Overview of Complications Occurring in The Post-Anesthesia Care Unit

Overview of complications occurring in the post-anesthesia care unit
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Overview of complications occurring in the post-anesthesia care unit Author David B Glick, MD, MBA Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Feb 2012. | This topic last updated: Out 20, 2011. INTRODUCTION Timely recognition and management of issues that arise in the immediate postoperative period saves lives, time, and money. The likelihood that a specific complication will arise for a given patient is determined by the nature of the procedure, the anesthetic techniques used, and the patient's preoperative comorbidities. The risk of some complications can be reduced with appropriate preoperative assessment and medical optimization. The most common postoperative problems encountered in the post-anesthesia care unit (PACU) will be reviewed here. Preoperative evaluation and preventive strategies are discussed elsewhere. (See "Preoperative medical evaluation of the healthy patient" and "Management of cardiac risk for noncardiac surgery" and "Evaluation of preoperative pulmonary risk".) INCIDENCE The most common complication in the PACU is postoperative nausea and vomiting (PONV), ranging between 10 and 30 percent [1,2]. A retrospective review involving 18,473 patients found an overall incidence of PACU complications of 23 percent [1]. The most common complication was (PONV) followed by upper airway problems (6.9 percent), hypotension (2.7 percent), dysrhythmias (1.4 percent), hypertension (1.1 percent), altered mental status (0.6 percent), and suspected or major cardiac events (0.6 percent). The complications of awareness during anesthesia and visual loss may first present in the PACU and, although rare, these have received considerable attention in both the medical and lay press. (See 'Intraoperative awareness' below and 'Visual disturbance' below.) POSTOPERATIVE NAUSEA/VOMITING Postoperative nausea and vomiting (PONV) is the most common complication in the immediate postoperative period. Control of nausea or vomiting is a necessary criterion for discharge from the PACU, regardless of whether the patient is going home or being admitted. Late PONV, which is PONV after discharge from the PACU, is associated with the diminishing effect of perioperative antiemetic dosing and/or dizziness from turning in hospital hallways during transport on a wheeled stretcher or the movements of a car during the ride home from the hospital following outpatient surgery [3]. PONV affects surgery in the following ways: PONV is reported to be the worst patient fear going into surgery [4]. Fear of PONV is worse than fear of potential surgical pain. Patient satisfaction following surgery is significantly decreased when PONV occurs [4]. A patient with severe PONV may require unplanned admission to the hospital [5]. Patients with PONV remain in the PACU longer than expected. Delays in discharging patients from the PACU, in turn, delay the ability to turnover patients in the operating room [5]. The development of late PONV during patient transport causes unnecessary patient discomfort. Risk factors for PONV The risk of postoperative nausea and vomiting is increased for certain anesthetic techniques, specific types of surgical procedures, and in certain subsets of patients [6]. General anesthesia using volatile anesthetics including halogenated agents (eg, sevoflurane, desflurane) and nitrous oxide is associated with an increased incidence of PONV compared with other anesthetic techniques [7,8]. Of the available choices for anesthesia, regional anesthetic techniques have the lowest risk. If general anesthesia is needed in a patient at high risk for PONV, total intravenous anesthesia (TIVA) can be used instead of volatile anesthetics. (See "Overview of anesthesia and anesthetic choices".) Procedures including gastrointestinal surgery, breast surgery, operations on the female reproductive organs, tympanoplasty, and tonsillectomy/adenoidectomy have higher rates of PONV [9-11]. Patient factors that are associated with higher rates of PONV include female gender, younger age, a history of motion sickness, absence of a history of smoking, and prior PONV [12]. The simplified Apfel scale, and others like it, attempts to predict the likelihood that a patient will suffer from PONV independent of anesthetic or procedure-related risk [7,13-16]. An increasing number of points correlates with an increased probability of developing postoperative nausea or vomiting. As an example, each of the following characteristics scores a point on the Apfel scale: female sex, history of motion sickness, nonsmoker, planned postoperative opioid treatment [13,17]. This patient scores four points and has a 78 percent chance of PONV. Score: probability of PONV (percent) 0 points: 10 1 point : 21 2 points: 39 3 points: 61 4 points: 78 Pharmacologic agents Preemptive pharmacologic treatment (prophylaxis) before the development of PONV significantly reduces the incidence of PONV. Treatment of PONV in a patient who was not given prophylaxis or who developed PONV in spite of prophylaxis is termed rescue therapy. Drugs classes that are available for prophylaxis or rescue therapy PONV include serotonin-receptor antagonists, corticosteroids, anticholinergic agents and neurokinin-receptor antagonists. The neurokinin-receptor antagonists (eg, aprepitant) are the latest class of antiemetic. Serotonin-receptor antagonists Selective serotonin-receptor (5-HT3) antagonists (eg, ondansetron, dolasetron, granisetron, ramosetron, tropisetron) can be used prophylactically or for rescue treatment of PONV. The serotonin-receptor antagonists are the most commonly used pharmacologic agents for PONV because they do not have sedative side effects and intravenous preparations are available. Two serotonin-receptor antagonists are available as generic drugs in United States (ondansetron and granisetron), which has decreased the cost associated with their use. (See "Characteristics of antiemetic drugs", section on 'Serotonin receptor antagonists'.) Section Editor Stephanie B Jones, MD Deputy Editor Kathryn A Collins, MD, PhD, FACS
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Serotonin receptor-antagonists suppress the initiation of nausea and vomiting by blocking serotonin peripherally at vagal afferents and centrally in the chemoreceptor trigger zone. EKG interval changes are a class effect of the first-generation 5-HT3 antagonists, including ondansetron, granisetron, and dolasetron. They appear to be most prominent one to two hours after a dose of these agents, are mostly small and clinically insignificant, and return to baseline within 24 hours. However, potentially fatal cardiac arrhythmias, including torsade de pointes, have been reported in association with QTc prolongation. In 2011 the US Food and Drug Administration (FDA) issued a warning concerning QTc prolongation due to ondansetron [18,19]. Revised ondansetron labeling includes a recommendation to avoid use in patients with congenital long-QT syndrome and to use ECG monitoring in certain patients, including those with hypokalemia or hypomagnesemia, heart failure, bradyarrhythmias, and in patients taking other medications that increase the risk of QTc prolongation. (See "Characteristics of antiemetic drugs", section on 'Serotonin receptor antagonists'.) Serotonin-receptor antagonists are most effective when given at the end of the surgical procedure [20]. The intravenous dosing for PONV prophylaxis is: ondansetron 4 mg dolasetron 12.5 mg granisetron 0.35 to 1.5 mg palonosetron 0.075 mg The intravenous dose needed to treat established PONV (rescue dose) in patients who have not received a serotonin antagonist for prophylaxis is lower than the dose needed for prophylaxis. However, patients who have failed one class of drug should be treated with another class as the rescue antiemetic [21]. Starting doses are generally as follows: ondansetron 1 mg dolasetron 12.5 mg granisetron 0.1 mg palonosetron 0.075 mg Glucocorticoids Glucocorticoids (eg, dexamethasone) can also be used prophylactically to control PONV. Dexamethasone is generally not useful for rescue therapy once PONV has developed. (See "Characteristics of antiemetic drugs", section on 'Glucocorticoids'.) The mechanism by which corticosteroids prevent PONV prophylaxis is uncertain; however, it is likely these agents exert their effects by reducing surgery-induced inflammation. The standard prophylactic dose of dexamethasone is 4 mg intravenously, at the induction of anesthesia. Anticholinergics Anticholinergic agents, and, specifically, transdermal scopolamine, are more commonly used for prophylaxis of PONV than for rescue therapy due to a slow onset of action. (See "Characteristics of antiemetic drugs", section on 'Anticholinergic agents'.) The exact mechanism by which scopolamine prevents PONV is also uncertain, but it may block cholinergic transmission from the vestibular nuclei to higher centers in the central nervous system, and from the reticular formation to the vomiting center. Common side effects of transdermal scopolamine include sedation, visual disturbances, dry mouth, and dizziness. The drug should be avoided in patients with narrow angle glaucoma. Scopolamine is applied as a patch (1.5 mg, to release 1 mg over three days) behind the ear four or more hours prior to the end of surgery [22,23]. The patch can also be applied the night before surgery. It is standard practice to apply the patch no sooner than one hour before cesarean section to reduce the exposure of the newborn to the drug. The time to onset of action is slow (two to four hours) but the effect is prolonged, which may be beneficial in preventing late PONV. Scopolamine patch is typically removed 24 hours after the end of surgery. Neurokinin-receptor antagonists Neurokinin is a naturally occurring pro-emetic substance. Aprepitant, which is a neurokinin receptor antagonist, is effective as a prophylactic agent for PONV. Because aprepitant is available only in oral form and has a long onset of action, it is not effective for rescue therapy. (See "Characteristics of antiemetic drugs", section on 'Neurokinin receptor antagonists'.) Similar to scopolamine, the long duration of action makes aprepitant a good choice for preventing late PONV. Aprepitant 40 mg orally may be administered within three hours before induction of anesthesia [24]. Preemptive analgesia Preemptive analgesia which minimizes the need for narcotic agents to manage postoperative pain decreases the incidence of PONV. (See "Management of postoperative pain", section on 'Preemptive analgesia'.) Other treatments Although there are no randomized trials to support their use, alternative therapies such as the more liberal use of intravenous fluids [25], or acupuncture/stimulation therapy may reduce the incidence of PONV [26-29]. Higher FiO (70 to 80 percent) has also been used as a supplemental therapy [30]. However, a systematic review that identified 10 trials comparing 80 percent
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oxygen with 30 to 40 percent oxygen found no significant differences in the early, late or overall incidence in PONV between the groups [31]. Efficacy of pharmacotherapy A systematic review evaluating 60 medications identified nine (ondansetron, dolasetron, granisetron, ramosetron, tropisetron, dexamethasone, metoclopramide, cyclizine and droperidol) that each significantly reduced the incidence of PONV compared with placebo [32]. Any one of these agents decreased the risk of PONV 20 to 40 percent compared with placebo (table 1). The use of more than one antiemetic agent confers additional benefit. The IMPACT study found that the effect of a given drug is independent of whether a drug is given alone or with one or two other drugs [2]. As an example, if one drug has a relative risk of 0.60 for PONV and another of 0.70, then, when administered together, the relative risk is 0.60 X 0.70 = 0.42. In the systematic review, trials comparing serotonin antagonists to other agents appeared to favor serotonin antagonists; however, the comparison studies were of poor methodological quality [32]. Similarly, no conclusions were drawn regarding comparisons of individual serotonin receptor antagonists (ondansetron, dolasetron, granisetron, ramosetron, tropisetron). A separate systematic review and metaanalysis identified 25 trials using transdermal scopolamine for prophylaxis and found a significantly reduced risk of PONV (relative risk 0.73, 95% CI 0.60-0.88) compared with placebo, similar to other agents [33]. Combination therapy using a scopolamine patch plus a serotonin antagonist was more effective than using a scopolamine patch alone [34]. Randomized trials have found that neurokinin receptor antagonists also reduce the risk of PONV compared with placebo [35,36]. Trials are underway evaluating differing dosing regimens [35,37-39]. A single trial comparing ondansetron and aprepitant found no significant differences for the primary endpoint (no vomiting and no rescue therapy) between aprepitant (40 or 125 mg) compared with ondansetron, but noted that aprepitant significantly increased the incidence of no vomiting (90 or 95 versus 74 percent) [40]. The authors noted, however, that ondansetron was administered at the time of induction and that it may have been more effective if administered at the end of surgery [20]. Approach to therapy Prevention of PONV is ideal and can be accomplished by choosing certain anesthetic techniques together with pharmacologic
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prophylaxis. Prior to surgery, the patients risk for PONV should be assessed. Based upon the number of risk factors, patients can be categorized as low (no risk factors), moderate (1 risk factor), or severe risk (>1 risk factor) [41]. (See 'Risk factors for PONV' above.) Prophylaxis We suggest the following for pharmacologic prophylaxis: Low risk for PONV - In general, patients with low risk for PONV do not require PONV prophylaxis. However, if the procedure is associated with the potential for significant complications if the patient develops PONV (eg, fundoplication, ventral hernia repair), or if increased intracranial pressure postoperatively would be detrimental, then prophylaxis is appropriate. Moderate risk for PONV - Patients at a moderate risk for PONV should receive a single prophylactic agent. Transdermal scopolamine, dexamethasone, or aprepitant are appropriate since each of these agents have a long duration of action which may also minimize late PONV. High risk for PONV - In patients who are at high risk for PONV, most clinicians use multiple (two or three) pharmacologic agents for prophylaxis. In addition, inhalational anesthetics should be avoided and postoperative opioids minimized. Rescue therapy Rescue therapy is not as effective as prophylaxis and is frequently needed in patients who were not given prophylaxis or developed PONV despite receiving prophylactic medication. When PONV develops in spite of pharmacologic prophylaxis, a different class of antiemetics is chosen for rescue therapy from the class used for prophylaxis [21,42]. The serotonin-receptor antagonists are the most commonly used agents for rescue therapy. (See 'Serotonin-receptor antagonists' above and 'Efficacy of pharmacotherapy' above.) RESPIRATORY COMPLICATIONS Respiratory problems are the second most common complication in the postoperative period. (See 'Incidence' above.) Patients with significant comorbidities, particularly neuromuscular, pulmonary or cardiac dysfunction, are at a higher risk for respiratory compromise, but any patient can develop hypoxemia following surgery. Hypoxemia (low PaO2) is due to hypoventilation (low PAO2) or compromised alveolar oxygen exchange which increase the alveolar to arterial (A-a) oxygen gradient. In the immediate postoperative period, the most common causes of hypoventilation include airway obstruction, the effects of anesthetics, analgesics (eg, opioids), sedatives, residual neuromuscular blockade and poorly controlled incisional pain impairing respiration. (See 'Airway obstruction' below and 'Residual effects of anesthesia' below.) Impaired oxygen exchange in the postoperative period can occur as a result of intrapulmonary shunting, pulmonary edema and pulmonary embolus. (See 'Compromised oxygen exchange' below.) Airway obstruction The most common cause of airway obstruction in the post-anesthesia care unit (PACU) is pharyngeal laxity due to weakness of the pharyngeal muscles. Other causes include laryngospasm, airway edema, hematoma, or a foreign body (eg, dentures). Postoperative stridor is an emergency that requires immediate evaluation by a healthcare provider experienced in advanced airway techniques. A surgical airway may be required in some cases. (See "Advanced emergency airway management in adults" and "Overview of tracheostomy".) Following the relief of acute airway obstruction, pulmonary edema termed "negative pressure pulmonary edema," may result. The incidence is about 0.1 percent of all anesthesia cases and it occurs more often in young adults. (See "Overview of the management of postoperative pulmonary complications", section on 'Pulmonary edema'.) Pharyngeal muscular weakness Loss of pharyngeal motor tone leading to muscular laxity is due to residual neuromuscular blockade, residual anesthetic effect, or opioids. Preoperative medical conditions such as obstructive sleep apnea can also predispose to airway obstruction in the post-anesthesia care unit (PACU). The diaphragm recovers more quickly from the effects of muscle relaxants than the pharyngeal musculature. Residual paralysis of pharyngeal muscles causes the base of the tongue and the tissues of the posterior oropharynx to move toward each other, obstructing the supraglottic inlet. As the patient attempts to draw in air, negative pressure generated in the thorax brings the pharyngeal tissues even closer together, further obstructing the airway. Clinically, the absence of airflow into the trachea is manifested as retraction at the sternal notch and paradoxical motion of the abdominal musculature. The treatment of airway obstruction due to decreased pharyngeal muscle tone is the classic jaw thrust maneuver that brings forward the mandible and the base of the tongue, which is attached to it, thus opening the inlet to the posterior oropharynx. Continuous positive airway pressure (CPAP) via a facemask can also be given to hold the airway open until pharyngeal muscle tone returns to normal. (See "Basic airway management in adults", section on 'Airway obstruction'.) If muscular weakness persists, the residual effects of muscle relaxants, sedatives, or opioids should be reversed. (See 'Residual effects of anesthesia' below.) Laryngospasm Laryngospasm as a cause of airway obstruction is more common in pediatric patients, but it can also occur in adults. Laryngospasm can occur abruptly following extubation in the patient who is no longer deeply anesthetized and not indifferent to laryngeal stimulation, but not awake enough to counteract the laryngeal reflex that results from vocal cord irritation (eg, tube removal, aspirate blood). Laryngospasm can also occur upon cessation of positive pressure ventilation via face mask, presumably due to sudden airway collapse. The treatment of laryngospasm is positive pressure ventilation. If bag-mask ventilation is not successful, a small dose of succinylcholine (0.1 mg/kg IV) can be given to relax the cords. Vocal cord paralysis Vocal cord paralysis due to bilateral recurrent laryngeal nerve injury can present in much the same way as laryngospasm and will not be apparent until the patient is extubated. Passage of air into the lungs is not possible. The vocal cords will be seen to be in apposition at the midline with the laryngoscope. Attempted intubation in this setting is traumatic and often unsuccessful. Emergent tracheostomy is the appropriate initial intervention. Airway edema The airway can become edematous due to direct tissue trauma from multiple intubation attempts or surgical manipulation, or because of decreased venous drainage resulting from prolonged head-down or prone positioning. (See "Endotracheal tube management and complications", section on 'Laryngeal injury'.) If airway edema is suspected, an endotracheal tube leak test can be performed once the patient is breathing spontaneously. The leak test is accomplished by deflating the cuff on the endotracheal tube and then covering the open end of the endotracheal tube to determine if the patient is capable of breathing around the tube. Alternatively, with the cuff deflated, the measured inspired volume can be compared with the exhaled volume on the ventilator. Significant airway edema is suggested if there is not a significant loss of tidal volume. The endotracheal tube should remain in place if airway edema is compromises the patency of the airway. The head is elevated to facilitate venous drainage. Steroids can also be given to decrease swelling associated with airway inflammation. Once an air leak around the endotracheal tube is apparent, extubation is reasonable.
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Postoperative cervical hematoma Following surgery in the neck, postoperative bleeding from vascular structures can lead to a cervical hematoma. As blood accumulates, it can compress against the thin posterior wall of the trachea and compromise the tracheal lumen. The lumen is often narrowed to less than 5 mm before the patient becomes clinically symptomatic Direct laryngoscopy will reveal only a dark mass along the posterior wall of the trachea. Attempts to intubate will be traumatic and unsuccessful. To secure a safe airway, the operative skin incision should be re-opened before attempting re-intubation. Ideally, the patient should be taken emergently to the operating room, the neck prepped and draped, and the sutures or staples removed. The hematoma can then be evacuated from the wound, sponges placed into the wound and pressure applied to control bleeding while the patient is intubated. Once the airway is secured, surgical exploration can be continued to identify and control the source of bleeding, irrigate the wound and re-close the incision. Foreign bodies Dentures, teeth, surgical packs, or instruments can also obstruct the airway. Direct laryngoscopy or rigid bronchoscopy may be necessary to extract the obstructing object. Digital sweep through the mouth risks pushing the foreign body deeper into the airway and/or converting a partial obstruction to a complete obstruction, and should not be performed. (See "Diagnosis and management of central airway obstruction", section on 'Foreign body extraction'.) Residual effects of anesthesia Following the completion of a procedure, the patients respiration is supported with positive pressure ventilation until the effects of the administered anesthetic agents wear off. (See 'Supportive care' below.) One of the effects of volatile anesthetics, many intravenous sedative/hypnotic agents, and opioids is a decrease in the sensitivity of the respiratory center to rises in carbon dioxide, which then diminishes the respiratory drive. Intravenous sedatives like ketamine and dexmedetomidine have less of a suppressive effect. A diminished respiratory drive manifests as a reduced respiratory rate and/or tidal volume. For example, the tidal volume is decreased but the respiratory rate may increase with the use of volatile anesthetic agents. In contrast, the respiratory rate decreases with the use of opioids while the tidal volume remains normal. The neuromuscular blockers have a direct effect on the musculature and reduce tidal volume because of reduced diaphragmatic movement. If prolonged, pharmacologic reversal may be necessary, as guided by the patients clinical condition. Patients with compromised renal or hepatic function are at an increased risk for persistent effects from sedatives, opioids and neuromuscular blocking agents due to reduced drug clearance. Hypothermia and/or acidosis also slow enzymatic degradation of some agents (eg, cisatracurium). Pharmacologic reversal There are no reversal agents for the volatile gases, barbiturates, and propofol. Specific antidotes are available to reverse the effects of benzodiazepines, anticholinergics, and neuromuscular blocking agents: Benzodiazepines Oversedation caused by benzodiazepines, which are administered as a premedication before surgery, has become uncommon since diazepam was replaced by midazolam, a shorter-acting agent. When reversal is needed, intravenous flumazenil is given. Because flumazenil is generally shorter-acting than the sedative it is reversing, the patient must be closely monitored for evidence of returning sedation, and additional doses of flumazenil given, as necessary. In adults, the recommended initial dose is 0.2 mg given intravenously (IV) over 30 seconds. Repeated doses of 0.2 mg, to a maximum dose of 1 mg, can be given until the desired effect is achieved [23]. In the event of re-sedation, dosing can be repeated, but no more than 3 mg of flumazenil should be given within a given hour. (See "Benzodiazepine poisoning and withdrawal", section on 'Antidote (Flumazenil)'.) Anticholinergics The sedative effects of the central-acting anticholinergics, atropine and scopolamine, can be antagonized with physostigmine, but this is not usually necessary. The recommended dose of physostigmine is 0.5 to 2 mg (0.02 mg/kg IV, up to a maximum of 0.5 mg per dose in pediatric patients). The drug should be given by slow intravenous push, generally over five minutes. Overly rapid infusion may result in cholinergic symptoms or seizures. The treatment of anticholinergic side effects is discussed in detail elsewhere. (See "Anticholinergic poisoning", section on 'Antidotal therapy with physostigmine'.) Neuromuscular blocking agents It is customary to reverse neuromuscular blockade using one of the pseudocholinesterase inhibitors (eg, neostigmine) in most patients who received nondepolarizing neuromuscular blocking agents (eg, vecuronium, rocuronium, cisatracurium). Complete recovery from neuromuscular blockade is correlated with a train-of-four (TOF) peripheral nerve stimulation ratio of 0.9, or the ability to hold a tongue depressor between the molars. The TOF ratio is defined as the amplitude of the twitch response to a fourth nerve stimulation relative to the twitch response of the first stimulation. If the patient is reversed before these signs are apparent, the neuromuscular blocking agent will still be circulating after the reversal agent has worn off. A second dose of the reversing agent can be given, but the patient needs to be observed carefully and should be reintubated if weakness persists. In some patients, persistent paralysis may be due to the administration of succinylcholine or mivacurium in a patient with pseudocholinesterase deficiency. (See "Neuromuscular blocking agents (NMBA) for rapid sequence intubation in adults", section on 'Contraindications and side effects'.) Opioids When hypoventilation is due to narcotics, treatment is supportive with positive pressure ventilation and, if needed, reversal using naloxone (40 micrograms every five minutes, intravenously, until adequate reversal is achieved). (See "Opioid intoxication in adults", section on 'Management'.) Reversal with naloxone is generally safe but is not without risks. Like the benzodiazepines, the half-life of the opioid being reversed may be longer than naloxone (half-life 1 to 1.5 hours), and thus, the patient must be monitored for re-sedation as the naloxone wears off. Repeat doses can be given, or, alternatively, a continuous infusion can be started. It is important to remember that, in addition to reversing the sedative and respiratory depressant effects, naloxone also reverses the analgesic effects of the narcotic, which can be extremely uncomfortable for the patient, and in patients with cardiac disease the associated sympathetic surge can lead to myocardial ischemia. Flash pulmonary edema has also been reported after large doses of naloxone in young, muscular patients [43]. Compromised oxygen exchange Inadequate exchange of oxygen from the alveoli into the pulmonary capillaries leading to hypoxemia can be due to intrapulmonary shunting, pulmonary edema, or pulmonary embolus. Intrapulmonary shunting Lung collapse (eg, atelectasis, pneumothorax) leads to regions of the lung that are perfused but not ventilated, which can result in significant hypoxemia if a large amount of blood is shunted. Treatment for atelectasis is supportive, consisting of adequate analgesia, deep breathing and coughing, incentive spirometry or, in some cases, positive pressure ventilation to open the collapsed segment. Treatment for pneumothorax requires evacuation of the air by placement of a chest tube. (See "Placement and management of thoracostomy tubes", section on 'Indications'.) Pulmonary edema Pulmonary edema diminishes the lung's capacity to move oxygen from the alveoli into the pulmonary capillaries and can also lead to hypoxemia. In the postoperative period, patients at risk for pulmonary edema often have preexisting heart failure, but pulmonary edema can also develop in otherwise healthy patients as a sequelae of airway obstruction (negative pressure pulmonary edema), or following narcotic reversal with naloxone (flash pulmonary edema). Treatment of pulmonary edema is supportive. Supplemental oxygen is given and positive pressure ventilation is added, as needed. The treatment of postoperative pulmonary edema and postoperative heart failure are discussed in detail elsewhere. (See "Overview of the management of postoperative pulmonary complications", section on 'Pulmonary edema' and "Perioperative heart failure in noncardiac surgery".) Pulmonary embolus Although uncommon in the early postoperative period, pulmonary embolus can occur due to vein thrombus, fat (eg, long bone
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surgery), or amniotic fluid (childbirth). A diagnosis of pulmonary embolus should be suspected in patients with suggestive clinical symptoms and signs which include chest pain, tachycardia, and hypoxemia resistant to supplemental oxygen. The diagnosis and treatment of pulmonary embolus is discussed elsewhere. (See "Diagnosis of acute pulmonary embolism" and "Treatment of acute pulmonary embolism".) Supportive care Supportive care of respiratory complications in the post-anesthesia care unit consists of pain control, supplemental oxygen, and positive pressure respiratory support. It is important to remember that hypoventilating patients can become hypoxic breathing room air. Pharmacologic reversal of the residual effects of anesthetic medication may be needed and is discussed separately. (See 'Pharmacologic reversal' above.) Patients who have incisions in the chest or upper abdomen often find it painful to breathe deeply. The best way to treat this cause of hypoventilation is to provide adequate analgesia, which will improve tidal volume. Non-sedating alternatives for pain control include nonnarcotic intravenous analgesics and regional analgesia (eg, epidural catheter placement, intercostal block, transversus abdominus plane block). (See "Management of postoperative pain" and "Strategies to reduce postoperative pulmonary complications".) Short-term positive pressure ventilation is provided using bag-mask ventilation. If a longer period of support will be required, noninvasive positive pressure ventilation (NIPPV) can be used. NIPPV uses a tightly fitting facemask to administer continuous positive airway pressure (CPAP) or a nasal mask to give bilevel positive airway pressure (BiPAP). CPAP, which delivers a steady plateau of pressure to the lungs, raises mean airway pressure, recruits collapsed alveoli, increases minute ventilation, and maintains upper airway patency. BiPAP provides a continuous level of pressure through the upper airway with all the benefits of CPAP, but it also delivers an incremental increase in pressure with inspiration. This additional level of airway support allows the respiratory muscles to rest. If noninvasive techniques are not adequate, reintubation may be required. The details and use of noninvasive positive pressure ventilation are discussed elsewhere. (See "Noninvasive positive pressure ventilation in acute respiratory failure in adults".) CARDIOVASCULAR COMPLICATIONS Cardiovascular complications in the postoperative patient are related to the severity of cardiovascular comorbidities (eg, coronary artery disease, hypertension), and the nature and course (eg, blood loss) of the operation. Surgical patients with ischemic heart disease or a history of heart failure are less tolerant of the stress that surgery places on the heart, and these patients are more likely to present with cardiovascular complications in the post-anesthesia care unit (PACU). The surgical procedure can lead to cardiovascular complications through indirect and/or direct effects. As an example, blood loss during surgery may result in hypotension and hypoperfusion with cardiovascular injury as an indirect consequence. On the other hand, operations near the heart or mediastinum (eg, cardiac, pulmonary, or esophageal surgeries) can cause myocardial irritability and postoperative arrhythmias. Hypotension There are many etiologies for hypotension in patients managed in the post-anesthesia care unit (PACU). The most significant of these include hypovolemia, heart failure, sepsis, drug effects, anaphylaxis, and pulmonary embolus. Hypovolemia Inadequate intravascular volume can be due to inadequate fluid replacement during the course of the operation. If intraoperative blood loss and/or ongoing blood loss is the cause of the hypovolemia, blood products are given as part of their ongoing resuscitation. It is important to remember that the postoperative hematocrit will not accurately reflect the degree of blood loss until adequate fluid resuscitation has occurred. (See "Maintenance and replacement fluid therapy in adults" and "Treatment of severe hypovolemia or hypovolemic shock in adults".) Myocardial ischemia/heart failure In the perioperative period, hypotension can also be due to myocardial ischemia/infarction, heart failure, cardiac valvular dysfunction, and cardiac arrhythmia. (See 'Arrhythmias' below.) Patients with preexisting coronary artery disease and patients with drug-eluting stents whose antiplatelet therapy was prematurely withheld are at increased risk for perioperative myocardial ischemia [44]. (See "Perioperative heart failure in noncardiac surgery" and "Perioperative myocardial infarction after noncardiac surgery" and "Coronary artery stent thrombosis: Prevention and management", section on 'Risk associated with premature cessation'.) Decreased vascular resistance Hypotension related to decreased systemic vascular resistance is due to the combined effects of decreased atrial filling and reduced afterload. Iatrogenic causes of decreased vascular resistance are related to the administration of various pharmacologic agents such as the vasodilators sodium nitroprusside or hydralazine to treat hypertension, or the prolonged effect of long-acting anti-hypertensives (eg, lisinopril) taken by the patient on the morning of surgery. Epidural and spinal anesthetics also decrease peripheral vascular resistance by causing venodilation. When treating hypotension in patients with an epidural or spinal anesthetic, vasoconstricting agents are preferred over additional fluid, particularly in patients who will have trouble clearing the fluid load when vascular tone returns to normal (eg, patients with renal insufficiency, history of heart failure). Many disease states also decrease vascular resistance and can lead to postoperative hypotension. As examples, endotoxins released during surgery for intraabdominal sepsis, spinal shock due to spinal cord injury, and histamine release from mast cells during anaphylaxis can all cause profound hypotension mediated by a decrease in vascular resistance. Treatment is directed at the underlying cause (eg, antibiotics for sepsis, epinephrine to stabilize the mast cells in anaphylaxis), and symptomatic therapy includes intravenous vasoconstrictors (eg, vasopressin, norepinephrine, or phenylephrine) and fluid resuscitation; high fluid volumes are often needed. (See "Management of severe sepsis and septic shock in adults" and "Acute traumatic spinal cord injury" and "Perioperative anaphylaxis: Clinical manifestations, etiology, and diagnosis".) Hypertension Patients who develop hypertension in the post-anesthesia care unit (PACU) are at a higher risk for postoperative complications (eg, unplanned intensive care unit admission) compared with patients who experience an episode of hypotension [45]. The most common cause of hypertension in the PACU is preoperative hypertension, particularly if the patient did not take their usual anti-hypertensive agent(s) on the morning of surgery. Other frequent causes of hypertension in the PACU include inadequate pain control, hypoventilation, urinary retention, and anxiety. Less commonly, delirium, which may be a manifestation of alcohol or drug withdrawal can also contribute. These are reviewed briefly below. The general treatment of hypertension in the perioperative period is discussed in detail elsewhere. (See "Perioperative management of hypertension".) Pain is a common cause of hypertension in the PACU. Inadequately treated surgical pain leads to sympathetic discharge which increases heart rate and blood pressure. A multimodal approach to pain management is preferred. Regional anesthetic techniques are useful when narcotics need to be avoided. (See "Management of postoperative pain" and "Pain control in the critically ill adult patient".) Urinary retention is an easily remedied cause of hypertension in the PACU, particularly for older men with known voiding problems due to prostatic hypertrophy or patients with decreased bladder muscle tone due to neuraxial anesthesia. If the patient has received a large volume of intravenous fluid and has not voided, the bladder should be palpated or scanned by ultrasound to determine if catheterization of the bladder is needed. (See 'Postoperative urinary retention' below.) Hypoventilation is initially associated with an increase in sympathetic tone leading to a rise in blood pressure. Treatment is supportive with positive pressure ventilation via bag-mask ventilation or reintubation until the patient's respiratory drive returns to normal. (See 'Respiratory complications' above.) Postoperative anxiety and emergence delirium can also lead to elevated blood pressures. This problem is far more common in children. Prior to giving any
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sedatives, other causes of anxiety (eg, pain, respiratory insufficiency) must be identified and treated first. (See 'Emergence delirium' below.) Drug or alcohol withdrawal can also lead to hypertension in the PACU. Alcohol withdrawal can begin as early as 24 hours after consumption of the last alcoholic beverage. Early signs of withdrawal include hypertension and tachycardia. Narcotic abusers who have not received their usual dose may require additional dosing of their narcotic to manage withdrawal symptoms. The treatment of drug and alcohol withdrawal is discussed elsewhere. (See "Opioid withdrawal in the emergency setting" and "Benzodiazepine poisoning and withdrawal".) Arrhythmias Cardiac arrhythmias in the postoperative period can be due to acute coronary insufficiency hypoxia, electrolyte abnormalities (eg, hypokalemia, hypomagnesemia), anesthetics, and other pharmacologic agents. The uncoordinated cardiac contraction can lead to marked hypotension, particularly if ventricular function is already compromised such as in the patient with poor preoperative cardiac contractility. (See 'Hypotension' above.) The most common postoperative ventricular arrhythmias are isolated premature ventricular contractions (PVCs) and ventricular bigeminy. These rhythms are unlikely to degenerate into life-threatening arrhythmias and they do not routinely require intervention. On the other hand, Torsade de Pointes (figure 1) is a polymorphic ventricular tachycardia that results from prolongation of the Q-T interval in susceptible patients who become hypomagnesemic or receive certain medications (eg, class IA or III anti-arrhythmics, droperidol). Torsade de Pointes can cause hypotension or degenerate into ventricular fibrillation and sudden cardiac death. (See "Overview of the acute management of tachyarrhythmias", section on 'Torsades de pointes'.) Atrial fibrillation is most likely to occur if a patient undergoes cardiac or thoracic surgery. The rate of new onset atrial fibrillation after pneumonectomy can be 50 percent or higher, and may be due to atrial irritability or the sudden cessation of chronic beta-blockade. (See "Arrhythmias after cardiac surgery: Atrial fibrillation and atrial flutter" and "Overview of the acute management of tachyarrhythmias".) New onset postoperative bradyarrhythmias are due to excess administration of antihypertensive agents (eg, beta-blockers, alpha-2 agonists), excess opioid dosing, or related to high neuraxial anesthesia (suppression of cardiac accelerator fibers originating at the level of the first through fourth thoracic vertebrae [T1-T4]). (See "Major side effects of beta blockers".) The treatment of arrhythmias in the PACU first requires identification and correction of the underlying cause of the rhythm disturbance and thus, hypoxia, hypercarbia, ischemia, and electrolyte imbalances must be addressed. Medical management of the arrhythmias is usually enough to correct the arrhythmias, but if the tachyarrhythmias cause hemodynamic instability, electrical cardioversion may be required. (See "Overview of the acute management of tachyarrhythmias".) Symptomatic bradyarrhythmias that are not corrected may require temporary pacing (transvenous or transcutaneous). (See "Temporary cardiac pacing".) IMPAIRED THERMOREGULATION Impaired thermoregulation resulting in hypothermia or hyperthermia has negative consequences. Decreases in body temperature as little as 2 C can slow drug metabolism (particularly degradation of neuromuscular blocking agents), and decrease platelet function impairing hemostasis. More profound decreases in body temperature cause somnolence. In contrast, excessive increases in body temperature cause a hypermetabolic state that increases the respiratory rate and heart rate, which can exacerbate underlying medical conditions. Maintenance of normothermia during recovery is important enough that the Joint Commission and the Surgical Care Improvement Project encourages warming all patients to 96.8 Fahrenheit (36 Celsius) within fifteen minutes of their arrival in the post-anesthesia care unit (PACU) [46]. Warming in the PACU is typically achieved using forced air warming devices. Shivering Shivering in the postoperative period can occur with hypothermia or normothermia. Shivering causes patient discomfort and markedly increases myocardial oxygen consumption. Shivering is treated with a single dose of meperidine, 12.5 to 25 mg, intravenously. Alpha-2 agonists including clonidine (150 micrograms intravenously) and dexmedetomidine are used as second-line therapy. Fever Fever is defined as a core body temperature 102.2 Fahrenheit (39 Celsius) (table 2). The most common causes for fever in the postoperative period are atelectasis, transfusion or drug reaction and infection (wound, urinary tract, pneumonia); however, fever due to infection does not typically manifest in the post-anesthesia care unit (PACU) unless an existing infection was the reason for the surgery (eg, drainage of an abscess, sepsis). Less common causes of postoperative fever that may manifest in the PACU include malignant hyperthermia and hyperthyroidism. Deep vein thrombosis (DVT) may also cause fever but DVT is more common in the later postoperative period. The differential diagnosis of postoperative fever is discussed in detail elsewhere. (See "Postoperative fever".) Atelectasis Atelectasis is more common following surgery of the chest or upper abdomen due to splinting from pain upon inspiration, which leads to lower lung collapse. Treatment consists of adequate analgesia, deep breathing, and coughing or incentive spirometry. A chest x-ray can help make the diagnosis, but is usually unnecessary. (See "Strategies to reduce postoperative pulmonary complications", section on 'Lung expansion'.) Drug or transfusion reaction Several pharmacologic agents associated with anesthesia can cause fever due to altered thermoregulation (eg, anticholinergics, sympathomimetic drugs), hypersensitivity (eg, antibiotics, heparin), and cytokine release (eg, antibiotics). Adverse reactions to blood transfusion can occur in anyone, but are more common in patients with hematologic and oncologic diseases. (See "Drug fever" and "Immunologic blood transfusion reactions".) Malignant hyperthermia Exposure of susceptible patients to succinylcholine or volatile anesthetics can cause malignant hyperthermia (MH). Fever usually occurs after other signs, such as hypercarbia and tachycardia, but fever more typically presents in the immediate postoperative period rather than later in the patients postoperative course. A blood gas demonstrating a mixed respiratory and metabolic acidosis differentiates MH from sepsis (table 3). (See "Susceptibility to malignant hyperthermia" and "Malignant hyperthermia: Clinical diagnosis and management of acute crisis".) Thyrotoxicosis Patients with a history of hyperthyroidism can present in a fashion very similar to those with malignant hyperthermia. It may be difficult to differentiate these entities if a diagnosis of hyperthyroidism is not confirmed preoperatively. (See "Overview of the clinical manifestations of hyperthyroidism in adults".) NEUROPSYCHIATRIC COMPLICATIONS The most common central nervous system manifestation in the postoperative care unit (PACU) is an altered state of consciousness. Postoperative patients can demonstrate excessive sedation or agitation, which, in some cases, may be alternating. (See 'Emergence delirium' below and 'Somnolence' below.) Other neurologic problems that may be encountered include visual disturbances, complications related to regional anesthesia (epidural hematoma, neurapraxia), and intraoperative recall of the events of the operation. Early identification and treatment is important to lessen the impact of these uncommon, but potentially devastating complications. Each is discussed briefly. Emergence delirium Emergence delirium, also known as emergence agitation, refers to a prolonged (hours) change in mental status characterized by a dissociated state of consciousness in which the patient is irritable, uncooperative, uncompromising, thrashing, moaning, incoherent, or crying. The incidence of emergence agitation in children can be as high as 30 percent and is most common in children age two to four. Emergence agitation is likely a response to a disorienting situation. Parental presence can smooth this transition and the child usually calms in less than 15 minutes. Pediatric emergence agitation has been attributed to the increased use of the rapid onset low-solubility inhaled anesthetic agents [47].
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In the adult population, emergence agitation is less common with an incidence of less than 5 percent. Transient agitation occurs in a wide range of adult postsurgical patients, but the development of delirium occurs most commonly in elderly patients, especially following major orthopedic procedures [48]. Emergence delirium can be a result of pain, hypoxia, hypercarbia, urinary retention, electrolyte imbalance (especially hyponatremia), and central, drug-induced anti-cholinergic activity. Preoperative substance abuse and poor functional status are also risk factors for postoperative delirium. Treatment should be directed first at the underlying cause. When needed, a small dose of midazolam (1 to 2 mg, intravenous in adults) can be given to help relax the patient and consequently will reduce blood pressure if elevated. (See "Prevention and treatment of delirium and confusional states", section on 'Postoperative setting'.) Somnolence Somnolence in the post-anesthesia care unit (PACU) is most often due to the persistent effects of pharmacologic agents used during surgery, typically sedatives and neuromuscular blocking agents. (See 'Residual effects of anesthesia' above.) It is important to rule out other causes of somnolence, such as hypotension, hypoxia, hypercarbia, hypoglycemia, and electrolyte abnormalities, before attributing the patients condition solely to a persistent anesthetic effect. A check of routine vital signs, complete blood count, blood gas analysis, and chemistry panel will differentiate most of the potential causes of postoperative somnolence. If a cerebrovascular injury is suspected, computed tomography (CT) of the head may be needed. Visual disturbance The most common cause of visual disturbance in the postoperative period is corneal abrasion. The patient typically complains of the sensation of a foreign body in the affected eye. The diagnosis is made by staining the cornea with fluorescein. Topical antibiotics and use of an eye patch typically result in full recovery. (See "Corneal abrasions and corneal foreign bodies".) Although rare, a patient may awaken from anesthesia with visual loss. Visual complications due to ischemic optic neuropathy or retinal artery occlusion can lead to total and permanent visual loss. Patients undergoing cardiac, spinal, and head and neck operations are at the highest risk. Risk factors include prone positioning, prolonged procedure duration, and significant blood loss or need for large volume resuscitation. An ophthalmology consultation is appropriate but there may be little to offer the patient who has suffered this complication. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Perioperative ION' and "Posterior ischemic optic neuropathy", section on 'Perioperative PION'.) Epidural hematoma Epidural hematoma is an uncommon complication of neuraxial anesthesia with a reported incidence of 1 in 150,000. The risk increases in the setting of systemic anticoagulation [49]. Epidural catheters are usually placed just prior to induction of anesthesia. If an epidural hematoma develops, it will not become apparent until the patient awakens in the post-anesthesia care unit (PACU). Symptoms include back pain or back pressure, which can progress to muscle weakness, sensory loss, and urinary or bladder dysfunction. If an epidural hematoma is suspected, an emergent MRI of the spine and neurosurgical evaluation for possible decompression should be obtained because permanent neurological injury can result in as little as six hours from the time of onset. Intraoperative awareness Awareness with recall following anesthesia refers to conscious awareness of intraoperative events and has become an important topic of discussion in the professional and lay press. As affected patients awaken from anesthesia, they may show evidence of awareness of the surgical procedure. Any patient suspected of having an awareness event should be offered psychiatric counseling. Awareness with recall following anesthesia is discussed in detail elsewhere. (See "Awareness with recall following anesthesia".) POSTOPERATIVE URINARY RETENTION Urinary retention is common following anesthesia. The incidence varies widely, ranging from 5 to 70 percent [50]. Postoperative urinary retention (POUR), in the absence of urologic pathology, is usually transient but on occasion can be prolonged. Risk factors Risk factors for POUR are patient-specific, procedure-specific, and anesthetic-specific. Patient Advanced age, male gender, pre-existing neurologic disease (eg, cerebral palsy, neuropathy, multiple sclerosis) Procedure Anorectal surgery, joint arthroplasty, hernia repair Anesthesia Medications Anticholinergic agents, beta-blockers, sympathomimetics Prolonged duration of anesthesia Excessive fluid administration Mode of anesthesia. Neuraxial anesthesia is more likely to cause POUR compared with general anesthesia (inhaled or intravenous) Evaluation and treatment Patients with POUR may or may not complain of bladder fullness or lower abdominal discomfort and physical examination is not sufficiently sensitive to detect bladder volumes before the development of overdistention [51]. Thus, the bladder is assessed directly. Bladder volume is measured by draining the bladder, which requires catheterization, or by using ultrasound. We prefer to use bladder ultrasound because ultrasound is noninvasive and urine volumes measured by ultrasound have shown a good correlation to volumes measured by bladder catheterization [52,53]. Patients with any of the risk factors who are unable to void four hours after surgery should have a bladder ultrasound performed. Patients with more than 600 cc of urine should undergo one-time catheterization, after which ambulatory patients may be discharged [50]. Ambulatory patients with less than 600 cc of urine in their bladder and patients without risk factors for POUR can be discharged without voiding. Patients who have not spontaneously voided prior to discharge are instructed to seek medical assistance if they have not spontaneously voided within eight hours of discharge. SUMMARY AND RECOMMENDATIONS Postoperative complications are estimated to occur in about 25 percent of patients undergoing anesthesia. Complications may require additional treatment and may delay discharge from the post-anesthesia care unit (PACU). (See 'Introduction' above.) The most common PACU complication is postoperative nausea or vomiting (PONV). The incidence following anesthesia ranges between 10 and 30 percent. Risk factors associated with higher rates of PONV include female gender, younger age, a history of motion sickness, absence of a history of smoking, prior PONV, gastrointestinal surgery, breast surgery, operations on the female reproductive organs, tympanoplasty, and tonsillectomy. (See 'Postoperative nausea/vomiting' above.) Prior to surgery, the patient should be assessed for their risk for PONV. We administer pharmacologic prophylaxis to patients with 1 risk factor for PONV. For patients with a single risk factor for PONV, a single agent is adequate, whereas patients with >1 risk factor generally require multiple agents. Prophylaxis is not necessary for patients who do not have risk factors. (See 'Risk factors for PONV' above and 'Approach to therapy' above.) Respiratory problems are the second most common complication arising in the PACU. Patients with significant comorbidities, particularly cardiac, neuromuscular, or pulmonary dysfunction are at a higher risk for hypoxemia due to hypoventilation or impaired oxygen exchange. In postoperative patients, hypoventilation can be due to airway obstruction, poorly controlled incisional pain, and the residual effects of anesthetics, analgesics (eg, opioids), sedatives, or neuromuscular blocking agents. Impaired oxygen exchange is most commonly due to atelectasis from pulmonary splinting, but other causes for impaired oxygen exchange include pulmonary edema, or, more rarely pulmonary embolus. (See 'Respiratory complications' above.)
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Cardiovascular complications in the postoperative patient are closely correlated to preexisting cardiovascular disease. Hypotension can be due to hypovolemia, heart failure, sepsis, drugs, cardiac arrhythmia, anaphylaxis, and pulmonary embolus. Postoperative hypertension is most commonly related to pre-existing hypertension. Inadequately controlled pain is another common cause of hypertension. Other causes include urinary retention, hypoventilation, and drug or alcohol withdrawal. Cardiac arrhythmias (tachycardia, bradycardia) can be due to cardiac ischemia, hypoxia, electrolyte abnormalities (eg, hypokalemia, hypomagnesemia), anesthetics, and other pharmacologic agents. (See 'Cardiovascular complications' above.) Disturbances in thermoregulation are common, including hypothermia and hyperthermia. Shivering can occur in hypothermic or normothermic patients. Within 15 minutes of arrival in the PACU, all patients should be warmed to 96.8 F (36 C). Postoperative fever in the PACU is most likely to be due to atelectasis, but can be due to drug or transfusion reaction, or more rarely, malignant hyperthermia or thyrotoxicosis. (See 'Impaired thermoregulation' above.) The most common central nervous system complication in the PACU is an altered state of consciousness (delirium, agitation, somnolence). Uncommon problems include visual disturbances, complications related to regional anesthesia (epidural hematoma, neurapraxia), and recall of intraoperative events. Early identification and treatment of these uncommon problems is important to lessen the impact of these potentially devastating complications. (See 'Neuropsychiatric complications' above.) Urinary retention is common following anesthesia. The incidence varies widely, ranging from 5 to 70 percent depending upon patient, procedure, and anesthesia-specific factors. Patients with more than one risk factor for urinary retention should undergo assessment of urinary volume to determine if one-time catheterization is needed prior to discharge. All patients who have not spontaneously voided prior to discharge should seek medical attention if they have not spontaneously voided within eight hours of discharge. (See 'Postoperative urinary retention' above.)
Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Hines R, Barash PG, Watrous G, O'Connor T. Complications occurring in the postanesthesia care unit: a survey. Anesth Analg 1992; 74:503. 2. Apfel CC, Korttila K, Abdalla M, et al. A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med 2004; 350:2441. 3. Wu CL, Berenholtz SM, Pronovost PJ, Fleisher LA. Systematic review and analysis of postdischarge symptoms after outpatient surgery. Anesthesiology 2002; 96:994. 4. Macario A, Weinger M, Carney S, Kim A. Which clinical anesthesia outcomes are important to avoid? The perspective of patients. Anesth Analg 1999; 89:652. 5. Gold BS, Kitz DS, Lecky JH, Neuhaus JM. Unanticipated admission to the hospital following ambulatory surgery. JAMA 1989; 262:3008. 6. Gan TJ. Risk factors for postoperative nausea and vomiting. Anesth Analg 2006; 102:1884. 7. Koivuranta M, Lr E, Snre L, Alahuhta S. A survey of postoperative nausea and vomiting. Anaesthesia 1997; 52:443. 8. Fernndez-Guisasola J, Gmez-Arnau JI, Cabrera Y, del Valle SG. Association between nitrous oxide and the incidence of postoperative nausea and vomiting in adults: a systematic review and meta-analysis. Anaesthesia 2010; 65:379. 9. Apfel CC, Kranke P, Eberhart LH. Comparison of surgical site and patient's history with a simplified risk score for the prediction of postoperative nausea and vomiting. Anaesthesia 2004; 59:1078. 10. Stadler M, Bardiau F, Seidel L, et al. Difference in risk factors for postoperative nausea and vomiting. Anesthesiology 2003; 98:46. 11. Ruiz JR, Kee SS, Frenzel JC, et al. The effect of an anatomically classified procedure on antiemetic administration in the postanesthesia care unit. Anesth Analg 2010; 110:403. 12. Sinclair DR, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted? Anesthesiology 1999; 91:109. 13. Apfel CC, Lr E, Koivuranta M, et al. A simplified risk score for predicting postoperative nausea and vomiting: conclusions from cross-validations between two centers. Anesthesiology 1999; 91:693. 14. van den Bosch JE, Kalkman CJ, Vergouwe Y, et al. Assessing the applicability of scoring systems for predicting postoperative nausea and vomiting. Anaesthesia 2005; 60:323. 15. Apfel CC, Kranke P, Eberhart LH, et al. Comparison of predictive models for postoperative nausea and vomiting. Br J Anaesth 2002; 88:234. 16. Eberhart LH, Hgel J, Seeling W, et al. Evaluation of three risk scores to predict postoperative nausea and vomiting. Acta Anaesthesiol Scand 2000; 44:480. 17. Apfel CC, Greim CA, Haubitz I, et al. A risk score to predict the probability of postoperative vomiting in adults. Acta Anaesthesiol Scand 1998; 42:495. 18. Charbit B, Alvarez JC, Dasque E, et al. Droperidol and ondansetron-induced QT interval prolongation: a clinical drug interaction study. Anesthesiology 2008; 109:206. 19. http://www.fda.gov/Drugs/DrugSafety/ucm271913.htm (Accessed on September 27, 2011). 20. Tang J, Wang B, White PF, et al. The effect of timing of ondansetron administration on its efficacy, cost-effectiveness, and cost-benefit as a prophylactic antiemetic in the ambulatory setting. Anesth Analg 1998; 86:274. 21. Habib AS, Reuveni J, Taguchi A, et al. A comparison of ondansetron with promethazine for treating postoperative nausea and vomiting in patients who received prophylaxis with ondansetron: a retrospective database analysis. Anesth Analg 2007; 104:548. 22. Kotelko DM, Rottman RL, Wright WC, et al. Transdermal scopolamine decreases nausea and vomiting following cesarean section in patients receiving epidural morphine. Anesthesiology 1989; 71:675. 23. Bailey PL, Streisand JB, Pace NL, et al. Transdermal scopolamine reduces nausea and vomiting after outpatient laparoscopy. Anesthesiology 1990; 72:977. 24. Emend (Aprepitant) Prescribing Information. Section 2. Dosage and Administration, 2.2 Prevention of postoperative nausea and vomiting (PONV). http://www.merck.com/product/usa/pi_circulars/e/emend/emend_pi.pdf (Accessed on October 20, 2011). 25. Yogendran S, Asokumar B, Cheng DC, Chung F. A prospective randomized double-blinded study of the effect of intravenous fluid therapy on adverse outcomes on outpatient surgery. Anesth Analg 1995; 80:682. 26. Lee A, Done ML. The use of nonpharmacologic techniques to prevent postoperative nausea and vomiting: a meta-analysis. Anesth Analg 1999; 88:1362. 27. Kim YH, Kim KS, Lee HJ, et al. The efficacy of several neuromuscular monitoring modes at the P6 acupuncture point in preventing postoperative nausea and vomiting. Anesth Analg 2011; 112:819. 28. Larson JD, Gutowski KA, Marcus BC, et al. The effect of electroacustimulation on postoperative nausea, vomiting, and pain in outpatient plastic surgery patients: a prospective, randomized, blinded, clinical trial. Plast Reconstr Surg 2010; 125:989. 29. Allen TK, Habib AS. P6 stimulation for the prevention of nausea and vomiting associated with cesarean delivery under neuraxial anesthesia: a systematic review of randomized controlled trials. Anesth Analg 2008; 107:1308.
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30. Greif R, Laciny S, Rapf B, et al. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology 1999; 91:1246. 31. Orhan-Sungur M, Kranke P, Sessler D, Apfel CC. Does supplemental oxygen reduce postoperative nausea and vomiting? A meta-analysis of randomized controlled trials. Anesth Analg 2008; 106:1733. 32. Carlisle JB, Stevenson CA. Drugs for preventing postoperative nausea and vomiting. Cochrane Database Syst Rev 2006; 3:CD004125. 33. Apfel CC, Zhang K, George E, et al. Transdermal scopolamine for the prevention of postoperative nausea and vomiting: a systematic review and meta-analysis. Clin Ther 2010; 32:1987. 34. Gan TJ, Sinha AC, Kovac AL, et al. A randomized, double-blind, multicenter trial comparing transdermal scopolamine plus ondansetron to ondansetron alone for the prevention of postoperative nausea and vomiting in the outpatient setting. Anesth Analg 2009; 108:1498. 35. Diemunsch P, Schoeffler P, Bryssine B, et al. Antiemetic activity of the NK1 receptor antagonist GR205171 in the treatment of established postoperative nausea and vomiting after major gynaecological surgery. Br J Anaesth 1999; 82:274. 36. Gan TJ, Gu J, Singla N, et al. Rolapitant for the prevention of postoperative nausea and vomiting: a prospective, double-blinded, placebo-controlled randomized trial. Anesth Analg 2011; 112:804. 37. Altorjay A, Melson T, Chinachoit T, et al. Casopitant and ondansetron for postoperative nausea and vomiting prevention in women at high risk for emesis: a phase 3 study. Arch Surg 2011; 146:201. 38. Singla NK, Singla SK, Chung F, et al. Phase II study to evaluate the safety and efficacy of the oral neurokinin-1 receptor antagonist casopitant (GW679769) administered with ondansetron for the prevention of postoperative and postdischarge nausea and vomiting in high-risk patients. Anesthesiology 2010; 113:74. 39. Kovac AL, Eberhart L, Kotarski J, et al. A randomized, double-blind study to evaluate the efficacy and safety of three different doses of palonosetron versus placebo in preventing postoperative nausea and vomiting over a 72-hour period. Anesth Analg 2008; 107:439. 40. Gan TJ, Apfel CC, Kovac A, et al. A randomized, double-blind comparison of the NK1 antagonist, aprepitant, versus ondansetron for the prevention of postoperative nausea and vomiting. Anesth Analg 2007; 104:1082. 41. Gan TJ, Meyer TA, Apfel CC, et al. Society for Ambulatory Anesthesia guidelines for the management of postoperative nausea and vomiting. Anesth Analg 2007; 105:1615. 42. Gmez-Arnau JI, Aguilar JL, Bovaira P, et al. [Postoperative nausea and vomiting and opioid-induced nausea and vomiting: guidelines for prevention and treatment]. Rev Esp Anestesiol Reanim 2010; 57:508. 43. Taff RH. Pulmonary edema following naloxone administration in a patient without heart disease. Anesthesiology 1983; 59:576. 44. Grines CL, Bonow RO, Casey DE Jr, et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. J Am Coll Cardiol 2007; 49:734. 45. Rose DK, Cohen MM, DeBoer DP. Cardiovascular events in the postanesthesia care unit: contribution of risk factors. Anesthesiology 1996; 84:772. 46. SCIP-Inf-7 www.qualitynet.org (Accessed on March 02, 2010). 47. Keaney A, Diviney D, Harte S, Lyons B. Postoperative behavioral changes following anesthesia with sevoflurane. Paediatr Anaesth 2004; 14:866. 48. Bitsch M, Foss N, Kristensen B, Kehlet H. Pathogenesis of and management strategies for postoperative delirium after hip fracture: a review. Acta Orthop Scand 2004; 75:378. 49. Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 2003; 28:172. 50. Baldini G, Bagry H, Aprikian A, Carli F. Postoperative urinary retention: anesthetic and perioperative considerations. Anesthesiology 2009; 110:1139. 51. Stallard S, Prescott S. Postoperative urinary retention in general surgical patients. Br J Surg 1988; 75:1141. 52. Pavlin DJ, Pavlin EG, Gunn HC, et al. Voiding in patients managed with or without ultrasound monitoring of bladder volume after outpatient surgery. Anesth Analg 1999; 89:90. 53. Ding YY, Sahadevan S, Pang WS, Choo PW. Clinical utility of a portable ultrasound scanner in the measurement of residual urine volume. Singapore Med J 1996; 37:365. Topic 14946 Version 4.0
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GRAPHICS
Anti-emetic agents for postoperative nausea and vomiting*
Relative risk (95% CI)
Nausea Droperidol Dexamethasone Cyclizine Metoclopramide Ondansetron Dolasetron Tropisetron Granisetron Romasetron 0.65 (0.60-0.71) 0.57 (0.48-0.69) 0.65 (0.47-0.90) 0.82 (0.76-0.88) 0.68 (0.63-0.74) 0.82 (0.76-0.90) 0.77 (0.71-0.84) 0.53 (0.45-0.63) 0.62 (0.40-0.96) Vomiting 0.65 (0.61-0.70) 0.51 (0.46-0.57) 0.57 (0.43-0.75) 0.75 (0.70-0.81) 0.55 (0.50-0.59) 0.63 (0.51-0.76) 0.59 (0.50-0.69) 0.40 (0.35-0.46) 0.42 (0.28-0.63) Nausea and vomiting 0.62 (0.58-0.67) 0.49 (0.44-0.54) 0.68 (0.58-0.80) 0.76 (0.70-0.82) 0.56 (0.50-0.63) 0.72 (0.62-0.83) 0.70 (0.61-0.81) 0.39 (0.31-0.48) 0.51 (0.39-0.68) Rescue antiemetic 0.53 (0.47-0.60) 0.50 (0.42-0.59) 0.27 (0.14-0.62) 0.78 (0.69-0.88) 0.55 (0.49-0.61) 0.67 (0.57-0.79) 0.62 (0.53-0.72) 0.29 (0.22-0.39) 0.38 (0.15-0.99)
Drug
* Placebo versus drug. Data from: Carlisle J, Stevenson CA. Drugs for preventing postoperative nausea and vomiting. Cochrane Database Syst Rev 2006; 3:CD004125.
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Example of torsades de pointes
Shown are three ECG leads (I, II, III); bradycardia and prolongation of the QT interval are present. Several runs of polymorphic ventricular tachycardia, called torsades de pointes (TdP) when associated with QT prolongation are seen (panel A); after several minutes, a rapid sustained ventricular tachycardia, sometimes called ventricular flutter, occurs (panel B). This is closely related to ventricular fibrillation. Reproduced with permission
by Samuel Levy, MD.
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Fahrenheit and Celsius temperature equivalents

Fahrenheit
96.0 96.2 96.4 96.6 96.8 97.0 97.2 97.4 97.6 97.8 98.0 98.2 98.4 98.6 98.8 99.0 99.2 99.4 99.6 99.8 100.0 100.2 100.4 100.6 100.8 101.0 101.2 101.4 101.6 101.8 35.6 35.7 35.8 35.9 36.0 36.1 36.2 36.3 36.4 36.6 36.7 36.8 36.9 37.0 37.1 37.2 37.3 37.4 37.6 37.7 37.8 37.9 38.0 38.1 38.2 38.3 38.4 38.6 38.7 38.8
Celsius
102.0 102.2 102.4 102.6 102.8 103.0 103.2 103.4 103.6 103.8 104.0 104.2 104.4 104.6 104.8 105.0 105.2 105.4 105.6 105.8 106.0 106.2 106.4 106.6 106.8 107.0
Fahrenheit
38.9 39.0 39.1 39.2 39.3 39.4 39.6 39.7 39.8 39.9 40.0 40.1 40.2 40.3 40.4 40.6 40.7 40.8 40.9 41.0 41.1 41.2 41.3 41.4 41.6 41.7
Celsius
To convert from Fahrenheit to Celsius: (Temperature - 32) x (5/9) To convert from Celsius to Fahrenheit: ((9/5) x Temperature) + 32
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Differential diagnosis of acute malignant hyperthermia

Hypercapnia
Cardiorespiratory Hypoventilation Sepsis Neurologic Hypoxic encephalopathy Meningitis Intracranial bleed Traumatic brain injury Endocrine Thyrotoxicosis Pheochromocytoma Toxicologic Serotonin syndrome Radiologic contrast neurotoxicity Anticholinergic syndrome Cocaine toxicity Amphetamine toxicity Alcohol withdrawal Salicylate toxicity Iatrogenic Faulty temp probe Overheating Absorption of CO
2
Tachycardia
Rigidity/myoclonus
Metabolic acidosis
Rhabdomyolysis
Hyperthermia
+ +
+ +
+/-
+/-
+/-
+/-
+/-
+/+/+/-
+ + +
+/+/+/-
+/+/+/-
+ +/+/-
+ +
+/-
+ +/-
+/-
+/-
+/-
+/-
+/-
+/-
+/-
+ +
+ +
+ +
+ +
+ +
+ +
+ -
+ +
+ +
+ + -
during laparoscopy Miscellaneous Neuroleptic malignant syndrome Heatstroke Extrapyramidal syndrome + + +/+
+/-
+ -
+ +
+ -
+ -
+ -
+: likely manifestation; +/-: possible manifestation; -: unlikely manifestation.
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Overview of Complications Occurring in The Post-Anesthesia Care Unit

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Overview of Complications Occurring in The Post-Anesthesia Care Unit

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Overview of complications occurring in the post-anesthesia care unit

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