Management of epiphora following parotid duct transposition for xerophthalmia.
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Vitamin A-deficient rabbits were used to evaluate the role of secondary bacterial infection in the development of keratomalacia and to describe the resultant clinical and morphologic alterations. The conjunctival sacs of vitamin A-deficient rabbits at different stages of corneal involvement were inoculated with Pseudomonas aeruginosa topically. Approximately two weeks after inoculation, corneal ulceration with stromal melting developed in one of three eyes with severe punctate keratitis and in four of seven eyes with xerosis. Ulceration did not develop in any of the eight eyes with early epithelial graying or mild punctate keratitis. Inflammatory cells (primarily polymorphonuclear leukocytes) infiltrated the anterior corneal stroma of infected corneas. Liquefaction of collagen was observed in association with bacteria alone, as well as in association with polymorphonuclear leukocytes. No signs of infection were observed after conjunctival inoculation of Pseudomonas in the eyes of nine control rabbits.
Six measures of nutritional status were studied in 162 consecutive cases of presumed nutritional keratopathy ranging from mild xerosis through full-thickness necrosis (keratomalacia) and in a variety of control subjects. The severity of corneal involvement was related to the severity of wasting, prevalence of edema, and serum levels of albumin, transferrin, and vitamin A. Even the most severe corneal alterations were compatible with normal indices of protein and anthropometric status, but not with normal serum vitamin A levels. Analysis suggests that interaction between vitamin A and protein status determines cellular adequacy of vitamin A metabolism, which virtually collapses in keratomalacia. Serum levels of holoretinol-binding protein were severely and uniformly depressed in all degrees of corneal involvement.
Detailed examinations were conducted on 162 consecutive children with nutritional keratopathy. Surface changes ranged from mild haziness through generalized xerosis and formation of thickened keratinized plaques. Diffuse stromal edema occured early in the disease. Stromal loss took two forms: relatively small, sharply demarcated, eccentric, noninfiltrated cylindrical ulcers of varying depth; and localized or generalized, usually full-thickness necrosis. All forms of involvement were sometimes present in the same individual or even the same eye. Traumatic separation of a keratinized plaque, or decompensation of a dellen, accounted for some instances of stromal baring. In other cases, stromal melting appeared to progress below an intact epithelium. Focal areas of necrosis healed rapidly, as adherent leukomas; larger lesions sloughed, forming extensive descemetoceles. With therapy, the vast majority of children retained central corneal clarity.
We studied the appearance of conjunctiva in 50 consecutive cases of vitamin A-responsive conjunctival xerosis (X1) and 162 consecutive cases of nutritional keratopathy (corneal xerosis [X2] and stromal loss [X3]). conjunctival xerosis, most extensive at or shortly after the onset of frank corneal involvement, was present in 101 (95%) of 106 eyes of cases of X2 but in only 99 (64%) of 155 ulcerated/necrotic eyes (X3A and X3B). Forty-four percent of involved eyes were inflamed, the percentage increasing with the severity of corneal disease. In 20 patients with nutritional keratopathy, conjunctival xerosis was monocular: inflammation was more prevalent and corneal involvement more severe in the nonxerotic eyes. In patients with precipitous deterioration of vitamin A status, clinically recognizable alterations of the cornea sometimes developed before any changes appeared in the conjunctiva.
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A countrywide prevalence survey of 9,508 children was conducted in El Salvador to determine the prevalence of anterior-segment abnormalities and magnitude of clinical vitamin A deficiency. Thirty-six children had corneal opacities, 56% of them secondary to trauma. Such traumatic corneal opacities were 19 times more frequent among urban than rural children, 57.6 vs. 3.1 per 1,000. Keratomalacia accounted for only 8% of all corneal opacities, and for one (and possibly two) of the five cases of bilateral anterior-segment blindness encountered. The prevalance of Bitot spots and vitamin-A-related corneal opacities was 5.3 and 3.2 per 10,000, respectively. There are an estimated 43 new surviving cases of vitamin-A-related corneal opacities in the country each year, one third of which result in bilateral blindness. Fifteen percent of all children examined had grossly purulent conjunctivitis.
The prevalence of presumed vitamin A-related corneal scars among 5,589 preschool-age Haitian children ranged from 1.2 per 1,000 in the south, to almost 1% in the famine-afflicted north. These scars accounted for at least 45% of all corneal scars, and all bilateral corneal blindness encountered. Most lesions were acquired during the first three years of life. There was no variation by sex or ecology of the sample site. This country of 5.5 million inhabitants acquires 345 new surviving cases of vitamin A-related corneal destruction, over one fourth bilaterally blind, each year, although local ophthalmologists rarely encounter the disease and Bitot's spots were absent from our study population. Countrywide clinical prevalence surveys are the only unbiased means of determining the magnitude, severity, and geographic distribution of vitamin A-related corneal destruction, prerequisites for the design of public health prevention programs.
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