Acute onset progressive hemiparesis in a case of head and neck injury.

Traumatic carotid artery injury is an increasingly recognized complication of severe blunt head or neck trauma in patients with motor vehicle accidents. A 22-year-old male presented after a high-velocity road traffic accident and sustained head, neck and systemic injuries. Initially the patient was neurologically stable and initial CT scan brain was also apparently normal. Few hours after the injury, the patient developed progressive left hemiparesis. MRI of brain was suggestive of acute infarct involving right internal carotid artery territory. In accordance with the literature and as in present case, it would be emphasized that the patients who develop gross neurological abnormalities after blunt trauma to the head or neck, there should be a high index of suspicion of having sustained injury to the carotid arteries.

INTRODUCTION

Traumatic carotid artery injury is an increasingly recognized complication of severe blunt head or neck trauma, more common in patients with motor vehicle accidents.[1] The carotid injury in these patients can easily be missed as clinical presentation can be overshadowed by significant intracranial injuries, effects of intoxication and other systemic injuries.[23]

CASE REPORT

A 22-year-old male patient presented two hours after a high-velocity road traffic accident (the vehicle collided with a lorry while he was driving the vehicle). There was history of transient loss of consciousness, oral and nasal bleed with multiple episodes of vomiting. There was no history of seizures. His general and systemic examination was unremarkable. Neurologically Glasgow coma scale was 14/15 (E3, V5, M6-eye opening to call, obeying command and oriented). He was moving all four limbs equally; pupils were bilaterally equal and reacting to light. Local examination revealed multiple lacerations over right side of the neck, massive bruising and swelling over right side of the neck, fracture mandible and massive swelling involving right upper limb [Figure 1]. His blood investigations were normal. X-ray chest was normal, x-ray right shoulder showed comminuted fracture of upper end of right humerus [Figure 2]. Initial computerized tomography scan (CT scan) of the brain showed anterior cranial fossa fractures and pneumocephalus [Figure 3]. CT scan of neck showed massive swelling involving right side of the neck and mandible fracture with normal vertebral column [Figure 4]. The patient was planned to be managed conservatively. Neck wounds were thoroughly cleaned and sutured. About six hours after the injury the patient developed progressively increasing weakness of left upper and lower limbs and became drowsier (GCS-E3, V4, M5). In view of new onset of neurological deficits and initial early normal CT scan a possibility of expanding intracranial hematoma was suspected. As the patient also had significant neck injury a differential diagnosis of blunt carotid injury with thrombo-embolic event was also suspected. Urgent repeat magnetic resonance imaging (MRI) showed evidence of the infarct in the right middle cerebral artery territory [Figure 5]. However, while the patient was recovering he suddenly developed hypotension and tachypnea and features suggestive of pulmonary embolism. In spite of aggressive management he did not recover and succumbed to it.

Figure 1

Clinical photograph showing massive bruising and swelling involving right side of the neck

Figure 2

X-ray right shoulder showing comminuted fracture of upper end of right if humerus

Figure 3

Initial CT scan brain showing anterior cranial fossa fractures and pneumocephalus and normal brain parenchyma

Figure 4

Initial CT scan showing massive swelling over right side of neck and fracture of mandible

Figure 5

MRI brain showing hyperintense signal changes in right internal capsule and basal ganglionic region

DISCUSSION

In spite of increasing awareness about the carotid dissection following blunt injury to the neck, the diagnosis may not be apparent initially and often delayed until the patients develop features of cerebral ischemia and focal neurological deficits.[4-7] The mechanism of injury to the carotids can be direct blow, hyperextension of neck with contralateral rotation of head, blunt intraoral trauma or skull base fracture.[3] The clinical presentation in patients with carotid injury is influenced by the extent of arterial damage and often there is a lucid interval between the injury and appearance of neurological symptoms (usually of less than 24 h).[7] Intimal damage can cause dissection and subsequent thrombosis that may present as transient ischemic attack or stroke.[58] At the time of presentation to the casualty the patient did not have any neurological deficits, however in view of significant systemic injuries and high-velocity impact mechanism a CT scan of brain and spine was performed that showed extensive neck swelling on right side and normal brain parenchyma and cervical spine.[8] In view of new neurological deficits in a patient of head and neck injury with initial normal CT scan, expanding intracranial hematomas (e.g. extradural or subdural) or contusions or as in present case thrombo-embolic event secondary to carotid artery injury were considered.[1-7] In literature the indications to investigate for carotid artery injury include “hemorrhage of potential arterial origin originating from the nose, ears, mouth, or a wound, expanding cervical hematoma, cervical bruit in a patient >50 years of age, evidence of acute infarct at brain imaging; unexplained central or lateralizing neurological deficit or transient ischemic attack, or Horner syndrome or neck or head pain”.[1] Non-invasive diagnostic modalities including carotid color Doppler ultrasound, computerized tomography angiography of the neck and magnetic resonance angiography with each method having its diagnostic limitations have been identified as the modalities of choice.[19] Duplex ultrasound can be used as the primary diagnostic modality; it would be cost-saving and have patient friendly characteristics.[10] As a rapid screening test for blunt carotid artery injury, in addition to a whole-body CT trauma scan, the integration of multidetector CTA is recommended.[1112] CT angiography is shown to be 98.6% sensitive and 100% specific, however it can underestimate subtle lesions such as intimal flaps.[13] MR angiography gives additional information on brain damage but it requires the patient to be stable and compliant. It is of limited value in depiction of concurrent osseous injuries, not readily available in all centers, and the degree of definition may not be adequate to recognize subtle injuries.[13-15] Still the catheter angiography is the gold standard diagnostic procedure in evaluating vascular trauma and can be combined with intervention where suitable expertise is available.[13] Management of blunt carotid artery injury depends on the type and extent of the injury.[16] The mainstay of treatment for these injuries is antithrombotic therapy and the majority of injuries will resolve with medical management.[7] Although anticoagulants and antiplatelet drugs may prevent ischemic stroke, but these may cause bleeding from traumatized tissues.[1] Surgical repair remains the gold standard in managing rupture of the carotid artery; however, emergency surgery in the setting of acute hemorrhage although very challenging will be life saving.[17] Apart from the surgical repair in centers where the required expertise and infrastructure is available, endovascular stenting have obvious advantage particularly in terms of morbidity.[17] In accordance with the literature and as in present case, it would be emphasized that in patients who develop gross neurological abnormalities after blunt trauma to the head or neck until proven otherwise, injury to the carotid arteries should be considered.[18]