Ординатура / Офтальмология / Английские материалы / Mechanisms of the Glaucomas_Shields, Tombran-Tink, Barnstable_2008

Although they can appear spontaneously (25%), most cases of carotid-cavernous fistula are caused by cranial trauma. They can also appear after neurological surgical procedures (107).

Although more than 50% of these patients have elevated IOP, the characteristic glaucomatous optic neuropathy is much less common. Ishijima et al. reported that among the 43 patients diagnosed with CCF, a total of 13 patients (14 eyes) showed ocular manifestations (108). CCF was idiopathic in 12 subjects and resulted from head trauma in one. Elevated IOP was observed in 64.3%, with maximum IOP ranging from 22 to 55 mmHg.

Theories of Glaucoma Mechanism

The CCF causes high pressure in the venous system of the orbit and globe similar to pressures in the arterial system. The resulting elevated EVP increases resistance to aqueous humor outflow, resulting in increased IOP and associated open-angle glaucoma. Patients with glaucoma and CCF often present with blood in the Schlemm’s canal although this may also be found in normal eyes, and the gonioscopic findings may be masked by heavy trabecular meshwork pigmentation.

Another mechanism of glaucoma is angle closure due to increased pressure in the vortex veins, leading to a forward displacement of the lens–iris diaphragm (109,110).

Yet another mechanism is neovascular glaucoma, in which neovascularization of the optic disc, rubeosis iridis, and ischemic ocular necrosis are caused by the reduced perfusion pressure in these cases. The patients who typically suffer severe vision loss are those with the ischemic optic neuropathy and chorioretinal dysfunction, including occlusion of the retina central vein (111–114).

Management

The medical treatment is similar to that for open-angle glaucoma; drugs that reduce aqueous production, such as beta blockers, alpha-2 agonists, and carbonic anhydrase inhibitors. Prostaglandins, as previously discussed, may have unique benefits in eyes with elevated EVP. However, medical treatment in these cases is often inadequate.

Fistulization surgery appears to be effective in these cases although they are associated with the higher incidence of choroidal effusion and expulsive hemorrhage with shallow or flat anterior chamber in the face of elevated EVP (115). In some cases, it may be necessary to close the abnormal vascular communication by neuro or vascular surgeons, although this is associated with a risk of apoplexy and stroke (108). Acute angle-closure glaucoma has been reported to develop in association with an oculomotor palsy following neurointervention (116).

IDIOPATHIC ELEVATED EPISCLERAL VENOUS PRESSURE

The glaucoma in this condition is associate with elevated EVP and dilated episcleral veins, without a detectable cause (117–121). Several reports suggest a familial predisposition (120,122,123). Although originally described by Minas and Podos (120), the same entity is termed the Radius–Maumenee syndrome in the German literature (118).

Glaucoma due to idiopathic elevated EVP is rare. Jorgensen and Guthoff (119) studied 64 patients with dilated episcleral vessels, open-angle glaucoma, and elevated

EVP and reported that in 10 of the cases they could not detect an explanation for the elevated EVP.

Ocular Features

The glaucoma is usually unilateral or asymmetrical, and the IOP is generally above 30 mmHg (117–121). Gonioscopically, Schlemm’s channel is often filled with blood. Extensive studies have failed to reveal the origin of the elevated EVP, with the only pathologic findings being increased tonographic resistance to outflow and increased arterial and venous episcleral flow on the color-coded Doppler sonography (117,121, 122,124).

Theories of Glaucoma Mechanism

As previously noted, glaucoma secondary to idiopathic EVP, with dilated vessels is typically unilateral or at least asymmetrical. Talusan et al. (122) described seven cases, only one of which was bilateral. In all six patients with apparently unilateral involvement, the IOP was higher in the eye with the dilated vessels, and EVP was measured to be twice the normal value in the affected eyes. Jorgensen and Guthoff described similar results in a study of five patients (125).

Jonas (6) studied ophthalmodynamometry in eyes with dilated episcleral veins and found that the central retinal vein collapses at pressure that was significantly higher in the study group with dilated episcleral veins, than in the control group (p < 0.001) [37.9 ± 33.8 vs. 5.1 ± 8.4 relative units (RU)]. For the central retinal artery, there was no significant difference in the diastolic collapse pressure between the study and control groups (78.2 ± 22.8 vs. 74.2 ± 18.8 RU, respectively; p = 0.74). He suggested that ophthalmodynamometric estimation of the central retina vein collapse pressure might be helpful in the assessment of patients with dilated episcleral veins.

Management

Management of the glaucoma in these patients is difficult although the majority of reports were prior to the introduction of uveoscleral drainage agents, for example, prostaglandins, which may be more effective than aqueous suppressants, as they bypass the episcleral venous drainage. Filtration surgery is frequently required to control the IOP (117) and one suggested alternative approach is non-penetrating, deep sclerectomy (126).

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POST-INFLAMMATORY ANGLE-CLOSURE GLAUCOMA

Iridocyclitis

Iridocyclitis is one of the main causes of PAS often resulting from idiopathic disease (2). Identifiable diseases typically resulting in iridocyclitis include ankylosing spondylitis, juvenile rheumatoid arthritis, interstitial keratitis, sarcoidosis, pars planitis, and uveitis-glaucoma-hyphema syndrome. Most cases of iridocyclitis are acute and selflimiting. Anterior synechiae do not usually form in these cases unless repeated episodes lead to the adhesions between the iris and trabecular meshwork–cornea complex. Recurrent subacute or chronic iridocyclitis, on the other hand, is much more likely to lead to iris and trabecular meshwork swelling with eventual PAS. Once PAS covers over 25% of the angle, aqueous outflow is frequently compromised and intraocular pressure (IOP) becomes elevated. In the subacute form, ocular examination may appear normal until gonioscopy reveals PAS. Attacks of elevated IOP may go unnoticed and be mistaken for migraines or stress headaches. The chronic form of iridocyclitis typically leads to sustained elevation of IOP, and patients often present with significant angle closure and optic neuropathy because of long-standing disease. These patients often fail medical therapy for IOP control and require filtration surgery.

Infectious Iridocyclitis

Synechiae formation may be associated with infectious keratitis, congenital infectious iridocyclitis, or disseminated ocular infections as in endophthalmitis. Common pathogens involved with anterior segment inflammation and PAS formation include herpes simplex, herpes zoster, and toxoplasmosis (3–5). The ultimate mechanism leading to drainage angle disruption is formation of PAS as a result of tissue swelling and deposition of inflammatory cells. Adhesions then form between iris and cornea leading to decreased aqueous outflow and IOP elevation. Early control of infection and inflammatory response lessens the chance of PAS formation.

Grant’s Syndrome

A form of acute open-angle glaucoma involving keratic precipitates (KPs) over the trabecular meshwork was described by Chandler and Grant (6). They noted gonioscopic evidence of gray or yellowish KPs associated with elevated IOP in otherwise quiet appearing eyes. The presentation is usually bilateral and resolves promptly with topical steroid drops. Recurring episodes could lead to synechiae formation and angle closure.

Traumatic Iridocyclitis

Ocular trauma may lead to elevation in IOP due to iridocyclitis and swelling of the trabecular meshwork cells. This is usually a transient phenomenon with no lasting sequelae. In more severe trauma, and particularly in cases involving hyphema, chronic inflammation may lead to PAS formation and eventual angle closure (7). Early treatment with topical steroids may decrease the incidence and severity of PAS formation.

A second anterior pulling mechanism of angle closure following trauma has been described. This form involves the formation of a Descemet’s-like membrane over the