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However 200MDI beconase aq overnight delivery allergy medicine 029, even if the taxonomy issues of incidence reporting are improved cheap 200MDI beconase aq with amex allergy kid, the problem of determining the true incidence rate remains generic beconase aq 200MDI on line allergy medicine 013. A comprehensively described and deconstructed incident only gives insight into the numerator; it does not provide information on the number of patients at risk and does not allow determination of true incidence rates order beconase aq 200MDI free shipping allergy bumps. The denominators are especially difficult to determine because these measurements have major impacts on interpretation [11]; for instance, C. The numerator data are equally challenging because of the time and expense of chart extraction needed for their collection. If the characteristics of the patient population change over time, then these factors must be accounted for as well. For example, if the patient population changes or new services such as transplantation are offered by a given hospital, then the patient mix will change and adjusted hazard rates will be needed. Although most of these indicators relate to surgical patients, newer indicators are being designed to measure the safety of care for medical patients with critical illnesses, such as myocardial infarction, stroke, and congestive heart failure. Although this method is powerful and can be quite useful, it is important to also recognize its limitations. Large data sets such as these also have limited data quality for clinically relevant covariates, so controlling for confounders is difficult. Because all of the clinically relevant covariates are not included, the problem of residual confounding is always a problem and caution should be exercised when interpreting results. Making interinstitutional comparisons is therefore difficult, and even when trending data over time, results must be analyzed with caution. When there is marked heterogeneity in terms of clinical problems and rapid changes in process of care over time, this approach will face difficulties. However, it may be difficult to isolate and ascertain the contributory effect of influential factors, such as adherence to best practice by the caregiving team, the role of complications, or level of care. Physicians and other clinicians often have a stronger sense of accountability toward a process measure than an outcome measure because the process measure can be more strongly linked to a particular care provider or team behaviors [30]. Physicians may also believe that outcomes can be overly influenced by severity of disease and prove resistant to quality improvement efforts. To serve as an accurate measure of safety and to influence quality improvement, process measures must have a causal relationship with the outcome they intend to represent. Computerized physician order entry (order- sets) for drugs has the potential to decrease the rate of serious medication errors [33] and to improve clinical outcomes when applied to antibiotic prescribing [34]. Process of care measurement is often very effective for certain types of problems (like computerized order entry), but it is important to recognize some of the limitations and difficulties inherent in this system when applied to more complex problems. When strong evidence-based clinical practice guidelines are available, it is a feasible strategy, but often this is not the case. In addition, properly identifying those patients eligible for a particular protocol during the appropriate time period is critical. Determining the numerator for such process of care measures is fairly easy (who actually received the drug), but determining the denominator can be more difficult and can be costly because of the time and expense needed for data collection (e. In addition, chart abstraction in such cases usually requires a high level of expert judgment, which makes it variable, difficult, and costly. Thus, process of care measurement, because of cost and time considerations, may be a suitable approach to improving safety for those problems in which there is a strong evidence base and for which the costs of identifying the patient population (both numerator and denominator) are sustainable and warranted by the value of information obtained. Additional structure measures of safety include the presence of resources to establish ongoing competency of medical staff and residents [39], adequate nurse staffing and skill sets [40,41], and appropriate technology resources, such as smart pumps and bar coding [42]. Pronovost and Sexton [45] recommend measuring the entire hospital annually with the full Safety Attitudes Questionnaire that has construct validity and sufficient reliability for measuring the single construct of safety culture. Trigger Tools Trigger tools refer to techniques used to detect organizational signals for adverse events. For instance, orders for flumazenil may identify patients who were given an overdose of a benzodiazepine drug. A trigger or set of triggers can be used to identify medical records for retrospective review to assess organizational safety, or used in “real time” as a tool to identify a specific patient at risk of an adverse outcome. Limitations of Existing Metrics and Their Applications Currently, the majority of data collected to measure safety is process oriented. However, there is only limited evidence that the use of current process measures translates into better outcomes [48,49]. In addition, risk adjustment to facilitate valid comparisons increases the amount and complexity of data abstraction required, further increasing costs. In such instances, proper measures require collecting information on a very large population, which constitutes the denominator of the rates being measured. It is also very important to consider carefully the attributes of performance measures and how the measures are arrived at. In addition, the magnitude and direction of bias for reporting can be greater than the true variation of outcomes. This is because most reporting systems, such as the Patient Safety Reporting System, provide data from a non-randomly selected sample and the population at risk is not known. When interpreting safety metrics, careful attention must be paid, bias must be considered, and all results should be viewed with caution. There are a variety of endorsed quality and safety measures currently available, some with a stronger evidence base than others, but which ones are best is not clear and will depend largely on local factors. The cost- effectiveness of even the best evidence-based measures and interventions is difficult to prove, and the potential benefits of implementation are likely to vary depending on the local context. The National Quality Forum measures for quality in intensive care serve to highlight some of the difficulties encountered. However, it is informative to note the measures that were previously sanctioned but are no longer authorized. These include severity-standardized average length of stay, the ventilator bundle, central line bundle compliance, and measures of glycemic control with intravenous insulin. The selection process should take into account whether the measures are valid rates, whether proportions are sufficient, whether the outcomes being measured are truly preventable with intervention, potential sources of bias, costs of implementation, and the strength of the evidence supporting a given intervention. Although the vast majority of the literature supports the value of intensivist-based critical care, a landmark study by Angus et al. Moreover, it was estimated that this gap between supply and demand will only widen in the coming decades [53]. The evidence base is still incomplete and when taken together, shows that having an intensivist onsite overnight is not associated with improvements in patient outcomes. However, for some, but not others, addition of such providers improved mortality for units with low daytime staffing intensity. A meta-analysis supported this lack of association of nighttime intensivists and meaningful patient outcomes [65]. Other studies found no association with the shiftwork model (including overnight onsite intensivist) and any measured patient outcome [66,67].
In addition generic beconase aq 200MDI amex allergy medicine comparison chart, tubes should be flushed with water before and after the administration of any medications discount beconase aq 200MDI visa allergy zapper. The tube can be irrigated with warm saline 200MDI beconase aq allergy treatment 5mm, a carbonated liquid discount 200MDI beconase aq with mastercard allergy testing scale, cranberry juice, or a pancreatic enzyme solution (e. Commonly, a mixture of lipase, amylase, and protease (Pancrease) dissolved in sodium bicarbonate solution (for enzyme activation) is instilled into the tube with a syringe and the tube clamped for approximately 30 minutes to allow enzymatic degradation of precipitated enteral feedings. The pancreatic enzyme solution was successful in restoring tube patency in 96% of cases where formula clotting was the likely cause of occlusion and use of cola or water had failed [36,37]. Prevention of tube clogging with flushes and pancreatic enzyme are, therefore, the methods of choice in maintenance of chronic enteral feeding tubes. Utility of Ultrasonography for Feeding Tube Insertion Ultrasonography has useful application related to insertion of a feeding tube. The insertion of a gastric tube may be facilitated with ultrasonography by identifying the nasogastric tube in the upper esophagus and confirming its placement in the stomach by direct visualization (Video 21. The tube may also be guided into a postpyloric position using real-time ultrasonography guidance (Video 21. For this application when compared to blind insertion technique, ultrasonography guidance has a higher success rate, takes less time, and reduces the need for postprocedure radiograph. Being a straightforward bedside technique, it has advantage over fluoroscopic, endoscopic, or electromagnetic guidance of postpyloric tube placement, given the simplicity of ultrasonography. The main disadvantage to ultrasonography guidance is that abdominal wounds and dressings can prevent its use, and patient specific factors such as obesity or intestinal gas may block visualization of the tube as it passes into the duodenum or the jejunem. Dhaliwal R, Cahill N, Lemieux M, et al: the Canadian critical care nutrition guidelines in 2013: an update on current recommendations and implementation strategies. Alhazzani W, Almasoud A, Jaeschke R, et al: Small bowel feeding and risk of pneumonia in adult critically ill patients: a systematic review and meta-analysis of randomized trials. Foster J, Filocarno P, Nava H, et al: the introducer technique is the optimal method for placing percutaneous endoscopic gastrostomy tubes in head and neck cancer patients. Trabal J, Leyes P, Hervas S, et al: Factors associated with nosocomial diarrhea in patients with enteral tube feeding. Gok F, Kilicaslan A, Yosunkaya A: Ultrasound-guided nasogastric feeding tube placement in critical care patients. Because proximal gastric varices and varices in the distal 5 cm of the esophagus lie in the superficial lamina propria, they are more likely to bleed and respond to endoscopic treatment [2]. Variceal rupture may be predicted by Child–Pugh class, red wale markings indicating epithelial thickness, and variceal size [1]. Although urgent endoscopy, sclerotherapy, and band ligations are considered first-line treatments, balloon tamponade remains a valuable intervention for the treatment of bleeding esophageal varices. Balloon tamponade is accomplished using a multilumen tube, approximately 1 m in length, with esophageal and gastric cuffs that can be inflated to compress esophageal varices and gastric submucosal veins, thereby providing hemostasis through tamponade, while incorporating aspiration ports for diagnostic and therapeutic usage. In 1947, successful control of hemorrhage by balloon tamponade was achieved by attaching an inflatable latex bag to the end of a Miller–Abbot tube. A triple-lumen tube with gastric and esophageal balloons, as well as a port for gastric aspiration, was described by Sengstaken and Blakemore in 1950. In 1955, Linton and Nachlas engineered a tube with a larger gastric balloon capable of compressing the submucosal veins in the cardia, thereby minimizing flow to the esophageal veins, with suction ports above and below the balloon. The Minnesota tube was described in 1968 as a modification of the Sengstaken–Blakemore tube, incorporating the esophageal suction port, which is described later. Several studies have published combined experience with tubes such as the Linton–Nachlas tube; however, the techniques described here are limited to the use of the Minnesota and Sengstaken–Blakemore tubes. Self-expanding metal stents as an alternative to balloon tamponade are promising and currently under investigation [4,5]. Emergent therapeutic endoscopy in conjunction with pharmacotherapy is more effective than pharmacotherapy alone and is also performed as soon as possible. Band ligation has a lower rate of rebleeding and complications when compared with sclerotherapy, and should be performed preferentially, provided that visualization is adequate to ligate or sclerose varices successfully [3,10]. Tissue adhesives such as polidocanol and cyanoacrylate delivered through an endoscope are being used and studied outside the United States though glue embolization remains a concern [5]. Balloon tamponade is performed to control massive variceal hemorrhage, with the hope that band ligation or sclerotherapy and secondary prophylaxis will then be possible. Other alternatives include percutaneous transhepatic embolization; emergent esophageal transection with stapling [13]; esophagogastric devascularization with esophageal transection and splenectomy; and hepatic transplantation. If at all possible, making an adequate anatomic diagnosis is critical before any of these balloon tubes are inserted. Severe upper gastrointestinal bleeding attributed to esophageal varices in patients with clinical evidence of chronic liver disease results from other causes in up to 40% of cases. The observation of a white nipple sign (platelet plug) during endoscopy is indicative of a recent variceal bleed. A balloon tube is contraindicated for patients with recent esophageal surgery or esophageal stricture [17]. Some authors do not recommend balloon tamponade when a hiatal hernia is present, but there are reports of successful hemorrhage control in some of these patients [18]. When there are no other options, it may be practical to titrate to the lowest effective balloon pressures especially when repeated endoscopic sclerotherapy has been performed, because there is increased risk of esophageal perforation [19]. The incidence of aspiration pneumonia is directly related to the presence of impaired mental status [20]. Suctioning of pulmonary secretions and blood that accumulates in the hypopharynx is facilitated in patients who have been intubated. Sedatives and analgesics are more readily administered to intubated patients, and may be required when balloon tamponade is poorly tolerated, because retching or vomiting may lead to esophageal rupture [21]. The incidence of pulmonary complications is significantly lower when endotracheal intubation is routinely used [22]. Hypovolemia, Shock, and Coagulopathy Adequate intravenous access should be obtained with large-bore venous catheters for blood product administration and fluid resuscitation with crystalloids and colloids. Packed red blood cells should be administered keeping four to six units available in case of severe recurrent bleeding, which commonly occurs among these patients. Clots and Gastric Decompression If time permits, placement of an Ewald tube and aggressive lavage and suctioning of the stomach and duodenum facilitates endoscopy, diminishes the risk of aspiration, and may help control hemorrhage from causes other than esophageal varices. Infection, Ulceration, and Encephalopathy Mortality is increased when infection is present in bleeding cirrhotic patients. Intravenous proton pump inhibitors are more efficacious than histamine-2-receptor antagonists for maintaining gastric pH at a goal of 7 or greater. Rifaximin, lactulose, or lacitol may be useful, because blood and ammonia-forming bacteria in the gastrointestinal tract may contribute to encephalopathy. Balloons, Ports, and Preparation All lumens should be flushed to assure patency and the balloons inflated underwater to check for leaks. Two clean 100-mL (or larger) Foley-tip syringes and two to four rubber-shod hemostats should be readied for inflation of the balloons. To ensure that the gastric balloon will not be positioned in the esophagus, preinsertion compliance should be tested by placing 100-mL aliquots of air up to the listed maximum recommended volumes into the gastric inflation port while recording the corresponding pressures using a manometer attached to the gastric pressure port. A portable handheld manometer allows for simpler continuous monitoring as well as patient transport and repositioning.
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The exact incidence is difficult to ascertain purchase 200MDI beconase aq visa allergy symptoms getting worse, because the definitions for endocarditis differ in many surveys cheap 200MDI beconase aq fast delivery xyz allergy medicine. This means that a primary care physician will encounter only 1-2 cases over a working lifetime discount beconase aq 200MDI allergy medicine not working for child. Endocarditis is more common in men than in women order beconase aq 200MDI line allergy medicine safe pregnancy, and the disease is increasingly becoming a disease of elderly individuals. In recent series, more than half of the patients with endocarditis were over the age of 50 years. With available rapid treatment for group A streptococcal infections, the incidence of rheumatic heart disease has declined, eliminating this important risk factor for endocarditis in the young. With life expectancy increasing worldwide, the percentage of elderly people will continue to rise, and the number of elderly patients with infective endocarditis can be expected to increase in the future. A rare disease; a primary care physician is likely to see just 1-2 cases in an entire career. This sterile lesion serves as an ideal site to trap bacteria as they pass through the bloodstream. Patients with congenital heart disease and rheumatic heart disease, those with an audible murmur associated with mitral valve prolapse, and elderly patients with calcific aortic stenosis are all at increased risk. The higher the pressure gradient in aortic stenosis, the greater the risk of developing endocarditis. Intravenous drug abusers are at high risk of developing endocarditis as a consequence of injecting bacterially contaminated solutions intravenously. Platelets and bacteria tend to accumulate in specific areas of the heart based on the Venturi effect. When a fluid or gas passes at high pressure through a narrow orifice, an area of low pressure is created directly downstream of the orifice. The Venturi effect is most easily appreciated by examining a rapidly flowing, rock-filled river. When the flow of water is confined to a narrower channel by large rocks, the velocity of water flow increases. As a consequence of the Venturi effect, twigs and other debris can be seen to accumulate on the downstream side of the obstructing rocks, in the area of lowest pressure. Similarly, vegetations form on the downstream or low-pressure side of a valvular lesion. In aortic stenosis, vegetations tend to form in the aortic coronary cusps on the downstream side of the obstructing lesion. In mitral regurgitation, vegetations are most commonly seen in the atrium, the low- pressure side of regurgitant flow. Upon attaching to the endocardium, pathogenic bacteria induce platelet aggregation, and the resulting dense plateletfibrin complex provides a protective environment. Phagocytes are incapable of entering this site, eliminating an important host defense. Colony 9 11 counts in vegetations usually reach 10 —10 bacteria per gram of tissue, and these bacteria within vegetations periodically lapse into a metabolically inactive, dormant phase. Venturi effect results in vegetation formation on the low-pressure side of high-flow valvular lesions. Disease of the mitral or aortic valve is most common; disease of tricuspid valve is rarer (usually seen in intravenous drug abusers). The frequency with which the four valves become infected reflects the likelihood of endocardial damage. Shear stress would be expected to be highest in the valves exposed to high pressure, and most cases of bacterial endocarditis involve the valves of the left side of the heart. The mitral and aortic valves are subjected to the highest pressures and are the most commonly infected. Right-sided endocarditis is uncommon (except in the case of intravenous drug abusers), and when right-sided disease does occur, it most commonly involves the tricuspid valve. The closed pulmonic valve is subject to the lowest pressure, and infection of this valve is rare. Patients with prosthetic valves must be particularly alert to the symptoms and signs of endocarditis, because the artificial material serves as an excellent site for bacterial adherence. Patients who have recovered from an episode of infective endocarditis are at increased risk of developing a second episode. Streptococci that express dextran on the cell wall surface adhere more tightly to dental enamel and to other inert surfaces. Streptococci that produce higher levels of dextran demonstrate an increased ability to cause dental caries and to cause bacterial endocarditis. Streptococcus viridans, named for their ability to cause green (“alpha”) hemolysis on blood agar plates, often have a high dextran content and are a leading cause of dental caries and bacterial endocarditis. This bacterium often enters the bloodstream via the gastrointestinal tract as a consequence of a colonic carcinoma. Whenever a mucosal surface heavily colonized with bacterial flora is traumatized, a small number of bacteria enter the bloodstream, where they are quickly cleared by the spleen and liver. Patients undergoing dental extraction or periodontal surgery are at particularly high risk, but gum chewing and tooth brushing can also lead to bacteremia. Oral irrigation devices such as the Waterpik should be avoided in patients with known valvular heart disease or prosthetic valves, because these devices precipitate bacteremia more frequently than simple tooth brushing. Other manipulations that can cause significant transient bacteremia include tonsillectomy, urethral dilatation, transurethral prostatic resection, and cystoscopy. Pulmonary and gastrointestinal procedures cause bacteremia in a low percentage of patients. In native valve endocarditis, in earlier series, Streptococcus species were the most common cause, representing more than half of all cases. However, Staphylococcus species are now the most common cause of native valve endocarditis followed by Streptococcal species. Staphy-lococcus aureus predominates, with coagulase-negative staphylococci playing a modest role. They may not be detected on routine blood cultures that are discarded after 7 days. Anaerobes, Coxiella burnetii (“Q fever endocarditis”) and Chlamydia species are exceedingly rare causes. In certain areas of the country—for example, Detroit, Michigan—methicillin-resistant S. Pseudomonas aeruginosa, found in tap water, is the most common gram-negative organism. The causes of prosthetic valve endocarditis depend on the timing of the infection (Table 7. The development of endocarditis within the first 2 months after surgery (“early prosthetic valve endocarditis”) is primarily caused by nosocomial pathogens. Staphylococcal species (coagulase-positive and -negative strains alike), gram-negative aerobic bacilli, and fungi predominate. In disease that develops more than 2 months after surgery (“late prosthetic valve endocarditis”), organisms originating from the mouth and skin flora predominate: S. Gram-negative aerobic bacilli and fungi are less common, but still important pathogens.
Other risk factors for seizures include a history of organic brain disease order beconase aq 200MDI overnight delivery allergy symptoms sore eyes, epilepsy discount beconase aq 200MDI on-line allergy cold, electroconvulsive therapy 200MDI beconase aq mastercard allergy medicine safe to take while pregnant, abnormal baseline electroencephalogram generic 200MDI beconase aq with amex allergy symptoms upper respiratory, polypharmacy, and initiation and rapid dose titration of neuroleptics [27]. After overdose, the incidence of seizures is as high as 60% and 10% for loxapine and clozapine, respectively, whereas the incidence for most other neuroleptics is approximately 1% [3,11]. Agranulocytosis (absolute neutrophil count < 500 cells per μL) is a serious idiosyncratic side effect of clozapine and phenothiazine therapy. The mechanism underlying clozapine-induced agranulocytosis may be both immune-mediated and the result of direct myelotoxicity from the drug. Neutropenia has also been associated with the therapeutic use of olanzapine, quetiapine, and risperidone [63]. Hepatotoxicity is idiosyncratic, often occurs within the first 3 months of treatment, and is usually mild and self-limiting (most patients remain asymptomatic). The patterns of hepatoxicity are both hepatitic (including nonalcoholic steatohepatitis) and cholestatic [63,64]. Several cases of fatal diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic coma have been reported among the patients taking clozapine and olanzapine [68,69]. Pancreatitis has been associated with the use of clozapine, and hypertriglyceridemia has been reported among patients treated with clozapine, olanzapine, and quetiapine [56,70–72]. Allergic dermatitis, cholestatic jaundice, irreversible pigmentary retinopathy, photosensitivity reactions, and priapism are uncommon idiosyncratic reactions associated with phenothiazine therapy [7]. Myocarditis and cardiomyopathy have been rarely associated with the use of clozapine; these conditions are idiosyncratic, frequently fatal, often occur within the first 2 weeks of treatment, and are likely the result of acute hypersensitivity [8,73]. Respiratory depression and arrest have been reported with the coadministration of clozapine and lorazepam or diazepam [75,76]. Exaggerated anticholinergic effects may occur with concurrent use of tricyclic antidepressants, certain skeletal muscle relaxants, antihistamines, and antiparkinson agents. The combination of antipsychotics with significant α1-adrenergic blockade and certain antihypertensive agents (e. Knowledge of antipsychotic-associated drug interactions facilitates recognition and treatment of these increasingly common iatrogenic events. For mild intoxication, findings include ataxia, confusion, lethargy, slurred speech, tachycardia, and hypertension or orthostatic hypotension. Other than sinus tachycardia, repolarization abnormalities are the earliest and most common electrocardiographic findings associated with neuroleptic poisoning [11,18,19,79]. Signs and symptoms of moderate poisoning include low-grade coma (see Chapters 145 and 146, respiratory depression, and hypotension). Miosis is more likely to occur following overdose of both atypical and typical agents; it has been described in 75% of the adults and 72% of the children after phenothiazine overdose [3,37,38,41,80]. Paradoxical agitation, delirium, hallucinations, psychosis, myoclonic jerking, and tachypnea may occur [3,38,41–43,81]. Central and peripheral anticholinergic stigmata frequently occur after overdose with chlorpromazine, clozapine, mesoridazine, olanzapine, and thioridazine [3,38,41–43]. With severe poisoning, high-grade coma with loss of most or all reflexes, apnea, hypotension, seizures, and a variety of cardiac conduction disturbances and arrhythmias may develop. Tachyarrhythmias include sinus and supraventricular tachycardias, supraventricular and ventricular premature beats, ventricular tachycardia and fibrillation, and TdP [3,11,18–20,24,82]. Serious cardiovascular toxicity occurs more commonly when piperidine phenothiazines have been ingested [11]. Electrocardiographic abnormalities or obvious cardiotoxicity should be evident within several hours of overdose. Although the overall seizure incidence is about 1% for patients that overdose on neuroleptics, the incidence is much greater following ingestion of chlorpromazine, clozapine, loxapine, mesoridazine, and thioridazine [3,10,11]. Pulmonary edema has been reported rarely as a complication of overdose with chlorpromazine, clozapine, haloperidol, and perphenazine [3,39,40]. Cardiovascular effects are mild or absent, but convulsions are common and often lead to rhabdomyolysis and subsequent renal failure [88]. Early deaths are due to respiratory arrest, arrhythmias, shock, or aspiration-associated respiratory failure. Later complications include cerebral and pulmonary edema, disseminated intravascular coagulation, rhabdomyolysis, myoglobinuric renal failure, and infection. They may be focal at the onset and then spread to contiguous muscles; occasionally, they are generalized [89]. Those involving muscles of the tongue and jaw (buccolingual crisis) produce trismus, protrusion of the tongue, dysphagia, dysarthria, and facial grimacing. Contractions of muscles of the neck or back result in abnormal head positioning (torticollic reactions) or arching and twisting of the torso (opisthotonic posturing), respectively. When muscles of the abdominal wall are involved, the patients present with abdominal wall pain and spasm, bizarre gait patterns, kyphosis, and lordosis (tortipelvic and gait crises). A complete history should be obtained from the patient as well as the person(s) who found or brought the patient (to corroborate the patient’s history). As with all drug ingestions, the name, quantity, and time of ingestion of the drug(s) should be determined. For patients who become toxic during chronic therapy, a recent medication or dose change or an illness may be responsible. Routine laboratory evaluation should include a complete blood cell count and electrolyte count and blood urea nitrogen, creatinine, and glucose tests. Measurements of serum acetaminophen and salicylate should be performed on all patients with intentional overdose. Among the patients with seizures, hyperthermia, and severe poisoning, laboratory evaluation should include urinalysis (routine and for myoglobin); creatinine phosphokinase, calcium, magnesium, and phosphate tests; and a coagulation profile. Toxicologic analyses of the urine and serum by immunoassay and chromatography–mass spectrometry may be performed to confirm the identity of the offending agent and to rule out other ingestants [92]. Quantitative drug levels are not helpful for predicting clinical toxicity or guiding treatment [29,30,33]. Although neither sensitive nor specific, or readily available, the Forrest, Mason, and Phenistix colorimetric tests are rapid urine screens that may be positive with phenothiazine ingestions [93]. A complete blood cell count should be performed for patients who develop a fever or infection while taking clozapine or phenothiazines. Those with mild toxicity can often be managed in the emergency department or a similarly equipped observation unit. Advanced life support measures should be instituted as necessary, and underlying metabolic abnormalities corrected. The patients with seizures or hyperthermia should have continuous (rectal probe) temperature monitoring. Central venous, intra-arterial, and echocardiographic monitoring may be necessary for optimal management of the patients who are hemodynamically unstable. If they are associated with hypotension, correction of this abnormality is often all that is necessary. Amiodarone and electrical cardioversion are alternative treatments for patients with ventricular tachyarrhythmias, depending on hemodynamic stability. The blood pressure should be carefully monitored during isoproterenol administration, as it may cause or worsen hypotension.
