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Reduction of vancomycin-resistant enterococcal infections by limitation of broad-spectrum cephalosporin use in a trauma and burn intensive care unit buy lamotrigine 50mg treatment of pneumonia. Association between antecedent intravenous antimicrobial exposure and isolation of vancomycin-resistant enterococci quality 50mg lamotrigine medications used to treat adhd. Effect of the increasing use of piperacillin/tazobactam on the incidence of vancomycin-resistant enterococci in four academic medical centers cheap 50mg lamotrigine amex medications used to treat ptsd. Impact of a formulary switch from ticarcillin-clavulanate to piperacillin-tazobactam on colonization with vancomycin-resistant enterococci order 25mg lamotrigine mastercard symptoms 6 year molars. Acquisition of rectal colonization by vancomycin- resistant Enterococcus among intensive care unit patients treated with piperacillin-tazobactam versus those receiving cefepime-containing antibiotic regimens. Costs and savings associated with infection control measures that reduced transmission of vancomycin-resistant enterococci in an endemic setting. Cost-effectiveness of perirectal surveillance cultures for controlling vancomycin-resistant Enterococcus. A cost-benefit analysis of gown use in controlling vancomycin-resistant Enterococcus transmission: is it worth the price? Cunha Infectious Disease Division, Winthrop-University Hospital, Mineola, New York, and State University of New York School of Medicine, Stony Brook, New York, U. The main clinical problem with the “septic” patient is to determine whether the patient is septic or has a dis- order noninfectious mimic of sepsis by hemodynamic or laboratory parameters. In the intensive care setting, it is of critical importance to differentiate between sepsis and its mimics (1–6). The most important clinical consideration in determining whether a patient is septic is to identify the source of infection. Infections limited to specific infections in a few organ systems are the only ones with septic potential. Lower gastrointes- tinal tract perforations, intra-abdominal/pelvic abscesses, pylephlebitis, commonly result clinically in sepsis. In contrast, gastritis and nonperforating gastric ulcer are rarely associated with sepsis. Cholangitis in the hepatobiliary tract results in sepsis, but rarely, if ever, complicates acute/chronic cholecystitis (6–13). It is almost always possible to identify the septic source by physical exam, laboratory, or radiology tests. Disorders that mimic sepsis should be recognized to treat the condition and not to avoid inappropriate treatment with antibiotics. Fever should not be equated with infection since the chemical mediators of inflammation and infection, i. All that is febrile is not infectious, and most, but not all diseases causing sepsis are accompanied by temperatures! With the exceptions of drug fever and adrenal insufficiency, the disorders that mimic sepsis and Clinical Approach to Sepsis and Its Mimics in Critical Care 129 Table 1 Clinical Conditions Associated with Sepsis Associated with sepsis (fevers! Genitourinary source Sinusitis Renal Mastoiditis Pyelonephritis Bronchitis Intra/perinephric abscess Otitis Calculi. Skin/soft tissue source Total Osteomyelitis Prostate Uncomplicated wound infections Abscess. Central nervous system source Tubo-ovarian abscess Bacterial meningitis (excluding meningococcal meningitis Pelvic septic thrombophlebitis with meningococcemia). Hypothermia is an important clinical clue to bacteremia, particularly in renal insufficiency. In normal hosts with fever, sepsis should not be a diagnostic consideration if temperatures are <1028For>1068F (22–25) (Table 2). As with hemodynamic parameters, laboratory data may mislead the unwary into incorrectly ascribing laboratory abnormalities to an infectious rather than a noninfectious process. An increase in white peripheral blood cell count with a shift to the left is a nonspecific reaction to stress, and is not specific for infection. An increase in white count with a shift to the left is a measure of the intensity of the systemic response to stress of infectious or noninfectious disorders. Laboratory parameters that are more indicative of infection include leukopenia or thrombocytopenia. The only laboratory abnormalities that are specific for sepsis are organisms in the blood, i. Positive buffy coat smears are not present in all patients with bacteremia, and when positive are diagnostic and rapid. The bacteria/fungi present in buffy coat smears are helpful in determining the origin of the septic process by their association with particular organ system involvement, i. The morphology/arrangement of the bacteria in buffy coat smears is also useful in selecting appropriate empiric antibiotic coverage (26–30) (Table 3). Because each organ has its normal resident flora that becomes the pathogenic flora when the organ function is disrupted, empiric coverage is directed against the normal resident flora (Table 4). Factors in antibiotic selection include hepatic/renal insufficiency, allergic status of the patient, tissue penetration of the antibiotic, safety profile of the antibiotic, resistance potential of the antibiotic, and cost. If the spectrum is appropriate for the source of sepsis, no regimen is superior to others in terms of clinical outcome. However, clinicians should utilize the most clinically/cost-effective regimens with a low resistance potential and begin therapy as soon as the diagnosis of sepsis is made. The basis of empiric therapy for sepsis depends on eliminating the source of sepsis and covering the patient with antibiotic therapy appropriate for the septic source (31–42). The use of steroids and anti-cytokine therapies remain controversial and of unproven benefit (43–46). Clinical Approach to Sepsis and Its Mimics in Critical Care 131 Table 3 Sepsis Vs. Microbiologic Negative blood cultures (excluding Positive buffy-coat smear skin contaminants) Bacteremia (excluding skin contaminants). Table 4 Empiric Therapy of Sepsis Based on Organ System Involved Empiric therapy usual organisms Source/usual organisms Monotherapy Combination therapy. Lung nosocomial pneumonia/vent- Meropenem Meropenem or cefepime plus either associated pneumonia Cefepime levofloxacin or aztreonam or (aerobic gram-negative bacilli) Cefoperazone amikacin Levofloxacin. Organism unknown Meropenem Piperacillin/tazobactam Tigacyclinea a if Proteus and P. The temperature of the patient is of key importance in determining if the patient has sepsis or a noninfectious mimic. Antibiotic therapy should be instituted as soon as there is a basis for the diagnosis of sepsis, i. Coverage should be based on the usual pathogens associated with the involved organ system. Antibiotics with appropriate spectrum, good safety profile, low resistance potential, and anti-endotoxin qualities are preferred. In sepsis related to perforation, obstruction, or abscess, surgical intervention is paramount and should be done as soon as the diagnosis is confirmed. Cardiogenic shock complicating acute myocardial infarction: expanding to paradigm. Clinical gram-positive sepsis: does it fundamentally differ from gram-negative bacterial sepsis?

Syndromes

• Usually starts on the head and spreads to other areas, moving down the body
• Fluids through a vein (by IV)
• Moth repellent
• Low blood pressure upon standing (orthostatic hypotension)
• Decreased urine output
• Take medications correctly and manage their side effects
• Renal tubular acidosis; proximal
• Pain with intercourse (much less common in men than women)
• Avoid carbonated beverages
• Nerve problems

In this case buy lamotrigine 200 mg with amex medications not to take with grapefruit, insulin and C-peptide levels would both be elevated order 25mg lamotrigine with visa medicine 027 pill, and a sulfonylurea screen is also appropri- ate in this patient order 50 mg lamotrigine otc medicine 3601. The most common hormone pattern is a decrease in total and unbound T3 levels as peripheral conversion of T4 to T3 is im- paired 200 mg lamotrigine otc medicine zolpidem. Teleologically, the fall in T3, the most active thyroid hormone, is thought to limit catabolism in starved or ill patients. This patient undoubtedly has ab- normal thyroid function tests as a result of his injuries from the motor vehicle acci- dent. Over the course of weeks to months, as the patient recovers, thyroid function will return to normal. However, measures of bone resorption may help in the prediction of risk of fracture in older patients. In women over 65 years old, even in the presence of normal bone den- sity, a high index of bone resorption should prompt consideration for treatment. Mea- sures of bone resorption fall quickly after the initiation of antiresorptive therapy (bisphosphonates, estrogen, raloxifene, calcitonin) and provide an earlier measure of response than does bone densitometry. Serum alkaline phosphatase is a measure of bone formation, not resorption, as are serum osteocalcin and serum propeptide of type I procollagen. Biochemical Markers of Bone Metabolism in Clinical Use Bone formation Serum bone-specific alkaline phosphatase Serum osteocalcin Serum propeptide of type I procollagen Bone resorption Urine and serum cross-linked N-telopeptide Urine and serum cross-linked C-telopeptide Urine total free deoxypyridinoline Urine hydroxyproline Serum tartrate-resistant acid phosphatase Serum bone sialoprotein Urine hydroxylysine glycosides X. It is most common in postmenopausal women, but the incidence is also increasing in men. Estrogen loss probably causes bone loss by activation of bone remodeling sites and exaggeration of the imbalance between bone formation and resorption. Clinical determinations of bone density are most commonly measured at the lum- bar spine and hip. The T-score compares an individual’s results to a young population, whereas the Z-score com- pared the individual’s results to an age-matched population. An evaluation for secondary causes of osteoporosis should be considered in individuals presenting with osteoporotic fractures at a young age and those who have very low Z-scores. Initial evalua- tion should include serum and 24-h urine calcium levels, renal function panel, hepatic function panel, serum phosphorous level, and vitamin D levels. Other endocrine abnor- malities including hyperthyroidism and hyperparathyroidism should be evaluated, and uri- nary cortisol levels should be checked if there is a clinical suspicion for Cushing’s syndrome. Follicle-stimulating hormone and luteinizing hormone levels would be elevated but are not useful in this individual as she presents with a known perimenopausal state. Her radiographs show characteristic changes of ac- tive disease in the pelvis, one of the most common areas for Paget disease to present. Her elevated alkaline phosphatase provides further evidence of active bone turnover. The normal serum calcium and phosphate levels are characteristic for Paget disease. Management of asymptomatic Paget disease has changed since effective treatments have become available. Treatment should be initiated in all symptomatic patients and in asymptomatic patients who have evidence of active disease (high alkaline phosphatase or urine hydroxyproline) or dis- ease adjacent to weight-bearing structures, vertebrae, or the skull. Second-generation oral bisphosphonates such as tiludronate, alendronate, and risedronate are excellent choices due to their ability to decrease bone turnover. They should be taken in the morning, on an empty stomach, sit- ting upright to minimize the risk of reflux. Duration of use depends upon the clinical response; typically 3–6 months are needed to see the alkaline phosphatase begin to normal- ize. The “gold- standard” for diagnosis is liver biopsy with quantitative copper assays. Kayser-Fleischer rings can be diagnosed definitively only with a slit-lamp examination and are highly spe- cific for the disease: they are present in >99% of patients who have concomitant neuropsy- chiatric manifestations of copper toxicity and in 30–50% of patients with liver involvement alone or who are presymptomatic. Serum cerulo- plasmin levels are an unreliable marker of illness and should not be used for diagnosis; they are normal in 10% of affected patients. Ceruloplasmin is a liver-derived acute-phase reac- tant that may be elevated in systemic inflammatory states, even in patients with Wilson dis- ease. A 24-h urine copper test can be helpful, particularly in patients who are already experiencing symptoms. Multiple viruses have been impli- cated, but none have been definitively identified as the trigger for subacute thyroiditis. Autoimmune hypothyroidism should be con- sidered; however, the tempo of her illness, the tenderness of the thyroid on examination, and her preceding viral illness make this diagnosis less likely. Ludwig’s angina is a poten- tially life-threatening bacterial infection of the retropharyngeal and submandibular spaces, often caused by preceding dental infection. Cat-scratch fever is a usually benign illness that presents with lymphadenopathy, fever, and malaise. It is caused by Bartonella henselae and is frequently transmitted from cat scratches that penetrate the epidermis. In the first phase of the disease, thyroid inflammation leads to follicle destruction and release of thyroid hormone. In the second phase, the thyroid is depleted of hormone and hypothyroidism results. A recovery phase typically follows in which decreased inflammation allows the follicles to heal and regenerate hormone. Large doses of aspirin (such as 600 mg by mouth every 4–6 h) or nonsteroidal anti-in- flammatory drugs are often sufficient for what is usually a self-limited illness. Thyroid function should be monitored closely; some patients may require low-dose thyroid hormone replacement. The intensive group received multiple administra- tions of insulin daily along with education and psychological counseling. Improvement in glycemic control resulted in a 47% reduction in retinopathy, a 54% reduc- tion in nephropathy, and a 60% reduction in neuropathy. There was a nonsignificant trend toward improvement in macrovascular complications. Individuals receiving intensive glycemic control had a reduction in microvascular events but no signif- icant change in macrovascular complications. However, hypoparathyroidism may occur even if the parathyroid glands are not removed by thyroidectomy due to devascularization or trauma to the parathy- roid glands. Hypocalcemia following removal of the parathyroid glands may begin any time during the first 24–72 h, and monitoring of serial calcium levels is recommended for the first 72 h. The earliest symptoms of hypocalcemia are typically circumoral paresthesias and pares- thesias with a “pins-and needles” sensation in the fingers and toes.

These treatments are also subject to constraints and complexities engen- dered by individual variability generic 200mg lamotrigine fast delivery medicine cups. It also involves the study of the mechanisms by which drugs change the expression of genes cheap lamotrigine 25 mg on line medications related to the integumentary system, including drug-metabolizing enzymes best 50 mg lamotrigine symptoms of anemia, a phenomenon known as induction cheap 100mg lamotrigine fast delivery treatment of tuberculosis. These same tools are applicable to study the diversity of drug effects in different populations. Pharmacogenomics promises to enable the development of safer and more effective drugs by helping to design clinical trials such that non-responders would be eliminated from the patient population and take the guesswork out of prescribing medications. It will also ensure that the right drug is given to the right person from the start. Pharmacogenomic studies are rapidly elucidating the inherited nature of these differences in drug disposition and effects, thereby enhancing drug discovery and providing a stronger scientific basis for optimizing drug therapy on the basis of each patient’s genetic constitution. Pharmacogenomics vs Pharmacogenetics Pharmacogenomics, a distinct discipline within genomics, carries on that tradition by applying the large-scale systemic approaches of genomics to understand the basic mechanisms and apply them to drug discovery and development. Pharmacogenomics now seeks to examine the way drugs act on the cells as revealed by the gene expression patterns and thus bridges the fields of medicinal chemistry and genomics. Some of the drug response markers are examples of interplay between pharmacogenomics and pharmacogenetics; both are playing an important role in the development of personalized medicines. The two terms – pharmacoge- netics and pharmacogenomics – are sometimes used synonymously but one must recognize the differences between the two as shown in Table 5. This scheme shows that genomic technologies and pharmacogenomics play an important role in drug discovery and development. Information obtained from study of the function of genes, their interactions, their role in biological pathways, as well as their variability among the population can be utilized in drug discovery. An under- standing of gene expression changes from normal tissues through the disease devel- opment process among different populations provides possible targets for drug development. These response profiles can be analyzed to uncover biomarkers that correlate with toxicity or efficacy. These biomarkers can help triage hepatotoxicity and car- diotoxicity among other response profiles and reduce the cost of drug development. Target selection in the future should be genetics-based rather than the currently popular target validation. Use of genetic evidence-based methods of target selection should reduce the testing of too many hypotheses that are eventually proven wrong. Reducing attrition and improving a product’s return on investment measure success in discovery. As molecules pass through the development pipelines, choices made in 2015 will undoubtedly play a role in the outcomes in 2020. At first, knowledge of the gene has to be translated into an understanding of the role the gene-encoded protein plays in the disease. Then one has to identify a disease-related tractable target – be it an enzyme, receptor or ion channel – using the best functional genomics tools available. Thus moving from a gene to an understanding of its functional role in disease, and mov- ing from there to optimal therapeutic targets and a therapeutic agent, is the next great challenge for drug development. Genomics is expected to increase the number of possible disease targets by a factor of 5–10. This increase will be driven mainly by the genetic heterogeneity of many diseases. Thus there will be a need to develop more potential medicines that are aimed at the patients’ underlying genotype, not just the disease phenotype. This increase in targets generated by genomics is being successfully met by the sophistication of technologies such as combinatorial chem- istry and high-throughput screening. Preclinical Prediction of Drug Efficacy Assays of drug action typically evaluate biochemical activity. However, accurately matching therapeutic efficacy with biochemical activity is a challenge. High-content cellular assays seek to bridge this gap by capturing broad information about the cel- lular physiology of drug action. Detailed information contained in genomic expres- sion data is usually sufficient to match the physiological effect of a novel drug at the cellular level with its clinical relevance. This capacity to identify therapeutic effi- cacy on the basis of gene expression signatures in vitro has potential utility in drug discovery and drug target validation relevant to personalized medicine. Knowledge of genetic variation in a target enables early assessment of the clinical significance of polymorphism through the appropriate design of preclinical studies and use of relevant animal models. A focused pharmacogenomic strategy at the pre- clinical phase of drug development can contribute to the decision-making process for Universal Free E-Book Store 154 5 Pharmacogenomics full development of compounds. Pharmacogenomics and Clinical Trials Examples of role of pharmacogenomics in clinical trials are listed in Table 5. Current applications of pharmacogenomics include development by prospective genotyping in phase I tri- als, to ensure that a subject population is representative with respect to drug metabo- lism phenotypes. The banking of genetic material from later stage trials for retrospective studies on drug response is becoming more frequent, but is not yet standard in the industry. Some examples of use of pharmacogenomics in clinical studies are shown in Table 5. In case of a genotype-specific drug, test groups should contain only the targeted phenotypes. Molecular genetic methods may be applied both for genetic profiling(polymorphisms, mutations, etc. Genotype/ phenotype correlations based on identification of mutations and polymorphisms are used for population segmentation. Pharmacogenomic tests used by the pharmaceutical companies themselves can be used to help identify suitable subjects for clinical trials, aid in interpretation of clinical trial results, find new markets for current products and speed up the devel- opment of new treatments and therapies. Universal Free E-Book Store 156 5 Pharmacogenomics It is anticipated that genotyping at different stages of clinical trials would change the approach to drug development. Currently there are four phases of clinical trials followed by postmarketing studies. Suggestions to shorten the clinical drug devel- opment process by reducing the number of phases are as follows: • Phase I. Detection of rare events and development of diagnostic tests tied in with the drug therapeutics. Some drawbacks of pharmacogenomics-based clinical trials are: • Exclusion of certain subjects from trials on the basis of genotype is interpreted s discrimination similar to exclusion of women and minorities • Stratification into smaller subgroups might confound statistical analysis and interpretation of results • Statistical differences may not be clinically significant • Misuse of the good results in a subgroup to portray the drug as a whole • Need to do separate clinical trials in different countries Limitations of the Pharmacogenomic-Based Clinical Trials Large prospective trials to demonstrate the value of genotyping in patient manage- ment will be required to support the introduction of pharmacogenomics into clinical practice. Some of the limitations to be considered are: • Such studies are costly and can be justified only if there is a reproducible association between genotype and a clinically relevant phenotype. It may reflect real population differences but multiple comparisons, biases and other design limitations suggest that many initial positive associations represent Type I errors. In selected situations, pharmacogenomic studies in healthy volunteers may sup- port a decision to perform such prospective association studies.

Vernaleo Division of Infectious Diseases order 200mg lamotrigine with visa aquapel glass treatment, Wyckoff Heights Medical Center lamotrigine 100 mg mastercard symptoms inner ear infection, Brooklyn buy generic lamotrigine 50 mg medications in spanish, New York discount 100 mg lamotrigine treatment whiplash, U. Wilkinson Department of Ophthalmology, Pennsylvania State University, College of Medicine, Hershey, Pennsylvania, U. Wilson Department of Surgery, University of California, Irvine School of Medicine, Orange, California, U. Wolf Division of Trauma and Emergency Surgery, Department of Surgery, University of Texas Health Science Center, San Antonio, and Burn Center, United States Army Institute of Surgical Research, San Antonio, Texas, U. Cunha Infectious Disease Division, Winthrop-University Hospital, Mineola, New York, and State University of New York School of Medicine, Stony Brook, New York, U. It is the task of the infectious disease consultant to relate aspects of the patient’s history, physical, laboratory, and radiological tests with the characteristics of the patient’s fever, which together determine differential diagnostic possibilities. After the differential diagnosis has been narrowed by analyzing the fever’s characteristics and the patient-related factors mentioned, it is usually relatively straightforward to order tests to arrive at a specific diagnosis. The infectious disease consultant’s clinical excellence is best demonstrated by the rapidity and accuracy in arriving at a causeforthepatient’sfever(Table1)(1–10). Both infectious and noninfectious disorders may cause acute/chronic fevers that may be low, i. There are relatively few disorders, all noninfectious, which are associated with extreme hyperpyrexia (Table 2) (1,3,5). Central nervous Meningitis Cerebral infarction Encephalitis Cerebral hemorrhage Seizures. Pulmonary Pneumonia Deep vein thrombosis Empyema Atelectasis Tracheobronchitis Chemical pneumonitis Sinusitis Pulmonary emboli/infarction. Gastrointestinal Intra-abdominal abscess Gastrointestinal hemorrhage Cholecystitis/cholangitis Acalculous cholecystitis Viral hepatitis Nonviral hepatitis Peritonitis Pancreatitis Diverticulitis Inflammatory bowel disease C. Skin/soft tissue Cellulitis Hematoma Wound infection Intramuscular injections Burns. Miscellaneous Sustained bacteremias Alcohol/drug withdrawal Transient bacteremias Drug fever Parotitis Postoperative/postprocedure Pharyngitis Blood/blood products transfusion Intravenous contrast reaction Fat emboli syndrome Neoplasms/metastasis Table 2 Causes of Extreme Hyperpyrexia (High Fevers! Tetanus The clinical approach to the noninfectious disorders with fever is usually relatively straightforward because they are readily diagnosable by history, physical, or routine laboratory or radiology tests. By knowing that noninfectious disorders are not associated with fevers >1028F, the clinician can approach patients with these disorders that have fevers >1028F by looking for an alternate explanation. The difficulty usually arises when the patient has a multiplicity of conditions and sorting out the infectious from the noninfectious causes can be a daunting task (Tables 3 and 4) (1–6,10). Infectious disease consultation also useful to evaluate mimics of infection (pseudosepsis) and interpretation of complex microbiologic data Low-grade fevers ( 1028F). While all infections do not manifest temperatures >1028F, they have the potential to be >1028F, e. The clinician should analyze the fever relationships in the clinical context and correlate these findings with other aspects of the patient’s clinical condition to arrive at a likely cause for the temperature elevation. The clinical approach utilizes not only the height of the fever but the abruptness of onset, the characteristics of the fever curve, the duration of the fever, and defervescence pattern, all of which have diagnostic importance (Table 5) (5). The causes of single fever spikes include insertion/removal of a urinary catheter, insertion/removal of a venous catheter, suctioning/manipulation of an endotracheal tube, wound packing/lavage, wound irrigation, etc. Pleural effusions l Bilateral effusions are never due to infection: look for a noninfectious etiology Uncomplicated wound infections l Except for gas gangrene and streptococcal cellulitis, temperatures are usually low grade l “Wounds” with temperatures! Such transient bacteremias are unsustained and because of their short duration, i. Single fever spikes of the transient bacteremias are a diagnostic not a therapeutic problem. Fever secondary to blood products/blood transfusions are a frequent occurrence, and are most commonly manifested by fever following the infusion. Most reactions occur within the first 72 hours after the blood/blood product transfusion, and most reactions within the 72-hour period occur in the first 24 to 48 hours. There are very few reactions after 72 hours, but there is a smaller peak five to seven days after the blood transfusion, which although very uncommon, may occur. The temperature elevations associated with late blood transfusion reactions are lower than those with reactions occurring soon after blood transfusion. The fever subsequent to the transient bacteremia results from cytokine release and is not indicative of a prolonged exposure to the infecting agent, but rather represents the post-bacteremia chemokine-induced febrile response. The temperature 8 Cunha elevations from manipulation of a colonized infected mucosal surface persist long after the bacteremia has ceased (1,3–5,24–27). In patients with fever spikes due to transient bacteremias following manipulation of a colonized or infected mucosal surface, or secondary to a blood/blood product transfusion, may be inferred by the temporal relationship of the event and the appearance of the fever. In addition to the temporal relationship between the fever and the transient bacteremia or transfusion-related febrile response is the characteristic of the fever curve, i. The clinician must rely upon associated findings in the history and physical, or among laboratory or radiology tests to narrow down the cause of the fever. Pulse–temperature relationships are also of help in differentiating the causes of fever in patients with multiple temperature spikes over a period of days (1–5,10). Assuming that there is no characteristic fever pattern, the presence or absence of a pulse–temperature deficit is useful. The diagnostic significance of relative bradycardia can only be applied in patients who have normal pulse–temperature relationships, i. Any patient on these medications who develop fever will develop relative bradycardia, thus eliminating the usefulness of this important diagnostic sign in patients with relative bradycardia (Table 6) (1,5,33–35). Fever secondary to acute myocardial infarction, pulmonary embolus, acute pancreatitis, are all associated with fevers of short duration. If present in patients with these underlying diagnoses, a fever >1028F or one that lasts for more than three days should suggest a complication or an alternate diagnosis. Clinicians should try to determine what noninfectious disorder is causing the fever so that undue resources will not be expended looking for an unlikely infectious disease explanation for the fever (1–10,24–30). Prolonged fevers that become high spiking fevers should suggest the possibility of nosocomial endocarditis related to a central line or invasive cardiac procedure. Prolonged high spiking fevers can also be due to septic thrombophlebitis or an undrained abscess. Physicians should always be suspicious of the possibility of drug fever when other diagnostic possibilities have been exhausted. Drug fever may occur in individuals who have just recently been started on the sensitizing medication, or more commonly who have been on a sensitizing medication for a long period of time without previous problems. Patients with drug fever do not necessarily have multiple allergies to medications and are not usually atopic. However, the likelihood of drug fever is enhanced in patients who are atopic with multiple drug allergies.

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