Carotid blowout syndrome (CBS) is defined as “a hemorrhage caused by the rupture of the extracranial carotid arteries or its major branches.”1,2 Recent retrospective data suggest a prevalence of 3.9% after oncological head and neck surgery.3 CBS occurs after this type of surgery, or after radiation therapy, when the weakened friable arterial wall cannot sustain its integrity against the shear stress caused by systolic blood pressure.4
Risk factors compromise the firmness of the carotid arterial wall as determined by the integrity of the vasa vasorum. These risk factors include a body mass index of <22.5 kg/m2 at the initial presentation, a primary tumor originating from the hypopharynx or oropharynx, extensive neck dissection, an open wound in the neck requiring wound care with wet dressing, or having received a total radiation dose of 70 Gy to the neck.1,3
CBS is a life-threatening situation that can be very challenging for anesthesiologists. After failed intubation, hemorrhagic shock is the leading preventable cause of death.5 Massive transfusion protocols have proven benefits in resuscitating hypovolemic patients with continuing blood loss.6,7 Endovascular strategies are generally considered to be the gold standard, whereas surgical treatment is typically the last resort in massive arterial bleeding.1,8
We describe the anesthetic strategy and the thromboelastometry (ROTEM®)-guided massive transfusion protocol we used. We discuss the treatment algorithm of CBS, including the extensive resuscitation using a predefined “massive transfusion pack” and ROTEM analysis. Written consent for publication was obtained from the patient.
A 44-year-old man was transported to our emergency department by the physician-based Helicopter Emergency Medical Service (HEMS) with pharyngeal hemorrhage effusing from the mouth 6 weeks after total laryngectomy, partial pharyngectomy, and extensive neck dissection. During this operation, the internal jugular vein and the external carotid artery were ligated. Reconstruction was performed with 2 pectoralis major flaps and a superficial circumflex iliac artery perforator flap. After this surgery, the patient was treated with adjuvant radiotherapy. The patient was treated in the outpatient clinic for a postoperative wound infection and a pharyngeal–cutaneous fistula.
On arrival of the HEMS, the patient was in severe hemorrhagic shock: confused but responsive, tachycardic (145 beats per minute), hypotensive (93/43 mm Hg), and tachypneic (50/min) with a peripheral oxygen saturation of 99%. The estimated amount of prehospital blood loss was 2 L. The HEMS physician administered 1.5 L of 0.9% saline and 2 g of tranexamic acid IV. A cutoff cuffed endotracheal tube was placed in the tracheostomy to secure the airway. His bleeding neck was bandaged, and the patient’s mouth was filled with HemCon Bandage® (HemCon Medical Technologies, Inc, Portland, OR). To minimize further blood loss during transport to the emergency department, permissive hypotension was allowed.9 The nearest university hospital was contacted (Erasmus MC, Rotterdam, the Netherlands) to notify the trauma team, including the head and neck surgeon. The patient remained conscious and cooperative during transport.
Shortly after arrival at the emergency department, the patient’s bleeding increased and his condition deteriorated. A predefined massive transfusion pack (Figure 1) was administered immediately.
We replaced the cutoff tube with a cuffed ShileyTM tracheostomy cannula size 6 (Covidien, Minneapolis, MN). In consultation with the head and neck surgeon, the decision was made to perform immediate damage control surgery at the emergency department, because the patient’s condition was too unstable for transport to the radiology intervention suite or the operating room.
Induction of anesthesia was performed with titration of fentanyl and midazolam (a total of 200 μg fentanyl and 10 mg midazolam was administered IV). The patient’s lungs were ventilated with an Fio2 of 1.0, bilevel positive airway pressure, with 25/5 cm H2O peak/positive end-expiratory pressure, frequency of 16 times/min. Muscle relaxation was established with 50 mg rocuronium bromide IV. Anesthesia was maintained with a propofol perfusor at 4 mg/kg/h. A norepinephrine perfusor was initiated at a low dosage (<0.1 μg/kg/min).
During surgical exploration of the neck, there was continuing arterial bleeding at the site of the carotid bifurcation. We continued damage control resuscitation with 2 Level 1® H-1025 Fast Flow Fluid Warmers (Smits Medical, Kent, UK) connected to 2 14-gauge IV catheters. Eight units of packed red blood cells (Sanquin, Amsterdam, the Netherlands), 10 pooled plasma (Sanquin), 2 platelet concentrates (Sanquin), and 6 g calcium gluconate were administered after the initial massive transfusion pack.
The head and neck surgeon successfully performed ligation of the left common carotid artery. Arterial blood was drawn, and the results were as follows: hemoglobin, 11.0 g/dL; international normalized ratio, 1.9; activated partial thromboplastin time, 33 seconds; platelet count, 170 × 109/L; fibrinogen, 2.7 g/L; ionized calcium, 0.98 mmol/L; pH, 7.13; Pco2, 55 mm Hg, ROTEM (Figure 2). The patient’s condition stabilized. We administered low-dose norepinephrine (<0.1 μg/kg/min) to establish a mean arterial blood pressure of 70 to 80 mm Hg. The patient’s temperature remained >35°C (95°F).
The patient was transferred to the intensive care unit where sedation was continued for 24 hours. The patient remained hemodynamically stable without any support. His respiratory acidosis normalized. He recovered without any neurologic sequelae, proving patency of the circle of Willis. After 8 days of recovery on the head and neck surgery ward, the patient was discharged from the hospital.
Since first being published in 1984, endovascular therapy has had a prominent role in the management of CBS.8 Before the implementation of this technique, exploration of the neck and surgical ligation of the affected artery was the treatment of choice. However, performing surgery on these patients has resulted in high mortality and neurologic morbidity (median estimates of 40% and 60%, respectively).1,10 This is because of several factors. First, a rupture of the carotid artery typically results in severe hemodynamic instability. Second, the anatomy can be dramatically changed after previous oncologic surgery and radiation therapy, often with pharyngocutaneous fistula formation and local infection. Third, neurologic complications can result from cerebral ischemia because of either an incomplete circle of Willis or thromboembolism from the occluded artery.1,11,12
During CBS, massive transfusion protocols should be used. The immediate resuscitation with our institute’s massive transfusion pack provided a balanced replenishment of coagulation factors, as demonstrated by conventional coagulation parameters and by thromboelastometry (ROTEM).
The use of viscoelastic hemostatic assays (TEG® or ROTEM) in patients presenting at the emergency department with acute bleeding is a topic of ongoing discussion. Recent studies suggest a decrease in use of blood products in ROTEM-guided massive transfusion protocols, but these settings cannot easily be compared with the acute setting at the emergency department, as described in this case. In a Cochrane review published in 2011 concerning the accuracy of viscoelastic assays in trauma, the authors concluded that there is insufficient evidence to justify the standard use of viscoelastic testing in trauma patients with bleeding.13 Despite this review, viscoelastic hemostatic assays have been incorporated in most massive blood loss protocols.
The results of the ROTEM analysis in this particular case ((Figure 2) were within the normal range after massive transfusion, with the exception of a slight prolongation of the clot formation time and a decreased α angle. These results indicate a decreased platelet count/function or a low fibrinogen level,a but considering the adequate hemostasis achieved at the surgical field, we did not intervene on the basis of the ROTEM results.
In their 2004 review, Cohen and Rad1 describe a comprehensive algorithm for the management of carotid blowout. Regarding surgical ligation, they state that operative intervention should be used only as a last resort if interventional angiography cannot be accomplished.
The case we describe demonstrates an unusual presentation of the CBS, because of the continuing bleeding into the oropharyngeal cavity and the subsequent inability to effectively tamponade the bleeding. Immediate surgery was necessary because adequate fluid resuscitation could not be achieved during massive ongoing blood loss. Stabilization or transport to interventional radiology was not an option. We recommend immediate surgery during CBS if stabilization or transport to an interventional radiology suite is not an option.
In summary, immediate surgical intervention in case of acute CBS should be performed if endovascular options are not viable. Early damage control resuscitation with predefined massive transfusion packs provides a balanced replenishment of coagulation parameters, as demonstrated by subsequent ROTEM analysis. Further transfusion strategies should be based on a massive transfusion protocol guided by point-of-care tests such as the ROTEM.
We thank Dr. D. Y. Lin, Anesthetic Resident, for her assistance.
1. Cohen J, Rad I. Contemporary management of carotid blowout. Curr Opin Otolaryngol Head Neck Surg 2004;12:1105.
2. Pampana E, Gandini R, Stefanini M, Fabiano S, Chiaravalloti A, Morosetti D, Spano S, Simonetti G. Coronaric stent-graft deployment in the treatment of carotid blowout. Interv Neuroradiol 2011;17:4904.
3. Chen YJ, Wang CP, Wang CC, Jiang RS, Lin JC, Liu SA. Carotid blowout in patients with head and neck cancer: associated factors and treatment outcomes. Head Neck 2015;37:26572.
4. McDonald MW, Moore MG, Johnstone PA. Risk of carotid blowout after reirradiation of the head and neck: a systematic review. Int J Radiat Oncol Biol Phys 2012;82:10839.
5. Holcomb JB, del Junco DJ, Fox EE, Wade CE, Cohen MJ, Schreiber MA, Alarcon LH, Bai Y, Brasel KJ, Bulger EM, Cotton BA, Matijevic N, Muskat P, Myers JG, Phelan HA, White CE, Zhang J, Rahbar MH; PROMMTT Study Group. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying treatment with competing risks. JAMA Surg 2013;148:12736.
6. Young PP, Cotton BA, Goodnough LT. Massive transfusion protocols for patients with substantial hemorrhage. Transfus Med Rev 2011;25:293303.
7. Cotton BA, Au BK, Nunez TC, Gunter OL, Robertson AM, Young PP. Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications. J Trauma 2009;66:418; discussion 489.
8. Osguthorpe JD, Hungerford GD. Transarterial carotid occlusion. Case report and review of the literature. Arch Otolaryngol 1984;110:6946.
9. Gourgiotis S, Gemenetzis G, Kocher HM, Aloizos S, Salemis NS, Grammenos S. Permissive hypotension in bleeding trauma patients: helpful or not and when? Crit Care Nurse 2013;33:1824.
10. Chaloupka JC, Roth TC, Putman CM, Mitra S, Ross DA, Lowlicht RA, Sasaki CT. Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges in a newly recognized subgroup of patients. AJNR Am J Neuroradiol 1999;20:106977.
11. Razack MS, Sako K. Carotid artery hemorrhage and ligation in head and neck cancer. J Surg Oncol 1982;19:18992.
12. Citardi MJ, Chaloupka JC, Son YH, Ariyan S, Sasaki CT. Management of carotid artery rupture by monitored endovascular therapeutic occlusion (1988–1994). Laryngoscope 1995;105:108692.
13. Hunt H, Hyde C, Stanworth S, Curry N, Perel P, Woolley T, Cooper C, Ukoumunne O. Thromboelastography (TEG) and thromboelastometry (ROTEM) for trauma induced coagulopathy in adult trauma patients with bleeding. Cochrane Database Syst Rev 2011:CD010438.