Internal carotid artery occlusion after trauma

Introduction to internal carotid artery occlusion after trauma After the neck or cervical vertebrae are directly or indirectly injured, the internal carotid artery or vertebral artery intima is damaged. On this basis, inflammation and oozing occur, and then a local thrombus is formed and spread to the distal end, causing cerebral infarction of the corresponding blood supply. After trauma, internal carotid artery occlusion can spread upward involving the ophthalmic artery, choroidal artery, until the front of the willis ring, even the anterior and middle cerebral arteries. In patients with mild neurological dysfunction, severe cases can cause large cerebral infarction and deep coma, and one third of them are often life-threatening. basic knowledge The proportion of sickness: 0.004% - 0.007% Susceptible people: no special people Mode of infection: non-infectious Complications: cerebral infarction edema

Causes of internal carotid artery occlusion after trauma

(1) Causes of the disease

In addition to the direct injury to the carotid artery in addition to the open neck injury, cranial and neck closed injury caused by traffic accidents is often the main cause of carotid injury. When the neck is excessively strong, the back and lateral flexion can make the neck The internal artery is on the third cervical vertebrae, causing damage to the vessel wall and intima and causing thrombosis. Sometimes it may be due to damage of the common carotid artery. After thrombosis, it continues to develop upward, and the carotid artery is occluded beyond the carotid bifurcation. Therefore, the occlusion of the neck segment is most common in the carotid bifurcation at 1 to 3 cm, accounting for about 70%, followed by the embolization of the siphon, that is, the base of the internal carotid artery, where the artery is relatively fixed and vulnerable to violence. Involvement and squeezing, or direct contusion of blood vessels due to skull base fracture, resulting in intimal detachment, shrinkage, wall bleeding, resulting in vascular stenosis, platelet wall and thrombosis, and further occlusion of the middle cerebral artery, especially The branch of the temporal lobe, which enters the brain parenchyma from the free cerebral cistern, is more likely to be impacted or squeezed on the sphenoid ridge to cause damage to the vascular portion. The cerebral artery wall is opposite to the artery in other parts of the body. And the inner membrane and the middle layer are easy to separate, so there are many opportunities to form inter-wall hematoma or dissection aneurysm. In addition, the occlusion of the posterior cerebral artery, the vertebral-basal artery and the deep communication branch of the brain is occasionally Occurrence, the former is often secondary to the cerebellar incision, because the brain stem is displaced downward, causing the posterior cerebral artery to be embedded in the cerebellar incision, resulting in occlusion, which can lead to hemianism; vertebral-basal artery occlusion More common in the impact of the neck and neck damage, due to the violent movement of the cerebellum, the vertebral artery is involved, squeezed, or the basilar artery directly hits the slope and injured, once the thrombosis, the patient often falls into a deep coma, mortality Very high, traumatic deep brain occlusion can cause basal focal infarction is rare, more accidentally found in CT scans, generally occur in children and young people, clinically only partial hemiplegia and partial sensory disturbance, It is easy to be confused with the brain damage and should be noted.

(two) pathogenesis

In recent years, studies on cerebral ischemia and hypoxia after traumatic brain injury have revealed that the mechanism of traumatic internal carotid artery occlusion is not only the main cause of mechanical damage to the cerebral vessels itself, but also some internal factors that contribute to cerebral vascular thrombosis. For example, the dysregulation of vasoactive substances after injury, the decrease of cerebral blood flow and the hypercoagulability of blood, etc., among which the substances causing cerebral vasospasm are particularly important, because many substances that promote vasospasm such as catecholamine (CA) after brain trauma , serotonin (5-HT), norepinephrine (NE), contractile prostaglandin (PG), oxyhemoglobin (OXYHb), lipid peroxide (LPO) and potassium ions are significantly elevated, Injury of vascular endothelial cells, due to the loss of barrier function, the permeability is significantly increased, so that the vasoactive substances serotonin, oxyhemoglobin, etc. can directly act on vascular smooth muscle and cause vasospasm. In addition, vascular endothelial cells also have The function of producing vasoactive substances and regulating vascular tone, when the endothelial cells are damaged, the imbalance between the vasospasm and the vasoconstriction is caused by blood. Endothelium-derived endothelium-derived vasoconstrictor (EDCF) is dominant, so that the cerebral blood vessels are in a state of sustained contraction, bringing together various factors that promote vasospasm, plus Hemorheological changes caused by traumatic brain injury, such as increased whole blood viscosity, decreased red blood cell deformability, increased aggregation, platelet activation, increased viscosity, and local cerebral vascular damage, will eventually occur in a variety of conditions. Under the influence of factors, cerebral vascular occlusion and infarction of the brain domain are involved.

Prevention of internal carotid artery occlusion after trauma

Early detection and early diagnosis and early treatment.

Complications of internal carotid artery occlusion after trauma Complications Cerebral infarction edema

Such as acute internal carotid artery thrombosis, the artery is completely blocked, and the collateral circulation of the brain is insufficient, acute cerebral infarction, diffuse cerebral edema, severe carotid artery embolization may be a large cerebral infarction.

Symptoms of internal carotid artery occlusion after trauma Common symptoms Neck and shoulder skin hard dysfunction Drowsiness hemian sensation Dysfunction cerebral membranous artery occlusion

The clinical manifestations of traumatic internal carotid artery occlusion mainly depend on the location of the injured blood vessels and the extent of vascular spread. The speed of thrombus development, the size of the affected blood vessels and the compensatory ability of surrounding blood vessels are related to the severity of cerebral infarction. Clinical signs can be Immediately after the injury, it can also be performed several days after the injury.

The clinical manifestations of traumatic internal carotid artery occlusion generally have the following conditions: If the thrombus is located at the bifurcation of the common carotid artery, only the beginning of the internal carotid artery is involved, and the patient has hemiplegia within a few hours to several days after the injury, aphasia. Decreased visual acuity and hemianopia, about 15% of patients have epilepsy, such as acute internal carotid artery thrombosis, the artery is completely blocked, and the collateral circulation of the brain is insufficient, resulting in severe ischemia of the lateral brain, acute cerebral infarction, diffuse Sexual cerebral edema, manifested as a progressive disturbance of consciousness after injury, severe internal carotid artery embolization is complete, rapid onset, due to large cerebral infarction, can enter the cerebral palsy crisis within a few hours, and even death, fundus examination visible The fundus side of the fundus artery is in a collapsed state, and some of the internal carotid artery occlusion, or limited to the extracranial segment, may be asymptomatic or mild in clinical due to the compensatory ability of the contralateral carotid artery system and good blood flow.

Examination of internal carotid artery occlusion after trauma

1. Cerebral angiography showed obstruction of the extracranial segment of the affected internal carotid artery, and the image of the brain and anterior cerebral artery disappeared.

2. MRI examination can be detected 1 hour after cerebral ischemia, cerebral edema has appeared in the ischemic area within the first 9 hours, low signal on T1 weighted image, high signal on T2 weighted image; necrosis in ischemic tissue after about 12h The T1 relaxation time is prolonged, which is characterized by a long T1 long T2 signal; when the ischemic area is softened, the signal is similar to the cerebrospinal fluid phase.

3. CT scan in the early stage of cerebral ischemic area within 6 ~ 24h, only a small number of patients with a slightly low-density area with unclear borders, the detection rate is slightly inferior to MRI, but after 24h, most of the low-density infarcts with clear boundaries can be seen. The morphology and location are consistent with the distribution of occluded arteries; at 2 to 15 days, the lower density of infarcted areas is particularly pronounced, with varying degrees of cerebral edema and mass effect; at 2 to 3 weeks, collateral circulation begins to form. Capillary enlargement and hyperemia, so there is a curved or nodular density or slightly higher density in the infarct area. At this time, the lesion range is rather blurred; after 4 to 5 weeks, the infarct area is cystic, and the density is similar to that of cerebrospinal fluid; The display of cerebral infarction is more characteristic. In the first week after arterial occlusion, there may be no enhancement due to severe ischemic attack. From 7 to 10 days, due to capillary proliferation, obvious linear, cerebral gyrus or annular enhancement images can be seen. Have important diagnostic value.

4. Doppler ultrasonography, positron emission tomography and radionuclide scintigraphy cerebral angiography can help to understand the situation of cerebral ischemia or infarction, and can be used as a means of auxiliary diagnosis.

Diagnosis and diagnosis of internal carotid artery occlusion after trauma

For patients with mild brain injury and internal carotid artery occlusion, the clinical manifestations and brain damage are often inconsistent with this disease, especially after 1 to 2 days after injury, the condition suddenly aggravates the signs of cerebral hemisphere ischemia, such as lethargy. Hemiplegia, partial sensation of the sensory side, symptoms of darkness or aphasia in the affected side. If the pulsation of one side of the carotid artery is weakened or disappeared, the arterial pressure of the fundus of the diseased side is decreased, and the pale or thinning of the retina is considered to be considered. In patients with severe brain injury and internal carotid artery occlusion, it is not easy to confirm the diagnosis before cerebral ischemia has reached irreversible damage. Only by closely observing the imaging examination can the early diagnosis be made. Cerebral angiography can directly show the specific location and extent of arterial occlusion, which is the most valuable diagnostic method for treatment. CT and MRI are helpful for diagnosis.

The mild onset is slower, and there are some collaterals on the distal end of the occluded artery. The scope of cerebral ischemia or infarction is small. The clinical situation is mostly partial hemiplegia. The patient's mind is still clear, and he can complain of headache. It is easy to be misdiagnosed. It is an intracranial lesion or is confused with brain damage.

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