Handbook of Clinical Anesthesia

Chapter 36

Anesthesia for Trauma and Burn patients

Approximately 75% of the hospital mortality from trauma occurs within 48 hours of admission, most commonly from thoracic, abdominal or retroperitoneal, vascular, or central nervous system injuries (Capan LM, Miller SM: Trauma and burns. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 889–926).

  1. Initial Evaluation and Resuscitation

The general approach to evaluation of an acute trauma victim includes three sequential components: rapid overview, primary survey, and secondary survey (Fig. 36-1). During this period, the anesthesiologist identifies injuries, pre-existing conditions, and the resulting functional abnormalities that require either immediate treatment or provision for resuscitative and anesthetic management. Universal infection control precautions are the standard because many trauma victims are carriers of hepatitis B, hepatitis C, or human immunodeficiency virus.

  1. Airway Evaluation and Intervention.The American Society of Anesthesiologists' difficult airway algorithm can be applied to trauma airway management scenarios.
  2. Airway Obstruction.If the patient can speak, serious airway obstruction is unlikely. Signs of upper and lower airway obstruction include dyspnea, hoarseness, stridor, dysphoria, subcutaneous emphysema, and hemoptysis. Cervical deformity, edema, crepitation, tracheal deviation, or jugular venous distention may be present before the appearance of symptoms.
  3. After immobilization of the cervical spine and administration of oxygen by face mask, airway management should include chin lift, jaw thrust, clearing of the

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oropharyngeal cavity, and placement of an oral or nasopharyngeal airway.

 

Figure 36-1. The general approach to evaluation of acute trauma patients includes the sequential steps of rapid overview, primary survey, and secondary survey. CT = computed tomography; ED = emergency department; ICU = intensive care unit.

  1. Ventilation is supported in inadequately breathing patients with a self-inflating bag.
  2. If these measures do not provide adequate ventilation, the trachea must be intubated using either direct laryngoscopy or cricothyroidotomy.
  3. Proper placement of devices, such as a laryngeal mask airway (LMA), Combitube, or endotracheal tube, by paramedics should be confirmed by capnometry as soon as possible after the patient enters the hospital.

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  1. Full stomachis a background condition in acute trauma, and the urgency of securing the airway often does not permit time for pharmacologic measures to decrease gastric volume and acidity.
  2. Excessive cricoid pressure may displace a vertebral bone fragment with potential damage to the spinal cord. Spinal cord injury may also accompany cricoid pressure and manual incline stabilization to cervical spine-injured patients.
  3. The LMA may be used temporarily to maintain airway patency (a full stomach precludes its sustained use) or to facilitate intubation aided by a fiberoptic laryngoscope.
  4. The presence of uncorrectable hypotension may preclude use of intravenous (IV) anesthetics. (Muscle relaxants alone may be sufficient in these patients.) If only a mild to moderate degree of hypovolemia is present, decreased doses (30% to 50%) of anesthetics should be administered.
  5. There is no consensus about the extent of the airway that can be safely anesthetized with topical drugs. (Avoidance of transtracheal anesthesia preserves the cough reflex even in the presence of an impaired glottic closure reflex owing to a superior laryngeal nerve block or topical anesthesia.)
  6. Agitated and uncooperative patients (topical anesthesia is not possible) may require a rapid sequence induction of anesthesia followed by direct laryngoscopy to secure the airway.
  7. Head, Open Eye, and Contained Major Vessel Injuries
  8. These conditions require deep anesthesia (opioids and IV anesthetics) and profound skeletal muscle relaxation before airway manipulation (this assumes a difficult tracheal intubation is not anticipated and the patient is not hypotensive).
  9. Hypertension, coughing, and reacting to the tracheal tube may adversely increase systemic blood pressure, intracranial pressure (ICP), and intraocular pressure.
  10. Hypotension dictates either reduced or no IV anesthetic administration.
  11. Cervical Spine Injury.Immobilization of the neck in a neutral position is indicated before airway management in all acute trauma patients suspected to have cervical spine injury. Intubation may theoretically cause spinal

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cord damage during manipulation of the neck, although the available literature attests to the rare, possibly nonexistent occurrence of this event.

Table 36-1 Five Criteria That Rule Out Cervical Spine Injury

No midline cervical tenderness
No focal neurologic deficit
Normally alert
Not intoxicated
No distracting painful injury

  1. Initial Evaluation.In a conscious patient with a suspected injury, the diagnosis is relatively easy (Table 36-1). Computed tomography (CT) scanning is the primary diagnostic measure for detection of fractures; magnetic resonance imaging [MRI] is used for ligamentous injury.
  2. Airway Management.Almost all airway maneuvers (jaw thrust, chin lift, head tilt, oral airway placement) result in some degree of cervical spine movement. Stabilization of the head, neck, and torso in a neutral position is best accomplished by manual in-line immobilization (a cervical collar does not provide absolute protection). The first operator stabilizes and aligns the head in a neutral position without applying cephalad traction, and the second operator stabilizes both shoulders by holding them against the supporting surface. Use of fiberoptic bronchoscopy in a sedated patient is a consideration when time constraints, a full stomach, and patient cooperation issues are not present.
  3. Direct Airway Injuries(Table 36-2)
  4. Management of Breathing Abnormalities
  5. Of the several causes that may alter breathing after trauma, tension pneumothorax, flail chest, and open pneumothorax are immediate threats to life and therefore require rapid diagnosis and treatment.
  6. A flail chest results from comminuted fractures of at least three adjacent ribs or rib fractures with associated costochondral separation or sternal fracture.
  7. An underlying pulmonary contusion with increased elastic recoil of the lung and work of breathing is

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the main cause of respiratory insufficiency or failure and resulting hypoxemia.

Table 36-2 Mechanisms of Direct Airway Injury

Maxillofacial Injuries
Soft tissue edema of the pharynx (hematoma or edema mayexpand during the 6–12 hours after injury; liberal fluidadministration may contribute to edema)
Blood and debris in the oropharyngeal cavity
Mandibular condylar fractures (if bilateral, they prevent openingof the mouth)
Cervical Airway Injuries
Blunt or penetrating trauma (hoarseness, dysphagia, flattening ofthe thyroid cartilage protuberance)
Thoracic Airway Injuries
Blunt injury usually involves the posterior membranous portion ofthe trachea and the mainstem bronchi (it should be suspectedwhen a seal around the tracheal tube cuff cannot be obtained)

  1. Respiratory failure often develops over a 3- to 6-hour period, causing gradual deterioration seen on chest radiography and arterial blood gas analysis.
  2. Tracheal intubation is often necessary in patients with pulmonary contusion or respiratory insufficiency or failure despite adequate analgesia.
  3. Positive end-expiratory pressure is used if ventilation is controlled.
  4. In intubated and spontaneously breathing patients, airway pressure release ventilation provides improved arterial oxygenation and maintenance of blood pressure, lower sedation requirements, and shorter periods of intubation.
  5. In bilateral severe contusions with life-threatening hypoxemia, high-frequency jet ventilation may enhance oxygenation as well as cardiac function, which may be compromised by concomitant myocardial contusion.
  6. The definitive diagnosis of tension pneumothorax is with chest radiography. When there is no time for radiologic confirmation, a 14-gauge angiocath can be placed through the fourth intercostal space in the midaxillary line.
  7. In the absence of significant gas exchange abnormalities, chest wall instability alone is not an indication

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for tracheal intubation and mechanical ventilation (Table 36-3). Effective pain relief (continuous epidural analgesia) by itself can improve respiratory function and often prevent the need for mechanical ventilation.

Table 36-3 Indications for Mechanical Ventilation in Patientswith Flail Chest

Clinical evidence of respiratory failure
Progressive fatigue or deterioration
Respiratory rate >35 breaths/min
PaO2 <60 mm Hg breathing at least 50% oxygen
PaCO2 >55 mm Hg
Vital capacity <15 mL/kg
Clinical evidence of shock
Associated severe head injury with need to hyperventilate the patient's lungs
Severe associated injury requiring surgery
Airway obstruction
Significant pre-existing chronic pulmonary disease

  1. Hypoxia and hypercarbia result from an open pneumothorax. (Occlusive dressing is the initial treatment.)
  2. Management of Shock.In the initial phase of trauma, hypotension has many causes, but hemorrhage is the most common (Table 36-4). Evaluation of the severity of hemorrhagic shock in the initial phase is based on a few relatively insensitive and nonspecific clinical signs (Table 36-5).
  3. Although heart rate is one of the earliest signs of hemorrhagic shock, the heart rate does not necessarily correlate with the blood loss. Tachycardia may be absent in up to 30% of hypotensive trauma patients because of increased vagal tone or chronic cocaine use.
  4. Equating a normal systemic blood pressure with normovolemia during initial resuscitation may lead to loss of valuable time for treating underlying hypovolemia.
  5. The response of the heart rate and blood pressure to initial fluid therapy also aids in assessment of the degree of hypovolemia (Table 36-6).

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Table 36-4 Causes of Hypotension in the Initial Phase of Trauma

Hemorrhage or Extensive Tissue Injury
Tachycardia, narrow pulse pressure, peripheral vasoconstriction
Crystalloid solution should be given initially and the patient should be transfused if 2000 mL in 15 minutes does not improve blood pressure
Cardiac Tamponade
Tachycardia, dilated neck veins, muffled heart sounds
Pericardiocentesis
Myocardial Contusion
Tachycardia, cardiac dysrhythmias
Crystalloids, vasodilators, inotropes
Pneumothorax or Hemothorax
Tachycardia, dilated neck veins, absent breath sounds, dyspnea, subcutaneous emphysema
Chest tube
Spinal Cord Injury
Hypotension without tachycardia, narrow pulse pressure, or vasoconstriction
Crystalloids, vasopressor, inotropes
Sepsis
Develops typically a few hours after colon injury (in normovolemic patients, it manifests as modest tachycardia, wide pulse pressure, and fever)
Antibiotics, crystalloids, inotropes

  1. Markers of organ perfusion to guide resuscitation include base deficit, blood lactate level, and sublingual capnometry (gut perfusion).
  2. During the initial phase of treatment, serial measurements of hematocrit (which are helpful if the first sample is obtained before administration of large volumes of fluid) help to determine the need for transfusion.
  3. A low hemoglobin determination (<8 g/dL) immediately after injury is a strong indicator of ongoing blood loss and poor prognosis.
  4. During fluid infusion, a reasonable transfusion threshold is a hematocrit below 25 mL/dL for young, healthy patients and below 30 mL/dL for older patients and those with coronary or cerebrovascular disease.

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Table 36-5 Advanced Trauma Life Support Classification of Hemorrhagic Shock

 

Class I

Class II

Class III

Class IV

Blood loss (mL)

≤750

750–1500

1500–2000

>2000

Blood loss (% of blood volume)

≤15

15–30

20–40

>40

Heart rate (bpm)

<100

>100

>120

>140

Systemic blood pressure

Normal

Normal

Decreased

Decreased

Pulse pressure increased

Normal or

Decreased

Decreased

Decreased

Capillary refill test

Normal

Positive

Positive

Positive

Respiratory rate (breaths/min)

14–20

20–30

30–40

<35

Urine output (mL/hr)

>30

20–30

5–15

Negligible

Mental status

Slightly anxious

Mildly anxious

Anxious and confused

Confused and lethargic

Fluid replacement

Crystalloid

Crystalloid and blood

Crystalloid and blood

Crystalloid (3:1 rule)

Table 36-6 Assessment of the Degree of Hypovolemia in Hypotensive and Tachycardic Patients

Decrease in Circulating Blood Volume Equivalent to 10%–20%
Administration of lactated Ringer's solution (2000 mL over 15 minutes in adults or 20 mL/kg in children) should normalize blood pressure.
Decrease in Circulating Blood Volume Equivalent to 20%–40%
Administration of lactated Ringer's solution produces a transientincrease in blood pressure.
More crystalloids with or without blood transfusions are needed.
Decrease in Circulating Blood Volume Exceeds 40%
Administration of lactated Ringer's solution does not improveblood pressure.
Rapid infusion of crystalloids, colloids, and blood is needed.
Blood typing and cross-matching requires 45 minutes versus typespecific, which can be available in about 15 minutes, versusimmediate transfusion with type O blood (Rh-negative bloodis preferred for women of child-bearing age).

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  2. The control of active bleeding has a higher priority than restoration of blood volume or placement of invasive monitors in the initial resuscitation.
  3. Rapid establishment of venous access with large-bore cannulas placed in peripheral veins that drain both above and below the diaphragm is essential for adequate fluid resuscitation in severely injured patients.
  4. Early Management of Specific Injuries
  5. Head Injury.Approximately 40% of deaths from trauma are caused by head injury. Prevention of progression of brain injury beyond the initial area is the primary objective of early management of patients with brain trauma. Of all the possible insults to the injured brain, hypotension has the greatest detrimental impact, followed by hypoxia.
  6. Diagnosis.A baseline neurologic examination should be performed before any sedative or muscle relaxant drugs are administered or the trachea is intubated, and the examination should be repeated at frequent intervals because the patient's condition may change rapidly (Table 36-7).
  7. Computed tomography scanningis used for the diagnosis (midline shift, distortion of the ventricles, presence of a hematoma, depressed skull fractures) of most head injuries. (MRI has the advantage of being able to demonstrate ischemia but is rarely

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used because of its cost and impracticality in injured patients.)

Table 36-7 Baseline Neurologic Examination of Trauma Patient

Level 1—AVPU System

A

Alert

V

Responds to verbal stimuli

P

Responds to painful stimuli (motor activity of extremities)

U

Unresponsive

Level 2—Glasgow Coma Scale

Score 8

Deep coma, severe head injury, poor outcome

Score 9–12

Conscious patient with moderate injury

Score 13–15

Mild injury

Table 36-8 Universally Accepted Aspects of Treatment for Head-Injured Patients

Normalization of systemic blood pressure (mean cerebralperfusion pressure >60 mm Hg)
Normalization of arterial oxygenation (SaO2 >95%)
Sedation and skeletal muscle paralysis as necessary
Mannitol and possibly a loop diuretic to shrink the brain anddecrease ICP
Drainage of CSF
Mechanical hyperventilation of the lungs if ICP remains increased(otherwise, normocapnia should be maintained)
High-dose barbiturates used only for refractory intracranialhypertension
Immediate surgical decompression if indicated (epiduralhematoma)

CSF = cerebrospinal fluid; ICP = intracranial pressure.

  1. Patients in a coma (Glasgow coma score <8) have a 40% likelihood of having an intracranial hematoma.
  2. Managementincludes therapeutic maneuvers intended to maintain cerebral perfusion pressure and oxygen delivery (Table 36-8).
  3. It is not known whether active normalization of hyperglycemia (which is common in head-injured patients) has any salutary effect.
  4. Measurement of jugular bulb oxygen saturation (<50% is considered critical desaturation) is a useful guide for treatment of head-injured patients (reflects demand of the brain for oxygen and its supply; [AvDO2] >6 is a sign of insufficient blood flow).
  5. Hyperventilation may enhance increased cerebral vascular resistance, which is responsible for the initial cerebral hypoperfusion likely to occur during the first 6 hours after head trauma. Use of hyperventilation is ideally guided by monitoring ICP and AvDO2.
  6. Mannitol (0.25–0.5 g/kg IV) produces an osmotic diuretic effect to decrease ICP and may improve

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cerebral blood flow by decreasing blood viscosity. There is a risk of hypovolemia and hypotension when therapeutic doses of mannitol are used. Hyponatremia reflects intravascular volume expansion.

  1. Because of a synergistic action between mannitol and loop diuretics, adding furosemide may be preferred to increasing doses of mannitol when intracranial hypertension persists.
  2. Steroids are no longer viewed as a necessary part of treatment of patients with severe head injuries.
  3. Maintenance of normovolemia rather than fluid restriction is desirable.
  4. Anesthetic considerationsinclude the likely occurrence of hypotension and the risk of administering succinylcholine to patients with spine injury.
  5. Spine and Spinal Cord Injury
  6. Initial Evaluation.The objective of the evaluation is to diagnose the instability of the spine and the extent of neurologic involvement. Often the urgency of the associated injuries precludes a definitive assessment, necessitating spine protection until a satisfactory diagnosis is established.
  7. In a comatose patient, flaccid areflexia, loss of rectal sphincter tone, diaphragmatic breathing, and bradycardia suggest the diagnosis of spinal cord injury.
  8. In cervical spine trauma, an ability to flex but not to extend the elbow and response to painful stimuli above but not below the clavicle suggest neurologic injury.
  9. Neurogenic shock describes the hypotension and bradycardia caused by the loss of vasomotor tone and sympathetic innervation of the heart as a result of functional depression of the descending sympathetic pathways of the spinal cord (usually present after high thoracic and cervical spine injuries and improves within 3–5 days).
  10. Initial Management
  11. Immobilization and Intubation.If a cervical spine fracture is suspected, immobilization or manual in-line stabilization of the neck is of paramount importance.
  12. Steroids.Treatment with methylprednisolone for 24 to 48 hours is an option.

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  1. Respiratory complicationsare common in all phases of the care of patients with spinal cord-injuries. Accessory respiratory muscle paresis may cause a significant loss of expiratory reserve, and pulmonary edema may occur after a catecholamine surge associated with spinal cord injury. Aspiration may also occur.
  2. Paradoxical respiration in patients with quadriplegia is aggravated when the patient is placed in the upright position.
  3. Unopposed vagal activity during tracheal intubation may result in severe bradycardia and cardiac dysrhythmias (instrumentation should be preceded by oxygen and 0.4–0.6 mg IV of atropine).
  4. Hemodynamic managementmay include assessment with a pulmonary artery catheter. Left ventricular dysfunction may contribute to hypotension in quadriplegic patients.
  5. Neck Injury.Penetrating and blunt trauma may injure major structures in the neck (vessels, respiratory, digestive, nervous system).
  6. Chest Injury
  7. Chest wall injury(ribs, sternum, scapula) can predict the likelihood and severity of internal injuries to a certain extent. (Patients with three or more fractured ribs have a greater likelihood of hepatic and splenic injury.)
  8. Pleural injurymanifesting as a closed pneumothorax most commonly develops as a result of lung puncture by a displaced rib fracture. (This is diagnosed with an upright [this position may be contraindicated in hypovolemic patients or those with suspected spine or head injury] or supine chest film that is obtained routinely in evaluation of all trauma victims.) CT is more reliable for detecting a small pneumothorax and should be performed in patients who require general anesthesia or mechanical ventilation of the lungs after thoracoabdominal trauma.
  9. Subcutaneous emphysema is suggestive of a coexisting pneumothorax.
  10. After it has been diagnosed, a traumatic pneumothorax, no matter how small, should be treated with thoracostomy drainage.
  11. Bleeding intercostal vessels are responsible for most hemothoraces. Initial drainage of more than

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1000 mL of blood or collection of more than 200 mL/hr is an indication for thoracotomy.

  1. Penetrating cardiac injurymay result in pericardial tamponade, which is diagnosed with transesophageal echocardiography (TEE).
  2. Blunt Cardiac Injury.Diagnosis (myocardial contusion) is based on clinical history (blunt chest trauma, angina, cardiac dysrhythmias) and results of TEE (segmental wall motion abnormalities), creatine phosphokinase-MB isoenzymes, and electrocardiography.
  3. Thoracic aortic injuryis suspected in patients with a history of high-impact trauma with deceleration, especially to the chest (a widened mediastinum should prompt search for this injury). TEE, contrast-enhanced CT, and ultrasound techniques are important tools for evaluating aortic trauma.
  4. Diaphragmatic injuryis suggested on the chest radiograph when the nasogastric tube is above the diaphragm.
  5. Abdominal and Pelvic Injuries
  6. Liver and spleen lacerations are the most common abdominal injuries after both blunt and penetrating abdominal trauma, presenting most often with signs of hemorrhage.
  7. Because of the unpredictable course of bullets in the body, exploratory laparotomy or laparoscopy (in selected cases) is required after all gunshot wounds to the abdomen.
  8. Abdominal ultrasonography and CT are useful for the evaluation of abdominal and pelvic injuries.
  9. Fractures of the pelvismay result in major hemorrhage, especially if there is disruption of the pubic symphysis.
  10. Extremity Injuries
  11. Surgical repair of extremity fractures (open or closed) should be performed as soon as possible to decrease the risk of deep vein thrombosis, fat embolism syndrome, pulmonary complications, and sepsis (likely when repair is delayed longer than 6 hours).
  12. Compartment syndromeis suggested by severe pain in the affected extremity, swelling, and tenseness. Profound analgesia in the presence of an extremity fracture may delay the diagnosis of this syndrome.

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III. Burns

Determination of the size of the burned area (rule of nines) and depth of the burn set the guidelines for resuscitation as well as the timing of surgical intervention. (A partial-thickness burn is red, blanches to the touch, and is painful, but a full-thickness burn does not blanche and is insensate.) Information about the mechanism of the injury (closed space is associated with airway damage; electrocution shows little external injury despite internal injury) facilitates the diagnosis of associated clinical abnormalities.

  1. Airway Complications
  2. Singed eyebrows or eyelashes and black soot in and around the nose or mouth should increase the suspicion of airway injury.
  3. The initial chest radiography, ABG analyses, and pulmonary function test results are usually normal in the immediate post-burn period, followed by the appearance of clinical symptoms reflecting pulmonary edema.
  4. Fiberoptic bronchoscopy is the best way to evaluate large airways.
  5. Ventilation and Intensive Care.Hypoxemia may persist despite tracheal intubation and ventilation. In the first 36 hours, hypoxemia reflects pulmonary edema; after 2 to 5 days, it reflects atelectasis and bronchial pneumonia.
  6. Carbon Monoxide Toxicity
  7. An increased inhaled oxygen concentration promotes elimination of carbon monoxide (100% oxygen decreases the blood half-time of carboxyhemoglobin from 4 hours to <1 hour) (Table 36-9).
  8. A normal oxygen saturation from a pulse oximeter does not exclude the possibility of carbon monoxide toxicity.
  9. Increased carboxyhemoglobin levels do not cause tachypnea because the carotid bodies are sensitive to arterial PaO2and not arterial oxygen content.
  10. Cyanide toxicity(which manifests as metabolic acidosis) is a possibility when cyanide or hydrocyanic acid is produced by incomplete combustion of synthetic materials. Pulse oximetry readings are accurate in the absence of carbon monoxide toxicity and nitrate therapy–induced methemoglobinemia.

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Table 36-9 Symptoms of Carbon Monoxide Toxicity

Blood Carboxyhemoglobin Level (%)

Symptoms

<15–20

Headache
Dizziness

 

Occasional confusion

20–40

Disorientation
Visual impairment

40–60

Agitation
Combativeness
Hallucinations
Coma and shock

>60

Death

  1. Fluid Replacement
  2. Fluid resuscitation is essential in the early care of burn patients, although overaggressive resuscitation may be deleterious (causing airway edema, pulmonary edema, or abdominal edema).
  3. If fluid resuscitation is successful, edema formation stops within 18 to 24 hours.
  4. Administration of fluids during the initial phase should be titrated to specific goals such as urine output of about 0.5 mL/kg/hr, heart rate of 110 to 120 beats/min, normal blood lactate level, and mixed venous oxygen partial pressure of above 35 mm Hg. An increase in the hematocrit during the first day of the burn injury suggests inadequate fluid resuscitation.
  5. Operative Management (Tables 36-10 and 36-11)
  6. Monitoring(Table 36-12)
  7. Hemodynamic Monitoring
  8. There is no effective substitute for direct intra–arterial monitoring, which permits beat-to-beat assessment of blood pressure (a hemodynamically stable patient may suddenly become hypotensive when the chest or abdomen is opened) and facilitates sampling for measurement of blood gases. During mechanical ventilation of the patient's lungs, the extent of systolic blood pressure variation can provide reliable information about the status of the intravascular fluid volume (Fig. 36-2).

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Table 36-10 Implications of Pre-existing Diseases for IntraoperativeManagement of Trauma Patients

Substance Abuse
Alcohol
Delayed gastric emptying
Vasodilation and myocardial depression
Potentiation of trauma-induced hypothermia
Hemostatic defect
Postoperative alcohol withdrawal
Cocaine use
Unpredictable hemodynamic response to hemorrhage
Cardiac dysrhythmias
Opioid use
Delayed gastric emptying
Vasodilation
Postoperative opioid withdrawal
Hypertension
Decreased tolerance to hypovolemia
Exaggerated hypertensive response to pain
Increased likelihood of myocardial ischemia and cardiac dysrhythmias
Ischemic Heart Disease
Increased likelihood of myocardial ischemia caused by trauma-induced changes
Anemia
Sickle Cell Disease
Coagulation Disorders
Diabetes Mellitus
Delayed gastric emptying
Decreased response to resuscitative measures in patients with autonomic neuropathy
Increased likelihood of ischemic heart disease
Electrolyte abnormalities
Asthma

  1. Placement of a central venous pressure or pulmonary artery catheter is not necessary in young patients in the absence of heart disease. (A reasonable assessment of the patient's blood volume can be made by repeated observation of systemic blood pressure, hematocrit, ABG analyses, and urine output.)

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Table 36-11 Specialized Equipment, Supplies, and Drugs That May Be Needed for Management of Trauma Patients

Equipment
Fiberoptic bronchoscope with a light source
Mechanical ventilator that is effective in patients with decreasedpulmonary compliance (lung contusion, aspiration)
Jet ventilator system
Positive end-expiratory pressure valves
Blood and fluid bag pressurizing systems
Fluid warming system
Rapid infusion system
Forced air warming device and heated humidifier for inspiredgases
Calibrated infusion pumps
Transesophageal echocardiography
Pneumatic tourniquet
Cardiopulmonary bypass
Supplies
Material for special airway management
Material for arterial and pulmonary artery catheter placement
Drugs
Vasopressors
Inotropes
Calcium chloride
THAM
Sodium bicarbonate
Topical anesthetics

THAM = tris-hydroxymethyl-aminomethane.

  1. Transesophageal echocardiographyprovides valuable diagnostic information in myocardial contusion, cardiac valvular dysfunction, pericardial fluid accumulation, intravascular fluid volume, cardiac output, myocardial contractility, and large vessel injury. (A probe should not be placed if there is a possibility of esophageal injury.)
  2. Urine Output
  3. As a rough guideline, urine output should be maintained at above 0.5 mL/kg/hr. (After prolonged shock, renal failure may already be present on the patient's arrival in the operating room.)
  4. Osmotic diuresis produced by preoperative radiopaque dye or mannitol decreases the value of urine output as a monitor of organ perfusion.

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Table 36-12 Monitoring of Trauma Patients

Physiologic Parameter

Degree of Importance

Monitoring Equipment

Specific Intraoperative Uses

Cardiac rate, rhythm, and ischemia

Essential

Electrocardiogram

Routine

Arterial blood pressure

Essential

Indirect (cuff, Doppler, oscillometric system)

Routine

Central venous pressure

Useful

Direct (intra-arterial catheter)

Hypovolemia
Pericardial tamponade
Myocardial contusion
Air embolism

Pulmonary artery and capillary wedge pressure

Selected

Pulmonary artery catheter

Blunt chest injury ARDS
Blunt cardiac injury (contusion)
Pulmonary edema

Cardiac output

Useful

Computer

Same as pulmonary artery catheter

Cardiac wall motion abnormalities, myocardial ischemia

Useful

TEE

Blunt cardiac injury (contusion)
Major vessel injuries

Ventilation

Essential

End-tidal carbon dioxide monitor

Routine
Head injury
Air embolism

Arterial oxygenation

Essential

Pulse oximetry
ABG analyses

Routine

Tissue oxygenation

Useful

Oximeter pulmonary artery catheter

Low perfusion states

Renal function

Essential

Foley catheter and graduated container

All major trauma patients

Temperature

Essential

Esophageal or rectal probe

Routine

Neuromuscular function

Essential

Peripheral nerve stimulator

Routine

Neurologic function

Useful

Bolt, catheter, or fiberoptic sensor

Head injury

Coagulation

Useful

Prothrombin time, partial thromboplastin time, platelets, fibrinogen
Tube test
Thromboelastography

Shock
Massive transfusions

ABG = arterial blood gas; ARDS = acute respiratory distress syndrome; TEE = transesophageal echocardiography.

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Figure 36-2. The magnitude of systolic blood pressure variation may provide valuable information about the status of the intravascular fluid volume.

  1. Cola-colored urine suggests hemoglobinuria from an incompatible blood transfusion (associated with pink-stained plasma) or myoglobinuria caused by skeletal muscle destruction, as after blunt or electrical trauma. Both of these conditions may result in acute renal failure (which can be prevented with mannitol diuresis). Red-colored urine usually indicates urinary tract injury in trauma patients.
  2. Oxygenation.Older generation pulse oximeters fail to provide accurate measurements in patients with oxygen saturations of 90% or below, hypothermia, hypotension, and decreased peripheral perfusion. Multi-wave length pulse oximeters can measure carboxyhemoglobin (acute burn injury management).
  3. Organ Perfusion and Oxygen Utilization
  4. Occult hypoperfusion may not be detected by traditional hemodynamic monitoring such as systemic blood pressure, heart rate, and urine output.
  5. Intestinal mucosa is particularly vulnerable to occult hypoperfusion (passage of luminal microorganisms

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into the circulation and release of inflammatory mediators causing sepsis and multiorgan failure).

Table 36-13 Information Obtained from the “Tube Test”

Coagulation: Clotting factor deficiency is likely if a clot does not form or does so only after 10 to 20 minutes.
Clot Retraction: Platelet depletion or dysfunction is likely if a clot fails to contract within 1 hour.
Clot Lysis: Fibrinolysis is likely if clot lysis occurs earlier than 6 hours.

  1. Markers of organ perfusion and oxygen utilization include oxygen transport variables (oxygen delivery, oxygen consumption, oxygen extraction ratio), base deficit, and blood lactate.
  2. Coagulation
  3. Conventional blood coagulation monitoring involves determination of prothrombin time, activated plasma thromboplastin time, platelet count, blood fibrinogen level, and fibrin degradation products.
  4. The “tube test,” which involves obtaining a plain tube of blood with no anticoagulant, is a practical intraoperative method of coagulation monitoring (Table 36-13).
  5. The results of coagulation tests have little primary impact on treatment. (Platelet and factor replacement are likely to be necessary when more than one blood volume is replaced.)
  6. Anesthetic and Adjunct Drugs.From the standpoint of anesthetic management, injuries may be placed in one of five categories.
  7. Airway Compromise.The primary issue is whether to manage the airway with or without the use of anesthetic drugs and muscle relaxants. As a general precaution, these drugs may be avoided if there is significant airway obstruction or if there is doubt as to whether the patient's trachea can be intubated because of anatomic limitations.
  8. Hypovolemia.Inhaled and IV anesthetics predictably further decrease blood pressure in the presence of hypovolemia. Two important principles in the use of anesthetic drugs are accurate estimation of the extent of

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hypovolemia and decrease of the anesthetic dose accordingly. Intraoperative use of bispectral index monitor and titrating anesthetics to levels below 60 whenever possible may prevent recall in trauma patients.

  1. Head and Open-Eye Injuries
  2. Deep anesthesia and adequate skeletal muscle relaxation for tracheal intubation are important principles.
  3. Drugs selected for management of patients with head injury should produce the least increase in ICP, the least decrease in mean arterial pressure, and the greatest decrease in cerebral metabolic requirements for oxygen. With the exception of ketamine, all IV drugs produce similar degrees of cerebral vasoconstriction and suppression of cerebral metabolism. The disadvantage of these drugs is depression of cerebral perfusion pressure.
  4. All inhaled anesthetics have the potential to increase cerebral blood flow, cerebral blood volume, and ICP while decreasing cerebral metabolic requirements for oxygen. (The uncoupling between blood flow and metabolism is greatest for halothane and least for isoflurane.) Desflurane and sevoflurane have effects similar to those of isoflurane on cerebral hemodynamics.
  5. In patients with severe head injury with associated loss of cerebral autoregulation and responsiveness to carbon dioxide, even isoflurane may increase cerebral blood flow and ICP. In these patients, anesthesia can be maintained until the skull is open with opioids plus thiopental, propofol, midazolam, or etomidate.
  6. Cardiac Injury
  7. Pericardial Tamponade.Preload, myocardial contractility, and heart rate should be maintained. If possible, the evacuation of the pericardial blood should be accomplished under local anesthesia. (All anesthetics decrease myocardial contractility and may cause peripheral vasodilation.) Ketamine is often recommended if anesthesia must be induced before evacuation of the tamponade.
  8. Blunt myocardial injury may put patients at risk for drug-induced decreases in myocardial contractility. (Use of inotropes may be necessary.)

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  1. Burns
  2. Extensive escharotomies may necessitate massive transfusions; temperature control; and management of fluid, electrolyte, and coagulation abnormalities.
  3. A hypermetabolic state necessitates increased oxygen, ventilation, and nutrition.
  4. Hypothermia is a risk in the operating room. (Room temperature should be maintained at 28°C to 32°C, fluid and blood-warming devices should be used, and inspired gases should be humidified.)
  5. After the first 24 hours, succinylcholine must be avoided for as long as 1 year because hyperkalemia may occur after its administration. (Large increases in serum potassium levels occur when the burn size exceeds 10% of the body surface area.)
  6. Resistance to nondepolarizing muscle relaxants develops in patients with more than 30% burns starting about 1 week after the burn injury and peaking in 5 to 6 weeks.
  7. For serial wound debridement, ketamine in intermittent doses, neuraxial or peripheral nerve blocks via an indwelling catheter, or sedation with opioids and IV agents may be used.
  8. Managment of Intraoperative Complications
  9. Persistent hypotensionis suggestive of bleeding, tension pneumothorax, neurogenic shock, or cardiac injury.
  10. Hypothermiathat accompanies trauma is associated with increased mortality.
  11. Convective warming forced dry air (Bair Hugger) can prevent a temperature decrease in most trauma patients but cannot effectively treat those with severe hypothermia.
  12. Administration of warm IV fluids is the most effective way to prevent and treat hypothermia in trauma patients.
  13. Coagulation abnormalitiesmay reflect dilutional effects from transfusions, tissue thromboplastin release, and hypothermia-induced platelet dysfunction. Hypothermia may also enhance fibrinolytic activity.
  14. Prompt platelet administration should be considered when abnormal clinical bleeding is noted (assuming surgical bleeding is controlled).

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Table 36-14 Needs and Concerns in the Early PostoperativePeriod in Trauma Patients

Sedation and analgesia (improves pulmonary function)
Propofol (1.5–6 mg/kg/hr), midazolam (0.1–0.2 mg/kg/hr), or both
Morphine (0.02–0.04 mg/kg/hr) or fentanyl (1–3 µg/kg/hr)
Acute renal failure (decreased urine output is not a good indicator, and BUN does not increase until at least 24 hours postoperatively)
Abdominal compartment syndrome (intra-abdominalhypertension from edema of abdominal organs produced byinflammatory mediators, fluid resuscitation, or surgicalmanipulation; it should be suspected if the patient has atense abdomen; its presence suggests the need to measureintravesical pressure)
Thromboembolism

BUN = blood urea nitrogen.

  1. After the replacement with coagulation-deficient fluids exceeds one blood volume, clinical coagulopathy is likely, even in the absence of shock, hypothermia, or other aggravating factors.
  2. Electrolyte and Acid–Base Disturbances
  3. Hyperkalemia may develop as a result of shock-induced alteration in permeability of cell membranes, release from ischemic tissues, or rapid transfusion of blood (faster than 1 U every 4 minutes).
  4. Metabolic acidosis is caused by shock in the majority of patients after trauma. Treatment of metabolic acidosis includes correction of the underlying cause (hypoxemia, hypovolemia, decreased cardiac output). Symptomatic treatment with sodium bicarbonate has several disadvantages, including leftward shift of the oxyhemoglobin dissociation curve, hyperosmolar state, and alkalosis.
  5. Base deficit parallels the degree of hypovolemia.
  6. Intraoperative deathis more likely during emergency trauma surgery than it is in any other operative procedure.
  7. Early Postoperative Considerations

Re-evaluation and optimization of the circulation, oxygenation, temperature, central nervous system function, coagulation, electrolyte and acid–base status, and renal function are the hallmarks of postoperative management (Table 36-14).

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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