Near-fatal heat stroke during the 1995 heat wave in Chicago.

BACKGROUND: In July 1995, Chicago sustained a heat wave that resulted in more than 600 excess deaths, 3300 excess emergency department visits, and a substantial number of intensive care unit admissions for near-fatal heat stroke. OBJECTIVE: To describe the clinical features of patients admitted to an intensive care unit with near-fatal classic heat stroke. Patients were followed for 1 year to assess delayed functional outcome and mortality. DESIGN: Observational study. SETTING: Intensive care units in the Chicago area. PATIENTS: 58 patients admitted to the hospital from 12 July to 20 July 1995 who met the case definition of classic heat stroke. MEASUREMENTS: The data collection tool was designed to compile demographic and survival data and to permit analysis of organ system function by abstracting data on physical examination findings, electrocardiography and echocardiography results, fluid resuscitation, radiography results, and laboratory findings. Data on functional status at discharge and at 1 year were collected by using a modified Stanford Health Assessment Questionnaire. RESULTS: Patients experienced multiorgan dysfunction with neurologic impairment (100%), moderate to severe renal insufficiency (53%), disseminated intravascular coagulation (45%), and the acute respiratory distress syndrome (10%). Fifty-seven percent of patients had evidence of infection on admission. In-hospital mortality was 21%. Most survivors recovered near-normal renal, hematologic, and respiratory status, but disability persisted, resulting in moderate to severe functional impairment in 33% of patients at hospital discharge. At 1 year, no patient had improved functional status, and an additional 28% of patients had died. CONCLUSIONS: Near-fatal classic heat stroke is associated with multiorgan dysfunction. A high percentage of patients had infection at presentation. A high mortality rate was observed during acute hospitalization and at 1 year. In addition, substantial functional impairment at discharge persisted 1 year. The degree of functional disability correlated highly with survival at 1 year.

Colloidal carbon as a combined ophthalmoscopic and microscopic probe of retinal and choroidal vascular integrity.

While studying an experimental retinal immunopathy, we searched for a vascular tracer that would permit us to test the anatomical and functional status of retinal and choroidal vessels by ophthalmoscopy, light microscopy, and electron microscopy in the same eye. We found that colloidal carbon, administered intravenously, can be seen ophthalmoscopically in the choroidal and retinal circulations, and abnormal deposits of it can be visualized in vivo. The ophthalmoscopic findings can be corroborated and extended by stereomicroscopy, and later the same specimens can be used for light and transmission electron microscopical studies. This tracer, thus, would allow the correlation of the ophthalmoscopic appearance of a clinical lesion with its histological and ultrastructural substrata.

Congenital retinitis in the rat following maternal exposure to lymphocytic choriomeningitis virus.

A combined clinical and histopathological study of the eyes of the offspring of females inoculated with LCMV shows that about two-thirds of the pups develop some degree of retinal inflammation. This may range from a mild, subclinical reaction to an overt retinitis characterized clinically by demonstrable inflammatory and degenerative changes. Histopathologically, the latter condition presents the picture of an inflammatory reaction with extensive loss of photoreceptors and retinal neurons in general, macrophagic invasion, mild microcystoid degeneration and total or subtotal retinal detachment. This vertically-transmitted disease does not show the relentless progression and hemorrhagic tendency characteristic of the retinitis which occurs after direct viral inoculation. However, in the most severe cases the final outcome is the same, namely severe retinal impairment subsequent to widespread loss of photoreceptors. In the presence of consistently negative virological data, the hypothesis is proposed that this retinitis could be the result of a vertically-transmitted autoimmune disease.

Chronic retinitis in rats infected as neonates with lymphocytic choriomeningitis virus: a clinical, histopathologic, and electroretinographic study.

The long-term sequelae to infection of neonatal rats with lymphocytic choriomeningitis virus were studied by a variety of approaches, including indirect ophthalmoscopic, electroretinographic, and histopathologic methods. Data from these studies demonstrated that a progressive chronic retinitis develops after the acute, virus-specific, immune-mediated retinopathy. This chronic inflammation eventually leads to a total destruction of the retinal architecture. An autoimmune reaction against normally sequestered retinal antigens, released during the acute state of necrotizing retinitis, is probably the initiating mechanism of the chronic disease. This experimental disease, triggered by infection with a relatively harmless virus, constitutes a very convenient animal model of chronic retinitis.