The postulated benefits of this treatment include decreasing the extent and duration of hypermetabolism and immunosuppression symptoms 2dpo generic 400 mg asacol with amex, shortening the length of the hospital stay medicine effexor order 400 mg asacol with amex, and improving survival symptoms 10 dpo order asacol 400 mg visa. Administration of propranolol has been effective in decreasing metabolic rate and cardiac work in burned children and adults; however medications names cheap asacol 400 mg on line, increased nitrogen loss was induced presumably from peripheral -receptor blockade medicine omeprazole asacol 800 mg without a prescription. Cardioselective -adrenergic blockers are currently being studied that may circumvent the nitrogen-wasting effects of nonselective agents symptoms 28 weeks pregnant cheap asacol 400mg amex. The selective 2-adrenergic agonist clenbuterol increased resting energy expenditure and normalized muscle protein content, muscle mass, and body weight gain in burned rats. Similar responses in burn patients were demonstrated with the administration of low-dose exogenous insulin and glucose. Oxandrolone, a weakly androgenic testosterone analogue, has been shown recently to decrease net daily nitrogen loss and weight loss in seriously burned patients. Complications were similar between groups, and no side effects directly attributed to the drug were identified. Herndon and colleagues evaluated the effect of -adrenergic blockade using orally administered propranolol on resting energy expenditure and muscle-protein catabolism in severely burned children. After 2 weeks of treatment, a dose sufficient to decrease the resting heart rate by 20% resulted in a 24% decrease in resting energy expenditure in the propranolol group compared with a 5% increase in a matched control group. The net muscle-protein balance increased by 82% over baseline values in the propranolol group, whereas it decreased by 27% in the control group. Further studies are required to determine if the apparent benefits of blockade of the hypermetabolic response result in decreased morbidity and mortality for the severely burned patient or whether they merely reflect short-term changes in protein metabolism. Tanaka H et al: Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration. Strong alkalis and acids found in common household cleaners are responsible for the majority of minor chemical injuries. More extensive injuries often result from industrial and laboratory accidents or from assaults. The amount of tissue damage incurred also depends on the nature of the specific agent. Strong alkalis react with tissues to produce saponification and liquefaction necrosis. Acids are water-soluble and penetrate easily into subcutaneous tissue and cause coagulation necrosis soon after contact. The exothermic reaction produced by contact with strong acids or bases also contributes to the depth of injury. Organic solvents and petroleum products, which are highly lipid-soluble, injure tissues by delipidation. Cutaneous absorption of certain chemical agents may cause systemic toxicity, which complicates subsequent therapy and makes identification of the causative agent imperative. Fluoride ion continues to penetrate the tissues until inactivated by calcium salt formation. Topical treatment with a calcium gluconate gel should be instituted, and if the pain does not subside, local injection of 10% calcium gluconate into the damaged tissue may provide prompt pain relief. Intraarterial infusion of calcium gluconate also has been used to limit tissue damage and relieve pain, but surgical excision of the damaged tissue may be necessary for complete pain control. Initial treatment consists of copious water lavage; however, owing to the poor water solubility of phenol, a lipophilic solvent such as polyethylene glycol (50% solution in water) may be more effective at removing the residual agent. Initial Care of Chemical Burns Chemical injuries, unlike other thermal injuries, require immediate care of the burn wound. All clothing, including shoes and gloves, must be removed and the wounds copiously irrigated with water. In the case of alkali burns, this treatment should continue for a minimum of 1 hour. If ocular injury is suspected, prompt and prolonged irrigation with saline or water should begin. A search for specific antidotes is unnecessary and may only delay the initiation of adequate water lavage. Assessing the depth of injury in chemical burns is difficult because many agents may produce a tanned or bronzed appearance of the skin, which remains pliable to the touch but may represent extensive full-thickness tissue necrosis. With the exception of the initial attention given to the burn wound, the resuscitation and later treatment of skin injury follow that of thermal burns. Hydrocarbons Cutaneous injury from immersion in gasoline and other hydrocarbons is often overlooked in victims of motor vehicle accidents who sustain prolonged exposure during extrication. Partial- and full-thickness injuries have been described, and systemic toxicity, similar to that produced by ingestion or inhalation, may occur. The pulmonary excretion of hydrocarbons may produce chemical pneumonitis and bronchitis. Systemic lead poisoning from cutaneous absorption of leaded gasoline also has been described. Inhalation of Aerosolized Chemicals Inhalation of aerosolized chemicals may produce pulmonary injury and systemic toxicity, thus requiring accurate diagnosis and aggressive treatment. Varying degrees of pulmonary insufficiency may be agent-specific and manifested by severe airway edema formation, mucosal sloughing, and bronchospasm. Systemic toxicity through pulmonary absorption may occur; thus the causative agents must be clearly identified to ensure appropriate diagnostic and treatment strategies. The degree of pulmonary support required is determined by the severity of pulmonary insufficiency. Specific Chemical Agents & Systemic Toxicities In general, the use of antidotes for specific chemicals is condemned, and copious water lavage is considered the appropriate form of initial therapy. However, several specific chemical agents exist for which treatment with a specific antidote has proved beneficial. Injury owing to hydrofluoric acid exposure is an occupational hazard of petroleum refinery workers, etchers, and those employed in the cleaning of air-conditioning equipment. Following contact with this agent, there is usually a pain-free interval followed by Ocular Injury If chemical eye injury is suspected, prompt and prolonged irrigation of the eye with water or saline should ensue. This "iceberg" effect may require the performance of fasciotomy-rather than escharotomy-to ensure adequate perfusion of the distal extremity and to evaluate the viability of the underlying subcutaneous tissue and muscle. With extensive muscle necrosis, hemochromogens may be liberated, resulting in the appearance of those pigments in the urine. Intravenous fluids are administered to achieve a urine output of 100 mL/h in adults. If the hemochromogenuria does not clear with an adequate urine output, 50 meq sodium bicarbonate should be added to each liter of intravenous fluid to promote alkalinization of the urine and prevent pigment precipitation in the renal tubules. If after aggressive fluid resuscitation the renal output does not reach 100 mL/h, an osmotic diuretic such as mannitol also may be administered (a bolus dose of 25 g with 12. When urine production is increased by the use of diuretics, invasive hemodynamic monitoring with a pulmonary artery catheter should be considered because urine output is no longer a reliable measure of intravascular volume and organ perfusion. Ophthalmology consultation should be obtained on all suspected chemical eye injuries. The severity of the injury depends on the voltage, the type of current (alternating or direct), the path of the current through the body, and the duration of contact. High- and low-voltage injuries are arbitrarily defined as those above and below 1000 V. Tissue damage from electrical injury may be obvious at the cutaneous contact site or sites but also may involve underlying tissues and organs along the path of the current. The amount of heat generated is proportionate to tissue resistance; however, the differences in tissue resistance (eg, bone, fat, nerve, etc. Current density then predominates as the main determinant of tissue damage, with severity of injury being inversely proportional to the cross-sectional area traversed by current. Thus severe injuries to the extremities are often encountered, and significant injuries to the torso are rare. Superficial tissues in a limb may be normal, whereas tissues near bone may be nonviable owing to longer duration of heating because of the slower heat dissipation from bone. Alternating current injuries may initiate ventricular fibrillation, whereas high-voltage injury and lightning injury are associated with asystolic cardiopulmonary arrest. Complications Associated injuries are more common in patients sustaining electrical injury than those injured by thermal burns. Owing to the titanic contractions of the paraspinal musculature induced by the electric current, compression fractures of the lumbar and thoracic spine may occur. Blunt traumatic injuries should be suspected and appropriate diagnostic measures initiated. A complete neurologic examination must be performed on admission and at scheduled intervals in all patients sustaining electrical injury. Immediate peripheral deficits owing to the damaging effects of electric current may be irreversible; however, early deficits in a distribution where there is no clear tissue damage are likely to resolve. Neurologic symptoms of delayed onset, often mimicking upper motor neuron disease, tend to be progressive and permanent. Progressive thrombosis of nutrient vessels of the spinal cord or nerve trunks may play a role in the pathogenesis of the late-occurring upper motor neuron deficits. Direct electrical injury to the viscera is rare; however, liver necrosis, intestinal perforation, focal pancreatic necrosis, and gallbladder necrosis have been reported in patients with high-voltage electric injury and truncal contact points. An increased occurrence of cholelithiasis has been reported in convalescent patients following electric injury. Delayed hemorrhage from moderate-sized to large blood vessels has been described following electrical injury and attributed by some to an "arteritis" produced by the electric current. The actual mechanism of this complication is unclear, but inadequate initial wound debridement and subsequent Treatment Cardiac arrest often occurs following an electrical contact and requires immediate cardiopulmonary resuscitation. In patients not sustaining an initial cardiac arrest, cardiac dysrhythmias occur in a small percentage of patients. All patients should have continuous electrocardiographic monitoring for at least 24 hours, and functionally significant dysrhythmias should be treated promptly if they occur. In patients in whom the electrical contact point involved the head or neck, the development of cataracts up to 3 years or more following injury has been described. Ophthalmologic slit-lamp examination should document the presence or absence of cataracts during the initial hospitalization. In 2002, the American Association of Poison Control Centers documented 2,112,774 episodes of toxin exposure resulting in poison center notification. This number actually underrepresents the true number of poisonings because 70% are never reported to poison control centers. Treating these patients requires a working understanding of the principles of stabilization and supportive care, decontamination, drug elimination, use of antidotes, and the pathophysiologic features specific to the poisons or toxins involved. This chapter will cover the general principles involved in caring for these patients and will discuss the details of treating the specific poisons typically encountered in the practice of critical care. It is important to remember, however, that the history may be unreliable in patients who intentionally ingest toxins. Careful physical examination is key, and laboratory evaluation and close observation are frequently required. Symptoms and Signs the physical examination can provide a wealth of information, even in patients unable to provide a useful history. An abbreviated physical examination, which could be called the toxidrome-oriented physical examination, focuses on the physical findings observed in patients exposed to particular types of poisons and offers rapid assessment and guides testing and treatment. However, there are several general guidelines for the evaluation and treatment of a patient with a potential ingestion or toxic exposure. Laboratory Studies A rapid bedside serum glucose concentration should be checked in all patients with altered mental status, and if it is found to be low, intravenous glucose should be administered. Other tests (eg, drug levels, methemoglobin level, and carboxyhemoglobin level) may be helpful in specific patients and will be discussed later in this chapter. As a general rule, toxicology screens are of limited value in evaluation of these patients and are expensive and Diagnosis of Poisoning History Obtaining a history from a patient with a potential ingestion or toxic exposure may be difficult if the patient is too young to communicate, is obtunded, or is reluctant to cooperate. Vital signs Temperature Blood pressure Respiratory rate Heart rate Brief neurologic examination Level of consciousness Pupillary examination Motor responses Skin examination: moisture, rash, cyanosis Lung examination Auscultation for bowel sounds time-consuming. A toxicology screen also may be helpful in patients with mixed-drug ingestions or those who present with signs of major toxicity. Finally, a sample of blood may be saved for future toxicology evaluation in patients in whom the diagnosis is unclear. Salicylate, acetaminophen, barbiturates, digoxin, ethanol, iron, lithium, and theophylline serum levels are available in most hospital laboratories on an urgent basis. This drug is found in many prescription and over-the-counter medications, and patients may ingest potentially lethal amounts but show minimal or nonspecific signs of toxicity. Head trauma or hypoxemia also may cause findings similar to those observed following toxin exposure. The heart rate, evidence of dysrhythmias, vector axes, and interval measurements are helpful in determining the presence or severity of several ingestions, and serial electrocardiographic evaluation can, in some cases, help to follow the progression of toxicity. This may require establishing an airway, ventilating and oxygenating the patient, and supporting circulation by normalizing and maintaining an adequate heart rate and blood pressure. These measures should be taken regardless of the toxin involved; more specific interventions can be made after stabilization is completed.
Digoxin should be a preferred agent in patients whose heart failure is associated with atrial arrhythmias 9 medications that can cause heartburn generic 400mg asacol otc. Although direct-acting vasodilators can produce favorable short-term hemodynamic effects in patients with heart failure treatment broken toe discount asacol 400 mg with amex, their long-term use has not improved symptoms and has increased the risk of heart failure and death in controlled clinical trials treatment zoster buy cheap asacol 400mg on-line. Of the agents evaluated symptoms jet lag discount asacol 400 mg with visa, only a combination of isosorbide dinitrate and hydralazine has produced some encouraging results medicine bow generic 400 mg asacol with amex. The combination of these two direct-acting vasodilators has been reported to reduce the risk of death in patients with heart failure receiving digitalis and diuretics medicine x topol 2015 generic asacol 400 mg fast delivery. However, this vasodilator combination has no effect on the frequency of hospitalizations, and many patients fail to tolerate long-term treatment with these drugs. There is little evidence to support the use of nitrates alone or hydralazine alone in the management of chronic heart failure. Drugs Used for the Treatment of Coexistent Cardiac Disorders Many patients with heart failure have coexistent cardiac disorders that require active management. Revascularization should be strongly considered in patients with heart failure who have angina, because it may reduce the risk of major cardiac events. Nitrates and beta-blockers and amlodipine may be used if revascularization cannot be performed or is unsuccessful. Atrial arrhythmias are common in patients with heart failure; and if accompanied by a rapid ventricular response, they can exacerbate the severity of symptoms and possibly accelerate progression of the underlying disease. Although the prevention of atrial arrhythmias would be highly desirable, this goal cannot be effectively or safely achieved with most antiarrhythmic drugs. The agent most likely to suppress atrial arrhythmias in patients with heart failure is amiodarone, but the substantial toxicity of the drug has justifiably discouraged its widespread use. As a result, many physicians do not attempt to restore sinus rhythm in patients with an established atrial arrhythmia but instead focus on controlling the rate of the ventricular response with digitalis and beta-blockers and reducing the risk of embolic events with anticoagulants. If a slow ventricular response cannot be achieved in this manner, amiodarone or radiofrequency ablative procedures (see Chapter 51) should be considered. Most patients with heart failure have frequent and complex ventricular arrhythmias; but when asymptomatic, these do not presage or contribute to the occurrence of sudden death and thus do not require therapy. The appearance of ventricular arrhythmias in these patients is likely to reflect the severity of the underlying cardiac disease and thus may respond to interventions that reduce the risk of disease progression. In addition, every effort should be made to correct electrolyte imbalances if these are found. In patients who have an immediate life-threatening ventricular arrhythmia (sustained ventricular tachycardia or ventricular fibrillation) or who have been resuscitated from sudden death, use of an implantable cardioverter-defibrillator may reduce the risk of a lethal recurrence (see Chapter 52). Because of stasis of blood in dilated hypokinetic cardiac chambers, patients with a dilated cardiomyopathy are at increased risk of cardiac thrombi and embolic events. Yet, it is unclear whether all patients with a depressed ejection fraction should receive treatment with anticoagulant drugs, even if they are known to harbor a cardiac thrombus. Most cardiac thrombi detected by echocardiography do not embolize, and most embolic events are related to thrombi that were not visualized. Anticoagulation is recommended primarily for patients with a previous embolic event or atrial fibrillation. Drugs To Be Avoided in Patients with Heart Failure Patients with heart failure can improve dramatically after the withdrawal of drugs that are known to affect cardiac function adversely or that interact unfavorably with drugs of established benefit. Prostaglandins play an important role in circulatory homeostasis and in the action of many drugs used to treat heart failure. These substances are endogenous vasodilators that act to unload the heart when peripheral vessels are constricted and can support glomerular filtration when renal perfusion is compromised. As a result, most patients with heart failure should not receive non-steroidal anti-inflammatory agents. Whether the recommendation to avoid inhibitors of prostaglandin synthesis applies to aspirin remains controversial. Aspirin is widely prescribed to patients with heart failure, either to reduce the risk of recurrent myocardial ischemic events in patients with coronary artery disease or to decrease the frequency of systemic embolic events in patients with normal coronary arteries. Although calcium channel blockers are peripheral vasodilators, these agents have not improved the symptoms of heart failure or enhanced exercise tolerance. Instead, the short- and long-term administration of these drugs has caused serious adverse cardiovascular reactions, including profound hypotension, worsening heart failure, pulmonary edema, and cardiogenic shock. These deleterious responses have been observed with short- or long-acting formulations of the same drug. As a result, clinicians should not use calcium channel blockers for the treatment of heart failure, and most calcium channel blockers should be avoided for the treatment of angina, atrial fibrillation, or hypertension in patients with heart failure. Of the available agents, only amlodipine has strong evidence supporting its safety in patients with advanced disease. Antiarrhythmic agents can suppress ventricular arrhythmias in patients with heart failure, but these agents have not been shown to reduce the risk of sudden death. Instead, the short- and long-term administration of these drugs has caused serious adverse cardiovascular reactions, including worsening heart failure, life-threatening proarrhythmia, and death. As a result, antiarrhythmic therapy should not be used to treat patients with heart failure who have asymptomatic ventricular arrhythmias, regardless of their frequency or complexity. Antiarrhythmic drugs may be useful for patients with rapid atrial fibrillation or for those with hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation. Such toxicity has been reported with all types of agents of this class (except for digitalis), whether these have been prescribed orally or intravenously or administered continuously or intermittently. Because of the lack of data demonstrating efficacy and important concerns about toxicity, the use of intermittent intravenous positive inotropic therapy cannot be recommended as a long-term treatment strategy, even in patients with end-stage heart failure. The major syndromes requiring hospitalization include (1) fluid overload resistant to orally administered diuretics. Each syndrome represents an exaggerated expression of each of the pathophysiologic mechanisms that play a role in the evolution of heart failure; that is, refractory edema reflects excessive sodium and water retention; acute pulmonary edema is the result of extreme vasoconstriction; and refractory symptoms associated with systemic hypoperfusion are the ultimate consequence of contractile failure. These syndromes share a common therapeutic approach: that is, because of their immediate life-threatening nature, physicians must rely on short-term hemodynamic interventions to achieve clinical stability as rapidly as possible. If the syndromes are the result of changes in diet or medications or the advent of a treatable complicating illness. However, if these syndromes represent the end-stage of a terminal disease that is refractory to medical therapy, hemodynamic support must be continued until a definitive mechanical solution can be devised. In either case, neurohormonal activation is not a therapeutic target in patients who are hospitalized for the treatment of decompensated heart failure. Indeed, by supporting cardiac contractility and systemic blood pressure, the activation of the sympathetic nervous system and renin-angiotensin system may help to maintain circulatory homeostasis in acutely ill patients. Fluid Overload Refractory to Oral Diuretics (Refractory Peripheral Edema) Patients with heart failure are frequently hospitalized for the treatment of edema that persists despite the use of diuretics. These patients typically present with a marked increase in body weight, associated with pleural effusions, ascites, and massive peripheral edema. The degree of fluid retention can become so severe that the edema itself becomes incapacitating and may require mechanical removal of fluid for relief of symptoms. However, in some patients, the occurrence of refractory edema is indicative of advancing right and left ventricular failure. By causing mesenteric congestion, right ventricular failure can impair the rate of absorption of diuretics; by causing renal hypoperfusion, left ventricular failure can impede the delivery of diuretics to active sites in the renal tubules. As a result, as heart failure advances, patients become increasingly resistant to the effects of diuretic drugs and require larger and larger doses to achieve a therapeutic response. Management of Refractory Peripheral Edema Several strategies should be considered in the management of patients with refractory edema. Non-steroidal anti-inflammatory drugs, which can decrease the efficacy and increase the risk of diuretics, should be withdrawn. If the patient fails to respond to the intravenous administration of large doses of furosemide, the physician may add a second diuretic with a different renal tubular site of action. A combination of two diuretics can produce a dramatic increase in urine output, but such a regimen is commonly accompanied by striking (and occasionally life-threatening) degrees of hypokalemia. If a combination of intravenous furosemide and oral metolazone proves ineffective, these diuretics should be co-administered with drugs that increase renal blood flow. Finally, if the edema becomes refractory to all pharmacologic interventions, hemofiltration or peritoneal dialysis may be useful in restoring fluid balance in selected patients. Regardless of the severity of fluid retention, every effort should be made to achieve dry weight, even if achievement of this goal requires a prolonged hospitalization. Patients discharged prematurely with residual edema due to an inadequate diuresis are commonly readmitted to the hospital for refractory edema within several weeks. In contrast, patients who achieve dry weight frequently become responsive to conventional treatments for heart failure and have a lower risk of recurrent hospitalization. Pulmonary Congestion (Acute Pulmonary Edema) One of the most common clinical presentations of advanced left ventricular failure is the syndrome of pulmonary congestion. These patients complain of dyspnea at rest and have pulmonary rales on physical examination. Pulmonary congestion may be the first evidence of heart failure in patients without a history of cardiac disease; it may appear in patients who are already hospitalized for an acute cardiac disorder. If severe, abrupt, and accompanied by clinical evidence of sympathetic overactivity (tachycardia, diaphoresis and vasoconstriction), the syndrome is designated as acute pulmonary edema. Acute pulmonary edema may also be triggered by non-cardiac disorders, including direct injury to the alveolar-capillary membrane, high-altitude stress, catastrophes of the central nervous system, narcotic overdose, or pulmonary embolism. Regardless of its cause, pulmonary edema reflects the transudation of fluid into the alveolar space and arises from an imbalance in the factors that regulate the transport of fluid from the pulmonary microcirculation to the interstitial space of the lung. When the cause of the syndrome is cardiac, pulmonary edema results from the rapid onset of intense peripheral vasoconstriction that leads to a marked increase in pulmonary venous pressures. The profound constriction of systemic arteries and veins causes a sudden and dramatic redistribution of blood from peripheral reservoirs to the pulmonary circuit, causing the pulmonary capillary hydrostatic pressure in the lung to exceed the capillary colloid osmotic pressure. However, the transudation of fluid into the alveoli cannot occur if pulmonary blood flow is impaired; thus, patients with an elevated pulmonary vascular resistance or depressed right ventricular function rarely develop acute pulmonary edema. Management of Pulmonary Edema Several general measures are advisable for most patients with pulmonary congestion. Every effort should be made to identify an underlying precipitating factor, because its correction is often critical to the success of treatment. Patients usually feel most comfortable resting in bed in the upright position with the legs dependent. Special attention should be devoted to maintaining adequate oxygenation, which can be achieved by increasing the concentration of 225 inspired oxygen or (if necessary) by endotracheal intubation and mechanical ventilation. Given the importance of peripheral vasoconstriction in the pathogenesis of pulmonary edema, pharmacologic dilation of peripheral vessels represents the critical element in any successful approach to management. This goal can be achieved with the use of (1) morphine; (2) loop diuretic drugs. Because of the need for rapid and reliable treatment, these interventions are generally administered intravenously. Morphine remains the most effective single agent for the treatment of acute cardiogenic pulmonary edema. The drug acts specifically to antagonize the peripheral vasoconstrictor effects of the sympathetic nervous system; the resultant vasodilatation leads to an immediate and dramatic decline in pulmonary arterial and venous pressures, leading directly to symptomatic improvement. The magnitude of venodilation produced by the drug in the limbs is insufficient to explain its effects on pulmonary flow and pressures; instead, morphine appears to act primarily to increase the pooling of blood in the splanchnic circulation. In addition, morphine blunts the chemoreceptor-mediated ventilatory reflexes that trigger the severe tachypnea that accompanies pulmonary edema; by doing so, the drug reduces the work of breathing and thereby oxygen demand. Morphine is administered in intermittent doses of 2 to 4 mg intravenously (up to 10-15 mg), until dyspnea is relieved and diaphoresis subsides. The former reflects the acute decline in pulmonary blood flow and pulmonary venous pressures; the latter indicates a decline in the activity of the sympathetic nervous system. Patients should be monitored for respiratory depression, which can be reversed by narcotic antagonists. All diuretics increase urine output in patients with pulmonary edema, but loop diuretics can produce dramatic clinical benefits even before a diuresis has materialized. These immediate benefits are related to the peripheral arterial and venous dilatation produced by these drugs, which results from their ability to enhance the release of prostaglandins from the kidney. Although loop diuretics act quickly to increase sodium excretion, the rapidity of diuresis does not determine the clinical response to treatment, because vasodilation (not diuresis) is the principal mechanism of symptom relief. Indeed, an increase in urine output is generally not seen until peripheral signs of vasoconstriction have resolved. Furosemide is the loop diuretic most commonly used in the treatment of pulmonary edema. The dose of the drug is determined by the prior exposure of the patient to diuretic therapy. In patients who have not received loop diuretics, treatment is usually begun with low doses (40-80 mg intravenously), whereas patients who have received long-term therapy may require large doses of the drug (120-200 mg intravenously). In such patients, pulmonary congestion may be primarily related to diastolic dysfunction. By stimulating guanylate cyclase within the vascular smooth muscle cell, both nitroprusside and nitroglycerin exert dilating effects on arterial resistance and venous capacitance vessels and thereby lower pulmonary blood flow and pulmonary venous pressures. Therapy with both nitroprusside and nitroglycerin is usually initiated as a continuous low-dose intravenous infusion, the rate of which is increased to achieve specific hemodynamic or clinical goals. Nitroglycerin (1-50 mug/kg/min) is considered the agent of choice in patients with underlying ischemic heart disease; nitroprusside (0. Hypotension is the most common side effect of both nitroprusside and nitroglycerin; thus, infusions of the drugs require close continuous monitoring of vital signs. Symptomatic hypotension is frequently associated with bradycardia (not tachycardia), particularly when nitroglycerin is used. Both drugs can cause pulmonary vasodilatation, which can aggravate arterial hypoxemia in patients with ventilation-perfusion abnormalities. If dyspnea, diaphoresis, and peripheral vasoconstriction persist or if the syndrome becomes immediately life threatening, mechanical ventilation can improve oxygenation and reduce the redistribution of blood into the pulmonary circuit. If this fails to stabilize the course of the patient, the removal of 250 to 500 mL of blood by phlebotomy can produce a rapid reduction in pulmonary blood volume and dramatic clinical improvement. Refractory Symptoms Associated With Systemic Hypoperfusion the most serious presentation of heart failure in the hospitalized patient is the syndrome of refractory heart failure, which is characterized by hemodynamic instability and systemic hypotension. Patients complain of dyspnea and fatigue at rest and have objective evidence of poor peripheral perfusion, as reflected by low systemic blood pressure, diminished mental alertness, cool extremities, and decreased urine output.
Potassium shifts from extracellular to intracellular fluids also may be enhanced by using aerosolized specific beta2 agonists; albuterol is a commonly used agent of this kind medicine ball abs asacol 400mg on line. Agents such as albuterol are most helpful in managing mild hyperkalemia in chronic disorders such as chronic renal failure and hyperkalemic periodic paralysis treatment varicose veins generic asacol 800 mg without a prescription. This approach should be undertaken with constant electrocardiographic monitoring and should be used with extreme caution in patients who have received digitalis symptoms of mono buy 400 mg asacol amex. In the latter circumstance medications not to be taken with grapefruit purchase asacol 400 mg fast delivery, calcium administration may unmask digitalis intoxication art of medicine purchase 800 mg asacol free shipping, especially if other agents are used simultaneously to reduce the serum potassium level treatment writing purchase asacol 800mg on line. Calcium salts should not be added to bottles of intravenous fluids containing bicarbonate, because water-insoluble calcium salts will form. The influence of calcium salts in minimizing the cardiotoxic effects of hyperkalemia may be understood by noting that depolarization of excitable tissues by elevating serum K+ concentrations inactivates sodium channels and that the extracellular sides of these sodium channels are electronegative. Divalent cations such as calcium provide a remarkably effective way of screening these electronegative sites. Thus, calcium salts raise the voltage gradient across sodium channels by screening electronegative surface charges of these channels on their extracellular fluid sides and consequently restoring the voltage-dependent excitability of these channels. Gastrointestinal potassium losses may be produced by the use of cation exchange resins in the sodium cycle, such as sodium polystyrene sulfonate (Kayexalate), or by agents that induce secretory diarrhea. Each gram of the resin contains approximately 1 mEq of sodium and exchanges for about 1 mEq of potassium. This stoichiometry is not precise, since the sodium form of the resin also exchanges for other cations in gastrointestinal secretions, including calcium. In chronic hyperkalemia, 20 g of Kayexalate may be given three or four times a day in a 70% solution of sorbitol. The sorbitol creates an osmotic diarrhea and enhances resin passage through the gastrointestinal tract. It must be stated that use of resin-cathartic therapy is relatively unpleasant for 558 the patient. Kayexalate may also be administered by enema, generally as 100 g of resin suspended in 200 g/mL of 20% sorbitol. The effect of single dose Kayexalate on fecal potassium output is minimal when compared to non-cation exchange agents that induce secretory diarrhea, however Kayexalate may be of benefit in management of hyperkalemia when given more chronically. The use of chronic Kayexalate therapy in patients with chronic renal failure carries with it the risk of sodium overload. Finally, acute hemodialysis or peritoneal dialysis provides another mechanism for potassium removal from the body. Study shows that standard-dose trimethoprim-sulfamethoxazole therapy consistently increases peak serum potassium concentrations. Nice article that discusses the reasons and mechanisms in management of hypokalemia. Data review showing that refractory K+ repletion is often associated with total body Mg2+ deficiency. Acidemia and alkalemia refer to blood hydrogen concentration and therefore to the pH of the blood. These terms do not refer to the mechanism by which a disturbance in pH is reached. Acidosis and alkalosis, on the other hand, refer to the mechanism by which a given acid-base disturbance is reached. Primary refers to the initiating process of acid-base disturbance, whereas secondary refers to a compensatory process. Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. These terms are defined early in this chapter for the sake of clarity and are developed in more detail later. Therefore, the Henderson-Hasselbalch equation becomes Primary changes in the numerator (blood bicarbonate concentration) refer to primary metabolic changes, whereas primary changes in the denominator (blood carbon dioxide tension) refer to primary respiratory changes. The largest source of endogenous acid production is from combustion of glucose and fatty acids to carbon dioxide and water or, in other words, to a volatile acid. During aerobic glycolysis, that is, cellular respiration, glucose oxidation involves oxygen utilization and carbon dioxide production according to the following reaction: Because red blood cells contain carbonic anhydrase (c. A simple way of calculating the daily rate of non-volatile acid production is to note, from the preceding reactions, that producing 1 mole of metabolic water and 1 mole of carbon dioxide represents, through dissociation of carbonic acid, the formation of 1 mole of hydrogen ions. Under normal circumstances, organic anions such as lactate and keto acids, which derive from incomplete combustion of carbohydrates and fatty acids, have plasma concentrations of approximately 5 mEq/L. In most circumstances, central medullary chemoreceptors provide the major impetus to altering ventilatory response, and the carotid body chemoreceptors serve as relatively minor stimuli to ventilation. On average, for every 1 mEq/L reduction in plasma bicarbonate produced by metabolic acidosis, increased minute ventilation will produce a 1. The major source for non-volatile acid production is the metabolism of sulfur-containing amino acids, such as cysteine and methionine, which results in sulfuric acid formation. Consequently, the daily rate of non-volatile acid production is closely related to dietary protein intake and to the rate of endogenous protein catabolism. Non-volatile acids also derive from oxidation of phosphoproteins and phospholipids, which results in phosphoric acid formation; nucleoprotein degradation, which yields uric acid; and incomplete combustion of carbohydrates and fatty acids, which produces lactic acid and the keto acids. The daily rate of non-volatile acid production under normal conditions is about 1 mEq/kg of body weight. Thus, daily non-volatile acid production would consume the total body fluid buffering capacity in about 2 weeks, were it not for the fact that the kidneys excrete non-volatile acids and, in so doing, regenerate bicarbonate. The kidneys also filter large quantities of bicarbonate daily: for a normal plasma bicarbonate concentration of 24 mEq/L and a glomerular filtration of 180 L/d, the net amount of bicarbonate filtered daily is approximately 4300 mEq, or about four times the total body buffering capacity. Thus, in addition to generating new bicarbonate, the renal tubules must also absorb filtered bicarbonate. Virtually all filtered bicarbonate is absorbed, together with sodium, by the proximal tubule. Apical membrane Na+ exchange permits H+ secretion into urine and Na+ entry into cells, with subsequent absorption of sodium bicarbonate to blood. The rate of proximal bicarbonate reabsorption is modulated by the same effectors that regulate proximal sodium absorption. Volume expansion, which resets glomerulotubular balance downward, reduces the fractional rate of proximal bicarbonate reabsorption. Conversely, volume contraction raises the bicarbonate threshold by increasing the fractional rate of proximal tubular sodium bicarbonate reabsorption. Two other effectors regulate, in operational terms, the rate of bicarbonate reabsorption. This factor accounts for the compensatory increase in plasma bicarbonate concentrations in respiratory acidosis. Second, hypokalemia also increases the rate of bicarbonate reabsorption, presumably by raising the intracellular hydrogen ion concentration. This factor accounts for the fact that in hypokalemic, hypochloremic metabolic alkalosis associated with volume contraction, alkalosis can persist after volume deficits are restored. In this circumstance, correcting potassium deficits is required to correct the alkalosis. The excretion of non-volatile acids and the simultaneous renal regeneration of bicarbonate occur principally in distal nephron segments. The secreted protons titrate urinary buffers, principally phosphate, while sodium is absorbed. Thus the overall reaction is as follows: Titratable acid formation normally accounts for about one third of renal acid excretion. Distal acid excretion and bicarbonate absorption are accompanied by sodium absorption. Consequently, effector systems that enhance distal sodium absorption, such as aldosterone or increased rates of sodium delivery to terminal nephron segments, also promote terminal nephron hydrogen ion excretion. These three last-named effector systems enhance renal acid excretion by creating a favorable situation for proton transfer from tubular cells to urine. Conversely, aldosterone deficiency, alkalosis, or reduced rates of salt delivery to terminal nephron segments reduce renal capacity for acid excretion. The ventilatory responses to pH changes mediated by respiratory processes or by metabolic processes therefore differ. Consequently, in the early stages of acute metabolic acidosis, there may be a 1- to 3-hour delay in the development of a maximal hyperventilatory response. In these situations, carotid body chemoreceptors, rather than central medullary chemoreceptors, provide the major stimulus to respiration driven by a reduced arterial pH. These data also provide an index to total-body acid-base balance, because, as indicated in the preceding section, the majority of body buffering occurs within cells. The graph on the right, labeled compensatory response, indicates the general trend of pH. Respiratory acidosis and alkalosis are accompanied by compensatory renal bicarbonate retention and loss, respectively. Metabolic acidosis and alkalosis are accompanied by compensatory hyperventilation and hypoventilation, respectively. Note that the compensatory response in each of the four acid-base disorders tends to restore arterial pH values toward the pH 7. A convenient way for considering these disturbances is illustrated in Figure 102-9, which illustrates pH isobars (for pH 7. Metabolic alkalosis occurs when increases in the plasma bicarbonate concentration raise pH, and metabolic acidosis occurs when reductions in plasma bicarbonate decrease pH. Any of these initial acid-base disturbances activates compensatory responses, illustrated in the right-hand panel of Figure 102-9, that tend to minimize the pH changes produced by the initial acid-base abnormality. By comparing the directional arrows in the left- and right-hand panels of Figure 102-9, it becomes evident that the initial disturbance in any of these four acid-base abnormalities tends to displace the arterial pH away from the pH 7. Renal and pulmonary mechanisms aggressively protect the body from changes in pH of arterial blood and interstitial fluid against primary acid-base disturbances that would threaten the optimal activity of various pH-dependent organ functions. These are known as "compensatory mechanisms" that blunt the effect of the initial insult or pH homeostasis. Although the magnitude and rate of the compensatory responses vary among individual patients and do not provide complete compensation for the initiating abnormality, they nevertheless are relatively predictable. The predicted compensatory responses to the primary acid-base disturbances are listed in Table 102-14. The sum of plasma chloride plus bicarbonate concentrations is less than the serum sodium concentration; the remaining anions required for electroneutrality, generally not reported with routine serum electrolyte measurements, are referred to as unmeasured anions, or as the serum anion gap. The anion serum gap includes primarily phosphates and sulfates derived from tissue metabolism, lactate and keto acids arising from incomplete combustion of carbohydrates and fatty acids, and negatively charged protein molecules, principally albumin. An increased serum anion gap generally indicates the presence of metabolic acidosis. The factors responsible for this kind of metabolic acidosis are discussed in the next section. The anion gap will be reduced if the sodium concentration falls while the chloride plus bicarbonate concentrations are unchanged or, in other words, when the concentration of another cation in serum is increased while the serum osmolality remains normal. This may occur in multiple myeloma of the immunoglobulin G (IgG) variety if the myeloma proteins are cationic at pH 7. Hyperviscosity syndromes also may result in a reduced anion gap because of a laboratory artifact: when serum is excessively viscous, automatic pumps deliver decreased volumes of serum to a flame photometer, producing artifactual reductions in sodium concentrations. Rarely, lithium intoxication, hypermagnesemia, and hypercalcemia raise non-sodium cation concentrations sufficiently high to reduce the anion gap. The serum anion gap also will be decreased if the serum sodium concentration remains normal while the serum chloride plus bicarbonate concentrations are increased. A low serum anion gap also occurs in bromide intoxication, since colorimetric techniques for serum chloride determinations give spuriously high values for chloride plus bromide when bromide is present in relatively high concentrations in serum. The urinary anion gap, defined as is useful in evaluating patients with hyperchloremic acidosis. Thus, in hyperchloremic metabolic acidosis, a normal renal response would be a negative urinary anion gap, generally in the range of 30 to 50 mEq/L. In such an instance, the hyperchloremic acidosis is probably due to gastrointestinal losses rather than a renal lesion. In contrast, a positive urinary anion gap implies a renal tubular disorder, as is discussed below. The urinary response to oral furosemide loading is another useful test for evaluating tubular acidifying capability. The rationale for the test is that in normal individuals blockade of sodium absorption in diluting segments by furosemide increases sodium delivery to distal nephron segments where potassium and protons are secreted (see earlier) and increases the excretion rate of the latter two moieties. Consequently, the oral administration of 40 to 80 mg of furosemide should be followed, in a subsequent 4- to 6-hour urinary collection, by an increase in urinary sodium excretion and fractional sodium excretion, an increase in urinary potassium excretion and fractional potassium excretion, and a reduction in urinary pH. In some renal tubular acidosis syndromes, proton and/or potassium excretion is impaired (Table 102-15). A convenient way to consider the metabolic acidoses is to divide them into two groups: normal anion gap and increased anion gap metabolic acidoses (Table 102-16). The metabolic acidoses having a normal anion gap result whenever there are abnormally high net bicarbonate losses. Ethylene glycol because there are extrarenal losses of bicarbonate, or because excessive amounts of substances yielding hydrochloric acid have been administered. The apparent threshold for bicarbonate in this disorder is set below the normal value of 26 mEq of bicarbonate per deciliter of glomerular filtrate and may be as low as 15 to 20 mEq of bicarbonate per deciliter of glomerular filtrate. Consequently, bicarbonate wasting occurs whenever the plasma bicarbonate level is raised above the apparent renal threshold for bicarbonate. Attempts to correct the acidosis of proximal renal tubular acidosis by bicarbonate administration are generally unrewarding, because increases in the plasma bicarbonate level produced by administering bicarbonate salts are accompanied by corresponding increases in bicarbonaturia.
Intubation results in laryngeal and tracheal irritation medicine 832 safe asacol 400mg, loss of effective cough lb 95 medications purchase asacol 400mg overnight delivery, and increased risk of infection symptoms 0f a mini stroke generic 400 mg asacol otc. With careful handling symptoms 9 days before period generic 800 mg asacol with mastercard, endotracheal tubes may be kept in place for at least 2 weeks (see Chapter 93) symptoms 1dp5dt buy 400mg asacol mastercard. When artificial ventilation is required for more than 2 weeks treatment example order 400mg asacol with amex, a tracheostomy is often required. The most important indication for early tracheostomy is the presence of copious, tenacious secretions that cannot be adequately removed through the endotracheal tube. Tracheostomy carries some risk of bleeding, pneumothorax, and local infection and an increased incidence of aspiration. Short-term outcome following acute hypoxic respiratory failure is generally good (see Table 88-1). The long-term prognosis is dictated by underlying disease and the functional impairment before acute respiratory failure developed. If historical information is not available, however, a specific diagnosis may be difficult, because many end-stage primary lung diseases overlap clinically. Obstruction can be separated from restriction (see Chapter 72), although patients may not be able to perform the necessary rigorous pulmonary function tests. At times, superimposed infection, pleural disease, or previous surgery also blurs these distinctions. In the most severe cases of chronic hypoxic respiratory failure, progressive lung destruction also impairs ventilation, and hypercapnia develops. Many patients with chronic hypoxic respiratory failure have end-stage fibrosis (honeycomb lung) (see Chapter 78). Supportive care includes oxygen for severe hypoxia and diuretics for excessive edema. Various O2 -conserving devices are available and may allow for more cost-effective supplementation and longer periods away from home. If patients are younger than 60 years and have no other significant problems, lung transplantation (see Chapter 89) should be considered. A variety of diseases lead to chronic hypercapnic respiratory failure (see Chapters 74 and 75). Using these devices during sleep may improve quality of life and prolong survival, especially in patients with neuromuscular diseases. Younger patients with alpha1 -antitrypsin deficiency (see Chapter 75), cystic fibrosis (see Chapter 76), and other causes of bronchiectasis (see Chapter 77) are good candidates for lung transplantation (see Chapter 89). Quality of life is always an issue for elderly patients, and relief of suffering may be the major therapeutic goal of both patient and physician. Mentzer the role of surgery in the diagnosis and therapy of lung disease has expanded greatly as lung transplantation has gained acceptance as a therapeutic option for selected patients with advanced lung disease. In addition, the concept of surgery to reduce lung volume in patients with emphysema has been reintroduced and is an area of active clinical investigation. Minimally invasive thoracic surgery has also created new options for lung biopsy and pulmonary resection. The annual number of lung transplant procedures increased steadily from 1982 through 1993, but it has recently remained constant at 1300 to 1400 patients annually because of limited donor availability. Transplant Types Currently, four types of lung transplantation procedures are performed. Single lung transplantation is typically performed through a posterolateral thoracotomy incision and requires three anastomoses: mainstem bronchus, pulmonary artery, and pulmonary veins/left atrium. The contralateral lung is not removed, so single lung transplantation is not performed in patients with bilaterally infected lungs. It requires six anastomoses: both mainstem bronchi, both pulmonary arteries, and both sets of pulmonary veins. It is the procedure of choice for patients with bilaterally infected lungs and is also performed in certain patients with emphysema, primary pulmonary hypertension, and other diseases. Heart-lung transplantation was initially the most common type of lung transplant procedure but is now performed infrequently. It is an en bloc procedure, with right atrial, aortic, and distal tracheal anastomoses. The most recently introduced lung transplant procedure is living donor lobar transplantation. This procedure involves the removal of a lower lobe from each of two living donors, with the implantation of one in each hemithorax of the recipient in a manner similar to bilateral lung transplantation. Diseases Treated with Lung Transplantation the most common indications for transplantation are diseases or conditions that share the following common features: they produce extreme disability in affected patients, they are unresponsive to medical therapy, and they are responsible for limited life expectancy in affected patients (Table 89-1). With the exception of a small number of cases of sarcoidosis and lymphangioleiomyomatosis, the original lung disease does not recur after lung transplantation. Considerations in the Evaluation of Potential Transplant Recipients the ideal candidate for lung transplantation has lung disease unresponsive to medical therapy but is in otherwise good health. In contrast to cardiac transplantation (see Chapter 71), patients who are critically ill are usually not appropriate candidates for lung transplantation. Patients who experience critical illness due to lung disease often have poor nutritional status, coexistent major organ dysfunction, refractory infection, or other contraindications to transplantation (Table 89-2) (Table Not Available). The specific recommendations for referral for transplant evaluation vary depending on the underlying disease (Table 89-3) (Table Not Available). As waiting times for transplantation lengthen because of the expansion of the potential number of recipients, patients will likely need to be referred earlier to have a reasonable chance of surviving until transplantation. Issues after Lung Transplantation Most of the medical issues that patients and physicians face after lung transplantation are the consequence of the transplant and post-transplant medication, rather than the underlying disease for which the transplant was performed. Examples include immunosuppression, infections and their prophylaxis, acute allograft rejection, chronic allograft rejection, and nonpulmonary complications of transplantation. The standard chemotherapeutic regimen for immunosuppression after lung transplantation consists of cyclosporine, azathioprine, and corticosteroids. Use of tacrolimus instead of cyclosporine may result in fewer episodes of acute rejection in the first year after transplantation. Some centers add an antilymphocyte antibody preparation in the first days after transplantation, but the effect of this practice on rates of acute and chronic rejection are unknown. Experience with mycophenolate mofetil is limited, and its role remains to be defined. Lung transplant recipients are at high risk for bacterial, viral, fungal, and protozoal infections; infections are the leading causes of death during the early post-transplant period. Additionally, patients are pharmacologically immunosuppressed, are in a catabolic state, have impaired defenses as the result of endotracheal intubation, and have arterial and central venous catheters, chest tubes, and a large surgical incision. In the first 3 months after transplantation, bacterial infections are responsible for the majority of deaths. Approximately one-third of patients are diagnosed with pneumonia in the first weeks after transplantation, with gram-negative organisms as the etiology in 75% of cases. Patients with chronic rejection often develop colonization and recurrent infections, usually with Pseudomonas species. Seronegative patients who have a seronegative donor are at low risk for infection, provided they are treated with seronegative blood products. Most programs now use prophylactic ganciclovir in patients at risk, although the optimal dosing regimen and duration of treatment are as yet undetermined. Herpes simplex infections are relatively unusual, in part due to the standard use of prophylactic antiviral medication (ganciclovir or acyclovir). Predisposing factors for such infection include preoperative colonization with Aspergillus, stenotic airways, or the presence of an airway stent. Due to the nature of the immunosuppressive chemotherapeutic regimen used, patients are at high risk for infection by the protozoan Pneumocystis carinii. The use of trimethoprim-sulfamethoxazole prophylaxis has virtually eliminated Pneumocystis pneumonia. Histologically, the initial manifestation of acute rejection is a lymphocyte-predominant inflammatory response, usually centered around blood vessels and/or airways. The vascular inflammation is accompanied by endothelial inflammation, and the lymphocyte infiltration can progress to involve alveolar walls. By convention, acute rejection is graded from 0 (normal) to 4 (severe), with subclasses defined by the presence or absence of airway inflammation. The risk of acute allograft rejection is highest in the early months after transplant and declines with time. Multiple episodes of acute rejection are the major risk factor for the subsequent development of chronic rejection. Because up to 25% of surveillance bronchoscopies reveal asymptomatic rejection, some programs perform surveillance biopsies at regular intervals with the goal of reducing the incidence of chronic rejection; however, the efficacy of this approach has not been established. Evaluation may demonstrate rales or rhonchi on chest examination, a decline in pulmonary function by spirometry, leukocytosis, opacities on chest radiography, and exertional desaturation. The clinical presentation is often indistinguishable from infectious pneumonia, and the clinical impression is accurate in only 50% of cases. Bronchoscopy with bronchoalveolar lavage and/or transbronchial biopsy is commonly needed to clarify the diagnosis. Treatment of acute rejection most often consists of high-dose corticosteroids administered intravenously for 3 days. In patients with persistent or recurrent acute rejection, therapeutic strategies include antilymphocyte antibodies, changing maintenance immunosuppressive drugs, and other attempts to augment immunosuppression. The bronchiolitis obliterans syndrome is thought to be a manifestation of chronic rejection. Pathologically, "early" lesions demonstrate inflammation and disruption of the epithelium of small airways followed by growth of granulation tissue into the airway lumen, resulting in complete or partial obstruction. The granulation tissue then organizes in a stereotypical pattern with resultant fibrosis that obliterates the lumen of the airway. Patients typically develop progressive exertional breathlessness, and pulmonary function testing usually demonstrates evidence of progressive airflow obstruction. In early stages, chest radiography is notable only for hyperinflation, but it may show bronchiectasis as the syndrome progresses. Later stages of bronchiolitis obliterans may include a syndrome of bronchiectasis with chronic productive cough and airway colonization with Pseudomonas species. The diagnosis of bronchiolitis obliterans is made both on clinical and pathologic grounds. Transbronchial biopsy has a low yield for demonstrating histologic evidence of bronchiolitis obliterans; but when such evidence is seen, it is diagnostic. In patients with a compatible clinical syndrome, the exclusion of anastomotic stenosis and occult pulmonary infection is sufficient to establish the diagnosis. A variety of types of therapy have been tried, including pulse corticosteroids, antilymphocyte antibodies, total lymphoid irradiation, photopheresis, and nebulized cyclosporine, but none is clearly effective. Most patients with bronchiolitis obliterans experience a progressive decline in pulmonary function despite augmentation of immunosuppression. Bronchiolitis obliterans is the leading cause of late mortality after lung transplantation. Most of the nonpulmonary medical complications that arise in patients after lung transplantation are the result of immunosuppressive therapy. Virtually all lung transplant recipients develop one or more of these complications. Osteoporosis is common owing to the chronic use of corticosteroids and cyclosporine. Bone density should be monitored periodically, and pharmacologic therapy should be instituted if excessive bone loss is identified (see Chapter 257). Chronic renal insufficiency is common and is the result of therapy with cyclosporine or tacrolimus, both of which affect afferent vascular tone in the kidneys and result in an average 50% drop in the glomerular filtration rate in the 12 months after lung transplantation. Calcium-channel blockers, which are often used to treat hypertension, raise serum cyclosporine levels; appropriate monitoring and dose adjustment are needed when starting such therapy. Both corticosteroids and tacrolimus contribute to the development of diabetes mellitus and hyperlipidemia. Organ transplantation is associated with an increased incidence of malignancy, thought to be due to pharmacologic immunosuppression and alteration in immune surveillance. Patients are at increased risk for lymphoproliferative malignancies and other types of cancer. Post-transplant lymphoproliferative disorders occur in about 4% of patients after organ transplantation; most are associated with Epstein-Barr virus. Reduction in immunosuppression is sometimes therapeutic in those with polyclonal disease. The prognosis in patients with monoclonal disease is poor, with little response to modification of immunosuppression or antineoplastic chemotherapy. Patients are also at increased risk for skin, cervical, anogenital, and hepatobiliary malignancy after solid organ transplantation. Outcomes after Lung Transplantation A comparison of survival data in lung transplants done before 1990 with those done between 1991 and 1993 shows that 1-year survival rates improved significantly (64. The subsequent rate of decline in survival (8 to 10% annually) has not changed and largely reflects the effects of bronchiolitis obliterans on patient survival. He proposed a procedure in which peripheral areas of emphysematous 478 lung were resected, postulating that the resulting reduction in lung volume would increase elastic recoil and radial traction on airways during expiration and also allow restoration of the normal configuration of the muscles of respiration. This procedure failed to achieve widespread acceptance, largely due to a reported mortality of about 15% and the lack of documented benefit. Cooper and colleagues reconsidered these concepts and in 1994 reported that lung volume reduction surgery produces a significant improvement in expiratory flow, exercise tolerance, and quality of life. The role of lung volume reduction surgery in the management of patients with emphysema is currently the subject of active investigation and several large clinical trials. Most experts believe that patients with other causes of airflow obstruction, including bronchiectasis, asthma, or chronic bronchitis, are unlikely to benefit. Types of Lung Volume Reduction Surgery A variety of approaches may be taken in the common goal of reducing lung volume by about 30%. In the absence of a specific contraindication, bilateral lung volume reduction surgery is currently the procedure of choice. Currently favored techniques include stapled resection of peripheral lung tissue, with or without the use of exogenous material to buttress the suture lines, and plication, in which the lung is rolled on itself and stapled without resection.
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References
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