Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

CHAPTER 17 – Trauma and Acute Care

Richard P. Dutton, MD, MBA,
Thomas E. Grissom, MD



Basic Considerations



Team Organization and Multi-trauma Priorities



Airway Management



Fluid Resuscitation



Specific Conditions



Traumatic Brain Injury



Spinal Cord Injury



Ocular Trauma



Complex Facial Injuries



Penetrating Trauma



Traumatic Aortic Injury



Orthopedic Injuries



Near Drowning



Smoke Inhalation and Carbon Monoxide Poisoning



The Pregnant Trauma Patient



Geriatric Trauma


Trauma—disruption of anatomy and physiology due to application of external energy—is the leading cause of death in Americans younger than 45 years old and the leading cause of lost years of life.[1]Anesthesiologists see trauma patients in the emergency department (ED), in the operating room (OR), in the intensive care unit (ICU), and in the pain clinic. Specialists in trauma anesthesia are rare, but every anesthesiologist will see trauma patients at times and must be aware of the specific medical issues associated with this challenging population. This chapter begins with an overview of issues common to most trauma patients—team organization, multi-trauma priorities, emergency airway management, and fluid resuscitation—and then presents a discussion of specific types of patients and injuries.

Team Organization and Multi-Trauma Priorities

Trauma care is a team sport, where outcomes depend as much on the coordination of services as on the quality of each individual practitioner. A number of studies have shown that the more organized and experienced a trauma service is, the better the outcomes it achieves. [2] [3] Practicing anesthesiologists must understand how the local trauma service is organized and how anesthesia personnel are expected to participate.

Trauma is considered a surgical disease, and seriously injured patients are usually managed by a trauma general surgeon. The surgeon will have responsibility for the sequencing of diagnostic and therapeutic procedures and for resource allocation among multiple patients. The anesthesiologist may be involved in initial airway management and hemodynamic resuscitation and will certainly be involved in the timing and extent of any surgery. Close communication with the surgeon is essential to the appropriate allocation of scarce operating room resources. As the gatekeeper to the OR, the anesthesiologist is required to determine how trauma cases will be accommodated in a busy elective schedule. Understanding surgical priorities is essential to this process.

Table 17-1 is an outline of trauma case priorities.[4] Emergent cases must reach the OR as soon as possible. While surgical airway access and resuscitative thoracotomy usually occur in the ED, immediate follow-up in the OR will be necessary if the patient survives. Also considered emergent are any exploratory surgeries (laparotomy or thoracotomy) in a hemodynamically unstable patient and craniotomy in a patient with a depressed or deteriorating mental status. Limb-threatening orthopedic and vascular injuries should undergo surgical exploration as soon as the necessary diagnostic studies have been performed and interpreted. Urgent cases are not immediately life threatening but require surgery as soon as possible to reduce the incidence of subsequent complications. Examples include exploratory laparotomy in stable patients with free abdominal fluid; irrigation, débridement, and initial stabilization of open fractures; and repair of contained rupture of the thoracic aorta. Early fixation of closed fractures, especially spine and long-bone fractures, has been shown to benefit trauma patients by reducing the incidence of subsequent pulmonary complications. Definitive repair within 24 hours is recommended in otherwise stable and non–brain-injured patients. Nonurgent cases are those that can be safely delayed until a scheduled OR time is available. Face, wrist, and ankle fracture fixation are not time dependent: early surgery will shorten the patient's length of stay but may be technically more difficult due to swelling and distortion of the surrounding tissue. These surgeries are commonly postponed and may be undertaken days to weeks after injury, when tissue edema has resolved and the patient's condition is otherwise stable.

TABLE 17-1   -- Surgical Priorities in Trauma Patients




Airway access

Available OR or at bedside

Thoracotomy or laparotomy to control hemorrhage


Evacuation of epidural or subdural hematoma


Perforated viscus

First available OR

Unstable spine with no deficit or a partial deficit


Decompressive craniotomy


Decompressive laparotomy


Fasciotomy or limb salvage procedure

As soon as possible

Open fractures

Next unscheduled OR

Irrigation and débridement of soft tissue wounds


Open globe injury or entrapped ocular muscle


Isolated closed long-bone fracture


Small bone fractures: wrist, ankle, hand, foot

Next scheduled OR

Facial surgery


“Second-look” laparotomy or thoracotomy


Acetabular reconstruction


Fixation of stable spinal fractures


Plastic surgery and wound reconstruction


Repeat irrigation and débridement of open wounds



In addition to facilitating timely surgery in those patients who require it, the anesthesiologist and surgeon working together must often determine the extent of surgery to be permitted. The concept of “damage control” has revolutionized surgical thinking in the past decade, limiting initial therapeutic procedures to those required for hemostasis while delaying reconstructive procedures until adequate resuscitation has been achieved.[5] In a typical example, the surgeon treating an unstable patient with blunt trauma might perform an exploratory laparotomy, rapid splenectomy, staple resection of injured bowel (without attempt at reanastomosis), ligation of bleeding large vessels, and packing of all four abdominal quadrants. The abdomen would be left open under a sterile watertight dressing and the patient taken to the ICU. Angiographic embolization might be used to facilitate hemostasis in the liver and retroperitoneum. After resolution of shock, warming, and normalization of laboratory values, the patient would return to the OR in 24 to 48 hours for débridement of nonviable tissue, reconstruction of the bowel, placement of enteral feeding access, and abdominal closure. The concept of damage control may also be applied to orthopedic injuries: initial external fixation of the pelvis and long bones is adequate for temporary stabilization of fractures, without imposing the additional physiologic burdens of intramedullary nailing or open fixation.[6] While objective indicators of the need for damage control have not been established, this approach should be considered in any patient with persistent hypoperfusion, elevated lactate, or transfusion requirement in excess of one blood volume.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Airway Management

The first priority in the care of any trauma patient is assurance of a patent airway and adequate oxygenation and ventilation.[7] Anesthesiologists are the acknowledged experts for airway management in most hospitals, including those in which trauma patients are managed initially by Emergency Medicine physicians. Whether in the ED or the OR, the ability to swiftly and safely intubate injured patients may be lifesaving.


Indications for intubation of the trauma patient are shown in Table 17-2 . Hypoxemia may be the result of impaired respiratory effort, obstruction of the upper airway, aspiration of blood or gastric contents, mechanical disruption of the chest cavity, or severe hemorrhagic shock. Traumatic brain injury (TBI) and intoxication with alcohol or other drugs contribute to impaired effort, upper airway obstruction, and aspiration, whereas direct trauma to the face, neck, or chest may cause bleeding, anatomic disruption of the airways, or pneumothorax.

TABLE 17-2   -- Indications for Intubation






Traumatic brain injury






Medication effect






Pulmonary injury












Cardiac contusion/ischemia with pulmonary edema



Neurologic injury with decreased cough or respiratory effort



Carbon monoxide poisoning



Airway Obstruction



Traumatic brain injury






Upper airway injury or hemorrhage



Airway burn



Need for Anesthesia



Painful injuries



Urgent surgical procedures



Combative or uncooperative patient



Ventilatory failure is common in trauma patients, both at initial presentation and in the days immediately following. Pulmonary contusion, with subsequent consolidation of alveolar space, may take hours to develop and may not be obvious until after fluid resuscitation and initial surgeries have been completed. Ventilatory failure may also be due to exacerbation of underlying chronic cardiac or pulmonary disease or to pulmonary embolus (PE). Trauma patients are at very high risk for PE, and this condition should be suspected in any patient with an abrupt decline in respiratory status. Multiply injured patients are likely to develop the systemic inflammatory response syndrome (SIRS), manifested by progressive respiratory compromise, recurrent sepsis, and multiple organ system failure.

All trauma patients are considered to have full stomachs, both because obtaining an accurate history in the injured patient is difficult and because trauma itself will lead to an immediate cessation of gastrointestinal motility, with ileus persisting for hours to days after injury.[8] Trauma patients are also at risk for aspiration of blood from open fractures or penetrating wounds of the face. Impaired mental status due to TBI or intoxication makes aspiration more likely, particularly when combined with the use of sedative or analgesic drugs given to facilitate diagnostic procedures (such as computed tomography [CT]) or minor surgical procedures (such as reducing a fracture or suturing a laceration).

Impairment of mental status is also the leading cause of combative or uncooperative behavior. Although it may be possible through history taking and physical examination to determine which patients have suffered a TBI and which are simply intoxicated, the similarities between the two conditions make absolute knowledge impossible before CT. Successful treatment of TBI is highly time dependent, meaning that the patient with impaired mental status must be treated as if an epidural hematoma is present, until proven otherwise.


Assessment of the patient before airway management is no different than assessment of an elective surgery patient, but it must be adjusted for the urgency of the situation. A thorough history and physical examination of the face, neck, and chest is appropriate when possible. Any suggestion that intubation will be difficult should suggest the need for additional equipment or personnel and a modification of the usual rapid-sequence protocol. When the urgency of the situation does not allow for a thorough assessment, the anesthesiologist must gather what information is immediately available from other providers and a quick look at the patient and then proceed as necessary. Factors predicting a difficult airway are summarized in Table 17-3 , in approximate order of importance.

TABLE 17-3   -- Factors Predicting a Difficult Intubation



Emergency setting



Presence of hypoxemia



Prior history of a difficult intubation (may be noted on a Medic-Alert bracelet)






History of sleep apnea



Presence of a cervical collar and backboard



Soft tissue injury to the neck or face



Known cervical spine injury (possibility of prevertebral edema)



Limited mouth opening



Limited neck extension (ankylosing spondylitis, previous cervical fusion)



Upper airway hemorrhage



Tongue injury



Foreign bodies in the airway



Previous attempts at intubation



The need for intubation in the combative or uncooperative patient is controversial, and the provider must carefully assess the risks and benefits of intervention. On the one hand, induction of anesthesia will allow for immediate diagnostic studies, and thus more rapid identification of life-threatening conditions such as epidural hematoma or splenic rupture. Induction and intubation may also prevent the patient from injuring himself or others and allow for deeper and safer levels of sedation during diagnostic studies. On the other hand, induction can precipitate hemodynamic instability and technical complications of rapid sequence intubation may be difficult to justify in the uninjured patient. Early intubation, diagnostic imaging, and rapid extubation of the intoxicated patient without significant trauma are possible in some settings but a substantial economic burden in others. Ultimately, the trauma team, including the anesthesiologist, must evaluate the potential for life-threatening trauma, the patient's ability to tolerate CT (with or without additional sedation), and the likely ease of intubation when deciding how to proceed with this sort of patient. No matter what course is elected, close monitoring of the patient's neurologic status and respiratory effort is required.

Preoperative Preparation.

Sufficient trained personnel must be on hand to physically manage the airway, administer induction drugs, provide cricoid pressure, and stabilize the cervical spine. The anesthesiologist must coordinate this process and must ensure that all participants are clear on their roles. When appropriate, the plan of care should be discussed with the patient and family ahead of time and any questions answered. Preoxygenation with a tight-fitting face mask (if tolerated) or assisted bag-valve-mask ventilation should be provided while preparations are underway. A high-flow suction device should be immediately available. All necessary intubating equipment, including emergency medications, should be close at hand and in good working order. Figure 17-1 is a picture of the trauma resuscitation unit intubating box used at the R. Adams Cowley Shock Trauma Center, provided as an example.


FIGURE 17-1  A typical intubation box, with its contents. Everything required for immediate emergent intubation is available, including a laryngoscope handle and blades, endotracheal tubes, an intubating stylet, a carbon dioxide detector, and prefilled syringes of sodium thiopental, succinylcholine, and lidocaine.



Patient positioning can greatly facilitate intubation and is often overlooked in the emergent situation. The bed or stretcher should be placed at a convenient height for the anesthesiologist and enough space provided at the head of the bed to allow room for unhindered motion. Ergonomic design of the trauma bay has been shown to improve the process of emergency intubation.[9]

The presence of cervical spine instability will be a possibility in most trauma victims requiring emergent intubation, because the exclusion of this condition requires a conscious, cooperative, pain-free patient who has undergone a number of diagnostic studies (see later). The traditional “sniffing position” is thus contraindicated, whereas the presence of a rigid cervical collar and the maintenance of in-line cervical stabilization also contribute to the difficulty of intubation.[10] Whereas some have advocated the routine use of fiberoptic intubation for all trauma patients with the potential for cervical instability, this approach is time and resource intensive. Direct laryngoscopy with manual in-line stabilization is unlikely to aggravate an existing cervical spine injury and has been judged safe and appropriate for the majority of trauma patients.[11]

Preprocedure preparation should include the availability of a device to facilitate intubation of an anterior larynx (e.g., a trigger tube or gum elastic bougie), rescue devices for impossible intubation (e.g., the laryngeal mask airway or Combitube), and an understanding of when cervical spine protection should be abandoned in favor of achieving a successful intubation. The likelihood of an anterior larynx argues for the routine use of a stylet in the endotracheal tube. Capnometry should be available to confirm endotracheal placement of the tube and adequacy of ventilation. Equipment should also be on hand for emergent cricothyroidotomy in the worst case.

Intraoperative Considerations.

A rapid-sequence intubation (RSI) technique is recommended, with the use of cricoid pressure from induction until confirmation of endotracheal tube placement. Although the consistency with which the Sellick maneuver prevents the aspiration of gastric contents has been called into question,[12] cricoid pressure is also beneficial in moving the larynx into a more posterior position, thus facilitating the laryngoscopic view of the vocal cords. If excessive pressure is distorting airway anatomy or preventing passage of the endotracheal tube, then it should be abandoned. Aspiration is unlikely during direct visualization of the airway, with a suction catheter immediately at hand.

Advantages and disadvantages of various induction drugs are shown in Table 17-4 . While agents that lack a negative inotropic effect (e.g., ketamine or etomidate) are more likely to preserve cardiovascular function in the euvolemic patient, any induction drug—and even the change to positive-pressure ventilation alone—can precipitate hemodynamic instability in the patient in shock. This is because the hypovolemic patient is relying on a high serum level of catecholamines to support the blood pressure. Any sedative or analgesic agent may impair the adrenal response to hemorrhage and “unmask” hypovolemia. Because internal hemorrhage may not be readily apparent at the time of induction, and because vital signs are only a crude indicator of fluid volume status, care should be used with any anesthetic agent. The use of smaller than normal doses, with titration against the patient's response, is recommended.

TABLE 17-4   -- Medications Used During Emergency Airway Management




Sodium thiopental


Fast, inexpensive, negative inotrope and vasodilator



Fast, expensive, fewer cardiovascular effects, may cause transient myoclonus



Fast, expensive, easily titrated, negative inotrope and vasodilator



Fast, inexpensive, positive inotrope, may cause “bad dreams” or dysphoric reactions



Blunts airway reactivity, negative inotrope



Expensive, slower onset, negative inotrope and vasodilator, may cause retrograde amnesia



Blunts airway reactivity, does not produce amnesia



Slower onset and longer half-life than fentanyl, may cause histamine release, has a euphoric effect



Most rapid onset, produces fasciculations, will cause potassium release in vulnerable patients (burns, spinal cord injury)



Slower onset and longer duration, no hemodynamic side effects



Intermediate onset and duration, but less predictable than vecuronium, no hemodynamic side effects

Note that any sedative or analgesic medication will reduce the endogenous catechol response and may precipitate hemodynamic instability.




Succinylcholine is the standard paralytic agent for rapid-sequence intubation and is recommended in the absence of obvious contraindications (previous neuromuscular disease, known or suspected hyperkalemia, burn or spinal cord deficit occurring more than 24 hours previously). High doses of rocuronium or vecuronium can be used in place of succinylcholine and will provide adequate intubating conditions in the majority of cases, at the cost of prolonged paralysis thereafter.

The administration of positive-pressure breaths by bag-valve-mask during RSI is controversial. In routine OR cases, in which RSI is undertaken in a cooperative, preoxygenated patient in a good sniffing position, positive-pressure ventilation is avoided because of concern that it will distend the stomach and increase the likelihood of aspiration. In the emergent setting, however, ventilation throughout RSI should be strongly considered. Preoxygenation may be difficult in the combative patient, anatomic positioning is not optimal, and even transient hypoxemia is dangerous to the patient with TBI or hemorrhagic shock. In the not-uncommon situation that the anesthesiologist is supervising a less skilled provider, the provision of a positive-pressure breath of 100% oxygen before laryngoscopy will allow for a longer and safer intubation effort.

With trained providers, RSI of the trauma patient is successful on the first attempt about 90% of the time. In the remaining cases, knowledge of the local difficult airway algorithm becomes essential. Providers vary in their skills, institutions vary in the available equipment, and the time pressure of an emergent intubation makes creative thought difficult, which is why it is incumbent on every anesthesiologist to pre-plan for the steps he or she intends to follow if a given intubation proves challenging. It is assumed that every anesthesiologist is acquainted with the difficult airway algorithm of the American Society of Anesthesiologists (ASA),[13] which should be followed in most cases. The algorithm for emergent intubations is considerably simpler, because waking the patient up is not usually a viable option. Figure 17-2 is the algorithm used at the R. Cowley Shock Trauma Center, as one example.


FIGURE 17-2  The emergency intubation algorithm of the R. Adams Cowley Shock Trauma Center. The algorithm assumes that oxygenation and/or ventilation are already failing and that airway access and mechanical ventilation are absolutely required. BVM, bag-valve-mask ventilation; LMA, laryngeal mask airway.



Successful intubation, by whatever route, must be confirmed by detection of CO2 in exhaled breaths. In areas where intubation and mechanical ventilation are common, such as the ED trauma bay, continuous waveform capnometry is highly recommended. For other areas a disposable CO2 detector should be part of the emergency intubation setup. Patients with no cardiac output may not exhale CO2, even with cardiopulmonary resuscitation in progress. In these cases, successful intubation should be confirmed by direct laryngoscopic inspection or by observation of lung motion if the chest has been opened.

After confirmation of successful intubation, the anesthesiologist is responsible for assessment of hemodynamic stability after induction, for initial ventilator settings, and for ongoing sedation and analgesia. Undesired patient awareness during mechanical ventilation is a significant problem in most EDs, particularly when paralytic agents are used to facilitate diagnostic studies or minor procedures. Even if not directly involved in this phase of care, the anesthesiologist can contribute substantially to the recognition of this problem and to the education of nursing and medical personnel.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Fluid Resuscitation

Airway and breathing are the first priorities in trauma care, followed closely by assessment of the circulation—the ABCs.[7] The anesthesiologist may share responsibility for hemodynamic management in the ED with other members of the trauma team, but in the OR this becomes a primary task.


Tissue injury causes disruption of blood vessels, and hemorrhage is a hallmark of trauma. While bleeding associated with some injuries stops spontaneously, in other cases active intervention is required to prevent exsanguination. Life-threatening hemorrhage occurs into one of five compartments, summarized in Table 17-5 .[4] Trauma is a surgical disease because early diagnosis and treatment of ongoing hemorrhage are essential. What is less obvious, but equally true, is the importance of nonsurgical hemorrhage control and ongoing resuscitation.

TABLE 17-5   -- Sites of Exsanguinating Hemorrhage: Diagnostic and Therapeutic Options


Diagnostic Mechanism

Therapeutic Options



Tube thoracostomy


Chest radiograph

Exploratory thoracotomy






Nonoperative management



Angiographic embolization



Exploratory laparotomy



Pelvic stabilization



Angiographic embolization

Thigh or thighs

Physical examination

Fracture reduction



Fracture fixation



Vascular exploration

“The street” (outside the body)

Physical examination

Direct pressure


Paramedic report

Surgical closure

CT, computed tomography; FAST, focused assessment by sonography for trauma.




Shock is the term used to describe the complex pathophysiology that arises from inadequate systemic oxygen delivery. Symptoms of shock are listed in Table 17-6 . Shock was first described in trauma patients because hemorrhage is a common and obvious cause.[14] Trauma patients may also be in shock from mechanical impairment of blood flow (tension pneumothorax or cardiac tamponade), cardiac dysfunction, spinal cord injury, ingestion of toxins, or a mixture of causes, but hemorrhage is considered to be the source until it is definitively ruled out. Much of the Advanced Trauma Life Support (ATLS) curriculum is devoted to this important diagnostic and therapeutic process.[7] Figure 17-3 is a rough algorithm for management of the trauma patient with active hemorrhage.

TABLE 17-6   -- Symptoms of Shock



Patient Appearance









Prolonged capillary refill



Poor skin turgor



Mental Status



Agitation, then progressive obtundation






Vital Signs



Hypotension (automated devices may be inaccurate)



Narrowed pulse pressure









Diminished or absent pulse oximeter signal



Laboratory Signs



Metabolic acidosis



Elevated serum osmolarity



Elevated serum lactate



Decreased hematocrit (takes time to develop)







FIGURE 17-3  Algorithm for management of active hemorrhage. BP, blood pressure; ABG, arterial blood gases; PRBC, packed red blood cells; FFP, fresh frozen plasma; BE, base excess.



Hemorrhage reduces circulating blood volume, leading to decreased preload and reduced cardiac output. Vasoconstriction and increased inotropy mediated by the sympathetic nervous system allow for continued blood flow to vital organs in the presence of blood loss as severe as 40% of normal intravascular volume (2 of 5 L in a 70-kg male). Acute blood loss in excess of this amount causes a critical reduction of perfusion to the heart and brain, manifesting as coma, pulseless electrical activity, and death. Blood loss less than this amount may also be lethal, because reduced perfusion leads to anaerobic metabolism and accumulation of lactic acid and other toxins. Individual cells react to ischemia by hibernation (reduction of all nonessential activities), apoptosis (“programmed cell death”), or outright necrosis, depending on the organ system in question.[15] Many ischemic cells—especially gut and muscle cells—react to ischemia by absorption of extracellular fluid.[16] The resulting tissue edema is both locally and systemically disruptive by clogging capillary pathways (the no-reflow phenomenon) and further depleting intravascular volume. Ischemic cells also release inflammatory mediators, triggering a chemical cascade that perpetuates the pathophysiology of shock long after adequate circulation is restored ( Fig. 17-4 ).[17] The “dose” of shock absorbed by the body, a summation of the depth of hypoperfusion and its duration, largely determines the patient's clinical outcome, ranging from a mild inflammatory response to organ system failure to death. The typical young male trauma patient has an enormous compensatory reserve and may achieve normal pulse and blood pressure while still significantly fluid depleted and highly vasoconstricted. This phenomenon, known as the occult hypoperfusion syndrome, is associated with a high incidence of organ system failure if not recognized and corrected.[18]


FIGURE 17-4  The shock cascade. A single episode of hypoperfusion can trigger a prolonged systemic response.



Isotonic crystalloid infusion increases preload and produces an immediate increase in cardiac output and blood pressure. Crystalloid therapy is a double-edged sword, however. Increased blood pressure leads to increased bleeding from open vessels and rebleeding from previously hemostatic injuries, due in part to decreased blood viscosity and relaxation of compensatory vasonstriction.[19] Aggressive crystalloid infusion dilutes red cell mass and clotting factor concentration and leads to hypothermia in most prehospital and ED settings. Studies of uncontrolled hemorrhagic shock in rats,[20] swine,[21]sheep,[22] and dogs[23] have all demonstrated improved survival when initial fluid therapy is titrated to a lower than normal systolic blood pressure (70 to 80 mm Hg). This finding is supported by two human trials conducted within the past decade. [24] [25]

Dilution of red cell mass is inevitable during early resuscitation, because losses to hemorrhage are compounded by intravascular recruitment of extracellular fluid and exogenous crystalloid administration. A hematocrit measured soon after hemorrhagic trauma may show little change, because whole blood is being lost and the percentage of red cells in the remaining volume does not change. The longer hemorrhage and resuscitation persist, however, the more the hematocrit will fall. Loss of red cells leads to decreased blood viscosity, allowing for more rapid flow of blood. Below a hematocrit of about 30%, however, this rheologic improvement in blood flow is overbalanced by the decrease in carrying capacity, and tissue oxygen delivery begins to decrease.


The diagnostic characteristics of hemorrhagic shock are listed in Table 17-6 . Control of bleeding is the first priority in treatment, and nothing must interfere with the indicated diagnostic or therapeutic procedures shown in Table 17-5 . Relevant patient physiology is assessed by continuous measurement of vital signs (facilitated by early placement of an arterial pressure catheter) and by immediate and repeated measurement of arterial blood gases, complete blood chemistry, clotting function, and serum lactate determination. Toxicology screening and electrocardiography may help to diagnose underlying intoxication or cardiac disease.

Response to fluid therapy will provide important diagnostic information. Most patients in shock will demonstrate an improvement in vital signs after bolus fluid administration. In those who have achieved spontaneous hemostasis (e.g., those with lung injury or peripheral orthopedic injuries), the improvement in vital signs will be sustained. In those with ongoing hemorrhage (e.g., abdominal visceral trauma, pelvic fracture) the response to fluid will be transient. These are the patients most in need of urgent diagnostic studies and therapeutic procedures. Those patients who do not respond at all to an initial fluid bolus either have a nonhemorrhagic source of shock (e.g., spinal cord injury, cardiac disease) or are bleeding very rapidly.


Resuscitation of the actively hemorrhaging patient requires large-bore, high-flow intravenous access through at least two separate catheters. Warmed intravenous fluids are highly recommended, especially early in resuscitation. Commercial fluid warming technology is highly effective and should be used as commonly (or more so) in the trauma bay as in the operating room. Rapid infusion systems are designed to warm and actively administer large fluid volumes quickly and may be lifesaving in the patient with rapid and uncontrolled hemorrhage.

The ability to rapidly administer uncrossmatched type O blood may be lifesaving. Many trauma center blood banks and emergency departments maintain a supply on hand for just this purpose. Crossmatched blood, plasma, and platelets should be requested at the earliest moment that a massive transfusion seems likely. OR nursing and anesthesia resources should be mobilized to allow for extra personnel to facilitate the early stages of emergency surgery and resuscitation.

Intraoperative Considerations.

Resuscitation must be carried out simultaneously with diagnostic and therapeutic procedures to control hemorrhage, in such a way that tissue perfusion is supported without making bleeding worse. Recent understanding of the potential for rebleeding and dilution has led to a change away from the traditional ATLS approach of rapid crystalloid infusion to one of deliberate, controlled fluid administration, titrated to specific physiologic end points ( Table 17-7 ).

TABLE 17-7   -- Goals for Fluid Resuscitation During Active Hemorrhage

Total Fluids

Adequate to prevent worsening of shock (increasing lactate or base deficit)

Vital Signs

Systolic blood pressure 80–100 mm Hg


Heart rate < 120 beats per minute


Pulse oximeter functioning

Blood Content

Hematocrit 20%-30%; higher if risk factors for ischemic coronary disease


Normal prothrombin and partial thromboplastin time


Platelet count > 50,000/mm3


Normal serum ionized calcium


Core > 35°C

Anesthetic Depth

Fluid therapy to allow appropriate anesthetic and analgesic depth

Overly aggressive resuscitation must be weighed against the risk of exacerbating hemorrhage.




Replacement of red cells is essential to limiting the depth and duration of shock after hemorrhage. Packed red blood cells should be administered early in the resuscitative process, using uncrossmatched type O units if necessary. Adverse reaction to this therapy is extremely unlikely: more than 100,000 units of uncrossmatched blood were administered during the Vietnam War without a single documented case of fatal transfusion reaction, as compared with the nine cases that occurred in the 600,000 crossmatched transfusions.[26] Immediate transfusion of type O blood is sufficiently safe and beneficial that it should be considered for any patient presenting in extremis from hemorrhagic shock. The most appropriate target hematocrit for resuscitation must be individualized on the basis of age, specific injury pattern, preexisting disease, and the potential for further hemorrhage. In previously healthy patients, 20% is an absolute minimum during resuscitation whereas 30% is an appropriate maximum value.

Coagulopathy due to acute consumption of coagulation factors is likely in any patient losing more than a single blood volume (5 L) or receiving more than 10 units of red blood cells.[27] Because coagulopathy is more easily prevented than treated, early administration of plasma to any patient who has lost or will lose this amount of blood is highly recommended. Plasma should be ordered from the blood bank for any patient presenting emergently to the OR with symptoms of acute hemorrhagic shock. A ratio of 1:1 replacement of red cells and plasma is appropriate for any patient who has lost or will lose more than a blood volume but should be guided when possible by both laboratory and clinical assessment. The same is also true of thrombocytopenia. Platelet count will usually remain adequate longer than coagulation factor concentration, and platelet therapy is thus less commonly required than plasma therapy. Transfused platelets have a very short functional life span in the circulation and represent a strong immune stimulus. For these reasons platelet therapy should be reserved for those trauma patients with both a platelet count of less than 50,000/mm3 and clinical evidence of bleeding. Coagulation factor concentrates and cryoprecipitate do not offer a benefit beyond that of plasma infusion in the hemorrhaging trauma patient, unless fluid overload is a significant risk (as in the coagulopathic elderly patient) or the patient is known to have a specific factor deficiency. Use of human factor VIIa may represent an exception to this principle, however, as recent anecdotal reports have described rapid resolution of traumatic coagulopathy after administration of 20 to 100 μg/kg.[28] Because of the expense of this therapy and the lack of prospectively collected safety data in trauma patients, however, it cannot be recommended unless conventional therapy has failed and exsanguination is likely.

Electrolyte abnormalities are common during resuscitation from hemorrhage. Hyperosmolarity may result from alcohol ingestion, dehydration, hypovolemia, or administration of normal saline. Mild hyperglycemia secondary to high circulating catecholamine levels is expected. Neither of these conditions mandates specific treatment during resuscitation, because both will resolve with restoration of adequate intravascular volume. Hyperchloremic metabolic acidosis is a significant risk of over-resuscitation, especially with mildly hypertonic solutions such as normal saline,[29] and can be managed with the titrated addition of hypotonic fluids. Hypocalcemia arises from chelation of circulating calcium by the citrate or adenosine additives found in banked blood products. Intravenous administration of calcium is indicated in patients with low serum ionized calcium levels, particularly in the presence of hemodynamic instability. Serum bicarbonate levels will be lower than normal in the hemorrhaging patient, owing to increased lactic acidosis and impaired renal blood flow. Administration of bicarbonate solutions has been recommended by some to increase systemic pH in very acidotic patients, to enhance the functioning of important protein systems, including coagulation and catecholamine receptors.[30] The clinical utility of this therapy has never been proven, however. Adequate fluid resuscitation remains the primary therapy for restoration of normal acid-base status.

Paradoxically, while early resuscitation has evolved toward less aggressive fluid administration, resuscitation after control of hemorrhage (usually in the ICU) has moved in the opposite direction. Late resuscitation is characterized by the need to completely restore and support perfusion. To do so requires the practitioner to look beyond the vital signs for a more direct measure of tissue perfusion. Placement of invasive monitoring or a transesophageal echocardiographic probe and administration of fluid until the cardiac output is maximized is one approach. Close observation of chemical markers is another. The speed with which serum lactate level normalizes after shock is strongly associated with the risk of death from organ system failure.[31] Those patients who do not show a significant downward trend in lactate after resolution of hemorrhage require more aggressive fluid therapy and closer monitoring.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier


Traumatic Brain Injury

Traumatic brain injury causes at least half of all deaths from trauma.[1] As with hemorrhagic shock, the pathophysiology of TBI consists of both the primary injury, in which tissue is disrupted by mechanical force, and a secondary physiologic response. Because prevention of secondary injury is critical to outcome, the anesthesiologist plays an important role in managing these patients both in the OR and in the ICU.


Traumatic brain injury is classified as mild, moderate, or severe, depending on the Glasgow Coma Scale (GCS) score on admission. Mild TBI (GCS 13 to 15) is the most common. Although mild TBI does not usually necessitate intensive treatment, patients may be significantly debilitated by postconcussive symptoms, including headaches, sleep and memory disturbances, and mood swings.[32] Progression of mild TBI is rare but may be catastrophic.

Moderate TBI (GCS 9 to 12) is more likely to be associated with intracranial lesions that require surgical evacuation. These patients have a higher potential for deterioration and are more susceptible to secondary insult if not carefully managed.

Severe TBI (GCS < 9) is a highly lethal condition, almost always associated with intraparenchymal or intraventricular hemorrhage or evidence of diffuse axonal injury on cranial CT. Patients with severe TBI are usually unable to maintain airway patency and may evidence diminished or absent respiratory drive, with inability to protect the airway from aspiration. Most patients presenting to the OR for surgical treatment will have severe TBI, with elevation of intracranial pressure (ICP) due to hemorrhage (epidural, subdural, or intraparenchymal), edema, or both. Failure to promptly relieve elevated ICP will lead to herniation of brain tissue, loss of brain blood flow, and death. The goal of surgical therapy is the resolution of increased ICP and the control of any active hemorrhage.


The neurologic examination is the most important component of preoperative assessment in the patient with TBI. Recovery from TBI is a gradual process, and the sedative effects of anesthetic medications may be exaggerated, meaning that the trauma patient will seldom improve immediately at the conclusion of cranial decompression. It is important to know when a deterioration has occurred, however, so that follow-up studies and appropriate ICU management can commence.

More controversial is the timing of noncranial surgery in the patient with TBI. Transient hypotension or hypoxemia associated with orthopedic surgery may lead to worsening of neurologic injury, whereas delay in repair of fractures increases the risk of pulmonary complications and sepsis.[33] Although no definitive prospective study has been conducted, more recent retrospective work suggests that early surgery with meticulous anesthetic care does not necessarily worsen TBI.[34]

Preoperative Preparation.

Early intubation of the TBI patient may be required owing to combative or agitated behavior, the need for diagnostic studies before reaching the OR, and the potentially catastrophic consequences of respiratory depression or pulmonary aspiration. In fact, most patients with moderate or severe TBI will present to the OR having been already intubated in the field or ED.

Arterial pressure monitoring is required for any intracranial procedure, because dramatic swings in the blood pressure can occur throughout the case. Large-bore intravenous access is necessary, because blood loss can become excessive, particularly in patients with severe TBI and early onset of coagulopathy. Supplemental medications likely to be needed include mannitol and/or hypertonic saline solution, phenytoin, and thiopental.

Intraoperative Management.

Patients with mild TBI pose few additional anesthetic risks but are more susceptible to the effects of sedative medication. Benzodiazepines should be used with care in the preoperative period. The anesthesiologist should strive to have the patient's sensorium as clear as possible as rapidly as possible after any anesthetic. Any change from the patient's preoperative mental status not attributable to anesthetic drugs is an indication for immediate repeat cranial tomography and neurosurgical reassessment.

The care of patients with moderate TBI consists of serial assessment of neurologic function, with repeat CT at regular intervals. If close monitoring is not possible, owing to the need for general anesthesia or sedating medications, then continuous invasive measurement of cerebral perfusion pressure (CPP) is indicated.[35] An ICP monitor is recommended in any patient with moderate or severe TBI undergoing noncranial surgery likely to last longer than 2 hours.

Patients with severe TBI represent a substantial anesthetic challenge. Early, rapid management focused on restoration of systemic homeostasis and perfusion-directed care of the injured brain is required to produce the best possible outcomes. The occurrence of hypoxemia (PaO2 < 60 mm Hg) or hypotension (systolic blood pressure < 90 mm Hg) in patients with severe TBI is associated with a significant increase in mortality.[36] Management requires a highly skilled facility, close cooperation among providers, and a stepwise implementation of therapies as shown in Figure 17-5 .


FIGURE 17-5  Critical pathway for treatment of cerebral perfusion pressure (CPP) for patients with severe traumatic brain injury. BP, blood pressure; Hct, hematocrit; ICP, intracranial pressure; IVC, intravenous catheter; CT, computed tomography; CSF, cerebrospinal fluid; CBF, cerebral blood flow.



Aggressive restoration of intravascular volume is indicated to maintain intracranial perfusion, especially if associated pulmonary injuries necessitate the use of high mean airway pressures to support oxygenation. Hyperventilation therapy, long a mainstay in the management of patients with TBI, is no longer an appropriate treatment, unless there are signs of imminent herniation. This is because hyperventilation lowers ICP by reduction of blood flow, putting ischemic brain tissue at further risk for necrosis or apoptosis. Hyperventilation is indicated only for those patients who present with strong lateralizing signs who are en route to CT and emergent decompressive surgery.

Patients with severe TBI should be maintained at a mean arterial pressure (MAP) greater than 90 mm Hg until invasive ICP monitoring is instituted and CPP (MAP - ICP) can be directly calculated. Placement of a ventriculostomy allows both continuous monitoring of CPP and therapeutic drainage of cerebrospinal fluid (CSF), and this approach is preferred over other invasive ICP monitors.[37]Current guidelines suggest maintenance of CPP at a minimum of 70 mm Hg at all times. Contrary to practice in the past, the patient with severe TBI should be maintained in a euvolemic state. Fluid resuscitation is the mainstay of therapy, followed by vasoactive infusions as needed. If surgery is indicated, care should be taken with the ventriculostomy drain; both failure of drainage and excessive loss of CSF can occur during transport. Familiarity is also beneficial for the more advanced monitors of jugular bulb and brain tissue oxygenation that are now coming into use.

Positional therapy is used in almost every case of severe TBI. Elevation of the head facilitates venous and CSF drainage from the cranium, lowering ICP and improving CPP as long as the patient is euvolemic. Pulmonary ventilation-perfusion (   ) matching may also improve in this position, making maintenance of cerebral oxygen delivery easier. The patient should be transported to the OR in this position and maintained with the head up during surgery if at all possible.

Analgesics are indicated for treatment of pain arising from coexisting injuries. Sedatives are useful for control of elevated ICP but may make serial examination difficult. Propofol is popular because it offers the most rapid return of neurologic function when discontinued, but the clinician must use this drug cautiously. Large doses of propofol sustained over days to weeks have recently been associated with the development of lethal rhabdomyolysis (the propofol infusion syndrome).[38] The use of sedatives to decrease ICP frequently mandates the use of vasoactive drugs to maintain MAP. Invasive hemodynamic monitoring with a pulmonary artery catheter and frequent assessment of lactate and base deficit may be necessary to maintain an appropriate intravascular volume in the presence of confounding pharmacologic agents and ongoing mechanical ventilation.

Osmotic diuretic agents are common first-line therapy for severe TBI. Mannitol decreases ICP by drawing edema fluid out of brain tissue and into the circulation and may have secondary benefit as a scavenger of free radicals and other harmful inflammatory compounds. Hypertonic saline has a similar osmotic effect and may also act as a beneficial immunologic agent. Use of either drug will lead to increased diuresis, necessitating greater attention to adequate volume replacement so that euvolemia can be maintained. Use of osmotic agents to reduce elevated ICP is usually titrated to a serum osmolarity of 310 to 230 mOsm/L.

Invasive physiologic monitoring, positional therapy, sedation, and osmotic diuresis will be applied to most patients with severe TBI.[35] The next tier of therapy is reserved for the subset of patients with intractable elevations of ICP. A small percentage may respond to barbiturate coma. In addition to lowering the cerebral metabolic rate, barbiturates have been shown to decrease excitatory neurotransmitters.[39] Management of barbiturate coma necessitates exquisite management of intravascular volume, usually requiring a pulmonary artery catheter, and the use of vasoactive and inotropic agents to maintain CPP.

Decompressive craniectomy is a surgical procedure that is gaining popularity in the management of intractable ICP elevations. Relieving pressure by removal of a piece of cranium and use of a dural patch may improve mortality and morbidity in patients who might not otherwise survive.[40] Decompressive laparotomy may also be indicated in patients with severe TBI, if coexisting injuries or vigorous volume infusion have increased intra-abdominal compartment pressure to greater than 20 mm Hg.[41] Elevated abdominal pressure causes elevated intrathoracic pressure, higher ventilator pressures, and increased ICP.

Although vigorous control of fever is an undisputed recommendation, deliberate hypothermia to reduce the cerebral metabolic rate remains controversial[42] and is not currently recommended. Corticosteroid therapy for severe TBI has not been proven beneficial and is now contraindicated owing to the high potential for deleterious side effects. A number of other drugs, monitors, and therapies for severe TBI are under investigation, offering the promise that the next decade will see significant improvement in outcomes from this challenging disease.

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Copyright © 2005 Saunders, An Imprint of Elsevier

Spinal Cord Injury


Spinal cord injury with complete or partial neurologic deficit occurs in approximately 8,000 Americans a year.[43] High energy falls or motor vehicle crashes cause the majority of serious spinal cord injuries. Incomplete deficits—known as “stingers”—commonly resolve within hours to days. Complete deficits represent a total disruption of the spinal cord and are much less likely to improve over time. Cervical spine injuries causing quadriplegia are accompanied by significant hypotension, owing to inappropriate vasodilatation and loss of cardiac inotropy (neurogenic shock). Autonomous functioning of the lower cord will return over days to weeks, with restoration of vascular tone but absence of sensory or motor transmission. Patterns of spinal cord injury are described in Table 17-8 .

TABLE 17-8   -- Types of Spine Fracture



Upper cervical spine (occiput to C2)

Usually fatal; considered to be unstable in survivors; Jefferson, hangman's, and odontoid fractures

Lower cervical spine (C3 to T1)

Flexion with axial loading produces vertebral body compression fractures with possible displacement of fragments; often with ligamentous injury; involvement with posterior elements can cause unilateral or bilateral jumped facets

Thoracic spine (T2-T10)

Flexion-extension injuries most common; with axial loading can produce burst fracture; displacement of fragments into canal frequently associated with complete cord injury secondary to smaller canal

Lumbar spine (T11-L1)

Classified by mechanism-compression fracture with flexion, burst fracture with axial loading, transverse process fracture, flexion-distraction injury, shear injury

Lower lumbar and sacral spine

Uncommon injuries; can occur with hyperflexion and axial loading; longitudinal sacral fracture may have radiculopathy while horizontal fracture is associated with injury to cauda equina

Ligamentous injury without bony injury

Plain radiographs with no evidence of bony injury do not preclude ligamentous injury; may be unstable and produce subsequent neurologic injury




Early intubation is almost universally required for patients with cervical spine fracture and quadriplegia. Ventilatory support is absolutely required for patients with a deficit above C4, who will lack diaphragmatic function. Patients with levels from C4 to C7 are also likely to require early intubation, because of lost chest wall innervation, paradoxical respiratory motion, and the inability to clear secretions. Atelectasis will develop quickly and may lead to rapid, progressive desaturation. Recurrent pneumonia is a common complication that will lead to tracheostomy in half of all patients with complete deficits at the C5 to C7 level.

Preoperative Preparation.

The urgency of surgery to stabilize the spine is determined by the neurologic status of the patient and the anatomic presentation. A patient with a partial deficit and visible impingement of the spinal canal is considered an emergency because of the potential for regaining neurologic function after decompression. Patients with no deficit or complete deficit may require surgical stabilization to facilitate mobilization but are less urgent cases. Surgery is more commonly required for cervical lesions, whereas supportive bracing of the torso is more common for thoracic and lumbar fractures.

Determining cervical spine stability can be difficult, and many trauma patients will present to the OR with a rigid cervical collar still in place. Protocols to rule out instability of the cervical spine are controversial and may vary substantially between centers. These protocols include plain films, CT, flexion-extension radiography, magnetic resonance imaging (MRI), and examination by orthopedic or neurosurgical specialists and may take days to complete.[44] Insistence on definitive clearance of cervical spine injury before proceeding with urgent or semiurgent surgery is not reasonable. The risk of pulmonary complications posed by delaying needed orthopedic procedures greatly outweighs the risk of worsening an unsuspected spine injury during intubation and anesthesia. For lower-risk patients and for patients who are uncooperative or hemodynamically unstable the preferred approach is an RSI with maintenance of manual inline axial stabilization throughout the procedure. The safety record of this approach is impressive.[11]

Intraoperative Management.

For the cooperative patient with a known or highly probable injury (existing deficit, suspicious radiographs, or substantial neck pain), maintaining the patient in a rigid collar or cervical traction while performing an awake fiberoptic intubation is the safest approach. When awake intubation is elected, the nasal route is usually easier. Oral intubation is more challenging technically but will be of greater value if the patient remains intubated postoperatively, because of a lower risk for sinusitis. Blind nasal intubation, transillumination with a lighted stylet, use of an intubating laryngeal mask airway or Bullard laryngoscope, and any of a variety of other instrument systems for indirect laryngoscopy are acceptable. The clinician is advised to use the equipment and techniques that are most familiar. The goal is to achieve tracheal intubation with the least possible motion of the cervical spine, while preserving the ability to assess neurologic function after intubation and patient positioning.

Hemodynamic instability may complicate urgent and emergent spinal surgery. Hypotension from neurogenic shock is characterized by bradycardia due to loss of cardiac accelerator function and unopposed parasympathetic tone but can still be difficult to distinguish from hypotension due to acute hemorrhage. Aggressive fluid administration is indicated, subject to the end points of resuscitation outlined earlier. Once hemorrhage has been ruled out or treated, some data exist that support maintenance of an elevated MAP greater than 85 mm Hg for 7 days after spinal cord injury, although this approach is highly controversial.[45] Fluid administration will help to expand the vascular volume and counter the effects of inappropriate vasodilatation but may produce an added strain on the heart. Any patient with a poor response to initial volume loading, particularly an elderly one, should receive pulmonary artery catheterization to guide subsequent resuscitation.

Almost all patients with a persistent deficit after spinal cord injury will be treated with high doses of methylprednisolone in the days after surgery.[46] Although this therapy is highly controversial, and the expected benefit to most patients is slight, no other alternatives are presently available. Corticosteroid infusions should be continued during operative interventions, and the clinician should be wary of the development of corticosteroid-related side effects, including adrenocortical insufficiency, gastric ulceration, and occult infections.

Autonomic hyperreflexia develops in 85% of patients with a complete injury above T5, owing to the loss of inhibitory control of vascular reflexes.[47] This condition mandates general or conduction anesthesia for any subsequent surgery in a quadriplegic or high-paraplegic patient, even if the planned procedure is in an insensate region.

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Copyright © 2005 Saunders, An Imprint of Elsevier

Ocular Trauma

Ocular trauma, both penetrating and nonpenetrating, is an important cause of visual loss and disability, with up to 90,000 injuries per year resulting in some degree of visual impairment.[48] Many of the patients with severe ocular injuries have concomitant head and neck trauma that delay initial recognition and evaluation of these problems. With current diagnostic methods, surgical techniques, and rehabilitation, vision can be salvaged in many patients. Despite a better understanding of anesthetic, medical, and surgical management, penetrating eye trauma continues to be a complicated and challenging condition.


Types of ocular trauma are listed in Table 17-9 . Severe concussive injury to the globe and orbit can cause damage to all of the ocular tissue. Force directed against the eye pushes the globe back into the orbit. The resulting compression of the eye stretches the softer tissues lining the eye, producing significant stretching vectors. Additionally, the thin bony medial wall and floor of the orbit are prone to movement, producing a “blowout” fracture. These fractures typically do not require emergent surgery unless visual impairment or globe injury is present. With penetrating injuries of the eye, closure of the laceration is the primary surgical goal due to concerns of infection and loss of intraocular contents, particularly from the posterior segment. Prognosis for penetrating eye injuries is related to a number of factors, including initial visual acuity, type and extent of injury, presence of retinal detachment, and presence of foreign bodies.

TABLE 17-9   -- Types of Ocular Trauma









Lid laceration






Facial fracture



Retrobulbar hemorrhage



Traumatic optic neuropathy



Superficial Ocular



Corneal abrasion



Foreign body



Chemical injury



Thermal injury












Iris injury



Retinal damage



Traumatic cataract



Subchoroidal hemorrhage



Lens subluxation






Globe rupture






Penetrating foreign body




Preoperative documentation of prior visual function and the degree of visual loss is important and may affect subsequent decisions and the timing of surgery. The documented examination should be as complete as possible, but any further injury to the globe should be avoided. Because many ocular injuries are associated with head and neck trauma, a thorough secondary survey should be accomplished, including CT for the evaluation of both intraocular and periocular structures. Also, CT may show whether a patient has sustained an intracranial injury, such as subdural hemorrhage. Although CT provides a helpful adjunct in penetrating ocular trauma, it may not be sensitive enough to be relied on as the sole means of evaluating a potential open globe injury.

Preoperative Preparation

Once a known or suspected globe injury has been identified, it becomes important to avoid significant increases in intraocular pressure (IOP) such as may occur during coughing, bucking, straining, or a Valsalva maneuver. This may require the judicious use of sedatives and narcotics in the preoperative period. In general, most of these agents will lower IOP and can be used if not contraindicated by other considerations. Additionally, the open globe should be protected with a shield and a broad-spectrum antibiotic may be administered to prevent infection. Optimal timing for surgical interventions is based on a number of factors, including concomitant injuries, coexisting disease, and operative factors ( Table 17-10 ). Because a large number of open globe injuries occur in children, pediatric considerations will frequently be required in their management.[49]

TABLE 17-10   -- Timing of Intervention in Various Forms of Ocular Trauma



Absolute emergency

Chemical injury (alkali > acid)


Threat of gas gangrene


Orbital abscess


Expulsive choroidal hemorrhage extruding intraocular tissues through the open wound


Vision loss because of expanding orbital hemorrhage




High-risk IOFB

Within 24 hours

Open wounds requiring surgical closure



Within a few days (24–72 hours preferred)

Thick submacular hemorrhage

Within 2 weeks



Secondary reconstruction if retina is detached


Media opacity in the amblyopic age group

Adapted from Kuhn F: Strategic thinking in eye trauma management. Ophthalmol Clin North Am 2002;15:171–177.

IOFB, intraocular foreign body.





Intraoperative Considerations.

While general anesthesia is used most commonly in the repair of penetrating eye injuries, local or regional anesthesia can be used safely with cooperative patients in the setting of limited corneal lacerations where the potential for extrusion of intraocular tissue is minimal. General anesthesia is indicated for cases of severe lacerating injuries, pediatric patients, or patients who are uncooperative because of alcohol or drug intoxication. This provides an immobile eye and eliminates the need for patient cooperation, while allowing for the control of factors affecting IOP. Care must be taken during anesthetic induction not to apply direct pressure to the globe with the face mask.

With the use of general anesthesia for the management of patients with potential or known open globe injuries, the management objectives include (1) overall patient safety, (2) avoidance of elevated IOP, (3) provision of a stable operative field, (4) avoidance of external ocular pressure, and (5) minimized bleeding. With most trauma patients, the anesthesiologist must assume that the stomach is full, making an RSI the technique of choice. As long as a deep level of anesthesia is provided during induction, any intravenous agent with the exception of ketamine is acceptable.

The choice of muscle relaxant for use in induction has been surrounded by controversy. Succinylcholine, which can cause contraction of extraocular muscles and choroidal congestion, has been shown to transiently increase IOP to a small degree. When given without intravenous or inhalational anesthetics, the IOP rise can be as high as 18 mm Hg.[50] Typically, however, the increase is 2 to 5 mm Hg with a high of 10 mm Hg with appropriate induction.[51] A recent review looking at the published studies and recommendations regarding the use of succinylcholine and open globe injuries cited only anecdotal reporting of vitreous loss associated with its use.[52] Several case series and animal studies have failed to demonstrate the extrusion of vitreous with the use of succinylcholine when used with a nondepolarizing pretreatment, although there is a lack of randomized controlled trials. [53] [54] Currently, it appears that the use of succinylcholine should be dictated by the need for rapid onset or termination of muscle relaxation rather than concerns about loss of ocular contents. Pretreatment with a small dose of a nondepolarizing muscle relaxant should precede the use of succinylcholine to blunt the expected increase in IOP. The use of intravenous lidocaine, β blockers, and short-acting narcotics may be useful at induction to blunt the hypertensive response to laryngoscopy and intubation, which are also associated with increases in IOP. [55] [56]

After induction and intubation, deep anesthesia with a combination of narcotics, inhalational anesthesia, and muscle relaxants will allow for the avoidance of extraocular pressure and choroidal congestion by eliminating coughing, straining, or movement. Although occurring infrequently during repair of eye lacerations, the oculocardiac reflex may occur during manipulation of the globe. Whereas use of a retrobulbar block will abolish or prevent this reflex, it should not be used with a potential open globe injury. If possible, maintenance of a head-up position will facilitate venous drainage.

During emergence from anesthesia, an increase in IOP is possible. While the concern for loss of intraocular contents is lessened, straining, emesis, coughing, and agitation may increase the risk of bleeding and affect the surgical outcome. Appropriate antiemetic therapy is indicated along with the use of narcotics for pain management. Shivering should also be avoided and can be treated with small doses of meperidine.

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Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Complex Facial Injuries

Although frequently distracting in appearance, severe maxillofacial trauma is not often life threatening unless there is involvement of the airway or, rarely, severe hemorrhage. The face and head are exposed to a broad range of physical trauma ( Table 17-11 ). An estimated 3 million patients require hospital treatment for facial injuries every year from motor vehicle crashes alone.[57] Life-threatening airway and bleeding problems; severe ocular, nasal, or jaw dysfunction; and significant cosmetic deformities are the potential consequences of facial trauma. The anesthesiologist must be familiar with these injuries to ensure appropriate initial management, to facilitate emergent treatment, and to support surgical correction.

TABLE 17-11   -- Major Causes of Facial Injuries



Vehicle crash: motorized and nonmotorized



Pedestrian accident



Industrial accident






Blunt force such as fist or club



Penetrating such as knife or gunshot









Thermal injury



Chemical injury




The type and severity of injury is determined by several factors, including the mechanism of injury, extent, direction and duration of force, and characteristics of the impacted facial structures. Significant bone trauma can coexist with only modest soft tissue injury; similarly, dramatic soft tissue injury may occur in the absence of facial fractures.

Each of the major mechanisms of injury produces not only distinctive patterns of injury but also necessitates a search for likely associated trauma. Blunt trauma typically has a greater effect on the facial skeleton than soft tissue. In cases of interpersonal violence or sports-related blunt trauma, edema and hematoma may be the only soft tissue findings with significant underlying facial fractures. Patients involved in motor vehicle crashes presenting with significant facial trauma should be presumed to have traumatic brain and cervical injury[58] until proven otherwise. With penetrating trauma from close range (e.g., shotguns, rifles, and high-velocity projectiles), there may be significant loss of soft tissue with massive facial destruction. Burns are associated with progressive cutaneous and mucosal edema, necessitating early management of a potentially compromised airway.

The direction of force applied to the facial structures determines the fracture location. Given the lower force requirements to produce fracture of the nasal bones, zygoma, frontal sinus, and mandibular ramus compared with other facial bones, these are the more common sites of injury. [59] [60] As would be expected with blunt trauma, the greater the change of velocity at the time of impact, the greater the severity of the resultant fracture. With penetrating trauma from gunshot wounds, the damage potential is directly related to the velocity of the projectile on impact. Fortunately, the structure of the midfacial skeleton provides some buttressing and protection for the thinner, laminar bones in this area. This allows for dispersal of traumatic forces and may prevent fracture of low-resistance facial bones and reduced energy transmission to the base of the skull. [61] [62]

The face can be divided into three anatomic regions. The lower third contains the mandible and includes the temporomandibular joint and coronoid process. The middle third comprises the maxilla, nasal bones, orbits, and zygomatic arch. The upper third contains the frontal bone, frontal sinuses, frontozygomatic process, and nasoethmoidal complex. A summary of signs, symptoms, and long-term complications associated with these fractures is found in Table 17-12 . Along with soft tissue injuries, this provides a framework for classification of facial injuries.

TABLE 17-12   -- Types of Facial Fractures


Signs and Symptoms

Long-Term Complications


Pain, obstruction, crepitus, swelling, epistaxis

Malunion, obstruction

Naso-orbital, ethmoid

Pain, visual change, epistaxis, swelling, telecanthus

Malunion, telecanthus

Frontal sinus

Pain, epistaxis


Zygomatic arch

Lateral pain, trismus, asymmetry, lateral depression

Unstable, recurrent depression


Numb cheek and/or lip, visual change, swelling entrapment, scleral hemorrhage, epistaxis, step-off, enophthalmos, associated globe injury

Asymmetry, entrapment, enophthalmos

Orbital blowout

See Zygoma; rarely, numbness, epistaxis, and step-off

Entrapment, enophthalmos


Malocclusion, trismus, numbness, visual changes, massive swelling, epistaxis, scleral hemorrhage, midface mobility

Malocclusion, malunion, dental loss, asymmetry, lacrimal obstruction


Lower lip numbness, trismus, pain referred to ear, crepitus, malocclusion, open bite

Malocclusion, malunion, osteomyelitis, ankylosis, dental loss, nerve injury

Adapted from Darian VB: Maxillofacial trauma. In Trunkey DD, Lewis FR (eds): Current Therapy of Trauma, 4th ed. St. Louis, Mosby, 1999.



Soft tissue injuries range from minor to severe, including contusions, abrasions, punctures, lacerations, avulsion flaps, and frank tissue loss. Early management usually consists of débridement, conversion of unfavorable to favorable wounds, and meticulous closure. Careful examination should be performed to evaluate for injury to other important structures such as the facial nerve, parotid gland, and the lacrimal apparatus. Lacerations in the vicinity of the zygomatic arch may include injury to the frontal branch of the facial nerve. Large hematomas, particularly involving the nasal septum and auricular cartilage, may require drainage to prevent subsequent cosmetic deformity.[63]

Mandibular fractures are the second most common form of facial fracture after the nasal bones. Because greater than 50% of mandibular fractures occur in two or more locations, a second fracture site should almost always be suspected when evaluating a patient.[63] The strong musculature attached to the mandible has a tendency to produce displacement of fractured bones along with malocclusion and asymmetry. In some cases this may produce compromise of the airway affecting surgical and anesthetic management.

Midface fractures include nasal, Le Fort, orbital, and zygomatic arch fractures. The nasal bones are the most commonly injured facial bones. Disruption of the nasal septum may result in airway obstruction and lead to significant hemorrhage. The classic midface fractures were described by Rene Le Fort in 1902 and were named Le Fort I, II, and III. Le Fort I is a dentoalveolar horizontal fracture that separates the maxillary alveolus from the midface. Le Fort II is a pyramidal or triangular fracture separating the maxilla from the zygoma, with the fracture lines demarcating a central fragment involving the maxillary alveolus, the medial portion of the orbit, and the nose. A Le Fort III fracture is a complete dislocation of the facial skeleton from the cranial skeleton running parallel to the skull base. This fracture involves the ethmoid bones and can extend into the cribriform plate, allowing a communication with the anterior fossa. Thus, the presence of rhinorrhea could signal the presence of a CSF leak. The absence of rhinorrhea, however, does not rule out the possibility of disruption of the cribriform plate and a skull base fracture. While useful in describing elements of a midface fracture, rarely are the classic patterns identified in isolation. Le Fort fractures are rarely bilateral and may be seen in combination with other facial fractures and soft tissue injury.

Zygomatic arch fractures are caused by blows to the lateral aspect of the midface. Trismus may occur due to swelling from hematoma or edema within the masseter muscle or direct mechanical impingement of the bone fragments of the arch onto the coronoid process of the mandible. Fractures of the zygoma and orbital walls may affect eye movement through entrapment of periorbital soft tissue, including extraocular muscles. Direct globe trauma may also occur and should be included in the initial evaluation.

Fractures involving the upper third of the facial structure include frontal sinus and frontal bone fractures. Concomitant nasoethmoidal, supraorbital, zygomatic, and cranial base fractures are commonly seen and may involve the anterior cranial fossa. Thus, particular attention must be paid to assessing for frontal lobe contusion, CSF rhinorrhea, and pneumocephalus.


Because facial trauma frequently occurs in the multiply injured patient, initial evaluation should focus on life-threatening problems and complete assessment of more emergent injuries. Upper and occasionally lower airway obstruction can occur with facial trauma, necessitating a detailed evaluation of the airway and potential for subsequent compromise. Patients with multiple mandibular fractures or combined maxillary, mandibular, and nasal fractures are more likely to experience early airway obstruction. [64] [65] The arch configuration of the mandible suspends the tongue anteriorly such that posterior displacement from a complex mandibular fracture allows the floor of the mouth to fall backward, causing airway obstruction. Obstruction of the nasopharynx may occur with some midface fractures. Although this will not produce complete airway compromise in the presence of mouth breathing, impaired consciousness with posterior collapse of oral structures can lead to severe obstruction. Alternatively, swelling of the tongue, pharynx, palate, or floor of the mouth from trauma, burns, or penetrating injuries may produce progressive airway occlusion.

The diagnosis of facial injuries is generally made by physical examination and radiographic analysis. Careful observation for soft tissue injuries, facial symmetry, gross deformities, eye movements, and alterations in muscle tone should be documented exactly. Palpation of the face may reveal pain, crepitus, numbness, and deformity suggestive of facial injury. Malocclusion is a very important sign of maxillofacial fracture. The ability of the patient to open the mouth should be ascertained, including the presence or absence of pain with opening. In the setting of limited mouth opening, it is important to determine if the cause is mechanical obstruction or pain/spasm. Anesthetics and muscle relaxants can relieve muscle spasm or trismus; however, their use in a patient with a mechanical obstruction may lead to loss of the airway and inability to perform direct laryngoscopy. Finally, a thorough airway examination should include an evaluation of the oral cavity to note the presence of loose or missing teeth, tongue mobility, and source of hemorrhage, if present.

Blunt trauma causing extensive facial injury should alert one to the possibility of concomitant cervical spine and/or closed-head injury. [58] [59] Extreme care needs to be taken with these patients in regard to subsequent airway management to avoid spinal cord injury. Radiographic analysis, including plain films and CT, are essential in evaluating the extent of facial injuries but will also provide information on associated injuries.

Preoperative Preparation.

The majority of penetrating facial injuries will require urgent exploration and surgical management. The timing of surgical repair of blunt facial injuries, however, is determined by many factors, including associated injuries, extent of soft tissue damage, edema, and overall patient condition. Definitive repair of these injuries is sometimes undertaken shortly after the time of injury, particularly if associated injuries require operative intervention. Many facial fractures can wait 7 to 10 days for definitive repair provided that soft tissue injuries are treated and intermaxillary fixation is applied, if necessary.

Airway management in the patient with significant facial trauma is the principal task of the anesthesiologist during the preoperative management phase. Decisions regarding airway management depend on many factors, including the significance of airway compromise, state of consciousness, etiology and type of injuries sustained, condition and anatomic distortion of the airway, identifiable or known premorbid conditions, and need for medical or surgical intervention. Partial airway obstruction is common for the reasons just described, and placement of an oral or nasal airway may alleviate the problem. A nasal airway is less likely to stimulate gagging if airway reflexes are present but should not be used in the presence of a nasal or skull base fracture.[66] Patients with severely distorted airway anatomy may be best managed with an elective tracheotomy, with or without first securing the airway through other means.

Preoperative preparation for emergent surgery should proceed as with any other traumatized patient, paying close attention to establishing adequate respiration and circulation while maintaining cervical spine immobilization. For cases of delayed surgical repair, attempts should be made to clear the cervical spine of injury to facilitate subsequent intraoperative management. Judicious use of sedatives and analgesics is indicated and may help with spasm of muscles associated with fractures through the temporomandibular joint, provided mechanical obstruction is ruled out.

Intraoperative Considerations.

Mask ventilation has only limited use in facial trauma; there are constant problems attaining appropriate seal and adequate airway opening without applying pressure to fracture sites or extending the cervical spine. In patients with a compromised but stable airway, an awake intubation technique may be the best choice for airway management. To optimize access to the surgical field, procedures involving the lower face, including the mandible, are best managed with nasal intubation if not contraindicated by other injuries or conditions. Conversely, procedures involving the midface are best managed with oral intubation or a surgical airway. The risks and benefits of approaching the airway with alternative blind techniques, either orally or nasally, must be strongly weighed.

Choice of anesthetic technique should take into consideration that facial reconstructions are long cases, have intermittent intervals of intense stimulation, and may involve significant blood loss. Surgeons will demand unencumbered access to the face and neck and may request controlled hypotension at times. In addition, monitoring of facial nerve function may be necessary.

After completion of surgery, postsurgical edema may further affect airway patency. Patients should be awake with intact reflexes before extubation. In cases of soft tissue edema, dexamethasone, 4 to 8 mg intravenously, may help reduce the tissue swelling, although the effect is not immediate. If intermaxillary fixation is applied, wire cutters should be available at the bedside and remain with the patient in the event of airway obstruction or hemorrhage.

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Penetrating Trauma

While fortunately rare in most hospitals, knife and gunshot wounds cause up to 30% of all admissions to busy urban trauma centers. Penetrating injuries can affect any region of the body, and considerations for the anesthetic care of penetrating trauma victims are not substantially different than for the victims of blunt trauma. When initially assessing the patient it is important to establish the trajectory and energy transmission of the injury, so as to estimate the organ systems at risk. Gunshot wounds, particularly from high-velocity weapons such as rifles, may cause concussive damage to organs in the proximity of the bullet path even in the absence of direct penetration. Patient intoxication with alcohol or narcotics may mask signs of pain, whereas youthful physiology and use of cocaine may lead to underestimation of blood loss.

Patients who are hemodynamically unstable after penetrating trauma should be taken immediately to the OR and undergo direct exploration, the only exception being patients with limited thoracic penetration who respond promptly to tube thoracostomy. Damage control principles are applied, with the goal of controlling hemorrhage as rapidly as possible, completing resuscitation, and then returning for definitive reconstruction after 24 to 48 hours of stability in the ICU. Patients who are initially stable may undergo diagnostic testing with plain radiographs, CT, and ultrasound. The number of hemodynamically stable penetrating trauma patients who require diagnostic surgery is decreasing in recent years, because of the increasing capability of diagnostic modalities such as CT and angiography to exclude operative injury. Exploration of neck wounds, the diagnostic pericardial window, and exploratory laparotomy for flank wounds are all performed less commonly today. Noninvasive technology is still not sufficiently sensitive to reliably exclude diaphragmatic or bowel penetration, however, and a penetrating wound that is likely to have violated the peritoneum is still a strong indicator for urgent exploratory laparotomy.

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Traumatic Aortic Injury


Any high-injury blunt trauma resulting in sudden acceleration or deceleration of the torso may result in a traumatic injury to the aorta, with catastrophic consequences for the patient. Shear forces are typically concentrated at the aortic isthmus, where the relatively free-floating heart and aortic arch are tethered to the descending thoracic aorta by the ligamentum arteriosum. The spectrum of anatomic injury ranges from “cracking” of the intima with creation of a small intravascular flap all the way to complete transection. Many patients with the latter condition are found dead at the scene of injury, but survival to hospital admission is not uncommon owing to the tamponading effect of the surrounding pleura and pericardium. These patients have a very high risk of free rupture and exsanguination during the hours immediately after injury. The natural history of small intimal flaps is unknown, although some of these patients go on to form pseudoaneurysms that may become symptomatic years after the initial injury.[67] Patients with underlying atherosclerotic disease may experience proximal or distal dissection of the aorta arising from the site of injury.


Diagnosis of aortic injury begins with a high degree of suspicion in any patient who has suffered a high-speed frontal or lateral impact motor vehicle collision (particularly when no airbag is present), any pedestrian struck by a motor vehicle, any motorcyclist, and any patient who has fallen more than 10 feet. Symptoms of aortic injury are nonspecific, consisting mainly of back pain in the thoracic region. The blood pressure is commonly labile, with exaggerated peaks and troughs in response to hemorrhage from other injuries, painful stimulation, and sedating medications. Common coexisting injuries include fractured ribs or sternum, left hemothorax, humeral fracture, splenic rupture, and left-sided femur or acetabular fracture, although none of these is a highly sensitive marker for aortic trauma. Chest radiography is indicated but often not discriminatory. If the aortic contour is normal and well visualized, the chance of aortic injury is small, but a confident interpretation of the anteroposterior chest radiograph is possible in less than 50% of patients at risk. Visible disruption of the aortic contour or other unusual shadowing of the mediastinal structures is caused by injury to small vessels in the vicinity of the aorta and is a strong indication for further diagnostic assessment. The traditional gold standard for aortic clearance is contrast aortography. Chest CT is gaining in resolution and accuracy for aortic injury and is now the standard in large centers with experienced radiographers.[68]Transesophageal echocardiography is also highly sensitive and specific and is an appropriate diagnostic approach when an experienced operator is available.

Preoperative Preparation.

Transfer of the patient to a trauma center with experience in aortic surgery is highly desirable if it can be expeditiously arranged. β-Blocker therapy is indicated in the presurgical interval to reduce sheer-force stresses on the proximal aorta. Large-bore intravenous access, right radial arterial pressure monitoring, and assessment of central pressures by pulmonary artery catheterization or transesophageal echocardiography are strongly indicated.

Intraoperative Management.

Surgical treatment of traumatic aortic injury is indicated in any patient who can tolerate the procedure. Angiographically guided vascular stenting is an investigational therapy at this time, although likely to play a larger role in the near future.[69] Aortic surgery should be approached on an urgent basis, following only emergent procedures such as damage control laparotomy or evacuation of intracranial hemorrhage. Intraoperative anesthetic management requires double lumen intubation to facilitate surgical exposure of the left pleural cavity. Partial cardiac bypass is commonly used to support systemic perfusion. A full description of this technique is beyond the scope of this chapter but can be found in an excellent paper by Read and associates.[70]

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Orthopedic Injuries

Orthopedic trauma produces life- and limb-threatening musculoskeletal injuries, including hemorrhage from wounds and fractures, infections from open fractures, limb loss from vascular damage and compartment syndrome, and loss of function from spinal or peripheral neurologic injuries. The management of these cases presents a wide variety of challenges for the anesthesiologist. Musculoskeletal injuries comprise the most common indication for operative management in most trauma centers. Because many procedures might be appropriately managed under regional anesthesia, familiarity with regional anesthetic techniques is essential. In addition to a familiarity with an array of regional anesthetic procedures, the anesthesiologist may need skill with fiberoptic intubation, hypotensive anesthesia, hemodilution, intraoperative cell saver techniques for minimizing intraoperative blood loss, and invasive hemodynamic and evoked potential monitoring. The length of many procedures, particularly with the presence of multiple extremity injuries, necessitates attention to body positioning, maintenance of normothermia, fluid balance, and preservation of peripheral blood flow, especially in reimplantation procedures.


For the past 15 years, the emphasis in trauma management of the multiply injured patient has included early stabilization of long bone, spine, pelvic, and acetabular fractures. Failure to do so results in increased morbidity, pulmonary complications, and length of hospital stay. [71] [72] In one study only 2% of patients with femoral shaft fractures stabilized within the first 24 hours of injury had pulmonary complications, as compared with 38% of patients in whom fracture stabilization was delayed for more than 48 hours.[73] Thus, the clinical picture, treatment plan, and anesthetic management of orthopedic trauma must be focused on early entry into the operating room.

Classification of orthopedic injuries takes into account the mechanism of injury, site, type of fracture, soft tissue involvement, vascular or nerve injury, and whether the fracture is open. The anticipated rate of and severity of fracture-related complications such as need for amputation, infection, nonunion, and prognosis are linked with the classification of open fractures ( Table 17-13 ). The mechanism of injury for a given site can predict potential complications that would affect or alter the anesthetic plan. For instance, approximate blood loss from fracture hemorrhage varies from 500 mL with a closed tibia fracture up to life-threatening hemorrhage with a pelvic fracture.

TABLE 17-13   -- Classification of Open Fracture Wounds




Clean wound less than 1 cm long


Laceration > 1 cm without extensive soft tissue damage, skin flaps, or avulsions


Extensive soft tissue lacerations or flaps with adequate soft tissue coverage of bone; result of high-energy trauma


Extensive soft tissue loss with periosteal stripping and bony exposure; usually contaminated


Arterial injury requiring repair regardless of size of soft tissue wound



Extremity injuries include fractures, dislocations, soft tissue damage, or a combination of these findings. An understanding of anatomy and the mechanism of injury can be helpful in predicting associated injuries such as nerve and vascular damage. For instance, displaced intracapsular femoral neck fractures have a high risk of avascular necrosis, and posterior dislocation of the knee is associated with popliteal vessel injury.

Pelvic fractures occur as the result of substantial force and can be associated with significant morbidity and mortality from direct pelvic trauma combined with other injuries. They can be classified as having anteroposterior compression, lateral compression injury, or vertical shear patterns. The mechanism of injury is important because the relative risk of hemorrhage from the internal iliac artery or posterior pelvic venous plexus damage is increased with anteroposterior compression and vertical shear injuries.[73] Early stabilization of the fracture with the use of external compressive devices or external fixation and/or angiography with selective embolization may be needed before operative repair while addressing other life-threatening injuries. In addition to significant hemorrhage, other direct injuries include nerve injury, rectal or vaginal laceration, bladder rupture, and urethral injury.

Damage to the spinal column is common in traumatic injury and is frequently associated with neurologic dysfunction. The level of injury is most commonly cervical (55%), with 30% at the thoracic level and 15% in the lumbar region.[74] The most basic classification of spinal cord injuries delineates complete or partial loss of function at a given level. A complete injury is defined as a total loss of sensory and motor function lasting for more than 48 hours in areas innervated more than two levels below the level of bony injury.[75] Late injury may still occur if stability has been compromised. Mechanism and site of injury produce typical fracture patterns and frequently determine the need for surgical stabilization (see Table 17-8 ). A more complete discussion of spinal cord injury can be found in Chapter 8 .


During evaluation of the orthopedic trauma patient, initial attention should be paid to the adequacy of the patient's airway, quality of ventilation, and status of perfusion, just as in any injured patient. Once these areas have been addressed and appropriate therapies initiated, subsequent evaluation should focus on the identification and treatment of associated injuries. In the multiply injured patient, this requires prioritization of the injuries and coordination of the care with the anesthetic team. Many orthopedic injuries require emergent intervention to attempt limb salvage, control of hemorrhage, nerve repair, or prevent infection.

A thorough history and examination is always vital. Time course of the injury is important because many orthopedic surgeons believe all open fractures require surgical débridement within 6 hours of the initial trauma. A history inconsistent with the extent of injury may suggest either a pathologic fracture or the possibility of abuse. After the initial assessment, a secondary examination should include documentation of a thorough neurologic examination with attention to function and sensation in injured extremities. This may be particularly important if regional anesthesia is chosen, because postoperative deficits may be inadvertently attributed to the anesthetic technique. Distal perfusion should also be well documented by assessment of distal pulses. Capillary refill is not, by itself, adequate clinical evidence of intact perfusion and does not exclude the presence of a compartment syndrome or vascular injury.

Preoperative Preparation.

The initial management of patients with orthopedic trauma is not substantially different from that of any injured patient. Airway management remains the highest priority. Consideration should be given to early definitive management in patients with multiple extremity fractures, serious pelvic injury, and high spine injuries with deficit. The evaluation process will often include multiple trips to remote locations such as the radiology suite, CT, and angiography, where there may not be suitable provisions for emergent airway management. Additionally, early intubation is frequently needed to allow for manipulation of fractures, treatment of dislocation, or placement of fixation pins. Ongoing assessment of adequacy of ventilation and oxygenation must be maintained throughout the evaluation process.

Maintaining adequate circulation becomes the next highest priority. Intravenous access should be established with large-bore peripheral catheters if possible, but extremities with known injuries should be avoided. Use of central venous lines may be necessary, although femoral or lower extremity cutdowns should be avoided with suspected pelvic injuries owing to the potential for pelvic venous injury. In addition, it is important to anticipate the need for blood products.[76] The mean 24-hour requirements in patients admitted with clear signs of shock is over 5 units, and approximately 20% of these patients will require more than 15 units.

Intraoperative Considerations.

Choice of anesthetic technique will depend on a multitude of factors, including associated injuries, ability to cooperate with the anesthetic plan, hemodynamic stability, coexisting disease, and patient preference. Because patients present with a continuum of injury severity, no anesthetic technique is clearly superior for all patients. Presentations range from minor injuries that can be managed with infiltration of a local anesthetic, to injuries that could be treated with a peripheral nerve or subarachnoid block, and finally to injuries that require general anesthesia with invasive monitoring. Typically, general anesthesia is the technique of choice for patients with multiple injuries. While regional anesthesia may seem attractive because it produces less interaction with the patient's cardiopulmonary function and avoids airway manipulation, patients with serious trauma benefit from endotracheal intubation and mechanical ventilation and are unlikely to cooperate with lying still during prolonged surgery. The use of neuraxial blockade can interfere with compensation for hemorrhage and produce hemodynamic instability. Thus, regional anesthesia is most useful for isolated limb trauma, for example, brachial plexus block for a hand fracture.

There are some specific considerations for the intraoperative management of patients requiring surgery for orthopedic trauma, including positioning, temperature management, use of tourniquets, potential for fat embolism, and development of deep venous thrombosis (DVT). Optimal outcome for an unstable multiply injured patient is achieved if all injuries can be corrected at the time of initial surgery. The victim of blunt trauma with multiple fractures especially benefits from early fracture fixation that reduces ongoing hemorrhage, intravascular release of bone marrow, and postoperative complications of immobilization. [71] [72] During prolonged surgery, the anesthesiologist must closely monitor electrolytes, coagulation abnormalities, fluid balance, and the adequacy of ventilation/oxygenation.


Many orthopedic surgical procedures require a nonsupine position. Care should be taken to ensure ventilation is not compromised, and positioning should allow for adequate diaphragmatic excursion and thoracic expansion without producing excessive airway pressure. All extremities should be placed in positions of comfort, preventing torsion or traction on neurovascular bundles, particularly the brachial plexus. All pressure points should be padded, especially where nerves are placed in the dependent position. The eyes, ears, nose, breasts, and genitalia should be protected when the patient is lateral or prone.


Hypothermia is a real risk in trauma patients, particularly those with multiple injured extremities. Many patients enter the trauma center with low body temperature resulting from environmental exposure. Further exposure to a cold operating room, evaporative heat loss from the respiratory tract, infusion of cold fluids, and loss of heat production secondary to shock can produce a further drop in core temperature or reduce the effectiveness of warming efforts. With recent therapy being directed toward early fracture stabilization and definitive repair, patients with multiple extremity fractures will have long operations and large fluid volume requirements. All skin surfaces not in the surgical field should be covered to reduce convective and radiant heat loss. The addition of forced-air warming should be used where possible. Humidification of inspired gases through the use of heat-moisture exchange units reduces evaporative heat loss from the lung. The use of active heating and saturation of inspired gases can produce active warming of the patient. Only warmed intravenous fluids should be used, and in situations where large volumes of fluid or blood will be used, heat exchangers capable of warming fluids to 37°C at very rapid infusion rates should be employed. Hypothermia is a potentially life-threatening condition in these patients owing to increased susceptibility to cardiac dysrhythmias, coagulopathies, central nervous system (CNS) depression, and altered liver and kidney function.

Tourniquet Problems.

Tourniquets are frequently used in extremity surgery to reduce blood loss and improve surgical visualization. When used for excessive durations or at excessive pressure tourniquets can cause injury to underlying nerves, muscle, and blood vessels, as well as producing systemic effects. Effects can be seen with initial inflation, during prolonged inflation, and on tourniquet deflation. Inflation of the tourniquet and exsanguination of the limb typically produces only small increases in central venous or arterial pressures. The application of bilateral lower extremity cuffs, however, may result in significant elevation of central venous pressure.[77] Forty-five to 60 minutes after tourniquet inflation patients under general anesthesia may develop systemic hypertension.[78] The mechanism for this elevated blood pressure is not clearly understood, and the hypertension does not always respond to deepening anesthetic depth. Deflation of the tourniquet with reperfusion of the ischemic limb may be associated with significant decreases in central venous and arterial pressures. The sudden reduction in peripheral vascular resistance with blood pooling in the extremity and the circulatory effects of ischemic metabolites most likely account for these changes.[79] Finally, awake patients undergoing regional anesthesia may complain of tourniquet pain despite an otherwise adequate block. Use of small doses of intravenous narcotics or transient deflation (10 to 15 minutes) may relieve the discomfort.

Recommended levels are 100 mm Hg above systolic pressure for thigh cuffs and 50 mm Hg above systolic pressure for upper extremity cuffs.[80] Duration of cuff inflation should generally not exceed 120 minutes. [81] [82] Anesthesiologists who use regional anesthesia may be implicated when postoperative nerve injuries are identified when in fact they are secondary to tourniquet injury.

Fat Embolism.

After long-bone fractures, some lung dysfunction occurs in almost all patients, ranging from minor laboratory abnormalities to full-blown fat embolism syndrome. A lack of universally accepted diagnostic criteria combined with concomitant pulmonary and cardiovascular dysfunction accounts for the varying incidences reported in the literature. Most studies suggest clinically significant fat embolism syndrome occurs in 3% to 10% of patients, although the presence of multiple long-bone fractures is associated with the higher incidence. Patients with coexisting lung injury are at additional risk of fat embolism. Signs include hypoxia, tachycardia, mental status changes, and petechiae on the upper portions of the body, including the axillae, upper arms and shoulders, chest, neck, and conjunctivae. Fat embolism syndrome should be considered whenever the alveolar-arterial oxygen gradient deteriorates in conjunction with loss of pulmonary compliance and CNS deterioration. Under general anesthesia, the CNS changes will be lost but may present as failure to wake up after surgery. If central hemodynamic monitoring is available, pulmonary artery pressures are elevated, often accompanied by decreases in cardiac index. Efforts to surgically correct fractures early and minimize trauma to the bone marrow lessen the degree of fat/bone marrow embolism, although extensive reaming of the medullary canals can contribute to perioperative morbidity and the severity of fat embolism syndrome.

Diagnosis in the operating room is largely based on the clinical presentation and ruling out other treatable causes of hypoxemia. Fat globules in the urine are nondiagnostic, but lung infiltrates seen on chest radiograph confirm the presence of lung injury and the need for appropriate ventilatory management. [83] [84]

Treatment includes early recognition, oxygen administration, and judicious fluid management. A change in the orthopedic procedure may be indicated, such as converting “rodding” of the femur to external fixation. Pulmonary arterial catheter monitoring may be necessary to optimize hemodynamics because maintenance of intravascular volume is critical. Acute right-sided heart failure due to elevated pulmonary pressures is possible and requires close attention to avoid fluid overload. Finally, the use of corticosteroids has been advocated early after fat embolism syndrome. [85] [86] [87] Although clinical evidence supports improved outcomes, corticosteroids are probably not necessary in most cases.

Deep Venous Thrombosis.

Deep venous thrombosis is a common problem after orthopedic trauma, with pulmonary embolism being a major contributor to postoperative mortality. The incidence of DVT varies by site and type of operative procedure ( Table 17-14 ). The thrombosis can form during surgery with periods of venous stasis in the presence of surgical trauma. Thus, it is important to institute preventive measures starting in the operating room and continuing into the postoperative period.

TABLE 17-14   -- Incidence of Deep Venous Thrombosis (DVT) by Fracture Site or Operative Procedure

Fracture Site

Rate of DVT (%)

Knee arthroscopy


Total hip replacement


Total knee replacement


Tibial plateau


Femoral shaft


Tibial shaft


Distal tibia




Mechanical nonpharmacologic prophylaxis methods, such as intermittent pneumatic compression devices and foot pumps, increase the speed of venous flow and the volume of blood returned from the extremity to the heart. They also produce endothelial-induced changes that decrease the risk of thromboembolic phenomenon. Because they do not affect the coagulation system, they should be used in all patients undergoing orthopedic procedures unless prevented by the presence of injury.

Epidural or spinal anesthesia reduces DVT rates after total-knee replacement by 20%[88] and after total-hip replacement by approximately 40%,[89] although postoperative epidural analgesia does not appear to provide additional benefit in reducing DVT rates.[90] Postoperative epidural analgesia may still be beneficial by allowing for earlier ambulation.

Current guidelines suggest that a low-molecular-weight heparin (LMWH) such as enoxaparin provides the best prophylaxis for venous thromboembolism in the high-risk trauma patient.[91] Once therapy has been started, LMWH should be withheld for 12 hours before surgery, if possible, and restarted a minimum of 3 hours after surgery. Recent guidelines for the use of neuraxial anesthesia and thromboprophylaxis have been published and provide clear guidance for timing of the anesthetic technique and the various agents used for thromboprophylaxis.[92] In very high-risk cases or when postoperative prophylaxis is contraindicated, vena cava filters may be placed perioperatively.

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Near Drowning

As an expert in airway management and pulmonary support, the anesthesiologist may be consulted in the care of patients who present with asphyxia secondary to near drowning. Prompt intubation and restoration of normal oxygen saturation is the obvious starting point. Subsequent management is symptomatic and consists of frequent assessment of arterial blood gases with ongoing titration of mechanical ventilation to achieve adequate recruitment of collapsed lung units with the lowest possible peak airway pressure. Laryngoconstrictive reflexes are among the strongest, and many near-drowning victims do not actually aspirate significant quantities of water. Those who do have evidence of aspiration have likely reached more significant levels of hypoxia. A significant pulmonary aspiration will both remove surfactant from the lungs and contaminate the alveoli, leading to significant acute lung injury and fluid volume loss.[93] Ventilatory support is indicated and may be required for hours to days after the acute event. Because the return of normal pulmonary function is likely, long-term outcomes are driven by the patient's neurologic status, secondary to the initial period of hypoxia.

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Smoke Inhalation and Carbon Monoxide Poisoning


Patients exposed to fire and toxic gases may be hypoxic from any of three mechanisms: thermal injury to the upper airway, with edema and stricture of the larynx; particulate inhalation with subsequent bronchoconstriction; and carboxyhemoglobin formation secondary to carbon monoxide (CO) poisoning. Pulse oximetry may not accurately reflect tissue oxygen delivery because oximeters cannot discriminate carboxyhemoglobin from normal oxyhemoglobin. Because the former compound does not actually transport oxygen, significant tissue hypoxia can occur. Early arterial blood gas sampling, with specific co-oximetric measurement of the fraction of carboxyhemoglobin, is essential.


While soot staining of the mucosa is common, patients with visible burns of the soft palate (blistering or erythema) should be promptly intubated, as should any patient with laryngeal edema, indicated by stridor or a progressive change in voice. Hypoxia may also be indicated by agitation or lethargy; any burn or CO-poisoning patient with an altered mental status should be intubated and mechanically ventilated until diagnostic studies have been completed. For less severely injured patients humidified oxygen and nebulized bronchodilator therapy will contribute to clearance of soot particles from the airways.

Perioperative Management.

Initial management follows the ABCs of trauma. CO poisoning is managed by administration of high concentrations of oxygen, which will competitively displace CO from hemoglobin. At an Fio2 of 1.0, the half-life of carboxyhemoglobin is approximately 90 minutes. For patients without neurologic symptoms, face mask therapy is generally adequate. For neurologically impaired patients or those with special risk factors (pregnant, pediatric, elderly, comorbid conditions) intubation may be useful simply to increase the Fio2. Hyperbaric therapy is indicated for severe CO poisoning cases and will significantly shorten the half-life of carboxyhemoglobin.[94]

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The Pregnant Trauma Patient

Trauma to the pregnant patient presents unique problems for the anesthesiologist and resuscitation team. Significant alterations in physiologic demand associated with pregnancy may confuse and complicate the evaluation, treatment, and management of these patients. Trauma has become the leading cause of maternal death in the United States, with 3 to 4 per 1000 pregnancies requiring hospital admission for trauma. [95] [96] Even minor trauma poses a significant risk to the fetus and requires extra vigilance during the most routine cases. The primary focus of resuscitation and early management is the mother, because there can be no fetal survival without maternal survival. Therefore, stabilization of the mother's condition takes priority over concerns about the fetus. One possible exception occurs during the third trimester, in the rare case in which the maternal prognosis is poor and immediate cesarean section may possibly save the fetus.


Physiologic changes associated with pregnancy alter the responses seen in traumatic injury. Table 17-15 summarizes the significant changes seen in the pregnant patient and their implications as related to trauma. During pregnancy, maternal plasma volume expands by 40% to 50% by the end of the first trimester and peaks by 30 to 34 weeks' gestation. Because red cell mass expands to a lesser degree, a dilutional anemia, referred to as the physiologic anemia of pregnancy, occurs with a normal hemoglobin range of 10.5 to 12.9 mg/dL, depending on individual variation and weeks of gestation. As a result of intravascular volume expansion, mild to moderate blood loss associated with traumatic injury may appear to be well tolerated by the mother. Subsequent alterations in uteroplacental circulation due to compensatory mechanisms, however, may have a significant impact on the fetus. Other hemodynamic alterations that may impact evaluation and management decisions include changes to baseline blood pressure and cardiac output. By 28 weeks, normal maternal blood pressure decreases by 15% to 20% owing to reductions in peripheral vascular resistance. At the same time, cardiac output increases by 35% to 50% above baseline, with a 17% increase in heart rate and a moderate increase in stroke volume. The increase in cardiac output has been attributed to a functional 20% to 30% arteriovenous shunt produced by the low-resistance placental circulation.

TABLE 17-15   -- Physiologic Changes of Pregnancy

Organ System




Decreased peripheral vascular resistance

Reduced baseline blood pressure


Increased cardiac output



Increased heart rate

Resting tachycardia


Aortocaval compression

Supine hypotension


Increased plasma volume

Dilutional anemia


Hypercoagulable state



Increased leukocyte count



Increased minute ventilation

Respiratory alkalosis


Decreased residual capacity



Elevated diaphragm

Abnormal chest radiograph


Decreased motility



Decreased lower esophageal sphincter tone



Increased filtration rate



Dilated collection system

Hydroureter, hydronephrosis


Pelvic ligament laxity

Widened pubic symphysis


Increased venous volume

Bleeding with fractures



An additional hemodynamic effect that may have significant impact on the pregnant trauma patient is the hypotensive effect from compression of the inferior vena cava secondary to the gravid uterus. By 24 weeks' gestation, the uterus is sufficiently enlarged to produce mechanical compression of the vena cava when the patient is in a supine position. This can be manifested by as much as a 25% effective reduction of cardiac output. In the case of significant hemorrhage or cardiac arrest, hemodynamic instability due to caval compression may become an acute problem. All efforts should be made to avoid supine positioning of the severely traumatized pregnant patient during the third trimester. This can be accomplished using the left lateral decubitus position. When the patient cannot be placed on the side due to injuries, a right hip wedge, manual displacement of the uterus laterally by hand, or lateral tilt of backboard or exam table/bed can be effective.

Beyond the cardiovascular changes associated with pregnancy, significant respiratory changes should also be anticipated. Minute ventilation is increased by almost 50%, secondary to an increase in tidal volume. The increase in effective ventilation produces a compensated respiratory alkalosis with a reduction in buffering capacity. A “normal” blood gas in a pregnant patient should prompt an evaluation of respiratory function. Because functional residual capacity is reduced by 15% to 20% at term and oxygen consumption is significantly elevated, pregnant patients are less tolerant of apnea.

During pregnancy, capillary engorgement of the mucosa occurring throughout the respiratory tract can produce edema in the nasopharynx, oropharynx, larynx, and trachea. Manipulation of the airway requires extra care, because further injury may worsen the underlying edema and lead to airway obstruction. Endotracheal intubation with a small, cuffed endotracheal tube (6.5 to 7.0 mm) is reasonable owing to the probability for moderate supraglottic edema.

Gastrointestinal function is also affected by pregnancy, and the risk of gastric reflux is increased in the gravid patient. While alterations in gastric motility are most prominent during labor, a decrease in lower esophageal sphincter tone and increased secretion of gastric acid suggest that the risk of aspiration is increased in any pregnant patient near term.

Physiologic changes of note include increased renal blood flow and creatinine clearance. A mild physiologic hydronephrosis of pregnancy may also be present and should be considered when evaluating the patient with abdominal or pelvic trauma. Hematologic function is altered by an estrogen-influenced increase in hepatic production of coagulation factors. Pregnancy places women at increased risk for thromboembolic disease caused by increased venous stasis, vessel wall injury, and changes in the coagulation cascade that lead to hypercoagulability. Fibrinogen is also increased by 50%, such that a normal level in a pregnant patient (300 mg/dL) may suggest an abnormal consumptive process. Finally, a moderate leukocytosis is normal in pregnancy and does not by itself suggest the presence of an inflammatory or infective process.

In addition to understanding the impact of maternal physiology on the response to trauma, the anesthesiologist must also consider the effects on the fetus. The consequences of trauma on pregnancy depend on the gestational age of the fetus, the type and severity of the trauma, and the extent of disruption of normal uterine and fetal relationships. Fetal survival depends on adequate uterine perfusion and delivery of oxygen. Because autoregulation is lacking in uterine circulation, uterine blood flow is related directly to maternal systemic blood pressure. Once the mother approaches a state of hypovolemic shock, further maternal vasoconstriction will compromise uterine perfusion. Once clinically measurable shock develops in the mother, the chances of saving the fetus are about 20%.

Fetal bradycardia or tachycardia, a decrease in baseline heart rate variability, absence of normal accelerations of fetal heart rate, or repetitive decelerations suggest that fetal oxygenation and/or perfusion have been compromised by trauma. An abnormal fetal heart rate may be the first indication of an important disruption in fetal homeostasis. Finally, direct or indirect uterine trauma can also injure the myometrium and lead to uterine contractions, with the possibility of inducing premature labor. When the maternal injuries are not lethal, placental abruption is the most common cause of fetal demise.[97]Because placental abruption can occur with low energy impacts, all patients with moderate blunt trauma should undergo fetal heart rate monitoring and close observation. [96] [98]


Involvement of anesthesia personnel in the care of the injured pregnant patient potentially requiring surgery should begin with the initial evaluation. Immediate consultation with an obstetrician or maternal-fetal specialist will allow for better coordination of care. The primary goal in treating a pregnant trauma victim is to stabilize the mother's condition. During the primary survey, the priorities for treatment of an injured pregnant patient remain the same as those for the nonpregnant patient. Given the increased risk of aspiration, decreased tolerance for apnea, and fetal distress associated with hypoxia, endotracheal intubation should be considered early. This must be balanced against the potential for encountering a difficult airway, particularly in the later stages of pregnancy. Although tachypnea is present at baseline in the pregnant patient, other causes of respiratory compromise should be sought. Assessment of perfusion and interpretation of all vital signs should take into consideration pregnancy-related changes. With a baseline elevation of 10 to 15 beats per minute above baseline, maternal heart rate may be difficult to correlate with volume status. Assessment of central and peripheral pulses, capillary refill, skin color and temperature, and mental status are still useful tools, although significant hypovolemia can be present with minimal change in these markers.

After initiation of lifesaving measures, a more thorough secondary survey of the stable pregnant patient must include some form of fetal assessment. If possible, a pregnancy history should be obtained with attention to determining the estimated gestational age, prenatal care, and complications, including diabetes or hypertension. Estimated gestational age and viability should be determined quickly, because the fetus is considered to be viable at 24 weeks' gestation. If the mother is unable to provide a history, the ability to palpate the uterine fundus at 3 to 4 cm above the umbilicus correlates with a viable gestational age. Cardiotocographic monitoring (CTM) should be initiated as early as possible. Fetal bradycardia is a sensitive indicator of maternal perfusion and can be the first measurable change in the presence of significant maternal hypovolemia. Uterine irritability and contractions monitored through CTM are sensitive in detecting placental abruption. [99] [100] The American College of Obstetricians and Gynecologists (ACOG) recommends that any pregnant woman sustaining trauma beyond 22 to 24 weeks' gestation should undergo fetal monitoring for a minimum of 24 hours.[99] In the presence of ruptured membranes, bleeding, fetal arrhythmia, fetal heart rate deceleration, or more than four contractions per hour, the patient should be admitted with continuous fetal monitoring for at least 24 hours.

Laboratory evaluation should include hemoglobin, hematocrit, type and crossmatch, urinalysis, coagulation parameters, lactate determination, and blood gas analysis. Interpretation of the results should take pregnancy-related changes into consideration. Physiologic anemia may be confused with that produced by hemorrhage in the pregnant trauma patient. A normal fibrinogen level may be an early indicator of disseminated intravascular coagulation due to placental abruption. Additionally, a normal or elevated Paco2 level may suggest pending respiratory failure. Use of lactate levels as a marker of resuscitation is not affected by the pregnant state.

In the Rh-negative patient, a Kleihauer-Betke test may be ordered to assess for Rh isoimmunization. Administration of RhO(D) immune globulin is indicated in the presence of fetomaternal hemorrhage in this subset of patients.

Preoperative Preparation.

Careful attention must be paid to the perioperative volume status of the gravid trauma patient to avoid decreases in fetal perfusion. As with all trauma patients, large-bore intravenous access is required. When large volumes of crystalloid are necessary, normal saline should be avoided because it may lead to maternal and fetal hyperchloremic acidosis. Coagulation defects should be corrected before surgery, keeping in mind pregnancy-related changes, including an elevated fibrinogen level. Prophylactic measures to reduce gastric pH and volume are warranted, because aspiration of gastric contents during general anesthesia is a major cause of maternal morbidity and mortality.

Intraoperative Considerations.

The choice of anesthetic technique in the traumatized pregnant patient will be determined by the operative procedure, concomitant injuries, preexisting conditions, and maternal preference. When feasible, regional anesthesia offers some advantages to general anesthesia, although there is no direct evidence showing a reduction in mortality. A decrease in the administration of systemic medications and subsequent reduction in fetal exposure is desirable. Additionally, the avoidance of airway manipulation reduces the risk of airway loss and maternal morbidity.

Nonetheless, general anesthesia will still be a necessity for many pregnant trauma patients requiring operative procedures. Preoxygenation before anesthetic induction must be accomplished for more than 3 minutes with 100% oxygen to blunt the rapid onset of hypoxia seen with apnea in these patients.[100] This is usually accomplished in conjunction with an RSI due to the increased risk of aspiration. Left uterine displacement must be continued throughout the induction and operative periods. Invasive hemodynamic monitoring is used as dictated by maternal conditions. Maternal arterial CO2 should be kept at 33 to 36 mm Hg. Further degrees of hyperventilation may be detrimental to fetal perfusion. Intraoperative fetal CTM can supplement other available information regarding maternal perfusion, although operative considerations may prohibit its use. CTM should be continued into the postoperative period to monitor for premature labor.

Concerns about the effects of anesthetic agents on the growth and development of the human fetus should be factored into the anesthetic plan. A more comprehensive review of pharmacologic considerations and potential teratogenicity is provided elsewhere in this text (see Chapter 19 ). Agents and techniques that have been widely used and evaluated should be employed for the care of the pregnant trauma patient whenever possible.

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Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Geriatric Trauma

Outcomes from trauma are dramatically worse in elderly patients, with significantly higher in-hospital morbidity and mortality rates after identical anatomic injuries.[101] Reasons for this difference are multifactorial but may include a decreased basal metabolic rate, limited cardiopulmonary reserve, impaired wound healing, and increased susceptibility to sepsis. Elderly patients are more likely than younger ones to have coexisting medical disease, such as diabetes or atherosclerosis, that contribute to delayed healing. Preexisting neurologic impairment, including untreated depression, is common in older trauma patients. For many elderly patients it is a traumatic event that signifies the transition from independent living to a requirement for chronic nursing care or assisted living.

For the anesthesiologist, close attention to detail is required to achieve the best possible results. This may include modalities such as nutritional support, continuous insulin infusion, and perioperative β blockade. The surgical procedures required by elderly patients are similar to those in other trauma patients, but determining the optimal timing for surgery may be more challenging. Bed-bound elderly trauma patients will suffer a predictable and progressive loss of pulmonary function owing to atelectasis and pneumonia, even in the presence of attentive nursing care, meaning that delaying surgery in an effort to improve ventilation or perform further diagnostic studies may be counterproductive. Similarly, the need for urgent operative repair of long bone fractures and open wounds should limit the pursuit of specialty consultation and risk stratification studies (e.g., stress cardiac imaging) to those situations in which there is a high likelihood of a change in management. Patients with active myocardial ischemia or cardiac dysrhythmias may benefit from angioplasty or electrophysiologic intervention before an orthopedic surgery, but in most other situations the patient will benefit more from prompt surgical correction of the traumatic injury.[33]

In general, the anesthesiologist is advised to assume the worst about the patient with an unclear history or unknown cardiac risk. Anesthetic medications, including induction agents, should be chosen with the intention of maintaining cardiovascular stability and should be carefully titrated to the patient's response. Many elderly patients will exhibit prolonged sedation and disorientation after intravenous anxiolysis, frequently necessitating postoperative mechanical ventilation. Invasive arterial pressure monitoring and frequent laboratory assessment of tissue perfusion should be considered in any patient likely to experience more than a minimal blood loss. Pulmonary artery catheterization and direct assessment of myocardial performance and fluid volume status may be beneficial,[102] although this technique is cumbersome in the operating room. Transesophageal echocardiography and newer noninvasive technologies may be more appropriate for elderly patients undergoing moderate risk procedures.

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Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Prehospital Anesthetic Care

The role of the anesthesiologist extends beyond the walls of a medical facility when he or she becomes involved in prehospital medical care. Many large trauma centers have established relationships with their local emergency medical service (EMS) to provide a field response or “Go Team” that is capable of providing extended medical support in the event of a disaster or accident where their services may be necessary for lifesaving or limb-saving interventions.[103] Physician involvement in prehospital management of trauma is limited to consultation and occasional scene response in North America, although Israel, Germany, France, and other countries have mobile ICUs staffed by anesthesiologists and other physicians. [104] [105]

Inclusion on a “Go Team” brings with it certain training requirements for the unique conditions found with medical disaster response. An effective approach to the challenges of disaster response is to break the response down to recognizable tasks ( Table 17-16 ). Although physicians involved in the response to a disaster scene will not be responsible for the majority of these tasks, familiarity with them will make their integration into the team smoother and establish a framework for their own unique skills. Individuals assigned to a “Go Team” must be familiar with a number of areas, including working with hazardous materials, use of personal protective gear, maintaining scene control, decontamination, use of rescue equipment, understanding of aeromedical considerations, and basic emergency medicine training.

TABLE 17-16   -- Disaster Response Tasks



Scene Assessment



Scene description



Scene safety



Patient conditions



Incident Management



Command and control






Victim Care



Search and rescue



Primary assessment and triage






Definitive care



The most common scenario for “Go Team” response is entrapment after a motor vehicle crash or building collapse. Field amputation is occasionally required to safely extract the patient. A familiarity with intravenous anesthesia and alternative airway techniques are essential for these types of cases. In addition, the “Go Team” usually has the ability to administer blood products as well as higher degrees of sedation than are possible under most EMS protocols.

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Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier


  1. Fingerhut LA, Warner M: Injury Chartbook. Health, United States, 1996-97,  Hyattsville, MD, National Center for Health Statistics, 1998.
  2. West JG, Cales RH, Gazzaniga AB: Impact of regionalization the Orange County experience.  Arch Surg1983; 118:740.
  3. Resources for optimal care of the injured patient: 1998,  Chicago, American College of Surgeons, 1998.
  4. Dutton RP, Scalea TM, Aarabi B: Prioritizing surgical needs in the multiply injured patient.  Trauma Care2002; 13(3):In Prough DS, Fleisher L (eds): Problems in Anesthesia
  5. Rotondo MF, Schwab CW, McGonigal MD, et al: ‘Damage control’: An approach for improved survival in exsanguinating penetrating abdominal injury.  J Trauma1993; 35:375-382.
  6. Scalea TM, Boswell SA, Scott JD, et al: External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: Damage control orthopedics.  J Trauma2000; 48:613-621.
  7. Committee on Trauma, American College of Surgeons : Advanced Trauma Life Support Program for Doctors,  Chicago, American College of Surgeons, 1997.
  8. Thierbach AR, Lipp MDW: Airway management in trauma patients.  Anesth Clin North Am1999; 17:63-81.
  9. Xiao Y, Hunter WA, Mackenzie CF, et al: Task complexity in emergency medical care and its implications for team coordination.  Hum Factors1996; 38:636-645.
  10. Todd MM, Hindman BJ, Brian JE: Cervical Spine Anatomy and Physiology for Anesthesiologists.  ASA Refresher Courses in Anesthesiology,  Chicago: American Society of Anesthesiologists; 2003:189-202.
  11. Talucci RC, Shaikh KA, Schwab CW: Rapid sequence induction with oral endotracheal intubation in the multiply injured patient.  Am Surg1988; 54:185-187.
  12. Brimacombe JR, Brain AIJ, Berry AM: Anatomical implications.   In: Brimacombe JR, Brain AIJ, ed. The Laryngeal Mask Airway: A Review and Practical Guide,  Philadelphia: WB Saunders; 1997:14-26.
  13. Practice guidelines for management of the difficult airway. An updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway.  Anesthesiology2003; 98:1269-1277.
  14. Crile GW: An Experimental Research into Surgical Shock,  Philadelphia, JB Lippincott, 1899.
  15. Peitzman AB: Hypovolemic shock.   In: Pinsky MR, Dhainaut JFA, ed. Pathophysiologic Foundations of Critical Care,  Baltimore: Williams & Wilkins; 1993:161-169.
  16. Shires GT, Cunningham N, Baker CRF, et al: Alterations in cellular membrane function during hemorrhagic shock in primates.  Ann Surg1972; 176:288-295.
  17. Dutton RP: Management of traumatic shock.  Trauma Care2002; 13(3):In Prough DS, Fleisher L (eds): Problems in Anesthesia
  18. Blow O, Magliore L, Claridge JA, et al: The golden hour and the silver day: Detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma.  J Trauma1999; 47:964-969.
  19. Stern A, Dronen SC, Birrer P, Wang X: Effect of blood pressure on haemorrhagic volume in a near-fatal haemorrhage model incorporating a vascular injury.  Ann Emerg Med1993; 22:155-163.
  20. Capone A, Safar P, Stezoski SW, et al: Uncontrolled hemorrhagic shock outcome model in rats.  Resuscitation1995; 29:143-152.
  21. Riddez L, Johnson L, Hahn RG: Central and regional hemodynamics during fluid therapy after uncontrolled intra-abdominal bleeding.  J Trauma1998; 44:1-7.
  22. Sakles JC, Sena MJ, Knight DA, Davis JM: Effect of immediate fluid resuscitation on the rate, volume, and duration of pulmonary vascular hemorrhage in a sheep model of penetrating thoracic trauma.  Ann Emerg Med1997; 29:392-399.
  23. Burris D, Rhee P, Kaufmann C, et al: Controlled resuscitation for uncontrolled hemorrhagic shock.  J Trauma1999; 46:216-223.
  24. Bickell WH, Wall MJ, Pepe PE, et al: Immediate versus delayed resuscitation for hypotensive patients with penetrating torso injuries.  N Engl J Med1994; 331:1105-1109.
  25. Dutton RP, Mackenzie CF, Scalea TM: Hypotensive resuscitation during active hemorrhage: Impact on in-hospital mortality.  J Trauma2002; 52:1141-1146.
  26. Camp, FR, Conte NF, Brewer JR: Military Blood Banking 1941-1973,  Fort Knox, KY: U.S. Army Medical Research Laboratory; 1973:20.
  27. Lorentz A, Frietsch T: Transfusion medicine.  N Engl J Med2002; 347:538-539.
  28. Martinowitz U, Kenet G, Segal E, et al: Recombinant activated factor VII for adjunctive hemorrhage control in trauma.  J Trauma2001; 51:1-9.
  29. Prough DS, Bidani A: Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline.  Anesthesiology1999; 90:1247.
  30. Otto CW: Cardiopulmonary resuscitation.   In: Barash PG, Cullen BF, Stoelting RK, ed. Clinical Anesthesia,  4th ed. Philadelphia: Lippincott-Raven; 2001:1498-1499.
  31. Abramson D, Scalea TM, Hitchcock R, et al: Lactate clearance and survival following injury.  J Trauma1993; 35:584-588.
  32. Evans RW: The postconcussion syndrome and the sequelae of mild head injury.  Neurol Clin1992; 10:815-847.
  33. Dunham CM, Bosse MJ, Clancy TV, et al: Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients: The EAST practice management guidelines work group.  J Trauma2001; 50:958-967.
  34. Kalb DC, Ney AL, Rodriguez JL, et al: Assessment of the relationship between timing of fixation of the fracture and secondary brain injury in patients with multiple trauma.  Surgery1998; 124:739-744.
  35. Guidelines for the management of severe traumatic brain injury. Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care.  J Neurotrauma2000; 17:451-627.
  36. Chestnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury.  J Trauma1993; 134:216-222.
  37. Kerr EM, Marion D, Sereika MS, et al: The effect of cerebrospinal fluid drainage on cerebral perfusion in traumatic brain injured adults.  J Neurosurg Anesthesiol2000; 12:324-333.
  38. Cremer OL, Moons KG, Bouman EA, et al: Long-term propofol infusion and cardiac failure in adult head-injured patients.  Lancet2001; 357:117-118.
  39. Masuzawa M, Nakao S, Miyamoto E, et al: Pentobarbital inhibits ketamine-induced dopamine release in the rat nucleus accumbens: A microdialysis study.  Anesth Analg2003; 96:148-152.
  40. Soukiasian HJ, Hui T, Avital I, et al: Decompressive craniectomy in trauma patients with severe brain injury.  Am Surg2002; 68:1066-1071.
  41. Joseph D, Dutton RP, Aarabi B, Scalea TM: Decompressive laparotomy to reduce intracranial pressure in patients with severe traumatic brain injury.  J Trauma2004; 57:687-693.
  42. Clifton GL, Emmy RM, Choi SC, et al: Lack of effect of induction of hypothermia after acute brain injury.  N Engl J Med2001; 344:556-563.
  43. Kiwerski JE: Neurological outcome from conservative treatment of cervical spinal cord injured patients.  Paraplegia1993; 31:192-196.
  44. EAST Practice Parameter Workgroup for Cervical Spine Clearance : Practice Management Guidelines for Identifying Cervical Spine Injuries Following Trauma. Eastern Association for the Surgery of Trauma 1998.  Available at http://east.org/tpg.html.
  45. American Association of Neurological Surgeons : Guidelines for the management of acute spinal cervical spine and spinal cord injuries.  Neurosurgery2002; 59:S58.
  46. Bracken MB, Shepard MJ, Holford TR, et al: Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury: Results of the third National Acute Spinal Cord Injury Study.  JAMA1997; 277:1597-1604.
  47. Kewelramani LS: Autonomic dysreflexia in traumatic myelopathy.  Am J Phys Med1980; 59:1.
  48. Zagelbaum BM, Tostanoski JR, Kerner DJ, Hersh PS: Urban eye trauma: A one-year prospective study.  Ophthalmology1993; 100:851-856.
  49. Blomdahl S, Norell S: Perforating eye injury in the Stockholm population: An epidemiological study.  Acta Ophthalmol (Copenh)1984; 62:378-390.
  50. Cunningham AJ, Barry P: Intraocular pressure physiology and implications for anaesthetic management.  Can Anaesth Soc J1986; 33:195-208.
  51. Pandey K, Badola RP, Kumar S: Time course of intraocular hypertension produced by suxamethonium.  Br J Anaesth1972; 44:191-196.
  52. Vachon CA, Warner DO, Bacon DR: Succinylcholine and the open globe: Tracing the teaching.  Anesthesiology2003; 99:220-223.
  53. Libonati MM, Leahy JJ, Ellison N: The use of succinylcholine in open eye surgery.  Anesthesiology1985; 62:637-640.
  54. Moreno RJ, Kloess P, Carlson DW: Effect of succinylcholine on the intraocular contents of open globes.  Ophthalmology1991; 98:636-638.
  55. Drenger B, Pe'er J, BenEzra D, et al: The effect of intravenous lidocaine on the increase in intraocular pressure induced by tracheal intubation.  Anesth Analg1985; 64:1211-1213.
  56. Stirt JA, Chiu GJ: Intraocular pressure during rapid sequence induction: Use of moderate-dose sufentanil or fentanyl and vecuronium or atracurium.  Anaesth Intensive Care1990; 18:390-394.
  57. Karlson TA: The incidence of hospital-treated facial injuries from vehicles.  J Trauma1982; 22:303-310.
  58. Hackl W, Hausberger K, Sailer R, et al: Prevalence of cervical spine injuries in patients with facial trauma.  Oral Surg Oral Med Oral Pathol Oral Radiol Endod2001; 92:370-376.
  59. Luce EA, Tubb TD, Moore AM: Review of 1,000 major facial fractures and associated injuries.  Plast Reconstr Surg1979; 63:26-30.
  60. Lee KF, Wagner LK, Lee YE, et al: The impact-absorbing effects of facial fractures in closed-head injuries: An analysis of 210 patients.  J Neurosurg1987; 66:542-547.
  61. Capan LM, Miller SM, Glickman R: Management of facial injuries.   In: Capan LM, Miller SM, Turndorf H, ed. Trauma Anesthesia and Intensive Care,  Philadelphia: JB Lippincott; 1991:385-408.
  62. Krohner RG: Anesthetic considerations and techniques for oral and maxillofacial surgery.  Int Anesthesiol Clin2003; 41:67-89.
  63. Shepherd SM, Lippe MS: Maxillofacial trauma: Evaluation and management by the emergency physician.  Emerg Med Clin North Am1987; 5:371-392.
  64. Rohrich RJ, Shewmake KB: Evolving concepts of craniomaxillofacial fracture management.  Clin Plast Surg1992; 19:1-10.
  65. Gruss JS: Complex craniomaxillofacial trauma: Evolving concepts in management: A trauma unit's experience 1989 Fraser B. Gurd lecture.  J Trauma1990; 30:377-383.
  66. Martin JE, Mehta R, Aarabi B, et al: Intracranial insertion of a nasopharyngeal airway in a patient with craniofacial trauma.  Milit Med2004; 169:496-497.
  67. Petty SM, Parker LA, Mauro MA, et al: Chronic posttraumatic aortic pseudoaneurysm.  Postgrad Med1991; 89:173-178.
  68. Mirvis SE, Shanmuganathan K, Miller BH: Traumatic aortic injury: Diagnosis with contrast-enhanced thoracic CT-five year experience at a major trauma center.  Radiology1996; 200:413.
  69. Dunham MB, Zygun D, Petrasek P, et al: Endovascular stent grafts for acute blunt aortic injury.  J Trauma2004; 56:1173-1178.
  70. Read RA, Moore EE, Moore FA, Haenel JB: Partial left heart bypass for thoracic aortic repair.  Arch Surg1993; 128:746.
  71. Johnson KD, Cadambi A, Seibert GB: Incidence of adult respiratory distress syndrome in patients with multiple musculoskeletal injuries: Effect of early operative stabilization of fractures.  J Trauma1985; 25:375-384.
  72. Bone LB, Johnson KD, Weigelt J, Scheinberg R: Early versus delayed stabilization of femoral fractures: A prospective randomized study.  J Bone Joint Surg Am1989; 71:336-340.
  73. Dalal SA, Burgess AR, Siegel JH, et al: Pelvic fracture in multiple trauma: Classification by mechanism is key to pattern of organ injury, resuscitative requirements, and outcome.  J Trauma1989; 29:981-1000.
  74. Burney RE, et al: Incidence, characteristics, and outcome of spinal cord injury at trauma centers in North America.  Arch Surg1993; 128:596-599.
  75. In: Rothman RH, Simeone FA, ed. The Spine,  Philadelphia: WB Saunders; 1992.
  76. Klein SR, Saroyan RM, Baumgartner F, Bonegard FS: Management strategy of vascular injuries associated with pelvic fractures.  J Cardiovasc Surg (Torino)1992; 33:349-357.
  77. Bradford EM: Haemodynamic changes associated with the application of lower limb tourniquets.  Anaesthesia1969; 24:190-197.
  78. Kaufman RD, Walts LF: Tourniquet-induced hypertension.  Br J Anaesth1982; 54:333-336.
  79. Kahn RL, Marino V, Urguhart B, Sharrock NE: Hemodynamic changes associated with tourniquet use under epidural anesthesia for total knee arthroplasty.  Reg Anesth1992; 17:228-232.
  80. Klenerman L: Tourniquet time how long?.  Hand1980; 12:231-234.
  81. Heppenstall RB, Scott R, Sapega A, et al: A comparative study of the tolerance of skeletal muscle to ischemia: Tourniquet application compared with acute compartment syndrome.  J Bone Joint Surg Am1986; 68:820-828.
  82. Sapega AA, Heppenstall RB, Chance B, et al: Optimizing tourniquet application and release times in extremity surgery: A biochemical and ultrastructural study.  J Bone Joint Surg Am1985; 67:303-314.
  83. Hutchins PM, Macnicol MF: Pulmonary insufficiency after long bone fractures: Absence of circulating fat or significant immunodepression.  J Bone Joint Surg Br1985; 67:835-839.
  84. Lindeque BG, Schoeman HS, Dommisse GF, et al: Fat embolism and the fat embolism syndrome: A double-blind therapeutic study.  J Bone Joint Surg Br1987; 69:128-131.
  85. Kallenbach J, Lewis M, Zaltman M, et al: Low-dose corticosteroid prophylaxis against fat embolism.  J Trauma1987; 27:1173-1176.
  86. Schonfeld SA, Ploysongsang Y, Dilisio R, et al: Fat embolism prophylaxis with corticosteroids: A prospective study in high-risk patients.  Ann Intern Med1983; 99:438-443.
  87. Alho A, Saikku K, Eerola P, et al: Corticosteroids in patients with a high risk of fat embolism syndrome.  Surg Gynecol Obstet1978; 147:358-362.
  88. Williams-Russo P, Sharrock NE, Haas SB, et al: Randomized trial of epidural versus general anesthesia: Outcomes after primary total knee replacement.  Clin Orthop1996; 331:199-208.
  89. Prins MH, Hirsh J: A critical review of the evidence supporting a relationship between impaired fibrinolytic activity and venous thromboembolism.  Arch Intern Med1991; 151:1721-1731.
  90. Sharrock NE, Hargell MJ, Urquhart B, et al: Factors affecting deep vein thrombosis rate following total knee arthroplasty under epidural anesthesia.  J Arthroplasty1993; 8:133-139.
  91. Rogers FB, Cipolle MD, Velmahos G, Rozycki G: Practice Management Guidelines for the Management of Venous Thomboembolism in Trauma Patients,  Atlanta, The Eastern Association for the Surgery of Trauma, 1999.
  92. Horlocker TT, Wedel DJ, Berzon H, et al: Regional anesthesia in the anticoagulated patient: Defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation).  Reg Anesth Pain Med2003; 28:172-197.
  93. Orlowski JP, Abulleli MM, Phillips JM: Effects of tonicities of saline solutions on pulmonary injury in drowning.  Crit Care Med1987; 1:126.
  94. Weaver LK, Hopkins RO, Chan KJ, et al: Hyperbaric oxygen for acute carbon monoxide poisoning.  N Engl J Med2002; 347:1057-1067.
  95. Connolly AM, Katz VL, Bosh KL, et al: Trauma and pregnancy.  Am J Perinatol1997; 14:331-336.
  96. Pearlman MD, Tintinalli JE: Evaluation and treatment of the gravida and fetus following trauma during pregnancy.  Obstet Gynecol Clin North Am1991; 18:371-381.
  97. Dahmus MA, Sibai BM: Blunt abdominal trauma: Are there any predictive factors for abruptio placentae or maternal-fetal distress?.  Am J Obstet Gynecol1993; 169:1054-1059.
  98. Pak LL, Reece EA, Chan L: Is adverse pregnancy outcome predictable after blunt abdominal trauma?.  Am J Obstet Gynecol1998; 179:1140-1144.
  99. American College of Obstetricians and Gynecologists : Obstetric Aspects of Trauma Management,  Washington, DC, ACOG, 2000. ACOG educational bulletin No. 251
  100. Archer GW, Marx GF: Arterial oxygen tension during apnoea in parturient women.  Br J Anaesth1974; 46:358-360.
  101. Osler T, Hales K, Baack B, et al: Trauma in the elderly.  Am J Surg1988; 156:537.
  102. Scalea TM, Simon HM, Duncan AO, et al: Geriatric blunt multiple trauma: Improved survival with early imaging and monitoring.  J Trauma1990; 30:129.
  103. Jaslow D, Barbera JA, Desai S, Jolly BT: An emergency department-based field response team: Case report and recommendations for a ‘go team.’.  Prehosp Emerg Care1998; 2:81-85.
  104. Einav S, Donchin Y, Weisman C, et al: Anesthesiologists on ambulances: Where do we stand?.  Curr Opin Anaesthesiol2003; 16:585-591.
  105. Benitez FL, Pepe PE: Role of the physician in prehospital management of trauma: North American perspective.  Curr Opin Crit Care2003; 8:551-558.