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Surgical guidelines
in acute cerebral vasculopathy

The ischaemic ictus consists of an abrupt appearing of neurologic signs resulting from the parenchyma damage caused by the sudden drop of tissue perfusion. It generally occurs after an artery occlusion.
Since the circuit arrest, the cerebral tissue fed by the occluded vessel suffers from several haemodinamic and metabolic modifications that fatally lead to the cellular death.
In some cases, the clinical onset shows the appearing of temporary ischaemia episodes that, on the other hand, repeat themselves at an increasingly frequent intervals, with additional symptoms at every new episode, until the final impairment of the function occurs resulting from the definitive cerebral tissue damage. The "crescendo TIA" are almost always secondary to multiple emboli that split from the surface of a complicated atheromatous plaque that may eventually cause the internal carotid occlusion.
On the contrary, in other cases we can have the appearing of moderate neurologic symptoms that tend to progressively increase within a few hours. The status of the stroke in evolution is sometimes really serious, because we experience the patient's progressive functional deterioration, frequently bound to exitus. Also in this case, the causes of this clinical form are often to be found in the carotid atheromatous pathology, responsible for the recurrent embolisms that at the end provoke the occlusion of one or more intracranial main vessels.
Another often abrupt cerebral ischaemia form, which sometimes includes the stroke in evolution, is the one called by the American authors "watershed infarction", that is the infarction of the border areas between the vascular territory and another zone where the vascularization depends on two or more main vessels instead of only one. This type of infarction, which is very much affected by the compensation circuit integrality¹, represents about 10% of all the cerebral infarctions². At least 40% of these infarctions occurs in patients suffering from stenosis or carotid occlusion.³
The border area between the anterior cerebral artery and the middle cerebral artery corresponds to the frontoparietal region relative to the areas in charge of the upper limb function, while the border area among the anterior, middle and posterior cerebral arteries is located in the further back area corresponding to the parieto-occipital region.
A cerebral infarction may especially affect a border area after a contemporaneous occlusion of two main vessels inside the cranium (as for example in case of massive embolism),⁴ during the bilateral occlusion of the internal carotids in the extracranial segment or for a severe stenosis of the two arteries with a subsequent drop of cerebral perfusion pressure due to a sudden blood pressure lowering. (Tab. 1A) (Tab 1B)
 

In normal conditions, the encephalon needs for its own energy demand about 50 ml of blood per minute for 100 grams of tissue.
When the flow reaches a level lower than 33 ml/min, it becomes already evident an initial slowing of the brain metabolic process, which corresponds to the perfusion drop with a reaction of dynamic and metabolic adjustment to the new situation (oligohaemia phase; Baron) ⁵ (Fig. 1). The dynamic adjustment is assured by the immediate functioning of the vascular compensations through the perilesional anastomotic circuit, and by the autoregulatory mechanisms ^5-6 leading to a reduction of the peripheral resistance in the hypovascularized areas for the vasodilation effect deriving from CO2 accumulation and contributing to sustain the parenchyma perfusion.
When the vasodilation is not able to assure the parenchymal perfusion anymore, the metabolic adjustment takes over and determines an increase of the oxygen extraction from the circulating blood, jumping from the normal O2 extraction rate of 30-40% to 80 or even 90%⁵.
These compensation mechanisms allow the ischaemic zone to safeguard the neuron homeostasis keeping the high intracellular potassium gradient and the extracellular sodium, calcium and chlorum ion gradient, and sustaining its vitality before suffering from the damages which could definitively compromise its functionality.
When the regional perfusion goes below 18-20 ml/min. the neurologic deficits appear. However, even if at this stage the cerebral parenchyma is already severely, damaged (as it is proved by the typical cerebral electric anomalies indicating an incipient irreversible cellular damage), it is not considered irrecoverable yet, because the increase of the cerebral flow to physiologic values may cause a fairly prompt regression of the symptoms (paralysis phase; Baron).
Only in case of a flow decrease below 10 ml/min values, irreversible parenchymial damages occur leading to cellular death (infarction phase ).
At these levels there is a severe alteration of the cellular membrane homeostasis due to the depletion of important high energy metabolites, such as ATP, responsible for the ionic pump functioning. While the extracellular potassium grows, the sodium and chlorum accumulate inside the cells and, attracting water, induce the neuron and glia swelling (cytotoxic oedema). The intracellular calcium increases. It is partly released by mitochondrions and endoplasma reticulum after ischaemia, and partly derives from the extracellular gaps (due to the action of some neurotransmitters, such as glutamate and aspartate activating the calcium channels). The increase determines a significant free Ca⁺⁺ that activates the phospholipases able to attack and destroy the cellular membranes, leading to cellular death. From the cellular membrane destruction comes a release of the arachidonic acid. It is a fatty acid which, through the eicosanoids and the leukotrienes, toxic free radicals produced by its metabolism, facilitates the thrombocytic aggregation and the vasoconstriction, thus enlarging and worsening the neuronal damage⁷.

After a main artery occlusion, the cerebral parenchyma perfused by this vessel suffers from an immediate anoxic damage. The most anoxia-affected tissue is the one corresponding to the central zone of the vascular area, which depends on the occluded vessel. The surrounding area, called penumbra, although affected by the hypoxia consequences, remains fairly vascularized and it is potentially able to retake its functionality after the regression of compressive phenomena and vasomotorial alterations (Fig. 2). Therefore, after a sudden and disabling onset, the surviving patients may present a gradual, though incomplete, recovery of the functions.
The cerebral flow in the ischaemic area is thus variable: in the central area of the lesion it drops with a consistent speed below 10 ml/100gr/min, while in the surrounding area, that is in the ischaemic penumbra area,^5-8 it stays above these values, though always within critical levels. The consequence is that the central area is bound to cellular degeneration within a few minutes after the ischaemic event, while the penumbra area still maintains a fair vitality which may be badly affected by the phenomena occurring after the cellular degeneration..
The vitality degree of parenchyma in the penumbra area depends on the level of the regional cerebral flow and, therefore, on the validity of the compensation circuits and on the local alterations following ischaemia.
Doubtless, as far as the connections among the different vascular areas are effective, the survival chances of the ischaemic penumbra area are higher because the flow to the infarcted periphery is more consistent.
Nevertheless, the severe slowing of the flow occurring in the centre of the infarcted area and the haemopexic mechanisms relative to the damaged vascular areas may facilitate thrombosis phenomena that prevent any possibility of reperfusing the surrounding areas, with a consequent progressive expansion to periphery of the cellular necrosis area. The necrosis determines the alteration of the haemato-encephalic barrier which facilitates the flowing of fluids and proteins out of the vascular compartment (also due to the hypertension following the contextual loss of cerebral autoregulation), thus provoking the onset of the vasogenic oedema which further affects the parenchyma perfusion and helps the degenerative expansion to the penumbra area.
If the artery has been occluded by an embolus, it may occur that the boost of blood current upstream the occlusion is able to push the embolus more distally, perfusing the artery which was occluded. In these cases, if the vascular structures have already been damaged and are degenerating, the reperfusion may cause a capillary and arteriole breaking, with a consequent blood outflow and the conversion of the ischaemic area in haemorrhage area. The haemorrhagic infarction, which occurs in about 60% of the cerebral infarctions, is a typical embolic lesion and only exceptionally it becomes apparent after the progressive occlusion of an intracranial artery caused by an atheromatous plaque.
 
 

The first works about the surgery on cerebral ictus at an acute phase were so particularly optimistic that Denman⁹ in 1955 and Rob and Wheeler in 1957¹⁰ reported some cases of patients affected by severe neurologic deficit consequent to an ischaemic cerebral ictus, in which the disoccluding intervention on the carotid bifurcation was followed by a complete neurologic recovery. On the contrary, Breutman¹¹ in 1963 and Wylie¹² in 1964 indicated the possibility of cerebral haemorrhage and death risks after a TEA following a recent infarction. Rob¹³ himself in 1969 indicated a consistent mortality rate after TEA in urgency (about 30%), while only 21 patients out of 125 received beneficial effects from the intervention.
In the Joint Study for Extracranial Arterial Occlusive Disease¹⁴ it was underlined that a two or three week minimum postponement of the surgical intervention after the ictal event showed an important reduction of the mortality rate, which went from 42% for interventions performed up to 10 days after the ictus to 1,7% for interventions performed after at least two weeks since the ischaemic event occurrence. Also the recent observations by Giordano¹⁵ confirm the sharp and outstanding mortality reduction in patients operated after five weeks. Nevertheless, Dosick ¹⁶ and Whittemore¹⁷ have emphasised the importance of precociously intervening at least on those patients having neurologic symptoms, whose cranial CT does not show significant parenchyma alterations, to prevent a new embolic episode onset during the waiting period for the clinical stabilisation of the infarcted area.
The ischaemic cerebral ictus caused by carotid emboli occurs with an elevate rate of recidives and some of them are mortal. (10%/year, Sacco¹⁸ - 7%/year, McCullough¹⁹) This is because the degenerated and ulcerated atheromatous plaques of the carotid bifurcation represent a potentially continuous source of emboli and, besides, they may facilitate the sudden acute thrombosis of the internal carotid.
The conservative medical treatment of crescendo TIA and stroke in evolution does not give encouraging results, as it is proved by the fact that the patients affected by these symptoms and treated only medically show a morbidity rate equal to 75% with a mortality rate of 14% within two weeks since the symptom onset.²⁰
An endarterectomy undertaken during the acute phase on patients suffering from recurrent neurologic symptoms that are slightly increasing or definitive, may doubtlessly represent a useful remedy to reduce the morbidity and mortality rate at least for selected groups of patients.²¹-²² Valid candidates for the intervention are those patients who are awake or do not show a severe alteration of the consciousness, have no significant CT detected densitometric alteration or shift to the medial line structures and are in fairly good general conditions. On the contrary, this is absolutely inadvisable in case of an important cardiorespiratory desease, especially, in case of a congestive heart condition or a severe renal insufficiency, where any surgical operation must be excluded.
Goldstone and Moore²¹ successfully treated 13 patients affected by stroke in evolution and 8 patients by crescendo TIA, while Mentzer²² achieved a complete recovery in seven patients affected by crescendo TIA and a significant neurological recovery in 12 out of 17 patients affected by stroke in evolution and operated in urgency. Among them only one died, while the other 4 showed a neurological status substantially stable compared to the pre-operation conditions.
However, since also the follow-up complications are particularly frequent and insidious, it is useful, if possible, to wait for the infarcted area stabilisation before proceeding to operate during the acute phase. If the atheromatous lesion appears stable and if the neurologic status does not show relevant pejorative oscillations, the patient can be monitored and checked for a three-six week period, that is the necessary time to allow a definitive stabilisation of a cerebral infarcted area.^19-23 On the contrary, the patient must be operated if we encounter a severe stenosis, responsible for severe dynamic alterations with an evident circuit slowing, or a not homogenous plaque with a large ulceration. The operation is necessary also when from the neurologic variations we can foresee a possible impairment secondary to the internal carotid occlusion or to a thrombus detachment from the plaque surface.
In case of stenosis, the patient prepared to the intervention must be operated to restore the normal intracranial dynamics and to prevent that the cerebral hypoxia may further aggravate the parenchyma damage with consequent worsening of the neurologic deficit.
In case of ulcerated plaques, the purpose of the intervention is to prevent further embolus detachment and, if possible, to facilitate the outflow of those clots still located in the internal carotid that have not reached the intracranial vessels yet, both by arterious defluxion and the use of Fogarty catheter.
 

The acute thrombosis of the internal carotid can be consequent to:

1. gradual reduction of the arterious lumen due to progressive thickening of an atheromatous plaque of the biforcation with a conclusive formation of a thrombus completely blocking the arterious lumen.
2. sudden degeneration of an atheromatous plaque secondary to an intramural haemorrhage with successive ulceration and fast formation of a clot blocking the arterious lumen.
3. fast formation of a clot on an endarterectomized area.
4. detachment of a embolus from the left heart valves or walls, which is occlusive in correspondence to the internal carotid ostium.

In the first case, the slow plaque transformation leading to the occlusion occurs with a gradual variation of the pressor gradients to the other arteries which usually ensure a sufficient perfusion to the involved area through the extra and intra cranial anastomotic circuits. In these circumstances, the occlusion is almost always tolerated, often it is asymptomatic because the progressive adjustment to the new dynamic conditions prevents the perfusion deficit onset and consequently the ischaemia, also when morphologic and functional anomalies of Willis circle are present.
On the contrary, in the other cases, the occlusion of the internal carotid occurs abruptly and it consists in a sudden, even if temporary, flow arrest in the dependent area, followed by a prompt reperfusion by other arteries through the communicating arteries and extracranial anastomosis. Naturally, since in the acute occlusion the dynamic adjustment must be fast, if the Willis circle is entire, the patient may have no symptoms or feel other than a temporary mild discomfort; on the contrary he will suffer from a focal neurologic syndrome, if the communicant arteries are not able to ensure an adequate compensation to the ischaemic areas.
Sometimes, before the definitive occlusion of the internal carotid, some emboli may reach and occlude the intracranial vessels. In these cases, the clinical onset is abrupt and the evolution is almost always very serious, even with a valid anastomotic intake by the communicating arteries (Tab. 2).
Unfortunately, it is often difficult to prove and document in the acute phase the embolic occlusion of one or more cerebral arteries in concomitance with the occlusion of the neck internal carotid, since the carotid selective angiography only emphasises the contrast arrest at the lower limit of the occlusion. Certainly, the current flowmetric and angiographic NMR methods could supply the documentation for such a situation, but they are often long to perform and thus, scarcely useful for the evaluation extempore of the cerebral circuit conditions.
 

The study of the natural history of the carotid occlusion does not allow to comes to significant conclusions about the clinical evolution of this pathology, since the largest case-records on the desease course of patients suffering from ischaemic lesions ²⁴,²⁵ lack of the fundamental diagnostic support of angiography or at least of the autopsy results.
The first significant case-record belongs to McDowell in 1961²⁶ in which the data related to 40 patients affected by carotid occlusion, ascertained by angiography and autopsy, were analysed. In this group the carotid occlusion emerged with a serious neurologic deficit only in 22 patients, while in the other 18 the onset symptomatology was absent or irrelevant. Out of the symptomatic patients 55% (12 patients.) died after the ischaemic event, 41% (9 patients) showed serious disabling neurologic outcomes and only 4% (1 patient) completely recovered every deficit.
Grillo and Patterson in 1975²⁷ assessed that out of 44 patients with angiographically proved carotid occlusion, the clinic onset had been abrupt in 26 subjects, while the other 18 had only showed signs of temporary ischaemia in the related carotid area. The mortality rate was 16% during the first two weeks after the ictal event.
The same mortality rate (9 patients) was reported by Norrving and Nilsson in 1981²⁸ out of 59 cases of internal carotid acute occlusion, documented angiographically and by autopsy.
The analysis of these results proves that the internal carotid occlusion can be asymptomatic or have an irrelevant clinical symptomatology, consisting in temporary ischaemic attacks in 40-45% of the cases. Besides, the continuous use of noninvasive examinations, especially the Ecodoppler, has proved that the rate of asymptomatic or carotid occlusions is surely higher than in the case above mentioned.
On the contrary, 55- 60% of patients shows a abrupt clinical onset with a definitive ictus or a stroke in evolution. In this group, the mortality rate is between 30 and 55%, depending on the case-records, the disabling morbidity is about 50%, while only a low percentage of patients (from 2 to 12%) has a satisfactory neurological recovery.
 

The surgical therapy for the internal carotid acute occlusion is a topic that keeps arousing great controversy.^29-34 The lack of a homogeneous approach depends on the substantially different positions of the surgeons toward this issue; also, the scarce positive results on a large scale have certainly contributed to gradually reduce the interest for this segment of the carotid surgery.
Frequently, the perfusion of an occluded carotid is followed by a symptom worsening due to a cerebral haemorrhage onset or, more precisely, to a haemorrhagic infarction secondary to the breakage of small vessels in the ischaemic area. In 1964 Wilie³⁵ assessed that this complication emerged in 5 out of 9 patients submitted to TEA for internal carotid acute occlusion, operated from three to nine days after the clinical onset.
Certainly, after the recent experiences and evaluations both clinical and experimental, the surgical treatment performed after many hours or even some days later the neurologic sign onset, seems to negatively affect the surgical outcomes.
In the Joint Extracranial Arterial Occlusive Disease Study, Blaisdell³⁶, recorded a mortality rate of about 40% in a series of 50 TEA performed on internal carotid acute occlusion and treated up to 13 days after the clinical onset.
However, in the therapeutic decision, the evaluation of the initial clinical status plays an important role, since it is clear that patients affected by serious deficits and by alteration of the consciousness show a high mortality rate, regardless of the treatment type.
Thompson³⁷ noticed a high mortality rate among the patients affected by serious deficit and he did not recommended the surgical treatment, because he considered improbable that the intervention could lead to a significant neurological recovery. Ojemann³⁸ and Weese³⁹ had the same position, they opposed the intervention for sudden and serious deficit, especially in the case of a unconsciousness condition, while they considered surgical those patients affected by internal carotid acute occlusion with irrelevant neurological deficit.
On the other hand, the possibility to precociously intervene after the occlusion and the symptom onset, gives a significant advantage in the results. Those patients urgently operated because timely taken to structures organised to provide a precocious diagnosis and with a good surgeon team, or because already hospitalised for a preocclusive carotid stenosis which later became an occlusion, or because the carotid occlusion developed after a angiographic examination, show a very low intervention mortality and, especially, a particularly high recovery index.
Hafner and Tew⁴⁰ maintained the opportunity to operate within two hours since the clinical onset also those patients affected by serious neurological deficit, on the basis of three occlusion cases resulted in a very positive way after a precocious intervention.
Out of 15 TEA performed after an occlusion following an angiographic exam and responsible for significant neurologic deficit, Najafi⁴¹ noticed a clinical enhancement in 53% of the patients (8 patients) versus 33% of negative results and that the mortality rate represented only 6% (1 patient). Out of five patients urgently operated for the withdrawing of a carotid murmur, he obtained a positive outcome in all cases.
Meyer and Sundt⁴² considered 34 patients already hospitalised and among them 33 were affected by neurological deficit. They obtained encouraging results, though they reported a mortality rate of 20,6%.
The fast perfusion of the carotid after the acute thrombosis is proved also in the post operation occlusions, in which the period of time elapsing between the clinical sign onset, the diagnosis and the reintervention seems to be very important in the recovery perspective. Certainly, the surgical interventions performed immediately after the symptom manifestation, when the patient is still in the operation room, result in brilliant outcomes. The clinical recovery appears more problematic if a few hours pass by since the neurologic symptom occurence to the awakening and the angiography.
Kwaan⁴³ noticed that out of 9 patients affected by postendarterectomic occlusion, the 3 people who were operated again within maximum 45 minutes had a brilliant desease course with a complete neurologic recovery. Out of the remaining 6 who had a tardive surgical intervention, about three hours after, due to a angiography carrying out, 4 resulted hemiplegic and 2 died.
In the cases where the carrying out of a angiography is considered necessary, the reintervention can be successfully performed if, besides fast radiological and surgical procedures, it becomes evident from the angiography the good perfusion of the carotid siphon by the ophthalmic artery or comunicating artery and the siphon retrocursive opacification toward the carotid channel.⁴⁴
Sundt,⁴⁵ starting from the analysis of his 34 patient group submitted to intervention in urgency maintains the positive result obtained in 38,3% of the cases (13 patients), with a mortality rate of 20,6%. To achieve a successful intervention of carotid deocclusion in acute phase he has emphasized that it is necessary to consider two fundamental elements:
1) the use of a angiographical study, to exclude the embolic occlusion of a middle cerebral artery
2) to be sure that there is a good compensation circuit able to feed the ischaemic area.
As it was above mentioned, the problem of the coexisting of intracranial embolic lesions has not been carefully considered by most authors. Therefore, it is not excluded that many of the unsuccessful surgical operations reported in the literature occurred in patients affected not only by internal carotid occlusion, but also by a concomitant occlusion of the middle cerebral artery or, more rarely, of the anterior cerebral artery. The coexistence of the embolic occlusion of the middle cerebral artery practically vanificates the deocclusion of the internal carotid. This is because the cerebral tissue depending on the sylvian artery, though peripherally perfused by the pial anastomotic vessel, inevitably shows a severe hypoxic central area, bound to a imminent necrosis that even the perfusion increase by the compensation circuits is unable to prevent.
The presence of a valid compensation circuit through the communicating arteries, according to Sundt, represents the second important factor to allow a surgical operation. In fact, a working blood flow toward the ischaemic zone through the anterior and the homolateral posterior communicating arteries, ensures a valid perfusion of the ischaemic penumbra area, preserving many cells from the irreversible damages consequent to the membrane alterations when the regional flow goes below 10 ml/100gr/minute.
Overall, Sundt suggests the intervention on patients whose angiographic exam undertaken in urgency shows a satisfying compensation circuit and excludes embolic obstructions of intracranial vessels. Furthermore, he emphasises the necessity to intervene on these cases within a very short time to limit the development of generative processes that lead to cerebral tissue death.
However, there is the need to raise some objections to Sundt's guidelines. First, it must be considered that many acute thrombosis stay asymptomatic due to the presence of the compensation circuits and it is not clear why, in the same situations, there is instead the onset of a seriously deficitary neurologic symptomatology. In these cases, it should not be excluded the hypothesis that the symptom onset can be secondary to an embolism affecting the Heuber or lenticulostriate arteries or to a widespread microembolism of the perforating arteries, which is difficult to angiographically identify in emergency situations. In this case, the effectiveness of the surgical intervention depends on a collateral flow enhancement in the border areas of the ischaemic zone.
Secondly, it should not be forgotten that when there are some morphologic anomalies of the Willis⁴⁶ circle, an intracranial carotid can be almost completely isolated from the other cerebral vessels. It behaves as a terminal vessel and its acute occlusion can be compared, from a clinical point of view, to the acute occlusion of the middle cerebral artery. (Fig. 3 A-C). In these cases, the cortical anastomosis and the extracranial connections are not enough to ensure a sufficient blood supply to the energy need of the ischaemic area and, thus the clinical onset is naturally abrupt and the ischaemia manifestations practically involve the entire cerebral hemisphere depending on the occluded carotid.
However, it is possible that the pial anastomosis and the intracranical circuit of the ophthalmic artery are able for a few hours to keep the perfusion pressure above the survival critical levels of the brain tissue which is globally hypoperfused but which does not show, as in the case of middle cerebral artery occlusion, central areas with a fast drop of the perfusion pressure where the cellular necrosis occurs after a few minutes. The entire cerebral hemisphere can behave as a large ischaemic penumbra area, functionally inactive but virtually recoverable. The internal carotid deocclusion, if timely performed, could determine the reperfusion of all the arteries located downstream, with the possibility of functionally recovering the cerebral parenchyma (Fig. 4).
After all, the surgical therapy could be effective in the symptomatic acute thrombosis, when there are communicating artery anomalies that prevent the perfusion of the hemisphere hit by ischaemia from the other cerebral vessels.
The internal carotid occlusion diagnosis is easy. It is necessary only a continuous mono or bidirectional Doppler to identify the lesion. What is important in order to consider a surgical treatment is to know the state of the communicating arteries and the patency or not of the cerebral arteries (Tab. 3).
Doubtless, the transcranial Doppler is an excellent noninvasive method to define this problem. Unfortunately, it is not always reliable, because it requires the patient's cooperation; the patient is often agitated or intolerant and this does not allow to follow the entire pathway of the anterior and middle cerebral arteries, but primarily, in case of the impossibility of their detection, it does not allow to establish whether they are occluded by emboli or the communicating arteries are insufficient or the temporal bone window is suitable to the ultrasound passage. Finally, the method could become long and complicated, with a relevant waste of time which makes useless the advantage of the noninvasiveness.
The noninvasive method able to offer a reliable feedback is the NMR that provides a much more precocious evaluation of the cerebral parenchyma state compared to the CT; also, and especially, it offers an excellent general view, with the angiographic sequences, of the neck and intracranial vessels. Unfortunately, often in the structures where it could be possible to perform a urgent treatment of the acute patients, the equipment is not available.
Since in emergency situations it is necessary for the instrumental examinations to ensure a fast and reliable diagnosis to undertake, wherever the conditions allow to do so, the surgical intervention in the least time possible, in most neurosurgery and vascular surgery centres it is the angiography to be performed. Obviously, the purpose of this examination must be to document the state of the intracranial vessels and the communicating arteries and it should be performed by selectively analysing the controlateral carotid artery and a vertebral artery. In case of the anterior communicating artery patency, a good spontaneous view of the controlateral vessels can be obtained with the consequent possibility of locating an embolic arrest, while in case of its inefficiency the vessels of the hemisphere depending on the occluded carotid are not or only slightly injected. The case is the same for the posterior communicating artery spontaneously feeding the carotid siphon when the internal carotid is occluded, allowing to check the state of the anterior and middle cerebral arteries .
In conclusion, as far as these considerations and our experience are taken into account, the surgical intervention of deocclusion on the internal carotid in case of acute thrombosis can be successfully performed only when we face ostium internal carotid thrombosis associated with communicating artery insufficiency and lack of occlusive emboli of the anterior and middle cerebral arteries.
 

The main difficulty in the internal carotid deocclusion in case of acute occlusion depends on the fact that the blood stasis often facilitates the thrombus expansion in the intracranial carotid till the origin of the ophthalmic artery. The consistent retrograde flow of this artery fed by the external carotid generally prevents the further progression of the clot (Fig. 5).
Special care must be taken to ensure a stable arterious pressure. The exposure of the carotid bifurcation is performed using the same technical criteria of the elective surgery, without any improper artery manipulation during the dissection to avoid the thrombus fragmentation. Since in the acute phase of the occlusion it is necessary to ensure a valid flow downstream the occlusion, some authors, once exposed the carotid bifurcation, do not close the external carotid but they directly clamp the internal carotid at the origin to ensure the direct blood outflow from the common carotid to the external carotid in order to maintain the collateral circuits (fig. 6A). On the contrary, other surgeons do not apply any clamp on the internal carotid, from the beginning of the deocclusion intervention till the end, in order to avoid the thrombus breaking (Fig. 6B).
The thrombus must always be gradually removed with special care, using a thin aspirator with a smoothed tip or a Fogarty catheter that must be softly inserted and removed after blowing the small balloon on top of it (Fig. 7A). Also, we can take advantage of the retrograde flow boost in the internal carotid that facilitates the thrombus expulsion.
The catheter must be used very carefully because it could cause severe damages to the internal carotid wall or even facilitate the development of a carotid-cavernous fistula.
Blaisdell^48,49 suggests the insertion of saline solution between the endarterium and the thrombus to facilitate its detachment from the wall and then its expulsion, but this method is considered too dangerous due to the frequently caused embolism (Fig. 7B).
Imparato⁴⁹ uses an helicoid disector which is always introduced between the endarterium and the thrombus in the internal carotid until it reaches the cariotid siphon. With this method, the author succeeded in completely extracting the clot in 10% of the cases (Fig. 7C).
If a perfusion of the artery is achieved, as it is proved by the onset of a satisfying run-off flow, the TEA and then an intraoperation angiography are undertaken to detect the possible presence of emboli located in the middle cerebral artery. They are used also to check the carotid siphon that frequently appears attacked by a severe atheromatous process or presents free intimal flaps which explain the frequent failure consequent to this type of surgery.
 

In case of failure in surgically disoccluding the internal carotid due to the thrombus excessive distal extension, the use of fibrinolytic drugs should be considered to facilitate clot disintegration and artery perfusion.
The conventional fibrinolytic treatment consists of injecting 250.000 I.U. of Streptokinase directly into the occluded internal carotid after performing the vessel clamping downstream the arterectomy. The drug is left to develop its action for about 20 minutes. After this period, the internal carotid is clamped and, if the thrombus has been dissolved, a valid run-off flow can be observed.
This method successfully used by Maiza,^50,51 has the advantage to greatly limit the cerebral haemorrhage risk caused by the fibrinolytic drugs. In fact, Streptokinase is introduced in an artery segment which is completely excluded by the circuit and thus not subjected to any dynamic stimulus by the blood flow. Therefore, even in case of fast clot dissolution and occluded vessel perfusion, the drug could not be distally pushed toward the brain, where its powerful action could facilitate the development of unrestrainable haemorrhage, but it is eliminated with the run-off blood after performing the internal carotid clamping.
If it is not possible to disocclude the artery, the alternative could be to perform a pterional craniotomy, largely exposing the carotid siphon after the removal of the anterior clinoid to allow the exposure of the ophthalmic artery. Then, a clip is applied on the siphon, upstream the posterior communicating artery, and another clip is placed on the ophthalmic artery. A brief arterectomy is performed on the carotid siphon along the major axis facilitating the clot outflow from the internal carotid intrapetrous and intracavernous segments by injecting a heparinate saline solution at a consistent pressure with a catheter inserted in the neck internal carotid. Once the internal carotid has been reperfused, another clip is applied upstream the arterectomy. After the temporary closure of the posterior communicating artery with a small clip, the clip previously placed on the siphon is removed in order to induce the blood retrograde outflow and the expulsion of possible clots. The clip is applied again and the siphon is sutured. After checking the suture accuracy, all the clips are removed letting the blood flow from the cranium toward the neck for a few seconds. After ensuring that all the possible clots have been extruded, it is possible to proceed to suture the neck internal carotid (Fig. 8).
Sometimes, after the carotid siphon opening, despite the washing with heparinate solution, it is impossible to disocclude the artery. In these cases a by-pass between the common carotid and the carotid siphon can be performed using a venous graft or a conic graft in PTFE, after checking the carotid siphon patency below the posterior communicating artery (Fig. 9).
Only rarely it is impossible to reperfuse the internal carotid. In this case the ostium internal carotid should be sutured to avoid the formation of a long and dangerous recess which could facilitate the external carotid thrombosis or the cerebral embolism through the ophthalmic artery.
In any case, it is useful to perform the external carotid TEA to eliminate every possible stenosis.
 

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