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Resuscitative Endovascular Balloon Occlusion of the Aorta and the Anesthesiologist: A Case Report and Literature Review

Conti, Bianca M. MD*; Richards, Justin E. MD*; Kundi, Rishi MD, RPVI; Nascone, Jason MD; Scalea, Thomas M. MD, FACS, MCCM§; McCunn, Maureen MD, MIPP, FCCM

doi: 10.1213/XAA.0000000000000461
Case Reports: Case Report

The most common preventable cause of death after trauma is exsanguination due to uncontrolled hemorrhage. Traditionally, anterolateral emergency department thoracotomy is used for temporary control of noncompressible torso hemorrhage and to increase preload after trauma. Resuscitative endovascular balloon occlusion of the aorta is a minimally invasive technique that achieves similar goals. It is therefore imperative for the anesthesiologist to understand physiologic implications during resuscitative endovascular aortic occlusion and after balloon deflation. We report a case of a patient with significant pelvic and lower-extremity trauma who required acute resuscitative endovascular balloon occlusion of the aorta deployment, aggressive resuscitation, and extensive intraoperative hemorrhage control.

From the *Division of Trauma Anesthesiology, R Adams Cowley Shock Trauma Center; Division of Vascular Surgery, Department of Surgery; Division of Orthopaedic Traumatology; §R Adams Cowley Shock Trauma Center; and Division of Trauma Anesthesiology, R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, Baltimore, Maryland.

Accepted for publication October 10, 2016.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Bianca M. Conti, MD, Division of Trauma Anesthesiology R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, 22 South Greene St, Baltimore, MD 21201. Address e-mail to bconti@umm.edu.

To control noncompressible torso hemorrhage (NCTH), particularly below the diaphragm, anterolateral emergency department thoracotomy (EDT) traditionally is performed to facilitate aortic cross-clamping.1 Ideally, this results in increased preload, temporary control of hemorrhage, and facilitates internal cardiac massage and defibrillation when needed. Endovascular aortic occlusion has been used to control hemorrhage in patients with ruptured abdominal aortic aneurysms.2 The original case series using an intra-aortic balloon by the U.S. military described its use in the Korean War on 3 injured soldiers3 and was slow to gain acceptance in trauma. With recent improvements, however, the use of resuscitative endovascular balloon occlusion of the aorta (REBOA) has become more common in the management of patients after traumatic hemorrhage.

Figure 1

Figure 1

REBOA is a supportive resuscitation technique, which, similar to EDT, should minimize distal hemorrhage while maintaining cerebral and myocardial perfusion.4 After cannulation of the common femoral artery and insertion of a vascular sheath, a guidewire is advanced retrograde to the distal aortic arch. A balloon catheter is then advanced over the wire to a specified anatomic position (zone 1: origin of the left subclavian artery to the celiac artery or zone 3: lowest renal artery to the aortic bifurcation), which is determined based on the likely source of hemorrhage (Figure 1). The balloon is then inflated to provide aortic occlusion, confirmed by radiographic images, and secured in place with a clamp so as not to migrate distally. Although the surgical approach for placement of the REBOA has been outlined, the anesthetic perspective of prolonged aortic occlusion has not been described. This case study describes REBOA use with an occlusion time of approximately 110 minutes.

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Written Consent Statement

The patient and family have given written permission for this published report.

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DESCRIPTION OF THE CASE: CLINICAL CARE

A 40-year-old, 75-kg male unrestrained driver who was ejected from a motor vehicle presented to the trauma center with a Glasgow Coma Score (GCS) of 15. He had an obvious deformity of his left upper extremity, bilateral open femur fractures, and an unstable pelvis. He had no palpable pulse in any extremity but was able to move his left lower extremity and was awake, alert, oriented, and conversant. His heart rate varied from 112 to 137 beats per minute, with an oxygen saturation of 100% on nasal cannula. Initially, the patient continued to demonstrate an appropriate and reassuring mental status (the inability to obtain peripheral pulses was likely because of the extent of extremity injuries). An automatic blood pressure recording could not be obtained, and, therefore, manual sphygmomanometry was used with the first reading of 74/48 mm Hg approximately 15 minutes after presentation. The focused assessment with sonography for trauma was negative for pericardial, abdominal, or pelvic fluid.

Figure 2

Figure 2

Fluid resuscitation, including red cell and thawed plasma transfusion was initiated. An arterial line was placed in the left femoral artery, and a pelvic binder was applied. Admission lactate was 8.4 mmol/L and the base deficit was 18.3 mmol/L. Because of continued hypotension and concern for hemorrhage from severe pelvic injury, a REBOA device was deployed in zone 3 (infrarenal) through the left femoral arterial line site 23 minutes after presentation. The patient ultimately was intubated with etomidate and rocuronium 30 minutes after arrival as the result of declining mental status. His pelvic X-ray showed an extensively displaced combined pelvic ring and acetabular fracture (Figure 2). The patient was transported emergently to the hybrid operating room (OR). Total balloon aortic occlusion time on presentation to the OR was 51 minutes.

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Intraoperative Course

A right brachial endovascular angiogram demonstrated a “blush” of the right proximal internal iliac artery, which was coil embolized. The right external iliac artery was occluded, and an external iliac-to-common femoral artery bypass was performed. Spanning external fixation was applied to the bilateral lower extremities and pelvic stability was maintained by internal rotation of bilateral femurs and bridging the femoral frames to reduce pelvic volume. The REBOA was removed and the femoral artery repaired. Total REBOA inflation time, including preoperative deployment, was 110 minutes (Figure 3). Throughout the 9-hour operative course, the patient required ongoing hemodynamic resuscitation that included 32 units of packed red blood cells, 28 units of plasma, 24 units of platelets (4 “6 packs”), 180 mL of cryoprecipitate, 1 g of tranexamic acid, 1 L of 5% albumin, 4 L of Plasma-Lyte® (Baxter Healthcare Corp, Deerfield, IL), intermittent boluses of phenylephrine, vasopressin, calcium chloride, sodium bicarbonate, and infusions of norepinephrine and vasopressin. His analgesic requirement consisted of a total of 800 μg of fentanyl, which was administered in 50- to 100-μg aliquots throughout the 9-hour operation. He also received 4 mg of midazolam: 2 mg before the start of the operation and 2 mg before the final deflation of the REBOA. The inhalation anesthetic concentration of isoflurane ranged from 0.2% to 0.5% throughout the operation. The Table outlines the intraoperative acid–base status via arterial blood gas analysis. Estimated blood loss in the OR was 4.5 L, although this did not account for preoperative estimated blood loss, nor the volume of blood and clots on the OR table.

Table

Table

Figure 3

Figure 3

In subsequent days, the patient underwent multiple operations for debridement of the right lower extremity as he had a combination of direct muscle injury and ischemia resulting in muscle necrosis. However, he ultimately developed acute kidney failure requiring continuous renal-replacement therapy and, to obtain source control of necrotic tissue, required a right lower extremity amputation, followed by a right hemipelvectomy. Two months after injury, the patient was discharged to a rehabilitation facility with a GCS of 15. The patient was seen in trauma clinic 3 months later: he was with a GCS of 15 and cognitively intact.

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DISCUSSION

Uncontrolled hemorrhage represents the leading cause of preventable death after injury.5 Despite recent advances in blood transfusion therapy,5 NCTH remains a common cause of death due to hemorrhagic shock. NCTH results from injuries that cause vascular disruption of axial torso vessels, solid organ damage (ie, spleen, liver, kidney), and/or injuries to the bony pelvis. Although EDT has been the standard therapeutic approach to temporize NCTH,1 it is morbid and the open chest is a source of heat and blood loss. Recent advances and availability of endovascular techniques, particularly the REBOA, have demonstrated promising results in the management of certain patients with NCTH after traumatic injury.4

The role of the anesthesiologist in the management of hemorrhagic shock is multifaceted, with attention paid to multiple organ systems. Deployment of the REBOA device and inflation of the occlusive balloon serve to augment coronary and carotid artery blood flow to maintain vital perfusion to the heart and brain, respectively. With proximal aortic occlusion, there is an increase in cardiac afterload and mean arterial pressure.6 Physiologically, this increase in afterload, while supporting coronary perfusion, may also increase myocardial transmural wall tension and cardiac pressure work.7 In a swine model of controlled hemorrhagic shock, Morrison et al6 demonstrated that there was no significant difference in vasopressor support or cardiac filling pressures among animals with increasing duration of aortic balloon occlusion; however, the exact clinical significance on subsequent cardiac performance after balloon deflation has yet to be elucidated in humans. It is paramount for the resuscitation team to remember that REBOA is a temporizing measure with dynamic physiologic changes, which aims to support vital organ perfusion but does not provide definitive hemorrhage control.

At present, there are few recommendations for optimal hemodynamic management during the period of aortic occlusion. Considering the increase in systemic vascular resistance and mean arterial pressure during balloon inflation,6,8 a balanced anesthetic technique that achieves judicious analgesia and appropriate sedation seems wise.9 Of note, our patient received a predominately narcotic-based anesthetic (approximately 10 mcg/kg of fentanyl) with an inhalational anesthetic of less than one-half of minimum alveolar concentration and supplemental midazolam. Aggressive hemodynamic resuscitation also must continue with transfusion of blood products and attention to the acute coagulopathy of trauma.9 With prolonged duration of aortic occlusion, there is a significant increase in lactate concentration and volume of resuscitative fluid requirements compared with nonballoon occlusive therapy.8 Similar to unclamping of the aorta during abdominal aortic aneurysm’s repair, reperfusion distal to the occlusion site may result in a washout of metabolites with subsequent hyperkalemia, lactic acidosis, and profound hypotension.7 Therefore, restoration of intravascular volume should be achieved before balloon deflation.

It is imperative that the anesthesiologist be in constant communication with the surgical operative team before and during the period of aortic balloon deflation to allow distal reperfusion without profound hemodynamic changes, and to rapidly reinitiate aortic occlusion should such decompensation occur. Similar to gradual release of an aortic cross-clamp, the REBOA balloon can be slowly deflated—and reinflated if necessary—while volume replacement or vasoactives are titrated to an optimal level.

Our patient sustained devastating anatomic injury. This injury pattern is associated with a high rate of morbidity and mortality related to hemorrhagic shock. Recent algorithms have been published to guide the decision-making process in patients with hemodynamically significant pelvic fractures, and the roles of angiography and external fixation.10 The addition of REBOA for temporary hemodynamic support has also been described recently in patients with hemorrhagic shock secondary to pelvic injuries and is now considered part of the armamentarium for the resuscitation team until definitive hemorrhage control is achieved.10 Considering the potential role of endovascular therapy in severe pelvic trauma, it would benefit the anesthesiologist to be well versed in the concepts of damage control resuscitation, damage control orthopedics, and endovascular aortic balloon occlusion. The concept of damage control anesthesia is also evolving to guide the anesthetic requirements in the setting of severe hemorrhagic shock.9

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CONCLUSIONS

Profound life-threatening hemorrhage due to NCTH remains a leading cause of death after certain injuries. Endovascular therapy is an emerging technique that is applicable to trauma patients with significant vascular injuries. Considering the role of the anesthesiologist in the preoperative and intraoperative resuscitation period, a thorough understanding of hemorrhage control and temporary supportive therapies, such as REBOA, is necessary to be fully engaged in the dynamic resuscitation process. Future research with REBOA techniques will further define the role of this technology in the multidisciplinary management of severe hemorrhagic shock.

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DISCLOSURES

Name: Bianca M. Conti, MD.

Contribution: This author helped write the manuscript.

Name: Justin E. Richards, MD.

Contribution: This author helped write the manuscript.

Name: Rishi Kundi, MD, RPVI.

Contribution: This author helped write the manuscript.

Name: Jason Nascone, MD.

Contribution: This author helped write the manuscript.

Name: Thomas M. Scalea, MD, FACS, MCCM.

Contribution: This author helped write the manuscript.

Name: Maureen McCunn, MD, MIPP, FCCM.

Contribution: This author helped write the manuscript.

This manuscript was handled by: Richard P. Dutton, MD.

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REFERENCES

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2. Arthurs ZM, Sohn VY, Starnes BW. Ruptured abdominal aortic aneurysms: remote aortic occlusion for the general surgeon. Surg Clin North Am. 2007;87:1035–1045.
3. Hughes CW. Use of an intra-aortic balloon catheter tamponade for controlling intra-abdominal hemorrhage in man. Surgery. 1954;36:65–68.
4. Brenner ML, Moore LJ, DuBose JJ, et al. A clinical series of resuscitative endovascular balloon occlusion of the aorta for hemorrhage control and resuscitation. J Trauma Acute Care Surg. 2013;75:506–511.
5. Holcomb JB, Tilley BC, Baraniuk S, et al; PROPPR Study GroupTransfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313:471–482.
6. Morrison JJ, Ross JD, Markov NP, Scott DJ, Spencer JR, Rasmussen TE. The inflammatory sequelae of aortic balloon occlusion in hemorrhagic shock. J Surg Res. 2014;191:423–431.
7. Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology. 1995;82:1026–1060.
8. Markov NP, Percival TJ, Morrison JJ, et al. Physiologic tolerance of descending thoracic aortic balloon occlusion in a swine model of hemorrhagic shock. Surgery. 2013;153:848–856.
9. Dutton RP. Haemostatic resuscitation. Br J Anaesth. 2012;109(suppl 1):i39–i46.
10. Costatinni TW, Coimbra R, Homcomb JB, et al; the AAST Pelvic Fracture Study GroupCurrent management of hemorrhage from severe pelvic fractures: results of an American association for the surgery of trauma multi-institutional trial. J Trauma Acute Care Surg. 2016;80:717–723.
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