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A 9 month-old boy developed secondary open-angle glaucoma associated with fever and multiple lytic bone lesions 2 1/2 months after cataract aspiration. An open bone biopsy provided a diagnosis of histiocytosis X. Hisiocytes similar to those in the bone were identified in a specimen of aqueous humor from the affected eye. No other cells were found. The abnormal histiocytes may have caused the glaucoma by infiltrating the trabecular angle structures and mechanically obstructing aqueous outflow from the eye.

Ninety-three patients received ruby laser panretinal photocoagulation in one eye for diabetic retinopathy and we examined them at an average time of 7.1 years later. In 14 patients, the untreated eye developed rubeosis iridis and the contralateral treated eye did not. In seven patients, the untreated eye developed angle neovascularization and the contralateral eye did not. The untreated eye developed neovascular glaucoma and the contralateral treated eye did not in four patients. Our findings suggest that eyes with proliferative retinopathy that received panretinal photocoagulation are less likely to develop rubeosis iridis, angle neovascularization, and probably neovascular glaucoma, than those eyes not receiving panretinal photocoagulation.

We examined trabeculectomy specimens obtained at the time of surgery for inadequately controlled open-angle glaucoma by scanning electron microscopy. Of the 50 specimens ten included a broad area of the trabecular meshwork. In these ten specimens the meshwork was obscured by material. We believe the degree of occlusion was significant in these specimens, which would lead to obstruction of aqueous outflow. No similar material was found in control specimens from persons of similar age.

Summary Clinical and investigative evidence indicated a glaucoma caused mainly by degenerated red blood cells, or ghost cells. These ghost cells, with altered shape, color, and pliability, accumulated in the vitreous cavity after hemorrhage. Following disruption of the anterior hyaloid face, they passed into the anterior chamber and caused severe glaucoma. In the anterior chamber, the tiny, khakicolored cells, circulating slowly, were frequently mistaken for white blood cells. They covered the trabecular meshwork or filled the inferior angle with a pathognomonic khaki-colored layer. They were identified by phase-contrast microscopic examination of anterior chamber aspirates. The decreased pliability of these degenerated cells seemed to account for their inability to pass easily through the human trabecular meshwork and, therefore, to cause severe glaucoma.

Enucleated eyes were perfused alternately via the anterior and vitreous chambers. At low intraocular pressure (IOP), vitreous humor presented considerable resistance to forward flow of perfusion fluid in calf eyes, but not in human eyes. In human eyes when the perfusion pressure was increased to 60 mm Hg, the resistance to flow forward from the vitreous body increased, but became practically nil again when the IOP was decreased. At high pressure the volume of the vitreous body apparently increases and the anterior hyaloid membrane probably presses against the ciliary body, reducing the area of hyaloid membrane through which fluid can flow. Whether increased perfusion pressure can in some other manner change the permeability of human vitreous to resemble that of the calf remains unanswered. Our results suggest that factors other than, or in addition to, simple diversion of aqeous humor must be important in malignant glaucoma.

Forty-nine patients with bilateral pigmentary dispersion syndrome (abnormal accumulation of pigment in the anterior chamber, principally from the posterior layers of the iris), including 31 patients with pigmentary glaucoma, underwent 10% phenylephrine testing in one eye for evaluation of liberation of pigment floaters into the anterior chamber and the influence of phenylephrine on the intraocular pressure. Ten patients with pigmentary glaucoma developed a 3+ to 4+ pigment response, but only two demonstrated a pressure rise greater than 2 mm Hg. The highest pressure rise observed was 7 mm Hg. Nine patients with pigmentary dispersion syndrome but without glaucoma also developed a 3+ to 4+ pigment response, but none of these had a pressure rise. The incidence of pigment liberation was higher in older patients and in pigmentary glaucoma patients receiving topical antiglaucoma therapy at the time of testing. The extent of iris transillumination did not correlate with the grade of phenylephrine-induced pigment liberation. Two pigmentary glaucoma patients, who did not liberate pigment or have a pressure rise when tested with phenylephrine, did exhibit spontaneous or exercise-induced liberations of pigment into the anterior chamber, with marked rises of intraocular pressure and obstruction of aqueous outflow.

During a nine-month period, we have seen seven patients with a rather uniform clinical picture of keratoconjunctivitis which ap­ pears to have been caused by a new form of Vick's VapoRub, marketed on a trial basis in Boston and Detroit. This new product has also proved injurious to the eyes of rabbits, whereas regular Vick's VapoRub has been innocuous. Although the new product has been with­ drawn from the market, publication of our observations seems worthwhile for several reasons. Of the several hundred thousand tubes that were distributed, many may re­ main in the hands of consumers, providing a potential cause of keratitis. In addition, de­ scription of the recognizable distinguishing characteristics of this keratitis should facili­ tate its diagnosis. The experience with this product provides additional evidence that preparations for the skin can readily con­ taminate the eyes without producing any warning discomfort unless, of course, a com­ ponent is present which immediately causes irritation. Mathalone and Easty and Brodkin and Bleiberg have recently reported a similar type of keratitis resulting from the use of Exolan cream in the treatment of psoriasis. A-200 Pyrinate, a pediculocide ap­ plied to the hair, has also caused severe tran­ sitory keratitis through accidental contami­ nation of the eyes, as described by Reinecke and Kinder, and continues to be a cause of eye injuries, particularly in children.