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Biomedical subjects

C D Phelps

Publications and source records attributed to C D Phelps.

At least 55 records · Page 3Linked to original sources

The pathogenesis of glaucoma in Sturge-Weber syndrome.

What is the cause of glaucoma in Sturge-Weber syndrome? Looking for the answer to this puzzling question, we examined 21 patients with the disease. Sixteen patients had gglaucoma: three bilateral and 13 unilateral. Episcleral hemangiomas were visible in all glaucomatous eyes. In general, the more extensive the hemangioma, the more severe was the glaucoma. During gonioscopy, blood could easily be made to reflux into Schlemm's canal of glaucomatous eyes. Often the canal separated into multiple fine channels. Episcleral venous pressure, which we measured in 11 patients, was high in all glaucomatous eyes. These observations suggest that glaucoma in Sturge-Weber syndrome is caused by elevated episcleral venous pressure. Most likely, veins draining aqueous from the canal of Schlemm are part of an intrascleral or episcleral hemangioma. The canal of Schlemm itself may be part of the hemangioma. Arteriovenous shunts in the hemangioma raise episcleral venous pressure, which in turn elevates intraocular pressure.

Adolescent↗

Perimetry.

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Aged↗

Glaucoma and retinal detachment.

In a survey of 817 patients undergoing primary operations for retinal detachment, glaucoma was present in 9.5%. Ocular hypertension (intraocular pressure [IOP] greater than 21 mm Hg) was present in an additional 6.5%. Primary open-angle glaucoma; the type of glaucoma most frequently encountered, occurred in 4% of the patients. Aphakic eyes and eyes with peripheral anterior synechiae had high prevalences of glaucoma. A high percentage of eyes with posttraumatic angle recessions had either glaucoma or elevated IOPs. Miotics used in the treatment of glaucoma could not be definitely implicated as a cause of retinal detachment. The rate of successful retinal reattachment was the same, whether or not glaucoma was present. However, a good visual result occurred less frequently in patients with glaucoma.

Eye Injuries↗

The clinical spectrum of posterior polymorphous dystrophy.

We examined 61 affected members of eight families with an inherited corneal dystrophy. The corneal abnormalities varied greatly from one member of a family to another. Some patients had only a few isolated endothelial vesicles, while others in the same family had severe secondary stromal and epithelial edema. In some patients edema was present at birth or in early childhood; in others it developed later in life. The wide variation of corneal abnormalities suggests the possibility that several conditions previously described as separate disease entities, such as grouped vesicles, Schnyder's posterior herpes, posterior polymorphous dystrophy, and congenital hereditary endothelial dystrophy, are part of the clinical spectrum of expression of a single familial corneal dystrophy. Some affected family members also had ocular hypertension or open-angle glaucoma. Broad iridocorneal adhesions were present in some of the patients with glaucoma and in others with normal intraocular pressures. Other ocular abnormalities present in a few patients include pupillary ectropion, "glass membranes" on the anterior iris surface, and bands in Descemet's membrane. The transmission in most of the families was autosomal dominant. In two families it appeared to be autosomal recessive.

Adolescent↗

Open-angle glaucoma following surgery for congenital cataracts.

Eighteen patients who, years earlier, had undergone operations for congenital cataracts were discovered to have high intraocular pressures. Several had profound glaucomatous loss of vision. All had deep anterior chambers with flat iris planes and wide open angles. The uveal meshwork was unusually coarse and pigmented in some cases. Nystagmus, aftercataracts, and small pupils made visual field testing and observation of optic discs difficult. Most cases were bilateral, which suggested a hereditary origin; some had a family history of glaucoma. In none did we observe signs of congenital glaucoma or rubella syndrome. The incidence of this disease is not yet known, but it is common enough in our clinic to indicate lifetime surveillance for glaucoma in all patients who undergo congenital cataract surgery.

Adolescent↗

Cardiac, skeletal and ophthalmologic abnormalities in relatives of patients with the Marfan syndrome.

Nine patients with the Marfan syndrome and 40 of their first degree relatives were evaluated for the presence of cardiac, skeletal and ophthalmologic abnormalities. Aortic root dilatation and mitral valve prolapse were sought by echocardiography, and the metacarpal index was calculated from hand X-rays. Abnormalities of all the tests performed were present in all nine index cases, except for one normal eye exam. Mitral prolapse was present in thirteen relatives (33%) and aortic root dilatation in seven (18%). At least one cardiac abnormality was present in nineteen (47%) relatives. Aortic root dilatation was more common in male relatives; the incidence of mitral prolapse was approximately equal in the two sexes. Abnormal metacarpal index (greater than 8.0) occurred in fifteen of twenty-six relatives examined (58%). Ophthalmologic abnormalities were found in only four relatives. Two relatives had abnormalities of all three organ systems evaluated, five others had abnormalities of two systems, and fourteen had abnormalities of one system. We conclude that cardiac and skeletal abnormalities are demonstrable in a high percentage of first degree relatives of patients with the Marfan syndrome.

Adolescent↗

Measurement of intraocular pressure: a study of its reproducibility.

Intraocular pressure was measured with Goldmann applanation tonometers by two independent examiners in 420 eyes. A difference between measurements of at least 3 mm Hg occurred in 30% of the eyes. Some evidence suggests that the differences between pressure measuremens were caused by actual changes of intraocular pressure rather than by instrument inaccuracy of technician error.

Humans↗

Hemolytic glaucoma.

The clinical manifestations of hemolytic glaucoma in five patients showed that the glaucoma began after a large intraocular hemorrhage. Gonioscopy revealed open angles in the anterior chamber and reddish-brown pigment covering the trabecular meshwork. Numerous red-tinted blood cells were floating in the aqueous humor; some of these were macrophages found by cytologic examination to contain golden-brown pigment granules. The presumed cause of hemolytic glaucoma is obstruction of the trabecular meshwork by fragments of hemolyzed red blood cells and hemoglobin-laden macrophages. Two patients, whose intraocular pressures were not decreased with medication, improved remarkably after irrigation of hemolytic debris from the anterior chamber.

Acetazolamide↗

Blood pressure and pressure amaurosis.

Susceptibility to pressure amaurosis was measured in young research subjects before and during blood pressure elevation induced by intravenous infusions of phenylephrine. Intraocular pressure elevations were produced by paralimbal suction; we measured the highest level to which intraocular pressure could be raised without obliterating perception of a slowly flickering stimulus in the nasal field of vision. Elevation of systemic blood pressure was accompanied in all subjects by a corresponding increase in the highest "safe" level of intraocular pressure. This observation confirms the commonly held hypothesis that pressure amaurosis is the result of pressure-induced neuroretinal ischemia.

Atropine↗