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Yibian
 Shen Yaozi 
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diseaseVitreous Hemorrhage
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bubble_chart Overview

Vitreous hemorrhage is a common complication caused by ocular trauma or retinal vascular diseases that poses a threat to vision. On one hand, the hemorrhage not only clouds the refractive medium, obstructing light from reaching the retina, but also causes severe damage to ocular tissues. On the other hand, the body's response to the hemorrhage can gradually clear the blood. The consequences of vitreous hemorrhage vary significantly among different cases. Appropriate clinical management should be provided in a timely manner based on the primary injury or disease, the amount of vitreous hemorrhage, the absorption of the hemorrhage, and the ocular response.

bubble_chart Etiology

In cases where the retina, choroid, blood vessels, or neovascular tissue proliferate due to any cause, neovascularization may occur within the vitreous cavity. Ocular trauma and vascular diseases of the fundus are the most common clinical causes of vitreous hemorrhage.

In ocular trauma, both penetrating injuries and blunt contusions of the eyeball can lead to traumatic vitreous hemorrhage. The incidence of vitreous hemorrhage is high in cases of corneal and scleral perforation injuries, as well as in retained foreign body injuries in the posterior segment of the eye. The instantaneous deformation of the eyeball caused by blunt contusion can lead to rupture of the retina and choroid, resulting in hemorrhage; anterior vitreous hemorrhage can be caused by injury to the ciliary body. According to our observation of a group of cases, traumatic vitreous hemorrhage can account for 25-45% of cases primarily involving blunt contusion of the posterior segment. Juan et al.'s statistical analysis of 453 hospitalized patients with ocular trauma showed that vitreous hemorrhage occurred in 145 cases, accounting for 32%.

There are many diseases that can cause spontaneous vitreous hemorrhage, including inflammatory, degenerative, or neoplastic diseases of the retina and choroid. According to a group of case statistics, diabetic retinopathy accounted for 34.1%; retinal holes without detachment accounted for 22.4%; rhegmatogenous retinal detachment accounted for 14.9%; and retinal vein occlusion accounted for 13.0%. These four conditions accounted for 84% of cases. Other diseases such as posterior vitreous detachment, retinal vasculitis, retinal periphlebitis, age-related macular degeneration, intraocular tumors, and retinopathy of prematurity also account for a significant proportion of cases with vitreous hemorrhage. Nitta et al. conducted a clinical analysis of 151 cases of unilateral vitreous hemorrhage excluding diabetes and ocular trauma, and found that the main causes of hemorrhage were retinal hole formation (42%) and branch retinal vein occlusion (37%). Some hematologic diseases such as leukemia and retinal schisis can also lead to vitreous hemorrhage, but these are relatively rare.

In diabetic patients, the appearance of neovascularization in the fundus is a precursor to vitreous hemorrhage. If no treatment is administered, approximately 27% of cases will develop vitreous hemorrhage within 5 years. About 60% of patients with vision loss due to hemorrhage cannot recover through spontaneous absorption of the blood.

Surgical vitreous hemorrhage can occur in cases of cataract surgery, retinal detachment repair surgery, and vitrectomy.

bubble_chart Pathogenesis

The accumulation of blood in the vitreous cavity can cause damage to the vitreous and retina; the body's response will gradually clear the blood and its breakdown products.

Damage to the vitreous by blood

According to clinical observations and experimental studies, a certain amount of blood entering the vitreous can cause the vitreous to condense, liquefy, and detach posteriorly. The vitreous loses its normal gel structure and support functions for the retina, and its generation and transformation characteristics also change accordingly.

Injecting 0.1 to 0.2 ml of autologous whole blood into the vitreous of a normal rabbit can lead to the separation between the vitreous and retina within a week, with the collapsed vitreous forming a thin membrane-like structure, pseudocystically surrounding the blood clot. This pseudomembrane attaches to the vitreous at the site of incomplete detachment.

After two weeks, the vitreous is almost completely detached, and the vitreous undergoes degeneration and liquefaction.

There is no complete consensus on the mechanism by which blood causes vitreous degeneration. ① For a long time, it has been believed that the iron ions released from hemoglobin after blood degradation play an important role in vitreous liquefaction. To test this hypothesis, we added ferrous chloride solution to the vitreous of isolated bovine eyes. The results showed that 0.1 ml of ferrous solution equivalent to a blood iron concentration of 10 mM could completely destroy the gel structure of the vitreous within 20 hours, causing all collagen fibers to condense and separate. Even 1% of this concentration of ferrous ions could cause partial collagen condensation. The specific destructive effect of iron ions on the vitreous is related to the production of hydroxyl radicals. In vivo experiments on rabbits confirmed that iron ions at concentrations equivalent to 0.3 to 0.7 mol/L (16.8 to 39.2 μg) could cause vitreous liquefaction in rabbits. Theoretically, 0.1 ml of blood contains more than 50 μg of iron ions, but in reality, only a small amount of free iron ions are released during vitreous hemorrhage. ② During vitreous hemorrhage, a large number of macrophages invade. Experiments have confirmed a decrease in the activity of superoxide dismutase in the vitreous, indirectly proving the existence of superoxide anion radicals (O﹒) released by macrophages during respiratory bursts. These radicals have a strong destructive effect on the vitreous matrix and cellular components. ③ From the perspective of enzymatic reactions, the inflammatory process caused by blood can activate lysosomal enzymes, which can hydrolyze vitreous collagen and hyaluronic acid. Therefore, the degeneration and liquefaction of the vitreous may be the combined result of the above three effects.

Posterior vitreous detachment is related to vitreous condensation and the action of macrophages. Injecting activated macrophages into the vitreous and examining with transmission electron microscopy shows macrophages attaching to the vitreoretinal interface, with the collagen at the interface becoming loose and disintegrating. After 8 days, the posterior surface of the vitreous separates from the inner limiting membrane, forming a posterior vitreous space, with the inner limiting membrane remaining intact and the space containing intact macrophages. Subsequently, the posterior vitreous membrane gradually moves away, and the separation area expands. This observation suggests that posterior vitreous detachment may be related to the hydrolytic action of elastase and collagenase secreted by macrophages.

bubble_chart Clinical Manifestations

The symptoms, signs, prognosis, and complications of vitreous hemorrhage mainly depend on the underlying disease causing the hemorrhage, the amount of bleeding, the frequency of bleeding, and other factors. Spontaneous hemorrhage often occurs suddenly and can be a small amount of bleeding or form dense blood clots in larger amounts. When there is a small amount of bleeding, the patient may not notice it or only experience "floaters"; when more bleeding occurs, the patient may notice dark shadows moving in front of their eyes or feel as if there is a red glass piece blocking their vision. Patients with recurrent bleeding may feel "smoke" and experience a significant decrease in vision. During an ophthalmologic examination, when the bleeding is minimal and does not affect the observation with a slit lamp, red blood cells can be seen aggregated in the vitreous gel framework, appearing as lemon-colored dust. Moderate amounts of fresh bleeding may appear as dense black streaks of opacity. A large amount of bleeding can result in the absence of red reflex in the fundus, with vision decreasing to light perception.

Over time, the blood in the vitreous diffuses, the color fades, and the vitreous gradually becomes transparent. The absorption of a larger amount of blood may take 6 months or even more than a year. In the absence of significant fundus lesions, vision may fully or mostly recover. In cases of posterior segment trauma combined with a large amount of vitreous hemorrhage, about half of the patients may lose useful vision.

bubble_chart Diagnosis

Ultrasound examination has significant diagnostic value for vitreous hemorrhage, especially when direct visualization is not possible. A small amount of diffuse hemorrhage may yield negative results with B-mode ultrasound due to the lack of sufficient echo interfaces within the vitreous. However, A-mode ultrasound scanning may show low baseline echoes. When the vitreous hemorrhage is more dense, both A-mode and B-mode ultrasound can reveal scattered echoes with low to grade II amplitude. High-sensitivity scanning can more clearly show the density and distribution of the hemorrhage; reducing the sensitivity of the scan can decrease the echo amplitude, and most echo points are eliminated, thus helping to determine whether there is concurrent retinal detachment. Vitreous hemorrhage-induced posterior vitreous detachment should be differentiated from retinal detachment in ultrasound imaging. The detached retina often shows high-amplitude echoes, and the retinal echoes change little when sensitivity is adjusted. The detached retina can often be traced back to its attachment site or the optic disc, and in cases of tractional retinal detachment, a tractional morphology is observed. In simple posterior vitreous detachment, the posterior vitreous interface shows significant posterior movement when the eye moves, and the echo amplitude weakens when the machine's sensitivity is reduced. Therefore, ultrasound examination can determine the extent of posterior segment trauma and vitreous hemorrhage, whether there is concurrent retinal detachment, and assess visual prognosis. Repeat examinations can be performed if necessary.

The diagnosis of vitreous hemorrhage should include the primary disease (or whether it is traumatic); for the amount of hemorrhage, we recommend classifying it into four levels based on the degree of vitreous opacity: "±" or grade I, indicating a very small amount of hemorrhage that does not affect fundus observation; "+" or grade II, indicating a significant red reflex in the fundus or visible retinal vessels in the upper peripheral area; "++" or grade III, indicating a partial red reflex in the fundus with no red reflex in the lower part; "+++" or grade IV, indicating no red reflex in the fundus.

bubble_chart Treatment Measures

In most cases, spontaneous absorption of vitreous hemorrhage takes 4 to 6 months, although preretinal hemorrhage may dissipate within a few days to weeks. Therefore, it is generally recommended to observe for 3 to 4 months before initiating treatment. If the vitreous opacity does not significantly decrease during this period, it suggests that spontaneous absorption is slow or the likelihood of complete absorption is low.

Drug therapy aims to promote blood absorption. However, no drug has been confirmed to have definitive efficacy. Due to the variability in cases of vitreous hemorrhage, it is difficult to conduct randomized controlled clinical trials to evaluate the effectiveness of a particular drug or non-surgical therapy. Urokinase intravitreal injection is frequently reported in the literature. The mechanism of urokinase is that it activates plasminogen in blood clots, causing the clots to dissolve and break apart, and may also increase the permeability of ocular capillaries, promoting blood absorption. Intravitreal injection can be performed under mydriasis and local anesthesia, with two rectus muscle traction sutures to fix the eyeball. Preoperatively, 0.5g of acetazolamide is administered orally to reduce intraocular pressure. Anterior chamber paracentesis may also be performed to soften the eyeball before injection. Then, 0.3ml of urokinase (25,000 Ploug units dissolved in distilled water) is injected into the vitreous through the pars plana. If the vitreous remains opaque after 6 to 8 weeks, the injection can be repeated once. Intravitreal injection of urokinase often causes hypopyon, which typically resolves within 3 to 6 days. Intraocular pressure may transiently increase, and 0.25g of acetazolamide can be administered orally four times daily for 1 to 2 weeks postoperatively. Campman-Smith treated 27 cases (34 eyes), with 10 eyes showing visual improvement, 10 eyes unchanged, and 3 eyes worsening. Chen Daoyu et al. used subconjunctival injection with results similar to the above. In animal experiments, Koziol et al. injected 22,500 CTA units of urokinase into monkey eyes, but found no significant effect on vitreous blood clearance. In reports without strict case controls, patients with slow blood absorption were given 6,000 to 10,000 IU of urokinase peribulbar injections once a week for 8 to 10 weeks, achieving some efficacy. Other drugs, including compound formula Chinese medicinal preparations with invigorating blood and resolving stasis effects, such as compound Salvia solution and compound anisodine, have also been used clinically, but their efficacy requires further evaluation.

Physical therapy has been reported for treating vitreous hemorrhage, but experiments show that full-dose ultrasound does not accelerate blood absorption. Coleman et al. believe that ultrasound can promote the absorption of vitreous membranes. Argon laser has also been tried to target intravitreal blood clots, causing qi transformation, loosening, and dissociation of the clots, red blood cell rupture, increased macrophage activity, and accelerated blood absorption. However, this may only be suitable for cases with obvious blood clots and transparent surrounding media.

Surgical treatment, specifically vitrectomy, is most suitable for cases of vitreous hemorrhage caused by ocular trauma (such as contusion, laceration, perforation, or rupture).

1. Early vitrectomy for traumatic vitreous hemorrhage: Experimental and clinical studies suggest that surgery within 1 to 2 weeks after injury is most appropriate. Removing blood clots and inflammatory products during this period can avoid excessive stimulation of the wound healing process, reduce intraocular fibrous tissue proliferation and the risk of tractional retinal detachment, and increase the likelihood of visual recovery.

2. Management of intraoperative or postoperative hemorrhage: Reports indicate that adding thrombin to the perfusion solution can reduce the incidence of hemorrhage. 6-Aminocaproic acid has some effect in preventing postoperative hemorrhage. Minor postoperative vitreous hemorrhage may not require special treatment and can be absorbed quickly. For more significant hemorrhage, aspiration or fluid-air exchange can be used to remove the blood clots.

Peripheral retinal membrane condensation surgery has been tried in cases of severe diabetic nature of disease retinal membrane lesions combined with vitreous hemorrhage, where vitreous surgery is no longer suitable. It can promote the absorption of vitreous blood to some extent, while also coagulating part of the retinal membrane tissue, which has a certain effect on controlling the condition.

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