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

Figure 10: Alternating suction and back-flushing facilitates clearing of the subretinal hemorrhage.

As previously mentioned macular hemorrhages in trauma can be located in different levels, so it can happen that part of the blood is localized in the retinal tissue. It is important to recognize these variants in these cases, because the surgeon must limit himself to attempting to extract only blood localized between the neurosensory retina and the retinal pigment epithelium. In patients who present with hemorrhages older than 7 days, it is possible to see

a yellowish change in the color of the blood (Figure 11).(47)

Figure 11: Fundus photograph of a young man who sustained blunt trauma to the right eye 20 days before. There is a choroidal rupture with a secondary subretinal hemorrhage (arrow).

After extracting the subretinal blood, the peripheral retina is inspected looking for holes or tears. In case any are found, we apply cryotherapy to the lesions. The placement of a scleral buckle is not necessary.

Finally a complete air-fluid exchange is made (Figure 12). The application of endolaser burns is not necessary unless the retinotomy is extensive and the surgeon considers there is a risk for retinal detachment. If the eye is phakic, we generally use a non expandable concentration of SF6 (18%). In aphakic or pseudophakic eyes we use 14% C3F8. Some authors have reported the use of air only, without an expandable gas mixture for postoperative tamponade.(23) Finally, the sclerotomies are sutured.

Postoperatively, the fundus is evaluated to detect the presence of recurrent bleeding. Remainingbloodremnantsgenerallydisappear after 2 weeks. As the gas bubble disappears, the peripheral retina must be carefully observed looking for subretinal fluid that can mean a tear or a peripheral hole. Visual acuity tends to improve after the first or second postoperative month (Figure 13a-c).

It is very important to discuss preoperatively the risk/benefit ratio of this surgery with the patient and his family. The more frequent complications of this kind of surgery include retinal detachment and postoperative cataract formation. Retinal detachment has been reported mainly in the cases in which extensive retinotomies were necessary.(31,33)

Lewis(38) suggests that tPA usage can decrease the presence of retinal detachment due to the smaller retinotomy that is necessary in these cases. Nevertheless, Moriarty(48) reported retinal detachment in 13% of the operated cases (15 patients) still with the usage of tPA. Cataract formation is a complication of vitrectomy, and is more frequent in patients older than 50 years of age.

McCannel et al(49) has reported the case of a patient in which choroidal neovascularization formation appeared in the retinotomy site made for the surgical removal of a neovascular membrane.

data about the management of this entity deals with SCH associated to intraocular surgery, and must sometimes be transpolated to the management of traumatic SCH.

Pathophysiology

Traumatic events may precipitate SCH by two means:

1. A mechanism unique to penetrating trauma: Trauma with an object that penetrates through the sclera, directly damaging the choroidal vessels, which in turn bleed into the suprachoroidal space, causing a SCH.

TRAUMATIC

SUPRACHOROIDAL

HEMORRHAGE

Suprachoroidal hemorrhage (SCH) is defined as an accumulation of blood within the space between the choroid and the sclera (known as the suprachoroidal space).(50) While normally a potential space, holding a very little amount of fluid (approximately 10 μl), it becomes a true space when filled with fluid or blood, with the scleral spur and the border of the optic disc as its anterior and posterior boundaries, respectively.(51)

Suprachoroidal hemorrhage may have different etiologies, such as blunt trauma, penetrating trauma, or intraocular surgery, the latter being the most frequent cause.(50,51) This chapter will deal with traumatic SCH, which behaves differently from intraoperative or postoperative SCH, although they share some characteristics. Furthermore, most published

2. A mechanism analogous to the one that precipitates SCH associated to intraocular surgery: Penetrating trauma to the anterior or posterior segment may cause the loss of intraocular fluids or tissue, leading to hypotony, which has been deeply implicated in the genesis of SCH. The exact mechanism by which hypotony causes SCH is unclear, but studies have shown the rupture of a necrotic long or short posterior ciliary artery after hypotony.(52) In a rabbit experimental model of expulsive hemorrhage, in which the central cornea, lens and anterior vitreous were removed, four stages in the development of SCH were described: 1) Engorgement of the choriocapillaris, (2) Suprachoroidal effusion, mainly near the posterior pole,

(3) Stretching and tearing of the choroidal vessels as the effusion enlarged, and (4) Massive extravasation of blood into the choroidal space.(53) These findings suggest that hypotony and/or the loss of intraocular tissue, by this mechanism, lead to a chain of events that culminates in SCH.

The genesis of SCH in closed blunt trauma is even less clear, since in theory, intraocular pressure may limit the extent to which the hemorrhage may increase in size. However, it is possible to observe very large SCH in cases in which trauma is purely blunt, without loss of intraocular tissue and/or hypotony. It has been hypotesized that since blunt trauma modifies the shape of the globe (anteroposterior shortening and equatorial expansion),(54) shearing forces are generated that tear and rupture the choroidal vessels, causing SCH.

Diagnosis

Suprachoroidal hemorrhage may be visible by ophthalmoscopic evaluation of the fundus, when the media are transparent enough to do so, in which case it appears as an elevated dome-shaped lesion or lesions at the level of the equator, and sometimes extending posteriorly; they can be small in size (known as “limited” SCH) or very large, with contact of the inner retinal surface of the lesions (known as “kissing”, “appositional” or “massive” SCH).

In most cases, however, traumatic damage to ocular structures (such as corneal opacities, vitreous or anterior chamber hemorrhage, or cataract)makesclinicalevaluationofthefundus impossible, in which case ocular ultrasound images are extremely useful.(55) Ecographic evaluation of a traumatized eye with media opacities must be done as soon as possible in order to evaluate intraocular structures. This procedure can be performed through the lids in eyes with suspected penetrating injury, or directly on the ocular surface.

Ultrasound can give information about the presence of vitreous hemorrhage, retinal detachment, intraocular foreign body, and/or SCH, as well as their extent and localization. Furthermore, it can differentiate if the contents of a choroidal detachment are hemorrhagic or serous in nature. In cases of SCH, a domeshaped separation of the choroid from the sclera is observed, and the suprachoroidal space is filled with hyperechoic signals denoting the presence of blood.

Ultrasound is also a very valuable tool for the evaluation of the liquefaction of suprachoroidal blood, which is of paramount importance to plan a drainage surgical procedure, since the blood must be liquefied in order to be drained. Early after trauma, suprachoroidal blood is seen as hyperechoic signals of irregular internal structure, indicating the presence of a disorganized clot (Figure 14). After some days, the intensity of the signals is lower and more regular, indicating the beginning of liquefaction (Figure 15). After more days, the ultrasound image of suprachoroidal blood is homogenous, withlow-reflectivemobileopacities.(55) Thetime from the appearance of SCH to liquefaction has been reported to be between 7 and 14

days.(51, 54-58)

Computed tomography(59, 60) and magnetic resonance imaging(61, 62) have also been found of aid in the diagnosis of SCH, allowing even for the differentiation between serous and hemorrhagic content, as well as other features. However, the amount of information that can be obtained from these diagnostic studies is still limited when compared to ultrasound. Furthermore, magnetic resonance

imaging is contraindicated in cases where a metallic foreign body is suspected.

Management

Management of traumatic SCH is somewhat similar to the management of intraoperative or delayed SCH. In fact, most of the criteria and techniques applied to the management of traumatic SCH must be transpolated from information available from non-traumatic SCH. The management of traumatic SCH depends on several factors, including the need to manage other lesions in the traumatized eye, the extent of the SCH (limited vs massive), and characteristics of the hemorrhage (solid clot vs liquefied hemorrhage).

Indication for Surgery

Limited or localized SCH (sometimes called suprachoroidal hematoma) most of the times does not require any surgical management, since the blood clot will liquefy and reabsorb in the matter of weeks (Figure 14).(63) If a patient needs surgical management for other ocular lesions, (e.g. cataract, retinal detachment, etc), no surgical maneuvers are performed to drain the SCH, since these maneuvers themselves may cause more damage to the eye.

Indications for surgical drainage of traumatic SCH include appositional configuration, and other indications for vitreoretinal surgery not directly related to SCH,

such as the presence of retinal detachment (Figure 16), vitreous hemorrhage, intraocular foreign body, retained lens material, etc, in which the size of the SCH is so large as to limit the intraoperative maneuvers.

The presence of appositional configuration has been traditionally regarded as the main indication for SCH drainage (Figure 17), since it has been reported that adherence of the retina may occur after apposition.(64) This view, however, has been challenged by other authors, who followed clinically and ecographically the natural history of appositional SCH of various etiologies in 18 patients, and found that apposition lasted for 10 to 25 days, and after that the hemorrhage reabsorbed without any sign of persistent retinal adherence.(55)

Regardless of the presence or absence of persistent retinal adherence, appositional configuration has been found in other studies to be a sign of bad prognosis. Reynolds et al reported the outcome of 20 eyes with appositional SCH.(57) Thirteen of these eyes underwent surgical drainage while the rest remained in observation. Forty six percent of the eyes that underwent surgery achieved visual acuity of 20/200 or better, compared to 0% of the ones that had no intervention. Scott et al reported a study in 51 eyes with appositional SCH, and found a negative correlation between duration of apposition and final visual acuity.(65) Other studies, although performed on postoperative rather than traumatic SCH, found that the presence and duration of apposition resulted in worse prognosis.(66,67)

Timing of Intervention

The timing between the appearance of SCH (which usually is the time of the traumatic event) and the surgical drainage is of paramount importance, since during the first days after trauma, blood within the suprachoroidal space is forming a clot,(55) which is very difficult to drain through a sclerotomy. Most authors agree that surgical drainage must be delayed 7 to 14 days or until ecographic evidence of clot lysis.

If other procedures (such as wound closure, etc) need to be urgently performed in a traumatized eye that also has considerable SCH, the drainage of the SCH must be delayed, since most attempts to drain a SCH before it has liquefied are usually unsuccessful, and surgical maneuvers to this effect most often result in further damage to the globe.(51)

Surgical Technique

Traumatic SCH is frequently associated to posterior segment pathology, such as vitreous hemorrhage, retinal detachment, subretinal hemorrhage, luxated lens or lens fragments, intraocular foreign body, retinal incarceration in the wound, etc., that need to be addressed during the same surgical procedure. For this reason, most of the times its management requires a vitreoretinal approach.

The first surgical objective is to create a drainage sclerotomy. The placement of the sclerotomy is very important, and should be placed in a quadrant where the SCH is largest,

551

in order to avoid damage to the inner choroid or to puncture the retina. The sclerotomy is usually created at approximately 6 mm behind the limbus with a 20G MVR blade, and can be orientated perpendicular or parallel to the limbus. A well-placed sclerotomy in an eye with a well-liquified SCH should result in immediate egress of suprachoroidal blood through the sclerotomy. The blood should be purple-brown in color (Figure 18).

The second surgical objective is to pressurize the vitreous cavity, and this can be achieved in several ways, depending on the extent of the SCH:

1.Anterior chamber infusion: If there is a very large SCH that totally precludes a pars plana incision, an infusion must be placed in the anterior chamber. This can be done by creating a clear corneal incision with a 15° blade, and placing an anterior chamber maintainer or a 23G infusion cannula. Since most patients are pseudophakic or aphakic, balanced saline solution (BSS) freely flows to the vitreous cavity. This can also be done, however, in phakic patients, since BSS can also flow through the zonular ligaments, although sometimes the anterior chamber deepens before this happens, resulting in zonular weakness (Figure 19).

2.Pars-plana infusion: If the SCH is limited to some quadrants, one quadrant may be available for the placement of a pars plana infusion, 3 to 4 mm behind the limbus, using a 6 mm infusion cannula. This procedure, however, carries some risks. In the presence of SCH, the pars plana, retina and vitreous base are not in their normal