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13 • Selective Aortic Arch Perfusion 155
Lactate levels at end of post-surgery observation period
HBOC-201FWB + Ca
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Large IVC clots
25
20
15
10
Contained pelvic hematoma
5
0
Fig. 13.8 Final lactate levels showing similar recovery for selective aortic arch perfusion with fresh whole blood (FWB) plus calcium versus hemoglobin-
based oxygen carrier -201 (HBOC-201) at 5 hours after resuscitation from hemorrhage-induced traumatic cardiac arrest in a porcine model. DCS, Damage
control surgery; IVC, inferior vena cava.
Died before 4 hours
Poor / worsening
Fair - Good / Improving
Excellent recovery
2+
Two failed Defib
Post-DCS bleed/
Improving after
control
Post-DCS bleed
Fig. 13.9 Illustration of selective aortic arch perfusion (SAAP) in peri-
cardial tamponade.
intravenous uid and blood resuscitation catch-up with
hemorrhage-induced intravascular volume loss. REBOA
is most effective when deployed while the heart is still beating
well and there is a discernible arterial blood pressure. When
patients become bradycardic and lose measurable blood pressure, this is a state of impending cardiac arrest. REBOA can
be effective at this point but only if the heart continues to
beat and intravenous blood transfusion rapidly corrects the
volume and perfusion decit. Traditionally, this is the point
at which resuscitative thoracotomy is either performed, or at
least considered, before cessation of resuscitation efforts.
Fig. 13.10 Hemodynamic response to selective aortic arch perfusion
(SAAP) in a porcine model of hemorrhage-induced traumatic cardiac
arrest with an associated 200 mL pericardial tamponade. SAAP infu-
sion results in return of electrocardiographic activity and spontaneous
cardiac contractility with measurable arterial pressure while the peri-
cardial tamponade remains. The central aortic pressure progressively
increases with removal of the pericardial tamponade blood in 50 mL
increments. Right atrial pressure drops with relief of the pericardial
tamponade. FWB, Fresh whole blood.
SAAP offers extracorporeal perfusion to aortic balloon
occlusion hemorrhage control in the setting of true cardiac
arrest due to hemorrhage or impending cardiac arrest with
rapidly dropping heart rate and extremely low, nonviable blood
pressure. The combination of thoracic aortic balloon occlusion
156 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
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(functional aortic cross-clamp), extracorporeal perfusion with
exogenous oxygen carrier (more effective than manual cardiac
compression), and rapid intravascular volume replacement
(equivalent to or better than intravenous infusion) provided
for by the SAAP technique can serve to promote ROSC without the need for a thoracotomy and bridge survival until the
patient can be transferred to the operating theater for denitive
hemorrhage control. Therefore, in the setting of hemorrhageinduced cardiac arrest, SAAP is an intervention between
REBOA and resuscitative thoracotomy that can potentially
achieve ROSC and obviate the need for thoracotomy.
In medical cardiac arrest, the potential role of SAAP lies
between standard resuscitation therapies of the present
day, the foundation of which is closed-chest CPR, and the
implementation of VA-ECLS during cardiac arrest or ECPR.
A proportion of medical cardiac arrest victims can be resuscitated with closed-chest CPR and debrillation, if bystander
CPR is initiated without delay and an automated debrillator is nearby and used appropriately. However, these two
conditions are infrequently met. Delays in CPR and debrillation lead to decreased effectiveness of CPR and degraded
electrical energy, respectively, that result in preventable
deaths just as uncontrolled hemorrhage with severe hypoperfusion does in trauma. VA-ECLS/ECPR provides extracorporeal perfusion that can effectively reverse the ischemic
debt that occurs during cardiac arrest and lead to ROSC and
long-term survival. Clinical reports are very promising with
remarkably high survival with good neurological recovery
in the patients that meet criteria for ECPR.
An important aspect of VA-ECLS is that once a patient
has been cannulated during cardiac arrest for ECPR and
had achieved ROSC, the patient remains on VA-ECLS. The
duration of VA-ECLS support after ROSC is typically several
days. In general, VA-ECLS is not an intervention that can be
quickly discontinued. It usually requires surgical decannulation and vascular repair in an operating theater. Although
some resuscitated patients need ongoing perfusion support
post-ROSC, some do not. This issue is faced when trying
to determine the appropriate criteria for committing the
resources required to perform VA-ECLS/ECPR. In some systems, standard therapy is continued for 20 minutes before
the patient is considered for VA-ECLS/ECPR in an effort to
avoid overutilization. There is a tension between waiting too
long to initiate VA-ECLS/ECPR and overutilization without
any clear parameters to distinguish the appropriate choice.
Temporary heart and brain perfusion during cardiac
arrest may be adequate to achieve ROSC and promote longterm survival without the need for prolonged ECLS support.
This is the niche that SAAP is designed to ll. The sequence
of SAAP interventions previously described could be initiated early in resuscitation after initial CPR and debrillation
have failed without committing to prolonged ECLS support.
If ROSC is achieved and the patient is hemodynamically stable post-ROSC, SAAP can be withdrawn rapidly. However,
if the patient’s condition shows a need for ongoing ECLS
support, SAAP interventions can be used to provide bridging support until cannulation for VA-ECLS can be accomplished. Thus, SAAP in medical cardiac arrest may promote
ROSC and favorable neurological recovery without committing patients to extended ECLS support post-ROSC. However,
if ongoing ECLS support is needed, SAAP serves as a bridge
to ECMO. Therefore, in the setting of medical cardiac arrest,
SAAP is an intervention between closed-chest CPR and
VA-ECLS that can potentially achieve ROSC and prevent
unnecessary prolonged ECLS support.
Implications for Trauma and
Vascular Surgery
The emergence of endovascular resuscitation in both medical cardiac arrest and severe hemorrhagic shock will lead
to many more emergency vascular access procedures being
performed under time pressure in suboptimal conditions.
This reality can be expected to result in a growing number
of vascular access–related and endovascular resuscitation
intervention–related complications that will require the
expertise and care of vascular surgeons. It is unrealistic to
think that these time-critical endovascular resuscitation procedures will be performed by vascular surgeons. Indeed, the
vast majority will not be performed by vascular surgeons and
it is likely that many of these procedures will be performed by
non-surgeons. For example, prehospital ECMO cannulations
in Paris for ECPR and prehospital REBOA catheterizations in
London for uncontrolled hemorrhage are performed by prehospital emergency physicians. In the United States, emergency department cannulations for ECPR are performed by
emergency physicians in some hospitals.
The positive approach to the emerging endovascular
resuscitation era is to foster collaboration between resuscitation physicians who will be performing these interventions
and vascular surgeons who may be involved in training and
will likely manage complications. The active involvement of
vascular surgeons in vascular access training, procedure
protocols, and case reviews will serve to improve care and
limit vascular complications for these endovascular resuscitation interventions. It should be kept in mind that these
interventions are an effort to save the lives of patients who
presently almost invariably die. Success in this arena will be
a major advance in resuscitation medicine, one that may
impact us personally someday.
Summary
SAAP has been developed over three decades of large animal
laboratory research as an advanced endovascular resuscitation technique aimed at transforming the survivability
of both medical cardiac arrest and hemorrhage-induced
cardiac arrest. SAAP is presently being advanced toward
clinical trials and implementation. During the development of SAAP, endovascular resuscitation technology has
signicantly advanced, which has both helped to understand the need for this innovation and made it important
to dene how SAAP segues with other interventions. The
use of escalating SAAP modalities complements REBOA,
VA-ECLS/ECPR, and EPR by providing a logical step-wise
approach that assists with clinical decision-making while
reducing the potential risks to the patient of endovascular
intervention by only delivering the least invasive intervention required for survival in a timely fashion.
13 • Selective Aortic Arch Perfusion 157
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14
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Endovascular to Extracorporeal
Organ Support for Vascular
Trauma and Shock
KEVIN K. CHUNG, ANDRIY I. BATCHINSKY, and IAN J. STEWART
Introduction
Mechanical trauma to major arteries often leads to signicant vascular compromise to large tissue beds which then
results in the reduction in oxygen delivery, cellular dysoxia,
and cell death. This occurs in varying degrees, depending
on the robustness of collateral blood ow to every anatomic
region and organ in the body (e.g., muscle, kidney, lungs,
liver, intestines, etc.). Regardless, it has been well documented that the degree and extent of tissue injury directly
correlates with the duration of the ischemic insult.
arterial vessels are repaired and blood ow is restored via
a variety of open and endovascular techniques described
in chapters throughout this textbook, varying degrees of
metabolic and end-organ consequences can be expected
and are widely characterized as “ischemia-reperfusion”
4,5
injury.
results in profound metabolic and inammatory derangements secondary to the release and circulation of cellular
contents. This often is compounded by concomitant direct
tissue injury, such as blunt force injury or crush, which
can augment the metabolic derangement several fold. Globally, the dysregulated immune-inammatory cascade that
ensues can trigger a distributive shock characterized by
capillary leak, hemodynamic instability, coagulopathy, and
end-organ failure (Fig. 14.1). Recent disruptive advances
in the eld of vascular surgery in the form of endovascular
occlusion techniques for hemorrhage control and a variety
of endovascular repair options have pushed the physiological limits of what is humanly possible to sustain life after
severe injury. As such, an increasing number of severely
injured patients are surviving longer into the hospitalization and are more metabolically deranged than ever with
varying degrees of end-organ injury.6 Fortunately, the eld
of critical care has experienced an equally formidable leap
in medical innovation in the form of various extracorporeal
organ support technologies.6 This chapter will review the
latest advances and techniques to assist vascular trauma
specialists in the management of metabolic derangements
and organ failure, with a focus on renal and lung support.
Reperfusion of damaged skeletal muscle often
1–3
As
Advances in Renal Support
Over the last three decades, major advancements have
been made in renal replacement therapy (RRT). The early
1990s saw the rst generation of continuous RRT (CRRT)
devices.7 These machines were based on technology from
chronic dialysis, but were a major advance from prior CRRT
therapies that relied on an assortment of pumps and dialyzers that were not an integrated unit.7 This was followed by
machines designed for the care of critically ill patients with
acute kidney injury (AKI), such as the PRISMAFLEX (Baxter International, Deereld, IL), and the NxStage System
One (NxStage Medical Inc., Lawrence, MA). These devices
were relatively simple to set-up and maintain, leading to
widespread adoption of the technology. Another major
advancement was the clarication of the proper “dose” of
RRT in the setting of AKI in two, large randomized controlled trials (RCTs) involving a mixed critically ill popula-
8,9
tion.
Based on these data, the Kidney Disease: Improving
Global Outcomes (KDIGO) guidelines recommends a minimum dose of 20 to 25 mL/kg per hour with CRRT therapy.
There are three major modalities of RRT used to treat
patients with AKI: intermittent hemodialysis (IHD), CRRT,
and slow low-efciency dialysis (SLED). Prior to discussing
the nuances between the modes of RRT, an explanation of
how clearance is achieved is important. The rst method by
which the blood is cleared is by diffusion, or hemodialysis.11
With diffusion, the blood and dialysate are separated in a
hollow ber dialyzer by a semipermeable membrane. The
difference in concentration of a particular solute between
the two compartments drives clearance and manages metabolic disturbances. For example, patients with ischemiareperfusion injury often have hyperkalemia and metabolic
acidosis. Compared to the blood, the dialysate is low in
potassium. Therefore, potassium goes down its concentration gradient from the blood into the dialysate and is thus
cleared from the body. Conversely, the dialysate has a relatively high concentration of bicarbonate compared to the
blood. This results in a net transfer from the dialysate to the
blood, which improves acid-base status. The second method
of clearance in RRT is convection, or hemoltration.11 With
this method of clearance, there is no dialysate. Instead,
the semipermeable membrane is used only to remove uid
and electrolytes from the blood. Separately, a replacement
uid is infused into the blood line. Similar to dialysate, the
replacement uid is low in concentration of things that need
to be removed (e.g., potassium) and high in concentration
of things that need to be added (e.g., bicarbonate).
The rst type of RRT used to treat patients with AKI is IHD
which primarily uses hemodialysis or diffusive clearance.
This method utilizes machines that are designed for use in
patients with end-stage renal disease and are on chronic
10
158
14 • Endovascular to Extracorporeal Organ Support for Vascular Trauma and Shock 159
n
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Inammatory
insult
↑ Oxidative stress
↓ Myocardial perfusion
Lung
Inammatory
insult
Myocardial infarction
↑ Oxidative stress
↓ O
transport
2
Hypoxia
Pulmonary HTN
↑
A-a gradient
Edema
ARDS
Kidney
Inammatory
insult
↑
Oxidation abcess
Direct dissect damage
↑ Endothelial dysfunctio
Imperial GFR
Kidney failure
Continued
ischemia
Reperfusion
↓ SVR
Distributive shock
End organ failure
or organ support technologies
Ischemia
↑ IL-6
↑ IL-8
↑ TNF-α
↑
CK
↑ LDH
Fig. 14.1 Anatomic schematic representing the cascade of events that occurs during an ischemia reperfusion insult. Ischemia results in cellular dysoxia
which leads to cell death and the local release of intracellular enzymes, inflammatory cytokines, and chemokines into the local tissue. Upon reperfusion
of the tissue bed, the compilation of the enzymes is released into the systemic circulation resulting in direct and indirect inflammatory injuries to various organs including the kidneys, heart, lungs, liver, and gastrointestinal tract. This ultimately leads to end-organ failure that can occur in isolation or
in combination.
lactate dehydrogenase;
RRT. With IHD, dialysate is made using concentrated electrolyte solutions and tap water that has been thoroughly
processed and puried.12 The second type of RRT is
CRRT, which can be subdivided into continuous venovenous hemoltration (CVVH), continuous veno-venous
hemodialysis (CVVHD), and continuous veno-venous
hemodialtration (CVVHDF).13 These techniques utilize
devices that were designed to be used in critically ill patients
with AKI. The primary difference between the modes of
CRRT is the method of clearance that is employed. CVVH uses
replacement uid for convective clearance (hemoltration),
whereas CVVHD uses dialysate for diffusive clearance
(hemodialysis). CVVHDF is a combination therapy that uses
both convective and diffusive clearance (hemodialtration).
CVVH, CVVHD, and CVVHDF are all dosed relative to the
patient’s body weight, and prescribed in mL/kg per hour. As
noted previously, the recommended minimum dose is 20
ARDS
, Acute respiratory distress syndrome; CK, creatine kinase;
SVR
, systemic vascular resistance;
TNF-
α, tumor necrosis factor-α.
GFR
, glomerular filtration rate;
HTN
, hypertension; IL, interleukin;
to 25 mL/kg per hour.14 For example, the proper dose for a
70-kg patient would be 1400 to 1750 mL/hour of replacement uid (if using CVVH), dialysate (if using CVVHD), or
a combination of the two (if using CVVHDF). The primary
difference between CRRT and IHD is time and clearance.
IHD typically lasts 3 to 4 hours, requiring a large amount of
clearance over that time period to meet the patient’s metabolic demand. Conversely, CRRT runs continuously, allowing time for much slower clearance. In contrast to IHD,
which generates dialysis using tap water and concentrated
electrolyte solutions, CRRT therapies utilize prepackaged
sterile solutions for dialysate or replacement uid.
The third type of RRT used to treat AKI is SLED.
SLED is also sometimes referred to in the literature as prolonged intermittent RRT or extended daily dialysis. SLED
uses standard IHD machines, but operates at lower blood
and dialysate ow rates. Whereas a typical IHD session has
LDH
15,16
,
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blood and dialysate ow rates of 200 to 400 and 400 to
700 mL/min, respectively, SLED treatments have dialysate
and blood ows of 100 to 200 mL/min. Although most SLED
treatments last 8 hours, sessions lasting 24 hours have been
described.17 The major advantage of SLED is that because
it leverages traditional IHD, it is relatively easy to institute
in hospitals that do not have sufcient patient volume for
formal CRRT programs. However, there are some concerns
regarding SLED when compared to CRRT and IHD. The rst
is electrolyte disturbances, particularly hypophosphatemia,
which can make it difcult to wean patients from mechanical ventilation.18 The second is that the optimal dosing of
antibiotics is unclear, especially when SLED treatments are
longer than 8 hours.
19
There are two theoretical benets to CRRT over IHD in
hemodynamically unstable patients. The rst is the slower
rate of volume removal. As noted previously, an IHD session typically lasts 3 to 4 hours. Over this relatively short
period of time, the entire amount of uid prescribed to be
removed that day must be taken off the patient. As CRRT
can remove the required volume over a 24-hour period,
the rate at which volume is removed is lower. For example,
if 3 L must be removed, the hourly rate would be 750 mL
with a 4-hour IHD treatment. With a 24-hour CRRT treatment, the hourly rate would be much lower at 125 mL. This
reduced hourly rate is postulated to improve hemodynamic
stability. A second theoretical benet to CRRT over IHD in
hemodynamically unstable patients is the slower rate of
clearance. The high clearances of IHD result in a decrease
of plasma osmolality.20 When this occurs, an osmotic gradient is established between the intravascular space and
the extra vascular space, drawing water into the extravascular compartment. This reduces blood volume and may
adversely impact hemodynamics. Another situation where
the slow clearance of CRRT can be advantageous is for
patients with traumatic brain injury (TBI). In patients with
TBI, the osmotic shifts involved with the greater clearance
of solute with IHD can result in increased intracranial
pressure and cerebral edema.21 Although solute is removed
quickly from the intravascular space with IHD, there is
a lag before it can re-equilibrate across the blood-brain
barrier, resulting in the intracranial compartment having
a higher osmolarity than the vascular compartment. This
concen tration gradient results in the transfer of water to
the intracranial compartment via osmosis.22 The slower
clearances provided by CRRT minimize this gradient and
may decrease cerebral edema.
23
Despite these theoretical benets, the results from observational and clinical trials have been mixed. A recent
metaanalysis of 21 studies (16 comparing CRRT with IHD
and 5 comparing CRRT with SLED) did not demonstrate
a difference between the modalities in terms of mortality,
dialysis dependence, or length of hospital and intensive care
unit (ICU) stays.24 In contrast, a previous metaanalysis of
23 studies found that IHD was associated with higher rates
of dialysis dependence than CRRT.25 These results were
largely driven by the results from the 16 observational studies. The seven RCTs did not demonstrate a signicant benet to CRRT. However, the total number of patients in the
RCTs was small (N = 240 for IHD and N = 232 for CRRT).
Despite this paucity of evidence, current opinion in the eld
is that CRRT is the preferred modality for hemodynamically
unstable patients, whereas IHD is the preferred modality for
hemodynamically stable patients.
10
The timing of RRT is controversial in the nephrology
and critical care elds. Early observational evidence was
mixed due primarily to different denitions of “early.” One
study did not nd a difference on timing of RRT when
early was dened by blood urea nitrogen concentration,
but found that when RRT was started within 2 days of ICU
admission there was an association with lower mortality
compared with patients who started RRT after ICU day 5.26
Similar ndings were observed in another retrospective
cohort, in which a lower risk of mortality was present
when RRT was initiated within 24 hours of the diagnosis
of severe AKI.27 This study found that early RRT was associated with decreased days on mechanical ventilation and
less time on RRT.
27
Recently, three RCTs have examined the optimal timing
of RRT. The rst of these was the Articial Kidney Initiation
in Kidney Injury (AKIKI) trial.28 The AKIKI trial randomized 620 subjects with severe AKI to early (within 6 hours)
or late (when the subject developed metabolic disturbances,
pulmonary edema, or oliguria) RRT. There was no difference in the primary end point of 60-day mortality. The
second study was the Effect of Early vs Delayed Initiation
of Renal Replacement Therapy on Mortality in Critically
Ill Patients with Acute Kidney Injury (ELAIN) trial.29 The
ELAIN trial was a single center study of 231 patients with
moderate AKI and an elevated plasma neutrophil gelatinase-associated lipocalin (a biomarker for AKI). Early was
dened as initiating RRT within 8 hours of moderate AKI
and late as initiating RRT within 12 hours of severe AKI. In
contrast to the AKIKI study, ELAIN found a decrease in mortality when RRT was initiated early. The third study was the
Initiation of Dialysis Early Versus Delayed in the Intensive
Care Unit (IDEAL-ICU).30 This multicenter trial randomized
488 patients with severe AKI to an early strategy (within
12 hours) or a late strategy (after a delay of 48 hours if
the patient did not recover renal function). Similar to the
AKIKI study, the IDEAL-ICU trial did not nd a difference in
mortality between the two arms. Although there is another
large multicenter trial ongoing,
31,32
the preponderance of
evidence currently points against the generalizability of
an early approach. However, it is important to note that
the only trial to show a benet (ELAIN) started RRT much
earlier than either the AKIKI study or the IDEAL-ICU study.
Furthermore, ELAIN involved mostly surgical patients and
included a novel biomarker to risk-stratify patients. It is
therefore possible that some patients could benet from an
early initiation strategy, especially when a biomarker is used
to stratify patients.
A variety of other extracorporeal treatment techniques
have been examined in an effort to improve mortality in
critically injured and ill patients with AKI. One of these
is high-volume hemoltration (HVHF). There is some evidence from small studies that HVHF improves surrogate
outcomes. For example, HVHF has been demonstrated
to decrease vasopressor dependency index and multiple
organ dysfunction syndrome score in critically ill patients
with burn injury.33 In the largest RCT done to date in 140
critically ill patients, no difference was observed in 28-day
mortality or hemodynamic proles.14 What is clear is
that this technique is relatively well-tolerated. Thus, in
14 • Endovascular to Extracorporeal Organ Support for Vascular Trauma and Shock 161
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select patients with profound metabolic derangements
being treated with CVVH, increasing the dose of therapy
to achieve metabolic control seems reasonable and should
be requested.
Since the early 2000s, CRRT has gained widespread
acceptance and has saved countless lives. Despite these
advances, the mortality rate of injured patients with AKI
requiring RRT is high at 40% to 67%.
34–36
Early initiation or
HVHF may have benet in postsurgical patients with profound metabolic derangements. However, the effect sizes
are likely to be small and these are difcult to generalize.
RRT will always have a role in the management of electrolyte disturbances and volume overload; however, future
advances in patient care will need to couple it with support
to other organs (such as extracorporeal membrane oxygenation [ECMO]) and other forms of blood purication targeted at immune-modulation and pathogen removal.
Advances in Lung Support
Acute lung injury and acute respiratory distress syndrome
(ARDS) are well-recognized problems following vascular
trauma and shock. In the United States, 200,000 patients
develop ARDS each year and it is anticipated that, by
2025, 300,000 cases will be seen per year.37 The causes of
ARDS are varied and classically include pneumonia, sepsis,
inhalation injury, thermal injury, chemical exposure, and
iatrogenesis in the form of overzealous mechanical ventilation and over exuberant uid resuscitation.
trauma, particularly, military unique trauma such as
vascular trauma with shock, burns, blast injury,40 chemical
weapons,41 and the medical care rendered to treat these
injuries
42,43
also are common causes of ARDS. Although the
precise molecular mechanism that initiates ARDS remains
enigmatic, the shared phenomenon of intense inammation
among these causes of ARDS is compelling. For this reason
it is not surprising that ischemia-reperfusion injuries also
produce ARDS. Unfortunately, despite decades of research
and numerous clinical trials, the reported mortality for
ARDS remains high, ranging from 11% to 44%.
At present, mechanical ventilation is the standard supportive intervention for ARDS and is highly effective in
most patients with mild ARDS. However, as the severity of
injury increases, lung function decreases. This is evidenced
clinically by impairment of oxygenation, ventilation, and
reductions in lung compliance. These changes often prompt
increases in ventilator pressures and/or volumes which, in
turn, place the patient at risk for ventilator-induced lung
injury (VILI).45 Also referred to as barotrauma or volutrauma, this mechanical insult is the result of increased
ventilator volumes and pressures delivered to a poorly compliant lung. This overstretching of the lung parenchyma
provokes activation of the inammatory cascade and leads
to multisystem organ failure.
46–48
Typically, early treatment of ARDS is focused on preventing VILI and was the focus of the landmark ARDSNet trial.
ARDSNet demonstrated that reduction in ventilator settings to a VT of 6 mL/kg of ideal body weight (IBW) and a
maximum end-inspiratory plateau pressure (P
H2O was able to decrease mortality to 31%, compared
with 39.8% in the conventional arm treated with a VT of
38,39
Similarly,
37,44
) of 30 cm
plat
12 mL/kg IBW.49 This strategy, known as lung-protective
ventilation, has become an important tool for treating ARDS,
but it has not been a panacea. Studies have shown that
despite using the ARDSNet strategy, lung hyperination,
and thus VILI, still occur in approximately 30% of patients.50
Furthermore, for patients in whom a lung-protective strategy is implemented, second-order consequences such as
hypoventilation, hypercarbia, and acidosis often complicate
management. This is particularly challenging in severely
injured trauma patients, acute or chronic renal failure, concomitant brain injury, and in those with severe cardiovascular or peripheral vascular disease.
51
Extracorporeal life support (ECLS) for adult lung failure
has become an increasingly valuable tool for the clinical
management of ARDS. In a practical sense, the role of ECMO
off-loads the lungs and spares pulmonary parenchyma from
exposure to VILI. As they apply to treatment of lung failure
and ARDS, the terms ECMO and ECLS are interchangeable.
Currently, ECMO is used to extend survival by providing for
both oxygenation and carbon dioxide clearance in critically
ill patients who have failed to improve on less invasive techniques such as ARDSNet strategies. Ultimately, the goal of
ECMO is to provide adequate time for the underlying clinical
condition to be resolved and, consequently, allow the ARDSinciting inammatory insult to abate.
Functionally, ECMO is a miniaturized form of cardiopulmonary bypass. Although there are multiple modes of
ECMO, all modes require cannulation of major vascular
structures, by either open or percutaneous means. Large
23- to 32-Fr catheters drain circulating blood into an
extracorporeal circuit and an articial membrane lung
which carries out gas exchange (delivers O2 and removes
CO2). Following gas exchange, oxygenated blood is returned
to the body via a return circuit. The most common modes
of ECMO are venovenous (VV) ECLS and venoarterial
(VA) ECLS. Although both techniques rely on the use of
an exchange membrane, VV ECLS returns the oxygenated
blood to the venous circulation, whereas VA ECLS returns
oxygenated blood to the arterial circulation.
52,53
The majority of ECMO circuits augment ow with a centrifugal pump
and heat the returning blood with an integral heating element.
Use of ECMO was shown to be benecial in adult trauma
victims as early as 197254 but subsequently received negative publicity after clinical trials from 1980 to 1990 showed
poor outcomes.
55,56
Criticisms of the early ECLS stem largely
from an inadequate appreciation of interactions between
the mechanical ventilation and ECLS, and an inadequate
reduction of mechanical ventilation settings which contributed to iatrogenic VILI that likely increased mortality. Furthermore, modern ECMO circuits avoid the use of
silicone-based membrane lungs and long, cumbersome
circuits made of biologically unfriendly polymers. These
technological differences led to unsustainable management
challenges such as transfusion of 1 to 2 L of blood and blood
products per patient per day in the early clinical studies.57
Whereas the blood losses alone could explain the adverse
outcomes observed in the early studies, ECMO patients were
also subjected to iatrogenic VILI and exposed to a high risk
of transfusion-related lung injury (TRALI).
42,58
Today these
complications are largely avoided with modern circuits. In
fact, today’s ECLS systems bear little physical resemblance
162 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
3000
16000
Annual runs
Cumulative runs
Annual runs Cumulative runs
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to their nascent predecessors (Fig. 14.2) and are clinically
separated by generations of technological advancement.
Lastly, access-related bleeding complications and subsequent transfusion-related coagulopathies in up to 70% of
patients led to a staggering rate of cerebral hemorrhage as
a cause of death.
55,56
For a combination of these reasons,
ECLS before the year 2000 (and in some centers still to date)
was often started too late and in patients who were older
and sicker, making them unlikely to benet from therapy.
Although early ECMO trials raised concerns of its efcacy
prior to the 2000s, more recent trials have supported the
lifesaving capabilities of modern ECLS centers. Two prominent trials have since evaluated ECMO for lung support. The
CESAR trial (conventional ventilatory support vs. extracorporeal membrane oxygenation for severe adult respiratory
failure)58 and the H1N1 trial.59 The H1N1 study was especially important for the renaissance of ECLS, as providers
were eager to initiate ECLS early when encountering fulminant ARDS due to the H1N1 virus in otherwise healthy
patients. Advancements in technology and increased user
experience have produced laudable improvements in outcomes for severely injured patients treated with ECLS.
52,58,59
Data from the ELSO registry shows that the number of
ECMO cases performed annually is increasing (Fig. 14.3).59
At the same time reported survival has increased to 70%
to 80% in patients with severe ARDS in whom mechanical
ventilation was no longer effective.59 These improvements,
interestingly, have occurred despite a continued bias favoring last-resort ECMO and are a direct reection of using better technology.
In trauma-induced ARDS, which is more analogous to
vascular patients who have sustained shock and ischemiareperfusion, similar improvements in outcomes have been
reported.
60,61
In a review of ECLS for cardiopulmonary failure in trauma from 1994 to 2015, survival to discharge
ranged from 50% to 79%.62 These improvements in survival have not gone unnoticed by those caring for the most
severely ill and injured in whom multisystem organ failure is
highly morbid and mortal. Evidence suggests combination
therapy with renal support may continue trends toward
Fig. 14.2 Representative images of early extracorporeal life support (ECLS) technology.
middle panel
and ECLS tools.
points to the smallest pediatric membrane lung in the modern modular NovaLung (Xenios/Fresenius) system which has a 0.19-L priming volume. (Left
panel, Picture adopted from the manuscript describing the first trauma patient treated using ECLS by Hill et al.,
Picture courtesy Luciano Gattinoni and Antonio Pesenti, Milan University, Italy.)
, a typical ECLS system from the 1990s is depicted.
Arrow
on the left points to the membrane lung used in the Hill study in 1972 which had a 30-L priming volume;
2500
2000
1500
1000
500
0
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
Right panel
2000
2001
1998
1999
depicts the modern modular Xenios/Fresenius family of membrane lungs
2003
2002
2004
2005
Left panel
2007
2006
2008
shows first trauma patient treated using ECLS. In the
arrow
on the right panel
ASAIO
. 1972;18(0):546–552. Middle panel,
14000
12000
10000
8000
6000
4000
2000
2009
2010
2011
2012
2013
2014
2015
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2017
0
Fig. 14.3 Sharp increase in extracorporeal life support cases for respiratory failure since the CESAR and H1N1 studies in 2006–2011. (Figure courtesy
Extracorporeal Life Support Organization [ELSO].)
14 • Endovascular to Extracorporeal Organ Support for Vascular Trauma and Shock 163
https://t.me/medicina_free
Fig. 14.4 Xenios-AG console and hot-swappable membranes of
neonatal, pediatric, and adult sizes. Circle denotes MiniLung. (Image
courtesy Xenios AG.)
improved survival.
6,63
However, in chronically ill patients
with vascular disease, tempered hopes may be warranted.
Evidence from combat casualties shows an improved probability of benet from ECMO relative to their civilian counterparts; a nding that is most likely attributable to their
relative youth, normal baseline physiology, and minimal
preexisting medical comorbidities.
64
Modern ECLS is also less invasive and more efcient in
gas exchange than devices even one generation older. Percutaneous vascular access using 13- to 19-Fr catheters
has become the preferred method of cannulation in specialized ECLS centers and has broadened the appeal of
ECMO initiation to nonsurgeon physicians.
58,65
Enhancements in efciency are owed to new highly exchangepermeable polymethylpentene (PMP)-based membrane
lungs that more closely mimic the abilities of native lung.
In the 2010s, the latest-generation mini-ECLS devices
have been developed, based on reengineering of old technology (Fig. 14.4). Although the functional principles
are identical to ECMO, the logistical burden, safety, and
efciency of the new-generation mini-ECLS devices are
in a class of their own.
53,66–68
These simplied devices are
comparable to existing bedside dialysis in both usability
and invasiveness.
Simplication of the machinery has lowered the bar to
early ECLS and expanded the settings where cannulation
and initiation of ECMO is acceptable. More facile cannulation, portable mini-ECMO devices, lower access-related
morbidity, and improved membrane lung efciency has led
to availability, though admittedly not widespread, of ECLS
in emergency departments, ICUs, and even in select prehospital and medical transport settings across the nation. In
turn, the potential patient population who may benet from
ECLS is increased and, consequently, the number of patients
exposed to VILI-producing ventilator settings is reduced.
66,69
In fact, there is potential to avoid intubation altogether for
select patients suffering exacerbations of CO2 retention.
Currently, at the cutting edge of ECLS technology are
recently developed devices capable of partial ventilatory
lung support. These devices provide extracorporeal CO2
removal (ECCO2R), function at dialysis-like low blood ows
(350–500 mL/min), and now have CE approval for use in
Europe.
68,69,71,72
To date, however, there are no ECCO2R
devices approved by the US Food and Drug Administration
(FDA). ECCO2R is to be distinguished from full ECMO, which
utilizes 23- to 32-Fr catheters and blood ows in the 2- to
7-L/min range. The primary role of the ECCO2R system is to
remove CO2, which is why it is particularly suited for reduction in mechanical ventilator settings during ARDS. To date,
studies have shown that ECCO2R can be performed safely
and effectively enabling low-tidal-volume ventilation, while
preventing deleterious shifts in pH and PaCO2.
53,67
is also effective in reducing pulmonary artery pressure and
reduces the work of the right heart in ARDS.73 ECCO2R is an
effective way to control hypoventilation, hypercarbia, and
acidosis, the main sequelae of the lung-protective ventilation in ARDS patients.66 ECCO2R has been used as a means
to minimize, replace, and avoid the use of mechanical venti-
69,70,74
lation.
This new approach is important for mitigation
of VILI as an increase in peak inspiratory pressure or in
driving pressure (ΔP), even in patients receiving lungprotective ventilation. Conversely, unloading the lung by
reducing mechanical ventilator settings and decreasing
ΔP is associated with survival in ARDS.
75,76
Batchinsky
et al. demonstrated the ability to reduce ventilator settings in
healthy animals, an approach that is behind the “respiratory
dialysis” concept for modern ECCO2R devices.
69,77
An example of this approach is the study by Terragni
et al., who achieved control of ventilatory pressures, hypercarbia, and pH in patients with mixed causes of ARDS.66
These authors studied two groups: (1) patients treated using
ARDSNet ventilation alone, and (2) patients receiving both
low-tidal-volume ventilation and ECCO2R as an adjunct.
In group 2, Terragni et al. minimized ventilator settings
using reductions of VT down to circa 4.2 mL/kg (below
the ARDSNet-recommended 6 mL/kg). This resulted in an
increase in PaCO2 and a concomitant decrease in pH in these
patients, but permitted plateau pressures under 25 cm H2O,
compared to 28 to 30 cm H2O in patients in group 1. Upon
initiation of ECCO2R, the PaCO2 and pH were normalized,
and patients had a lower level of circulating inammatory
mediators.66 The Terragni study substantiates the concept
that ECCO2R can be effectively used as adjunct to mechanical
ventilation in humans with ARDS. Together with work from
translational research laboratories, this lung protective
strategy at dialysis-like invasiveness will be a promising new
therapy in hospitals around the world.
69,74,78–80
Combining Techniques
As in many other critically ill or injured populations, the
support of patients having sustained major vascular trauma
continues to evolve. Extracorporeal organ support is rapidly
culminating in an ability to support multiple failing organ
systems at the same time.6 The ultimate goal of multiorgan support therapy would be to link all of these therapies
70
ECCO2R
164 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
(RRT, blood purication, as well as lung and cardiovascular
support) into one multifaceted intervention and delivery
platform. Of note, the device used in the Terragni study
combined a unique approach to multiorgan failure mitigation in that it combined an ECCO2R and dialysis membranes
in a single set up.66 This is fortuitous and likely more externally valid among vascular patients whose complex pathophysiology often results in multiorgan failure which will
most benet from a multiorgan support strategy. Combining extracorporeal modalities in the management of multiple organ failure is not new. RRT is already often combined
with ECMO and recent reports have demonstrated that
therapeutic plasma exchange and molecular adsorbent
recirculating system may be helpful for acute liver support
(i.e., a form of “liver dialysis”).
81,82
The concept of a multiorgan
extracorporeal support platform is within reach and further
advances in these technologies will push the physiologic
limits of what is possible in efforts to save the lives of severely
ill and injured patients.
Acknowledgments
The authors would like to thank Dr. John Fletcher for his
assistance with manuscript formatting, editing, and reference management.
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