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A hemorrhaging patient does not have the luxury of time generic methotrexate 2.5 mg overnight delivery, and delayed recognition of shock often results in death purchase methotrexate 2.5mg. Immediate threats to life must be identified early cheap 2.5 mg methotrexate fast delivery, and minor injuries or findings must not derail the primary goal of addressing potentially lethal matters. Basic physical examination skills utilized in context often form a clinical impression that leads to the diagnosis. Heart rate and blood pressure, which are often used in the incorrect definition of shock, may be normal. A narrowed pulse pressure, however, is typically present, and often missed owing to a normal systolic value. Anxiety or belligerence may be a sign of shock, and can easily be confused for intoxication or isolated brain injury. Cool, clammy extremities in a patient at risk for shock are clinical markers for peripheral vasoconstrictive compensation. Hypothermia, a key component of the lethal triad (hypothermia, coagulopathy, and acidosis) is an independent predictor of mortality in hemorrhaging patients. For example, hemoglobin and hematocrit levels are frequently normal, because the laboratory result is a measure of concentration—which remains unchanged until compensatory mechanisms and interstitial to intravascular fluid shifts have occurred. However, when a hemoglobin of less than 11 g per dL is present, it is associated with a mortality rate of nearly 40% [21]. This makes the arterial blood gas quite useful, because any acid– base abnormality can be presumed to be caused by the event that brought the patient to the hospital, and not underlying medical conditions. Tissue oxygen saturation continues to be investigated as a simple, reliable, and early marker of the presence of hemorrhagic shock [23]. For the injured patient, chest and pelvic radiographs may be of great utility because they can help identify major hemorrhage in two of the five key locations where deadly hemorrhage may occur. In nontrauma cases, a nasogastric tube may be inserted for suspected gastrointestinal hemorrhage to aid in localization. Endoscopy and interventional radiologic methods may also be employed emergently as conditions warrant. Transient response conveys ongoing hemorrhage, and beseeches health care providers to act quickly to obtain hemorrhage control. Many studies of hemorrhagic shock identification scoring systems use the necessity for transfusion as the outcome of interest. The Emergency Transfusion Score involves the use of nine markers, with a weighted coefficient assigned to each marker. A simplified method of identifying the probability of life-threatening hemorrhage was developed from military experience. Tachycardia, hypotension, acidosis, and acute anemia are all independent risk factors for the need of massive transfusion. The validity of this model, however, rests on a weighted evaluation, with pH carrying the most value, and thus is difficult to rapidly calculate. Utility of Ultrasonography for Diagnosis of Hemorrhagic Shock As discussed earlier, early control of the site of bleeding is an essential part of the management of hemorrhagic shock. Ultrasonography has utility for this purpose, because it can be deployed at the point of care for urgent evaluation of the critically ill patient. Ultrasonography has the advantage of immediate application by the frontline clinical team who can integrate the results of the examination into the other key elements of emergency evaluation: the history, physical examination, and initial laboratory results. The ultrasonography examination is performed by a member of the trauma team while other key elements of initial resuscitation are ongoing. Modern bedside ultrasonography machines are small enough that they can be brought to the bedside without blocking access to the patient by other members of the trauma team. The machine has multiple uses beyond examination for life-threatening hemorrhage, such as vascular access, airway management, and assessment for alternative causes for shock. It has replaced intra-abdominal lavage as the technique of choice for management of abdominal trauma and is standard practice for evaluation for intra-abdominal bleeding in trauma [39]. On the right side, the probe is placed in the midaxillary line on the lower chest wall in order to obtain a transcostal view of the liver in a coronal imaging plane (see Chapter 44 Critical Care of the Patient with Abdominal Trauma). Once the appropriate intercostal space is found, the probe is angled and tilted to achieve a clear image of the hepatorenal space. The examiner also checks for prehepatic fluid, and, using the liver as an acoustic window, examines the subdiaphragmatic space for fluid (Video 37. The scan is repeated on the left with examination of the splenorenal, presplenic, and subdiaphragmatic spaces (Video 37. The probe is placed just above the level of the iliac crest in the midline using a transverse scanning plane and angled downward through the bladder to search for fluid in the pelvis (Video 37. In the presence of hemorrhagic shock, a positive examination indicates intra-abdominal bleeding and the need for urgent source control. In addition, the examination has utility to examine for pneumothorax and pericardial effusion on an emergency basis. Scanning Technique With the patient is supine position, fluid will distribute in the dependent thorax owing to gravitational effect. On both the right and left sides, the probe is placed in the midaxillary to posterior axillary line on the chest in a coronal imaging plane and moved over adjacent interspaces to examine for pleural effusion. The examination for pleural fluid may be performed by extending the scan performed for intra-abdominal fluid to the area above the diaphragm. The finding of significant pleural fluid in a patient with hemorrhagic shock indicates hemothorax and the need for consideration of urgent source control (Video 37. Examination for Retroperitoneal Bleed Retroperitoneal bleeding is a potentital cause of hemorrhagic shock that may be difficult to identify by physical examination. For this reason, in patients who present in hemorrhagic shock with no identifiable cause, a retroperitoneal source should be considered, and expedient operative intervention should proceed in instances where a high index of suspicion exists. Identification of retroperitoneal fluid collection indicates retroperitoneal bleeding and the urgent need for consideration of source control (Video 37. In hemorrhagic shock, the trauma team may reasonably assume that the fluid represents hemorrhage and takes action based upon this supposition. Competence in scanning during emergency situations, such as for the evaluation of hemorrhagic shock, requires effective training for competence [40] because inaccurate results may have severe consequence in the unstable patient. Perhaps the greatest limitation of using ultrasonography to identify sources of hemorrhagic shock, is misinterpretation of a negative result. Patients who exhibit signs of hemodynamic compromise related to hemorrhage may have a completely normal ultrasound examination. Despite these limitations, ultrasonography is an effective tool for the initial and ongoing evaluation of the patient with hemorrhagic shock. It can be fully integrated into the team effort at the bedside, and it gives immediate and valuable clinical information. As such, it is an essential component of the imaging strategy for the evaluation and management of hemorrhagic shock.

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Treatment of exacerbations or severe persistent asthma may require the addition of a short course of oral or intravenous corticosteroids discount 2.5 mg methotrexate with amex. However buy methotrexate 2.5mg on line, as with all inhaled medications purchase methotrexate 2.5 mg amex, appropriate inhalation technique is critical to the success of therapy (see section on Inhaler Technique). Oral/systemic Patients with a severe exacerbation of asthma (status asthmaticus) may require intravenous methylprednisolone or oral prednisone to reduce airway inflammation. In most cases, suppression of the hypothalamic–pituitary–adrenal cortex axis does not occur during the oral prednisone “burst” (short course) typically prescribed for an asthma exacerbation. Patients should be instructed to rinse the mouth in a “swish-and-spit” method with water following use of the inhaler to decrease the chance of these adverse events. Alternative Drugs Used to Treat Asthma These drugs are useful for treatment of asthma in patients who are poorly controlled by conventional therapy or experience adverse effects secondary to corticosteroid treatment. They should not be used in situations where immediate bronchodilation is required. Leukotriene receptor antagonists have also shown efficacy for the prevention of exercise-induced bronchospasm. Zileuton and its metabolites are excreted in urine, whereas zafirlukast, montelukast, and their metabolites undergo biliary excretion. Adverse effects Elevations in serum hepatic enzymes may occur with these drugs, requiring periodic monitoring and discontinuation when enzymes exceed three to five times the upper limit of normal. Coadministration with drugs that are substrates of these isoenzymes may result in increased effects and/or toxicity. It is an alternative therapy for mild persistent asthma and is available as a nebulized solution. Because cromolyn is not a bronchodilator, it is not useful in managing an acute asthma attack. Due to its short duration of action, this agent requires dosing three or four times daily, which affects adherence and limits its use. Cholinergic antagonists the anticholinergic agents block vagally mediated contraction of airway smooth muscle and mucus secretion (see Chapter 5). Adverse effects such as xerostomia and bitter taste are related to local anticholinergic effects. It may also possess anti-inflammatory activity, although the mechanism of action is unclear. Previously, the mainstay of asthma therapy, theophylline has been largely replaced with β agonists and2 corticosteroids due to its narrow therapeutic window, adverse effect profile, and potential for drug interactions. Serum concentration monitoring should be performed when theophylline is used chronically. This leads to decreased binding of IgE to its receptor on the surface of mast cells and basophils. Reduction in surface-bound IgE limits the release of mediators of the allergic response. These agents are indicated for the treatment of severe persistent asthma in patients who are poorly controlled with conventional therapy. Adverse effects include serious anaphylactic reactions (rare), arthralgias, fever, rash, and increased risk of infections. These may include cough, excess mucus production, chest tightness, breathlessness, difficulty sleeping, and fatigue. Unfortunately, with currently available care, many patients still experience a decline in lung function over time. The combination of an anticholinergic and a β agonist may be helpful in patients who have2 inadequate response to a single inhaled bronchodilator and are at risk of exacerbations. Roflumilast is not a bronchodilator and is not indicated for the relief of acute bronchospasm. Its use is limited by common adverse effects including weight loss, nausea, diarrhea, and headache. Proper technique is critical to the success of therapy, and inhaler technique should be assessed regularly. Patients should be instructed to exhale before they actuate the inhaler, and then begin to inhale slowly as they press the canister and continue inhaling slowly and deeply throughout actuation. This technique avoids impaction of the medication onto the laryngeal mucosa and facilitates the drug reaching the site of action in the bronchial smooth muscle. A large fraction (typically 80% to 90%) of inhaled medication (for example, corticosteroids) is either deposited in the mouth and pharynx or swallowed (ure 39. The remaining 10% to 20% of a dose of inhaled glucocorticoids that is not swallowed reaches the site of action in the airway. Patients should be instructed to inhale quickly and deeply to optimize drug delivery to the lungs. Patients using any type of inhaled corticosteroid device should be instructed to rinse the mouth after use to prevent the development of oral candidiasis. The chamber reduces the velocity of the aerosol before entering the mouth, allowing large drug particles to be deposited in the device. The smaller, higher-velocity drug particles are less likely to be deposited in the mouth and more likely to reach the target airway tissue (ure 39. Patients should be advised to wash and/or rinse spacers to reduce the risk of bacterial or fungal growth that may induce an asthma attack. Drugs Used to Treat Allergic Rhinitis Rhinitis is an inflammation of the mucous membranes of the nose and is characterized by sneezing, itchy nose/eyes, watery rhinorrhea, nasal congestion, and sometimes a nonproductive cough. An attack may be precipitated by inhalation of an allergen (such as dust, pollen, or animal dander). The foreign material interacts with mast cells coated with IgE generated in response to a previous allergen exposure. The mast cells release mediators, such as histamine, leukotrienes, and chemotactic factors that promote bronchiolar spasm and mucosal thickening from edema and cellular infiltration. Antihistamines and/or intranasal corticosteroids are preferred therapies for allergic rhinitis. Antihistamines Oral antihistamines (H receptor antagonists; see Chapter 37) have a fast onset of action and are useful for the1 management of symptoms of allergic rhinitis caused by histamine release, such as sneezing, watery rhinorrhea, and itchy eyes/nose. However, they are more effective for prevention of symptoms in mild or intermittent disease, rather than treatment once symptoms have begun. First-generation antihistamines, such as diphenhydramine and chlorpheniramine, are usually not preferred due to adverse effects, such as sedation, performance impairment, and other anticholinergic effects. The second-generation antihistamines (for example, fexofenadine, loratadine, desloratadine, cetirizine) are generally better tolerated. Ophthalmic and nasal antihistamine delivery devices are available for targeted, topical tissue delivery.

Ito H buy methotrexate 2.5mg amex, Tomooka T generic 2.5 mg methotrexate with visa, Sakai N generic 2.5 mg methotrexate amex, et al: Lack of myocardial perfusion immediately after successful thrombolysis. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Kastrati A, Dibra A, Spaulding C, et al: Meta-analysis of randomized trials on drug-eluting stents vs. Palmerini T, Biondi-Zoccai G, Della Riva D, et al: Stent thrombosis with drug-eluting and bare-metal stents: evidence from a comprehensive network meta-analysis. Valgimigli M, Gagnor A, Calabró P, et al: Radial versus femoral access in patients with acute coronary syndromes undergoing invasive management: a randomised multicentre trial. Widimsky P, Groch L, Zelízko M, et al: Multicentre randomized trial comparing transport to primary angioplasty vs immediate thrombolysis vs combined strategy for patients with acute myocardial infarction presenting to a community hospital without a catheterization laboratory. Widimsky P, Budesínský T, Vorβc D, et al: Long distance transport for primary angioplasty vs immediate thrombolysis in acute myocardial infarction. Zeymer U, Uebis R, Vogt A, et al: Randomized comparison of percutaneous transluminal coronary angioplasty and medical therapy in stable survivors of acute myocardial infarction with single vessel disease: a study of the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausarzte. Nielsen N, Wetterslev J, Cronberg T, et al: Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. Roux S, Christeller S, Ludin E: Effects of aspirin on coronary reocclusion and recurrent ischemia after thrombolysis: a meta- analysis. Antithrombotic Trialists Collaboration: Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Yusuf S, Peto R, Lewis J, et al: Beta blockade during and after myocardial infarction: an overview of the randomized trials. Pitt B, Remme W, Zannad F, et al: Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. Wilson K, Gibson N, Willan A, et al: Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. The latter condition is usually caused by acute total obstruction of a coronary artery [2,3], and urgent reperfusion is the mainstay of therapy. The five broad etiologies are (a) plaque rupture or erosion with superimposed nonocclusive thrombus; (b) dynamic obstruction (i. Plaque Rupture and Erosion Atherosclerosis is a silent process that usually begins 20 to 30 years prior to a patient’s clinical presentation [10,11]. Plaque rupture and erosion can be precipitated by multiple factors, including endothelial dysfunction [12], plaque lipid content [13], local inflammation [14], coronary artery tone at the site of irregular plaques and local shear stress forces, platelet function [15,16], and the status of the coagulation system (i. Thrombosis occurs in two interrelated stages: (a) primary hemostasis and (b) secondary hemostasis [27,28]. The first stage of hemostasis is initiated by platelets as they adhere to damaged vessels and form a platelet plug. After adhering to the subendothelial matrix, the platelet undergoes a conformational change from a smooth discoid shape to a spiculated form, which increases the surface area on which thrombin generation can occur. Secondary Hemostasis Simultaneous with the formation of the platelet plug, the plasma coagulation system is activated. Following plaque rupture or ulceration, the injured endothelial cells on the vessel wall become activated and release protein disulfide isomerase, which acts to cause a conformational change in circulating tissue factor [29–32]. With the activation of factor X (to factor Xa), thrombin is generated and acts to cleave fibrinogen to form fibrin. The process is identified in three settings: (a) vasospasm in the absence of obstructive plaque, (b) vasoconstriction in the setting of atherosclerotic plaque, and (c) microcirculatory angina. Vasospasm can occur among patients without coronary atherosclerosis or among those with a nonobstructive atheromatous plaque. Vasospastic angina appears to be caused by hypercontractility of vascular smooth muscle and endothelial dysfunction occurring in the region of spasm. Prinzmetal’s variant angina, with intense focal spasm of a segment of an epicardial coronary artery, is the prototypical example [33]. Vasoconstriction more commonly occurs in the setting of significant coronary atherosclerotic plaque, especially those with superimposed thrombus. Vasoconstriction can occur as the result of local vasoconstrictors released from platelets, such as serotonin and thromboxane A2 [34–36]. Vasoconstriction can also result from a dysfunctional coronary endothelium, which has reduced the production of nitric oxide and increased the release of endothelin. Adrenergic stimuli, cold immersion [37], cocaine [38,39], or mental stress [40] can also cause coronary vasoconstriction among susceptible vessels. In this condition, ischemia results from constriction of the small intramural coronary resistance vessels [41]. Although no epicardial coronary artery stenoses are present, coronary flow is usually slowed and does not increase appropriately in response to a variety of signals. This change could occur either as a result of an increase of myocardial oxygen demand or as a decrease of coronary blood flow. Ischemic chest pain is usually described as a discomfort or pressure (rarely as a pain) that is brought on by exertion and relieved by rest. It is generally located in the retrosternal region but sometimes in the epigastrium and frequently radiates to the anterior neck, left shoulder, and left arm. Signs that suggest ischemia are sweatiness, pale cool skin, sinus tachycardia, and a fourth heart sound. The biomarker criteria include at least one value greater than the 99th percentile of the upper reference range. If the initial value is positive, a subsequent value must demonstrate an increase or decrease of ≥20% [7,49]. More sensitive assays show better diagnostic performance for patients presenting early after symptom onset [52,53]. Using a high-sensitivty assay, values below the 99th percentile at presentation and 1 hour later have a negative predictive value >99. Moreover, values below the limit of detection at presentation (seen in ~25% of patients) have a negative predictive value of >99. Risk assessment using clinical, electrocardiographic, and laboratory markers identifies which patients are at highest risk for adverse outcomes. Risk assessment can similarly be used to determine the most appropriate level of care and monitoring (i. The “management strategy” refers to whether early angiography is performed (with revascularization as appropriate) directly following the index event or whether a conservative or ischemia-driven strategy is carried out, first with noninvasive assessment of residual ischemia, followed by angiography and revascularization only if recurrent ischemia is demonstrated (see section on, “Early Routine Invasive” vs. Risk Assessment Using Clinical Predictors the initial clinical evaluation can be used to risk-stratify patients quickly and to assist with triage and early management strategy [7,8,65]. In addition to age, gender, and significant comorbidities, certain aspects of the clinical presentation can yield valuable information. High-risk patients can be identified by the presence of pain at rest and increasing frequency of symptoms leading up to the index event. Given the enhanced sensitivity and specificity, troponin is the preferred marker of myocardial necrosis for both diagnosis and prognosis [7,8]. Thus, there is evidence from multiple trials that the use of troponins can assist in both assessing the risk and determining which patients will accrue the most benefit from more potent antithrombotic agents and an invasive management strategy.

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