Trauma Anesthesia Challenges
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Key action points for anesthesia in the setting of trauma include the following:
Through decisive action and communication with the trauma team, the anesthesiologist proves critical in reducing the morbidity and mortality of the acute trauma patient.
Trauma is among the leading causes of morbidity and mortality worldwide. In fact, it is the leading cause of death in the United States for individuals between the ages of 1 and 46 years, accounting for a staggering 47% of deaths in this group. [1] Trauma patients presenting to the operating room (OR) for emergency treatment generally have been subjected either to blunt force or to penetrating injury, and their care poses specific challenges for the anesthetic provider, including the following:
The anesthesiologist plays a critical role in stabilizing the patient and maintaining safe conditions during this dynamic period and frequently will find it necessary to shift management strategies as the case evolves.
In trauma cases, unlike many scheduled and urgent anesthesia cases, the patient commonly presents to the OR with an unknown past medical history and is already involved in an evolving spectrum of care that may have been initiated in the prehospital setting or in the emergency department (ED). Examples range from a patient who is already orotracheally intubated with large-bore venous access and is undergoing massive transfusion resuscitation to a combative patient who is in systemic shock with little or no access and whose vital signs are faltering.
In the face of the special challenges posed by trauma, it is imperative that the anesthesiologist be able to call upon his or her training in a well-equipped environment (ie, one that includes advanced airway equipment, rapid transfusion devices, vasoactive agents with infusion pumps, and warming devices) and act quickly to accomplish the following:
Induction of anesthesia and selection of anesthetics
A rapid sequence induction is required for trauma patients presenting to OR with an unsecured airway. As noted, induction of anesthesia is particularly challenging in the setting of trauma, both because the extent of the patient’s injuries is often undetermined or underappreciated (as when there is significant blood loss in closed compartments such as the retroperitoneal space or the lower extremities) and because comorbid conditions frequently are unknown and unoptimized.
Accordingly, careful selection of induction and maintenance agents is critical. [2] Commonly used agents include the following:
It must be kept in mind, however, that even with careful selection, hemodynamic instability can be encountered in the administration of any anesthetic to a trauma patient, given that the injured patient may be extremely hypovolemic and vasodilated with impaired compensatory mechanisms. In this situation, the anesthetic dosage must be titrated downward, at the expense of increased risk of awareness; anesthetic depth can be increased only as hemodynamic stability is obtained during damage control surgery. [3]
Etomidate, a gamma-aminobutyric acid (GABA) agonist, offers a stable hemodynamic profile with minimal disruption of vascular tone. [4] Furthermore, its ability to decrease cerebral blood flow, cerebral metabolic requirements, and intracranial pressure (ICP) make it particularly useful in unstable trauma patients with known intracranial injury. [2] On the other hand, etomidate has its disadvantages. It has been associated with increased mortality in septic patients on the basis of its known adrenal suppression; it has also been shown to increase trauma patients’ susceptibility to pneumonia, which potentially limits its utility. [5]
Ketamine, a noncompetitive N-methyl-d-aspartic acid (NMDA) inhibitor, is another induction and maintenance agent that is commonly used in trauma patients. Through its ability to raise sympathetic tone and release endogenous catecholamines, ketamine can actually increase cardiovascular tone; this makes it particularly appealing in the hypovolemic, hypotensive trauma patient. In addition, because ketamine’s lipophilicity and formulation permit intramuscular (IM) injection, this agent can be administered to combative patients without vascular access.
However, ketamine is not without its own disadvantages. Despite its ability to increase cardiovascular tone, it is also a direct myocardial depressant, and its use can lead to significant hypotension in the catecholamine-depleted patient. [6] Ketamine is also known to raise ICP, an effect that raises questions about its applicability in patients with traumatic intracranial injuries; however, some studies have suggested that it may in fact have a neuroprotective effect. [7]
Propofol, a lipid-soluble GABA agonist, is one of the most widely used induction agents in the United States; consequently, most US anesthesia providers are familiar with it and have expertise in using it. However, propofol, though ideal for hemodynamically stable patients by virtue of its quick onset of action and deep levels of amnesia, causes a significant reduction in systemic vascular tone and has mild myocardial depressant effects, which make it potentially dangerous in the trauma setting. Nonetheless, this agent can still play a role in trauma anesthesia if administered in reduced doses, in conjunction with other induction agents, or with vasoactive support.
Neuromuscular blockade
Once amnesia has been induced, neuromuscular blockade often is also needed to facilitate endotracheal intubation. Both depolarizing and nondepolarizing neuromuscular blocking agents can be used, with the recognition that a quick onset of action is of primary importance. The two agents most commonly used for neuromuscular blockade are succinylcholine and rocuronium.
Succinylcholine, a depolarizing agent, is characterized by its quick onset and short duration of action for a single dose. It must be used cautiously in patients with known neuromuscular disease and denervation injuries because it can lead to life-threatening hyperkalemia. Rocuronium, a nondepolarizing agent, can achieve similar intubation conditions in a rapid sequence induction at a higher dose without the associated hyperkalemic response. However, even though rocuronium is one of the shortest-acting nondepolarizing agents, its duration of action is significantly longer than that of succinylcholine.
Airway management
Securing the airway in a trauma patient can include multiple challenges that may require the anesthesiologist to move quickly along a modified difficult airway algorithm. [8] As noted, trauma patients can present to the OR at any of numerous points along a spectrum of consciousness, resuscitation, and initiation of care; accordingly, they are often less able, or even entirely unable, to cooperate with preoperative evaluation and airway assessment.
Furthermore, there is an extremely high likelihood that the patient either will have a cervical spine (C-spine) injury or will still be observing full C-spine precautions, either of which will limit the ability to flex or extend the neck as well as potentially hinder mouth opening. [9] In addition, the patient may have maxillofacial or intraoral injuries that distort the normal anatomy and thus make intubation via traditional methods difficult or impossible. [10] In this setting, blood or vomitus in the airway can render video and fiberoptic laryngoscopy futile.
In these scenarios, unlike difficult airway scenarios for nontrauma surgical procedures, the patient’s relative inability to tolerate or cooperate with an awake fiberoptic intubation, coupled with the time needs for securing the airway to facilitate stabilization, eliminates the option of “waking the patient up” when the airway cannot be secured. This creates a situation where a surgical airway must be considered early on, possibly as the primary technique, so as not to delay surgical intervention or induce hypoxia in an already compromised patient.
In short, airway management can be highly challenging in trauma patients, and the anesthesiologist must have a plan in place with multiple backup methods that often must be employed in an accelerated manner to facilitate the ongoing emergency care of these patients. The anesthesiologist must act quickly and decisively to determine whether direct laryngoscopy is possible or video laryngoscopy is viable, as well as to initiate surgical control of the airway if necessary.
Hemodynamic stabilization and resuscitation
Once anesthesia is induced and the airway is secured, the anesthesiologist’s role shifts to establishing hemodynamic stabilization and resuscitating the patient. This role also may differ in the setting of trauma, in that the anesthesiologist may need to observe lower MAP goals if there is acute hemorrhage or may need to delay or modify fluid replacement therapy.
For damage control surgery in patients with hemodynamic instability caused by uncontrolled hemorrhage, the literature supports an MAP goal of approximately 65 mm Hg and the delayed use of large crystalloid volumes to help minimize blood loss and keep from diluting the coagulation cascade. [8, 11] Once hemodynamic control has been established, the MAP goal can be raised to a higher level, as deemed appropriate.
In lieu of administration of large crystalloid volumes as recommended by advanced trauma life support (ATLS) guidelines, early administration of balanced PRBC:FFP:Plt ratios has been suggested as a means of lowering morbidity and mortality in trauma patients. [12] These patients often have coagulopathies (see below), and it is critical to reduce risk factors that might disturb clot formation. [13] Replacing the lost whole-blood components with balanced-ratio PRBC:FFP:Plt, as well as using real-time coagulopathy monitors (eg, thromboelastography [TEG]) to further guide therapy with other factors (eg, cryoprecipitate), can help achieve the control of bleeding that is critical for maintaining hemodynamic stability.
Management of coagulopathy
Finally, trauma patients frequently experience coagulopathies, for any of a multitude of reasons. Hess et al described this traumatic coagulopathy as follows [14] :
Traumatic coagulopathy is a complex multifactorial process, contrary to the simplistic, reductionist explanations which pervade and underpin current clinical practice. There appear to be six primary mechanisms involved in the development of traumatic coagulopathy: tissue trauma, shock, hemodilution, hypothermia, acidemia, and inflammation. Shock is the main driver of early coagulopathy, but requires tissue injury as an initiator. As shock progresses and intravenous therapy is initiated, hemodilution exacerbates the established hemostatic derangements. Where bleeding is unchecked, severe hypothermia and acidemia aggravate the established coagulopathy. The clinical importance of inflammation in the development of trauma coagulopathy has not been fully elucidated.
The anesthesiologist has the ability to intercede at several key points to minimize the impact of several of these factors, as follows:
The anesthesiologist plays an integral role in combating the coagulopathies seen in major trauma; both vigilance and aggressive action are needed to minimize their many inciting causes.
A 29-year-old man with an unknown past medical history presents after an altercation in which he was struck with a baseball bat and stabbed multiple times. The primary survey in the ED reveals free air in the abdomen, and the patient is booked for emergency laparotomy. On inspection, he has an extremely swollen face with distorted anatomy and a very bloody oropharynx.
After a rapid sequence induction with etomidate and succinylcholine, the anesthesiologist is able to obtain only a grade IV view on direct laryngoscopy, and video laryngoscopy fails because of the copious amount of blood present. The anesthesiologist is able to carry out mask ventilation with tidal volumes between 200 and 300 mL and to maintain oxygen saturation in the mid-90s (%).
What can be done at this point to secure the airway?
Given the patient’s need for emergency surgery (laparotomy in the setting of free air in the abdomen) and the presumed extensive facial fractures and dental injury leading to inability to secure the airway definitively, the anesthesiologist should quickly move along the modified difficult airway algorithm discussed above (see Management).
Specifically, the anesthesiologist should maintain oxygenation and ventilation via mask ventilation while having the trauma surgeon perform an urgent tracheostomy to secure the airway definitively, both for the emergency surgical procedure at hand and for the future operations presumed to be necessary to address the maxillofacial damage.
An elderly patient presents as a case of pedestrian vs car. Her past medical history is unclear, but she has known unstable pelvic fractures and worrisome vital signs. On examination, the patient is petite and frail-appearing, with a Glasgow Coma Scale (GCS) score of 9. Her heart rate is in the 100s (beats/min) to 110s, her systolic BP in the 80s (mm Hg) to 90s, and her diastolic BP in the 50s to 60s. The patient comes to the OR with one 20-gauge peripheral IV and one 16-gauge peripheral IV, a hematocrit of 0.19, and normal saline wide open.
What should be the plan for access, induction, and resuscitation?
The anesthesiologist should begin volume resuscitation with a balanced-ratio PRBC:FFP:Plt formulation while placing an arterial line before induction. Once adequate monitoring is in place, the anesthesiologist should perform a rapid sequence induction with etomidate and succinylcholine to help reduce the risks of hemodynamic collapse and then should maintain anesthesia with a combination of volatile anesthetic and IV agents (eg, midazolam) to the extent that the patient’s BP will permit.
Hemodynamic goals should focus on reduced MAPs (65-70 mm Hg) until hemodynamic control has been achieved. Once hemodynamic control is obtained, the anesthesiologist can raise the target MAP and deepen anesthesia while maintaining resuscitation with blood products, as guided by surgical losses and values from laboratory tests and evaluative procedures (eg, hematocrit, international normalized ratio [INR], and TEG).
A 45-year-old male cyclist presents to the OR for repair of an open left femur fracture after being struck by a car. He is currently awake and oriented and is in a cervical collar. He has sustained multiple abrasions and lacerations. In addition to the open femur fracture, the patient has multiple rib fractures, a nondisplaced clavicle fracture, and a small subdural hematoma. His HR is 110 beats/min; his systolic BP is in the 150s; his diastolic BP is in the 80s; his respiratory rate (RR) is 24 breaths/min; and his oxygen saturation is 93% on 10 L of oxygen via face mask.
After American Society of Anesthesiologist (ASA) monitors are placed, a rapid sequence induction is performed with ketamine, propofol and succinylcholine. The airway is secured via video laryngoscopy. Shortly after induction, the patient’s BP falls to 80s/50s, his oxygen saturation decreases to 88% despite a 100% fraction of inspired oxygen (FiO2), and on inspection, only the left side of the chest is noted to have breath sounds, despite the endotracheal tube being secured at 20 cm at the teeth.
Given the constellation of decreased breath sounds, hypotension, and desaturation developing shortly after initiation of positive-pressure ventilation (PPV) in a trauma patient with known rib fractures, emergency treatment of a tension pneumothorax is indicated. The anesthesiologist should support BP with vasoactive agents while performing a needle decompression in the midclavicular line at the second intercostal space. Alternatively, if time permits, the anesthesiologist can consult with the trauma surgeon for emergency chest tube placement.
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Vanderhave KL, Chiravuri S, Caird MS, Farley FA, Graziano GP, Hensinger RN, et al. Cervical spine trauma in children and adults: perioperative considerations. J Am Acad Orthop Surg. 2011 Jun. 19 (6):319-27. [Medline].
Robertson CG, Doucet JC. Helping anesthesiologists understand facial fractures. Oral Maxillofac Surg Clin North Am. 2013 Nov. 25 (4):561-72. [Medline].
Bickell WH, Wall MJ Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994 Oct 27. 331 (17):1105-9. [Medline]. [Full Text].
Tapia NM, Suliburk J, Mattox KL. The initial trauma center fluid management of penetrating injury: a systematic review. Clin Orthop Relat Res. 2013 Dec. 471 (12):3961-73. [Medline]. [Full Text].
Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma. 2003 Jun. 54 (6):1127-30. [Medline].
Hess JR, Brohi K, Dutton RP, Hauser CJ, Holcomb JB, Kluger Y, et al. The coagulopathy of trauma: a review of mechanisms. J Trauma. 2008 Oct. 65 (4):748-54. [Medline].
Christopher Painter, MD Clinical Assistant Professor, Department of Anesthesiology, Stanford University School of Medicine
Christopher Painter, MD is a member of the following medical societies: American Society of Anesthesiologists, California Society of Anesthesiologists
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Sheela Pai Cole, MD Clinical Associate Professor of Cardiothoracic Anesthesiology and Critical Care Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine
Sheela Pai Cole, MD is a member of the following medical societies: American Medical Association, American Society of Anesthesiologists, American Society of Echocardiography, California Society of Anesthesiologists, International Anesthesia Research Society, Pennsylvania Society of Anesthesiologists, Society of Cardiovascular Anesthesiologists, Society of Critical Care Anesthesiologists, Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Trauma Anesthesia Challenges
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