Sudden death due to primary diffuse leptomeningeal gliomatosis.

Tumors of the central nervous system are an unusual cause of sudden death. This report describes the sudden death of a presumed healthy 28-year-old woman from primary diffuse leptomeningeal gliomatosis. She presented to an emergency room with headache and vomiting, subsequently became unresponsive and was pronounced dead 14 h later. Autopsy revealed a diffuse extensive infiltrate of well-differentiated astrocytoma in the leptomeninges of the brain and spinal cord without an underlying parenchymal tumor. Primary diffuse leptomeningeal gliomatosis is a rare tumor that arises within the leptomeninges from small neuroglial heterotopic rests that undergo neoplastic transformation. Grossly. this tumor can mimic leptomeningeal carcinomatosis, pachymeningitis, tuberculosis, sarcoidosis, and fungal infections. However, the histologic features of primary diffuse leptomeningeal gliomatosis should allow it to be readily distinguished from grossly similar conditions. The mechanism of death in this case is most likely tumor obstruction of cerebrospinal fluid outflow resulting in the usual complications seen with increased intracranial pressure. Although this tumor is aggressive and is associated with a rapidly progressive fatal course, it has not been previously associated with sudden death.

Fatal "crack" cocaine ingestion in an infant.

This report describes a 10-month-old infant girl who died of cocaine poisoning. The infant was found apneic and in ventricular fibrillation after the parents summoned rescue personnel and claimed she had ingested rat poison. The parents later admitted that 2 hours before calling for assistance, the infant's 2-year-old brother was found eating "crack" cocaine and also feeding it to the infant. Investigators found "crack" cocaine throughout the house and in the infant's crib. At autopsy, the infant had two pieces of "crack" cocaine in the duodenum. The brain exhibited a markedly thinned corpus callosum. Toxicologic examination showed high concentrations of cocaine in the blood and in other specimens. The manner of death was classified as homicide because the infant was willfully placed in a hazardous environment with an easily accessible toxic substance, medical attention was deliberately delayed for 2 hours, and medical personnel were deceived when they were falsely told she had ingested rat poison. These features were thought to constitute neglect. The toxicologic characteristics of this case are unique. There are numerous reports of passive cocaine inhalation in infants and children less than 5 years of age, but ingestion of cocaine in this age group has rarely been documented. This age group also has no reported deaths due to cocaine ingestion and no cases of "crack" cocaine ingestion. The high concentrations of cocaine seen in this case, combined with the "crack" cocaine found in the duodenum, indicate ingestion as the route of exposure. The thinned corpus callosum in this case may be a consequence of intrauterine cocaine exposure.

Pulmonary capillary hemangiomatosis-like foci. An autopsy study of 8 cases.

Pulmonary capillary hemangiomatosis (PCH) typically occurs in young patients who have signs and symptoms of pulmonary hypertension. It commonly is misdiagnosed in life as pulmonary veno-occlusive disease, and the correct diagnosis usually is not made until autopsy. Autopsy records, including reports, gross photographs, histologic slides, clinical histories, and radiographic images, were reviewed to identify cases with morphologic changes characteristic of PCH. The previous case reports describe PCH as a diffuse process throughout both lung fields. All patients were symptomatic, and most died of the disease. This article details 8 cases of PCH-like foci that were incidental findings at autopsy in which the patients did not have symptoms of pulmonary hypertension nor did PCH contribute in any way to death. This is the first case series that describes pathologic changes of PCH occurring in this setting, and we hope to provide more interest in PCH and its natural history.

Solitary fibrous tumor of the orbit with a t(9;22)(q31;p13).

Solitary fibrous tumors are well-described neoplasms found predominantly in the subpleural region but also in many other body sites. They generally behave in a benign fashion, although a few cases that exhibit a malignant course have been reported. Genetic information on solitary fibrous tumors is sparse. This case illustrates a previously unreported finding of a tumor-specific t(9;22)(q31;p13) in a solitary fibrous tumor of the orbit of a 58-year-old man.

Elevated free fosphenytoin concentrations in uremic sera: uremic toxins hippuric acid and indoxyl sulfate do not account for the impaired protein binding of fosphenytoin.

Fosphenytoin is a new phosphate ester prodrug of phenytoin. Impaired protein binding of phenytoin in uremia has been extensively documented, which prompted us to investigate the protein binding of fosphenytoin in uremic sera. Also studied was the role of uremic toxins hippuric acid and indoxyl sulfate as potential inhibitor of the protein binding of fosphenytoin because these compounds impair protein binding of phenytoin in uremia. Five serum pools were prepared from normal volunteers and five pools from patients with uremia. None of them received phenytoin. The normal serum pools were diluted with saline to mimic the albumin concentration of uremic pool. Both the diluted normal pool and the uremic pool were supplemented with fosphenytoin; after incubation at room temperature for 30 minutes, total and free fosphenytoin concentrations as phenytoin equivalents were measured using fluorescence polarization immunoassay (Abbott Laboratories; Abbott Park, IL, U.S.A.). The authors observed significantly elevated free fosphenytoin concentration in uremic sera compared with that of normal sera in all cases. Because both normal and uremic sera had the same concentrations of albumin, the elevated free fosphenytoin concentration in uremic sera was not caused by hypoalbuminemia. Both indoxyl sulfate and hippuric acid cause significant displacement of phenytoin from protein binding. In contrast, none caused any displacement of fosphenytoin from protein binding.

The CARDIA dietary history: development, implementation, and evaluation.

To meet the objectives for dietary assessment in the Coronary Artery Risk Development in Young Adults (CARDIA) prospective study, we developed a dietary history to provide accurate and reliable quantitative data on habitual individual nutrient intakes at baseline. The CARDIA dietary history was an interviewer-administered method that included a short questionnaire regarding general dietary practices followed by a comprehensive food frequency questionnaire about typical intake of foods using the previous month as a reference for recall. For each broad category of foods, participants were questioned in detail about specific foods only if they indicated that they consumed foods from that category. Follow-up questions for selected foods concerned serving size, frequency of consumption, and common additions to these foods. Provision was made for reporting foods not found in the food frequency list. The interview took approximately 45 minutes. Cue cards prompted responses and plastic food models assisted in estimating usual amounts consumed. A precoded format standardized coding for reported items and established the detail needed for recall during the interview. Baseline nutrient analyses from the CARDIA dietary history provided estimates that agreed reasonably well with expected caloric intake for body mass index according to the age- and sex-specific Recommended Dietary Allowances, but were higher than those reported from 24-hour recalls for comparable age, sex, and race groups in the second National Health and Nutrition Examination Survey. The CARDIA dietary history is a comprehensive assessment tool that can provide a dietitian with detailed information regarding habitual eating patterns and nutrient intakes among adults.