ANESTHESIA INDUCTION AND MAINTENANCE

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ANESTHESIA INDUCTION AND MAINTENANCE Niels N. Chapman, MD and Bruce F. Cullen, MD

INDUCTION OF GENERAL ANESTHESIA The goals of any general anesthetic are the safe establishment of an airway and provision of sufficient analgesia, amnesia, and perhaps neuromuscular blockade to prevent patient awareness or movement during surgery. In the case of trauma, some of these steps may have already been accomplished by other health care providers. This article is thus arbitrarily divided into two major sections, the first discussing management of the patient with an airway that has not been instrumented (nonintubated) and the second discussing the patient with an endotracheal tube in place (intubated). As airway management has been reviewed elsewhere in this issue, only a few comments will be made regarding the implications of a compromised airway on the induction of anesthesia. A brief summary of anesthetic concerns for the pregnant trauma patient is also included. Although this article is limited to a discussion of general anesthesia, it is important to note that in select cases, after thorough review of the pathophysiology at hand (including the potential for hypovolemia and coagulopathies),regional anesthesia (such as for extremity surgery) may be a preferred alternative in the trauma setting. The Nonintubated Patient Before proceeding, two basic questions must be addressed: how to establish a secure airway and which pharmacologic agents to use. From the Department of Anesthesiology, University of New Mexico School of Medicine, Albuquerque, New Mexico (NNC); and the Department of Anesthesiology, University of Washington School of Medicine, Harborview Medical Center, Seattle, Washington (BFC) ~

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ANESTHESIOLOGY CLINICS OF NORTH AMERICA

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VOLUME 14 NUMBER 1 MARCH 1996

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Examination of airway patency and anatomy, chest and cardiac auscultation, determination of hemodynamic parameters after placement of appropriate monitors, and, very importantly, assessment of neurologic status are parts of the Advanced Trauma Life Support (ATLS) protocol.* Ideally, they should be performed before the decision for surgical intervention is made. It must be emphasized that in the scenario of a severely injured patient being rushed to the operating room, the cervical spine cannot be "cleared" of fractures or ligamentous injury, even with the usual lateral radiograph. Therefore, strict maintenance of the cervical spine in a neutral position, especially when managing the airway, is indicated. If time permits, types of information derived from the mnemonic AMPLE in the ATLS guidelines should be elicited: allergies, medications, past medical and surgical history,62,90 last meal, and events and environment of the accident. Cervical spine and chest radiographs should be reviewed as well as pertinent laboratory tests (hematocrit, serum electrolytes, coagulation parameters, and, where indicated, arterial blood gases, P-human chorionic gonadotropin (hCG) and toxicologic screens). With this information and data on the patient's volume status and fluid requirements, the anesthesiologist can reach some conclusions concerning the patient's physiologic reserves. As a matter of routine, the trauma operating room should be prepared before the trauma patient arrives because induction of anesthesia may of necessity be precipitous. The following should be available and functioning: pertinent invasive and noninvasive monitors, devices for rapid administration and warming of intravenous (IV) blood products and clear solutions,", 33, 71, 84 red cell-saving devices, warming devices such as a heating blanket or a heated humidifier included in the respirator circuit, and appropriate airway-management equipment. The room temperature should be above 75°F.85 Many trauma centers store low anti-A,B titer 0 negative blood for female patients and 0 positive blood for male patients for use until type-specific blood is available. The availability of these units should be ascertained and cross-matching for type-specific blood initiated as soon as the patient arrives at the hospital. A primary concern when managing the nonintubated trauma patient is the potential for aspiration of gastric contents. An accident victim must be considered to have a "full stomach" irrespective of the last time of consumption of food or beverage, as trauma delays gastric emptying. The presence of a nasogastric tube, a routine requirement in the ATLS protocol, by no means guarantees an empty stomach. The risks of passive reflux of gastric contents during unconsciousness, ethanol intoxication, or anesthetic induction as well as active vomiting during awake intubation or as a consequence of increased intracranial pressure (ICP) must be taken into account when planning airway management. Securing the airway while maintaining pressure on the cricoid cartilage78and having strong suction available at all times are essential. The designation of preferred induction agents for the trauma patient continues to be a source of debate owing to the fact that no agent

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ensures loss of consciousness while preserving adequate perfusion in the face of severe hypovolemia. Standard doses of many induction agents may cause profound hypotension. In shock there is a reduced volume of distributionlooand cardiac output, leading to greater plasma concentrations of drug than in normovolemic patients. Hypoalbuminemia resulting from the dilution of plasma proteins by large quantities of resuscitation fluids and hypoperfusion of the liver40may also result in higher drug concentrations. In addition, anesthetic requirements may loo be reduced by hypoperfusion, cerebral hypoxia, and hyp~thermia.~~, Finally, many trauma patients have ingested drugs such as ethanol or cocaine before the trauma occurred,12,32, 67 adding to the uncertainty about the hemodynamic response to induction agents. Some of the physiologic effects of ethanol are listed in Table 1.

Table 1. EFFECTS OF ALCOHOL IN TRAUMA ~

Cardiovascular and respiratory system

Gastrointestinal system

Blood and hemostasis

Central nervous system (CNS), anesthetic effects

Musculoskeletal Metabolism and thermoregulation

Direct cardiac depression, diuresis by blockage of ADH Facilitation of atrial and ventricular arrhythmias through a direct effect and electrolyte disturbances Exacerbation of myocardial contusion and reduced threshold for electromechanical dissociation Blunting of vascular response to norepinephrine, vasodilation despite enhancement of norepinephrine release Decreased airway sensitivity with increased risk for pulmonary aspiration of foreign bodies Decreased mobility of alveolar macrophages with increased risk for pneumonia Increased pulmonary vascular resistance with increased risk for the development of post-traumatic ARDS Abdominal wall laxity with increased risk for blunt abdominal injury, masking of signs of abdominal injury In cirrhosis, portal hypertension and splenomegaly with increased risk of splenic rupture Thrombocytopenia Folate deficiency in alcoholism with leukopenia, thrombocytopenia and microcytic/macrocytic anemia. Also, decreased production of thromboxane, factors 11, VII, IX, X, vitamin K deficiency. Higher degree of brain and spinal cord injury with worse neurologic recovery, enhanced CNS edema formation Altered sensorium making neurologic evaluation difficult Alteration of hepatic metabolism and generation of cross tolerance Decreased anesthetic requirements in acute intoxication Increased risk for orthopedic injuries during intoxication In alcoholism, increased urinary losses of calcium and magnesium and reduced bone density Depression of hypothalamic thermoregulation and shivering Peripheral vasodilation with increased heat loss Hypoglycemia in alcoholics after fasting

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The decision as to what quantity of which drug(s) to use for induction of anesthesia, if any, depends on such variables as the patient’s hemodynamic status, the presence or absence of a closed head injury or an open globe, the potential for airway problems, and the presence of allergies or prior adverse reactions to anesthetics. This decision must also consider a significant past medical history of preexisting cardiac, pulmonary, neurologic, renal, or hepatic condition^.^^ If the patient is obtunded, there may be no need to administer anesthetics. Ventilation and oxygenation, with or without concomitant use of a muscle relaxant, may be all that is required. Similarly, if the patient is severely hypotensive, it may be unwise to administer anesthetic drugs; however, it is obviously important to be wary of the potential for patient recall. Despite hypotension, acidosis, and high blood ethanol levels, some patients have reported recall.’O Also, even if the patient is obtunded, it may be advisable to administer an IV anesthetic before tracheal intubation to avoid the associated increase in intracranial pressure. Thiopental has proved to be a remarkably safe induction agent with limited cardiovascular and respiratory depression when used in most elective situation^.^^, 22 The initial application of thiopental in trauma was disastrous. Early in World War 11, it was administered to soldiers who had been inadequately fluid resuscitated, and they subsequently died.39 Their deaths are not surprising because thiopental causes dilation of terminal arterioles and capacitance vessels, release of histamine, decreases in cardiac output and mean arterial pressure through a direct negative inotropic effect, and decreases in central sympathetic outflow.26 If patients are fluid resuscitated before they receive thiopental and the dose is reduced somewhat, serious hypotension need not result. In an animal model of hypovolemia, the effect of thiopental was not different from that of ketamine in terms of causing reductions in systemic vascular resistance, mean arterial pressure, cardiac output, and heart rate while maintaining stroke volume and producing less acidosis.102 Thiopental is particularly advantageous for patients with head injuries because of its ability to reduce ICP and the cerebral metabolic rate of oxygen consumption (CMRO,). Ketamine is best known for its release of catecholamines, minimal respiratory depression, and occasionally causing emergence hallucinations. Its property of releasing catecholamines suggests that it might be the ideal agent to use in profound hypovolemia and shock.16,51, 74, yl, “I6 Experimental work has shown ketamine to be a powerful direct cardiac depres~ant.~~, 92 In hypovolemic animals, an effective drop in mean arterial pressure, stroke volume, and heart rate is accompanied by the release of epinephrine, norepinephrine, and renin.48,Io2 This effect persists for 30 minutes and is accompanied by substantially higher lactic acid levels than with thiopental or inhalation anesthetics.1o4Increased ICP as a consequence of increased cerebral blood flow and stimulation of thalamic and limbic centers suggests that ketamine should be used with caution in the presence of head injuriesHX Cerebral autoregulation

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and CO, responsiveness remain preserved during ketamine anesthesia. Intraocular pressure increases with the use of ketamine, and its use in open-globe injuries is cautioned.62In pregnant patients ketamine elicits contractions similar to erg~tamine”~, and therefore should be avoided unless a cesarean section or emergency delivery is planned. Etomidate has found clinical application in patients with significant cardiac and coronary disease. It lacks direct cardiac depressant effect+ 66 but can cause decreased peripheral vascular resistance and a small decrease in blood pressure in patients with heart disease.I8 The most serious side effect of etomidate consists of temporary dose-dependent, reversible inhibition of 11 P-hydroxylation during steroidogenesis, resulting in adrenocortical suppression for 3 to 5 hours after an induction dose.98The associated risk appears to be more theoretic than real. Myoclonic movements, which occur frequently after induction with etomidate, may limit its use in open-eye injuries8 Etomidate does, however, offer excellent cerebral protection through a decrease in CMRO, and Although it offers more cardiovascular stability than thiopental, etomidate should also be used with caution in the presence of uncompensated hemorrhagic shock; however, no clinical or experimental data have been reported in this context. Propofol is notable for its short action, pleasant emergence, antiemetic properties, and cerebral protective effects of lowering CMRO, and ICP. Compared with thiopental, propofol causes less depression of cardiac contractility4,65 but greater depression of systemic vascular resistance.68In euvolemic geriatric patients, cardiac output was maintained, but the mean arterial pressure fell by 25% to 30% through a loss of systemic vascular re~istance.~~ These qualities make propofol unattractive for any trauma victim suspected of being hypovolemic. Propofol has, however, been successfully used as a substitute for barbiturates for intraoperative control of increased ICP in otherwise stable patients. Muscle relaxants are frequently an indispensable adjunct to endotracheal intubation, especially if a ”rapid sequence” intubation is attempted in view of a high risk of aspiration of gastric contents. The relaxant employed most often and with great success55is succinylcholine (SCh). Its short duration of action and rapid onset have so far not been matched by nondepolarizing agents. Rocuronium, a new nondepolarizing muscle relaxant, has a comparable speed of onset in the range of 65 to 80 seconds when used in doses of 0.9 to 1.2 mg/kg, but it concomitantly has prolonged action, similar to vecuronium and a t r a c ~ r i u mA . ~recent ~ study comparing SCh with high-dose vecuronium (0.4 mg/kg) demonstrated good intubation conditions for SCh at 53 seconds, in contrast to 100 seconds for v e c ~ r o n i u mIn .~~ a double-blind study comparing SCh and vecuronium, good intubating conditions were encountered with both drugs after 60 The use of muscle relaxants can significantly improve the chances for successful first-attempt tracheal intubation of trauma victims.*8The safety of SCh in the presence of an open-globe injury is still debated.lSrs7

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A small but measurable increase in intraocular pressure may follow administration of SCh, but the clinical risk is minimal, particularly if a "defasciculating" dose of a nondepolarizing relaxant is given beforehand. A large series of patients with open-globe injuries received SCh with induction without adverse 99 Intraocular pressures may, however, increase after SCh administration and tracheal intubation, in part by mechanisms unrelated to extraocular muscle contraction,5O such as coughing or increases in arterial or venous pressures. A small increase in ICP with the use of SCh suggests that its use in patients with head injuries may be relatively contraindicated. Frequently, however, the more rapid control of the airway and reduced apnea time with SCh as a muscle relaxant may easily outweigh this consideration, especially if hyperventilation is required quickly or if hypoventilation and a poorly controlled airway precede the attempted intubation. As with intraocular pressure, ICP can also be significantly increased by coughing and by increases in arterial or venous pressure associated with tracheal intubation. Of the nondepolarizing muscle relaxants, vecuronium offers virtuIo7 For rapid-sequence inducally complete cardiovascular ~tabi1ity.l~~ tions, doses up to 0.4 mg/kg have been used without hemodynamic or cardiac changes re~u1ting.I~ High-dose vecuronium prolongs its duration of action; so a single bolus as previously described may act for as long as 138 minutes.36Mivacurium, a short-acting nondepolarizing relaxant that depends on pseudocholinesterase for breakdown, has onset times similar to those of vecuronium and causes systemic vasodilation through histamine release if injected too rapidly. Rocuronium has an onset time similar to that of SCh, but it has not been clinically available long enough to determine its ultimate role in the care of the trauma patient. Rocuronium, similar to vecuronium, offers hemodynamic stability, although an increase in heart rate has occurred when 0.6 mg/kg is given to healthy, anesthetized, normocapnic patients; blood pressure was not lowered.59 Recently, new long-acting, nondepolarizing agents with a variety of cardiovascular responses and onset times have been introduced to practice, offering alternatives to pancuronium if reliable, longterm neuromuscular blockade is desired. If time permits, appropriate monitors should be placed before anesthesia is induced and should include an arterial line unless the trauma is minor, the patient is hemodynamically stable, or the patient is combative. The value of preoxygenation in permitting safe extension of the 49, 53 apnea period during induction has been sufficiently doc~mented.~, Some trauma centers prepare and drape trauma victims completely before induction to allow for emergent left thoracotomy and aortic cross clamping should the patient decompensate with induction. During tracheal intubation the anesthesiologist should assign reliable assistants to maintain axial stabilization of the cervical spine and provide cricoid pressure as described by S e l l i ~ kMost . ~ ~ victims of deceleration injuries are maintained in cervical collars to immobilize the spine. In our experience, airway management is facilitated by the temporary removal of

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such devices (particularly the anterior portion of such) as they tend to restrict the mask fit and mandibular range of motion. Obviously, axial stabilization needs to be maintained by an assistant while these collars are removed. Because many experienced health care workers may have confusion about how long cricoid pressure needs to be maintained, the person assigned to this task should be given clear instructions to hold the pressure until specifically relieved of this function by the anesthesiologist after unequivocally correct placement of the endotracheal tube. It has been established that the effectiveness of the Sellick maneuver is not compromised by the presence of a nasogastric tube, which therefore yh Suctioning of the does not need to be removed before laryngos~opy.~~, nasogastric tube before induction and leaving it open to air may facilitate gastric decompression.y6 It is obvious that resuscitation of an exsanguinating patient needs to be continued during induction. A large-bore infusion should be established (if not done earlier), proper function of existing IV access assured, and fluid resuscitation continued by assistants assigned to this task. In the trauma setting, except under exceedingly rare circumstances, general anesthesia should be started by IV induction. Inhalation induction may be appropriate in selected pediatric patients or in situations where gradual induction is indicated for control of the airway. In virtually all cases where general anesthesia is induced intravenously, a socalled rapid-sequence technique, with expeditious administration of IV anesthetics and neuromuscular blockers, followed by placement of an endotracheal tube at the earliest safe opportunity, is indicated. The classic teaching prohibits mask ventilation between loss of consciousness and tracheal intubation, mostly because of concern about possible insufflation of gas into the stomach and resultant regurgitation of gastric contents. In view of the data generated by Sellick and mask ventilation can be performed safely while maintaining cricoid pressure and may actually be desirable in certain circumstances. A buildup of carbon dioxide in the presence of a head injury will cause an increase in ICP, and morbidly obese or pregnant patients may experience precipitous oxygen desaturation when apneic despite preoxygenation. If a nondepolarizing neuromuscular blocking agent with a slower onset has been employed, mask ventilation is indicated until good intubating conditions are established. Following verification of proper placement of the endotracheal tube and implementation of ventilation or hyperventilation, maintenance anesthetics should be added if this can be done safely. The anesthesiologist should then address, if indicated, issues such as further fluid resuscitation, placement of invasive monitoring devices, establishment of additional vascular access, implementation of warming devices, and updating pertinent laboratory data. In the context of the ATLS protocol, cardiopulmonary and neurologic parameters should be constantly reevaluated. After implementation of positive pressure ventilation, tension pneumothoraces can develop insidiously and will occasionally be her-

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alded by increased ventilation pressures or hypotensionz4,83; it is important that the staff is alert to this possibility. The lntubated Patient

With more aggressive prehospital care being provided by paramedical personnel, many trauma victims will arrive at the hospital with an artificial airway already in place. Whereas esophageal obturator airways were used frequently in the past, they are rarely used today because they do not eliminate the need for eventual tracheal intubation, and emesis almost always accompanies their withdrawal. Endotracheal intubations in the field often must be performed under dramatic circumstances so that the first step when an intubated patient is admitted to the emergency room should be to ascertain correct placement of the endotracheal tube by auscultation, possibly capnography, and ultimately chest radiography. On rare occasions, the endotracheal tube placed in the field may prove inadequate because of insufficient size, a ruptured cuff, or the need for special tubes, such as armored or double-lumen tubes, for the impending surgical procedure. In this circumstance, the entire armament of tricks and techniques of airway management may be required. Pediatric trauma victims (aged 10 years or younger) present an especially serious problem with respect to the optimal size of an endotracheal tube. Although under elective circumstances uncuffed endotracheal tubes are chosen for use in this population, the traumatic event may ultimately require that the patient be ventilated with high airway pressures. Many pediatric intensivists have therefore introduced the use of cuffed endotracheal tubes, which allow variation of the pressure exerted on the trachea tailored to the ventilatory requirements. The possibility of a pneumothorax or severe pulmonary injury involving the trachea or bronchi must be kept in mind when assessing severely injured patients.43Muscle paralysis, positive pressure ventilation, or airway instrumentation may convert a tenuous but stable situation to a life-threatening crisis. In the case of a complete bronchial rupture with loss of the entire tidal volume into the pleural space, effective ventilation may require placement of a double-lumen tube and ventilation of the unaffected side only or jet ventilation distal to the rupture via a catheter or rigid broncho~cope.~~ Depending on the prehospital choice of muscle relaxant, the patient may recover from the neuromuscular blockade on arrival in the hospital, which provides an excellent opportunity to assess the patient’s mental and neurologic status before neuromuscular blockade is (possibly) reimplemented. Despite the fact that sedatives or hypnotics may appear unnecessary in an already intubated patient, rapid establishment of anesthesia with IV agents is desirable not only to provide amnesia before the commencement of painful procedures but also to prevent hemodynamic reactions or coughing induced by the endotracheal tube or other stimuli. If pa-

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tients demonstrate serious hemodynamic instability, they may not tolerate routine doses of sedatives, opioids, or anesthetic gases. In this circumstance, one may have to rely on small doses of IV amnestic drugs (benzodiazepines or scopolamine) plus muscle relaxants.

The Compromised Airway

Determination of which drugs and techniques to use when managing a patient with a suspected or obviously compromised airway is challenging. A variety of anatomic and pathologic conditions will render an airway difficult to manage, including abnormal craniofacial proportions, reduced mobility of the mandible, anterior positioning of the larynx, orofacial fractures with loss of upper airway anatomy, a fractured larynx, or tracheobronchial rupture. Safe management or’ the airway of the traumatized patient demands a detailed examination of the patient, and, if available, of the past medical history. Frequently, the mechanism of injury may suggest the nature of the airway injury. Observation of the patient’s respiratory efforts may reveal obstruction or inspiratory stridor; on some occasions, patients may ”fight for their lives” by positioning themselves in such a way as to permit ventilation through otherwise collapsing airways. Gross bleeding from the oropharynx or nasopharynx suggests serious maxillofacial injuries. Hoarseness, anterior neck hematomas, or gross injuries to the anterior neck suggest laryngeal injuries. Cricothyroid, tracheal, or bronchial rupture is more subtle and not easily diagnosed. The presence of any such condition may mandate a departure from a routine rapid sequence induction and formulation of a careful strategy for airway management. Although the anesthesiologist is the first authority on airway management in such patients, other specialists should also be consulted. Surgeons may be asked to stand by for emergency tracheostomies, and especially in the case of trauma to the larynx, an otolaryngologist should be consulted before potentially irreversible damage to the larynx is imparted by orotracheal 76 int~bation.~~, Anesthetic drugs, especially muscle relaxants, must be used judiciously in the presence of a near obstructed airway. Although great success using succinylcholine to facilitate intubation in the emergency room was reported in a prospective other techniques may prove safer: for example, awake laryngoscopy or fiberoptic bronchoscopy after topical anesthesia to the airways or techniques such as blind nasal intubation or retrograde wire intubations. Sometimes, performing an awake tracheostomy with the patient under local anesthesia is the safest method, especially if the patient would eventually undergo such a procedure for extensive maxillofacial fractures.

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The Pregnant Patient

Trauma is the leading cause of maternal mortality in the United States.', 28, 31,6y Seriously injured pregnant patients, however, constituted less than 1%of all trauma admissions in one making it difficult to develop a routine in such cases. Maternal physiologic changes pertinent to trauma anesthesia are listed in Table 2. The risk of anesthetic induction is increased by numerous factors, such as increased metabolic rate, decreased functional residual capacity and total lung capacity, increased gastric acidity, reduced gastric emptying, and a frequently incompetent gastroesophageal junction. The enlarged uterus causes craniad displacement of the diaphragm, causing faster development of pneumothoraces and increasing the risk of diaphragmatic or abdominal injuries with chest-tube placement. Diffuse tissue edema may cause narrowing of the patient's airway and may necessitate intubation with smaller endotracheal tubes. Other factors, such as an increase in blood volume and red-cell mass, provide a physiologic reserve for the mother but not for the fetus.69The need for left lateral displacement of the uterus, either manually or by tilting the backboard or operating room

Table 2. PHYSIOLOGIC CHANGES IN PREGNANCY Parameter

Increase

Decrease

Minute ventilation Alveolar ventilation Tidal volume Airway resistance Compliance Chest wall compliance Total lung capacity FRC Arterial PO, Arterial PCO, Oxygen consumption Blood volume Plasma volume Red blood cell volume Cardiac output Stroke volume Heart rate Mean arterial pressure MAC Renal plasma flow GFR BUN Serum cholinesterase Gastroesophageal reflux Gastric motility

50% 70% 40%

-

-

36%

-

20%

10 mm Hg

-

20% 35% 45% 20%

40% 30% 15%

-

30% 45% 5% -

10 mm Hg

-

-

-

15 mm Hg 40%

50% 50%

-

-

40% 33%

-

+++

+++

-

FRC, fundamental reserve capacity; MAC, maximum alveolar concentration; GFR, glomerular filtration rate; BUN, blood urea nitrogen.

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table, to avoid the vena cava compression syndrome should be kept in mind. Because of a large gradient in oxygenation between maternal and fetal blood, provision of supplemental oxygen to the mother is critical. As the uterine vasculature is very sensitive to catecholamines, the first end organ to suffer from centralization of blood volume during hemorrhage is the uterus; however, physiologic vasodilation of epidermal vessels significantly delays maternal pallor and loss of capillary refill.hyThis fact stresses the importance of electronic fetal monitoring, which may also serve as a gauge of maternal resuscitation. An obstetrician should be consulted as early as possible for fetal ultrasound, monitoring of fetal heart tones, and possibly uterine contractions and to render an opinion regarding the need for emergency delivery. As the onset of premature contractions or other complications is most likely during the first 6 hours, uterine contractions and fetal heart tones should be monitored in patients beyond 20 weeks' gestation during this period. If more than one uterine contraction occurs within 15 minutes, this period should be extended to 24 hours. Because maternal well-being is crucial to fetal survival, the use of almost every drug, monitoring device, and radiographic study necessary for maternal diagnosis or treatment is acceptable. With the exception of chemotherapeutic agents and certain antibiotics, such as tetracycline, sulfonamides, nitrofurantoin,7(' and anticonvulsant most drugs used in treating the trauma patient are unlikely to have significant teratogenic effects. Benzodiazepines and nitrous oxide have been implicated as teratogenic if administered during the first trimester and should be avoided if alternatives are possible. Large retrospective cohort studies of pregnant patients undergoing nonobstetric surgery during the first and second trimester failed to substantiate a correlation between anesthetic agents or technique and the rate of fetal malformation^^^ but showed an increased risk for spontaneous abortions2s and low birth weight and early neonatal death.57These data suggest that, if possible, regional anesthesia should be chosen in such cases. Lastly, ketamine is known to induce contractions in the earlier stages of pregnancy and should be avoided.34,63 MAINTENANCE OF GENERAL ANESTHESIA Selection of Anesthetics

The dilemma of how best to provide analgesia and amnesia in the presence of hemorrhage-induced hemodynamic instability has not been successfully resolved. With neuromuscular blockers available to achieve immobilization, intraoperative recall of events by the patient remains an entity that is difficult to predict or diagnose.loThe cardiovascular and other effects of common anesthetic agents in traumatized humans have not been studied. It is difficult to carry out 'sound research protocols when one must consider ethical issues (such as how to get informed

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consent) and the fact that the degree of injury and the clinical outcome are difficult if not impossible to standardize. Potent volatile anesthetics are frequently the anesthetics of choice for the trauma patient because at appropriate concentrations they provide analgesia, amnesia, and some degree of immobilization, combined with rapid titratability. The minimum alveolar concentration (MAC) for these agents may be decreased by anemia and hypoxemia,2°,21 but the magnitude of this effect in the individual trauma patient is unpredictable. Conversely, the use of vasopressors such as ephedrine may increase MAC by release of brain noradrenalin.s2 In young volunteers, in the absence of a surgical stimulus, enflurane causes the most cardiovascular depression and should be avoided, at least in high concentrations, in unstable patients. Halothane lacks significant peripheral vasodilation but exerts stronger cardiac depression than isoflurane. One side effect of halothane, the sensitization of the myocardium to catecholamine-induced dysrhythmias, is a concern for patients who are likely to develop dysrhythmias caused by hypothermia, hypotension, anemia, and high levels of endogenous and iatrogenic vasoactive amines. Another risk of halothane is hepatic injury, which may be confused with (transfusion) hepatitis and surgical hepatic injury. In euvolemic humans, isoflurane produces profound peripheral vasodilation but maintains hemodynamic stability through an increase in heart rate. Trauma victims already have an increased heart rate, and their ability to compensate for a reduction in peripheral resistance may be impaired. Under these circumstances, isoflurane could cause further hypotension. Like all anesthetics, the dose of isoflurane must be carefully titrated. Desflurane, a new addition to the potent volatile agents that is notable for its low solubility in blood, has cardiovascular effects similar to those of isoflurane.60In lower doses, hemodynamic stability appears to depend less on an increase in heart rate than during isoflurane anesthesia, suggesting a lower degree of myocardial depression than observed with other halogenated agents.lo3The ability to titrate rapidly the concentration of desflurane in the face of changing hemodynamic conditions in the trauma patient may provide a significant advantage. Irrespective of the volatile anesthetic chosen for the trauma patient, reduced doses of these agents may be all that is tolerated. The use of other amnestic substances may be advisable. Nitrous oxide administered to normovolemic humans produces minimal cardiovascular changes through a balance between mild sympathetic stimulation and direct myocardial depression. In hypovolemic swine, nitrous oxide causes physiologically significant hernodynamic and metabolic deterioration similar to that induced by equipotent doses of halothane.lol Nitrous oxide carries the well-known risk of causing volume or pressure increases in enclosed airspaces such as the pneumothorax, pneumomediastinum, pneumencephalos, and intestine. Finally, it may be unwise to use nitrous oxide and decrease the fraction of

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inspired oxygen when caring for patients whose pulmonary function is rapidly deteriorating. There are few, if any, indications for the use of nitrous oxide in the patient with multiple traumas. If IV or inhaled anesthetic agents cannot be administered, amnesia can often be achieved by using various agents, such as benzodiazepines, low-dose ketamine, neuroleptics, and central anticholinergic drugs. Benzodiazepines administered in low doses can induce amnesia with relatively little hemodynamic compromise, although these drugs have not been studied in the setting of trauma and hemorrhage in humans6,72, 86, 87, lo7 In general, benzodiazepines cause a dose-related myocardial depression, a fall in blood pressure, and a decrease in peripheral resistance, but these are minimal in healthy, normovolemic individuals. The least researched and probably best suited amnestic for the unstable trauma patient is scopolamine. Frequently used for anesthetic premedication, it is a powerful amnestic in doses of 5 to 10 pg/kg. Its cardiac effects can range from negative chronotropy to a transient increase in heart rate, usually limited to 30 minutes.I3 In one study, its use as an amnestic for induction of anesthesia with sufentanil for coronary revascularization was associated with higher increases in blood pressure and heart rate after laryngoscopy compared with lorazepam and sufentanil.14 Scopolamine is used as a model for transient global amnesia.13 Given the half-life of this drug, it should be redosed, if still required, in 4-hour intervals in younger patient^.^ Redosing may not be necessary in older patients because the drug is longer lasting, some patients have a documented anticholinergic hypersensitivity, and others have developed symptoms resembling dementia after administration of scopolamine. Opioids frequently must be withheld until the patient is stabilized and “has a blood pressure.” It should be kept in mind that opioids, although they have minimal cardiovascular effects in the euvolemic patient, can cause a decrease in central sympathetic outflow with concomitant hemodynamic decompensation. Furthermore, opioids have no documented amnestic properties. Opioids do provide excellent analgesia, and most trauma patients do experience severe pain. If inhaled anesthetics are not well tolerated by the patient, an acceptable alternative is to administer small doses of opioids in conjunction with an amnestic agent. Thus, if the patient has recall, it should be for auditory events only, not for pain.

Positioning Traumatized patients will often undergo a variety of procedures while under a single anesthetic. Not only may the anesthetic be prolonged but it may be necessary to turn the patient intraoperatively; in addition, special devices (fracture tables, head holders, splints) may be required to align, expose, or stabilize body parts. As insignificant as

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these facts may appear in the face of life-threatening trauma, serious additional injuries to the patient may result. The patient's spine must be kept straight ("spinal precautions") throughout hospitalization until it has been determined that the entire spine is free of injury. This determination may require a combination of spine radiographs; physical examination of an awake, cooperative, nonmedicated sober patient; or an MR imaging scan of the spine. These studies are done to rule out ligamentous injuries, which can present as serious a risk to the patient as bony injuries but are undetectable on radiographs or CT scans. Despite the need to observe precautions against spinal injury, the transport backboard should be removed before any but the shortest procedures to avoid pressure injuries and skin breakdown. Logrolling, or the use of sliding boards or long rollers, with constant in-line stabilization of the patient's head is advisable. Certain special situations, such as the lateral decubitus position, the placement of head prongs for neurosurgical interventions, or the use of a fracture table, demand the utmost caution by all participants; in addition, the patient should be attended by as many assistants as possible for positioning. The hypoperfusion and anemia of trauma also predispose patients to peripheral nerve injuries incurred by localized pressure points or undue tension on structures such as the axillary plexus, ulnar and median nerves, sciatic nerve, and common peroneal nerve. A high central venous pressure in conjunction with pressure on the globe may lead to blindness. Careful reassessment of adequate padding and positioning is therefore necessary throughout the procedure, even if most of the attention is focused on resuscitation of the patient. Finally, some positions may interfere with the placement or use of invasive catheters or monitors. Prevention of such difficulties requires careful thought and action before positioning. Thermoconservation and Rewarming

Hypothermia is a potentially life-threatening condition for trauma victims. Hypothermia is categorized as mild (33.6-36.5"C), deep (1733.5"C), or profound (4-16.5"C).73A number of factors may contribute to the development of hypothermia after an accident, including environmental exposure, immobilization, infusion of unwarmed fluids,'* and the absence of shivering in severe hypotension.sOThe presence of hypothermia correlates with the trauma severity score, a low systolic blood pressure (< 90 mm Hg), a low base deficit, and the amount of unwarmed fluid administered. One study established a 100% mortality rate for patients undergoing emergency laparotomy who have a core temperature of 32°C or lower (Fig. l).45 The physiologic effects of hypothermia, although beneficial used under elective circumstances in cardiac and neurologic surgery, are life-threatening in trauma and include an increased susceptibility to cardiac dysrhythmias, atrial and ventricular fibrillation, cardiac depression, coagulopathies, central nervous system

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depression, and reduced hepatic and renal organ function. Transthoracic defibrillation is frequently impossible at temperatures below 30°C. Vital signs are difficult to establish at temperatures below 27°C because of cardioplegia and central nervous system d e p r e s ~ i o n . ~ ~ Various strategies have been suggested for rewarming the patient and preventing hypothermia. These strategies include minimizing exposure to the environment (the E in the mnemonic AMPLE in the ATLS protocol); even though it is a transient necessity for patient evaluation and later positioning. Surface heating via fluid-filled ”warming blankets” or heated air convection blankets may be of some benefit, although the unfavorable surface-to-volume ratio in adults limits their

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effectiveness. Room temperatures below 21°C are associated with the development of hypothermiag5and should therefore be raised as much above this level as technically feasible. Heated humidifiers in anesthesia and ventilator circuits may add significantly to rewarming Gastric, peritoneal, and bladder lavage with warm fluids have been attempted with moderate results and, especially in the case of gastric lavage, may present an increased risk to the patient. Most importantly, IV fluids should be infused through fluid-warming devices. Unwarmed IV fluids and lavage fluids, when used for this purpose, are the most significant sources of thermal loss in the trauma scenario in the operating room." Highly effective invasive methods have been developed to actively rewarm hypothermic patients and include partial venovenous bypass, extracorporeal venous or arterioven~us~~ rewarming, and full cardiopulmonary bypass. These techniques can result in temperature increases of 1°C to 5°C per hour. The effect of hypothermia on surgical blood loss and coagulopathies 30, y4 The enzymatic process of coagulation, the is well doc~mented.~, function of platelets, and the hepatic clearance of fibrinogen split products and other circulating anticoagulants are reduced in hypothermia. Increased transfusion of blood and components, albeit often unsuccessful, may be necessary to manage a coagulopathy under such circumstances. Finally, the hepatic clearance of drugs is reduced in hypothermia. From an anesthetic point of view, muscle relaxants and IV anesthetics may have a prolonged duration of action. In view of the adverse metabolic effects of hypothermia in awake patients (shivering, increased oxygen consumption, and the need for an increased cardiac output and minute ventilation),4*early extubation of a hypothermic patient is usually unwarranted. Volume Replacement and Transfusion

Restoration of intravascular volume, oxygen-carrying capacity, and coagulation factors are among the foremost priorities in the anesthetic management of the critically injured patient. The process of resuscitation is necessarily a combined effort in which the underlying condition (e.g., cessation of hemorrhage) is expeditiously addressed while its pathophysiologic consequences (e.g., fluid infusion) are treated. Fluid resuscitation must be preceded by an in-depth assessment of the patient's hemodynamic status, the pathophysiology at hand, and the pertinent laboratory data. In the course of a preoperative physical examination, assessment should include the patient's mental status (as an indicator of cerebral perfusion, hypoxia, head injury, or intoxication), color (especially of the gingiva, conjunctival sac, or nailbeds as a sign of anemia), and the presence of peripheral pulses (as a sign of vasoconstriction or "centralization" of blood volume). Chest auscultation can help

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to rule out pericardial tamponade or a significant pneumothorax, both of which can critically interfere with cardiac output. Bulging neck veins may also suggest pericardial tamponade, fulminant right heart failure, or a traumatic ventricular septa1 defect. Gathering hemodynamic data, information on fluid requirements, and data on urine output before the patient arrives in the emergency room help to complete the picture. Securing adequate intravascular access and invasive monitoring is a high priority. Short, large-bore, peripheral IV cannulas allow higher flow rates than most central venous catheters (with the notable exception of 8.5 F introducer cannulas). The anatomic site of IV access is equally important. Volume infused into lower-extremity veins may extravasate into the abdomen if the patient has abdominal vascular trauma; cannulation of a vein in an extremity with bony injuries may add to the risk of a compartment syndrome. Double cannulation of a single central vein, following the technique described by Fabian et al,29is possible without serious compromise of venous drainage. The speed of infusion or transfusion necessary to stabilize a victim in hemorrhagic shock often requires active pumping of fluids. To free the anesthesiologist’s hands, a number of devices have been marketed, ranging from simple pressure bags to roller-pump-operated rapid infusion systems. Obviously, the expense of disposable materials and the need for trained operators increase with the technical complexity of the system involved. Whereas simple pressure bags require no special tubing and can be operated by anyone, as long as care is taken not to press air out of containers into the patient, they require constant attention and are time consuming to deflate, load, and reinflate. Commercial systems with hard-shell, hinge-operated compression chambers connected to a pressurized air outlet allow much faster delivery of fluids. Devices such as the Level One, which combine the technology of pressure-infusion devices with countercurrent heated-water cartridge heat exchangers, significantly aid in the prevention and treatment of hypothermia. If the previously mentioned rapid transfusion systems are combined with a cardiotomy reservoir and the roller pump of an extracorporeal circulation device, infusion rates as high as 1000 mL/min are attainable. The ability to infuse warmed fluids efficiently and rapidly is far greater with these sophisticated devices than with older standard “blood warmers.” (Fig. 2).93 In most cases, clear fluids should constitute the mainstay of fluid resuscitation in trauma. The question of whether to use crystalloid, as opposed to colloid solutions remains unsettled. A recent meta-analysis of the subject demonstrated slightly better survival of acutely traumatized patients with the use of crystalloid ~olutions,9~ but the decision to employ either crystalloids or colloids clearly must be individualized. A significant capillary leak frequently develops after trauma. This process of ”third-spacing” may not only compromise the patient’s hemodynamic status through loss of intravascular volume but may also increase lung water, decrease lung compliance and impair pulmonary function. Recently this problem has been approached by vigorously

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using blood products and crystalloid solutions in combination with continuous infusion of inotropic drugs to maximize cardiac output and oxygen delivery to supranormal levels.7yThe effectiveness of this regimen in reducing mortality and morbidity has been q~estioned.~’

SUMMARY Considerations regarding the anesthetic management of the traumatized patient cannot be limited to simple airway management and the administration of anesthetic drugs. The induction of anesthesia must be

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preceded, within the constraints of time, by assessment of the patient’s airway and breathing (whether the patient is intubated or not), the circulatory status (including a briefing on fluid requirements and hemodynamics before arrival in the hospital), and assessment of the patient’s neurologic status. If possible, the medical history, including allergies and medications, should be elicited. Without interruption of resuscitation, the patient’s airway should be secured while protecting the patient’s spine and minimizing the risk of pulmonary aspiration of gastric contents. Inhaled and IV anesthetic agents might not be tolerated by the patient because of hemodynamic instability, thus narrowing the selection of drugs to amnestics, perhaps low doses of opioids, plus muscle relaxants. Pregnant patients beyond the 20th week of gestation should receive electronic fetal monitoring for at least 6 hours and otherwise receive any drug or treatment, including radiographic studies, indicated. Despite the presence of hypotension, hypothermia, and acidosis or the use of low doses of anesthetics or amnestic agents, there is a substantial risk for recall in severely traumatized patients. Spinal precautions, accessibility of lines, and avoidance of pressure points are important considerations for positioning. Hypothermia must be avoided or vigorously treated by all modalities available. Frequent assessment of the patient’s volume status as indicated by invasive monitoring, the establishment of sufficient IV access, and use of efficient rapid infusion and warming devices establish the framework for resuscitation of the patient with blood, crystalloid, or colloid, guided by frequent laboratory studies of blood coagulation and arterial blood gases.

References 1. ACOG (American College of Obstetrics and Gynecology): Trauma during pregnancy. ACOG Technical Bulletin 161-Nov 1991. Int J Gynecol Obstet 40165-170, 1993 2. Alexander RH, Proctor HJ (eds): Initial assessment and management. In Advanced Trauma Life Support, ed. 5. Chicago, American College of Surgeons, 1993, pp 17-37 3. Ardila A, Morena C: Scopolamine intoxication as a model of global transient amnesia. Brain Cogn 15:236-245, 1991 4. Azari DM, Cork RC: Comparative myocardial depressive effects of propofol and thiopental. Anesth Analg 77:324-329, 1993 5. Batjer HH: Cerebral protective effects of etomidate: Experimental and clinical aspects. Cereb Brain Metab Rev 5:17-32, 1993 6. Benson KT, Tomlinson DL, Goto H Cardiovascular effects during sufentanil anesthesia. Anesth Analg 67996-998, 1988 7. Bernabei AF, Levison MA, Bender JS. The effects of hypothermia and injury severity on blood loss during trauma laparotomy. J Trauma 33:835-839, 1992 8. Berry JM, Merin RG: Etomidate myoclonus and the open globe. Anesth Analg 69:256259, 1989 9. Berthoud MC, Peacock JE, Reilly CS: Effectiveness of preoxygenation in morbidly obese patients. Br J Anaesth 767464466, 1991 10. Bogetz MS, Katz J A Recall of surgery for major trauma. Anesthesiology 61:6-9, 1984 11. Boyan CP: Cold or warmed blood for massive transfusions. Ann Surg 160:282-284, 1963 12. Brookoff D, Campbell E, Shaw L The underreporting of cocaine related trauma:

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35. George ER, Vanderkwaak T, Scholten DJ: Factors influencing pregnancy outcome after trauma. Am Surg 58:594-598, 1992 36. Ginsberg 8, Glass PS, Shafron D, et a1 Onset and duration of neuromuscular blockade following high dose vecuronium administration. Anesthesiology 71:201-205, 1989 37. Goldrick KE: The open globe: is an alternative to succinylcholine necessary? J Clin Anesth 5:14, 1993 38. Gooding JM, Corssen G: Effect of etomidate on the cardiovascular system. Anesth Analg 56:717-719, 1977 39. Halford FJ: A critique of intravenous anesthesia in war surgery. Anesthesiology 4:6749, 1943 40. Haljamae H: The physiology of shock. Acta Anaesthesiol Scand 373-6, 1993 41. Hayes MA, Timmins AC, Yau EHS, et al: Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 330:1717-1722, 1994 42. Hemingway A: Shivering. Physiol Rev 43397-422, 1963 43. Jackimczyk K Blunt chest trauma. Emerg Med Clin North Am 11:81-96, 1993 44. Jones DR, Hill RC, Vasilakis A, et a1 The successful resuscitation of a hypothermic multitrauma patient. WV Med J 87298-301, 1991 45. Jurkowich GJ, Geiser WB, Luterman A: Hypothermia in trauma victims: an ominous predictor of survival. 1 Trauma 271019-1024, 1987 46. Kammerer W S Nonobstetric surgery during pregnancy. Med Clin North Am 63:11571164, 1979 47. Kaneko S, Otani K, Fukushima Y, et al: Teratogenicity of antiepileptic drugs: Analysis of possible risk factors. Epilepsia 29:459467, 1988 48. Kashimoto S, Doursout MF, Hartley C, et al: Effects of thiopental and ketamine on cardiac function during moderate hemorrhage in chronically instrumented rats. J Cardiovasc Pharmacol 21:829-833, 1993 49. Keller ML, Watson TR Polarographic study of arterial oxygenation during apnea in man. N Engl J Med 264:32&330, 1961 50. Kelly RE, Dinner M, Turner LS, et al: Succinylcholine increases intraocular pressure in the human eye with the extraocular muscles detached. Anesthesiology 79:948952, 1993 51. Knox JWD, Bovill JG, Clarke RSJ, et al: Clinical studies of induction agents XXXVI: Ketamine. Br J Anaesth 42:875-885, 1970 52. Koller Me, Husby P: High dose vecuronium may be an alternative to suxamethonium for rapid sequence intubation. Acta Anesthesiol Scand 37465468, 1993 53. Kung MC, Hung CT, Ng KP, et al: Arterial desaturation during induction in healthy adults: Should preoxygenation be a routine. Anaesth Intensive Care 19:192-196, 1991 54. Libonati MM, Leahy JJ, Ellison N: The use of succinylcholine in open eye surgery. Anesthesiology 62637440, 1985 55. Ligier B, Buchman TG, Breslow MJ, et al: The role of anesthetic induction agents and neuromuscular blockade in the endotracheal intubation of trauma victims. Surg Gynecol Obstet 173:477481, 1991 56. Magorian T, Flannery KB, Miller R D Comparison of rocuronium, succinylcholine an vecuronium for rapid sequence induction of anesthesia in adult patients. Anesthesiology 79~913-918, 1993 57. Mazze RI, Kallen B: Reproductive outcome after anesthesia and operation during pregnancy: a registry study of 405 cases. Am J Obstet Gynecol 161:1178-1185, 1989 58. Minard G, Kudsk KA, Croce MA, et al: Laryngotracheal trauma. Am Surg 58:181187, 1992 59. Mirakhur RK: Newer neuromuscular blocking drugs. Drugs 44:182-199, 1992 60. Moore MA, Weiskopf RB, Eger EL, et al: Arrhythmogenic doses of epinephrine are similar during desflurane or isoflurane anesthesia in humans. Anesthesiology 79:943-947, 1993 61. Morris JA, MacKenzie EJ, Edelstein SL: The effect of preexisting conditions on mortality in trauma patients. JAMA 263:1942-1946, 1990 62. Murphy DF: Anesthesia and intraocular pressure. Anesth Analg 64:520-530, 1985 63. Oats JN, Vasey DP, Waldron BA: Effects of ketamine on the pregnant uterus. Br J Anaesth 51:1163-1166, 1979

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64. Page1 PS, Kampine JP, Schmeling WT, et al: Ketamine depresses myocardial contractility as evaluated by the preload recruitable stroke work relationship in chronically instrumented dogs with autonomic nervous system blockade. Anesthesiology 76:564572, 1992 65. Park WK, Lynch C: Propofol and thiopental depression of myocardial contractility: a comparative study of mechanical and electrophysiologic effects in isolated guinea pig ventricular muscle. Anesth Analg 74395405, 1992 66. Pascoe PJ, Ilkiw JE, Haskins SC: Cardiopulmonary effects of etomidate in hypovolemic dogs. Am J Vet Res 53:2178-2182, 1992 67. Pavlin EG: Ethanol and substance abuse in trauma patients. In Grande CM (ed): Textbook of Trauma Anesthesia and Critical Care. St Louis, Mosby 1993, pp 744-752 68. Pensado A, Molins N, Alvarez J: Effects of propofol on mean arterial pressure and systemic vascular resistance during cardiopulmonary bypass. Acta Anaesthesiol Scand 37498-501, 1993 69. Pimentel L. Mother and child: trauma in pregnancy. Emerg Med Clin North Am 9:549-563, 1991 70. Piper JM, Baum C, Kennedy DL, et al: Maternal use of prescribed drugs associated with recognized fetal adverse drug reactions. Am J Obstet Gynecol 159:1173-1176, 1988 71. Plaisier BR, McCarthy MC, Canal DF: Autotransfusion in trauma: A comparison of two systems. Am Surg 58:562-566, 1992 72. Raza SMA, Masters RW, Zsigmaond EK. Comparison of the hemodynamic effects of midazolam and diazepam in patients with coronary occlusion. Int J Clin Pharmacol Ther Toxicol 271-6, 1989 73. Reitz B, Ream A: Use of hypothermia in cardiovascular surgery. In Ream A, Fogdall RP (eds): Acute Cardiovascular Management: Anesthesia and Intensive Care. Philadelphia, JB Lippincott, 1982, pp 830-851 74. Restall J, Tully AM, Ward PJ, et al: Forum: total intravenous anaesthesia for military surgery. A technique using ketamine, midazolam and vecuronium. Anaesthesia 43:4649, 1988 75. Salem MR, Sellick BA, Elam J O The historical background of cricoid pressure in anesthesia and resuscitation. Anesth Analg 53230-232, 1974 76. Schaefer SD: The acute management of external laryngeal trauma: A 27 year experience. Arch Otolaryngol Head Neck Surg 118:598404, 1992 77. Sebel PS, Lowdon JD: Propofol: a new intravenous anesthetic. Anesthesiology 71:260277, 1989 78. Sellick BA: Contents during induction of anaesthesia. Lancet 2:404406, 1961 79. Shoemaker WC, Appel PL, Kram HB: Oxygen transport measurements to evaluate tissue perfusion and titrate therapy: dobutamine and dopamine effects. Crit Care Med 19:672-688, 1991 80. Sori AJ, El-Assuooty A, Rush BF: The effect of temperature on survival in hemorrhagic shock. Am Surg 53706-710, 1987. 81. Stanski DR Recall and wakefulness. In Miller RD, (ed): Anesthesia, ed 3. New York, Churchill Livingstone, 1990, 1004 82. Steffey EP, Eger EI: The effect of seven vasopressors on halothane MAC in dogs. Br J Anaesth 47435438, 1975 83. Steier M, Ching N, Roberts B, et a1 Pneumothorax complicating continuous ventilatory support. J Thorac Cardiovasc Surg 6717-23, 1974 84. Steinemann S, Shackford SR, Davis JW: Implications of admission hypothermia in trauma patients. J Trauma 30:200-201, 1990 85. Stone DR, Downs JB, Paul WL, et al: Adult body temperature and heated humidification of anesthetic gases during general anesthesia. Anesth Analg 60:736-741, 1981 86. Stowe DF, Bosnjak ZJ, Kampine JP: Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts. Anesth Analg 74~547-558,1992 87. Sunzel M, Paalzow L, Berggren L, et al: Respiratory and cardiovascular effects in relation to plasma levels of midazolam and diazepam. Br J Clin Pharmacol 25:561569, 1988

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88. Takeshita H, Okuda Y, Sari A: The effects of ketamine on cerebral circulation and metabolism in man. Anesthesiology 36:69-75, 1972 89. Tarantino DP, Bernhard W N Anesthetic considerations in thoracic trauma. Semin Thorac Cardiovasc Surg 4:187-194, 1992 90. Taylor RW, Dellinger RP: Preexisting medical problems in the trauma patient: Do they matter? Int Anesthesiol Clin 25:1143-1161, 1987 91. Traber DL, Wilson RD: Involvement of the sympathetic nervous system in the pressor response to ketamine. Anesth Analg 48248-252, 1966 92. Traber DL, Wilson RD, Priano LL: Differentiation of the cardiovascular effects of CI581. Anesth Analg 47:769-778, 1968 93. Uhl L, Pacini D, Kruskall MS: A comparative study of blood warmer performance. Anesthesiology 771022-1028, 1992 94. Valeri CR, Feingold H, Cassidy G, et al: Hypothermia induced platelet dysfunction. Ann Surg 205:175-181, 1987 95. Vanner RG, Pryle BJ: Regurgitation and oesophageal rupture with cricoid pressure: A cadaver study. Anaesthesia 47:732-735, 1992 96. Vanner RG, Pryle BJ: Nasogastric tubes and cricoid pressure. Anaesthesia 48:11121113, 1993 97. Velanovich V: Crystalloid vs colloid fluid resuscitation: A meta-analysis of mortality. Surgery 105:65-70, 1989 98. Wagner RL, White PF, Kan PB, et al: Inhibition of adrenal steroidogenesis by the anesthetic etomidate. N Engl J Med 310:1415-1421, 1984 99. Wang ML, Seiff SR, Drasner K: A comparison of visual outcome in open globe rcpair: Succinylcholine with d-tubocurarine vs nondepolarizing agents. Ophthalmic Surg 23:746-751, 1992 100. Weiskopf RB, Bogetz MS: Haemorrhage decreases the anaesthetic requirement for ketamine and thiopentone in the pig. Br J Anaesth 571022-1025, 1985 101. Weiskopf RB, Bogetz MS: Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine. Anesthesiology 63:509-516, 1985 102. Weiskopf RB, Bogetz MS, Roizen MF, et al: Cardiovascular and metabolic sequelae of inducing anesthesia with ketamine or thiopental in hypovolemic swine. Anesthesiology 60:214-219, 1984 103. Weiskopf RB, Cahalan MK, Eger EI, et al: Cardiovascular actions of desflurane in normocarbic volunteers. Anesth Analg 73:143-156, 1991 104. Weiskopf RB, Townsley MI, Riordan KK, et al: Comparison of cardiopulmonary responses to graded hemorrhage during enflurane, halothane, isoflurane and ketamine anesthesia. Anesth Analg 60:481-491, 1981 105. White PF: Comparative evaluation of intravenous agents for rapid sequence induction-thiopental, ketamine, and midazolam. Anesthesiology 57279-284, 1982 106. White PF, Way WL, Trevor AJ: Ketamine-its pharmacology and therapeutic uses. Anesthesiology 56:119-136, 1982 107. Wierda JMKH, Maestrone E, Bencini AF, et al: Haemodynamic effects of vecuronium. Br J Anaesth 62194-198, 1989 Address reprint requests to Niels N. Chapman, MD 2211 Lomas NE Albuquerque, NM 87131