Part 2 book “Essentials of trauma anesthesia” has contents: Anesthetic considerations for adult traumatic brain injury, anesthetic considerations for spinal cord injury, anesthetic considerations for ocular and maxillofacial trauma, anesthetic considerations for chest anesthetic considerations for chest,… and other contents.
Section Chapter 11 Core Principles in Trauma Anesthesia Coagulation Monitoring of the Bleeding Trauma Patient Marc P Steurer and Michael T Ganter Introduction Blood coagulation is a complex and tightly regulated physiologic network of interacting proteins and cells If deranged, it may dramatically influence outcome A comprehensive understanding of normal hemostasis and its pathophysiology is necessary for anesthesiologists working in the perioperative field Treatment of a massive trauma bleeding requires an interdisciplinary approach for both trauma surgeons and anesthesiologists Modern transfusion strategies and coagulation management are based on a detailed understanding of coagulation physiology and specific coagulation monitoring Besides the patients’ medical history, clinical presentation and laboratory tests, bedside coagulation analyses (point-of-care, POC) are increasingly being used to assess hemostasis Consequently, specific, individualized, and goal-directed hemostatic interventions are becoming more and more feasible Abnormal hemostasis is not limited to bleeding Hypercoagulability and thrombosis are further phenotypes of disturbed hemostasis The coagulation system represents a delicate balance of forces supporting coagulation (coagulation, antifibrinolysis) and forces inhibiting coagulation (anticoagulation, fibrinolysis) (Figure 11.1) The distinctive challenge is to assess and quantify both sides of this balance and to maintain an equilibrium Specific coagulation interventions can be made on either side, with the goal of preventing both overt bleeding and thrombosis Figure 11.1 Coagulation balance Normal blood coagulation exists when procoagulant and anticoagulant forces are in balance 154 18:17:51, subject to the Cambridge Core 012 Chapter 11: Coagulation Monitoring 155 Current Concepts of the Coagulation System Hemostasis is the process that causes bleeding to stop after a vessel injury It is maintained in the body by three interacting mechanisms: the vasculature, primary hemostasis, and secondary hemostasis In addition, hemostasis initiates sore healing of the injured vessel while preserving the general rheologic qualities of the blood The vascular part of hemostasis is the first step after a vessel injury It is mediated in a paracrine way by the endothelium, the vessel wall, and the immediate environment of the vessel By immediate vasoconstriction of the damaged vessel, blood flow and pressure temporarily decreases within the vessel Primary hemostasis describes the cellular part of clotting and is primarily mediated by platelets and von Willebrand factor (VWF) Platelet activation (with release of coagulation-active substances), adhesion, aggregation, and finally stabilization result in a mechanical blockage of the damaged vessel wall by a platelet plug Secondary hemostasis illustrates the plasmatic portion of blood clotting and describes the complex interaction of different clotting factors that finally result in a stable fibrin network To protect the organism against thrombosis and embolism, the natural anticoagulant pathway restrains overt clot formation at different levels, and the fibrinolytic system prevents excessive clot formation and promotes lysis of inadvertently formed blood clots In vivo, the coagulation system becomes primarily activated by tissue factor (TF) Tissue factor exists beyond the blood vessels on smooth muscle cells and fibroblasts Therefore, the coagulation system is not activated in a healthy individual Tissue damage, however, brings TF in contact with blood and activates the clotting system to protect the organism from exsanguination Under certain pathologic circumstances like sepsis, TF can be intravascularly expressed on endothelial cells, monocytes, and circulating microparticles (cell fragments) The resulting uncontrolled and overt coagulation activation can lead to the syndrome of disseminated intravascular coagulation (DIC) The key enzyme of secondary hemostasis is thrombin (FIIa), a serin-protease similar to trypsin Besides transformation of fibrinogen to soluble fibrin, thrombin facilitates numerous other biochemical reactions such as coagulation and immune system activation The net effect of thrombin depends on the context and the molecules that are present locally Thrombin promotes activation of clotting Factors V, VIII, and XI, thereby activating the intrinsic pathway and finally amplifying its own production Thrombin further activates the thrombin-activated fibrinolysis inhibitor (TAFI), Factor XIII, as well as platelets, endothelial cells, and perivascular smooth muscle cells During this process, two regulatory mechanisms are important for the protection from an overshooting thrombin formation: the antithrombin and protein C system Antithrombin does so by irreversibly binding and inactivating thrombin Activated protein C has strong anticoagulatory and pro-fibrinolytic properties that further help balance thrombosis The historical cascade model of blood coagulation published in 1964 with its intrinsic and extrinsic activation pathways describes the complexity of hemostasis inadequately It limits itself to the phenomena of in vitro secondary hemostasis and permits no explanation of certain coagulation disorders in vivo Nevertheless, this model can still be pulled up even today for the simplistic visualization of the process of plasmatic coagulation tests, e.g., the prothrombin time (PT)/international normalized ratio (INR) and the activated partial thromboplastin time (aPTT) 18:17:51, subject to the Cambridge Core 012 156 Section 1: Core Principles in Trauma Anesthesia A more recent and accurate model of blood clotting is the cell-based coagulation model In contrast to the cascade model, it assumes that coagulation takes place on activated cell surfaces Besides platelets and endothelial cells, the cell surface of erythrocytes, leukocytes, and microparticles play a central role Different steps are distinguished: The clotting process is described by the initiation, amplification, and propagation phase To strengthen the immature clot, it will be stabilized in the next phase (mediated by FXIII) Regulatory mechanisms are present for the termination of coagulation activation (mediated by TF pathway inhibitor, antithrombin and the protein C pathway) and the elimination of overt clot formation (mediated by plasmin) This model illustrates the in vivo coagulation better than the classical cascade model For example, it can explain the bleeding defects observed with Factors XI, IX, and VIII deficiencies, because these proteins are required for generation of Factor Xa (and subsequently thrombin) on platelet membranes It further suggests that the extrinsic and intrinsic systems are in fact parallel generators of Factor Xa that occur on different cell surfaces, rather than redundant pathways Therefore, the classic plasmatic coagulation tests like PT/INR and aPTT only fragmentarily represent this model The cell-based coagulation model can be illustrated much better with whole blood, viscoelastic coagulation analyzers Assessment of Coagulation To best assess and quantify the status of a patient’s coagulation system, information on the following four mainstays of perioperative coagulation monitoring should be collected and combined for clinical interpretation Medical History The patient’s focused medical history is crucial for the assessment of the individual bleeding risk and should be carried out with specific questionnaires This standardized approach has been shown to be superior to preoperative routine laboratory coagulation studies Accordingly, national societies have published recommendations on standardized preoperative assessment of hemostasis Clinical Presentation The clinical presentation of abnormal hemostasis (e.g., certain phenotypes of bleeding or thrombosis) is critical for the differential diagnosis and gives valuable information on possible etiologies of the underlying coagulation disorder Also, abnormal laboratory coagulation studies must always be correlated with the current clinical presentation, before any hemostatic therapy is initiated Without clinically relevant bleeding (e.g., “dry” surgical area) no procoagulant therapy should be initiated due to the risk of adverse thrombotic events Instead, the patient must be closely observed and reassessed When a patient is bleeding, the question often arises whether the cause of bleeding is “surgical” or “non-surgical.” Advanced coagulation monitoring can help distinguish both types of bleeding If “surgical” bleeding is present, the patient requires surgical re-exploration to control the bleeding A diffuse, microvascular, “non-surgical” bleed, however, requires rapid, individualized, and goal-directed treatment 18:17:51, subject to the Cambridge Core 012 Chapter 11: Coagulation Monitoring 157 Standard Laboratory Coagulation Tests Standard or conventional laboratory coagulation tests include PT/INR, aPTT, and platelet count Depending on local circumstances, other laboratory values, such as fibrinogen concentration, D-dimer, Factor XIII, Anti-Xa, and thrombin time, may be part of a standard laboratory coagulation panel Patients presenting with complex hemostatic disorders require in-depth laboratory coagulation studies under the direction of a hematologist Discussion of advanced laboratory coagulation tests is beyond the scope of this article Standard laboratory coagulation tests play a central role in the initial diagnostic steps of patients with deranged hemostasis Like other analyses, these tests only answer certain questions, although they are of value in monitoring the effects of warfarin and heparin, and other conditions Bedside Point-of-Care (POC) Coagulation Tests There are several methods available to analyze blood coagulation at the patient’s bedside According to their main objective and function, POC coagulation analyzers can be categorized into devices focusing on the analysis of: Primary (cellular) hemostasis, mainly platelet function Tests analyzing primary hemostasis measure platelet count and function as well as VWF activity Several bedside tests are available, e.g., PFA-200 and modified platelet aggregometry Secondary (plasmatic) hemostasis These bedside tests are used to monitor anticoagulant therapy Examples include the ACT, whole blood PT/INR, and heparin management devices Entire hemostasis, from initial thrombin generation to maximum clot formation up to fibrinolysis Viscoelastic coagulation monitoring devices like thromboelastography (TEG), rotational thromboelastometry (ROTEM), and Sonoclot assess the hemostatic system globally, analyzing primary and secondary hemostasis, clot strength, and fibrinolysis In the trauma setting, POC monitoring of the entire coagulation process is most useful TEG, ROTEM, and Sonoclot measure the clot’s physical property under low shear conditions and graphically display the changes in viscoelasticity of the blood sample after initiating the coagulation cascade POC Monitoring of the Entire Coagulation Process Bedside coagulation tests, especially the viscoelastic tests such as TEG and ROTEM, may help to avoid unnecessary administration of procoagulant substances (e.g., plasma, platelets, and coagulation factor concentrates) and enable the clinicians to distinguish between a surgical and non-surgical cause of bleeding These tests may also reduce interventional delays and the need for surgical re-explorations, and ultimately reduce mortality TEG and ROTEM TEG is a method to study the entire coagulation potential of a single whole blood specimen and was first described by Hartert in 1948 Because TEG assesses the viscoelastic properties of blood, it is sensitive to all interacting cellular and plasmatic components After starting 18:17:51, subject to the Cambridge Core 012 158 Section 1: Core Principles in Trauma Anesthesia Figure 11.2 Working principle of viscoelastic POC devices TEG, ROTEM, and Sonoclot working principle Figure 11.3 Standard graphical output of viscoelastic POC devices TEG, ROTEM, and Sonoclot standard graph the analysis, the thrombelastograph measures and graphically displays all stages of the coagulation process: the time until initial fibrin formation, the kinetics of fibrin formation and clot development, and the ultimate strength and stability of the clot as well as the clot lysis In TEG, whole blood is added to a heated cuvette at a set temperature, typically 37°C A disposable pin connected to a torsion wire is suspended in the blood sample and the cup is oscillated through an angle of 4°45’ (rotation cycle 10 seconds; Figure 11.2) As the blood sample starts to clot, fibrin strands connect and couple the cup with the pin The rotation of the cup is transmitted to the pin The rotation movement of the pin is converted by a mechanical-electrical transducer to an electrical signal, and displayed as the typical TEG tracing (Figure 11.3) ROTEM technology avoids some limitations of traditional TEG and offers advantages: measurements are less susceptible to mechanical shocks, four samples can be run at the same time (TEG can only run two), and pipetting is made easier by provision of an electronic pipette In ROTEM, the disposable pin (not the cup) rotates back and forth 4°75’ (Figure 11.2) The rotating pin is stabilized by a high precision ball-bearing system Signal transmission is carried out via an optical detector system (not a torsion wire) The exact position of the pin is detected by reflection of light on a small, embedded mirror on the shaft of the pin Data obtained from the reflected light are then processed and graphically displayed (Figure 11.3) Although TEG and ROTEM tracings appear similar, the nomenclature and reference ranges are not comparable The systems use different materials: ROTEM cups and pins are composed of a plastic with a greater surface charge resulting in higher contact activation compared to those used in TEG Furthermore, the systems involve different proprietary formulas of coagulation activators (e.g., composition, concentration) For example, if the same blood specimen is analyzed by TEG and ROTEM with their proprietary intrinsic coagulation activator, kaolin or inTEM reagent (partial thromboplastin phospholipids), 18:17:51, subject to the Cambridge Core 012 Chapter 11: Coagulation Monitoring 159 respectively, the results obtained are significantly different TEG and ROTEM cannot be used interchangeably, and treatment algorithms have to be specifically adapted for each device In the perioperative setting, most coagulation analyses are performed in citrated whole blood that is recalcified and specifically activated to reduce variability and running time Several commercial reagents are available that contain different coagulation activators, heparin neutralizers, platelet blockers, or antifibrinolytics to answer specific questions on the current coagulation status Blood samples can be extrinsically (tissue factor; e.g., exTEM reagent) and intrinsically (contact activator; e.g., inTEM reagent) activated To determine functionality and levels of fibrinogen, reagents incorporate platelet inhibitors (e.g., cytochalasin D in fibTEM reagent) This concept has been proven to work and a good correlation of this modified maximum amplitude (MA)/maximum clot firmness (MCF) with levels of fibrinogen measured in the laboratory has been demonstrated Finally, by adding an antifibrinolytic drug to the activating reagent (e.g., aprotinin in apTEM), the test can provide information on the current fibrinolytic state, especially when compared to a test run without antifibrinolytics, and help guide antifibrinolytic therapy The repeatability of measurements by both devices has shown to be acceptable, provided they are performed exactly as outlined in the user’s manuals TEG and ROTEM have become the gold standard for the detection and quantification of coagulopathy in trauma patients There is also evidence that these assays may predict transfusion need and mortality in the trauma population Sonoclot Coagulation and Platelet Function Analyzer The Sonoclot analyzer was introduced in 1975 by von Kaulla and associates and measures viscoelastic properties of a blood sample A hollow, oscillating probe is immersed into the blood and the change in impedance to movement imposed by the developing clot is measured (Figure 11.2) Different cuvettes with different coagulation activators and inhibitors are commercially available Normal values for tests run by the Sonoclot analyzer depend largely on the type of sample (whole blood vs plasma; native vs citrated sample), cuvette, and activator used The Sonoclot analyzer provides information on the entire hemostasis both in a qualitative graph, known as the Sonoclot signature (Figure 11.3), and as quantitative results: the activated clotting time (ACT), clot rate, and platelet function The ACT is the time in seconds from activation of the sample until fibrin formation This onset of clot formation is defined as a certain upward deflection of the Sonoclot signature and is detected automatically by the machine Sonoclot’s ACT corresponds to conventional ACT, provided that cuvettes containing a high concentration of typical activators (e.g., celite, kaolin) are being used The clot rate, expressed in units/minute, is the maximum slope of the Sonoclot signature during initial fibrin polymerization and clot development Platelet function is reflected by the timing and quality of the clot retraction Platelet function is a calculated value, derived by an automated numeric integration of changes in the Sonoclot signature after fibrin formation has completed To obtain reliable results for platelet function, cuvettes containing glass beads for specific platelet activation (gbACT+) should be used The nominal range of values for the platelet function goes from 0, representing no platelet function (no clot retraction and flat Sonoclot signature after fibrin formation), to approximately 5, representing strong platelet function (clot retraction occurs sooner and is very strong, with clearly defined, sharp peaks in the Sonoclot signature after fibrin formation) 18:17:51, subject to the Cambridge Core 012 160 Section 1: Core Principles in Trauma Anesthesia Simplified Interpretation for TEG/ROTEM Readouts While the TEG and ROTEM results may look a bit challenging when seen for the first time, one can get used to reading them very quickly and intuitively in a relatively short period of time The readout of TEG/ROTEM can be divided into three phases: Pre-clot formation phase Clot formation phase Clot stability phase The first phase starts with the addition of reagents (e.g., calcium, coagulation activator) that trigger the plasma coagulation cascade and activate platelets (Figure 11.4) It ends with a thrombin burst and the beginning of clot formation This part of the curve lasts less than minutes and can inform the user about the functional state of the coagulation cascade If there are deficiencies in this phase, prothrombin complex concentrates (PCC, typically containing vitamin K-dependent coagulation factors) and/or FFP can usually correct them In patients receiving anticoagulants (e.g heparin, dabigatran), specific reversal (e.g protamine, idarucizumab) is recommended The second phase starts with the beginning of clot formation and ends when the maximum clot firmness is reached (Figure 11.5) It depends mostly on the Figure 11.4 Phase of the TEG/ROTEM graph 18:17:51, subject to the Cambridge Core 012 Chapter 11: Coagulation Monitoring 161 Figure 11.6 Phase of the TEG/ ROTEM graph functional platelet mass and the availability of fibrinogen, and to a minor degree, on the functionality of Factor XIII Any defects in this phase are usually readily visible after a few more minutes and can be corrected with the transfusion of cryoprecipitate and/or fibrinogen concentrate and/or platelet concentrates The last phase depicts clot stability and will detect hyperfibrinolysis (Figure 11.6) Viscoelastic tests are essentially the only clinically available tests that can detect and quantify hyperfibrinolysis Standard Laboratory Coagulation Tests versus Viscoelastic Coagulation Tests in Trauma Standard laboratory coagulation tests can be of high value to determine levels of oral anticoagulation with vitamin K antagonists, the degree of heparin effect, and the bleeding likelihood of a patient with genetic or acquired thrombophilia All of those conditions can be complicating factors for patients, and they need to be evaluated with the proper standard laboratory coagulation tests On the other hand, standard coagulation tests fail to reliably quantify both overall perioperative bleeding risk and a specific cause for coagulopathy Most studies fail to document any usefulness of standard laboratory coagulation tests in the setting of perioperative coagulopathic bleeding Standard laboratory coagulation tests represent historically established thresholds that were utilized for lack of alternatives and are not supported by current evidence Aside from these validation concerns, results of standard laboratory coagulation tests are not rapidly available In most centers, the delay in obtaining results is 25–60 minutes, which may render results that are out of context in the setting of significant bleeding Lastly, there are no standard tests that would detect hyperfibrinolysis and hypercoagulability The former not only has a significant prevalence in trauma patients, but it also lends itself to intervention by administering an antifibrinolytic Hypercoagulability is a major concern in the days after survival from severe trauma The ability to measure and quantify the hypercoagulable state has the potential to guide further intervention The viscoelastic coagulation tests overcome many of the above listed constraints The following attributes make TEG and ROTEM ideal tests for perioperative and traumatic coagulopathy: Validated tests in the setting of perioperative and traumatic coagulopathy Turnaround time for most of the relevant information in less than 10 minutes Can detect both hyperfibrinolysis and hypercoagulability Economic Aspects of the Utilization of POC Viscoelastic Coagulation Testing The argument of increased cost is frequently mentioned with the utilization of POC ular While the purchase 18:17:51, subject to the Cambridge Core 012 162 Section 1: Core Principles in Trauma Anesthesia and implementation of a thromboelastometry device is associated with significant cost ($50,000–$100,000 USD), their utilization will result in significant direct and indirect savings There have been a number of recent publications focusing on the cost savings that can be achieved by deploying a thromboelastometry-based algorithm in the setting of trauma or cardiac surgery Even when performed in addition to standard coagulation tests, they produce significant cost reductions for the respective organizations The main mechanism of cost savings is reduction in utilization of blood products and coagulation factors Most studies found that deploying a transfusion/coagulation management algorithm based on POC coagulation testing resulted in a 25–50% reduction of the overall cost of blood and coagulation products These savings include the offsetting of the additional testing cost Not included in the calculation were the potential indirect savings that result from better patient outcomes (e.g., less complications, less days in the ICU, lower incidence of organ failure) Treatment of Coagulopathy With the information from the aforementioned four mainstays of perioperative coagulation assessment (medical history, clinical presentation, standard and POC coagulation tests) bleeding patients can be treated individually on a goal-directed basis according to defined algorithms Evidence-based guidelines, like the one from Task Force for Advanced Bleeding Care in Trauma (see Rossaint et al 2016), are helpful in developing locally adapted treatment algorithms (see Figure 11.7) It must be emphasized that procoagulant therapy should always be applied with caution A deficient coagulation system should never be excessively corrected because of the serious risk for thromboembolic adverse events Therapy should be titrated carefully and stopped if bleeding is no longer clinically relevant A specific, goal-directed coagulation management in combination with clearly defined algorithms can lead to decreased transfusion needs, diminished costs, and a better outcome Therefore, transfusion algorithms have been introduced in different clinics recently Algorithms consider the physiology and pathophysiology of the developing coagulopathy in massively bleeding patients and serve as clearly structured guidelines for individualized coagulation therapy Figure 11.7 Coagulation management algorithm based on ROTEM at Zuckerberg San Francisco General Hospital and Trauma Center CT = clotting time, MCF = maximum clot formation, ML = maximum lysis, exTEM = extrinsically activated essay (using tissue factor), fibTEM = fibrinogen-only essay (suppressing platelet contribution to clot by 18:17:51, subject to the Cambridge Core 012 Chapter 11: Coagulation Monitoring 163 Conclusions Hemostasis is a complex vital system of our body Normal blood coagulation exists when procoagulant and anticoagulant forces are in balance Clinically relevant phenotypes of hemostasis, bleeding, and thrombosis occur immediately if the system is no longer in equilibrium Disturbed perioperative coagulation may have different causes For specific diagnosis, information must be gathered from the four mainstays of perioperative coagulation assessment: medical history, clinical presentation, and standard and POC coagulation tests Modern coagulation management relies on this assessment and is specific, goaloriented, and individualized to the patient’s needs Key Points Hemostasis, the process which causes bleeding to stop, consists of three interacting mechanisms: vascular, primary (cellular), and secondary (plasmatic) hemostasis The historic cascade model with its intrinsic and extrinsic pathway is inadequate to describe the complexity of hemostasis The cell-based coagulation model is a more accurate and comprehensive model of the coagulation system This model accounts for the pivotal role of platelets and endothelial cells A thorough assessment of any perioperative coagulopathy includes the patient’s medical history, clinical presentation of the hemorrhage, standard laboratory coagulation tests, and POC coagulation testing Standard laboratory coagulation tests in isolation have significant shortcomings in the perioperative setting Viscoelastic POC coagulation tests (TEG/ROTEM) have become the mainstay for assessing the nature and magnitude of perioperative coagulopathy Whenever possible, disturbances of a given patient’s coagulation system should be treated on an individual, goal-directed basis using an appropriate algorithm Further Reading Da Luz LT, Nascimento B, Shankarakutty AK, et al Effect of thromboelastography (TEG) and rotational thromboelastometry (ROTEM) on diagnosis of coagulopathy, transfusion guidance and mortality in trauma: descriptive systematic review Crit Care 2014;18:518 Ganter MT, Hofer CK Coagulation monitoring: current techniques and clinical use of viscoelastic point-of-care coagulation devices Anesth Analg 2008;106:1366–1375 Gonzalez E, Moore EE, Moore HB, et al Goal-directed hemostatic resuscitation of trauma-induced coagulopathy: a pragmatic randomized clinical trial comparing a viscoelastic assay to conventional coagulation assays Ann Surg 2016;263:1051–1059 Haas T, Fries D, Tanaka KA, et al Usefulness of standard plasma coagulation tests in the management of perioperative coagulopathic bleeding: is there any evidence? Br J Anaesth 2015;114: 217–224 Nardi G, Agostini V, Rondinelli B, et al Trauma-induced coagulopathy: impact of the early coagulation support protocol on blood product consumption, mortality and costs Crit Care 2015;19:83 Rossaint R, Bouillon B, Cerny V, et al The European guideline on management of major bleeding and coagulopathy following trauma: fourth edition Crit Care 2016;20:100 Steurer MP, Ganter MT Trauma and massive blood transfusions Curr Anesthesiol Rep 2014;4:200–208 18:17:51, subject to the Cambridge Core 012 Table 22.3 Checklist for anesthetic management of the pregnant trauma patient PREMEDICATION • Sodium citrate or H2-receptor antagonist POSITIONING • Sniffing position • Elevate upper back and shoulders if necessary so that external auditory meatus is at level of sternum • Left uterine displacement: wedge under right hip INDUCTION & AIRWAY MANAGEMENT • Backup help available; present in OR if difficult airway anticipated • Videolaryngoscope available • Advanced airway equipment available (e.g., flexible bronchoscope, LMA) • Rapid sequence induction • Cricoid pressure • TT 6.0 and 6.5 available ANESTHESIA MAINTENANCE • Volatile agents, depolarizing and non-depolarizing neuromuscular blockers, fentanyl, morphine all safe during pregnancy IV ACCESS • 1–2 large bore (at least 16 G) • Placement above diaphragm INTRAOPERATIVE MATERNAL MONITORING • Arterial line if indicated due to maternal condition • Keep SBP >100 mmHg to maintain uteroplacental blood flow • Both ephedrine and phenylephrine are acceptable vasopressors during pregnancy INTRAOPERATIVE FETAL MONITORING • Indication determined by obstetricians • If indicated, a labor nurse is present to monitor CESAREAN DELIVERY PREPARATION • If FHR monitoring is being done (possibility for cesarean delivery), have available oxytocin 20–40 units/1 L crystalloid (first-line uterotonic) and methylergonovine 0.2 mg IM and carboprost 0.25 mg IM (second-line uterotonics) if cesarean delivery is done EMERGENCE (avoid aspiration) • Confirm full reversal of non-depolarizing muscle relaxants • Patient must be fully awake and responsive prior to extubation DISPOSITION • PACU or ICU depending on maternal status • Intermittent FHR monitoring by labor nurse or obstetrician Abbreviations: FHR = fetal heart rate; ICU = intensive care unit; IM = intramuscular; IV = intravenous; LMA= laryngeal mask airway; OR = operating room; PACU = postanesthesia care unit; SBP = systolic blood pressure; TT = tracheal tube 18:31:01, subject to the Cambridge Core 023 Chapter 22: Management of the Pregnant Trauma Patient 315 Table 22.4 Checklist for initial multidisciplinary management of the pregnant trauma patient ANESTHESIA TEAM • H&P • Trauma history • Maternal vital signs, severe ranges include: BP 120 FiO2 0.5 Abbreviations: HR = heart... complications of trauma are often seen in cases of both penetrating and blunt trauma and are of concern when massive resuscitation is required The strategy of damage control surgery calls for control of