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By: Bertram G. Katzung MD, PhD

  • Professor Emeritus, Department of Cellular & Molecular Pharmacology, University of California, San Francisco

The shoes or inserts must be prescribed by a podiatrist (foot doctor) or other qualifed doctor and provided by a podiatrist cheap 10 mg namenda with amex, orthotist order namenda 10 mg without a prescription, prosthetist purchase namenda 10 mg otc, pedorthist cheap namenda 10 mg line, or other qualifed individual. Other diabetic services and supplies: See Diabetes services and Diabetes supplies on pages 30?31. Traction equipment Part B covers traction equipment that your doctor prescribes for use in your home. Section 2: Items & services 105 Transitional Care Management Services Medicare may cover these services if you?re returning to your community afer a stay at certain facilities, like a hospital or skilled nursing facility. You?ll also be able to get an in-person ofce visit within 2 weeks of your return home. They will work with you and your family and caregiver(s), as appropriate, and with your other health care providers. Help you with referrals or arrangements for follow-up care or community resources. Help you with scheduling and managing your medications More information Visit Medicare. Tere are some exceptions, including some cases where Part B may pay for services that you get on board a ship within the territorial waters adjoining the land areas of the U. Medicare may pay for inpatient hospital, doctor, or ambulance services you get in a foreign country in these rare cases. In the situations described above, you pay 20% of the Medicare-approved amount, and the Part B deductible applies. Virgin Islands, Guam, the Northern Mariana Islands, and American Samoa are considered part of the U. Section 2: Items & services 107 Vaginal cancer screenings See Cervical & vaginal cancer screenings on pages 17?18. The walker must be medically necessary and prescribed by your doctor or other treating provider for use in your home. You must have a face-to-face examination and a written prescription from a doctor or other treating provider before Medicare helps pay for a power wheelchair. X-rays Part B covers medically necessary diagnostic X-rays when ordered by your treating doctor or other health care provider. Costs You pay 20% of the Medicare-approved amount, and the Part B deductible applies. To request Medicare or Marketplace information in an accessible format you can: 1. Note: If you?re enrolled in a Medicare Advantage Plan or Medicare Prescription Drug Plan, contact your plan to request its information in an accessible format. Rhodes z Introduction Central venous oxygen saturation (ScvO)2 and mixed venous oxygen saturation (SvO) have been used in the assessment and management of the critically ill for2 many years. ScvO2 refers to hemoglobin saturation of blood in the superior vena cava and SvO2 refers to the same measurement in blood from the proximal pulmo nary artery. The earliest clinical reports of the use of such data were of ScvO2 in the coronary care unit [1]. Since that time various authors have utilized SvO2 and ScvO2 as therapeutic goals in clinical trials, initially without success [3]. However, as our understanding of the clinical relevance of ScvO2 and SvO2 has improved, use of these parameters has been associated with marked improvements in outcome [4]. As a result, there is renewed interest in the use of venous saturation, in particular as a hemodynamic goal in the use of goal-directed therapy. The aim of this chapter is to give an ac count of the physiology of SvO2 and ScvO2 in health and disease, describe the rela tionshipbetween the two and explore the use of these parameters in interventional trials. Either a sample of blood from the correct anatomical position can be taken and the venous saturation then measured (intermittent) or a continuous invasive catheter is used that mea sures the saturation of blood in vivo. Intermittent Blood Sampling the saturation of hemoglobin with oxygen is measured by spectrophotometry. The pattern of light absorption differs for oxygenated and de-oxygenated hemoglobin. The relative concentrations of each form may be calculated from absorption of light comprising two or more discrete wavelengths and a measurement of hematocrit. This technique, known as a co-oximetry, is employed in modern blood gas analy zers and allows the presence of methemoglobin and carboxyhemoglobin to be quantified as well. Mixed and Central Venous Oxygen Saturation 593 Co-oximetry is a reliable technique, the main sources of error being the use of a diluted or unhomogenized blood sample. Prior to the introduction of spectrophotometry, PvO2 and PcvO2 were measured and SvO2 and ScvO2 then calculated with the use of a nomogram [6]. This technique does not take account of changes either in hemoglobin affinity for oxygen or the presence of carboxyhemoglobin and methemoglobin, which may be clinically significant in the critically ill. Some older studies describing ScvO2 and SvO2 are therefore subject to a greater margin of error than subsequent re search which utilized spectrophotometric techniques. Indwelling Fiberoptic Catheter By incorporating optical fibers into pulmonary artery and central venous catheters, the oxygen saturation of venous blood may be measured continuously without the need for intermittent blood sampling. The main sources of error with this approach are malposition of the catheter and the catheter tipabutting a vessel wall. The latter is indicated by a signal on the display provided by some continuous spectrophotometry systems. Factors influencing mixed and central venous oxygen saturation Factors affecting oxygen delivery Factors affecting oxygen consumption Cardiac output Cytopathic hypoxia z Cardiogenic shock z Sepsis z Reduced circulating blood volume z Cyanide poisoning z Exercise Increased consumption Oxygen content z Pyrexia z Hypoxia/O2 therapy z Exercise z Hyperbaric O2 exposure z Shivering z Anemia/hemorrhage Reduced consumption z Carbon monoxide poisoning z Sedation/anesthesia 594 R.

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Silica particles can accumulate in the kidney discount 5mg namenda with amex, leading to cheap 10mg namenda with amex localized inflammatory responses and fibrotic lesions similar to order namenda 10mg line those observed in pulmonary silicosis (Slavin et al order namenda 5mg with visa. Alternatively, circulating autoantibodies may deposit in the kidney, resulting in immune complex glomerulonephritis. There is little information on the duration of exposure and dose required for silica-related autoimmune effects, and it is not currently known whether peak or cumulative dose is more predictive of disease development. Silica exposure may often occur in the presence of other exposures that may interact mechanistically to modify the risk of developing autoimmune disease. For example, even trace contam ination of quartz dust with iron particles may augment inflammatory effects in the lung (Castranova et al. Smoking is another common exposure in many silica-exposed workers and has been shown to modify the association of high and moderate-level silica exposure for risk of systemic lupus erythematosus (Parks et al. Silica dust exposure may be associated with a wide range of autoimmune diseases and immune abnormalities. Although some studies have explicitly focused on only one disease, several indicate an increased occurrence of several different diseases within the same study population. In addition to exploring the possibility of shared mechanisms, risk analyses should consider the impact of silica dust exposure across multiple diseases. There is also a need to consider the potential for effect modification by genetic or sex differences in disease susceptibility, as well as the modifying effects of other environmental exposures. Polymorphisms in tumour necrosis factor and other cytokine genes may be related to severity of silicosis in humans (Corbett et al. As allelic variation in these genes has also been linked to other autoimmune diseases, it is plausible that differences in silica related autoimmunity might be modified by these factors as well. Given that women have higher rates of many autoimmune diseases compared with men, it will be important to learn if they are more or less vulnerable to the effects of silica. It would seem likely that these heavy metals have the same effects on humans, presumably by a similar mechanism. Autoimmune manifestations induced by heavy metals include lupus-type nephritis, autoimmune haemolytic anae mia, and skin diseases, such as pemphigus and scleroderma-like lesion. Some manifestations of immune-mediated nephritis and elevation of circulating autoantibodies have been noted in case studies of persons exposed to gold and cadmium as well as mercury (Ohsawa, 1993; Bigazzi, 1994, 1999). The lack of a clear correlation between mechanistic research on mercury toxicity and sublethal non-cytotoxic effects and lack of consideration of mercury induced immunotoxicity as an important health outcome have limited the application of science-based risk assessment on this issue (Silbergeld & Devine, 2000). Occupational exposure to mercury, in spite of immunological changes described even in workers with relatively low urinary mercury concentrations (Queiroz et al. The suggestion that mercury may cause autoimmune response and disease in humans is based mainly on several cases of nephrotic syndrome associated with mercury-containing drugs that were in use until the mid-20th century, in which renal histopathological lesions and the presence of autoantibodies bound to the renal membrane in kidney biopsies were reported. The use of mercury for the production of dental silver amalgam restorations and the subsequent release of mercury have been a matter of concern over the last 30 years (Clarkson et al. In a recent epidemio logical study of 20 000 people (84% males) with detailed exposure data, a consistent level of amalgam treatment across the cohort, and investigation of a wide range of possible health outcomes, an association was evidenced only with multiple sclerosis, and this association was relatively weak (adjusted hazard ratio of 1. Additional epidemiological studies are needed to fully address the question of autoimmune-related health effects of dental amalgams (Weiner et al. The organic alkylmercury compound thimerosal (sodium ethyl mercury thiosalicylate) is another modern facet of mercury. Mercury has two types of immunotoxic effects, both of which have been described in humans, primates, and rodents. First, in rodents, subtoxic doses of mercury may induce a characteristic systemic autoimmune syndrome associated with three major patho logical sequelae: lymphoproliferation, hypergammaglobulinaemia, and the development of autoimmunity. Autoimmunity is manifested as the formation of antinuclear antibodies and highly specific anti nucleolar autoantibodies, which are deposited within the kidney and eventually disrupt renal function, causing clinical disease (Bagen stose et al. The mechanism for mercury-induced autoimmunity probably involves the modification of the autoantigen fibrillarin by mercury followed by a T cell-dependent immune response driven by the modified fibrillarin (Arnett et al. Antinucleolar antibodies present a virtually identical specificity of response to that of autoantibodies found with high titres in sera of patients with systemic scleroderma, the human autoimmune disease most often associated with exposure to environmental agents (Takeuchi et al. The second type of mercury immunotoxic effects is immunosuppression, which occurs at relatively low doses of mercury and methylmercury that directly impair Th1 responses and augment Th2 responses (Lawrence & McCabe, 1995; Silbergeld & 132 Chemical/Physical Agents and Autoimmunity Devine, 2000; Bagenstose et al. Apoptosis has been sug gested as a possible mechanism for immunosuppression (Shenker et al. The induction and development of autoimmune responses in susceptible strains vary across species. Rats become resistant to mercury induced autoimmunity after a subsequent challenge, whereas mice do not show resistance to subsequent mercury exposures (see also chapter 10). The question remains whether Th1 cells participate in both the induction and the regulation of the disease (Bagenstose et al. Recent studies have raised the possibility that both genetic and environmental factors act synergically at several stages of autoim munity pathogenesis. These studies predict that individuals suscep tible to spontaneous autoimmunity should be more susceptible following xenobiotic exposure by virtue of the presence of pre disposing background genes (Cooper et al. In this regard, recent discussions regarding the autoimmune effect of mercury are not only, or even mainly, concerned with the risk of inducing de novo autoimmune conditions, but further the possibility that mercury might accelerate or aggravate spontaneously occurring systemic autoimmune conditions (Havarinasab et al. Rowley & Monestier (2005) reviewed mechanisms of the induction of autoimmunity by the heavy metal mercury in the rat and mouse. In contrast to the rat autoimmune model, in the mouse model for autoimmunity induced by mercury, the autoantibody response is specifically targeted towards nucleolar antigens and is associated with induction of antifibrillarin autoantibodies. Second, exposure to low doses of mercury can dramatically worsen the development of autoimmune responses in lupus mouse models. A third difference is the nature of the interaction of heavy metals such as mercury with thiol groups and the role of this affinity in the availability of certain thiol-containing molecules for immature cells. They examined data available that suggest that mercury can behave as an adjuvant and trigger autoimmunity responses. This supports the notion that mercury acts by promoting differentiation of autoreactive T cells towards pathological pathways through a bystander effect.

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In cardiac arrest proven 10 mg namenda, the clinician should specifically examine for the presence or absence of cardiac contractions discount namenda 10 mg visa. If contractions are seen cheap namenda 5 mg with mastercard, the clinician should look for the coordinated movements of the mitral and aortic valves buy 5mg namenda with visa. In this scenario, the absence of coordinated opening of mitral and aortic valves will require chest compres sions to maintain cardiac output. This aspect is predominantly a cause of the muscular hypertrophy that takes place in the myocar dium of the left ventricle after birth, with the closure of the ductus arteriosus. The left ventricle is under considerably more stress than the right ventricle, to meet the demands of the higher systemic pressure, and hypertrophy is a normal compensatory mechanism. On bedside echocardiography, the normal ratio of the left to right ventricle is 1:0. The subxiphoid view can be used, but care must be taken to fan through the entire right ventricle, as it is easy to underestimate the true right ventricular size in this view. Any condition that causes pressure to suddenly increase within the pulmonary vascular circuit will result in acute dilation of the right heart in an effort to maintain forward flow into the pulmonary artery. The classic cause of acute right heart strain is a large central pulmonary embolus. Due to the sudden obstruction of the pulmonary outflow tract by a large pulmonary embolus, the right ventricle will attempt to compen sate with acute dilation. This process can be seen on bedside echocardiography by a right ventricular chamber that is as large, or larger, than the left ventricle (Fig. Acute right heart strain thus differs from chronic right heart strain in that although both conditions cause dilation of the chamber, the ventricle will not have the time to hypertrophy if the time course is sudden. Previous published studies have looked at the sensitivity of the finding of right heart dilation in helping the clinician to diagnose a pulmonary embolus. The results show that the sensitivity is moderate, but the specificity and positive predictive value of this finding are high in the correct clinical scenario, especially if hypotension is present. The literature suggests that in general, patients with a pulmonary embolus should be immediately started on heparin. However, a hypotensive patient with a pulmonary embolus should be considered for thrombolysis. The aorta will often come quickly into view from this plane as a thicker walled and deeper structure. This respiratory variation can be further augmented by having the patient sniff or inspire forcefully. Using a high-frequency linear array transducer, the internal jugular veins can first be found in the short-axis plane, then evaluated more closely by moving the probe into a long-axis configuration. The location of the superior closing meniscus is determined by the point at which the walls of the vein touch each other. In traumatic conditions, the clinician must quickly determine whether hemoperitoneum or hemothorax is present, as a result of a hole in the tank, leading to hypovolemic shock. In nontrau matic conditions, accumulation of excess fluid into the abdominal and chest cavities often signifies tank overload, with resultant pleural effusions and ascites that may build-up with failure of the heart, kidneys, and/or liver. However, many patients with intrathoracic or intra-abdominal fluid collections are actually intravascularly volume depleted, confusing the clinical picture. In infectious states, pneumonia may be accom panied by a complicating parapneumonic pleural effusion, and ascites may lead to spontaneous bacterial peritonitis. Depending on the clinical scenario, small fluid collections within the peritoneal cavity may also represent intra-abdominal abscesses leading to a sepsis picture. The peritoneal cavity can be readily evaluated with bedside ultrasound for the pres ence of an abnormal fluid collection in both trauma and nontrauma states. This examination consists of an inspection of the potential spaces in the right and left upper abdominal quadrants and in the pelvis. Specific views include the space between the liver and kidney (hep atorenal space or Morison pouch), the area around the spleen (perisplenic space), and the area around and behind the bladder (rectovesicular/rectovaginal space or pouch of Douglas). A dark or anechoic area in any of these 3 potential spaces represents free intraperitoneal fluid (Fig. These 3 areas represent the most common places for free fluid to collect, and correspond to the most dependent areas of the peritoneal cavity in the supine patient. Trendelenburg positioning will cause fluid to shift to the upper abdominal regions, whereas an upright position will cause shift of fluid into the pelvis. In both the hepatorenal and perisplenic views, the diaphragms appear as bright or hyperechoic lines immediately above, or cephalad to, the liver and spleen respectively. Aiming the probe above the diaphragm will allow for identifi cation of a thoracic fluid collection. If fluid is found, movement of the probe 1 or 2 inter costal spaces cephalad provides a better view of the thoracic cavity, allowing quantification of the fluid present. In the normal supradiaphragmatic view, there are no dark areas of fluid in the thoracic cavity, and the lung can often be visualized as a moving structure. In the presence of an effusion or hemothorax, the normally visu alized lung above the diaphragm is replaced with a dark, or anechoic, space. Pleural effusions often exert compression on the lung, causing hepatization, or an appearance of the lung in the effusion similar to a solid organ, like the liver. The literature supports the use of bedside ultrasound for the detection of pleural effusion and hemothorax. Several studies have found Emergency Department ultrasound to have a sensitivity in excess of 92% and a specificity approaching 100% in the detection of hemothorax. Free fluid in the peritoneal or thoracic cavities in a hypotensive patient in whom a history of trauma is present or suspected should initially be presumed to be blood, leading to a diagnosis of hemorrhagic shock.

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Diagnose cor triatriatum using available laboratory tests and recognize important anatomic features that could affect surgical management 7 buy namenda 5 mg without a prescription. Recognize the anatomic features of pulmonary venous stenosis/atresia and associated lesions 3 purchase namenda 10mg free shipping. Recognize the implications of increasing pulmonary blood flow in a patient with occult pulmonary venous obstruction b buy namenda 10 mg line. Recognize and interpret hemodynamic and angiographic findings in a patient with pulmonary venous stenosis/atresia using available laboratory tests and recognize important anatomic features that could affect surgical management 7 10 mg namenda otc. Plan the medical and transcatheter or surgical management for a patient with pulmonary venous stenosis/atresia b. Understand complications that may occur with therapy of pulmonary venous stenosis/atresia E. Understand the etiology, epidemiology, and embryology of situs abnormalities and relationships between cardiac and visceral situs 2. Know anatomic features and variations in atrial situs and commonly associated lesions b. Recognize the anatomic features of superior-inferior ventricles and criss-cross hearts 3. Understand physiologic consequences of lesions associated with asplenia/polysplenia syndromes 4. Recognize features of abnormal atrial and visceral situs using available diagnostic tests and recognize important anatomic features that could affect surgical management b. Know the prognosis and natural history of patients with the major forms of situs abnormalities 5. Recognize the clinical findings of various cardiac lesions associated with situs abnormalities and associated cardiac and extracardiac abnormalities 6. Know what supplemental testing might be necessary in patients with situs abnormalities and how to interpret 7. Be able to advise immunization and antibiotic prophylaxis in a patient with situs abnormalities F. Recognize anatomic types and associated cardiac and noncardiac anatomic features of ectopia cordis 2. Recognize features associated with ectopia cordis using available laboratory tests and recognize important anatomic features that could affect surgical management 3. Cardiomyopathies (including systolic dysfunction, diastolic dysfunction, and hypertrophic) 1. Understand the role of protein and genetic defects in familial hypertrophic cardiomyopathy b. Identify the types of mutations and inheritance pattern associated with hypertrophic cardiomyopathy 2. Know gross and histologic features of the specific types of cardiomyopathies (dilated, restrictive, hypertrophic, arrhythmic right ventricular) b. Know gross and histologic features and natural history of secondary cardiomyopathies c. Know the morphologic changes associated with myocardial dilatation and hypertrophy d. Know the effects of myocardial dilatation and hypertrophy on ventricular wall tension and stress b. Know the pathophysiology of congestive heart failure, including causes and functional consequences of abnormal loading conditions and altered contractility c. Know the causes of alterations in heart rate causing congestive cardiac failure d. Understand the physiology of dilated cardiomyopathy, including the effects on systemic and pulmonary vasculature and pulmonary function f. Understand the effect of restrictive cardiomyopathy on systemic or pulmonary vasculature, including the effects on the liver, kidneys, and lungs g. Understand the effect of hypertrophic cardiomyopathy on systemic or pulmonary vasculature, including the effects on the liver, kidneys, and lungs h. Know the effects of end organ congestive heart failure on systemic systems (growth, development, skin, skeletal muscle, gastrointestinal, renal, hepatic, etc) c. Know the principles of medical therapy for congestive heart failure, including the use of digitalis, other inotropic drugs, vasodilators, diuretics, and other therapeutic options d. Know the pathology of cardiac viral infection as it relates to myocarditis and cardiomyopathy f. Know the major nutritional causes of cardiomyopathy, including hypocalcemia, hypercalcemia, hypocupremia, iron deficiency, and selenium deficiency h. Understand the physiologic and anatomic significance of abnormal clinical and physical findings in a patient in whom dilated, hypertrophic, or restrictive cardiomyopathy is suspected and describe the details of a general examination for this patient j. Know the details of the general and cardiac examination of dilated, hypertrophic, and restrictive cardiomyopathy and understand the physiologic and anatomic significance of abnormal physical findings k. Know the role of noninvasive imaging in dilated, hypertrophic, and restrictive cardiomyopathy c. Know the cardiac catheterization features of dilated, hypertrophic, and restrictive cardiomyopathy, and relate them to physiologic and/or anatomic features of the condition. Understand the significance of ambulatory and exercise monitoring results in dilated, hypertrophic, and restrictive cardiomyopathy f. Relate abnormal electrocardiographic features to physiologic and/or anatomic details of dilated, hypertrophic, or restrictive hypertrophic cardiomyopathy g. Know the role of natriuretic peptide in congestive heart failure, including the utility of monitoring serum B-type natriuretic peptide 6.

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This increases renal vasoconstriction via both the renin?angiotensin?aldosterone pathway and sympathetic nervous system activation generic namenda 5 mg line. The diagnosis is based on the absence of primary kidney disease discount namenda 10 mg free shipping, proteinuria purchase namenda 5 mg with amex, or systemic hypovolemia causing renal hypoperfusion purchase namenda 5mg otc. There is normal urinary sediment, low urinary sodium (<10 mEq/L), uremia, and oligu ria. Despite low platelet counts, platelet adhesion and aggregation might be normal, because of increased endothelial production of von Willebrand factor. Thrombin then triggers the formation of a strong clot made of fibrinogen and platelets that can withstand fibri nolysis. Thromboelastography/thromboelastometry can determine the quality of clot forma tion (generation of thrombin), clot strength (the effect of fibrinogen and platelets), and fibrinolysis. Other common causes include portal hypertension and varices, endothelial dysfunction, renal failure, and disseminated intravascular coagulation. Basic intraoperative monitoring includes central venous and intraarterial pressure monitoring. Echocardiography is a powerful tool to assess major hemodynamic changes and guide inotropic therapy. It also can detect major complications early such as intracardiac thromboembolism or air embolism. Anesthesia for Liver Transplantation 503 response laboratory service with rapid turnaround times and blood bank services are essential. The operation is divided into 3 phases: preanhepatic, anhepatic, and the neohepatic phases. Compression or occlu sion of major blood vessels can cause further hemodynamic compromise. This phase ends in the clamping of the inferior vena cava, portal vein and hepatic artery, and removal of the liver. The presence of portal varices and other new vessels in patients with longstanding cirrhosis can ameliorate this effect. Care must be taken not to overcompensate with significant volume expansion, because this volume will return to the circulation upon unclamping. The resulting hypervolemia can lead to venous congestion and poor function of the new liver. With partial return of blood from the inferior vena cava to the heart, hemo dynamics are usually more stable than with a full clamp. Venovenous bypass: Venous blood from the inferior vena cava and femoral vein is returned into the internal jugular vein using extracorporeal venovenous cannulas and a centrifugal pump. As the vena cava is unclamped, adequate return of venous blood volume to the heart is restored. The portal vein is then opened, causing the cold, acidotic, hyperkalemic blood from below the clamp and from the liver graft itself to circulate directly into the right heart. This can cause a significant decrease in blood pressure, bradycardia, other arrhythmias, and occa sionally cardiac arrest. Severe hypotension upon unclamping is called reperfusion syndrome and can be ameliorated by administration of calcium chloride, bicarbonate, epinephrine, and vasopressin. Warm ischemia is very damaging to the graft, and thus limiting warm ischemia time is critical to graft function. The neohepatic phase consists of the hepatic artery and bile duct anastomoses, often with a concomitant cholecystectomy. During this time, the anesthesiologist is looking for signs that the new liver is beginning to function?improvement in acidosis and clearing of lactic acid, and improved hemostasis and production of bile. Hemosta sis requires excellent surgical skills, temperature control and the early diagnosis and treatment of fibrinolysis. Failure to do so leads to breakdown of existing clots and the development of diffuse bleeding. Maintenance of a low central venous pressure may reduce venous bleeding during hepatectomy. Treatment of abnormal laboratory values such as low platelet counts, low fibrin ogen, and high prothrombin times is only required if there is clinical bleeding. These laboratory values frequently normalize as the new graft functions and platelets return to the circulation from the spleen. In case of bleeding, patients are treated with factor replacement, blood, and platelets. Approaches to resuscitation and treatment of high blood loss differ by institution. Renal dysfunction, with poor urine output and rising creatinine, may occur during transplantation, especially after a full caval clamp, long anhepatic time, or prolonged hypotension. Patients with volume overload, hyperkalemia, or hyponatremia may benefit from continuous venovenous hemodialysis that can be instituted in the oper ating room or upon arrival to the intensive care unit. They must meet usual standard Anesthesia for Liver Transplantation 505 extubation criteria. In some institutions, extubated patients with good liver function can bypass the intensive care unit and are sent to the postoperative recovery unit and then to a regular surgical floor or step-down unit. Occasionally, the abdominal distension owing to an especially large organ or tissue swelling might prevent primary closure of the surgical wound.

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