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6 • Damage Control and Immediate Resuscitation for Vascular Trauma 75
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Ketamine with short acting opiates (alfentanil/fentanyl)
is the preferred choice of most trauma anesthetists and prehospital practitioners, particularly within the UK setting.
Ketamine has the advantage of maintaining sympathetic
drive and cardiac inotropy, thereby maintaining cardiac
output. It also has analgesic properties due to its action as an
N-methyl-D-aspartate (NMDA) antagonist, which reduces
pain burden during recovery. Ketamine is not frequently
used in day-to-day anesthetic practice and, unlike the other
induction agents, it achieves anesthesia by disassociation.
Dosing errors, inadequate or overzealous hypnosis, and
increased risk of adverse outcomes are potential hazards
when used by those who are unfamiliar with ketamine. It
increases cerebral blood ow and raises intracranial pressure, which would be detrimental in head injured patients.
Hallucinations, particularly on emergence, are a possibility
and therefore the operator should maintain a calm environment during induction/emergence, as well as having readily
deployable rescue strategies to deal with associated combativeness.
Etomidate has a very advantageous cardio-stability prole, as well as providing rapid onset of anesthesia. When
rst introduced in the 1970s, it rapidly gained in popularity as the “ideal” induction agent.47 However, by the 1980s
it was noted that that etomidate inhibits 11β-hydroxylase,
a key enzyme in adrenal cortisol production, and was
shown to lead to poorer mortality outcomes in critically ill
patients.48 For this reason, it is often avoided in routine clinical practice and certainly would be particularly harmful in
a patient who is likely to undergo a prolonged period within
critical care.
E—Everything Else (Including Transfer)
Hypothermia worsens coagulopathy. Efforts must be made
not only to deliver heat, but also to limit heat loss. The
removal of wet clothing, ensuring adequate ambient temperatures as well as the use of forced air warmers/blankets
will help prevent loss, whereas the use of warmed uids will
aid in the delivery of heat. Other more invasive techniques
such as intravesical washout and extracorporeal warming
are available in theory, but in practice are rarely used, particularly in the acute setting.
The primary survey should also be completed to ensure
all other major life-threatening injuries are found, with the
head-to-toe examination (secondary survey) conducted
only once all issues found during the primary survey have
been addressed.
This patient will need an escorted transfer (to CT or Theatres), which will require an anesthetist, particularly if the
patient is under general anesthesia. The same standard of
care (i.e., monitoring and physiological support) should
be adhered to throughout the process of the transfer. This
means there must be the means to maintain safe anesthesia
(i.e., infusions and oxygen, with resilience in case of entrapment), as well as emergency drugs and equipment at hand
for the transferring team to respond to patient deterioration at any point during the transfer. A good rule of thumb
is to take double the amount of drugs and oxygen anticipated for the expected duration of transfer. Throughout the
transfer, the team must be mindful of the location of the
nearest places of safety, which includes returning to ED if
required.
MANAGEMENT BEYOND THE EMERGENCY
DEPARTMENT
The operating theatre is fraught with human factor challenges that pose hazards to the unstable patient. Urgency
for intervention combined with clinical uncertainty and
patient instability serve to compound stress and the potential for error. Good communication—not just between
the surgeon and anesthetist, but amongst all team members—is an essential attribute of good surgical and anesthetic management. Both sides of the surgical drape need
to understand each other’s roles and how they may help
each other. Surgeons and anesthetists are equally prone to
task xation, which leads to the loss of global situational
awareness. Although consultants have authority to direct
the ow of care, the team should be managed with as at a
hierarchy as possible, such that all are empowered to speak
up, fully participate in decision-making, and anticipate
their own requirements to perform optimally.
Checklists can enhance team function. Although some
checklists have arguably become cumbersome, when used
correctly they reduce the incidence of never events.49 A
well-drilled and rehearsed team will use the checklist as
an opportunity to give everyone an insight into the global
picture and allow voicing of concerns. Momentum can be
maintained by using an abbreviated version of the welldescribed WHO surgical safety checklist known as a Snap
Brief:
n Patient
n Conrm patient ID
n Clinical ndings
n Surgical
n Surgical plans
n Time required
n Anesthetic
n STACK brief (physiological status)
n Systolic BP
n Temperature
n Acidosis/base excess
n Coagulation/calcium
n Kit (blood products/drugs given)/potassium
Intraoperatively, this same format can be used to facilitate regular team briefs, with the “S” standing for “surgical
progress.”
During surgery, anesthetic concerns fall broadly in to (1)
ensuring cardiovascular stability; (2) optimizing coagulation through the treatment of coagulopathy; and (3) facilitating surgical treatment.
Cardiovascular Management
Blood pressure—readily available and measurable—is often
used as a resuscitation end point during the early stage of
resuscitation. Mean arterial pressure (MAP) is intimately
linked to cardiac output and systemic vascular resistance as
demonstrated by the equation below:
MAP = Cardiac Output × Systemic Vascular Resistance
This equation forms the basis of how pharmacological cardiovascular support can be provided in the form of
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vasopressors, which cause vasoconstriction, and inotropes,
which increase heart muscle contractility.
Vasopressors predominately have an effect on the capacitance vessels (i.e., arterioles) by increasing the vasomotor
tone (therefore vascular resistance), leading to greater perfusion pressure. The vasopressor of choice is noradrenaline,
which is easily titratable and widely used; however, this does
require central access, and phenylephrine or metaraminol
may be used to bridge the period until central access is available. At some point, however, vasopressors alone can lead
to excessive vasoconstriction, inhibiting global ow, which
may cause end organ damage.50 The early use of vasopressors in trauma has proven controversial. In theory, the use
of vasopressors may limit the amount of volume required
to maintain a higher blood pressure and thereby reduce
the risk of TIC and other deleterious effects of excessive
uid. A recent systematic review of predominantly observational studies found a lack of suitably robust evidence
to determine whether vasopressors are of benet in early
trauma.51 Vasopressors were associated with worse outcomes and increased use of uids, indicating that patients
requiring vasopressors are more likely to be physiologically
deranged.
52–54
Similarly, the single RCT included in this
review did not nd any benet with vasopressor use when
compared to placebo, although it was underpowered and
prone to methodological bias.55 The results of ongoing RCTs
examining this therapeutic question are awaited.
Inotropes increase cardiac contractility, thereby increasing stroke volume and cardiac output. Increased contractility incurs an increased demand for oxygen and potential
for oxidative stress in the cardiac myocytes, which increases
the risk of ischemia. Many inotropes are chronotropic (act
to increase the rate of contraction), which not only adds to
oxygen demand but also potentiates arrhythmia, decreasing cardiac efciency and therefore reducing cardiac output.
Though important, blood pressure is only a surrogate
marker for tissue perfusion and is not a particularly reliable
metric in hemorrhagic shock. Perfusion may deteriorate as
compensatory increases in vascular resistance maintain
measured blood pressure and the latter can mislead.56 Ideally, oxygen delivery, which is calculated as:
O2 Delivery = Arterial O2 Content ×Cardiac Output
is the variable that is of most utility as an end point. Cardiac
output is the most inuential component of this formula as
arterial oxygen content is usually not decient if appropriate transfusion has been rendered. The gold standard for
cardiac output measurement utilizes pulmonary artery
catheterization, which in itself divides opinion. Suggestions
of increased complication rate,57 difculties with interpretation of data,58 and the lack of mortality benet59 have led
to calls for less invasive means to measure cardiac output.60
These may include bioimpedance, esophageal Doppler, and
pulse waveform analysis, which have shown to be reasonably accurate,61 with the latter applicable within the prehospital phase,62 although whether availability of these metrics
affects outcomes is unknown.
Other markers for adequacy of oxygen delivery include
acid-base status and serum lactate. Although lactate is
affected by many other factors, it is widely available in
any hospital and offers real time feedback. Severe acidosis
impedes coagulation and is negatively inotropic, which compounds inadequate tissue perfusion63; correction of acidosis
(“lactate clearance”) is a useful predictor of mortality.
31,64
Optimizing Coagulation
Optimization of coagulation comes in two parts: the management of TIC and the mitigation of the untoward effects
of blood product administration and massive transfusion.
The pathophysiology of TIC is multifaceted and not
fully understood. Coagulation function is conventionally
measured using established assays such as prothrombin
time and international normalized ratio. These tests were
initially developed for the screening of heritable coagulopathies such as hemophilia, and as means to monitor
anticoagulant therapy.65 The results of these tests represent
the time, in seconds, until the earliest formation of brin is
detected. They do not assess the maturity of the clot beyond
the formation of the rst strands of brin and correlate
poorly with risk of bleeding in elective general and vascular
surgeries.
66
New approaches include point of care (POC) testing in
the form of viscoelastic assays such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM). In
the trauma setting, TEG was rst used as a research tool to
investigate trauma coagulopathy67; it is now an increasingly
important technique in managing TIC.
68–70
TEG and ROTEM
both measure clot strength, thereby allowing functional
assessment of coagulation. Both employ a vertical pin held in
a blood sample contained within a cup (cuvette). In TEG, the
cup oscillates clockwise and anticlockwise as the blood clots’
viscosity increases and the degree of frictional torque force
on the pin changes, allowing a dynamic picture of clot development and strength to be obtained (Fig. 6.1).71 In ROTEM,
the oscillatory force is applied to the pin rather than the
cuvette—the latter is held stationary—and as the clot develops, pin movement is reduced; this is measured by the angle
of deection of a beam of light directed at the pin. Newer TEG
technology assesses clot formation using a different, innovative approach where the blood vibrates at a xed frequency,
and a light detector measures meniscus motion to generate
the clot formation tracing.72 TEG and ROTEM depict changes
in viscosity (and thus clot strength) via a trace, characterized
by a number of descriptors (Fig. 6.2).
73
R-Time. The reaction (R)-time represents the time from
the beginning of the test to the establishment of a brin
mesh with measurable rigidity of amplitude of 2 mm. This
variable has also been referred to as the clot initiation time.
R-time is measured in minutes and reects coagulation
factor activity. This variable is currently used in clinical
algorithms and protocols to trigger plasma transfusion.
74
Alpha (α) Angle. This is thought to signify the clot
strengthening, which in this phase of clotting is mostly
achieved by brinogen cleavage and brin polymerization.
A lower angle represents a decreased rate of clot strength
growth, whereas a higher angle represents a greater rate
of clot strength growth. The α-angle is used clinically as a
marker of brinogen concentration and is currently used in
trauma protocols to trigger brinogen replacement in the
way of cryoprecipitate or brinogen concentrate.
75,76
Maximal Amplitude (MA). This represents the maximal
strength achieved by the clot, depicted by the width in
Time (min)
Clot
Amplitude (Mm)
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6 • Damage Control and Immediate Resuscitation for Vascular Trauma 77
More tailored use of blood products may also incur less
complications, such as immunosuppression (where the
mechanism is not fully understood)83; citrate toxicity with
hypocalcemia (mitigated via intravenous calcium supplementation with every shock pack and measurement of
ionized calcium levels), hypomagnesaemia, and alkalosis;
hypothermia (mitigated with blood warming devices); and
hyperkalemia. Regarding the latter, whereas prolonged
storage (more than 10 days) or irradiated blood is thought
to increase the risk of hemolysis, there is no evidence that
mortality is signicantly affected by the age of stored blood
that is used prior to standard expiry times.84 Regular POC
testing and timely dextrose/insulin infusion intervention for hyperkalemia (greater than 7.0 mmol/L or 6.0 to
6.9 mmol/L + ECG changes) represents the best means of
Fig. 6.1 Normal thromboelastography trace.
71
managing this sequela of massive transfusion.
Facilitating Surgical Treatment
Keys to good anesthetic planning (and thus facilitating the
surgical agenda) include (1) a realistic appraisal of the likely
length of surgery; (2) likely blood loss; and (3) potential for
deviation from the surgical plan. Regular situation reports
Clot
formation
propagation
Clot
strength
Clot
lysis
(STACK brief) on progress or difculty allows the anesthetist
0 angle
MA (mm)
LY30,%
and the wider team to gain a global view about the direction of management and the rationale for the surgical plan.
Knowing when surgical hemostasis has been achieved pre-
R time (min)
vents over-resuscitation. Similarly, the forewarning of key
surgical steps (clamping and de-clamping of major vessels)
allows the anesthetist to pre-emptively manage circulating
volume, inotrope strategy, and deal with ischemia-reperfusion and washout of metabolites.
Another consideration for the anesthetist is to decide
on the merits of waking the patient following completion
Fig. 6.2 Viscoelastic trace and parameters of the various stages of the
clotting process.73 See text for explanation.
of surgery. Physiological stability (acid-base status, vasopressor support), probability of returning to theatre, and
likelihood of a successful analgesia plan are some of the
factors that are considered. In the authors’ experience, DCS
millimeters of the widest space in the TEG tracing. Clinically,
MA reects a combination of platelet count and function,
as well as brinogen activity and the interaction between
the two. Although not solely reecting platelet function,
MA is currently used in clinical algorithms and protocols to
patients, by denition, remain physiologically deranged and
will require further surgical exploration. Therefore, in vascular trauma patients, a period of sedation in critical care
and preparations for transfer of an anesthetized patient will
need to be made.
trigger platelet transfusion.
Amplitude at 30 Minutes (LY30). This is the standard
measure of brinolysis by TEG. LY30 is determined
Ethics of Resuscitation
by calculating the percent reduction of clot strength
(amplitude) 30 minutes after reaching MA.
Fig. 6.377 gives examples of traces, their explanations,
and suggested treatment options to guide coagulation
optimization. Being a POC test, viscoelastometry assessments can be continued from the trauma bay to theatre,
recovery, and critical care. There is some evidence that
better outcomes are obtained when these tests are used
to inform transfusion practice78 in trauma, guiding the
hemostatic resuscitation79 and reducing blood product
consumption as compared to standard assays.80 As such,
uptake has increased accordingly; in 2014 the American
Association for the Surgery of Trauma noted that only 9%
of institutions used TEG,81 but it is now endorsed by The
American College of Surgeons Trauma Quality Improvement Program82 and is included in the general surgical
resident curriculum.
The ethics of resuscitation following major vascular trauma
and hemorrhagic shock presents challenges, particularly so
when set against the resource-constrained environment of a
military eld hospital or humanitarian surgical team. Decisions surrounding initiation of resuscitation or surgery in
the gravely injured, declaration of futility following cardiac
arrest, and the denition of ceilings of care and/or blood
product expenditure are vexing and cannot be satisfactorily
answered by the application of a triage algorithm. Senior
clinical decision-makers, who can navigate the often-emotional pressures of these conundrums, are an important
resource in implementing an evidence-based approach.
For instance, knowing that the outcome from cardiac
arrest following vascular trauma and cardiovascular collapse
is likely to be an adverse outcome can help guide the duration of resuscitation attempt. Even in the best well-resourced
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Fig. 6.3 Abnormal viscoelastometry values/traces and their explanations.76 D.I.C., Disseminated intravascular coagulopathy; N/S, 0.9% normal saline.
civilian series, a survival rate of 7% (physician-led London
Helicopter Emergency Medical Service) was observed.85
Results in well-resourced and staffed role 3 hospitals, working in a mature military trauma system, are better (24%
survival in a select group of injured, in whom the dominant
challenges in advance with their own teams. The goals are
to manage expectations, maintain organizational norms,
respect the conventions of ethical clinical management,
and deliver humane and respectful medical care that allevi-
ates suffering.
cause of cardiac arrest was hypovolemia1), but the likelihood
of achieving these results during warfare, characterized by
remote and dispersed medical facilities, is not high.
Future Development of DCR
Context is therefore the foundation for approaching
many of these questions. Context will dictate expectations
and inform boundary setting, as will a clear understanding
of the organizational Medical Rules of Eligibility for treatment. Similarly, the professional obligations of the physician (mandated through national law, statutory policy,
and professional regulation) and their duty to the chain of
command form part of a decision framework for contentious issues. Any appraisal of potential ethical challenges
caused by the necessity to treat the civilian population must
also consider the capacity and capability of host nation
health systems; familial, cultural, and societal expectations;
and the spectrum of opinion that will be held by Medical
Treatment Facility staff. The threshold for sustaining local
patients and transferring them to their own health-care
facilities is often an ethical quandary.
Answers to these dilemmas are beyond the scope of this
chapter, but it is appropriate for those who manage major
vascular trauma in the resource-constrained or deployed
setting to consider these questions and then discuss the
Whole blood transfusion was established in World War II
and the Vietnam War; however, the need for a more tailored
approach and longer storage times leads to development of
the standardized component therapy that is a highly effective and efcient treatment in elective surgical circumstances. In military major trauma settings, especially those
that cannot access component platelet therapy, the case for
whole blood is increasingly clear.
86,87
The risk of increased
risk of plasma-associated transfusion reactions can be mitigated using leuko-reduction lters. The logistics of providing a prescreened, low-titer emergency donor panel are
complicated but feasible. Evidence from civilian trials is
awaited.
The early use of high-dose brinogen concentrates
(cryoprecipitate) as a treatment option for TIC is also being
investigated. Following encouraging results from a feasibility study (CRYOSTAT,88 which suggested that early use of
cryoprecipitate and maintaining brinogen levels may lead
to reduced mortality), a multicenter RCT (CRYOSTAT-2) is
6 • Damage Control and Immediate Resuscitation for Vascular Trauma 79
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being conducted to investigate benet, with results expected
by 2021.
Another aspect of tailoring DCR and personalizing transfusion strategy to the individual patient is to make better
diagnostic and prognostic predictions, whether these arise
from more sophisticated assays or via insights generated
from application of computer science. Health-care systems
generate huge quantities of structured and unstructured
data pertaining to all manner of input and outcome criteria. The use of articial intelligence (AI) technologies to
develop machine-learning algorithms to better understand
relationships between data points and aid in prediction and
prognostication, thereby aiding clinical decision-making, is
attracting increasing attention.
89
Summary
The overarching principal of DCR in vascular trauma
patients is to manage the pathophysiology of hemorrhage,
hypoperfusion, and coagulopathy, through the careful application of balanced, timely transfusion of blood products
and anesthetic technique that is calibrated to the severity of
physiological insult and the demands of surgical intervention. Physiological derangement may be causally related to
the effects of the injury and exacerbated by poorly chosen
interventions and inadequately monitored parameters.
Although our understanding of the mechanisms underlying TIC and endothelial dysfunction is not fully developed,
taking all necessary steps to ensure adequate oxygen delivery to the tissues will prevent further physiological deterioration.
Resuscitation is a continuum of care and applies
through out the ED and surgical phases of management.
Adjuncts to good resuscitation include a well-developed
understanding of the physiology of shock; prior preparation of the receiving team and planning for contingency;
excellence in communication between anesthetic, surgical, and theatre teams; anticipation of complications; and
effective coordination of effort. By so doing the optimal care
for the compromised patient can be delivered and best outcomes achieved.
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7
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Diagnosis of Vascular Injury
MICHAEL J. SISE
Introduction
Vascular trauma presents in a variety of settings and results in
ndings that range from life-threatening hemorrhage secondary to major torso or extremity vessel disruption to no detectable signs in occult injuries. Effective management is based
upon early diagnosis and prompt treatment. Isolated vascular
injuries are becoming less common at modern urban trauma
centers. There is a growing prevalence of multisystem trauma
that includes vascular injury, making early diagnosis more of
a challenge.
timely fashion requires an organized approach with attention
to the mechanism of injury, presence of hemorrhage at the
scene or during transport, a thorough physical examination
augmented, when needed, with Doppler extremity pressure
measurements, and nally, the effective use of multidetector
CT angiography (MDCTA). Imaging techniques are discussed
at length in subsequent chapters.
Several analyses of human error suggest that three factors play a role in most major errors: familiarity, distraction,
and fatigue.4 The modern trauma center creates an environment where all three factors are constantly interplaying.
Trauma care is, therefore, an error prone process. Avoiding
error in the care of the injured requires not only an organized approach, but the use of short but effective checklists
which assure the application of that organized approach.
Unfortunately, most physicians are overly familiar with
long, detailed, and all-inclusive checklists that were not
developed in conjunction with them or by colleagues who
actually provide trauma care. Most physicians do not nd
these types of checklists useful and they are not often used.
In contrast, the experience of military and civilian aviation
communities strongly supports the use of short and practical checklists created by experienced air crews and thoroughly tested at the point of service until they are effective.4
The essential history and physical elements that lead to
the prompt diagnosis of vascular injury are displayed as a
checklist in Box 7.1.
1–3
Successfully identifying vascular trauma in a
The Mechanism, Setting, and
Patterns of Injury
The evaluation of an injured patient must begin with a consideration of the mechanism of injury and the setting in
which that injury occurred.5 This is particularly important
in patients injured in high-speed motor vehicle crashes. The
advent of modern automobile passenger restraint systems
resulted in many occupants surviving what were previously
fatal crashes. However, this also resulted in a rising incidence
of blunt cerebrovascular and thoracic arterial injuries.6
These injuries are often asymptomatic, associated with few
physical ndings on presentation, and occur in the setting of
a variety of injury patterns. They can only be found with further imaging studies. Thus, considering both the mechanism
and setting of injury will lead to the appropriate diagnostic
evaluation. Further consideration of injury patterns will also
prompt appropriate early workup and timely recognition,
and result in successful management.
Penetrating vascular injuries are rarely occult and usually present with clear signs of hemorrhage including local
hematoma, active bleeding, and shock.7 The nature of bleeding at the scene should always be determined. Initial pulsatile
ow or large amounts of blood at the scene may be indicative of signicant vascular injury. Bleeding during prehospital transport should also be considered a sign of vascular
trauma. This information may not be readily available when
patients are transported by bystanders or if they ee the scene
of the injury. In the shocked patient, redirecting attention to
apparently nonbleeding wounds may reveal an underlying
extremity vascular injury which has ceased bleeding.
Injury Pattern Recognition
The early diagnosis of vascular injuries requires a high
index of suspicion based upon both mechanism of injury
and injury patterns. The following discussion reviews each
anatomic area and the important considerations of both
mechanism and injury pattern that will lead to attention
to diagnostic measures that identify vascular injuries in a
timely fashion. The goal of this review is to generate pattern
recognition and decisive action.
HEAD AND NECK VASCULAR INJURIES
The neck and face are areas of relatively supercial major
vascular structures. Additionally, the neck is a zone of
multiaxis motion with cerebrovascular arterial structures
in close proximity to boney prominences. This is a highrisk zone for both blunt and penetrating vascular injury.2
Although penetrating injuries are usually obvious because
of hemorrhage, blunt injuries are almost always occult. Low
velocity gunshot wounds may cause injuries other than the
typical penetrating laceration hemorrhage. Partial arterial
wall disruption from bullets passing in proximity may cause
arterial thrombosis. Pattern recognition of both blunt force
loading and associated injuries is essential for prompt diagnosis of blunt cerebrovascular injury.
The most common underlying mechanism of signicant
blunt cerebrovascular injury in the neck and at the skull base
is stretching of the vessel, often across a boney prominence,
or from direct compression by a fracture fragment.
likely is focal blunt force with direct compression and partial
arterial rupture. There are key anatomic areas where these
events occur. At the base of the skull, fracture of the temporal
6,8
Less
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Box 7.1 Checklist for Prompt Recognition of
Vascular Injury
Review following questions in the trauma bay and consider further evaluation for vascular injury for any positive answer
1. High-Risk Mechanism of Injury
n Significant blunt force loading and anatomic extent across
major vessels?
n Penetrating path in area of major vessels?
2. Blood Loss at the Scene
n History of pulsatile bleeding from wound?
n Significant blood at scene, on clothing, trail of blood?
n Fled the scene and history of significant bleeding from
wounds?
3. Bleeding Indicators
n Prehospital hypotension present and trauma in area of
major vessel?
n Shock unexplained with nonbleeding extremity or neck
lacerations?
4. Physical Examination
n Pulsatile bleeding, copious venous bleeding, or large
hematoma?
n Extremity pulses absent, Doppler signals absent, or injured
extremity index <0.9?
n Bruit or thrill over injury site?
n Major deficit in peripheral nerve located in proximity to
major vessel?
5. High-Risk Fractures, Joint Dislocations?
n Cervical spine fracture—vertebral artery injury
n Thoracic spine fracture—thoracic aortic injury
n Supracondylar humerus fracture—brachial artery injury
n Knee dislocation—popliteal artery injury
n Tibial plateau fracture—calf compartment syndrome
bone in the area of the carotid canal may be associated with
internal carotid artery dissection. Hyperextension of the neck
may stretch the internal carotid artery across the transverse
process of C2, also causing dissection. Hyperexion may lead
to compression of the internal carotid between the angle of
the mandible and the transverse process of C2 with arterial
thrombosis (Fig. 7.1). Hyperrotation of C1 on C2 can cause
a stretch injury of the vertebral artery, resulting in dissection
and thrombosis. Any cervical spine fracture that involves
transverse processes may cause vertebral artery injury. At
the prominent transverse process of C6, direct blunt force
trauma may compress the common carotid artery, creating
a partial wall disruption and pseudo-aneurysm.
Direct trauma to the neck also requires attention to the
possibility of vascular injury.
direct blows to the neck may disrupt the carotid artery.
Attempted hanging or strangulation may cause blunt carotid
disruption. The shoulder harness of an automobile passenger restraint system may also compress the common carotid
artery and cause disruption and thrombosis. Signs of direct
neck trauma should direct attention to the possibility of
carotid injury. Particular attention should be paid to direct
lower neck trauma and hoarseness in the absence of direct
laryngeal trauma. The vagus nerve lies adjacent to the common carotid artery and trauma sufcient to cause injury to
the vagus proximal to the take-off of the recurrent laryngeal
trauma may also injure the common carotid artery (Fig. 7.2).
6,8
Handlebar trauma and other
THORACIC VASCULAR INJURIES
Penetrating trauma to the thorax with major vascular
injury presents with life-threatening hemorrhage that
requires immediate operative intervention to identify the
injury and control hemorrhage. In contrast, blunt injuries
are often occult and early diagnosis requires attention to
both mechanism and injury pattern. Rapid deceleration
or acceleration can create visceral rotation and stretch of
the mediastinal structures, causing sheer stress at transition points between relatively mobile and xed vessel seg-
2,9
ments.
The heart and proximal great vessels have been
described as moving like a “bell clapper” in the chest in
certain high-speed impacts, with the result that the aorta
is partially torn at the isthmus, a transition point between
mobile and xed elements.9 This type of movement can also
stretch and partially tear the branches of the aortic arch.
Direct trauma from compression and fracture of the sternum, manubrium, or clavicles can cause vascular injuries.
This type of direct compression may injure the aortic arch
and its proximal branches or the pulmonary artery at its
bifurcation area (Fig. 7.3).
A variety of fracture patterns have been described with
blunt thoracic aortic injury. Although rst rib fracture is
often described as a harbinger of blunt aortic injury, thoracic spine fracture is the most commonly associated fracture nding.
9,10
This type of fracture is the result of major
force loading on the thorax and indicative of the risk of
great vessel injury. Although clavicle fractures are very
common, blunt subclavian artery and venous injuries are
rarely associated with this nding.
1,2
The portable anterior-posterior chest radiograph is an
important tool in the early recognition of occult mediastinal
vascular injury. Despite a wide variety of ndings described
to be associated with thoracic aortic injury, two are of
particular importance.
9,10
Increased width of the superior
mediastinum and the absence of a normal left side aortic
contour are both indications of a mediastinal hematoma
and warrant additional CT scan imaging to rule out vascular injury. Finding of rib fractures, thoracic spine fractures,
and sternal fractures are less strongly associated with thoracic aorta and great vessel injuries, but should also prompt
additional imaging with CT scanning.
ABDOMINAL VASCULAR INJURIES
Penetrating abdominal vascular injuries present in a manner similar to thoracic vascular injuries.
nal hemorrhage and shock require immediate operative
intervention to both identify and control the site of hemorrhage. Blunt vascular injuries occur in a fashion similar
to thoracic injuries.11 The major difference in the abdomen
is the paucity of motion segments in major arteries due to
the retroperitoneal location of the aorta and its proximal
branches. The renal hilum is an exception and blunt stretch
injuries of the renal arteries are not uncommon.
abdominal aorta and proximal mesenteric arteries may be
injured by direct blunt force trauma such as a lap belt passenger restraint compression of the distal aorta against the
sacral promontory in a high-speed motor vehicle crash.
Survivable blunt tears of the celiac and superior mesenteric
artery occur infrequently.
2,10,11
10,11
Intraabdomi-
2,10,11
The
84 SECTION 2 • Immediate Management and Diagnostic Approaches
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Right
1.91cm
Fig. 7.1 Internal carotid artery thrombosis from gunshot wound transiting retromandibular area and lodging adjacent to mastoid process. There was a
lack of hemorrhage or hematoma and the patient had a normal neurologic examination.
UPPER EXTREMITY VASCULAR INJURIES
Penetrating upper extremity vascular injuries typically produce either signicant external hemorrhage or acute limb
ischemia and are usually obvious at initial presentation
(Fig. 7.4). Blunt injuries, although less obvious, are usually
associated with musculoskeletal injuries.
distraction of the shoulder with brachial plexus stretch
1,2
Blunt posterior
Right
injury can result in tearing and thrombosis of the axillary
artery with absent pulses at the wrist. Proximal fracture of
the humerus or humeral head dislocation rarely causes brachial artery occlusion. However, supra-condylar humeral
fracture is associated with distal brachial artery occlusion
and forearm ischemia.
1,2
Other fractures of the upper arm
are infrequently associated with major vascular injuries
unless they involve a crush injury.
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