Chapter 71. Postoperative Complications

1. Complications in the postanesthesia care unit (PACU) are common. Despite pharmacologic and medical advances over the last 10 years, the incidence of postoperative complications appears largely unchanged. Even minor postoperative complications are important to patients, and greater efforts at preventing and treating such complications should lead to improved postoperative recovery and patient satisfaction.

2. Knowledge of the expected postoperative course for a given operation is essential to identifying and managing problems when they occur. Awareness of the temporal patterns of complications is important to anticipating periods of increased perioperative risk.

3. Airway obstruction is common in the postoperative period. Upper airway obstruction arises in the pharynx (posterior tongue displacement, soft tissue collapse), larynx (laryngeal edema, laryngospasm, vocal cord paralysis), or trachea due to extrinsic compression. Anesthetics, and even minimal residual neuromuscular blockade, may lead to upper airway obstruction.

4. Hypoxemia is common in postoperative patients not receiving supplemental oxygen (O2). Following general anesthesia or sedation, all patients should receive supplemental O2 during their transport from the operating room and during their initial PACU stay. Continuous monitoring of O2 saturation with pulse oximetry is essential for early detection of hypoxemia.

5. Several conditions may necessitate continued intubation after surgery. They include delayed emergence from general anesthesia, inadequate reversal of neuromuscular blockade, potential for airway obstruction, inadequate gas exchange, and hemodynamic instability.

6. Hypotension is a common postoperative complication that results from hypovolemia (most common), decreased vascular tone, and/or reduced cardiac output. Causes of hypovolemia in the PACU include inadequate fluid replacement, ongoing hemorrhage, and fluid sequestration ("third spacing"). Clinical evaluation of a patient's intravascular volume status requires consideration of preoperative status, type and duration of surgery, estimated blood loss, fluid replacement, and evidence of hemostasis.

7. Cardiac dysrhythmias are common during the perioperative period, and most dysrhythmias are benign. The precipitating factor is usually a transient imbalance such as hypoxia, ischemia, increased catecholamines, altered acid–base status, or electrolyte abnormalities. The management strategy for a new dysrhythmia is focused on stabilizing hemodynamics and treating the underlying problem.

8. Hypertension is a very common problem in the postoperative period. Sympathetic nervous system activation resulting from noxious stimuli, such as pain, anxiety, bladder distension, fluid overload, hypoxemia, hypercarbia, and hypothermia, are common precipitants. The decision to treat hypertension should take into consideration the patient's baseline blood pressure, coexisting diseases, and perceived risk of complications.

9. Urinary retention and oliguria are common problems in the PACU. Oliguria is most commonly caused by hypovolemia (prerenal) in the immediate postoperative period, but postrenal and intrinsic renal causes should also be considered.

10. Patients who develop bleeding postoperatively require rapid evaluation to differentiate poor surgical hemostasis (which may require immediate reoperation) or from a diffuse coagulopathy. It is important to appreciate that surgical and nonsurgical bleeding often coexist. If there is evidence of significant bleeding, diagnosis and treatment usually occur simultaneously. Adequate intravenous (IV) access should be established, availability of appropriate blood products ensured, and a diagnostic evaluation performed.

11. Hypothermia remains a common PACU problem. Even mild hypothermia (core temperature between 34°C and 36°C) has been associated with adverse outcomes, including myocardial ischemia, arrhythmias, coagulopathy, wound infection, decreased drug metabolism, and poor patient satisfaction.

12. The major causes of delayed awakening after general anesthesia can be divided into 3 groups: (1) prolonged pharmacologic effects, (2) metabolic abnormalities, and (3) neurologic injury.

13. Awareness with recall of intraoperative events is an infrequent but recognized complication of general anesthesia that can result in significant distress to patients and long-term psychological sequelae. In cases of possible awareness, the patient should be offered counseling and psychological support.

Complications in the PACU are common. In a study of 18,473 patients entering the PACU at a university teaching hospital, Hines et al1 reported a complication rate of 23%, with nausea and vomiting (9.8%), need for upper airway support (6.9%), and hypotension (2.7%) the most frequently encountered problems (Fig. 71-1). Despite pharmacologic and medical advances over the last 10 years, the incidence of postoperative complications appears largely unchanged.2 Even minor postoperative complications are important to patients (Table 71-1), and greater efforts at preventing and treating complications should lead to improved postoperative recovery and patient satisfaction.3,4

This chapter focuses on postoperative complications commonly encountered in the PACU setting, with emphasis on early diagnosis and treatment. Naturally there is some overlap with events that occur during routine recovery (see Chapter 70). Many of the specific details of diagnosis and management are covered in other chapters of this book and are not repeated here.

As with intraoperative anesthetic care, knowledge of the expected postoperative course for a given operation is essential for identifying and managing problems when they occur including awareness of the perioperative risk (Table 71-2).5 When complications do occur, early communication with the surgical team is essential.

Upper Airway Obstruction

Upper airway obstruction can arise in the pharynx from posterior tongue displacement or soft tissue collapse; the larynx from laryngeal edema, laryngospasm, or vocal cord paralysis; or the large airways from extrinsic compression. Anesthetics, and even minimal residual neuromuscular blockade, may lead to upper airway obstruction.6 Principal signs are lack of adequate air movement, intercostal and suprasternal retractions, and discoordinate abdominal and chest wall movements during inspiration.

Pharyngeal Obstruction

Usually simple maneuvers such as a chin lift, jaw thrust, and lateral decubitus positioning, as well as decreasing the level of sedation, are successful in relieving pharyngeal obstruction. Oropharyngeal or nasopharyngeal airways are useful adjuncts. Nasopharyngeal airways are better tolerated than oral airways at light levels of sedation because they are less likely to provoke a gag reflex. Careful insertion of nasal airways is necessary to avoid creating a nosebleed.

Laryngeal Obstruction

Laryngeal Edema

Laryngeal or subglottic edema can create airway obstruction. This is particularly true in children because of the smaller airway diameter and in patients recovering from neck surgery. Treatment of partial airway obstruction resulting from airway edema includes head-up positioning to promote venous drainage and administration of steroids and nebulized epinephrine. Treatment of severe airway edema may require emergency reintubation or tracheostomy.

Prolonged surgery in a head-down position can result in significant swelling of the airway. The common practice of listening for an air leak with a positive pressure breath after deflation of the endotracheal cuff is a reliable method to determine that extubation will likely be successful if a leak is present.7 However, a failed leak test does not preclude uneventful extubation.8 Patients at risk for significant swelling should be evaluated (using direct or fiberoptic laryngoscopy) before extubation because they are at risk for complete airway obstruction. Patients with significant obstruction should remain intubated until airway edema resolves.

Laryngospasm

Laryngospasm is a reflex resulting from prolonged glottic closure. Although the cords are adducted, the primary obstruction is caused by tonic contraction of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet. Laryngospasm may be precipitated by light anesthesia and the presence of an airway irritant such as secretions, blood, or a foreign body. It also can be caused by stimulation from an elongated uvula, may be sleep related, or may be stimulated by distal esophageal afferents.9 Partial laryngospasm allows for some air movement and may be difficult to distinguish from other causes of upper airway obstruction. Complete laryngospasm prevents all air movement and is a prominent cause of negative pressure pulmonary edema (see later section on pulmonary edema). Management of laryngospasm consists of jaw thrust, positive pressure ventilation, and possibly administration of intravenous propofol or a small dose of succinylcholine (0.1 mg/kg).

Vocal Cord Paralysis

Vocal cord paralysis can be due to either nerve injury or mechanical injury and may be unilateral or bilateral. Injury to the recurrent laryngeal nerve prevents abduction of the ipsilateral vocal cord, which becomes fixed in a paramedian position because of the unopposed action of the cricothyroid muscle. An inflated endotracheal tube cuff in the subglottic larynx can compress the anterior branch of the recurrent laryngeal nerve as it enters between the cricoid and thyroid cartilage, resulting in nerve injury. Recurrent laryngeal nerve injury may occur after operations such as a rigid bronchoscopy, thyroid and parathyroid surgery, or laryngeal and thoracic surgery. Arytenoid avulsion can result in vocal cord immobility.10

Hoarseness usually is noted immediately after extubation. Healthy patients generally tolerate the resulting increased airway resistance, but it may become a problem in patients with preexisting pulmonary compromise. Bilateral recurrent laryngeal nerve injuries result in inadequate glottic opening and require emergent reintubation or tracheostomy. Vocal cord paralysis usually is associated with spontaneous recovery, but it may take a period of days to months. Otolaryngologic evaluation in the acute setting is generally warranted.

Extrinsic Airway Compression

Acute extrinsic neck compression from an expanding neck hematoma can be life threatening. Neck hematomas can develop after carotid endarterectomy, thyroid or parathyroid surgery, or other neck surgery. Although many neck hematomas can be treated conservatively, they should be closely monitored for progression and signs of airway compromise. A rapidly expanding hematoma can cause marked tracheal deviation and make emergency reintubation extremely difficult. If possible, subcutaneous clot should be decompressed by removing surgical sutures. Definitive treatment usually requires returning to the operating room for hematoma evacuation and exploration.11,12

General anesthesia inhibits hypoxic and hypercapnic ventilatory drive and reduces the lung's functional residual capacity. These changes may persist for variable periods of time postoperatively and predispose to hypoventilation and hypoxemia. Additional causes of hypoxemia and hypercapnia encountered in the PACU include aspiration, pulmonary edema, pulmonary embolism (PE), and pneumothorax.

Hypoxemia

Hypoxemia is common in postoperative patients not receiving supplemental O2. In a study of patients undergoing transfer from the operating room to the PACU, Tyler et al13 found that 30% of patients had O2 saturations (SpO2) less than 90% while breathing air. The most common causes of hypoxemia in the early postoperative period include hypoventilation and atelectasis. Patients with preexisting lung disease or obesity and those recovering from thoracic and upper abdominal surgery are at increased risk (Fig. 71-2).14

Following general anesthesia or sedation, all patients should receive supplemental O2 during transport from the operating room and during their initial PACU stay. Continuous monitoring of O2 saturation with pulse oximetry is essential to early detection of hypoxemia. It is important to remember that supplemental O2 can prolong the time to desaturation, which may delay the detection of hypoventilation. Hypoxemia is treated by increasing the inspired O2, elevating the head of the bed, performing lung expansion maneuvers, and eliminating other reversible causes (eg, bronchospasm, secretions, and mucus plugs). Continuous positive airway pressure may be effective in treating more severe hypoxemia in some patients and decrease the need for endotracheal intubation (Fig. 71-3).15,16

Hypoventilation

Hypoventilation is characterized by an inappropriately low minute ventilation with resulting hypercapnia and respiratory acidosis. Severe hypoventilation results in hypoxemia, carbon dioxide (CO2) narcosis, and ultimately apnea. Causes of postoperative hypoventilation include decreased ventilatory drive, respiratory muscle insufficiency, increased CO2 production, and acute or chronic lung disease.

Decreased Ventilatory Drive

The typical combination of inhaled anesthetics, opioids, and benzodiazepines can depress both the hypercarbic and hypoxic drive, resulting in hypoventilation. Development of postoperative hypercarbia can be deceptive because patients may appear awake and even complain of pain while experiencing significant hypoventilation. Ventilatory depression from opioids and sedatives will become significantly worse, however, if the patient falls asleep (see Chapter 41). A balance must be achieved between adequate analgesia and an acceptable level of respiratory depression. Opioid-induced hypoventilation can be reversed by small incremental doses of naloxone (0.04-0.08 mg) while preserving some analgesia. Reversal of narcosis usually occurs within 1 to 2 minutes and lasts for 30 to 60 minutes. Caution should be exercised because the duration of action of naloxone is shorter than that of most opioids, and repeated doses of naloxone or an infusion may be required. Flumazenil can reverse the sedative effects of benzodiazepines, but it does not reverse the depression of hypoxic drive (see Chapter 40). Flumazenil does not reverse opioid-induced respiratory depression.

Respiratory Muscle Insufficiency

Incomplete reversal of neuromuscular blockade can result in airway obstruction and hypoventilation. The patient may exhibit discoordinated movements, generalized weakness, hypoxemia, or shallow breathing. The frequency of residual blockade ranges between 4% and 50% is more common in patients who receive long-acting muscle relaxants such as pancuronium and those not treated with reversal agents (Fig. 71-4).17-19 Residual blockade is associated with muscle weakness, O2 desaturation, atelectasis, and respiratory failure.

Limited chest expansion may be caused by pain (splinting) after thoracic and upper abdominal surgery, resulting in atelectasis and consequently right-to-left shunting. Better analgesia (particularly that produced by neuraxial and intercostal blocks) facilitates deep breathing and significantly reduces hypercapnia and hypoxemia.

Many factors increase the work of breathing for postoperative patients. For example, functional residual capacity can be reduced by airway closure and collapse; significant muscular effort is required to reexpand the lung. Other intrathoracic factors, such as pulmonary edema, pneumothorax, restrictive lung diseases, and skeletal abnormalities, can reduce lung compliance and increase energy expenditure for breathing. Obesity, gastric distension, and restrictive dressings on the chest or abdomen are extrathoracic factors that result in increased work of breathing and the potential for inadequate ventilation. Incentive spirometry, chest physiotherapy, upright positioning, and continuous positive airway pressure may be effective therapeutic maneuvers for these patients.

Acute or Chronic Lung Disease

Preexisting pulmonary disease is an important risk factor for developing postoperative pulmonary complications.20 Respiratory diseases usually are categorized according to the manner in which they alter pulmonary mechanics, producing either a limitation of expiratory airflow (obstructive disease) or a limitation of lung expansion (restrictive disease). Exacerbations of obstructive diseases, such as asthma and chronic obstructive pulmonary disease (COPD), are frequently accompanied by increasing hypercapnia and worsening hypoxemia. The key management issues are similar in both acute asthma and COPD exacerbations. They include treating bronchospasm and airway inflammation, correcting hypoxemia and respiratory acidosis, clearing secretions, and removing/treating precipitating factors. The concern for CO2 retention and respiratory depression resulting from administration of supplemental O2 to patients with COPD has been overemphasized.21 In all cases, correction of hypoxemia should take precedence over concerns for CO2 retention.

Restrictive pulmonary disorders are characterized by decreased lung compliance resulting from intrinsic disease of the lungs (eg, pulmonary fibrosis, pulmonary edema) or extrinsic disorders (eg, pleural effusions, obesity, scoliosis, abdominal distension, massive ascites) that impair normal lung expansion. Management is directed at treating the underlying disease process (eg, steroids for pulmonary fibrosis, draining the pleural space, etc) and supportive respiratory care.

Aspiration

General anesthesia and surgery depress airway protective reflexes and predispose patients to aspiration. Gastric contents or objects such as dislodged teeth can enter the trachea during induction or emergence and even after PACU admission. Perioperative pulmonary aspiration is an infrequent event (1 in 2000-3000 general anesthetics), but it can result in severe morbidity and mortality.22 Signs of significant aspiration include bronchospasm, hypoxemia, atelectasis, tachypnea, tachycardia, and hypotension. Radiographic evidence of aspiration (usually infiltrates in the upper lobes of supine patients) may take some time to appear.

The severity of symptoms depends on the type and volume of material aspirated. Aspiration pneumonitis (Mendelson syndrome) is a chemical injury to the lungs caused by inhalation of sterile acidic gastric contents, whereas aspiration pneumonia refers to inhalation of contents colonized by pathogenic bacteria.23 Initial treatment of a significant aspiration consists of oropharyngeal suctioning, administration of bronchodilators for bronchospasm, and supplemental O2. Plans should be made for transfer of the patient to an intensive care unit (ICU). Bronchoscopy may be of benefit to remove particulate matter from the tracheobronchial tree, but pulmonary lavage with large volumes of saline is generally believed to be detrimental. Mechanical ventilatory support with positive end-expiratory pressure may be necessary if hypoxemia is severe. Administration of empirical antibiotics for aspiration is not recommended unless the material aspirated has a high bacterial load, as with a small bowel obstruction. Steroids are of no benefit in treatment if administered after an aspiration has occurred.24 In cases of mild or uncertain aspiration, close postoperative observation should be undertaken with continuous pulse oximetry monitoring and chest radiography. Patients with clinical evidence of aspiration who do not develop signs or symptoms (cough, wheeze, hypoxia on room air, or radiologic abnormalities) within 2 hours of aspiration are unlikely to develop pulmonary complications (Fig. 71-5).25,26

Pulmonary Edema

Pulmonary edema is the accumulation of fluid in the interstitium and alveoli of the lungs that can hinder gas exchange. Cardiogenic pulmonary edema results from increased pulmonary capillary pressure secondary to elevated left atrial pressure that may be precipitated by fluid overload, left ventricular dysfunction, or mitral valve disease. A careful physical examination, chest x-ray film, electrocardiography (ECG), and arterial blood gas analysis are useful for diagnosis. Evaluation by a cardiologist may be indicated when myocardial ischemia or acute valvular disease is considered the cause of the pulmonary edema. Noncardiac pulmonary edema usually is due to increased pulmonary capillary permeability. Mainstays of treatment include supplemental O2, diuretics, vasodilators, and mechanical ventilatory support with positive end-expiratory pressure.

Pulmonary edema can occur in the operating room or PACU most commonly secondary to acute upper airway obstruction (negative-pressure pulmonary edema). During upper airway obstruction, forceful inspiratory efforts against a closed glottis can result in large negative intrathoracic pressures with an increased left ventricular preload and afterload. In addition, hypoxia and increased circulating catecholamine levels may elevate pulmonary and systemic vascular resistance, shift the intraventricular septum to the left, and cause left ventricular diastolic dysfunction. These result in negative-pressure pulmonary edema, a rapid onset of copious pink fluid with bubbles due to acute fluid filtration into the lung, and capillary failure resulting in alveolar hemorrhage and hemoptysis.27,28 Negative pressure pulmonary edema generally resolves within 12 to 48 hours when recognized early and respiratory support and diuresis are instituted promptly.29

Pulmonary Embolism

Pulmonary embolism (PE) contributes to 50,000 to 200,000 deaths annually.30 The mortality rate exceeds 15% in the first 3 months after the diagnosis is made, and in nearly 25% of patients with PE, the initial clinical sign is sudden death.31 Under pathologic conditions, thrombi escape the normal fibrinolytic system, propagate in the deep veins of the lower extremities and pelvis, and then dislodge and embolize, blocking pulmonary vessels. Thrombosis is triggered by venous stasis, hypercoagulability, and vessel wall inflammation (Virchow triad). The diagnosis of PE can be challenging because the clinical presentation can vary substantially. Dyspnea is the most frequent symptom, although patients may be asymptomatic. A patient with a massive PE may present with hypotension, severe hypoxemia, cardiogenic shock, or cardiac arrest. ECG may reveal signs of right ventricular strain but may be entirely normal in previously healthy patients, and the chest x-ray film is often normal. Chest computed tomography (CT) has become the primary diagnostic imaging modality to evaluate suspected PE. Alternative imaging modalities include a ventilation-perfusion lung scan, magnetic resonance angiography, echocardiography, and pulmonary angiography. Treatment of PE is supportive (volume infusion, vasopressors, and mechanical ventilation) because anticoagulation or thrombolytic therapy often is not an option in the immediate postoperative period. Inhaled nitric oxide has been given experimentally to reverse pulmonary vasospasm following pulmonary embolism.32 Insertion of an inferior vena cava filter may be beneficial to prevent further embolism in patients in whom anticoagulation is contraindicated. In patients with severe hypoxemia and/or hypotension, emergency pulmonary embolectomy may be required.

Pneumothorax

Pneumothorax is the accumulation of gas within the pleural space. It can result from surgical entrance into the pleural space during thoracic, upper abdominal, or retroperitoneal surgery, tracheostomy, or surgery on the chest wall or neck. Other causes include blunt or penetrating trauma, rupture of blebs or bullae, barotrauma from positive pressure ventilation, and as a complication of procedures such as central line placement, thoracentesis, or upper extremity neural blockade.33

A tension pneumothorax occurs when the site of pulmonary air leak forms a 1-way valve, allowing airflow into the pleural space during inspiration but preventing its elimination during expiration. The rapid unilateral increase in intrathoracic pressure can be life threatening because it can produce a contralateral mediastinal shift with a rapid deterioration in gas exchange, diminished cardiac output, and marked hemodynamic instability. Diminished or absent chest sounds on auscultation may be present over 1 hemithorax. If a tension pneumothorax is suspected and hemodynamic or respiratory status is compromised, then decompression should be performed immediately, without waiting for confirmation of the diagnosis by chest radiography. A 14-gauge Angiocath can be placed through the chest wall in the second intercostal space at the midclavicular line or the fourth intercostal space at the midaxillary line. The needle is removed, and the catheter is held securely in position until a tube thoracostomy can be performed. A rush of released air and immediate improvement in respiratory and hemodynamic status should occur when decompression is successful.

A disposable 1-piece suction device (eg, Pleurovac) is commonly used for chest tube drainage. The underlying principle of drainage is the same as the original 3-bottle system, but the apparatus is more compact with fewer connections. The proximal compartment collects drainage, the middle prevents flow of air back into the thorax by forming a water seal, and the distal compartment regulates the amount of suction that is applied to the pleural cavity (Fig. 71-6). Generally, the chest tube initially is given active suction of 20-cm water. If no bubbles are observed in the water seal (ie, no air leak is detected), active suction may not be necessary.

Chest tubes should be monitored continuously to ensure that they are functioning properly and achieving the desired therapeutic effect. The position of the chest tube, lung expansion, and fluid content of the pleural space should be evaluated by chest radiography.

Prolonged Intubation

Several conditions may require continued intubation after surgery. These include delayed emergence from general anesthesia, inadequate reversal of neuromuscular blockade, potential for airway obstruction, inadequate gas exchange, and hemodynamic instability.

Delayed emergence from general anesthesia due to volatile or IV agents is an indication to delay extubation (see later section on delayed awakening). Although reversal of narcosis may be facilitated with naloxone, it is prudent to provide support with controlled or assisted ventilation until the patient emerges spontaneously. Spontaneous ventilation of the intubated patient through a T-piece may be sufficient when prolonged emergence is not expected. To minimize the risk of aspiration, the presence of a full stomach mandates that laryngeal reflexes and consciousness are fully recovered before extubation.

The potential for airway obstruction is highest after surgical procedures of the head and neck, drainage of pharyngeal abscesses, or when the jaws are wired closed following facial trauma. As stated previously, obstruction from glottic edema can occur after prolonged surgery, especially in the prone or head-down position. Hemodynamic instability, when severe, may be associated with a variable degree of impaired gas exchange or impaired consciousness that requires continuation of mechanical ventilation. Marginal oxygenation or ventilation provides additional stresses to a cardiovascular system subjected to hypovolemia, hypothermia, or myocardial ischemia. Early admission to an ICU should be considered for patients who are not anticipated to improve after a few hours in the PACU.

Hypotension

Hypotension is a common postoperative complication that can result from hypovolemia, decreased systemic vascular tone, and/or reduced cardiac output. Hypotension can result in myocardial ischemia or infarction, stroke, acute renal failure, and bowel ischemia. During hypotension, the body attempts to redirect blood flow toward the brain, heart, and kidneys: Signs of hypoperfusion of these organs suggest that compensatory mechanisms have failed. Hypotension may be defined as a more than 20% decline of blood pressure from baseline or evidence of end-organ hypoperfusion.

Accurate measurement of blood pressure is essential to making a correct diagnosis of hypotension. An inappropriately large blood pressure cuff or an arterial transducer that is improperly zeroed, positioned, or dampened will provide falsely low blood pressure readings.

Hypovolemia

Causes of hypovolemia in the PACU include inadequate fluid replacement, ongoing hemorrhage, and fluid sequestration ("third spacing"). Clinical evaluation of a patient's intravascular volume status requires consideration of preoperative status and comorbid conditions, type and duration of surgery, estimated blood loss, fluid replacement, and evidence of hemostasis. Signs of hypovolemia include hypotension, tachycardia, orthostasis, decreased skin turgor, oliguria, and dry mucous membranes. Administration of a fluid bolus during the initial assessment is generally a safe maneuver. Persistent hypotension despite seemingly adequate fluid replacement requires further assessment and may require monitoring of central venous and pulmonary artery pressures or echocardiography.

Systemic Vasodilatation

Neuraxial anesthesia, residual inhalation agents, administration of vasodilators, rewarming after hypothermia, transfusion reactions, systemic inflammation, and sepsis can cause hypotension by decreasing systemic vascular resistance and impairing venous return. Hypovolemia increases systemic hypotension due to vasodilatation, but fluid resuscitation often does not fully restore the blood pressure. Pharmacologic treatment includes administration of a peripheral vasoconstrictor. A pure α1-agonist, such as phenylephrine, often is chosen because it is unlikely to cause dysrhythmias and can be administered through a peripheral intravenous line. More potent pressor agonists, such as norepinephrine, usually require central venous access for administration. Diagnosis and treatment of the specific etiology of the vasodilatation should be concurrent with symptomatic treatment.

Myocardial Ischemia and Infarction

A variety of factors in the perioperative period may alter the balance between myocardial O2 supply and demand. The body's physiologic response to surgery is an increase circulating catecholamines; these increase myocardial demand by increasing heart rate, myocardial contractility, and peripheral vascular resistance. Myocardial O2 supply may be decreased by perioperative factors such as hypoxemia and hypotension. Patients with coronary artery disease or those at risk for coronary disease have significantly higher rates of perioperative myocardial ischemia, infarction, and cardiac death.34 Mangano et al35 reported that the incidence and severity of perioperative myocardial ischemia was greatest during the first 48 hours after surgery. Badner et al36 reported the peak incidence of perioperative myocardial infarction (MI) occurred during the first 24 hours following surgery.

The diagnosis of perioperative ischemia can be difficult because often the condition is silent. Postoperative chest pain may be masked by residual anesthesia or analgesics, and pain perception may be altered by the competing stimulus of incisional pain. The patient at high risk for perioperative myocardial ischemia and infarction should be assessed by ECG preoperatively, immediately after surgery, and on the first 2 postoperative days.37 In patients with ECG changes or chest pain typical of an acute coronary syndrome, serial markers of myocardial injury (troponin, creatine phosphokinase) should be followed. Therapy for perioperative ischemia or MI is similar to that for other medical patients with MI and includes aggressive pain control, β-blockade, aspirin, and nitrates. Administration of anticoagulants is generally reserved for cases of acute coronary stent thrombosis or ST elevation MI and requires weighing the risks of surgical bleeding with the benefits of anticoagulation.

Dysrhythmias

Cardiac dysrhythmias are common during the perioperative period; transient dysrhythmias reportedly occur in 62% to 84% of patients.38 Most perioperative dysrhythmias are benign. They are most likely to occur in patients with underlying structural heart disease; however, the precipitating factor is usually a transient event such as hypoxia, ischemia, increased circulating catecholamine levels, altered acid–base status, or electrolyte abnormalities. The clinical significance of a dysrhythmia depends on the patient's underlying cardiac function. Bradycardia may cause a clinically significant reduction in cardiac output in a patient with relatively fixed stroke volume. Tachycardia may reduce cardiac output by decreasing diastolic filling time and increasing myocardial O2 consumption, resulting in myocardial ischemia. Loss of atrial contraction in atrial fibrillation may decrease cardiac output by decreasing diastolic filling. The management strategy for a new dysrhythmia is focused on stabilizing hemodynamics and treating the underlying problem. Significant hemodynamic instability that results from dysrhythmia is an indication for emergent cardioversion.

Specific antiarrhythmic therapy in the postoperative setting is similar to that in the nonoperative setting, but generally therapy will not be effective unless the precipitating factors are identified and treated.

Tachycardia

Tachyarrhythmias usually are classified according to their anatomic origin as either supraventricular or ventricular. Supraventricular arrhythmias include sinus tachycardia, atrial fibrillation and flutter, ectopic atrial tachycardia, multifocal atrial tachycardia, junctional tachycardia, atrioventricular nodal reentrant tachycardia, and accessory pathway reciprocating tachycardias. Ventricular arrhythmias consist of ventricular premature beats, ventricular tachycardia, and ventricular fibrillation. For a comprehensive discussion of cardiac arrhythmias, see Chapters 44 and 51.

Sinus tachycardia is the most common dysrhythmia in the immediate postoperative period. Increased sympathetic discharge resulting from pain, hypovolemia, anemia, anxiety, hypoxia, and hypercarbia are common causes. Sinus tachycardia usually is benign; however, it may precipitate myocardial ischemia in a patient with coronary artery disease. Treatment of the underlying cause(s) (eg, analgesics for pain, intravenous fluids for hypovolemia, sedatives for anxiety) usually is adequate for resolution. In patients at risk for myocardial ischemia, β-blockade usually is effective in reducing the heart rate.

Supraventricular tachyarrhythmias are more common after thoracic surgery than after other types of noncardiac surgery with a reported incidence of 15% or more.39 In these patients, prophylaxis with calcium channel blockers or β-blockers significantly reduces the occurrence of atrial fibrillation.39

Atrial fibrillation is the most common supraventricular dysrhythmia after both cardiac and noncardiac surgery and has the greatest potential for serious consequences.40,41 For unstable patients with atrial fibrillation and a rapid ventricular rate, urgent cardioversion is indicated. In hemodynamically stable patients, β-blockers, calcium channel blockers, or amiodarone are alternatives for rate control. In most patients, atrial fibrillation resolves within 36 to 48 hours. New-onset atrial fibrillation raises increased risk of stroke from cerebral embolism; anticoagulation may not be possible in a postoperative patient at risk for bleeding.

Bradycardia

Bradycardia usually is associated with sinus node or atrioventricular node dysfunction. The various possible presentations are sinus bradycardia, sinus pause, sinoatrial block, sinus arrest, junctional rhythms, and varying degrees of heart block. At sufficiently slow heart rates, ventricular escape beats may be seen. In the postoperative setting, bradycardia is often due to increased vagal tone as a result of hypoxemia, pain, nausea, drugs (eg, neostigmine, β-blockers, or opioids) or the effects of neuraxial anesthesia. Sinus bradycardia can be a normal rhythm in a young healthy patient. Bradycardia without hypotension usually is benign and no treatment is necessary. If bradycardia is associated with hemodynamic compromise (hypotension, low cardiac output), treatment with antimuscarinic agents (glycopyrrolate or atropine) or β-agonists (ephedrine) can restore normal sinus rhythm.

Development of complete heart block can occur in patients with preexisting conduction disorders, and the resulting idioventricular bradycardia often compromises systemic hemodynamics. Treatment includes atropine to improve atrioventricular nodal conduction and permit supraventricular impulse transmission, or epinephrine, isoproterenol, or ventricular pacing to increase ventricular rate. In the setting of complete heart block, the need to provide either external or internal pacing must be anticipated; consultation with a cardiologist in anticipation of requirement for pacing is recommended.

Ectopy

Ectopic beats, whether atrial or ventricular, are common and by themselves do not necessarily imply underlying cardiac disease. In the postoperative period, ectopic beats often are associated with electrolyte imbalances, hypoxia, acid–base abnormalities, and hypertension. They may result from drug therapy (eg, digitalis toxicity) or cardiac irritation from central venous catheters. Hypokalemia and hypomagnesemia are the most common electrolyte abnormalities associated with ectopy. Care should be taken when correcting these abnormalities because rapid administration of large quantities of either potassium or magnesium can produce hemodynamic and rhythm disturbances more deleterious than simple ectopy.

Frequent premature atrial contractions are usually of minor hemodynamic significance but may be harbingers of supraventricular tachycardia or atrial fibrillation. Medical therapy is generally not needed, but patients should be monitored closely.

Similarly, premature ventricular contractions in an asymptomatic patient generally do not require treatment. Preoperative ventricular ectopy usually reoccurs postoperatively and does not predict an adverse outcome.42

Postoperative ECG Changes

ECG changes are common after anesthesia and surgery. Changes in P- or T-wave morphology, intraventricular conduction, or ST segments may occur in the absence of a cardiac abnormality or ischemia. These changes can result from cardiac effects of anesthetics and other drugs, increased sympathetic tone, hypothermia, and electrolyte imbalances. Breslow et al43 reported an 18% incidence of T-wave changes in a postoperative population; changes occurred with equal frequency in all age groups and were not more common in patients with preexisting coronary artery disease. These patients did not demonstrate any evidence of postoperative myocardial ischemia or injury, and most of the ECG changes resolved with 24 hours. If there is a suspicion of perioperative ischemia, T-wave changes should be treated as a potential MI; therapeutic control of heart rate and blood pressure, serial ECGs and cardiac enzyme levels, as well as a cardiology consultation are indicated.

Hypertension

Hypertension is a very common problem in the postoperative period. Typical onset is early, usually within 2 hours after surgery, and generally requires treatment for 6 hours or less. It occurs most commonly after vascular, head and neck, and neurosurgical procedures (Table 71-3).44 Patients with preexisting hypertensive disease are more likely to develop postoperative hypertension, especially if antihypertensive medications are withheld preoperatively. Noxious stimuli, including pain, anxiety, bladder distension, fluid overload, hypoxemia, hypercarbia, and hypothermia, activate the sympathetic nervous system producing hypertension. Complications of severe postoperative hypertension include myocardial ischemia/infarction, dysrhythmias, congestive heart failure, stroke, and increased surgical bleeding.

The decision to treat hypertension requires consideration of the patient's baseline blood pressure, coexisting diseases, and perceived risk of complications: systolic or diastolic blood pressure more than 20% above baseline, signs or symptoms of complications such as chest pain or dysrhythmias, or a perceived increased risk of complications are indications for treatment.45 Reversible causes of hypertension (eg, pain, anxiety, bladder distension) should be ruled out before initiation of antihypertensive therapy. For patients with preexisting hypertension, resumption of chronic antihypertensive therapy is a sensible option. Short-term control of blood pressure in the PACU is best accomplished with drugs that have a rapid onset and possess a short to intermediate duration of action. Intravenous agents such as labetalol, esmolol, propranolol, and hydralazine are commonly used for short-term control of blood pressure. For persistent or refractory hypertension, continuous infusions of vasodilators such as nitroprusside, nitroglycerin, nicardipine, or fenoldopam may be required.

Postoperative bladder distension with associated urinary retention may induce pain, restlessness, and delirium and may delay PACU discharge. Furthermore, severe or prolonged bladder distension may cause permanent damage to the detrusor muscle.46 The prevalence of postoperative bladder distension ranges from 1% to more than 50% of patients and depends on the population, type of surgery, and method of estimating bladder distension.47 A study of predictive factors for early postoperative urinary retention in the PACU found older age (≥50 y), bladder volume on entry to PACU (≥270 mL), and quantity of intraoperative fluids administered (>750 mL) each independently increased risk of urinary retention.48 Based on these results, regular evaluation of bladder volume with ultrasound in the PACU was suggested, especially in patients with the enumerated risk factors.

Oliguria, defined as a urine output less than<0.5 mL/kg/h, is a frequent postoperative occurrence. Oliguria may be a sign of acute kidney injury (AKI), a condition associated with a markedly increased morbidity and mortality in the postoperative patient.49,50

• Prerenal AKI is caused by decreased renal perfusion due to decreased effective circulating blood volume or impaired renal hemodynamics. Hypovolemia is the most common prerenal cause of oliguria in this setting. Administration of a 250- to 500-mL IV fluid bolus helps to rule out hypovolemia. Maintenance of adequate systemic blood pressure (based on preoperative values) is essential for sufficient renal perfusion. If urine output does not improve despite what appears to be adequate fluid resuscitation and blood pressure, a more extensive investigation is warranted. Central venous pressure monitoring and/or echocardiography may provide better assessment of intravascular volume status and cardiac function.
• Postrenal AKI is caused by obstruction of urinary flow. In patients without a bladder catheter, it is important to determine the time since last voiding. Placement of a urinary catheter helps differentiate insufficient urine production from the inability to void. Irrigation of the urinary catheter to assess for kinking, obstruction, or migration is important to exclude these common postrenal causes of oliguria.
• Intrinsic AKI is divided into tubular (acute tubular necrosis), interstitial, glomerular, and vascular etiologies. Analysis of urine electrolytes, osmolality, and cast formation may be helpful in this assessment. Diuretics should be given sparingly because they may worsen preexisting renal injury, and forced diuresis does not improve the prognosis of AKI. Intraoperative events that may cause AKI (eg, extended aortic crossclamping, prolonged systemic hypotension, possible ureteral ligature, or trauma) should be investigated. Imaging studies such as ultrasonography, CT, angiography, or radionuclide scanning may be indicated to clarify renal status and exclude reversible causes of injury. Early consultation with a nephrologist is indicated.

Absorption of irrigation fluid into the intravascular space during cystoscopy may lead to substantial fluid overload and electrolyte shifts. This condition is referred to as transurethral resection of the prostate (TURP) syndrome.51 A similar syndrome has been described in women undergoing transcervical endometrial ablation.52 In both cases, irrigation is performed with an isotonic nonconductive glycine-containing solution that permits use of electrocautery for the procedure. Signs and symptoms result from acute increase in intravascular volume, increased levels of plasma glycine, and rapid decreases in plasma sodium concentration. At the extreme, hyponatremia may produce convulsions, coma, and death. Cardiovascular findings can include hypertension (from hypervolemia) or hypotension (from congestive heart failure), dysrhythmias, pulmonary edema, and cardiac arrest. The diagnosis is confirmed by measuring plasma sodium and osmolality. Management involves providing supportive care, including diuretics for volume overload and administration of isotonic saline. Hypertonic saline therapy may be necessary when plasma sodium decreases below 120 mmol/L or in the event of acute neurologic deterioration.53 Caution should be exercised when infusing hypertonic saline because rapid correction of sodium has been linked to central pontine myelinolysis.

Delirium

Delirium is a transient, fluctuating disturbance of consciousness, attention, cognition, and perception. Postoperative delirium is a common problem in the PACU with a reported incidence in adults of 3% to 5%.54,55 The delirious patient often is hypertensive and tachycardic, and the accompanying agitation can have serious consequences, including trauma, disruption of suture lines or surgical repairs, and accidental removal of catheters, tubes, and drains. Health care providers are also at risk for injury. Postoperative delirium is more common in the elderly and may delay recovery and prolong hospital stay.56,57 Other preoperative risk factors include organic brain disease, withdrawal from alcohol and sedatives, anxiety, and depression. Intraoperative risk factors include specific types of surgery (eg, cardiac, orthopedic, ophthalmologic) and administration of certain drugs (eg, anticholinergics, barbiturates, benzodiazepines). Perioperative hypoxemia, hypotension, and sepsis are believed to be risk factors. There appears to be no difference in the incidence of postoperative delirium with either neuraxial or general anesthesia.58

The first priority in management of postoperative delirium is to rule out physiologic causes, including hypoxemia, hypotension, and acidemia. Postoperative pain often plays a significant role and should be treated adequately.59 Other treatable causes include hypoglycemia, electrolyte disturbances, sepsis, and sensory overload. Bladder or gastric distension, or other nonsurgical pain sources (eg, corneal abrasion, infiltrated IV, poor positioning) should be excluded. Delirium should be treated supportively with verbal reassurance that the surgery is over and that the patient is doing well. Medications may be indicated in some circumstances; physostigmine is helpful when delirium is believed to be the result of central anticholinergic drugs such as scopolamine. Haloperidol is the most widely used agent to treat delirium; benefits include reducing severity and duration of delirium episodes.60

Delayed Awakening

The major causes of delayed awakening after general anesthesia can be divided into 3 groups: (1) prolonged pharmacologic effects, (2) metabolic abnormalities, and (3) neurologic injury.61 The residual effects of anesthetic drugs are the most common cause of delayed awakening. It is important to obtain information on the patient's preoperative level of consciousness, the timing and dosage of administered sedatives and opioids, and use of volatile anesthetics and muscle relaxants. Volatile anesthetics, especially those with high solubility, are more likely to result in delayed awakening after longer procedures or in obese patients. If residual sedative effects of opioids or benzodiazepines are suspected, then pharmacologic reversal with naloxone or flumazenil, respectively, can be used for evaluation as well as treatment. Administration of physostigmine (1.25 mg IV) nonspecifically reverses the anesthetic effects of some sedative and inhalational agents.62,63 The effects of profound neuromuscular blockade can mimic unconsciousness by preventing a motor response to stimuli. In this situation, spontaneous ventilation and movement will be absent and autonomic responses may remain. Possible causes of prolonged paralysis include an overdosage of neuromuscular blocking agents, impaired clearance, drug interaction (eg, with certain antibiotics), or a failure to reverse. The possibility that the patient has pseudocholinesterase deficiency or an unrecognized neuromuscular disease also should be considered. Evaluation with a train-of-four nerve stimulation is recommended.

Metabolic causes of delayed awakening include hypoxemia, hypercapnia, hepatic, renal or endocrine dysfunction, and glucose and electrolyte abnormalities. Hypoglycemia should be considered early, and 50% dextrose should be administered immediately if hypoglycemia is suspected. Hyperglycemia, resulting in hyperosmolar coma or diabetic ketoacidosis, can reduce level of consciousness. Obtaining arterial blood gas and plasma chemistries are the first steps to identify a metabolic etiology.

Sleep deprivation and disruption of normal sleeping patterns in children can result in difficult arousal (see Chapter 64). Profound hypothermia (<33°C) can cause unconsciousness and increase the sedative effects of anesthetics. Extreme hypothermia can cause fixed dilated pupils and areflexia. Overdosage with local anesthetics or inadvertent subarachnoid injection during retrobulbar block can cause unconsciousness.

If the diagnosis remains uncertain, neurologic consultation should be sought. Urgent radiologic imaging (eg, CT, magnetic resonance imaging [MRI]) can be performed to rule out an intracranial process, including stroke, hemorrhage, or hypoxic injury. Trauma patients may be found to have unrecognized intracranial injury. Cerebral vascular accidents, although uncommon after general surgery, can occur in the perioperative period.64,65 Subclinical generalized seizures are an uncommon cause of postoperative unconsciousness. Patients often are slow to awaken after long intracranial procedures; however, consideration should be given to the occurrence of complications such as intracranial hemorrhage or increased intracranial pressure. Rarely, psychiatric causes can result in impaired consciousness.66

Stroke

The incidence of perioperative stroke varies with the type and complexity of the surgical procedure with the reported incidence ranging from as low as 0.08% after general surgical procedures to more than 9% in complicated cardiac and vascular surgery.65,67 Perioperative strokes are predominately embolic and ischemic. Approximately half of perioperative strokes are identified within the first postoperative day.65 These early strokes generally result from emboli generated by manipulations of the heart, aorta, or the carotid, or from particulate matter emanating from cardiopulmonary bypass. Strokes occurring after the first postoperative day generally are caused by emboli resulting from atrial fibrillation, MI, or cerebral hypoperfusion and coagulopathy. Preexisting renal disease, history of stroke, and cardiac valvular disease are additional risk factors for stroke in patients undergoing noncardiac, nonvascular surgery.67 Surgery-induced hypercoagulopathy, general anesthesia, dehydration, bed rest, and perioperative withholding of antiplatelet and anticoagulant medications may also contribute to thrombogenic events such as stroke. Early diagnosis and management is essential to improving outcome after stroke. However, diagnosis may be difficult because symptoms such as somnolence, slurred speech, visual changes, agitation, confusion, numbness, and muscular weakness or paralysis may overlap with the effects of residual anesthetics. Neurologic consultation in conjunction with radiologic imaging is mandatory to guide therapy. Administration of IV thrombolytics may be contraindicated in patients who have recently undergone major surgery. However, intra-arterial administration of tissue plasminogen activator and endovascular mechanical clot disruption are potentially safer options in the postoperative period.68,69

Awareness with recall of intraoperative events is an infrequent but recognized complication of general anesthesia, with a reported incidence of 0.1% to 0.2%.70 Awareness can result in significant distress to patients and long-term psychological sequelae, including symptoms associated with posttraumatic stress disorder.71 Certain patient characteristics (eg, younger age, higher American Society of Anesthesiologists [ASA] physical status, history of alcohol or drug tolerance, history of difficult intubation), types of procedures (eg, cesarean delivery, cardiac surgery, trauma surgery), and anesthetic techniques (eg, rapid sequence induction, reduced anesthetic doses) are associated with an increased risk of intraoperative awareness.72 A questionnaire such as proposed by Brice et al73 is a useful screen for intraoperative awareness in the PACU and during the postoperative visit.

For the patient indicating possible awareness, the clinician should speak with the patient to obtain specific details of the event and to ascertain potential causes.74 A structured interview instrument may be useful to obtain a detailed account of the patient's experience.75 An occurrence report regarding the event should be completed for the purpose of quality management. The patient should be offered counseling and psychological support.

Despite increased knowledge of the mechanisms of acute pain and increased emphasis on pain management programs, postoperative pain continues to be undermanaged (Fig. 71-7).76,77 Inadequate pain relief may have harmful physiologic and psychologic consequences, resulting in increased postoperative morbidity. In addition, inadequate, pain control delays PACU recovery and discharge to home, may result in development of a chronic pain syndrome, and increases resource utilization and health care costs.78,79

For patients to function well postoperatively, they must have adequate pain relief at rest and with movement. Multimodal analgesic approaches that combine regional techniques, nonsteroidal anti-inflammatory drug (NSAID), and opioid therapies are recommended to provide pain relief during movement while producing a low incidence of side effects.80,81 Procedure-specific guidelines for pain therapy may be helpful because pain intensity, as well as the risks and benefits of different analgesics, clearly are procedure related.82,83 Chapter 72 provides a thorough discussion of acute postoperative pain management.

Patients who are opioid tolerant (either from substance abuse or legitimate medical therapy) often present a management challenge in the immediate postoperative period. These patients may be receiving large doses of long-acting oral opioid agonists or even high doses of the opioid partial agonist buprenorphine (see Chapters 23 and 41). When possible, regional anesthetic techniques and nonopioid adjuncts (eg, NSAIDs, clonidine) should be used to provide multimodal therapy. If a regional technique is used as the primary anesthetic in a patient known to be physically dependent on opioids, it is important to provide a supplemental opioid to prevent the symptoms of withdrawal.

Frequently opioid-tolerant patients require parenteral opioids as a primary mode of analgesia after surgery. Tolerant and nontolerant patients are at similar risk for opioid-induced respiratory depression if comparable levels of pain relief are achieved (see Chapter 48). Unfortunately, assessing pain relief in opioid-tolerant patients can be difficult and sometimes inaccurate. Relying on a "pain score" as an analgesic end point may be unwise because these individuals report higher pain scores even when quite sedated.84 For this reason, patients requiring very large doses of opioids should undergo careful monitoring of O2 saturation and respiratory rate for signs of respiratory depression. Patients with coexisting respiratory diseases such as sleep apnea may be best managed in an ICU during the early postoperative period.85 In addition, consultation with a specialist in addiction medicine may assist with acute management as well as follow-up during or after patient hospitalization.

Patients who develop bleeding postoperatively require rapid evaluation to differentiate poor surgical hemostasis (perhaps requiring immediate reoperation) from a diffuse coagulopathy. It is important to appreciate that surgical and nonsurgical bleeding often coexist. Visible bleeding from wounds or drains makes the diagnosis easier, whereas bleeding into the chest, pelvis, thigh, or retroperitoneum can be difficult to detect. Drains can become blocked, kinked, or malpositioned, resulting in a false sense of security.

The patient should be examined for tachycardia, diminished urine output, and delayed capillary refill. Blood pressure may be preserved, especially in the young patient, despite loss of up to 40% of total blood volume.86 Orthostatic hypotension, narrow pulse pressure, and tachycardia may provide an early indication of intravascular volume depletion. Hemoglobin levels may remain stable for a time, and initial declines may be attributed to hemodilution despite significant hemorrhage.

If there is evidence of significant bleeding, diagnosis and treatment usually occur simultaneously. Adequate IV access should be established and the availability of appropriate blood products ensured. Diagnostic studies include measurement of filling pressures (ie, central venous pressure or pulmonary capillary wedge pressure) and imaging (ultrasound, CT) of body cavities. Angiography eventually may be required for definitive diagnosis, localization, and therapy by embolization.

The diagnosis of a coagulopathy in the surgical setting commonly occurs with a dilutional thrombocytopenia and decline in clotting factors. Coagulation tests should be guided by knowledge of preexisting medical illnesses (eg, hepatic disease, bone marrow suppression) or specific surgical factors (eg, sepsis leading to disseminated intravascular coagulation). Hypothermia if present should be corrected because it can cause platelet dysfunction. Laboratory test results can change rapidly, and serial measurements are often required.

Hypothermia

Hypothermia remains a common postoperative problem despite the ASA requirement for the "availability" of intraoperative temperature monitoring and the improved technology for patient warming in the operating room. Multiple sources of heat loss, decreased heat production, and impairment of thermoregulatory control all contribute to intraoperative hypothermia. Even mild hypothermia (core temperature between 34°C and 36°C) has been associated with adverse outcomes, including myocardial ischemia, arrhythmias, coagulopathy, wound infection, and decreased drug metabolism.87 Furthermore, hypothermia can result in substantial discomfort, rated by some patients as worse than their surgical pain.88 Mild hypothermia may increase the duration of PACU stay by 40 minutes or more.89 Violent shivering may increase the risk of trauma or subcutaneous bleeding. It also may dislodge medical devices and interfere with ECG and pulse oximetry monitoring.

Restoration of normothermia is an important goal during the postoperative period. For patients with mild hypothermia, warm blankets and verbal reassurance usually are adequate treatment. Forced-air warming devices are more efficient, if available. Shivering can be rapidly suppressed with small doses of meperidine, which acts by stimulating α2B receptors (see Chapter 41). This will decrease heat production but will make the patient more comfortable. Clonidine, dexmedetomidine, and doxapram also have been used successfully to treat shivering.90

Hyperthermia

Although fever is common during the first few days after surgery, significant hyperthermia is relatively uncommon in the PACU. Most early postoperative fever is caused by cytokine release in response to surgery and resolves spontaneously.91 A 1.4°C average increase in core temperature set point occurs in patients undergoing major surgical procedures (Fig. 71-8).92 Brief periods of hyperthermia also can occur when patients are closely draped and subjected to aggressive warming techniques in the operating room. Infection is always a concern; this is less likely in the PACU unless the patient had a preexisting infection or bacteremia was provoked by the surgical procedure. A febrile reaction to a medication or blood product given during surgery can occur. Less common etiologies include hyperthyroidism, malignant hyperthermia, and the neuroleptic malignant syndrome. Fever can be associated with other adverse events, including PE, adrenal insufficiency, and ethanol withdrawal.

Evaluation of fever in the early postoperative period begins with a careful review of the and physical examination. Preoperative fever or leukocytosis, preoperative and intraoperative medications, and surgery that involves abscess drainage or fecal spillage can all contribute to postoperative fever. Routine use of blood and urine cultures, urinalysis, and chest radiography is costly, and these tests should be ordered only when indicated by the history and physical examination. The decision to administer antibiotics depends on the perceived urgency of treatment and the level of clinical suspicion of infection. Symptomatic treatment with rectal or oral acetaminophen is useful for patient comfort and minimizes increased metabolic demands of fever.

Hyperglycemia due to diabetes, impaired glucose tolerance/fasting glucose or "stress induced" is common in the adult population.93 Hyperglycemia in perioperative patients has been identified as a risk factor for morbidity and mortality. Whether tight glycemic control improves mortality in the perioperative period remains controversial. Several studies suggest that intensive insulin therapy may have a favorable impact on outcome in specific subpopulations, including improved survival after cardiac surgery, decreased infection rates, improved outcome after neurologic injury, and decreased rejection in cadaveric renal transplantation.94 However, recent evidence of severe hypoglycemia and adverse events associated with intensive insulin therapy calls into question both safety and efficacy. Concerns have been raised over the optimal glucose level, accuracy of measurements, the resources required to achieve tight glycemic control, and the impact of tight glycemic control across the heterogeneous surgical population of diabetic and nondiabetic patients.95 There is currently insufficient evidence to support the routine use of tight glycemic control in the perioperative period. However, maintaining blood glucose less than 150 mg/dL and reducing blood glucose variability may be effective.94 Other strategies to maintain glycemic control in the perioperative period include avoiding oral hypoglycemic agents when not on a regular diet, providing basal insulin doses for patients who are insulin deficient, and implementing a program to prevent and manage hypoglycemia.96 These issues are covered more extensively in Chapters 12 and 59.

Ocular

Visual changes after anesthesia for nonocular surgery are relatively infrequent, with an incidence of 0.0008% after all noncardiac surgery and 0.2% following spine surgery.97,98 Severity ranges from transient blurring of vision to irreversible blindness. Transient blurring of vision can be due attributed to cycloplegia from anticholinergic medications, use of ocular lubricants, excessive corneal drying, or a corneal abrasion.99 Corneal abrasion is suggested by symptoms of tearing, miosis, photophobia, and the sensation of a foreign body in the eye. The diagnosis is confirmed by fluorescein staining of the cornea. Ophthalmologic consultation is recommended, and management usually consists of patching and administration of topical antibiotics, anesthetics, and cycloplegics.

Prolonged or permanent visual loss is a recognized complication after head/neck, neurovascular, cardiopulmonary bypass, and spine surgery.100 Impairment of retinal perfusion may result from direct ocular compression, but it also is associated with acute anemia, hypotension, emboli, and large-volume crystalloid administration in the absence of direct compression.101 The risk is higher in patients with preexisting vascular disease and in those receiving long anesthetics and surgery in the prone position.102

If there is a postoperative concern regarding potential visual loss, urgent ophthalmologic consultation should be obtained to determine its cause. Optimizing hemodynamics, hemoglobin levels, and arterial oxygenation may improve recovery, but this has not been confirmed prospectively. MRI may be needed to detect intracranial causes of vision loss.103

Oropharyngeal

Sore throat, hoarseness, and dysphagia are common postoperative complaints following tracheal intubation and laryngeal mask airway (LMA) insertion. In most cases, the laryngeal or pharyngeal trauma is minor, and symptoms resolve without treatment. Gargling with viscous lidocaine may provide symptomatic relief but increases the risk of aspiration during recovery. Severe or persistent pain, dysphagia, or hoarseness may suggest more significant pathology warranting otolaryngologic consultation. Pathologic changes from laryngoscopy and intubation include epithelial loss, glottic hematoma and edema, submucosal tears, and granuloma formation. Oropharyngeal injuries resulting from LMA insertion include pharyngeal abrasion, nerve palsy, arytenoid dislocation, epiglottitis, and uvular bruising.104

Dental

Perioperative dental injury has a reported incidence of 1 in 4500 general anesthetics.105 Risk factors include preexisting poor dentition and a difficult laryngoscopy/intubation.106,107 The upper incisors are most often involved. Damage to teeth should be carefully documented and a dental consultation obtained. If a tooth is missing and cannot be found, a chest x-ray should be obtained to rule out a pulmonary aspiration.

Nerve

Sixteen percent of claims in the ASA closed claims project database were for anesthesia-related nerve injuries.108 Nerve injury may result from improper intraoperative positioning, direct surgical damage, or as a complication of needles and drugs used in regional anesthesia. Preexisting nerve abnormalities also may play a role.109 Many perioperative neuropathies have no identifiable cause. Examination of the patient in the PACU may lead to earlier recognition of a peripheral neuropathy.110 The patient should be positioned in a manner to prevent further compression or stretch of the involved nerve. Evaluation for potentially treatable sources of injury, such as constrictive dressings or improperly applied casts, is important. Prompt neurologic consultation should be obtained when a new deficit is identified to document the patient's status, arrange additional testing or intervention, and provide follow-up. Neurophysiologic assessment, such as nerve conduction studies, evoked potentials, and electromyography, may be helpful in localizing the injury and establishing the diagnosis and prognosis. This information may be helpful in directing a treatment plan.

Major neurologic complications after spinal or epidural anesthesia are rare but can be devastating. The etiology may be traumatic injury to the spinal cord or nerve roots during needle or catheter placement, spinal hematoma or abscess, or a direct toxic effect of injected medications or contaminants.111 Several of these possibilities require urgent MRI and neurologic evaluation. Lack of recovery from spinal or epidural anesthesia may indicate spinal cord compression from a hematoma. Persistent motor blockade after recovery of sensory anesthesia may be due to spinal artery occlusion or spasm. In both cases, prompt diagnosis with MRI and early intervention greatly increase the likelihood of a successful outcome.

Hearing

Hearing loss has been reported after general and neuraxial anesthesia, but it is often subclinical and goes unnoticed unless audiometry is performed. Hearing loss after spinal anesthesia or lumbar puncture is reported most frequently, with 10% to 50% of patients experiencing an audiometrically measurable low-frequency hearing loss.112 The etiology appears to be related to cerebrospinal fluid leak; likelihood of impairment is increased with use of larger-gauge and cutting-tip needles. Hearing loss after dural puncture generally resolves completely within days to weeks. In severe cases, an epidural blood patch may hasten recovery.113

Hearing loss after general anesthesia has been reported after both cardiac and noncardiac surgery. The etiology often is unclear but may be related to changes in middle ear pressure, injury to the inner ear microcirculation, embolism, or the effects of ototoxic drugs. Some patients who received nitrous oxide may actually have developed hyperacusis (increased sensitivity to sound), presumably from changes in middle ear pressure.

Extravasation Injury

Extravasation injury can result from unintentional injection or leakage of IV fluids or medications into the perivascular or subcutaneous space. The amount of injury depends on the specific drug and concentration, the site of injury, the infusion pressure, and the duration of tissue exposure.114 Extravasation of vasoconstrictors, alkaline solutions such as thiopental, and hyperosmolar or concentrated electrolyte solutions may cause significant tissue necrosis. Pain, swelling, and local hyperthermia are not reliable predictors of the degree of tissue damage. The IV infusion should be stopped immediately. Conservative measures such as elevating the involved extremity or applying heat or cold have not been shown to be beneficial, although early aspiration of the intravenous cannula and flushing with saline may be useful. In the case of extravasation of vasopressors, early infiltration with phentolamine may be effective. Surgical consultation and radiologic imaging (eg, MRI) may be helpful if there is concern regarding tissue damage (Fig. 71-9).

A compartment syndrome may result from extravasation of fluid into an extremity. If the amount of extravasated fluid is sufficiently large, blood flow to the distal portion of the extremity may be compromised with resulting tissue ischemia. Untreated ischemia may result in reversible changes in nerve function within 30 minutes and irreversible changes after 12 to 24 hours.115 Impairment in muscle function can be seen during the first 4 hours with irreversible impairment thereafter. Measurement of elevated compartment pressures in conjunction with the clinical examination is used to make the diagnosis of compartment syndrome. Fasciotomy may be required for perfusion to the compromised extremity.

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