Trauma, 7th Ed.

CHAPTER 17. Principles of Anesthesia and Pain Management

Dirk Younker

Providing an anesthetic for the trauma victim is among the greatest challenges for an anesthesiologist. In many cases, care must be rendered to a patient about whom one knows very little, who may be physiologically unstable, who may possess obvious comorbidities that increase anesthetic risk, and for whom one has very little time to prepare. Additionally, necessity may demand that an anesthetic be provided with nothing more than basic monitoring modalities, using the simplest of anesthetic techniques. Consequently, it is helpful for the surgical practitioner to possess a basic working knowledge of anesthetic principles and practice.


The anesthetic plan must encompass preoperative, intraoperative, and postoperative care. During the preoperative phase, the fitness of the patient for the intended anesthetic and surgical procedure is determined; the urgency of surgery determines much of the time devoted to this phase. The postoperative period includes monitoring the recovery of the patient from the anesthetic, maintaining an attitude of vigilance in respect to the development of postoperative complications and managing postoperative pain. The American Society of Anesthesiologists has published specific guidelines that outline the provision of care during these periods, which can be modified as circumstances demand. The responsibility for the preoperative and postoperative care of a patient is shared by nursing personnel, surgeons, and anesthesiologists, who work together for the benefit of their patient. In contrast, the intraoperative phase of the anesthetic care plan is the realm of the anesthesia professional. It has three components: induction, maintenance, and emergence. An anesthetic plan of action arises from the needs of the patient, the experience of the anesthesiologist and the constraints placed upon both by the proposed surgical procedure. In particular, a trauma anesthetic needs to be dynamic and responsive to rapid changes in patient condition. The design of such a plan is aided through the employment of a decision tree, which is constructed by answering three questions: “why,” “what else,” and “what if.”

The “Why?” Question One seeks the answers to any number of questions, from “How did the injury occur?” to “Why are these lab values abnormal?” to “Is my plan still what this patient needs—and if not, why not?”

The “What else?” Question Questions posed include, but are not limited to, those such as “If general anesthesia is not an option, what else can I do” or “If succinylcholine is contraindicated, what else can I use?” or “If my patient gets nauseated when he gets opiates, what else can I do for his pain?”

The “What if?” Question Of course, the classic question is “What if I can’t intubate the patient?”, and there are innumerable others, including “What if my block fails,” “What if he arrests when the aortic clamp comes off,” and “What if he develops malignant hyperthermia?”

The successful execution of the plan requires vigilance, adaptability, and a thorough understanding of the basic principles pharmacology, physiology, and monitoring modalities, as applied to the victim of trauma.


The goals of an anesthetic plan may include some or all of the following: anxiolysis, analgesia, amnesia, unconsciousness, control of sympathetic reflexes, maintenance of homeostasis, and muscle relaxation. The anesthesia professional achieves these goals through pharmacologic manipulation of basic physiologic processes. The drugs employed to accomplish are divided into two general categories: anesthetic agents and anesthetic adjuvants. Anesthetic agents include general and local anesthetic agents; anesthetic adjuvants include sedatives, narcotics, and muscle relaxants.

General Anesthetic Agents These include volatile inhalational (halothane, enflurane, isoflurane, sevoflurane, desflurane) and intravenous (thiopental, methohexital, propofol, etomidate, ketamine) agents. The volatile agents possess simple halogenated alkane or ether structures. Nitrous oxide is usually considered an adjuvant to general inhalational techniques because it can produce surgical anesthesia only under hyperbaric conditions. All of these drugs share the ability to inhibit spinal and supraspinal neural transmission through either the activation or the inhibition of specific receptors. With the exception of ketamine, they are able to produce suppression of cortical electrical activity and inhibition of spinal reflexes. Burst suppression on the electroencephalogram may be achieved in clinically useful doses, and isoelectricity (and cardiovascular depression) may result if these doses are exceeded.

The effects of these drugs usually dissipate following their metabolism and excretion. In the case of volatile inhalational agents, this is very rapid because they are, in general, metabolically inert and are removed by reversing their concentration gradients. The majority of intravenous anesthetic agents follow time-dependent pathways of metabolism through the liver and kidneys. The mechanism of action of general anesthetic agents is not uniform and is the subject of intense study.1,2 Pertinent physicochemical characteristics are summarized in Tables 17-1 and 17-2.

TABLE 17-1 General Anesthetic Agents Delivered by Inhalation


TABLE 17-2 General Anesthetic Agents Administered Intravenously


Local Anesthetic Agents These include the amino-amide (lidocaine, mepivacaine, bupivacaine, ropivacaine) and amino-ester (cocaine, tetracaine, benzocaine) local anesthetic agents. They are used to produce topical anesthesia of mucous membranes, infiltration anesthesia of superficial skin wounds, blockade of the neuraxis using the spinal or epidural approach, and peripheral nerve blockade. Appropriately administered neuraxial or peripheral nerve blockade generally produces surgical anesthesia to the target dermatomes. Their mechanism of action is thought to involve inhibition of sodium conductance in excitable membranes, which suppresses the transmission of neural impulses. Amino-amide local anesthetic agents are metabolized in the liver and excreted by the kidneys; amino-ester agents are inactivated by plasma cholinesterase.

Unintentional intravenous injection or overdosage generally results in seizure activity, cardiovascular collapse and, in the case of bupivacaine or ropivacaine, a particularly malignant form of torsade de pointes. Intravenous intralipid administration may be helpful in treating this dysrhythmia, should it occur in the setting of toxicity involving these two agents.3,4 Excessive doses of benzocaine are well known to produce methemoglobinemia, a side effect that may be avoided through careful attention to dosing requirements. Cocaine inhibits the reuptake of catecholamines at noradrenergic nerve terminals; therefore, adrenergic agents must be administered with caution in its presence. Interestingly, the concept of regional anesthesia is expanding outside the immediate intraoperative period to include techniques suitable for postoperative pain control. This is a particularly attractive concept for many trauma patients. Pertinent physicochemical characteristics are summarized in Table 17-3.

TABLE 17-3 Local Anesthetic Agents


Sedative-Hypnotic Agents Although almost any intravenous or inhalational agent may be administered in very low doses to produce sedation or hypnosis, it is the benzodiazepine class of minor tranquilizers that are most commonly used for this purpose. They produce reliable amnesia and anxiolysis; they have no analgesic potency. In combination with an opiate, benzodiazepines (most commonly midazolam) are the linchpins of the technique of conscious sedation. Intense amnesia can be achieved with the co-administration of small doses of a benzodiazepine and ketamine, with the ketamine providing additional, substantial analgesia. These drugs are reliable anticonvulsants and should be at hand whenever local anesthetic agents are being administered. Midazolam has a relatively short duration of action, although its effects can be prolonged in the presence of hepatorenal impairment or systemic acidosis. In large doses, it is possible to achieve a plane of relatively deep general anesthesia with benzodiazepines.

Flumazenil is considered to be a specific benzodiazepine antagonist; its duration of activity, however, is much shorter than that of most benzodiazepines and it should be administered with careful attention to this limitation.

Neuromuscular Blocking Agents There are two broad categories of muscle relaxants: those that produce competitive inhibition of impulse transmission at the junctional endplate and those that do not. Competitive inhibitors of neuromuscular transmission are further subdivided into two groups, which are distinguished by their chemical structures. These groups are the benzylisoquinoline curariform alkaloids (curare, atracurium, mivacurium, cis-atracurium) and the 4-aminosterol compounds (pancuronium, vercuronium, rocuronium). The sole noncompetitive inhibitor of neuromuscular transmission in contemporary clinical use is succinylcholine. All of these drugs are generally used to facilitate endotracheal intubation and to enhance the muscle relaxation produced by general anesthetics.

Plasma cholinesterase rapidly cleaves the succinylcholine molecule and terminates its activity; its duration of action may be prolonged in the rare patient who possesses a genetic deficiency of this enzyme. Terminating the activity of competitive neuromuscular blocking agents is more complex. Curare and each of the 4-amino sterol compounds must first be displaced from the junctional endplate by acetylcholine and then be transported in the plasma to the liver for metabolism and excretion, usually by the kidneys. Plasma cholinesterase assists in terminating the activity of mivacurium. A complex, pH-dependent process known as “Hoffmann degradation” assists the inactivation of atracurium and its isomer cis-atracurium. No similar assistive processes exist for terminating the activity of the 4-aminosterol compounds.

With competitive inhibitors, these time-dependent processes of inactivation may be hastened by transiently increasing the concentration of acetylcholine at the junctional endplate, which through mass effect displaces a greater amount of relaxant and makes it available for metabolism and excretion. This displacement is usually produced by the simultaneous administration of a cholinesterase inhibitor and an anticholinergic agent; neostigmine and glycopyrrolate are generally used to accomplish this objective. This practice is commonly known as “reversal,” which is a misleading term, because it is more precisely an example of time-dependent pharmacologic antagonism. The duration of activity of most cholinesterase inhibitors is relatively brief and their effect may dissipate prior to complete termination of a profound neuromuscular block. If this should occur, re-paralysis of the patient may ensue.

The mechanism of action of sugammadex represents a novel approach to the concept of antagonism; however, its efficacy is greatest only for rocuronium, and it is currently not available in the United States.5,6 Neuromuscular blockade monitors (“twitch monitors”) are routinely used to assess the depth of paralysis and the efficacy of antagonism. It should be clear by now that these complex drugs are potentially lethal and that their effects must be carefully monitored. Pertinent physicochemical characteristics are summarized in Table 17-4.

TABLE 17-4 Neuromuscular Blocking Agents


Analgesic Agents Drugs commonly employed to facilitate analgesia fall into two general categories: those that stimulate inhibitory opiate receptors and those that block excitatory N-methyl-D-aspartate (NMDA) receptors. Nonsteroidal anti-inflammatory drugs are also used, as are nerve blocks produced by local anesthetics. Stimulation of the inhibitory, G-protein–linked opiate receptor is accomplished with agents possessing either a morphinan nucleus (morphine, codeine, hydromorphone, hydrocodone, oxycodone) or a phenylpiperidine nucleus (meperidine, fentanyl, sufentanil). Blockade of the excitatory NMDA receptor is achieved with ketamine, dextromethorphan, or nitrous oxide. Methadone constitutes a special case: broadly speaking, it is a phenylpiperidine derivative and its racemic mixture has activity at both opiate and NMDA receptors. Its potency and duration of activity make it a very useful analgesic; however, recent reports of its association with a drug-induced prolonged QT syndrome are troubling.710

Most analgesic agents are dependent upon hepatic metabolism and renal excretion for the termination of their effects; dosages must be adjusted for the extremes of age or in the presence of hepatorenal impairment. Morphine and meperidine may also accumulate potent active metabolites in the presence of renal insufficiency. Opiate agonists are notorious for producing an array of side effects, such as meiosis, respiratory depression, constipation, dysphoria, urinary retention, and generalized pruritus. The side effects of the NMDA antagonist ketamine include agitation, hallucinosis, hypersalivation, and sympathetic stimulation. There is a “ceiling effect” to the analgesia produced by both classes of drugs, and there is no point in their further administration if side effects are developing. Smaller doses of both classes of drugs, for example morphine and ketamine, may be given together to provide a synergistic response characterized by intense analgesia with less frequent side effects.11,12

Naloxone produces reliable antagonism of the narcosis and respiratory depression produced by opiate agonists. However, it is a very short-acting drug and care must be taken not to antagonize the analgesic effects of the opiate agonist. A massive sympathetic discharge producing cardiac arrest may ensue if a patient abruptly awakens from an opiate-induced narcosis and has the sudden perception of extreme pain. There is no reliable antagonist for ketamine.


Anesthesia Machines Anesthesia delivery systems range from the simple (an open drop ether cone) to the complex (the modern electronic anesthesia machine); however, all incorporate certain basic features. These include a means to supply calibrated flows of gases such as oxygen, air, or nitrous oxide (flow meters); a mechanism for the vaporization and controlled delivery of volatile anesthetic agents (vaporizers); devices to monitor the concentrations of inspired oxygen and expired carbon dioxide; an absorber to remove carbon dioxide from exhaled gases; and a method to support ventilation of the lungs. They are constructed with one-way valves, which inhibit re-breathing of carbon dioxide, and they have internal cutoff failsafe valves, which are designed to prevent the delivery of a hypoxic mixture to the patient. They possess distinctive, audible warning alarms. Cylinders of compressed oxygen, air and nitrous oxide are present; these are used to maintain essential gas flows in the event of pipeline failure.

Contemporary anesthesia machines contain complex electronic circuitry and substantial amounts of ferrous metal, which render them useless in an MRI suite; anesthetics in this hostile environment are conducted using specially constructed machines and shielded monitors. The American Society of Anesthesiologists has published guidelines for the appropriate daily checkout and maintenance of contemporary anesthesia machines.13 Rugged, reliable anesthesia machines, stripped down to their essential components, are available for use in the field. A brief review of any of these will provide the nonanesthesiologist with a more complete idea of what an anesthesia machine is meant to accomplish.14

Monitoring Systems The American Society of Anesthesiologists has published specific minimum requirements for the monitoring of patients who receive anesthetic care. These include, but are not limited to, methods of assessing the adequacy of oxygenation, ventilation, and circulation. These requirements are normally interpreted to mean the routine use of a blood pressure cuff, electrocardiography, stethoscope, temperature probe, pulse oximetry, and capnography on all patients. Extended monitoring includes the use of invasive hemodynamic monitoring, transesophageal echocardiography, and monitors of neuromuscular or cerebral function.

The routine use of cerebral function monitors (“processed EEGs”) is controversial; however, they may be helpful in identifying those trauma patients at risk for intraoperative awareness.15 Also, it is difficult to accurately place their electrodes in the face of traumatic intracranial procedures. In addition, the administration of ketamine will reduce the reliability of the signal. Transesophageal echocardiography is very useful in the detection and monitoring of traumatic injuries to the heart and great vessels;16 nonetheless, both its institution and the accurate interpretation acquired images may require the presence of an additional, experienced anesthesia caregiver.


The Full Stomach Trauma patients rarely, if ever, enjoy the luxury of an overnight fast; therefore, pulmonary aspiration of gastric contents presents a very real risk for them. In addition, the stress of trauma or the administration of opiate analgesics will profoundly inhibit gastric emptying. Induction of general anesthesia in these cases is usually accomplished with a “rapid sequence” technique and the use of Sellick’s maneuver (“cricoid pressure”).17,18 This induction sequence is performed with airway rescue devices at hand and the “difficult airway algorithm,” developed by the American Society of Anesthesiologists, is invoked if it fails.19 Institution of regional anesthesia in a trauma patient does not remove the risk of pulmonary aspiration; the patient may aspirate at any time if he loses consciousness and his protective airway reflexes become obtunded.

Rapid Sequence Induction and the Suspected Cervical Spine Injury Virtually every experienced trauma anesthesiologist has his own “tried and true” method of securing the airway in these patients, many of whom present for intubation in the emergency room.20 Common characteristics of emergent orotracheal intubation include Sellick’s maneuver, maintenance of the neck of the patient in the neutral position and removal of the anterior portion of the cervical collar in order to facilitate laryngoscopy. Airway rescue devices are usually at hand, as should be the resources needed to perform a tracheotomy.

The Field Intubation Many trauma anesthesiologists will confirm the appropriate position of an endotracheal tube, which they themselves have not inserted, using one or more of the following techniques: auscultation of breath sounds, capnography, repeat direct laryngoscopy, or fiberoptic bronchoscopy. The desire to immediately reintubate a patient with a functioning esophageal obturator already in place must be tempered by the knowledge that its insertion may have produced substantial upper airway trauma. If possible, any exchange of airway devices may best be reserved for the formal operating room environment.

The Extremes of Age Pediatric and geriatric patients possess substantial deviations from what is considered “normal adult” cardiovascular, pulmonary, hepatic, and renal physiology. They may respond to volume depletion with precipitate hypotension, apnea may be poorly tolerated and drug clearance may be unpredictable (it is generally reduced) in the presence of immature or senescent hepatorenal function. They share an inability to maintain normal body temperature under conditions of stress and an impressive coagulopathy may develop in the presence of hypothermia.

The Morbidly Obese Patient Even under optimal circumstances, the anesthetic care of the morbidly obese patient presents many challenges. At the top of the list are airway considerations: obese patients may be difficult to ventilate, difficult to intubate, and may possess a markedly reduced functional residual capacity, resulting in rapid arterial desaturation in the presence of ineffective ventilation of the lungs. Their body habitus may make effective arterial or venous access very difficult to achieve. They may present with numerous medical comorbidities, including hypertension, coronary artery disease, congestive heart failure, obstructive or restrictive lung disease, diabetes mellitus, deep vein thrombosis, and hepatic steatosis; these may be in varying states of compensation at the time of injury. Considerations such as these accompany the patient into the postoperative period, complicating the recovery phase.

The Pregnant Patient Unique physiologic changes complicate the care of the pregnant trauma patient. Circulating progesterone relaxes the lower esophageal sphincter, allowing free reflux of gastric contents into the hypopharynx; even in the absence of traumatic injury, a rapid sequence induction with Sellick’s maneuver is essential in order to prevent massive aspiration. Circulating plasma volume is increased, producing an edematous upper airway and extremities; intubation may be difficult and reliable vascular access may be a challenge to secure. Tracheotomy may be rendered hazardous by an enlarged, hypervascular thyroid gland. Also, the gravid uterus exerts upward pressure on the bases of the lungs, reducing functional residual capacity; this results in rapid arterial desaturation if ventilation is ineffective. In addition, when the patient is supine, the gravid uterus rests upon her aorta and inferior vena cava, reducing venous return to the heart. Therefore, profound hypotension and fetal asphyxia may occur if she is not positioned on her side, or at least with the left hip elevated, for transport, induction and surgery itself.

Of course, not all pregnant trauma victims are healthy prior to injury: gestational diabetes mellitus, pregnancy-induced hypertension, seizure disorders, gestational asthma, deep vein thrombosis, various coagulation abnormalities, and morbid obesity may be present, with all of their medical, surgical, and anesthetic implications. Also, one must remember that there are two patients who require attention: the mother and the fetus. Emergent evacuation of the uterus should always be anticipated and may be necessary in the event of maternal arrest. The fetus cannot survive in the absence of effective uteroplacental perfusion and the mother cannot be effectively resuscitated as long as the gravid uterus reduces venous return to the heart.

Traumatic Brain Injury Open or closed brain trauma may occur as an isolated finding or as one of several injuries in a victim of multiple trauma. In most of these patients, the blood-brain barrier is disrupted and cerebral edema is present. Many of these patients will be obtunded, lack protective airway reflexes and possess ineffective spontaneous ventilation. The resulting hypoxemia and hypercarbia will increase intracranial pressure and will have detrimental effects on the viability of injured neural tissue. They are also clearly at risk for pulmonary aspiration of gastric contents. Consequently, emergent endotracheal intubation is usually indicated in order to protect the airway and to control oxygenation and ventilation. Since the salvage of cells within the ischemic penumbra of injured neural tissue is of paramount importance, maintenance of a normal perfusion pressure and oxygen carrying capacity in the blood essential. The institution of hyperventilation in indicated for the control of intracranial hypertension, if present, as is the administration of osmotic diuretics. These considerations should be kept in mind from the time of initial intubation in the emergency room, through the period of diagnostic imaging, into the operating room and in the postoperative recovery phase.

Acute Spinal Cord Injury Many of the considerations for traumatic brain injury also are present in the patient with acute spinal cord injury. Succinylcholine may be used to facilitate emergent intubation in these patients at the time of their initial presentation; however, its administration is contraindicated later in their hospital course due to the risk of abrupt, fatal hyperkalemia.

The Open Globe The administration of succinylcholine to the patient with an open globe injury is now considered by many to be safe.21 Used to facilitate endotracheal intubation, it does not result in the extrusion of vitreous humor and it is the muscle relaxant of choice if the patient requires a rapid sequence induction. Patient movement or “bucking” during the course of the anesthetic, however, will place the patient at risk for this complication and it must be avoided.

Malignant Hyperthermia Patients with this disease may develop fatal hyperthermia, skeletal muscle rigidity, rhabdomyolysis, and dysrhythmias when exposed to inhaled anesthetic agents or succinylcholine. The disease is caused by inherited or spontaneous mutations of the RYR1 or CAC1NAS genes, which regulate calcium ion transport in the sarcoplasmic reticulum. Definitive diagnosis is made by subjecting biopsied muscle to the halothane- or caffeine-contracture test. Most anesthesiologists will consider any member of a kindred afflicted with malignant hyperthermia to be at risk for developing the reaction, even in the absence of a personal history, and will avoid the administration of triggering agents to these individuals.22 Malignant hyperthermia presents with a spectrum of reactions, ranging from mild to severe, and it is treated by immediately discontinuing any inhaled anesthetics or succinylcholine and by administering dantrolene sodium. The Joint Commission for the Accreditation of Hospital Organizations requires that a supply of dantrolene sodium be present in every surgical suite. Supportive measures include cooling the patient, hydration, and the treatment of acid–base disturbances. Other genetic disorders that are associated with malignant hyperthermia include hypokalemic periodic paralysis, central core disease, multiminicore disease, and Duchenne’s muscular dystrophy. Treatment protocols and resources for patients may be quickly accessed on the website of The Malignant Hyperthermia Association of the United States.23

Drug Intoxications Many trauma victims present with a documented history of substance abuse. Common intoxicants include ethanol, cocaine, marijuana, phencyclidine, ketamine, opiates, and any one of a number of amphetamine compounds. Of compelling concern to the anesthesiologist are the pulmonary and cardiovascular effects of central nervous system stimulants, in particular, when they are inhaled. The inhalation of “crack cocaine” or “crystal meth” can produce pulmonary thermal injury, abrupt hypertension, myocardial ischemia, and malignant ventricular dysrhythmias.24 Also, chronic abuse of “crystal meth” has been linked to the development of a severe dilated cardiomyopathy, thought to be the result of continual catcholamine elevation.25 In addition, severe intoxication with cocaine, amphetamines and certain major tranquilizers may produce muscle rigidity and an elevation of core body temperature; these signs and symptoms may be confused with malignant hyperthermia.26 In most of these clinical situations, the administration of dantrolene sodium is generally ineffective.

Laparoscopic Procedures The course of an anesthetic for a “screening laparoscopy” in a healthy, stable trauma patient is generally uneventful. However, the associated pneumoperitoneum may be poorly tolerated in patients with limited myocardial or pulmonary reserve: abrupt hypotension, hypoxemia, or both may develop, and may not resolve until deflation of the abdomen.27 The institution of invasive monitoring or the use of transesophageal echocardiography may be helpful if pneumoperitoneum cannot be avoided.

The Prone Position Most healthy, stable trauma patients will compensate for the reductions in cardiac output and functional residual capacity that occur during movement from the supine to the prone position.28 However, patients with limited myocardial or pulmonary reserve may develop abrupt, profound hypotension, or hypoxemia, or both, after prone positioning; this is particularly evident in the morbidly obese patient. In addition, the obese patient may become very difficult to ventilate because of increases in intra-abdominal and intrathoracic pressure. The simplest remedy is to avoid the prone position in an unstable patient and to use the lateral position, if at all possible. If the prone position is essential for surgical access, one may consider the use of an operating table that does not inhibit the free excursion of thorax and abdomen; an example of this is the orthopedic spine table.

Ophthalmic complications may occur following the use of the prone position for surgery. Postoperative blindness is the most devastating of these; it may be caused by central retinal artery occlusion, ischemic optic neuropathy and rarely, ischemia of the visual cortex. Its incidence has increased as the number of lengthy spine procedures has increased.29,30 Associated factors include intraoperative anemia or hypotension, operative procedures of long duration, diabetic or hypertensive retinal vascular disease, excessive in fluid administration, and pressure on the globe. A national registry exists, the purpose of which is to monitor the incidence of this complication.31

Single-lung Ventilation The use of single lung ventilation delivered by a double lumen tube will facilitate surgery on the thoracic aorta. These large endotracheal tubes are relatively inflexible and intubation with this airway device requires an experienced anesthesiologist. Experience is particularly important should the patient also possess an associated injury to the cervical spine or be at risk for aspiration of gastric contents. Fiberoptic bronchoscopy is essential for the confirmation of appropriate endotracheal tube placement following initial intubation. It is also helpful in repositioning a tube that has slipped out of position during the course of surgery. Patients with traumatic injuries to the thoracic aorta may also have associated pulmonary contusions; if substantial injury to the nonoperative lung is present, it may be impossible to effectively oxygenate or ventilate the patient once the operative lung is deflated. This may be detected prior to positioning and the initiation of surgery by simply collapsing the operative lung and observing the oximeter for signs of arterial desaturation.

Mass Casualties and Disasters The administration of anesthesia in the face of mass casualties presents any number of logistic and medical challenges. Supplies may be limited, standard equipment or facilities poorly functional and conventional anesthetic techniques impossible to institute. Recent eyewitness reports from medical volunteers in Haiti illustrate these problems.32 If general inhalation anesthesia cannot be administered, continuous infusions of etomidate or ketamine produce relatively reliable hemodynamic stability and are the cornerstones of total intravenous anesthesia delivered under extreme conditions.33Etomidate lacks analgesic potency and does not produce muscle relaxation; analgesics and adjuvant muscle relaxation must be administered if it is used. Adrenocortical suppression may also occur if large doses are given over a long period of time. Ketamine infusions produce reliable anesthesia, amnesia, analgesia and modest muscle relaxation. However, in anesthetic doses the drug produces an increase in intracranial and intraocular pressure and should be used with caution, if at all, in the presence of head trauma or an open globe injury. Also, large doses of ketamine may produce a prolonged emergence from general anesthesia, accompanied by impressive psychomimetic side effects. With both of these drugs, the airway should be secured with a cuffed endotracheal tube should the patient be at risk for aspiration of gastric contents.

If resources are limited, regional anesthesia may present as the only safe option for anesthetic care.34 Neuraxial anesthesia and simple peripheral nerve blocks may be employed to produce surgical anesthesia; however, careful patient selection for these techniques in this setting is of paramount importance.35,36 Contraindications to the use of regional anesthesia in the extreme trauma setting include hemodynamic instability, infection at the site of needle insertion, sepsis, abnormal coagulation, and known allergy to the proposed local anesthetic agent.


In the presence of traumatic injury, the primitive protective pain reflex is activated, which results in both the cognitive perception of pain and a well-defined neuroendocrine physiologic response. Thickly myelinated Aδ and nonmyelinated C-fibers carry afferent impulses from the peripheral tissues to synapses in the spinal cord and brain. Aδ fibers form the fast response and C-fibers form the slow response limbs of this feedback loop. The neurotransmitters involved in initiating, transmitting, and modulating this reflex include endogenous opiates, NMDA, and substance P. For purposes of pain management, these neurotransmitters are present in peripheral tissues (substance P), the substantia gelatinosa of the spinal cord (endogenous opiates), the nucleus proprius of the spinal cord (NMDA receptors), and in the limbic system, hypothalamus, and floor of the fourth ventricle in the brain.

Stimulation of opiate receptors and blockade of NMDA receptors will tend to suppress transmission of pain impulses. Local anesthetic agents, delivered by a number of regional anesthetic techniques, will block the afferent limb of the pain loop, thereby inhibiting the transmission of pain impulses. Therefore, the pain reflex may be manipulated in the periphery, spinal cord, and brain through the stimulation or blockade of any number of receptors. Early and aggressive pain management, beginning in the preoperative period, will assist in controlling both the neuroendocrine responses to pain and the development of debilitating posttraumatic chronic pain syndromes.

The most rational approach to the management of acute traumatic pain involves the utilization of nonsteroidal anti-inflammatory agents, opiates, NMDA-receptor antagonists, anticonvulsants, antidepressants, and local anesthetics, which are then employed according to a plan that is tailored to specific patient needs.37,38 Targeted blockade of the neuraxis or peripheral nerves has long been used to provide surgical anesthesia as well as lingering postoperative analgesia. In this sense, the development of ultrasound-guided, indwelling continuous catheter techniques for regional anesthesia and analgesia has revolutionized the management of pain in trauma patients and their postoperative rehabilitation.36,39 Both “single shot” and continuous catheter techniques have been designed to access the thoracic epidural and paravertebral spaces, the lumbar paravertebral space, the sheath of the brachial plexus, the femoral sheath, and the sheath that surrounds the sciatic and popliteal nerves. With catheter-based techniques, analgesia is provided by the continuous infusion of dilute concentrations of local anesthetic agent, which may be supplemented by the admixture of small-dose opiates or ketamine.


1. Campagna JA, Miller KW, Forman SA. Mechanisms of actions of inhaled anesthetics. N Engl J Med. 2003;348:2110–2124.

2. Nemergut EC, Lynch C. Mechanisms of general anesthetic action. Adv Anesth. 2003;21:115–161.

3. Leskiw U, Weinberg GL. Lipid resuscitation for local anesthetic toxicity: is it really lifesaving? Curr Opin Anaesthesiol. 2009;22(5):667–671.

4. Weinberg G. Lipid rescue resuscitation from local anaesthetic cardiac toxicity. Toxicol Rev. 2006;25(3):139–145.

5. Yang LP, Keam SJ. Sugammadex: a review of its use in anaesthetic practice. Drugs. 2009;69(7):919–942.

6. Abrishami A, Ho J, Wong J, et al. Sugammadex, a selective reversal medication for preventing postoperative residual neuromuscular blockade. Cochrane Databse Syst Rev. 2009;(4):CD007362.

7. Gupta A, Lawrence AT, Krishnan K, et al. Current concepts in the mechanisms and management of drug-induced QT prolongation and torsade de pointes. Am Heart J. 2007;153(6):891–899.

8. Ehret GB, Desmeules JA, Broers B. Methadone-associated long QT syndrome: improving pharmacotherapy for dependence on illegal opioids and lessons learned for pharmacology. Expert Opin Drug Saf. 2007;6(3): 289–303.

9. Andrews CM, Krantz MJ, Wedam EF, et al. Methadone-induced mortality in the treatment of chronic pain: role of QT prolongation. Cardiol J. 2009;16(3):210–217.

10. Fredheim OM, Moksnes K, Borchgrevink PC, et al. Clinical pharmacology of methadone for pain. Acta Anaesthesiol Scand. 2008;52(7):879–889.

11. Berti M, Baciarello M, Troglio R, et al. Clinical uses of low-dose ketamine in patients undergoing surgery. Curr Drug Targets. 2009;10(8):707–715.

12. Bell RF, Dahl JB, Moore RA, et al. Perioperative ketamine for acute postoperative pain. Cochrane Databse Syst Rev. 2009;(3):CD004603.

13. Guidelines for effective anesthesia apparatus checkout recommendations. Available at: Park Ridge, IL. Accessed February 21, 2010.

14. Petty WC. Military anesthesia machines. In: Zajtchuk R, Grande CM, eds. Textbook of Military Medicine: Anesthesia and Perioperative Care of the Combat Casualty. Washington, DC: Office of the Surgeon General, Borden Institute, Walter Reed Army Medical Center; 1995:141–174.

15. American Society of Anesthesiologists Task Force on Intraoperative Awareness. Practice advisory for intraoperative awareness and brain function monitoring: a report by the American Society of Anesthesiologists Task Force on Intraoperative Awareness. Anesthesiology. 2006;104: 847–864.

16. American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophgeal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography: a report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophgeal Echocardiography. Anesthesiology. 1996;84(4):986–1006.

17. Rice MJ, Mancuso AA, Gibbs C, et al. Cricoid pressure results in compression of the postcricoid hypopharynx: the esophageal position is irrelevant. Anesth Analg. 2009;109(5):1546–1552.

18. Ovassapian A, Salem MR. Sellick’s maneuver: to do nor not do. Anesth Analg. 2009;109(5):1360–1362.

19. American Society of Anesthesiolgists Task Force on Management of the Difficult Airway. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiolgists Task Force on Management of the Difficult Airway. Anesthesiology. 2003;98:1269–1277.

20. Bonhomme V, Hans P. Management of the unstable cervical spine: elective versus emergent cases. Curr Opin Anaesthesiol. 2009;22: 579–585.

21. Vachon CA, Warner DO, Bacon DR. Succinylcholine and the open globe: tracing the teaching. Anesthesiology 2003;99:220–223.

22. Larach MG, Gronert GA, Allen GC, et al. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 19887 to 2006. Anesth Analg. 2010;110:498–507.

23. The Malignant Hyperthermia Association of the United States. Available at: Accessed February 21, 2010.

24. Devlin RJ, Henry JA. Clinical review: major consequences of illicit drug consumption. Critical Care. 2008;12:202–209.

25. Yeo KK, Wijetunga M, Ito H, et al. The association of methamphetamine use and cardiomyopathy in young patients. Am J Med. 2007;120(2): 165–171.

26. Altman CS, Jahangiri MF. Serotonin syndrome in the perioperative period. Anesth Analg. 2010;110:526–528.

27. Hirvonen EA, Poikolainen EO, Paakkonen ME, et al. The adverse hemodynamic effects of anesthesia, head-up tilt, and carbon dioxide pneumoperitoneum during laparoscopic cholecystectomy. Surg Endosc. 2000;14:272–277.

28. Edgcombe H, Carter K, Yarrow S. Anaesthesia in the prone position. Br J Anaesth. 2008;100(2):165–183.

29. Chang S-H, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery. Spine. 2005;30(11):1299–1302.

30. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol. 2008;145:604–610.

31. Practice advisory for the perioperative visual loss associated with spine surgery: a report by the American Society of Anesthesiolgists Task Force on Perioperative Blindness. Anesthesiology. 2006;104:1319–1328.

32. Sontag S. Foreign doctors are haunted by Haitians they couldn’t aid. The New York Times. 2010;159(54950):A1,A8.

33. Fox DJ, Saunders LD, Menk EJ, et al. Intravenous anesthesia. In: Zajtchuk R, Grande CM, eds. Textbook of Military Medicine: Anesthesia and Perioperative Care of the Combat Casualty. Washington, DC: Office of the Surgeon General, Borden Institute, Walter Reed Army Medical Center; 1995:211–233.

34. Bruckenmaier CC, McKnight GM, Winkley JV, et al. Continuous peripheral nerve block for battlefield anesthesia and evacuation. Reg Anesth Pain Med. 2005;30:202–205.

35. The Defense & Veterans Pain Management Initiative. Available at: Washington, DC. Accessed February 21, 2010.

36. The Defense & Veterans Pain Management Initiative: MARAA Book Project. Available at: Washington, DC. Accessed February 21, 2010.

37. Buvanendran A, Kroin JS. Multimodal analgesia for controlling acute postoperative pain. Curr Opin Anaesthesiol. 2009;22:588–593.

38. Heitz JW, Witkowski TA, Viscusi ER. New and emerging analgesics and analgesic technologies for acute pain management. Curr Opin Anaesthesiol. 2009;22:608–617.

39. Clark L, Varbanova M. Regional anesthesia in trauma. Adv Anesth. 2009:27:191–222.

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