Highlights from the Hill: needlestick prevention and reduction in medical errors.
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Biomedical subjects
Publications and source records attributed to J F Adams.
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According to research data from both the USDA and private companies, Americans consume approximately one serving of whole grain foods per day. Current guidelines recommend three or more servings a day. The health benefits of whole grains are well documented. However, convincing Americans to eat them, especially in the amount recommended, has been unsuccessful. Adults and children give a variety of reasons for not choosing whole grain foods, including these: a lack of understanding of the health benefits of whole grain foods, an inability to identify whole grain foods at the point of purchase, their taste, their cost, the time it takes to prepare them and the availability of whole grain foods in stores. This paper addresses some of the misconceptions surrounding whole grain foods and offers strategies for helping consumers choose more whole grain products. In addition, we present historical information on the consumption trends of whole grains as well as educational and promotional opportunities that industry and health professionals can use to encourage the public to eat more whole grains.
As nurses and voters in the United States, we have a professional responsibility to keep abreast of issues that affect health care delivery. We must be aware of who our legislators are and how to contact them regarding the issues at hand. This article tells you how to do that and brings to the forefront the current bills and legislative issues impacting nursing.
BACKGROUND: Infection with Mycobacterium tuberculosis induces a type-1 immune response, whereas intestinal parasites elicit a type-2 response. Given that type-1 and type-2 responses inhibit each other, we investigated if M tuberculosis downregulates serum IgE, a marker of a type-2 response. METHODS: A prospective study was done in the Western Cape Province of South Africa, where tuberculosis and intestinal-parasite infection are common. Total serum IgE was determined for 37 controls and for 33 adolescent patients at presentation with tuberculosis and after successful completion of treatment. IgE specific for ascaris and allergens were measured in a subset of these individuals. Mantoux skin tests were done on 35 controls and on 31 patients at diagnosis. FINDINGS: Total IgE concentrations were high in controls (mean 313 kU/L) and in patients before treatment (mean 457 kU/L, p=0.085) and declined in all patients following successful treatment (mean 175 kU/L, p<0.0001). Posttreatment IgE concentrations did not differ from concentrations in controls. Ascaris-specific IgE was lower in controls (mean 1.73 kU/L) than in patients before treatment (4.62 kU/L, p=0.023) and was 2.39 kU/L in patients after treatment (p=0.0625). Tuberculin induration correlated inversely with IgE in patients but not in controls. INTERPRETATION: Infection with M tuberculosis as such is not incompatible with a prominent IgE response. IgE concentrations decreased after successful treatment of tuberculosis, showing that IgE concentrations in human beings can be downregulated under these circumstances, presumably due to enhancement of a type-1 response.
OBJECTIVE: Squamous cell carcinoma (SCC) of the head and neck is rare in patients younger than 45 years. Patients aged 18 to 45 years with SCC of the oral cavity (OC) and oropharynx (OP) were retrospectively compared with older control subjects. METHODS: Twenty of 127 patients with OC/OP SCC were young adults. Thirteen patients (10 men) comprise the present series; 9 had OC lesions. Seven case controls were identified. RESULTS: Overall, 15.75% of patients with OC/OP SCC were 18 to 45 years old. Seven OC lesions were early stage, and 2 were late stage; OP lesions were evenly divided. Eleven of 13 patients were disease free at the time of their last visit; 2 died of disease. Thirty-one percent of young patients were heavy drinkers; 77% of them smoked. CONCLUSIONS: Young adults' survival rate resembles that reported for all patients with head and neck cancer stage for stage. Tobacco and alcohol abuse prevention among young people is imperative. Health care providers who encounter a young patient with a suspicious head or neck lesion must include malignancy in their differential diagnosis.
PURPOSE: Second malignancies have been reported among patients who were treated by radiation therapy or chemotherapy alone or in combination. Studies have implied an increased risk of breast cancer in women who received radiotherapy as part of their treatment for Hodgkin's disease. This review was performed to determine if there is an association between splenectomy and subsequent breast cancer. METHODS AND MATERIALS: One hundred and thirty-six female patients with histologically proven Hodgkin's disease were seen in the Division of Radiation Oncology between 1962 and 1985. All patients received mantle or mediastinal irradiation as part of their therapy. The risk of breast cancer was assessed and multiple linear regression analysis was performed on the following variables: patient age, stage, dose and extent of radiation field, time after completing radiation therapy, splenectomy, and chemotherapy. RESULTS: Breast cancer was observed in 11 of 74 splenectomized patients and in none of 62 patients not splenectomized. The mean follow-up was 13 years in splenectomized patients and 16 years, 7 months in nonsplenectomized patients. Nine patients developed invasive breast cancer and two developed ductal carcinoma in situ. Splenectomy was the only variable independently associated with an increased risk of breast cancer (p < 0.005) in multiple linear regression analysis; age, latency, and splenectomy considered together were also associated with an increased risk of breast cancer (p < 0.01). CONCLUSION: Our data show an increased risk of breast cancer in splenectomized patients who had treatment for Hodgkin's disease. A multiinstitutional survey may better define the influence of splenectomy relative to developing breast cancer in patients treated for Hodgkin's disease. The risk of breast cancer should be considered when recommending staging laparotomy, and we recommend close follow-up examination including routine mammograms for female patients successfully treated for Hodgkin's disease.
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Medicinal leech therapy is recorded as early as 200 B.C. to treat everything from mental illness to headaches. The medicinal leech (Hirudo medicinalis) is used today as a successful treatment for venous congestion following replantation or transplantation of tissue. This paper discusses specific leeching properties, indications for use, nursing care and expected outcomes of leech therapy.
The present study extends previous reports of hepatic damage 24 h after halothane anaesthesia in the phenobarbitone pretreated hypoxic rat model by fully characterizing the lesion during the time course of its onset and recovery. Phenobarbitone treated animals exposed to halothane (1% for 2 h in 14% inspired oxygen) were killed 1, 2, 4, 6, 12 and 24 h and 2, 3, 5, 10, 15 and 30 days after commencement of the anaesthetic period. Blood was collected 1 day before the administration of halothane and at the time of killing for determination of serum alanine aminotransferase (ALT), a biochemical index of hepatic damage. Liver tissue was obtained immediately at post-mortem for histological examination. Serum ALT was increased at the end of the anaesthetic period, i.e. 2 h, with peak levels occurring at 12-24 h and remaining elevated for 3 days after exposure. Minor changes in liver histology were evident at 2 h in 50% of the animals and by 6 h all animals had mild hepatic injury. The extent of the necrosis was maximal at 24 h and this was sustained until 3 days. By 5 days after exposure minimal evidence of liver damage was observed and animals killed at 30 days had morphologically normal livers. Elevation of serum ALT or changes in liver histology were not observed in other treatment groups. The early onset of damage at 2-6 h is in keeping with direct hepatotoxicity associated with the biotransformation of halothane.
Tetrazolium salts, histochemical indicators of mitochondrial respiratory enzymes, have been used by some pathologists to detect infarcts in myocardium. We explored the utility of this technique in detecting experimental brain infarcts and report our findings. Infarcts were produced in cats, gerbils, and rats by unilateral temporal and permanent cerebral vessel occlusion. After various time periods the animals were killed, and their brains were reacted with 2,3,5, triphenyl, 2H-tetrazolium chloride (TTC). The experimental and contralateral hemispheres were examined by light and electron microscopy. The TTC-stained tissue was correlated with histology. In some situations the histological condition of the tissue correlated well with the TTC staining results. Brain regions supplied by temporarily occluded vessels and judged infarcted by light and electron microscopy did not stain. In these regions less than 6% of the mitochondria were intact. In brain tissue from animals with permanent vessel occlusion (no reflow) mitochondria were intact despite the fact that other cellular organelles, such as nuclei, were destroyed. TTC stained such mitochondria and as a result could not distinguish infarcted brain in complete ischemia situations (no reflow). Another draw back to this staining procedure was 36 h after infarction macrophages with intact mitochondria would replace damage neurons and be stained. Under ideal conditions though this technique can detect irreversibly damaged brain as early as 2.5 h after artery occlusion.
In a survey of 46 randomly selected diabetic patients on biguanide therapy, 30% had malabsorption of vitamin B12. Withdrawal of the drug resulted in normal absorption in only half of those with malabsorption. In most patients with persistent malabsorption, the results of absorption tests with exogenous intrinsic factor suggested the diagnosis of coincidental intrinsic factor deficiency. Further considerations, however, led to the concept that biguanides can induce malabsorption by two different mechanisms. One of these is temporary and unrelated to intrinsic factor secretion and the other is permanent and mediated by depression of intrinsic factor secretion.
The conventional method of measuring vitamin B12 absorption using a whole-body counter normally involves a delay of fourteen days before complete faecal excretion of unabsorbed B12 tracer can be assumed. A modified technique has been used which reduces the delay to four days. A non-absorbable tracer, 51Cr-chromic chloride, was administered firstly with 58Co-labelled vitamin B12 and then three hours later with 57Co-labelled vitamin B12 and then three hours later with 57Co-labelled vitamin B12 plus 50 mg hog intrinsic factor which normalises B12 malabsorption in patients with pernicious anaemia. Three days later, the residual whole-body activities of the three radionuclides were measured. The retention of 51Cr indicated the efficiency of faecal excretion of unabsorbed B12 tracer and could be used to quantify vitamin B12 absorption before complete excretion of unabsorbed B12 tracer. Vitamin B12 absorption values were measured at four days by this technique and compared with the corresponding values at fourteen days in 38 tests on 33 subjects, 16 of whom had pernicious anaemia. Excellent correlations between the results obtained at four and 14 days were obtained for both B12 tracers.
In vivo studies were undertaken to determine whether free radical formation in the liver during administration of various halogenated anesthetics is associated with hepatotoxicity of these agents in an animal model. In addition to the anesthetics halothane, enflurane, and isoflurane, carbon tetrachloride was studied as an example of a hepatotoxic halogenated compound acting by a free radical mechanism. Free radicals were trapped in vivo during anesthesia as stable adducts using the spin trap, alpha-phenyl-t-butyl nitrone. These adducts were extracted from the liver and studied by electron spin resonance spectrometry. Free radicals were detected after administration of halothane or carbon tetrachloride, compounds which were hepatotoxic under the conditions of the experiment, but were not found after anesthesia induced with enflurane or isoflurane, anesthetics which were not hepatotoxic under identical conditions. The free radical trapped after alpha-phenyl-t-butyl nitrone treatment of halothane-anesthetized rats appeared to be a metabolic intermediate of halothane.
The assay procedure described in this paper allows the calculation of pharmacokinetic data of antipyrine disposition to be obtained from a single animal with minimal disturbance in hematocrit. A sample volume (100 microliters) allows the repeated use of the same rat for studies of hepatic drug metabolism. The lower limit of sensitivity is 5 micrograms/ml, with a range of linearity extending to 100 micrograms/ml. This allows for various dosing regimens. The GLC assay is rapid and accurate as shown by comparison with previously published values for the half-life of antipyrine in rats.
The relationship between the reductive metabolism of halothane and hepatotoxicity was examined in three rat strains (Fischer 344, Sprague-Dawley, and black hooded Wistar) to determine if there were genetic differences in 1) the reductive metabolism of halothane under identical exposure conditions, and 2) the susceptibility to the hepatotoxic effects of halothane. Halothane hepatotoxic was produced in all rat strains by exposing phenobarbital-pretreated rats to 1 per cent halothane under mild hypoxia (14 per cent oxygen, inspired) for 2 h. Generally the levels of both 2-chloro-1,1,1-trifluoroethane (CTF) and 2-chloro-1,1-difluoroethylene (CDF), two volatile metabolites of halothane, increased from the onset of anesthetic exposure and reached a plateau after approximately 60 min. The exception to this trend were phenobarbital-pretreated Wistar rats (exposed to 1 per cent halothane with 14 per cent oxygen) where the levels of either CDF or CTF were high initially (10-min sample) and decreased in subsequent samples to reach a plateau after 80 min. The plateau levels of both CDF (approximately 6 ppm) and CTF (approximately 20 ppm) were not significantly different among the three rat strains exposed to halothane (1 per cent) and hypoxia with prior enzyme induction. There were, however, significant differences in both biochemical and pathological changes among the three strains exposed under the above identical conditions when the rats were killed 24 h after anesthetic exposure. For example, serum alanine aminotransferase (ALT) was increased fourfold in the Fischer strain but only doubled for the other two strains. Moreover, while all three strains had various amounts of hepatocyte damage in the vicinity of the central veins when the rats were exposed to halothane, hypoxia, and enzyme induction, only the Fischer strain showed hepatocyte damage under the exposure conditions of halothane (1 per cent) and normoxia (21 per cent oxygen, inspired) with prior enzyme induction. The results support the role of reductive metabolism of halothane in the etiology of halothane hepatotoxicity. Furthermore, they suggest that genetic variations in the susceptibility of the liver to the reactive intermediates or metabolites formed during reductive metabolism of halothane may be a significant factor in halothane hepatotoxicity.
The effect on intrinsic factor (IF) secretion of eight weeks' continuous treatment with a clinically relevant oral dose of ranitidine hydrochloride, a new histamine H2-receptor antagonist, has been studied in 11 patients with duodenal ulcer. There was no significant difference between the mean IF output during treatment of after drug withdrawal as compared with the control value, despite highly significant (p less than 0.001) reduction in acid output during treatment. In the short term this potent drug is unlikely to cause pernicious anemia from interference with IF secretion, although further study is necessary to exclude this possibility after long-term use.
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1. The long-term clearance of radioactive vitamin B12 from serum and from whole body was measured in control subjects and patients with treated pernicious anaemia and the data were analysed by the occupancy principle to provide estimates of dietary intake, daily requirements and whole-body mass of vitamin B12. 2. In six cases the daily requirement for vitamin B12 ranged from 0.15 to 1.9 microgram with an average of 1.0 microgram. The whole-body vitamin B12 in four cases ranged from 780 to 1350 microgram with an average of 1060 microgram. 3. Estimates of the whole-body vitamin B12 on the assumption of single-pool equilibrium gave constantly changing results, which, together with discrepant half-lives for serum radioactivity and whole-body radioactivity, constitute evidence against the concept of single-pool equilibrium.