Biomedical subjects
Publications and source records attributed to D L Knox.
A 30-year-old man under treatment for acute leukemia died of Candida sepsis and Pneumocystis carinii pneumonia. A small granuloma containing Pneumocystis carinii was found in one optic nerve.
PURPOSE: To define the histopathologic features of eyes in which a pathologic diagnosis of ischemic optic neuropathy had been made in the years 1951 through 1998. METHODS: The following data were documented: age of patient, race, sex, source of tissue, cause of death, clinical history, interval from loss of vision to death, enucleation, exenteration, and biopsy. The histopathologic criteria for diagnosis of ischemic optic neuropathy were the presence of localized ischemic edema, cavernous degeneration, or an area of atrophy located superior or inferior in the optic nerve. Cases with history of abrupt loss of vision were combined with reports from the literature to construct a time table of histopathologic features and associated conditions. RESULTS: Ischemic optic neuropathy was present in 193 eyes. There were 88 females and 65 males. The average age was 71.6 years. Ischemic edema without (early) and with (later) gitter macrophages was present in 26 (13.5%). Cavernous degeneration was present in 69 nerves (36%). Mucopolysaccharide (MPS) was present in 37 cavernous lesions 1 month or longer after loss of vision. Cavernous lesions were seen in 3 eyes in which peripapillary retinal nerve fiber layer hemorrhage had been observed prior to death. Atrophic lesions, the most common pattern, were observed in 133 optic nerves (66.8%). More than 1 ischemic lesion was seen in 38 optic nerves (19.7%). Bilateral ischemic lesions were seen in 50 (35.2%) of 142 paired eyes. CONCLUSIONS: Ischemic optic nerve lesions are initially acellular and later show macrophage infiltration. Cavernous lesions with MPS are present 4 weeks or longer after vision loss. The location of MPS posteriorly and along the internal margin suggests that MPS is produced at the edges of lesions. Progressive vision loss in ischemic optic neuropathy may be secondary to compression of intact nerve from ischemic edema and cavernous swelling, or a second ischemic lesion.
Alan C. Woods, Sr. was born in Baltimore in 1889 and died there in 1963 after living a full life. He excelled in ophthalmology and medical school leadership, patient care, scientific investigation, promulgation of ideas, clear thinking and writing, love of literature and most dramatic of all, he made a life of fun and play for his family, friends, colleagues and the ophthalmologists he trained. Late in his professional life, 1958, the year he received the Gonin Medal in recognition of his work, he made his most important contribution, recognition and clarification of the Ocular Histoplasmosis Syndrome.
A 47-year-old white man with dementia, supranuclear ophthalmoplegia, and myoclonic ocular and facial jerks died in 1931. The case report in 1936 by Ford and Walsh diagnosed encephalitis. In 1993, we made a clinical diagnosis of Whipple's disease on the basis of the 1936 publication. We restudied the pathologic material and found, in addition to extensive encephalitis, PAS-positive material in only the eye, brain, spinal cord, and pituitary. Electron microscopy demonstrated free and intracytoplasmic microorganisms in the eye and brain. We review the history of cerebral ocular Whipple's disease and the implications from this case, which occurred before the development of antibiotics.
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Myasthenia gravis (MG) commonly presents with weakness and fatigability of the lids and extraocular muscles, which respond to treatment with anticholinesterase medication. However, certain intracranial mass lesions may mimic these features of MG; alternatively, MG may mask the signs of a coexistent intracranial mass. We describe 8 patients originally diagnosed as having MG by knowledgeable clinicians, in whom an intracranial lesion instead of, or in addition to, MG was later identified. The lesions included parasellar tumors and aneurysms. In patients presenting with clinical features of ocular MG, it is therefore essential to establish a definite diagnosis of MG, to exclude other possible causes of "pseudomyasthenia," and to exclude other diseases that might be masked by coexisting myasthenic weakness. We recommend that patients with clinical features of MG limited to the ocular or cranial musculature be thoroughly evaluated for intracranial mass lesions, using CT or MRI if warranted.
Vision loss progressing over several days, reduced pupil reactions to light, and swollen optic nerves were the clinical features in six patients with severe renal disease manifested by uremia, anemia, and (in four patients) moderately or severely elevated blood pressure. In two patients pale edema of the optic nerve head extended into the macula. One patient with renal transplant rejection was in the early phases of cryptococcal meningitis that went undiagnosed for two weeks. Medical management with hemodialysis was followed by improvement of vision in four patients. In one patient, resumption of oral corticosteroid therapy was followed by improvement in vision. The patient whose vision improved the most rapidly was managed by prompt use of both dialysis and oral corticosteroid therapy. The patient with cryptococcal meningitis did not recover vision.
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Diagnosis and management of the child with an ocular inflammation demands that all of the standard tools of medicine be employed: family and individual history, particularly of allergy, social and diet history, system review, physical examination, and basic laboratory testing with special tests for certain microorganisms and allergies. Close cooperation among pediatrician, ophthalmologist, and family is important. Cases are rare, and management often requires special experience.
The authors report 32 cases of histologically proven ocular reticulum cell sarcoma (RCS). Follow-up data are available for all patients. Twenty-six patients (81%) have died and the mean survival time was 20 months from the time of diagnosis of RCS. Diagnosis of ocular involvement was made by vitreous biopsy in 56% of cases, enucleation in 13%, and postmortem examination in 31%. The mean age at the time of diagnosis was 60 years. Central nervous system (CNS) involvement was present in 56% of patients, visceral involvement in 16%, and both CNS and visceral involvement in 6%. Isolated ocular disease occurred in 22% of patients. Results of head computed tomography (CT) and cerebrospinal fluid examination more often disclosed evidence of RCS than did body CT or nuclear medicine scans. Responses to treatment were variable, but prognosis for survival is poor.
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The acute retinal necrosis (ARN) syndrome is a morphologically defined necrotizing retinitis, occurring in apparently otherwise healthy patients. It has been shown that the varicella zoster virus is at least one cause of the ARN syndrome; treatment with acyclovir has proven to be effective for the infectious component of ARN. We report three immunocompromised patients who developed cutaneous herpes zoster and a necrotizing retinitis that was morphologically similar to the ARN syndrome. All three patients responded promptly to treatment with acyclovir, an agent highly effective against varicella zoster and herpes simplex viruses, but ineffective in the treatment of cytomegalovirus. While cytomegalovirus retinitis is more common in immunocompromised patients, these patients may occasionally develop an ARN-like retinitis, presumably as a result of the varicella zoster virus, which responds to treatment with acyclovir.
The clinicopathologic features of a 62-year-old woman with the aortic arch syndrome who presented with ischemic ocular inflammation, followed by complete loss of vision, is presented. The pathophysiology and ocular manifestations of chronic ocular ischemia are discussed.
This article presents the clinicopathologic features of five patients with ocular involvement secondary to carotid artery disease. Three patients had the features of hypotensive retinopathy and two had panocular ischemia. In demonstrating the possible ocular and nonocular sequelae of carotid artery disease, this study stressed the importance of the recognition of the variable ocular features associated with carotid artery occlusive disease.
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Patients with granulomatous enterocolitis, a disorder which can affect the whole alimentary tract, have a 10% chance of having an ocular complication. Experience with 47 patients seen over 20 years found different types of ocular complications. Definition of the type of complication aids in diagnosis and management of both the eye and intestine. Primary ocular complications are those which occur with activity of Crohn's disease and respond to treatment for the Crohn's disease. Secondary ocular complications occur because of some other primary, systemic, or ocular complication. Coincidental ocular complications are unrelated to Crohn's disease.
A 13-year-old boy with severe, active granulomatous ileocolitis presented with bilateral conjunctival nodules and infiltrates, iritis, and uniocular corneal infiltrates. Gastrointestinal biopsy revealed deep focal ulcers of the bowel wall with adjacent granulomas. Conjunctival biopsy disclosed non-caseating granulomatous inflammation.