INTRODUCTION — Although the most critically injured patients are ideally transported to a designated trauma center, anesthesiologists in other hospitals may provide care for a patient who requires immediate surgical or other interventions after traumatic injury [1].
This topic reviews anesthetic management of adult patients with severe or multitrauma injuries. Anesthetic management for other types of trauma (eg, isolated orthopedic upper or lower extremity trauma, burn injuries) is addressed in separate topics. (See "Anesthesia for orthopedic trauma" and "Anesthesia for patients with burn injuries".)
Other topics address immediate management of trauma patients upon arrival to the emergency department (ED) and initial decisions regarding diagnostic, surgical, and other interventions:
●(See "Initial management of trauma in adults".)
●(See "Approach to shock in the adult trauma patient".)
●(See "Overview of damage control surgery and resuscitation in patients sustaining severe injury".)
GENERAL APPROACH — A clear, simple, and organized approach to the trauma patient is used in both the emergency department (ED) and operating room (OR), including assessment of airway, breathing, circulation, disability (eg, neurologic evaluation and cervical spine stabilization), and exposure (eg, hypothermia, smoke inhalation, intoxicants) [2]. An example is the Advanced Trauma Life Support (ATLS) tool. Participation of the anesthesiologist at an early stage (eg, at the time of trauma response activation or patient arrival in the ED) provides continuity of care before and after transition to the OR [3]. (See "Initial management of trauma in adults", section on 'Primary evaluation and management'.)
Goals — Primary goals in both the ED and the OR include:
●Airway management. (See 'Airway management' below.)
●Management of hemodynamic instability. This includes management of hemorrhagic hypovolemic shock and its sequelae (eg, coagulopathy, hemodilution, hypothermia, and electrolyte and acid-base derangements), as well as other etiologies of shock after trauma. (See 'Management of hemodynamic instability' below.)
●Lung-protective ventilation. (See 'Lung-protective ventilation' below.)
●Maintenance of normothermia. (See 'Temperature management' below.)
●Maintenance of adequate cerebral blood flow, oxygenation, and ventilation is prudent to avoid secondary brain injury. Even in the absence of overt evidence of traumatic brain injury (TBI), concussion is common in trauma patients and may be associated with significant changes in cerebral hemodynamics and metabolism [4,5]. (See "Anesthesia for patients with acute traumatic brain injury", section on 'Goals for anesthetic management'.)
●Prevention of unpleasant experiences during painful interventions (eg, by employing local or regional anesthesia, sedation, or general anesthesia). (See 'Management of general anesthesia' below.)
PATIENT STABILIZATION
Airway management — Initial airway management for trauma patients by emergency department (ED) clinicians is discussed in other topics for specific types of airway injury:
●(See "Approach to advanced emergency airway management in adults".)
●(See "Emergency airway management in the adult with direct airway trauma".)
Airway management after trauma caused by burn injuries and details regarding general management of difficult airway problems in the operating room are found in separate topics:
●(See "Management of the difficult airway for general anesthesia in adults".)
●(See "Anesthesia for patients with burn injuries", section on 'Airway management'.)
Urgent airway management in trauma patients may be challenging due to maxillofacial injury or burns, blunt or penetrating neck injury, laryngeal or major bronchial disruption, cervical spine instability, compression of the airway, bleeding due to the initial traumatic injury or multiple subsequent intubation attempts that impair direct visualization of the upper airway, or oropharyngeal and/or laryngeal edema due to burn injury. These acute injuries may create a "difficult airway," or may worsen a pre-existing anatomical predisposition to a difficult airway. The American Society of Anesthesiologists Committee on Trauma and Emergency Preparedness has developed guidance for difficult airway management in trauma patients (algorithm 1) [6].
A clearly defined, sequential approach to a patient with airway injury or abnormality is critical, since preoxygenation may be difficult and any delay in securing the airway may lead to rapidly progressing hypoxemia [7]. Also, prolonged efforts to secure the airway may delay definitive treatment of other life-threatening injuries [8]. Details regarding management of a difficult airway in specific trauma conditions (eg, airway disruption, oral and maxillofacial trauma, airway compression, closed head injury) are described in the tables (table 1 and table 2 and table 3 and table 4) [6,9]. Management in patients who may have a cervical spine injury is discussed in another topic (figure 1). (See "Anesthesia for adults with acute spinal cord injury", section on 'Airway management'.)
In a patient with life-threatening injuries or hypoxemia, inability to obtain a definitive airway is an absolute indication for emergency cricothyroidotomy or surgical tracheostomy, particularly if a "cannot ventilate, cannot intubate" scenario develops [10]. If airway injury is extensive, a joint decision to place a surgical airway distal to the site of injury may be made by the anesthesiologist and the ED clinician and/or trauma surgeon. Factors influencing this decision include the specific airway injury, presence of other traumatic injuries, the patient's overall condition, clinician expertise, and types of immediately available airway equipment. (See "Emergency cricothyrotomy (cricothyroidotomy)".)
In stable patients without airway compromise, conservative airway management may be suitable. In one review, immediate establishment of a definitive airway was necessary in approximately 50 percent of patients with penetrating trauma and in 80 percent of those with blunt trauma [10]. In another review, approximately one-third of traumatized patients did not require immediate endotracheal intubation in the ED, but were instead intubated after transport to the operating room (OR) [11].
We avoid hyperoxemia by continuously monitoring pulse oximetry and intermittently obtaining arterial blood gases to check the partial pressure of arterial oxygen (PaO2); our target values are an arterial oxygen saturation (SpO2) >92 percent or a PaO2 >65 mmHg. Systematic reviews have found that liberal oxygen therapy resulting in hyperoxemia is associated with increased mortality in acutely ill patients with traumatic brain injury (TBI), recent cardiac arrest, or stroke [12-16]. There is limited evidence suggesting benefits of a high fraction of inspired oxygen (FiO2) in trauma patients, and no evidence for those with spontaneous respirations [17], Nevertheless, many trauma patients treated with supplemental oxygen will develop hyperoxemia [18]. We recommend an SpO2 range of greater than 92 percent but less than 98 percent [12,13,19,20].
Monitoring and intravenous access — An intra-arterial catheter and a central venous catheter (CVC) are inserted in most hemodynamically unstable trauma patients undergoing general anesthesia, if not previously inserted in the ED. Two large-bore peripheral intravenous (IV) catheters (eg, 16 G or larger) can be rapidly inserted instead of or in addition to a CVC for initial administration of fluid, blood transfusions, and IV vasoactive and anesthetic agents. Although all intravascular catheters are ideally inserted before anesthetic induction, placement should not unduly delay emergency surgical intervention. If obtaining reliable IV access is difficult, intraosseous (IO) access can be rapidly and reliably achieved, and can be used for (blood and fluid) resuscitation and to administer medications (see "Intraosseous infusion") [21,22]. Additional considerations for intraoperative monitoring are discussed separately. (See "Intraoperative management of shock in adults", section on 'Intraoperative monitoring'.)
Management of hemodynamic instability — Initial resuscitation efforts in a hemodynamically unstable trauma patient may occur in the ED, interventional radiology (IR) suite, and/or OR [23]. The goal is to prevent organ damage by restoring tissue perfusion pressure, normal oxygen delivery, and adequate microcirculatory flow [24]. (See "Intraoperative management of shock in adults", section on 'Initial resuscitation' and "Approach to shock in the adult trauma patient".)
Point-of-care (POC) ultrasound (eg, the focused assessment with sonography for trauma [FAST] examination) is the standard screening examination performed by ED or other clinicians to diagnose common life-threatening injuries that may otherwise be undetected in trauma patients [25]. FAST involves assessments of the pericardium to look for hemopericardium and tamponade; and of the right flank, left flank, and pelvis to look for intraperitoneal free fluid, often with an extended evaluation looking for pneumothorax (E-FAST). (See "Emergency ultrasound in adults with abdominal and thoracic trauma".)
Treatment of hemorrhagic shock
General principles — The most common cause of shock for patients admitted to the trauma bay is hemorrhage. There are formal scores for predicting the likelihood of requiring a massive transfusion; however, it is highly likely that any hypotensive patient who does not respond to a fluid bolus has a hemorrhagic cause and will likely require blood products (see "Massive blood transfusion" and "Initial management of moderate to severe hemorrhage in the adult trauma patient"). Care for these patients should follow damage control resuscitation (DCR) principles until hemorrhage can be arrested [26-30].
Further descriptions on the pathophysiology and evaluation of hemorrhagic shock can be found elsewhere. (See "Approach to shock in the adult trauma patient".)
In addition to early surgical control of hemorrhage, initial strategies to limit ongoing blood loss include maintenance of a low to normal systolic blood pressure (BP) at approximately 90 mmHg (or ≤110 mmHg in older adults) and/or mean arterial pressure (MAP) at 50 to 65 mmHg. Once hemostasis has been achieved, higher BP values are targeted (eg, systolic BP ≥90 mmHg and/or MAP ≥65 mmHg). Although increasing BP indicates increasing macro-circulatory pressure, micro-circulatory flow may still be abnormal. (See 'High-dose opioid supplementation' below and "Initial management of trauma in adults", section on 'Circulation'.)
Information rapidly derived from intraoperative laboratory tests allows rational decision-making regarding transfusion of RBCs and other blood components. POC tests of hemostatic function allow rapid assessment of causes of coagulopathy and responses to interventions, including transfusion of blood products. The most commonly used POC tests for overall hemostatic function are thromboelastography (TEG) or rotational thromboelastometry (ROTEM) [31-33]. (See "Coagulopathy in trauma patients", section on 'Thromboelastography' and "Coagulopathy in trauma patients", section on 'Thromboelastography-based transfusion'.)
An intraoperative blood salvage system is often used [34]. In a 2015 systematic review of patients undergoing emergency abdominal or thoracic trauma surgery (one trial; n = 44), the reduction in the use of allogeneic red blood cells in the cell salvage group was 4.7 units (95% CI 1.31-8.09 units), compared with controls [35]. (See "Surgical blood conservation: Blood salvage".)
Total blood and fluid administration is limited by employing dynamic parameters to assess intravascular volume status and guide fluid administration in the OR (eg, transesophageal echocardiography [TEE] to assess changes in left ventricular cavity size (movie 1) or respirophasic variation in the intra-arterial pressure waveform during positive pressure ventilation (table 5 and figure 2 and figure 3) [36-38]. Fluid overload is avoided [39,40]. (See "Intraoperative fluid management", section on 'Goal-directed fluid therapy'.)
Our approach focuses on limiting crystalloids and administering blood products as soon as practicable for patients with a high likelihood for hemorrhagic shock. Further details are available in other topics:
●(See "Intraoperative management of shock in adults", section on 'Hypovolemic shock management'.)
●(See "Treatment of severe hypovolemia or hypovolemic shock in adults".)
●(See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)
●(See "Novel tools for hemodynamic monitoring in critically ill patients with shock".)
It is critically important to warm all IV fluids and blood in order to maintain normothermia and avoid hypothermia-induced exacerbation of coagulopathy. (See 'Temperature management' below.)
Specific blood products and other therapies — For patients with severe or ongoing hemorrhage, red blood cells (RBCs) and other appropriate blood products are transfused as soon as they are available, rather than continuing administration of crystalloid or colloid [41]. Current ATLS guidelines recommend no more than 1 L of warm 0.9% saline prior to administration of blood components [2]. Availability should not rely on a full crossmatch in patients with hemorrhagic shock since uncrossmatched blood can be administered until crossmatched blood is available. The incidence of a hemolytic reaction in a patient with a negative screen receiving type-specific blood is less than 1/50,000 and 1 percent in uncross-matched O-type blood, while the risk of mortality increases by 13 percent when the hemoglobin falls from a range of 5 to 6.9 g/dL to 3 to 4.9 g/dL and mortality risk increases by 28 percent at <3 g/dL [42,43].
●Control of coagulopathy – A ratio of 1:1:1 or 2:1:1 (RBCs:plasma:platelet packs) is targeted for blood product transfusion [44-46]. Although this ratio mirrors the content of whole blood, superior viscoelastic maximal clot formation is achieved with transfusion of whole blood compared with 1:1:1 component transfusion [47].
Fresh whole blood has been used in the military for combat injuries, and some institutions (including ours) have developed protocols for its use in civilian trauma [48-51]. The use of low-titer whole blood appears to be generally safe in several retrospective studies [52-57]. A 2021 systematic review concluded that use of whole blood was not associated with a significant survival benefit or reduced blood product utilization, but did confer logistical advantages during massive transfusion (five studies) [57]. Similar results were noted in a 2020 systematic review (27 studies) [54]. Ongoing trials will likely inform indications, advantages, and complications associated with transfusion of whole blood versus blood components in severely bleeding trauma patients [54].
Control of coagulopathy is critically important, particularly in a patient with TBI. Acute coagulopathy after severe traumatic injury has multifactorial etiologies including acidosis related to tissue injury and shock, hypothermia related to exposure and fluid administration, systemic anticoagulation with activation of Protein C and Protein S, hyperfibrinolysis from amplification of tissue plasminogen activator, platelet dysfunction following platelet activation, hemodilution due to fluid or component blood product administration, consumption of clotting factors manifesting as disseminated intravascular coagulation, and other biochemical processes [58,59]. (See "Coagulopathy in trauma patients", section on 'Etiologies'.)
●Point-of care and standard laboratory testing – Management of coagulopathy is guided by POC tests such as TEG or ROTEM, if available, as well as standard laboratory tests [60-66]. Turnaround is rapid with POC tests, and a single tracing result provides information regarding clot initiation, kinetics of clot formation, clot strength, and fibrinolysis (figure 4 and figure 5 and table 6). (See "Coagulopathy in trauma patients", section on 'Thromboelastography' and "Intraoperative transfusion of blood products in adults", section on 'Intraoperative diagnostic testing'.)
Fibrinogen supplementation by administration of cryoprecipitate or fibrinogen concentrate may improve outcomes following major trauma, particularly if low fibrinogen levels are documented or strongly suspected [65-70]. The guidelines of the European Society of Anaesthesiology and the European Task Force for Advanced Bleeding Care in Trauma suggest a target fibrinogen concentration >150 to 200 mg/dL [69,70]. Proponents argue that baseline fibrinogen concentrations are relatively low and there are no fibrinogen stores to be mobilized; thus, fibrinogen is the first procoagulant to become critically low in a hemorrhaging patient [71]. Low fibrinogen concentration <100 mg/dL or fibrinolysis evident on POC laboratory tests is generally treated with cryoprecipitate or fibrinogen concentrate. However, whether replacement of fibrinogen is optimally accomplished with cryoprecipitate of fibrinogen concentrate in severe traumatic hemorrhage remains controversial [72,73]. (See "Coagulopathy in trauma patients" and "Intraoperative transfusion of blood products in adults", section on 'Indications and risks for specific blood products'.)
Limited data suggest that administration of 3-factor or 4-factor prothrombin complex concentrate (PCC), alone or in combination with fibrinogen or fresh frozen plasma (FFP), reduces transfusion of RBCs and other blood components and international normalized ratio (INR), as well as reductions in trauma patients [74-78]. If available, POC viscoelastic testing of hemostasis may be used to dose these agents (eg, a dose of 2 to 6 g fibrinogen concentrate for a FIBTEM CA10 value <7 mm; or a dose of 6 to 8 g with 20 to 30 units/kg prothrombin concentrates for an EXTEM CA10 value <30 mm) [79]. (See "Coagulopathy in trauma patients", section on 'Thromboelastography'.)
●Management of fibrinolysis – The use of tranexamic acid (TXA) in trauma remains controversial. TXA is part of "massive transfusion protocols," in most major trauma centers in the United States. The benefit of TXA seems to be time dependent, since some studies have shown reduced efficacy with later administration [80,81]. It has been suggested that since the onset of hyperfibrinolysis occurs rapidly in severely injured trauma patients, antifibrinolytic therapy (typically TXA) should be administered as soon as hyperfibrinolysis is noted on POC testing, and to patients with active hemorrhage if TEG or ROTEM is unavailable [80,82-84]. In the CRASH-2 study, TXA was administered as an initial 1 g IV bolus over 10 minutes, followed by 1 g infusion over 8 hours [80]. Current military guidelines recommend an initial dose of 2 g TXA IV or interosseus (IO) [85]. Each subsequent dose is guided by POC viscoelastic testing. (See "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Antifibrinolytic agents'.)
There are several pathological forms of fibrinolysis after severe trauma: fibrinolysis shutdown (34 to 54 percent), hyperfibrinolysis (18 to 42.9 percent), and physiologic fibrinolysis (18 to 22.9 percent) [86-89]. Additional categories should be considered since timing of viscoelastic testing will affect results, such as hypofibrinolysis in patients who never generate increased fibrinolytic activity and acute fibrinolysis shutdown in patients who generate increased fibrinolytic activity, but more quickly start generating more stable clots [88].
Some investigators caution that trauma patients should be carefully selected for TXA administration since fibrinolysis is a natural process that enables clot degradation and maintains patency of the microvasculature [90]. Endogenous or exogenous inhibition (shutdown) of the fibrinolysis system may have an adverse effect on survival and may be recognized on TEG or ROTEM viscoelastic tests [91,92]. However, published data regarding fibrinolysis and TXA are difficult to interpret due to variations in study design that includes differences in type and quantity of concomitantly administered blood products. For example, administration of platelets and red blood cells also affects fibrinolytic activity [93,94]. (See "Coagulopathy in trauma patients", section on 'Thromboelastography-based fibrinolytic phenotypes'.)
Assessment for other causes of shock — In addition to hemorrhagic shock, a trauma patient may have other known or unrecognized causes of shock. Examples include spinal cord injury causing neurogenic (ie, vasoplegic) shock, severe ischemic myocardial dysfunction causing cardiogenic shock, or tension pneumothorax, pericardial tamponade, or increased intra-abdominal pressure causing obstructive shock. Perioperative management of these causes of shock are discussed in detail in separate topics:
●(See "Approach to shock in the adult trauma patient".)
●(See "Approach to shock in the adult trauma patient".)
●(See "Intraoperative management of shock in adults".)
Ongoing resuscitation — After control of acute hemorrhage, ongoing intraoperative resuscitation includes reestablishment of normothermia and continuing assessment and treatment of coagulopathy, hypothermia, electrolyte abnormalities, elevated serum lactate level, and acid-base derangements in order to maintain hemodynamic stability [46,95,96]. Correction of metabolic acidosis is initially accomplished with adequate fluid resuscitation rather than with administration of sodium bicarbonate [97,98]. Continuous infusion of a vasopressor or inotropic agent may be necessary to maintain blood pressure and restore adequate tissue perfusion (table 7). (See "Intraoperative management of shock in adults", section on 'Initial interventions'.)
We do not use vasopressors in the early stages of hemorrhagic shock. However, in patients with vasoplegia or insufficient vasoconstrictive response (eg, patients with neurogenic shock, systemic inflammatory response syndrome), we administer low dose norepinephrine 0.01 to 0.09 mcg/kg per minute and/or vasopressin 0.3 units/minute to maintain desired blood pressure targets (table 8). Early use of vasopressors in hemorrhagic shock is more prevalent practice in Europe compared with the United States. Vasopressor use in hemorrhagic shock has been historically discouraged due to concerns regarding worsening vasoconstriction and organ failure in the absence of adequate volume resuscitation [99,100]. In several small studies of patients in hemorrhagic shock, infusions of vasopressin have been shown to maintain serum vasopressin levels, decrease fluid requirements after injury, and decrease blood product requirements [101-103]. Conversely, other small studies have noted that administration of various vasopressor agents was associated with increased mortality [100,104-107].
MANAGEMENT OF GENERAL ANESTHESIA
General principles — Operating rooms in trauma centers should have full monitoring capabilities and be stocked with routine and advanced airway capabilities, equipment for rapid transfusion, and a variety of catheters for intravascular and intra-arterial access. Equipment to warm blood and intravenous (IV) fluids and devices to warm the patient should be readily available, and the operating room itself is kept warm to avoid development or exacerbation of hypothermia.
General anesthesia is nearly always employed during the intraoperative period in severely injured trauma patients, rather than regional anesthetic techniques (eg, neuraxial anesthesia or peripheral nerve blocks). However, a multimodal approach to analgesia that includes regional anesthetic techniques is used to decrease postoperative opioid dosing requirements when feasible. (See "Anesthesia for thoracic trauma in adults", section on 'Regional analgesic techniques' and "Overview of peripheral nerve blocks".)
Anesthetic agents with minimal hemodynamic effects are selected, and doses are reduced and carefully titrated to avoid exacerbation of hypotension [108,109]. Patients with barely compensated or decompensated hemorrhagic shock have a lower volume of distribution for all anesthetic agents. Even after hemodynamic stability has been achieved, careful titration is necessary since the patient's clinical condition may rapidly change. For example, a trauma patient may have unrecognized bleeding into the retroperitoneum after a severe pelvic injury, or into muscle and fascial compartments after bilateral femur fractures.
Induction — The goal of induction of general anesthesia is to produce an unconscious state while maintaining adequate organ perfusion. However, induction may result in profound hypotension and/or cardiac arrest in a patient with barely compensated or decompensated hemorrhagic shock. Before beginning induction, a vasopressor infusion should be connected "in line" in the IV tubing so that it is ready for immediate administration (table 7). In a hemodynamically unstable patient, we administer a bolus dose of a vasopressor concurrently with the induction agents to prevent exacerbation of hypotension. (See "Intraoperative management of shock in adults", section on 'Induction'.)
For most trauma patients, rapid sequence induction and intubation (RSII) is indicated (see "Rapid sequence induction and intubation (RSII) for anesthesia"). Either etomidate or ketamine is typically selected as the primary induction agent for a hemodynamically unstable patient. A 2019 systematic review noted no differences in outcomes (mortality, length of hospital stay, or number of blood transfusions) when ketamine (n=634) rather than etomidate (n=699) was selected to induce anesthesia in trauma patients (one randomized trial and two nonrandomized trials) [110] (see "General anesthesia: Intravenous induction agents", section on 'Etomidate' and "General anesthesia: Intravenous induction agents", section on 'Ketamine'). The shock index may be considered as a guide for administering lower doses of induction agents.
Propofol is generally avoided since administration of an IV bolus may further reduce blood pressure (BP) by causing dose-dependent venous and arterial dilation and decreased contractility [109]. However, in a hemodynamically stable trauma patient, a reduced dose of propofol (eg, 0.5 mg/kg) may be administered. Adjuvant induction agents (eg, opioids, lidocaine, midazolam) are eliminated in hemodynamically unstable patients, or reduced if hemodynamic stability has been achieved (table 9). (See "Rapid sequence induction and intubation (RSII) for anesthesia" and "Intraoperative management of shock in adults", section on 'Induction'.)
We typically select succinylcholine as the neuromuscular blocking agent (NMBA) for RSII, administered at a dose of 1.5 mg/kg IV (or 3 to 4 mg/kg intramuscularly [IM] if IV access is not available) (table 10) or rocuronium 1.2 mg/kg IV. Dosing for RSII is discussed separately. (See "Rapid sequence induction and intubation (RSII) for anesthesia", section on 'Neuromuscular blocking agents (NMBAs)'.)
Maintenance
Inhalation anesthetic agents
●Volatile inhalation agents – A volatile inhalation anesthetic agent (eg, desflurane, isoflurane, sevoflurane) is typically selected for maintenance of anesthesia. Administration is initiated at a lower concentration than in healthy patients due to dose-dependent cardiovascular effects of the volatile anesthetic agents. Subsequently, the agent is carefully titrated to maintain anesthesia while avoiding hypotension that may further decrease end-organ perfusion. In patients with multiple injuries or multiple episodes of severe hemodynamic instability, agents with a low blood-gas partition coefficient (eg, desflurane, sevoflurane) are preferred to permit rapid titration. If systolic BP improves to ≥90 mmHg, the selected volatile agent may be increased to ≥0.5 minimum alveolar concentration (MAC) (table 11). (See "Maintenance of general anesthesia: Overview", section on 'Inhalation anesthetic agents and techniques'.)
In patients with multiple traumatic injuries that may include brain injury, the volatile agent is maintained ≤1 MAC to avoid dose-dependent increases in cerebral blood flow (CBF) and intracranial pressure (ICP). (See "Anesthesia for patients with acute traumatic brain injury", section on 'Choice of anesthetic agents'.)
Although volatile inhalation anesthetics are effective modulators of the inflammatory response after tissue injury and may have beneficial effects on organ function in humans and animal models, studies have focused on ischemia-reperfusion injury and biomarkers of organ dysfunction rather than on clinical outcomes [111-118].
●Nitrous oxide gas – We generally avoid nitrous oxide (N2O) in trauma patients for several reasons [119-121] (see "Inhalation anesthetic agents: Clinical effects and uses", section on 'Nitrous oxide'):
•N2O expands all gas spaces and can worsen a traumatic pneumothorax or pneumocephalus.
•In patients with TBI, N2O may increase the cerebral metabolic rate of O2 consumption (CMRO2), and may also increase ICP.
•N2O increases pulmonary vascular resistance and may worsen pulmonary hypertension.
•N2O may cause apoptosis and altered immunologic responses to infection [121-124].
High-dose opioid supplementation — When systolic BP is consistently maintained ≥90 mmHg and surgical hemostasis is assured, we add doses of fentanyl during the maintenance phase of anesthesia, particularly if the patient will remain intubated and sedated with controlled ventilation in the immediate postoperative period. Fentanyl may cause beneficial dilation of the microcirculation and has minimal myocardial depressant effects [125-127].
Initially, we administer 50 to 150 mcg bolus doses of fentanyl, with close monitoring of the hemodynamic response. Additional resuscitation may be necessary during fentanyl administration (eg, additional volume or vasopressor administration). If systolic BP is maintained ≥90 mmHg, fentanyl dosing is incrementally increased until the patient tolerates a single bolus of approximately 250 mcg. Use of this high-dose opioid technique typically results in administration of a total fentanyl dose of 10 to 30 mcg/kg during the surgical procedure. However, plasma fentanyl levels and total dose vary considerably if the patient's blood volume is constantly changing due to ongoing bleeding and transfusion.
If evidence of tissue hypoperfusion (eg, elevated lactate concentration and/or base deficit) persists after these relatively high doses of fentanyl, we add another opioid to achieve additional vasodilatation. We typically select methadone as the second-line opioid when the patient's electrocardiogram (ECG) reveals a normal QT interval (<440 ms). Methadone is administered in 10 mg IV increments to a total dose of 20 to 30 mg. Hydromorphone is an alternative opioid, titrated in 0.2 to 0.4 mg increments to a total dose of approximately 2 mg. Morphine is generally avoided due to concern regarding histamine release, which may exacerbate hypotension.
Strategies to minimize risk of awareness — Since it may be unsafe to administer sufficient anesthesia during all phases of damage control surgery and other interventions, trauma patients are at risk for intraoperative awareness with postoperative recall. (See "Accidental awareness during general anesthesia", section on 'Risk factors'.)
We administer incremental doses of one or more adjuvant agents during periods of light anesthetic depth to potentially limit the traumatic effect of an intraoperative awareness event, particularly if the patient is hemodynamically unstable and unable to tolerate a volatile anesthetic agent [128]. We typically administer a benzodiazepine (eg, midazolam 1 to 4 mg or diazepam 2 to 10 mg) to produce amnesia [129], and/or an opioid to decrease pain. (See 'High-dose opioid supplementation' above and "Accidental awareness during general anesthesia", section on 'Administration of adjuvant medications'.)
Scopolamine is an anticholinergic amnestic that has been used to prevent intraoperative awareness in hemodynamically unstable patients, although data regarding dosing and effectiveness are lacking [130]. However, IV preparations of scopolamine are no longer available in the United States. In countries where IV scopolamine is available, it is avoided in patients with traumatic brain injury (TBI) because it has a long half-life (4.5 hours); thus, subsequent neurologic examinations are confounded by its side effect of pupillary dilation.
Lung-protective ventilation — An intraoperative lung-protective strategy is used during controlled ventilation for patients with trauma and shock, with low tidal volumes of 6 to 8 mL/kg. Mild permissive hypercapnia with partial pressure of carbon dioxide (PaCO2) of 40 to 45 mmHg is allowed, unless the patient has metabolic acidosis or known or suspected TBI. In such cases, a faster respiratory rate may be temporarily employed to achieve a PaCO2 or 30 to 35 mmHg. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia' and "Anesthesia for patients with acute traumatic brain injury", section on 'Intraoperative ventilation and oxygenation'.)
Initial positive end-expiratory pressure (PEEP) is set at 0 cm H2O until hemodynamic stability and control of hemorrhage and adequate resuscitation has been achieved. Subsequently, PEEP may be slowly and incrementally increased to 5 to 10 cm H2O if tolerated without provoking hypotension, and FiO2 is concurrently weaned to maintain arterial saturation >90 percent. The goal is to provide an optimal balance between minimizing lung injury and preventing hemodynamic instability. Hyperoxia is also avoided [16,131].
In patients with hemorrhagic shock, it is particularly important to avoid high levels of PEEP and dynamic hyperinflation with development of auto-PEEP [132]. PEEP and auto-PEEP increase intrathoracic pressure, and decrease venous return, cardiac output, and systemic BP. (See "Physiologic and pathophysiologic consequences of mechanical ventilation", section on 'Hemodynamics'.)
In rare cases, venovenous extracorporeal membrane oxygenation (ECMO) may be employed to treat trauma-related refractory respiratory distress syndrome, or venoarterial ECMO may be employed in a trauma patient with cardiogenic shock after cardiac arrest [133-136]. (See "Extracorporeal membrane oxygenation (ECMO) in adults".)
Temperature management — Perioperative temperature management is accomplished with warming devices to maintain normothermia (temperature ≥35.5°C) in patients with trauma and shock, as discussed separately. (See "Intraoperative management of shock in adults", section on 'Temperature management'.)
POSTOPERATIVE CONSIDERATIONS — After emergency trauma surgery, most patients remain intubated and sedated with controlled ventilation (see 'High-dose opioid supplementation' above). The anesthesiologist should continuously monitor the electrocardiogram (ECG), pulse oximetry (SpO2), and intra-arterial blood pressure during transport to the intensive care unit (ICU) [137]. (See "Intraoperative management of shock in adults", section on 'Transport to the intensive care unit'.)
Upon arrival in the ICU, a clear, simple, and organized handoff is critically important. We prefer to use a cognitive aid such as the ABCDE communication tool (table 12).
Reassessment of the extent of unresolved shock is necessary shortly after arrival in the ICU. Ongoing resuscitation and management of respiratory, cardiovascular, metabolic, and immunologic consequences of traumatic injury and massive transfusion may be necessary [138]. Most trauma patients require controlled ventilation and hemodynamic support, and many require correction of critical acid-base and electrolyte abnormalities, restoration of normothermia, or efforts to minimize secondary central nervous system injury. Frequent postoperative reassessments for the possibility of missed injuries or inadequately treated pain are important after surgery for traumatic injuries. (See 'Assessment for other causes of shock' above and "Overview of inpatient management of the adult trauma patient", section on 'Consider other potential injuries'.)
SPECIAL POPULATIONS — Unique anesthetic considerations exist for certain injury-specific or patient–specific situations.
Resuscitative endovascular balloon occlusion of the aorta — In selected patients (eg, those with noncompressible torso hemorrhage following traumatic injury), resuscitative endovascular balloon occlusion of the aorta (REBOA) is a temporizing measure to support vital organ perfusion, decrease the amount of bleeding distal to the occluded site, and provide a window of opportunity for resuscitation and definitive hemorrhage control (figure 6) [136,139-141]. However, REBOA does not provide definitive hemorrhage control. REBOA indications and techniques are discussed separately. (See "Endovascular methods for aortic control in trauma".)
Anesthetic management during REBOA includes insertion of an intra-arterial catheter and a central venous catheter (CVC) [142]. The intra-arterial catheter is placed in an upper extremity since perfusion to the lower extremity arteries will be temporarily interrupted during balloon occlusion of the aorta. Similar to intraoperative monitoring during endovascular aortic repair, transesophageal echocardiography (TEE) is particularly useful to assess changes in regional and global ventricular function as well as intravascular volume status before, during, and after balloon occlusion [140,143]. TEE can also be used to monitor position of the endovascular balloon [139,141].
During REBOA, critical hemodynamic changes occur with balloon inflation and deflation [139,140,143]:
●Inflation – Similar to application of an aortic crossclamp during abdominal aortic aneurysm (AAA) repair, proximal aortic occlusion during REBOA increases systemic vascular resistance (SVR), blood pressure (BP), and cardiac afterload, thereby increasing cerebral and myocardial perfusion (figure 6) [140,141,143]. Physiologically, the increased afterload, while supporting coronary perfusion, may also increase myocardial transmural wall tension and cardiac pressure work (figure 7) [141,144,145]. Although published recommendations for anesthetic management in this setting are lacking, careful increases in volatile inhalation anesthetic concentration to produce some degree of vasodilation is prudent if systolic BP is higher than desired during proximal aortic occlusion. (See "Anesthesia for open abdominal aortic surgery", section on 'Management of aortic cross-clamping' and "Endovascular methods for aortic control in trauma", section on 'Inflate the balloon catheter'.)
●Deflation – REBOA balloon deflation is attempted when hemostasis has been achieved or to check for sources of ongoing hemorrhage [139,141,143]. Similar to aortic unclamping during open AAA repair, deflation of the intra-aortic balloon catheter may result in severe hypotension due to a sudden decrease in SVR, decreased preload due to venodilation, hypoxia-mediated reactive hyperemia, and decreased myocardial contractility due to metabolic (lactic) acidosis (figure 8) [139,143,145,146]. Metabolic acidosis and washout of ischemic muscle tissue may also result in hyperkalemia, malignant arrhythmias, and cardiac arrest. (See "Anesthesia for open abdominal aortic surgery", section on 'Management of aortic unclamping'.)
Clear team communication is required in preparation for deflation [139,140,143]. In some cases, it is clinically necessary for the surgeon to transiently, partially, or gradually deflate the balloon to permit reperfusion between occlusion periods, or to allow the anesthesiologist to increase intravascular volume and add vasopressor and/or inotropic agents as needed to avoid precipitous cardiovascular collapse after full balloon deflation. (See "Endovascular methods for aortic control in trauma", section on 'Duration of inflation and balloon deflation'.)
Following balloon deflation, metabolic derangements are typically present during the period of reperfusion (eg, hypoxemia, hypercarbia, acidosis, hyperkalemia, anemia, disorders of hemostasis), similar to reperfusion after aortic surgery [139,140,143,146]. In addition to obtaining standard point-of-care (POC) laboratory tests, serum lactate is monitored to assess successful reversal of shock as intraoperative resuscitation is completed [95,147]. (See "Anesthesia for open abdominal aortic surgery", section on 'Point-of-care testing'.)
Acute traumatic brain injury — The care for patients with acute traumatic brain injury (TBI) is focused on limiting secondary injury to vulnerable brain tissue, reducing intracranial pressure to maintain tissue perfusion, and preventing seizures. Anesthetic management of patients with acute TBI shares these goals which are summarized in the table (table 8). Clinicians should be mindful of altered cerebral autoregulation. Additional information about anesthetic management for TBI is discussed elsewhere. (See "Anesthesia for patients with acute traumatic brain injury" and "Anesthesia for craniotomy".)
Acute traumatic spinal cord injury — Acute spinal cord injuries may present with cardiovascular and pulmonary complications, and can affect airway management. Anesthetic management of acute spinal cord injury is discussed separately. In patients with high cervical spinal cord injuries (ie, injuries above C5), we prefer early intubation to avoid complications related to acute respiratory failure and/or airway compression from edema or hematoma expansion. (See "Anesthesia for adults with acute spinal cord injury" and "Acute traumatic spinal cord injury".)
Traumatic injury in pregnant patients — Every female trauma victim of reproductive age should be considered pregnant until proven otherwise by a definitive pregnancy test. Approximately 1 in 12 women with known pregnancy experience physical trauma, which can cause maternal and fetal morbidity or mortality [148]. Specific considerations for pregnant trauma patients include:
●Airway management – If intubation is necessary, we suggest a rapid sequence induction and intubation (RSII) with application of cricoid pressure, and placement of a smaller sized endotracheal tube [148,149]. Also, a nasal or orogastric tube should be placed before or after intubation to prevent aspiration of acidic gastric contents [148]. Pregnant patients have increased risk for difficulties with airway management, including a difficult intubation, as well as aspiration of gastric contents [148-150]. (See "Initial evaluation and management of major trauma in pregnancy", section on 'Airway, breathing, and ventilation'.)
●Uterine displacement – If the uterus is at or above the umbilicus, it should be displaced to the left (off the aortocaval vessels) to increase venous return to maximize cardiac output. This is best accomplished by placing the patient on her left side; an alternative method is placement of a wedge or rolled towel under her right hip (or under the spinal board, if appropriate) to achieve a 15 to 30 degree left lateral tilt (see "Initial evaluation and management of major trauma in pregnancy", section on 'Uterine displacement'). Alternatively, manual leftward displacement of the uterus may also be effective as left lateral tilting to reduce the incidence of hypotension and/or requirement for vasopressors [151].
●Volume replacement and transfusion – Volume replacement after trauma with blood loss should be aggressive due to the physiologic hypervolemia of pregnancy. Volume replacement is preferable to vasopressor administration to support BP (figure 9). If transfusion is indicated in a Rh-negative pregnant patient, O-negative blood should be transfused until cross-matched blood becomes available (to avoid rhesus D [Rh] alloimmunization). Anti-D (RhoGAM) immune globulin should also be administered, per standard protocols. (See "Initial evaluation and management of major trauma in pregnancy", section on 'Volume replacement' and "RhD alloimmunization: Prevention in pregnant and postpartum patients".)
●Use of vasopressors – We administer phenylephrine boluses rather than ephedrine to treat hypotension in the absence of maternal bradycardia, aiming for a maternal blood pressure close to baseline. Limited data also support the safety and efficacy of norepinephrine in obstetrical anesthesia [152]. (See "Anesthesia for cesarean delivery", section on 'Hemodynamic management' and "Anesthesia for cesarean delivery", section on 'Vasopressors'.)
●Cesarean delivery – The fetus may be viable at ≥23 weeks gestation if delivery is likely. A multidisciplinary approach with involvement of obstetricians, neonatal intensive care unit staff, and maternal fetal medicine specialists is ideal for management of mother and fetus. In the event of maternal cardiac arrest, a cesarean delivery is recommended for viable pregnancies ≥23 weeks, if possible no later than four minutes following arrest [148]. This facilitates both maternal resuscitation and fetal salvage. (See "Initial evaluation and management of major trauma in pregnancy", section on 'Delivery'.)
Other considerations for anesthetic management of a pregnant patient who must undergo nonobstetric surgery are discussed elsewhere. (See "Anesthesia for nonobstetric surgery during pregnancy".)
Anesthesia for burn patients — Many patients arrive at trauma centers with concomitant burns. Burn injuries are not only caused by open flame and contact with hot substances, but also include etiologies such as electrical, chemical, and inhalation of gases. Size, thickness, and location of the burns affect resuscitation and treatment strategies. The clinician should remain vigilant for signs and symptoms of inhalation injury. Additional information about the systemic effects of burns and the anesthetic management is discussed elsewhere. (See "Overview of the management of the severely burned patient" and "Anesthesia for patients with burn injuries".)
Trauma to the thorax — The thorax contains the heart and lungs, along with their connecting structures. Injuries in this area can lead to nuances in care which will affect anesthetic management. Specific descriptions of the injuries, evaluation, and anesthetic management are described elsewhere. (See "Anesthesia for thoracic trauma in adults".)
Geriatric trauma — Management of older adult trauma victims is discussed elsewhere. (See "Geriatric trauma: Initial evaluation and management" and "Anesthesia for the older adult".)
Orthopedic trauma — Orthopedic trauma such as fractures may cause hemorrhage, neurovascular compromise, or compartment syndrome. When multiple traumatic injuries are present in a hemodynamically unstable patient, temporizing measures may reduce blood loss from the fractures. Delaying surgery for definitive treatment in order to perform urgently necessary procedures to stabilize the patient's condition may be appropriate. Anesthetic management of orthopedic trauma is discussed in a separate topic. (See "Anesthesia for orthopedic trauma".)
Substance use disorder or acute intoxication — Acute intoxication is frequently associated with trauma, and some patients may be intoxicated with multiple substances of abuse. Anesthetic management of these patients is discussed in a separate topic. (See "Anesthesia for patients with substance use disorder or acute intoxication".)
Management during the COVID-19 pandemic — During the novel coronavirus disease 2019 (COVID-19) pandemic, anesthetic management of trauma patients involves the following principles [153,154]:
●Ensuring screening and testing patient for COVID-19 infection on admission.
●Rigorously adhering to the use of personal protective equipment (PPE) during anesthetic care for emergency surgery, regardless of screening status. (See "COVID-19: Perioperative risk assessment and anesthetic considerations, including airway management and infection control", section on 'PPE during airway management or aerosol generating procedures'.)
●In patients with uncertain status, collecting bronchoalveolar lavage specimens at the time of endotracheal intubation.
●Performing emergency surgical procedures in a negative pressure operating room when feasible.
●Selecting a rapid sequence intubation technique for general anesthesia. Preoxygenation is accomplished with a surgical mask over the patient's mouth. Positive pressure mask ventilation is avoided or minimized.
●Employing lung-protective ventilation. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia'.)
●Using goal-directed fluid therapy to restore and maintain euvolemia. (See "Intraoperative fluid management", section on 'Goal-directed fluid therapy'.)
●Considering the potential for coagulation disorders in COVID-19 patients. (See "COVID-19: Hypercoagulability".)
●Considering potential for dysrhythmias in COVID-19 patients taking chloroquine or hydroxychloroquine. (See "COVID-19: Perioperative risk assessment and anesthetic considerations, including airway management and infection control", section on 'Infection control during patient transport'.)
●Extubating the patient's trachea with a minimal number of people in the room, then immediately covering the patient's mouth and nose with a surgical mask previously positioned around the chin, and an oxygen mask if needed. If oxygen is to be administered via nasal cannula, it should be positioned before extubation.
●Transporting directly to a dedicated COVID-19 unit for intensive care or recovery when feasible. Transporting patients who need oxygen via face mask in a demistifier tent.
●Using postoperative nausea and vomiting (PONV) prophylaxis for extubated patients.
Further details regarding anesthetic care of patients with suspected or known COVID-19-positive status are available in a separate topic. (See "COVID-19: Perioperative risk assessment and anesthetic considerations, including airway management and infection control".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Transfusion and patient blood management" and "Society guideline links: Thoracic trauma" and "Society guideline links: Airway management in adults" and "Society guideline links: Traumatic abdominal and non-genitourinary retroperitoneal injury" and "Society guideline links: Use of point-of-care echocardiography and ultrasonography as a monitor for therapeutic intervention in critically ill patients".)
SUMMARY AND RECOMMENDATIONS
●Patient stabilization and goals – Specific goals during stabilization of trauma patients in the emergency department (ED) and the operating room (OR) include (see 'Goals' above and 'Patient stabilization' above):
•Airway management – A clearly defined, sequential approach to a patient with airway injury or abnormality is critical, since delay in securing the airway may lead to rapidly progressing hypoxemia (algorithm 1 and table 1 and table 2 and table 3 and table 4 and figure 1). (See 'Airway management' above.)
•Management of hemodynamic instability and/or hemorrhagic shock – Resuscitation of hypotensive patients to a targeted systolic blood pressure (BP) ≥90 mmHg is the primary goal until hemostasis has been achieved. Other goals for patients with hemorrhagic hypovolemic shock and its sequelae include management of coagulopathy (figure 4 and figure 5 and table 6), hemodilution, hypothermia, electrolyte abnormalities, and acid-base derangements, as well as management of coexisting etiologies of shock after trauma. (See 'Management of hemodynamic instability' above.)
•Lung-protective ventilation – We employ low tidal volumes of 6 to 8 mL/kg, low plateau pressure ≤30 cm H2O, and initial positive end-expiratory pressure (PEEP) at 0 cm H2O. When the patient is hemodynamically stable, we incrementally increase PEEP to 5 to 10 cm H2O and concurrently wean FiO2 to maintain arterial oxygenation. (See 'Lung-protective ventilation' above.)
•Maintenance of normothermia – We employ warming devices to maintain temperature ≥35.5°C. (See 'Temperature management' above.)
•Prevention of unpleasant experiences – We employ strategies to minimize risk of awareness since it may be unsafe to administer sufficient anesthesia during all phases of trauma surgery. (See 'Strategies to minimize risk of awareness' above.)
●Intravascular access and monitoring – An intra-arterial catheter and a central venous catheter (CVC) are usually inserted in hemodynamically unstable patients, ideally before anesthetic induction. However, insertion should not unduly delay emergency surgical intervention and large-bore peripheral intravenous (IV) catheters may be used rather than a CVC. (See 'Monitoring and intravenous access' above.)
●General anesthesia
•General principles – Anesthetic induction and maintenance agents with minimal hemodynamic effects are selected, and doses are reduced and carefully titrated to avoid exacerbation of hypotension. (See 'General principles' above.)
•Induction – A rapid sequence induction and intubation (RSII) technique with either etomidate or ketamine is typically employed; propofol is avoided in hypotensive patients (table 13). We typically select succinylcholine 1.5 mg/kg as the neuromuscular blocking agent (NMBA) for RSII; rocuronium 1.2 mg/kg is a reasonable alternative, particularly if sugammadex is immediately available (table 10). (See 'Induction' above.)
•Maintenance
-Inhalation anesthetic agents – We typically employ a volatile inhalation anesthetic agent (eg, desflurane, isoflurane, sevoflurane) for maintenance of anesthesia, administered at a lower concentration than in healthy patients due to dose-dependent cardiovascular effects, and titrated to maintain anesthesia while avoiding hypotension. We generally avoid nitrous oxide. (See 'Inhalation anesthetic agents' above.)
-High-dose opioid supplementation – When systolic BP is consistently maintained ≥90 mmHg and surgical hemostasis is assured, we add fentanyl in 50 to 150 mcg increments to a total dose of 10 to 30 mcg/kg during the surgical procedure, in order to beneficially dilate the microcirculation. If evidence of tissue hypoperfusion persists (eg, elevated lactate concentration and/or base deficit), we add another opioid such as methadone or hydromorphone to achieve additional vasodilatation. (See 'High-dose opioid supplementation' above.)
●Postoperative considerations – In the postoperative period, most patients remain intubated and sedated with controlled ventilation. The electrocardiogram (ECG), pulse oximetry (SaO2), and intra-arterial blood pressure are continuously monitored during transport. A formal handoff process (table 12) and reassessment of the extent of unresolved shock are necessary upon arrival in the ICU. (See 'Postoperative considerations' above.)
●Special populations – Injury-specific or patient–specific situations that require additional resuscitative and anesthetic considerations include:
•Resuscitative endovascular balloon occlusion of the aorta (REBOA) (figure 6 and figure 7 and figure 8) – (see 'Resuscitative endovascular balloon occlusion of the aorta' above)
•Thoracic trauma (see "Anesthesia for thoracic trauma in adults")
•Orthopedic trauma – (see "Anesthesia for orthopedic trauma")
•Acute traumatic brain injury (TBI) (see "Anesthesia for patients with acute traumatic brain injury")
•Acute traumatic spinal cord injury (see "Anesthesia for adults with acute spinal cord injury" and "Acute traumatic spinal cord injury")
•Traumatic injury in pregnant patients (see 'Traumatic injury in pregnant patients' above)
•Traumatic injury in older patients – (see "Geriatric trauma: Initial evaluation and management" and "Anesthesia for the older adult")
•Burn injury (see "Anesthesia for patients with burn injuries")
•Acute intoxication (see "Anesthesia for patients with substance use disorder or acute intoxication")
•COVID-19 infection (see 'Management during the COVID-19 pandemic' above)
