Vitreous Hemorrhage

Vitreous hemorrhage is the most common cause of progressive visual disturbance in patients with cavernous hemangioma.

From: Retina (Fifth Edition), 2013

Related terms:

Learn more about Vitreous Hemorrhage

Download as PDFSet alert

Darin R. Goldman, in Atlas of Retinal OCT: Optical Coherence Tomography, 2018


Spontaneous vitreous hemorrhage is a common disorder of the vitreous cavity, occurring in approximately 7 per 100,000 people (Spraul & Grossniklaus 1997). The appearance of vitreous hemorrhage develops secondary to bleeding from normal or neovascular blood vessels within the retina/vitreous and also may occur as a result of extension from layers underneath the retina. The most common causes for nontraumatic, spontaneous vitreous hemorrhage include diabetic retinopathy, retinal tear/detachment, vitreoretinal traction resulting from posterior vitreous detachment, retinal venous occlusive disease, ruptured retinal macroaneurysm, and exudative age-related macular degeneration. Spontaneous vitreous hemorrhage is a common cause for visual impairment and often will resolve without treatment in mild cases. More severe cases may require surgical vitrectomy. In the setting of severe vitreous hemorrhage and no visualization of the fundus, B-scan ultrasound is the imaging modality of choice. However, when vitreous hemorrhage is present with sufficient visualization of the fundus, OCT can be helpful to identify underlying macular abnormalities. Additionally, in cases of very subtle vitreous hemorrhage, OCT can be useful to confirm its presence.

Adrienne W. Scott, ... Morton F. Goldberg, in Retina (Fifth Edition),2013

Stage IV

Vitreous hemorrhage represents Goldberg stage IV. Sea fans grow or are pulled into the vitreous chamber, and vitreous traction on the delicate neovascular fronds may cause bleeding into the vitreous. Vitreous hemorrhage may be localized over the sea fan, and an individual may remain asymptomatic. However, dramatic, sudden vision loss may occur as the hemorrhage disseminates into the vitreous gel. Vitreous hemorrhage occurs more commonly in the Hb SC than the Hb SS genotype (23% versus 3%).70,88,92 The risk of recurrent vitreous hemorrhage also increases if an eye has more than 60° of circumferential retinal neovascularization, or if a patient initially presents with vitreous hemorrhage.107 Chronic vitreous hemorrhage may give rise to fibroglial membranes and vitreous strands, which may produce traction and resultant retinal detachment.48,57

Simon Brunner, Susanne Binder, in Retina (Fifth Edition), 2013

Vitreous hemorrhage

Postoperative vitreous hemorrhage after vitrectomy is common. A single postoperative vitreous hemorrhage occurs in about 65% of patients, whereas 35% will suffer two or more recurrences of vitreous hemorrhage.61,171,205,216 However, the vast majority of immediate postoperative vitreous hemorrhages are mild and do not impair fundus visualization; 80% of them will occur in the first postoperative year.216 Vitreous hemorrhages may also occur in association with iris or angle neovascularizations, retinal fibrovascular proliferations, or an anterior hyaloidal fibrovascular proliferation (AHFVP).12 A careful control of intraoperative hemorrhages may prevent or reduce postoperative vitreous hemorrhage (see above). The management of postoperative vitreous hemorrhage includes observation, vitreous cavity lavage or repeated vitrectomy. A slight hemorrhage might occur in eyes where silicone oil has not been used. If it clears within 1–3 weeks, no further treatment is necessary. If the hemorrhage is massive, a washout procedure might be indicated after 3 weeks in eyes where the retina is attached. Serial ultrasound tests are mandatory in eyes without fundus visualization. If the retinal situation is unclear, repeated vitrectomy is necessary. Only 4–10% of cases will finally require another vitrectomy, which includes removal of blood and probably residual fibrovascular tissue, additional photocoagulation treatment, and most likely silicone oil tamponade.25,30,163,217,218

Eoin O'Sullivan, Elizabeth Graham, in Neurology and Clinical Neuroscience, 2007

Terson's Syndrome

Vitreous hemorrhage occurring in association with subarachnoid hemorrhage is known as Terson's syndrome.262 However, intraocular hemorrhages of any type (retinal, subhyaloid, or vitreous) have been documented in 10% to 40% of individuals with subarachnoid hemorrhage,263 and reports have not always made a distinction between such types of hemorrhage (Fig. 24-25).264 Furthermore, preretinal hemorrhage may precede vitreous hemorrhage.263,265Terson's syndrome is present in between 3% and 13% of patients with a subarachnoid hemorrhage266 and carries an increased mortality rate in relation to patients who have had a subarachnoid hemorrhage but not vitreous hemorrhage.266 It has also been suggested that mild retinal hemorrhages are associated with a better prognosis than are large preretinal hemorrhages or vitreous hemorrhages.267 An urgent vitrectomy may be required for visual rehabilitation in patients with bilateral vitreous hemorrhage.

Franco M. Recchia, Paul SternbergJr, in Retina (Fifth Edition), 2013

Vitreous hemorrhage

Vitreous hemorrhage may result from damage to blood vessels in the ciliary body, retina, or choroid. Vitreous hemorrhage from blunt trauma may be associated with a retinal tear, and indirect ophthalmoscopy with scleral depression should be performed with great care in attempting to identify retinal abnormalities. Vitreous hemorrhage often is limited immediately after injury, with the initial fundus examination allowing best visualization of retinal detail. Subsequent diffusion of the hemorrhage or further bleeding may compromise later examinations. If the physician suspects an occult scleral rupture, scleral depression should be deferred.

If vitreous hemorrhage obscures examination of the retina, ultrasonography plays a critical role in decision-making. With combined contact A-scan and B-scan techniques, many details of the posterior segment can be determined, including presence of retinal detachment, posterior vitreous detachment, occult scleral rupture, hemorrhagic or serous choroidal detachment, and giant retinal tear (Fig. 110.5). For example, if ultrasound demonstrates vitreous strands emanating from an equatorial location, an occult scleral rupture with vitreous incarcerated in the wound can be inferred, requiring conjunctival peritomy and exploration.

Fig. 110.5. In the presence of vitreous hemorrhage, contact B-scan ultrasonography can demonstrate a retinal detachment and can sometimes also identify the causative retinal tear.

In general, patients with a nonpenetrating ocular injury and a vitreous hemorrhage without associated retinal tear or detachment should be observed. In cases of minimal diffuse hemorrhage, indirect ophthalmoscopy may be sufficient to establish retinal attachment. However, if the blood does not settle, the patient should be followed every few weeks with ultrasonography repeated to confirm retinal attachment. If retinal detachment is seen or suspected on ultrasonography, pars plana vitrectomy should be performed.

If pars plana vitrectomy is performed for a nonclearing vitreous hemorrhage caused by nonpenetrating trauma, we recommend a standard three-port technique. After the infusion cannula is sutured in place and confirmed to be in the vitreous cavity, a core vitrectomy should be performed to remove hemorrhagic vitreous. In most cases a PVD will have developed in the interim between injury and surgery. After one cuts through the detached posterior hyaloid face with the vitrectomy instrument, subhyaloid blood can be aspirated from the preretinal space. A blunt cannula connected either to the vitrectomy system for powered extrusion or to a fluted handle for passive extrusion will allow controlled removal of the blood. Residual vitreous, including posterior hyaloid, is then excised with the vitrectomy instrument. The retinal periphery should be examined carefully to identify retinal tears or dialyses that could have led to the original vitreous hemorrhage.

If a PVD is not present, the surgeon should attempt to create one, by using gentle suction from the vitrectomy instrument. If this is not successful, the posterior hyaloid can be engaged with a powered soft-tipped extrusion cannula. The vitreous detachment can be extended using an illuminated vitreoretinal pick while the hyaloid is elevated with either the extrusion cannula or vitrectomy instrument. Other techniques include using a vitreoretinal pick or carefully incising the posterior hyaloid with a myringotomy blade over the periphery of the optic nerve. If the posterior hyaloid remains adherent in certain locations, it should be freed from surrounding vitreous so that all localized vitreoretinal traction is relieved. Residual posterior cortical vitreous can be easily visualized by instilling triamcinolone (either full-strength or diluted 20% in balanced salt solution) following core vitrectomy. If traction persists, it may be necessary to place a local scleral buckle. Areas of persistent vitreoretinal traction should be scrutinized carefully because they may represent sites of occult scleral rupture where the vitreous became incarcerated in the laceration.

Smaller-gauge vitrectomy instrumentation can be used successfully for cases of traumatic vitreous hemorrhage, especially those without associated retinal detachment, proliferative vitreoretinopathy, and with some visualization of the retinal periphery. The surgeon should remember several aspects of transconjunctival small-gauge surgery that are especially relevant to traumatized eyes. First, since the infusion cannula is not sutured in place, it may slip backwards into the suprachoroidal space, even after being well-visualized at initial placement. This risk is higher in eyes with choroidal hemorrhage, choroidal congestion, or dense accumulation of blood or fibrin at the anterior vitreous base. This risk can be minimized by preoperative ultrasonographic confirmation of an absence of choroidal detachment, by choosing a quadrant of the eye with a relatively clearer periphery, and by selecting the longest infusion cannula available. Second, smaller-gauge vitreous cutters (especially earlier-generation 25G cutters) may become clogged with dense hemorrhage or vitreous debris. Third, additional instrumentation (such as intraocular forceps, scissors, lighted instruments, or equipment for oil infusion) may be required for treatment of associated vitreoretinal pathology. The surgeon must have as much information regarding the ocular anatomy as possible and have readily available the surgical instruments that may be required.

The visual prognosis for eyes with vitreous hemorrhage associated with nonpenetrating trauma depends on associated macular damage (from choroidal rupture, traumatic macular hole, Berlin's edema, or macular contusion), retinal dysfunction from associated retinal detachment, and occlusional amblyopia in young children. In a study of 33 eyes with severe vitreous hemorrhage associated with closed-globe injury, best-corrected visual acuity following resolution and/or treatment of hemorrhage was <20/200 in 54%. The most common cause of poor visual outcome was macular scar. Poor prognostic factors included presenting visual acuity of light perception or worse, hyphema, traumatic cataract, and age 55 years or younger.33

Chris Steele BSc (Hons) FCOptom DCLP DipOC FBCLA, ... Colin Waine OBE MBBS FRCGP FRCPath, in Diabetes and the Eye, 2008

Potential consequences of untreated PDR

Vitreous haemorrhage occurs as a result of vitreous traction on any pre-retinal neovascular proliferation. This may result in obscuration of the fundus view in severe cases. Where the fundus cannot be visualized a B scan ultrasound can be performed to exclude any other significant pathology such as retinal detachment.

Fibrovascular tissue may shrink causing contraction and distortion of the normal retinal tissue. Combined with the process of vitreous detachment, this may progress to a tractional retinal detachment and normally affects the temporal arcades first. Temporal tractional detachments may remain more localized and do not significantly affect vision.

Tractional retinal detachments may also develop retinal tears and breaks which often result in a rapidly progressing combined tractional-rhegmatogenous retinal detachment.

Tractional retinal detachments are typically concave compared with rhegmatogenous retinal detachments that are usually convex. Also, tractional retinal detachments tend not to extend beyond the orra serrata.

Vision is significantly affected if there is foveal involvement following detachment. The vision may also be affected in other situations such as when fibrovascular tissue grows over the foveal area but with the fovea still attached. In other situations, extra-foveal fibrovascular tissue may cause tangential tractional forces giving rise to displacement of the fovea horizontally.

Rubeosis iridis is a complication of PDR in response to significant ischaemia. New vessels grow over the surface of the iris. It is therefore important to check the iris-pupil margin carefully for any signs of rubeosis in diabetics. If the new vessels obstruct the anterior chamber angles, this may lead to neovascular glaucoma.

Baha'a N Noureddin, ... John F Salmon, in Glaucoma (Second Edition), 2015

Hemolytic Glaucoma.

Traumatic vitreous hemorrhage is a prerequisite for causing this rare type of secondary open-angle glaucoma, and the similar pathophysiology to phacolytic glaucoma is responsible for the name.

Reddish-brown blood cells are seen in the anterior chamber, as well as on the trabecular meshwork, especially inferiorly. The increase in IOP is caused by the obstruction of the trabecular meshwork by red blood cell debris, free hemoglobin, and hemoglobin-laden macrophages.39

The clinical picture is similar to that of ghost-cell glaucoma. However, anterior chamber aspirates show macrophages containing golden-brown pigment, but no ghost cells.1 Other histologic studies show degenerative changes in the trabecular endothelial cells, which also have phagocytized blood.1

The IOP increase is transient, occurring days to weeks following the trauma, and usually responds well to medical treatment with topical β-blockers, α2 agonists, and carbonic anhydrase inhibitors. Only rarely does anterior chamber washout or vitrectomy become indicated.1

Rudolf F. Guthoff, ... Oliver Stachs, in Retina (Fifth Edition), 2013

Vitreous hemorrhages

An acute vitreous hemorrhage is an important indication for ultrasonography. Acute hemorrhages can fill the vitreous cavity with small opacities from the particles of the red blood cells. These opacities usually accumulate after a few hours in the lower circumference of the vitreous base (Fig. 9.17).

Fig. 9.17. (A) Conspicuous bleeding into syneretic vitreous; erythrocytes within the vitreous create reflective opacities. A static picture may give the impression of a solid lesion. (B) After a few hours the opacities usually accumulate in the lower aspect of the vitreous cavity. (C) Schematic drawing.

If a detachment of the posterior hyaloid membrane precedes a vitreous hemorrhage, the erythrocytes frequently precipitate on to a vitreous strand (Fig. 9.18). This strand may be responsible for the development of a retinal tear, and its traction can be demonstrated directly in acoustic sectioning (Fig. 9.19). A circumscribed thickening of the ocular wall in cross-section may indicate the presence of a retinal operculum (Fig. 9.20). This area should be localized echographically and then carefully scrutinized with ophthalmoscopy if possible.

Fig. 9.18. Fresh vitreous hemorrhage. In a cross-sectional echogram the vitreous framework converges towards the ocular wall. Blood precipitates increase the acoustic reflectivity of the vitreous. Traction has to be assumed where the vitreous is in contact with the ocular wall.
Fig. 9.19. (A) Recent vitreous hemorrhage. The low reflecting membranes float freely with ocular movement. A newly formed horseshoe tear may be present at their connection point to the wall. (B) Schematic drawing.
Fig. 9.20. (A,B) Recent vitreous hemorrhage. Erythrocytes have precipitated on to the partly detached posterior hyaloid membrane, increasing its acoustic reflectivity. (C) Schematic drawing.

In larger hemorrhages, the blood can also disseminate into multiple pre-existing vitreous compartments. In the early phase of this process, the erythrocytes will collect in the retrovitreal space (Fig. 9.21). The retrovitreal space may completely clear after a few days or weeks due to its high fluid exchange rate; however, blood on the vitreous framework absorbs much more slowly (Fig. 9.22).

Fig. 9.21. (A) Vitreous hemorrhage with posterior vitreous detachment emphasizing the retrovitreal space. (B) In the early stage after the hemorrhage, erythrocytes accumulate in the retrovitreal space. They may ensheath the part of the vitreous that was free of blood and had a normal structure. (C) Schematic drawing.
Fig. 9.22. The retrovitreal space may completely clear after a few days or weeks due to its high fluid exchange rate; however, blood on the vitreous framework or located subretinally absorbs much more slowly (A). (B) Schematic drawing.

Vitreous hemorrhage from neovascularization

Hemorrhages that develop from proliferative changes in patients with diabetic retinopathy and retinal neovascularization will always be accompanied by pathologic changes in the vitreous. Vitreous membranes tent rectilinearly between the adhesions to the retina. The normal aftermovements that should occur in the vitreous after eye movements are extinguished in the presence of peripheral neovascular tufts. The vitreous tufts create adhesions that encircle the posterior pole. This is an ominous sign, which is indicative of early retinal tractional detachment from these circular adhesions (Fig. 9.23). Choroidal neovascularization from age-related macular degeneration will have hemorrhage in multiple layers of the eye (Fig. 9.24).

Fig. 9.23. (A) Beginning traction detachment at the posterior pole with vitreous contraction and proliferative diabetic retinopathy, which is hidden behind a diffuse vitreous hemorrhage. A springboard-like, taut, detached hyaloid membrane is still adherent to the retina at the posterior pole and has led to a traction detachment in several places. (B) Schematic drawing.
Fig. 9.24. (A) Extensive vitreous hemorrhage from disciform macular degeneration. The blood dissipates into the preretinal or intrachoroidal space, into the area of the macular lesion and into the detached vitreous. The retrovitreal space is echo-free because of its high fluid exchange. (B) Schematic drawing.