The role of inflammation in CW Nd:YAG contact transscleral photocoagulation and cryopexy.

Cyclodestructive modalities in humans have been shown to be effective when applied 3.5 mm or more posterior to the limbus. Therefore, CW Nd:YAG contact transscleral laser and cryopexy were applied 6 mm posterior to the limbus of pigmented rabbits. The intraocular pressure (IOP), flare, iritis, cells and conjunctival hyperemia were monitored clinically up to 3 weeks. The pressure lowering effect was -7.5 +/- 7.7 mm Hg for laser retinopexy and -14.2 +/- 6.0 mm Hg for retinocryopexy at 3 weeks and was comparable to application of the same modalities directly over the ciliary body. Similarly, induction of intraocular inflammation by injecting 10 micrograms of endotoxin intravitreally lowered IOP significantly. These findings suggest that hypotension may not be directly due to cyclodestruction but may be related to the ocular irritative response and extent of neuroepithelial defect, irrespective of its distance from the limbus.

A comparison of CW Nd:YAG contact transscleral cyclophotocoagulation with cyclocryopexy.

The cyclodestructive and inflammatory effects of CW Nd:YAG contact laser were compared to those of conventional cryopexy. CW Nd:YAG light transmitted by fiber optic cable and sapphire crystal was applied transsclerally to the ciliary body of pigmented and albino rabbits. Cyclocryopexy was given to a comparable second group. The intraocular pressure (IOP), flare, iritis, cells and conjunctival hyperemia were monitored clinically up to 3 weeks. The breakdown of the blood-aqueous barrier and time course of ocular inflammation was similar for both modalities and IOP was -12.2 +/- 4.2 mm Hg for laser cyclopexy and -15.1 +/- 5.4 mm Hg for cyclocryopexy at 3 weeks. Ciliary body lesions were noted in both groups. Overall, albino rabbits showed less histological damage and faster recovery of IOP. Contact cyclophotocoagulation and cyclocryopexy can be considered models of ocular injury. The similarities in ocular irritative response suggest a similar pathophysiologic mechanism underlying the pressure behavior in both thermal mode injuries.

Endothelial repair following Nd:YAG laser injury.

Effects of different energy levels (1.2, 2.0, 2.8, 4.0 mj) of a mode-locked Nd:YAG laser beam focused directly on the corneal endothelium were evaluated in rabbit, cat, and owl monkey. The endothelial lesion observed by specular microscopy at 10 min; 8, 16, and 24 hr; 3, 5, 7, and 21 days measured up to 0.8 mM in diameter. It showed focal destruction of Descemet's membrane and a larger area of endothelial denudation corresponding probably to the shock wave generated by the plasma. The size of the defect correlated with the amount of energy delivered. Even though healing was characterized by a phase of rapid endothelial migration during the first 24 hr, only about one-half of the defect was covered after 1 week in all animals. This lesion persisted with minimal endothelial proliferation for 3 weeks in the rabbit and for 3 months in the cat. The monkey was followed for only 1 week. Our findings indicate that the laser-tissue interaction is different from mechanical or thermal modes of injury and interferes with the specific endothelial functions in repair.

Changes in aqueous outflow after in vitro neodymium: yttrium aluminum garnet laser cyclophotocoagulation.

To examine the possible role of transscleral outflow routes, enucleated human and porcine eyes underwent noncontact neodymium:yttrium aluminum garnet (Nd:YAG) laser cyclophotocoagulation 3 mm posterior to the limbus. Pars plana lesions were verified histologically. The eyes were perfused with saline solution at 50 mm Hg perfusion pressure, placing the tip of the needle into the hyaloid orbicular space. The outflow facility was 0.072 microliter/min/mm Hg in paired controls and 0.105 microliter/min/mm Hg in human lasered eyes, a difference of 31%. In porcine eyes the difference was 43%. Since concepts of aqueous production, impaired circulation, and inflammation do not apply to enucleated eyes, the increase may be related to pars plana transscleral flow facilitated by disruption of the neuroepithelial barrier.

Interaction of ultraviolet laser light with the cornea.

The effect of pulsed ultraviolet (UV) laser light on the cornea depends on wavelength (photon energy), irradiance (photon flux), and pulse firing rate. At the available excimer laser wavelengths of 193, 249, 308, and 351 nanometers, the authors have varied the irradiance per pulse (10 to 2000 mj/cm2) as well a pulse frequency (1, 10, 25 Hz) and determined the thresholds for coagulation and ablation of the corneal stroma. The latter ablative action creates a groove resembling an incision and was present at all wavelengths studied. The threshold for ablation increased for longer wavelengths and lower pulse frequencies, except for 193-nm exposure, which was characterized by a constant threshold independent of laser pulse rate. The grooves at 193 nm were both biomicroscopically and histologically smooth and no coagulation effects were noted. Some degree of coagulation of adjacent tissues was noted at 249, 308, and 351 nm.

The role of the vitreous in the intraocular pressure rise after neodymium-YAG laser capsulotomy.

Autologous liquid vitreous injected into the anterior chamber of the phakic owl monkey eye leads to markedly increased intraocular pressure (IOP) peaking at one to two hours. In contrast, neodymium-YAG laser shock waves focused in the center of the anterior chamber of the same animal led to a mild decrease in IOP. Debris produced by laser pulses focused on the residual cortex of owl monkey eyes that had undergone extracapsular surgery failed to increase the IOP. Similarly, injection of dialyzed vitreous did not have any significant influence on IOP. We conclude that the disruption of the integrity of the anterior cortical gel and the subsequent release of a dialyzable intravitreal substance with a molecular weight of less than 10,000 daltons into the anterior chamber may contribute to the IOP rise after surgical discission, including neodymium-YAG laser posterior capsulotomy.

A history of intraocular pressure rise with reference to the Nd:YAG laser.

The rise in intraocular pressure after Nd:YAG laser capsulotomy is presently thought to be due to laser specific shockwaves and debris. Glaucoma has also been a frequent complication of mechanical discission as shown by a review of 84 cases from 1865-1932. Most authors have ascribed the pressure rise to vitreous or a quality of vitreous. Focusing on the disruption of the barrier between aqueous and vitreous as a common link between knife and laser discission, an attempt is made to combine the historical and recent views. It appears that apart from radiation effects, the Nd:YAG laser functions as a sharp knife and therefore shares the complications of mechanical discission, namely, glaucoma, injury to the vitreous and retinal detachment.

Postsurgical hypotony: relationship to fistulization, inflammation, chorioretinal lesions, and the vitreous.

Hypotony is a natural occurrence, symptom, and complication of surgical treatment. With more sophisticated and aggressive techniques, postsurgical hypotony recently has been given increased attention as an obstacle to success of surgery for glaucoma and retinal detachment. Whereas two standard deviations below normal pressure (15.9-5.8 = 10.1 mm Hg) can be called hypotonous, most eyes, depending on scleral rigidity, lid pressure, eye rubbing, or corneal or retinal edema, will be symptomatic at < 5 mm Hg. Hypotony can be defined as the low pressure (whether acute, transient, chronic or permanent) which, in an individual eye, leads to functional changes (whether asymptomatic or symptomatic) and structural changes (whether reversible or irreversible). Depending on its duration and degree, postsurgical hypotony produces characteristic tissue changes that often are modified by, but separate from, the tissue changes caused by an underlying disease or its surgical treatment. This review summarizes the situations, variably associated with hypotony, that occur after such interventions as cataract extraction, filtering surgery, cyclodialysis, cyclodestruction, and vitreoretinal surgery, in addition to the reported pathomechanisms of hypotony and its proposed treatments.

Neurilemmoma of the anterior ethmoidal nerve encroaching upon the nasolacrimal duct.

The clinical, light microscopic, ultrastructural, and immunohistologic findings of a neurilemmoma encroaching upon the nasolacrimal duct are presented. This is the first reported case of this rare tumour of the nasolacrimal duct where the diagnosis has been confirmed by electron microscopy and immunohistochemical techniques.

Retinotomy and silicone oil for detachments complicated by anterior inferior proliferative vitreoretinopathy.

AIM: To describe a subset of patients with recurrent retinal detachments caused by anterior intraretinal and subretinal proliferative vitreoretinopathy (PVR), which required greater than 180 degrees retinotomy and silicone oil tamponade. METHODS: Interventional case series. Forty-one patients underwent >180 degrees retinotomy, anterior retinectomy, removal of subretinal membranes, laser to the retinotomy edge and silicone oil tamponade. Risk factors for detachment, prior surgical history and PVR location were examined. Main outcomes included change in visual acuity, recurrent detachment and postoperative complications. RESULTS: Cataract extraction (49%), high myopia (29%) and lattice degeneration (27%) were preoperative risk factors. The average number of prior procedures for retinal attachment was 2.3 (SD 0.9). The majority of detachments were inferior and related to anterior intraretinal and subretinal PVR. Twenty-four patients (59%) saw 20/200 or better. Eleven patients (27%) had poor vision (<20/400) at the end of follow-up. Thirty-seven retinas (90%) remained attached. Increased rates of postoperative corneal decompensation (p<0.0001) and silicone oil in the anterior chamber (p<0.0001) were statistically significant markers of poor visual outcome. CONCLUSIONS: Patients with complex PVR requiring a large retinotomy often had similar presurgical conditions. A large inferior retinotomy effectively addressed proliferations where they most frequently occur, and silicone oil was beneficial.

Cystoid macular edema: the apparent role of mechanical factors.

CME is the final common pathway of many intraocular and systemic diseases. It involves the retinal vasculature and often has a choroidal and vitreal component. Obviously, at some level of this complex pathophysiological process, mediators must be involved. The question is whether the characteristic distribution of vascular leakage and retinal edema is best explained by the diffusion of mediators released by from a remote site, as proposed by Miyake (see Miyake et al., 1989), or whether it reflects the distribution of pre-existing anatomical structures causing the local release of mediators by exerting mechanical stress. The fact that vitreous adhesions are present at the lens and vitreous base anteriorly and at the major vessels, optic disc, and macula posteriorly support the mechanical concept. The anatomic sites of vitreo-retinal attachments have in common the thinness of their basal lamina and firmness of their fibrous vitreal attachments to the Muller cells. Although adhesion at two opposite sites is the precondition for the development of traction, it will only be generated through intrinsic or extrinsic pathologic changes in the vitreous. In a normal anatomical situation, many vitreous fibers distribute tractional forces evenly to numerous Muller cell attachments. In partial PVDs, fewer fibers and Muller cells endure most of the traction. This may lead to chronic Muller cell irritation and local release of a variety of mediators which, in turn, may facilitate vascular leakage. Vitreous shrinkage and possibly chronic Muller cell irritation may, therefore, facilitate abnormal leakage at all sites of attachment. A typical example is pars planitis, with leakage at the peripheral retina and around major blood vessels, the disc and macula. This pattern of leakage suggests that vitreous traction may be a co-factor in many cases. Most traction develops slowly, passing through stages of partial PVD. The occurrence of a traumatic macular hole and vitreous base avulsion as a result of trauma is the exception. While the pattern of PVD in vivo has not been investigated in detail, PVD with normal adhesions is frequently found in age-related liquefaction and collapse of the vitreous. PVD with abnormal adhesions and shrinkage is found in association with diabetes, proliferative vitreoretinopathy, and inflammation. As to the macula itself, two types of attachment are suggested, a firm central foveolar attachment and a larger, weaker perifoveal attachment, corresponding to the nuclear and cortical vitreous and to two types of pathologic traction; anteroposterior and tangential.(ABSTRACT TRUNCATED AT 400 WORDS)

Intraocular pressure after peripheral retinal cryopexy in normotensive human eyes.

Intraocular pressure (IOP) was measured before and after peripheral retinal cryopexy given for lattice degeneration and small retinal breaks. During the period of observation the IOP of treated eyes decreased, suggesting that freezing of areas remote from the ciliary body may lower IOP through mediation and/or transscleral outflow.

Noncontact and contact pars plana transscleral neodymium: YAG laser cyclophotocoagulation in postmortem eyes.

Transscleral neodymium:YAG (Nd:YAG) laser energy (5 J), noncontact at 20 msec and contact at 0.5 sec exposure time, was applied to enucleated porcine and human eyes 3 mm posterior to the limbus. Coagulative pars plana lesions were noted in all cases. Related to focus and exposure time, noncontact lesions were larger, more homogeneous, and affected primarily the pigment epithelium, whereas contact lesions showed more full-thickness thermal effects, including sclera. Because the corona ciliaris was unharmed when laser applications were made 3 mm from the limbus, this commonly used clinical focus raises questions about cyclo "destruction." Future clinical research will have to show which phenotype of pars plana lesion correlates best with long-term lowering of pressure.

Vitreoretinal changes associated with rise in intraocular pressure after Nd:YAG capsulotomy.

In a chart review of 100 consecutive Nd:YAG laser capsulotomies, six presumed risk factors of the rise in intraocular pressure (IOP) after capsulotomy were identified. A group of 15 patients in which the pressure rose to at least 10 mmHg above baseline postoperatively showed a significant (P less than or equal to 0.01) association with myopia, vitreoretinal disease, and vitreous prolapse into the anterior chamber. The previously known association of high pressures with glaucoma, a large capsular opening, or absence of a posterior chamber lens were also confirmed. There was no correlation between the energy used and IOP. These retrospective findings are suggestively consistent with the concept that injury to a liquefied vitreous may contribute to the IOP rise after capsulotomy.

Schisis-like rhegmatogenous retinal detachment associated with choroidal colobomas.

BACKGROUND: The breaks that cause retinal detachments in colobomatous eyes are often hidden within the lesion and difficult to find. METHOD: To elucidate the pathoanatomy and possible pathomechanism of such detachments, histological sections of eight choroidal colobomas were reviewed. RESULTS: Sections of the margin showed central continuation of the inner neuroblastic layer (the intercalary membrane) and eversion and separation of the outer neuroblastic layer. The opposite direction of continuity of the neuroblastic layers created a schisis-like configuration between the intercalary membrane and the everted outer retina. The zone of duplication was a point of retinal adhesion, but also a locus minoris resistentiae due to vitreous attachments and variable glial support at the margin. CONCLUSION: The subset of coloboma-associated retinal detachments requires both a central break in the inner layer and a break in the outer layer at the margin of the coloboma. The inner layer break may be precipitated by retinovascular ischemia or scleral stretching; that in the outer layer may be caused by vitreous traction on the margin of the coloboma or extension of the formerly isolated detachment through the outer marginal zone of decreased glial support.