ED evaluation of the pediatric trauma patient by ultrasonography.

The purpose of this study was to determine the accuracy of ultrasound examination of pediatric trauma patients by emergency physicians. Pediatric (age less than 18 years) trauma patients presenting to the emergency department of a level I trauma center were prospectively examined with bedside ultrasound during the secondary survey of their trauma resuscitation. Examinations were performed by emergency medicine residents and attending physicians who had completed an 8-hour course on trauma ultrasonography. Trauma physicians providing care to the patient were blinded to the results of the examination. In 47 children (median age 9 years) computed tomography of the abdomen/pelvis or laparotomy were also performed and served as gold standards to verify the presence or absence of free fluid in the abdomen. Sensitivity, specificity, and accuracy of the ultrasound examination for the detection of free fluid in the abdominal cavity was 75% (95% confidence interval [CI] 36% to 95%), 97% (95% CI 81% to 100%), and 92% (95% Cl 77% to 98%). Positive and negative predictive values were 90% (95% CI 46% to 100%) and 92% (95% CI 74% to 99%), respectively. Ultrasound examinations took an average of 7 minutes and 36 seconds, although this did not take into consideration delays created by interruptions for other diagnostic tests or procedures. An emergency physician and radiologist agreed on blinded interpretations of 83% of the examinations (kappa = 0.56). Bedside ultrasonography is a reliable and rapid method for screening traumatized children for the presence or absence of free fluid in the peritoneum even in the hands of novice sonographers.

Arthrogryposis multiplex congenita and bilateral parietal polymicrogyria in association with the intrauterine death of a twin.

A case of neurogenic arthrogryposis multiplex congenita (AMC) with associated neuronal migration abnormalities is described. A child with neurogenic AMC and developmental delay presented with late onset of seizures. The first trimester of the mother's pregnancy was marked by an episode of gastro-enteritis and the intrauterine death of a twin fetus. Computer tomography (CT) and magnetic resonance (MR) imaging demonstrated abnormal neuronal migration consisting of bilateral parietal polymicrogyria, and an isolated grey matter heterotopia.

Antibiotic prophylaxis in patients undergoing radiological procedures who are at risk of infective endocarditis--do radiologists know what they are doing?

The British Society for Antimicrobial Chemotherapy has published guidelines recommending that all patients with prosthetic heart valves, or those with a previous history of bacterial endocarditis, should receive prophylactic antibiotics before procedures likely to cause a bacteraemia, due to the potential risk of bacterial endocarditis. The guidelines are widely available, notably in the British National Formulary. Two separate and independent surveys of radiologists in this Region showed that there was poor awareness of these guidelines and their implications for radiology departments.

Biochemical basis of warfarin and bromadiolone resistance in the house mouse, Mus musculus domesticus.

Danish mice (Mus musculus domesticus) genetically resistant to the anticoagulant action of two 4-hydroxycoumarins, warfarin and bromadiolone, were examined to determine their mechanism of resistance. The hepatic vitamin K epoxide reductase in the bromadiolone-resistant mice and in one phenotype of warfarin-resistant mice was highly insensitive to in vitro inhibition by warfarin and bromadiolone. The kinetic constants for the epoxide reductase from bromadiolone-resistant mice were also altered. The Vmax for this enzyme was decreased by 40%, and the Km for the reaction reductant, dithiothreitol, was 70% lower than that of normal mice. This phenotype of Danish resistant mice appears to have a resistance mechanism that is similar to that reported for a Welsh strain of warfarin-resistant rats. The other phenotype of Danish resistant mice had a hepatic epoxide reductase that was only slightly less sensitive to warfarin inhibition than normal. The mechanism of warfarin resistance in these mice is not apparent from the available data.

Cyclic AMP inhibits secretion from bovine adrenal chromaffin cells evoked by carbamylcholine but not by high K+.

The role of cAMP in the control of secretion from bovine adrenal chromaffin cells was examined using the adenylate cyclase activator, forskolin. Treatment of chromaffin cells with forskolin resulted in a rise in cAMP levels. Forskolin inhibited catecholamine release elicited by carbamylcholine or nicotine but had no effect on secretion evoked by 55 mM K+. Inhibition of carbamylcholine-stimulated release by forskolin was half-maximal at 10 microM forskolin. The inhibition by forskolin of secretion evoked by carbamylcholine was at a step distal to the rise in intracellular free calcium concentration ([Ca2+]i), since this rise was not inhibited by forskolin, which itself produced a small rise in [Ca2+]i. The results suggest that secretion evoked by carbamylcholine is due to the activation of an additional second messenger pathway acting with the rise in [Ca2+]i. This additional pathway may be the target for cAMP action.

Metabolism of ascorbic acid and ascorbic-2-sulfate in man and the subhuman primate.

Man does not catabolize ascorbate to CO2, whereas the monkey does catabolize ascorbate and ascorbate sulfate to CO2 when these compounds are given orally. However, it takes the same length of time to produce frank scurvy in both man and the monkey, thus indicating that the comparative storage, rate of use, and mode of metabolism of ascorbate is similar in both species. Preliminary feeding and isotope studies conducted on monkeys are in agreement with the fact that only a small amount of labeled ascorbate or ascorbate sulfate equilibrated with body stores. These results are in agreement with published ascorbic acid requirements of 10 mg/kg body weight. In our experiments, 250 mg/day had to be fed to a 10-kg monkey to completely clear all signs of scurvy and return blood ascorbate levels to normal. Ascorbic acid administered intravenously to monkeys appears to equilibrate completely with the ascorbate pool(s). Ascorbate sulfate was found to be a urinary metabolite of both ascorbic-1-14C acid and ascorbic-6-14C acid fed orally to monkeys.

Ascorbate sulfate: a urinary metabolite of ascorbic acid in man.

Ascorbate-3-sulfate is a significant metabolite of ascorbic acid excreted in human urine. The characteristics of this compound were determined in experiments in which labeling with carbon-14 and tritium was used coupled with cochromatography with synthetic ascorbate-3-sulfate (both labeled and not labeled with sulfur-35) in a variety of solvent and absorbent systems.