Supraortic trunks (TSAO) are born from the aortic arch: on the right the
anonymous artery, which gives rise to the common carotid and subclavian; on the
left, separately, the common carotid and the subclavian. The subclavians
arteries give origin to the vertebral arteries, that they come together to form
the basic artery and enter in the skull where they contribute to the posterior
circuit.
The common carotid, about the height of the thyroid cartilage, presents a
fusiform dilatation, the carotid bulb, and is divited in to the external carotid
artery (for the neck and face) and in the internal carotid artery, which enters the
skull through the homonymous foramen and provides for the vascularization of
the brain through the cerebral arteries, of which, the most conspicuous, is the average.
About 80% of the cerebral spraying is sustained by the internal carotid
arteries and the
remaining 20% by the vertebral arteries.
Even in pathological conditions of occlusion or tight stenosis of one of the
cerebro-afferent blood vessels, there are ample possibilities of compensation between
the two systems, the carotid and vertebral arteries, and between the two hemispheres through
the Willis polygon, actually completely represented only in about one third of
the cases. Other systems of substitution are activated through the periorbital
branches of the external carotid artery and the ophthalmic, the first branch of the
internal intra-cranial carotid, where the flow is reversed; or through the
branches of vertebral arteries with cervical vessels.
Most of the cerebral ischemia is of an embolic type and much more rarely of a thrombotic type starting from complicated plaques. Atheromatous plaques that assume hemodynamic relevance, and as such at compile risk, are located, in over 90% of cases, to the carotid bulb and the first part of the internal carotid. Intracranial localizations (carotid siphon, middle cerebral, basic) or intra-thoracic (anonymous, common carotid) affect not more than 10%. Thrombosis can generally occur at the internal carotid, vertebral or small intracerebral vessels (the latter cause lacunar infarcts, generally not very relevant in terms of symptoms). In the case of steno-occlusions involving multiple cerebral vessels, a haemodynamic mechanism for cerebral hypo-affux during hypotensive episodes or the passage from clinius to orthostatism is also possible. The atheromatous plaque in its growth can become unstable and prone to acute complications: intraplaque haemorrhage with softening and increase in volume, rupture of the fibrous cap with release of emboli and formation of an ulcer. Therefore, at the plaque complication an atheroma embolism can be achieved, and at the ulcer a thrombus can be overlapped, in turn capable of determining a thrombotic embolism or a complete acute occlusion. Plaque instability is related to the extent of the stenosis it determines and its structure (fibrous, mixed, calcified). If thrombosis stops at the ophthalmic and if the Willis polygon is efficient the occlusion of the internal carotid artery with a small proximal proximal ulcer and recent ulcer from intra-plaque hemorrhage. it can also be asymptomatic or paucisintomatic. If thrombus or thrombus propagation involves the middle cerebral, profound hemiplegia can occur up to coma and death.
The clinical expression of cerebral ischemia is extremely variable in duration (TIA,
prolonged TIA and stroke), type (sensory syndromes, amaurosis paresis,
non-hemispheric symptoms) and entities (mone or hemiparesis, etc.). The TIAs are
transient emi or monoparesi, amaurosi fugax, dysarthria, drop attacks, generally
lasting a few tens of minutes and which however completely reverse within 24
hours. They may or may not be associated with the evidence of generally small
ischemic areas at CT. RINDs are longer lasting deficits, which can become
permanent or even regress completely or in part. Deficits of the carotid
territory involve contralateral motor paralysis, which can vary them simple
motor embarrassment of an upper or lower limb or both, up to the plegia of the
whole hemisome; it is not rare the only pafacciale, to be distinguished from
paralysis to the frigore, the amaurosi, usually fleeting, is another important
symptom that the patient feels as a sudden defect veil on the visual field
ipsilateral vascular territory concerned, up to make a patient temporarily blind.
Other emic symptoms are dysarthria and aphasia when the dominant hemisphere is
affected.
Ischemias in the territory of the middle cerebral artery, the most important, we
can highlight hemiplegia and contralateral hemianesthesia, ipsilateral
hemianopsia, global aphasia if concerned dominant hemisphere. If the occlusion
concerns the anterior cerebral circuit, the clinic is represented by motor
disturbances of the
contralateral lower limb, associated with sensory deficit and mild hyposthenia
of the upper limb. In the case of posterior cerebral occlusion, the expression
varies from complete parcelular paralysis of the third cranial nerve,
contralateral hypoaesthesia, haemoreo-atetosis or hemiballism, contralateral
homonymous hemianopsia. Deficit vertebro-basilar territory are the "drop attacks"
(abrupt loss of tone of the lower limbs during erect or at the beginning of
walking, without loss of consciousness, vertigo, diplopia and campimetric
disturbances Transient hemispheric symptoms (vertigo, lipotymie, obnubilates,
syncopes) are more likely to be linked to non-ischemic pathologies or to diffuse
perfusion disorders, rather than to focal deficits typical of thromboembolism.
The ultrasounds are reflected with different echogenicity depending on the
composition of the vessel wall: the lipid component is the least echogenic one;
the echogenicity increases parallel to the increase in collagen, typical of
fibrous plaques; the presence of calcifications makes the hyperechoic plaque.
Usually the structure of the mature plaques is inhomogeneous due to the presence
of hemorrhages, thrombotic material, lipid deposits and calcifications inside it:
this results in a heterogeneity of the echoes.
Fibrous or calcified plaques are considered relatively stable, those soft and inhomogeneous unstable and with higher complicative risk. According to a study of patients with significant or severe stenosis, at three years, only 10% of those with calcified plaque had developed symptoms, in contrast to 90% of those with soft plaque. The presence of ulcers is an indication of asymptomatic embolism, and as such indicates an increased thrombo-embolic risk. One of the main limitations of the ecodoppler difficulty of appropriately evaluating the intrathoracic of TSAOs and the intracrar vessel reality, the first point is quite superior because indirect assessments of the go flow are exclude major lesions from the TSAO origin. The second problem is also partially overcome by the introduction of the transcranial doppler, which allows to evaluate the flow on the first cerebral vessels, in particular the cerebral cortex. The modern multislice CTs, through software (angio-CT) allow visualization of the cervical vascular district and intracranial providing images and three-dimensional reconstructions, which are similar to those of angiography. The advantages of the method are the minimun invasion (only injection of contrast medium), the speed of execution (few min good demonstration of plaques with the possibility of subtraction, obtaining a direct visualization of the residual lumen.) It can not provide information on the type of Nuclear magnetic resonance applied to the brain themselves as indications of the CT, but allows the early visualization of the ischemic areas lesions of smaller size.The angio-RM allows to acquire images without ionizing radiation, or contrast media similar to those provided from angio-CT The stenosis less than 50% of the lumen section, haemodynamically significant between 50 and 70%, severe when above 70%, sub-occlusive when greater than 90% are considered mild or moderate. stenosis is for now the main indicator of the risk of ischemic events: patients with mild stenoses face an annual stroke risk of 0 , 4%, those with moderate stenosis 0.9%; severe stenosis 2.3%; sub-occlusive 9%. The risk rises to 16.2% if severe stenosis has already caused symptoms. In recent years, plaque structure has also entered the normal ultrasound evaluation. The ultrasounds are reflected with different echogenicity depending on the composition of the vessel wall: the lipid component is the least echogenic one; the echogenicity increases parallel to the increase in collagen, typical of fibrous plaques; the presence of calcifications makes the hyperechoic plaque. Usually the structure of the mature plaques is inhomogeneous due to the presence of hemorrhages, thrombotic material, lipid deposits and calcifications inside it: this results in a heterogeneity of the echoes. Fibrous or calcified plaques are considered relatively stable, those soft and inhomogeneous unstable and with higher complicative risk. According to a study of patients with significant or severe stenosis, at three years, only 10% of those with calcified plaque had developed symptoms, in contrast to 90% of those with soft plaque.
Extensive
prospective and randomized studies in symptomatic patients (NASCET, ECST) and
asymptomatic patients (ACAS, ACST) compared the outcome of antiplatelet therapy
with surgical treatment, almost always an endarterectomy of carotid bifurcation.
They have shown that surgery can significantly reduce the risk of disabling or
fatal strokes in symptomatic patients and with> 70% of the lumen section
stenosis, compared to patients treated with medical therapy alone. This
advantage also exists for severe asymptomatic strictures, but is less striking.
All this provided that postoperative mortality and morbidity are contained
within 2-3%. Indications to surgery are therefore stenosis higher than this,
both in symptomatic and asymptomatic subjects, especially if determined by soft
or inhomogeneous, ulcerated and already symptomatic plaques. Contraindications
to surgery are too recent ischemies (less than 3-4 weeks) due to the risk of
worsening periwound ischemia, extensive stabilized cerebral infarcts and the
thrombosis of the internal carotid, which is a stabilized condition. Surgical
treatment consists of carotid endarterectomy, rarely in a replacement graft. The
choice of type of anesthesia is fundamental, since it is connected to the type
of brain monitoring to verify the tolerance to the carotid clamping. Under
general anesthesia the most used monitoring technique is the continuous EEG with
loco-regional anesthesia (plutum with C2-C4 block or cervical peridural C6-C7)
the control of the conscience and of the contralateral motility is sufficient.
In the case of demonstrated blockage intolerance (EEG abnormalities, loss of
consciousness or decreased consciousness) the insertion of a temporary shunt
between the common and internal carotid is able to ensure cerebral perfusion.
Through an incision on the anterior edge of the sterno-cleido-mastoid and
accurately respecting the cranial nerves (vague and recurrent, glosso,
glosso-pharyngeal), the common carotidide is isolated, the internal and the
external, avoiding maneuvers at risk of cause embolism (safety technique).
In systemic heparinization, the vessels are clamped and the neurologic tolerance to
the clamping is checked. A longitudinal arteriotomy is performed on the bulb and
the first part of the internal carotid and the plaque is removed by
endarterectomy. It is preferably reconstructed using an enlargement angioplasty
with patches in the saphenous vein, dacron or PTFE. Endarterectomy can also be
performed by completely dissecting the internal carotid to its origin and
removing the atheromatous cylinder.
The transluminal angioplasty with stents (CAS) in fact remains burdened by immediate risks of embolism and non-negligible cardiac complications and is followed by results not well known at a distance. The procedure is carried out under angiographic guidance through femoral access and consists in the dilation of the stenosis with a balloon catheter and release of a metal stent. The risk of embolism has decreased, but not canceled, by the insertion of a protective filter upstream of the stenosis, always through catheterization. Given the extreme delicacy of the cerebral region, the patient should be carefully monitored under the resuscitation and cardiology aspect, since the stretching of the carotid day can cause bradycardia up to the cardiac arrest (atropine). In the best centers, technical success is achieved in 98% of cases with complications in about 6%. Recent randomized trials have shown short-term results almost equivalent to surgery, but not long-term, since restenosis seems somewhat more frequent. Although some believe that CAS is a valid alternative to surgical endarterectomy, it is probably best to reserve it for groups of patients selected for high-risk clamping, fibrodysplasia, arteritis, stenosis of the distal internal carotid, hostile neck or reoperative. Relative contraindications are roughly calcified stenoses, particularly if asymmetric.