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Nonpenetrating glaucoma surgeries include several different, but related, surgical techniques, including sinusotomy, ab externo or external trabeculectomy, deep sclerectomy with or without implants, and viscocanalostomy, all of which target the site of maximum outflow resistance.
Aqueous egress occurs at the level of SC and its efferents, and the selective removal of the inner wall of Schlemm's canal and the adjacent trabecular meshwork results in increase in outflow facility.
The retained intact membrane (comprised of the anterior and posterior trabecular meshwork, the internal endothelium of Schlemm's canal and Descemet's membrane) results in residual outflow resistance thereby minimizing complications and improving safety.
Absorbable and nonabsorbable implants may be used to maintain the intrascleral bleb, and to avoid a secondary collapse of the superficial flap over the TDM, thereby allowing optimal filtration.
In primary open-angle glaucoma (POAG), the primary outflow resistance is located within the trabecular meshwork(TM), and therefore, nonpenetrating glaucoma surgeries, based on the selective microsurgical dissection of trabecular meshwork, have become the focus of attention among glaucoma surgeons for the past two decades.
Nonpenetrating glaucoma surgeries include several different, but related, surgical techniques, including sinusotomy, ab externo or external trabeculectomy, deep sclerectomy with or without implants, viscocanalostomy, and canaloplasty.
The optimal surgical algorithm for these surgeries is still under refinement, and there is insufficient evidence about their mechanism of action, and aqueous outflow mechanisms. There is however, sufficient evidence to establish them as an important therapeutic option for patients of open-angle glaucoma, in terms of both efficacy and safety.
Nonpenetrating glaucoma surgeries are based on two essential principles:
Aqueous egress occurs at the level of SC and its efferents, and the selective removal of the inner wall of Schlemm's canal (SC) and the adjacent trabecular meshwork results in an increase in outflow facility ( Fig. 96-1 ).
The retained intact membrane (comprised of the anterior and posterior trabecular meshwork, the internal endothelium of Schlemm's canal and Descemet's membrane) results in residual outflow resistance thereby minimizing complications like hyphema, choroidal effusions, shallow anterior chamber, postoperative infections and cataract formation.
Sinusotomy was first described by Krasnov and consisted of excising the bulk sclera overlying Schlemm's canal, on the assumption that the maximum resistance to aqueous outflow was at the level of scleral aqueous veins. The trabecula and inner wall of SC were left in situ.
Zimmerman proposed ‘ ab-externo trabeculectomy ’, the removal of the juxtacanalicular (JXT) meshwork and the inner wall of SC under a scleral flap to decrease aqueous outflow resistance. Deep sclerectomy, as performed by Fyodorov and Koslov, consisted of removal of corneal stroma behind the anterior trabeculum and the Descemet membrane under a scleral flap.
Modern day nonpenetrating deep sclerectomy combines both of these procedures, and its complete nomenclature therefore is ‘ deep sclerectomy with external trabeculectomy ’.
Viscocanalostomy, developed by Stegmann, involves the additional injection of viscoelastic substance in the SC ostia in order to dilate it, together with removal of a homogenous external trabecular membrane. The aqueous filters through the trabeculo-Descemet’s membrane (TDM) into the intrascleral space, as in deep sclerectomy; but as the superficial scleral flap is tightly closed, no intrascleral bleb results. From the intrascleral space, the aqueous humor is presumed to reach SC ostia, and from there into the aqueous episcleral veins.
Canaloplasty is a modification of the older viscocanalostomy in which a microcatheter is used for circumferential viscodilation and tensioning of Schlemm's canal, instead of clearing only a segment. After 360 degrees of canal cannulation, a 10-0 prolene suture is inserted and the ends tied together to provide tension to the inner wall of the canal and the associated trabecular meshwork. This suture tension is presumed to stretch the trabecular meshwork, resulting in an increase in the outflow facility.
The trabecular meshwork is a porous structure that bridges the scleral sulcus, converting it into a circumferential channel, called the Schlemm's canal. The TM consists of connective tissue surrounded by endothelium and is divided into three components: uveal meshwork, corneoscleral meshwork, and juxtacanalicular meshwork.
The uveal meshwork extends from the iris root and ciliary body to the peripheral cornea, and consists of bands of connective tissue, with irregular openings that measure between 25 to 75 microns. It forms the lateral border of the anterior chamber.
The corneoscleral meshwork is the most extensive portion of the TM and is composed of perforated sheets that become progressively smaller as the SC is approached. It extends from the scleral spur to the anterior wall of the scleral sulcus.
The juxtacanalicular meshwork is the outermost part of the TM, and consists of a layer of non-fenestrated connective tissue lined on either side by endothelium. The outer endothelial layer comprises the inner wall of SC.
The outermost juxtacanalicular or cribriform region has several cell layers immersed in a loose web of extracellular matrix (ECM) which contains basement membrane material, proteoglycans, and glycosaminoglycans, providing significant outflow resistance. The matrix has no collagenous beams, but small tortuous aqueous pathways (that appear as empty spaces) have been noted under electron microscopy.
SC endothelium, surrounded by connective tissue like a vein, has the highest hydraulic conductivity of any endothelium in the body. It constitutes a leaky lining probably because of the numerous micron-sized transcellular pores in the endothelium and the associated giant vacuoles. It has several internal collector channels and is connected to episcleral and conjunctival veins through the external collector channels, the intrascleral venous plexus, the deep scleral plexus, and the aqueous veins.
The ‘conventional’ outflow pathway (via the anterior chamber to the trabecular meshwork, SC, and collector channels) accounts for 70% of aqueous outflow. The remaining 30% is attributed to the uveoscleral, or ‘unconventional,’ outflow pathway, which is a passive fluid movement into the ciliary muscle, and then through the supraciliary space and across the anterior or posterior sclera, through the emissarial canals around the vortex veins, or into the choroidal vessels.
In humans, 75% of the resistance to the aqueous humor outflow is localized to the TM and 25% beyond SC, in the outer wall of SC or tissue surrounding it. The major site of resistance within the TM structure is yet to be accurately determined, but most investigators agree that up to 75% is localized in the JXT portion.
The major mechanisms through which resistance across the conventional outflow pathway may be regulated are:
The Schlemm's canal, normally, is not known to be the site of considerable outflow resistance. As IOP increases, however, the TM expands into the lumen of the canal, causing its concomitant narrowing, with a significant increase in outflow resistance. It is also postulated that a safeguard against this collapse and collector channel occlusion is provided by the collagenous septae between the inner and outer walls.
The collapse of SC may be considered contributory to the increase in outflow resistance, though the evidence for this is not conclusive.
Deep sclerectomy with external trabeculectomy may function via a variety of possible mechanisms: removal of JXT tissue; vaulting of residual trabecular meshwork toward the intrascleral cavity leading to widening of the cribriform interspaces; and development of new aqueous veins in the intrascleral space ( Fig. 96-2 ).
Viscocanalostomy involves the injection of a high-molecular-weight viscoelastic in the ostia of the open SC to dilate the canal. Several mechanisms are presumed to increase aqueous outflow: drainage from dilated SC to capillaries and veins within the intrascleral canals and episcleral veins as well as focal ruptures in the inner and outer endothelial walls of the canal; extending into the JXT and direct communication of the juxtacanalicular extracellular spaces with the lumen of SC ( Fig. 96-3 ).
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