Ординатура / Офтальмология / Английские материалы / Textbook of Vitreoretinal Diseases and Surgery_Natarajan, Hussain_2008
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Textbook of Vitreoretinal Diseases and Surgery
FIGURE 7-5: Hemorrhage at the macula, the fundus image does not allow differentiating between subhyaloidal hemorrhage (preretinal hemorrhage) or sub-ILM hemorrhage (intraretinal hemorrhage)
FIGURE 7-6: Schematic diagram of a subhyaloidal hemorrhage
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FIGURE 7-7: Schematic diagram of a sub-ILM hemorrhage |
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Hemorrhage at the Macula: Classifications and Treatment Options
diseases like arteriosclerosis, hypertension, retinal artery or vein occlusion, diabetic retinopathy, blood disorders, shaken baby syndrome, retinal macroaneurysm, chorioretinits, age-related macular degeneration, trauma or spontaneously.7-14
Although some authors identified a sub ILM hemorrhage by glistening reflexes and surface striae,15,16 others, however, disputed the reliability of biomicroscopy in locating the plane of hemorrhage.7,17,18 Several authors were able to demonstrate the localization of hemorrhage as subILM. In these cases the cleavage plane could be identified by ophthalmoscopy due to already detached vitreous at the area of the sub-ILM hemorrhage, by echography, optical coherence tomography (OCT) or by histological analyses of the surgically removed anterior wall of the hemorrhage.4, 7–9, 17-28
The lack of a definitive differentiating biomicroscopic characteristic emphasizes the difficulty in detecting clinically the location of tissue separation. But this distinction could have an implication for eventual treatment regimen. In selected cases OCT may be helpful. In general an OCT scan through the center of a hemorrhage at the macula does not illustrate whether the hemorrhage is
FIGURE 7-8A: Hemorrhage at the macula, the fundus image does not allow differentiating between subhyaloidal hemorrhage (preretinal hemorrhage) or sub-ILM hemorrhage (intraretinal hemorrhage); the white arrow demonstrates the area, length and direction of the OCT scan that is shown in Figure 7-8B
FIGURE 7-8B: Corresponding OCT scan; The scan through the center
of the hemorrhage does not allow to state the exact location of the 79 hemorrhage
Textbook of Vitreoretinal Diseases and Surgery
subhyaloidal or sub-ILM. Moreover, it does not even allow the differentiation between preor subretinal hemorrhage as the underlying structures are severely attenuated (Figures 7-8A and B).29 Shukla et al21 performed the OCT scans just above the level of sedimented blood and in case of partial detached vitreous these scans displayed two distinct membranes. A single highly reflective band corresponded to the ILM and an overlying membrane with low optical reflectivity demonstrated the posterior hyaloid. Previously we deomonstrated a selective A-scan analysis and identified numerous hyper-reflective spikes whereas a highly reflective band corresponded to the anterior wall of the prior hemorrhage corresponding to the ILM. In cases where OCT did not allow to differentiate between subhyaloidal and sub-ILM location we performed OCT after performing argon laser puncture to release the hemorrhage into the vitreous. When the optical media cleared up – in most cases one or two days after laser puncture – OCT was performed. Hereby, the anterior wall of the hemorrhage could be visualized as there was a hyporeflective area beneath, representing the cavity of prior blood accumulation. The reflectivity of the A-scan was measured (Figure 7-9A) and compared to the reflectivity of the posterior hyaloid (Figure 7-9B).
FIGURE 7-9A: OCT scan and measurement of A-scan reflectivity in a case of subhyaloidal hemorrhage. The OCT scan is performed in the upper part of the hemorrhage. The distinct membrane is marked with cursor 2 and the surface of 80 the neuroretina is marked with cursor 1. The difference is 1.1 dB. Therefore the distinct membrane represents a high
reflective membrane
Hemorrhage at the Macula: Classifications and Treatment Options
FIGURE 7-9B: OCT A-scam measurement of a posterior vitreous detachment. Cursor 1 represents the posterior hyaloid, whereas cursor 2 demonstrates the surface of the neuroretina. The difference of these two spikes is 15.4 dB. The posterior hyaloid appear with low reflectivity
Treatment Options
Treatment options should consider the underlying disease.
In the natural course of history, spontaneous reabsorption of the hemorrhage may occur slowly within one to two months.12, 16, 24, 25, 28 The possible complications of persistence of blood may cause irreversible retinal damage and permanent visual loss due to preretinal tractional membrane formation and proliferative vitreoretinopathy. Moreover, the toxic effect of longstanding preretinal blood is a concern which is even more toxic in macular hemorrhage.25, 30 It should be considered in the decision of treatment that the hemorrhage beneath the ILM tends to remain longer than the subhyaloid hemorrhage.8, 31
Laser drainage, introduced in 1973 by Heydenreich,12 can be used to provide the entrapped blood, by creating a focal opening, into the vitreous cavity which may result in accelerated clearing and visual improvement. As a complication of this procedure epimacular membrane (ERM) formation has been described.18-20 The hemorrhage contains growth factors stimulating proliferation of entrapped cells along the outer ILM and retinal surface.7 Probably, this occurs in cases where the hemorrhage
is located beneath the ILM so that laser drainage requires disruption of the basal lamina of sensory 81 retina with a consequent gliotic wound healing response.18, 32
Textbook of Vitreoretinal Diseases and Surgery
Vitrectomy allows the effective removal of the hemorrhage without any delay. By this method the surgically removed anterior wall of the hemorrhage cavity can be analyzed and the location definitely stated.18, 22 However, even though vitrectomy is a routine procedure, it is associated with numerous risks and side effects. Formation of a nuclear sclerotic cataract is a well known and relatively common complication, especially in patients over the age of 50 years.33 Intraoperative retinal breaks, postoperative proliferative vitreoretinopathy that may result in retinal detachment and severe loss of visual function and endophthalmitis are possible side effects.
Summary
First, the synonym “premacular hemorrhage” was used in the literature for the subhyaloidal as well as the sub-ILM hemorrhage, as in most cases a differentiation was not possible. The term “subhyaloidal” actually describe the location between hyaloid and retina. If the hemorrhage is located beneath the ILM, sub-ILM hemorrhage, macular hemorrhage or macular hematoma seems to be an adequate description. If the exact location can not be determined, “hemorrhage at the macula” represents an appropriate description.
Second, in consideration of the exact location of the hemorrhage, in selected cases we differ these by ophthalmoscopy (evaluation of the vitreous and surface of the retina), echography, OCT, staining with dyes intraoperatively and histological analyses postoperatively. Third, the period of waiting for the natural course and the time point of intervention as well as the best treatment option is speculative. Fourth, laser drainage has shown very good functional results, nevertheless secondary membrane formation has also been reported in selected cases and required additonal sugery with vitrectomy. For these cases the location of hemorrhage has been demonstrated beneath the ILM. Further studies are necessary to clarify whether laser drainage is more eligible for subhyaloidal hemorrhage and vitrectomy for sub-ILM hemorrhage.
References
1.Mennel S. Subhyaloidal and macular haemorrhage: localisation and treatment strategies. Br J Ophthalmol. 2007; 91: 850-2.
2.Ossoinig KC. Echographic detection and classification of posterior hyphemas. Ophthalmologica 1984; 189: 2-11.
3.Duke-Elder S, Dobree JH. System of Ophthalmology. Vol.10. St. Louis: C.V.Mosby, 1967: 145-7.
4.Morris R, Kuhn F, Witherspoon CD. Hemorrhagic macular cysts. Ophthalmology 1994; 101: 1.
5.Schubert HD. Hemorrhagic macular cyst or hematoma? Ophthalmology 1994; 101: 1477-8.
6.De Maeyer K, Van Ginderdeuren R, Postelmans L, Stalmans P, Van Calster J. Sub-inner limiting membrane haemorrhage: causes and treatment with vitrectomy. Br J Ophthalmol 2007; 91: 869-72.
7.Russell SR, Hageman GS. Hemorrhagic detachment of the internal limiting membrane after penetrating ocular injury. Retina 1992; 12: 346-50.
8.Iijima H, Satoh S, Tsukahara S. Nd:YAG laser photodisruption for preretinalhemorrhage due to retinal macroaneurysm. Retina 1998; 18: 430-4.
9.Meier P, Schmitz F, Wiedemann P. Vitrectomy for pre-macular hemorrhagic cyst in children and young adults. Graefes Arch Clin Exp.Ophthalmol 2005; 243: 824-8.
10.Kroll P, Busse H. Therapy of preretinal macular hemorrhages. Klin Monatsbl Augenheilkd 1986; 188: 610–2.
11.Kroll P, Le Mer Y. Treatment of preretinal retrohyaloidal hemorrhage: value of early argon laser photocoagulation. J Fr Ophtalmol 1989; 12: 61-6.
12.Heydenreich A. Treatment of preretinal haemorrhages by means of photocoagulation. Klin Monatsbl Augenheilkd 1973; 163: 671-6.
13.Ulbig MW, Mangouritsas G, Rothbacher HH, Hamilton AM, McHugh JD. Long-term results after drainage of
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premacular subhyaloid hemorrhage into the vitreous with a pulsed Nd:YAG laser. Arch Ophthalmol 1998; 116: |
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1465-9. |
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Hemorrhage at the Macula: Classifications and Treatment Options
14.Kaynak S, Eryildirim A, Kaynak T, et al. Nd:YAG laser posterior hyaloidotomy in subhyaloid hemorrhage. Ophthalmic Surg 1994; 25: 474-6.
15.Gass JDM. Traumatic retinopathy. In: Stereoscopic atlas of macular diseases: diagnosis and treatment. St Louis: Mosby, 1997: 737–74.
16.Keithahn MA, Bennett SR, Cameron D, Mieler WF. Retinal folds in Terson syndrome. Ophthalmology 1993; 100: 1187-90.
17.Spraul CW, Grossniklaus HE. Vitreous Hemorrhage. Surv Ophthalmol 1997; 42: 3-39.
18.Kwok AK, Lai TY, Chan NR. Epiretinal membrane formation with internal limiting membrane wrinkling after Nd:YAG laser membranotomy in valsalva retinopathy. Am J Ophthalmol 2003; 136:763-6.
19.Meyer CH, Mennel S, Rodrigues EB et al. Persistent premacular cavity after membranotomy in valsalva retinopathy evident by optical coherence tomography. Retina 2006; 26: 116-8.
20.Meyer CH, Mennel S, Rodrigues EB et al. Is the location of valsalva hemorrhages submembranous or subhyaloidal? Am J Ophthalmol. 2006; 141: 231-2.
21.Shukla D, Naresh KB, Kim R. Optical coherence tomography findings in valsalva retinopathy. Am J Ophthalmol 2005; 140: 134-6.
22.Arroyo JG, Bula DV. Immunohistochemical study of the internal limiting membrane in Terson syndrome. Retina 2004; 24: 155-7.
23.Srinivasan S, Kyle G. Subinternal limiting membrane and subhyaloid haemorrhage in Terson syndrome: the macular ‘double ring’ sign. Eye 2006; 20: 1099-101.
24.Kuhn F, Morris R, Witherspoon CD, Mester V. Terson syndrome. Results of vitrectomy and the significance of vitreous hemorrhage in patients with subarachnoid hemorrhage. Ophthalmology 1998; 105: 472-7.
25.Morris R, Kuhn F, Witherspoon CD et al. Hemorrhagic macular cysts in Terson’s syndrome and its implications for macular surgery. Dev Ophthalmol 1997; 29: 44-54.
26.Friedman SM, Margo CE. Bilateral subinternal limiting membrane hemorrhage with Terson syndrome. Am J Ophthalmol 1997; 124: 850-1.
27.Arroyo JG, Bula DV. Immunohistochemical study of the internal limiting membrane in Terson syndrome. Retina 2004; 24: 155-7.
28.Messmer EP, Wessing A, Ruprecht K, Naumann GO. Solitary intraretinal macular hemorrhage. Graefes Arch Clin Exp Ophthalmol 1984; 222: 9-12.
29.Blaise P, Duchateau E, Comhaire Y, Rakic JM. Optical coherence tomography in the diagnosis of premacular hemorrhage. Retina 2006; 26: 232-4.
30.Velikay M, Datlinger P, Stolba U, et al. Retinal detachment with severe proliferative vitreoretinopathy in Terson syndrome. Ophthalmology 1994; 101: 35-7.
31.Shukla D. Is the Location of Valsalva Hemorrhages Submembranous or Subhyaloidal? Authors Reply. Am J Ophthalmol 2006; 141: 231-2.
32.Garcia-Arumi J, Corcostegui B, Tallada N, Salvador F. Epiretinal membranes in Terson’s syndrome. A clinicopathologic study. Retina 1994; 14: 351-5.
33.Kroll P: Passagere Linsentrübung bei intraokularer Gastamponade. Ber Dtsch Ges 1981;78:1067-8.
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Textbook of Vitreoretinal Diseases and Surgery
Introduction
The vitreous body with a total volume of about 4 ml makes up two-thirds of the intraocular space and consists of 98% water and 2 % hyaluronic acid and collagen-fibers. The collagen-fibers form a scaffold, which is arranged loosely in the vitreous and condenses preretinally to form the posterior vitreous cortex. This structure is especially dense in the area of the ora serrata, the so-called vitreous base. The collagen-fibers also insert into the inner retinal layer, the so-called internal limiting membrane (ILM). This connection seems to be very tight at the posterior pole, around the optic disc as so-called Weissring and in the foveal area. In the periphery, this connection is especially adherent at the vitreous base.1
The Adherence of Retina and Vitreous Cortex:
Interdependence Diseases
The tight adherence of retina and vitreous cortex is the reason why, changes of the vitreous can also influence the retina and vice versa. The normal vitreous is subject to degeneration. As a consequence this leads to a condensation of collagen-fibres. Finally, water-filled lacunae develop, that can pass through the posterior vitreous cortex and separate it from the retina. This characteristically happens at the central retina and is called “posterior vitreous detachment (PVD)”.
Influencing factors include higher age, myopia, after cataract removal, trauma and intraocular diseases, such as uveitis. This physiological ageing process may be complicated by the fact that posterior vitreous detachment may remain incomplete, thus leading to anterior-posterior traction to the retina.
Tangential retinal tractions can also be found in cases with adherent posterior vitreous, when vitreous condenses and shrinks.2 A completely or partially attached vitreous may be the cause of many diseases of the central retina, such as the macular traction syndrome, or it may influence the course of the disease, such as in diabetic maculopathy.3-6
Examination of the Vitreous by Biomicroscopy Ultrasound and OCT
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The vitreous is examined biomicroscopically with a 90 or 78 diopter lens, by ultrasound or optical |
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coherence tomography (OCT). If the optical media are clear, a floating peripapillary ring (Martegiani) |
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is a sign for PVD. Preretinal traction may either be recognized by a condensed posterior vitreous or |
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a distortion of the underlying retina. |
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With ultrasound (USG), different vitreous densities can be demonstrated (Figures 8-1A and B). |
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The border between vitreous-cortex and posterior hyaloid are characterized by a fluctuating structure |
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particularly in cases of PVD where cellular precipitates are enhancing this border. Vitreous tractions |
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inserting in the retina in retinal detachments can be visualized by ultrasound even in the presence of |
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cloudy optical media (Figure 8-2). |
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The OCT yields high resolution images of retinal structures. Clear optical media and cooperative |
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patients are required in order to perform this examination. With this technique retinal thickness and |
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ultra-structure of the retina with its different layers can be demonstrated as well as the posterior |
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vitreous and vitreo-retinal tractions (Figure 8-3). |
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Additionally, the posterior vitreous is also visualised during pars plana vitrectomy (Figure 8-4) |
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using a white angle viewing system such as the binocular indirect ophthalmoscope (BIOM) which |
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Retinal Stress by Vitreous Traction
FIGURES 8-1A AND B: (A) Ultrasound: opacification of the vitreous cavity, the vitreous is attached, but no focal vitreous traction is visible; (B) Ultrasound: focal vitreoretinal traction
FIGURE 8-2: Fundus image; due to vitreous hemorrhage the retina is not visible in detail
allows good fundus overview.
The posterior pole can be examined using a Kilb contact lens which has only a small viewing angle but greatly enhances fine preretinal structures, such as a Martegiani ring and tractions induced by suction with a vitreous cutter. The extent of a posterior vitreous detachment can thus easily be recognized. Furthermore, dyeing of the border layers using triamcinolone can help judging whether a posterior vitreous detachment is present or not (Figure 8-5).
PosteriorVitreousAdherenceinProliferativeDiabeticVitreoretinopathy
Since 1999, the presence or absence of a PVD was documented in all 3300 vitrectomies performed at 87