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93
setting [58]. In the future, Partial-REBOA aims to decrease distal ischemia by
allowing titrated, controlled, low-volume ow distal to aortic occlusion while
maintaining physiologic carotid ow [60].
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© Springer Nature Switzerland AG 2020
T. Hörer et al. (eds.), Endovascular Resuscitation and Trauma Management,
Hot Topics in Acute Care Surgery and Trauma,
https://doi.org/10.1007/978-3-030-25341-7_7
A. J. Davidson
Department of Surgery, University of California Davis Medical Center,
Sacramento, CA, USA
e-mail: ajdavidson@ucdavis.edu
T. K. Williams (
*)
Vascular and Endovascular Surgery, Wake Forest Baptist Health, Winston-Salem, NC, USA
7
Partial REBOA
AndersJ.Davidson andTimothyK.Williams
7.1 Introduction
Resuscitative endovascular balloon occlusion of the aorta (REBOA) has emerged as
a feasible technique for modern hemorrhage control and trauma resuscitation [1, 2].
REBOA results in decreased bleeding below the level of complete occlusion and
augmentation of blood pressure and blood ow to the heart, lungs, and brain [3].
While initially advocated for trauma patients in extremis as an alternative to emer-
gency thoracotomy, the indications for REBOA have continued to expand [4]. Its
use has been described as a prophylactic hemorrhage control adjunct in major elec-
tive surgery, for the management of postpartum hemorrhage, and in nontraumatic
cardiac arrest [5–10].
Despite its increasing utilization and broadening applications, REBOA carries
several negative physiologic consequences primarily related to the profound distal
ischemia created by complete aortic occlusion. Additionally, REBOA can pro-
duce severe supraphysiologic proximal hypertension and cardiac afterload, which
may have detrimental effects [11, 12]. One proposed alternative to complete aortic
occlusion is a technique of partial REBOA (P-REBOA) [13]. The application of
partial aortic occlusion allows a limited amount of blood ow beyond the occlu-
sion balloon. This technique maintains the benets of increased perfusion created
above the level of occlusion, while simultaneously allowing some blood ow to
areas distal to the level of occlusion. The purpose of P-REBOA is to minimize
distal ischemia and limit proximal hypertension, while simultaneously limiting
downstream bleeding. This may serve to extend the duration of intervention,
98
allowing prolonged application in scenarios where hemorrhage control will be
delayed beyond the ischemia threshold of complete REBOA (Figs.7.1, 7.2, 7.3,
7.4, 7.5, and 7.6, Table7.1).
Complete
Partial
None
abc
Fig. 7.1 (a–c) P-REBOA is partial aortic balloon occlusion and can occur anywhere between 0%
and 100% occlusion. This makes P-REBOA dynamic and able to respond to physiologic changes,
but makes comparison of studies difcult
Intravascular
volume
Cardiac
output
Regional
ischemia
Circulating
catecholamines
Vasoconstriction
Blood
pressure
Amount
of aortic
occlusion
Aortic diameter
Aortic
flow
Fig. 7.2 Determinants of aortic ow. Reliably predicting aortic ow at a given degree of occlusion
is difcult given complex interactions between physiologic, mechanical, and metabolic factors
A. J. Davidson and T. K. Williams
99
Fig. 7.3 Establishing arterial access is key for P-REBOA.Distal pressure can be transduced through
the femoral sheath through which a REBOA catheter is placed, or though the contralateral femoral
artery. Proximal pressure can be transduced through a radial arterial line or directly from more mod-
ern occlusion catheters such as the ER-REBOA™. The black arrow denotes arterial sheath with
REBOA (note integrated arterial pressure port). The white arrow denotes contralateral femoral access
30 cc “course
adjustment” syringe
Distal arterial pressure
monitoring via sheath
5 cc “fine adjustment”
syringe
Fig. 7.4 Our preferred
setup for REBOA.Note
“course ination” syringe,
“ne adjustment” syringe,
and distal arterial pressure
monitoring through arterial
sheath. This example
utilizes an ER-REBOA™
catheter, which can also
transduce proximal arterial
pressure
7 Partial REBOA
100
Complete
Proximal aortic pressure
150
100
MAP (mmHg)
60
50
0
030
Time (min)
60 90
Partial
Control
Fig. 7.5 Effects of REBOA, P-REBOA, and no occlusion on proximal blood pressure during
intervention in a translational animal model of trauma. Note supraphysiologic pressures created by
REBOA with more physiologic blood pressures in the P-REBOA group. The vertical red line at
90min indicates balloon deation. The horizontal red line indicates mean arterial pressure of 60
Metabolic burden over time
Complete
Partial
Control
BSL
2
4
6
Lactate (mmol/L)
8
10
12
0153045
Time (min)
60 75 90 95 100 105
Fig. 7.6 Effects of REBOA, P-REBOA, and no occlusion on circulating lactic acid over time. The
red line at 90min indicates balloon deation
A. J. Davidson and T. K. Williams
101
This chapter will discuss the technique of P-REBOA including the physiology of
partial aortic occlusion, translational and early clinical data of P-REBOA, as well as
future considerations for continued renement of the technique.
7.2 Physiology
7.2.1 The Effects ofComplete Aortic Occlusion
Occlusion of the descending aorta is associated with a complex hemodynamic
response with several intended and unintended physiologic consequences.
It creates a relative arterial hypertension proximal to the level of occlusion with
a redistribution of blood ow in order to preserve perfusion to vital proximal organs
[14]. Although some scant collateral arterial blood ow remains, this is insufcient
to maintain organ viability over prolonged periods [15]. Therefore, aortic occlusion
creates an “on the clock” phenomenon, with progressive ischemia as a function of
the duration of occlusion [16]. Ultimately, this can result in irreversible ischemia
once a critical time threshold has been passed [17]. Additionally, once aortic blood
ow is restored, these distal tissue beds experience a reperfusion injury with a wash-
out of ischemic metabolites such as potassium and lactic acid. This ischemia-
reperfusion injury is quite dramatic and is the primary reason that aortic occlusion
is a time-sensitive modality [18]. Notably, patients experience worse outcomes the
longer aortic occlusion is maintained due to this phenomenon [19].
The primary intended consequence of aortic occlusion is a near instantaneous
increase in blood pressure proximal to the level of occlusion with a resultant
increase in blood ow to organs cranial to the level of occlusion. In the shock
state, this has the ability to promote and maintain perfusion to critical organs such
as the heart, lungs, and brain [20]. The development of arterial hypertension is the
most consistent and dramatic nding that occurs during aortic occlusion. This
increase in blood ow has the desired effect of maintenance of perfusion; how-
ever, often this dramatic increase in pressure can create an additional burden on
the heart and may exacerbate injuries such as traumatic brain injury or pulmonary
contusions [21, 22].
Table 7.1 Comparison of REBOA and P-REBOA
REBOA
P-REBOA
Proximal blood pressure Supraphysiologic More physiologic
Distal ischemia Near complete Relative ischemia
Metabolite washout Immediate with return of distal blood
ow
More protracted
Degree of aortic occlusion Static: Only complete Dynamic 0–99%
Potential for ongoing
bleeding
Minimal Considerable
Ease of use Simpler: Single provider Difcult: multiple
providers
Tolerable duration of use Shorter Longer
7 Partial REBOA
102
The two primary physiologic limitations of aortic occlusion are ischemia and
reperfusion. This pathologic condition is characterized by an initial restriction of
blood supply followed by subsequent restoration of perfusion and oxygenation. The
ischemic period is associated with impaired endothelial cell barrier function with a
concomitant increase in blood vessel permeability and leakage. In the short term,
this causes a cellular transition to anaerobic metabolism in the affected tissues with
inhibition of key enzymes that require oxygen as a cofactor. This is associated with
alterations to transcription and gene expression. As the duration of ischemia is
increased, activation of cell death (apoptosis) occurs. This in turn causes a release
of proteases, lysosomes, and key intracellular electrolytes (i.e., potassium) into the
extracellular compartment. These ischemic metabolites will continue to collect as
the duration of ischemia increases. Eventually, an organ reaches an ischemic thresh-
old of irreversibility beyond which recovery cannot occur [23]. Reperfusion then
reintroduces blood ow into the area. This creates an abrupt “washout” of these
ischemic metabolites to the systemic circulation. If the duration of ischemia is short,
this may be of limited physiologic consequence. However, if the duration is longer,
there may be severe consequences such as cardiac arrest or multiorgan failure.
Resistance to ischemic injury is dependent on the organ type and its metabolic
requirements for oxygen (i.e., skeletal muscle is more resistant and kidneys are less
resistant) [24].
7.2.2 The Effects ofPartial REBOA
The physiologic rationale for P-REBOA is to decrease distal ischemia by allowing
limited blood ow beyond the level of occlusion, while simultaneously reducing
proximal hypertension and cardiac afterload. This limited downstream blood ow
created by P-REBOA generates a “relative” ischemia as opposed to “complete”
ischemia created by REBOA, which serves to extend the duration of intervention
and limit the reperfusion injury that occurs at the time of full balloon deation.
Furthermore, P-REBOA may mitigate the “washout” of ischemic metabolites expe-
rienced during reperfusion by continuously clearing some metabolites through con-
tinued low volume distal ow. Additionally, P-REBOA may lessen the potentially
detrimental effects of proximal arterial hypertension and increased afterload associ-
ated with complete aortic occlusion. In theory, this will decrease the strain on the
heart, and may reduce the potential for pulmonary or cerebral edema.
In the context of uncontrolled injury, P-REBOA does create the potential for
ongoing bleeding by perpetuating blood ow to injured vascular beds. This is inher-
ently unpredictable and inuenced by factors such as the extent and location of
injury, tamponade and thrombus formation at the injury site, and overall coagulation
status. It is conceivable that hemorrhage may ensue, particularly from injuries
involving large blood vessels such as the aorta and its primary branches. However,
this bleeding may occur at tolerable levels that can be met by ongoing resuscitation
efforts. This concept is supported by the notion of permissive hypotension after
traumatic injury [25]. The theory is that low arterial blood pressures may support
A. J. Davidson and T. K. Williams