Ebook Essentials of trauma anesthesia (2/E): Part 2

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.

Marc P Steurer and Michael T Ganter

Introduction

Blood coagulation is a complex and tightly regulated physiologic network of interactingproteins and cells If deranged, it may dramatically influence outcome A comprehensiveunderstanding of normal hemostasis and its pathophysiology is necessary for anesthesiol-ogists working in the perioperative field

Treatment of a massive trauma bleeding requires an interdisciplinary approach for bothtrauma surgeons and anesthesiologists Modern transfusion strategies and coagulationmanagement are based on a detailed understanding of coagulation physiology and specificcoagulation monitoring Besides the patients’ medical history, clinical presentation andlaboratory tests, bedside coagulation analyses (point-of-care, POC) are increasingly beingused to assess hemostasis Consequently, specific, individualized, and goal-directed hemo-static interventions are becoming more and more feasible

Abnormal hemostasis is not limited to bleeding Hypercoagulability and thrombosis arefurther phenotypes of disturbed hemostasis The coagulation system represents a delicatebalance of forces supporting coagulation (coagulation, antifibrinolysis) and forces inhibit-ing coagulation (anticoagulation, fibrinolysis) (Figure 11.1) The distinctive challenge is

to assess and quantify both sides of this balance and to maintain an equilibrium Specificcoagulation interventions can be made on either side, with the goal of preventing both overtbleeding and thrombosis

Figure 11.1 Coagulation balance Normal blood coagulation exists when procoagulant and anticoagulant forces are in balance.

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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, andsecondary hemostasis In addition, hemostasis initiates sore healing of the injured vesselwhile 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 aparacrine way by the endothelium, the vessel wall, and the immediate environment ofthe 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 byplatelets 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 describesthe complex interaction of different clotting factors that finally result in a stable fibrinnetwork

To protect the organism against thrombosis and embolism, the natural anticoagulantpathway restrains overt clot formation at different levels, and the fibrinolytic system preventsexcessive clot formation and promotes lysis of inadvertently formed blood clots

In vivo, the coagulation system becomes primarily activated by tissue factor (TF) Tissuefactor exists beyond the blood vessels on smooth muscle cells and fibroblasts Therefore, thecoagulation 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 fromexsanguination Under certain pathologic circumstances like sepsis, TF can be intravascularlyexpressed on endothelial cells, monocytes, and circulating microparticles (cell fragments).The resulting uncontrolled and overt coagulation activation can lead to the syndrome ofdisseminated intravascular coagulation (DIC)

The key enzyme of secondary hemostasis is thrombin (FIIa), a serin-protease similar totrypsin Besides transformation of fibrinogen to soluble fibrin, thrombin facilitates numer-ous other biochemical reactions such as coagulation and immune system activation The neteffect 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 theintrinsic pathway and finally amplifying its own production Thrombin further activates thethrombin-activated fibrinolysis inhibitor (TAFI), Factor XIII, as well as platelets, endothe-lial cells, and perivascular smooth muscle cells During this process, two regulatory mech-anisms are important for the protection from an overshooting thrombin formation: theantithrombin and protein C system Antithrombin does so by irreversibly binding andinactivating thrombin Activated protein C has strong anticoagulatory and pro-fibrinolyticproperties that further help balance thrombosis

The historical cascade model of blood coagulation published in 1964 with its intrinsicand extrinsic activation pathways describes the complexity of hemostasis inadequately Itlimits 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 eventoday for the simplistic visualization of the process of plasmatic coagulation tests, e.g., theprothrombin time (PT)/international normalized ratio (INR) and the activated partialthromboplastin time (aPTT)

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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 cellsurfaces 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 byFXIII)

 Regulatory mechanisms are present for the termination of coagulation activation(mediated by TF pathway inhibitor, antithrombin and the protein C pathway) and theelimination of overt clot formation (mediated by plasmin)

This model illustrates the in vivo coagulation better than the classical cascade model Forexample, it can explain the bleeding defects observed with Factors XI, IX, and VIIIdeficiencies, because these proteins are required for generation of Factor Xa (and subse-quently thrombin) on platelet membranes It further suggests that the extrinsic andintrinsic systems are in fact parallel generators of Factor Xa that occur on different cellsurfaces, rather than redundant pathways Therefore, the classic plasmatic coagulationtests like PT/INR and aPTT only fragmentarily represent this model The cell-basedcoagulation model can be illustrated much better with whole blood, viscoelastic coagula-tion analyzers

Assessment of Coagulation

To best assess and quantify the status of a patient’s coagulation system, information on thefollowing four mainstays of perioperative coagulation monitoring should be collected andcombined for clinical interpretation

1 Medical History

The patient’s focused medical history is crucial for the assessment of the individual bleedingrisk and should be carried out with specific questionnaires This standardized approach hasbeen shown to be superior to preoperative routine laboratory coagulation studies Accord-ingly, national societies have published recommendations on standardized preoperativeassessment of hemostasis

2 Clinical Presentation

The clinical presentation of abnormal hemostasis (e.g., certain phenotypes of bleeding orthrombosis) is critical for the differential diagnosis and gives valuable information onpossible etiologies of the underlying coagulation disorder Also, abnormal laboratorycoagulation studies must always be correlated with the current clinical presentation, beforeany hemostatic therapy is initiated Without clinically relevant bleeding (e.g.,“dry” surgicalarea) no procoagulant therapy should be initiated due to the risk of adverse thromboticevents 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 bothtypes of bleeding If“surgical” bleeding is present, the patient requires surgical re-exploration

to control the bleeding A diffuse, microvascular,“non-surgical” bleed, however, requiresrapid, individualized, and goal-directed treatment

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3 Standard Laboratory Coagulation Tests

Standard or conventional laboratory coagulation tests include PT/INR, aPTT, and plateletcount Depending on local circumstances, other laboratory values, such as fibrinogen concen-tration, D-dimer, Factor XIII, Anti-Xa, and thrombin time, may be part of a standardlaboratory coagulation panel

Patients presenting with complex hemostatic disorders require in-depth laboratorycoagulation studies under the direction of a hematologist Discussion of advanced labora-tory coagulation tests is beyond the scope of this article

Standard laboratory coagulation tests play a central role in the initial diagnostic steps ofpatients with deranged hemostasis Like other analyses, these tests only answer certainquestions, although they are of value in monitoring the effects of warfarin and heparin, andother conditions

4 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 categor-ized 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 bedsidetests 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 heparinmanagement devices

 Entire hemostasis, from initial thrombin generation to maximum clot formation up tofibrinolysis Viscoelastic coagulation monitoring devices like thromboelastography(TEG), rotational thromboelastometry (ROTEM), and Sonoclot assess the hemostaticsystem 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 condi-tions and graphically display the changes in viscoelasticity of the blood sample afterinitiating the coagulation cascade

POC Monitoring of the Entire Coagulation Process

Bedside coagulation tests, especially the viscoelastic tests such as TEG and ROTEM, mayhelp to avoid unnecessary administration of procoagulant substances (e.g., plasma, platelets,and coagulation factor concentrates) and enable the clinicians to distinguish between asurgical and non-surgical cause of bleeding These tests may also reduce interventionaldelays 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 specimenand 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

Chapter 11: Coagulation Monitoring 157

the analysis, the thrombelastograph measures and graphically displays all stages of thecoagulation process: the time until initial fibrin formation, the kinetics of fibrin formationand 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 isoscillated through an angle of 4°45’ (rotation cycle 10 seconds; Figure 11.2) As the bloodsample starts to clot, fibrin strands connect and couple the cup with the pin The rotation ofthe cup is transmitted to the pin The rotation movement of the pin is converted by amechanical-electrical transducer to an electrical signal, and displayed as the typical TEGtracing (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 thesame time (TEG can only run two), and pipetting is made easier by provision of anelectronic pipette In ROTEM, the disposable pin (not the cup) rotates back and forth4°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) Theexact position of the pin is detected by reflection of light on a small, embedded mirror onthe shaft of the pin Data obtained from the reflected light are then processed andgraphically displayed (Figure 11.3)

Although TEG and ROTEM tracings appear similar, the nomenclature and referenceranges are not comparable The systems use different materials: ROTEM cups and pins arecomposed of a plastic with a greater surface charge resulting in higher contact activationcompared to those used in TEG Furthermore, the systems involve different proprietaryformulas of coagulation activators (e.g., composition, concentration) For example, if thesame blood specimen is analyzed by TEG and ROTEM with their proprietary intrinsiccoagulation activator, kaolin or inTEM reagent (partial thromboplastin phospholipids),

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.

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respectively, the results obtained are significantly different TEG and ROTEM cannot be usedinterchangeably, and treatment algorithms have to be specifically adapted for each device.

In the perioperative setting, most coagulation analyses are performed in citrated wholeblood 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 onthe current coagulation status Blood samples can be extrinsically (tissue factor; e.g., exTEMreagent) and intrinsically (contact activator; e.g., inTEM reagent) activated To determinefunctionality and levels of fibrinogen, reagents incorporate platelet inhibitors (e.g., cytocha-lasin D in fibTEM reagent) This concept has been proven to work and a good correlation ofthis modified maximum amplitude (MA)/maximum clot firmness (MCF) with levels offibrinogen measured in the laboratory has been demonstrated Finally, by adding an anti-fibrinolytic drug to the activating reagent (e.g., aprotinin in apTEM), the test can provideinformation on the current fibrinolytic state, especially when compared to a test run withoutantifibrinolytics, and help guide antifibrinolytic therapy

The repeatability of measurements by both devices has shown to be acceptable, providedthey are performed exactly as outlined in the user’s manuals

TEG and ROTEM have become the gold standard for the detection and quantification ofcoagulopathy in trauma patients There is also evidence that these assays may predicttransfusion 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 measuresviscoelastic properties of a blood sample A hollow, oscillating probe is immersed into theblood and the change in impedance to movement imposed by the developing clot ismeasured (Figure 11.2) Different cuvettes with different coagulation activators and inhibi-tors are commercially available Normal values for tests run by the Sonoclot analyzerdepend 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 tive graph, known as the Sonoclot signature (Figure 11.3), and as quantitative results: theactivated clotting time (ACT), clot rate, and platelet function The ACT is the time inseconds from activation of the sample until fibrin formation This onset of clot formation isdefined as a certain upward deflection of the Sonoclot signature and is detected automatic-ally by the machine Sonoclot’s ACT corresponds to conventional ACT, provided thatcuvettes containing a high concentration of typical activators (e.g., celite, kaolin) are beingused The clot rate, expressed in units/minute, is the maximum slope of the Sonoclotsignature during initial fibrin polymerization and clot development Platelet function isreflected by the timing and quality of the clot retraction Platelet function is a calculatedvalue, derived by an automated numeric integration of changes in the Sonoclot signatureafter 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 plateletfunction (no clot retraction and flat Sonoclot signature after fibrin formation), to approxi-mately 5, representing strong platelet function (clot retraction occurs sooner and is verystrong, with clearly defined, sharp peaks in the Sonoclot signature after fibrin formation)

qualita-Chapter 11: Coagulation Monitoring 159

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 oftime The readout of TEG/ROTEM can be divided into three phases:

1 Pre-clot formation phase

2 Clot formation phase

3 Clot stability phase

The first phase starts with the addition of reagents (e.g., calcium, coagulation activator) thattrigger the plasma coagulation cascade and activate platelets (Figure 11.4) It ends with athrombin burst and the beginning of clot formation This part of the curve lasts less than

5 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, typicallycontaining vitamin K-dependent coagulation factors) and/or FFP can usually correct them Inpatients receiving anticoagulants (e.g heparin, dabigatran), specific reversal (e.g protamine,idarucizumab) is recommended The second phase starts with the beginning of clot formationand ends when the maximum clot firmness is reached (Figure 11.5) It depends mostly on the

Figure 11.4 Phase 1 of the TEG/ROTEM graph.

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functional platelet mass and the availability of fibrinogen, and to a minor degree, on thefunctionality of Factor XIII Any defects in this phase are usually readily visible after a fewmore minutes and can be corrected with the transfusion of cryoprecipitate and/or fibrinogenconcentrate and/or platelet concentrates The last phase depicts clot stability and will detecthyperfibrinolysis (Figure 11.6) Viscoelastic tests are essentially the only clinically availabletests 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 oagulation with vitamin K antagonists, the degree of heparin effect, and the bleedinglikelihood of a patient with genetic or acquired thrombophilia All of those conditions can

antic-be complicating factors for patients, and they need to antic-be evaluated with the proper standardlaboratory coagulation tests On the other hand, standard coagulation tests fail to reliablyquantify both overall perioperative bleeding risk and a specific cause for coagulopathy Moststudies fail to document any usefulness of standard laboratory coagulation tests in the setting

of perioperative coagulopathic bleeding Standard laboratory coagulation tests representhistorically established thresholds that were utilized for lack of alternatives and are notsupported by current evidence Aside from these validation concerns, results of standardlaboratory coagulation tests are not rapidly available In most centers, the delay in obtainingresults is 25–60 minutes, which may render results that are out of context in the setting ofsignificant bleeding Lastly, there are no standard tests that would detect hyperfibrinolysis andhypercoagulability The former not only has a significant prevalence in trauma patients, but italso lends itself to intervention by administering an antifibrinolytic Hypercoagulability is amajor concern in the days after survival from severe trauma The ability to measure andquantify the hypercoagulable state has the potential to guide further intervention

The viscoelastic coagulation tests overcome many of the above listed constraints Thefollowing attributes make TEG and ROTEM ideal tests for perioperative and traumaticcoagulopathy:

 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 TestingThe argument of increased cost is frequently mentioned with the utilization of POC

Figure 11.6 Phase 3 of the TEG/

ROTEM graph.

Chapter 11: Coagulation Monitoring 161

and implementation of a thromboelastometry device is associated with significant cost($50,000–$100,000 USD), their utilization will result in significant direct and indirectsavings There have been a number of recent publications focusing on the cost savings thatcan be achieved by deploying a thromboelastometry-based algorithm in the setting oftrauma or cardiac surgery Even when performed in addition to standard coagulation tests,they produce significant cost reductions for the respective organizations The main mech-anism 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 andcoagulation products These savings include the offsetting of the additional testing cost Notincluded in the calculation were the potential indirect savings that result from better patientoutcomes (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 coagulationassessment (medical history, clinical presentation, standard and POC coagulation tests)bleeding patients can be treated individually on a goal-directed basis according to definedalgorithms Evidence-based guidelines, like the one from Task Force for Advanced BleedingCare in Trauma (see Rossaint et al 2016), are helpful in developing locally adaptedtreatment 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 seriousrisk for thromboembolic adverse events Therapy should be titrated carefully and stopped ifbleeding is no longer clinically relevant

A specific, goal-directed coagulation management in combination with clearly definedalgorithms can lead to decreased transfusion needs, diminished costs, and a better outcome.Therefore, transfusion algorithms have been introduced in different clinics recently Algorithmsconsider the physiology and pathophysiology of the developing coagulopathy in massivelybleeding 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

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Hemostasis is a complex vital system of our body Normal blood coagulation exists whenprocoagulant and anticoagulant forces are in balance Clinically relevant phenotypes ofhemostasis, bleeding, and thrombosis occur immediately if the system is no longer inequilibrium Disturbed perioperative coagulation may have different causes For specificdiagnosis, information must be gathered from the four mainstays of perioperative coagula-tion assessment: medical history, clinical presentation, and standard and POC coagulationtests Modern coagulation management relies on this assessment and is specific, goal-oriented, and individualized to the patient’s needs

 Standard laboratory coagulation tests in isolation have significant shortcomings in theperioperative setting

 Viscoelastic POC coagulation tests (TEG/ROTEM) have become the mainstay forassessing the nature and magnitude of perioperative coagulopathy

 Whenever possible, disturbances of a given patient’s coagulation system should betreated on an individual, goal-directed basis using an appropriate algorithm

Further Reading

1 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

2 Ganter MT, Hofer CK Coagulation

monitoring: current techniques and clinical

use of viscoelastic point-of-care

coagulation devices Anesth Analg

2008;106:1366–1375

3 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

4 Haas T, Fries D, Tanaka KA, et al

Usefulness of standard plasma coagulationtests in the management of perioperativecoagulopathic bleeding: is there anyevidence? Br J Anaesth 2015;114:

217–224

5 Nardi G, Agostini V, Rondinelli B, et al.Trauma-induced coagulopathy: impact ofthe early coagulation support protocol onblood product consumption, mortality andcosts Crit Care 2015;19:83

6 Rossaint R, Bouillon B, Cerny V, et al TheEuropean guideline on management ofmajor bleeding and coagulopathyfollowing trauma: fourth edition Crit Care2016;20:100

7 Steurer MP, Ganter MT Trauma andmassive blood transfusions CurrAnesthesiol Rep 2014;4:200–208

Chapter 11: Coagulation Monitoring 163

Jack Louro and Albert J Varon

Disposition and Transport from the Operating Room (OR)

The decision of where the patient will be taken for the immediate postoperative course is akey multidisciplinary discussion where the trauma anesthesiologist must be involved In themajority of acute trauma cases the decision is based on the patient’s hemodynamic profile,extent of the injuries, and whether the surgical procedure was able to definitely correct theinjuries or not

 Hemodynamically stable patients without airway and ventilatory issues who sustainminor injuries generally can recover in the postanesthesia care unit (PACU)

 Patients with hemodynamic instability or respiratory compromise should be recovered

in a dedicated ICU for continued resuscitation and mechanical ventilation

ICUs capable of dealing with polytrauma patients are a necessity for any hospital withtrauma capabilities New paradigms in critical care are being developed with subspecialtyICUs A dedicated trauma ICU that specializes in the care of trauma patients may affordbetter outcomes in terms of mortality and post-injury complications

Postoperative care may require continuing anesthetic management if the patient needsdiagnostic or therapeutic procedures at the completion of surgery prior to transport to theICU For example, patients with active bleeding in the pelvis or liver may require transport

to the angiography suite for endovascular control of bleeding with continued care by theanesthesiologist The availability of hybrid ORs where both surgical and angiographicprocedures can be performed may obviate the need for transporting an unstable patient toanother location In cases where the bleeding has been controlled but there is concern abouthead injury, the patient may be transported directly from the OR to the CT suite to performbrain CT scan and immediately return to the OR if emergent neurosurgical intervention isrequired However, not all patients who receive a damage control laparotomy need to be164

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taken immediately for CT imaging The incidence of missed abdominal injury requiringreoperation after damage control surgery is less than 5% and there is no difference in the re-exploration rates or time to re-exploration in patients who undergo early abdominal CTcompared to those who do not The key is to identify those few patients with a high suspicion

of a missed injury with need for further imaging and intervention, while transporting themajority directly to the ICU for secondary resuscitation

Secondary Resuscitation

In the operative management of traumatic injury, blood component therapy is initiatedearly and guided by the paradigm of balanced resuscitation with the early use of plasma andplatelets along with red blood cells As the initial resuscitation carries on, the ratio of bloodproducts can shift due to blood product preparation times or limited IV transfusion access.When the surgery concludes, secondary resuscitation must follow in the PACU or ICU toensure adequate repletion of coagulation factors and platelets to prevent worsening of thetrauma-associated coagulopathy As the time for thawing and preparation of plasma islonger than that for red blood cells (RBCs), this usually involves a catch-up of fresh frozenplasma (FFP) transfusion as the patient is leaving the OR

 The correction of coagulopathy, hypothermia, and acidosis are important goals of thepostoperative care team in the setting of trauma, especially following damage controlsurgery

 As part of the early resuscitation in the OR, a 1 g loading dose of tranexamic acid (TXA)

is usually indicated in hemorrhaging patients within the first 3 hours from injury(ideally<1 hour) followed by a second dose of the antifibrinolytic over 8 hours

 TXA administration is usually initiated in the OR or emergency department and

continued in the ICU

 Once hemodynamic parameters are stable, the need for empiric ratio-driven transfusion

of blood products should be replaced with targeted hemostatic therapy

Both traditional and viscoelastic coagulation testing such as thromboelastography (TEG)and rotational thromboelastometry (ROTEM) can help guide coagulation therapy in theimmediate postoperative period (see also Chapter 11) Secondary resuscitation will alsoinclude measurement of laboratory values and correction of acidosis and hypothermia (ifpresent) Heat loss from general anesthesia is accentuated in trauma patients due to largesurgical exposure and the requirement of large amounts of fluid and blood products.Temperature management includes the use of forced air warming blankets and IV fluidwarmers In addition to close respiratory monitoring, continued assessment of metabolicacidosis should be undertaken during the postoperative resuscitation until normalization ofthe acidosis

Postoperative Pain Management and Sedation

Sedation and pain control can significantly impact the trauma patient’s recovery and risk ofpulmonary complications Patients who are unstable and require tracheal intubation andmechanical ventilation after surgery will need sedation and analgesia

 An opioid-first approach is usually well tolerated and can reduce the need for othersedatives by providing adequate analgesia

 Opioids are the mainstay of analgesia in the postoperative period

Chapter 12: Postoperative Care of the Trauma Patient 165

Hydromorphone is preferred over morphine due to the lack of active metabolites andhistamine release With all pain medication regimens, a multimodal approach is favored tominimize the adverse effects of opioids and increase analgesic efficacy The use of potentparenteral non-steroidal anti-inflammatory drugs (NSAIDs) such as ketorolac can lead to adecrease in opioid use Intravenous oral, and rectal formulations of acetaminophen areavailable to also work synergistically with opioids and may be used in the acute setting.Adjuncts such as dexmedetomidine and ketamine can be useful in select populations as theywill reduce the amount of sedatives and opioids required Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that can provide sedation as well as analgesia vianon-opioid receptor pathways and has a safe hemodynamic profile in subanesthetic doses.Dexmedetomidine, an alpha-2 agonist, stimulates natural sleep pathways and providessynergism with opioids for analgesia Dexmedetomidine has been associated with decreasedincidence of ICU delirium Both ketamine (at subanesthetic doses) and dexmedetomidinemay also be used for analgesia in non-intubated patients Table 12.1 lists options forpostoperative pain management.

Propofol is a useful sedative drug due to its short context-sensitive half-life; however, thevasodilation that occurs at higher doses of propofol is not well tolerated in unstable patients.Although the use of benzodiazepines in the acute setting can provide a stable hemodynamicprofile, care has to be taken if used in patients with renal failure or the elderly Caution isalso advised for long-term benzodiazepine use, as ICU delirium may result The develop-ment of delirium in the ICU is a major concern, as patients who develop delirium haveworse outcomes and higher mortality There is very little prophylactic pharmacologictreatment for ICU delirium, but early mobilization is key to prevention When deliriumdoes develop, the use of a second-generation antipsychotic along with aggressive reorien-tation is the preferred approach over the use of sedatives or benzodiazepines

Table 12.1 Options for postoperative pain management

Opioids Central acting opioid

receptor agonists

Fentanyl, hydromorphone, morphine (PCApreferred over intermittent dosing)NSAIDs Peripherally acting anti-

Synergistic effects and opioid sparing

Available PO, rectal, and IVCalcium channel

modulators

Inhibits nociceptiveneurotransmitter release

Subanesthetic doses up to 10μg/kg/min

Local anesthetics Na channel blockers Can be infiltrated locally or directed to sensory

nervesAbbreviations: PCA = patient-controlled analgesia; NSAIDs = non-steroidal anti-inflammatory drugs; NMDA = N-methyl-D-aspartate.

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 For stable patients who will have their tracheas extubated postoperatively, adequateanalgesia to allow normal breathing is crucial.

Patients with rib fractures or upper abdominal surgery will commonly have shallowbreathing and refrain from coughing due to pain The use of thoracic epidural catheterscan be effective for both rib fracture pain as well as thoracic and upper abdominal surgerypostoperative pain control (see also Chapter 8) The use of paravertebral nerve blocks inpatients who undergo unilateral thoracic surgery seems to be as effective as epiduralanalgesia and may carry less risk Patients with significant limb injuries can benefit fromperipheral nerve blocks to reduce the requirement for opioids

to bacterial contamination from penetrating injuries

 Ventilation strategies entail the use of positive end-expiratory pressure (PEEP) that isadequate to prevent atelectasis with the lowest tolerated oxygen concentration Tidalvolumes should be based on predicted body weight and limited to no more than 8 mL/

kg, with many recommending 6 mL/kg in patients who have developed ARDS

Efforts should be made to limit duration of positive pressure ventilation and extubate thetrachea as quickly as possible to reduce the incidence of ventilator-associated infections andlung injury Appropriate selection of patients for ventilatory support and taking steps tominimize the duration of mechanical ventilation are key to reducing these untoward outcomes.The need for mechanical ventilation needs to be assessed daily in the postoperative period anddifferentiated from the need for postoperative airway protection In some cases, mechanicalventilation will not be necessary if a definitive airway can be established via tracheostomy.Patients with traumatic brain injury (TBI) or neck trauma frequently require airwayprotection postoperatively, which puts the native airway in danger Although large randomizedcontrolled trials (RCTs) in the general ICU population have shown no benefit of earlytracheostomy, certain subsets of trauma patients, such as those with significant maxillofacialfractures requiring multiple surgical procedures, may benefit from early tracheostomy to limitthe duration of mechanical ventilation In cases with significant burns as part of the trauma, theairway may develop significant edema that requires prolonged intubation or even tracheos-tomy Patients with thoracic trauma requiring thoracotomy may need postoperative ventilationbecause the emergent nature of the surgery prevents adequate pre-emptive analgesia and giventhe fact that pulmonary contusions can progress to edema and acute respiratory distresssyndrome (ARDS), especially when there is a need for massive resuscitation

Patients who are hemodynamically stable, have return of mental status to baseline, andmeet respiratory criteria should have their tracheas extubated without delay Respiratorycriteria for extubation in the ICU are similar to intraoperative criteria, including fullrecovery of neuromuscular function, adequate tidal volume to respiratory rate ratio, andnegative inspiratory force less than–20 mmHg in order to have adequate cough, as well asstrength to lift head or legs for 5 seconds Since these criteria can be more challenging to

Chapter 12: Postoperative Care of the Trauma Patient 167

assess in a polytrauma patient, a spontaneous breathing trial with blow-by oxygen orminimal pressure support for 30 to 120 minutes should be considered (Table 12.2).

Neurologic Considerations

Patients presenting to the trauma center with altered mental status and hemodynamicinstability will likely proceed to the OR without the benefit of a detailed neurologic exam.These patients will require early brain imaging immediately post-op if the presentingGlasgow Coma Scale (GCS) score was consistent with moderate to severe TBI There could

be urgent need for neurosurgical intervention in the setting of an intracranial hemorrhage.Patients who will remain intubated in the postoperative period should have sedation heldearly to allow neurologic examination Even patients with mild TBI (GCS>12) may needbrain CT if their neurologic function is not at baseline after the emergency surgery Patientswho suffer TBI should be supported by maintaining adequate oxygenation and normalblood pressure in the early postoperative period Although there is some debate on the use

of hypotensive resuscitation in bleeding patients, it is clear that TBI patients require normalblood pressure to protect brain perfusion and oxygen delivery

Along with brain imaging, patients who have depressed mental status or major ing injury will require imaging of the spine if there was the potential for injury This isespecially true in blunt trauma since an adequate clinical exam will be unreliable in a patientimmediately after surgery Until imaging of the spine can be performed, full spine precau-tions should remain in place including the use of a cervical hard collar In hemodynamicallyunstable patients with blunt injury and no evidence of hemorrhage, neurogenic shock could

distract-be the culprit due to a missed spinal cord injury For these patients the use of vasopressorsand inotropes may need to be initiated early and adequate fluid repletion administered tocompensate for the vasodilatory state

 RR <35 breaths per minute

 ABG without acidosis and PaCO2<60 mmHg

 PF >60 L/min

 PaO2/FiO2>120

 FiO20.5Abbreviations: HR = heart rate; SBP = systolic blood pressure; TV = tidal volume; RR = respiratory rate; ABG = arterial blood gas; NIF = negative inspiratory force; PF = peak flow; PEEP = positive end-expiratory pressure.

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blood loss and remains in shock, cardiac etiologies have to be ruled out in the immediatepostoperative period Myocardial contusion is uncommon even in blunt trauma (incidence

~5%), but may occur more frequently in the setting of chest trauma with associated sternal

or anterior rib fractures Myocardial contusions may result in cell damage and cause rightand left ventricular wall motion abnormalities and decreased ventricular function Theinjured myocardium may also be predisposed to the development of arrhythmias, especially

if electrolyte abnormalities are present (e.g., acute kidney injury [AKI], massive transfusion,rhabdomyolysis) An admission electrocardiogram (ECG) should be performed in patientswith suspected blunt cardiac injury If the admission ECG reveals new abnormalities thepatient should receive continuous ECG monitoring in the acute phase of injury Myocardialcontusions with hemodynamic compromise will demonstrate functional deficits on echo-cardiography (see Chapter 10) Echocardiography can also identify signs of tamponadephysiology including pericardial effusion and cardiac chamber compression or collapse.However, routine echocardiography is not useful as a primary screening modality formyocardial contusion, but rather as a diagnostic test for patients who have unexplainedhypotension or arrhythmias

As the population ages and advances are made in the treatment of chronic cardiacconditions, the percentage of elderly trauma patients with multiple comorbidities willcontinue to increase In a patient with underlying heart failure, the initial volume resusci-tation during ongoing blood loss may not unmask the heart failure However, once damagecontrol surgery has stopped blood loss and secondary resuscitation progresses, patients maydevelop decompensated heart failure In these scenarios, hemodynamic monitoring could

be helpful in patient management (see also Chapter 9) Invasive hemodynamic monitorsinclude the use of arterial, central venous, and, in select cases, pulmonary artery catheters.Echocardiography can help elucidate the cardiac etiology of shock as well as guide shockmanagement, and is rapidly becoming the preferred method for hemodynamic monitoringdue to its non-invasive nature and portability With the use of echocardiography, patientsdisplaying cardiac dysfunction postoperatively can be identified and inotropic supportinitiated to optimize ventricular function and systemic perfusion

Renal and Acid/Base Considerations

In the immediate postoperative period after resuscitation and damage control surgery,metabolic acidosis is common and can be associated with complications and increasedmortality Efforts should be made to restore the body’s acid–base balance by ensuringadequate tissue perfusion and providing intravascular volume with not only the necessaryblood products but also balanced electrolyte solutions Measuring and correcting basedeficit and lactate levels in a timely manner, usually within the first 12–36 hours, will allowfor definitive interventions and could result in fewer complications The initial intraopera-tive course and severity of injury will dictate the amount of secondary resuscitation, but keyelectrolyte derangements should be suspected and treated Calcium and potassium levelsneed to be monitored for patients who receive massive transfusion after trauma Tissueinjury and ischemia along with lysis of red blood cells can result in life-threateninghyperkalemia, which could present in the postoperative period as tissues are beingreperfused and red blood cell administration continues Hypocalcemia is common inthe setting of massive transfusion after trauma and this will need continuing correctionand monitoring

Chapter 12: Postoperative Care of the Trauma Patient 169

Acute kidney injury is a prevalent problem in the post-traumatic patient The etiologycould result from tissue injury leading to rhabdomyolysis but more evidence is pointing torenal hypoperfusion that accompanies the shock state Multiple factors such as crush injury,head injury, and the use of furosemide have been linked to AKI in trauma ICU patients.Patients who develop AKI tend to have a higher mortality and length of stay than traumapatients who do not suffer AKI Restoring adequate renal perfusion quickly after hemor-rhage will help prevent the propagation of renal insult In patients with AKI, adjustmentsmust be made to medications including antibiotics in the postoperative period to preventtoxic doses or worsening of renal failure.

Special consideration must be made for patients with TBI and elevated intracranialpressure (ICP) Hyperosmolar treatment is usually initiated intraoperatively in the manage-ment of ICP With the use of hypertonic saline or mannitol, fluid shifts will be common inthe postoperative period TBI itself can lead to a deficiency in antidiuretic hormone (ADH)causing diabetes insipidus and electrolytes and fluid alterations When mannitol is used,the hyperosmolar state may cause transient hyperkalemia and eventual loss of potassiumthrough the urine, which often leads to hypokalemia Due to mannitol’s high osmolarity,there is concern for initial fluid overload However, patients can become hypovolemic ifkidney function is preserved, as mannitol is a potent osmolar diuretic Hypernatremia can becaused by iatrogenic administration of hypertonic saline or the development of diabetesinsipidus in brain injury patients The latter is managed by providing adequate volumereplacement and vasopressin receptor agonists Correction should be gradual to avoidworsening brain edema

Gastrointestinal and Nutritional Support

Gastrointestinal complications of trauma are often seen in cases of both penetrating andblunt trauma and are of concern when massive resuscitation is required The strategy ofdamage control surgery calls for control of bleeding and intra-abdominal contaminationand keeping the abdomen open These patients must have a fine balance of adequate fluidresuscitation but avoidance of fluid overload that can impair the ability to close theabdomen within the recommended time frame of 8 days Patients who do not requiredamage control laparotomy but require massive resuscitation can develop bowel edema inthe postoperative period The ICU care of patients receiving large-volume resuscitationrequires close monitoring for signs of intra-abdominal hypertension and abdominal com-partment syndrome Peak airway pressures and urine output along with bladder pressurescan be used to detect rising intra-abdominal pressure

Nutrition in the postoperative course of the trauma patient needs to be started as early

as possible Patients who receive nutrition within 48 hours of trauma have less related complications Enteral nutrition is the preferred route and should be started oncethe patient is hemodynamically stable, unless contraindicated by bowel obstruction, boweldiscontinuity, perforation, or bleeding Patients who have an initial damage control surgerywill need to return to the OR for definitive procedures These patients will likely have feedsheld multiple times in the postoperative course One consideration in the intubated andmechanically ventilated patient is to continue enteral feeds until the time of surgery as there

infection-is a secure airway in place In these patients, the rinfection-isk of aspiration infection-is low and the benefit ofcontinued nutrition outweighs the risk of aspiration For patients who have bowel injuriesand must be left in discontinuity or have multiple anastomoses and fistulas, early parenteral

170 Section 1: Core Principles in Trauma Anesthesia

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nutrition should be considered Starting parenteral nutrition early (within 1 week) would bepreferable over delaying nutrition until the enteral route is available In certain circum-stances, low-dose enteral feeds can be used concurrently to protect the gastrointestinalmucosa and maintain normal flora while nutritional needs are being met mostly throughthe parenteral route.

Postoperative Infection and Sepsis

Patients who survive the initial phase of trauma can develop dysregulation of the inflammatorysystem which has been implicated in a host of complications Of these complications, infec-tions and sepsis are still prevalent in the trauma patient and have continued to be a significantcause of morbidity and mortality Sepsis is a common diagnosis in ICU patients and can bedeadly if not recognized and treated early Infection and sepsis tend to be related to the severity

of the injuries in trauma patients Those with higher injury severity will likely end up in theICU and be exposed to mechanical ventilation as well as indwelling catheters and monitors.The incidence of sepsis in trauma patients has been decreasing, but still remains approxi-mately 10% in multiply injured patients Although mortality from trauma in general hasdecreased over the past few decades, the subset of trauma patients who develop sepsis afterinjury has not experienced a similar reduction in mortality The systemic inflammatoryresponse can cause multiorgan failure independent of the presence of infection

Sepsis is a common diagnosis in ICU patients and can be deadly if not recognized andtreated early Over the past decade, early goal-directed therapy has been commonlyemployed to ensure adequate oxygen delivery with the use of fluids, red cell transfusion,vasopressors, and inotropes The early recognition and aggressive protocol-driven manage-ment has led to a decrease in sepsis mortality over the past 20 years Early recognition andinitiation of antibiotics as well as supportive care are paramount However, recent studieshave challenged the need to adhere to a specific protocol requiring the measurement ofCVP or mixed venous saturation as endpoints The consensus seems to be that aggressivetreatment must be started as soon as the patient meets sepsis criteria

Trauma patients have a high incidence of lung infection as a primary source This isoften expected in patients who require prolonged ventilation due to lung contusions, TBI,and ongoing resuscitation The main pathogens in the trauma ICU patients tend to begram-negative organisms unlike the non-trauma ICU patients, where the predominantpathogens are gram-positive Trauma ICU patients also tend to be colonized and/orinfected with bacteria that are multi-drug resistant Early recognition and initiation ofantibiotics as well as supportive care are paramount Careful selection of antibiotics isrequired when treating patients empirically The goal is to prevent the propagation of multi-drug resistance while adequately covering the most common organisms

Key Points

 The postoperative care of the trauma patient begins with patient disposition and

initiating transport from the OR to the PACU or ICU Anesthesiologists must beinvolved in this process

 Aggressive secondary resuscitation must be initiated early to prevent the lethal triad ofcoagulopathy, acidosis, and hypothermia

 The use of viscoelastic coagulation tests can facilitate individualized therapy with bloodproducts and hemostatic agents

Chapter 12: Postoperative Care of the Trauma Patient 171

 Postoperative pain control should entail multimodal analgesia Minimizing

postoperative sedation may prevent ICU delirium and decrease morbidity

 Trauma patients who sustain major injury are at risk of developing ARDS Therefore,ventilator management should incorporate lung-protective strategies with low tidalvolumes, PEEP, limited plateau pressures, and as low an inspired oxygen concentration

as the patient will tolerate

 Spine precautions (including a cervical collar) must remain in place in blunt traumapatients until imaging or reliable clinical exam can exclude injury

 Echocardiography is a useful tool to detect cardiac injuries and evaluate cardiac function

in the patient who remains hypotensive despite adequate resuscitation

 Hypoperfusion during the initial shock state can lead to AKI Therefore, adequate renalperfusion should be ensured along with monitoring electrolyte imbalances

 Abdominal compartment syndrome may develop after damage control laparotomy ormassive transfusion Monitoring peak airway pressures and urine output can help makethe diagnosis

 Early nutrition is essential in the postoperative period for trauma patients Enteralnutrition is preferred, but nutrition should not be delayed even if the enteral route isunavailable

 Sepsis and infection continue to pose high mortality in the trauma ICU population.Early aggressive therapy should be initiated and includes appropriate broad spectrumantibiotics and fluid repletion

Further Reading

1 Curry N, Davis PW What’s new in

resuscitation strategies for the patient

with multiple trauma? Injury

2012;43:1021–1028

2 Dobson GP, Letson HL, Sharma R,

Sheppard FR, Cap AP Mechanisms of early

trauma-induced coagulopathy: The clot

thickens or not? J Trauma Acute Care Surg

2015;79:301–309

3 Eriksson M, Brattström O, Mårtensson J,

Larsson E, Oldner A Acute kidney injury

following severe trauma: risk factors and

long-term outcome J Trauma Acute Care

Surg 2015;79:407–412

4 Fowler MA, Spiess BD Postanesthesia

recovery In: Barash P, Cullen B,

Stoelting R, Cahalan M, Stock MC, Ortega

R, eds Clinical Anesthesia, 7th edition.Philadelphia, PA: Lippincott Williams &Wilkins; 2013

5 Ramsamy Y, Hardcastle TC, Muckart DJ.Surviving sepsis in the intensive careunit: The challenge of antimicrobialresistance and the trauma patient

World J Surg 2016: 016–3531-0

doi:10.1007/s00268-6 Schmidt GA, Hall JB Management of theventilated patient In: Hall JB, Schmidt GA,Kress JP, eds Principles of Critical Care, 4thedition New York, NY: McGraw-Hill;2015

7 Slutsky AS, Ranieri VM induced lung injury N Engl J Med2013;369:2126–2136

Ventilator-172 Section 1: Core Principles in Trauma Anesthesia

18:18:59, subject to the Cambridge Core

K H Kevin Luk and Armagan Dagal

Introduction

Traumatic brain injury (TBI) is an acquired insult to the brain due to an externalmechanical force and can lead to transient or permanent impairment of cognitive, physical,and psychosocial functions Anesthesiologists are most often involved in the care of patientswith moderate to severe TBI for a variety of procedures including but not limited to initialevaluation and resuscitation, diagnostic imaging, surgical intervention, and intensive careunit (ICU) management

Epidemiology

 The global incidence of TBI is estimated at 200 per 100,000 people per year

 In 2010, about 2.5 million (87%) emergency department (ED) visits were associated withTBI in the United States

 ED visits led to 283,630 (11%) hospitalizations and 52,844 (2%) deaths

 This translates to a 70% increase in ED visits, 11% increase in hospitalizations, and 7%reduction in deaths between the years 2001 and 2010

 TBI continues to be responsible for approximately 30% of all injury-related deaths

 Falls (40.5%) are the leading cause of TBI followed by motor vehicle collisions (MVCs,14.3%), struck by/against events (15.5%), assaults (10.7%), and unknown/other (19%)causes

 The leading cause of TBI-related death varies by age:

: Falls are the major cause of death for elderly persons (age>65)

: MVCs are responsible for the majority of deaths in children and young adults (ages5–24)

: Assaults are the leading cause of death for children (ages 0–4)

 There are potential gender differences in TBI outcomes:

: Male gender is associated with a higher rate of hospitalization as well as a three-foldincrease in death from TBI

: After mild TBI, females use more healthcare services and may have a higher risk ofepilepsy and suicide

Pathophysiology

TBI has been described in two distinct yet interrelated epochs: the initial primary injury andsubsequent secondary injuries

173

 Primary injury is the consequence of the initial trauma, resulting in mechanical

deformation on the skull and the brain tissue

: Disruption of the vascular structures results in intracranial hematomas

: Shearing and compression of neuronal, glial, and vascular tissues result in

hemorrhagic brain contusions

Axonal tissue is more vulnerable to TBI than vascular tissue Thus, focal injuriesare usually superimposed upon more diffuse neuronal injury At the cellular level,primary injury results in physical disruption of tissue architecture, compression ofvascular structures, and disturbance of ionic homeostasis secondary to cell

membrane disruption and increased permeability, which ultimately leads to celldeath

 Secondary injury is described as the consequence of progressive insult to the neurons inthe penumbral region and starts immediately after TBI

: Secondary injury results in astrocytic and neuronal swelling, relative hypoperfusion,perturbation of cellular calcium homeostasis, increased free radical generation andlipid peroxidation, mitochondrial dysfunction, inflammation, glutaminergic

excitotoxicity, cellular necrosis, apoptosis, and diffuse axonal degeneration

: Systemic insults such as hypotension (SBP<90 mmHg), hypoxemia (PaO2<60mmHg), hypoglycemia, hyperglycemia, hypocarbia, and hypercarbia are majorcontributors of secondary injury

: The early management of TBI is directed toward minimizing secondary insults.Although cerebral ischemia appears to be the major common pathway of secondarybrain damage, reperfusion hyperemia may also occur and is equally detrimental.The Marshall classification is frequently utilized for classifying TBI based on CT character-istics (Table 13.1)

Table 13.1 Marshall’s classification of traumatic brain injury

Diffuse injury I No visible intracranial pathology on CT scan

Diffuse injury II Cisterns are present with midline shift<5 mm and/or lesion densities

present

No high- or mixed-density lesion>25 mL, may include bone fragmentsand foreign bodies

Diffuse injury III Cisterns compressed or absent with midline shift 0–5 mm

No high- or mixed-density lesion>25 mLDiffuse injury IV Midline shift>5 mm

No high- or mixed-density lesion>25 mLEvacuated mass

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Preoperative Considerations

In any trauma patient, priority must first be given to general evaluation and stabilization ofvital body functions, with particular attention to the airway, breathing, and circulationduring the primary survey A baseline neurologic assessment should be performed using theGlasgow Coma Scale (GCS) score (Table 13.2) Traumatic brain injury is classified as severe

if the GCS score is8 and is associated with higher morbidity and mortality It is classified

as moderate if the GCS score is 9–12 and mild if the GCS score is 13–15 Secondary surveyswill identify other injuries

Knowledge of the mechanism of injury is important for prognostication as well as foranticipation of associated injuries Penetrating injuries have a worse outcome than blunttrauma Females may fare less well Pedestrians and cyclists do worse than vehicle occupants

in motor vehicle accidents, and ejection from the vehicle leads to a higher risk of TBI.Surgical procedures for TBI include:

 Craniotomy for the evacuation of epidural, subdural, or intracerebral hematomas

 Decompressive hemicraniectomy for the treatment of intracranial hypertension (ICH)refractory to medical treatment

Anesthesia providers should actively look for manifestations of increased intracranialpressure (ICP) including Cushing’s triad of hypertension, bradycardia, and irregular res-piration Patients with high preoperative ICPs are at risk of cerebral ischemia and hypoten-sion following evacuation of an intracranial hematoma Issues related to urgent or emergent

Table 13.2 Glasgow Coma Scale score a

a Total Glasgow Coma Scale score (range 3 –15) is summation of best eye + verbal + motor response scores.

Chapter 13: Considerations for Adult Traumatic Brain Injury 175

craniotomy include need for adequate vascular access, availability of blood products, and abilityfor rapid resuscitation Management of the patient with TBI can be challenging and compli-cated by associated extracranial injuries and coexisting hypovolemic and neurogenic shock.The preoperative anesthetic assessment checklist for patients with TBI focuses on:

 Airway and cervical spine stability

 Adequacy of oxygenation and ventilation

 Blood pressure, heart rate, and rhythm

 Baseline neurologic status

 Associated extracranial injuries

 Available medical, surgical, and anesthetic history, and allergies

 Current medications including anticoagulant/antiplatelet use (e.g., clopidogrel, aspirin,

or warfarin) and herbal supplements

 Relevant laboratory data (e.g., hematocrit, coagulation profile, blood gas, glucose,electrolytes)

 Planning of the postoperative management and discharge destination (e.g., ICU)Medically unstable conditions warranting further evaluation are rare since craniotomy forTBI is typically urgent or emergent Hence, delaying surgery is seldom indicated However, anumber of TBI patients suffer from concomitant injuries and may require extracranialsurgery The decision of which surgery should be performed first depends on several factorsincluding severity of TBI, severity of associated injuries, and hemodynamic stability Forexample, if the polytrauma patient with possible TBI is hemodynamically stable during initialevaluation, abdominal and head CT may be performed prior to management of extracranialinjury Patients with possible TBI who are hemodynamically unstable and have abdominaltrauma typically require emergency laparotomy Intraoperative ICP monitoring may beinitiated prior to a head CT if coagulation parameters are normal and the index of suspicionfor TBI is high In this case, head CT is obtained after extracranial surgery In rarecircumstances (e.g., hemodynamic instability, positive FAST, positive neurologic signs),patients may require simultaneous emergency craniectomy and laparotomy

Coexisting conditions may impact the surgical and postoperative course For elderlypatients who sustain falls, particular attention should be paid to pre-injury cardiac, pulmon-ary, and endocrine status since congestive heart failure, hypertension, chronic obstructivepulmonary disease (COPD), and type II diabetes mellitus are common in this population.These coexisting conditions may result in perioperative complications such as worseningcongestive heart failure, COPD exacerbation, pulmonary edema, or hyperglycemia

Medications used to manage the aforementioned pre-injury conditions can result inintraoperative complications:

 Antihypertensive drugs: Diuretics can cause electrolyte imbalance resulting in

arrhythmias Patients receiving beta-blockers prior to surgery may experience bradycardiaand fail to increase their heart rate in response to acute blood loss Calcium channelblockers and angiotensin-converting enzyme inhibitors or angiotensin II antagonists maycause hypotension, especially when combined with beta-blockers and diuretics

 Antiplatelet and oral anticoagulant drugs: Patients who receive antiplatelet or

anticoagulant drugs may have an increased risk of bleeding and transfusion

Transfusion of platelet or other coagulation products may be required Four factor

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prothrombin complex concentrate (4-Factor PCC) is the preferred option for rapid andpredictable warfarin reversal Fresh frozen plasma can be used if 4-Factor PCC is notavailable, although it may lead to volume overload or incomplete reversal Dabigatran

is a direct thrombin inhibitor that can be reversed effectively with Idarucizumab, aspecific monoclonal antibody While currently there is no specific reversal for Factor Xinhibitors (rivaroxaban, edoxaban, and apixaban) 4-Factor PCC has been used withsome success and should be considered

 Herbals: Garlic, ginseng, ginger, and gingko may interfere with platelet function,

particularly when combined with non-steroidal anti-inflammatory drugs or warfarin,and increase the risk of bleeding

 Oral hypoglycemic drugs: Patients who receive oral hypoglycemic drugs may developperioperative hypoglycemia

Laboratory Investigations

Preoperative tests may be ordered selectively for guiding or optimizing perioperativemanagement on the basis of a patient’s clinical characteristics and urgency of surgicalprocedure However, these investigations should not delay the start of surgical manage-ment For rapid assessment, prothrombin time, fibrinogen, platelet count, and hematocritobtained together, as an “emergency hemorrhage panel”, and viscoelastic point-of-carecoagulation tests may facilitate timely transfusion therapy Preoperative hyperglycemiamay portend intraoperative hyperglycemia and poor outcome Therefore, glucose levelsshould be obtained prior to surgery and hourly during surgery Patients with TBI may haveelectrolyte disturbances and the treatment for these should be initiated while the patientproceeds to surgery

Intraoperative Management

There are no formal intraoperative guidelines for the management of TBI Intraoperativecare is largely based on physiologic optimization and may be guided by the 2016 recom-mendations from the Brain Trauma Foundation (Table 13.3)

A minimum of two large-bore, peripheral, intravenous catheters should be placedpreferably in the upper extremities General anesthesia with tracheal intubation is requiredfor control of oxygenation and ventilation (see Chapter 7) Some patients with TBI requir-ing emergency craniotomy may have their trachea intubated when they arrive in theoperating room In these patients, adequate positioning of the tracheal tube must beconfirmed In patients whose tracheas are not intubated, expedient tracheal intubation isoften necessary based on the patient’s clinical condition Airway management can bechallenging because of several factors, including:

 Urgent/emergent nature of the procedure

 Potential for aspiration

 Potential instability of the cervical spine

 Potentially complicated airway (airway injury, blood, skull base fracture)

 Elevated ICP

 Uncooperative or combative patient

 Existing impaired oxygenation, ventilation, or hemodynamic status

Chapter 13: Considerations for Adult Traumatic Brain Injury 177

Table 13.3 Brain Trauma Foundation recommendations for severe TBI

Systolic blood pressure SBP100 mmHg for patients 50–69 years old

SBP110 mmHg for patients 15–49 or >70 years oldIntracranial pressure Treatment of ICP>22 mmHg

monitoring

Jugular bulb monitoring of AVDO2, as a source of information formanagement decisions, may be considered to reduce mortality andimprove outcomes

Cerebral perfusion

pressure

Target CPP between 60 and 70 mmHg (Avoid aggressive attempts tomaintain CPP>70 mmHg with fluids and vasopressors due to risk ofrespiratory failure)

Not recommended to improve outcomes

Hyperosmolar therapy Mannitol (0.25–1 g/kg) is effective in reducing ICP, but should be

reserved for transtentorial herniation or progressive neurologicdeterioration prior to ICP monitoring

Ventilation strategies Prolonged prophylactic hyperventilation (PaCO225) is not

recommended, and hyperventilation should be avoided during the first

24 hours of injury Hyperventilation should only be used as atemporizing measure for ICP reduction If hyperventilation is used, SjvO2

or BtpO2measurements are recommendedAnesthetics/analgesics/

sedatives

Prophylactic burst suppression using barbiturates is not recommended.High-dose barbiturates can be considered for treatment of refractoryICP elevation Propofol is recommended for ICP control (but high-doseuse can cause significant morbidity)

Steroids Routine use is not recommended (High-dose methyl-prednisolone

administration associated with increased mortality)Seizure prophylaxis Phenytoin is recommended to decrease early seizure (<7 days), but

long-term prophylaxis is not recommendedDeep vein thrombosis

prophylaxis

Intermittent pneumatic compression stockings and low-dose heparin

or low-molecular-weight heparin are recommendedAbbreviations: AVDO 2 = arteriovenous oxygen content difference; BtpO 2 = brain tissue O 2 partial pressure; CPP = cerebral perfusion pressure; CSF = cerebrospinal fluid; CT = computed tomography; GCS = Glasgow Coma Scale; ICH = intracranial hypertension; ICP = intracranial pressure; PaCO 2 = partial pressure of arterial carbon dioxide; SBP = systolic blood pressure; S jv O 2 = jugular venous oxygen saturation; TBI = traumatic brain injury.

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The choice of intubation technique is determined by urgency, personnel experience, andavailable resources (see Chapter 3) In general, rapid sequence induction (RSI) and intub-ation with manual in-line immobilization is recommended If the cervical collar is in place,the anterior portion is removed to allow greater mouth opening and facilitate laryngoscopy.Cervical collars have not been shown to significantly reduce neck movement by themselvesand may, in fact, make intubation more difficult due to decreased mouth opening Sincethe injured brain has minimal tolerance to hypoxia, hypercarbia, and increased ICP, it isimportant to have a variety of emergency airway equipment immediately available, includ-ing videolaryngoscopy (e.g., Glidescope), gum elastic bougie, laryngeal mask airway, andemergency surgical airway equipment Nasotracheal intubation should be avoided inpatients with base of skull fractures, severe facial fractures, or bleeding diatheses.

Oxygenation and Ventilation

Hypoxia, hypercarbia, and hypocarbia should be avoided to prevent secondary injuries afterTBI Oxygenation should be monitored and maintained at PaO2 >60 mmHg or oxygensaturation >90% Hyperventilation causes cerebral vasoconstriction and can result inischemia The current guidelines for managing TBI indicate that prolonged prophylactichyperventilation (PaCO225 mmHg) is not recommended and hyperventilation should beavoided during the first 24 hours after TBI when cerebral blood flow (CBF) is oftencritically reduced Hyperventilation is only recommended as a temporizing measure forthe reduction of elevated ICP and may be utilized briefly during emergent evacuation ofexpanding intracranial hematoma When hyperventilation is used, jugular venous oxygensaturation (SjvO2) or brain tissue oxygen partial pressure (BtpO2) measurements arerecommended to monitor oxygen delivery

Anesthetic Technique

Anesthetic agents, including sedative/hypnotic agents used to facilitate intubation, canaffect cerebral physiology in multiple ways Choice of induction agent depends on thehemodynamic status Thiopental and propofol are indirect cerebral vasoconstrictors, redu-cing cerebral metabolic rate of oxygen (CMRO2) coupled with a corresponding reduction ofCBF Both autoregulation and CO2 reactivity are preserved However, propofol and thio-pental can cause cardiovascular depression and venodilation leading to hypotension, espe-cially in the presence of uncorrected hypovolemia Etomidate decreases the cerebralmetabolic rate, CBF, and ICP At the same time, because of minimal cardiovascular effects,cerebral perfusion pressure (CPP) is well maintained However, etomidate has been shown

to inhibit adrenal hormone synthesis with persisting low cortisol levels for approximately

12–24 hours after administration and may necessitate vasopressor use The effect of a singleinduction dose of etomidate on TBI outcome is not clear Ketamine is a weak noncompe-titive N-methyl-D-aspartate (NMDA) antagonist that has sympathomimetic properties Itscerebral effects are complex and are partly dependent on the action of other concurrentlyadministered drugs Recent studies have reported that ketamine does not result in increasedICP, and in fact may lower it in selected cases

The effects of anesthetic technique (inhalation versus total intravenous anesthesia) on TBIoutcome have not conclusively revealed superiority of one technique over another However,

in general, low-dose volatile agents preserve cerebral hemodynamics compared to high-dosevolatile agents The cerebral effects of inhaled anesthetic agents appear to be two-fold; at low

Chapter 13: Considerations for Adult Traumatic Brain Injury 179

doses, they preserve flow–metabolism coupling whereas at doses >1 minimum alveolarconcentration (MAC), direct cerebral vasodilation may cause cerebral hyperemia andincreased ICP With the exception of sevoflurane, which appears to preserve cerebral auto-regulation at all clinically relevant doses, other inhalational agents impair cerebral autoregu-lation in a dose-dependent manner Nitrous oxide is generally avoided due to increasedCMRO2and increased ICP from cerebral vasodilatation Preexisting pneumocephalus may

be aggravated by the use of nitrous oxide

Neuromuscular blocking agents have little or no effect on CBF and ICP Succinylcholineand rocuronium are both suitable options for neuromuscular blockade (see Chapter 7).Succinylcholine is unlikely to cause increased ICP in the setting of RSI On the other hand,increases in ICP secondary to hypoxia and hypercarbia are well documented and muchmore likely to be clinically important Coughing and bucking during intubation can alsocause a large increase in ICP Hence, in patients with TBI, anesthesiologists should notavoid using succinylcholine when difficulty in airway management is anticipated

In general, opioids are safe to use in patients with TBI receiving mechanical ventilation.However, opioids may cause hypercarbia and ICP elevation if the airway is not secured and thepatient is hypoventilated There is no evidence of direct opiate-mediated cerebral vasodilatoryaction in the presence of controlled ventilation However, in patients with decreased intracra-nial compliance, opioid-induced systemic hypotension can also lead to secondary increase inICP from compensatory vasodilatation Opioids with short duration of action are preferred

Intraoperative Monitoring

In addition to the standard American Society of Anesthesiologists (ASA) monitors, arterialcatheterization is recommended for beat-to-beat blood pressure monitoring and for bloodgas analysis, glucose, and blood electrolyte sampling during surgery Central venouscatheterization may be useful for resuscitation and when vasopressors are administeredbut should not delay surgical decompression, as vascular access may be obtained usingfemoral or intraosseous catheters, should peripheral intravenous access prove to be difficult.Ultrasound guidance should be used to facilitate internal jugular vein cannulation, therebyreducing the need for Trendelenburg positioning, which may increase ICP

In general, ICP monitoring is recommended in all salvageable patients with severe TBI(GCS 8) and an abnormal CT scan (hematomas, contusions, swelling, herniation, orcompressed basal cistern), and in patients with severe TBI with a normal CT scan if two ormore of the following features are noted at the admission: age >40 years, unilateral orbilateral motor posturing, or SBP<90 mmHg For patients with TBI undergoing extracra-nial surgeries, intraoperative ICP monitoring is desirable to optimize cerebral physiologyand avoid secondary increases in ICP Intraoperative placement of ICP monitors is notdesirable if significant coagulopathy is present (see also Chapter 9) However, ICP monitorinsertion is feasible in patients with mild coagulopathy when the international normalizedratio (INR)1.6 and platelet count >100,000

Despite their increasing application in ICUs, advanced neuromonitoring techniqueshave not gained widespread acceptance for intraoperative management of patients undergo-ing urgent/emergent surgical decompression Jugular venous oximetry may be performed

in select patients as it allows assessment of the global oxygenation status of the brain as well

as adequacy of CBF Normal SjvO2ranges between 55 and 75% The ischemic threshold hasbeen reported to be a SjvO2<50% for at least 10 minutes In TBI, SjvO2is most commonly

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used for the detection of reduced cerebral perfusion and titration of hyperventilation inpatients with increased ICP Both transcranial Doppler ultrasonography and brain tissueoxygenation monitoring have been used to optimize CBF and cerebral oxygenation.

Hemodynamic Management

Several studies have documented worsened outcome in TBI patients who have experiencedepisodes of hypotension (SBP<90 mm Hg) after TBI Thus, continuous monitoring andoptimization of blood pressure and CPP is a fundamental part of TBI management TheBrain Trauma Foundation currently recommends a CPP of 60–70 mmHg in patients withsevere TBI It is worth noting that there is a lack of intraoperative data and it is unclear as towhat the optimal intraoperative hemodynamic goals should be However, cerebral auto-regulation may be impaired after TBI and this is important because when blood pressure islow–normal, cerebral ischemia may result; whereas in the presence of normal–high bloodpressures, cerebral hyperemia may ensue Therefore, cerebral autoregulation is one import-ant mediator of CBF and outcome after TBI

Fluid Management

Isotonic crystalloid solution (e.g., normal saline and Plasma-Lyte) is preferable in TBI for fluidreplacement Glucose-containing and colloid solutions should be avoided According to theSaline versus Albumin Fluid Evaluation (SAFE) study, resuscitation with albumin is associatedwith a higher mortality rate and unfavorable outcome in TBI patients A multicenter, clinicalrandomized control trial to determine whether out-of-hospital administration of hypertonicfluids would improve neurologic outcome following severe TBI was terminated early due topresumed futility The investigators concluded that initial fluid resuscitation of patients withsevere TBI with either hypertonic saline/dextran or hypertonic saline (HTS) was not superior to0.9% saline with respect to 6-month neurologic outcome or survival In addition, the use ofstarch-based colloid solutions is associated with coagulopathy and renal failure

Osmotherapeutics have been shown to decrease ICP and improve CPP Mannitol is thefirst-line osmotic agent for the treatment of ICH in TBI The recommended dose of mannitol

is 0.25 to 1 g/kg body weight administered over 20 minutes Its use prior to ICP monitoringshould be restricted to patients with signs of transtentorial herniation or progressive neuro-logic deterioration due to intracranial pathology However, due to osmotic diuresis, mannitoladministration may result in hypovolemia and hypotension Reverse osmotic shift frommannitol overdose can lead to worsening cerebral edema and acute kidney injury Therefore,serum osmolality should be monitored and should not exceed 320 mOsm In addition, whencompared to HTS, mannitol is more likely to contribute to coagulopathy There is limitedevidence regarding the benefit and favorable side effect profile of HTS over mannitoladministration in TBI However, HTS has been shown to have beneficial vasoregulatory,immunomodulatory, and neurochemical effects on the injured brain while improving braintissue oxygenation and hemodynamics (higher CPP and cardiac output) when used as asecond-tier therapy after mannitol administration for elevated ICP

Anemia

Evidence suggests that both anemia and packed red blood cell (RBC) transfusion areassociated with poor neurologic outcome in TBI While anemia is associated with increasedin-hospital mortality, lower hospital discharge GCS score, and lower discharge Glasgow

Chapter 13: Considerations for Adult Traumatic Brain Injury 181

outcome score, RBC transfusion is associated with acute lung injury, longer ICU andhospital stay, and mortality in TBI.

Mechanisms proposed for anemia-induced brain injury include tissue hypoxia, reactiveoxygen species, disruption of blood–brain barrier function, vascular thrombosis, andanemic cerebral hyperemia However, a number of cerebro-protective physiologic mechan-isms become effective with anemia, which include aortic chemoreceptor activation,increased sympathetic activity leading to increased heart rate, stroke volume and cardiacindex, reduced systemic vascular resistance, and enhanced oxygen extraction Moreover, anumber of cellular mechanisms of cerebral protection become effective during acuteanemia These include hypoxia-inducible factors, increased nitric oxide synthase and nitricoxide in the brain (nNOS/NO), erythropoietin, and vascular endothelial growth factor-mediated angiogenesis and vascular repair

The overall effects of anemia on the brain, therefore, depend on the relative balancebetween these competing protective and harmful factors of anemia and RBC transfusion It

is unclear whether the transfusion trigger in patients with TBI should be any different fromother critically ill patients and whether the injured brain is more susceptible to thedeleterious effects of anemia The optimal hemoglobin level in TBI patients is unclear,but there is no benefit of a liberal transfusion strategy in moderate to severe TBI patients.Monitoring modalities such as brain tissue oxygen tension, near infrared spectroscopy,and jugular bulb catheter sampling can be used to monitor the regional or global oxygen-ation, and may help determine transfusion needs Their effectiveness in patient outcome,however, remains to be proven The anesthesiologist should individualize the decision fortransfusion during craniotomy based on preexisting comorbidities and ongoing blood loss,and after weighing risks versus benefits

Coagulopathy

Coagulopathy is common after TBI Coagulation disorders can cause secondary braininjury from ongoing intracranial bleeding and worsen outcome TBI is associated withthe release of tissue thromboplastin that activates the extrinsic coagulation pathway Theactivation of clotting cascades may lead to the formation of intravascular fibrin and theconsumption of procoagulants and platelets, which results in disseminated intravascularcoagulation (DIC) (Table 13.4)

At present, there is no standard guideline for treatment of coagulopathy in TBI Themanagement of DIC includes platelets and blood component replacement Plasma, plateletconcentrates, heparin, antithrombin III, procoagulant drugs like Recombinant Factor VIIa(rFVIIa), and antifibrinolytic agents such as tranexamic acid have been tested usingdifferent protocols to correct coagulopathy in patients with TBI Not all studies returnedwith significant benefit on outcome There is no strong evidence supporting the benefit ofrFVIIa in TBI patients Two tranexamic acid (TXA) trials demonstrated no statisticallysignificant improvement in clinical outcome but a reduction in intracranial hematomaprogression in the TXA groups An international multicenter randomized clinical trial(CRASH-3) is currently evaluating the use of TXA in patients with TBI

Glucose Control

Hyperglycemia is a stress response after TBI and is associated with increased morbidity andmortality Blood glucose levels are known to increase during anesthesia even in patients

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who do not have preexisting diabetes mellitus Approximately 15% of adults and 23% ofchildren undergoing emergent/urgent craniotomy for TBI have intraoperative hypergly-cemia Risk factors for intraoperative hyperglycemia include age <4 years or >65 years,severe TBI (GCS <9), presence of subdural hematoma on CT scan, and preoperativehyperglycemia.

Intraoperative hyperglycemia is associated with increased mortality after TBI However,the benefit of tight glucose control is unproven In the NICE-SUGAR trial, intense glucosecontrol (<140 mg/dL) showed no benefit in critically ill patients and increased the inci-dence of hypoglycemia In the absence of strong evidence for tight control, it is recom-mended to maintain intraoperative glucose values between 100 and 180 mg/dL Moreimportantly, glucose should be monitored at least hourly during general anesthesia sincehypoglycemia is detrimental to the injured brain Development and clinical implementation

of continuous or frequent glucose monitoring devices and“closed-loop” glycemic controlsystems coupled with algorithm-driven treatment protocols may reduce both extremes ofhypoglycemia and hyperglycemia

Therapeutic Hypothermia

Proposed mechanisms by which hypothermia protects the brain include reduction in brainmetabolic rate, attenuation of blood–brain barrier permeability, reduction of the criticalthreshold for oxygen delivery, calcium antagonism, blockade of excitotoxic mechanisms,preservation of protein synthesis, reduction of intracellular acidosis, modulation of theinflammatory response, decrease in edema formation, suppression of free radicals andantioxidants, and modulation of apoptotic cell death Furthermore, hypothermia lowersthe cerebral metabolic rate by 6–7% for every 1°C decrease in core temperature, whichconsequently improves oxygen supply to the areas of ischemic brain and decreases ICP.However, multicenter phase III trials failed to demonstrate a benefit of hypothermia in TBI.One randomized, multicenter clinical trial (NABIS: H II) of very early mild hypothermia

Table 13.4 International Society of Thrombosis and Homeostasis diagnostic criteria for DIC

<5 points Suggestive (but not confirmative) for non-overt DICAbbreviations: PT = prothrombin time; DIC = disseminated intravascular coagulation.

Chapter 13: Considerations for Adult Traumatic Brain Injury 183

maintained for 48 hours was terminated early due to no significant difference in outcome inpatients treated with hypothermia compared with those treated with normothermia Cur-rent Brain Trauma Foundation guidelines do not recommend the use of therapeutichypothermia in TBI In addition, intraoperative hypothermia may exacerbate ongoingcoagulopathy and increase the incidence of infections It is important to note that althoughhypothermia has not proven to be beneficial, hyperthermia is clearly detrimental to theinjured brain and should be prevented or treated.

Decompressive Craniectomy

Persistent uncontrolled ICH results in poor outcomes following TBI Up to 15% of severe TBIpatients with ICH do not respond to maximum medical management and may need second-tier therapies including decompressive craniectomy In addition, decompressive craniectomymay improve cerebral compliance, CBF, and brain oxygenation The Australian multicenterDECRA (Decompressive Craniectomy in Patients with Severe Traumatic Brain Injury) studyreported on 155 adults with severe diffuse TBI and refractory ICH According to the study,early bifronto-temporoparietal decompressive craniectomy lowered ICP and length of stay inthe ICU, but leads to more unfavorable outcomes Rates of death were found to be similar inboth the craniectomy group (19%) and the standard-care group (18%) at 6 months Morerecently, the RESCUEicp (Randomized Evaluation of Surgery with Craniectomy for Uncon-trollable Elevation of Intracranial Pressure) study demonstrated that decompressive craniect-omy in refractory ICH patients resulted in lower mortality (26.9% vs 48.9%) but higher rates

of vegetative state (8.5% vs 2.1%) and severe disability There was no difference in rates ofmoderate disability and good recovery The decompressive craniectomy group had shorterduration of ICP>25 mmHg, but had a higher rate of adverse events (16.3% vs 9.2%) Thedecision of proceeding with decompressive craniectomy should be individualized taking intoaccount life expectancy and the patient’s current versus expected quality of life

Non-neurologic Surgery in Neurologically Injured Patients

Eighty percent of TBI patients develop multiorgan dysfunction As a result, TBI patientsrequire a thorough assessment and may necessitate further treatment in the ICU prior

to any other semiurgent surgical intervention Temporizing procedures, such as damagecontrol surgery, should be favored over definitive procedures in the early phase oftrauma

Non-emergent procedures in patients with severe TBI should be postponed and thepatient’s medical condition optimized to minimize secondary injury

Emergence from Anesthesia

The management of emergence from anesthesia in the TBI patient is dictated by multiplefactors:

 Need for ongoing resuscitation

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The decision to extubate the trachea in the operating room in TBI patients must beindividualized During emergence, blood pressure and PaCO2are important as hypertensionand hypercarbia may be deleterious and may warrant aggressive control Patients planned fordelayed tracheal extubation because of aforementioned factors should be taken directly to theICU Multimodal monitoring, ICP control, brain protective strategies, and optimization ofCPP are fundamental objectives for the ICU team Adequate analgesia and sedation reducesanxiety, agitation, and pain as they can increase ICP Commonly used sedatives includepropofol, midazolam, and dexmedetomidine Adequate analgesia can be provided withcontinuous intravenous infusion of short-acting opioids such as remifentanil or fentanyl.Coughing, straining, and hypertension during transport may lead to intracranial bleeding andelevation of ICP; neuromuscular relaxants help to prevent this Hypertension (e.g., SBP>160mmHg) can be treated with nicardipine, labetalol, or esmolol, and supplemental barbiturates

or short-acting benzodiazepines, such as midazolam, can be given for sedation In manycenters, it is prudent to obtain an immediate postoperative CT scan to rule out remediablesurgical complications Patients with severe TBI are often transported with the head of bedelevated to prevent ICP increase

Key Points

 Cornerstones of severe TBI management consist of careful pre-anesthesia evaluation,physiologic optimization according to Brain Trauma Foundation guidelines, andmultimodal cerebral monitoring

 Data on the impact of anesthetic technique (inhalation versus total intravenous

anesthesia) on TBI outcome have not conclusively revealed superiority of one techniqueover another

 Prophylactic hyperventilation (PaCO225 mmHg) is not recommended and

hyperventilation should be avoided during the first 24 hours after severe TBI Low andhigh blood pressures may result in cerebral ischemia and cerebral hyperemia,

respectively, and should be avoided Maintaining a CPP between 60–70 mmHg isrecommended in patients with severe TBI

 Isotonic crystalloid solutions are preferable to hypotonic solutions The role of

colloids is controversial The optimal hemoglobin level in TBI patients is unknown, butthere is no benefit of a liberal transfusion strategy in moderate to severe TBI patients

 Glucose-containing solutions should be avoided Continuous or frequent glucosemonitoring devices with algorithm-driven treatment protocols may reduce both

extremes of hypoglycemia and hyperglycemia

 Normothermia should be maintained and there is no advantage of therapeutic

hypothermia in patients with TBI However, hyperthermia is clearly detrimental andshould be prevented and/or treated

 Decompressive craniectomy lowers ICP, duration of ICU stay, and mortality, but doesnot appear to improve functional outcome after severe TBI

Acknowledgment

The authors are grateful to Deepak Sharma and Monica S Vavilala for their contributions

to the 2012 chapter“Anesthetic Considerations for Adult Traumatic Brain Injury” in thefirst edition of“Essentials of Trauma Anesthesia.”

Chapter 13: Considerations for Adult Traumatic Brain Injury 185

Further Reading

1 Cancelliere C, Donovan J, Cassidy JD Is

sex an indicator of prognosis after mild

traumatic brain injury: A systematic

analysis of the findings of the World Health

Organization Collaborating Centre Task

Force on mild traumatic brain injury and

the International Collaboration on Mild

Traumatic Brain Injury Prognosis Arch

Phys Med Rehabil 2016;97:S5–18

2 Carney N, Totten AM, OʼReilly C, et al

Guidelines for the Management of Severe

Traumatic Brain Injury, Fourth Edition

Neurosurgery 2017;80:6–15

3 Clifton GL, Valadka A, Zygun D, et al Very

early hypothermia induction in patients with

severe brain injury (the National Acute Brain

Injury Study: Hypothermia II): a randomised

trial Lancet Neurol 2011;10:131–139

4 Cooper DJ, Rosenfeld JV, Murray L, et al;

DECRA Trial Investigators; Australian and

New Zealand Intensive Care Society

Clinical Trials Group Decompressive

craniectomy in diffuse traumatic brain

injury N Engl J Med 2011;364:1493–1502

5 Faul M, Xu L, Wald MM, Coronado VG

Traumatic Brain Injury in the United

States: Emergency Department Visits,

Hospitalizations, and Deaths Atlanta, GA:

Centers for Disease Control and

Prevention, National Center for Injury

Prevention and Control; 2010

6 Frontera JA, Lewin JJ 3rd, Rabinstein AA,

et al Guideline for reversal ofantithrombotics in intracranialhemorrhage: a statement for healthcareprofessionals from the Neurocritical CareSociety and Society of Critical CareMedicine Neurocrit Care 2016;24:6–46

7 Hutchinson PJ, Kolias AG, Timofeev IS,

et al Trial of decompressive craniectomyfor traumatic intracranial hypertension

N Engl J Med 2016;375:1119–1130

8 Myburgh J, Cooper DJ, Finfer S, et al SAFEStudy Investigators; Australian and NewZealand Intensive Care Society ClinicalTrials Group; Australian Red Cross BloodService; George Institute for InternationalHealth Saline or albumin for fluidresuscitation in patients with traumaticbrain injury N Engl J Med

2007;357:874–884

9 NICE-SUGAR Study Investigators, Finfer

S, Chittock DR, et al Intensive versusconventional glucose control in critically illpatients N Engl J Med

186 Section 2: Anesthetic Considerations for Trauma

00:58:57, subject to the Cambridge Core

K H Kevin Luk and Armagan Dagal

Epidemiology

Motor vehicle collisions (MVCs) and falls are the leading causes of spinal cord injury (SCI).Spinal column fractures are usually the result of high-energy trauma, which tends to result

in patients having multiple injuries SCI occurs in up to 2–5% of all major trauma cases and

at least 14% of these cases have the potential to have an unstable spine In addition,concomitant SCI is found in 7.5–10% of head-injured patients It is estimated that patientswith cervical spine (C-spine) fractures have a 20% risk of a secondary fracture somewhereelse in the spine Twenty to 60% of SCIs are associated with a concurrent traumatic braininjury In the United States, the estimated annual incidence of SCI is approximately 54 casesper million or about 17,000 new cases per year An estimated 282,200 people (about 900 permillion) in the United States live with SCI The age of the victims with SCI follows abimodal distribution, with a first peak occurring between the ages of 15 and 29, and then asecond peak at age>65 The median age of injury has recently increased to 42 The USspinal cord injury population demographics are listed in Table 14.1

With the advancements in medical care, SCI is becoming a more survivable condition,which in turn, increases the societal morbidity in caring for the survivors of SCI The lifeexpectancy of individuals who survived the initial insult for at least 1 year varies with ageand level of injury For tetraplegics with cervical 1–4 level injury, life expectancy 1-year-post-injury is 36.9% at 20, 21% at 40, and 8.7% at 60 years of age Regardless of the level ofinjury, ventilator dependence reduces the life expectancy significantly (25.3%, 12.6%, and

Table 14.1 Spinal cord injury population demographics

4% for patients aged 20, 40, and 60 years, respectively) Septicemia and pneumonia remainthe leading causes of death among individuals with SCI.

In developed countries, the economic impact of SCI is becoming an increasingly importanttopic In the United States, SCI care is estimated to cost $9.7 billion annually In 2011,estimates for average first-year healthcare and living expenses vary from $347,896 for anincomplete motor function at any level to $1,065,980 for high tetraplegia (C1–C4) Thesubsequent recurring annual cost is reported to be well below first-year costs but is nonetheless

a significant economic burden on healthcare systems Lifetime cost can be from $1,580,148 for

an incomplete motor function at any level to $4,729,788 for high tetraplegia (C1–C4)

be divided into two interrelated categories: an initial primary injury and the subsequentsecondary injuries

 Primary injury: This is the immediate consequence of the trauma, which can be due tocompression, contusion, shear, hyperextension, transection, and frank hemorrhage ofthe spinal cord

 Secondary injury: Minutes to hours after the initial insult, neurons in the penumbralregion are exposed to the risk of secondary injury Mechanistically, secondary injury isthe result of spinal cord compression due to edema and the surrounding rigid spinalcanal, and it tends to peak between 4 and 6 days post-injury

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Clinical Presentation and Classification of Spinal Cord Injury

The severity of SCI is graded based on the American Spinal Injury Association (ASIA)impairment scale (AIS) (see Figure 14.1)

Several incomplete spinal cord syndromes offer insights into lesion site, prognosis, andthe potential for early, targeted treatment or interventions (see Table 14.2)

Initial Assessment

The essential management principles of spine trauma include early detection and tion of secondary injury through maintenance of adequate oxygenation, blood pressuresupport (volume replacement and cardiovascular support), and immobilization The cer-vical cord is the least protected segment of the spinal cord and it is involved in half oftraumatic SCI cases, with resulting quadriparesis or quadriplegia Concomitant injuries(e.g., traumatic brain injury, abdominal, thoracic, and pelvic injuries) in a multisystemtrauma patient can mask the presence of SCI This can potentially delay diagnosis andadversely affect patient outcome Up to 8% of maxillofacial fractures are associated with SCIwhich can greatly affect airway management (see Chapters 3 and 15)

preven-The function of the spinal cord is generally examined during the secondary survey(see Figure 14.1) The patient should be evaluated for any midline back pain, tenderness topalpation, motor weakness, and loss of sensation and anal tone In the presence of alteredmental status, SCI should be assumed until proven otherwise Spinal immobilization

is recommended for all trauma patients with a C-spine or spinal cord injury or with amechanism of injury that has the potential to cause these injuries In penetrating trauma,spinal immobilization is not recommended due to its potential to delay resuscitation In theprehospital setting, neck immobilization with a cervical collar, lateral supports, straps, andspinal backboard should be used (spinal motion restriction) Patients should be transferredoff the backboard as soon as it is practical and safe, to minimize pressure injury In thehospital, C-spine immobilization should continue by these methods and must be applieduntil appropriately trained clinicians clear the spine

predomin-at the cervico-thoracic junction The pressure exerted by the laryngoscope blade on airwaysoft tissue is generally transmitted to the spinal column Instability of the occiput–atlas–axiscomplex may lead to anterior movement of the atlas during direct laryngoscopy, resulting

in additional narrowing of the spinal canal

In trauma patients with altered sensorium, a full stomach should be assumed and rapidsequence induction (RSI) and intubation is routinely done However, succinylcholineshould be avoided between 3 days and 9 months following SCI due to the risk ofhyperkalemia caused by muscle denervation-related upregulation of acetylcholine receptors.Rocuronium is a reasonable alternative Limited jaw thrust and chin lift should be used, andearly employment of an oral or nasal airway helps to reduce the force required to maintain

Chapter 14: Considerations for Spinal Cord Injury 189

airway patency The urgent nature of airway interventions usually requires direct scopy or videolaryngoscopy with manual in-line stabilization (MILS) The goal of MILS is

laryngo-to apply sufficient stabilizing force laryngo-to the head and neck laryngo-to limit spine movement duringairway intervention MILS provides better cervical stability but may impair the view of thevocal cords during conventional laryngoscopy Use of increased laryngoscope blade force toovercome poor views does have the potential to increase cervical motion at an unstablefracture site when MILS is applied Nevertheless, when MILS is utilized, the incidence ofneurologic impairment due to tracheal intubation is extremely rare The gum elastic bougie

is a well-established adjunct to direct laryngoscopy, allowing successful intubation of thetrachea in more limited views, and application of less force during laryngoscopy RSI, MILSwith the front of the cervical collar removed, cricoid pressure (CP), and gentle directlaryngoscopy or videolaryngoscopy are suitable in the emergency setting Cricoid pressureshould be applied during induction and maintained through intubation until tube place-ment is confirmed However, MILS and CP can be altered or removed if they impedeventilation, intubation, or insertion of a laryngeal mask airway

In non-urgent circumstances, careful planning is required for safe airway manipulation.The presence of traction/halo device may further impede access to the airway Certain

Table 14.2 Spinal cord syndromes

Central cord

syndrome

Most common incomplete SCI Disproportionate weakness in upperextremities below the level of the lesion compared with the lowerextremities More common in elderly patients with preexistingarthropathy after minor trauma

Brown–Sequard

syndrome

A result of hemisection of the spinal cord with disruption ofcorticospinal, dorsal column, and spinothalamic tracts on one side ofthe spinal cord Ipsilateral hemiplegia and contralateral painand temperature sensation deficits More common with penetratingtrauma

Anterior cord

syndrome

Compromised blood supply to the anterior two-thirds of the spinalcord Paraplegia/quadriplegia with pain and temperature sensation loss,but preserved fine touch and proprioception Often occurs as aconsequence of direct compression by a herniated intervertebral disc

or bone fragment, but can also occur during thoracoabdominal aorticsurgery, if the artery of Adamkiewicz is compromised

Posterior cord

syndrome

Disruption of one of the posterior spinal arteries, which supplies thedorsal column of the spinal cord Isolated ipsilateral loss of fine touch,vibration, and proprioception

Cauda equina

syndrome

Compression of the spinal nerves in the cauda equina Characterized bydull pain in the lower back and upper buttocks and loss or alteredsensation in the buttocks, genitalia, and thigh Also associated withdisturbances of bowel and bladder function

Spinal shock/

transient paralysis

A state of flaccid paralysis, complete anesthesia, absent bowel/bladdercontrol, areflexia, and possible bradycardia and hypotension after anSCI Some patients, especially younger athletes, can make completerecoveries However, most patients progress to some form ofspastic paresis

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conditions, including spondylosis, rheumatoid arthritis, Klippel–Feil syndrome, ankylosingspondylitis, spinal tumor, and prior spinal instrumentation may increase the difficulty ofairway management Several options are available, but none are proven to be superior

to others:

 Awake flexible bronchoscopic intubation: Allows for a neurologic exam to be performedafter intubation and positioning, but requires patient cooperation and may increasestress and discomfort

 Direct laryngoscopy (with gum elastic bougie for Grade III views): Applicable in

patients with preexisting deficits and acceptable radiologic findings

 Videolaryngoscopy: The view of the vocal cords is usually superior compared to directlaryngoscopy Popular for managing patients with known or suspected C-spine

injury However, this technique may still cause cervical displacement Thus, MILS isrequired Can be used in both awake and asleep intubation attempts

The most suitable strategy will often depend on the anesthesiologist’s experience with aparticular technique and the specifics of the clinical situation In our center, a combin-ation technique of asleep (general anesthesia plus remifentanil or short-acting neuromus-cular blockade) videolaryngoscopy and flexible bronchoscopy is often employed forintubating patients with SCI Several supraglottic airway devices can facilitate placement

of a tracheal tube using flexible bronchoscopy

The decision to extubate the trachea postoperatively is influenced by many factors.These include the ease of intubation, extent and duration of surgery, surgical complications(e.g., recurrent laryngeal nerve injury), prone positioning, blood loss, subsequent fluidresuscitation, and other associated injuries and comorbidities The presence of a cuff leakdemonstrated on either inspiration or expiration in the spontaneously breathing patient hasnot consistently been shown to predict subsequent airway obstruction Extubating thetrachea with an airway exchange catheter in situ may facilitate emergent reintubation inthe event of an obstruction from airway edema or hematoma Clinical judgment isparamount, and if there is concern, the trachea should be extubated at a later time

Cardiovascular Management

Traumatic SCI is frequently complicated by systemic hypotension and reduced spinal cordperfusion pressure (SCPP) This, in turn, may contribute to secondary ischemic injury andshould be avoided SCPP is determined by the difference in mean arterial pressure (MAP)and cerebrospinal fluid pressure (CSFP) (SCPP = MAP CSFP) Spinal cord perfusion

is autoregulated over a wide range of systemic blood pressure (BP) similar to cerebralperfusion, but the relationship can become altered in an injured cord Sympathectomy andsystemic vasodilation occur in increasing severity with ascending levels of spinal cord injuryabove L2, leading to hypotension Injuries above T6 are generally accompanied by brady-cardia due to compromise of the sympathetic cardiac accelerator fibers

Hypovolemia, hemorrhage, cardiac dysrhythmia, and sympathectomy can result inhypotension Volume resuscitation and source control are essential for restoration ofcirculatory volume If the patient continues to be hypotensive despite correction toeuvolemia, neurogenic shock should be suspected, and vasoactive infusions (see below)should be employed to restore vascular tone An anticholinergic drug may be required forbradycardia A urinary catheter should be placed to monitor urine output, and to relievebladder distension

Chapter 14: Considerations for Spinal Cord Injury 193