Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

Figure 5. Recent Invasive Vitreous Haemorrhage (H). Initially the haemorrhage has a red appearance preserved for a considerable period of time. Months later it turns into a yellowish dark color usually difficult to reabsorb, and the formation of fibrous tissue

(P). (Art from Jaypee - Highlights Medical Publishers).

the vitreous hemorrhage such as trauma or a uveitic process, especially one associated with peripheral retinal ischemia and secondary neovascularization.

It is essential that the fellow eye be examined when possible, since any findings there (or lack thereof) can significantly alter the likelihood of underlying etiologies in the differential diagnosis of the eye with the vitreous hemorrhage. The presence of diabetic retinopathy, retinopathy of sickle cell disease, or age-related macular degeneration may dramatically increase the probably of conditions in the fellow eye affecting the

eye with the vitreous hemorrhage. Such confounding factors may significantly alter the timing of intervention and frequency of repeat examinations for the eye with the vitreous hemorrhage.

Diagnostic Testing

B-scan ultrasonography is the test most commonly used to manage vitreous hemorrhages because this test may provide the underlying diagnosis and indicate whether a vitrectomy is needed and when. Ultrasonography is particularly critical for patients

whose medical histories are unavailable or whose physical examination findings do not suggest a particular disease process and there is no view of the fundus (Figure 6). The foremost task of the ultrasonographer is to assess whether a retinal detachment or a retinal tear or break is present. Prompt vitrectomy is required for retinal tears or breaks and for retinal detachments that do not involve the macula. A hyperechogenic lesion in the macula suggests that the etiology may be exudative age-related macular degeneration,

or, less likely, a neoplastic process which may be encountered elsewhere as well.

For patients with risk factors for diabetes mellitus and no history of recent screening, a fasting serum glucose, glucose tolerance test, or glycosylated hemoglobin laboratory evaluation should be considered. For patients whose histories suggest a diagnosis of sickle cell disease or trait or thalassemia, hemoglobin electrophoresis may be considered.

Management

The management of vitreous hemorrhages can be straightforward when diagnostic ultrasonography clearly reveals a retinal detachment, tear or break. The management of a vitreous hemorrhage is typically conservative for diabetic patients. For patients with type II diabetes mellitus, observation every few months is indicated; for patients with type I diabetes mellitus, observation is generally indicated more often.1 Generally after six months of a non-clearing vitreous hemorrhage in a type II diabetic, the benefits of surgical intervention (vitrectomy) outweigh the risks. The most significant factors in determining when a vitrectomy is indicated

for a non-clearing vitreous hemorrhage in a diabetic patient not previously examined are the type of diabetes mellitus (type I or II) and the age of the patient, since these factors relate directly to the presence or absence of a posterior vitreous detachment and the potential aggressiveness or rate of growth of the neovascularization (Figure 7). In young patients with type I diabetes mellitus, the posterior hyaloid is often attached and the rate of maturation of the neovascularization is generally rapid; the opposite is generally the case in older patients with type II diabetes. Bilateral vitreous hemorrhages with significant reduction in visual acuity are also an indication for more prompt intervention to obtain visual improvement.

Not since the advent of vitrectomy has the management of vitreous hemorrhage been altered more than with the widespread use of anti-VEGF (vascular endothelial growth factor) agents, which are particularly useful in diabetic patients or others with known risk factors for retinal (or choroidal) neovascularization. Before proceeding with vitrectomy, an intravitreal anti-VEGF agent is now commonly employed to regress neovascularization. While a non-clearing vitreous hemorrhage is a common indication for vitrectomy, the term “non-clearing” may be a misnomer, given the growing experience using anti-VEGF agents.2 It appears that in many patients with vitreous hemorrhages that were previously considered to be non-clearing, the hemorrhages continue to occur subclinically. A significant number of these hemorrhages improve when the anti-VEGF agent is used, suggesting that the regression of neovascularization achieved with the anti-VEGF agent halts subclinical active hemorrhaging; the “non-clearing” vitreous hemorrhage is no longer clinically observed.

Oftentimes ultrasonography will not provide definitive diagnostic findings (e.g., no retinal detachment, tumor, or evidence of a tear or break), especially in the absence of a history of retinal pathology in the affected or contralateral eye. One exception may be the patient who has been evaluated routinely by an experienced eye-care practitioner who notes thepresenceofaposteriorvitreousdetachment, which may be identified as the etiology of the hemorrhage. There is a paucity of data to clearly guide the clinician in the management of patients with vitreous hemorrhages who have no history of or known risk factor

for diabetes mellitus or another predisposing condition. Clinicians have a highly variable approach in such circumstances, based on the clinician’s own experience and the patient’s particularsituation. Dependingonthepatient’s general medical condition and the associated risks of surgical intervention, relatively prompt vitrectomy is considered by some vitreoretinal surgeons. Repeat evaluation is generally a matter of days among those clinicians who manage such patients conservatively. Even if empirical data were available, it may be difficult to apply the information to the specific clinical circumstance presented, as multiple factors (e.g., history of systemic vasculitis) can significantlyincreaseordecreasetheprobability of a particular underlying pathology. Such factors can increase or decrease the risk-benefit ratio with regard to the timing of vitrectomy and the frequency of repeat examinations. For example, if patients develop symptoms of worsening acuity or photopsia, it may be less appropriate to defer vitrectomy.

Etiology of Vitreous

Hemorrhage

Retinal neovascularization is a common etiology for vitreous hemorrhages. The most common causes of retinal neovascularization are proliferative diabetic retinopathy and venous occlusive disease. Other, less common conditions that may cause neovascularization include sickle cell disease, sickle cell trait, thalassemia, radiation retinopathy, and inflammation. In addition, central or branch retinal artery occlusion may give rise to ischemia and secondary retinal neovascularization (Figure 8).

If a history of diabetes mellitus is reported by the patient, the history should be probed to determine the time since diagnosis, the degree of glycemic control and the presence of other microvascular complications of the disease. For the vast majority of patients with diabetes mellitus, neovascularization secondary to diabetic retinopathy will probably be the culprit, and therefore conservative management is usually most appropriate. An etiology of proliferative diabetic retinopathy should be viewed with some skepticism for patients with diabetes mellitus who have a history of a normal recent eye examination and are not pregnant or have had no recent

change in their glycemic control. For patients with known proliferative diabetic retinopathy, especially with a history of previous vitreous hemorrhage, the primary diagnosis of proliferative diabetic retinopathy for the current vitreous hemorrhage can be presumed the absence of contrary findings on examination and with B-scan ultrasonography. Additional testing for competing etiologies is probably not necessary unless unusual circumstances exist, such as a history of trauma or unusual findings on examination.

Almost universally, patients that present with a central retinal artery occlusion have

histories of such occlusions. It is possible, however, that some patients with poor premorbid (i.e., before the occlusion) vision, amblyopia, or other disease in a non-dominant eye may have a cilio-retinal artery supplying the fovea, which can lead to an asymptomatic central retinal artery occlusion. Patients with central retinal vein occlusion, branch retinal vein occlusion, or branch retinal arteriolar occlusions are often unaware of the underlying pathology until they become symptomatic with the vitreous hemorrhage, usually weeks after the neovascularization has begun to mature. On examination, it is often possible with indirect ophthalmoscopy and an adequate view of the retina to make the diagnosis of a retinal vein occlusion. After an arteriolar occlusion, in the convalescent period it is often difficult, if not impossible, to make a diagnosis of the occlusion as the retina often appears essentially normal on examination. After central retinal artery or branch retinal arteriolar occlusions, the minimal amount of retinal sequelae found with ophthalmoscopy warrant clinical contemplation regarding a diagnosis, but if neovascularization can be directly visualized then diagnosis is aided. Where an adequate view is possible, clues to the underlying etiology may be present, such as a thrombus, embolus, or arteriovenous crossing abnormality, although such clues are rare. Diagnosis is greatly aided by retinal angiography if an adequate view is possible.

Knowing the age of the patient may also be helpful for diagnosis. Etiologies such as retinal tears or breaks and posterior vitreous detachments usually present in the sixth and

seventh decades of life, which is also the most common time for retinal vascular occlusive disease to occur. Age is most helpful for diagnosing patients that are in their fourth and fifth decades of life, when typically patients do not have retinal vascular occlusions. In these patients, consideration of an etiology other than retinal occlusive disease is appropriate.

Evaluation for competing diagnoses such as hemoglobinopathies or radiation retinopathy with neovascularization is guided by the history. Hemoglobin electrophoresis can be useful, and anti-VEGF agents for sickle cell disease can be considered.3 Deciding when to perform a vitrectomy should be based on the risks and benefits for each individual patient; the procedure should be performed based on knowledge of the patient’s preexisting retinopathy and the duration and severity of the vitreous hemorrhage.

Other etiologies of retinal neovascularization that may result in vitreous hemorrhage can include any disorder that may result in retinal ischemia, such as retinopathies associated with the hemoglobinopathies and multiple heterogenic inflammatory disorders. Inflammation may cause ischemia indirectly,4 or may take the form of an autoimmune attack specifically against the retinal vasculature (i.e., phlebitis or arteritis).5

A vitreous hemorrhage without a preexisting risk factor is most worrisome in terms of management. A careful history is essential in these patients. Occasionally a history of symptoms consistent with a

posterior vitreous detachment or retinal tear or break, such as photopsia, is obtained. If this is the case, then it may be likely that a retinal break or tear is present in addition to a posterior vitreous detachment. A careful inspection of the peripheral retina with the indirect ophthalmoscope is necessary in these patients; examination can be improved with scleral indentation. However, the hemorrhage often prevents or limits this examination, in which case obtaining B-scan ultrasonography is critical.

Choroidal neovascularization, most commonly from exudative age-related macular degeneration, may rarely result in a significant vitreous hemorrhage—occasionally massive enough to prohibit a view of the posterior pole. In such cases, examination of the contralateral eye can be more useful than ultrasonography in helping to support the diagnosis. It is important to conduct follow up with such patients, as choroidal melanoma in the macula may mimic this presentation. Choroidal neovascularization from other etiologies that allow egress of vessels through pathology in Bruch’s membrane should also be considered, but are rare (e.g., myopic degeneration, angioid streaks6). Of those disorders in which large vitreous hemorrhage may result, the most common may be idiopathic peripheral choroidal neovascularization.7

The presence of intraocular neoplasia is seldom the etiology of vitreous hemorrhages,

but it can be the presenting symptom of an intraocular malignancy.

Conclusion

Vitreous hemorrhage is a common condition seen in the retina clinic. In many patients the underlying etiology and subsequent management is discernable from the history, physical examination and ancillary testing such as B-scan ultrasonography. However, for many other patients the etiology of the vitreous hemorrhage is not easily identified; for these patients, management can be appropriately recommended based upon the most likely and most consequential diagnoses in the differential. The timing of vitrectomy and the frequency of follow-up observation in patients with a vitreous hemorrhage varies among physicians and should be customized for each patient based on the probable diagnoses.

References

1.Diabetic Retinopathy Vitrectomy Study Research Group. Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy: two-year results of a randomized trial. Diabetic Retinopathy Vitrectomy Study Report 2. Arch Ophthalmol. 1985; 103:1644.

2.Spaide RF, Fisher YL. Intravitreal bevacizumab (Avastin) treatment of proliferative diabetic retinopathy complicated by vitreous hemorrhage. Retina

206 Mar;26(3):275-8.

Suprachoroidal hemorrhage is a rare but potentially devastating event that can occur spontaneously, or as a consequence of trauma or ocular surgery. It was first reported to have occurred during ophthalmic surgery by Baron de Wetzel in 1760.1 Successful management of suprachoroidal hemorrhage was first described by Verhoeff in 1915.2

Anatomy and Pathophysiology

The suprachoroidal space is a potential space between the choroid and the sclera and normally contains about 10μl of fluid. When filled with blood it becomes a true space with boundaries at the scleral spur anteriorly and the optic disc posteriorly. The choroid is also attached to the sclera at the ampullae of the vortex veins, thus giving choroidal detachments their characteristic lobular appearance (Figures 1 and 2).

Many authors have described the mechanism leading to development of non-traumatic suprachoroidal hemorrhage.3-5 Hypotony appears to be the major precipitating event, leading to anterior displacement of the lens-iris diaphragm and in turn the retina and choroid. This can result in traction of a long or short posterior ciliary arteries, leading to rupture and hemorrhage.4 Hypotony can also cause serous choroidal effusion that can contribute to rupture of a long or a short posterior ciliary artery.6 In a rabbit model, four sequential stages in the development of suprachoroidal hemorrhage have been described.3

1.Engorgement of the choroidal capillaries.

2.Serous effusion into the suprachoroidal space.

3.Stretching and tearing of the blood vessels at the ciliary body base.

4.Massive hemorrhage from the torn vessels into the suprachoroidal space.

The long posterior ciliary arteries are especially prone to rupture during ciliochoroidal effusion due to their short connections between the scleral exit and outer choroid.7

Risk Factors

Risk factors for the development of suprachoroidal hemorrhage can be classified as ocular and systemic. Ocular risk factors includeglaucoma,elevatedintraocularpressure (IOP), increased axial length, aphakia, pseudophakia, inflammation and ocular surgery.8 Systemic risk factors include advanced age, atherosclerosis, diabetes mellitus, hypertension and blood dyscrasias.

Glaucoma, elevated IOP and increased axial length were found to be highly significant risk factors in the development of suprachoroidal hemorrhage by more than one author.8 These ocular conditions promote vascular necrosis and weaken the integrity of the long posterior ciliary arteries, making them more vulnerable to rupture. In axial myopia, loss of scleral rigidity and choroidal vascular fragility is presumed to be responsible for the development of suprachoroidal hemorrhage. In aphakia, more stretching and separation of the uvea from the sclera occurs during ciliochoroidal effusion due to loss of support from the lens and zonular apparatus.

Suprachoroidal hemorrhage can occur during ocular surgery or in the post-operative period. It has been reported with all types of intraocular procedures including cataract extraction, glaucoma filtration procedures, penetrating keratoplasty and vitrectomy. Older methods of cataract surgery and secondary

intraocular lens implantation procedures were associated with higher incidence of expulsive suprachoroidal hemorrhage, probably due to larger wounds and more prolonged hypotony. Phacoemulsification cataract extraction has reduced the incidence of suprachoroidal hemorrhage due to reduced manipulation and less pronounced fluctuations of intraoperative intraocular pressure. Glaucoma filtration procedures have a higher incidence of delayed suprachoroidal inflammation due to prolonged postoperative hypotony and inflammation. General anesthesia and intraoperative pulse rate greater than 90 beats per minute have also been implicated in the development of suprachoroidal hemorrhage.9,10

Valsalva-type maneuvers (either from bucking during general anesthesia or vomiting in the post-operative period) result in an increase in the pressure gradient across the wall of a necrotic ciliary vessel, which can lead to rupture and subsequent suprachoroidal hemorrhage.11

Preventive Measures

Preventive measures can be undertaken preoperatively and intraoperatively in patients at high risk for suprachoroidal hemorrhage. A thorough ocular and systemic evaluation should be performed preoperatively to look for evidence of hypertension, atherosclerosis, liver disease and blood dyscrasias. Diabetics should have their blood glucose under adequate control. Patients should also refrain from the use of aspirin and other non-steroidal anti-inflammatory agents in the immediate preoperative period.