MINISTRY OF PUBLIC HEALTH OF UKRAINENATIONAL O.O. BOGOMOLETS MEDICAL UNIVERSITY

CHAIR OF ANAESTHESIOLOGY AND INTENSIVE THERAPY

“Affirmed”Head of the Chair of

Anaesthesiology and Intensive TherapyProfessor F.S. Glumcher

“____” _________ 2009

STUDY GUIDE FOR PRACTICAL WORKFOR TEACHERS AND STUDENTS

CLASSES IN ANAESTHESIOLOGY AND INTENSIVE THERAPY

THEME:«ANAESTHESIOLOGY: CLINICAL ASPECTS»

Kyiv2009

1. Theme Actual Significance

Anaesthesiology is unique in that it requires a working familiarity with most other specialties, including surgery and its subspecialties, internal medicine, pediatrics, and obstetrics as well as clinical pharmacology, applied physiology, and biomedical technology. There are a lot of special considerations in different fields of Surgery. The purposes of this topic is to familiarize students with features of anaesthesia in some special fields.

2. Educational purposes of practical class

The Core Topics are:1. Anesthesia for the Trauma Patient1.1. Initial Assessment (Primary Survey, Secondary Survey, Tertiary Survey)1.2. Anesthetic Considerations1.2.1. General Considerations1.2.2. Head and Spinal Cord Trauma1.2.3. Chest Trauma1.2.4. Abdominal Trauma1.2.5. Exremity Trauma2. Anesthesia for Thoracic Surgery2.1. Special Consideretions (The Lateral Decubitus Position, Positive-Pressure Ventilation, Open Pneumothorax, Mediastinal Shift, One-Lung Ventilation)2.2. Postoperative Management2.3. Postoperative Complications3. Anesthesia for Orthopedic Surgery3.1. Special Considerations in Orthopedic Surgery (Bone Cement, Pneumatic Tourniquets)3.2. Special Complications (Fat Embolism Syndrome, Deep Venous Thrombosis and Thromboembolism)4. Obstetric Anesthesia4.1. Anesthesia for Labor and Vaginal Delivery4.1.1. Psychological and Nonpharmacological Techniques4.1.2. Parenteral Agents4.1.3. Pudendal Nerve Block4.1.4. Regional Anesthetic Techniques (Lumbar Epidural Anaglesia, Combined Spinal and Epidural (CSE) Analgesia, Spinal Anesthesia)4.1.5. General Anesthesia4.2. Anesthesia for Cesarean Section4.2.1. Regional anesthesia4.2.2. CSE Anesthesia4.2.3. General Anesthesia5. Pediatric Anesthesia5.1. Pharmacological Differences (Inhalational Anesthetics, Nonvolatile Anesthetics, Muscle Relaxants)

5.2. Pediatric Anesthetic Risk5.3. Pediatric Anesthetic Techniques (Preoperative Interview, Preoperative Fasting, Premedication, Monitoring, Intravenous Access, Regional Anesthesia, Sedation for Procedures in and out of the Operating Room)5.4. Emergence and Recovery5.4.1. Laryngospasm5.4.2. Postintubation Croup5.4.3.Postoperative Pain Management6. Geriatric Anesthesia6.1. Age-Related Anatomic and Physiological Changes6.2. Age-Related Pharmacological Changes (Inhalational Anesthetics, Nonvolatile Anesthetic Agents, Muscle Relaxants)7. Postanesthesia Care7.1. Emergence from General Anesthesia7.1.1. Delayed Emergence8Routine Recovery: General Anesthesia7.1.2 Routine Recovery: Regional Anesthesia7.2.Pain Control7.3. Nausea and Vomiting7.4. Shivering and Hypothermia 7.5. Discharge from ICU or Recovery Room

3. Contents of a theme

Anesthesia for the Trauma Patient

Trauma is the leading cause of death in the world from the first to the thirty-fifth year of age. Up to one-third of all hospital admissions are directly related to trauma. Fifty percent of trauma deaths occur immediately, with another 30% occurring within a few hours of injury (the "golden hour"). Because many trauma victims require immediate surgery, anesthesiologists can directly affect their survival. In fact, the role of the anesthesiologist is often that of primary resuscitator, with provision of anesthesia a secondary activity. It is important for the anesthesiologist to remember that these patients may have an increased likelihood of being drug abusers, acutely intoxicated, and carriers of hepatitis or human immunodeficiency virus (HIV). This chapter presents a framework for the initial assessment of the trauma victim and anesthetic considerations in the treatment of patients with injuries of the head and spine, chest, abdomen, and extremities.

Initial Assessment

The initial assessment of the trauma patient can be divided into primary, secondary, and tertiary surveys. The primary survey should take 2–5 min and consists of the ABCDE sequence of trauma: Airway, Breathing, Circulation, Disability, and Exposure. If the function of any of the first three systems is

impaired, resuscitation must be initiated immediately. In critically ill patients, resuscitation and assessment proceed simultaneously by a team of trauma practitioners. Basic monitoring including the electroencephalograph (ECG), noninvasive blood pressure, and pulse oximetry can often be initiated in the field and is continued during treatment. Trauma resuscitation includes two additional phases: control of hemorrhage and definitive repair of the injury. More comprehensive secondary and tertiary surveys of the patient follow the primary survey.

Primary Survey

Airway

Establishing and maintaining an airway is always the first priority. If a patient can talk the airway is usually clear, but if unconscious the patient will likely require airway and ventilatory assistance. Important signs of obstruction include snoring or gurgling, stridor, and paradoxical chest movements. The presence of a foreign body should be considered in unconscious patients. Advanced airway management (such as endotracheal intubation, cricothyrotomy, or tracheostomy) is indicated if there is apnea, persistent obstruction, severe head injury, maxillofacial trauma, a penetrating neck injury with an expanding hematoma, or major chest injuries.

Cervical spine injury is unlikely in alert patients without neck pain or tenderness. Five criteria increase the risk for potential instability of the cervical spine: (1) neck pain, (2) severe distracting pain, (3) any neurological signs or symptoms, (4) intoxication, and (5) loss of consciousness at the scene. A cervical spine fracture must be assumed if any one of these criteria is present, even if there is no known injury above the level of the clavicle. Even with these criteria, the incidence of cervical spine trauma is approximately 2%. The incidence of cervical spine instability increases up to 10% in the presence of a severe head injury. To avoid neck hyperextension, the jaw-thrust maneuver is the preferred means of establishing an airway. Oral and nasal airways may help maintain airway patency. Unconscious patients with major trauma are always considered to be at increased risk for aspiration, and the airway must be secured as soon as possible with an endotracheal tube or tracheostomy. Neck hyperextension and excessive axial traction must be avoided, and manual immobilization of the head and neck by an assistant should be used to stabilize the cervical spine during laryngoscopy ("manual in-line stabilization" or MILS). The assistant places his or her hands on either side of the head, holding down the occiput and preventing any head rotation. Studies have demonstrated neck movement, however, particularly at C1 and C2, during mask ventilation and direct laryngoscopy despite attempts at stabilization (eg, MILS, axial traction, sandbags, forehead tape, soft collar, Philadelphia [hard] collar). Of all these techniques, MILS may be most effective, but it also makes direct laryngoscopy more difficult. For this reason, some clinicians prefer nasal

intubation (blind or fiberoptic) in spontaneously breathing patients with suspected cervical spine injury, although this technique may be associated with a higher risk of pulmonary aspiration. Others advocate use of a lightwand, Bullard laryngoscope, WuScope, or an intubating laryngeal mask airway. Clearly, the expertise and preferences of individual clinicians affect the choice of technique, together with the need for expediency and risks of complications in a given patient. Most practitioners have greater familiarity with oral intubation, and this technique should be considered in patients who are apneic and require immediate intubation. Furthermore, nasal intubation should be avoided in patients with midface or basilar skull fractures. If an esophageal obturator airway has been placed in the field, it should not be removed until the trachea has been intubated because of the likelihood of regurgitation.

Laryngeal trauma makes a complicated situation worse. Open injuries may be associated with bleeding from major neck vessels, obstruction from hematoma or edema, subcutaneous emphysema, and cervical spine injuries. Closed laryngeal trauma is less obvious but can present as neck crepitations, hematoma, dysphagia, hemoptysis, or poor phonation. An awake intubation with a small endotracheal tube (6.0 in adults) under direct laryngoscopy or fiberoptic bronchoscopy with topical anesthesia can be attempted if the larynx can be well visualized. If facial or neck injuries preclude endotracheal intubation, tracheostomy under local anesthesia should be considered. Acute obstruction from upper airway trauma may require emergency cricothyrotomy or percutaneous or surgical tracheostomy.

Breathing

Assessment of ventilation is best accomplished by the look, listen, and feel approach. Look for cyanosis, use of accessory muscles, flail chest, and penetrating or sucking chest injuries. Listen for the presence, absence, or diminution of breath sounds. Feel for subcutaneous emphysema, tracheal shift, and broken ribs. The clinician should have a high index of suspicion for tension pneumothorax and hemothorax (see below), particularly in patients with respiratory distress. Pleural drainage may be necessary before the chest X-ray can be obtained.

Most critically ill trauma patients require assisted—if not controlled—ventilation. Bag-valve devices (eg, a self-inflating bag with a nonrebreathing valve) usually provide adequate ventilation immediately after intubation and during periods of patient transport. A 100% oxygen concentration is delivered until oxygenation is assessed by arterial blood gases.

Circulation

Adequacy of circulation is based on pulse rate, pulse fullness, blood pressure, and signs of peripheral perfusion. Signs of inadequate circulation include tachycardia, weak or unpalpable peripheral pulses, hypotension, and pale, cool, or cyanotic extremities. The first priority in restoring adequate circulation is to stop

bleeding; the second priority is to replace intravascular volume. Cardiac arrest during transport to the hospital or shortly after arrival following penetrating chest injuries and possibly blunt chest is an indication for emergency room thoracotomy (ERT). The latter, which is also called resuscitative thoracotomy, allows rapid control of obvious bleeding, opens the pericardium, and allows suturing of cardiac injuries and cross-clamping of the aorta above the diaphragm. Some trauma surgeons also advocate ERT for cardiac arrest during transport or shortly after arrival at the hospital following penetrating or blunt injuries to the abdomen. Pregnant patients at term who are in cardiac arrest or shock often can be resuscitated properly only after delivery of the baby.

Hemorrhage

Obvious sites of hemorrhage should be identified and controlled with direct pressure on the wound. Bleeding from the extremities is easily controlled with pressure dressings and packs; tourniquets can cause reperfusion injuries. Bleeding due to chest trauma is usually from intercostal arteries and often slows or stops when the lung is expanded following chest tube drainage. Bleeding due to intraabdominal injuries, depending on its severity, may tamponade itself, allowing a variable period of fluid and blood resuscitation while surgical evaluation is completed. Pneumatic antishock garments can decrease bleeding in the abdomen and lower extremities, increase peripheral vascular resistance, and augment perfusion of the heart and brain. Bleeding wounds above the level of the suit (eg thorax or head) contraindicate the use of these garments because of the risk of increasing hemorrhage.

The term shock denotes circulatory failure leading to inadequate vital organ perfusion and oxygen delivery. Although there are many causes of shock, in the trauma patient it is usually due to hypovolemia. Physiological responses to hemorrhage range from tachycardia, poor capillary perfusion, and a decrease in pulse pressure to hypotension, tachypnea, and delirium. Serum hematocrit and hemoglobin concentrations are often not accurate indicators of acute blood loss. Peripheral somatic nerve stimulation and massive tissue injury appear to exacerbate the reductions in cardiac output and stroke volume seen in hypovolemic shock. The hemodynamic lability of these patients demands invasive arterial blood pressure monitoring. In severe hypovolemia, the pulse waveform can almost disappear during the inspiratory phase of mechanical ventilation. The degree of hypotension on presentation to the emergency room and operating room correlates strongly with the mortality rate.

Disability

Evaluation for disability consists of a rapid neurological assessment. Because there is usually no time for a Glasgow Coma Scale, the AVPU system is used: awake, verbal response, painful response, and unresponsive.

Exposure

The patient should be undressed to allow examination for injuries. In-line immobilization should be used if a neck or spinal cord injury is suspected.

Secondary Survey

The secondary survey begins only when the ABCs are stabilized. In the secondary survey, the patient is evaluated from head to toe and the indicated studies (eg, radiographs, laboratory tests, invasive diagnostic procedures) are obtained. Head examination includes looking for injuries to the scalp, eyes, and ears. Neurological examination includes the Glasgow Coma Scale and evaluation of motor and sensory functions as well as reflexes. Fixed dilated pupils do not necessarily imply irreversible brain damage. The chest is auscultated and inspected again for fractures and functional integrity (flail chest). Diminished breath sounds may reveal a delayed or enlarging pneumothorax that requires chest tube placement. Similarly, distant heart sounds, a narrow pulse pressure, and distended neck veins may signal pericardial tamponade, calling for pericardiocentesis. A normal initial examination does not definitively eliminate the possibility of these problems. Examination of the abdomen should consist of inspection, auscultation, and palpation. The extremities are examined for fractures, dislocations, and peripheral pulses. A urinary catheter and nasogastric tube are also normally inserted.

Basic laboratory analysis includes a complete blood count (or hematocrit or hemoglobin), electrolytes, glucose, blood urea nitrogen (BUN), and creatinine. Arterial blood gases may also be extremely helpful. A chest X-ray should be obtained in all patients with major trauma. The possibility of cervical spine injury is evaluated by examining all seven vertebrae in a cross-table lateral radiograph and a swimmer's view. Although these studies detect 80–90% of fractures, only a normal computed tomographic scan reliably rules out significant cervical spine trauma. Additional radiographic studies may include skull, pelvic, and long bone films. A focused assessment with sonography for trauma (FAST) scan is a rapid, bedside, ultrasound examination performed to identify intraperitoneal hemorrhage or pericardial tamponade. The FAST scan, which has become an extension of the physical examination of the trauma patient, examines four areas for free fluid: perihepatic/hepatorenal space; perisplenic space; pelvis; and pericardium. Depending on the injuries and the hemodynamic status of the patient, other imaging techniques (eg, chest computed tomography [CT] or angiography) or diagnostic tests such as diagnostic peritoneal lavage (DPL) may also be indicated.

Tertiary Survey

Many trauma centers also advocate a tertiary trauma survey (TTS) to avoid missed injuries. Between 2% and 50% of traumatic injuries may be missed by primary and secondary surveys, particularly following blunt multiple trauma (eg, car accident). A tertiary survey is defined as a patient evaluation that identifies and

catalogues all injuries after initial resuscitation and operative interventions. It typically occurs within 24 h of injuries. This delayed evaluation normally results in a more awake patient who is able to fully communicate all complaints, more detailed information on the mechanism of injury, and a detailed examination of the medical record to determine preexisting comorbidities.

The tertiary survey occurs prior to discharge to reassess and confirm known injuries and identify occult ones. It includes another "head-to-toe examination" and a review of all laboratory and imaging studies. Missed injuries can include extremity and pelvic fractures, spinal cord and head injuries, and abdominal and peripheral nerve injuries.

Anesthetic Considerations

General Considerations

Regional anesthesia is usually impractical and inappropriate in hemodynamically unstable patients with life-threatening injuries.

If the patient arrives in the operating room already intubated, correct positioning of the endotracheal tube must be verified. Patients with suspected head trauma are hyperventilated to decrease intracranial pressure. Ventilation may be compromised by pneumothorax, flail chest, obstruction of the endotracheal tube, or direct pulmonary injury.

If the patient is not intubated the same principles of airway management described above should be followed in the operating room. If time permits, hypovolemia should be at least partially corrected prior to induction of general anesthesia. Fluid resuscitation and transfusion should continue throughout induction and maintenance of anesthesia. Commonly used induction agents for trauma patients include ketamine and Na oxybutiras. Studies suggest that even after adequate fluid resuscitation, the induction dose requirements for propofol are greatly (80–90%) reduced in patients with major trauma. Even drugs such as ketamine and nitrous oxide, which normally indirectly stimulate cardiac function, can display cardiodepressant properties in patients who are in shock and already have maximal sympathetic stimulation. Hypotension may also be encountered following etomidate induction.

Maintenance of anesthesia in unstable patients may consist primarily of the use of muscle relaxants (also called neuromuscular blocking agents), with general anesthetic agents titrated as tolerated (mean arterial pressure > 50–60 mm Hg) in an effort to provide at least amnesia. Intermittent small doses of ketamine (25 mg every 15 min) are often well tolerated and may help reduce the incidence of recall, particularly when used with low concentrations of a volatile agent (< 0.5 minimum alveolar concentration). Other adjuncts that may be useful in preventing recall include midazolam (intermittent 1 mg) or scopolamine (0.3 mg). Many clinicians

avoid nitrous oxide entirely in these patients because of the possibility of a pneumothorax and because it limits inspired oxygen concentration. Obviously, drugs that tend to lower blood pressure (eg, histamine release from atracurium and mivacurium) should generally be avoided in patients in hypovolemic shock. The rate of rise of the alveolar concentration of inhalational anesthetics is greater in shock because of lower cardiac output and increased ventilation. Higher alveolar anesthetic partial pressures lead to higher arterial partial pressures and greater myocardial depression. Similarly, the effects of intravenous anesthetics are exaggerated as they are injected into a smaller intravascular volume. The key to the safe anesthetic management of shock patients is to administer small incremental doses of whichever agents are selected.

Invasive monitoring (direct arterial, central venous, and pulmonary artery pressure monitoring) can be extremely helpful in guiding fluid resuscitation, but insertion of these monitors should not detract from the resuscitation itself. Serial hematocrits (or hemoglobin), arterial blood gas measurement, and serum electrolytes (particularly K+) are invaluable in protracted resuscitations.

Head and Spinal Cord Trauma

Any trauma victim with altered consciousness must be considered to have a brain injury. The level of consciousness is assessed by serial Glasgow Coma Scale evaluations. Common injuries requiring immediate surgical intervention include epidural hematoma, acute subdural hematoma, and some penetrating brain injuries and depressed skull fractures. Other injuries that may be managed conservatively include basilar skull fracture and intracerebral hematoma. Basilar skull fractures are often associated with bruising on the eyelids ("raccoon eyes") or over the mastoid process (Battle's sign), and cerebrospinal fluid (CSF) leaks from the ear or nose (CSF rhinorrhea). Other signs of brain damage include restlessness, convulsions, and cranial nerve dysfunction (eg, a nonreactive pupil). The classic Cushing triad (hypertension, bradycardia, and respiratory disturbances) is a late and unreliable sign that usually just precedes brain herniation. Hypotension is rarely due to head injury alone. Patients suspected of sustaining head trauma should not receive any premedication that will alter their mental status (eg, sedatives, analgesics) or neurological examination (eg, anticholinergic-induced pupillary dilation).

Brain injuries are often accompanied by increased intracranial pressure from cerebral hemorrhage or edema. Intracranial hypertension is controlled by a combination of fluid restriction (except in the presence of hypovolemic shock), diuretics (eg, mannitol, 0.5 g/kg), barbiturates, and deliberate hypocapnia (PaCO2 of 28–32 mm Hg). The latter two require endotracheal intubation, which also protects against aspiration caused by altered airway reflexes. Hypertension or tachycardia during intubation can be attenuated with intravenous lidocaine or fentanyl. Awake intubations cause a precipitous rise in intracranial pressure. Nasal

passage of an endotracheal tube or nasogastric tube in patients with basal skull fractures risks cribriform plate perforation and CSF infection. A slight elevation of the head will improve venous drainage and decrease intracranial pressure. The role of corticosteroids in head injury is controversial; most studies have shown either an adverse effect or no benefit. Anesthetic agents that increase intracranial pressure should be avoided (eg, ketamine). Hyperglycemia should also be avoided and treated with insulin if present. Mild hypothermia may prove beneficial in a patient with a head injury because of its proven value in preventing ischemia-induced injury.

Because autoregulation of cerebral blood flow is usually impaired in areas of brain injury, arterial hypertension can worsen cerebral edema and increase intracranial pressure. In addition, episodes of arterial hypotension will cause regional cerebral ischemia. In general, cerebral perfusion pressure (the difference between mean arterial pressure at the level of the brain and the larger of central venous pressure or intracranial pressure) should be maintained above 60 mm Hg.

Patients with severe head injuries are more prone to arterial hypoxemia from pulmonary shunting and ventilation/perfusion mismatching. These changes may be due to aspiration, atelectasis, or direct neural effects on the pulmonary vasculature. Intracranial hypertension may predispose patients to pulmonary edema because of an increase in sympathetic outflow.

The degree of physiological derangement following spinal cord injury is proportional to the level of the lesion. Great care must be taken to prevent further injury during transportation and intubation. Lesions of the cervical spine may involve the phrenic nerves (C3–C5) and cause apnea. Loss of intercostal function limits pulmonary reserve and the ability to cough. High thoracic injuries will eliminate sympathetic innervation of the heart (T1–T4), leading to bradycardia. Acute high spinal cord injury can cause spinal shock, a condition characterized by loss of sympathetic tone in the capacitance and resistance vessels below the level of the lesion, resulting in hypotension, bradycardia, areflexia, and gastrointestinal atony. In fact, venous distention in the legs is a sign of spinal cord injury. Hypotension in these patients requires aggressive fluid therapy—tempered by the possibility of pulmonary edema after the acute phase has resolved. Succinylcholine is reportedly safe during the first 48 h following the injury but is associated with life-threatening hyperkalemia afterward. Short-term high-dose corticosteroid therapy with methylprednisolone (30 mg/kg followed by 5.4 mg/kg/h for 23 h) improves the neurological outcome of patients with spinal cord trauma. Autonomic hyperreflexia is associated with lesions above T5 but is not a problem during acute management.

Chest Trauma

Trauma to the chest may severely compromise the function of the heart or lungs, leading to cardiogenic shock or hypoxia. A simple pneumothorax is an accumulation of air between the parietal and visceral pleura. The ipsilateral collapse of lung tissue results in a severe ventilation/perfusion abnormality and hypoxia. The overlying chest wall is hyperresonant to percussion, breath sounds are decreased or absent, and a chest film confirms lung collapse. Nitrous oxide will expand a pneumothorax and is contraindicated in these patients. Treatment includes placement of a chest tube in the fourth or fifth intercostal space, anterior to the midaxillary line. A persistent air leak following chest tube placement may indicate injury to a major bronchus.

A tension pneumothorax develops from air entering the pleural space through a one-way valve in the lung or chest wall. In either case, air is forced into the thorax with inspiration but cannot escape during expiration. As a result, the ipsilateral lung completely collapses and the mediastinum and trachea are shifted to the contralateral side. A simple pneumothorax may develop into a tension pneumothorax when positive-pressure ventilation is instituted. Venous return and expansion of the contralateral lung are impaired. Clinical signs include ipsilateral absence of breath sounds and hyperresonance to percussion, contralateral tracheal shift, and distended neck veins. Insertion of a 14-gauge over-the-needle catheter (3–6 cm long) into the second intercostal space at the midclavicular line will convert a tension pneumothorax to an open pneumothorax. Definitive treatment includes chest tube placement as described above.

Multiple rib fractures may compromise the functional integrity of the thorax, resulting in flail chest. Hypoxia is often worsened in these patients by underlying pulmonary contusion or hemothorax. Pulmonary contusion results in worsening respiratory failure over time. Hemothorax is differentiated from pneumothorax by dullness to percussion over silent lung fields. Hemomediastinum, like hemothorax, can also result in hemorrhagic shock. Massive hemoptysis may require isolation of the affected lung with a double-lumen tube (DLT) to prevent blood from entering the healthy lung. Use of a single-lumen endotracheal tube with a bronchial blocker may be safer whenever laryngoscopy is difficult or problems are encountered with the DLT. A large bronchial injury also requires lung separation and ventilation of the unaffected side only. High-frequency jet ventilation may alternately be used to ventilate at lower airway pressures and help minimize the bronchial air leak when the bronchial leak is bilateral or the lung separation is not possible. Air leakage from traumatized bronchi can track an open pulmonary vein causing pulmonary and systemic air embolism. The source of the leak must be quickly identified and controlled. Most bronchial ruptures are within 2.5 cm of the carina.

Cardiac tamponade is a life-threatening chest injury that must be recognized early. When a FAST scan or bedside echocardiography is not available, the presence of Beck's triad (neck vein distention, hypotension, and muffled heart tones), pulsus paradoxus (a > 10 mm Hg decline in blood pressure during

spontaneous inspiration), and a high index of suspicion will help make the diagnosis. Pericardiocentesis provides temporary relief. This is performed by directing a 16-gauge over-the-needle catheter (at least 15 cm long) from the xiphochondral junction toward the tip of the left scapula at a 45° angle, under the guidance of transthoracic echocardiography or the electrocardiogram. Electrocardiographic changes during pericardiocentesis indicate overadvancement of the needle into the myocardium. Definitive treatment of pericardial tamponade requires thoracotomy. Anesthetic management of these patients should maximize cardiac inotropism, chronotropism, and preload. For these reasons, ketamine is a favored induction agent. Penetrating injuries to the heart or great vessels require immediate exploration without delay. Repeated manipulation of the heart often results in intermittent episodes of bradycardia and profound hypotension.

Myocardial contusion is usually diagnosed by electrocardiographic changes consistent with ischemia (ST-segment elevation), cardiac enzyme elevations (creatine kinase MB or troponin levels), or an abnormal echocardiogram. Wall motion abnormalities may be observed with transthoracic echocardiography. Patients are at increased risk for dysrhythmias, such as heart block and ventricular fibrillation. Elective surgery should be postponed until all signs of heart injury resolve.

Other possible injuries following chest trauma include aortic transection or aortic dissection, avulsion of the left subclavian artery, aortic or mitral valve disruption, traumatic diaphragmatic herniation, and esophageal rupture. Aortic transection usually occurs just distal to the left subclavian artery following a severe deceleration injury; it classically presents as wide mediastinum on the chest radiograph and may be associated with a fracture of the first rib.

Acute respiratory distress syndrome (ARDS) is usually a delayed pulmonary complication of trauma that has multiple causes: sepsis, direct thoracic injury, aspiration, head injury, fat embolism, massive transfusion, and oxygen toxicity. Clearly, the trauma patient is often at risk for several of these factors. Even with advances in technology, the mortality rate of ARDS approaches 50%. In some cases, ARDS may present early in the operating room. Similarly, aspiration pneumonia, following aspiration in the field prior to intubation, may first present in the operating room and could be confused with ARDS. Mechanical ventilators on anesthesia machines are often incapable of sustaining adequate gas flows in patients who rapidly develop poor lung compliance; use of an intensive care unit ventilator capable of sustaining adequate gas flows at high airway pressure may be necessary.

Abdominal Trauma

Patients involved in major trauma should be considered to have an abdominal injury until proved otherwise. Up to 20% of patients with

intraabdominal injuries do not have pain or signs of peritoneal irritation (muscle guarding, percussion tenderness, or ileus) on first examination. Large quantities of blood (acute hemoperitoneum) may be present in the abdomen (eg, hepatic or splenic injury) with minimal signs. Abdominal trauma is usually divided into penetrating (eg, gunshot or stabbing) and nonpenetrating (eg, deceleration, crush, or compression injuries).

Penetrating abdominal injuries are usually obvious with entry marks on the abdomen or lower chest. The most commonly injured organ is the liver. Patients tend to fall into three subgroups: (1) pulseless, (2) hemodynamically unstable, and (3) stable. Pulseless and hemodynamically unstable patients (those who fail to maintain a systolic blood pressure of 80–90 mm Hg with 1–2 L of fluid resuscitation should be rushed for immediate laparotomy. They usually have either major vascular or solid organ injury. Stable patients with clinical signs of peritonitis or evisceration should also undergo laparotomy as soon as possible. In contrast, hemodynamically stable patients with penetrating injuries who do not have clinical peritonitis require close evaluation to avoid unnecessary laparotomy. Signs of significant intraabdominal injuries may include free air under the diaphragm on the chest X-ray, blood from the nasogastric tube, hematuria, and rectal blood. Further evaluation of hemodynamically stable patients may include serial physical examinations, local wound exploration, diagnostic peritoneal lavage (DPL), FAST scans, abdominal CT scan, or diagnostic laparoscopy. The use of FAST scans and abdominal CT has reduced the need for DPLs.

Blunt abdominal trauma is the leading cause of morbidity and mortality in trauma, and the leading cause of intraabdominal injuries. Splenic tears or ruptures are most common. A positive FAST scan in a hemodynamically unstable patient with blunt abdominal trauma is an indication for immediate surgery. If the FAST scan is negative or equivocal in an unstable patient, particularly without peritoneal signs, a search is indicated for other sites of blood loss or causes of nonhemorrhagic shock. Management of hemodynamically stable patients with blunt abdominal trauma is based on the FAST scan. If the FAST scan is positive, the decision to proceed to laparoscopy or laparotomy is usually based on an abdominal CT. If the FAST scan is negative, continued observation with serial examinations and repeat FAST scans is usually indicated.

Profound hypotension may follow opening of the abdomen as the tamponading effect of extravasated blood (and bowel distention) is lost. Whenever time permits, preparations for immediate fluid and blood resuscitation with a rapid infusion device should be completed prior to the laparotomy. Nitrous oxide is avoided to prevent worsening of bowel distention. A nasogastric tube (if not already present) will help prevent gastric dilation but should be placed orally if a cribriform plate fracture is suspected. The potential for massive blood transfusion should be anticipated, particularly when abdominal trauma is associated with vascular, hepatic, splenic, or renal injuries, pelvic fractures, or retroperitoneal

hemorrhage. Transfusion-induced hyperkalemia is equally as lethal as exsanguination and must be treated aggressively.

Massive abdominal hemorrhage may require packing of bleeding areas and/or clamping of the abdominal aorta until bleeding sites are identified and the resuscitation can catch up with the blood loss. Prolonged aortic clamping leads to ischemic injury to the liver, kidneys, intestines, and, in some instances, a compartment syndrome of the lower extremities; the latter can produce rhabdomyolysis and acute renal failure. The use of a mannitol infusion and a loop diuretic (prior to aortic cross-clamping), along with resuscitation fluid may prevent renal failure in such instances but is controversial. Rapid resuscitation with fluids and blood products via a rapid transfusion device, together with control of the bleeding, shortens cross-clamp time and likely reduces the incidence of such complications.

Progressive bowel edema from injuries and fluid resuscitation may preclude abdominal closure at the end of the procedure. Tight abdominal closures markedly increase intraabdominal pressure, resulting in an abdominal compartment syndrome that can produce renal and splanchnic ischemia. Oxygenation and ventilation are often severely compromised, even with complete muscle paralysis. Oliguria and renal shutdown follow. In such cases, the abdomen should be left open (but sterilely covered—often with intravenous bag plastic) for 48–72 h until the edema subsides and secondary closure can be undertaken.

Extremity Trauma

Extremity injuries can be life-threatening because of associated vascular injuries and secondary infectious complications. Vascular injuries can lead to massive hemorrhage and threaten extremity viability. For example, a femoral fracture can be associated with 2–3 units of occult blood loss, and closed pelvic fractures can cause even more occult blood loss resulting in hypovolemic shock. Delay of treatment or indiscriminate positioning can worsen dislocations and further compromise neurovascular bundles. Fat emboli are associated with pelvic and long-bone fractures and may cause pulmonary insufficiency, dysrhythmias, skin petechiae, and mental deterioration within 1–3 days after the traumatic event. The laboratory diagnosis of fat embolism depends on elevation of serum lipase, fat in the urine, and thrombocytopenia.

A compartment syndrome can also occur following large intramuscular hematomas, crush injuries, fractures, and amputation injuries. An increase in internal fascial pressure together with a reduced arterial pressure results in ischemia, tissue hypoxia, and progressive swelling. As previously discussed, rhabdomyolysis and renal failure may result. Reperfusion when blood pressure is restored can aggravate the injury and edema. The forearm and lower leg are most at risk. The diagnosis may be made clinically or based on direct measurement of

compartment pressures: greater than 45 mm Hg or within 10–30 mm Hg of diastolic blood pressure. Early fasciotomy to save the limb is recommended.

Modern surgical techniques frequently allow the reimplantation of severed extremities and digits. A cooled, amputated, limb part may be reimplanted up to 20 h following amputation; a noncooled part has to be implanted within 6 h. If the injury is isolated, a regional technique (eg, brachial or interscalene plexus block) is often recommended to increase peripheral blood flow by interrupting sympathetic innervation. During general anesthesia, the patient should be kept warm, and emergence shivering must be avoided to maximize perfusion.

Anesthesia for Thoracic Surgery

Indications and techniques for thoracic surgery have continually evolved since its origins. Common indications are no longer restricted to complications of tuberculosis and suppurative pneumonitis but now include thoracic malignancies (mainly of the lungs and esophagus), chest trauma, esophageal disease, and mediastinal tumors. Diagnostic procedures such as bronchoscopy, mediastinoscopy, and open-lung biopsies are also common. Anesthetic techniques for separating the ventilation to each lung have allowed the refinement of surgical techniques to the point that many procedures are increasingly performed thoracoscopically. High-frequency jet ventilation and cardiopulmonary bypass (CPB) now allow complex procedures such as tracheal resection and lung transplantation, respectively, to be performed.

Thoracic surgery presents a unique set of physiological problems for the anesthesiologist that requires special consideration. These include physiological derangements caused by placing the patient with one side down (lateral decubitus position), opening the chest (open pneumothorax), and the frequent need for one-lung ventilation.

The Lateral Decubitus Position

The lateral decubitus position provides optimal access for most operations on the lungs, pleura, esophagus, the great vessels, other mediastinal structures, and vertebrae. Unfortunately, this position may significantly alter the normal pulmonary ventilation/perfusion relationships. These derangements are further accentuated by induction of anesthesia, initiation of mechanical ventilation, neuromuscular blockade, opening the chest, and surgical retraction. Although perfusion continues to favor the dependent (lower) lung, ventilation progressively favors the less perfused upper lung. The resulting mismatch markedly increases the risk of hypoxemia. The effect of anesthesia on lung compliance in the lateral decubitus position: the upper lung assumes a more favorable position and the lower lung becomes less compliant.

Positive-Pressure Ventilation

Controlled positive-pressure ventilation favors the upper lung in the lateral position because it is more compliant than the lower one. Neuromuscular blockade enhances this effect by allowing the abdominal contents to rise up further against the dependent hemidiaphragm and impede ventilation of the lower lung. Using a rigid "bean bag" to maintain the patient in the lateral decubitus position further restricts movement of the dependent hemithorax. Finally, opening the nondependent side of the chest further accentuates differences in compliance between the two sides because the upper lung is now less restricted in movement.

All these effects worsen ventilation/perfusion mismatching and predispose to hypoxemia.

The Open Pneumothorax

The lungs are normally kept expanded by a negative pleural pressure—the net result of the tendency of the lung to collapse and the chest wall to expand. When one side of the chest is opened, the negative pleural pressure is lost and the elastic recoil of the lung on that side tends to collapse it. Spontaneous ventilation with an open pneumothorax in the lateral position results in paradoxical respirations and mediastinal shift. These two phenomena can cause progressive hypoxemia and hypercapnia, but, fortunately, their effects are overcome by the use of positive-pressure ventilation during general anesthesia and thoracotomy.

Mediastinal Shift

During spontaneous ventilation in the lateral position, inspiration causes pleural pressure to become more negative on the dependent side but not on the side of the open pneumothorax. This results in a downward shift of the mediastinum during inspiration and an upward shift during expiration. The major effect of the mediastinal shift is to decrease the contribution of the dependent lung to the tidal volume.

Spontaneous ventilation in a patient with an open pneumothorax also results in to-and-from gas flow between the dependent and nondependent lung (paradoxical respiration [pendeluft]). During inspiration, the pneumothorax increases, and gas flows from the upper lung across the carina to the dependent lung. During expiration, the gas flow reverses and moves from the dependent to the upper lung.

One-Lung Ventilation

Intentional collapse of the lung on the operative side facilitates most thoracic procedures but greatly complicates anesthetic management. Because the collapsed lung continues to be perfused and is deliberately no longer ventilated, the patient develops a large right-to-left intrapulmonary shunt (20–30%). During one-lung ventilation, the mixing of unoxygenated blood from the collapsed upper lung with oxygenated blood from the still-ventilated dependent lung widens the PA–a (alveolar-to-arterial) O2 gradient and often results in hypoxemia. Fortunately, blood flow to the nonventilated lung is decreased by hypoxic pulmonary vasoconstriction (HPV) and possibly surgical compression of the upper lung.

Factors known to inhibit HPV and thus worsen the right-to-left shunting include (1) very high or very low pulmonary artery pressures; (2) hypocapnia; (3) high or very low mixed venous PO2; (4) vasodilators such as nitroglycerin, nitroprusside, adrenergic agonists (including dobutamine and salbutamol), and calcium channel blockers; (5) pulmonary infection; and (6) inhalation anesthetics.

Factors that decrease blood flow to the ventilated lung can be equally detrimental; they counteract the effect of HPV by indirectly increasing blood flow to the collapsed lung. Such factors include (1) high mean airway pressures in the ventilated lung due to high positive end-expiratory pressure (PEEP), hyperventilation, or high peak inspiratory pressures; (2) a low FIO2, which produces hypoxic pulmonary vasoconstriction in the ventilated lung; (3) vasoconstrictors that may have a greater effect on normoxic vessels than hypoxic ones; and (4) intrinsic PEEP that develops due to inadequate expiratory times.

Elimination of CO2 is usually not affected by one-lung ventilation provided minute ventilation is unchanged and preexisting CO2 retention was not present while ventilating both lungs; arterial CO2 tension is usually not appreciably altered

Postoperative Management

Most patients are extubated early to decrease the risk of pulmonary barotrauma (particularly "blowout" [rupture] of the bronchial suture line) and pulmonary infection. Patients with marginal pulmonary reserve should be left intubated until standard extubation criteria are met; if a double-lumen tube was used for one-lung ventilation, it should be replaced with a regular single-lumen tube at the end of surgery. A catheter guide ("tube exchanger") should be used if the original laryngoscopy was difficult (above).

Patients are observed carefully in the intensive care unit (ICU) in most instances, at least overnight or longer Postoperative hypoxemia and respiratory acidosis are common. These effects are largely caused by atelectasis from surgical compression of the lungs and "shallow breathing ('splinting')" due to incisional pain. Gravity-dependent transudation of fluid into the dependent lung (above) may also be contributory. Reexpansion edema of the collapsed nondependent lung can also occur, particularly with rapid reinflation of the lung.

Postoperative hemorrhage complicates about 3% of thoracotomies and may be associated with up to 20% mortality. Signs of hemorrhage include increased chest tube drainage (> 200 mL/h), hypotension, tachycardia, and a falling hematocrit. Postoperative supraventricular tachyarrhythmias are common and should be treated aggressively. Acute right ventricular failure is suggested by a low cardiac output, elevated CVP, oliguria, and a normal pulmonary capillary occlusion pressure.

Routine postoperative care should include maintenance of a semiupright (> 30°) position, supplemental oxygen (40–50%), incentive spirometry, close electrocardiographic and hemodynamic monitoring, a postoperative radiograph, and aggressive pain relief.

Postoperative Analgesia

The balance between comfort and respiratory depression in patients with marginal lung function is difficult to achieve with parenteral opioids alone. Patients who have undergone thoracotomy clearly benefit from the use of other techniques described below that may obviate the need for any parenteral opioids. If parenteral opioids are used alone, small intravenous doses are superior to large intramuscular doses and probably are best administered via a patient-controlled analgesia (PCA) device.

A long-acting agent such as 0.5% ropivacaine (4–5 mL), injected two levels above and below the thoracotomy incision, typically provides excellent pain relief. These blocks may be done under direct vision intraoperatively or via the standard technique postoperatively. Intercostal or paravertebral nerve blocks improve postoperative arterial blood gases and pulmonary function tests and shorten hospital stay.

Epidural opioids with or without a local anesthetic can also provide excellent analgesia. Equally satisfactory analgesia may be obtained with either a lumbar or thoracic epidural catheter when morphine is used. Injection of morphine 5–7 mg in 10–15 mL of saline usually provides 6–24 h of analgesia without autonomic, sensory, or motor blockade. The lumbar route may be safer because it is less likely to traumatize the spinal cord or puncture the dura, but the latter is more of a theoretical concern because it may occur (although infrequently) during cautious and correct placement of a thoracic epidural. Epidural injections of a lipophilic opioid, such as fentanyl, are more effective via a thoracic catheter than a lumbar catheter. Some clinicians prefer fentanyl given epidurally because it is less likely to cause delayed respiratory depression. In either case, patients should be closely monitored for this complication.

Postoperative Complications

Postoperative complications following thoracotomy are relatively common, but fortunately most are minor and resolve uneventfully. Blood clots and thick secretions readily obstruct the airways and result in atelectasis; aggressive but gentle suctioning may be necessary. Significant atelectasis is suggested by tracheal deviation and shifting of the mediastinum to the operative side following segmental or lobar resections. Therapeutic bronchoscopy should be considered for persistent atelectasis, particularly when associated with thick secretions. Air leaks from the operative hemithorax are common following segmental and lobar resections because fissures are usually incomplete; resection therefore often leaves the small channels responsible for collateral ventilation open. Most air leaks stop after a few days. Bronchopleural fistula presents as a sudden large air leak from the chest tube that may be associated with an increasing pneumothorax and partial lung collapse. When it occurs within the first 24–72 h, it is usually the result of inadequate surgical closure of the bronchial stump. Delayed presentation is usually

due to necrosis of the suture line associated with inadequate blood flow or infection.

Some complications are rare but deserve special consideration because they can be life-threatening, require a high index of suspicion, and may require immediate exploratory thoracotomy. Postoperative bleeding was discussed above. Torsion of a lobe or segment can occur as the remaining lung on the operative side expands to occupy the hemithorax. The torsion usually occludes the pulmonary vein to that part of the lung, causing venous outflow obstruction. Hemoptysis and infarction can rapidly follow. The diagnosis is suggested by an enlarging homogeneous density on the chest radiograph and a closed lobar orifice on bronchoscopy. Acute herniation of the heart into the operative hemithorax can occur through the pericardial defect that may be left following a radical pneumonectomy. A large pressure differential between the two hemithoraxes is thought to trigger this catastrophic event. Herniation into the right hemithorax results in sudden severe hypotension with an elevated CVP because of torsion of the central veins. Herniation into the left hemithorax following left pneumonectomy results in sudden compression of the heart at the atrioventricular groove, resulting in hypotension, ischemia, and infarction. A chest radiograph shows a shift of the cardiac shadow into the operative hemithorax.

Extensive mediastinal dissections can injure the phrenic, vagus, and left recurrent laryngeal nerves. Postoperative phrenic nerve palsy presents as elevation of the ipsilateral hemidiaphragm together with difficulty in weaning the patient from the ventilator. Large en bloc chest wall resections may also involve part of the diaphragm, causing a similar problem, in addition to a flail chest. Paraplegia can rarely follow thoracotomy for lung resection. Sacrificing the left lower intercostal arteries can produce spinal cord ischemia. Alternately, an epidural hematoma may form if the surgical dissection enters the epidural space through the chest cavity.

Anesthesia for Orthopedic Surgery

Orthopedic surgery challenges the anesthesiologist with its diversity. The degree of surgical trespass varies from minor finger surgery to hemipelvectomy. Orthopedic patients range from neonates with congenital anomalies to healthy young athletes to immobile geriatric patients with end-stage multiorgan failure. Long bone fractures predispose to fat embolism syndrome. Patients may be at high risk for venous thromboembolism, particularly following pelvic, hip, and knee operations. Use of bone cement during arthroplasties can cause hemodynamic instability. Limb tourniquets limit blood loss but introduce additional risks. Neuraxial and other regional anesthetic techniques play an important role in decreasing the incidence of perioperative thromboembolic complications, providing postoperative analgesia, and facilitating early rehabilitation and hospital discharges. Advances in surgical techniques, such as minimally invasive

approaches to hip replacement utilizing computer-assisted surgery, are necessitating modifications in anesthetic management to allow for overnight or even same day discharge of patients undergoing procedures that used to require a week or more in the hospital. After reviewing problems that are frequently encountered in orthopedic surgery, this chapter discusses the anesthetic management of patients undergoing some common orthopedic operations.

Special Considerations in Orthopedic Surgery

Bone Cement

Bone cement, polymethylmethacrylate, is frequently required for joint arthroplasties. The cement interdigitates within the interstices of cancellous bone and strongly binds the prosthetic device to the patient's bone. Mixing polymerized methylmethacrylate powder with liquid methylmethacrylate monomer causes polymerization and cross-linking of the polymer chains. This exothermic reaction leads to hardening of the cement and expansion against the prosthetic components. The resultant intramedullary hypertension (> 500 mm Hg) causes embolization of fat, bone marrow, cement, and air into the femoral venous channels. Residual methylmethacrylate monomer can produce vasodilation and a decrease in systemic vascular resistance. The release of tissue thromboplastin may trigger platelet aggregation, microthrombus formation in the lungs, and cardiovascular instability as a result of the circulation of vasoactive substances.

The clinical manifestations of bone cement implantation syndrome include hypoxia (increased pulmonary shunt), hypotension, dysrhythmias (including heart block and sinus arrest), pulmonary hypertension (increased pulmonary vascular resistance), and decreased cardiac output. Emboli most frequently occur during insertion of a femoral prosthesis. Strategies to minimize the effects of this complication include increasing inspired oxygen concentration prior to cementing, maintaining euvolemia by monitoring central venous pressure, creating a vent hole in the distal femur to relieve intramedullary pressure, performing high-pressure lavage of the femoral shaft to remove debris (potential microemboli), or using an uncemented femoral component.

Another major disadvantage of cement is the potential for gradual loosening of the prosthesis resulting from breakage of small pieces of cement over the years. Components of cementless implants are made of a porous material that allows the natural bone to grow into them. Cementless prostheses generally last longer and may be advantageous for younger, active patients, even though full recovery may be longer compared to cemented joint replacements. Unfortunately, cementless implants require healthy active bone formation. Therefore cemented prosthesis are still preferred for older (> 80 years) and less active patients who often have osteoporosis and/or thin bone (cortex). Practices continue to evolve regarding selection of cemented versus cementless joint replacements, depending on the joint

replaced, patient, and surgical technique. In many cases cemented and cementless components are used in the same patient (eg, total hip arthroplasty). Articular surfaces on modern prostheses may be metal, plastic, or ceramic.

Pneumatic Tourniquets

Use of a pneumatic tourniquet on the upper or lower extremity creates a bloodless field that greatly facilitates surgery. Unfortunately, tourniquets are associated with potential problems of their own, including hemodynamic changes, pain, metabolic alterations, arterial thromboembolism, and even pulmonary embolism. Inflation pressure is usually about 100 mm Hg over systolic blood pressure. Prolonged inflation (> 2 h) routinely leads to transient muscle dysfunction and may be associated with permanent peripheral nerve injury or even rhabdomyolysis. Tourniquet inflation has also been associated with increases in body temperature in pediatric patients undergoing leg surgery.

Exsanguination of a lower extremity and tourniquet inflation cause a shift of blood volume into the central circulation. Although this is usually not clinically significant, bilateral Esmarch bandage exsanguination can cause a rise in central venous pressure and arterial blood pressure that may not be well tolerated in patients with left ventricular dysfunction.

Anyone who has had a tourniquet on the thigh inflated to 100 mm Hg above systolic blood pressure for more than a few minutes appreciates tourniquet pain. Although the mechanism and neural pathways for this severe aching and burning sensation defy precise explanation, unmyelinated, slow-conduction C fibers, which are relatively resistant to local anesthetic blockade, probably play a critical role. Tourniquet pain gradually becomes so severe over time that patients may require substantial supplemental analgesia, if not general anesthesia, despite a regional block that is adequate for surgical incision. Even during general anesthesia, tourniquet pain is often manifested as a gradually increasing mean arterial blood pressure beginning about ¾ to 1 h after cuff inflation. Signs of progressive sympathetic activation include marked hypertension, tachycardia, and diaphoresis. The likelihood of tourniquet pain and its accompanying hypertension may be influenced by many factors, including anesthetic technique (intravenous regional > epidural > spinal > general anesthesia), intensity and level of regional anesthetic block, choice of local anesthetic (hyperbaric spinal with tetracaine > isobaric bupivacaine), and supplementation of the block with opioids.

Cuff deflation invariably and immediately relieves the sensation of tourniquet pain and its hypertension. In fact, cuff deflation can be accompanied by a significant fall in central venous pressure and arterial blood pressure. Heart rate usually increases and core temperature decreases. Washout of accumulated metabolic wastes in the ischemic extremity increases PaCO2, ETCO2, and serum lactate and potassium levels. These metabolic alterations can cause an increase in

minute ventilation in the spontaneously breathing patient and, rarely, dysrhythmias. Ironically, cuff deflation and blood reoxygenation have been demonstrated to worsen ischemic tissue injury due to the formation of lipid peroxides. This reperfusion injury may be attenuated by propofol, which has been reported to limit superoxide generation.

Tourniquet-induced ischemia of a lower extremity may lead to the development of deep venous thrombosis. Transesophageal echocardiography has detected subclinical pulmonary embolism (miliary emboli) following tourniquet deflation in cases as minor as diagnostic knee arthroscopy. Rare episodes of massive pulmonary embolism during total knee arthroplasty have been reported during leg exsanguination, after tourniquet inflation, and following tourniquet deflation. Tourniquets are generally contraindicated in patients with significant calcific arterial disease. They have been safely used in patients with sickle cell disease, although particular attention should be paid to maintaining oxygenation, normocarbia or hypocarbia, hydration, and normothermia.

Fat Embolism Syndrome

Although some degree of fat embolism probably occurs in all cases of long-bone fracture, fat embolism syndrome is a less frequent but potentially fatal (10–20% mortality) event that can complicate anesthetic management. Fat embolism syndrome classically presents within 72 h following long-bone or pelvic fracture, with the triad of dyspnea, confusion, and petechiae. This syndrome can also be seen following cardiopulmonary resuscitation, parental feeding with lipid infusion, and liposuction. Two theories have been proposed for its pathogenesis. The most popular theory holds that fat globules are released by the disruption of fat cells in the fractured bone and enter the circulation through tears in medullary vessels. An alternative theory proposes that the fat globules are chylomicrons resulting from the aggregation of circulating free fatty acids caused by changes in fatty acid metabolism. Regardless of their source, the increased free fatty acid levels can have a toxic effect on the capillary–alveolar membrane leading to the release of vasoactive amines and prostaglandins and the development of acute respiratory distress syndrome. Neurological manifestations (agitation, confusion, stupor, or coma) probably represent capillary damage to the cerebral circulation and cerebral edema and may be exacerbated by hypoxia.

The diagnosis of fat embolism syndrome is suggested by petechiae on the chest, upper extremities, axillae, and conjunctiva. Fat globules may be found in the retina, urine, or sputum. Coagulation abnormalities such as thrombocytopenia or prolonged clotting times are occasionally present. Serum lipase activity may be elevated, but bears no relationship to disease severity. Pulmonary involvement typically progresses from mild hypoxia and a normal chest radiograph to severe hypoxia and a chest film showing diffuse patchy pulmonary infiltrates. Most of the classic signs and symptoms of fat embolism syndrome occur 1–3 days after the

precipitant event. Signs during general anesthesia may include a decline in ETCO2 and arterial oxygen saturation or a rise in pulmonary artery pressures. Electrocardiography may show ischemic-appearing ST-segment changes and right-sided heart strain.

Treatment is 2-fold: prophylactic and supportive. Early stabilization of the fracture decreases the incidence of fat embolism syndrome. Supportive treatment consists of oxygen therapy with continuous positive airway pressure ventilation. Treatment with heparin or alcohol has generally been disappointing. High-dose corticosteroid therapy may be beneficial, particularly in the presence of cerebral edema.

Deep Venous Thrombosis and Thromboembolism

Deep vein thrombosis (DVT) and pulmonary embolism (PE) can be major causes of morbidity and mortality following orthopedic operations on the pelvis and lower extremities. Additional risk factors include obesity, age > 60 years, procedures lasting > 30 min, use of a tourniquet, lower extremity fracture, and immobilization for more than 4 days. Patients at highest risk are those undergoing hip surgery and knee reconstruction, where DVT rates in older studies were as high as 50%. The incidence of clinically significant pulmonary embolism following hip surgery in some studies was reported to be as high as 20%, whereas that of fatal pulmonary embolism was as much as 1–3%. Major pathophysiological mechanisms likely include venous stasis and a hypercoagulable state due to localized and systemic inflammatory responses to surgery. Prophylactic anticoagulation and use of intermittent pneumatic (leg) compression (IPC) devices have been shown to significantly decrease the incidence of DVT and PE.

Although most clinicians agree that full anticoagulation or fibrinolytic therapy (eg, urokinase) represents an unacceptable risk for spinal or epidural hematoma following neuraxial anesthesia, the danger for patients already receiving low-dose anticoagulation preoperatively is somewhat controversial. Placement of an epidural needle or catheter (or removal) should generally not be undertaken within 6–8 h of a subcutaneous "minidose" of unfractionated heparin, or within 12–24 h of LMWH. Although potentially less traumatic, spinal anesthesia may represent a similar risk. Concomitant administration of an antiplatelet agent may further increase the risk of a spinal hematoma. Another major concern is that a regional anesthetic could mask the hallmarks of an expanding hematoma and spinal cord compression (eg, lower back pain and lower extremity weakness), thus delaying diagnosis and treatment.

Obstetric Anesthesia

Obstetric anesthesia is a demanding but gratifying subspecialty of anesthesiology. The widespread acceptance and use of regional anesthesia for labor has made obstetric anesthesia a major part of most anesthetic practices. The

guidelines of the American College of Obstetricians and Gynecologists and American Society of Anesthesiologists require that anesthesia service be readily available continuously and that cesarean section be started within 30 min of the recognition for its need. Moreover, high-risk patients, such as those undergoing a trial of vaginal birth after a previous cesarean delivery (VBAC), may require the immediate availability of anesthesia services.

Although most parturients are young and healthy, they nonetheless represent a high-risk group of patients for all the reasons discussed in the preceding chapter.

Anesthesia for Labor and Vaginal Delivery

Psychological and Nonpharmacological Techniques

Psychological and nonpharmacological techniques are based on the premise that the pain of labor can be suppressed by reorganizing one's thoughts. Patient education and positive conditioning about the birthing process are central to such techniques. Pain during labor tends to be accentuated by fear of the unknown or previous unpleasant experiences. The parturient also concentrates on an object in the room and attempts to focus her thoughts away from the pain. Less common nonpharmacological techniques include hypnosis, transcutaneous electrical nerve stimulation, biofeedback, and acupuncture. The success of all these techniques varies considerably from patient to patient, but most patients require additional forms of pain relief.

Parenteral Agents

Nearly all parenteral opioid analgesics and sedatives readily cross the placenta and can affect the fetus. Concern over fetal depression limits the use of these agents to the early stages of labor or to situations in which regional anesthetic techniques are not available. Central nervous system depression in the neonate may be manifested by a prolonged time to sustain respirations, respiratory acidosis, or an abnormal neurobehavioral examination. Moreover, loss of beat-to-beat variability in the fetal heart rate (seen with most central nervous system depressants) and decreased fetal movements (due to sedation of fetus) complicate the evaluation of fetal well-being during labor. Long-term fetal heart variability is affected more than short-term variability. The degree and significance of these effects depend on the specific agent, the dose, the time elapsed between its administration and delivery, and fetal maturity. Premature neonates exhibit the greatest sensitivity. In addition to maternal respiratory depression, opioids can also induce maternal nausea and vomiting and delay gastric emptying.

Intravenous fentanyl, 25–100 mkg/h, has also been used for labor. Fentanyl in 25–100 mkg doses has a 3- to 10-min analgesic onset that initially lasts about 60 min, and lasts longer following multiple doses. However, maternal respiratory depression outlasts the analgesia. Lower doses of fentanyl may be associated with

little or no neonatal respiratory depression and are reported to have no effect on Apgar scores. Morphine is not used because in equianalgesic doses it appears to cause greater respiratory depression in the fetus than meperidine and fentanyl.

Benzodiazepines, particularly longer acting agents such as diazepam, are not used during labor because of their potential to cause prolonged neonatal depression. The amnestic properties of benzodiazepines make them undesirable agents for parturients because they usually want to remember the experience of delivery.

Low-dose intravenous ketamine is a powerful analgesic. In doses of 10–15 mg intravenously, good analgesia can be obtained in 2–5 min without loss of consciousness. Unfortunately, fetal depression with low Apgar scores is associated with doses greater than 1 mg/kg. Large boluses of ketamine (> 1 mg/kg) can be associated with hypertonic uterine contractions. Low-dose ketamine is most useful just prior to delivery or as an adjuvant to regional anesthesia. Some clinicians avoid use of ketamine because it may produce unpleasant psychotomimetic effects.

Pudendal Nerve Block

Pudendal nerve blocks are often combined with perineal infiltration of local anesthetic to provide perineal anesthesia during the second stage of labor when other forms of anesthesia are not employed or prove to be inadequate. Paracervical plexus blocks are no longer used because of their association with a relatively high rate of fetal bradycardia; the close proximity of the injection site (paracervical plexus or Frankenhäuser's ganglia) to the uterine artery can result in uterine arterial vasoconstriction, uteroplacental insufficiency, and high levels of the local anesthetic in the fetal blood.

Regional Anesthetic Techniques

Regional techniques employing the epidural or intrathecal route, alone or in combination, are currently the most popular methods of pain relief during labor and delivery. They can provide excellent pain relief, yet allow the mother to be awake and cooperative during labor. Although spinal opioids or local anesthetics alone can provide satisfactory analgesia, techniques that combine the two have proved to be the most satisfactory in most parturients. Moreover, the apparent synergy between the two types of agents decreases dose requirements and provides excellent analgesia with few maternal side effects and little or no neonatal depression.

Spinal Opioids Alone

Preservative-free opioids may be given intraspinally as a single injection or intermittently via an epidural or intrathecal catheter. Relatively high doses are required for analgesia during labor when spinal opioids are used alone. For

example, the ED50 during labor is 124 mkg for epidural fentanyl and 21 mkg for epidural sufentanil. The higher doses may be associated with a high risk of side effects, most importantly respiratory depression. For that reason combinations of local anesthetics and opioids are most commonly used.

Intrathecal Opioids

Intrathecal morphine in doses of 0.25–0.5 mg may produce satisfactory and prolonged (4–6 h) analgesia during the first stage of labor. Unfortunately, the onset of analgesia is slow (45–60 min), and these doses may not be sufficient in many patients. Higher doses are associated with a relatively high incidence of side effects. Morphine is therefore rarely used alone. The combination of morphine, 0.25 mg, and fentanyl, 12.5 mkg, (or sufentanil, 5 mkg) may result in a more rapid onset of analgesia (5 min). Early reports of fetal bradycardia following intrathecal opioid injections (eg, sufentanil) are not supported by subsequent studies. Spinal meperidine has some weak local anesthetic properties and therefore can decrease blood pressure. Hypotension following intrathecal sufentanil for labor is likely related to the analgesia and decreased circulating catecholamine levels.

Epidural Opioids

Again relatively high doses (7.5 mg) of morphine are required for satisfactory analgesia during labor, but doses larger than 5 mg are not recommended because of the increased risk of delayed respiratory depression and because the analgesia is effective only in the early first stage of labor. The onset of analgesia may take 30–60 min but lasts up to 12–24 h (as will the risk of delayed respiratory depression). Epidural fentanyl, 50–150 mkg, or sufentanil, 10–20 mkg, usually produces analgesia within 5–10 min with few side effects, but it has a short duration (1–2 h). Although "single-shot" epidural opioids do not appear to cause significant neonatal depression, caution should be exercised following repeated administrations. Combinations of a lower dose of morphine, 2.5 mg, with fentanyl, 25–50 mkg (or sufentanil, 7.5–10 mkg), may result in a more rapid onset and prolongation of analgesia (4–5 h) with fewer side effects.

Local Anesthetic/Local Anesthetic–Opioid Mixtures

Epidural and spinal (intrathecal) analgesia more commonly utilizes local anesthetics either alone or with opioids for labor and delivery. Pain relief during the first stage of labor requires neural blockade at the T10–L1 sensory level, whereas pain relief during the second stage of labor requires neural blockade at T10–S4. Continuous lumbar epidural analgesia is the most versatile and most commonly employed technique, because it can be used for pain relief for the first stage of labor as well as analgesia/anesthesia for subsequent vaginal delivery or cesarean section, if necessary. "Single-shot" epidural, spinal, or combined spinal epidural analgesia may be appropriate when pain relief is initiated just prior to vaginal delivery (the second stage). Obstetric caudal injections have largely been

abandoned because of less versatility (they are most effective for perineal analgesia/anesthesia), the need for large volumes of local anesthetic, early paralysis of the pelvic muscles that may interfere with normal rotation of the fetal head, and a small risk of accidental puncture of the fetus.

Absolute contraindications to regional anesthesia include infection over the injection site, coagulopathy, thrombocytopenia, marked hypovolemia, true allergies to local anesthetics, and the patient's refusal or inability to cooperate for regional anesthesia. Preexisting neurological disease, back disorders, and some forms of heart disease are relative contraindications.

Before performing any regional block, appropriate equipment and supplies for resuscitation should be checked and made immediately available. Minimum supplies include oxygen, suction, a mask with a positive-pressure device for ventilation, a functioning laryngoscope, endotracheal tubes (6 or 6.5 mm), oral or nasal airways, intravenous fluids, ephedrine, atropine, thiopental (or propofol), and succinylcholine. The ability to frequently monitor blood pressure and heart rate is mandatory. A pulse oximeter and capnograph should also be readily available.

Lumbar Epidural Anaglesia

Traditionally epidural analgesia for labor is administered only when labor is well established. However, recent studies suggest that when dilute mixtures of a local anesthetic and an opioid are used epidural analgesia has little if any effect on the progress of labor. Concerns about increasing the likelihood of an oxytocin augmentation, operative (eg, forceps) delivery, or cesarean sections appear to be unjustified. It is often advantageous to place an epidural catheter early, when the patient is comfortable and can be positioned easily. Moreover, should emergent cesarean section become necessary the presence of a well-functioning epidural catheter makes it possible to avoid general anesthesia.

Epidural analgesia should generally be initiated when the parturient wants it (on demand) and the obstetrician approves it. A more conservative approach is to wait until labor is well established. Although exact criteria vary, commonly accepted conservative criteria include no fetal distress; good regular contractions 3–4 min apart and lasting about 1 min; adequate cervical dilatation, ie, 3–4 cm; and engagement of the fetal head. Even with a conservative approach, epidural anesthesia is often administered earlier to parturients who are committed to labor, eg, ruptured membranes and receiving an oxytocin infusion once a good contraction pattern is achieved.

Some clinicians advocate the midline approach, whereas others favor the paramedian approach. If air is used for detecting loss of resistance, the amount injected should be limited as much as possible; injection of excessive amounts of air (> 2–3 mL) in the epidural space has been associated with patchy or unilateral analgesia and headache. The average depth of the epidural space in obstetric

patients is reported to be 5 cm from the skin. Placement of the epidural catheter at the L3–4 or L4–5 interspace is generally optimal for achieving a T10–S5 neural blockade. If unintentional dural puncture occurs, the anesthetist has two choices: (1) place the epidural catheter in the subarachnoid space for continuous spinal analgesia and anesthesia (see below), or (2) remove the needle and attempt placement at a higher spinal level.

Choice of Local Anesthetic Solutions

The addition of opioids to local anesthetic solutions for epidural anesthesia has dramatically changed the practice of obstetric anesthesia. The synergy between epidural opioids and local anesthetic solutions appears to reflect separate sites of action, namely, opiate receptors and neuronal axons, respectively. When the two are combined, very low concentrations of both local anesthetic and opioid can be used. More importantly, the incidence of adverse side effects, such as hypotension and drug toxicity, is likely reduced. Although local anesthetics can be used alone, there is rarely a reason to do so. Moreover, when an opioid is omitted, the higher concentration of local anesthetic required (eg, bupivacaine 0.25% and ropivacaine 0.2%) can impair the parturient's ability to push effectively as the labor progresses. Bupivacaine or ropivacaine in concentrations of 0.0625–0.125% with either fentanyl 2–3 mkg/mL or sufentanil 0.3–0.5 mkg/mL is most often used. In general, the lower the concentration of the local anesthetic the higher the concentration of opioid that is required. Very dilute local anesthetic mixtures (0.0625%) generally do not produce motor blockade and may allow some patients to ambulate ("walking" or "mobile" epidural). The long duration of action of bupivacaine makes it a popular agent for labor. Ropivacaine may be preferable because of possibly less motor blockade and its reduced potential for cardiotoxicity. Systemic absorption of the opioid can decrease fetal heart rate variability due to transient sedation of the fetus.

The effect of epinephrine-containing solutions on the course of labor is somewhat controversial. Many clinicians use epinephrine-containing solutions only for intravascular test doses because of concern that the solutions may slow the progression of labor or adversely affect the fetus; others use only very dilute concentrations of epinephrine such as 1:800,000 or 1:400,000. Studies comparing these various agents have failed to find any differences in neonatal Apgar scores, acid–base status, or neurobehavioral evaluations.

Combined Spinal and Epidural (CSE) Analgesia

Techniques using CSE analgesia and anesthesia may particularly benefit patients with severe pain early in labor and those who receive analgesia/anesthesia just prior to delivery. Intrathecal opioid and local anesthetic are injected and an epidural catheter is left in place. The intrathecal drugs provide almost immediate pain control and have minimal effects on the early progress of labor, whereas the

epidural catheter provides a route for subsequent analgesia for labor and delivery or anesthesia for cesarean section. Addition of small doses of local anesthetic agents to intrathecal opioid injection greatly potentiates their analgesia and can significantly reduce opioid requirements. Thus, many clinicians will inject 2.5 mg of preservative-free bupivacaine or 3–4 mg of ropivacaine with intrathecal opioids for analgesia in the first stage of labor. Intrathecal doses for CSE are fentanyl 4–5 mkg or sufentanil 2–3 mkg. Addition of 0.1 mg of epinephrine prolongs the analgesia with such mixtures but not for intrathecal opioids alone. Some studies suggest that CSE techniques may be associated with greater patient satisfaction than epidural analgesia alone. A 24- to 27-gauge pencil-point spinal needle is used to minimize the incidence of PDPH.

Spinal Anesthesia

Spinal anesthesia given just prior to delivery—also known as saddle block—provides profound anesthesia for operative vaginal delivery. A 500- to 1000-mL fluid bolus is given prior to the procedure, which is performed with the patient in the sitting position. Use of a 22-gauge or smaller, pencil-point spinal needle (Whitacre, Sprotte, or Gertie Marx) decreases the likelihood of PDPH. Hyperbaric tetracaine (3–4 mg), bupivacaine (6–7 mg), or lidocaine (20–40 mg) usually provides excellent perineal anesthesia. Addition of fentanyl 12.5–25 mkg or sufentanil 5–7.5 mkg significantly potentiates the block. A T10 sensory level can be obtained with slightly larger amounts of local anesthetic. The intrathecal injection should be given slowly over 30 s and between contractions to minimize excessive cephalad spread. Three minutes after injection, the patient is placed in the lithotomy position with left uterine displacement.

General Anesthesia

Because of the increased risk of aspiration, general anesthesia for vaginal delivery is avoided except for a true emergency. If an epidural catheter is already in place and time permits, rapid-onset regional anesthesia can often be obtained with alkalinized lidocaine 2% or chloroprocaine 3%. Table 1 lists indications for general anesthesia during vaginal delivery. Many of these indications share the need for uterine relaxation. Intravenous nitroglycerin, 50–100 mkg, has been shown to be effective in inducing uterine relaxation and may obviate the need for general anesthesia in these cases.

Table 1. Possible Indications for General Anesthesia during Vaginal Delivery.

Fetal distress during the second stage

Tetanic uterine contractions

Breech extraction

Version and extraction

Manual removal of a retained placenta

Replacement of an inverted uterus

Psychiatric patients who become uncontrollable

Suggested Technique for Vaginal Delivery

1. Place a wedge under the right hip for left uterine displacement. 2. Preoxygenate the patient for 3–5 min as monitors are applied. Defasciculation with a nondepolarizing muscle relaxant is usually not necessary, because most pregnant patients do not fasciculate following succinylcholine. Moreover, fasciculations do not appear to promote regurgitation, because any increase in intragastric pressure is matched by a similar increase in the lower esophageal sphincter. 3. Once all monitors are applied and the obstetrician is ready, proceed with a rapid-sequence induction while cricoid pressure is applied and intubate with a 6- to 6.5-mm endotracheal tube. Propofol, 2 mg/kg, or thiopental, 4 mg/kg, and succinylcholine, 1.5 mg/kg, are most commonly used unless the patient is hypovolemic or hypotensive, in which case ketamine, 1 mg/kg, is used as the induction agent. 4. After successful intubation, use 1–2 minimum alveolar concentration (MAC) of any potent volatile inhalational agent in 100% oxygen while carefully monitoring blood pressure. 5. If skeletal muscle relaxation is necessary, a short- to intermediate-acting, nondepolarizing muscle relaxant (eg, mivacurium or atracurium) is used. 6. Once the fetus and placenta are delivered, the volatile agent is decreased to less than 0.5 MAC or discontinued, an oxytocin infusion is started (20–40 U/L of intravenous fluid), and a nitrous oxide–opioid technique or propofol infusion can be used to avoid recall. 7. An attempt to aspirate gastric contents may be made via an orogastric tube to decrease the likelihood of pulmonary aspiration on emergence. 8. At the end of the procedure, the skeletal nondepolarizing muscle relaxant is reversed, the gastric tube (if placed) is removed, and the patient is extubated while awake.

Anesthesia for Cesarean Section

The choice of anesthesia for cesarean section is determined by multiple factors, including the indication for operating, its urgency, patient and obstetrician preferences, and the skills of the anesthetist. Cesarean section rates between institutions generally vary between 15 and 25%. Offten it performed under regional anesthesia, nearly evenly split between spinal and epidural anesthesia. Regional anesthesia has become the preferred technique because general anesthesia

has been associated with higher maternal mortality. Deaths associated with general anesthesia are generally related to airway problems, such as inability to intubate, inability to ventilate, or aspiration pneumonitis, whereas deaths associated with regional anesthesia are generally related to excessively high neural blockade or local anesthetic toxicity.

Other advantages of regional anesthesia include (1) less neonatal exposure to potentially depressant drugs, (2) a decreased risk of maternal pulmonary aspiration, (3) an awake mother at the birth of her child, with the father also present if desired, and (4) the option of using spinal opioids for postoperative pain relief. The choice between spinal and epidural anesthesia is often based on physician preferences. Epidural anesthesia is preferred over spinal anesthesia by some clinicians because of the more gradual decrease in blood pressure associated with epidural anesthesia. Continuous epidural anesthesia also allows better control over the sensory level. Conversely, spinal anesthesia is easier to perform, has a more rapid, predictable onset, may produce a more intense (complete) block, and does not have the potential for serious systemic drug toxicity (because of the smaller dose of local anesthetic employed). Regardless of the regional technique chosen, the ability to administer a general anesthetic at any time during the procedure is mandatory. Moreover, administration of a nonparticulate antacid 1 h prior to surgery should also be considered.

General anesthesia offers (1) a very rapid and reliable onset, (2) control over the airway and ventilation, and (3) potentially less hypotension than regional anesthesia. General anesthesia also facilitates management in the event of severe hemorrhagic complications such as placenta accreta. Its principal disadvantages are the risk of pulmonary aspiration, the potential inability to intubate or ventilate the patient, and drug-induced fetal depression. Present anesthetic techniques, however, limit the dose of intravenous agents such that fetal depression is usually not clinically significant with general anesthesia when delivery occurs within 10 min of induction of anesthesia. Regardless of the type of anesthesia, neonates delivered more than 3 min after uterine incision have lower Apgar scores and acidotic blood gases.

Regional Anesthesia

Cesarean section requires a T4 sensory level. Because of the associated high sympathetic blockade, all patients should receive a 1000- to 1500-mL bolus of lactated Ringer's injection prior to neural blockade. Crystalloid boluses do not consistently prevent hypotension but can be helpful in some patients. Smaller volumes (250–500 mL) of colloid solutions, such as albumin or hetastarch, are more effective. After injection of the anesthetic, the patient is placed supine with left uterine displacement; supplemental oxygen (40–50%) is given; blood pressure is measured every 1–2 min until it stabilizes. Intravenous ephedrine, 10 mg, should be used to maintain systolic blood pressure > 100 mm Hg. Small intravenous doses

of phenylephrine, 25–100 mkg, or an infusion up to 100 mkg/min may also be used safely. Some studies suggest less neonatal acidosis with phenylephrine compared to ephedrine. Prophylactic administration of ephedrine (5 mg intravenous or 25 mg intramuscular) has been advocated by some clinicians for spinal anesthesia, as precipitous hypotension may be seen but is not recommended for most patients because of a risk of inducing excessive hypertension. Hypotension following epidural anesthesia typically has a slower onset. Slight Trendelenburg positioning facilitates achieving a T4 sensory level and may also help prevent severe hypotension. Extreme degrees of Trendelenburg may interfere with pulmonary gas exchange.

CSE Anesthesia

The technique for CSE is described in the above section on combined spinal epidural analgesia. For cesarean section, it combines the benefit of rapid, reliable, intense blockade of spinal anesthesia with the flexibility of an epidural catheter. The catheter also allows supplementation of anesthesia and can be used for postoperative analgesia. As mentioned previously, drugs given epidurally should be administered and titrated carefully because the dural hole created by the spinal needle increases the flux of epidural drugs into CSF and enhances their effects.

General Anesthesia

Pulmonary aspiration of gastric contents (incidence: 1:500–400 for obstetric patients versus 1:2000 for all patients) and failed endotracheal intubation (incidence: 1:300 versus 1:2000 for all patients) during general anesthesia are the major causes of maternal morbidity and mortality. Every effort should be made to ensure optimal conditions prior to the start of anesthesia and to follow measures aimed at preventing these complications.

All patients should possibly receive prophylaxis against severe nonparticulate aspiration pneumonia with 30 mL of 0.3 M sodium citrate 30–45 min prior to induction. Patients with additional risk factors predisposing them to aspiration should also receive intravenous ranitidine, 50 mg, and/or metoclopramide, 10 mg, 1–2 h prior to induction; such factors include morbid obesity, symptoms of gastroesophageal reflux, a potentially difficult airway, or emergent surgical delivery without an elective fasting period. Premedication with oral omeprazole, 40 mg, at night and in the morning also appears to be highly effective in high-risk patients undergoing elective cesarean section. Although anticholinergics theoretically may reduce lower esophageal sphincter tone, premedication with a small dose of glycopyrrolate (0.1 mg) helps reduce airway secretions and should be considered in patients with a potentially difficult airway.

Pediatric Anesthesia

Pediatric patients are not small adults. Neonates (0–1 months), infants (1–12 months), toddlers (1–3 years), and small children (4–12 years of age) have differing anesthetic requirements. Safe anesthetic management depends on full appreciation of the physiological, anatomic, and pharmacological characteristics of each group. These characteristics, which differentiate them from each other and adults, necessitate modification of anesthetic equipment and techniques. Indeed infants are at much greater risk of anesthetic morbidity and mortality than are older children; risk is generally inversely proportional to age, neonates being at highest risk. In addition, pediatric patients are prone to illnesses that require unique surgical and anesthetic strategies.

Pharmacological Differences

Pediatric drug dosing is typically based on a per-kilogram recommendation.Weight, however, does not take into account the disproportionately larger pediatric intravascular and extracellular fluid compartments, the immaturity of hepatic biotransformation pathways, increased organ blood flow, decreased protein binding, or higher metabolic rate. These variables must be considered on an individual basis.

Neonates and infants have a proportionately higher total water content (70–75%) than adults (50–60%). Total body water content decreases as fat and muscle content increase with age. As a direct result, the volume of distribution for most intravenous drugs is disproportionately higher in neonates, infants, and young children, and the dose (per kilogram) is usually higher than in older children and adults. A disproportionately smaller muscle mass in neonates prolongs the clinical termination of action by redistribution to muscle for drugs such as thiopental and fentanyl. Neonates also have a relatively lower glomerular filtration rate and hepatic blood flow, as well as immature renal tubular function and immature hepatic enzyme systems. Increased intraabdominal pressure and abdominal surgery further reduce hepatic blood flow. All these factors impair renal drug handling, hepatic metabolism, or biliary excretion of many drugs in neonates and young infants. Neonates also have decreased or impaired protein binding for some drugs, most notably thiopental, bupivacaine, and many antibiotics. In the first instance, increased free drug enhances potency and reduces the induction dose compared to older children. In the second instance, an increase in free bupivacaine may enhance systemic toxicity.

Inhalational Anesthetics

Neonates, infants, and young children have relatively higher alveolar ventilation and lower FRC compared with older children and adults. This higher minute ventilation-to-FRC ratio with relatively higher blood flow to vessel-rich organs contributes to a rapid rise in alveolar anesthetic concentration and speeds inhalation induction. Furthermore, the blood/gas coefficients of volatile anesthetics

are lower in neonates than in adults, resulting in even faster induction times and potentially increasing the risk of overdosing.

The minimum alveolar concentration (MAC) for halogenated agents is higher in infants than in neonates and adults. Unlike other agents, sevoflurane has the same MAC in neonates and infants. For unknown reasons, use of nitrous oxide in children does not augment the effects (lower MAC requirements) of desflurane and to some extent sevoflurane as it does for other

The blood pressure of neonates and infants tends to be more sensitive to volatile anesthetics, probably because of not fully developed compensatory mechanisms (eg, vasoconstriction, tachycardia) and an immature myocardium that is very sensitive to myocardial depressants. As with adults, halothane also sensitizes the heart to catecholamines; the maximum recommended dose of epinephrine in local anesthetic solutions during halothane anesthesia is 10 mkg/kg. Cardiovascular depression, bradycardia, and arrhythmias are significantly less with sevoflurane than with halothane. Halothane and sevoflurane are least likely to irritate the airway and cause breath holding or laryngospasm during. Volatile anesthetics appear to depress ventilation more in infants than in older children. Sevoflurane is associated with the least respiratory depression. Prepubertal children are at much less risk for halothane-induced hepatic dysfunction than are adults. There are no reported instances of renal toxicity from inorganic fluoride production during sevoflurane anesthesia in children. Overall, sevoflurane appears to have a greater therapeutic index than halothane and has become a preferred induction agent in pediatric anesthesia.

The rate of emergence is fastest following desflurane and sevoflurane anesthesia, but both agents are associated with an increased incidence of agitation or delirium upon emergence, particularly in young children. Because of the latter, many clinicians switch to either isoflurane or halothane for maintenance anesthesia following a sevoflurane induction. The speed of emergence from halothane and isoflurane anesthesia appears to be similar for procedures lasting less than 1 h.

Nonvolatile Anesthetics

Based on weight, infants and young children require larger doses of propofol because of a larger volume of distribution compared to adults. Children also have a shorter elimination half-life and higher plasma clearance for propofol. Whereas recovery from a single bolus is not appreciably different from adults, recovery following a continuous infusion may be more rapid. For the same reasons, children may require higher rates of infusion for maintenance of anesthesia (up to 250 mkg/kg/min). Propofol is not recommended for sedation of critically ill pediatric patients in the intensive care unit (ICU). The drug has been associated with higher mortality compared to other agents, and a controversial "propofol infusion syndrome" has been described. Its essential features are metabolic acidosis,

hemodynamic instability, hepatomegaly, rhabdomyolysis, and multiorgan failure. Although appearing primarily in critically ill children, this rare syndrome has been reported in adults and in patients undergoing long-term propofol infusion (> 48 h) for sedation at high doses (> 5 mg/kg/h).

Children require relatively higher doses of thiopental compared to adults. The elimination half-life is shorter and the plasma clearance is greater than in adults. In contrast, neonates, particularly those depressed at birth, appear to be more sensitive to barbiturates and have less protein binding, a longer half-life, and impaired clearance. The thiopental induction dose for neonates is 3–4 mg/kg compared to 5–6 mg/kg for infants.

Opioids appear to be more potent in neonates than in older children and adults. Possible explanations include easier entry across the blood–brain barrier, decreased metabolic capability, or increased sensitivity of the respiratory centers. Morphine sulfate should be used with caution in neonates because hepatic conjugation is reduced and renal clearance of morphine metabolites is decreased. The cytochrome P-450 pathways mature at the end of the neonatal period. Older pediatric patients have relatively high rates of biotransformation and elimination as a result of high hepatic blood flow. Sufentanil, alfentanil, and, possibly, fentanyl clearances may be higher in children than in adults. Remifentanil clearance is increased in neonates and infants but elimination half-life is unaltered compared to adults. Neonates and infants may be more resistant to the hypnotic effects of ketamine, requiring slightly higher doses than adults; pharmacokinetics do not appear to be significantly different from adults. The combination of ketamine and fentanyl is more likely to cause hypotension in neonates and young infants than ketamine and midazolam. Midazolam has the fastest clearance of all the benzodiazepines; however, midazolam clearance is significantly less in neonates than in older children. Moreover, the combination of midazolam and fentanyl can cause profound hypotension.

Muscle Relaxants

All muscle relaxants generally have a shorter onset (up to 50% less) in pediatric patients because of shorter circulation times than adults. Nonetheless, intravenous succinylcholine (1–1.5 mg/kg) has the fastest onset. Infants require significantly higher doses of succinylcholine (2–3 mg/kg) than older children and adults because of the relatively larger volume of distribution (extracellular space). This discrepancy disappears if dosage is based on body surface area. With the notable exclusion of succinylcholine, mivacurium, and possibly cisatracurium, infants require significantly less muscle relaxant than older children. Moreover, based on weight, older children require higher doses than adults for some neuromuscular blocking agents (eg, mivacurium and atracurium).

The response of neonates to nondepolarizing muscle relaxants is quite variable. Immaturity of the neuromuscular junction (particularly in premature neonates) tends to increase sensitivity, whereas a disproportionately large extracellular compartment dilutes drug concentration. The relative immaturity of neonatal hepatic function prolongs the duration of action for drugs that depend primarily on hepatic metabolism (eg, pancuronium, vecuronium, and rocuronium). In contrast, atracurium and cisatracurium, which do not depend on hepatic biotransformation, reliably behave as intermediate acting muscle relaxants. Breakdown of mivacurium also does not appear to be significantly altered in neonates.

Children are more susceptible than adults to cardiac arrhythmias, hyperkalemia, rhabdomyolysis, myoglobinemia, masseter spasm, and malignant hyperthermia after administration of succinylcholine. If a child unexpectedly experiences cardiac arrest following administration of succinylcholine, immediate treatment for hyperkalemia should be instituted. Prolonged and heroic (eg, cardiopulmonary bypass) resuscitative efforts may be required. For this reason, succinylcholine is best avoided for routine elective surgery in children and adolescents. Unlike in adult patients, profound bradycardia and sinus node arrest can develop in pediatric patients following the first dose of succinylcholine without atropine pretreatment. Atropine (0.1 mg minimum) must therefore always be administered prior to succinylcholine in children. Generally accepted indications for succinylcholine in children are rapid sequence induction with a full stomach, laryngospasm, and rapid muscle relaxation prior to intravenous access (eg, regurgitation). Intramuscular succinylcholine (4–6 mg/kg) can be used for the latter; in this situation, atropine (0.02 mg/kg intramuscularly) should be administered at the same time to prevent bradycardia. Some clinicians advocate intralingual administration (2 mg/kg in the mid-line to avoid hematoma formation) as an emergency alternate route.

Pediatric Anesthetic Risk

Perhaps the most current database for assessing pediatric anesthetic risk is the Pediatric Perioperative Cardiac Arrest (POCA) Registry. This registry includes reports based on approximately one million pediatric anesthetic cases administered since 1994. All cardiac arrests and deaths of pediatric patients during the administration of or recovery from anesthesia were analyzed to investigate the possible relationship of anesthesia to these incidents. Nearly all patients received general anesthesia alone or combined with regional anesthesia. In a preliminary analysis of the data that included 289 cases of cardiac arrest, 150 arrests were judged to be related to anesthesia. Thus the risk of cardiac arrest in pediatric anesthetic cases would appear to be approximately 1.4 in 10,000. Moreover, an overall mortality of 26% was reported following cardiac arrest. Approximately 6% suffered permanent injury, with the majority (68%) having either no or temporary injury. Mortality was 4% in American Society of Anesthesiologists (ASA)

physical status 1 and 2 patients compared to 37% in ASA physical status 3–5 patients. It is important to note that 33% of patients who suffered a cardiac arrest were ASA physical status 1–2. Moreover, infants accounted for 55% of all anesthesia-related arrests with those less than 1 month (ie, neonates) having the highest risk. As with adults, two major predictors of mortality were ASA physical status 3–5 and emergency surgery.

Most (82%) arrests occurred during induction of anesthesia; bradycardia, hypotension, and a low SpO2 were frequent preceding events. The most common mechanism of cardiac arrest was judged to be medication related. Cardiovascular depression from halothane, alone or in combination with other drugs, was believed to be responsible in 66% of all medication-related arrests. Another 9% was due to intravascular injection of a local anesthetic, most often following a negative aspiration test during a caudal injection. A presumed cardiovascular mechanism was most often of unclear etiology, but in more than 50% of those cases the patient had congenital heart disease. Where a cardiovascular mechanism could be identified, it was most often related to hemorrhage, transfusion, or inadequate/inappropriate fluid therapy.

A respiratory mechanism was most often due to laryngospasm, airway obstruction, and difficult intubation (in decreasing order). In most cases the laryngospasm occurred during induction. Nearly all patients who had airway obstruction or were difficult to intubate had significant underlying disease.

The most common equipment-related mechanism that led to a cardiac arrest was complications from placement of a central venous catheter (eg, pneumothorax, hemothorax, or cardiac tamponade).

Pediatric Anesthetic Techniques

Preoperative Interview

Depending on age, past surgical experiences, and maturity, children suffer from varying degrees of terror when faced with the prospect of surgery. In contrast to adults, who are usually most concerned about the possibility of death, children are principally worried about pain and separation from their parents. Presurgical preparation programs—such as brochures, videos, or tours—can be very helpful in preparing many children and parents. Unfortunately, outpatient and morning-of-admission surgery together with a busy operating room schedule often make it difficult for an anesthesiologist to have enough time to break through the barriers erected by pediatric patients. For this reason, premedication (below) can be extremely helpful. A key strategy is to demystify the process of anesthesia and surgery by explaining in age-appropriate terms what lies ahead. For example, the anesthesiologist might bring an anesthesia mask for the child to play with during the interview and describe it as something the astronauts use. Alternatively, in some centers, someone who the child trusts (eg, a parent, nurse, other physician)

may be allowed to be in attendance during preanesthetic preparations and induction of anesthesia. This can have a particularly calming influence on children undergoing repeated procedures (eg, examination under anesthesia following glaucoma surgery).

Recent Upper Respiratory Tract Infection

Children frequently present for surgery with evidence—a runny nose with fever, cough, or sore throat—of a coincidental viral upper respiratory tract infection (URTI). Attempts should be made to differentiate between an infectious cause of rhinorrhea and an allergic or vasomotor cause. A viral infection within 2–4 weeks before general anesthesia and endotracheal intubation appears to place the child at an increased risk for perioperative pulmonary complications, such as wheezing (10-fold), laryngospasm (5-fold), hypoxemia, and atelectasis. This is particularly likely if the child has a severe cough, high fever, or a family history of reactive airway disease. The decision to anesthetize children with URTIs remains controversial and depends on the presence of other coexisting illnesses, the severity of URTI symptoms, and the urgency of the surgery. If surgery cannot be deferred, consideration should be given to an anticholinergic premedication, mask ventilation, humidification of inspired gases, and a longer-than-usual stay in the recovery room.

Most asymptomatic patients with murmurs do not have significant cardiac pathology. Innocent murmurs may occur in more than 30% of normal children. They are usually soft, short systolic ejection murmurs that are best heard along the left upper or left lower sternal border without significant radiation. Innocent murmurs at the left upper sternal border are due to flow across the pulmonic valve (pulmonic ejection) whereas those at the lower left border are due to flow from the left ventricle to the aorta (Still's vibratory murmur). The pediatrician and possibly a cardiologist should carefully evaluate patients with a newly diagnosed murmur, particularly in infancy. An echocardiogram should be obtained if the patient is symptomatic (eg, poor feeding, failure to thrive, or easy fatigability); the murmur is harsh, loud, holosystolic, diastolic, or radiates widely; or pulses are either bounding (eg, with aortic runoff lesions) or markedly diminished.

Preoperative Fasting

Because pediatric patients are more prone to dehydration, their preoperative fluid restriction has always been more lenient. Several studies, however, have documented low gastric pH (< 2.5) and relatively high residual volumes in pediatric patients scheduled for surgery, suggesting that children may be at a higher risk for aspiration than previously thought. The incidence of aspiration is reported to be approximately 1:1000. Prolonged fasting does not necessarily decrease this risk. In fact, several studies have demonstrated lower residual volumes and higher gastric pH in pediatric patients who received clear fluids a few

h before induction. Depending on age, regular formula feedings or solid foods are continued until 4–8 h before surgery. More specifically, infants younger than 6 months are fed formula up to 4 h before induction, whereas infants 6–36 months of age can be given formula or solids up to 6 h before induction. Clear fluids are offered until 2–3 h before induction. These recommendations are for healthy neonates, infants, and children without risk factors for decreased gastric emptying or aspiration.

Premedication

There is great variation in the recommendations for premedication of pediatric patients. Sedative premedication is generally omitted for neonates and sick infants. Children who appear likely to exhibit uncontrollable separation anxiety can be given a sedative, such as midazolam (0.3–0.5 mg/kg, 15 mg maximum). The oral route is generally preferred because it is less traumatic than intramuscular injection, but it requires 20–45 min for effect. Smaller doses of midazolam may be used with the addition of oral ketamine (4–6 mg/kg), but the combination may not be suitable for outpatients. For uncooperative patients, intramuscular midazolam (0.1–0.15 mg/kg, 10 mg maximum) and/or ketamine (2–3 mg/kg) with atropine (0.02 mg/kg) may be helpful. Rectal midazolam (0.5–1 mg/kg, 20 mg maximum) or rectal methohexital (25–30 mg/kg of 10% solution) may also be administered in such cases while the child is in the parent's arms. The nasal route can be used with some drugs but is unpleasant, and some concerns exist over potential neurotoxicity of nasal midazolam. Fentanyl can also be administered as a lollipop (Actiq 5–15 mkg/kg); fentanyl levels continue to rise intraoperatively and can contribute to postoperative analgesia. Older agents such as chloral hydrate and pentobarbital are rarely used.

Some anesthesiologists routinely premedicate young children with anticholinergic drugs (eg, atropine 0.02 mg/kg intramuscularly) to decrease the likelihood of bradycardia during induction. Atropine reduces the incidence of hypotension during induction in neonates and in infants less than 3 months. Atropine can also prevent accumulation of secretions that can block small airways and endotracheal tubes. Secretions can be particularly problematic for patients with URTIs or those who have been given ketamine. Atropine is often administered orally (0.05 mg/kg), intramuscularly, or occasionally rectally. Many anesthesiologists prefer to give atropine intravenously at or shortly after induction.

Temperature must be closely monitored in pediatric patients because of a higher risk for malignant hyperthermia and the potential for both iatrogenic hypothermia and hyperthermia. Hypothermia can be prevented by maintaining a warm operating room environment (26°C or higher), warming and humidifying inspired gases, using a warming blanket and warming lights, and warming all intravenous fluids. The room temperature required for a neutral thermal environment varies with age; it is highest in premature newborns. Note that care

must be taken to prevent unintentional skin burns and iatrogenic hyperthermia from overzealous warming efforts.

Invasive monitoring (eg, arterial cannulation, central venous catheterization) requires considerable expertise and extreme caution. All air bubbles should be removed from pressure tubing and only small volume flushes should be used to prevent air embolism, inadvertent heparinization, and fluid overload. Pulmonary artery catheters are usually not used in pediatric patients because of the predictable relationship between right- and left-sided filling pressures. The right radial artery is often chosen for cannulation in the neonate because its preductal location mirrors the oxygen content of the carotid and retinal arteries. A femoral artery catheter may be a suitable alternative in very small neonates. Critically ill neonates may still have an umbilical artery catheter in place. Urinary output is an important measure of volume status.

Neonates who are premature or small for gestational age, who have received hyperalimentation, or whose mothers are diabetic may be prone to hypoglycemia. These infants should have frequent serum glucose determinations: levels < 30 mg/dL in the neonate and < 40 mg/dL in older children indicate hypoglycemia. Blood sampling (from an arterial or central venous catheter) for arterial blood gases, hemoglobin, potassium, and ionized calcium concentration can be invaluable in critically ill patients, particularly when transfusion is necessary.

Intravenous Access

Cannulation of tiny pediatric veins can be a trying ordeal. This is particularly true for infants who have spent weeks in a neonatal intensive care unit and have few veins left unscarred. Even healthy 1-year-old children can prove a challenge because of extensive subcutaneous fat. Veins usually become more accessible after 2 years of age. The saphenous vein has a consistent location at the ankle and, with experience, the practitioner can usually cannulate it even if it is not visible or palpable. Twenty-four-gauge over-the-needle catheters are adequate in neonates and infants when blood transfusions are not anticipated. All air bubbles should be removed from the intravenous line, as a high incidence of patent foramen ovale increases the risk of paradoxical air embolism. In emergency situations where intravenous access is impossible, fluids can be effectively infused through an 18-gauge needle inserted into the medullary sinusoids within the tibial bone. This intraosseous infusion can be used for all medications normally given intravenously with almost as rapid results.

Anesthesia can be maintained in pediatric patients with the same agents as in adults. Many clinicians switch to either isoflurane or halothane following a sevoflurane induction to help reduce the likelihood of postoperative delirium or agitation on emergence (see above). If sevoflurane is continued for maintenance, administration of an opioid (eg, fentanyl 1–1.5 mkg/kg) 15–20 min before the end

of the procedure can reduce the incidence of emergence delirium and agitation. Although the MAC is higher in children than in adults, neonates may be particularly susceptible to the cardiodepressant effects of general anesthetics. Nondepolarizing muscle relaxants are often required for optimal surgical conditions; this is particularly true in neonates and sick infants who may not tolerate higher doses of volatile agents.

Regional Anesthesia

The primary uses of regional techniques in pediatric anesthesia have been to supplement and lower general anesthetic requirements and provide good postoperative pain relief. Blocks range in complexity from the relatively simple peripheral nerve blocks described (eg, penile block, ilioinguinal block) to major conduction blocks (eg, spinal anesthesia).

Caudal blocks have proved useful in a variety of surgeries, including circumcision, inguinal herniorrhaphy, hypospadias repair, anal surgery, clubfoot repair, and other subumbilical procedures. Contraindications include infection around the sacral hiatus, coagulopathy, or anatomic abnormalities. The patient is usually lightly anesthetized or sedated and placed in the lateral position.

Sedation for Procedures in and out of the Operating Room

Sedation is often requested for pediatric patients inside and outside the operating room for nonsurgical procedures. Cooperation and motionlessness may be required for imaging studies, bronchoscopy, gastrointestinal (GI) endoscopy, cardiac catheterization, dressing changes, and minor procedures (eg, casts and bone marrow aspiration). Requirements vary depending on the patient and the procedure, ranging from anxiolysis (minimal sedation), to conscious sedation (moderate sedation and analgesia), to deep sedation/analgesia, and finally to general anesthesia. For all practical purposes, the same standards and guidelines that are provided for general anesthesia are also applied to moderate and deep sedation. This includes preoperative preparation (eg, fasting), assessment, monitoring, and postoperative care. Airway obstruction and hypoventilation are the most commonly encountered problems. With deep sedation and general anesthesia, cardiovascular depression can also be a problem. Supplemental oxygen and close monitoring of the airway, ventilation, and other vital signs are mandatory (as with other agents). A laryngeal mask airway is usually well tolerated at higher doses.

Emergence and Recovery

Pediatric patients are particularly vulnerable to two postanesthetic complications: laryngospasm and postintubation croup. As with adult patients, postoperative pain should be aggressively managed.

Laryngospasm

Laryngospasm is a forceful, involuntary spasm of the laryngeal musculature caused by stimulation of the superior laryngeal nerve. It may occur at induction, emergence, or any time in between without an endotracheal tube. Laryngospasm is more common in young pediatric patients (almost 1 in 50) than in adults, being highest in infants 1–3 months old. Laryngospasm at the end of a procedure can usually be avoided by extubating the patient either awake (opening the eyes) or while deeply anesthetized (spontaneously breathing but not swallowing or coughing); both techniques have advocates. Extubation during the interval between these extremes, however, is generally recognized as hazardous. A recent URTI or exposure to secondhand tobacco smoke predisposes patients to laryngospasm on emergence. Treatment of laryngospasm includes gentle positive- pressure ventilation, forward jaw thrust, intravenous lidocaine (1–1.5 mg/kg), or paralysis with intravenous succinylcholine (0.5–1 mg/kg) or rocuronium (0.4 mg/kg) and controlled ventilation.

Postintubation Croup

Croup is due to glottic or tracheal edema. Because the narrowest part of the pediatric airway is the cricoid cartilage, this is the most susceptible area. Croup is less common with endotracheal tubes that are uncuffed and small enough to allow a slight gas leak at 10–25 cm H2O. Postintubation croup is associated with early childhood (age 1–4 years), repeated intubation attempts, large endotracheal tubes, prolonged surgery, head and neck procedures, and excessive movement of the tube (eg, coughing with the tube in place, moving the patient's head). Intravenous dexamethasone (0.25–0.5 mg/kg) may prevent formation of edema, and inhalation of nebulized racemic epinephrine (0.25–0.5 mL of a 2.25% solution in 2.5 mL normal saline) is an effective treatment. Although postintubation croup is a complication that occurs later than laryngospasm, it almost always appears within 3 h after extubation.

Postoperative Pain Management

Pain in pediatric patients has received considerable attention in recent years, particularly the use of regional anesthetic techniques (above). Commonly used parenteral opioids include fentanyl 1–2 mkg/kg, morphine 0.05–0.1 mg/kg, hydromorphone 0.015 mg/kg, and meperidine 0.5 mg/kg. Ketorolac (0.5–0.75 mg/kg) significantly lowers opioid requirements. Rectal acetaminophen (40 mg/kg) may also be helpful.

Patient-controlled analgesia can also be successfully used in patients as young as 6–7 years old, depending on their maturity and on preoperative preparation. The most commonly used opioids are morphine and hydromorphone. With a 10-min lockout interval, the recommended interval dose is either morphine 20 mkg/kg or hydromorphone 5 mkg/kg. As with adults, continuous infusions increase the risk of respiratory depression; recommended continuous infusion

doses are morphine 0–12 mkg/kg/h or hydromorphone 0-3 mkg/kg/h. The subcutaneous route may be used with morphine.

As with adults, epidural infusions for postoperative analgesia usually consist of a local anesthetic plus an opioid. Bupivacaine 0.1–0.125% or ropivacaine 0.1–0.2% are used with fentanyl 2–2.5 mkg/mL. Recommended infusion rates depend on the size of the patient, the final drug concentration, and the location of the epidural catheter, and range from 0.1 to 0.4 mL/kg/h.

Geriatric Anesthesia

Optimal anesthetic management of geriatric patients depends on an understanding of the normal changes in physiology, anatomy, and response to pharmacological agents that accompany aging. In fact, there are many similarities between elderly and pediatric patients. Compared with pediatric patients, however, older people show a wider range of variation in these parameters. The relatively high frequency of serious physiological abnormalities in elderly patients demands a particularly careful preoperative evaluation.

Age-Related Anatomic and Physiological Changes

Cardiovascular System

It is important to distinguish between changes in physiology that normally accompany aging and the pathophysiology of diseases common in the geriatric population. For example, atherosclerosis is pathological—it is not present in healthy elderly patients. On the other hand, a reduction in arterial elasticity caused by fibrosis of the media is part of the normal aging process. Reduced arterial compliance results in increased afterload, elevated systolic blood pressure, and left ventricular hypertrophy. The left ventricular wall thickens at the expense of the left ventricular cavity. Some myocardial fibrosis and calcification of the valves are common. In the absence of coexisting disease, diastolic blood pressure remains unchanged or decreases. Baroreceptor function is depressed. Similarly, whereas cardiac output typically declines with age, it appears to be maintained in well-conditioned healthy individuals. In the absence of disease, resting systolic cardiac function appears to be preserved even in octogenarians. Increased vagal tone and decreased sensitivity of adrenergic receptors lead to a decline in heart rate; maximal heart rate declines by approximately one beat per minute per year of age over 50. Fibrosis of the conduction system and loss of sinoatrial node cells increase the incidence of dysrhythmias, particularly atrial fibrillation and flutter.

Elderly patients undergoing evaluation for surgery have a high incidence of diastolic dysfunction that can be detected with Doppler echocardiography. Marked diastolic dysfunction may be seen with systemic hypertension, coronary artery disease, cardiomyopathies, and valvular heart disease, particularly aortic stenosis. Patients may be asymptomatic or complain of exercise intolerance, dyspnea,

cough, or fatigue. Diastolic dysfunction results in relatively large increases in ventricular end-diastolic pressure with small changes of left ventricular volume; the atrial contribution to ventricular filling becomes even more important than in younger patients. Atrial enlargement predisposes patients to atrial fibrillation and flutter. Patients are at increased risk for developing congestive heart failure.

Diminished cardiac reserve in many elderly patients may be manifested as exaggerated drops in blood pressure during induction of general anesthesia. A prolonged circulation time delays the onset of intravenous drugs but speeds induction with inhalational agents. Like infants, elderly patients have less ability to respond to hypovolemia, hypotension, or hypoxia with an increase in heart rate.

Respiratory System

Elasticity is decreased in lung tissue also, allowing overdistention of alveoli and collapse of small airways. The former reduces the alveolar surface area, which decreases the efficiency of gas exchange. Airway collapse increases residual volume (the volume of air remaining in the lungs at the end of a forced expiration) and closing capacity (the volume of air in the lungs at which small airways begin to close). Even in normal persons, closing capacity exceeds functional residual capacity (the volume of air remaining in the lungs at the end of a normal expiration) at age 45 years in the supine position and age 65 in the sitting position. When this happens, some airways close during part of normal tidal breathing, resulting in a mismatch of ventilation and perfusion. The additive effect of these emphysema-like changes is said to decrease arterial oxygen tension by an average rate of 0.35 mm Hg per year. There is a wide range of arterial oxygen tensions in elderly preoperative patients. Both anatomic and physiological dead space increase.

Mask ventilation may be more difficult in edentulous patients, whereas arthritis of the temporomandibular joint or cervical spine may make intubation challenging. On the other hand, the absence of upper teeth often improves visualization of the vocal cords during laryngoscopy.

Prevention of perioperative hypoxia includes a longer preoxygenation period prior to induction, a higher inspired oxygen concentrations during anesthesia, small increments of positive end-expiratory pressure, and aggressive pulmonary toilet. Aspiration pneumonia is a common and potentially life-threatening complication in elderly patients. One reason for this predisposition is a progressive decrease in protective laryngeal reflexes with age. Ventilatory impairment in the recovery room is more common in elderly patients. Therefore, patients with severe preexisting respiratory disease and those who have just had major abdominal surgery should generally be left intubated postoperatively. In addition, pain control techniques that facilitate postoperative pulmonary function should be seriously considered (eg, epidural local anesthetics and opioids, intercostal nerve blocks).

Metabolic and Endocrine Function

Basal and maximal oxygen consumption declines with age. After reaching peak weight at about age 60, most men and women begin losing weight; the average elderly man and woman weigh less than younger counterparts. Heat production decreases, heat loss increases, and hypothalamic temperature-regulating centers may reset at a lower level. Increasing insulin resistance leads to a progressive decrease in the ability to handle glucose loads. The neuroendocrine response to stress appears to be preserved or slightly decreased in most healthy elderly patients. Aging is associated with a decreasing response to beta-adrenergic agents ("endogenous beta-blockade"). Circulating norepinephrine levels are reported to be elevated in elderly patients.

Renal Function

Renal blood flow and kidney mass (eg, glomerular number and tubular length) decrease with age. These changes are particularly prominent in the renal cortex where they are replaced by fat and fibrotic tissue. Renal function as determined by glomerular filtration rate and creatinine clearance is reduced. The serum creatinine level is unchanged because of a decrease in muscle mass and creatinine production, whereas blood urea nitrogen gradually increases (0.2 mg/dL per year). Impairment of sodium handling, concentrating ability, and diluting capacity predisposes elderly patients to dehydration or fluid overload. The response to antidiuretic hormone and aldosterone is reduced. The ability to reabsorb glucose is decreased. The combination of reduced renal blood flow and decreased nephron mass increases the risk of elderly patients for acute renal failure in the postoperative period.

As renal function declines, so does the kidney's ability to excrete drugs. The decreased capacity to handle water and electrolyte loads makes proper fluid management more critical; elderly patients are more predisposed to developing hypokalemia and hyperkalemia. This is further complicated by the common use of diuretics in the elderly population. To this end, serum electrolytes, cardiac filling pressures, and urinary output are more frequently monitored.

Gastrointestinal Function

Liver mass declines as a person ages, with a corresponding decrease in hepatic blood flow. Hepatic function (reserves) declines in proportion to the decrease in liver mass. Thus, the rate of biotransformation and albumin production decreases. Plasma cholinesterase levels are reduced in elderly men. Gastric pH tends to rise, whereas gastric emptying is prolonged, although some studies suggest elderly patients have lower gastric volumes than younger patients.

Nervous System

Brain mass decreases with age; neuronal loss is prominent in the cerebral cortex, particularly the frontal lobes. Cerebral blood flow also decreases about 10–20% in proportion to neuronal losses. It remains tightly coupled to metabolic rate; autoregulation is intact. Neurons decrease in size and lose some complexity of their dendritic tree and number of synapses. The synthesis of some neurotransmitters, such as dopamine, and the number of their receptors are reduced. Serotonergic, adrenergic, and gamma-aminobutyric acid (GABA) binding sites are also reduced. Astrocytes and microglial cells increase in number.

Degeneration of peripheral nerve cells results in prolonged conduction velocity and skeletal muscle atrophy.

Aging is associated with an increasing threshold for nearly all sensory modalities, including touch, temperature sensation, proprioception, hearing, and vision. Changes in pain perception are complex and poorly understood; central and peripheral processing mechanisms are likely altered. Dosage requirements for local (Cm: minimum anesthetic concentration) and general (MAC: minimum alveolar concentration) anesthetics are reduced. Administration of a given volume of epidural anesthetic tends to result in more extensive cephalad spread in elderly patients, but with a shorter duration of analgesia and motor block. In contrast, a longer duration of action should be expected from a spinal anesthetic.

In the absence of disease, decreases in cognitive function are normally modest but variable. Short-term memory appears to be most affected. Continued physical and intellectual activity appears to have a positive effect on preservation of cognitive functions.

Elderly patients often take more time to recover completely from the central nervous system effects of general anesthesia, particularly if they were confused or disoriented preoperatively. This is important in geriatric outpatient surgery, where socioeconomic factors such as the lack of a caretaker at home necessitate a higher level of self-care. Many elderly patients experience varying degrees of an acute confusional state, delirium, or cognitive dysfunction postoperatively. The etiology of postoperative cognitive dysfunction (POCD) is likely multifactorial and includes drug effects, pain, underlying dementia, hypothermia, and metabolic disturbances. Low levels of certain neurotransmitters, such as acetylcholine, may be contributory. Elderly patients are particularly sensitive to centrally acting anticholinergic agents such as scopolamine and atropine. Interestingly, the incidence of postoperative delirium appears similar with both regional and general anesthesia; it may be less following regional anesthesia without any sedation. Some patients suffer from prolonged or permanent POCD after surgery and anesthesia. Some studies suggest that POCD can be detected in 10–15% of patients > 60 years of age up to 3 months following major surgery. In some settings, eg, following cardiac and major orthopedic procedures, intraoperative arterial emboli may be contributory. Animal studies suggest that anesthesia without surgery can

impair learning for weeks, particularly in older animals. Elderly inpatients appear to have a significantly higher risk for POCD than elderly outpatients. Although the etiology remains unclear, both anesthetic and nonanesthetic factors are likely responsible for POCD.

Musculoskeletal

Muscle mass is reduced. At the microscopic level, neuromuscular junctions thicken. There also appears to be some extrajunctional spread of acetylcholine receptors. Skin atrophies with age and is prone to trauma from adhesive tape, electrocautery pads, and electrocardiographic electrodes. Veins are often frail and easily ruptured by intravenous infusions. Arthritic joints may interfere with positioning (eg, lithotomy) or regional anesthesia (eg, subarachnoid block). Degenerative cervical spine disease can limit neck extension potentially making intubation difficult.

Age-Related Pharmacological Changes

Aging produces both pharmacokinetic (the relationship between drug dose and plasma concentration) and pharmacodynamic (the relationship between plasma concentration and clinical effect) changes. Unfortunately, disease-related changes and wide interindividual variations even in similar populations lead to inconsistent generalizations.

A progressive decrease in muscle mass and increase in body fat (more pronounced in older women) results in decreased total body water. The reduced volume of distribution for water-soluble drugs can lead to higher plasma concentrations; conversely, an increased volume of distribution for lipid-soluble drugs can lower their plasma concentration. These changes in volume of distribution may affect elimination half-life. If a drug's volume of distribution expands, its elimination half-life will be prolonged unless the rate of clearance is also increased. However, because renal and hepatic functions decline with age, reductions in clearance prolong the duration of action for many drugs. Studies suggest that unlike those who are ill, healthy, active, elderly patients have little or no change in plasma volume.

Inhalational Anesthetics

The MAC for inhalational agents is reduced by 4% per decade of age over 40 years. For example, the MAC of halothane in an 80-year-old person would be expected to be 0.65 (0.77 – [0.77 x 4% x 4]). Onset of action will be more rapid if cardiac output is depressed, whereas it will be delayed if there is a significant ventilation/perfusion abnormality. The myocardial depressant effects of volatile anesthetics are exaggerated in elderly patients, whereas the tachycardiac tendencies of isoflurane and desflurane are attenuated. Thus, in contrast to its effects on

younger patients, isoflurane reduces cardiac output and heart rate in elderly patients. Recovery from anesthesia with a volatile anesthetic may be prolonged because of an increased volume of distribution (increased body fat), decreased hepatic function (decreased halothane metabolism), and decreased pulmonary gas exchange. The rapid elimination of desflurane may make it the inhalation anesthetic of choice for elderly patients.

Nonvolatile Anesthetic Agents

In general, elderly patients display a lower dose requirement for propofol, etomidate, barbiturates, opioids, and benzodiazepines. For example, the typical octogenarian may require less than half the induction dose of propofol or thiopental than that required by a 20-year-old patient.

Although propofol may be close to an ideal induction agent for elderly patients because of its rapid elimination, it is more likely to cause apnea and hypotension than in younger patients. Concomitant administration of midazolam, opioids, or ketamine further decreases propofol requirements. Both pharmacokinetic and pharmacodynamic factors are responsible for this enhanced sensitivity. Elderly patients require nearly 50% lower blood levels of propofol for anesthesia than younger patients. Moreover, both the rapidly equilibrating peripheral compartment and systemic clearance for propofol are significantly reduced in elderly patients. In the case of thiopental, enhanced sensitivity appears to be primarily due to pharmacokinetics factors.

Enhanced sensitivity to fentanyl, alfentanil, and sufentanil is primarily pharmacodynamic. Pharmacokinetics for these opioids are not significantly affected by age.

Aging increases the volume of distribution for all benzodiazepines, which effectively prolongs their elimination half-lives. In the case of diazepam, the elimination half-life can be as long as 36–72 h. Enhanced pharmacodynamic sensitivity to benzodiazepines is also observed. Midazolam requirements are generally 50% less in elderly patients; its elimination half-life is prolonged from about 2.5 to 4 h.

Muscle Relaxants

The response to succinylcholine and nondepolarizing agents is unaltered with aging. Decreased cardiac output and slow muscle blood flow, however, may cause up to a 2-fold prolongation in onset of neuromuscular blockade in elderly patients. Recovery from nondepolarizing muscle relaxants that depend on renal excretion (eg, metocurine, pancuronium, doxacurium, tubocurarine) may be delayed due to decreased drug clearance. Likewise, decreased hepatic excretion from a loss of liver mass prolongs the elimination half-life and duration of action

of rocuronium and vecuronium. The pharmacological profiles of atracurium and pipecuronium are not significantly affected by age.

Postanesthesia Care

Recovery rooms have been in existence for less than 50 years in most medical centers. Prior to that time, many early postoperative deaths occurred immediately after anesthesia and surgery. The realization that many of these deaths were preventable emphasized the need for specialized nursing care immediately following surgery. As surgical procedures became increasingly complex and were performed on sicker patients, recovery room care was often extended beyond the first few hours after surgery, and some critically ill patients were kept in the recovery room overnight. The success of these early recovery rooms was a major factor in the evolution of modern surgical intensive care units (ICU).

Following general anesthesia, if the patient was intubated and if ventilation was judged adequate, the endotracheal tube is also usually removed prior to transport. Patients are also routinely observed in the ICU following regional anesthesia, and in most instances following monitored anesthesia care (local anesthesia with sedation). Most procedure guidelines require that a patient be admitted to the ICU following any type of anesthesia, except by specific order of the attending anesthesiologist. After a brief verbal report to the ICU nurse, the patient is left in the ICU until the major effects of anesthesia are judged to have worn off. This period is characterized by a relatively high incidence of potentially life-threatening respiratory and circulatory complications.

Emergence from General Anesthesia

Recovery from general or regional anesthesia is a time of great physiological stress for many patients. Emergence from general anesthesia should ideally be a smooth and gradual awakening in a controlled environment. Unfortunately, it often begins in the operating room or during transport to the recovery room and is frequently characterized by airway obstruction, shivering, agitation, delirium, pain, nausea and vomiting, hypothermia, and autonomic lability. Even patients receiving spinal or epidural anesthesia can experience marked decreases in blood pressure during transport or recovery; the sympatholytic effects of regional blocks prevent compensatory reflex vasoconstriction when patients are moved or when they sit up.

Following an inhalational-based anesthetic, the speed of emergence is directly proportionate to alveolar ventilation but inversely proportionate to the agent's blood solubility. As the duration of anesthesia increases, emergence also becomes increasingly dependent on total tissue uptake, which is a function of agent solubility, the average concentration used, and the duration of exposure to the anesthetic. Recovery is therefore fastest with desflurane and nitrous oxide and slowest from prolonged deep anesthesia with halothane and enflurane. Hypoventilation delays emergence from inhalational anesthesia.

Emergence from an intravenous anesthetic is a function of its pharmacokinetics. Recovery from most intravenous anesthetic agents is dependent primarily on redistribution rather than on elimination half-life. As the total administered dose increases, however, cumulative effects become apparent in the form of prolonged emergence; the termination of action becomes increasingly dependent on the elimination or metabolic half-life. Under these conditions, advanced age or renal or hepatic disease can prolong emergence. Use of short and ultra- short-acting anesthetic agents such as propofol and remifentanil significantly shortens emergence, time to awakening, and discharge. Moreover, the use of a Bispectral Index Scale (BIS) monitor reduces total drug dosage and shortens recovery and time to discharge. The use of laryngeal mask airways may also allow lighter levels of anesthesia that could speed emergence.

The speed of emergence can also be influenced by preoperative medications. Premedication with agents that outlast the procedure may be expected to prolong emergence. The short duration of action of midazolam makes it a suitable premedication agent for short procedures. The effects of preoperative sleep deprivation or drug ingestion (alcohol, sedatives) can also be additive to those of anesthetic agents and can prolong emergence.

Delayed Emergence

The most frequent cause of delayed emergence (when the patient fails to regain consciousness 30–60 min after general anesthesia) is residual anesthetic, sedative, and analgesic drug effect. Delayed emergence might occur as a result of absolute or relative drug overdose or potentiation of anesthetic agents by prior drug ingestion (alcohol). Administration of naloxone (0.04 mg increments) and flumazenil (0.2 mg increments) readily reverses and can exclude the effects of an opioid and benzodiazepine, respectively. Physostigmine 1–2 mg may partially reverse the effect of other agents. A nerve stimulator can be used to exclude significant neuromuscular blockade in patients on a mechanical ventilator who have inadequate spontaneous tidal volumes.

Less common causes of delayed emergence include hypothermia, marked metabolic disturbances, and perioperative stroke. Core temperatures less than 33°C have an anesthetic effect and greatly potentiate the effects of central nervous system depressants. Forced-air warming devices are most effective in raising body temperature. Hypoxemia and hypercarbia are readily excluded by blood gas analysis. Hypercalcemia, hypermagnesemia, hyponatremia, and hypoglycemia and hyperglycemia are rare causes that require laboratory measurements for diagnosis. Perioperative stroke is rare except after neurological, cardiac, and cerebrovascular surgery; diagnosis requires neurological consultation and radiological imaging.

Routine Recovery: General Anesthesia

Airway patency, vital signs, and oxygenation should be checked immediately on arrival. Subsequent blood pressure, pulse rate, and respiratory rate measurements are routinely made at least every 5 min for 15 min or until stable, and every 15 min thereafter. Pulse oximetry should be monitored continuously in all patients recovering from general anesthesia, at least until they regain consciousness. The occurrence of hypoxemia does not necessarily correlate with the level of consciousness. Neuromuscular function should be assessed clinically, eg, head-lift. At least one temperature measurement should also be obtained. Additional monitoring includes pain assessment (eg, numerical or descriptive scales), the presence or absence of nausea or vomiting, and fluid input and output including urine flow, drainage, and bleeding.

All patients recovering from general anesthesia should receive 30–40% oxygen during emergence because transient hypoxemia can develop even in healthy patients. Patients at increased risk for hypoxemia, such as those with underlying pulmonary dysfunction or those undergoing upper abdominal or thoracic procedures, should continue to be monitored with a pulse oximeter even after emergence and may need oxygen supplementation for longer periods. A rational decision regarding continuing supplemental oxygen therapy at the time of discharge from the PACU can be made based on SpO2 readings on room air. Arterial blood gas measurements can be obtained to confirm abnormal oximetry readings. Oxygen therapy should be carefully controlled in patients with chronic obstructive pulmonary disease and a history of CO2 retention. Patients should generally be nursed in the head-up position whenever possible to optimize oxygenation. However, elevating the head of the bed before the patient is responsive can lead to airway obstruction. In such cases, the oral or nasal airway should be left in place until the patient is awake. Deep breathing and coughing should be encouraged periodically.

Routine Recovery: Regional Anesthesia

Patients who are heavily sedated or hemodynamically unstable following regional anesthesia should also receive supplemental oxygen. Sensory and motor levels should be periodically recorded following regional anesthesia to document dissipation of the block. Precautions in the form of padding or repeated warning may be necessary to prevent self-injury from uncoordinated arm movements following brachial plexus blocks. Blood pressure should be closely monitored following spinal and epidural anesthesia. Bladder catheterization may be necessary in patients who have had spinal or epidural anesthesia for longer than 4 h.

Pain Control

Mild to moderate pain can be treated orally with acetaminophen plus codeine, hydrocodone, or oxycodone. Alternatively, an opioid agonist–antagonist (butorphanol, 1–2 mg, or nalbuphine, 5–10 mg) or ketorolac tromethamine, 30 mg,

may be used intravenously. The latter is particularly useful following orthopedic and gynecological procedures.

Moderate to severe postoperative pain can be managed with parenteral or intraspinal opioids, regional anesthesia, or specific nerve blocks. When opioids are used, titration of small intravenous doses is generally safest. Although considerable variability may be encountered, most patients are quite sensitive to opioids within the first hour after general anesthesia. Adequate analgesia must be balanced against excessive sedation. Opioids of intermediate to long duration, such as morphine, 2–4 mg (0.025–0.05 mg/kg in children), are most commonly used. Analgesic effects usually peak within 4–5 min. Maximal respiratory depression, particularly with morphine and hydromorphone, may not be seen until 20–30 min later. When the patient is fully awake, patient-controlled analgesia (PCA) can be instituted for inpatients. Intramuscular administration of opioids has the disadvantage of delayed and variable onset (10–20 min) and delayed respiratory depression (up to 1 h).

When an epidural catheter has been left in place, epidural administration of fentanyl, 50–100 mkg or morphine, 3–5 mg, can provide excellent pain relief in adults; however, the risk of delayed respiratory depression with morphine mandates special monitoring precautions for 12–24 h afterward. Intercostal, interscalene, femoral, epidural, or caudal anesthesia is often helpful when opioid analgesia alone is unsatisfactory.

Nausea and Vomiting

Postoperative nausea and vomiting (PONV) are a common problem following general anesthesia, occurring in 20–30% of all patients. Moreover, PONV may occur only at home within 24 h of an uneventful discharge (postdischarge nausea and vomiting) in a significant number of additional patients. The etiology of PONV is usually multifactorial, involving anesthetic agents, the type of procedure, and patient factors. It is important to recognize that nausea is a common complaint that is reported at the onset of hypotension, particularly following spinal or epidural anesthesia.

Selective 5-hydroxytryptamine (serotonin) receptor 3 (5-HT3) antagonists such as ondansetron 4 mg (0.1 mg/kg in children) are effective in preventing PONV and in treating established PONV.

Controversy exists regarding routine prophylaxis for PONV in all patients. Clearly patients with multiple risk factors should receive prophylaxis. Additionally, use of two or more agents is more effective than single agent prophylaxis. Outcome studies and satisfaction surveys suggest little or no difference between routine prophylaxis and treat-as-needed strategies.

Shivering and Hypothermia

Shivering can occur as a result of intraoperative hypothermia or the effects of anesthetic agents. It is also common in the immediate postpartum period. The most important cause of hypothermia is a redistribution of heat from the body core to the peripheral compartments. A cold ambient temperature in the operating room, prolonged exposure of a large wound, and the use of large amounts of unwarmed intravenous fluids or high flows of unhumidified gases can also be contributory. The shivering occasionally can be intense enough to cause hyperthermia (38–39°C) and a significant metabolic acidosis, both of which promptly resolve when the shivering stops. Both spinal and epidural anesthesia also lower the shivering threshold and vasoconstrictive response to hypothermia; shivering may also be encountered in the recovery room following regional anesthesia. Other causes of shivering should be excluded, such as sepsis, drug allergy, or a transfusion reaction. Hypothermia should be treated with a forced-air warming device, or (less satisfactorily) with warming lights or heating blankets, to raise body temperature to normal. Intense shivering causes precipitous rises in oxygen consumption, CO2 production, and cardiac output. These physiological effects are often poorly tolerated by patients with preexisting cardiac or pulmonary impairment. Hypothermia has been associated with an increased incidence of myocardial ischemia, arrhythmias, increased transfusion requirements, and increased duration of muscle relaxant effects.

Discharge from ICU or Recovery Room

Before discharge from ICU, patients should have been observed for respiratory depression for at least 20–30 min after the last dose of parenteral narcotic. Other minimum discharge criteria for patients recovering from general anesthesia usually include the following:

(1) Easy arousability (2) Full orientation (3) The ability to maintain and protect the airway (4) Stable vital signs for at least 15–30 min (5) The ability to call for help if necessary (6) No obvious surgical complications (such as active bleeding).

Controlling postoperative pain, controlling nausea and vomiting, and reestablishing normothermia prior to discharge are also highly desirable. Scoring systems are widely used. Most assess SpO2 (or color), consciousness, circulation, respiration, and motor activity

Key Concepts

Venous air embolism can occur when the pressure within an open vein is subatmospheric. These conditions may exist in any position (and during any procedure) whenever the wound is above the level of the heart.

Optimal recovery of air following venous air embolism is provided by a multiorificed catheter positioned high in the atrium at its junction with the superior vena cava.

In a patient with head trauma, correction of hypotension and control of any bleeding take precedence over radiographic studies and definitive neurosurgical treatment because systolic arterial blood pressures of less than 80 mm Hg correlate with a poor outcome.

Techniques to minimize intraoperative blood loss include supplementation with cocaine or an epinephrine-containing local anesthetic, maintaining a slightly head-up position, and providing a mild degree of controlled hypotension.

As always, if there is serious doubt regarding potential airway problems, an intravenous induction should be avoided in favor of awake direct or fiberoptic laryngoscopy (cooperative patient) or an inhalational induction, maintaining spontaneous ventilation (uncooperative patient). In any case, the equipment and personnel required for an emergency tracheostomy must be immediately available.

Manipulation of the carotid sinus and stellate ganglion during radical neck dissection (right side more than the left) has been associated with wide swings in blood pressure, bradycardia, dysrhythmias, sinus arrest, and prolonged QT intervals. Infiltration of the carotid sheath with local anesthetic will usually ameliorate these problems. Bilateral neck dissection may result in postoperative hypertension and loss of hypoxic drive because of denervation of the carotid sinuses and bodies.

Patients undergoing maxillofacial reconstruction or orthognathic surgical procedures often pose the greatest airway challenges to the anesthesiologist. If there are any anticipated signs of problems with mask ventilation or tracheal intubation, the airway should be secured prior to induction.

If there is a chance of postoperative edema involving structures that could obstruct the airway (eg, tongue), the patient should be carefully observed and perhaps should be left intubated.

Any factor that normally increases intraocular pressure will tend to decrease intraocular volume by causing drainage of aqueous or extrusion of vitreous through the wound. The latter is a serious complication that can permanently worsen vision.

Succinylcholine increases intraocular pressure by 5–10 mm Hg for 5–10 min after administration, principally through prolonged contracture of the extraocular muscles.

Traction on extraocular muscles or pressure on the eyeball can elicit a wide variety of cardiac dysrhythmias ranging from bradycardia and ventricular ectopy to sinus arrest or ventricular fibrillation.

The key to inducing anesthesia in a patient with an open eye injury is controlling intraocular pressure with a smooth induction. Specifically, coughing during intubation must be avoided by achieving a deep level of anesthesia and profound paralysis.

The postretrobulbar apnea syndrome is probably due to injection of local anesthetic into the optic nerve sheath, with spread into the cerebrospinal fluid.

Regardless of the technique employed for intravenous sedation, ventilation and oxygenation must be carefully monitored, and equipment to provide positive-pressure ventilation must be immediately available.

During one-lung ventilation, the mixing of unoxygenated blood from the collapsed upper lung with oxygenated blood from the still-ventilated dependent lung widens the PA–a (alveolar-to-arterial) O2 gradient and often results in hypoxemia.

If epidural opioids are to be used postoperatively, their intravenous use should be limited during surgery to prevent excessive postoperative respiratory depression.

Postoperative hemorrhage complicates about 3% of thoracotomies and may be associated with up to 20% mortality. Signs of hemorrhage include increased chest tube drainage (> 200 mL/h), hypotension, tachycardia, and a falling hematocrit.

Bronchopleural fistula presents as a sudden large air leak from the chest tube that may be associated with an increasing pneumothorax and partial lung collapse.

Nitrous oxide is contraindicated in patients with cysts or bullae because it can expand the air space and cause rupture. The latter may be signaled by sudden hypotension, bronchospasm, or an abrupt rise in peak inflation pressure and requires immediate placement of a chest tube.

The initial assessment of the trauma patient can be divided into primary, secondary, and tertiary surveys. The primary survey should take 2–5 min and consists of the ABCDE sequence of trauma: Airway, Breathing, Circulation, Disability, and Exposure. Resuscitation and assessment proceed simultaneously. Trauma resuscitation includes two additional phases: control of hemorrhage and definitive repair of the injury. More comprehensive secondary and tertiary surveys of the patient follow the primary survey.

Five criteria increase the risk for potential instability of the cervical spine: (1) neck pain, (2) severe distracting pain, (3) any neurological signs or symptoms, (4) intoxication, and (5) loss of consciousness at the scene. A cervical spine fracture must be assumed if any one of these criteria is present. Even with these criteria, the incidence of cervical spine trauma is

approximately 2%. The incidence of cervical spine instability increases up to 10% in the presence of a severe head injury.

Neck hyperextension and excessive axial traction must be avoided whenever cervical spine instability is suspected. Manual immobilization of the head and neck by an assistant should be used to stabilize the cervical spine during laryngoscopy ("manual in-line stabilization" or MILS).

The mainstay of therapy of hemorrhagic shock is intravenous fluid resuscitation and transfusion. Multiple short (1.5–2 in), large-bore (14–16 gauge or 7–8.5F) catheters are placed in whichever veins are easily accessible.

Rapid-infusion systems that use large-bore tubing and rapidly warm fluids are invaluable during massive transfusions. A convection forced-air warming blanket and heated humidifier will also help maintain body temperature. Hypothermia worsens acid–base disorders, coagulopathy, and myocardial dysfunction.

Hypotension in patients with hypovolemic shock should be aggressively treated with intravenous fluids and blood products, not vasopressors unless there is profound hypotension that is unresponsive to fluid therapy, coexisting cardiogenic shock, or cardiac arrest.

Commonly used induction agents for trauma patients include ketamine and Na oxybutiras. Even after adequate fluid resuscitation, the induction dose requirements for propofol are greatly (80–90%) reduced in patients with major trauma. Even drugs such as ketamine and nitrous oxide that normally indirectly stimulate cardiac function can display cardiodepressant properties in patients who are in shock and already have maximal sympathetic stimulation.

Invasive monitoring (direct arterial, central venous, and pulmonary artery pressure monitoring) can be extremely helpful in guiding fluid resuscitation but insertion of these monitors should not detract from the resuscitation itself. Serial hematocrits (or hemoglobin), arterial blood gas measurement, and serum electrolytes (particularly K+) are invaluable in protracted resuscitations.

Any trauma victim with altered consciousness must be considered to have a brain injury. The level of consciousness is assessed by serial Glasgow Coma Scale evaluations.

The most common morbidities encountered in obstetrics are severe hemorrhage and severe preeclampsia.

Regardless of the time of last oral intake, all obstetric patients are considered to have a full stomach and to be at risk for pulmonary aspiration.

Nearly all parenteral opioid analgesics and sedatives readily cross the placenta and can affect the fetus. Regional anesthetic techniques are preferred for management of labor pain.

Using a local anesthetic–opioid mixture for lumbar epidural analgesia during labor significantly reduces drug requirements, compared with using either agent alone.

Optimal analgesia for labor requires neural blockade at T10–L1 in the first stage of labor and T10–S4 in the second stage.

Continuous lumbar epidural analgesia is the most versatile and most commonly employed technique, because it can be used for pain relief for the first stage of labor as well as analgesia/anesthesia for subsequent vaginal delivery or cesarean section, if necessary.

When dilute mixtures of a local anesthetic and an opioid are used epidural analgesia has little if any effect on the progress of labor.

Even when aspiration does not yield blood or cerebrospinal fluid, unintentional intravascular or intrathecal placement of an epidural needle or catheter is possible.

Hypotension is the most common side effect of regional anesthetic techniques and must be treated aggressively with ephedrine and intravenous fluid boluses to prevent fetal compromise.

Techniques using combined spinal epidural analgesia and anesthesia may particularly benefit patients with severe pain early in labor and those who receive analgesia/anesthesia just prior to delivery.

Spinal or epidural anesthesia is preferred to general anesthesia for cesarean section because regional anesthesia is associated with lower maternal mortality.

Spinal anesthesia for cesarean section is easier to perform and results in more rapid and intense neural blockade than epidural anesthesia. Epidural anesthesia allows greater control over sensory level and results in a more gradual fall in arterial blood pressure.

Systemic, local anesthetic toxicity during epidural anesthesia may be best avoided by slowly administering dilute solutions for labor pain and fractionating the total dose for cesarean section into 5-mL increments.

In general anesthesia for cesarean section, if endotracheal intubation fails, the life of the mother takes priority over delivery of the fetus.

Maternal hemorrhage is one of the most common severe morbidities complicating obstetric anesthesia. Causes include placenta previa, abruptio placentae, and uterine rupture.

Pregnancy-induced hypertension describes one of three syndromes: preeclampsia, eclampsia, and the HELLP syndrome.

Common causes of postpartum hemorrhage include uterine atony, a retained placenta, obstetric lacerations, uterine inversion, and use of tocolytic agents prior to delivery.

Intrauterine asphyxia during labor is the most common cause of neonatal depression. Fetal monitoring throughout labor is helpful in identifying which babies may be at risk, detecting fetal distress, and evaluating the effect of acute interventions.

The small and limited number of alveoli in neonates and infants reduces lung compliance; in contrast, their cartilaginous rib cage makes their chest wall very compliant. The combination of these two characteristics promotes

chest wall collapse during inspiration and relatively low residual lung volumes at expiration. The resulting decrease in functional residual capacity (FRC) is important because it limits oxygen reserves during periods of apnea (eg, intubation) and readily predisposes them to atelectasis and hypoxemia.

Neonates and infants have a proportionately larger head and tongue, narrow nasal passages, an anterior and cephalad larynx, a long epiglottis, and a short trachea and neck. These anatomic features make neonates and most young infants obligate nasal breathers until about 5 months of age. The cricoid cartilage is the narrowest point of the airway in children younger than 5 years of age.

Stroke volume is relatively fixed by a noncompliant and poorly developed left ventricle in neonates and infants. The cardiac output is therefore very dependent on heart rate.

Thin skin, low fat content, and a higher surface relative to weight allow greater heat loss to the environment in neonates. This problem is compounded by cold operating rooms, wound exposure, intravenous fluid administration, dry anesthetic gases, and the direct effect of anesthetic agents on temperature regulation. Hypothermia has been associated with delayed awakening from anesthesia, cardiac irritability, respiratory depression, increased pulmonary vascular resistance, and altered drug responses.

Neonates, infants, and young children have relatively higher alveolar ventilation and lower FRC compared with older children and adults. This higher minute ventilation-to-FRC ratio with relatively higher blood flow to vessel-rich organs contributes to a rapid rise in alveolar anesthetic concentration and speeds inhalation induction.

Children are more susceptible than adults to cardiac arrhythmias, hyperkalemia, rhabdomyolysis, myoglobinemia, masseter spasm, and malignant hyperthermia (MH) after administration of succinylcholine. If a child unexpectedly experiences cardiac arrest following administration of succinylcholine, immediate treatment for hyperkalemia should be instituted.

Unlike in adult patients, profound bradycardia and sinus node arrest can develop in pediatric patients following the first dose of succinylcholine without atropine pretreatment.

A viral infection within 2–4 weeks before general anesthesia and endotracheal intubation appears to place the child at an increased risk for perioperative pulmonary complications, such as wheezing, laryngospasm, hypoxemia, and atelectasis.

Temperature must be closely monitored in pediatric patients because of their higher risk for MH and the potential for both iatrogenic hypothermia and hyperthermia.

Meticulous fluid management is required in small pediatric patients because of extremely limited margins of error. A programmable infusion pump or a buret with a microdrip chamber should be used for accurate measurements.

Drugs are flushed through low dead-space tubing to minimize unnecessary fluid administration.

Laryngospasm can usually be avoided by extubating the patient either awake or while deeply anesthetized; both techniques have advocates. Extubation during the interval between these extremes, however, is generally recognized as hazardous.

In the absence of coexisting disease, resting systolic cardiac function appears to be preserved even in octogenarians. Increased vagal tone and decreased sensitivity of adrenergic receptors lead to a decline in heart rate.

Elderly patients undergoing evaluation for surgery have a high incidence of diastolic dysfunction that can be detected with Doppler echocardiography.

Diminished cardiac reserve in many elderly patients may be manifested as exaggerated drops in blood pressure during induction of general anesthesia. A prolonged circulation time delays the onset of intravenous drugs but speeds induction with inhalational agents.

Elasticity is decreased in lung tissue, allowing overdistention of alveoli and collapse of small airways. Airway collapse increases residual volume and closing capacity. Even in normal persons, closing capacity exceeds functional residual capacity at age 45 in the supine position and age 65 in the sitting position. When this happens, some airways close during part of normal tidal breathing, resulting in a mismatch of ventilation and perfusion.

Aging is associated with a decreasing response to beta-adrenergic agents ("endogenous beta-blockade").

Impairment of sodium handling, concentrating ability, and diluting capacity predisposes elderly patients to dehydration or fluid overload. As renal function declines, so does the kidney's ability to excrete drugs.

Hepatic function (reserves) declines in proportion to the decrease in liver mass.

Dosage requirements for local (minimum anesthetic concentration) and general (minimum alveolar concentration) anesthetics are reduced. Administration of a given volume of epidural anesthetic tends to result in more extensive cephalad spread in elderly patients, but with a shorter duration of analgesia and motor block. A longer duration of action should be expected from a spinal anesthetic.

Many elderly patients experience varying degrees of an acute confusional state, delirium, or cognitive dysfunction postoperatively.

Aging produces both pharmacokinetic and pharmacodynamic changes. Disease-related changes and wide interindividual variations even in similar populations lead to inconsistent generalizations.

Elderly patients display a lower dose requirement for propofol, barbiturates, opioids, and benzodiazepines.

Patients should not leave the operating room unless they have a stable and patent airway, have adequate ventilation and oxygenation, and are hemodynamically stable.

Before the patient is fully responsive, pain is often manifested as postoperative restlessness. Serious systemic disturbances (such as hypoxemia, acidosis, or hypotension), bladder distention, or a surgical complication (such as occult intraabdominal hemorrhage) should always be considered as well.

Intense shivering causes precipitous rises in oxygen consumption, CO2

production, and cardiac output. These physiological effects are often poorly tolerated by patients with preexisting cardiac or pulmonary impairment.

Respiratory problems are the most frequently encountered serious complications in the postanesthesia care unit (PACU). The overwhelming majority are related to airway obstruction, hypoventilation, or hypoxemia.

Hypoventilation in the PACU is most commonly due to the residual depressant effects of anesthetic agents on respiratory drive.

Obtundation, circulatory depression, or severe acidosis (arterial blood pH < 7.15) is an indication for immediate endotracheal intubation in patients suffering from hypoventilation.

Following administration of naloxone to increase respiration, patients should be watched carefully for recurrence of opioid-induced respiratory depression (renarcotization), as naloxone has a shorter duration than most opioids.

Increased intrapulmonary shunting from a decreased functional residual capacity relative to closing capacity is the most common cause of hypoxemia following general anesthesia.

The possibility of a postoperative pneumothorax should always be considered following central line placement, intercostal blocks, rib fractures, neck dissections, tracheostomy, nephrectomies, or other retroperitoneal or intraabdominal procedures (including laparoscopy), particularly when the diaphragm might be penetrated.

Hypovolemia is by far the most common cause of hypotension in the PACU. Noxious stimulation from incisional pain, endotracheal intubation, or

bladder distention is usually responsible for cases of postoperative hypertension.