Foregoing life-sustaining treatment in an Israeli ICU.

OBJECTIVE: To determine whether physicians in Israel withhold and/or withdraw life-sustaining treatments. DESIGN: A prospective, descriptive study of consecutively admitted patients. Patients were prospectively evaluated for diagnoses, types and reasons for foregoing life-sustaining treatment, mortality and times from foregoing therapy until mortality. SETTING: A general intensive care unit of a university hospital in Israel. RESULTS: Foregoing life-sustaining treatment occurred in 52 (13.5%) of 385 patients admitted and 5 (1%) had cardiopulmonary resuscitation. Withholding therapy occurred in 48 patients. Four patients with brain death had all treatments withdrawn. No patient had antibiotics, nutrition or fluids withheld or withdrawn. Time from foregoing therapy until death was 2.9 +/- 0.6 days. Thirty-one of 48 (65%) patients who had therapy withheld died within 48 h. CONCLUSIONS: Withholding life-prolonging treatments is common in an Israeli intensive care unit whereas withdrawing therapy is limited to brain dead patients. Terminal patients die soon after withholding, even if the therapy is not withdrawn. Withholding treatments should be an option for patients and professionals who object to withdrawing therapies.

A water-extractable toxic compound in vinyl upholstery fabric.

A compound, highly toxic to goldfish, was found to be released from a vinyl (polyvinyl chloride) automotive upholstery fabric when the material was immersed in their water. The compound, a flame retardant used in such material, was identified by specific detector gas chromatography and mass spectrometry as triphenyl phosphate. Fish exposed to the immersed fabric or pure triphenyl phosphate showed neurologic intoxication and extensive histopathologic lesions.

Caryospora cheloniae sp. n.: a coccidial pathogen of mariculture-reared green sea turtles (Chelonia mydas mydas).

Caryospora cheloniae sp. n. is described from mariculture-reared green sea turtles (Chelonia m. mydas). The sporulated oocyst has a thin, transparent, single-layered wall which often ruptures, leaving a naked sporulated sporocyst. Oocysts measured 33.8 to 40.1 micrometer by 11.0 to 14.6 micrometer (mean 37.4 by 12.8 micrometer). Greatest concentrations of developmental stages of C. cheloniae were found in the hindgut. Transverse binary fission was observed in dividing tissue stages. Pathologic alterations were most pronounced in the posterior third of the intestines (hindgut). The hindgut lumen was greatly dilated and filled with blood, oocysts and tissue debris. The hindgut wall was thinner than normal and the mucosal folds had sloughed into the intestinal lumen. Free blood escaped from the blood vessels of the tunica propria into the intestinal lumen. Epithelial hyperplasia was pronounced at the margins of denuded mucosal areas. Numerous inflammatory cells infiltrated the infected mucosal surface.

Toxicity to fish of flame retardant fabrics immersed in their water. Part I.

A number of commercial and candidate flame retardants were studied with regard to their toxicity to fish when released from fabrics immersed in their water. Immersion of laundered or unlaundered flame retardant 100% polyester or polyester blend fabrics used in children's sleepwear in water containing goldfish resulted in release of the anticholin-esterase flame retardant TDBPP (tris (2, 3-dibromopropyl) phosphate) and death of all fish within 24 hours. TDBPP undergoes loss of HBr in water and production of a metabolite.

Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs.

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.