M. Cruz. Lake Forest Graduate School of Management.
Symptoms of other foci of infection order hytrin 2mg with visa pulse pressure 60 mmhg, such as pneumonia buy hytrin with amex arteria definicion, otitis quality hytrin 1mg blood pressure ranges nhs, or sinusitis, may also be present . Any history of head trauma (including remote events) or recent clear nasal or ear discharges should be obtained. A history of exposure to a patient with known meningococcal disease is usually forthcoming if present. The initial neurologic examination should evaluate the mental status and the presence of focal deficits. A thorough ear, nose, and throat examination can reveal possible foci leading to contiguous extension to the meninges. Petechiae or purpuric lesions strongly suggest meningococcal disease, though they may also be seen in other bacterial infections or in aseptic meningitis caused by enteroviruses or rickettsiae. Needle aspiration or punch biopsy of skin lesions should be used to obtain material for Gram stain and culture. Neutrophil counts greater than 1,000 cells per μL are strongly associated with bacterial meningitis . Rapid deterioration should lead to consideration of subdural empyema, a collection between the dura and the arachnoid membrane [44,51]. A new focal neurologic abnormality, decreased level of consciousness, or cerebrovascular accident with a nonarterial distribution should prompt imaging for venous thrombophlebitis [44,51]. Differential Diagnosis Several pathogens other than pyogenic bacteria can cause clinical presentations and/or spinal fluid formulas that overlap with bacterial meningitis. Viral meningitis can have initial clinical presentations similar to bacterial meningitis, with an early neutrophil predominance and a shift to lymphocytes over time . However, some cases have a total leukocyte count in the range of purulent meningitis with a polymorphonuclear predominance . A history of tuberculosis, risk factors for exposure, or the presence of an immunocompromising condition should raise suspicion, particularly in the setting of a subacute meningitis presentation . Nucleic acid amplification tests may facilitate earlier diagnosis, but there is a wide variability in their availability and sensitivity . Primary amebic meningitis with Naegleria fowleri is acquired through freshwater exposure and presents similarly to acute bacterial meningitis. The nematode Strongyloides stercoralis is capable of establishing a cycle of autoinfection in immunosuppressed hosts, including those on oral corticosteroids. Cryptococcus neoformans is a major cause of meningitis in patients with immunosuppressive conditions, though it can occur in normal hosts; Cryptococcus gatti is an emerging cause of cryptococcal meningitis in immunocompetent hosts . Parameningeal foci of infection, including epidural abscess, can present a purulent picture, usually with elevated protein and a normal glucose concentration . Brain abscess that has ruptured into the ventricles may duplicate the clinical picture of bacterial meningitis. Therapy Bacterial meningitis requires prompt initiation of antimicrobial and anti- inflammatory therapy, aggressive control of the potential complications, and prevention of disease spread . Initial therapy is usually selected empirically based on the age and underlying condition of the patient. The third-generation cephalosporins (ceftriaxone or cefotaxime) are the mainstays of therapy for community-acquired meningitis. Initial therapy for postneurosurgical bacterial meningitis should include vancomycin plus either ceftazidime or cefepime to provide adequate coverage for methicillin-resistant staphylococci and P. Resistance to antimicrobials, either at the outset or developing during treatment, can complicate therapy for Gram-negative organisms . An increasing number of cases due to multidrug-resistant hospital-acquired organisms such as Acinetobacter sp. Consequently, a trial of the third-generation cephalosporins (or meropenem) should be strongly considered unless there is a documented, serious intolerance. For resistant organisms, vancomycin and cephalosporin should be continued and the addition of rifampin considered . The recommended duration of antimicrobial therapy for meningitis depends on the etiology and the clinical response. Gram-negative bacillary meningitis is typically treated for 3 weeks and staphylococcal disease, when accompanied by bacteremia, for 4 to 6 weeks . Anti-Inflammatory Therapy the role of endogenous mediators of inflammation in the pathogenesis of meningitis has provided a rationale for the use of anti-inflammatory agents. Dexamethasone therapy should be initiated before or simultaneously with the first antimicrobial dose in patients with suspected or confirmed pneumococcal meningitis [3,67]. The recommended duration of steroid therapy is 4 days, but some studies in children suggest that 2 days may be adequate [42,76]. Supportive Therapy Treatment of meningitis also requires management of seizures and increased intracranial pressure. Seizures should be controlled by anticonvulsants as necessary (see Chapter 151), and aspiration and hypoxia must be prevented. One stage removal with immediate replacement of the device followed by antibiotics is associated with a 65% rate of cure. Ceftriaxonea 125 mg for children or 250 mg for adults as a single meningitidis intramuscular injection Ciprofloxacinb 500 mg as a single dose in adults Rifampin 10 mg/kg (maximum dose, 600 mg) by mouth twice a day for 2 d H. Rifampin 20 mg/kg (maximum dose, 600 mg) by mouth once a influenzae day for 4 d a Preferred agent in pregnant women. Primary rifampin resistance is similarly rare but may develop secondarily in individuals who receive rifampin for prophylaxis . Meningococcal vaccines (quadrivalent or serogroup B, depending on the setting) can be used as an adjunct to chemoprophylaxis to prevent late secondary cases in contacts or to control outbreaks of disease [16,17]. In addition, if two or more cases have occurred in the same day-care group within 60 days, chemoprophylaxis is recommended. Although a specific diagnosis provides important prognostic and epidemiologic information, there are only a handful of treatable causes of encephalitis. Infections of the brain that do not present as acute encephalitis but rather as subacute to chronic processes are not discussed further in this chapter. Etiology For almost half of all encephalitis cases in the United States, the etiology is not identified. With improved diagnostic techniques, there is increased recognition of viruses such as Jamestown Canyon virus  and Powassan virus  as well as newly identified causative agents . Many nonviral pathogens, including Mycobacterium tuberculosis, rickettsiae, Mycoplasma pneumoniae, Bartonella sp. Despite the favorable prognosis, encephalitis caused by organisms listed in group 1 may be extremely severe, with prolonged unresponsiveness followed by gradual clearing. By the time encephalitic symptoms develop, the virus has usually been cleared from the circulation and specific antibody is present, facilitating diagnosis . Eastern equine encephalitis is the most virulent, causing death or severe neurologic sequelae in more than 60% of cases . Rabies virus reaches the brain by spreading up neural pathways from its site of inoculation, a process that may take weeks to years.
Thus cheap hytrin 1mg online prehypertension workout, an effusion should be suspected if there is increased homogeneous density over the lower lung fields compared to the upper lung fields 1 mg hytrin mastercard pulse pressure lower than 20. However order hytrin 2 mg with amex blood pressure variability, failure of chest wall tissue to move laterally, cardiomegaly, prominent epicardial fat pad, and lung collapse or consolidation may obscure a pleural effusion on a supine radiograph. An absent pectoral muscle, prior mastectomy, unilateral hyperlucent lung, scoliosis, previous lobectomy, hypoplastic pulmonary artery, or pleural or chest wall mass may lead to unilateral homogeneous increased density and mimic an effusion. Approximately 175 to 525 mL of pleural fluid results in blunting of the costophrenic angle on an erect radiograph. This quantity of effusion can be detected on a supine radiograph as an increased density over the lower lung zone. Failure to visualize the hemidiaphragm, absence of the costophrenic angle meniscus, and apical capping are less likely to be seen with effusions of less than 500 mL . The major radiographic finding of a pleural effusion in a supine position is increased homogeneous density over the lower lung field that does not obliterate normal bronchovascular markings, does not show air bronchograms, and does not show hilar or mediastinal displacement until the effusion is massive. C: A complex, septae pleural effusion seen in a patient with severe sepsis owing to the presence of an empyema. D: A complex pleural effusion with an anechoic area assoicated with an increased echogenic density in the dependent area of the fluid collection. This is called the “hematocrit sign” and occurred in a patient who developed a hemothorax as a result of extravascular migration of a central line into the pleural space. Patients with multiple lines or compromised hemodynamic and oxygenation status will be difficult to position sitting upright in bed. One option is for the examiner to place the transducer in the posterior axillary line while angling the probe up toward the center of the body to visualize smaller effusions. For unstable patients who have effusions that are difficult to visualize, positioning the patient in a lateral decubitus position may be helpful. The examiner should always use a systematic approach to identify the following three findings to confirm the presence of a pleural effusion (see Video 1-25 in Chapter 12 Cases). Anatomic boundaries: An identification of the diaphragm and subdiaphragmatic organs (the liver or the spleen, depending on the side), the chest wall, and the lung, which should be clearly differentiated from the pleural effusion. Echo-free space: the relatively echo-free space surrounded by typical anatomic boundaries is the pleural effusion. Another characteristic sign of pleural effusions is the plankton sign, which is caused by swirling debris agitated by cardiac or respiratory motion in a pleural effusion. In the case of parapneumonic effusions, these findings typically indicate the presence of a complicated parapneumonic effusion or an empyema . The base, lateral chest wall, and juxtacardiac area should be carefully visualized for evidence of pneumothorax. An erect or a decubitus (suspected hemithorax up) radiograph should be obtained to assess for the presence of a pneumothorax. Among individuals without pneumothorax, the lung– chest wall interface, which represents a to-and-fro movement synchronized with respiration, can be identified. However, the absence of lung sliding may be caused by the presence of large bullae or pleural symphysis caused by previous pleurodesis or pleural adhesions as a result of previous pleural disease. Hence, the absence of lung sliding is not specific for pneumothorax, but detection of lung sliding reliably excludes the presence of pleural air in the examined area. We recommend that preprocedural scanning be performed to determine the presence of lung sliding prior to the placement of a central venous line. The presence of lung sliding before and after the placement of a central venous catheter is reassuring for excluding an iatrogenic pneumothorax. Underlying lung disease may prevent total lung collapse, even if tension is present; for patients on mechanical ventilation, little or no midline mediastinal shift may result from the tension. Among the latter, a depressed ipsilateral diaphragm is a more reliable sign of tension than mediastinal shift. Pleural adhesions and relative compressibility and mobility of surrounding structures, in addition to the supine position, probably account for these loculated tension pneumothoraces. A study of 88 critically ill patients with 112 pneumothoraces found that the anteromedial and subpulmonic recesses were involved for 64% of patients in the supine and semierect positions . Furthermore, in 30% of the pneumothoraces of this study that were not initially detected by the clinician or radiologist, half of the patients progressed to tension pneumothorax. Factors that may contribute to an improved ability to diagnose this potentially lethal problem include (a) familiarity with atypical locations of pneumothoraces in critically ill patients, usually caused by the supine or semierect position; (b) the consequence of underlying cardiopulmonary disease; and (c) knowledge of other risk factors contributing to misdiagnosis (e. Pleural effusions are most commonly caused by primary lung disease but may also result from disease in the gastrointestinal tract, liver, kidney, heart, or reticuloendothelial system. Although disease of any organ system can cause a pleural effusion in critically ill patients, the diagnoses listed in Table 176. When a pleural effusion is suspected on physical examination and confirmed radiologically, a diagnostic thoracentesis under ultrasonographic guidance should be performed in an attempt to establish the cause. Observation may be warranted in these situations, but thoracentesis should be performed if there are adverse changes . In fact, establishing the diagnosis quickly for these critically ill patients may be more important and life-saving than in noncritically ill patients. Pneumothorax, the most clinically important complication of thoracentesis , is no more likely to occur during mechanical ventilation; however, when a pneumothorax does develop, the patient on mechanical ventilation is likely to develop a tension pneumothorax. If clinical judgment dictates that the information gained from the pleural fluid analysis may help in diagnosis and therapy, thoracentesis should be performed (see Chapter 12). Diagnostic thoracentesis with a small-bore needle can be performed safely in virtually any patient if meticulous technique is used. A patient with a small amount of pleural fluid and a low benefit to risk ratio also represents a relative contraindication. Complications Complications of diagnostic thoracentesis include pain at the needle insertion site, bleeding (local, intrapleural, or intra-abdominal), pneumothorax, empyema, and spleen or liver puncture (see Chapter 12). However, when ultrasound-guided thoracentesis is performed by experienced physician sonographers, pneumothorax or other injuries caused by organ puncture appear to be rare events. Liver or spleen puncture tends to occur when the patient is not sitting absolutely upright because movement toward recumbency causes cephalad migration of the abdominal viscera. However, even if the liver or the spleen is punctured with a small-bore needle, generally the outcome is favorable if the patient is not receiving anticoagulants and does not have a bleeding diathesis. Therapeutic Thoracentesis Indications and Contraindications the primary indication for therapeutic thoracentesis is relief of dyspnea. However, there appears to be an increased risk of pneumothorax, thus making a therapeutic thoracentesis in patients on mechanical ventilation potentially hazardous. The technique for therapeutic thoracentesis is essentially the same as for diagnostic thoracentesis, except that a blunt-tip needle or plastic catheter, rather than a sharp-tip needle, should be used (see Chapter 12). This reduces the risk of pneumothorax, which may occur because fluid is removed and the lung expands toward the chest wall. The amount of fluid that can be removed safely from the pleural space at one session is controversial. As long as intrapleural pressure does not fall to less than −20 cm H O, fluid removal2 can continue .
No difference was noted in graft function cheap hytrin 5mg with mastercard blood pressure healthy numbers, patient and graft survival purchase 1mg hytrin mastercard zofran arrhythmia, biopsy-proven acute rejection buy discount hytrin 1 mg heart attack 5 hour energy, or chronic allograft nephropathy between the two groups . Polyclonal antibodies directed against lymphocytes were developed first and have been used in transplantation since the 1960s. The production of monoclonal antibodies was later made possible, and, in turn, allowed for the development of targeted therapy. A number of different monoclonal antibodies (mAbs) are currently under development or in various phases of clinical testing; several have been tested and are now in clinical use. To address this problem, recent efforts have focused on the development of so-called humanized versions of mAbs, either by replacing the murine constant portion (Fc) with a human Fc component, and/or by replacing the hypervariable region of the antibody that determines antigen specificity, thus in both instances creating a chimeric antibody. The advantages of these humanized mAbs are a very long half-life, reduced immunogenicity, and the potential for indefinite and repeated use to confer effects over months rather than days . Owing to their efficacy, biologic induction agents are currently used in about 85% of all kidney transplants in the United States . After administration, the transplant recipient’s total lymphocyte count will fall, and hence these are known as depleting antibodies. Polyclonal antibodies have been successfully used to prevent rejection and to treat acute rejection episodes. Side effects include fever, chills, arthralgia, thrombocytopenia, leukopenia, and a serum sickness–like illness. If a significant drop in platelets or white blood cells is noted, the dosage should be halved or the drug temporarily withheld. Monoclonal Antibodies the hybridization of murine antibody–secreting B lymphocytes with a nonsecreting myeloma cell line produces mAbs. The description herein, therefore, will be brief, but it warrants discussion owing to its historical importance. The most serious side effect was a rapidly developing, noncardiogenic pulmonary edema that could be life threatening. It was also associated with a wide spectrum of neurologic complications (headache, aseptic meningitis, and encephalopathy). Daclizumab was withdrawn from clinical use in 2009, leaving basiliximab the only available agent for clinical use. Basiliximab is humanized (75% of the antibody is of human origin), the half-life of which is about 7 days. Clinical trials in kidney recipients have shown these agents to be effective in preventing acute rejection , but it is not indicated for the treatment of acute rejection episodes. In all clinical trials to date, basiliximab has been shown to be remarkably safe, with minimal side effects ascribed directly to its use. It stopped from being commercially available for transplantation in September 2012, but remains available for appropriate patients via the producer (Genzyme). Alemtuzumab facilitates reduced-maintenance immunosuppression requirements, without an increase in infections or malignant complications in kidney, pancreas, lung, and liver transplantations as compared with historical controls [82–86]. Rituximab has a role in the treatment of Banff 2 and 3 rejection and in reducing antibody formations . Fusion Proteins These are made by the fusion of a single receptor targeting a ligand of interest with a secondary molecule, which is typically the Fc portion of an IgG molecule. Fusion proteins can be composed of humanized components limiting their immune clearance and allowing prolonged administration. Costimulation-Based Agents Costimulatory molecules alter the threshold for activation of naive T lymphocytes without having a primary activating or inhibitory function. It is intended for use as an induction agent as well as for maintenance immunosuppression, but may have increased risk of acute rejection. Being expressed only on immune cell makes it an important target for developing new immunosuppressants. Major emphasis has been in the area of reduction of toxicities of immunosuppressive agents/combinations. Another major advantage of the availability of several immunosuppressive agents is that immunosuppression can now be tailored for the individual patient. Those having drug-specific toxicity can be switched to another drug with similar efficacy but differing side effects. 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Chan L, Mulgaonkar S, Walker R, et al: Patient-reported gastrointestinal symptoms burden and health-related quality of life following conversion from mycophenolate mofetil to enteric-coated mycophenolate sodium. Zucker K, Tsaroucha A, Olson L, et al: Evidence that tacrolimus augments the bioavailability of mycophenolate mofetil through the inhibition of mycophenolic acid glucuronidation. Neylan J: Immunosuppressive therapy in high-risk transplant patients: dose-dependent efficacy of mycophenolate mofetil in African-American renal allograft recipients. Pescovitz M, Conti D, Dunn J, et al: Intravenous mycophenolate mofetil: safety, tolerability and pharmacokinetics. Sartelet H, Toupance O, Lorenzato M, et al: Sirolimus-induced thrombotic microangiopathy is associated with decreased expression of vascular endothelial growth factor in kidneys. Dittrich E, Schmaldienst S, Soleiman A, et al: Rapamycin-associated post-transplantation glomerulonephritis and its remission after reintroduction of calcineurin-inhibitor therapy. Kahan B, Napoli K, Kelly P, et al: Therapeutic drug monitoring of sirolimus: correlations with efficacy and toxicity. Hong J, Kahan B: Sirolimus-induced thrombocytopenia and leukopenia in renal transplant recipients: risk factors, incidence, progression, and management. Singer S, Tiernan R, Sullivan E: Interstitial pneumonitis associated with sirolimus therapy in renal-transplant recipients. Cullis B, D’Souza R, McCullagh P, et al: Sirolimus-induced remission of posttransplantation lymphoproliferative disorder. Stallone G, Schena A, Infante B, et al: Sirolimus for Kaposi’s sarcoma in renal-transplant recipients. Alarcon-Zurita A, Ladefoged J: Treatment of acute allograft rejection with high doses of corticosteroids. Pascual J, Quereda C, Zamora J, et al: Steroid withdrawal in renal transplant patients on triple therapy with a calcineurin inhibitor and mycophenolate mofetil: a meta-analysis of randomized, controlled trials.