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Also of importance was the consideration that the recommendations would be or are also in concert with some of the other specialties participating in the Choosing Wisely campaign. Clinical policy: neuroimaging and decision-making in adult mild traumatic brain injury in the acute setting. Estimating the proportion of healthcare-associated infections that are reasonably preventable and the related mortality and costs. Strategies to prevent catheter-associated urinary tract infections in acute care hospitals. Appropriateness of use of indwelling urinary catheters in patients admitted to the medical service. The association between indwelling urinary catheter use in the elderly and urinary tract infection in acute care. Overutilization of indwelling urinary catheters and the development of nosocomial urinary tract infections. Inappropriate use of urinary catheters in elderly patients at a midwestern community teaching hospital. Reducing cost at the end of life by initiating transfer to inpatient hospice in the emergency department. Half of older Americans seen in emergency department in last month of life; most admitted to hospital, and many die there. Management of pediatric skin abscesses in pediatric, general academic and community emergency departments. Randomized, controlled trial of antibiotics in the management of community-acquired skin abscesses in the pediatric patient. National Hospital Ambulatory Medical Care Survey: 2007 Emergency Department Summary. The role of oral ondanestron in children with vomiting as a result of acute gastritis/gastroenteritis who have failed oral rehydration therapy: a randomized controlled trial. Oral versus intravenous rehydration for treating dehydration due to gastroenteritis in children. Diagnostic patterns and temporal trends in the evaluation of adult patients hospitalized with syncope. Current diagnosis of venous thromoboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Is the ordering of imaging for suspected venous thromboembolism consistent with D-dimer result? Evaluation of pulmonary embolism in the emergency department and consistency with a national quality measure. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. European guidelines for the management of acute nonspecific low back pain in primary care. Diagnostic imaging practice guidelines for musculoskeletal complaints in adults -an evidence-based approach part 3: spinal disorders. Guidelines for lumbar spine radiography in acute low back pain: effect of implementation in an accident and emergency department. Balancing the benefits and risks of empirical antibiotics for sinusitis: A teachable moment. Unenhanced helical computed tomography vs intravenous urography in patients with acute flank pain: accuracy and economic impact in a randomized prospective trial. A Government Services Chapter represents emergency physicians employed by military branches and other government agencies. Emergency physicians are recognized and valued for their commitment to high quality patient care, teaching, leadership, research and innovation. Prior to ordering a genetic test for an inherited condition, the health care provider should ask a patient about prior genetic testing and review the medical record for previously performed genetic tests. The relative risk conferred by the 4 allele is confounded by the presence of other risk alleles, gender, environment and possibly ethnicity.

Clinical evidence In a series of studies in healthy subjects, drinking 200 mL of coffee with various test meals containing radiolabelled iron resulted in a 39% to 83% reduction in the absorption of iron. No decrease was observed if the coffee was drunk one hour before the meal, but when the coffee was given one hour after the meal the reduction was the same as taking it simultaneously with the meal. Almost a quarter of the mothers were considered to have iron-deficiency anaemia (haemoglobin levels of less than 11 g/dL), compared with none among the control group of non-coffee drinkers. The coffee drinkers drank more than 450 mL of coffee daily, equivalent to more than 10 g of ground coffee. Mechanism It is suggested that polyphenolics in coffee might interfere with the absorption of iron. Note that coffee is not generally considered to be a suitable drink for babies and children, because of its effects on iron absorption. Coffee + Phenylpropanolamine A case report describes mania in a patient who drank coffee and took phenylpropanolamine. Evidence, mechanism, importance and management A case report describes mania with psychotic delusions in a healthy woman (who normally drank 7 to 8 cups of coffee daily) within 3 days of her starting to take a phenylpropanolamine-containing decongestant. She recovered within one week of stopping both the coffee and the phenylpropanolamine. However, case reports have described other severe reactions with caffeine, see Caffeine + Phenylpropanolamine, page 103. Coffee + Tetracycline Coffee does not appear to affect the absorption of tetracycline. Evidence, mechanism, importance and management A study in 9 healthy subjects found that 200 mL of coffee (milk content, if any, unstated) did not significantly affect the bioavailability of a single 250-mg dose of tetracycline. Influence of liquids (coffee and orange juice) on the bioavailability of tetracycline. The influence of coffee with milk and tea with milk on the bioavailability of tetracycline. For information on the pharmacokinetics of individual flavonoids present in cola, see under flavonoids, page 186. Interactions overview Cola contains significant amounts of caffeine, therefore the interactions of caffeine, page 97, should be applied to cola, unless the product is specified as decaffeinated. By virtue of its caffeine content cola may also cause serious adverse effects if used with other drugs or herbs with similar effects, such as ephedra, page 176. Cola may reduce the bioavailability of halofantrine and increase the risk of developing hypertension. For information on the interactions of individual flavonoids present in cola, see under flavonoids, page 186. Carbonated cola beverages are acidic, and they can therefore interact with drugs by altering gastric acidity. The best example of this is that they can increase the absorption of the azole antifungal drugs ketoconazole and itraconazole. However, this mechanism is not going to be applicable to herbal medicines containing cola extracts, and these interactions are not therefore covered here. Other constituents include flavonoids from the flavanol group (such as catechin and epicatechin), amines, an anthocyanin pigment (kola red) and betaine. Use and indications the main use of cola seed is as a stimulant for depression, tiredness and poor appetite, and as a diuretic. Evidence, mechanism, importance and management There is a possibility that the effect of cola on blood pressure might differ from that of pure caffeine. There appear to be very few published studies of the effect of cola on blood pressure; however, in the Nurses Health prospective cohort studies, both sugared cola and diet cola beverages were associated with an increased risk of developing hypertension with increased intake. However, the modest hypertensive effects of the caffeine content of cola may be of importance. See Caffeine + Antihypertensives, page 99, for further discussion of the adverse effect of caffeine on blood pressure.

A comprehensive review, including medical conditions, should be done at periodic intervals, at least annually, to determine if the medications are still needed and if any medications can be discontinued. The patient or caregiver should be the sole source of truth when taking the medication history. The patient or caregiver should be interviewed by someone with medication-use knowledge, ideally a pharmacist, and medications should be continued only if there is an associated patient indication. If a pharmacist is not available, then at a minimum, the healthcare worker taking the history should have access to robust drug information resources. The history should include the drug name, dose, units, frequency, and the last dose taken; and indication if available. Unnecessary medications should be discontinued, duplicate or overlapping therapies should be changed, and the specific changes should be clearly communicated to the patient. The Joint Commission recommends a thorough medication review at admission and discharge to prevent any unnecessary medications being continued. Serious medication errors, including patient deaths, have occurred because oral liquids are prescribed and/or administered using English measurement units such as the teaspoon or tablespoon. For medical professionals, best practice is using units and volume when prescribing a single-agent liquid medication, to be sure the dose is clear; but for administering, use only mL for measuring the amount. Prescribing using the metric system and dispensing with a metric measuring device will help avoid these preventable errors. Released June 1, 2017 How this List Was Created A task force made up of pharmacists from all practice settings was formed. The task force was oriented to the criteria used to establish Choosing Wisely lists and already established recommendations. Based on this information and on their knowledge of how medications are prescribed, dispensed, and administered, the task force developed an initial list of recommendations. Through a consensus process over time the list was prioritized down to a total of five recommendations. Economic value of pharmacist-led medication reconciliation for reducing medication errors after hospital discharge. Multidisciplinary approach to inpatient medication reconciliation in an academic setting. Unnecessary transfusion generates costs and exposes patients to potential adverse effects without any likelihood of benefit. Thrombophilia testing is costly and can result in harm to patients if the duration of anticoagulation is inappropriately prolonged or if patients are incorrectly labeled as thrombophilic. Blood products can cause serious harm to patients, are costly and are rarely indicated in the reversal of vitamin K antagonists. In non-emergent situations, elevations in the international normalized ratio are best addressed by holding the vitamin K antagonist and/or by administering vitamin K. By ensuring a patient receives an appropriate regimen of anticoagulation, clinicians may avoid unnecessary harm, reduce health care expenses and improve quality of life. In particular, they experience an increased risk of alloimmunization to minor blood group antigens and a high risk of iron overload from repeated transfusions. Moreover, there is no evidence that transfusion reduces pain due to vaso-occlusive crises. Do not discontinue heparin or start a non-heparin anticoagulant in these low-risk patients because presumptive treatment often involves an increased risk of bleeding, and because alternative anticoagulants are costly. Unnecessary treatment exposes patients to potentially serious treatment side effects and can be costly, with little expectation of clinical benefit. In the pediatric setting, treatment is usually not indicated in the absence of mucosal bleeding regardless of platelet count. In the adult setting, treatment may be indicated in the absence of bleeding if the platelet count is very low. In patients preparing for surgery or other invasive procedures, short-term treatment may be indicated to increase the platelet count prior to the planned intervention and during the immediate post-operative period.

Isoflavones + Benzodiazepines the interaction between isoflavones and benzodiazepines is based on experimental evidence only. Evidence, mechanism, importance and management In two experimental studies,1,2 the isoflavone puerarin has been shown to be a weak benzodiazepine antagonist. It is therefore theoretically possible that puerarin might reduce the effects of benzodiazepines if given concurrently. The fact that the information relates to an isolated isoflavone, and the effect was only weak, suggests that a clinically important interaction between isoflavones and benzodiazepines is unlikely. Inhibition of [3H] flunitrazepam binding to rat brain membranes in vitro by puerarin and daidzein. Isoflavones + Cardiovascular drugs; Miscellaneous the interaction between isoflavones and miscellaneous cardiovascular drugs is based on experimental evidence only. Evidence, mechanism, importance and management Some experimental studies have shown that isoflavones from kudzu, page 267, may inhibit of platelet aggregation. Some have interpreted these studies to indicate that, theoretically, kudzu might increase the risk of bleeding when used with antiplatelet drugs or anticoagulants, and that caution is warranted on concurrent use. Given the nature of the evidence, and the fact that it relates to isolated isoflavone constituents of kudzu, this appears to be a very cautious approach. Note that puerarin injection is used in China to treat angina and cardiovascular disease. Clinical studies comparing standard Western treatment (nitrates, beta blockers, calcium-channel blockers, aspirin, anticoagulants, etc. It was concluded that, although adverse events were inadequately reported, treatment including the injection tended to result in more adverse effects. Antithrombotic and antiallergic activities of daidzein, a metabolite of puerarin and daidzin produced by human intestinal microflora. I Isoflavones + Antidiabetics the interaction between isoflavones and antidiabetics is based on experimental evidence only. Evidence, mechanism, importance and management In various studies in animal models of diabetes, a couple of which are cited for information,1,2 puerarin, an isoflavone found in kudzu, page 267, has demonstrated blood glucose-lowering effects. Some have interpreted these studies to indicate that kudzu might have additive effects with antidiabetic drugs, and that the dose of antidiabetic medications might need to be adjusted. Given the nature Isoflavones 261 Isoflavones + Digoxin the interaction between isoflavones and digoxin is based on experimental evidence only. Biochanin A may modestly inhibit P-glycoprotein, resulting in a moderate increase in oral bioavailability of digoxin. Importance and management There appears to be no clinical data regarding an interaction between biochanin A and digoxin, and the clinical relevance of the experimental data needs to be determined. However, until more is known, because of the narrow therapeutic index of digoxin, it may be prudent to be cautious if patients taking digoxin also wish to take supplements containing high doses of biochanin A. Patients should be alert for any evidence of adverse effects, such as bradycardia, and if these occur it may be prudent to monitor digoxin levels. Isoflavones + Food No interactions found Isoflavones + Herbal medicines No interactions found. Isoflavones + Nicotine Soya isoflavones slightly decrease the metabolism of nicotine. Clinical evidence the effects of soya isoflavones on nicotine metabolism were investigated in a study in 7 healthy Japanese subjects who were non-smokers. This was when compared with nicotine metabolism after abstaining from soya foods for one week. Importance and management Although evidence is limited to one study, it is a well-designed clinical study. The minor change in nicotine metabolism when the subjects were taking isoflavones suggests that isoflavone supplements are unlikely to have a clinically relevant effect on the efficacy of nicotine replacement therapy. Nakajima M, Itoh M, Yamanaka H, Fukami T, Tokudome S, Yamamoto Y, Yamamoto H, Yokoi T.

Platelet transfusion is generally indicated either with platelet counts < 20,000 regardless of bleeding or when bleeding is present with a subnormal platelet count. Multiple processes result in platelet dysfunction, that may promote bleeding in the setting of a normal platelet count. Many of these are iatrogenic, since as discussed, anti-platelet pharmacotherapy is common [206]. Uremia results in impaired platelet function and hemostasis via mechanisms that are unclear. Hemophilia B; and disease states with global depression of coagulation factor levels, such as: 1. Patients with these disorders present with a history of easy bruising and late bleeding (early hemostasis with subsequent bleeding). This results in impaired coagulation via both the extrinsic and intrinsic pathway. Bleeding in end-stage liver disease results in considerable morbidity and mortality. Treatment in the acute setting involves transfusion of platelets (in patients with thrombocytopenia secondary to splenic sequestration), plasma, and cryoprecipitate [167]. Additionally, treatment of the etiology of the underlying liver disease, as well as liver transplantation (when indicated) are important elements in the treatment of bleeding complications. Initially, microvascular thromboses may be appreciated, whereas late, bleeding complications (for example, at venipuncture sites) are found. Finally, it is important to note that there are multiple non-blood product measures that are used to prevent bleeding. These include: Ca2+ (a requisite cofactor for many coagulation reactions), bicarbonate (as coagulation cascade reactions are impaired by acidosis), warming (since these reactions are also impaired by hypothermia), and anti-fibrinolytic agents (aprotinin [147]; [150], aminocaproic acid [97]; [114]) [171]. The flux boundary conditions govern the concentration of the various reactants in the flow domain and regulate the threshold response of the system. A model for the clot as a (highly viscous) viscoelastic fluid within which the reactants involved in clot formation and dissolution are uniformly present. Clot dissolution occurs due to either a decrease in fibrin concentration below 600nM (which may be due to fibrinolysis being well advanced)or due to attainment of a critical shear stress, the value of this shear stress depending on the concentration of platelets and fibrin at every point in the clot. We model whole blood and the clot within a framework that recognises that viscoelastic fluids possess multiple natural (stress-free) configurations. More importantly, our models arise in a thermodynamic setting that involves specifying the manner of the rate of dissipation and the manner in which energy is stored by the material in question. The procedure also guarantees constitutive relations that automatically meet the second law of thermodynamics and in order to ensure this we do not appeal to a procedure that is often used to place restrictions on allowable constitutive relations that presumes that the body can be subject to arbitrary processes (see [175] for a detailed discussion of these issues). We ensure that the rate of dissipation is non-negative and we maximize the rate of dissipation to select the final constitutive equation (see [174]). Let R (B) and t (B) denote the reference and the current configuration of the body B at time t, respectively. We let p(t) (B) denote the stress-free configuration that is reached by instantaneously unloading the body which is at the configuration t (B) (Figure 1). As the body continues to deform these natural configurations p(t) (B) can change (the suffix p(t) is used in order to highlight that it is the preferred stress free state corresponding to the deformed configuration at time t. See Rajagopal [173] for a detailed discussion of the notion of natural configurations). By the motion of a body we mean a one to one mapping that assigns to each point X R (B), a point x t (B), for each t, i. This model has been corroborated over the range of flow conditions expected in the human vasculature, and is an improvement over many of the models mentioned in the surveyed literature including the one in [229]. The model is defined through the following set of equations: T = -p1 + S, b S = µb Bp (t) + 1 D, µb 1+2n Bp(t) = -2 b tr(Bp(t)) - 3 3 =, tr(B-1) p(t) nb = b - 1; nb > 0. Upon rearranging the terms in the above expressions, the model can be expressed through: T = -p1 + S, S+ Here b S = µb Bp (t) + 1 D, 1 b Bp (t) = S - 1 D, µb b µb 1+2n (S, D) = (Bp (t)) = 2 b tr(Bp(t)) - 3 3 =. S = 1 D + D + (S, D) (S, D) tr(S - 1 D)-1 (18) (19) nb (20) (21) We see that the model as given through Equations (16) and (17) is very similar, in form, to the classical Oldroyd-B model as written in Equations (22) and (23) except for the extra term associated with the identity tensor, and the absence of a separate retardation time: T = -p1 + S, S + 1 S = D + 2 D.