Rajesh Gutta, BDS, MS

• Assistant Professor, Division of Oral and Maxillofacial
• Surgery, Department of Surgery, University of Cincinnati
• Cincinnati, Ohio

Sodium bicarbonate is often used antibiotic yeast cheap roxithromycin on line, particularly for persistent severe metabolic acidosis (pH <7 antibiotics for sinus infection how long purchase roxithromycin australia. Calcium chloride may be necessary when symptomatic hypocalcemia follows massive transfusion of citrated blood products antibiotic resistance rates roxithromycin 150mg mastercard. The incidence of transient postoperative deficits and postoperative paraplegia are 11% and 6% antibiotic bladder infection discount roxithromycin 150mg with visa, respectively do they give antibiotics for sinus infection order roxithromycin with amex. Increased rates are associated with cross-clamping periods longer than 30 min treatment for upper uti buy roxithromycin 150 mg otc, extensive surgical dissections, and emergency procedures. The classic deficit is an anterior spinal artery syndrome with loss of motor function and pinprick sensation but preservation of vibration and proprioception. Anatomic variations in spinal cord blood supply are responsible for the unpredictable occurrence and variable nature of deficits. The spinal cord receives its blood supply from the vertebral arteries and from the thoracic and abdominal aorta. Intercostal arteries feed the anterior and posterior arteries in the upper thoracic aorta. Textbook descriptions suggest that in the lower thoracic and lumbar cord, the anterior spinal artery is supplied by the thoracolumbar artery of Adamkiewicz. It may be damaged during surgical dissection or occluded by the aortic cross-clamping. Monitoring motor and somatosensory evoked potentials may be useful in preventing paraplegia, but clearly surgical technique and speed are most important. It is usually positioned proximally in the left ventricular apex and distally in a femoral artery. The excessive use of vasodilators to control the hypertensive response to cross-clamping may be a contributing factor in spinal cord ischemia, as drug actions also occur distal to the cross-clamp. Excessive reduction in blood pressure above the cross-clamp should therefore be avoided to prevent inadequate blood flow and excessive hypotension below it. A variety of "cocktails" have been employed in the hope of reducing the risk of kidney failure, including infusion of mannitol (0. Surgery on the Abdominal Aorta Stents are most often placed via catheters inserted in a femoral artery. When an open technique is chosen, either an anterior transperitoneal or an anterolateral retroperitoneal approach can be used to access the abdominal aorta. Depending on the location of the lesion, the cross-clamp can be applied to the supraceliac, suprarenal, or infrarenal aorta. In general, the more distally the clamp is applied to the aorta, the less the effect on left ventricular afterload. In fact, occlusion of the infrarenal aorta frequently results in minimal hemodynamic changes. In contrast, release of the clamp usually produces hypotension; the same techniques that were described earlier may be used to counteract the effects of unclamping. The large incision and extensive retroperitoneal surgical dissection increase fluid requirements beyond intraoperative blood loss. We recommend colloid to maintain intravascular volume and crystalloid for maintenance fluids. Clamping of the infrarenal aorta decreases renal blood flow, which may contribute to postoperative kidney failure. Some centers use continuous epidural anesthesia combined with general anesthesia for abdominal aortic surgery. This combined technique decreases the general anesthetic requirement and appears to suppress the release of stress hormones. It also provides an excellent route for administering postoperative epidural analgesia. Postoperative Considerations Those undergoing stenting may not require intubation either during or after the procedure. Most patients undergoing open surgery on the ascending aorta, the arch, or the thoracic aorta will remain intubated and ventilated for 1 to 24 h postoperatively. As with cardiac surgery, the initial emphasis in their postoperative care should be on hemodynamic stability and monitoring for postoperative bleeding. Patients undergoing open abdominal aortic surgery may be extubated at the end of the procedure. Ischemic strokes are usually the result of embolism or (less commonly) thrombosis in one of the blood vessels supplying the brain. By convention, a stroke is defined as a neurological deficit that lasts more than 24 h; its pathological correlate is typically focal infarction of brain. When a stroke is associated with progressive worsening of signs and symptoms, it is frequently termed a stroke in evolution. A second distinction is also often made between complete and incomplete strokes, based on whether the territory involved is completely affected or additional brain remains at risk for focal ischemia (eg, hemiplegia versus hemiparesis). The mechanism may be embolization of platelet-fibrin or plaque material, stenosis, or complete occlusion. Emboli distal to regions lacking collateral blood flow are more likely to produce symptoms. Small emboli in the ophthalmic branches can cause transient monocular blindness (amaurosis fugax). Larger emboli usually enter the middle cerebral artery, producing contralateral motor and sensory deficits that primarily affect the arm and face. Emboli in the anterior cerebral artery territory typically result in contralateral motor and sensory deficits that are worse in the leg. In the past, carotid endarterectomy was recommended for asymptomatic but significantly stenotic lesions (>60%). Operative mortality for open surgery is 1% to 4% and is primarily due to cardiac complications (myocardial infarction). Perioperative morbidity is 4% to 10% and is principally neurological; patients with preexisting neurological deficits have the greatest risk of perioperative neurological events. Studies suggest that age greater than 75 years, symptomatic lesions, uncontrolled hypertension, angina, carotid thrombus, and occlusions near the carotid siphon increase operative risk. Preoperative Anesthetic Evaluation & Management Most patients undergoing carotid endarterectomy are elderly and hypertensive, with generalized arteriosclerosis. Most postoperative neurological deficits appear to be related to surgical technique. Patients should receive their usual cardiac medications on schedule until the time of surgery. Angina should be stable and controlled, and signs of overt congestive heart failure should be absent. Because most patients are elderly, enhanced sensitivity to premedication should be expected. General Anesthesia 18 the emphasis of anesthetic management dur- ing carotid surgery is on maintaining adequate perfusion to the brain and heart. Traditionally, this is accomplished by close regulation of arterial blood pressure and avoidance of tachycardia. Carotid endarterectomy is not usually associated with significant blood loss or fluid shifts. Propofol and etomidate are popular choices for induction because they reduce cerebral metabolic rate proportionately more than cerebral blood flow. Small doses of an opioid or -adrenergic blocker can be used to blunt the hypertensive response to endotracheal intubation. In theory, isoflurane may be the volatile agent of choice because it appears to provide the greatest protection against cerebral ischemia. However, we do not regard the differences in neuroprotection among inhaled agents as clinically important. Intraoperative hypertension is common and generally necessitates the use of an intravenous vasodilator. Nitroglycerin is usually a good choice for mild to moderate hypertension because of its beneficial effects on the coronary circulation. Marked hypertension requires a more potent agent, such as nicardipine, nitroprusside, or clevidipine. Many clinicians consider phenylephrine the vasopressor of choice; if selected, it should be administered in small increments to prevent excessive hypertension. Pronounced or sustained reflex bradycardia or heart block caused by manipulation of the carotid baroreceptor can be treated with atropine. To prevent this response, some surgeons infiltrate the area of the carotid sinus with lidocaine, but the infiltration itself can induce bradycardia. Maintenance intravenous fluids should consist of glucose-free solutions because of the potentially adverse effects of hyperglycemia. Rapid emergence from anesthesia is desirable because it allows immediate neurological assessment, but the clinician must be prepared to treat hypertension and tachycardia. Postoperative hypertension may be related to surgical denervation of the ipsilateral carotid baroreceptor. Following extubation, patients should be observed closely for the development of a wound hematoma. When an expanding wound hematoma compromises the airway, the initial treatment maneuver may require opening the wound to release the hematoma. Transient postoperative hoarseness and ipsilateral deviation of the tongue may be noted; they are due to intraoperative retraction of the recurrent laryngeal or hypoglossal nerves, respectively. Monitoring Cerebral Function Unless regional anesthesia is used, indirect methods must be relied upon to assess the adequacy of cerebral perfusion during carotid cross-clamping. A distal stump pressure of less than 50 mm Hg has traditionally been used as an indication for a shunt. Electrophysiological signs of ischemia (or a marked decline in cerebral oxygen saturation) after cross-clamping dictate the use of a shunt; changes lasting more than 10 min may be associated with a new postoperative neurological deficit. Other techniques, including measurements of regional cerebral blood flow with radioactive xenon-133, transcranial Doppler measurement of middle cerebral artery flow velocity, cerebral oximetry, jugular venous oxygen saturation, and transconjunctival oxygen tension, are also not sufficiently reliable. Regional anesthesia for carotid surgery requires the cooperation of the surgeon and patient. It is not effective for arrhythmias from enhanced automaticity (multifocal atrial tachycardia) or triggered activity (digitalis toxicity). Specific indications for cardioversion of patients with atrial fibrillation include symptomatic fibrillation, recent onset, and no response to medications. Patients with long-standing fibrillation, a large atrium, chronic obstructive lung disease, congestive heart failure, or mitral regurgitation have a high recurrence rate. Such clots are typically located in the left atrial appendage and can be embolized by the cardioversion procedure or by sinus rhythm. Emergency cardioversion is indicated for any tachyarrhythmia associated with hypotension, congestive heart failure, or angina. Anesthesiologists Regional Anesthesia Carotid surgery may be performed under regional anesthesia. A substantial fraction of patients will require administration of local anesthetic by the surgeon into the carotid sheath (whether or not a deep cervical block is performed). The principal advantage of regional anesthesia (and it is a tremendous advantage) is that the patient can be examined intraoperatively; thus, the need for a temporary shunt can be assessed and any new neurological deficits diagnosed immediately during surgery. In fact, intraoperative neurological examination may be the most reliable method for assessing the adequacy of cerebral perfusion during carotid cross-clamping. The examination minimally consists of level of consciousness, speech, and contralateral handgrip. Experienced clinicians use minimal sedation and "cocktail conversation" with the patient to monitor the neurological status. Larger paddles help reduce any shock-induced myocardial necrosis by distributing the current over a wider area. The energy output should be kept at the minimally effective level to prevent myocardial damage. In the first position, one electrode is placed on the right second intercostal space next to the sternum and the other is placed on the left fifth intercostal space in the midclavicular line. When pads are used for the anteroposterior technique, one is placed anteriorly over the ventricular apex in the fifth intercostal space and the other underneath the patient in the left infrascapular region. For supraventricular tachycardias, with the notable exception of atrial fibrillation, energy levels of 25 to 50 J can successfully reestablish normal sinus rhythm. Synchronized shocks should be used for all tachyarrhythmias except ventricular fibrillation. All medical personnel should stand clear of the patient and the bed during the shock. Atrial fibrillation usually requires a minimum of 50 to 100 J, and larger energy levels are often used. Hemodynamically stable ventricular tachycardia can often be terminated with 25 to 50 J, but ventricular fibrillation and unstable ventricular tachycardia require 200 to 360 J. Regardless of the arrhythmia, a higher energy level is necessary when the first shock is ineffective. Elective cardioversion can be performed in any setting in which full provisions for cardiopulmonary resuscitation, including cardiac pacing capabilities, are immediately available. The patient should be fasted, evaluated, and treated as though he were receiving a general anesthetic in the operating room. If not corrected preoperatively, they can reinitiate the tachycardia following cardioversion. An antiarrhythmic agent is often started in patients with atrial fibrillation 1 to 2 days prior to the procedure to help maintain normal sinus rhythm.

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Intensive care unit-acquired hypernatremia is an independent predictor of increased mortality and length of stay antibiotics kills good bacteria order roxithromycin pills in toronto. Vomiting or continuous loss of gastric fluid by gastric drainage (nasogastric suctioning) can result in marked metabolic alkalosis antibiotic herbs infections roxithromycin 150 mg with visa, extracellular volume depletion antimicrobial jacket order 150mg roxithromycin with mastercard, and hypokalemia antibiotics invented buy 150 mg roxithromycin otc. Nearly all biochemical reactions in the body are dependent on maintenance of a physiological hydrogen ion concentration antibiotics for sinus infection in horses roxithromycin 150 mg for sale, and alterations beyond normal hydrogen ion concentration are associated with widespread organ dysfunction antibiotics long term effects order roxithromycin 150mg free shipping. A strong acid is a substance that readily and almost irreversibly gives up an H+ and increases [H+], whereas a strong base avidly binds H+ and decreases [H+]. In contrast, weak acids reversibly donate H+, whereas weak bases reversibly bind H+; both weak acids and bases tend to have less of an effect on [H+] (for a given concentration of the parent compound) than do strong acids and bases. Hydrogen ions are created or consumed based on changes in the dissociation of water. A buffer is a solution that contains a weak acid and its conjugate base or a weak base and its conjugate acid (conjugate pairs). Buffers minimize any change in [H+] by readily accepting or giving up hydrogen ions. Moreover, the conjugate pair must be present in significant quantities in solution to act as an effective buffer. The suffix "-osis" is used here to denote any pathological process that alters arterial pH. Thus, any disorder that tends to reduce pH to a less than normal value is an acidosis, whereas one tending to increase pH is termed an alkalosis. Secondary compensatory responses (discussed in the next section) should be referred to as just that and not as an "-osis. The suffix "-emia" is used to denote the net effect of all primary processes and compensatory physiological responses (described next) on arterial blood pH. The effectiveness of these buffers in the various fluid compartments is related to their concentration. Hemoglobin, though restricted inside red blood cells, also functions as an important buffer in blood. Other proteins probably play a major role in buffering the intracellular fluid compartment. Buffering of the extracellular compartment can also be accomplished by the exchange of extracellular H+ for Na+ and Ca2+ ions from bone and by the exchange of extracellular H+ for intracellular K+. Buffering by plasma bicarbonate is almost immediate, whereas that due to interstitial bicarbonate requires 15 to 20 min. Up to 50% to 60% of acid loads may ultimately be buffered by bone and intracellular buffers. The respiratory response to lower the Paco2 occurs rapidly but may not reach a predictably steady state until 12 to 24 h; pH is never completely restored to normal. Hemoglobin as a Buffer Hemoglobin is rich in histidine, which is an effective buffer from pH 5. The resulting alveolar hypoventilation tends to elevate Paco2 and restore arterial pH toward normal. The respiratory response to metabolic alkalosis is generally less predictable than the respiratory response to metabolic acidosis. Hypoxemia, as a result of progressive hypoventilation, eventually activates oxygen-sensitive chemoreceptors; the latter stimulates ventilation and limits the compensatory respiratory response. Consequently, Paco2 usually does not increase above 55 mm Hg in response to 4 metabolic alkalosis. Minute ventilation increases 1 to 4 L/min for every (acute) 1 mm Hg increase in Paco2. Respiratory compensatory responses are also important in defending against marked changes in pH during metabolic disturbances. The kidneys are responsible for eliminating the approximately 1 mEq/kg per day of sulfuric acid, phosphoric acid, uric acid, and incompletely oxidized organic acids that are normally produced by the metabolism of dietary and endogenous proteins, nucleoproteins, and organic phosphates (from phosphoproteins and phospholipids). Incomplete metabolisms of fatty acids and glucose produces keto acids and lactic acid. Endogenous bases are produced during the metabolism of some anionic amino acids (eg, glutamate and aspartate) and other organic compounds (eg, citrate, acetate, and lactate), but the quantity is insufficient to offset the endogenous acid production. Respiratory Compensation During Metabolic Acidosis Decreases in arterial blood pH stimulate medullary respiratory centers. Although these mechanisms are probably activated immediately, their effects are generally not appreciable for 12 to 24 h and may not be maximal for up to 5 days. The proximal tubules normally reabsorb 80% to 90% of the filtered bicarbonate load along with sodium, whereas the distal tubules are responsible for the remaining 10% to 20%. Unlike the proximal H+ pump, the H+ pump in the distal tubule is not necessarily linked to sodium reabsorption and is capable of generating steep H+ gradients between tubular fluid and tubular cells. As a result, the kidneys are highly effective in protecting against metabolic alkalosis, which therefore generally occurs only in association with concomitant sodium deficiency or mineralocorticoid excess. Sodium depletion decreases extracellular fluid volume and enhances Na+ reabsorption in the proximal tubule. Similarly, increased mineralocorticoid activity augments aldosterone-mediated Na+ reabsorption in exchange for H+ secretion in the distal tubules. Metabolic alkalosis is commonly associated with increased mineralocorticoid activity, even in the absence of sodium and chloride depletion. Renal tubule Peritubular capillary Base Excess Base excess is defined as the amount of acid or base (expressed in mEq/L) that must be added for blood pH to return to 7. A positive value indicates metabolic alkalosis, whereas a negative value reveals metabolic acidosis. Base excess is usually derived from a nomogram and requires measurement of hemoglobin concentration. The overall effects of acidemia represent the balance between the direct biochemical effects of H+ and the effects of acidemia-induced sympathoadrenal activation. Severe acidosis can lead to tissue hypoxia, despite a rightward shift in hemoglobin affinity for oxygen. Both cardiac and vascular smooth muscle become less responsive to endogenous and exogenous catecholamines, and the ventricular fibrillation threshold is decreased. The movement of K+ out of cells in exchange for increased extracellular H+ results in hyperkalemia that is also potentially lethal. Central nervous system depression is more prominent with respiratory acidosis than with metabolic acidosis. Chronic Respiratory Acidosis Renal compensation in respiratory acidosis is appreciable only after 12 to 24 h and may not be maximal 6 until 3 to 5 days have elapsed. Tromethamine has the added advantage of lacking sodium and may be a more effective intracellular buffer. Oxygen therapy must also be carefully controlled, because the respiratory drive in these patients may be dependent on hypoxemia, not Paco2. Potential temporizing measures aimed at improving alveolar ventilation (in addition to controlled mechanical ventilation) include bronchodilation, reversal of narcosis, or improving lung compliance via diuresis. An increased inspired oxygen concentration is also usually necessary, as coexistent hypoxemia is common. Note that differential diagnosis of metabolic acidosis may be facilitated by calculation of the anion gap. Using normal values, Anion gap = 140 - (104 + 24) = 12 mEq/L (Normal range = 7 - 14 mEq/L) In reality, an anion gap cannot exist because electroneutrality must be maintained in the body; the sum of all anions must equal the sum of all cations. Plasma albumin normally accounts for the largest fraction of the anion gap (approximately 11 mEq/L). Any process that increases "unmeasured anions" or decreases "unmeasured cations" will increase the anion gap. Conversely, any process that decreases "unmeasured anions" or increases "unmeasured cations" will decrease the anion gap. Mild elevations of plasma anion gap up to 20 mEq/L may not be helpful diagnostically during acidosis, but values greater than 30 mEq/L usually indicate the presence of a high anion gap acidosis. Metabolic alkalosis can also produce a high anion gap because of extracellular volume depletion, an increased charge on albumin, and a compensatory increase in lactate production. A low plasma anion gap may be encountered with hypoalbuminemia, bromide or lithium intoxication, and multiple myeloma. Failure to Excrete Endogenous Nonvolatile Acids Endogenously produced organic acids are normally eliminated by the kidneys in urine (as described earlier). Glomerular filtration rates below 20 mL/min (kidney injury or failure) typically result in progressive metabolic acidosis from the accumulation of these acids. Increased Endogenous Nonvolatile Acid Production Severe tissue hypoxia following hypoxemia, hypoperfusion (ischemia), or an inability to utilize oxygen (cyanide poisoning) can result in lactic acidosis. Decreased utilization of lactate by the liver, and, to a lesser extent by the kidneys, is less commonly responsible for lactic acidosis; causes include hypoperfusion, alcoholism, and liver disease. Acidosis resulting from D-lactic acid, which is not recognized by -lactate dehydrogenase (and not measured by routine assays), may be encountered in patients with short bowel syndromes; D-lactic acid is formed by colonic bacteria from dietary glucose and starch and is absorbed systemically. An absolute or relative lack of insulin can result in hyperglycemia and progressive ketoacidosis from the accumulation of -hydroxybutyric and acetoacetic acids (diabetic ketoacidosis). The pathophysiology of the acidosis often associated with severe alcoholic intoxication and nonketotic hyperosmolar coma is complex and may represent a buildup of lactic, keto, or other unknown acids. Some inborn errors of metabolism, such as maple syrup urine disease, methylmalonic aciduria, propionic acidemia, and isovaleric acidemia, produce a high anion gap metabolic acidosis as a result of accumulation of abnormal amino acids. Normal Anion Gap Metabolic Acidosis Metabolic acidosis associated with a normal anion gap is typically characterized by hyperchloremia. Calculation of the anion gap in urine can be helpful in diagnosing a normal anion gap acidosis. Ingestion of Exogenous Nonvolatile Acids Ingestion of large amounts of salicylates may result in metabolic acidosis. Salicylic acid and other acid intermediates rapidly accumulate and produce a high anion gap acidosis. Because salicylates also produce direct respiratory stimulation, most adults develop mixed metabolic acidosis with superimposed respiratory alkalosis. Ingestion of methanol (methyl alcohol) frequently produces acidosis and retinitis. Symptoms are typically delayed until the slow oxidation of methanol by alcohol dehydrogenase produces formic acid, which is highly toxic to the retina. The high anion gap represents the accumulation of many organic acids, including acetic acid. The toxicity of ethylene glycol is also the result of the action of alcohol dehydrogenase to produce glycolic acid. Loss of large volumes of these fluids can lead to hyperchloremic metabolic acidosis. Patients with ureterosigmoidostomies and those with ileal loop neobladders that are too long or that become partially obstructed frequently develop hyperchloremic metabolic acidosis. The ingestion of chloride-containing anion-exchange resins (cholestyramine) or large amounts of calcium or magnesium chloride can result in increased absorption of chloride and loss of bicarbonate ions. The nonabsorbable resins bind bicarbonate ions, whereas calcium and magnesium combine with bicarbonate to form insoluble salts within the intestines. These defects are encountered in patients taking carbonic anhydrase inhibitors, such as acetazolamide, and in those with renal tubular acidosis. The kidneys are unable to adequately acidify the urine, and urinary pH is inappropriately high relative to the systemic acidemia. Other Causes of Hyperchloremic Acidosis Dilutional hyperchloremic acidosis may occur when extracellular volume is rapidly expanded with a bicarbonate-free, chloride-rich fluid such as normal saline. Amino acid infusions (parenteral hyperalimentation) contain organic cations in excess of organic anions and can produce hyperchloremic metabolic acidosis because chloride is commonly used as the anion for the cationic amino acids. Lastly, the administration of excessive quantities of chloride-containing acids, such as ammonium chloride or arginine hydrochloride (usually given to treat a metabolic alkalosis), can cause hyperchloremic metabolic acidosis. In either case, serial blood gas measurements are mandatory to avoid complications (eg, overshoot alkalosis and sodium overload) and to guide further therapy. Profound or refractory acidemia may require acute hemodialysis with a bicarbonate dialysate. Specific therapy for diabetic ketoacidosis includes replacement of the existing fluid deficit resulting from a hyperglycemic osmotic diuresis first, as well as insulin, potassium, phosphate, and magnesium. The treatment of lactic acidosis should be directed first at restoring adequate oxygenation and tissue perfusion.

A mechanism to ensure the timely arrival of anesthesia personnel capable of airway rescue must likewise be incorporated into such policies antibiotics for cats buy roxithromycin once a day. Post-procedure disposition (whether discharge or admission) needs appropriate coordination by the anesthesiologist for postanesthesia care or safe transport from the remote unit antibiotic stewardship buy generic roxithromycin 150mg line, or both antibiotics for dogs safe for humans 150mg roxithromycin amex. Patients undergoing cardiac catheterization are routinely sedated by cardiologists without involvement of an anesthesiologist infection knee replacement symptoms 150mg roxithromycin for sale. Occasionally bacteria vaginosis icd 9 generic 150mg roxithromycin with visa, a patient with significant comorbidities (eg antibiotics for sinus infection bronchitis order 150mg roxithromycin mastercard, morbid obesity) requires the presence of a qualified anesthesia provider. General anesthesia is sometimes required for placement of aortic stents, which are increasingly performed by cardiologists in the cardiac catheterization laboratory. Specially built hybrid surgical suites enable both open and catheter-based vascular repairs. Increasingly, patients for transcatheter aortic valve replacement are managed with local anesthesia and sedation rather than general anesthesia. Institutional protocols and patient characteristics determine the anesthetic/sedation management of these patients. General anesthesia is frequently administered to patients in the neurointerventional suite for treatment of cerebral aneurysms and ischemic strokes. Patients requiring electrophysiology procedures for catheter-mediated arrhythmia ablation often need general anesthesia. Such patients may have both systolic and diastolic heart failure, leading to potential hemodynamic difficulties perioperatively. Sudden hypotension can herald the development of pericardial tamponade secondary to catheter perforation of the heart. During testing, deeper levels of sedation are required, as the defibrillation shock can be frightening and very uncomfortable. Likewise, anesthesia staff are called upon to provide anesthesia for cardioversion of patients in atrial fibrillation. These patients usually have associated cardiac diseases and require brief intravenous anesthetics to facilitate cardioversion. Oftentimes, a transesophageal echocardiogram must be performed prior to cardioversion to rule out clot in the left atrial appendage. Determination as to whether a patient needs sedation or general anesthesia with or without intubation is dependent upon routine patient assessment. Most institutions have policies and training protocols to prevent catastrophes (eg, oxygen tanks flying into the scanner). Both deep sedation and general anesthesia approaches with intubation or supraglottic airways can be used, depending on practitioner preference and patient requirements. Patients often require general anesthesia and tight blood pressure control to facilitate coiling and embolization of cerebral aneurysms, arteriovenous malformations, or stenting and clot removal for acute strokes. Patient comorbidity, drug interactions with various psychotropic medications, multiple anesthetic procedures, and effects of anesthetic agents on the quality of electroconvulsive therapy also need to be considered (see Chapter 28). Given the usual need for long immobilization, potential risk of aspiration, and significant comorbidity, general anesthesia is often the recommended anesthetic plan. Preoperative considerations include risk of aspiration, gastrointestinal bleeding, decreased functional residual capacity from ascites, pleural effusions, coagulopathy, thrombocytopenia, and hepatic encephalopathy. Intraoperative considerations should include careful hemodynamic monitoring (usually via arterial catheter) and frequent measurement of blood gases, electrolytes, and coagulation parameters. Altered pharmacokinetics of anesthetic agents from liver failure should also be kept in mind. The patient is induced with etomidate, fentanyl, and succinylcholine, using rapid sequence induction; atraumatic intubation is accomplished uneventfully. Administration of albumin may mitigate the hemodynamic effects of large volume paracentesis. Hemodynamically, this allows immediate decompression of portal hypertension by partial or complete diversion of portal flow from hepatic sinusoids into the inferior vena cava and the systemic circulation. Society of Anesthesia and Sleep Medicine guidelines on preoperative screening and assessment of adult patients with obstructive sleep apnea. Society for Ambulatory Anesthesia consensus statement on preoperative selection of adult patients with obstructive sleep apnea scheduled for ambulatory surgery. A systemic review of obstructive sleep apnea and its implications for anesthesiologists. Perioperative complications in obstructive sleep apnea patients undergoing surgery; a review of the legal literature. Risks of anesthesia or sedation outside the operating room: the role of the anesthesia care provider. Ambulatory anesthesia for the cardiac catheterization and electrophysiology laboratories. Beta blockers, calcium channel blockers, angiotensin converting enzyme inhibitors and angiotensin receptor blockers: Should they be stopped or not before ambulatory anaesthesia The effects of oral ibuprofen and celecoxib in preventing pain, improving recovery outcomes and patient satisfaction after ambulatory surgery. Neuraxial anesthesia may also be used simultaneously with general anesthesia or afterward for postoperative analgesia. Performing a lumbar (subarachnoid) spinal puncture below L1 in an adult (L3 in a child) usually avoids potential needle trauma to the spinal cord. The principal site of action for neuraxial blockade is believed to be the nerve root, at least during initial onset of block. Differential blockade typically results in sympathetic blockade (judged by temperature sensitivity) that may be two segments or more cephalad than the sensory block (pain, light touch), which, in turn, is usually several segments more cephalad than the motor blockade. Interruption of efferent autonomic transmission at the spinal nerve roots during neuraxial blocks produces sympathetic blockade. Neuraxial blocks typically produce variable decreases in blood pressure that may be accompanied by a decrease in heart rate. Deleterious cardiovascular effects should be anticipated and steps undertaken to minimize the degree of hypotension. However, volume loading with 10 to 20 mL/kg of intravenous fluid in a healthy patient before initiation of the block has been shown repeatedly to fail to prevent hypotension (in the absence of preexisting hypovolemia). Major contraindications to neuraxial anesthesia include lack of consent, coagulation abnormalities, severe hypovolemia, elevated intracranial pressure, and infection at the site of injection. Spinal, caudal, and epidural blocks were first used for surgical procedures at the turn of the twentieth century. These central blocks were widely used worldwide until reports of permanent neurological injury appeared, most prominently in the United Kingdom. However, a large-scale epidemiological study conducted in the 1950s proved that complications were rare when these blocks were performed skillfully, with attention to asepsis, and when newer, safer local anesthetics were used. Today, neuraxial blocks are routinely employed for labor analgesia, cesarian delivery, orthopedic surgery, perioperative analgesia, and chronic pain management. However, they are still associated with various complications, and much literature has examined the incidence of complications following neuraxial blocks associated with different disease states. Neuraxial anesthesia may be used simultaneously with general anesthesia or afterward for postoperative analgesia. Neuraxial blocks can be performed as a single injection or with a catheter to allow intermittent boluses or continuous infusions. Adverse reactions and complications associated with regional anesthesia range from self-limited back soreness to debilitating permanent neurological deficits and even death. The practitioner must therefore be thoroughly familiar with the anatomy involved and the pharmacology and toxic dosages of the agents employed. The practitioner must diligently employ sterile techniques and quickly address physiological derangements arising from neuraxial techniques. Some less convincing studies suggest that neuraxial blocks are associated with reduced perioperative mortality. Neuraxial blocks may also allow earlier return of gastrointestinal function following surgery. Proposed mechanisms (in addition to avoidance of larger doses of anesthetics and opioids) include reducing the hypercoagulable state associated with surgery, increasing tissue blood flow, improving oxygenation from decreased splinting, enhancing peristalsis, and suppressing the neuroendocrine stress response to surgery. Reduction of parenteral opioid administration may decrease the incidence of atelectasis, hypoventilation, and aspiration pneumonia and reduce the duration of ileus. Postoperative epidural analgesia may also significantly reduce both the need for mechanical ventilation and the time until extubation after major abdominal or thoracic surgery. Deep anesthesia can readily cause hypotension, whereas light anesthesia relative to the level of stimulation causes hypertension and tachycardia. Research is ongoing to discern if neuraxial techniques offer survival and other benefits to patients compared with general anesthetics for major operations such as open reduction and internal fixation of femoral neck fractures. The Obstetric Patient Currently, epidural anesthesia is widely used for analgesia in women in labor and during vaginal delivery. Large population studies in Great Britain and the United States have shown that regional anesthesia for cesarean delivery is associated with less maternal morbidity and mortality than is general anesthesia. This may be largely due to a reduction in the incidence of pulmonary aspiration and failed intubation when neuraxial anesthesia is employed. Fortunately, the increased availability of video laryngoscopes may also reduce the incidence of adverse outcomes related to airway difficulties associated with general anesthesia for cesarean delivery. The Sick Elderly Patient Anesthesiologists are all too familiar with situations in which a consultant "clears" a sick elderly patient with significant cardiac disease for surgery "under spinal anesthesia. Unfortunately, many patients will require some sedation during the procedure, either for comfort or to facilitate cooperation. Is spinal anesthesia always safer in a patient with severe coronary artery disease or with a decreased ejection fraction Ideally, an anesthetic technique should produce neither hypotension (which decreases myocardial perfusion pressure) nor hypertension and tachycardia (which increase myocardial oxygen consumption). Administration of large intravenous volumes may lead to fluid overload in the elderly patient with diastolic dysfunction, especially after the sympathetic block resolves postoperatively. General anesthesia, on the other hand, also poses potential problems for patients with cardiac compromise. The sacrum is a fusion of 5 sacral (S) vertebrae, and there are small rudimentary coccygeal vertebrae. The spine as a whole provides structural support for the body and protection for the spinal cord and nerves and allows a degree of mobility in several spatial planes. The first cervical vertebra, the atlas, lacks a body and has unique articulations with the base of the skull and with the second vertebra. The second vertebra, called the axis, consequently has atypical articulating surfaces. The laminae extend between the transverse processes and the spinous processes, and the pedicle extends between the vertebral body and the transverse processes. There are four small synovial joints at each vertebra, two articulating with the vertebra above it and two with the vertebra below. The pedicles are notched superiorly and inferiorly, these notches forming the intervertebral foramina from which the spinal nerves exit. Sacral vertebrae normally fuse into one large bone, the sacrum, but each one retains discrete anterior and posterior intervertebral foramina. Ligamentous elements provide structural support, and, together with supporting muscles, help to maintain the unique shape. Dorsally, the ligamentum flavum, interspinous ligament, and supraspinous ligament provide additional stability. The pia mater is adherent to the spinal cord, whereas the arachnoid mater is usually adherent to the thicker and denser dura mater. The spinal subdural space is generally a poorly demarcated, potential space that exists between the dura and arachnoid membranes. At the cervical level, the nerves arise above their respective vertebrae, but starting at T1, exit below their vertebrae. As a result, there are eight cervical nerve roots, but only seven cervical vertebrae. But, because the spinal cord normally ends at L1, lower nerve roots course some distance before exiting the intervertebral foramina. Note the end of the spinal cord rises with development from approximately L3 to L1. Nerve blocks close to the intervertebral foramen therefore carry a risk of subdural or subarachnoid injection. The dural sac and the subarachnoid and subdural spaces usually extend to S2 in adults and often to S3 in children, important considerations in avoiding accidental dural puncture during caudal anesthesia. The anterior spinal artery is formed from the vertebral artery at the base of the skull and courses down along the anterior surface of the cord. The anterior spinal artery supplies the anterior two-thirds of the cord, whereas the two posterior spinal arteries supply the posterior one-third. The posterior spinal arteries arise from the posterior inferior cerebellar arteries and course down along the dorsal surface of the cord medial to the dorsal nerve roots. The anterior and posterior spinal arteries receive additional blood flow from the intercostal arteries in the thorax and the lumbar arteries in the abdomen. It is typically unilateral and nearly always arises on the left side, providing the major blood supply to the anterior, lower two-thirds of the spinal cord. Injury to this artery can result in the anterior spinal artery syndrome (see Chapter 22). B: Cross-sectional view through the spinal cord showing paired posterior spinal arteries and a single anterior spinal artery. In contrast, neuraxial block is achieved only with much larger volumes and quantities of local anesthetic molecules during epidural and caudal anesthesia. The injection site (level) for epidural anesthesia is ideally sited in the middle of the nerve roots that must be anesthetized. Blockade of neural transmission (conduction) in the posterior nerve root fibers interrupts somatic and visceral sensation, whereas blockade of anterior nerve root fibers prevents efferent motor and autonomic outflow.

Risk factors for postanesthetic apnea include a low gestational age at birth antibiotics for uti for elderly order roxithromycin 150mg online, anemia (<30%) antibiotic allergy cheap roxithromycin 150 mg without a prescription, hypothermia antibiotics for uti sulfa allergy buy generic roxithromycin 150 mg on line, sepsis infection treatment roxithromycin 150 mg online, and neurological abnormalities virus game buy roxithromycin 150 mg otc. The risk of postanesthetic apnea may be decreased by intravenous administration of caffeine (10 mg/kg) or aminophylline infection specialist doctor quality 150mg roxithromycin. Thus, elective (particularly outpatient) procedures should be deferred until the preterm infant reaches the age of at least 50 weeks postconception. A 6-month symptom-free interval has been suggested for infants with a history of apneic episodes or bronchopulmonary dysplasia. If surgery must be performed earlier, monitoring with pulse oximetry for 12 to 24 h postoperatively is mandatory for infants less than 50 weeks postconception; infants between 50 and 60 weeks postconception should be closely observed in the postanesthesia recovery unit for at least 2 h. Sick, premature neonates often receive multiple transfusions of blood during their stay in the intensive care nursery. Their immunocompromised status predisposes them to cytomegalovirus infection following transfusion. Preventive measures include transfusing only with leukocyte-reduced red blood cells. Most patients with malrotation of the midgut present during infancy with symptoms of bowel obstruction. Coiling of the duodenum with the ascending colon can produce complete or partial duodenal obstruction. The most serious complication of malrotation, a midgut volvulus, can rapidly compromise intestinal blood supply causing infarction. Midgut volvulus is a true surgical emergency that most commonly occurs in infancy, with up to one third occurring in the first week of life. Typical symptoms are bilious vomiting, progressive abdominal distention and tenderness, metabolic acidosis, and hemodynamic instability. Abdominal ultrasonography or upper gastrointestinal imaging confirms the diagnosis. Anesthetic Considerations Surgery provides the only definitive treatment of malrotation and midgut volvulus. Depending on the size of the patient, rapid sequence induction (or awake intubation) should be employed. Patients with volvulus are usually hypovolemic and acidotic, and may be prone to hypotension. Postoperative ventilation will often be necessary, making an opioid-based anesthetic a reasonable choice. Fluid resuscitation, likely including blood products, with correction of acidosis is usually necessary. Surgical treatment includes reducing the volvulus, freeing the obstruction, and resecting any obviously necrotic bowel. Bowel edema can complicate abdominal closure and has the potential to produce an abdominal compartment syndrome. The latter can impair ventilation, hinder venous return, and produce acute kidney injury; delayed fascial closure or temporary closure with a Silastic "silo" may be necessary. A second-look laparotomy may be required 24 to 48 h later to ensure viability of the remaining bowel and close the abdomen. Diaphragmatic hernia, often accompanied by marked pulmonary hypertension, is associated with 40% to 50% mortality. Cardiopulmonary compromise is primarily due to pulmonary hypoplasia and pulmonary hypertension rather than to the mass effect of the herniated viscera. Treatment is aimed at immediate stabilization with sedation, paralysis, and moderate hyperventilation. Some centers employ permissive hypercapnia (postductal Paco2 < 65 mm Hg) and accept mild hypoxemia (preductal Spo2 > 85%) in an effort to reduce pulmonary barotrauma. Inhaled nitric oxide may be used to lower pulmonary artery pressures, but it does not appear to improve survival. If the pulmonary hypertension stabilizes and there is little right-to-left shunting, early surgical repair may be undertaken. Hallmarks of diaphragmatic herniation include hypoxia, a scaphoid abdomen, and evidence of bowel in the thorax by auscultation or radiography. Congenital diaphragmatic hernia is often diagnosed antenatally during a routine obstetric ultrasound examination. A reduction in alveoli and bronchioli (pulmonary hypoplasia) and malrotation of the intestines are almost always present. The ipsilateral lung is particularly Anesthetic Considerations Gastric distention must be minimized by placement of a nasogastric tube and avoidance of high levels of positive-pressure ventilation. The neonate is preoxygenated and typically intubated without the aid of muscle relaxants. Anesthesia is maintained with low concentrations of volatile agents or opioids, muscle relaxants, and oxygen-enriched air. A sudden fall in lung compliance, blood pressure, or oxygenation may signal a contralateral (usually rightsided) pneumothorax and necessitate placement of a chest tube. Arterial blood gases are monitored by sampling a preductal artery if an umbilical artery catheter is not already in place. Surgical repair is performed via a subcostal incision of the affected side; the bowel is reduced into the abdomen and the diaphragm is closed. The extent of pulmonary hypoplasia and the presence of other congenital defects determine the prognosis. Breathing results in gastric distention, whereas feeding leads to choking, coughing, and cyanosis (three Cs). The diagnosis is suspected by failure to pass a catheter into the stomach and confirmed by visualization of the catheter coiled in a blind, upper esophageal pouch. Aspiration pneumonia and the coexistence of other congenital anomalies (eg, cardiac) are common. Preoperative management is directed at identifying all congenital anomalies and preventing aspiration pneumonia. This may include maintaining the patient in a head-up position, using an oral-esophageal tube, and avoiding feedings. Definitive surgical treatment is usually postponed until any pneumonia clears or improves with antibiotic therapy. Anesthetic Considerations these neonates tend to have copious pharyngeal secretions that require frequent suctioning before and during surgery. Positive-pressure ventilation is avoided prior to intubation, as the resulting gastric distention may interfere with lung expansion. Ideally, the tip of the tube lies distal to the fistula and proximal to the carina, so that anesthetic gases pass into the lungs instead of the stomach. In these situations, intermittent venting of a gastrostomy tube may permit positive-pressure ventilation without excessive gastric distention. Suctioning of the gastrostomy tube and upper esophageal pouch tube helps prevent aspiration pneumonia. A precordial stethoscope should be placed in the dependent (left) axilla, since obstruction of the mainstem bronchus during surgical retraction is not uncommon. A drop in oxygen saturation indicates that the retracted lung needs to be reexpanded. Surgical retraction can also compress the great vessels, trachea, heart, and vagus nerve. Postoperative complications include gastroesophageal reflux, aspiration pneumonia, tracheal compression, and anastomotic leakage. Most patients must remain intubated and receive positivepressure ventilation in the immediate postoperative period. Neck extension and instrumentation (eg, suctioning) of the esophagus may disrupt the surgical repair and should be avoided. A one-stage closure (primary repair) is often not advisable, as it can cause an abdominal compartment syndrome. A staged closure with a temporary Silastic "silo" may be necessary, followed by a second procedure a few days later for complete closure. Persistent vomiting depletes potassium, chloride, hydrogen, and sodium ions, causing hypochloremic metabolic alkalosis. Initially, the kidney tries to compensate for the alkalosis by excreting sodium bicarbonate in the urine. Later, as hyponatremia and dehydration worsen, the kidneys must conserve sodium even at the expense of hydrogen ion excretion (paradoxic aciduria). Omphaloceles occur at the base of the umbilicus, have a hernia sac, and are often associated with other congenital anomalies such as trisomy 21, diaphragmatic hernia, and cardiac and bladder malformations. In contrast, the gastroschisis defect is usually lateral to the umbilicus, does not have a hernia sac, and is often an isolated finding. Antenatal diagnosis by ultrasound can be followed by elective cesarean section at 38 weeks and immediate surgical repair. Perioperative management focuses on preventing hypothermia, infection, and dehydration. These problems are usually more serious in gastroschisis, as the protective hernial sac is absent. Anesthetic Considerations Surgery should be delayed until fluid and electrolyte abnormalities have been corrected. The stomach should be emptied with a nasogastric or orogastric tube; the tube should be suctioned with the patient in the supine and lateral positions. Diagnosis often requires contrast radiography, and all contrast media must be suctioned from the stomach before induction. Techniques for intubation and induction vary, but in all cases the Anesthetic Considerations the stomach is decompressed with a nasogastric tube before induction. Experienced clinicians have variously advocated awake intubation, rapid sequence intravenous induction, and even careful inhalation induction in selected patients. These neonates may be at increased risk for respiratory depression and hypoventilation in the recovery room because of persistent metabolic (measurable in arterial blood) or cerebrospinal fluid alkalosis (despite neutral arterial pH). Anesthetic Considerations Patients with croup are managed conservatively with oxygen and mist therapy. Indications for intubation include progressive intercostal retractions, obvious respiratory fatigue, and central cyanosis. Anesthetic management of a foreign body aspiration is challenging, particularly with supraglottic and glottic obstruction. Experts recommend careful inhalational induction for a supraglottic object and gentle upper airway endoscopy to remove the object, secure the airway, or both. When the object is subglottic, a rapid-sequence or inhalational induction is usually followed by rigid bronchoscopy by the surgeon or endotracheal intubation and flexible bronchoscopy. Surgical preferences may vary according to the size of the patient and the nature and location of the foreign body. Children with impending airway obstruction from epiglottitis present in the operating room for definitive diagnosis by laryngoscopy followed by intubation. A preoperative lateral neck radiograph may show a characteristic thumblike epiglottic shadow, which is very specific but often absent. The radiograph is also helpful in revealing other causes of obstruction, such as foreign bodies. Rapid onset and progression of stridor, drooling, hoarseness, tachypnea, chest retractions, and a preference for the upright position are predictive of airway obstruction. Total obstruction can occur at any moment, and preparations for a possible tracheostomy must be made prior to induction of general anesthesia. Laryngoscopy should not be performed before induction of anesthesia because of the increased risk of laryngospasm. In most cases, an inhalational induction is performed with the patient in the sitting position, using a volatile anesthetic and oxygen. Oral intubation with an endotracheal tube one-half to one size smaller than usual is attempted as soon as an adequate depth of anesthesia is established. Foreign body aspiration is typically encountered in children aged 6 months to 5 years. Commonly aspirated objects include peanuts, coins, small batteries, screws, nails, tacks, and small pieces of toys. Onset is typically acute and the obstruction may be supraglottic, glottic, or subglottic. Stridor is prominent with the first two, whereas wheezing is more common with the latter. Acute epiglottitis is a bacterial infection (most commonly Haemophilus influenzae type B) classically affecting 2- to 6-year-old children but also occasionally appearing in older children and adults. It rapidly progresses from a sore throat to dysphagia and complete airway obstruction. The term supraglottitis has been suggested because the inflammation typically involves all supraglottic structures. Epiglottitis has increasingly become a disease of adults because of the widespread use of H influenzae vaccines in children. If intubation is impossible, rigid bronchoscopy or emergency tracheostomy must be performed. Sleep apnea and recent infection increase the risk of postoperative complications and may necessitate admission. Although these extremes of pathology are unusual, all children undergoing tonsillectomy or adenoidectomy should be considered to be at increased risk for perioperative airway problems. Causative organisms are usually bacterial and include pneumococcus, H influenzae, Streptococcus, and Mycoplasma pneumoniae.

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