Jose Miguel Risco

Choroidal Microvascular Repair after Argon Laser Photocoagulation

We studied the repair process of the choriocapillaris after argon laser retinal photocoagulation in the domestic cat with a plastic injection-corrosion technique and scanning electron microscopy. Retinal scatter photocoagulation was applied to the tapetum at threshold-, moderate-, and high-intensity levels and specimens prepared one, ten, and 30 days later. At 24 hours after photocoagulation, obstruction of the choriocapillaris was always present regardless of the power used. In lesions produced by higher-intensity energy levels, choriocapillaris defects had larger diameters and larger vessels were affected more severely. At ten days, there were early signs of choriocapillaris repair. At 30 days, choriocapillaris occupied almost the entire area of the defect, although the normal lobular architecture was not present.

Congenital Hereditary Endothelial Dystrophy Associated with Glaucoma

BACKGROUND Three children, ranging in age from 2 to 6 months, had diffuse and homogeneously opaque corneas, clinically consistent with congenital hereditary endothelial dystrophy. Bilateral elevated intraocular pressure (IOP) was a feature in all three children. METHODS Initially, all patients underwent glaucoma surgery to reduce IOP. Subsequently, a penetrating keratoplasty was performed in one eye of each patient to clear the visual axis. The excised corneal button was examined by light microscopy and by transmission and scanning electron microscopy. RESULTS Postoperatively, all patients maintained clear corneal grafts. Results of histopathologic examination showed an absence of the endothelial cell layer in all patients. The presence of a variably thick collagenous layer posterior to the anterior banded zone of Descemets membrane and the absence of endothelial cells were noted on transmission electron microscopy. Scanning electron microscopy confirmed absent, or scanty, and abnormal endothelial cells. CONCLUSION The authors describe three patients with a clear association between congenital glaucoma and congenital hereditary endothelial dystrophy. This combination should be suspected where persistent and total corneal opacification fails to resolve after normalization of IOP.

Keratoconjunctivitis sicca associated with achalasia of the cardia, adrenocortical insufficiency, and lacrimal gland degeneration: Keratoconjunctivitis sicca secondary to lacrimal gland degeneration may parallel degenerative changes in esophageal and adrenocortical function.

OBJECTIVE/DESIGN This study aimed to examine and describe three siblings with alacrima, the eldest of whom had associated achalasia and adrenocortical insufficiency. PARTICIPANTS Three affected siblings and four age-matched control subjects participated. INTERVENTION/MAIN OUTCOME MEASURES: The three children underwent complete ophthalmologic examinations; computed tomographic scanning of brain, orbit, chest, and abdomen; and measurement of serum cortisol. All three were subjected to a short synacthen challenge. Lacrimal gland biopsies were performed on the two younger subjects, and specimens were studied by light and electron microscopy. RESULTS All three children showed virtually absent tear secretion as tested by the Schirmer test. The resulting keratopathy was most severe in the oldest child, who developed bilateral corneal melting. The two younger children showed interpalpebral corneal staining with rose bengal. All three children improved after punctal occlusion. Addisons disease was present in the oldest child. Computed tomographic scanning showed absent lacrimal and shrunken adrenal glands in association with achalasia of the cardia in the oldest child. The lacrimal glands were found to be reduced in size in the next eldest child. When evaluated by electron microscopy, the lacrimal gland biopsy specimens from the two younger children showed neuronal degeneration associated with depletion of secretory granules in the acinar cells. CONCLUSION In this disease, radiologic evidence of reducing lacrimal gland size with increasing age could represent a degenerative process. This may be paralleled by other signs and the possibility of adrenocortical insufficiency and achalasia of the cardia should be investigated in all children presenting with dry eyes. These children appear to have a progressive neuronal disease.