The effect of flumazenil on patient recovery and discharge following ambulatory surgery.

Midazolam is a short-acting agent used for preoperative and conscious sedation. Despite a relatively short half-life, midazolam sedation contributes to postoperative sedation, delays in discharge, and increased costs. Administration of flumazenil, a benzodiazepine antagonist, can reverse the centrally mediated effects of midazolam and facilitate patient recovery and discharge, thereby reducing costs. The purpose of this multicenter study was to determine whether flumazenil antagonism of midazolam decreased the length of postoperative stay following intravenous sedation during local and selected regional procedures. A prospective, double-blinded, and randomized convenience sample of 110 adult patients who underwent procedures lasting 90 minutes or less was used. After receiving institutional review board approval and informed consent, patients received up to 150 micrograms of fentanyl and unlimited midazolam titrated intravenously to effect. Flumazenil or a placebo was administered at the conclusion of the surgical procedure. Cognitive scores were assessed by using the Digital Symbol Substitution Test and picture recall, while sedation scores were assessed by using the Observer's Assessment of Alertness/Sedation Scale. The time between the end of the surgical procedure until the patient met discharge criteria in phases I and II was recorded. Statistical analyses revealed no significant difference in age, height, weight, sex, ASA physical status, amount of midazolam and fentanyl received, time for each group to achieve phase I and phase II discharge criteria, or postoperative congnitive scores. The flumazenil group exhibited less amnesia and sedation than the placebo group on initial arrival in the postanesthesia care unit. Discharge times between the groups were not significantly different. Factors such as staffing and institutional discharge policies were identified as determinants of discharge times.

Encephalopathy in cattle experimentally infected with the scrapie agent.

Ten 8- to 10-month-old cattle were each inoculated intramuscularly, subcutaneously, intracerebrally, and orally with the scrapie agent to determine whether cattle are susceptible to it. Two inocula, both 10% homogenates of cerebrum, were used. One inoculum was from a sheep used for the second experimental ovine passage of the agent from 4 naturally affected Suffolk sheep. The other inoculum was from a goat used for the first experimental caprine passage of the agent from 2 naturally affected dairy goats living with the Suffolk sheep, the source of their infection. Between 27 and 48 months after inoculation, neurologic disease was observed in 1 of 5 cattle given the sheep brain homogenate and in 2 of 5 given the goat brain homogenate. In all 3 affected cattle, the disease was expressed clinically as increasing difficulty in rising from recumbency, stilted gait of the pelvic limbs, disorientation, and terminal recumbency during a 6- to 10-week course. Neurohistologic changes, though consistent with those of scrapie, were slight and subtle: moderate astrocytosis with sparse rod cells, some neuronal degeneration, a few vacuolated neurons, and scant spongiform change. Clinically and neurohistologically, the experimentally induced disease differed from bovine spongiform encephalopathy. The differences emphasize that such infections in cattle induce diverse responses, presumably depending largely on the strain of the agent. Pathologists should keep this variability in mind when looking for microscopic evidence of a scrapie-like encephalopathy in cattle.

Prevention of scrapie transmission in sheep, using embryo transfer.

Reciprocal embryo transfers were made between scrapie-inoculated and scrapie-free sheep (Cheviot and Suffolk breeds) to measure scrapie transmission via the embryo (using offspring from embryos of scrapie-inoculated donors and scrapie-free recipients) and via the uterus (using offspring from embryos of scrapie-free donors and scrapie-inoculated recipients taken by cesarean section). Two control groups of offspring, 1 from scrapie-free parents (negative) and 1 from scrapie-inoculated parents (positive), also were included. All sheep were observed for clinical signs of scrapie until death or for a minimum of 60 months. Final diagnosis was made on the basis of histopathologic findings or results of mouse inoculation and/or proteinase-K-resistant protein analysis. Thirty to 61% of the scrapie-inoculated donor/recipient sheep within groups developed scrapie within 8 to 44 months after inoculation. None of the scrapie-free donor/recipients, including those gestating embryos from scrapie-inoculated donors, developed scrapie. Also, none of the offspring observed to > or = 24 months of age from reciprocal cross, via embryo (0/67), or via the uterus (0/25), or from the negative-control group (0/33) developed scrapie. Fifty-six of the offspring via embryo, 19 of these via the uterus, and 31 negative controls survived to > or = 60 months of age. Of the 21 sheep in the positive-control group, 2 (9.5%) developed scrapie, 1 at 31 months of age and 1 at 42 months of age. In the Cheviot offspring, the percentage of sheep carrying the short incubation allele ranged from 24 to 44% and the percentage in the Suffolk offspring ranged from 61 to 83%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bluetongue: the disease in cattle.

Most researchers in South Africa found that although BT virus could be isolated from apparently healthy cattle and from inoculated cattle the virus did not produce overt clinical disease in cattle. However, when epizootics were reported outside Africa, clinical signs were observed in cattle in Israel, Palestine, Syria, Portugal, and Spain. Most natural BT infections in cattle in the United States do not result in overt clinical signs. However, in certain infected herds, approximately 5% of the cattle show from mild to severe disease. Except for severe cases, spontaneous recovery is usual. The clinical diagnosis of BT in cattle is difficult and requires laboratory assistance. Culicoides variipennis can serve as a vector of BT virus from cattle to cattle, cattle to sheep, sheep to cattle, and sheep to sheep. In utero transmission occurs in cattle and can result in abortion, hydraencephaly, congenital deformity, and birth of viraemic calves which may or may not develop BT antibody. Calves inoculated in utero or those born to infected dams may have a persistent viraemia with or without BT antibody. tone such animal has been held in insect-secure quarters and has continued to harbour virus for 3 years. Bluetongue virus was isolated from the semen of experimentally infected bulls. Calves inoculated with BT virus and also given an immuno-suppressant developed marked clinical disease in 8 to 12 days. Bluetongue virus is very closely associated with the erythrocytes of infected cattle, sheep, and goats. Cattle are considered important and relatively long-term virus reservoirs. In attempts to determine the maximum period of viraemia in cattle it is necessary to inoculate washed erythrocytes, rather than whole blood, and to use susceptible sheep as the assay system rather than embryonated chicken eggs.

Epizootiology of bluetongue: the situation in the United States of America.

Bluetongue was first reported in the United States in 1948 in sheep in Texas. The virus has now been isolated from sheep in 19 States. When the disease first occurs in a flock, the morbidity may reach 50 to 75% and mortality 20 to 50%. In subsequent years, the morbidity may be only 1 to 2% with very few deaths. Difference in breed susceptibility has not been observed. Natural bluetongue infection has not been observed in Angora or dairy goats. Bluetongue virus was first isolated from cattle, in Oregon, in 1959. The virus has now been isolated from cattle in 13 States. In cattle, the disease is usually inapparent but can cause mild to severe clinical disease and neonatal losses. Natural clinical bluetongue has also been reported in bighorn sheep, exotic ruminants in a zoo, mule deer, and white-tailed deer. Serological evidence of exposure to the virus has also been found in other species of ruminants in the wild. Inoculation of virulent bluetongue virus, vaccine virus, or natural disease can cause congenital deformities and neonatal losses in calves, lambs, and white-tailed deer fawns. Culicoides is considered the important insect vector of bluetongue. The virus has also been isolated from sheep keds and cattle lice. U.S. field strains of the virus fit into four serologic groups. No cross reactions were found between bluetongue and epizootic haemorrhagic disease of deer viruses. Cattle are considered significant virus reservoirs. It is necessary to use washed erythrocytes, rather than whole blood, and to inoculate susceptible sheep, rather than embryonated chicken eggs, to detect longer-term viraemia in cattle.