Stab injury to the preauricular region with laceration of the external carotid artery without involvement of the facial nerve: a case report

The first description of a penetrating neck injury dates back to 5000 years ago in The Edwin Smith Surgical Papyrus [1]. Ambroise Paré is credited with the first surgical repair of a major cervical bleeding in the neck region by ligating the carotid artery and the internal jugular vein of a wounded French soldier [1‐5]. Nowadays, penetrating head and neck injuries are relatively rare in most countries, representing 2–10% of all trauma admissions [2, 3, 5]. Among these injuries, major arterial lesions are also increasingly infrequent in most developed countries [3]. However, although rare, they can immediately jeopardize life, mandating prompt diagnosis and repair of the severed arteries and neighboring anatomical structures [5‐7].

In particular, open injuries to the face involving the external carotid artery (ECA) are relatively uncommon [8]. They are normally associated with compromise of the facial nerve (FN), owing to the more superficial position of this last structure [9]. Hence, ECA lesions are usually associated with FN dysfunction [10]. However, even penetrating injuries to the FN are very rare [11]. For example, in a 16-year retrospective study in which authors reported 456 consecutive patients with 557 peripheral nerve injuries, no cases of open section of the FN in the preauricular region were described [11]. Furthermore, Feldt et al., in reviewing 37,523 head and neck war injuries, found only 35 FN injuries [12].

We present an unusual case report in that the patient presented with an injury to the ECA inside the parotid region with no FN compromise. There is a large consensus in the literature that cases such as this one pose a significant clinical challenge because they involve large and important vascular and/or nerve structures in an emergent scenario [7, 13, 14]. Moreover, clinicians in most centers report limited experience with handling similar cases, which, in turn, causes considerable anxiety in medical personnel [7, 15]. Finally, because these cases are rare, scarce information regarding the surgical anatomy of these wounds is available [16]. The aim of the presentation of this clinical case, as well as of an anatomical dissection study performed to explain the clinical findings observed, is to add to the scant literature on emergent lesions to the ECA and the FN.

A 25-year-old Portuguese man with an unremarkable medical, social, family, and environmental history sustained a stab wound injury to his right preauricular region with a broken glass while he was sitting in a bar. Immediate profuse bleeding ensued. Provisory tamponade of the wound was achieved at the place of aggression by two off-duty doctors, who pressed a piece of clothing against the wound. The patient was initially transferred to a district hospital, where profuse arterial bleeding was observed by the general surgeon on call. A temporary compressive dressing was applied under local anesthesia. Subsequently, the patient was transferred to a tertiary hospital.

At admission in the emergency room, 2 hours after the injury, the patient was slightly diaphoretic and presented with slightly pale skin and mucosae. The patient’s left radial pulse was strong, regular, and had a frequency of 101 beats per minute. The patient presented with a pulsating lesion in the right preauricular region and mild weakness in the territory of the inferior buccal branch of the FN (Fig. 1). The remaining territory of the FN presented no changes. Pin-prick and light touch sensibility in the head and neck did not present changes. There were no signs of dysfunction of the other cranial nerves. The patient’s arterial blood pressure measured in his left arm was 110/75 mmHg. His physical examination was otherwise unremarkable.

However, in the operating theater, after the compressive dressing was removed, a large arterial bleeding was noted. Immediately, the bleeding was tamponaded, and a preauricular incision was made just deep to the subcutaneous musculoaponeurotic system of the face to expose the parotid gland. This gland presented an opening through which a section of the posterior and lateral flanks of the ECA was identified. To avoid inadvertent injury to the FN, the superficial lobe of the parotid gland was dissected posteriorly to anteriorly, thus exposing the FN and its branches. No lesion of the FN was observed. To minimize arterial bleeding, the incision was extended into a right lateral cervicotomy to expose the ECA after its origin in the carotid triangle (Fig. 2), and this vessel was temporarily clamped. At the same time, the superficial temporal and posterior auricular arteries were digitally compressed at the tragus and at the mastoid apex, respectively, by the surgeon’s assistant. The ECA was repaired deep to the FN with interrupted 6/0 nylon stitches.

The surgery took 7 hours in total. At the beginning of the surgery, the patient’s relevant blood test results were as follows: normal coagulation tests and blood sodium, potassium, and chloride; hemoglobin concentration of 7.2 g/dl (normal range 13.0–17.0 g/dl); hematocrit of 26.7% (normal range 40.0–50.0%); red blood cell count of 2.9 million/mm (normal range 4.4–5.9 million/mm); white blood cell count of 8500/mm (normal range 4.5–11.0 × 10⁴/mm); normal differential leukocyte counts; and normal renal and liver function tests. The patient received 3 red blood cell units during surgery because of intraoperative anemia. No further blood transfusions were needed postoperatively. At the end of surgery, the patient presented with the following significant blood tests results: normal coagulation tests and blood sodium, potassium, and chloride; hemoglobin concentration of 10.5 g/dl (normal range 13.0–17.0 g/dl); normal differential leukocyte counts; hematocrit of 31.1% (normal range 40.0–50.0%); red blood cell count of 3.28 million/mm (normal range 4.4–5.9 million/mm); white blood cell count of 9600/mm (normal range 4.5–11.0 × 10⁴/mm); neutrophilia (8,590/mm [normal range 2.0–8.5 × 10⁴/mm]); and normal renal and liver function tests. In the postoperative period, the patient was transferred to an intensive care unit and was nasotracheally intubated and ventilated. On the second day after surgery, a computed tomographic (CT) scan of the head and neck revealed marked edema and copious liquid in the right cervical-facial spaces. This, in turn, exerted a mass effect over the airways, with almost complete obliteration at the soft palate level (Fig. 3). For this reason, the patient was kept intubated for 8 days. On the third postoperative day, the patient developed a salivary fistula through the preauricular wound that was treated conservatively with the placement of a nasogastric tube, a nil by mouth regimen, and compressive dressings. On the seventh day after surgery, saliva emission through the wound ceased. Only then was the nasogastric tube removed and food intake reinstated. On the eighth postoperative day, a CT scan of the head and neck revealed that the airway swelling had largely subsided, and the patient was extubated. He has remained eupneic on atmospheric air ever since. On the ninth day of hospitalization, the patient was transferred to the plastic surgery department. His wounds healed well. Seven days afterward, he was discharged to home with no deficits in the territory innervated by the FN. The results of all blood tests performed at that time were within normal values. No serological or microbiological tests were done during the treatment of the patient.

Two years after surgery, at his last follow-up visit, the patient had an inconspicuous scar and presented with no motor deficits in the territory of the FN. He claimed to be happy with the functional and aesthetic outcomes.

This report describes an uncommon clinical situation in which there was a penetrating injury to the ECA in the parotid region. Reviewing the literature on penetrating injuries of the head and neck with major vascular lesions, we found very few reports of ECA injury in the parotid region, compared with lesions of the carotid and/or vertebral arterial system in the neck [2, 3, 6, 12, 17‐21]. Moreover, Tachmes et al., in reviewing parotid gland trauma in a tertiary referral center over a 10-year period, found only four cases of FN injury. In none of these cases was ECA injury present [10]. Furthermore, in the present case report, we describe a very unlikely clinical situation in which the ECA was injured without involvement of the FN. It is well known that when the ECA enters the parotid gland, it lies deep to the FN [22]. Thus, the initial clinical presentation of a large preauricular arterial bleeding with no significant motor deficits in the territory of the FN suggested an arterial lesion superficial to this nerve [22‐27].

The cadaveric study that we conducted revealed a small triangular space between the two main branches of division of the FN in which the ECA was not covered by the FN. In the case described, the glass fragment pierced this space and reached the deeper ECA (Fig. 5). This is obviously very improbable. We believe this to be the reason why we found no other such case in the literature, despite our best efforts. As far as we could determine, this triangular space has not been described before [22, 25, 28].

Even today, penetrating injuries to the head and neck region associated with significant arterial bleeding constitute surgical emergencies that are frequently very difficult to handle [2, 3, 5, 29]. The literature suggests that about 25% of penetrating neck trauma cases are associated with vascular injuries, with the internal carotid being the most frequently affected artery [5, 30]. In a 10-year retrospective study in which authors reported the data of 401 patients with penetrating neck trauma, the ECA was the third mostly commonly injured vessel, after the internal carotid and vertebral arteries [31]. Demetriades et al., reporting 223 patients in another large retrospective study, demonstrated that penetrating injuries to the ECA were less common than those involving the internal carotid, common carotid, and vertebral arteries [2, 3].

In contemporary times, penetrating injuries to the head and neck are much more common in war zones and in countries with higher violence rates [3, 4, 6, 12, 14, 18, 20, 21, 30, 32‐44]. In other countries, iatrogenic injuries are the main culprits for ECA lesions. Medical procedures most commonly involved in ECA injury are orthognathic surgery, head and neck oncological surgery, and temporomandibular joint invasive procedures [29, 45].

Historically, penetrating injuries to the head and neck were frequently associated with wars. These wounds have been associated with significant mortality rates. For example, during the American Civil War, it is estimated that 15% of the more than 4000 soldiers with these wounds died [1]. Mortality rates dropped to 11% in World War I and to approximately 7% in World War II, then remaining stable around this level for the remainder of the 20th century [6, 8, 12, 18, 20]. Recently, researchers in the Joint Facial and Invasive Neck Trauma (J-FAINT) Project, Iraq and Afghanistan, reported 37,523 facial and penetrating neck injuries in 7177 service members during the period of 2003–2011. These injuries were associated with an overall mortality rate of 3.5%.

It is widely believed that in the observed reduction of mortality, one of the most important contributing factors was the mandatory exploration of all wounds deep to the platysma muscle practiced by most military surgeons since World War II [1]. In 1956, Fogelman and Stewart published a seminal paper in the field, reporting a 6% mortality rate among patients who underwent immediate surgical exploration. This was in stark contrast to the astounding 35% mortality rate among patients who were not treated surgically or whose surgery was initially postponed [46]. Since then, in most trauma centers, mandatory exploration of deep penetrating head and neck injuries has become the gold standard for treatment [1].

Prompt control of bleeding in an ECA lesion is of paramount importance to prevent hemodynamic instability and eventual death [47]. Hemostasis should ideally be achieved through vessel exposure and direct suture of the severed segment [47]. However, this is not always possible, owing to difficulty in surgical access or to the extent of the vascular damage, which may require the use of autologous or synthetic vascular grafts [47]. In cases of difficult access to the severed segment or in cases of multisegment injuries, definitive control of bleeding can be achieved with ECA ligation or selective embolization [8, 47]. The choice is often determined by the availability of a skilled interventional radiologist and the experience of the surgeon in performing ECA ligation [8]. There are many ways to perform an ECA ligature. Most involve ligation of the vessel at its proximal portion just distal to the bifurcation of the common carotid artery. Ligation of the ECA at this level is estimated to reduce blood flow by approximately three-fourths [29]. The concomitant ligation of the superior thyroid, ascending pharyngeal, lingual, and facial arteries has been shown to reduce hemorrhage by roughly 85%. When the posterior auricular artery is additionally ligated, hemorrhage is seen to decrease to approximately 99% of the original carotid blood flow [29]. Selective ECA catheterization and embolization provide the significant advantage of avoiding the morbidity and iatrogenic potential associated with surgical exposure and manipulation of the ECA and surrounding structures. However, they also require catheterization of a large vessel, usually the femoral artery, as well as the use of a contrast agent to detect the bleeding sites and to deposit a thrombogenic agent. All these steps can have potential complications. In addition, selective embolization can be technically challenging in cases of small and tortuous vessels, particularly in the presence of hemorrhage-induced vasospasm [29].

The surgery in the clinical case presented in this report had an unusual level of complexity because the intact FN and its branches represented a fragile nerve mesh over the ECA bleeding site deep in the parotid gland. This made surgical access to the severed artery particularly difficult. Moreover, the numerous anastomoses between the branches of the two ECAs and their neighboring arteries made complete hemorrhage control using proximal arterial clamping impossible [16, 29, 48].

To the best of our knowledge, this is the first report in the literature of a section of the ECA in the preauricular region without involvement of the FN. The cadaveric dissection study we performed demonstrates that the anatomical basis for this clinical scenario is the existence of a triangular space between the cervicofacial and temporofacial nerve trunks, in which the ECA is not covered by the FN or its branches.

Furthermore, we believe that this case report eloquently demonstrates that in the presence of major penetrating injuries to the head and neck, sound anatomical knowledge is instrumental in establishing a presumptive diagnosis of the severed structures and of the level of the injury. This knowledge is also the basis for instituting adequate therapeutic measures to prevent potentially fatal hemorrhage while preserving functionally significant structures such as the FN [49‐56]. This avoided the subsequent need to repair the FN either primarily or with resort to nerve grafts or nerve flaps [24, 57].