Successful Surgical Management of Intracranial Carotid Artery Trauma Following Penetrating Facial Injury: A Case Report

Introduction

The face protects several exquisitely vital structures such as the carotid arteries. Carotid artery injury has an incidence of 0.2% in the National Trauma Data Bank [1]. The true incidence of traumatic intracranial carotid artery injury is unknown. One single-institution retrospective review found that intracranial carotid artery injury was observed in 10 out of 18 123 patients (0.6%) admitted for multiorgan trauma [2]. The most recent nationwide American data characterizing penetrating carotid injury (PCI), whether extracranial or intracranial, reported 3319 adult patients over a 15-year period who survived beyond the emergency department – roughly 221 cases per year [3]. Operatively managed PCI is associated with an 18.5% mortality rate and a 10.5% risk of stroke [3]. Of operative approaches to PCI, open repair accounts for 88.6% and endovascular repair accounts for 11.4% [3]. Finally, only 1.9% of PCI is due to a non-gunshot, non-stab “other” mechanism of injury [3]. This report details the diagnosis, multidisciplinary operative treatment, and postoperative course of a 74-year-old woman who suffered penetrating midface trauma with intracranial injury to the right internal carotid artery (RICA) and right optic nerve due to a wooden foreign body following a fall into a honeysuckle bush.

Case Report

A 74-year-old woman presented to the hospital after a ground level fall into a honeysuckle bush. She was found to have penetrating left facial trauma via wooden foreign body (Figure 1). The patient presented to a community hospital awake and oriented with Glasgow Coma Score (GCS) of 15 but with new-onset blindness of the right eye. Computed tomography (CT) imaging of the head revealed a wooden branch 1 cm in diameter penetrating the left maxillary sinus and terminating in the basal right forebrain adjacent to the RICA (Figure 2). Telephone neurosurgical consultation was obtained, and it was recommended that the branch be left in place until formal neurosurgical evaluation was performed. The patient was transferred to a tertiary trauma center by fixed wing aircraft. Upon arrival, examination showed GCS of 12 (Eyes 2, Verbal 4, Motor 6), right pupil 4.13 mm with neurological pupillary index (NPi) of 1.1, left pupil 4.55 mm with NPi of 2.6, and purposeful movements in all limbs. Visual acuity testing was limited due to sedation. CT angiography (CTA) of the head and neck was performed which demonstrated stable hemorrhage in the suprasellar cistern with no change in volume from 5 hours prior (Figure 2). There was no contrast extravasation. The decision was made to proceed immediately to surgery for a combined approach involving neurosurgery and otolaryngology.

The patient was transferred to the operating room. General anesthesia was induced with sevoflurane and propofol. Neuromonitoring was established with electroencephalography (EEG) and somatosensory evoked potentials. A right cervical exploration was performed by the head and neck surgeon to achieve proximal and distal control of the RICA. Some subcutaneous fat was put aside for skull base reconstruction. Simultaneously, a right pterional craniotomy was performed. Bone and dural flaps were created. The Sylvian fissure was exposed via microdissection and the internal carotid artery (ICA) complex was revealed. Prior to clamping, a bolus of 20% mannitol was given. Other neuroprotective medicines were employed including continuous propofol, continuous clevidipine, and a 2 mg bolus of midazolam. Temporary clips were applied to the artery for 10 minutes, then removed. No changes in intraoperative neuromonitoring were observed, which indicated RICA sacrifice could be tolerated if necessary. The foreign body was identified. It had pierced completely through the right optic nerve and the tip was deforming the RICA (Figure 3). At this stage, the foreign body was pulled out (Figure 4). Immediate brisk bleeding was encountered. Temporary clips were applied proximally at the cervical RICA and distally at the choroid segment of the RICA. Bleeding ceased. The RICA was found to have a small laceration in the carotid cave area which was packed with Surgicel then repaired with DuraSeal. Electrocautery was used judiciously. The temporary clips were removed. No further bleeding was visualized (Figure 5). A small amount of parasellar subarachnoid hemorrhage was evacuated with suction. Doppler auscultation confirmed good flow within the right-sided ICA, anterior cerebral artery, and middle cerebral artery (MCA). Endoscopic endonasal transsphenoidal surgery (EETS) was then used to perform posterior septectomy. There was obvious trauma to the left face of the sphenoid, the right roof of the sphenoid, and in the opticocarotid recess. The area was cleaned, and the skull base defect was closed with a fat graft obtained from the cervical exploration. The dura was closed primarily with suture, then onlay duraplasty was performed with a type I collagen matrix graft and an airtight seal was obtained with fibrin sealant. The bone flap was secured. The wound was irrigated until clear. Drains were left in subgaleal and submuscular spaces and suction was applied. The galea and skin were closed, and the craniotomy incision was dressed. The neck was washed out with saline and a 15 Fr Blake drain was placed prior to closure. The patient awoke and was extubated without complication.

Postoperative CTA and magnetic resonance imaging (MRI) of the head showed no signs of large vascular territory infarction; however, right frontotemporal cytotoxic edema was observed on MRI (Figure 6). A strict systolic blood pressure goal range of 90 to 100 mmHg was achieved with appropriate titration of continuous nicardipine and norepinephrine. Serum sodium was kept above a goal of 140 mmol/L and vasospasm prophylaxis was implemented with nimodipine. Antimicrobial meningitis prophylaxis was initiated with ceftriaxone and metronidazole. The patient was kept in deep sedation for the first 2 postoperative days. Transcranial doppler ultrasound was performed daily throughout the first postoperative week. No clinically significant vasospasm was noted. Ophthalmology was consulted on postoperative day 5, and examination showed a fixed right pupil. The patient confirmed blurry right eye vision which gradually improved throughout the remainder of her hospitalization. She was definitively extubated on postoperative day 9 and discharged on postoperative day 14 to a skilled nursing facility. She completed 10 days total of antimicrobial prophylaxis.

Telephone follow-up was conducted 1 year after the injury. There were no major motor sequelae. The patient reported persistent blurry vision of the right eye. She said, “My left eye was good until the third day after [the accident], and then it started to mimic my right eye.” Her left eye vision has improved somewhat over the past year but remains worse than before the accident. She says that her right eye can, “see colors and see a television screen, but cannot make out the closed captioning.” Her left eye can read large text. Her handwriting has notably worsened. She denies headaches but says she often gets dizzy while standing up. Dizziness was not an issue prior to the injury. She denies any other ongoing symptoms. She wears glasses and plans to follow up with optometry soon. She reports she has been in discussion with her primary care provider about potentially seeing an ophthalmologist.

Discussion

This case details the use of endoscopic skull base surgery combined with open craniotomy in the uncommon setting of penetrating trauma to the paraclinoid ICA and the optic nerve. Immediate surgical management was indicated due to the involved anatomy. The endoscopic endonasal transsphenoidal approach was chosen in this case to afford the best possible visualization of the sphenoid sinus injury and of any potential cerebrospinal fluid leak upon removal of the foreign body. Reconstruction of skull base defects, whether traumatic or iatrogenic in origin, is essential to seal off the intracranial space and reduce the risk of complications such as meningitis, encephalitis, and tension pneumocephalus [4]. In our case, reconstruction of the sphenoid defects was done with fat grafting and bioresorbable dressing. Free-graft reconstructions are thought to be noninferior to vascularized pedicle flaps in the closure of small or low-flow defects [4]. Vascularized reconstructions do provide benefit when managing large or high-flow defects [4]. Tissue sealants and dissolvable hemostatic packings are appropriate adjuncts for reinforcing around the edges of grafts and also for performing arterial repair [5,6].

The involvement of an ear-nose-throat (ENT) surgeon during EETS facilitates the identification and navigation of nasal anatomical variants which are present in a robust proportion of patients. A 2019 2-armed nonrandomized study found that EETS performed collaboratively between an ENT surgeon and a neurosurgeon is associated with shorter time to sphenoidotomy and lower risk of intraoperative complications, as opposed to when performed solely by a neurosurgeon [7]. ENT surgeon participation also facilitates proximal vessel control in the setting of carotid trauma through the use of cervical exploration.

With respect to the ICA injury, we were able to achieve hemostasis with compressive hemostatic gauze packing, tissue seal-ants, and electrocautery. For cases in which packing proves inadequate, endovascular methods or endoscopic vessel clipping should be considered. Unilateral ICA sacrifice is associated with rates of permanent neurologic deficit upwards of 20% but may be deemed necessary depending on the size of the vessel injury [4]. Proximal vessel control, a prerequisite for ICA sacrifice, is rapidly obtained through neck dissection, as our case and others illustrate [8]. Neck dissection additionally provides a source of graft for skull base closure if the EETS approach is chosen. The feasibility of sacrificing the ICA can be assessed preliminarily by angiography of collaterals and more definitively by intraoperative neuromonitoring and temporary vessel clipping, as in our case. If preoperative imaging produces absolutely no suspicion for vascular injury, transsphenoidal foreign bodies can potentially be removed with EETS alone and without open approaches to vessel control [9]. However, the open approach may not always be ideal. Khosla et al demonstrated that endovascular intervention should be prioritized when imaging suggests that arterial injury is too extensive to allow for safe distal control in the open operative setting [10]. Dubose et al performed a comprehensive literature review of endovascular stenting of traumatic ICA injuries and found 113 cases as of 2008 [11]. Stenting tends to be implemented in cases of blunt trauma and for injury to the high extracranial ICA where an open approach is particularly difficult. Rates of operative mortality and postoperative stroke seem to be lower for stents than for open surgical techniques, although conclusions are limited by sample size and the retrospective nature of available data.

Pharmacologic neuroprotection was enforced throughout the case with propofol, sevoflurane, mannitol, clevidipine, and midazolam. Propofol intensifies GABAA receptor activity. It reduces both cerebral metabolism and cerebral blood flow without compromising oxygen delivery to tissue beds [12]. Sevoflurane, an inhaled anesthetic, produces dose-dependent reductions in cerebral metabolic rate [13]. Mannitol is a sugar alcohol that reduces cerebral edema and alleviates endothelial cell stress by drawing free water into the intravascular compartment. Clevidipine is a calcium channel antagonist that reduces influx of calcium into cells and thereby prolongs structural integrity under ischemic conditions. Finally, midazolam (like propofol) is an allosteric modulator of the GABAA receptor. Midazolam has shown neuroprotective and antiapoptotic effects in animal models of cerebral ischemia, and its benefit is thought to be linked to suppression of glutaminergic excitotoxicity [14,15]. In our case, the administration of propofol, sevoflurane, and clevidipine was continuous throughout and boluses of mannitol and midazolam were administered within 10 minutes prior to carotid clamping.

Arterial vasospasm, a known sequela of subarachnoid hemorrhage, is thought to arise from free radical damage to vessel endothelium secondary to breakdown of blood products [16]. Vasospasm contributes to cerebral ischemia. The incidence of vasospasm is estimated at around 30–40% of patients with traumatic brain injury [17]. Transcranial doppler ultrasound is the ideal first-line method for diagnosing vasospasm because it is portable, noninvasive, and cost-efficient [18]. The Lindegaard index of anterior cerebral circulation – the ratio of maximum flow velocity in the MCA compared with the extracranial ICA – is useful for distinguishing vasospasm from hyperemia, with a ratio greater than 3 representing true vasospasm [19]. Calcium channel blockers have historically been first-line prophylaxis (oral route) and treatment (intravenous or intrathecal routes) for cerebral vasospasm [18]. Endovascular angioplasty is recommended as salvage therapy in the setting of vasospasm refractory to medical management [18].

Conclusions

The management of facially penetrating foreign bodies begins with assessment for neurologic deficits and vascular injury. We recommend leaving such objects in place and not removing them until definitive imaging is obtained. We present an interesting case of penetrating trauma to the intracranial carotid artery – an extremely rare injury. A retained foreign body was removed with satisfactory patient outcome using a combined endoscopic and open surgical approach along with cervical exploration for vessel control.