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   Table of Contents      
ORIGINAL ARTICLE
Year : 2001  |  Volume : 49  |  Issue : 4  |  Page : 255-9

The trabecular meshwork in acute and chronic angle closure glaucoma.


Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS, Ansari Nagar, New Delhi, India

Correspondence Address:
R Sihota
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS, Ansari Nagar, New Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 12930118

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  Abstract 

PURPOSE: To determine the effect of acute and chronic primary angle closure glaucoma (PACG) on the trabecular meshwork. METHODS: Trabecular specimens of 16 consecutive patients with primary angle closure glaucoma (PACG)--6 acute PACG eyes, and 10 chronic PACG eyes without an acute attack--were studied by light and electron microscopy. RESULTS: Acute PACG: The trabecular meshwork revealed a generalised oedema and an accumulation of pigment in the widened trabecular spaces and Schlemm's canal. Attenuated trabecular endothelial cells appeared to be devoid of subcellular components. Chronic PACG: In chronic PACG eyes the trabecular architecture had lost its regular arrangement, with fewer and narrower trabecular spaces and fusion of the trabecular beams in areas. There were numerous electron-dense bodies in the trabecular tissues, both within the trabecular beams and in the extracellular spaces, which had a banded fibrillar structure. An overall loss of endothelial cells was noted; the remaining cells were crowded together and were polymorphic. Melanin pigment was present both within the stroma and in the endothelial cells. CONCLUSIONS: Pigment accumulation in the trabecular spaces and within the cells and a noninflammatory degeneration appeared to be the primary changes in the trabecular meshwork after acute angle closure glaucoma. In chronic PACG eyes, there was evidence of loss of endothelial cells and reactive repair processes. These changes were present in areas away from visible peripheral anterior synechiae. A gonioscopic evaluation of the extent of peripheral anterior synechiae alone may not reflect the extent of trabecular meshwork damage in acute and chronic PACG. Patients experiencing an acute attack of PACG require a long-term follow up, because the intraocular pressure (IOP) may rise later, due to ongoing changes compromising the outflow facility, or due to the effects of aging in the trabecular meshwork.

Keywords: Acute Disease, Chronic Disease, Female, Glaucoma, Angle-Closure, pathology, surgery, Humans, Male, Microscopy, Electron, Middle Aged,


How to cite this article:
Sihota R, Lakshmaiah N C, Walia K B, Sharma S, Pailoor J, Agarwal H C. The trabecular meshwork in acute and chronic angle closure glaucoma. Indian J Ophthalmol 2001;49:255

How to cite this URL:
Sihota R, Lakshmaiah N C, Walia K B, Sharma S, Pailoor J, Agarwal H C. The trabecular meshwork in acute and chronic angle closure glaucoma. Indian J Ophthalmol [serial online] 2001 [cited 2019 Dec 7];49:255. Available from: http://www.ijo.in/text.asp?2001/49/4/255/14692

Studies of the histopathology of the trabecular meshwork in primary angle closure glaucoma (PACG) have been sparse. The few available reports on PACG, have all reported areas of iris stromal adhesion over the surface of the trabecular meshwork.[1-5] Rodrigues et al also have described reduced or obliterated intertrabecular spaces and a considerable narrowing of the Schlemm's canal.[2] These studies have not examined the different subtypes of PACG, in which the time frame and the magnitude of the intraocular pressure (IOP) rise is significantly different. Acute PACG eyes have a sudden, severe rise in IOP, while in chronic PACG the rise in IOP is prolonged and more moderate. The effect of such variations on the trabecular meshwork would be expected to differ.

We studied the trabeculectomy specimens using both light and electron microscopy, to determine the histopathological changes in the trabecular meshwork of eyes with acute and chronic PACG.


  Materials and Methods Top


Trabecular block specimens were obtained at trabeculectomy from 16 consecutive eyes with clinically confirmed acute or chronic PACG. A trabeculectomy was planned when the IOP was not controlled on topical medications alone; commonly a beta-blocker with either pilocarpine or dorzolamide. All the patients were 55 - 65 years of age, without a history of any other ocular disease or surgery. None of the patients with chronic PACG gave a prior history of an acute attack, and clinical features suggestive of an acute episode were not present.

All patients were administered intravenous mannitol preoperatively, and at the time of surgery all the eyes, had an IOP between 18 and 24 mmHg. During the trabeculectomy, we excised the trabecular block away from the gonioscopically visible peripheral anterior synechiae.

The specimens that contained both the trabecular meshwork and Schlemm's. canal were studied by light and transmission electron microscopy. The tissue for transmission electron microscopy was fixed in buffered glutaraldehyde, processed and embedded in epon resin. Sections 1 μm thick were stained with toluidine blue. The area of interest was identified, the blocks were trimmed, and sections cut and examined on a transmission electron microscope (Philips, Model CM 10, Eindhoven, The Netherlands). All light microscopy specimens were stained with haematoxylin and eosin. We also used elastic van Gieson's stain, to study the elastic and collagenous structures in the trabecular meshwork.


  Results Top


Trabecular specimens from 6 eyes with acute PACG, and10 eyes with chronic PACG without an acute attack met our selection criteria. All the acute PACG patients were female, while 6 of 10 patients were male in the chronic PACG group. The mean age was 61.4 ± 3.2 years. All the acute PACG patients recorded an IOP of 54- 62 mmHg, and a 2-4 day duration of symptoms prior to the surgery. IOP was controlled using intravenous mannitol, maximal medical therapy and topical corticosteroids. The duration of the chronic PACG in nonacute eyes could not be determined. Four chronic PACG eyes had received prior YAG iridotomy.


  Acute PACG Top


The outflow channels of acute PACG eyes had widened spaces between the trabecular beams, with a significant accumulation of pigment granules and occasional red blood cells, seen under both light and electron microscopy [Figure - 1] and [Figure - 2]. Light microscopy showed a swelling of some of the endothelial cells. A number of melanophages were present. On electron microscopy, the long, tapering, attenuated trabecular endothelial cells appeared devoid of subcellular components seen in normal endothelial cells. Desquamated endothelial cells were frequently encountered between the trabecular beams and occasional activated endothelial cells were also seen. The trabecular beams appeared widened with hypodense areas within. The central core of the beam was condensed and electron dense on electron microscopy [Figure - 2]. The canal of Schlemm was open in all eyes, and red blood cells were seen in 3 eyes. Elastic van Gieson staining of the light microscopy specimens in acute angle closure glaucoma revealed a regular, relatively parallel distribution of the elastic and collagen constituents of the trabecular meshwork, the elastic tissue surrounded by the collagen.


  Chronic PACG Top


Chronic PACG eyes, showed a gross alteration of the architecture and arrangement of the trabecular sheets and fewer, narrower and more irregular trabecular spaces. On light microscopy, endothelial cell crowding could be seen within relatively immature collagen, and melanin pigments were seen within the stroma of fused trabecular beams. There was polymorphism of the endothelial cells with some cells being rounded and larger. Small tags of iris stromal tissue were adherent to the surface of the trabecular meshwork in three specimens. Electron microscopy showed that the trabecular meshwork characteristically had numerous electron dense bodies of varying shapes and sizes, which were present both within the trabecular beam and in the extracellular spaces. On magnification these electron-dense bodies had a variably banded fibrillar structure.

The trabecular endothelial cells in chronic PACG contained membrane-bound pigment granules and vesicles. Some cells had numerous ill-defined vesicles with heterogenous contents and no intracytoplasmic organelles, suggestive of the onset of degenerative changes. The endothelial cells appeared polymorphic and were unevenly distributed over the trabecular beams. There were areas in which endothelial cells did not line the trabecular beams, thus leading to an apposition/fusion of adjacent trabecular beams. Schlemm's canal was minimally compressed, but open and easily identified. Endothelial cells lining Schlemm's canal were attenuated; there were pinocytic vesicles present in the endothelium of the inner wall, but giant vacuoles were not seen. There was a thickening of the amorphous layer beneath the endothelium of the inner wall of Schlemm's canal the subendothelial extracellular matrix.

Elastic van Gieson staining of the light microscopy specimens from chronic angle closure glaucoma, showed an absence of the regular layering of the trabecular sheets but the linear elastic tissue structures were seen to have an angled or branching pattern between the thickened and fused trabecular beams.


  Discussion Top


There are only a few histopathological reports of primary angle closure glaucoma in the literature. Spencer has described the occurrence of progressive fibrosis and degeneration in the trabecular meshwork, with a compressed and obliterated Schlemm's canal beneath iris adhesions in angle closure glaucoma.[4] Rodrigues et al have also described reduced or obliterated intertrabecular spaces and a considerable narrowing of the Schlemm's canal.[2] Kerman et al suggested the possibility of trabecular damage secondary to prolonged iris-trabecular contact.[5] Tripathi studied an eye with absolute angle closure glaucoma, after intermittent attacks of pain. He described a compact trabecular meshwork, with all other features resembling those of open angle glaucoma.[3]

We found that the electron-dense bodies in chronic PACG appeared larger and denser than the POAG eyes. They were present within the beams and in the extracellular spaces and were not necessarily confined to the juxtacanalicular tissues. The beams were apparently fused in sections from all over the meshwork; this was not confined to the posterior meshwork as has been reported for POAG.[5] Age-related changes such as thickening of the amorphous layer beneath the endothelium of the inner wall of Schlemm's canal was seen in PACG eyes as well. In our study, the trabecular meshwork of acute PACG eyes revealed evidence of acute pigment release and a noninflammatory degeneration of the endothelial cells and trabecular tssue. Chronic PACG eyes had an altered trabecular architecture with fewer spaces and fused trabecular beams. The latter was evidenced by the presence of pigment granules within fused beams, reduction of endothelial cells, and pleomorphism of remaining endothelial cells. Since the patients included in the study did not have a history or evidence of acute angle closure glaucoma, these changes were presumably the result of mild, recurrent, subacute attacks of angle closure that lead to chronic angle closure glaucoma.

Excessive phagocytosis of foreign material by trabecular endothelial cells causes them to grow larger and desquamate,[6] as was seen in the eyes with acute and chronic primary angle closure glaucoma. In pigmentary glaucoma repeated occurrence of such pigment phagocytosis has been associated with trabecular cell loss. Similarly in chronic angle closure glaucoma, repetitive episodes of pigment release during subacute attacks of PACG could affect the number and the normal functions of the endothelial cells. One of the major functions that gets affected is the synthesis and maintenance of the surrounding connective tissue. Fusion of the trabecular beams is seen in older eyes and is also related to endothelial cell cover. Therefore, changes in the endothelial cells could affect the compliance of the trabecular beams and alter the resistance to outflow.

Our study highlights the presence of extensive trabecular changes in acute and chronic PACG, even in areas without peripheral anterior synechiae. Prior iridotrabecular touch could also leave residual iris tissue attached to the trabecular surface. This may not be visible on gonioscopy. Therefore, gonioscopic evaluation of the extent of peripheral anterior synechiae may not truly reflect the extent of trabecular meshwork damage in acute and chronic PACG. After an acute attack of angle closure glaucoma it has been observed that some eyes continue to have raised IOP, despite a patent iridotomy and reversal of iridocorneal apposition. We found noninflammatory acute degeneration of the trabecular meshwork in the trabecular tissues in acute PACG. This probably leads to reactive repair processes similar to those seen in chronic PACG. In chronic PACG, the IOP is controlled in a third of the eyes with an iridotomy and medical therapy.[7]

The widespread changes in the trabecular structures noted by us in chronic angle closure glaucoma eyes could themselves impede the outflow of aqueous or could augment the known effects of aging. It is therefore important that all patients with an apparently resolved acute or subacute angle closure episode have longterm follow-up. The reactive trabecular changes after such an event would amplify the ongoing age-related changes in the trabecular meshwork and could lead to uncontrolled IOP in the future.[8]

 
  References Top

1.
Lee WR. The pathology of the outflow system in primary and secondary glaucoma. Eye 1995;9:l-23.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.
Rodrigues MM, Spaeth GL, Sivalingam E, Weinreb S. Histopathology of 150 trabeculectomy specimens in glaucoma. Trans Ophthalmol Soc UK 1976;96:245-55.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.
Tripathi RC. Aqueous outflow pathway in normal and glaucomatous eyes. Br J Ophthalmol 1978;56:157-74.  Back to cited text no. 3
    
4.
Spencer WH. Glaucoma. In: Spencer WH, editor. Ocular Pathology, An Atlas and Textbook. Philadelphia: WB Saunders;1985, pp 480-547.  Back to cited text no. 4
    
5.
Kerman KR, Christensen RE, Foos RY. Angle closure glaucoma. A clinicopathological correlation. Am J Ophthalmol 1973;76:887-95.  Back to cited text no. 5
    
6.
Alvarado JA, Murphy CG. Outflow obstruction in pigmentary and open angle glaucoma. Arch Ophthalmol 1992;110:1769-72.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.
Sihota R, Agarwal H C. Profile of the subtypes of angle closure glaucoma in a tertiary hospital in North India. Indian J Ophthalmol 1998;46:25-29.  Back to cited text no. 7
    
8.
Joseph JP, Grierson I. Anterior segment changes in glaucoma. In: Garner A, editor. Ocular Pathology. 1994. pp 433-68.  Back to cited text no. 8
    


    Figures

  [Figure - 1], [Figure - 2]


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