait until the patient is medically cleared for surgery before giving the anti-VEGF agent. Intravitreal injection of an anti-VEGF agent is usually indicated when the cause of vitreous hemorrhage is neovascular age-related macular degeneration.
The Early Treatment of Diabetic Retinopathy Study [4] showed that aspirin did not increase risk of vitreous hemorrhage, and no anticoagulant has been definitively shown to increase risk of vitreous hemorrhage. One report showed that patients taking aspirin, clopidogrel, or warfarin who develop an acute PVD are more likely to develop a vitreous hemorrhage, although the difference was small [3].
Most clinicians do not recommend discontinuation of anticoagulation with the goal of resolving a vitreous hemorrhage, especially when the anticoagulation is medically indicated. Patients with systemic causes of vitreous hemorrhage are followed closely by an internist or endocrinologist in addition to close ophthalmology follow up. Pars plana vitrectomy is indicated for vitreous hemorrhage accompanied by retinal detachment or break seen on B-scan, nonclearing vitreous hemorrhage, many cases of intraocular foreign body, vitreous hemorrhage with iris neovascularization or associated with hemolytic or ghost-cell glaucoma.
Pars plana vitrectomy is also indicated in cases of dense vitreous hemorrhage of unknown etiology. In these cases, pars plana vitrectomy can be both diagnostic and therapeutic. Depending on the etiology of vitreous hemorrhage, endolaser may also be placed intraoperatively. Some surgeons will also perform a concurrent air-fluid exchange after the vitrectomy or may even inject intravitreal anti-VEGF at the conclusion of case, but there is no substantial evidence that this prevents post-operative recurrent vitreous hemorrhage, a frustrating occurrence seen in some patients, especially diabetic patients.
In cases of open globe injury with vitreous hemorrhage but without intraocular foreign body, most surgeons close the eyewall first and address the vitreous hemorrhage as a second stage procedure. The prognosis is variable according to the etiology, status of optic nerve, and macular involvement.
For example, patients with vitreous hemorrhage secondary to proliferative diabetic retinopathy or age-related macular degeneration will have a more guarded prognosis compared to those with vitreous hemorrhage resulting from posterior vitreous detachment. Bleeding from other parts of the eye Occasionally, blood from another source can cause a vitreous haemorrhage.
Vitreous haemorrhage sometimes goes away by itself, or it can be removed with vitrectomy surgery, which may also be required to treat the cause of the haemorrhage. When blood leaks into this gel, usually from blockage or damage to the blood vessels of the retina, is known as a vitreous haemorrhage. This usually results in blurred vision, as the leaked fluids block the light that passes into the eye.
If you experience any of the symptoms of a vitreous haemorrhage, you should contact Eye Institute straight away on 99 20 20 for an appointment with one of our eye specialists. Symptoms Vitreous haemorrhage normally occurs suddenly, and without any pain.
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