Vascular Injury and Parenchymal Changes

CHAPTER 26 Vascular Injury and Parenchymal Changes

The spectrum of cerebrovascular trauma includes arterial occlusion, dissection, pseudoaneurysm, arteriovenous fistula, vasospasm, and venous thrombosis. Vascular trauma is the most common cause of stroke in individuals younger than 45 years of age1 and often has devastating consequences. Fortunately, newer diagnostic modalities such as CT angiography (CTA) have facilitated rapid diagnosis and treatment.


Extracranial vascular trauma may be blunt or penetrating. Blunt vascular trauma is most likely to occur with motor vehicle accidents, whereas penetrating trauma is usually secondary to assault with a sharp object or firearm.

Blunt Trauma


Blunt injury to the carotid and vertebral arteries is reported in fewer than 1% of motor vehicle collisions.2 The injury may lead to disabling or lethal infarcts, especially in younger individuals. The true frequency of vascular injury is likely to be higher than reported, because 23% of patients with carotid or vertebral injury have no related symptoms at the time of presentation3 and the diagnosis is often overlooked in the presence of concurrent severe head injuries.

Clinical Presentation

Vertebral artery dissections may present acutely or first become evident hours to weeks later.4 Physical findings include neck hematoma, bruit, palpable thrill, and Horner’s syndrome.5 However, as many as 50% of patients with blunt carotid injury show no external evidence of neck trauma.6 Damage to the intimal surface of the vessel can lead to platelet aggregation and subsequent embolization, so antiplatelet or anticoagulant drugs may be administered, provided there are no contraindications.2 Frank dissections and occlusions may lead to embolism/infarction of the brain stem, cerebellum, and posterior cerebral artery territory.


The internal carotid artery is vulnerable to intimal tearing, dissection, and subsequent occlusion as a result of rapid acceleration/deceleration of the head (Fig. 26-1). Intimal tears tend to occur where the internal carotid artery becomes stretched over the transverse processes of the upper cervical vertebrae or where the artery enters the skull base. Traumatic intimal tears may heal spontaneously or progress to dissection/occlusion.

The long course of the vertebral artery through the foramen transversarium from C6 to C1 makes this vessel prone to traumatic dissection from motor vehicle accidents, sports injuries, and chiropractic neck manipulation. The C1-C2 articulation is the most mobile segment of the cervical spine, so C1-C2 is also the most common site of vertebral dissection. From C2 to C6, fracture-dislocation may injure the vertebral artery within the foramen transversarium, resulting in dissection or occlusion (Fig. 26-2).


CT Angiography

Multidetector CT angiography (MDCTA) is highly accurate for detecting blunt cerebrovascular injury, with sensitivities of 97.7% and specificities of 100%.7,8 Therefore, MDCTA has replaced catheter angiography as a screening tool for blunt cerebrovascular injury at many level I trauma centers. Duplex ultrasonography, although accurate, cannot evaluate the carotid arteries at and above the skull base. Screening by MR angiography (MRA) presents logistical problems in the patient with multiple trauma, such as immediate MRI availability, lengthy examination time, patient motion, and incompatibility of many life support devices with MRI.

On contrast-enhanced CT, arterial injuries have varied appearances. With dissections, an intimal flap may be seen (Fig. 26-3), followed distally by tapering of the vessel. Maximum intensity pixel projection (MIPP) images confirm the abnormal morphology of the vessel lumen (Fig. 26-4). Pseudoaneurysms appear as collections of contrast material outside the wall of the injured artery (Fig. 26-5). Occlusions often present as a smoothly tapered artery that ends in a point. Thrombus may be seen as a filling defect within the artery (see Fig. 26-4C).

Penetrating Trauma


Injury to the great vessels of the neck is much more common with penetrating wounds than with blunt trauma, with an incidence approaching 25%.10 Gunshot and stab wounds are the most common mechanisms of penetrating injury. Blunt trauma and penetrating trauma cause similar lesions, including intimal flaps, dissection, occlusion, pseudoaneurysm, and arteriovenous fistula.


Intracranial vascular injury includes dissection, occlusion, hemorrhage, and fistula that involves the intracranial carotid and vertebral arteries, their branches, and any intracranial venous structures.

Pathophysiology and Clinical Presentation


When injury disrupts all three layers of an arterial wall the resulting hemorrhage may become contained by the surrounding soft tissue. The blood within the hematoma remains in contact with turbulent flow in the parent artery.5 With time, the wall of the hematoma organizes, becomes lined with fibrous tissue, and forms a pseudocapsule around the pseudoaneurysm. Pseudoaneurysms are unstable lesions that can rupture and present as sudden intracranial hemorrhage. They often rupture at 2 to 8 weeks after the traumatic event (Fig. 26-11) but may not rupture until years after the injury. Mortality after pseudoaneurysm rupture is 30% to 40%.13 Treatment usually consists of occlusion of the lumen with detachable coils or trapping of the parent artery. Covered stents are a promising future alternative.



In patients with carotid-cavernous fistula, contrast-enhanced CT may show dilatation of the ipsilateral superior ophthalmic vein (>4 mm), outward convexity of the cavernous sinus, engorgement of the extraocular muscles, proptosis, and preseptal soft tissue swelling. CTA may demonstrate irregularity of the cavernous carotid artery (Fig. 26-12). If the fistula has very high flow, CTA may also show involvement of both orbits. MRI and MRA more clearly depict the patterns of venous outflow, including the superior and inferior petrosal sinuses, emissary veins to the pterygoid plexus, and sphenoparietal sinuses. Despite the recent advances in noninvasive imaging, catheter angiography with rapid filming rates is still required to demonstrate the location and size of the fistula definitively (see Fig. 26-12D) and to plan interventional therapy. Currently, the treatment of choice is transarterial occlusion of the fistula with detachable balloons. Advances in covered stent technology may allow for bridging the tear in the carotid artery while preserving vessel patency.14,15


The assessment and management of traumatic brain injury require some understanding of cerebral physiology, specifically the interrelationships among cerebral blood volume (CBV), cerebral blood flow (CBF), intracranial pressure (ICP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP).

The normal adult ICP is 0 to 15 mm Hg. The adult intracranial volume is approximately 1500 mL. Intracranial compliance is defined as the change in intracranial volume divided by the change in ICP.16 Treatment of head injury is based on how the treatment affects ICP and compliance.16

The skull is a rigid, nondistensible structure. In adults, the brain occupies 85% to 90% of intracranial volume, the CBV about 10%, and cerebrospinal fluid (CSF) the remaining 5%. As edema and hemorrhage expand the traumatized brain, the ICP rises. Initially, the increase in ICP is accommodated by displacement of CBV and CSF from inside to outside the skull. However, this compensatory mechanism is very limited. Further increases in intracranial mass effect cause a rapid increase in the ICP.

Cerebral perfusion pressure is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP): CPP = MAP − ICP. Stated differently, CPP is the net pressure at which blood perfuses the brain. In a healthy individual with a normal MAP of 50 to 150 mm Hg, CBF is held constant through autoregulation by brain arterioles. When MAP falls below 50 mm Hg, compensatory mechanisms are no longer adequate. The CBF decreases, and ischemic injury is possible. Conversely, when MAP exceeds 160 mm Hg, excessive CBF may occur and lead to increased ICP. Autoregulation works well in the noninjured brain but is often impaired in the traumatized brain,16 so ICP rises with intracranial injury. The brain has very limited tolerance for increases in ICP, especially rapid increases. Uncontrollable rise in ICP is the single most frequent cause of death in traumatic brain injury. The elevated ICP poses two dangers. First, increased ICP can lead to decreased CPP and ischemic infarction; indeed, 80% to 90% of patients who die of traumatic brain injury have evidence of ischemic injury at autopsy.17 Second, very elevated ICP can lead to brain herniation.

Management of the acutely brain-injured patient requires control of ICP and maintenance of adequate CBF. In the adult, the ICP is ideally kept below 20 mm Hg. This is accomplished by elevating the head to 30 degrees, administering osmotic diuretics (mannitol), using hyperventilation to blow off CO2, and draining CSF through a ventricular catheter. The CPP is kept at 60 mm Hg or higher to ensure adequate CBF. This is accomplished by keeping the patient euvolemic and supporting the patient’s blood pressure.


Cerebral edema is an increase in brain tissue volume resulting from an increase in tissue water content.18 It may be focal or diffuse.


The pathogenesis of brain swelling after traumatic brain injury is unclear. Conventional wisdom held that vascular engorgement caused an increase in CBV that then elevated the ICP. However, the vascular engorgement “etiology” has not been substantiated in animal studies.19 Until recently it had not been possible to measure brain water content or CBV in the living brain-injured patient. Brain tissue water content can now be calculated using phase-sensitive inversion recovery slices, from which a pure T1W image can be calculated.20,21 The calculated T1W image is then converted into a brain water image. CBV is measured using a combination of stable xenon CT and contrast-enhanced CT.22 The xenon CT scan is used to obtain CBF. Dynamic contrast-enhanced CT is used to determine mean transit time. CBV is then calculated from these two parameters using the equation: CBV = mean transit time × CBF.

Marmarou and colleagues studied 31 patients with severe traumatic brain injury who had determinations of both brain tissue water and CBV. They found that brain water was increased but CBV was actually decreased.23 They concluded that the brain swelling associated with traumatic brain injury is caused by brain edema not increased CBV. An increase of only 1% in brain water content causes an increase in brain volume of 4.4%, which can elevate the ICP above 20 mm Hg.24


The cerebral edema associated with severe traumatic brain injury is both intracellular (cytotoxic edema) and extracellular (vasogenic edema) (Fig. 26-13). MRI study of patients with diffuse brain injury showed restricted diffusion and decreased ADC values, indicating intracellular edema.24 The CBF values of the study patients were all well above the ischemic threshold, eliminating ischemia as the cause of restricted diffusion.24 Alternatively, in a case with focal brain injury, the core of a contusion and the area immediately surrounding it showed increased apparent diffusion coefficient, indicating vasogenic edema (Fig. 26-14). The brain more distant from the contusion showed decreased apparent diffusion coefficient, indicating cytotoxic edema. Thus, the cerebral edema seen in traumatic brain injury is both intracellular and extracellular, with cytotoxic edema predominating.

The mechanism by which the cytotoxic edema forms remains unknown but may be related to mitochondrial dysfunction.24 The cellular edema develops slowly and becomes dominant at 1 or 2 weeks after injury.25 The vasogenic edema is thought to result from breakdown in the blood-brain barrier immediately after traumatic brain injury. It predominates in the first hour or so after injury. Animal studies show that the blood-brain barrier is usually reestablished within 30 minutes after the trauma.25 The type of edema present in traumatized brains therefore also varies with the time after injury.


Herniation is displacement of brain tissue from one compartment into another. It is a dreaded complication of mass effect, regardless of the cause, because it may result in infarction, coma, or death. The major types of brain herniation include subfalcine, transtentorial, and tonsillar (Fig. 26-15). Transtentorial herniation is subdivided into lateral (uncal, hippocampal) and central types and then described as descending or ascending in accordance with the direction of brain shift. Most central transtentorial herniation is directed inferiorly, but significant ascending central herniation can result from masses situated inferior to the tentorium. Herniations are readily detected by both CT and MRI and must be recognized to prevent or limit serious neurologic sequelae (Table 26-1).

Jan 22, 2016 | Posted by in NEUROLOGICAL IMAGING | Comments Off on Vascular Injury and Parenchymal Changes
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