vitreous hemorrhage
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Vitreous Hemorrhage
Vitreous hemorrhage
Presence of extravasated blood within the space outlined by the internal limiting membrane of the retina posteriorly and laterally, the nonpigmented epithelium of the ciliary body antero-laterally and the lens zonules and the posterior lens capsule anteriorly
Pathogenesis
Retinal vascular disorders that cause retinal ischemia
Retinal vascular abnormality not associated with retinal ischemia
Rupture of a normal retinal vessel Breakthrough bleeding
Retinal vascular disorders that cause retinal ischemia
Proliferative diabetic retinopathy Ischemic retinal vein occlusion Eales' disease Familial exudative vitreoretinopathy
(FEVR)
Proliferative diabetic retinopathy
HARD EXUDATES
Central retinal vein occlusion
Optic disc swelling
Venous tortuosity
Macular edema
NFL hemorrhage
Eales’ disease
an idiopathic retinal periphlebitis that primarily affects the peripheral retina in young adults
characterized by avascular areas in the retina periphery, followed posteriorly by microaneurysms, dilatation of capillary channels, tortuosity of neighboring vessels, and spontaneous chorioretinal scars
Eales’ disease
Retinal vein occlusion
Macular edema
Periphlebitis
Familial exudative vitreoretinopathy an inherited disease characterized by
aberrant retinal development in non-premature infants
Hallmark features: peripheral retina non-perfusion retinal neovascularization subretinal exudation formation of an abnormal vitreoretinal interface retinal detachment
Familial exudative vitreoretinopathy
temporal macular dragging
Familial exudative vitreoretinopathy
Peripheral nonperfusion
Retinal vascular abnormality not associated with retinal ischemia
Rupture of retinal arteriole macroaneurysm associated with systemic hypertension
Hemorrhage from a retinal angioma
Rupture of retinal arteriole macroaneurysm
Rupture of a normal retinal vessel
Retinal tears Retinoschisis
Tersons' syndrome Valsalva retinopathy
Retinal tear
Horshoe retinal tear
Vitreous hemorrhage
Tersons’ syndrome
originally defined by the occurrence of vitreous hemorrhage in association with subarachnoid hemorrhage
now encompasses any intraocular hemorrhage associated with intracranial hemorrhage and elevated intracranial pressures development of subretinal, retinal, preretinal,
subhyaloidal (classic presenation), or vitreal blood
Tersons’ syndrome
Valsalva retinopathy
Immediately following a Valsalva maneuver, a sudden rise in intraocular venous pressure causes retinal capillaries to spontaneously rupture.
The prognosis for Valsalva retinopathy is generally good, with newer treatment modalities speeding recovery time.
Valsalva retinopathy
Breakthrough bleeding
Subretinal haemorrhage following choroidal neovascular membrane secondary to age-related macular degeneration
Choroidal malignant melanoma
Choroidal neovascular membrane
Choroidal malignant melanoma
Fate of vitreous hemorrhage Rapid clot formation Slow lysis of fibrin Extracellular lysis of RBCs Persistence of intact RBCs for months Lack of early polymorphonuclear
response
Fate of vitreous hemorrhage Spontaneous clearance of blood from the
vitreous is a slow and constant process, and is much more common in cases which have no tendency of recurrent bleeding, syneresis of the vitreous gel, and in elderly and pahakic patients.
Vitreous blood does not clear as spontaneously in patients with diabetic retinopathy.
Fate of vitreous hemorrhage Long-standing vitreous hemorrhage with the
accumulated red cells and red cell debris suspended in and mixed with vitreous collagen ochre membrane
Fate of vitreous hemorrhage Complications occurring due to non-
clearing vitreous haemorrhage retinal damage glial and fibrovascular proliferation glaucoma
Evaluation of a patient with vitreous hemorrhage Symptoms
sudden painless decrease in vision sudden appearance of floaters flashes of light visual haze cloudy vision photophobia perception of shadows and cobwebs
Evaluation of a patient with vitreous hemorrhage Past Medical History
diabetes mellitus systemic hypertension drug intake cerebral stroke
Ocular Examination
• Best-corrected visual acuity• Anterior segment evaluation
– iris and angle neovascularisation– keratic precipitates– cells
• RAPD• Tonometry• Fundus evaluation• B-scan
Khaki-colored cells
Management
Factors to consider:• patient's age• duration of disease• visual acuity• intraocular pressure• amount of haemorrhage• retinal status• presence or absence of neovascularisation of iris• adequacy of photocogaulation if done before the
onset of haemorrhage• lens status (phakic or aphakic/pseudophakic)• presence or absence of posterior vitreous detachment
(PVD)
Principles of Management
Observation Laser photocoagulation Vitrectomy
Observation
Unknown etiology, attached retina on B-scan Rest the head in an elevated position. Reevealuate after 3-7 days to ascertain the
possible source of hemorrhage.
Observation
Known cause and source of hemorrhage, attached retina Reevaluate after 3-4 weeks Post laser or post-virectomy recurrent
vitreous hemorrhage, vitreous hemorrhage in Tersons’ syndrome or after acute PVD and hemorrhage associated with bleeding diathesis
Observation
Attached macula Wait for 2-3 weeks for PVD to occur to
enhance technical ease and outcomes of surgery
Macula-off Immediate surgery
Laser photocoagulation
Should start as soon as possible as any part of retina is visible in proliferative vasculopathies
Vitrectomy
• Attached retina, good PVD, non-clearing vitreous hemorrhage over 2-3 months
• Advanced proliferative retinopathy with non-clearing vitreous hemorrhage in 6-8 weeks after adequate laser therapy
• Vitreous hemorrhage in RD especially when associated with giant retinal tears or open globe injury and vitreous hemorrhage due to AMD and IPCV
Vitrectomy
• In general, early vitrectomy is indicated in situations where the underlying pathology is likely to progress fast if left untreated.
• Surgery can be delayed in eyes with well lasered proliferative retinopathy and attached retina where the reurrent hemorrhage is due to traction on elevated vessels and not secondary to active proliferation.
Enzymatic Vitreolysis for Retinal Disorders Vitreous liquefaction
in which the drug causes central liquefaction of the vitreous gel, collapse of the vitreous body, and secondary separation of the posterior hyaloid from the neural retina
Targeted enzymatic posterior vitreous detachment enzyme selectively cleaves the anatomic
attachment between the posterior hyaloid and the inner surface of the retina
Enzymatic Vitreolysis for Retinal Disorders
Plasmin Microplasmin Chondroitinase Hyaluronidase
Dispase
Plasmin
an autologous serum protease that is a key component of the fibrinolysis cascade
a non-specific protease usually present in human serum, and it is responsible for degrading a variety of plasma proteins
specific physiologic role is to degrade fibrin clots
Microplasmin
truncated form of plasmin contains the active site of plasmin and
has a similar mechanism of action in vitreolysis
Microplasmin
Unlike TPA, microplasmin is a direct acting thrombolytic, as compared to most other thrombolytics which dissolve clots indirectly by activating the plasmin precursor, plasminogen.
May have neuroprotective features and have a reduced risk of bleeding compared to indirect-acting thrombolytics.
Microplasmin
Once microplasmin enters into the systemic circulation, it is rapidly inactivated by a blood protein (alpha-2 anti-plasmin) thus reducing the risk of bleeding in locations away from the intended treatment area.
Hyaluronidase
substrate-specific enzyme that induces synchisis by acting on proteoglycans in the vitreous
appears to alter the diffusion and movement of substances through the vitreous and, simultaneously, is important in the development of posterior vitreous detachment
Hyaluronidase
Intravitreal injection of 1 IU of intravitreal hyaluronidase is sufficient for partial vitreolysis andis non-toxic to the rabbit retina (Gottlieb et al., 1990).
Intravitreal injection of hyaluronidase in doses of 10 IU or higher induces posterior vitreous detachment in rabbits over a period of 5 weeks.
Intravitreal doses of 20 IU or less do not appear to affect the microscopic morphology or function of ocular structures adversely.
Hyaluronidase
Ovine hyaluronidase accelerated the clearing of vitreous hemorrhage.
No serious safety issues were reported
after a single intravitreal injection of ovine hyaluronidase.
Kuppermann et al., 2005a
Chondroitinase
Proteolytic enzyme with specificity for chondroitin sulfate proteogylcan
Despite the presence of chondroitin sulfate proteoglycan in human vitreous, there is conflicting evidence on the ability of chondroitinase to induce a posterior vitreous detachment.
Chondroitinase
Chondroitinase failed to induce a posterior vitreous detachment in the porcine eye, which is known to have a particularly thick and tenacious posterior hyaloid; plasmin was able to induce a posterior vitreous detachment in this animal model
Hermel and Schrage, 2006
Chondroitinase
Although chondroitinase was not sufficient to induce a posterior vitreous detachment acting on its own, simultaneous intravitreal injection of chondroitinase ABC and matrix metalloproteinase-3 has been used in an experimental study of 24 rabbit eyes to induce posterior vitreous detachment.
Meng and Zeng, 2004
Dispase
The only agent that has been used to specifically attack the surface between the posterior hyaloid and inner limiting membrane with the goal of cleaving this attachment.
Dispase
35.9 kD protease obtained from Bacillus polymyxa which cleaves the basal membrane in various tissues including skin, testis, and retinal pigment epithelium
acts on type IV collagen and fibronectin, whereas other components of the extracellular matrix such as laminin, type V and VII collagens are resistant to the enzyme
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