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Pregnancy is associated with decreased lower esophageal sphincter tone and decreased gastric motility; therefore order 20 mg cialis super active overnight delivery, nasoduodenal tubes are preferred over nasogastric tubes to decrease the likelihood of reflux and aspiration buy cialis super active 20 mg lowest price, although scientific evidence for this is lacking discount 20mg cialis super active mastercard. Blood glucose levels should be measured, along with serum electrolyte concentrations, acid–base status, and renal and hepatic function. Periodic nutritional assessment should include evaluation of nitrogen balance, lymphocyte counts, transferrin, maternal weight, and fetal growth by ultrasound. Deficiencies of these vitamins may lead to fetal neural tube defects, eye abnormalities, and intracerebral hemorrhage [58]. Anticoagulation should be instituted immediately in all patients without clear contraindications, such as active bleeding, rather than delaying therapy pending conclusive diagnostic studies. Patients with extremes of weight <50 kg or >90 kg, should be considered for anti-Xa monitoring every 4 to 6 weeks, so that twice-daily regimens achieve anti-Xa levels of 0. A recent review identified 189 pregnant women who received thrombolytics during pregnancy for venous thromboembolism. Tissue plasminogen activator does not cross the placenta, and the risk of allergic reactions is lower than that of streptokinase. If thrombolytic therapy is used during pregnancy, it seems reasonable to limit the duration of therapy to the time needed for restoration of acceptable hemodynamic function and to discontinue therapy at least 4 to 6 hours antepartum. Continuous uterine massage and methylergonovine maleate should be used postpartum if thrombolytic therapy was only recently discontinued. Aminocaproic acid crosses the placenta readily and is teratogenic, so this should not be used when rapid reversal of the lytic state is needed before delivery. Laboratory monitoring of the lytic state during thrombolytic infusion is not recommended, because clot lysis and risk of bleeding do not correlate well with laboratory measurement of the lytic state [65]. If delivery is anticipated in the next 6 hours, initiation of heparin is delayed until after delivery. Thrombolysis is contraindicated during delivery and the immediate postpartum state because of the bleeding risk. There were no maternal deaths, although fetal death was reported in six cases and preterm delivery in four cases [64]. Surgical embolectomy should be reserved as a lifesaving measure for the mother because of the high incidence of fetal loss [64]. Catheter-directed therapy may include catheter-directed mechanical embolectomy and/or catheter-directed thrombolytic therapy. Among four cases using these techniques during pregnancy, one fetal death and one preterm delivery were reported [65]. Once the patient has stabilized, continuous intravenous heparin can be transitioned to subcutaneous therapy. The patient should be anticoagulated for the remainder of the pregnancy and for at least 6 weeks postpartum [60]. The timing of reinstitution of anticoagulation following delivery will vary depending upon the type of delivery, the presence of bleeding, and the presence of a neuraxial anesthesia catheter. As long as significant bleeding has not occurred, anticoagulation with a heparin may be resumed 6 hours after a vaginal birth or 12 hours after a cesarean section. If pulmonary capillary wedge pressures are elevated, it seems reasonable to use a diuretic to reduce hydrostatic pressures across the injured capillary endothelium. In addition to fluid resuscitation to reverse hypotension, vasopressor therapy is frequently required. For active bleeding, transfusion with red blood cells, fresh-frozen plasma, cryoprecipitate, platelets, and factor replacement is indicated. When uterine bleeding is refractory to these interventions, exploration for uterine tears or retained placenta should be considered. Venous Air Embolism The goals of treatment are to identify the source of air entry, prevent further air entrainment, restore circulation, and remove embolized air. Placing the patient in the left lateral decubitus position may restore forward blood flow by causing the bubble of air to migrate away from the right ventricular outflow tract to a nonobstructing position [19,29]. Aspiration of air from the right atrium, right ventricle, or pulmonary outflow tract can be attempted with a central venous or pulmonary artery catheter [19,20]. Air bubble resorption may be accelerated by ventilating the patient with 100% oxygen to facilitate diffusion of nitrogen from the embolus. When air embolism occurs during general anesthesia, nitrous oxide should be discontinued because it has a high solubility and tends to increase the size of air bubbles in the pulmonary vasculature [19,20]. Patients with continued evidence of neurologic deficits or cardiopulmonary compromise because of air embolism should be considered for hyperbaric oxygen therapy. Hyperbaric oxygen accelerates nitrogen resorption, decreases air bubble size, and increases the arterial oxygen content [19,20]. Use of anticoagulation with heparin has been suggested to treat fibrin microemboli, but has not been formally evaluated [19]. Aspiration of Gastric Contents For patients with permeability pulmonary edema because of aspiration of gastric contents during labor and delivery, the main treatment is supportive care. Prophylactic antibiotics have not been found to be beneficial for aspiration pneumonitis [22]; therefore, antibiotics should be prescribed only when infection complicates the initial chemical pneumonitis. If the patient’s clinical course suggests development of bacterial pneumonia, the choice of antibiotic should be guided by appropriate bacteriologic evaluation of respiratory secretions, pleural fluid (if present), and blood cultures. For patients who have been in the hospital for 48 hours or less, clindamycin or a β-lactam–β-lactamase inhibitor combination is a reasonable empiric choice to treat anaerobic organisms. Glucocorticoids are not recommended in the treatment of aspiration events because of a lack of benefit found by two large multicenter randomized trials [22]. Respiratory Infections Antibacterial agents to treat pneumonia during pregnancy should be selected according to the same principles used for nonpregnant patients [4,24,25]. For community-acquired pneumonia in pregnancy, penicillins, ceftriaxone, azithromycin, and erythromycin (excluding the estolate, which is associated with an increased risk of cholestatic jaundice in pregnancy) are probably safe. Tetracycline is contraindicated because it is teratogenic and causes hepatic toxicity when administered intravenously in pregnancy. The aminoglycosides have the potential of causing eighth nerve toxicity in the fetus and should be used only when strong clinical indications exist. Clindamycin has no reported adverse fetal effects, but experience is limited and it should be used with caution. Vancomycin hydrochloride may cause fetal renal and auditory toxicity and should be used with caution, with close monitoring of serum drug levels. Clarithromycin and levofloxacin are pregnancy risk factor class C and, therefore, should be used judiciously, weighing potential risks and benefits. The predominant treatment of influenza pneumonia is supportive care, following the same practices as outlined for other causes of respiratory failure in pregnancy.

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Although this method broke the siege cheap cialis super active 20 mg online, all but two of the 41 terrorists and 129 hostages died from opiate toxicity [9] cheap 20mg cialis super active with visa. The most recent use of chemical weapons occurred in the early morning hours of August 21 discount cialis super active 20mg amex, 2013 in the Ein Tarma and Zamalka suburbs of Damascus, Syria. Social media reports and videos as well as satellite imagery demonstrated large numbers of sick adults and children with no visible trauma; medical personnel described the symptoms as most consistent with exposure to a nerve agent [10]. Three Damascus hospitals received over 3,000 casualties where the principle antidote atropine was in short supply and exposure to contaminated patients at one hospital resulted in 41 staff members, including 10 doctors, becoming contaminated [11]. However, hospital-based critical care physicians should understand basic concepts of these topics to better care for their patients and protect themselves and their facilities from potential harm. The most important tool for detecting the use of these agents is accurate and timely intelligence from military or law enforcement agencies. Unfortunately, hospitals are not usually in the information- sharing and decision-making circles with these groups. As a result, initial awareness of a chemical agent attack typically occurs with the first patient presenting to the emergency department. Hospitals and physicians can improve their preparedness for the management of chemical agent casualties by actively participating in disaster-planning activities at their respective communities. At the present time, all commercially available detection equipment uses point source technology; that is, proximity to the substance is required. The handheld Chemical Agent Monitor uses ion mobility spectrometry to detect mustard and nerve agents. Chemical agent detection papers, such as the M8 and M9 papers (Anachemia, Lachine, Quebec, Canada), can be used to detect mustard and nerve agents. The M256 Detection Kit (Anachemia, Lachine, Quebec, Canada) can detect mustard, nerve agents, phosgene, and cyanide. Standoff capability, that is, detecting agents from as far away as 5 km, has been developed to detect contaminated areas without being exposed [14]. Many of the readily available detection strategies cannot detect lower levels of chemical agent, thus being less useful to confirm successful decontamination or detect chemical agents remotely from the site of exposure. Most hospitals will not have capability to confirm exposure or nature of chemical agents used in a timely manner to influence patient care or protect their facilities. As health care providers, use of samples from patients rather than environmental sampling may be helpful for clinical and forensic purposes. Sulfur mustard exposure can also be determined from hair analysis of patients with suspected exposure [16]. Further development of rapid, easy, and affordable technology to help hospitals detect and identify chemical weapon agents is expected to make new technologies available. Unfortunately, most disaster victims bypass emergency medical system transport and arrive unannounced at the closest hospital. As a result, hospitals must be prepared to decontaminate chemical agent casualties prior to admission. Such processes are needed to protect the victims from further exposure and to prevent the spread of chemical agents within the hospital and among health care providers. Critical care physicians, nurses, and support personnel may be called on to help develop decontamination protocols and assist in the decontamination process. It is imperative that all individuals designated to serve on decontamination teams be thoroughly trained in the procedures, precautions, and protective clothing required by the decontamination process. Attempting to provide help in a contaminated environment without prior training puts the health care provider at risk of being exposed to a chemical agent and could impede the delivery of effective medical care for the victims of a chemical attack. One common (and potential fatal) error made by health care providers is to rely on personal protective equipment effective for protection from biologic hazards (such as N95 respirators) which provide insufficient protection during decontamination or care of contaminated chemical agent exposed casualties. The sarin gas release in Tokyo provides a clear example of the need for preparation and training prior to a chemical attack. None of the first responders wore protective clothing or face masks and off-gassing of the chemical agent from clothing of victims played a significant role in their complaints. It was reported that 23% of the staff at the hospital that received the patients also experienced symptoms [17]. It provides guidance for the use of personal protective equipment and requires that written plans be developed for hospitals to train teams for the use of personal protective equipment to receive contaminated victims [18]. Recurrent training and drills in the use of available and appropriate personal protective equipment by hospital staff is recommended to ensure readiness in the event of a chemical agent event. Mechanical removal without deactivation may result in spread of some agents at the decontamination area and create contaminated waste. For most situations, effective chemical decontamination can be performed by carefully removing the victim’s clothing and thoroughly washing the victim with soap and water. It has been reported that removing contaminated clothing alone can eliminate 85% to 90% of chemical contaminants [19]. The M291 Skin Decontamination Kit has been in use by the military for many years, and can facilitate mechanical removal and partial deactivation of some agents. It is not used for prophylactic protection or total body decontamination, but, if applied early following exposure, is effective for neutralizing chemical warfare agents and T2 mycotoxins [21]. In addition to skin and wound decontamination products, other strategies may be used to decontaminate personal protective equipment and external surfaces. Normally employed as a foam, it effectively neutralizes a variety of chemical agents including nerve gases and mustard [23]. A recent study from the Czech Republic provides an excellent example of a comparative approach to chemical agent decontamination strategies, taking into consideration multiple factors relevant to different operating environments and expected exposures [24]. Finally, medical facilities must consider environmental variables such as wind direction, wind velocity, temperature, and water runoff when setting up decontamination areas. These environmental considerations are important for protecting patients and employees from exposure to chemical agents, as well as minimizing the risk of contaminating buildings and equipment during the patient decontamination process. The most common classification scheme divides them into the following categories: Nerve agents Vesicants Cyanide agents or “blood” agents Pulmonary agents or “choking” agents Nonlethal incapacitating agents Nerve Agents Because they are the most toxic, nerve agents are the most feared of chemical agents. The decrease of acetylcholinesterase activity results in the accumulation of acetylcholine at both muscarinic and nicotinic receptors in the central nervous system and neuromuscular junctions of the peripheral nervous system. Cholinergic overstimulation resulting from the accumulation of excess acetylcholine at these sites is responsible for the clinical manifestations of nerve agent toxicity [26]. Compounds that were originally developed in Germany have been designated as the “G” series of nerves agents. The “V” series of agents are better absorbed through the skin than the “G” agents and are so designated because they are more “venomous. Inhalation of nerve gas is the most effective means of producing clinical effects, although it can also be ingested.

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Arthropathy is uncommon buy 20mg cialis super active with visa, but arthralgia and arthritis are reported with fluoroquinolone use in pediatric patients discount 20 mg cialis super active otc. Use in the pediatric population should be limited to distinct clinical scenarios (for example buy 20 mg cialis super active with mastercard, cystic fibrosis exacerbation). Hepatotoxicity or blood glucose disturbances (usually in diabetic patients receiving oral hypoglycemic agents or insulin) have been observed. Identification of any of these events should result in prompt removal of the agent. Serum concentrations of medications such as theophylline, tizanidine, warfarin, ropinirole, duloxetine, caffeine, sildenafil, and zolpidem may be increased (ure 31. Examples of clinically useful fluoroquinolones Due to increasing resistance and boxed warnings, fluoroquinolones should be used with caution in select circumstances. They may be considered in patients who do not tolerate other agents (for example, severe beta-lactam allergies) or as definitive therapy once susceptibilities are available. Ciprofloxacin is used in the treatment of traveler’s diarrhea, typhoid fever, and anthrax. It is a second-line agent for infections arising from intra-abdominal, lung, skin, or urine sources. Of note, high-dose therapy should be employed when treating Pseudomonas infections. It may be considered for mild-to-moderate intra- abdominal infections, but should be avoided if patients have fluoroquinolone exposure within previous three months, due to increasing B. Moxifloxacin may be considered as a second-line agent for management of drug-susceptible tuberculosis. Due to its spectrum of activity, it is an option for managing acute bacterial skin and skin structure infections. Humans use dietary folate to synthesize the critical folate derivative, tetrahydrofolic acid. By contrast, many bacteria are impermeable to folate derivatives, and rely on their ability to synthesize folate de novo (ure 31. Sulfonamides (sulfa drugs) are a family of antibiotics that inhibit de novo synthesis of folate. A second type of folate antagonist, trimethoprim, prevents microorganisms from converting dihydrofolic acid to tetrahydrofolic acid. The combination of the sulfonamide sulfamethoxazole with trimethoprim (the generic name for the combination is cotrimoxazole) provides a synergistic effect. Sulfonamides Sulfa drugs were among the first antibiotics used in clinical practice. Today, they are seldom prescribed alone except in developing countries, where they are employed because of low cost and efficacy. Antibacterial spectrum Sulfa drugs have in vitro activity against gram-negative and gram-positive organisms. Common organisms include Enterobacteriaceae, Haemophilus influenzae, Streptococcus spp. Resistance Bacteria that obtain folate from their environment are naturally resistant to sulfa drugs. Acquired bacterial resistance to the sulfa drugs can arise from plasmid transfers or random mutations. Absorption Most sulfa drugs are well absorbed following oral administration (ure 31. It is not absorbed when administered orally or as a suppository and, therefore, is reserved for treatment of chronic inflammatory bowel diseases. Absorption of sulfapyridine can lead to toxicity in patients who are slow acetylators. Because of the risk of sensitization, sulfa drugs are not usually applied topically. Distribution Sulfa drugs are bound to serum albumin in circulation and widely distribute throughout body tissues. Sulfa drugs penetrate well into cerebrospinal fluid (even in the absence of inflammation) and cross the placental barrier to enter fetal tissues. The acetylated product is devoid of antimicrobial activity but retains the toxic potential to precipitate at neutral or acidic pH. This causes crystalluria (“stone formation”; see below) and potential damage to the kidney. Excretion Unchanged sulfa drug and metabolites are eliminated via glomerular filtration and secretion, requiring dose adjustments with renal impairment. Adequate hydration and alkalinization of urine can prevent the problem by reducing the concentration of drug and promoting its ionization. Hypersensitivity Hypersensitivity reactions, such as rashes, angioedema, or Stevens-Johnson syndrome, may occur. When patients report previous sulfa allergies, it is paramount to acquire a description of the reaction to direct appropriate therapy. Fatal reactions have been reported from associated agranulocytosis, aplastic anemia, and other blood dyscrasias. Kernicterus Bilirubin-associated brain damage (kernicterus) may occur in newborns, because sulfa drugs displace bilirubin from binding sites on serum albumin. Contraindications Due to the danger of kernicterus, sulfa drugs should be avoided in newborns and infants less than 2 months of age, as well as in pregnant women at term. Sulfonamides should not be given to patients receiving methenamine, since they can crystallize in the presence of formaldehyde produced by this agent. Mechanism of action Trimethoprim is a potent inhibitor of bacterial dihydrofolate reductase (see ure 31. Inhibition of this enzyme prevents the formation of the metabolically active form of folic acid, tetrahydrofolic acid, and thus, interferes with normal bacterial cell functions. Trimethoprim binds to bacterial dihydrofolate reductase more readily than it does to human dihydrofolate reductase, which accounts for the selective toxicity of the drug. Antibacterial spectrum The antibacterial spectrum of trimethoprim is similar to that of sulfamethoxazole. Resistance Resistance in gram-negative bacteria is due to the presence of an altered dihydrofolate reductase that has a lower affinity for trimethoprim. Because the drug is a weak base, higher concentrations of trimethoprim are achieved in the relatively acidic prostatic and vaginal fluids.