IntroductionNeurological alterations are common in polytraumatised patients and, in most cases, can be explained by direct traumatic brain injury. On the contrary,

potentially life-threatening blunt cervical artery injuries (BCVI), usually consisting of arterial dissection, are relatively unfrequent after a major trauma, as theincidence of traumatic dissection of the internal carotid artery ranges from 0,08 to 3,7%. The overall mortality is reported to be 21% to 31%; moreover, 37% to58% of patients suffer a permanent neurological deficit at hospital discharge1. A latent asymptomatic period of variable duration has long been recognized asa unique feature of cervical artery injury2 and more than half patients with dissection suffer from delayed cerebral infarction or transient ischemic episodes.Early diagnosis and treatment are therefore of the utmost importance to reduce the risk of hemispheric stroke and the subsequent morbidity and mortality2.Given the rarity of these lesions, the delayed clinical presentation and the simultaneous presence of other critical injures requiring immediate attention, thedetection of this complication before neurological damage has occurred remains a great challenge and requires a high index of suspicion. The case of apatient with massive cerebral infarction related to an undetected carotid artery dissection leading to cerebral death is reported below.

Case presentationA 41 year old otherwise healthy woman was admitted to a general community hospital after a severe trauma due to a high speed car accident. At the first

clinical examination the patient was conscious, with normal vital signs and a GCS of 10 (E3-V1-M6) and a slight bilateral hypertone localised at the lowerlimbs. Whole body CT scan at admission showed bilateral fractures of the I, II, III, IV, V, VI ribs, of the VII left rib and the right clavicle and a fracture of thetransverse process of the VI cervical vertebra. Considering the severe chest trauma, the patient was admitted to a General ICU. Ten hours after the trauma, asudden deterioration of consciousness was observed, associated with a diffuse hypertone. An emergent head CT scan showed multiple contusions of the leftcerebellum and punctiform hemorrhages of the right cerebral hemisphere; the patient was kept sedated and mechanically ventilated. Twelve hours later, acontrol head CT scan showed extended infarction of the right cerebral hemisphere, associated with oedema, effacement of the sulci and compression of thehomolateral ventricle. Therefore, a diagnosis of traumatic carotid dissection was suspected, prompting an urgent angio-MRI scan and an angiographic studywhich demonstrated the presence of right arterial dissection and an 18 mm extended thrombus in the extracranial tract of internal right carotid artery,located about two cm above the bifurcation. Considering the clinical picture and the time elapsed since the onset of the symptoms, the vascular surgeon’sconsult ruled out the immediate need for surgery. A medical management with dipiridamol, mannitol and furosemide was immediately started and thepatient was deeply sedated; furthermore, an intracranial pressure monitoring was instituted. Four days later, the intracranial pressure became elevated andunresponsive to medical treatment; therefore, the patient was transferred to the neurosurgical hospital to undergo decompressive craniotomy and was thenadmitted to our ICU after surgery. Despite the decompression, the neurological function did not improve and three days later the diagnosis of cerebral deathwas established.

DiscussionIn the reported case, the first clinical examination was not suggestive of a

traumatic cervical artery dissection, and normal CT scan led to overlook theunspecific neurological signs; consequently, targeted investigations of thebrain-supplying arteries were not performed. A ten hours delayed suddenneurological deterioration occurred, and the presence of mild haemorragiclesions at the head CT scan performed at that point probably contributed tothe even further delayed diagnosis, that was suspected only after the thirdhead CT. Overall, the diagnosis of right carotid dissection was established

POST-TRAUMATIC CAROTID ARTERY DISSECTION: a case reportSpano F.*, Isoni P.**, Sanna M.* ,Tolu C.*, Atzeni D.** Castaldi P.***

* Scuola di Specializzazione Anestesia e Rianimazione Università degli Studi di Cagliari - **Dir. Medico Rianimazione P.O. Marino ASL 8 Cagliari - ***Direttore Rianimazione P.O. Marino ASL 8 Cagliari

a

head CT. Overall, the diagnosis of right carotid dissection was establishedthirty-three hours after ICU admission, when the surgical treatment of thevascular lesion was deemed not necessary. Despite the medicalmanagement and even after decompressive craniotomy, the patient died.This case illustrates the potential disastrous consequences of anunrecognized traumatic carotid dissection and underscores the importanceof awareness of its risk factors, as the diagnosis of this complication beforethe onset of the stroke-related signs and symptoms results in a remarkableimprovement of the outcome2. Four-cerebral artery angiogram is the goldstandard for evaluation of brain supplying arteries; unfortunately, itsinvasiveness and complications preclude its indiscriminate application. CTangiography (CTA) is a less invasive though less accurate diagnostic tool,therefore it has been proposed to obtain CTA of the neck during CT scanevaluation of other body parts. Angiography should only be performed inpatients with a high suspicion index and a CTA negative result1. Since BCVIhas been recognized as a challenging as well as a life-saving diagnosis,several authors have identified different screening criteria; moreover, twoscreening protocols have been developed, namely the Denver and theMemphis screening protocols3,4,5. In order to improve diagnostic accuracy,this screening criteria have been even more expanded, notably including allpetrous bone fracture4,6, mandible fracture, thoracic injury, complex skullfracture with orbital involvement, scalp degloving injuries and cardiac andgreat vessel injury. However, a recent meta analysis found that only cervicalspine injury (OR 5.45) and thoracic injury (OR 1,98) were significantlyassociated, with a 5-fold and 2-fold greater likelihood of BCVI, respectively8;moreover, several studies have found that risk factors are absent in as manyas 20-30% of patients diagnosed with BCVI4,7. Remarkably, the latter strongpredictors identified by the meta-analysis were both present in this case.Even though the small number of strong BCVI predictors may suggest theopportunity of a restricted screening protocol, given the disastrousconsequences of a missed diagnosis, a growing number of authors advocatea liberalized screening, including all injuries instead of injuries highlysuspected for BCVI8; furthermore, an increasing conviction rising from thepast two decades experience highlights the importance of incorporation ofthe injury mechanism, specifically consisting of cervicalrotation/hyperextension, hyperflexion, or direct blow, combined withpatient injuries instead of the presence of risk factors alone4. Clinicalacumen and high index of suspicion, based on the awareness of risk factorsand injury mechanism, seem therefore to be equally of the utmostimportance for BCVI screening and diagnosis.

Conclusions.In summary, traumatic cervical lesions are a relatively rare event and often

occur asymptomatically during the first hours after the polytrauma. Delayedneurological signs and symptoms are often severe, potentially leading topermanent deficits or even cerebral death. This emphasizes the importanceto accurately search for risk factors, as the consequent early diagnosis andtreatment of such insidious injuries can reduce morbidity and mortality,finally improving the outcome. From this standpoint, the latentasymptomatic period should be considered as a potentially advantageousfeature, if every effort is made to timely identify and treat the silent arterialinjury during this time.

Memphis screening protocol5

Denver screening protocol3,4

Risk factors for BCVI Risk factors for BCVI Signs and symptoms of BCVI

Cervical spine fracture High-energy transfer mechanism with:

Arterial hemorrage

Neurological exam not explained by brain imaging

Le Fort II or III fracture Cervical bruit

Horner’s Syndrome Cervical-spine fracture patterns: subluxation, C1-C3 fractures, fractures involving tranverse foramen

Expanding cervical hematoma

Le Fort II or III facial fracture Petrous bone fracture Focal neurological deficit

Skull base fracture involving the foramen lacerum

Diffuse axonal injury with GCS<6 Neurologic examination incongrous with head CT scan findings

Neck soft tissue injury (ex. Seat belt injury)

Near hanging with anoxic brain injury Stroke on secondary CT scan

References1.Baker WE et al. – Unsuspected vascular trauma: blunt arterial injuries – Emerg Med Clin N Am; 2004 Nov: 22(4): 1081-98.2.Biffl WL et al. – The unrecognised epidemic of blunt carotid arterial injuries. Early diagnosis improves neurologic outcome – Annals of surgery. Vol 228. No 4, 462-470.3.Biffl WL et al. – Optimizing screening for blunt cerebrovascular injuries – Am J Surg. 1999; 178: 517-522.4.Burlew CC et al. – Blunt cerebrovascular injuries: redefining screening criteria in the era of noninvasive diagnosis – J Trauma Acute Care Surg. 2012 Feb; 72(2):330-5.5.Miller PR et al. – Prospective screening for blunt cerebrovascular injuries. Analysis of diagnostic modalities and outcomes -- Annals of surgery 2002 Sep; 236 (3): 386-93.6.Ciapetti M.et al. – Diagnosis of carotid arterial injury in major trauma using a modification of Memphis criteria – Scand J of Trauma, Resuscitation and Emergency Medicine 2010 Nov 22; 18:61.7.Bruns BR et al. – Blunt cerebrovascular injury screening guidelines: what are we willing to miss? – J Trauma Acute Care Surg. 2014 Mar; 76(3): 691-5.8.Rendall WF et all. – A systematic review and meta-analysis of diagnostic screening criteria for blunt cerebrovascular injuries – J Am Coll Surg. 2012 Mar; 214(3):313-27.

Table 1: The Denver and Memphis screening protocols

bc

d

Figure 1: angiorgraphic findings (a, b, c) and CT findings after decompressive craniotomy (d)