Surgical Factors
Peripheral iridotomy
It is rare for malignant glaucoma to develop as a result of peripheral iridectomy alone, probably because the procedure is less irritating to the iridociliary body, but if malignant glaucoma has developed in one eye, extra care should be taken when performing peripheral iridectomy in the other eye. In cases of malignant glaucoma after peripheral iridectomy, a noteworthy phenomenon can be observed in which the anteriorly displaced ciliary process can be seen abutting the equatorial portion of the lens through the peripheral iridectomy. And when the IOP decreases, the lens and ciliary process separate again, which further supports the inference that malignant glaucoma is ciliary ring block glaucoma.
In recent years, cases of malignant glaucoma occurring after Nd:YAG and laser iridotomy have been reported. However, some have questioned this suggestion, arguing that cases in which laser perforation was performed often had a history of using pilocarpine eye drops, so the exact mechanism remains to be studied.
Total retinal photocoagulation
High intraocular pressure may occur both simultaneously with laser treatment of retinal disease and for several hours after treatment, but this high intraocular pressure resolves with time and, in a few cases, requires medication. Notably, in the treatment of diabetic fundopathy with total retinal photocoagulation, Mensher et al. reported that in 44 of 45 patients, the anterior chamber became shallow, atrial angle closure occurred in 14 (31%), and edema or detachment of the choroid and ciliary flat was visible under the examining eye, the ciliary body thickened on ultrasound, and intraocular pressure reached 55 mmHg, and treatment with pupil reduction agents was ineffective. It is presumed to be caused by choroidal exudate entering the vitreous cavity and anterior displacement of the lens-iris septum due to cricoidal choroidal detachment.
Retinal detachment surgery
Weiss et al. reported a case of retinal detachment two days after scleral buckling, with shallow anterior chamber and extensive choroidal detachment, which became even more shallow after glycerol and trichothecene drops, and failure to control glaucoma by discharging suprachoroidal fluid, which was slightly relieved by ciliary muscle paralytics and finally controlled by scleral dissection, lens extraction and iridotomy. The ciliary process was found to be overlying the lens during surgery. smith reported a 4% incidence of malignant glaucoma in 1000 cases of scleral shortening.
Non-surgical factors
Use of pupil constricting agents
accounts for the first of the non-surgical triggers, and 24.7% of malignant glaucoma was reported in China. Not only can the application of pupil constricting agents alone induce malignant glaucoma, but the postoperative application of pupil constricting agents can also cause malignant glaucoma. In China, it was reported that 14.12% of malignant glaucoma was induced by the application of pupil reduction agents after surgery. Initially, it was reported that malignant glaucoma was induced in closed-angle glaucoma with pupil-reducing agents, and later it was also reported that malignant glaucoma was induced in open-angle glaucoma with pupil-reducing agents. The pathogenesis of glaucoma is that while pupil constricting agents can open up the interstitial space and increase atrial aqueous flow, they reduce the amount of atrial aqueous discharge between the uvea and the sclera and increase the pressure difference between the anterior and posterior chambers, causing the anterior chamber to become more shallow and the lens-iris septum to shift forward. At the same time, pupil constricting agents cause spasm of the ciliary muscle, thus narrowing the ciliary ring and contributing to the onset of malignant glaucoma.
Uveitis
Both anterior and posterior segments of uveitis can induce malignant glaucoma. Domestically, it accounts for 7.4% of malignant glaucoma, and its pathogenesis is related to ciliary edema, thickening and detachment due to inflammation. In addition, the direct cause of rheumatic and Harada’s disease causing malignant glaucoma is related to inflammation of the uvea.
Ocular trauma
Levene reported that malignant glaucoma due to trauma is caused by ciliary body edema due to inflammation or lens cortex, resulting in narrowing of the ciliary ring and resulting in ciliary ring blockage. Certain severe ocular traumas can cause mutual adhesions between the lens, ciliary process, and vitreous humor, preventing the atrial aqueous humor from entering the anterior chamber through its normal orbit and flowing into the vitreous humor.
Central retinal vein obstruction
Hyams (1972) and Grant (1973) reported that closed-angle glaucoma induced malignant glaucoma due to central venous obstruction; Weber (1987) reported that open-angle glaucoma induced malignant glaucoma due to central venous obstruction. Eisner used fundus fluorescence angiography to confirm significant leakage into the retina and vitreous. bloom (1977) used atrial angiography to find an enlarged ciliary bulge and suggested that the pathogenesis was caused by swelling and displacement of the ciliary body.
Fungal endophthalmitis
Jones (1955) introduced the concept of fungal endophthalmitis. Mclean (1963) suggested that vitreous abscesses could lead to shallow anterior chamber, and Lass (1981) reported a case of Nocardia asteroides infection with a shallow anterior chamber and increased intraocular pressure, in which partial iridectomy was ineffective, and vitreous aspiration combined with anterior chamber gas injection was performed. Accordingly, early surgical treatment is recommended for bacterial vitreous abscess and endophthalmitis with malignant glaucoma-like changes.
Retinopathy of prematurity
The proliferative retinopathy of prematurity is associated with ciliary adhesions that, when contracted, pull the lens-iris septum anteriorly and can lead to malignant glaucoma; Hittner (1979) et al. and Pollard (1980) suggested that glaucoma is caused by anterior displacement of the lens-iris septum. In contrast, Kushner et al. reported that atrial angle closure could be released with ciliary muscle paralyzing agents, and that aspiration of the vitreous and lens extraction cured this type of glaucoma.
In summary, we believe that no matter which type of ocular disease is present, as soon as the condition progresses to the point where it interferes with the normal circulation and drainage of atrial aqueous, the normal atrial aqueous pathway is intercepted and the atrial aqueous becomes disoriented and takes another wrong route – into the vitreous, causing its volume to gradually expand and increase. The watery and swollen vitreous body is then crowded forward, pushing the anterior structures further forward and exacerbating the vicious cycle of shallow/no anterior chamber and continued elevation of IOP.
As seen in the analysis, the anatomical factors of the anterior segment of the eye are of great importance to the development of malignant glaucoma; and the abnormal changes in the relationship between the lens, ciliary body, and vitreous, which play an immeasurable role in the regression and development of malignant glaucoma; lens removal combined with vitrectomy and anterior-posterior communication is the key to successful surgery.