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G. A. Richards et al.
• End-tidal CO2, especially if there is a concomitant traumatic brain injury
• Optimal endotracheal or tracheostomy tube positioning
and cuff pressure
13.8 Longer-Term ICU Airway Management
13.8.1 Tracheostomy
There are two main indications for tracheostomy, long-term
airway support as is the case with facial fractures, severe
traumatic brain (TBI), and laryngeal injury and prolonged
requirement for ventilatory support. Essentially a tracheostomy is performed to facilitate nursing care and oral hygiene,
as there is controversy surrounding the overall benet, with
some suggesting that there might be reduced ventilatorassociated pneumonia (VAP) and a shortened ICU stay.
Either a percutaneous or an open procedure (with difcult
neck anatomy or need for other operative procedures) may
be performed, either primarily or around day 3 for patients
with compromised airways or neuromuscular dysfunction.
A tracheostomy for cardiopulmonary dysfunction is com-
monly performed at around day 10, depending on the degree
of persistent pulmonary compromise and as to whether extubation is likely in the near future.
ble, as this leads to loss of PEEP and actually increases the
work of breathing, risking higher failure rates and loss of
recruitment.
When all reversible issues have been addressed and the
patient remains persistently ventilator dependent, the
approach will depend on available resources. A heart and/or
lung transplant may be considered where resources are available, but with limited resources, a family meeting, including
the patient where possible, should frankly discuss the situation with the likely transition from curative to palliative care.
Important Points
• Airway and ventilation go hand in hand but should be
independently assessed.
• Early resuscitative ventilation is different from ICU ven-
tilation as the goals differ.
• Hypercarbia is to be avoided in the TBI patient.
• Tracheostomy should be considered on an individual
patient basis.
• Weaning should be performed when the patient pathology
is reversed and the ventilator requirements have been
reduced to minimal levels.
• Remove chest tubes as soon as reasonable.
Suggested Reading
13.8.2 Weaning
Weaning is facilitated by early mobilization and reduced use
of sedation.
There are three main causes of weaning failure:
• Weakness (ICU-associated weakness, cord injury, thoracic cage injury, low GCS)
• Persistent hypoxemia due to due to unresolved or irreversible pulmonary injury
• Myocardial dysfunction (myocardial brosis after a contusion or infarct or a preexisting cardiomyopathy)
As described above, early conversion to spontaneous ven-
tilation with pressure support is suggested with a gradual
reduction of PSV rst and thereafter PEEP to a predened
baseline such as 6–8cmH2O for both. If the patient tolerates
this without elevation of RSBI above 80, hypoxemia (saturation<90%), and hypercarbia (with acidosis) with no signs of
distress (sweating, agitation) and is awake, then the patient
should be extubated. If the patient is fully conscious but is
considered to be high risk for failure or still requires PSV,
one may extubate to a noninvasive PSV mode, avoiding the
risks of prolonged intubation, while simultaneously optimizing oxygenation. A T-piece trial should be avoided if possi-
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patients. Curr Opin Crit Care. 2006;12:3–7.
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ECMO intheTrauma Patient: APractical
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Approach
JeromeCrowley
14
14.1 Introduction
This chapter will provide the trauma surgeon with an overview of extracorporeal membrane oxygenation (ECMO).
Indications for ECMO will be discussed as well as the basics
of cannulation strategies. Troubleshooting of common
ECMO scenarios will be discussed as well as the basics of
weaning from ECMO.
14.2 Background onECMO
ECMO is fundamentally the provision of gas exchange for
the blood outside the body. There are three main types of
ECMO of interest to the acute trauma population: venoarterial (V-A), veno-pulmonary arterial (V-P), and veno-venous
(V-V) ECMO.By convention, letters listed before the hyphen
refer to cannula draining blood from the patient to the ECMO
circuit, and letters listed after the hyphen refer to cannula
returning blood from the ECMO circuit to the patient. The
three subtypes of ECMO support differ what type of support
is provided to the patient. V-V ECMO is indicated for respiratory failure, either hypoxic, hypercapnic, or mixed. V-V
ECMO does not provide any signicant hemodynamic support, but by correcting the respiratory acidosis and reversing
the hypoxemia, there may be improvement in myocardial
function, particularly on the right side of the heart. V-P
ECMO is indicated for the scenario of signicant isolated
right ventricular dysfunction and is able to provide respiratory as well as right ventricular support. Finally, V-A ECMO
is primarily indicated to provide hemodynamic support to
the systemic circulation in the setting of cardiac pump failure. As discussed in a later section, the amount of respiratory
support provided by V-A ECMO is variable and depends on
native lung function and cannulation strategy.
J. Crowley (*)
Anesthesia, Critical Care, and Pain Medicine, Massachusetts
General Hospital, Boston, MA, USA
e-mail: jccrowley@mgh.harvard.edu
An ECMO circuit consists of four main components: a
drainage cannula removing blood from a large central vein, a
pump to move blood through the circuit, an oxygenator to
provide gas exchange, and a return cannula that is placed in
the patient to return oxygenated blood. The amount of
ECMO support a patient is on is described by three variables:
the ow through the circuit, the percentage of oxygen in the
gas in the oxygenator known as the delivered oxygen fraction (FdO2), and the ow rate of the gas in the oxygenator
known as the sweep ow. The FdO2 is analogous to the fraction of inspired oxygen on the ventilator and is one of the
determinants of the oxygenation of blood. The sweep ow
rate determines the rate of carbon dioxide removal and is
analogous to the minute ventilation. The ow through the
circuit is determined by several factors: the rotations per
minute of the centrifugal pump (RPMs), the resistance to
drainage through the venous cannula, and the resistance to
return through the return cannula. Increasing the RPMs will
increase the ow to a point; however it is always important to
remember that the ECMO pump is both preload dependent
and afterload sensitive, so the ow may vary at the same
RPMs due to different loading conditions.
Oxygenation of the blood via the ECMO circuit is related
to two factors: the fraction of delivered gas that is oxygen
and the total ow of the ECMO circuit. Approximately 70%
of blood must participate in efcient gas exchange to maintain an arterial saturation of 90–94%, so assuming 1.0 FdO2,
then the ECMO circuit ow must be ∼70% of the cardiac
output to achieve this goal. This is particularly relevant for
veno-venous ECMO when deciding the goal ow rates.
14.3 Veno-venous ECMO
V-V ECMO is indicated for respiratory failure refractory to
maximal medical management. The trauma patient presents
a unique challenge as all available medical therapies may not
be appropriate (proning may be contraindicated, for example, or due to a traumatic bronchopleural stula, lung-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
E. Degiannis et al. (eds.), Penetrating Trauma, https://doi.org/10.1007/978-3-031-47006-6_14
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J. Crowley
protective ventilation may not be feasible). Common
indications that are encountered in the trauma population
include severe acute respiratory distress syndrome, severe
pneumonia or aspiration, pulmonary contusions, inhalational
injuries, refractory status asthmaticus, airway obstruction,
severe air leak syndrome, or intraprocedural need for lung
isolation that is tolerated by conventional means. Most contraindications to veno-venous ECMO are relative, but care
should be taken in patients with severe cardiogenic shock
(may need venoarterial ECMO), patients with signicantly
elevated body mass index (>40–45) as this will be challenging to support due to the high ow rates needed, as well as
patients with signicant underlying comorbidities (end-stage
renal disease, cirrhosis, chronic lung disease, severe intracranial pathology) as it is unlikely that these patients will survive an ECMO course.
14.4 Cannulation forVeno-venous ECMO
V-V ECMO cannulation is almost always done peripherally
(not directly in the thorax). There are multiple congurations
available; the most important concept to keep in mind is that
blood must be drained from a large central vein (usually the
inferior vena cava) and returned to a large central vein (usually the superior vena cava or the right atrium). Dictating the
positioning of the cannula for V-V ECMO is a balance
between obtaining adequate drainage to obtain the goal ow
rate (for V-V ECMO, the drainage is almost always the limiting factor unless the return cannula is grossly undersized)
and avoiding the phenomenon of recirculation. Recirculation
is when blood passes directly from the return cannula back to
the drainage cannula rather than through the circulation of
the patient. This reduces both the efciency of the ECMO
circuit and the percentage of oxygenated blood available to
the patient. In order to minimize this phenomenon, it is ideal
to position the tip of the return cannula 10cm or greater from
the tip of the drainage cannula.
Cannulation for V-V ECMO is most commonly accomplished percutaneously, ideally using ultrasound guidance to
identify a safe location to access the vein. Options for cannulation include femoral/internal jugular, femoral/femoral,
femoral/subclavian, or dual-lumen single-site cannulation.
Common to all forms of cannulation is meticulous avoidance
of air in the ECMO circuit using “wet to wet” connections
and robust securing of cannula with multiple sutures to prevent inadvertent dislodgement.
Femoral/internal jugular and femoral/subclavian are similar. Under ultrasound guidance, the common femoral vein is
identied (preferentially the right as this is a straighter path
to the inferior vena cava although anatomic conditions may
dictate choice of the left) and access in the standard fashion,
and a small sheath is placed. Via this sheath a long (180cm
or 260cm) wire is passed to the right atrium. This is ideally
accomplished under imaging guidance: uoroscopy, transesophageal echocardiography, or transthoracic echocardiography; if not available a plain X-ray may sufce to conrm
appropriate wire placement. In the busy setting of an acute
trauma patient, a 180cm wire may be preferred as this can
reduce redundant wire and compromise of sterility. Over this
wire, using serial dilation and Seldinger technique, a venous
drainage cannula is placed. For adult patients, a 25Fr cannula
is usually sufcient in any patient over 40 kg. In smaller
patients a 23Fr cannula may be sufcient but will limit drainage. The tip of this cannula is ideally placed close to the right
atrial/IVC junction. If imaging guidance is available, it is
often advantageous to place a stiff wire from the femoral
location to act as a more stable access rail for the long venous
cannula. The benets of a stiff wire need to be balanced with
an increased risk of vascular perforation if imaging is not
available and providers are not experienced with endovascular procedures. If possible, it is desirable to place the tip at
least past the hepatic vein so the proximal drainage ports are
in the intrahepatic IVC which is more resistance to collapse
from intra-abdominal factors than the more distal IVC and
will provide more reliable drainage without needing excessive uid administration. If traumatic injury precludes such
placement, then shorter cannula can be used. In order to
compensate for less ideal positioning of the femoral cannula,
it may be necessary to place two femoral drainage cannula
and connect them together to ensure adequate drainage for
the ECMO circuit. The return cannula is a shorter arterial/
jugular cannula that in most adults is a 19 or 21Fr (allowing
for ows >5LPM if needed). The easiest location for the
return cannula is the right internal jugular vein where placement is analogous to normal central venous cannulation. The
right internal jugular vein is identied under ultrasound and
accessed in the normal fashion. This access is used to place a
wire to the right atrium over which the cannula is placed with
tip in the superior vena cava after serially dilating the tract. If
the right internal jugular vein is not feasible, then the left
subclavian vein is another option with placement being similar. The left internal jugular vein and right subclavian vein
are only recommended if uoroscopic guidance is available
due to the higher risk for cannula malposition with these
locations.
Femoral/femoral cannulation is an attractive cannulation
strategy in patients with potential neck trauma or traumatic
brain injury as it does not affect cerebral venous drainage
signicantly and allows for cannulation to be performed
away from the airway. Access of the femoral vessels is as
described above. A long wire is passed from the left femoral
vein to the right atrium; this is either a standard stiffness wire
or a stiff wire, or if a stiff wire does not pass easily, a soft
wire is placed and then exchanged over a pigtail catheter for
a stiff wire. Next a wire is advanced from the right femoral
vein to the right atrium. It is preferred to place the left-sided
cannula rst as the right-sided cannula will straighten the

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vena cava and may make the left-sided access more acute in
angle increasing the risk of vascular perforation. The left
femoral cannula is a 25Fr drainage cannula and the right
femoral cannula is a long (55cm) 19 or 21Fr return cannula
(tip placed in the right atrium). Based on patient anatomy,
smaller cannula may be needed which will reduce maximal
ows. This represents one of the limitations of femoral/femoral V-V ECMO: lower maximal ow than other cannulation
strategies. The other drawbacks include a higher rate of
recirculation (due to proximity of cannula) and a high rate of
deep venous thrombosis around the cannula.
Dual-lumen cannulation represents an attractive option as
it allows for single-site access and as it is supradiaphragmatic allows for easier patient mobilization. It is also appropriate for patients who cannot have a femoral cannula placed
(severe pelvic trauma, presence of an IVC lter, signicant
caval distortion from injury). Drawbacks are that it is more
time-consuming and prone to malposition necessitating
repositioning which requires echocardiography. Dual-lumen
cannulation is not recommended as rst line for an emergent
cannulation due to more nesse required for appropriate
positioning. The dual-lumen cannula has drainage holes in
both the SVC and IVC and returns blood to the right atrium
ideally directed at the tricuspid valve. It is most commonly
placed via the right internal jugular vein but can be placed
from either jugular vein or subclavian if anatomy is favorable. Positioning of the cannula is determined by both uoroscopy and transesophageal echocardiography. Attempts to
place the cannula without image guidance run a high risk of
right ventricular perforation and are not recommended.
After cannulation, the ECMO circuit is appropriately connected ensuring no air in the lines. It is recommended that an
“ECMO Initiation Checklist” be performed in order to ensure
appropriate direction of tubing, adequate fresh gas supply,
and appropriate levels of oxygen are conrmed. Support
should be initiated slowly in order to minimize abrupt temperature shifts (exercise extreme caution using a circuit that
has not been warmed as rapid infusion of cold uid can cause
the heart to brillate) and to ensure appropriate stability.
Cannulation can trigger a vasodilatory response, so vasopressors should be available to support the blood pressure.
Conversely, correction of the respiratory acidosis/hypoxia
may lead to rapid improvement in vasomotor tone and cardiac function, so close monitoring is essential. Once ECMO
support is established satisfactorily, ventilatory support
should be weaned to lung-protective settings in order to minimize further lung injury.
14.5 Veno-pulmonary Arterial ECMO
V-P ECMO is indicated to support the failing right ventricle
as well as providing veno-venous ECMO support. This conguration is not commonly used, but due to the availability
of percutaneous dual lumen, cannula is not becoming more
prevalent. Advantages include a low rate of recirculation
(drainage is in the right atrium and return in the pulmonary
artery; the tricuspid and pulmonic valves serve to minimize
mixing) and the ability to support a failing right heart as well
as potentially help decongest the liver and kidneys in the setting of right ventricular failure. It is important to remember
that this conguration is not ideal in the setting of any degree
of left ventricular dysfunction as the independent right-sided
support will rapidly overwhelm the failing left ventricle
leading to severe pulmonary edema.
Placement is almost always via the right internal jugular
vein. Under uoroscopic guidance, a balloon-tipped, owdirected catheter is placed into the pulmonary artery and
exchanged for a stiff wire. Over this wire, using serial dilation, the cannula is advanced and appropriately positioned. It
cannot be emphasized enough that placement cannot be
readily adjusted once the wire is removed, so all efforts
should be made to ensure satisfactory location before leaving
the uoroscopy suite.
ECMO support is initiated as above with additional attention paid to the left ventricular function to avoid overloading
the pulmonary circulation. In the setting of isolated right
ventricular dysfunction, improvement in cardiac output
should be noted with a reduced need for inotropic support.
14.6 Venoarterial ECMO
V-A ECMO is indicated in patients with hemodynamic
compromise related to inadequate cardiac function. The
most common indications are acute myocardial infarction,
myocarditis, massive pulmonary embolism, or decompensated heart failure. Trauma patients may benet from V-A
ECMO if they show evidence of impaired myocardial function due to contusions, severe acidosis, volume overload,
overdoses, or electrolyte abnormalities. Anatomic contraindications to V-A ECMO include signicant aortic insufciency and aortic dissection. Similar contraindications exist
as related to V-V ECMO with the additional caveat that
patients on V-A ECMO can “live” on ECMO for a prolonged period of time even with no reasonable chance of
recovery. This can be incredibly distressing on both health
care providers and patient’s families, and early discussion
of feasibility of recovery is critical. Exit strategies from
V-A ECMO include recovery, durable left ventricular support devices, heart transplant, or additional mechanical
support devices designed to act as a further bridge to intervention. The candidacy of most trauma patients for these
advanced therapies will be unknown, so best practice would
be to choose patients likely to recover as most patients suffering traumatic injury would need to have signicant
recovery before being considered for advanced cardiac
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Cannulation for V-A ECMO is dened as either central
(in the thorax) or peripheral. Central ECMO has been
described for trauma patients; however it is most commonly
only due in the cardiac surgical operating room, and techniques are beyond the scope of this text. Focus will be made
on peripheral V-A ECMO which is the most common cannulation strategy in an emergency. Peripheral cannulation is
accomplished via the femoral vessels by either an open or
percutaneous technique. Open techniques have the advantages of a higher success rate, easier method of ensuring limb
perfusion, and potentially easier removal of cannula.
Drawbacks include higher rates of bleeding, infection, and
slower cannulation times. Ultrasound-guided percutaneous
cannulation is rapidly becoming the standard of care. In
either strategy, the common femoral artery is identied
below the inguinal ligament but above the bifurcation of the
supercial and deep femoral arteries. A small sheath is
placed and used to introduce a J-wire into the descending
aorta over which serial dilation is used to place an appropriately sized cannula. Cannula size is determined by the vessel
size and by the goal ow. Goal ow on V-A ECMO is targeted to a cardiac index of 2.4 (so goal ow is body surface
area multiplied by 2.4). In an acute trauma situation this is
not often known, so a rough guide is to use a 17Fr cannula in
most adult patients (capable of ∼4.5LPM of ow). A 19Fr
cannula can be chosen in larger patients who are >180cm
(allowing for ∼5.5LPM of ow), and a 15Fr cannula can be
chosen in smaller patients (allowing for ∼3.5LPM of ow).
The venous cannula is placed analogous to the method
described in the V-V ECMO section, with most adult patients
accommodating a 25Fr cannula (and smaller patients tolerating a 23Fr cannula). It is critical to ensure that the venous
cannula is in the vein and not the artery as the large venous
cannula has a high likelihood of causing catastrophic vessel
injury if misplaced.
After cannulation, the ECMO circuit is appropriately connected ensuring no air in the lines. It is recommended that an
“ECMO Initiation Checklist” be performed in order to ensure
appropriate direction of tubing, adequate fresh gas supply,
and appropriate levels of oxygen are conrmed. Support
should be initiated slowly in order to minimize abrupt temperature shifts (exercise extreme caution using a circuit that
has not been warmed as rapid infusion of cold uid can cause
the heart to brillate) and to ensure appropriate stability.
Cannulation can trigger a vasodilatory response, so vasopressors should be available to support the blood pressure.
Conversely, correction of the low-output state may allow for
rapid weaning of vasopressors, and close monitoring of
blood pressure is critical.
Other considerations unique to peripheral V-A ECMO
are north/south syndrome (or differential hypoxia) and left
ventricular venting. Due to the retrograde nature of the ow
on V-A ECMO (ECMO ow owing retrograde up the aorta
from the femoral arterial cannula), there is a location of
mixing in the aorta where “ECMO blood” meets “native
blood” that has been ejected from the heart and has been
oxygenated via the lungs. If the patient’s native lung function is severely compromised, then this blood has the potential to be signicantly hypoxic. This is problematic as the
coronaries and the cerebral circulation are more likely to see
native blood and consequently will suffer hypoxic injury
despite adequate performance of the ECMO circuit. Close
vigilance for this phenomenon is critical and includes arterial blood gas sampling from the right upper extremity as
this will reect the blood entering the cerebral circulation
and will give warning of differential hypoxia in a patient on
peripheral V-A ECMO. An additional complication on
peripheral V-A ECMO is left ventricular distension. Due to
the retrograde ow on ECMO, the left ventricle will see
increased afterload which in the setting of impaired left ventricular function may lead to distension. This distension of
the left ventricle will lead to further left ventricular stress in
the setting of increased wall tension as well as the potential
for signicant pulmonary edema which will reduce the likelihood of liberation from ECMO.Monitoring for left ventricular distension includes frequent echocardiography to
assess for aortic insufciency, left ventricular function,
mitral regurgitation, and left ventricular size, chest X-rays
to look for pulmonary edema progression, and consideration of a pulmonary artery catheter to monitor left ventricular lling pressures.
In all forms of ECMO, it is optimal to maintain a reasonable degree of anticoagulation to reduce the risk of thrombosis in the circuit and thrombotic complications in the patient.
Targeted levels vary by institution and usually involve targeting an aPTT range, a Xa range, or an activated clotting time.
Trauma patients may not tolerate heparinization and this
becomes a risk-benet discussion. One possibility is that
anticoagulation is felt to be safe and standard protocols can
be followed (usually a bolus of 100units/kg of heparin or a
similar efcacy bolus of bivalirudin followed by an infusion
to maintain a therapeutic level). If the risk of bleeding is felt
to be too high, then either just a bolus dose for cannulation
(likely the highest initial risk portion due to stasis in the cannula) or anticoagulation can be avoided all together. There
are multiple reports of ECMO cannulation and circuits running without anticoagulation, so in the appropriate patient,
this is reasonable acknowledging the likely increased risk of
thrombotic complications. In order to mitigate these risks in
a trauma patient, it is reasonable to consider a strategy to
reduce any periods of blood stasis. This may include preferentially owing the circuit at higher rates, having two providers perform cannulation simultaneously to avoid
prolonged periods where a cannula is left clamped with no
ow, and ushing of cannulas with saline to avoid any blood
sitting in them while ECMO is being prepared.

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14.7 Troubleshooting
14.7.1 Recirculation onV-V ECMO
Recirculation is the phenomenon where blood that has been
oxygenated via the ECMO circuit passes back into the
ECMO circuit rather than through the systemic circulation.
This can be suspected when the patient’s arterial saturation
remains low despite what should be adequate ECMO ow. In
order to diagnose this, the saturation of the blood on the
drainage limb should be checked. The closer this to the arterial saturation, the more likely that recirculation is occurring
(assuming the oxygenator is functioning well). Another hallmark of this phenomena is that increasing the ECMO ow
has minimal effect on the oxygen saturation. In order to rectify this situation, the cannula likely need to be adjusted.
Ideally, under imaging guidance, the cannula can be retracted
slightly so that a separation of at least 10 cm is obtained.
Remember, the initial goal location of the drainage cannula
is in the IVC just below the right atrium, and the return cannula is in the SVC just above the right atrium. If the patient
has a single-site dual-lumen catheter, a transesophageal
echocardiogram is likely indicated to ensure appropriate
positioning. Plain lm radiographs may also be helpful to
determine if there has been cannula migration since catheter
placement.
14.7.2 Progressive Hypoxemia onV-V ECMO
One of the most common complications of ECMO is sepsis
(also a common fear in trauma patients). As sepsis commonly presents with elevated cardiac output, the required
V-V ECMO ow rates will increase as the patient becomes
more hyperdynamic. This will manifest as worsening of
hypoxemia despite stable ECMO ows and no change in
recirculation. The treatment is to increase ECMO ows;
however this may require the placement of additional drainage cannula, and it is important to note that most adult
ECMO oxygenators are not capable of oxygenating blood at
a rate greater than 7LPM.Vigilance for sepsis is critical and
early antibiotic therapy is important.
14.7.3 Dierential Hypoxia
As described above, differential hypoxia results from competing native cardiac ejection and ECMO ow in the setting
of impaired lung function. This is seen in trauma patients
who have recovery of their cardiac function faster than their
lung function. Diagnosis is made by sampling blood from
the right upper extremity arterial system. Management of
this depends on the severity of the lung injury. As a rst
maneuver, ventilatory support can be optimized in order to
improve native blood oxygenation. This is not ideal however
if it results in injurious settings that can potentiate further
lung injury and reduce the likelihood of recovery. A second
option is to create a hybrid circuit, known as venoarteriovenous ECMO (V-AV). Here, an additional return
cannula is placed in one of the jugular or subclavian veins
and y-connected to the femoral arterial cannula so that some
oxygenated blood is returned to the venous system, “preoxygenating” the blood before it passes into the native lungs.
In effect the patient is now on both V-V and V-A ECMO.This
conguration can be challenging to maintain as it requires
higher total drainage to support the ows needed as well as a
partial occluding clamp in order to adjust the relative venous
vs arterial ow.
14.7.4 Left Ventricular Distension
Left ventricular distension results from an impaired left ventricle facing the elevated afterload resulting from retrograde
ECMO ow. If left untreated this can lead to irreversible left
ventricular injury, pulmonary edema, and stasis in the left
ventricle leading to thrombotic complications. An initial
maneuver can be to increase inotropic support to encourage
left ventricular contraction. In addition, ECMO ow can be
increased further to decrease blood returning to the left ventricle. It should be noted, however, that this is not ideal in a
trauma patient who is not on anticoagulation as a noncontractile left ventricle will quickly develop thrombosis with a
high likelihood of stroke. Additional methods of decompressing the left ventricle are more invasive: placement of an
intra-aortic balloon pump (less likely to efcacious in
younger patients with compliant aortas), placement of a percutaneous left ventricular assist device, atrial septostomy, or
placement of a surgical vent via the left ventricular apex or
the left upper pulmonary vein.
14.7.5 ECMO Flow Issues
Commonly referred to as “chatter,” this refers to intermittent
uctuations in ECMO ow that can lead to cut outs and poor
circuit performance. This is usually due to problems with
venous drainage. If the drainage pressure is being measured,
commonly it will be dropping to −100 mmHg or greater
implying insufcient drainage. The problem can often be
temporized with volume resuscitation. The next step is to
check cannula position. If the cannula is adequately positioned, then causes of hypovolemia should be addressed
(gastrointestinal bleeding, over diuresis, etc.). If volume status is adequate and the cannula is adequately positioned,
then the problem may be that the drainage cannula cannot

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support the goal ow rates in which case an additional drainage cannula may be needed.
14.7.6 Weaning
Weaning from V-V ECMO can be prolonged, but the concept
is relatively straight forward. The patient must have sufcient
recovery of native lung function in order to liberate from the
ECMO circuit. This can be detected by improvements in
imaging, lung compliance, and resolution of the underlying
disease process. As the patient’s native lung function
improves, the required sweep gas ow and FdO2 will decrease.
Once these are minimal, then the patient can be placed on
standard ventilatory settings, and the sweep gas turned to
0LPM.This effectively means the patient is off ECMO.Flow
is maintained in the ECMO circuit in order to prevent thrombosis; however no gas exchange is occurring. If the patient
tolerates this for a prescribed period of time (6–24h depending on the fragility of their respiratory status), then they can
be decannulated. Decannulation from V-V ECMO can usually be performed at the bedside with cannula removed and
hemostasis obtained with sutures at the skin site and manual
pressure. Patients who do not show signs of lung recovery
should be considered for referral to a lung transplant center
that has experience with prolonged ECMO weans and the
possibility of lung transplant if the patient fails to wean.
Weaning for V-A ECMO is more complicated as the
sweep ow can never be reduced to zero (this would create
a large shunt) and that even at lower ow rates some hemodynamic support is maintained. For some patients, cardiac
recovery is obvious. For others a more deliberate approach
is needed. Once a patient can tolerate anticoagulation, a
ramp trial can be attempted if there are signs of myocardial
recovery. The ECMO ows are slowly decremented to
2LPM over a period of 12–24h, and an echocardiogram is
obtained. If this study is promising, then the patient can be
further anticoagulated and the ows further reduced until
the circuit is clamped and the patient is observed off of
ECMO.Caution must be taken in the setting of right ventricular failure as often the right ventricle only needs partial
unloading and failure to wean may not be apparent immediately. If the wean is successful, the patient can be decannulated from V-A ECMO which is commonly done via
surgical cut down and direct repair of the femoral artery.
14.8 Final Thoughts
ECMO can be a life-saving intervention in appropriate
patients, and comparative reviews of trauma patients have
shown similar outcomes to non-trauma patients. The most
important piece of developing an ECMO program is to recognize that it is a team-based system. Attempting to implement an ECMO service without having the appropriate
support will not be successful. In addition, it is recommended
that frequent review of ECMO patients is undertaken to
determine appropriateness of candidacy, management, and
complication rates. This is important as ECMO is often an
expensive and limited resource that should be used
appropriately.
Suggested Reading
Akoumianaki E, Jonkman A, Sklar MC, etal. A rational approach on
the use of extracorporeal membrane oxygenation in severe hypoxemia: advanced technology is not a panacea. Ann Intensive Care.
2021;11:107.
Mazzef MA, Rao VK, Dodd-O J, Del Rio JM, Hernandez A, Chung M,
Bardia A, Bauer RM, Meltzer JS, Satyapriya S, Rector R, Ramsay
JG, Gutsche J. Intraoperative Management of Adult Patients on
extracorporeal membrane oxygenation: an expert consensus statement from the Society of Cardiovascular Anesthesiologists-Part I,
technical aspects of extracorporeal membrane oxygenation. Anesth
Analg. 2021;133(6):1459–77.
Mazzef MA, Rao VK, Dodd-O J, Del Rio JM, Hernandez A, Chung M,
Bardia A, Bauer RM, Meltzer JS, Satyapriya S, Rector R, Ramsay
JG, Gutsche J. Intraoperative Management of Adult Patients on
extracorporeal membrane oxygenation: an expert consensus statement from the Society of Cardiovascular Anesthesiologists-Part II,
Intraoperative Management and Troubleshooting. Anesth Analg.
2021;133(6):1478–93.
Rao P, Khalpey Z, Smith R, Burkhoff D, Kociol RD.Venoarterial extra-
corporeal membrane oxygenation for cardiogenic shock and cardiac
arrest. Circ Heart Fail. 2018;11(9):e004905.
Sidebotham D.Troubleshooting adult ECMO.J Extra Corpor Technol.
2011;43(1):P27–32.
Squiers JJ, Lima B, DiMaio JM.Contemporary extracorporeal mem-
brane oxygenation therapy in adults: fundamental principles and
systematic review of the evidence. J Thorac Cardiovasc Surg.
2016;152(1):20–32.
Wang C, Zhang L, Qin T, et al. Extracorporeal membrane oxygen-
ation in trauma patients: a systematic review. World J Emerg Surg.
2020;15:51.
Zonies D, Codner P, Park P, Martin ND, Lissauer M, Evans S,
Cocanour C, Brasel K. AAST critical care committee clinical consensus: ECMO, nutrition. Trauma Surg Acute Care Open.
2019;4(1):e000304.

Sepsis andSeptic Shock
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MervynMer andMartinW.Dünser
15
15.1 Introduction andDenitions
Sepsis is dened as life-threatening organ dysfunction
caused by a dysregulated host response to infection. Septic
shock is a specic subset of sepsis in which profound circulatory, cellular and metabolic abnormalities are associated
with a greater risk of mortality than sepsis alone. With mortality rates ranging from 10% to 50%, sepsis makes up one of
the major disease burdens worldwide accounting for almost
one fth of all global deaths. Notably, the highest agestandardised incidence of sepsis occurred in regions with
low socio-demographic indices, such as sub-Saharan Africa,
Oceania, South Asia, East Asia and Southeast Asia. The
short- and long-term morbidity as well as the social and economic burden caused by sepsis remain to be fully elucidated
but are likely to be substantial.
Trauma patients are one of the populations at the highest
risk of developing sepsis. Sepsis is also the most frequent
cause of delayed death following severe trauma. The incidence of post-traumatic sepsis has been estimated to be as
high as 22%, with higher rates seen in patients with greater
injury severities. Sepsis following trauma does not only
result in a signicantly increased mortality but also prolonged intensive care unit and hospital lengths of stay. Age,
premorbid conditions, injury severity, spinal and chest injury,
shock, need for blood transfusion and a low Glasgow Coma
Scale score and positive alcohol concentrations at admission
are independent risk factors for the development of posttraumatic sepsis. Of note, the risk of sepsis increases in a
M. Mer (*)
Divisions of Critical Care and Pulmonology, Department of
Medicine, Charlotte Maxeke Johannesburg Academic Hospital and
Faculty of Health Sciences, University of the Witwatersrand,
Johannesburg, South Africa
e-mail: mervyn.mer@wits.ac.za
M. W. Dünser
Department of Anesthesiology and Intensive Care Medicine,
Kepler University Hospital and Johannes Kepler University Linz,
Linz, Austria
e-mail: martin.duenser@kepleruniklinikum.at
dose- dependent manner, with the number of blood transfusions received. Patients with penetrating trauma appear to be
at a particularly high risk for sepsis as these types of injuries
are commonly associated with a high injury severity, major
blood loss, direct inoculation of bacteria into deep tissue
structures and intestinal or hollow organ perforation.
15.2 Pathogenesis ofPosttraumatic
Infection andSepsis
Infectious complications in patients sustaining penetrating
injuries follow a biphasic pattern. A small peak occurs during the rst week after trauma, with a second and larger peak
encountered during later stages of the disease course. Early
infections typically include primary bacteremia, pleural or
mediastinal infection, meningitis or secondary peritonitis
due to gastrointestinal or other hollow organ injuries.
Infections occurring after the rst week mostly follow a similar pattern to that seen in a general critically ill population.
The respiratory tract is a frequent focus of infection. Devicerelated infections (e.g. central line-associated bloodstream
infections, urinary catheter-associated infections or ventricular drain-associated ventriculitis), surgical site infections and
deep tissue abscess formations (e.g. abdominal) are other
common sources of infections during this time frame. Early
infections following penetrating trauma are often the consequence of direct inoculation of pathogens into deep tissue
structures at the time of injury or during emergency surgery
(e.g. pleural infection, meningitis, secondary peritonitis) or
result from bacterial translocation in the gastrointestinal tract
during periods of severe systemic hypoperfusion (e.g. primary bacteremia). Immunosuppression due to a compensatory anti-inammatory response to severe injury makes
trauma patients highly susceptible to hospital-acquired and
device-associated infections at later stages. Unlike in
community- acquired infections, infections in penetrating
trauma victims are mostly due to bacterial pathogens.
Particularly, during the second peak of infectious complica-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
E. Degiannis et al. (eds.), Penetrating Trauma, https://doi.org/10.1007/978-3-031-47006-6_15
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M. Mer and M. W. Dünser
tions, extensively or multidrug-resistant bacteria (e.g.
Pseudomonas spp., Acinetobacter spp., methicillin-resistant
Staphylococcus aureus) are common pathogens causing
infections. Fungal infections (e.g. Candida albicans and
non-albicans) are on the increase and typically arise during
the second week or later. Re-activations of latent viral infections (e.g. cytomegalo-, herpes or Epstein-Barr virus) are
also encountered in trauma patients, but their pathogenic role
remains unknown, and therapy is generally not
recommended.
The exact reasons why infectious complications induce a
dysregulated host response, acute organ dysfunction and
thereby sepsis in some trauma patients while not in others
remain incompletely understood. Genetic factors, injury
severity, site and timing of infection all appear to play a role.
The pathogenesis of the dysregulated host response to infection is complex and does not only involve the immune system. Figure15.1 simplies pathways currently believed to be
involved in the dysregulated host response to infection and
which nally result in acute organ dysfunction and sepsis.
An interesting recent observation is that organ dysfunction in
sepsis appears to occur in four distinct clusters (i.e. shock
with acute kidney injury, minimal multi-organ dysfunction,
shock with acute lung injury and altered mental state, and
hepatic disease and thrombocytopenia). These clusters may
reect underlying pathophysiological differences and could
potentially dictate different therapeutic approaches in the
future. In addition to acute organ dysfunctions in patients
with sepsis, other body functions such as the endocrine and
metabolic systems are also compromised.
15.3 Diagnosis andInvestigations
In line with the denition of sepsis, the diagnosis of posttraumatic sepsis relies on recognition of both the underlying
infection and acute organ dysfunction.
15.3.1 Diagnosis oftheUnderlying Infection
Clinical signs are usually the rst to draw the physician’s
attention to the potential presence of a post-traumatic infection. While fever is a highly non-specic indicator of infec-
Fig. 15.1 Simplied pathogenetic pathway from infection to sepsis. ARDS acute respiratory distress syndrome, CNS central nervous system, GFR
glomerular ltration rate, LOC level of consciousness, PAMP pathogen-associated molecular pattern. Icons by Flaticom.com
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