Resuscitative endovascular balloon occlusion of the aorta

Resuscitative endovascular balloon occlusion of the aorta (REBOA) reduces sub-diaphragmatic haemorrhage while increasing proximal perfusion in non-compressible truncal exsanguination.¹ A catheter-borne balloon is inflated in the descending aorta, initially to complete occlusion then partially deflated, the aim being to optimise coronary and cerebral perfusion, while minimising distal haemorrhage and ischaemia. Resuscitative endovascular balloon occlusion of the aorta can be considered in blunt or penetrating sub-diaphragmatic injury with life-threatening bleeding or traumatic cardiac arrest in centres with an established, protocolised system for its deployment.^2,3

There is currently a lack of high-grade evidence demonstrating superiority over conventional manual aortic occlusion (AO) via thoracotomy;² the ongoing UK-REBOA trial is the first RCT to assess its efficacy. Nonetheless, REBOA is used at an increasing number of international centres. Although mostly deployed in major trauma, it has also been used in sub-diaphragmatic haemorrhage of other aetiologies and in non-traumatic cardiac arrest.^4,5

Relevant anatomy

The descending aorta is divided into three zones⁶:

• (i)Zone 1 (Z1): origin of left subclavian artery to coeliac artery
• (ii)Zone 2 (Z2): origin of coeliac artery to caudal renal artery
• (iii)Zone 3 (Z3): origin of caudal renal artery to aortic bifurcation

Balloon inflation in Z1 reduces bleeding from sub-diaphragmatic sources and augments coronary perfusion pressure, thereby increasing the probability of return of spontaneous circulation after cardiac arrest. Zone 3 deployment reduces bleeding from pelvic or junctional sources (e.g. groin wounds). The balloon is never intentionally inflated in Z2.

Deployment

The primary REBOA operator is an experienced member of the trauma team who has undergone specific training. The therapeutic window for REBOA is narrow. Too early deployment may expose patients who do not have the degree of haemorrhage to warrant it to the risks of REBOA. Too late deployment delays AO, worsening blood loss and physiological derangement. To address these concerns, early femoral access is advocated in patients with sub-diaphragmatic haemorrhage who are deemed at risk of progression to exsanguination (Fig. 1). The common femoral artery (CFA) is cannulated with a small (4 Fr) sheath using ultrasound guidance; the cannula can be replaced later with a larger size if required.

Fig 1.

Simplified decision tree for the deployment of REBOA in cases of sub-diaphragmatic haemorrhage.

In patients with established exsanguination, an 8 Fr sheath is inserted into the CFA, either directly or upsized from a 4 Fr sheath. The 6 Fr ER-REBOA™ catheter (Prytime Medical, Texas, USA) is then inserted to the appropriate length, after measuring the distance from the insertion site to the mid-sternum (Z1) or the umbilicus (Z3). The balloon is inflated with saline while observing the blood pressure (BP) response proximal (via the catheter tip) and distal (via the sheath side port) to the balloon. Inflation endpoint (complete [C]-REBOA) is improvement in proximal BP and distal waveform flatline. After inflation to C-REBOA (restricted to 15 or 20 min in Z1 or Z3, respectively), partial REBOA (P-REBOA) is targeted as soon as possible to minimise distal ischaemia. This procedure entails sequential balloon deflation until distal pulsatility is restored and distal MAP reaches 10 mmHg above that observed during C-REBOA (Fig. 2).

Fig 2.

a) Diagram of key anatomy and equipment for REBOA, b) illustration of arterial pressure changes before inflation, during complete REBOA (C-REBOA) and partial REBOA (P-REBOA). Red arterial line waveform (proximal) from above the balloon, blue (distal) waveform from below. The proximal and distal arterial pressures are equal before inflation so the waveforms are superimposed and appear purple. See https://prytimemedical.com/clinical/videos/ for further details.

Perioperative management of patients undergoing REBOA

Resuscitation management and targets are equivalent to those for other patients with traumatic haemorrhage. This includes permissive hypotension before definitive haemostasis and is guided by the proximal BP and arterial blood gas analysis from the proximal port of the REBOA catheter. Ideally, anaesthesia should be induced after balloon deployment to offset the cardiovascular effects of the i.v. anaesthetic agents and positive-pressure ventilation. Drugs to facilitate intubation may be limited to rocuronium 1 mg kg⁻¹ in a patient who is exsanguinating and peri-arrest, with the judicious addition of ketamine 0.5–1 mg kg⁻¹ in conscious patients.

Tasks include close coordination with the REBOA operator and surgeon regarding the patient's physiological state, the impact of any changes at balloon deflation, keeping track of deployment timings and troubleshooting the transducer and monitoring equipment. The transducer lines need manual flushing regularly when dampening of the pressure waveform occurs, and after blood sampling, as the catheter and sheath clot more frequently than standard arterial catheters.

The increased proximal afterload and relative reduction in intravascular space may lead to hyperaemia in proximal organs, especially if transfusion is overly aggressive.⁷ The patient's lungs can become congested with reduced pulmonary compliance. Improved cerebral perfusion pressures may increase patients' requirements for anaesthetic agents, which can typically be met with sevoflurane 0.3–0.5 minimum alveolar concentration and incremental doses of fentanyl.

Once haemostasis is achieved, the priority is balloon deflation. Reperfusion syndrome is typical. Severity depends on the degree of ischaemic burden, which is contingent on the duration of C-REBOA and P-REBOA, and time in Z1 and Z3. The circulating volume should be optimised in advance and drugs prepared to address vasoplegia and arrhythmias, precipitated by ischaemic metabolites and increases in serum potassium. Pre-emptive treatment with sodium bicarbonate and calcium chloride is often required, as guided by point-of-care testing. Hyperkalaemia is common and often needs treatment with an infusion of insulin in dextrose.

On confirming haemostasis after balloon deflation, the aim is restoration of normal physiology. A standard arterial cannula will be required as the 8 Fr sheath is removed as soon as possible to improve limb perfusion.

Complications and contraindications

Resuscitative endovascular balloon occlusion of the aorta is associated with significant complications.⁸ At our centre, surgical closure of the insertion site is performed to allow concurrent open thrombectomy, as the sheath is highly thrombogenic and thrombus is universally present.

Arterial access difficulties and balloon malposition may result in procedure failure or vascular injuries and subsequent death or amputation. Protracted balloon deployment will cause infarction of abdominal viscera and spinal cord. Zone 1 C-REBOA for 45 min has been reported as consistently fatal.⁹ Contraindications include suspected thoracic vascular injury and unidentifiable CFA at ultrasound.¹⁰ Rigorous multidisciplinary training and governance pathways are necessary.

Non-technical considerations

Favourable outcomes depend on restricting AO time to the minimum necessary. It is critical that momentum is maintained via task anticipation and prioritisation. Situational awareness must be preserved by delegating ‘head-down’ tasks (e.g. checking blood products) and care taken not to neglect trauma resuscitation anaesthesia standards (e.g. temperature management) during REBOA deployment.

Summary

Resuscitative endovascular balloon occlusion of the aorta is a complex, evolving technique that requires a concerted effort by the whole trauma team. Although supporting evidence is currently limited, its use is expanding and is likely to widen to include other aetiologies of truncal exsanguination. Anaesthetists have a central role in its safe and efficacious use.

Declaration of interests

The authors declare that they have no conflicts of interest.

Biographies

Harvey Parsons FRCA MRCP is a specialty registrar in anaesthesia in the Central London School of Anaesthesia.

Andrew Wood FRCA FIMC is a consultant anaesthetist with the Trauma Anaesthesia Group of the Royal London Hospital and consultant prehospital care physician with London's Air Ambulance.

Andrew Milne FRCA DMCC is a consultant anaesthetist with the Trauma Anaesthesia Group of the Royal London Hospital and prehospital care physician with the Greater Sydney Area Helicopter Emergency Medicine Service. He is on the board of directors of the Trauma Anesthesiology Society.

Matrix codes: 1A01, 1B04, 1I02, 1I03, 2A02, 2C04, 3A10