Causes
Vitreous hemorrhage can occur when blood flows out of the retina and accumulates in the vitreous cavity due to rupture of the retinal vessels or neovascularization for any reason. In normal people, the vitreous body is not vascularized, but retinal neovascularization can grow into the vitreous body or develop vitreous fibrovascular tissue proliferation. Ocular trauma and fundus vascular disease are common clinical causes of vitreous hemorrhage.
1, vitreous hemorrhage caused by ocular trauma or surgery. Ocular penetrating injuries or blunt contusions can cause traumatic vitreous hemorrhage. The incidence of vitreous hemorrhage is high in corneoscleral penetrating injuries, scleral penetration and foreign body injuries to the posterior segment of the eye. Instantaneous deformation of the eye due to ocular stenosis can lead to retinal choroidal rupture and hemorrhage; anterior vitreous hemorrhage can be caused by injury to the ciliary body area.
Surgical vitreous hemorrhage can be seen in cataract surgery, retinal detachment repair surgery, vitreous surgery, etc.
2.Spontaneous vitreous hemorrhage. There are more diseases included. The main ones are retinal vascular disease, such as diabetic retinopathy, retinal vein obstruction, Eales disease, retinal macroaneurysm, etc.; posterior vitreous detachment or retinal fissure formation; wet age-related macular degeneration; inflammation, degeneration or tumor of the retinal choroid. A clinical analysis of 151 cases of monocular vitreous hemorrhage with the exception of 2 etiologies such as diabetes mellitus and ocular trauma found that the main cause of hemorrhage was retinal fissure formation in 42% of cases; retinal vein branch obstruction in 37%. Some hematologic diseases such as leukemia and retinal schwannoma can also cause vitreous hemorrhage, but are less common. In diabetic patients, the presence of retinal neovascularization is a precursor to vitreous hemorrhage. If left untreated, vitreous hemorrhage occurs in approximately 27% of cases within 5 years. Vision loss due to hemorrhage does not recover by self-absorption of blood in about 60% of patients.
Pathogenesis
Vitreous hemorrhage can come from the posterior retina, optic disc and choroid, or from the iris and ciliary body in the anterior segment of the eye. In aphakic eyes, the hemorrhage is more likely to enter the vitreous posteriorly. Small amounts of hemorrhage are easily absorbed without sequelae, while larger amounts of hemorrhage are difficult to absorb and may result in cholesterol deposition, hemoglobin deposition, partial liquefaction of the vitreous, partial concentration, and posterior detachment. Heavy bleeding can also lead to the degeneration of red blood cells to form ghost cells, which can lead to hemophagocytic or hemolytic glaucoma. Repeated hemorrhage can stimulate a proliferative reaction in the eye, resulting in a dense, fibrous proliferative membrane with neovascularization. This membrane is prone to rupture and cause repeated hemorrhage, and it can contract to produce retinal fissures and retinal detachment, which can lead to complications of cataract and even eye atrophy.
Symptoms and signs
The symptoms, signs, course, prognosis and complications of vitreous hemorrhage depend mainly on the primary cause of the hemorrhage and the amount and frequency of the hemorrhage.
Spontaneous bleeding often occurs suddenly and can be a very small amount of bleeding or, in more cases, form a dense blood clot. When a small amount of bleeding occurs, the patient may not be aware of it, or only have “flying mosquitoes”; when more bleeding occurs, the patient may find dark shadows floating in front of the eyes, or seem to be covered by red glass, and patients with repeated bleeding may feel “smoke” and have a significant loss of vision. On ophthalmic examination, when the hemorrhage is small and does not interfere with the slit-lamp view, red blood cells can be seen aggregated in a lemon-colored dusty scaffold of vitreous gel. Moderate amounts of fresh hemorrhage may appear as dense black streaks of cloudiness. A large amount of hemorrhage results in no red light reflection from the fundus and vision loss to light perception.
Over time, the blood within the vitreous dissipates, the color fades, and the vitreous gradually becomes clear. The absorption of more blood takes 6 months or up to 1 year or more. In the absence of significant fundus lesions, vision may be fully or mostly restored. In cases of posterior segment trauma combined with massive vitreous blood accumulation, half of the patients may lose useful vision.
1. Determine the primary cause. Diagnosis is based on the cause of the hemorrhage and clinical manifestations, and examination of the contralateral eye is of great value. The diagnosis should include the primary cause, or be traumatic as well as comorbidities.
2.Definition of the amount of hemorrhage. For the amount of hemorrhage, according to the degree of vitreous opacity can be divided into 4 levels, “±” or grade I, refers to a very small amount of hemorrhage does not affect the fundus observation grade II, refers to the fundus red light reflection is obvious, or the retinal vessels are visible in the peripheral part above grade III, refers to part of the fundus with red light reflection, the lower half without red light reflection grade IV, refers to the fundus without red light reflection.
Examination and differentiation
For certain primary diseases causing vitreous hemorrhage, some necessary laboratory tests can be performed, such as blood routine, bleeding and coagulation indexes.
Ultrasound has a greater diagnostic value, especially when the fundus cannot be seen directly.
1. A small amount of diffuse hemorrhage may yield negative results with B-mode ultrasound because of the lack of sufficient echogenic interface in the vitreous. A-mode ultrasound scans may show low baseline echogenicity in this regard.
2. When the vitreous accumulation is dense, scattered echoes of low to moderate amplitude may be seen on either A- or B-mode ultrasonography. When scanned with high sensitivity, the densities and distribution of the hemorrhage are shown more clearly; scans with reduced sensitivity can result in a decrease in echogenic amplitude, and most of the echogenic points are cleared away, so that the presence of concurrent retinal detachment can be determined.
3.Posterior vitreous detachment caused by vitreous hemorrhage should be differentiated from retinal detachment in the diagnosis of ultrasound image.
Posterior vitreous detachment caused by blood accumulation in the vitreous should be distinguished from retinal detachment when diagnosed by ultrasound images. The detached retina often shows high amplitude echoes with little change in retinal echoes when sensitivity is changed. The detached retina can often be traced to the attachment or optic disc, and in retractive retinal detachments will show a retractive pattern. In simple posterior vitreous detachment, the posterior vitreous interface has significant posterior motion when the eye is turned, reducing the sensitivity of the machine when the echo amplitude is diminished. Therefore, ultrasonography can determine the extent of trauma to the posterior segment of the eye with vitreous hemorrhage and whether there is a combination of retinal detachment and other lesions, and can determine the prognosis of vision, which can be repeated if necessary.
Treatment of vitreous hemorrhage
Western medical treatment.
1, drug therapy: some drugs were tried in the past to try to promote the absorption of blood, but none of them have been confirmed to have positive efficacy. It is clinically difficult to conduct a randomized controlled clinical trial to evaluate the effect of a particular drug or non-surgical therapy. Intravitreal injections of urokinase or t-PA have been reported to activate fibrinogen in the clot, causing the clot to dissolve and break up, and may also increase the permeability of the ocular capillaries. Other drugs, including those with blood-activating and stasis-restoring effects early on may be given orally as Yunnan Baiyao 0.5 g three times daily to activate the hemostatic effect. Hemostatic drugs are applied, such as hemostatic minerals, anloin, etc. After 48-72 hours, anticoagulant drugs can be given to promote the absorption of bleeding, such as aspirin, compound thrombopoietin, and antoiodine, etc.
2.Physical therapy: Some reports use ultrasound to treat vitreous hemorrhage, but experiments show that ultrasound does not accelerate the role of blood absorption. Argon laser has also been tried to shoot the clot in the vitreous, which can make the clot vaporize and loosen. In addition, there are still ion introduction method attempts. These methods, in clinical application is not much.
3.Surgical treatment: Vitrectomy is most suitable for cases of vitreous hemorrhage caused by ocular trauma (such as contusion, laceration, penetrating injury or rupture injury), as well as persistent spontaneous hemorrhage or combined retinopathy.
(1) Traumatic vitreous hemorrhage: (1) When caused by penetrating eye injury, early vitrectomy can be performed. Experimental and clinical studies have shown that it is more appropriate to operate within 1 to 2 weeks after injury. Removal of blood clots and inflammatory products in the eye during this period can avoid excessive stimulation of blood to the repair process of trauma and reduce the chance of fibrous tissue proliferation and retinal detachment by traction. ②Choroidal retinal rupture due to blunt contusion can wait for a period of time if it is not accompanied by retinal detachment. Surgery will be considered when it cannot be spontaneously absorbed and affects the recovery of vision. (3) Bleeding during or after surgery can be treated without special treatment when it is small and can be absorbed quickly; when it is large, it can be treated by surgery again.
(2) Spontaneous vitreous hemorrhage: The timing of surgery should be decided according to the characteristics of the primary disease. In recent years, it is believed that the occurrence of vitreous hemorrhage in diabetic retinopathy is an indication for surgery, and the results of earlier surgery are better. Because the accumulation of blood hinders retinal photocoagulation therapy, and retinal ischemic lesions may continue to deteriorate, early surgery with effective photocoagulation can not only deal with complications, but also be beneficial to control retinal ischemia. Other ischemic lesions are similar.
In addition, the application of peripheral retinal condensation can help control severe diabetic retinopathy combined with vitreous blood accumulation in cases that are not amenable to vitreous surgery by promoting the absorption of vitreous blood to some extent while coagulating some retinal tissue.
Chinese medicine treatment.
1, blood heat delusion
Treatment: Clearing heat and diarrhea, cooling the blood and stopping bleeding.
Prescription: Sheng Pu Huang Tang (Chen Dafu’s experienced formula) with added flavor. If there is hyperactivity of the liver and yang, add Shijiao Ming and Xia Ku Cao; if the headache is severe, add Wu Ling Li and Dai Ochre; if there is a lot of bleeding, add Xian He Cao and Blood Yu Char.
2. Yin deficiency and fire inflammation
Treatment: Nourish Yin and lower fire, tonify liver and kidney.
Remedy: Zhi Bai Di Huang Tang (“Medical Jinguan”) with flavour. The above can be added to the appropriate Wu Wei Zi, Qing Cockscomb, mulberry leaf, mother of pearl, etc. to clear the liver and brighten the eyes.
3, heart and spleen deficiency
Treatment: nourish the heart and strengthen the spleen.
Remedies: GUI Spleen Tang (“Jisheng formula”) plus flavor. Atractylodes Macrocephalae 9g, Astragali 9g, Longan 9g, Fried Jujube 9g, Ginseng (or Dang Shen) 9g, Mu Xiang 2g, Roasted Licorice 5g, Radix Angelicae Sinensis 9g, Yuan Zhi 9g. Aconite, Blood Yu Tan, Tian San Qi can be added to help stop bleeding and resolve blood stasis.
4.Qi stagnation and blood stasis
Treatment: Promote the flow of Qi and Blood, break down stasis and disperse nodules.
Remedy: Blood Mansion and Blood Stasis Soup (“Medical Lin Reform”) plus or minus. Add Danshen and Yujin to strengthen the effect of promoting Qi and dispersing blood stasis; if the accumulated blood is thick or organic, use the products that promote blood circulation and resolve blood stasis, and add Sanguine, Curcuma, Seaweed and Kunbu to break blood stasis and soften the knots; if there is If there is heat depression, we can add Dampi and Gardenia to clear heat and disperse knots.
Acupuncture and moxibustion: take the points of foot solar bladder, foot Yangming stomach, hand Yangming large intestine, foot Taiyin kidney and Governor’s meridian mainly, more needles and less moxibustion. Selected points: Qingming, Hegu, Sibai, Sanyinjiao, Dazhi. If blood heat is delusional, optional addition of ear tip, Guanchong, Shaochong, Zhongchong, Yin Tang, the use of trigeminal leaf prick blood, the amount of 1 to 2 drops, each time the choice of 2 to 3 points, once between days, alternating. In case of deficiency fire injury to the ligament, Kidney Yu, Liver Yu, Brightness, Sun, Xingma, Taixi, and Shen Vessel; in case of deficiency of the heart and spleen, Spleen Yu, Stomach Yu, Diaphragm Yu, Foot Sanli, Zhonggui, and Qihai; in case of internal stasis of blood, Fengchi, Sun, Chengwei, Fenglong, Dachong, Brightness, Shen Vessel, and Zhaohai can be used.
Prognosis: In the absence of complications, timely removal of vitreous blood accumulation is beneficial for vision recovery, but attention should be paid to the treatment of the primary disease to prevent recurrence.