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

The basic LASIK procedure is based upon concepts and patients operated on by Barraquer.36 During the procedure, a lamellar corneal flap must be made to allow intrastromal ablation by the excimer laser beam. In order to obtain a consistent flap of the optimal thickness, the cornea is stabilized by a suction ring which is placed just behind the limbus and which sucks the anterior segment into a vacuum device firming the eye and the cornea. This device, the suction ring, has not changed in basic principle in the last 35 years. The following sequence of events might occur during the LASIK procedure. When the suction ring induces an increase in IOP (65 mmHg) and after that it is suddenly released, the anterior segment is rapidly drawn into a vacuum chamber with it’s shape changed rapidly, and all structures posterior to the suction ring are also compressed and decompressed in sequence. This type of “trauma” is in some ways analogous to what happens in a closed eye injury37-38 (“closed-suction injury”). A mechanism for development of peripheral retinal tears or macular disease could be anterior-posterior compression and expansion. The eye elongates along the anterior-posterior axis and the diameter of the globe may increase. At the same time, because the eye is a closed system, the eye is constricted in the equatorial plane (Figure 7A). As the anterior segment is drawn into a vacuum, the lens may be displaced forward along with the anterior hyaloid. This might accelerate vitreous detachment or cause traction at the vitreous base. When the suction suddenly is released, decompression leads to a dynamic overshoot with equatorial expansion and shortening in the anterior-posterior dimension (Figure 7B). These events may cause acute vitreo-retinal traction at the vitreous base and posterior pole.

Lens displacement could be responsible for cases of cataracts after LASIK. During compression there is traction posteriorly that may be responsible for the anecdotal reports of macular holes and macular hemorrhages. It is possible that there is deformation and traction near the vitreous base, which lies just posterior to the suction ring, this can be a cause of retinal breaks. We have measured the marks left immediately after the suction ring is applied in the sclera and its posterior border is at a mean of 4-mm posterior to the limbus. The elevation in IOP as well as the potential for deformation of the globe in the macula might also lead to exacerbation of macular pathology that can be present in high myopes such as defects in Bruch’s membrane (lacquer cracks).

Another potential source of damage to the vitreous and retina is from the pulsed energy applied to the cornea (Figure 7C). The excimer laser light ablates tissue; energy is released anteriorly as a plume of ablated tissue and is thrown into the air in front of the cornea. In addition, it has been reported that particulate mater was ejected from the cornea for up to 18 inches. Certainly such a powerful force might also be associated with backwards force into the vitreous. Hahn et al showed that most of the ablation particles seen to be launched in the air are water spherules. The particle diameter is 100-800 microns.39 Posteriorly, energy is transmitted in the form of a shockwave on the order of 10 atmospheres of pressure (Seiler and Krueger, unpublished observations). The effect of shockwaves and posteriorly-radiated energy on the vitreous integrity is unknown.

The incidence of vitreo-retinal pathology after LASIK in our studies was 0.06% (annual incidence 0.02%).24 This number is much

lower than the incidence of RRD in myopes in general.32 This finding may be explained by the fact that refractive surgery patients in the institutions involved underwent preoperative examinationsincludingaverythoroughdilated indirect funduscopy with scleral depression and treatment of any peripheral retinal lesion predisposing for the development of a RRD before LASIK. In this study extensive lattice degeneration, flap tears, atrophic holes, and retinal tufts were prophylactically treated regardless of symptoms. Such indication is justified by the fact that vitreo-retinal surgery causes changes in corneal shape thus damaging the refractive surgeon’s results as demonstrated by Azar-Arevalo and Arevalo.40 We suggest that cryopexy, argon laser retinopexy, pneumatic retinopexy or small-guage (25 or 23-gauge) vitrectomy without a scleral band be performed when appropriate because they tend not to change the shape or length of the globe. Another option in case of scleral buckling procedures is to remove the exoplants early, as suggested by Rodriguez and Camacho6, after being sure that all breaks have sealed and that no retinal detachment is present anywhere in the fundus.

We cannot determine whether treatment prophylactically is indicated. At the current time it is not possible to scientifically determine whether peripheral retinal lesions should be treated in a way different from standard practice just because a patient is to undergo LASIK. Mostpractitionerssuggestthatpatients scheduled for LASIK be carefully examined with indirect ophthalmoscopy and scleral depression under pupillary dilatation to detect any myopic peripheral lesion that requires

treatment before LASIK is performed. One could argue that this is prudent in myopes whether or not they undergo LASIK; given the potential of the procedure to exacerbate pre-existing pathology, it might be wise to treat such pathology more aggressively.

Another important factor to take into consideration when we evaluate our state of knowledge in this area is duration of follow up. It is reasonable to expect that the incidence of RRD in the initial cohort of patients that had LASIK will rise with time. It is possible that LASIK induced trauma might accelerate vitreous liquefaction and that over the years these patients might have a higher incidence of retinal detachments and other vitreo-retinal problems. It is equally likely that with the current practice patterns, we ophthalmologist would be unaware of this.

Macular diseases may be a relative contraindication to LASIK. Patients with high myopia and lacquer cracks in the macula are at high risk to develop macular hemorrhage or CNV after the intraocular pressure is raised with the suction ring during the procedure. Patients with angioid streaks and traumatic choroidal ruptures are in the same category of risk. Stage 1 macular holes may progress due to traction in the posterior pole during LASIK. In addition, eyes that are at risk of needing vitreoretinal surgery in the future have a relative contraindication to LASIK. On the other hand, in eyes with stable macular disease (scars), LASIK may be performed depending on the refractive surgeon’s criteria if the patient is aware and accepts his visual acuity limitations.

Summary

Serious complications after LASIK are infrequent. It is very important to inform patients that LASIK only corrects the refractive aspect of myopia. Vitreoretinal complications in these eyes will occur and only careful and large prospective studies in patients can determine if the procedure exacerbates myopic pathology. Such studies will need to be performed using careful prospective examinations including determination of risk factors, echography of the vitreous, indirect ophthalmoscopy and scleral depression and possible photography and angiography of the macula region to determine whether the LASIK procedure itself can exacerbate pathologic changes in the myopic eye. In addition, our studies show that results may be not as good as expected after RRD surgery. Reasons for poor VA include the development of epiretinal membrane, proliferative vitreo-retinopathy, chronicity of RRD, new retinal breaks, and cataract formation. Final VA may be limited by myopic degeneration, amblyopia, or delayed referral to a vitreoretinal specialist.

References

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Introduction

This chapter discusses intraocular hemorrhage of interest to the retina specialist and posterior-segment surgeon, with a focus on vitreous hemorrhage. Issues related to hyphema and other anterior segment hemorrhages will not be discussed. Additionally, small hemorrhages within the retina, most commonly seen with diabetes mellitus and systemic hypertension as well as a myriad of other less commonly associated disorders, will not be addressed, although technically these do qualify as intraocular hemorrhages. Subretinal and suprachoroidal hemorrhages, which are relatively uncommon, also are not covered in this chapter.

A vitreous hemorrhage is one of the most common disorders presenting to a retina practice. Its underlying etiology is variable although most often related to proliferative

diabetic retinopathy. Other pathologies in the differential diagnosis for vitreous hemorrhage include vascular occlusive disease, retinal breaks or tears, a posterior vitreous detachment, exudative macular degeneration, as well as rare neoplasia. Additional uncommon causes of vitreous hemorrhage include trauma, radiation retinopathy, retinopathies secondary to hemoglobinopathies and inflammation. Table 1 lists the etiologies of vitreous hemorrhages, in order of relative incidence.

First, we will discuss the management of patients with vitreous hemorrhage and then discuss the underlying disease states that are the primary pathologies responsible for vitreous hemorrhages. Although this order of presentation may seem backwards, often vitreous hemorrhage requires management without certitude of the underlying pathology responsible, which may be unclear or presumptive (e.g., in the case of diabetes mellitus). Fortunately, the clear media of

intraocular tissues allows the ophthalmologist to often see intraocular pathology directly. Thus ophthalmologists commonly are able to eliminate (or mitigate) the uncertainty of diagnosis much of the time. The patient history, diagnostic testing, and to a lesser extent the physical examination are more critical in managing vitreous hemorrhages than for other ocular conditions that can be visualized directly.

Patient History

Management of a vitreous hemorrhage generally requires more emphasis on the

patient history than in patients with other retinal diseases. For vitreous hemorrhages, the time from onset of symptoms to presentation is typically a matter of hours or days, since hemorrhages are typically, though not exclusively, dramatically symptomatic. With large vitreous hemorrhages, symptoms typically occur suddenly with significant loss of vision; these hemorrhages also typically obscure the view of the examiner as well as the patient. With smaller vitreous hemorrhages, symptoms of black floaters can occur which commonly appear to rise from inferior to superior visual space, secondary to the inverted real image projected on the

retina. Movement of floaters may be reported as resembling air bubbles underwater as in an aquarium, owing to the blood’s circuitous track in the irregularly syneretic vitreous body. Some patients report symptoms as a myriad of small objects obscuring vision in the affected eye, or looking through a screen door or window (Figure 1).

Pain is universally absent with the exception of patients for whom the etiology is trauma, which would be generally obvious from the history. A history of any known ophthalmic disease should be elicited. Review of the patient’s medical history may include a pre-existing ocular disease such as recent ophthalmic surgery, diabetic retinopathy or

ocular neoplasm. Often, however, no such history is reported, with the common exception of diabetes mellitus. In much of the industrialized world, undiagnosed diabetes mellitus is relatively unlikely if effective widespread screening has been conducted. However, in the United States routine screening for diabetes mellitus is not extensive due to high costs, and in much of the developing world screening is generally unavailable. In any case, eliciting a history of diabetes mellitus specifically is critical. If a patient presenting with a vitreous hemorrhage with no known predisposing risk factor responds that he or she does not have diabetes mellitus, followup questioning regarding a family history of diabetes mellitus and the date and method

of the patient’s most recent screening test is important (Figure 2). Such tests can include a routine urinalysis or serum glucose test. Comprehensive questioning regarding routine medications, other health conditions, family history and social circumstance is necessary in essentially all patients; in addition, specific clues regarding thalassemia or sickle cell disease or trait can be particularly helpful in patients with vitreous hemorrhage without an underlying likely etiology. A history of a malignancy or thyroid eye disease may uncover a history of radiation exposure. Multiple risk factors for cardiovascular dis-

ease will increase the likelihood of commonly encountered diagnoses of vascular occlusive disease.

Patients with vitreous hemorrhages who are asymptomatic (and therefore visit an eyecare provider much later than symptomatic patients) typically have underlying ocular pathology. Encountering patients with asymptomatic long-standing vitreous hemorrhages is unusual except for patients with poor acuity associated with a long history of an underlying risk factor for vitreous hemorrhage such as diabetic retinopathy (Figure 3).

Physical Examination

A direct or partial view of the underlying cause of a vitreous hemorrhage can in some circumstances be seen on physical examination. This view is usually available in less severe cases, when the patient may be asymptomatic. Examination alone may establish the diagnosis. Examination usually involves an indirect ophthalmoscope, which can be used with scleral indentation to obtain a kinetic examination of the peripheral fundus and observe clues regarding the presence of a peripheral break or tear if not observable

directly (Figure 4). Caution in this regard is necessary as the lamellar nature of the partially synergetic, gelatinous vitreous can commonly create, in a cleft of syneretic vitreous, the illusion of a break when none actually exists. Alternatively, the slit lamp (biomicroscope) may be used with various lenses capable of providing a highly magnified view of the retina to observe directly the culpable retinal or choroidal neovascularization, for example.

Commonly, however, on examination there is no view of the posterior segment other than that of the hemorrhage. The

hemorrhage typically has a red appearance in the acute phase, and this red color may be preserved in longstanding hemorrhages as well (Figure 5). In long-term hemorrhages, the hemorrhage may appear white or gray after hemoglobin degradation. Often this phenomenon is noted in the inferior vitreous as gravity consolidates the hemorrhage. It may be more difficult to make the diagnosis of vitreous hemorrhage in patients with longstanding disease, and the differential diagnosis in these circumstances may expand to include posterior segment uveitities and neoplasia. Typically blood in the vitreous cavity is removed by macrophage digestion over time.

Patients may notice, and the ophthalmologist may observe on examination, that subtle abnormalities in the vitreous remain after the hemorrhage has cleared, but typically, the hemorrhages are entirely resorbed over time. The patient’s age and the degree of vitreous syneresis influence the time needed for resorption. Other factors which affect the speed of resolution (also related to the extent of syneresis) are refractive error (i.e., vitreous volume), previous vitreous surgery or procedures, and the presence of comorbid inflammation. The etiology of the inflammation also must be considered as it may be secondary to the underlying etiology of