Medical Instructor, Northwestern University Feinberg School of Medicine
Abruptio placentae accounts for approximately one third of third-trimester hemorrhages and occurs in 0 blood sugar to a1c order 2.5 mg micronase otc. Diagnosis is made before delivery using ultrasonography and at delivery by examination of the placenta definition of reversing diabetes cheap micronase 2.5 mg overnight delivery. Delivery may be vaginal if the abruption is not jeopardizing maternal or fetal well-being blood glucose jobs cheap 2.5mg micronase amex. Perinatal mortality is 25-fold higher if a term pregnancy is complicated by abruption diabetes education purchase micronase 5 mg otc. If maternal hypotension is absent, clotting study results are acceptable, and there is no evidence of fetal distress due to uteroplacental insufficiency; epidural analgesia is useful to provide analgesia for labor and vaginal delivery. When the magnitude of placental separation and resulting hemorrhage are severe, emergency cesarean delivery is necessary; most often, general anesthesia is used, because regional anesthesia may be unwise in a patient with hemodynamic instability. It is not uncommon for blood to dissect between layers of the myometrium after premature separation of the placenta. As a result, the uterus is unable to contract adequately after delivery, and postpartum hemorrhage occurs. Clotting parameters usually revert to normal within a few hours after delivery of the fetus. Conditions associated with uterine atony include multiple parity, multiple births, polyhydramnios, a large fetus, and a retained placenta. Uterine atony may occur immediately after delivery or may manifest itself several hours later. Treatment is with intravenous oxytocin, which results in contraction of the uterus. Methylergonovine, administered intravenously or intramuscularly, or intramuscular or intrauterine carboprost tromethamine (or misoprostol) may also be used to control hemorrhage. Retained placenta occurs in approximately 1% of all vaginal deliveries and usually necessitates a manual exploration of the uterus. If epidural analgesia has been used for vaginal delivery, manual removal of the retained placenta may be attempted under epidural anesthesia. Spinal anesthesia (saddle block) or low-dose intravenous ketamine may provide adequate analgesia if an epidural catheter is not in place. Low doses of intravenous nitroglycerin (40-mcg boluses, as needed) are used to relax the uterus for placental removal when indicated. Uterine rupture and dehiscence represent a spectrum ranging from incomplete rupture or gradual dehiscence of surgical scars to explosive rupture with intraperitoneal extrusion of uterine contents. Visual examination of the uterus at cesarean delivery will detect rupture or dehiscence. Also, induction of labor, fetal gestational age of more than 40 weeks, fetal weight of more than 4000 g, and poor cervical dilation may be predictive of failure. The suggestion that neuraxial analgesia will mask the signs and symptoms of uterine rupture is unfounded. The pain of uterine rupture is constant (does not resolve between contractions), is much more intense, and has a different quality than the pain of contractions. Worsening of the fetal heart rate tracing will alert obstetric and anesthesiology teams to abnormality as well. The opioid-based epidural solutions used for labor provide only analgesia and cannot mask the pain of uterine rupture because these solutions do not provide anesthesia. Amniotic Fluid Embolism Amniotic fluid embolism is a rare catastrophic and life-threatening complication of pregnancy that occurs when there is a disruption in the barrier between the amniotic fluid and the maternal circulation. The three most common sites for entry of amniotic fluid into the maternal circulation are the endocervical veins, the placenta, and a uterine trauma site. Multiparous parturient women experiencing tumultuous labors are at increased risk of amniotic fluid embolism. As a result, pulmonary artery pressures increase, arterial hypoxemia develops owing to ventilation/perfusion mismatching, and hypotension occurs, reflecting decreased cardiac output and congestive heart failure caused by right ventricular outflow obstruction and acute cor pulmonale. Conditions that can mimic amniotic fluid embolism include inhalation of gastric contents, pulmonary embolism, venous air embolism, and local anesthetic toxicity. Pulmonary aspiration is more likely when bronchoconstriction accompanies the clinical signs and symptoms. Indeed, bronchospasm is rare in parturient women who experience amniotic fluid embolism. High sensory levels produced by spinal or epidural anesthesia may be confused with amniotic fluid embolism. Compared with cephalic presentations, there is a greater likelihood of cervical lacerations, perineal injury, retained placenta, and shock resulting from hemorrhage. These infants are more likely to experience arterial hypoxemia and acidosis during delivery because of umbilical cord compression. Prolapse of the umbilical cord occurs with increased frequency in breech presentations and is presumed to reflect failure of the presenting part to fill the lower uterine segment. In parturient patients undergoing elective cesarean delivery for breech presentation spinal anesthesia is generally used, as is routine for elective cesarean delivery. Vaginal delivery may be complicated by umbilical cord prolapse or fetal head entrapment, which necessitates emergency anesthesia for cesarean or instrumented vaginal delivery. Dense perineal anesthesia is needed for vaginal instrumentation and must be administered rapidly, either by using 3% 2-chloroprocaine if an epidural catheter is in place, or by inducing general anesthesia. The use of positive end-expiratory pressure is often helpful for improving oxygenation. Dopamine, dobutamine, and norepinephrine have been recommended as inotropes to treat acute left ventricular dysfunction and associated hypotension. Fluid therapy is guided by central venous pressure monitoring, but it must be kept in mind that these patients are vulnerable to developing pulmonary edema. Even with immediate and aggressive treatment, mortality resulting from amniotic fluid embolism remains higher than 80%.
Particular care is needed when selecting drugs for patients with acute intermittent porphyria or clinically active forms of porphyria and when prescribing drugs in combination diabetic chicken recipes order 5mg micronase, because exacerbation of porphyria is more likely under these circumstances diabete test order micronase with a mastercard. Acute Intermittent Porphyria Of all the acute porphyrias diabète yeux symptomes discount micronase 2.5 mg with visa, acute intermittent porphyria affecting the central and peripheral nervous system produces the most serious symptoms (systemic hypertension diabetic diet app purchase discount micronase on line, renal dysfunction) and is the one most likely to be life threatening. The defective enzyme is porphobilinogen deaminase, and the gene encoding this enzyme is located on chromosome 11. Variegate Porphyria Variegate porphyria is characterized by neurotoxicity and cutaneous photosensitivity in which bullous skin eruptions occur on exposure to sunlight as a result of the conversion of porphyrinogens to porphyrins. The enzyme defect is at the level of protoporphyrinogen oxidase, and the gene encoding this enzyme is on chromosome 1. Hereditary Coproporphyria Acute attacks of hereditary coproporphyria are less common and less severe than attacks of acute intermittent porphyria or variegate porphyria. These patients typically experience neurotoxicity and cutaneous hypersensitivity, although these signs tend to be less severe than is seen in variegate porphyria. The defective enzyme is coproporphyrinogen oxidase, encoded by a gene on chromosome 9. It is not possible to predict which drugs will be porphyrinogenic, although chemical groupings such as the allyl groups present on barbiturates and certain steroid structures have been incriminated in the induction of porphyria. It is not clear why the manifestations of nonacute porphyrias are apparently unaffected by enzyme-inducing drugs. Signs and symptoms of porphyria cutanea tarda most often appear as photosensitivity reactions, especially in men older than 35 years of age. Porphyrin accumulation in the liver can be associated with hepatocellular necrosis. Anesthetic drugs are not hazardous in affected patients, although the choice of drugs should take into consideration the likely presence of liver disease. Neurotoxicity and abdominal pain do not occur, and administration of barbiturates does not adversely alter the course of the disease. Erythropoietic Protoporphyria Erythropoietic protoporphyria is a more common, but less debilitating, form of erythropoietic porphyria. Signs and symptoms include photosensitivity, vesicular cutaneous eruptions, urticaria, and edema. In occasional patients cholelithiasis develops secondary to increased excretion of protoporphyrin. Administration of barbiturates does not adversely affect the course of the disease, and survival to adulthood is common. Erythropoietic Uroporphyria Erythropoietic uroporphyria is a rare form of porphyria transmitted as an autosomal recessive trait. Laboratory identification of porphyric individuals is not easy since many show only subtle or even no biochemical abnormalities during an asymptomatic phase. In the presence of a suggestive family history, determination of erythrocyte porphobilinogen activity is the most appropriate screening test for patients with suspected acute intermittent porphyria. A careful family history should be obtained and a thorough physical examination performed (although there is often no clinical evidence or only subtle skin lesions), and the presence or absence of peripheral neuropathy and autonomic nervous system instability should be noted. Guidelines for drug selection include the following: (1) There is evidence that a single exposure to a potent inducer can be well tolerated, but not during an acute attack. Note that the American Porphyria Foundation maintains up-to-date information on all aspects of these diseases, and a drug database with information about drugs and acute porphyria can be found at. If an acute exacerbation of porphyria is suspected during the perioperative period, particular attention must be given to skeletal muscle strength and cranial nerve function, since these symptoms and signs may predict impending respiratory failure and an increased risk of pulmonary aspiration. Cardiovascular examination may reveal systemic hypertension and tachycardia, which necessitate treatment before induction of anesthesia. Postoperative mechanical ventilation may be required during an acute porphyric crisis. Patients experiencing an acute porphyric crisis must be assessed carefully for fluid balance and electrolyte status, especially the presence of hyponatremia. Preoperative starvation should be minimized, but if a prolonged fast is unavoidable, administration of a glucose-saline infusion should be considered, since caloric restriction has been linked to the precipitation of attacks of acute porphyria. If oral feedings are not possible, then infusion of 10% glucose in saline is an option. Management of Anesthesia Anesthesia has been implicated in triggering acute attacks of porphyria. However, most patients with porphyria can be safely anesthetized if appropriate precautions are taken. Patients with evidence of active porphyria or a history of acute porphyric crises are at increased risk. Short-acting anesthetic drugs are presumed to be safe because their rapid elimination limits the time of exposure for enzyme induction. However, repeated or prolonged use of these drugs, such as by continuous intravenous infusion, could result in a different clinical outcome. A number of case reports have described the successful use of intermittent propofol administration in patients with porphyria, but there are not enough data to validate propofol administration by continuous infusion in porphyria patients. It is likely that exposure to several potential enzymeinducing drugs may be more dangerous than exposure to any one drug, so the anesthetic plan must take this into account. However, if a regional anesthetic is being considered, it is essential to perform a neurologic examination before initiating the blockade to minimize the likelihood that worsening of any preexisting neuropathy would be erroneously attributed to the regional anesthetic.
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Etomidate may transiently decrease the synthesis and release of cortisol by the adrenal cortex diabetes type 1 bcg vaccine safe micronase 5 mg. Doses of muscle relaxants should probably be decreased initially in view of the skeletal muscle weakness that frequently accompanies hypercortisolism diabetes type 2 effects on body order micronase with american express. In addition diabetes insipidus while pregnant buy generic micronase 5 mg online, the presence of hypokalemia may influence responses to nondepolarizing muscle relaxants blood sugar record sheet purchase 2.5 mg micronase otc. Regional anesthesia is acceptable, but the likely presence of osteoporosis, with possible vertebral body collapse, is a consideration. Plasma cortisol concentrations decrease promptly after microadenomectomy or bilateral adrenalectomy, and replacement therapy is recommended. Likewise, patients with metastatic disease involving the adrenal glands may develop acute adrenal insufficiency, which requires the initiation of supplemental therapy. Transient diabetes insipidus and meningitis may also occur after microadenomectomy. A syndrome exhibiting all the features of hyperaldosteronism (systemic hypertension, hypokalemia, suppression of the renin-angiotensin system) may result from long-term ingestion of licorice (glycyrrhizic acid). Occasionally, primary aldosteronism is associated with pheochromocytoma, primary hyperparathyroidism, or acromegaly. Secondary hyperaldosteronism is present when increased circulating serum concentrations of renin, as are associated with renovascular hypertension, stimulate the release of aldosterone. The prevalence of primary aldosteronism in patients with essential hypertension appears to be less than 1%. Skeletal muscle weakness resulting from hypokalemia may require treatment with intravenous potassium. Accentuation of hypokalemia caused by drug-induced diuresis is decreased by use of a potassiumsparing diuretic such as triamterene. Bilateral adrenalectomy may be necessary if multiple aldosteronesecreting tumors are found. Symptoms may reflect systemic hypertension (headache) or hypokalemia (polyuria, nocturia, skeletal muscle cramps, skeletal muscle weakness). Systemic hypertension (diastolic blood pressure is often 100 to 125 mm Hg) is a function of aldosterone-induced sodium retention and increase in extracellular fluid volume. Aldosterone promotes renal excretion of potassium, which results in hypokalemic metabolic alkalosis. Increased urinary excretion of potassium (more than 30 mEq/day) in the presence of hypokalemia suggests primary aldosteronism. Hypokalemic nephropathy can result in polyuria and loss of urine-concentrating ability. Plasma renin activity is suppressed in almost all patients with untreated primary aldosteronism and in many with essential hypertension; with secondary aldosteronism, however, the plasma renin activity is high. A plasma aldosterone concentration of less than Management of anesthesia for the surgical treatment of hyperaldosteronism is facilitated by preoperative correction of hypokalemia and treatment of systemic hypertension. Persistence of hypokalemia may modify responses to nondepolarizing muscle relaxants. The use of sevoflurane is questionable, however, if hypokalemic nephropathy and polyuria are present preoperatively. Measurement of cardiac filling pressures via a right atrial or pulmonary artery catheter may be useful during surgery for adequate evaluation of the intravascular fluid volume and the response to intravenous infusion of fluids. Indeed, aggressive preoperative preparation can convert the excessive intravascular fluid volume status of these patients to unexpected hypovolemia, manifesting as hypotension in response to administration of vasodilating anesthetic drugs, positive pressure ventilation, changes in body position, or surgical blood loss. The detection of orthostatic hypotension during the preoperative evaluation is a clue to underlying hypovolemia. Acid-base status and plasma electrolyte concentrations should be measured frequently. Supplementation with exogenous cortisol is probably unnecessary for surgical excision of a solitary adenoma in the adrenal cortex. Bilateral mobilization of the adrenal glands to excise multiple functional tumors, however, may introduce the need for exogenous cortisol administration. A continuous intravenous infusion of cortisol, 100 mg every 24 hours, may be initiated on an empirical basis if transient hypocortisolism resulting from surgical manipulation is a consideration. Hypoaldosteronism Hyperkalemia in the absence of renal insufficiency suggests the presence of hypoaldosteronism. Heart block secondary to hyperkalemia, orthostatic hypotension, and hyponatremia may also be present. Hyporeninemic hypoaldosteronism typically occurs in patients older than 45 years of age with chronic renal disease and/or diabetes mellitus. Indomethacin-induced prostaglandin deficiency is a reversible cause of this syndrome. Treatment of hypoaldosteronism includes liberal sodium intake and daily administration of fludrocortisone. All steroids except dexamethasone must be discontinued for 24 hours before testing. The most common cause of this rare endocrinopathy is bilateral adrenal destruction from autoimmune disease. In the majority of cases the cause is iatrogenic, such as pituitary surgery, pituitary irradiation, or most commonly the use of synthetic glucocorticoids. These patients lack cutaneous hyperpigmentation and may demonstrate only mild electrolyte abnormalities. It participates in carbohydrate and protein metabolism, fatty acid mobilization, electrolyte and water balance, and the antiinflammatory response.
If such an event occurs blood sugar keeps going up purchase genuine micronase line, midazolam or diazepam is likely to be a useful treatment blood sugar 67 cheap 5mg micronase free shipping. Numerous factors have been proposed to explain the high incidence of substance abuse among anesthesiologists diabetes diet overview best order micronase. Inhalation of marijuana smoke produces euphoria diabetes type 1 lifespan micronase 2.5 mg discount, with signs of increased sympathetic nervous system activity and decreased parasympathetic nervous system activity. Long-term marijuana abuse leads to increased tar deposits in the lungs, impaired pulmonary defense mechanisms, and decreased pulmonary function. Although physical dependence on marijuana is not believed to occur, abrupt cessation after long-term use is characterized by mild withdrawal symptoms, such as irritability, insomnia, diaphoresis, nausea, vomiting, and diarrhea. The one medical use for marijuana is as an antiemetic in patients receiving cancer chemotherapy. This curriculum notes the following demographic characteristics of anesthesiologists who are addicted to drugs: n n n n n n n Fifty percent are younger than 35 years of age, but this may reflect the age distribution within the specialty. It may be that, because of increased awareness of the high risk of substance abuse among anesthesiologists, training programs are looking more carefully for signs of addiction in this group. Interestingly, a higher proportion of anesthesiology residents who are addicted are members of the Alpha Omega Alpha Honor Society. Thirty-three percent have a family history of addictive disease, most frequently alcoholism. Sixty-five percent of anesthesiologists with a documented history of addiction are associated with academic departments. Substance Abuse as an Occupational Hazard in Anesthesiology Anesthesiologists represent 3. However, they are overrepresented in addiction treatment programs, enrolling at a rate approximately three times higher than that of any other physician group. In addition, anesthesiologists are at highest risk of relapse after drug addiction treatment. At the present time, 12% to 15% of all physicians in treatment are anesthesiologists. Fentanyl and sufentanil are the most commonly abused drugs, followed by meperidine and morphine. This choice is particularly evident among anesthesiologists younger than 35 years of age. Alcohol is the abused substance in older anesthesiologists, probably because the time to produce impairment is significantly longer than that observed with opiate addiction. Other agents that have been abused include cocaine, benzodiazepines (midazolam), and, more recently, propofol. Over the past 5 years, there has been a major switch to "needleless" delivery of commonly abused drugs. This approach provides a cleaner alternative to the more traditional intravenous or intramuscular routes. Every possible route of administration has been tried, including unusual intravenous sites (hidden veins in the feet, groin, thigh, and penis), oral-nasal administration (benzodiazepines), and sublingual and rectal routes. Regardless of the drug initially abused, after 6 months there is an increasing incidence of polydrug abuse. The principal risks to the anesthesia provider with addictive disease are an increased risk of suicide by drug overdose and drug-related death. Unfortunately, the relapse rate for anesthesiologists is the highest among all physicians with a history of narcotic addiction. The risk of relapse is greatest in the first 5 years and decreases as time in recovery increases. The positive news is that 89% of anesthesiologists who complete treatment and commit to aftercare remain abstinent for longer than 2 years. However, death is the primary presenting sign of relapse in opiate-addicted anesthesiologists! The data show that impaired physicians (those who are actively abusing drugs) are at increased risk of malpractice suits. Data from both California and Oklahoma revealed a dramatic decrease in both the number and dollar value of claims filed after treatment for substance abuse. Most states have laws requiring that hospital and medical staff report any suspected addictive behavior. Failure to report may have significant consequences depending on individual state statutes. The most frequently employed methods are falsely recording drug administration, improperly filling out the anesthesia record, and keeping rather than wasting leftover drugs. In addition, recent reports have highlighted a new practice involving secretly accessing multidose vials and then refilling and resealing them with other substances. It is important to be wary of the faculty member or resident who is too anxious to give breaks to others or who volunteers to take late cases. One of the most frequently reported retrospective markers of addictive behavior was the desire to work overtime, particularly during periods when supervision might be reduced, such as evenings and weekends. Classically, these behaviors include wide mood swings, such as periods of depression, anger, and irritability alternating with periods of euphoria. Key points to remember about addictive behavior include the following: n n n n n Denial is universal. Symptoms at work are the last to appear (symptoms appear first in the community and then at home). The following is a list of the most frequently overlooked symptoms of addictive behavior: n n n Desire to work alone Refusal of lunch relief or breaks Frequent offers to relieve others the process for dealing with suspected substance abuse by an anesthesiologist will be significantly affected by the presence or absence of a physician assistance committee. If an institution does not have such a committee, one should be formed and policies developed so that the support required by an impaired physician is in place when it is needed. In addition, this group should have a consulting agreement with local addiction specialists with experience in treating and referring physicians.
Cerebrovascular accidents may result from air or thrombotic emboli that occur during surgical resection of the diseased aorta diabetes test pancreas buy generic micronase 5mg online. Patients with co-existing cerebrovascular disease may be more vulnerable to the development of new central nervous system complications diabetes testing supplies order micronase 5mg amex. Spinal cord injury may manifest during the period immediately after surgery as paraparesis or flaccid paralysis diabetes test at doctors generic micronase 5 mg on line. Delayed appearance of paraplegia (12 hours to 21 days postoperatively) has been associated with postoperative hypotension in patients with severe atherosclerotic disease in whom marginally adequate collateral circulation to the spinal cord is present diabetes mellitus type 2 epocrates buy discount micronase 2.5 mg. Systemic hypertension is not uncommon and may jeopardize the integrity of the surgical repair and/or predispose to myocardial ischemia. Institution of antihypertensive therapy with drugs such as nitroglycerin, nitroprusside, and labetalol may be appropriate. Some patients benefit from concomitant administration of -blockers to attenuate manifestations of a hyperdynamic circulation. A familial component has also been identified, because 12% to 19% of first-degree relatives (usually men) of a patient with an abdominal aortic aneurysm will develop an aneurysm. Specific genetic markers and biochemical changes that produce this pathologic condition remain to be elucidated. Diagnosis Abdominal aortic aneurysms are usually detected as asymptomatic, pulsatile abdominal masses. Abdominal ultrasonography is a very sensitive test for the detection of abdominal aortic aneurysms. Treatment Surgery is usually recommended for abdominal aortic aneurysms larger than 5. This recommendation is based on clinical studies indicating that the risk of rupture within a 5-year period is 25% to 41% for aneurysms larger than 5 cm. Each patient must be evaluated for the presence of risk factors for accelerated aneurysm growth and rupture, such as tobacco use and family history. Surgical risk and overall health are also part of the evaluation to determine the timing of aneurysm repair. This atherosclerosis involves several highly interrelated processes, including lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, vascular smooth muscle cell activation, altered matrix metabolism, remodeling, and genetic factors. Atherosclerosis represents a response to vessel wall injury caused by processes such as infection, inflammation, increased protease activity within the arterial wall, genetically regulated defects in collagen and fibrillin, and mechanical factors. The primary event in the development of an abdominal aortic aneurysm is proteolytic degradation of the extracellular matrix proteins elastin and collagen. Various proteolytic enzymes, including matrix metalloproteinases, play critical roles during degradation and remodeling of the aortic wall. Oxidative stress, lymphocytic and monocytic infiltration with immunoglobulin deposition in the aortic wall, and biomechanical wall stress also contribute to the Preoperative Evaluation Co-existing medical conditions, especially coronary artery disease, chronic obstructive pulmonary disease, and renal dysfunction, are important to identify preoperatively in an attempt to minimize postoperative complications. Myocardial ischemia or infarction is responsible for most postoperative deaths following elective abdominal aortic aneurysm resection. Other postoperative cardiac events include cardiac dysrhythmias and congestive heart failure. Preoperative evaluation of cardiac function might include exercise or pharmacologic stress testing with or without echocardiography or radionuclide imaging. Rupture of an Abdominal Aortic Aneurysm the classic triad (hypotension, back pain, and a pulsatile abdominal mass) is present in only approximately half of patients who have a ruptured abdominal aortic aneurysm. Renal colic, diverticulitis, and gastrointestinal hemorrhage may be confused with a ruptured abdominal aortic aneurysm. Although hypovolemic shock may be present, exsanguination may be prevented by clotting and the tamponade effect of the retroperitoneum. Euvolemic resuscitation may be deferred until the aortic rupture is surgically controlled in the operating room, because euvolemic resuscitation and the resultant increase in blood pressure without surgical control of bleeding may lead to loss of retroperitoneal tamponade, further bleeding, hypotension, and death. Patients in unstable condition who have a suspected ruptured abdominal aortic aneurysm require immediate operation and control of the proximal aorta without preoperative confirmatory testing or optimal volume resuscitation. Management of Anesthesia Management of anesthesia for resection of an abdominal aortic aneurysm requires consideration of commonly associated medical conditions in this patient group: ischemic heart disease, hypertension, chronic obstructive pulmonary disease, diabetes mellitus, and renal dysfunction. Monitoring of intravascular volume and cardiac, pulmonary, and renal function is essential during the perioperative period. Pulmonary artery catheterization is indicated in most patients, because it is not always possible to predict whether central venous pressure will parallel left ventricular filling pressure, particularly in patients with previous myocardial infarction, angina pectoris, or congestive heart failure. If appropriate personnel and equipment are available, echocardiography can be very useful for evaluating the cardiac response to aortic cross-clamping and unclamping, and assessing left ventricular filling volume and regional and global myocardial function. No single anesthetic drug or technique is ideal for all patients undergoing elective abdominal aortic aneurysm repair. Combinations of volatile anesthetics and/or opioids are commonly used with or without nitrous oxide. Continuous epidural anesthesia combined with general anesthesia may offer advantages by decreasing overall anesthetic drug requirements, attenuating the increased systemic vascular resistance associated with aortic cross-clamping, and facilitating postoperative pain management. Nevertheless, there is no evidence that the combination of epidural anesthesia and general anesthesia decreases postoperative cardiac or pulmonary morbidity compared with general anesthesia alone in high-risk patients who undergo aortic surgery. Postoperative epidural analgesia may favorably influence the postoperative course, however. Administration of anticoagulants during abdominal aortic surgery raises the controversial issue of placement of an epidural catheter and the remote risk of epidural hematoma formation. Patients undergoing abdominal aortic aneurysm repair usually experience significant fluid and blood losses. Administration of a combination of balanced salt and colloid solutions (and blood if needed) guided by appropriate monitoring of cardiac and renal function facilitates maintenance of adequate intravascular volume, cardiac output, and urine formation. Balanced salt and/or colloid solutions should be infused during aortic cross-clamping to build up an intravascular volume reserve and thereby minimize unclamping hypotension.
