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

Section 1
Chapter

11

Core Principles in Trauma Anesthesia

Coagulation Monitoring of the
Bleeding Trauma Patient
Marc P. Steurer and Michael T. Ganter

Introduction
Blood coagulation is a complex and tightly regulated physiologic network of interacting
proteins and cells. If deranged, it may dramatically influence outcome. A comprehensive
understanding of normal hemostasis and its pathophysiology is necessary for anesthesiologists working in the perioperative field.
Treatment of a massive trauma bleeding requires an interdisciplinary approach for both
trauma surgeons and anesthesiologists. Modern transfusion strategies and coagulation
management are based on a detailed understanding of coagulation physiology and specific
coagulation monitoring. Besides the patients’ medical history, clinical presentation and
laboratory tests, bedside coagulation analyses (point-of-care, POC) are increasingly being
used to assess hemostasis. Consequently, specific, individualized, and goal-directed hemostatic interventions are becoming more and more feasible.
Abnormal hemostasis is not limited to bleeding. Hypercoagulability and thrombosis are
further phenotypes of disturbed hemostasis. The coagulation system represents a delicate
balance of forces supporting coagulation (coagulation, antifibrinolysis) and forces inhibiting coagulation (anticoagulation, fibrinolysis) (Figure 11.1). The distinctive challenge is
to assess and quantify both sides of this balance and to maintain an equilibrium. Specific
coagulation interventions can be made on either side, with the goal of preventing both overt
bleeding and thrombosis.

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

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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, and
secondary hemostasis. In addition, hemostasis initiates sore healing of the injured vessel
while preserving the general rheologic qualities of the blood.
 The vascular part of hemostasis is the first step after a vessel injury. It is mediated in a
paracrine way by the endothelium, the vessel wall, and the immediate environment of
the vessel. By immediate vasoconstriction of the damaged vessel, blood flow and
pressure temporarily decreases within the vessel.
 Primary hemostasis describes the cellular part of clotting and is primarily mediated by
platelets and von Willebrand factor (VWF). Platelet activation (with release of
coagulation-active substances), adhesion, aggregation, and finally stabilization result in
a mechanical blockage of the damaged vessel wall by a platelet plug.
 Secondary hemostasis illustrates the plasmatic portion of blood clotting and describes
the complex interaction of different clotting factors that finally result in a stable fibrin
network.
To protect the organism against thrombosis and embolism, the natural anticoagulant
pathway restrains overt clot formation at different levels, and the fibrinolytic system prevents
excessive clot formation and promotes lysis of inadvertently formed blood clots.
In vivo, the coagulation system becomes primarily activated by tissue factor (TF). Tissue
factor exists beyond the blood vessels on smooth muscle cells and fibroblasts. Therefore, the

coagulation system is not activated in a healthy individual. Tissue damage, however, brings
TF in contact with blood and activates the clotting system to protect the organism from
exsanguination. Under certain pathologic circumstances like sepsis, TF can be intravascularly
expressed on endothelial cells, monocytes, and circulating microparticles (cell fragments).
The resulting uncontrolled and overt coagulation activation can lead to the syndrome of
disseminated intravascular coagulation (DIC).
The key enzyme of secondary hemostasis is thrombin (FIIa), a serin-protease similar to
trypsin. Besides transformation of fibrinogen to soluble fibrin, thrombin facilitates numerous other biochemical reactions such as coagulation and immune system activation. The net
effect of thrombin depends on the context and the molecules that are present locally.
Thrombin promotes activation of clotting Factors V, VIII, and XI, thereby activating the
intrinsic pathway and finally amplifying its own production. Thrombin further activates the
thrombin-activated fibrinolysis inhibitor (TAFI), Factor XIII, as well as platelets, endothelial cells, and perivascular smooth muscle cells. During this process, two regulatory mechanisms are important for the protection from an overshooting thrombin formation: the
antithrombin and protein C system. Antithrombin does so by irreversibly binding and
inactivating thrombin. Activated protein C has strong anticoagulatory and pro-fibrinolytic
properties that further help balance thrombosis.
The historical cascade model of blood coagulation published in 1964 with its intrinsic
and extrinsic activation pathways describes the complexity of hemostasis inadequately. It
limits itself to the phenomena of in vitro secondary hemostasis and permits no explanation
of certain coagulation disorders in vivo. Nevertheless, this model can still be pulled up even
today for the simplistic visualization of the process of plasmatic coagulation tests, e.g., the
prothrombin time (PT)/international normalized ratio (INR) and the activated partial
thromboplastin time (aPTT).
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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 cell
surfaces. Besides platelets and endothelial cells, the cell surface of erythrocytes, leukocytes,
and microparticles play a central role. Different steps are distinguished:
 The clotting process is described by the initiation, amplification, and propagation phase.
 To strengthen the immature clot, it will be stabilized in the next phase (mediated by
FXIII).
 Regulatory mechanisms are present for the termination of coagulation activation
(mediated by TF pathway inhibitor, antithrombin and the protein C pathway) and the
elimination of overt clot formation (mediated by plasmin).
This model illustrates the in vivo coagulation better than the classical cascade model. For
example, it can explain the bleeding defects observed with Factors XI, IX, and VIII
deficiencies, because these proteins are required for generation of Factor Xa (and subsequently thrombin) on platelet membranes. It further suggests that the extrinsic and
intrinsic systems are in fact parallel generators of Factor Xa that occur on different cell
surfaces, rather than redundant pathways. Therefore, the classic plasmatic coagulation
tests like PT/INR and aPTT only fragmentarily represent this model. The cell-based
coagulation model can be illustrated much better with whole blood, viscoelastic coagulation analyzers.

Assessment of Coagulation
To best assess and quantify the status of a patient’s coagulation system, information on the
following four mainstays of perioperative coagulation monitoring should be collected and
combined for clinical interpretation.

1. Medical History
The patient’s focused medical history is crucial for the assessment of the individual bleeding
risk and should be carried out with specific questionnaires. This standardized approach has
been shown to be superior to preoperative routine laboratory coagulation studies. Accordingly, national societies have published recommendations on standardized preoperative
assessment of hemostasis.

2. Clinical Presentation

The clinical presentation of abnormal hemostasis (e.g., certain phenotypes of bleeding or
thrombosis) is critical for the differential diagnosis and gives valuable information on
possible etiologies of the underlying coagulation disorder. Also, abnormal laboratory
coagulation studies must always be correlated with the current clinical presentation, before
any hemostatic therapy is initiated. Without clinically relevant bleeding (e.g., “dry” surgical
area) no procoagulant therapy should be initiated due to the risk of adverse thrombotic
events. Instead, the patient must be closely observed and reassessed.
When a patient is bleeding, the question often arises whether the cause of bleeding is
“surgical” or “non-surgical.” Advanced coagulation monitoring can help distinguish both
types of bleeding. If “surgical” bleeding is present, the patient requires surgical re-exploration
to control the bleeding. A diffuse, microvascular, “non-surgical” bleed, however, requires
rapid, individualized, and goal-directed treatment.
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3. Standard Laboratory Coagulation Tests
Standard or conventional laboratory coagulation tests include PT/INR, aPTT, and platelet
count. Depending on local circumstances, other laboratory values, such as fibrinogen concentration, D-dimer, Factor XIII, Anti-Xa, and thrombin time, may be part of a standard
laboratory coagulation panel.
Patients presenting with complex hemostatic disorders require in-depth laboratory
coagulation studies under the direction of a hematologist. Discussion of advanced laboratory coagulation tests is beyond the scope of this article.
Standard laboratory coagulation tests play a central role in the initial diagnostic steps of
patients with deranged hemostasis. Like other analyses, these tests only answer certain
questions, although they are of value in monitoring the effects of warfarin and heparin, and
other conditions.

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 categorized into devices focusing on the analysis of:
 Primary (cellular) hemostasis, mainly platelet function. Tests analyzing primary
hemostasis measure platelet count and function as well as VWF activity. Several bedside
tests are available, e.g., PFA-200 and modified platelet aggregometry.
 Secondary (plasmatic) hemostasis. These bedside tests are used to monitor
anticoagulant therapy. Examples include the ACT, whole blood PT/INR, and heparin
management devices.
 Entire hemostasis, from initial thrombin generation to maximum clot formation up to
fibrinolysis. Viscoelastic coagulation monitoring devices like thromboelastography
(TEG), rotational thromboelastometry (ROTEM), and Sonoclot assess the hemostatic
system globally, analyzing primary and secondary hemostasis, clot strength, and
fibrinolysis.
In the trauma setting, POC monitoring of the entire coagulation process is most useful.
TEG, ROTEM, and Sonoclot measure the clot’s physical property under low shear conditions and graphically display the changes in viscoelasticity of the blood sample after
initiating the coagulation cascade.

POC Monitoring of the Entire Coagulation Process
Bedside coagulation tests, especially the viscoelastic tests such as TEG and ROTEM, may
help to avoid unnecessary administration of procoagulant substances (e.g., plasma, platelets,
and coagulation factor concentrates) and enable the clinicians to distinguish between a
surgical and non-surgical cause of bleeding. These tests may also reduce interventional
delays and the need for surgical re-explorations, and ultimately reduce mortality.

TEG and ROTEM
TEG is a method to study the entire coagulation potential of a single whole blood specimen
and was first described by Hartert in 1948. Because TEG assesses the viscoelastic properties
of blood, it is sensitive to all interacting cellular and plasmatic components. After starting

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Figure 11.2. Working principle of viscoelastic POC devices. TEG, ROTEM, and Sonoclot working principle.

Figure 11.3. Standard graphical output of viscoelastic POC devices. TEG, ROTEM, and Sonoclot standard graph.

the analysis, the thrombelastograph measures and graphically displays all stages of the
coagulation process: the time until initial fibrin formation, the kinetics of fibrin formation
and clot development, and the ultimate strength and stability of the clot as well as the clot lysis.
In TEG, whole blood is added to a heated cuvette at a set temperature, typically 37°C.
A disposable pin connected to a torsion wire is suspended in the blood sample and the cup is
oscillated through an angle of 4°45’ (rotation cycle 10 seconds; Figure 11.2). As the blood
sample starts to clot, fibrin strands connect and couple the cup with the pin. The rotation of
the cup is transmitted to the pin. The rotation movement of the pin is converted by a
mechanical-electrical transducer to an electrical signal, and displayed as the typical TEG
tracing (Figure 11.3).
ROTEM technology avoids some limitations of traditional TEG and offers advantages:
measurements are less susceptible to mechanical shocks, four samples can be run at the
same time (TEG can only run two), and pipetting is made easier by provision of an
electronic pipette. In ROTEM, the disposable pin (not the cup) rotates back and forth
4°75’ (Figure 11.2). The rotating pin is stabilized by a high precision ball-bearing system.
Signal transmission is carried out via an optical detector system (not a torsion wire). The
exact position of the pin is detected by reflection of light on a small, embedded mirror on
the shaft of the pin. Data obtained from the reflected light are then processed and

graphically displayed (Figure 11.3).
Although TEG and ROTEM tracings appear similar, the nomenclature and reference
ranges are not comparable. The systems use different materials: ROTEM cups and pins are
composed of a plastic with a greater surface charge resulting in higher contact activation
compared to those used in TEG. Furthermore, the systems involve different proprietary
formulas of coagulation activators (e.g., composition, concentration). For example, if the
same blood specimen is analyzed by TEG and ROTEM with their proprietary intrinsic
coagulation activator, kaolin or inTEM reagent (partial thromboplastin phospholipids),
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respectively, the results obtained are significantly different. TEG and ROTEM cannot be used
interchangeably, and treatment algorithms have to be specifically adapted for each device.
In the perioperative setting, most coagulation analyses are performed in citrated whole
blood that is recalcified and specifically activated to reduce variability and running time.
Several commercial reagents are available that contain different coagulation activators,
heparin neutralizers, platelet blockers, or antifibrinolytics to answer specific questions on
the current coagulation status. Blood samples can be extrinsically (tissue factor; e.g., exTEM
reagent) and intrinsically (contact activator; e.g., inTEM reagent) activated. To determine
functionality and levels of fibrinogen, reagents incorporate platelet inhibitors (e.g., cytochalasin D in fibTEM reagent). This concept has been proven to work and a good correlation of
this modified maximum amplitude (MA)/maximum clot firmness (MCF) with levels of
fibrinogen measured in the laboratory has been demonstrated. Finally, by adding an antifibrinolytic drug to the activating reagent (e.g., aprotinin in apTEM), the test can provide
information on the current fibrinolytic state, especially when compared to a test run without
antifibrinolytics, and help guide antifibrinolytic therapy.
The repeatability of measurements by both devices has shown to be acceptable, provided

they are performed exactly as outlined in the user’s manuals.
TEG and ROTEM have become the gold standard for the detection and quantification of
coagulopathy in trauma patients. There is also evidence that these assays may predict
transfusion need and mortality in the trauma population.

Sonoclot Coagulation and Platelet Function Analyzer
The Sonoclot analyzer was introduced in 1975 by von Kaulla and associates and measures
viscoelastic properties of a blood sample. A hollow, oscillating probe is immersed into the
blood and the change in impedance to movement imposed by the developing clot is
measured (Figure 11.2). Different cuvettes with different coagulation activators and inhibitors are commercially available. Normal values for tests run by the Sonoclot analyzer
depend largely on the type of sample (whole blood vs. plasma; native vs. citrated sample),
cuvette, and activator used.
The Sonoclot analyzer provides information on the entire hemostasis both in a qualitative graph, known as the Sonoclot signature (Figure 11.3), and as quantitative results: the
activated clotting time (ACT), clot rate, and platelet function. The ACT is the time in
seconds from activation of the sample until fibrin formation. This onset of clot formation is
defined as a certain upward deflection of the Sonoclot signature and is detected automatically by the machine. Sonoclot’s ACT corresponds to conventional ACT, provided that
cuvettes containing a high concentration of typical activators (e.g., celite, kaolin) are being
used. The clot rate, expressed in units/minute, is the maximum slope of the Sonoclot
signature during initial fibrin polymerization and clot development. Platelet function is
reflected by the timing and quality of the clot retraction. Platelet function is a calculated
value, derived by an automated numeric integration of changes in the Sonoclot signature
after fibrin formation has completed. To obtain reliable results for platelet function,
cuvettes containing glass beads for specific platelet activation (gbACT+) should be used.
The nominal range of values for the platelet function goes from 0, representing no platelet
function (no clot retraction and flat Sonoclot signature after fibrin formation), to approximately 5, representing strong platelet function (clot retraction occurs sooner and is very
strong, with clearly defined, sharp peaks in the Sonoclot signature after fibrin formation).
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Simplified Interpretation for TEG/ROTEM Readouts
While the TEG and ROTEM results may look a bit challenging when seen for the first time,
one can get used to reading them very quickly and intuitively in a relatively short period of
time. The readout of TEG/ROTEM can be divided into three phases:
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) that
trigger the plasma coagulation cascade and activate platelets (Figure 11.4). It ends with a
thrombin burst and the beginning of clot formation. This part of the curve lasts less than
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, typically
containing vitamin K-dependent coagulation factors) and/or FFP can usually correct them. In
patients receiving anticoagulants (e.g. heparin, dabigatran), specific reversal (e.g. protamine,
idarucizumab) is recommended. The second phase starts with the beginning of clot formation
and ends when the maximum clot firmness is reached (Figure 11.5). It depends mostly on the

Figure 11.4. Phase 1 of the TEG/ROTEM graph.

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Figure 11.6. Phase 3 of the TEG/
ROTEM graph.

functional platelet mass and the availability of fibrinogen, and to a minor degree, on the
functionality of Factor XIII. Any defects in this phase are usually readily visible after a few
more minutes and can be corrected with the transfusion of cryoprecipitate and/or fibrinogen
concentrate and/or platelet concentrates. The last phase depicts clot stability and will detect
hyperfibrinolysis (Figure 11.6). Viscoelastic tests are essentially the only clinically available
tests that can detect and quantify hyperfibrinolysis.

Standard Laboratory Coagulation Tests versus Viscoelastic Coagulation
Tests in Trauma
Standard laboratory coagulation tests can be of high value to determine levels of oral anticoagulation with vitamin K antagonists, the degree of heparin effect, and the bleeding
likelihood of a patient with genetic or acquired thrombophilia. All of those conditions can
be complicating factors for patients, and they need to be evaluated with the proper standard
laboratory coagulation tests. On the other hand, standard coagulation tests fail to reliably
quantify both overall perioperative bleeding risk and a specific cause for coagulopathy. Most
studies fail to document any usefulness of standard laboratory coagulation tests in the setting
of perioperative coagulopathic bleeding. Standard laboratory coagulation tests represent
historically established thresholds that were utilized for lack of alternatives and are not
supported by current evidence. Aside from these validation concerns, results of standard
laboratory coagulation tests are not rapidly available. In most centers, the delay in obtaining
results is 25–60 minutes, which may render results that are out of context in the setting of
significant bleeding. Lastly, there are no standard tests that would detect hyperfibrinolysis and
hypercoagulability. The former not only has a significant prevalence in trauma patients, but it
also lends itself to intervention by administering an antifibrinolytic. Hypercoagulability is a
major concern in the days after survival from severe trauma. The ability to measure and
quantify the hypercoagulable state has the potential to guide further intervention.
The viscoelastic coagulation tests overcome many of the above listed constraints. The

following attributes make TEG and ROTEM ideal tests for perioperative and traumatic
coagulopathy:
 Validated tests in the setting of perioperative and traumatic coagulopathy
 Turnaround time for most of the relevant information in less than 10 minutes
 Can detect both hyperfibrinolysis and hypercoagulability

Economic Aspects of the Utilization of POC Viscoelastic Coagulation Testing
The argument of increased cost is frequently mentioned with the utilization of POC
ular. While the purchase
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and implementation of a thromboelastometry device is associated with significant cost
($50,000–$100,000 USD), their utilization will result in significant direct and indirect
savings. There have been a number of recent publications focusing on the cost savings that
can be achieved by deploying a thromboelastometry-based algorithm in the setting of
trauma or cardiac surgery. Even when performed in addition to standard coagulation tests,
they produce significant cost reductions for the respective organizations. The main mechanism of cost savings is reduction in utilization of blood products and coagulation factors.
Most studies found that deploying a transfusion/coagulation management algorithm based
on POC coagulation testing resulted in a 25–50% reduction of the overall cost of blood and
coagulation products. These savings include the offsetting of the additional testing cost. Not
included in the calculation were the potential indirect savings that result from better patient
outcomes (e.g., less complications, less days in the ICU, lower incidence of organ failure).

Treatment of Coagulopathy

With the information from the aforementioned four mainstays of perioperative coagulation
assessment (medical history, clinical presentation, standard and POC coagulation tests)
bleeding patients can be treated individually on a goal-directed basis according to defined
algorithms. Evidence-based guidelines, like the one from Task Force for Advanced Bleeding
Care in Trauma (see Rossaint et al. 2016), are helpful in developing locally adapted
treatment algorithms (see Figure 11.7).
It must be emphasized that procoagulant therapy should always be applied with caution.
A deficient coagulation system should never be excessively corrected because of the serious
risk for thromboembolic adverse events. Therapy should be titrated carefully and stopped if
bleeding is no longer clinically relevant.
A specific, goal-directed coagulation management in combination with clearly defined
algorithms can lead to decreased transfusion needs, diminished costs, and a better outcome.
Therefore, transfusion algorithms have been introduced in different clinics recently. Algorithms
consider the physiology and pathophysiology of the developing coagulopathy in massively
bleeding patients and serve as clearly structured guidelines for individualized coagulation therapy.

Figure 11.7. Coagulation management algorithm based on ROTEM at Zuckerberg San Francisco General Hospital
and Trauma Center. CT = clotting time, MCF = maximum clot formation, ML = maximum lysis, exTEM = extrinsically
activated essay (using tissue factor), fibTEM = fibrinogen-only essay (suppressing platelet contribution to clot by
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Conclusions
Hemostasis is a complex vital system of our body. Normal blood coagulation exists when
procoagulant and anticoagulant forces are in balance. Clinically relevant phenotypes of

hemostasis, bleeding, and thrombosis occur immediately if the system is no longer in
equilibrium. Disturbed perioperative coagulation may have different causes. For specific
diagnosis, information must be gathered from the four mainstays of perioperative coagulation assessment: medical history, clinical presentation, and standard and POC coagulation
tests. Modern coagulation management relies on this assessment and is specific, goaloriented, and individualized to the patient’s needs.

Key Points
 Hemostasis, the process which causes bleeding to stop, consists of three interacting
mechanisms: vascular, primary (cellular), and secondary (plasmatic) hemostasis.
 The historic cascade model with its intrinsic and extrinsic pathway is inadequate to
describe the complexity of hemostasis.
 The cell-based coagulation model is a more accurate and comprehensive model of the
coagulation system. This model accounts for the pivotal role of platelets and
endothelial cells.
 A thorough assessment of any perioperative coagulopathy includes the patient’s medical
history, clinical presentation of the hemorrhage, standard laboratory coagulation tests,
and POC coagulation testing.
 Standard laboratory coagulation tests in isolation have significant shortcomings in the
perioperative setting.
 Viscoelastic POC coagulation tests (TEG/ROTEM) have become the mainstay for
assessing the nature and magnitude of perioperative coagulopathy.
 Whenever possible, disturbances of a given patient’s coagulation system should be
treated on an individual, goal-directed basis using an appropriate algorithm.

Further Reading
1.

2.

3.

Da Luz LT, Nascimento B, Shankarakutty
AK, et al. Effect of thromboelastography
(TEG) and rotational thromboelastometry
(ROTEM) on diagnosis of coagulopathy,
transfusion guidance and mortality in
trauma: descriptive systematic review. Crit
Care 2014;18:518.
Ganter MT, Hofer CK. Coagulation
monitoring: current techniques and clinical
use of viscoelastic point-of-care
coagulation devices. Anesth Analg
2008;106:1366–1375.
Gonzalez E, Moore EE, Moore HB, et al.
Goal-directed hemostatic resuscitation of
trauma-induced coagulopathy: a pragmatic
randomized clinical trial comparing a
viscoelastic assay to conventional coagulation
assays. Ann Surg 2016;263:1051–1059.

4.

Haas T, Fries D, Tanaka KA, et al.
Usefulness of standard plasma coagulation
tests in the management of perioperative
coagulopathic bleeding: is there any
evidence? Br J Anaesth 2015;114:
217–224.

5.

Nardi G, Agostini V, Rondinelli B, et al.
Trauma-induced coagulopathy: impact of
the early coagulation support protocol on
blood product consumption, mortality and
costs. Crit Care 2015;19:83.

6.

Rossaint R, Bouillon B, Cerny V, et al. The
European guideline on management of
major bleeding and coagulopathy
following trauma: fourth edition. Crit Care
2016;20:100.

7.

Steurer MP, Ganter MT. Trauma and
massive blood transfusions. Curr
Anesthesiol Rep 2014;4:200–208.
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Section 1
Chapter

12

Core Principles in Trauma Anesthesia

Postoperative Care of the Trauma
Patient
Jack Louro and Albert J. Varon

Introduction
In the trauma population, the initial surgical procedure is only the beginning of perioperative care as many patients will require aggressive postoperative management and admission
to an intensive care unit (ICU). There are numerous physiologic alterations after trauma,
many of which persist in the postoperative period. The care of the postoperative trauma
patient requires coordinated effort between surgeon, anesthesiologist, intensivist, nursing,
and other personnel. An organ systems-based approach to critical care paradigms is often
employed. In this chapter we will discuss the immediate postoperative considerations for
the trauma patient as well as some of the major concerns during the early ICU care of
patients after major surgery including damage control surgery.

Disposition and Transport from the Operating Room (OR)
The decision of where the patient will be taken for the immediate postoperative course is a
key multidisciplinary discussion where the trauma anesthesiologist must be involved. In the
majority 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 the
injuries or not.
 Hemodynamically stable patients without airway and ventilatory issues who sustain
minor 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 with
trauma capabilities. New paradigms in critical care are being developed with subspecialty
ICUs. A dedicated trauma ICU that specializes in the care of trauma patients may afford
better outcomes in terms of mortality and post-injury complications.
Postoperative care may require continuing anesthetic management if the patient needs
diagnostic or therapeutic procedures at the completion of surgery prior to transport to the

ICU. 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 the
anesthesiologist. The availability of hybrid ORs where both surgical and angiographic
procedures can be performed may obviate the need for transporting an unstable patient to
another location. In cases where the bleeding has been controlled but there is concern about
head injury, the patient may be transported directly from the OR to the CT suite to perform
brain CT scan and immediately return to the OR if emergent neurosurgical intervention is
required. However, not all patients who receive a damage control laparotomy need to be
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taken immediately for CT imaging. The incidence of missed abdominal injury requiring
reoperation after damage control surgery is less than 5% and there is no difference in the reexploration rates or time to re-exploration in patients who undergo early abdominal CT
compared 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 the
majority directly to the ICU for secondary resuscitation.

Secondary Resuscitation
In the operative management of traumatic injury, blood component therapy is initiated
early and guided by the paradigm of balanced resuscitation with the early use of plasma and
platelets along with red blood cells. As the initial resuscitation carries on, the ratio of blood
products 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 to
ensure adequate repletion of coagulation factors and platelets to prevent worsening of the

trauma-associated coagulopathy. As the time for thawing and preparation of plasma is
longer than that for red blood cells (RBCs), this usually involves a catch-up of fresh frozen
plasma (FFP) transfusion as the patient is leaving the OR.
 The correction of coagulopathy, hypothermia, and acidosis are important goals of the
postoperative care team in the setting of trauma, especially following damage control
surgery.
 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 the
immediate postoperative period (see also Chapter 11). Secondary resuscitation will also
include measurement of laboratory values and correction of acidosis and hypothermia (if
present). Heat loss from general anesthesia is accentuated in trauma patients due to large
surgical exposure and the requirement of large amounts of fluid and blood products.
Temperature management includes the use of forced air warming blankets and IV fluid
warmers. In addition to close respiratory monitoring, continued assessment of metabolic
acidosis should be undertaken during the postoperative resuscitation until normalization of
the acidosis.

Postoperative Pain Management and Sedation
Sedation and pain control can significantly impact the trauma patient’s recovery and risk of
pulmonary complications. Patients who are unstable and require tracheal intubation and
mechanical ventilation after surgery will need sedation and analgesia.
 An opioid-first approach is usually well tolerated and can reduce the need for other
sedatives by providing adequate analgesia.

 Opioids are the mainstay of analgesia in the postoperative period.
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Hydromorphone is preferred over morphine due to the lack of active metabolites and
histamine release. With all pain medication regimens, a multimodal approach is favored to
minimize the adverse effects of opioids and increase analgesic efficacy. The use of potent
parenteral non-steroidal anti-inflammatory drugs (NSAIDs) such as ketorolac can lead to a
decrease in opioid use. Intravenous oral, and rectal formulations of acetaminophen are
available 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 they
will reduce the amount of sedatives and opioids required. Ketamine is an N-methyl-Daspartate (NMDA) receptor antagonist that can provide sedation as well as analgesia via
non-opioid receptor pathways and has a safe hemodynamic profile in subanesthetic doses.
Dexmedetomidine, an alpha-2 agonist, stimulates natural sleep pathways and provides
synergism with opioids for analgesia. Dexmedetomidine has been associated with decreased
incidence of ICU delirium. Both ketamine (at subanesthetic doses) and dexmedetomidine
may also be used for analgesia in non-intubated patients. Table 12.1 lists options for
postoperative pain management.
Propofol is a useful sedative drug due to its short context-sensitive half-life; however, the
vasodilation 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 hemodynamic
profile, care has to be taken if used in patients with renal failure or the elderly. Caution is
also advised for long-term benzodiazepine use, as ICU delirium may result. The development of delirium in the ICU is a major concern, as patients who develop delirium have
worse outcomes and higher mortality. There is very little prophylactic pharmacologic
treatment for ICU delirium, but early mobilization is key to prevention. When delirium

does develop, the use of a second-generation antipsychotic along with aggressive reorientation is the preferred approach over the use of sedatives or benzodiazepines.
Table 12.1. Options for postoperative pain management

Drug

Mechanism of action

Example/comments

Opioids

Central acting opioid
receptor agonists

Fentanyl, hydromorphone, morphine (PCA
preferred over intermittent dosing)

NSAIDs

Peripherally acting antiinflammatory

Ketorolac is the only parenterally available
NSAID

Acetaminophen

Cyclooxygenase
inhibition?

Synergistic effects and opioid sparing.

Available PO, rectal, and IV

Calcium channel
modulators

Inhibits nociceptive
neurotransmitter release

Gabapentin, pregabalin

Dexmedetomidine

Selective alpha-2
adrenergic agonist

Stimulates natural sleep; reduces opioid
requirements

Ketamine

NMDA receptor
antagonist

Subanesthetic doses up to 10 μg/kg/min

Local anesthetics

Na channel blockers

Can be infiltrated locally or directed to sensory

nerves

Abbreviations: 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, adequate
analgesia to allow normal breathing is crucial.
Patients with rib fractures or upper abdominal surgery will commonly have shallow
breathing and refrain from coughing due to pain. The use of thoracic epidural catheters
can be effective for both rib fracture pain as well as thoracic and upper abdominal surgery
postoperative pain control (see also Chapter 8). The use of paravertebral nerve blocks in
patients who undergo unilateral thoracic surgery seems to be as effective as epidural
analgesia and may carry less risk. Patients with significant limb injuries can benefit from
peripheral nerve blocks to reduce the requirement for opioids.

Ventilator Management
Continued mechanical ventilation in the postoperative period is common after major
trauma surgery.
 Patients who require postoperative mechanical ventilation should be managed with
lung-protective strategies, since many will have risk factors for the development of
ARDS including lung contusions, multiple transfusions, and inflammatory reaction due
to bacterial contamination from penetrating injuries.

 Ventilation strategies entail the use of positive end-expiratory pressure (PEEP) that is
adequate to prevent atelectasis with the lowest tolerated oxygen concentration. Tidal
volumes 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 the
trachea as quickly as possible to reduce the incidence of ventilator-associated infections and
lung injury. Appropriate selection of patients for ventilatory support and taking steps to
minimize 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 and
differentiated from the need for postoperative airway protection. In some cases, mechanical
ventilation will not be necessary if a definitive airway can be established via tracheostomy.
Patients with traumatic brain injury (TBI) or neck trauma frequently require airway
protection postoperatively, which puts the native airway in danger. Although large randomized
controlled trials (RCTs) in the general ICU population have shown no benefit of early
tracheostomy, certain subsets of trauma patients, such as those with significant maxillofacial
fractures requiring multiple surgical procedures, may benefit from early tracheostomy to limit
the duration of mechanical ventilation. In cases with significant burns as part of the trauma, the
airway may develop significant edema that requires prolonged intubation or even tracheostomy. Patients with thoracic trauma requiring thoracotomy may need postoperative ventilation
because the emergent nature of the surgery prevents adequate pre-emptive analgesia and given
the fact that pulmonary contusions can progress to edema and acute respiratory distress
syndrome (ARDS), especially when there is a need for massive resuscitation.
Patients who are hemodynamically stable, have return of mental status to baseline, and
meet respiratory criteria should have their tracheas extubated without delay. Respiratory
criteria for extubation in the ICU are similar to intraoperative criteria, including full
recovery of neuromuscular function, adequate tidal volume to respiratory rate ratio, and
negative inspiratory force less than –20 mmHg in order to have adequate cough, as well as
strength to lift head or legs for 5 seconds. Since these criteria can be more challenging to
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Table 12.2. Extubation criteria for spontaneous breathing trial

Criteria

Parameters

Circulatory compensation




HR increase <20 beats per minute
SBP increase <20 mmHg

Appropriate ventilation





TV >5 mL/kg
RR <35 breaths per minute
ABG without acidosis and PaCO2 <60 mmHg

Adequate cough strength




NIF <–20 cmH2O
PF >60 L/min

Adequate oxygenation





PEEP 5 cmH2O
PaO2/FiO2 >120
FiO2 0.5

Abbreviations: 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.

assess in a polytrauma patient, a spontaneous breathing trial with blow-by oxygen or
minimal 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 hemodynamic
instability 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 presenting
Glasgow 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 held

early to allow neurologic examination. Even patients with mild TBI (GCS>12) may need
brain CT if their neurologic function is not at baseline after the emergency surgery. Patients
who suffer TBI should be supported by maintaining adequate oxygenation and normal
blood 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 normal
blood pressure to protect brain perfusion and oxygen delivery.
Along with brain imaging, patients who have depressed mental status or major distracting injury will require imaging of the spine if there was the potential for injury. This is
especially true in blunt trauma since an adequate clinical exam will be unreliable in a patient
immediately after surgery. Until imaging of the spine can be performed, full spine precautions should remain in place including the use of a cervical hard collar. In hemodynamically
unstable patients with blunt injury and no evidence of hemorrhage, neurogenic shock could
be the culprit due to a missed spinal cord injury. For these patients the use of vasopressors
and inotropes may need to be initiated early and adequate fluid repletion administered to
compensate for the vasodilatory state.

Cardiovascular Concerns
The etiology of shock in a trauma patient is usually hemorrhage and hypovolemia. In cases
where the patient has undergone surgical exploration without a clear source of ongoing
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blood loss and remains in shock, cardiac etiologies have to be ruled out in the immediate
postoperative 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 right
and left ventricular wall motion abnormalities and decreased ventricular function. The

injured 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 patients
with suspected blunt cardiac injury. If the admission ECG reveals new abnormalities the
patient should receive continuous ECG monitoring in the acute phase of injury. Myocardial
contusions with hemodynamic compromise will demonstrate functional deficits on echocardiography (see Chapter 10). Echocardiography can also identify signs of tamponade
physiology including pericardial effusion and cardiac chamber compression or collapse.
However, routine echocardiography is not useful as a primary screening modality for
myocardial contusion, but rather as a diagnostic test for patients who have unexplained
hypotension or arrhythmias.
As the population ages and advances are made in the treatment of chronic cardiac
conditions, the percentage of elderly trauma patients with multiple comorbidities will
continue to increase. In a patient with underlying heart failure, the initial volume resuscitation during ongoing blood loss may not unmask the heart failure. However, once damage
control surgery has stopped blood loss and secondary resuscitation progresses, patients may
develop decompensated heart failure. In these scenarios, hemodynamic monitoring could
be helpful in patient management (see also Chapter 9). Invasive hemodynamic monitors
include 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 shock
management, and is rapidly becoming the preferred method for hemodynamic monitoring
due to its non-invasive nature and portability. With the use of echocardiography, patients
displaying cardiac dysfunction postoperatively can be identified and inotropic support
initiated 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 increased
mortality. Efforts should be made to restore the body’s acid–base balance by ensuring
adequate tissue perfusion and providing intravascular volume with not only the necessary
blood products but also balanced electrolyte solutions. Measuring and correcting base
deficit and lactate levels in a timely manner, usually within the first 12–36 hours, will allow

for definitive interventions and could result in fewer complications. The initial intraoperative course and severity of injury will dictate the amount of secondary resuscitation, but key
electrolyte derangements should be suspected and treated. Calcium and potassium levels
need to be monitored for patients who receive massive transfusion after trauma. Tissue
injury and ischemia along with lysis of red blood cells can result in life-threatening
hyperkalemia, which could present in the postoperative period as tissues are being
reperfused and red blood cell administration continues. Hypocalcemia is common in
the setting of massive transfusion after trauma and this will need continuing correction
and monitoring.
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Acute kidney injury is a prevalent problem in the post-traumatic patient. The etiology
could result from tissue injury leading to rhabdomyolysis but more evidence is pointing to
renal 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 trauma
patients who do not suffer AKI. Restoring adequate renal perfusion quickly after hemorrhage will help prevent the propagation of renal insult. In patients with AKI, adjustments
must be made to medications including antibiotics in the postoperative period to prevent
toxic doses or worsening of renal failure.
Special consideration must be made for patients with TBI and elevated intracranial
pressure (ICP). Hyperosmolar treatment is usually initiated intraoperatively in the management of ICP. With the use of hypertonic saline or mannitol, fluid shifts will be common in
the 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 potassium
through 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 if
kidney function is preserved, as mannitol is a potent osmolar diuretic. Hypernatremia can be
caused by iatrogenic administration of hypertonic saline or the development of diabetes
insipidus in brain injury patients. The latter is managed by providing adequate volume
replacement and vasopressin receptor agonists. Correction should be gradual to avoid
worsening brain edema.

Gastrointestinal and Nutritional Support
Gastrointestinal complications of trauma are often seen in cases of both penetrating and
blunt trauma and are of concern when massive resuscitation is required. The strategy of
damage control surgery calls for control of bleeding and intra-abdominal contamination
and keeping the abdomen open. These patients must have a fine balance of adequate fluid
resuscitation but avoidance of fluid overload that can impair the ability to close the
abdomen within the recommended time frame of 8 days. Patients who do not require
damage control laparotomy but require massive resuscitation can develop bowel edema in
the postoperative period. The ICU care of patients receiving large-volume resuscitation
requires close monitoring for signs of intra-abdominal hypertension and abdominal compartment syndrome. Peak airway pressures and urine output along with bladder pressures
can 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 infectionrelated complications. Enteral nutrition is the preferred route and should be started once
the patient is hemodynamically stable, unless contraindicated by bowel obstruction, bowel
discontinuity, perforation, or bleeding. Patients who have an initial damage control surgery
will need to return to the OR for definitive procedures. These patients will likely have feeds
held multiple times in the postoperative course. One consideration in the intubated and
mechanically ventilated patient is to continue enteral feeds until the time of surgery as there
is a secure airway in place. In these patients, the risk of aspiration is low and the benefit of
continued nutrition outweighs the risk of aspiration. For patients who have bowel injuries
and must be left in discontinuity or have multiple anastomoses and fistulas, early parenteral
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nutrition should be considered. Starting parenteral nutrition early (within 1 week) would be
preferable over delaying nutrition until the enteral route is available. In certain circumstances, low-dose enteral feeds can be used concurrently to protect the gastrointestinal
mucosa and maintain normal flora while nutritional needs are being met mostly through
the parenteral route.

Postoperative Infection and Sepsis
Patients who survive the initial phase of trauma can develop dysregulation of the inflammatory
system which has been implicated in a host of complications. Of these complications, infections and sepsis are still prevalent in the trauma patient and have continued to be a significant
cause of morbidity and mortality. Sepsis is a common diagnosis in ICU patients and can be
deadly 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 the
ICU 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 approximately 10% in multiply injured patients. Although mortality from trauma in general has
decreased over the past few decades, the subset of trauma patients who develop sepsis after
injury has not experienced a similar reduction in mortality. The systemic inflammatory
response 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 and
treated early. Over the past decade, early goal-directed therapy has been commonly
employed to ensure adequate oxygen delivery with the use of fluids, red cell transfusion,
vasopressors, and inotropes. The early recognition and aggressive protocol-driven management has led to a decrease in sepsis mortality over the past 20 years. Early recognition and
initiation of antibiotics as well as supportive care are paramount. However, recent studies
have challenged the need to adhere to a specific protocol requiring the measurement of
CVP or mixed venous saturation as endpoints. The consensus seems to be that aggressive
treatment 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 is
often 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 be
gram-negative organisms unlike the non-trauma ICU patients, where the predominant
pathogens are gram-positive. Trauma ICU patients also tend to be colonized and/or
infected with bacteria that are multi-drug resistant. Early recognition and initiation of
antibiotics as well as supportive care are paramount. Careful selection of antibiotics is
required when treating patients empirically. The goal is to prevent the propagation of multidrug 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 be
involved in this process.
 Aggressive secondary resuscitation must be initiated early to prevent the lethal triad of
coagulopathy, acidosis, and hypothermia.
 The use of viscoelastic coagulation tests can facilitate individualized therapy with blood
products and hemostatic agents.
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 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 tidal
volumes, 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 trauma
patients 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 renal
perfusion should be ensured along with monitoring electrolyte imbalances.
 Abdominal compartment syndrome may develop after damage control laparotomy or
massive transfusion. Monitoring peak airway pressures and urine output can help make
the diagnosis.
 Early nutrition is essential in the postoperative period for trauma patients. Enteral
nutrition is preferred, but nutrition should not be delayed even if the enteral route is
unavailable.
 Sepsis and infection continue to pose high mortality in the trauma ICU population.
Early aggressive therapy should be initiated and includes appropriate broad spectrum
antibiotics 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 care
unit: The challenge of antimicrobial
resistance and the trauma patient.
World J Surg 2016: doi:10.1007/s00268016–3531-0.

6.

Schmidt GA, Hall JB. Management of the
ventilated patient. In: Hall JB, Schmidt GA,
Kress JP, eds. Principles of Critical Care, 4th
edition. New York, NY: McGraw-Hill;
2015.

7.

Slutsky AS, Ranieri VM. Ventilatorinduced lung injury. N Engl J Med
2013;369:2126–2136.

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Section 2
Chapter

13

Anesthetic Considerations for Trauma

Anesthetic Considerations for Adult
Traumatic Brain Injury
K. H. Kevin Luk and Armagan Dagal

Introduction
Traumatic brain injury (TBI) is an acquired insult to the brain due to an external
mechanical force and can lead to transient or permanent impairment of cognitive, physical,
and psychosocial functions. Anesthesiologists are most often involved in the care of patients

with moderate to severe TBI for a variety of procedures including but not limited to initial
evaluation and resuscitation, diagnostic imaging, surgical intervention, and intensive care
unit (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 with
TBI 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 (ages
5–24).
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-fold
increase in death from TBI.
After mild TBI, females use more healthcare services and may have a higher risk of
epilepsy and suicide.

Pathophysiology
TBI has been described in two distinct yet interrelated epochs: the initial primary injury and
subsequent secondary injuries.
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 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 injuries
are usually superimposed upon more diffuse neuronal injury. At the cellular level,
primary injury results in physical disruption of tissue architecture, compression of

vascular structures, and disturbance of ionic homeostasis secondary to cell
membrane disruption and increased permeability, which ultimately leads to cell
death.

 Secondary injury is described as the consequence of progressive insult to the neurons in
the 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 and
lipid peroxidation, mitochondrial dysfunction, inflammation, glutaminergic
excitotoxicity, cellular necrosis, apoptosis, and diffuse axonal degeneration.
Systemic insults such as hypotension (SBP <90 mmHg), hypoxemia (PaO2 <60
mmHg), hypoglycemia, hyperglycemia, hypocarbia, and hypercarbia are major
contributors 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 secondary
brain damage, reperfusion hyperemia may also occur and is equally detrimental.

The Marshall classification is frequently utilized for classifying TBI based on CT characteristics (Table 13.1).
Table 13.1. Marshall’s classification of traumatic brain injury

Category

Definition

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 fragments
and foreign bodies

Diffuse injury III

Cisterns compressed or absent with midline shift 0–5 mm
No high- or mixed-density lesion >25 mL

Diffuse injury IV

Midline shift >5 mm
No high- or mixed-density lesion >25 mL

Evacuated mass
lesion

Any lesion surgically evacuated

Non-evacuated mass
lesion

High- or mixed-density lesion >25 mL, not surgically evacuated

Abbreviation: CT = computed tomography.

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Preoperative Considerations
In any trauma patient, priority must first be given to general evaluation and stabilization of
vital body functions, with particular attention to the airway, breathing, and circulation
during the primary survey. A baseline neurologic assessment should be performed using the
Glasgow Coma Scale (GCS) score (Table 13.2). Traumatic brain injury is classified as severe
if the GCS score is 8 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 surveys
will identify other injuries.
Knowledge of the mechanism of injury is important for prognostication as well as for
anticipation of associated injuries. Penetrating injuries have a worse outcome than blunt
trauma. 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 intracranial
pressure (ICP) including Cushing’s triad of hypertension, bradycardia, and irregular respiration. Patients with high preoperative ICPs are at risk of cerebral ischemia and hypotension following evacuation of an intracranial hematoma. Issues related to urgent or emergent

Table 13.2. Glasgow Coma Scale scorea

Score
Best eye response

Best verbal response

Best motor response

a

Spontaneous

4

To speech

3

To pain

2

None

1

Oriented

5

Disoriented

4

Inappropriate words

3

Incomprehensible sounds

2

None

1

Obeys verbal orders

6

Localize pain

5

Flexion (withdrawal) to pain

4

Flexion (decortication) to pain

3

Extension (decerebration) to pain

2

None (flaccid)

1

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

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craniotomy include need for adequate vascular access, availability of blood products, and ability
for rapid resuscitation. Management of the patient with TBI can be challenging and complicated 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 for
TBI is typically urgent or emergent. Hence, delaying surgery is seldom indicated. However, a
number of TBI patients suffer from concomitant injuries and may require extracranial
surgery. The decision of which surgery should be performed first depends on several factors
including severity of TBI, severity of associated injuries, and hemodynamic stability. For
example, if the polytrauma patient with possible TBI is hemodynamically stable during initial
evaluation, abdominal and head CT may be performed prior to management of extracranial
injury. Patients with possible TBI who are hemodynamically unstable and have abdominal
trauma typically require emergency laparotomy. Intraoperative ICP monitoring may be
initiated prior to a head CT if coagulation parameters are normal and the index of suspicion
for TBI is high. In this case, head CT is obtained after extracranial surgery. In rare
circumstances (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 elderly
patients who sustain falls, particular attention should be paid to pre-injury cardiac, pulmonary, and endocrine status since congestive heart failure, hypertension, chronic obstructive
pulmonary disease (COPD), and type II diabetes mellitus are common in this population.
These coexisting conditions may result in perioperative complications such as worsening

congestive heart failure, COPD exacerbation, pulmonary edema, or hyperglycemia.
Medications used to manage the aforementioned pre-injury conditions can result in
intraoperative complications:
 Antihypertensive drugs: Diuretics can cause electrolyte imbalance resulting in
arrhythmias. Patients receiving beta-blockers prior to surgery may experience bradycardia
and fail to increase their heart rate in response to acute blood loss. Calcium channel
blockers and angiotensin-converting enzyme inhibitors or angiotensin II antagonists may
cause 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 and
predictable warfarin reversal. Fresh frozen plasma can be used if 4-Factor PCC is not
available, although it may lead to volume overload or incomplete reversal. Dabigatran
is a direct thrombin inhibitor that can be reversed effectively with Idarucizumab, a
specific monoclonal antibody. While currently there is no specific reversal for Factor X
inhibitors (rivaroxaban, edoxaban, and apixaban) 4-Factor PCC has been used with
some 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 develop
perioperative hypoglycemia.

Laboratory Investigations
Preoperative tests may be ordered selectively for guiding or optimizing perioperative
management on the basis of a patient’s clinical characteristics and urgency of surgical
procedure. However, these investigations should not delay the start of surgical management. For rapid assessment, prothrombin time, fibrinogen, platelet count, and hematocrit
obtained together, as an “emergency hemorrhage panel”, and viscoelastic point-of-care
coagulation tests may facilitate timely transfusion therapy. Preoperative hyperglycemia
may portend intraoperative hyperglycemia and poor outcome. Therefore, glucose levels
should be obtained prior to surgery and hourly during surgery. Patients with TBI may have
electrolyte disturbances and the treatment for these should be initiated while the patient
proceeds to surgery.

Intraoperative Management
There are no formal intraoperative guidelines for the management of TBI. Intraoperative
care is largely based on physiologic optimization and may be guided by the 2016 recommendations from the Brain Trauma Foundation (Table 13.3).
A minimum of two large-bore, peripheral, intravenous catheters should be placed
preferably in the upper extremities. General anesthesia with tracheal intubation is required
for control of oxygenation and ventilation (see Chapter 7). Some patients with TBI requiring emergency craniotomy may have their trachea intubated when they arrive in the
operating room. In these patients, adequate positioning of the tracheal tube must be
confirmed. In patients whose tracheas are not intubated, expedient tracheal intubation is
often necessary based on the patient’s clinical condition. Airway management can be
challenging 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

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178

Section 2: Anesthetic Considerations for Trauma

Table 13.3. Brain Trauma Foundation recommendations for severe TBI

Systolic blood pressure

SBP 100 mmHg for patients 50–69 years old
SBP 110 mmHg for patients 15–49 or >70 years old

Intracranial pressure

Treatment of ICP >22 mmHg

Intracranial pressure
monitoring

Recommended for severe TBI patients with abnormal head CT to
reduce in-hospital and 14-day mortality
Severe TBI patients with normal head CT and 2 of the
following features: age >40 years, motor posturing, or SBP
<90 mm Hg

Advanced cerebral
monitoring

Jugular bulb monitoring of AVDO2, as a source of information for
management decisions, may be considered to reduce mortality and
improve outcomes

Cerebral perfusion
pressure

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

Cerebrospinal fluid
drainage

Continuous CSF drainage using an external ventricular drain may be
considered to lower ICP in patients with initial GCS <6

Prophylactic
hypothermia

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 neurologic
deterioration prior to ICP monitoring

Ventilation strategies

Prolonged prophylactic hyperventilation (PaCO2 25) is not
recommended, and hyperventilation should be avoided during the first
24 hours of injury. Hyperventilation should only be used as a
temporizing measure for ICP reduction. If hyperventilation is used, SjvO2
or BtpO2 measurements are recommended

Anesthetics/analgesics/
sedatives

Prophylactic burst suppression using barbiturates is not recommended.
High-dose barbiturates can be considered for treatment of refractory
ICP elevation. Propofol is recommended for ICP control (but high-dose
use 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 recommended

Deep vein thrombosis
prophylaxis

Intermittent pneumatic compression stockings and low-dose heparin
or low-molecular-weight heparin are recommended

Abbreviations: AVDO2= arteriovenous oxygen content difference; BtpO2 = brain tissue O2 partial pressure; CPP =
cerebral perfusion pressure; CSF = cerebrospinal fluid; CT = computed tomography; GCS = Glasgow Coma Scale;
ICH = intracranial hypertension; ICP = intracranial pressure; PaCO2 = partial pressure of arterial carbon dioxide;
SBP = systolic blood pressure; SjvO2 = jugular venous oxygen saturation; TBI = traumatic brain injury.

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