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MINISTRY OF PUBLIC HEALTH OF UKRAINE
 NATIONAL O.O. BOGOMOLETS MEDICAL UNIVERSITY
CHAIR OF ANAESTHESIOLOGY AND INTENSIVE THERAPY


                                      “Affirmed”
                                 Head of the Chair of
                         Anaesthesiology and Intensive Therapy
                               Professor F.S. Glumcher

                               “____” _________ 2009



         STUDY GUIDE FOR PRACTICAL WORK
            FOR TEACHERS AND STUDENTS
CLASSES IN ANAESTHESIOLOGY AND INTENSIVE THERAPY

                   THEME:
      «ANAESTHESIOLOGY: CLINICAL ASPECTS»




                      Kyiv
                      2009
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 Patient
1.1. Initial Assessment (Primary Survey, Secondary Survey, Tertiary Survey)
1.2. Anesthetic Considerations
1.2.1. General Considerations
1.2.2. Head and Spinal Cord Trauma
1.2.3. Chest Trauma
1.2.4. Abdominal Trauma
1.2.5. Exremity Trauma
2. Anesthesia for Thoracic Surgery
2.1. Special Consideretions (The Lateral Decubitus Position, Positive-Pressure
Ventilation, Open Pneumothorax, Mediastinal Shift, One-Lung Ventilation)
2.2. Postoperative Management
2.3. Postoperative Complications
3. Anesthesia for Orthopedic Surgery
3.1. Special Considerations in Orthopedic Surgery (Bone Cement, Pneumatic
Tourniquets)
3.2. Special Complications (Fat Embolism Syndrome, Deep Venous Thrombosis
and Thromboembolism)
4. Obstetric Anesthesia
4.1. Anesthesia for Labor and Vaginal Delivery
4.1.1. Psychological and Nonpharmacological Techniques
4.1.2. Parenteral Agents
4.1.3. Pudendal Nerve Block
4.1.4. Regional Anesthetic Techniques (Lumbar Epidural Anaglesia, Combined
Spinal and Epidural (CSE) Analgesia, Spinal Anesthesia)
4.1.5. General Anesthesia
4.2. Anesthesia for Cesarean Section
4.2.1. Regional anesthesia
4.2.2. CSE Anesthesia
4.2.3. General Anesthesia
5. Pediatric Anesthesia
5.1. Pharmacological Differences (Inhalational Anesthetics, Nonvolatile
Anesthetics, Muscle Relaxants)
5.2. Pediatric Anesthetic Risk
5.3. 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 Recovery
5.4.1. Laryngospasm
5.4.2. Postintubation Croup
5.4.3.Postoperative Pain Management
6. Geriatric Anesthesia
6.1. Age-Related Anatomic and Physiological Changes
6.2. Age-Related Pharmacological Changes (Inhalational Anesthetics, Nonvolatile
Anesthetic Agents, Muscle Relaxants)
7. Postanesthesia Care
7.1. Emergence from General Anesthesia
7.1.1. Delayed Emergence8Routine Recovery: General Anesthesia
7.1.2 Routine Recovery: Regional Anesthesia
7.2.Pain Control
7.3. Nausea and Vomiting
7.4. 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).
Bohomolets anaesthesiology clinical
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Bohomolets anaesthesiology clinical

  • 1. MINISTRY OF PUBLIC HEALTH OF UKRAINE NATIONAL O.O. BOGOMOLETS MEDICAL UNIVERSITY CHAIR OF ANAESTHESIOLOGY AND INTENSIVE THERAPY “Affirmed” Head of the Chair of Anaesthesiology and Intensive Therapy Professor F.S. Glumcher “____” _________ 2009 STUDY GUIDE FOR PRACTICAL WORK FOR TEACHERS AND STUDENTS CLASSES IN ANAESTHESIOLOGY AND INTENSIVE THERAPY THEME: «ANAESTHESIOLOGY: CLINICAL ASPECTS» Kyiv 2009
  • 2. 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 Patient 1.1. Initial Assessment (Primary Survey, Secondary Survey, Tertiary Survey) 1.2. Anesthetic Considerations 1.2.1. General Considerations 1.2.2. Head and Spinal Cord Trauma 1.2.3. Chest Trauma 1.2.4. Abdominal Trauma 1.2.5. Exremity Trauma 2. Anesthesia for Thoracic Surgery 2.1. Special Consideretions (The Lateral Decubitus Position, Positive-Pressure Ventilation, Open Pneumothorax, Mediastinal Shift, One-Lung Ventilation) 2.2. Postoperative Management 2.3. Postoperative Complications 3. Anesthesia for Orthopedic Surgery 3.1. Special Considerations in Orthopedic Surgery (Bone Cement, Pneumatic Tourniquets) 3.2. Special Complications (Fat Embolism Syndrome, Deep Venous Thrombosis and Thromboembolism) 4. Obstetric Anesthesia 4.1. Anesthesia for Labor and Vaginal Delivery 4.1.1. Psychological and Nonpharmacological Techniques 4.1.2. Parenteral Agents 4.1.3. Pudendal Nerve Block 4.1.4. Regional Anesthetic Techniques (Lumbar Epidural Anaglesia, Combined Spinal and Epidural (CSE) Analgesia, Spinal Anesthesia) 4.1.5. General Anesthesia 4.2. Anesthesia for Cesarean Section 4.2.1. Regional anesthesia 4.2.2. CSE Anesthesia 4.2.3. General Anesthesia 5. Pediatric Anesthesia 5.1. Pharmacological Differences (Inhalational Anesthetics, Nonvolatile Anesthetics, Muscle Relaxants)
  • 3. 5.2. Pediatric Anesthetic Risk 5.3. 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 Recovery 5.4.1. Laryngospasm 5.4.2. Postintubation Croup 5.4.3.Postoperative Pain Management 6. Geriatric Anesthesia 6.1. Age-Related Anatomic and Physiological Changes 6.2. Age-Related Pharmacological Changes (Inhalational Anesthetics, Nonvolatile Anesthetic Agents, Muscle Relaxants) 7. Postanesthesia Care 7.1. Emergence from General Anesthesia 7.1.1. Delayed Emergence8Routine Recovery: General Anesthesia 7.1.2 Routine Recovery: Regional Anesthesia 7.2.Pain Control 7.3. Nausea and Vomiting 7.4. 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
  • 4. 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
  • 5. 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
  • 6. 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.
  • 7. 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
  • 8. 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
  • 9. 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
  • 10. 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
  • 11. 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
  • 12. 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
  • 13. 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
  • 14. 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
  • 15. 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.
  • 16. 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.
  • 17. 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.
  • 18. 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
  • 19. 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
  • 20. 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
  • 21. 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
  • 22. 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
  • 23. 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
  • 24. 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
  • 25. 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
  • 26. 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
  • 27. 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
  • 28. 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
  • 29. 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
  • 30. 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
  • 31. 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
  • 32. 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
  • 33. 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
  • 34. 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
  • 35. 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,
  • 36. 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).