CASE REPORT

A previously healthy, 52-year-old male in hemorrhagic shock, from a high-speed, side-impact motor vehicle collision at 06:50, underwent initial resuscitation at a non-trauma centre, including intubation and a massive blood-based resuscitation. Upon arrival, the patient was profoundly hypotensive (blood pressure [BP] 55/30) and Glasgow Coma Scale (GCS) of 8 (eyes 1, verbal 2, and motor 4). Basic investigations included a chest X-ray and pelvis X-ray, demonstrating bilateral pneumothoraces and an unstable open-book pelvis fracture (anteroposterior compression II, Young Burgess Classification). Management prior to transfer included insertion of bilateral chest tubes, application of a pelvic binder, and administration of 1 gram of tranexamic acid (TXA). He received 4 litres of 0.9% normal saline, 10 units of packed red blood cells (pRBCs), and 1 unit of fresh frozen plasma (FFP). Despite this massive resuscitation, an epinephrine infusion (1 mcg/kg/min) was initiated prior to transfer to our trauma centre because of persistent hypotension (BP 60/40).

The patient was received at our trauma centre at 09:50, under the care of a Royal College emergency medicine (FRCP-EM)-trained trauma team leader (TTL) in charge of a multi-disciplinary trauma team including anesthesia and orthopedic residents, a trauma surgery resident and fellow, a staff trauma surgeon, three trauma nurses, and two respiratory therapists. On repeat assessment, the airway remained secure, and an X-ray demonstrated bilateral lung re-expansion. A FAST exam was positive in the abdominal views, and the pelvis, previously bound, was not re-examined. During transfer, the patient had required the addition of a norepinephrine infusion; both norepinephrine and epinephrine infusions were dosed at 1 mcg/kg/min, with the systolic blood pressure (sBP) remaining between 45 and 60 mm Hg, heart rate of 102 bpm, and temperature of 33.2°C (91.8°F). Initial investigations included a pH of <6.8 (normal 7.35–7.42), lactate of >15.0 mmol/L (normal 0.5–2.3), fibrinogen 0.5 g/L (normal 1.8–4.0), hemoglobin of 143 g/L (normal 130–170), and platelets of 106 × 10⁹/L (normal 140–400).

Our massive transfusion protocol was activated, and the patient received six additional units of pRBCs, three units of FFP, one additional gram of TXA, and one pool of platelets upon arrival at our centre. His sBP did not increase above 60 mm Hg; however, he continued to demonstrate neurologic function with reactive pupils and a GCS of 7T (E2VTM5), localizing the endotracheal tube with both hands.

The TTL and trauma surgeon considered options for this patient, including an urgent transfer to the OR, resuscitative thoracotomy, and/or REBOA. While this patient, who was in profound hemorrhagic shock with a positive FAST exam, had indications for immediate surgery, transfer to the OR at our institution requires approximately 10 minutes because of the distance and travel by elevator. Given the persistent shock state (sBP < 60 mm Hg) and concern for cardiac arrest despite substantial resuscitative efforts, the transfer was deemed unsafe. Approximately one hour after the patient arrived at our institution (10:55), as an alternative to resuscitative thoracotomy with aortic cross-clamping, the surgeon-TTL team collaboratively elected to place a Zone 1 REBOA device as a temporizing measure to facilitate transfer to the OR (Figure 1).

Figure 1.

REBOA placement algorithm (A). Aortic zones of occlusion (B), adapted from Stannard, Eliason, and Rasmussen.Reference Stannard, Eliason and Rasmussen⁹ Zone 1 between the left subclavian artery and celiac artery is the recommended location for suspected intra-abdominal hemorrhage; Zone 2 between the celiac arteries and renal arteries is not a recommended placement location; and Zone 3, from the lowest renal artery to the aortic bifurcation, is the recommended location for suspected pelvic hemorrhage. Following the decision to proceed with REBOA placement, the clinician must determine where to position the occlusive balloon (Figure 1A). In this case, the patient had a positive FAST, and following the algorithm in Figure 1A, we placed the device in Zone 1.

While the TTL continued to guide resuscitation, the surgery team obtained central venous access in the right subclavian vein for blood product administration. The REBOA procedure began at 10:58 with ultrasound-guided puncture of the left common femoral artery, followed by the advancement of a 0.035 inch, 260 cm guidewire using a modified Seldinger technique. Serial dilation allowed insertion of a 14 Fr vascular access sheath. A Coda 46 mm balloon catheter (Cook Incorporated, Bloomington, IN, USA) was inserted into the distal thoracic aorta, followed by guidewire removal. The balloon was inflated with sterile saline until the sBP suddenly increased from 60 mm Hg to 105 mm Hg; a total of 7 cc of saline was used for inflation. Shortly after that, the epinephrine infusion was stopped, and the norepinephrine dose was decreased to 0.5 mcg/kg/min. Seven minutes elapsed from decision to REBOA and successful aorta occlusion.

The patient was transferred urgently to the OR and underwent a splenectomy, a small bowel resection, and pre-peritoneal pelvic packing. The largest volume of blood and most likely source of persistent hemodynamic instability was felt to be the pelvic injuries. After surgical hemostasis, but while still in the OR, the Coda balloon was deflated by the surgical team, with no change in mean arterial pressure (60–65 mm Hg). There was resistance upon attempting to remove the device that may have occurred because the balloon did not fully retract into the introducer sheath. To ensure complete deflation of the balloon and facilitate removal of the device, the catheter was transected, severing the lumen communicating with the balloon, and was then successfully removed without resistance.

A temporary abdominal closure was performed because of persistent coagulopathy (international normalised ratio [INR] of 2.25–3.7), followed by immediate pelvic angiography. There was no evidence of injury or REBOA complication in any Zone 1 or 2 vessels. Bleeding from bilateral internal iliac artery injuries required proximal embolization. The left external iliac artery demonstrated absent flow with clinical signs of ischemia including a pulseless and pale left foot two hours after removal of the REBOA catheter. Seven hours after arrival at our institution (and 12 hours post-injury), he was returned to the OR for vascular sheath removal, arteriorrhaphy, left femoral thrombectomy, and four-compartment fasciotomies of the left leg. The patient demonstrated increasing hemodynamic instability and worsening multi-organ dysfunction, prompting a repeat laparotomy. Several unnamed mesenteric vessels at the site of a prior bowel resection were ligated; however, the patient continued to bleed because of profound coagulopathy despite laboratory-guided blood product administration. Unfortunately, the patient died of his injuries 18 hours after his arrival at our institution. This report was approved by St. Michael's Hospital Research Ethics Board (18-081).