By F. Jens. The Julliard School.
Outcome of occupational asthma due to platinum salts after transferral to low-exposure areas 20 mg deltasone visa. Five year longitudinal study of workers employed in a new toluene diisocyanate manufacturing plant discount deltasone 10 mg with amex. Many of these practices are offered for patients with real or suspected allergy ( 2) buy deltasone 40mg line. They are especially popular today, even though there is no evidence that they are either alternative or complementary to rational scientifically based medical practice. Accurate diagnosis and effective therapy of allergic disorders based on sound theory and clinical research can be accomplished efficiently, safely, and cost effectively. There is little if any justification today for an empirical approach to the allergic patient. However, the clinician who treats allergic patients must be sufficiently knowledgeable about both accepted and unproved techniques and theories in order to practice rationally and successfully. Terminology Standard practice is generally defined as the methods of diagnosis and treatment used by reputable physicians in a particular subspecialty or primary care practice. In general, physicians who are knowledgeable, trained, and experienced in allergy may prefer certain diagnostic and therapeutic methods while at the same time recognizing that other methods are acceptable. Acceptable methods are based on, or consistent with, current scientifically established mechanisms of allergy. In addition, they have stood the test of time through a sufficient period of usage and an evaluation by properly conducted scientifically based clinical trials demonstrating efficacy and safety. Experimental procedures are potentially new methods of practice arising from the results of scientific studies or from chance empiric observation. Experimental methods of diagnosis and treatment are those that are used in clinical trials on subjects who are informed of the experimental nature of the procedure, their potential risks, and their potential benefits. Controversial methods refer to those procedures that lack scientific credibility and have not been shown to have clinical efficacy, even though they may be used by a few physicians in their practices. Most of the controversial methods discussed in this chapter have been tested in clinical trials; the published results show either ineffectiveness or insufficient data to establish effectiveness. The expression unproved is another term for procedures that are controversial, as defined above. The terms alternative and complementary are not appropriate because they tend to obscure the real issue of whether or not a particular procedure has been validated for clinical use by proper scientific scrutiny. The terms fraud and quackery generally equate to medical practices performed by those individuals who knowingly, deliberately, and deceitfully use unproven and controversial methods for profit. Many physicians who use controversial procedures in allergy practice, however, do so because they sincerely believe that these practices are worthwhile and are unwilling to accept evidence to the contrary. Laboratory testing is used selectively to supplement the history and physical findings, especially when objective measurement of a functional abnormality such as airway obstruction is desired, or when other diseases must be ruled out of consideration. Allergy tests such as skin-prick or intradermal tests, patch tests, or in vitro antibody tests are in fact tests for the presence of an immune response of a particular type [e. For example, the in vitro histamine release test has been widely used in allergy research, where it has been invaluable in furthering knowledge of disease, but it cannot be recommended for clinical use at this time. It may eventually be modified to assume a place in allergy practice in the future. Categories of inappropriate procedures Diagnostic Procedures of No Value Under Any Circumstances The procedures included in this category are not based on sound scientific principles, and they have not been shown by proper controlled clinical trials to be capable of assisting in diagnosis for any condition. The Cytotoxic Test This is also known as the leukocytotoxic test or Bryan test ( 3,4). It is the microscopic examination of an unstained wet mount of whole blood or buffy coat on a slide that had been previously coated with a dried food extract. Reproducibility of identifying unstained leukocyte morphologic changes has not been established. There are no known allergic diseases caused by leukocyte cytotoxicity from foods, either directly or immunologically. Some drugs do cause immunologically mediated cytotoxicity of leukocytes, but there have been no studies to show that this can be demonstrated in vitro by the Bryan test. Several controlled clinical trials have reported that the cytotoxic test is not reproducible, and it does not correlate with any clinical evidence of food allergy ( 5,6). The test is performed by giving the patient a test dose of an extract of one of these substances by either intracutaneous injection, subcutaneous injection, or by sublingual drop. The patient then records any subjective sensations appearing during the next 10 minutes. Any reported symptom constitutes a positive test result, that is, evidence for allergy to the substance. If the test is negative, it is repeated with higher concentrations of the substance until the patient reports a sensation or symptom. When the test is performed by intradermal injection, increasing wheal diameter with increasing dose is considered corroborative evidence of a positive test result. Some proponents measure change in pulse rate during the test, but there is disagreement about its significance. Published reports of provocation neutralization testing yield conflicting results ( 16). Studies have included subjects with varying clinical manifestations, different testing methods, and variable criteria for a positive test result. Many lack placebo controls, reflecting the absence of standardization and the subjective nature of provocation neutralization. Modern concepts of immunologic disease provide no rationale for the provocation of subjective symptoms and their immediate neutralization under the conditions used in this procedure ( 17). A placebo-controlled double-blind evaluation of provocation neutralization for diagnosis of food allergy in 18 patients showed that symptoms were provoked with equal frequency by food extracts and by placebo (18), showing that results are based on suggestion (19). Furthermore, there is a potential danger of causing a local reaction in the mouth or even a systemic reaction ( 20) in a patient tested with an allergen to which there is a significant IgE sensitivity. The procedure is time consuming, because only a single concentration of a single allergen can be tested at one time. In the United States, there are several environmental control units in which patients are subjected to airborne exposure to chemicals in testing booths ( 21). Unlike bronchial provocation testing in asthma, a positive test for environmental illness is designated by the appearance of self-reported symptoms only. Electrodermal Diagnosis This procedure purports to measure changes in skin resistance after the patient is exposed to an allergen ( 22). The allergen extract, usually a food, is placed in a glass vial that is then put on a metal plate inserted into the electrical circuit between the skin and a galvanometer. A decrease in skin electrical resistance is said to be a positive test indicating allergy to the food. This procedure is without any rational basis, and there have been no studies to support its use. Proponents use acupuncture points on the skin when performing this bizarre procedure, often referred to as electroacupuncture. A recent controlled study reported that it was incapable of detecting specific allergic sensitivities ( 23).
The frequency cheap deltasone 20 mg otc, severity deltasone 40 mg fast delivery, and duration of smoke exposures appear to be important determinants of clinical outcomes generic 40 mg deltasone amex, as well as individual host susceptibility factors. Although the complexities of exposure assessment and unpredictable nature of fires have permitted only limited evaluation of acute dose-response relationships and even less refined assessments of the long-term effects of smoke inhalation, many important observations have been made about the acute and chronic effects of smoke inhalation in fire fighters. Several studies have examined changes in fire fighters lung function in conjunction with measures of airway reactivity. Sheppard and co-workers measured baseline airway reactivity to methacholine in 29 fire fighters, and then followed pre-shift, post-shift, and post-fire spirometry over an eight-week period. Sherman and co-workers performed spirometry and methacholine challenge testing before and after firefighting activities in 18 Seattle fire fighters. The finding of increased airway responsiveness in fire fighters suggests that they may be at risk for accelerated loss of ventilatory function. Chia and co-workers exposed 10 new fire fighter recruits and 10 experienced fire fighters with normal airway reactivity to smoke in a chamber without respiratory protection. However, 80% of the experienced fire fighters developed increased airway reactivity. The authors suggested smoke-induced chronic injury or inflammation of the pulmonary epithelium in experienced fire fighters might lead to increased risk of airway reactivity. The authors speculated that airway obstruction following smoke inhalation might be more common and persistent than generally recognized. Recent studies of fire victims using bronchoalveolar lavage have provided insights into the cellular and biochemical effects of smoke inhalation. Following smoke inhalation, significant numbers of neutrophils are recruited to the airways. In patients with inhalation injury and cutaneous burns, increased numbers of both alveolar macrophages and neutrophils have been demonstrated in the airways; the alveolar macrophage may further contribute to the inflammatory response by elaborating additional cytokines such as tumor necrosis factor and interleukin-1, interleukin-6, and leukotriene B4. Although preliminary, these findings suggest potential mechanisms for the decrements in lung function and increases in airway reactivity demonstrated in epidemiologic investigations. Longitudinal studies of lung function in fire fighters have provided conflicting results. The authors concluded that selection factors within the fire department and increased use of personal respiratory protective equipment were important in reducing the effects of smoke inhalation; significant attrition in follow-up cohorts may also have influenced the results. It is important to note that the participants in these studies were evaluated before routine use of respiratory protective equipment, and may have sustained very significant smoke exposures. Two more recent studies of fire fighters from the United Kingdom have not shown evidence for longitudinal decline in lung function. It is important to note that wildland fire fighters, who are not provided with or do not typically wear protective respiratory equipment, have been shown to have decrements in lung function and increased airway responsiveness after a season of fighting fires. However, these results may be due to the healthy worker effect, where selections of healthy workers results in mortality rates lower than a general reference population. In a study of New Jersey fire fighters, Feuer and Rosenman found an excess of chronic respiratory disease compared to police controls (Proportionate Mortality Ratio = 1. Disasters other than fires have also been responsible for significant exposure to aerosolized respirable particles and gases. Helens eruption in 1980, hospital visits for pediatric asthma were increased in Seattle, Washington. After the explosion of the Union Carbide Chemical Plant in Bhopal, India, studies documented an increased loss of pulmonary function compared to normal aging and increased presence and severity of obstructive airways disease. Respiratory health consequences after exposure to a high-concentration particulate during a disaster can be grouped into three major categories: (1) inflammation-related aerodigestive syndromes (i. Mechanicalventilation was needed in 67% (median use seven days); two died; the remainder responded to corticosteroidsor supportive care; and post-treatment all had normal or near normalspirometry. Taken together, these findings strongly argue for providing improved respiratory protection at future disasters and other significant environmental/occupational exposures. Following any urban disaster, those exposed will naturally be concerned about their risk for developing malignancies due to their potential exposures to multiple combustion or pyrolysis products, many of which are known carcinogens (e. In contrast, thyroid cancer and leukemia resulting from radiation or certain chemical exposures have short latency periods, especially in children. It is important to consider the biologic plausibility and latency periods in post-disaster exposure counseling and planning. Hydrogen Cyanide Cyanide is a ubiquitous compound that is widely used in industry in its salt form and therefore, can be easily exploited by terrorists. Most information regarding cyanide toxicity comes from accidental disasters such as fires, explosions, industrial accidents, and poisonings (including consumption of apricot pits and cassava roots). Cyanide poisons aerobic metabolism by binding to the ferric ion (Fe3+) of mitochondrial cytochrome oxidase a. Cyanide binds 3 reversibly through the action of the enzymes rhodanese, 3-mercaptopyruvate sulfurtransferase, and thiosulfate reductase. Cyanide can readily diffuse through the epithelium and therefore is toxic through inhalation, ingestion, or topical contact. The clinical presentation of cyanide toxicity results from progressive tissue hypoxia. Additional signs and symptoms not specific for cyanide toxicity include diaphoresis, flushing, weakness, and vertigo. The odor of bitter almonds, which is commonly thought to be characteristic, is described by fewer than 60% of persons exposed to cyanide. Therefore, treatment is often empiric and should be considered from known or suspected exposures when symptoms are severe and not responding to conservative therapy. The primary goal of treatment is displacement of cyanide from cytochrome oxidase a3 through the formation of methemoglobin by sodium nitrite. Owing to a lack of sulfur donors during acute intoxication, sodium thiosulfate is administered as additional therapy to enhance clearance of cyanide. Sodium thiosulfate combines with sequestered cyanide to form thiocyanate, which is excreted from the body. A potential advantage is that methemoglobinemia is not a consequence of hydroxocobalamin therapy. Although automobile exhaust systems, faulty heating systems and fires are the common sources of carbon monoxide intoxication, the improper use of temporary home generators during blackouts is the most common cause in disaster environments. The affinity of the hemoglobin for carbon monoxide is over 200 times greater than that for oxygen. Cyanosis is not found in carbon monoxide poisoning due to the cherry-red color of the carboxyhemoglobin. Moderate exposures (20 - 30 ppm) commonly present with more severe headaches, fatigue and shortness of breath often accompanied by confusion, blurred vision, nausea and vomiting. This results from the increased minute ventilation (respiratory rate multiplied by tidal volume).
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