Can the Diameter of Endoluminal Shunt Influence the Risk of Hyperperfusion Syndrome After Carotid Endarterectomy?

Written By: Sam Savage

Published Date: August 22, 2008 Last Edited: August 22, 2008

By Bakoyiannis, C N Tsekouras, N; Georgopoulos, S; Tsigris, C; Filis, K; Skrapari, I; Bastounis, E

Aim. The aim of this study was to evaluate if there is a possible relation between the size of endoluminal shunt, in carotid endarterectomy (CEA), and the risk of postoperative hyperperfusion syndrome. Methods. We retrospectively studied prospectively collected data from 156 patients, who were subjected to CEA using shunting and vein patch angioplasty. One hundred and thirty-eight of the patients had bilateral, high grade (>90%) internal carotid lesions and the remaining 18 had a highgrade stenosis (>90%) and a contralateral internal carotid artery (ICA) occlusion. In 81 patients varying diameters of shunts were used (8-14 Fr) according to the diameter of ICA (group A) and in the other 75 patients (group B) only the smallest shunt was used (8 Fr). Development of hyperperfusion syndrome was evaluated both clinically and radiologically with magnetic resonance imaging.

Results. Fifteen patients developed hyperperfusion syndrome (9.6%), between 0 to 6 days postoperatively. Thirteen belonged to group A (86.6%), and 2 (13.3%) belonged to group B (P

Conclusions. During CEA in patients with high-grade bilateral lesions, we recommend the use of a shunt with small diameter: this aims at reducing the risk of hyperperfusion syndrome.

[Int Angiol 2008;27:260-5]

Key words: Endarterectomy, carotid – Postoperative complications – Carotid stenosis.

Hyperperfusion syndrome is a rare, but potentially lethal, complication after carotid endarterectomy (CEA). The classic triad of the syndrome includes: unilateral severe migraine symptoms (head, face and eye pain), focal deficits and focal seizures, due to cerebral edema or intracerebral hemorrhage (ICH).1,2 This triad is not always complete. Migraine symptoms and seizures are more common 3 and ICH is reported to occur in only 0.4% to 2% 4, 5 of the patients. The pathogenesis of the syndrome is still obscure: paralysis of normal vascular autoregulatory mechanisms, in a chronically hypoperfused hemisphere of a patient with high-grade carotid stenosis, combined with an acute and pronounced increase in cerebral blood flow (CBF), after endarterectomy, is the main hypothesis.1, 2, 6

We suggest that using a smaller size of endoluminal shunt during endarterectomy, as opposed to the size that could normally be fitted to the internal carotid artery (ICA), we can achieve lower risk of hyperperfusion syndrome, since the increase in blood flow of ICA, till its maximum value just after declamping, is more gradual.

Materials and methods

We retrospectively reviewed prospectively collected data from the Vascular Department of our clinic of 169 consecutive patients that were subjected to CEA because of bilateral high-grade (?90%) carotid stenoses or a high-grade lesion (?90%) and a contralateral ICA occlusion, during the period 1998 to 2004. Complete data were available for 156 of these patients (138 with bilateral high-grade stenoses and 18 with a high-grade lesion and a contralateral ICA occlusion). Stenoses were measured using cerebral digital subtraction angiography according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) study.7 Symptomatic lesions were first treated. In asymptomatic patients, with an equal degree of stenosis, characteristics of angiography (plaque ulcers, kinks, coils) were taken into account to decide which lesion to treat first. Preoperative neurological staging was done by the same consultant neurologist.

All CEA procedures were performed under general anesthesia by the same surgical team according to the standard technique: gentle dissection of the carotid bifurcation, systemic use of heparin (100 U/kg), careful insertion of an endoluminal shunt (Argyle, Sherwood Med., St. Louis, MO, USA), in all cases, and tacking sutures at the distal and proximal end of the endarterectomized internal/common carotid arteries, when needed. The arteriotomy was closed using a patch angioplasty (vein patch) in all cases. In 81 initial patients (group A), we decided who got which kind of shunt according to the diameter of ICA. So, the diameter of shunt in these patients was analogous to the diameter of ICA and shunts with varying diameters were used (from 8 Fr to 14 Fr). In a later group of 75 patients (group B), the smallest diameter of shunt was used (8Fr), even if a bigger one could be normally fitted to the ICA (Table I). All shunts of our study were of equal length (15 cm).

We studied the postoperative course of the patients only after the initial operations (in cases of bilateral stenoses). After CEA, all patients were clinically examined for neurological symptoms by the same certified neurologist who did the preoperative neurological staging. Clinical suspicion for hyperperfusion syndrome was set from the presence of the following symptoms: focal seizures (contralateral to the side of CEA), deterioration of consciousness levels at least 8 h postoperatively or focal neurological signs such as motor weakness (also contralateral to the side of CEA). Depending on the particular patient, duplex scanning or arteriography were performed to evaluate the patency of the endarterectomy site in all patients with the above clinical presentation.

All symptomatic patients were subjected to magnetic resonance imaging (MRI) examination with diffusion-weighted imaging (DWI) and perfusionweighted imaging (PWI), within 24 h after the onset of symptoms. The diagnosis of hyperperfusion syndrome required: any one of the above clinical symptoms, the absence of findings of ischemic lesions on MRI study with DWI, and finally the presence of a relative interhemisphere difference (RID) of CBF on MRI study with PWI.8

Statistical analysis

Immediate intensive control of arterial systolic blood pressure between 100 and 140 mmHg was instituted after establishment of diagnosis of hyperperfusion syndrome with intravenous administration of antihypertensive drugs. The chi2 test was used to evaluate the correlation between the diameter of shunt and the risk for hyperperfusion syndrome. A P value of

Results

Mean ages and other demographic data, such as symptomatic lesions, did not differ significantly between the two study groups (Table II). Overall, there were significantly more males than females, but their distribution was similar between the two groups.

All patients were awakened, noted to have no new gross neurological deficits. There was no 30-day mortality and new neurological symptoms or signs were observed 0 to 6 days postoperatively in 21 patients. Six of them had only transient deterioration of consciousness of a duration

Postoperative arteriography in 4 patients and duplex scanning in the remaining 11 patients did not show thrombosis or any technical deficit that could cause embolization from the site of endarterectomy. Furthermore, MRI did not demonstrate any additional ischemic cerebral infract ipsilateral to CEA. In one patient (0.6% of the study group) a 4 cm in diameter ICH was demonstrated in MRI on the 3rd postoperative day. His clinical presentation was with focal seizures and focal deficits contralateral to the side of operation. The patient belonged to group A and a 14 Fr shunt was used. In all 15 patients (including the patient with the ICH), MRI study with DWI demonstrated absence of acute ischemia or cytotoxic edema and MRI study with PWI demonstrated presence of RID of CBF. So, all 15 patients met the clinical and imaging criteria that were mentioned before and thus they were considered to have hyperperfusion syndrome (9.6% of the study group). Thirteen of them (85%) had a symptomatic carotid stenosis and all of them had a history of hypertension. Elevated blood pressure during symptoms of hyperperfusion was observed in 11 of the 15 patients (73.3%) and was managed immediately in all cases.

Thirteen of the patients with hyperperfusion syndrome belonged to group A (86.6%), where shunts with various diameters were applied. In group B, where the smallest shunt (8 Fr) was applied in all cases, 2 patients presented the syndrome (13.3%). The chi2 test demonstrated that the patients, where the smallest shunt was used, were protected against the risk of postoperative hyperperfusion syndrome. The value of chi2 was 6.55 after Yates’ correction (significant at P

Discussion

Post-CEA neurological deficits may rarely be related to a major increase in ipsilateral CBF after removal of a tight carotid stenosis1, 2 (hyperperfusion syndrome). A high-grade stenosis and a contralateral carotid occlusion are considered to be important risk factors of this syndrome.9 Other risk factors include long-standing hypertension and poor collateral blood flow to the brain.9 The patients of our study had bilateral high-grade stenoses or a high- grade stenosis and an occluded contralateral ICA. We chose a subgroup of patients that underwent CEA with a high risk of developing hyperperfusion syndrome, in order to collect cases and study the syndrome. Pre-existing cerebral hypoperfusion can be evaluated by measuring the degree of cerebrovascular reserve capacity (CRC), which is termed as the ability of further vasodilation of cerebral vessels after a sudden rising of CBF. We did not perform preoperatively any test of this kind. Nevertheless, existence of cerebral hypoperfusion is established in symptomatic stenoses and in asymptomatic occlusions10 as it happens in patients of our two groups. Many studies have concluded to the point that the impaired CRC is a significant risk factor of hyperperfusion syndrome.10,13

Moreover, 13 out of the 15 patients with hyperperfusion syndrome had a symptomatic carotid stenosis (85%). This result is in accordance with the greater hemodynamic impairment in symptomatic patients with a significant carotid stenosis or occlusion.14, 15 Yonas et al.16 claim that an impaired cerebrovascular reactivity, which is used to evaluate the collateral capacity of cerebral circulation, has a predictive value for post-CEA stroke only in symptomatic patients.

Postoperatively, we studied the syndrome using MRI images. All 15 patients with the clinical syndrome were subjected to MRI studies with DWI and PWI, which proved to be very useful in establishing the diagnosis. Absence of abnormal DWI hyperintensity in the hemisphere ipsilateral to the site of endarterectomy suggested absence of acute cerebral infraction.8 Furthermore, PWI demonstrated a moderate relative hyperperfusion in the hemisphere ipsilateral to the operated side.8 According to Karapanayiotides et al.8 hyperperfusion syndrome can occur even in the presence of relative hyperperfusion of the ipsilateral hemisphere.

Hemodynamic complications of ICA stenoses that can lead to hyperperfusion syndrome have not yet clearly been defined. Nevertheless, it is claimed that the drop of pressure ipsilateral to the lesion is compensated by collateral arteries, such as arteries of the circle of Willis (anterior and posterior communicating arteries) and ophthalmic or leptomeningeal arteries.17, 18 Thus, high-grade stenoses and poor collateral blood flow, because of a high degree of contralateral stenosis or a contralateral carotid occlusion, are considered to be risk factors of hyperfusion syndrome. The suggestion for collateral compensation is consistent with the clinical observations of Ouriel et al.19 about the predictive factors of the syndrome and with hemodynamic studies in patients with severe carotid stenoses with or without contralateral carotid occlusion.14, 15. 20-22

If collateral capacities are not sufficient, a second step of compensation mechanism is the increase of oxygen extraction from the circulating blood.17, 18 Cerebral tissue tries this way to satisfy its metabolic demands.

Moreover, if all above compensation capacities become insufficient, vasodilation of the cerebral arterioles occurs to improve cerebral perfusion10 (third step of compensation). This autoregulatory vasodilation lessens the ability of the arterioles for a further vasodilation and for this reason they are more prone to damage if rapid restoration of blood flow is achieved through them, after removal of tight ICA stenosis. Rupture of the hyperperfused vessels leads to ICH;19 nevertheless, the most common consequence of hyperperfusion syndrome is not rupture of arterioles, but a mildly leaky capillary bed that leads to brain edema.23 The ability of further vasodilation, as we mentioned above, is known as the CRC, which is an important risk factor for hyperperfusion syndrome.

Hyperperfusion syndrome usually presents in its mild form, with relatively slight symptoms, such as headaches, temporary seizures, temporary deteriorations in consciousness levels, or temporary focal deficits. In these cases, a mild cerebral edema is the cause for the characteristic clinical presentation.23. In our study, the incidence of the syndrome was 9.6%. The incidence that is referred to literature is 8-12%.2, 11, 24, 25 Florid symptoms and ICH are much rarer conditions as mentioned in the introduction. In our study only 1 patient out of 156 (0.6%) suffered from a major ICH, which fortunately proved not to be fatal. Mortality of patients with post- CEA ICH has been estimated to be approximately 36%.26

We were very cautious with the management of postoperative blood pressure, using intravenous antihypertensive drugs in all occasions of hyperperfusion syndrome. Long-standing hypertension is considered to be another independent risk factor for the syndrome, because of the possible damage in cerebral arterioles.27 It is known that hyperperfusion syndrome can occur even in normotensive patients,2, 25, 27, 28 after CEA, but elevation of blood pressure is a more common occurrence. In our study all patients with hyperperfusion syndrome had a history of hypertension and 11 of them (73.3%) had elevated blood pressure during onset of symptoms. Meticulous and continuous control of postoperative blood pressure is considered extremely important in preventing the syndrome.2, 11. 12, 24

The significant result of our study was the relation between the diameter of shunt and the incidence of hyperperfusion syndrome. It is known that liquid flow through a linear tube can be estimated from Poiseuilles law: Q=piDeltaPr^sup 4^ (Delta=3.14; DeltaP: P2- P1; P2: pressure at the distal end of the tube; Pl : pressure at the proximal end of the tube; r: diameter of the tube; n: viscosity of liquid; 1: length of tube). The characteristic of Poiseuille’s law is that the diameter of the tube is much more important for liquid flow, compared with the other mentioned factors that affect it. Flow is analogous with the fourth force of the tube s diameter. For instance, if we double the diameter of a tube the flow through it increases 16 times.

In our study, if we suggest that the only significant variable is the diameter of the shunt and all the others (DeltaP, n, 1) are approximately stable, we can see the great differences in blood flow between certain shunts (Table V). Using a small shunt during endarterectomy, means that we avoid an abrupt increase of blood flow through cerebral arteries after declamping. This “preconditioning” is useful for a more gradual rise in blood flow after removal of significant stenosis which seems to be a protective factor for a possible postoperative hyperperfusion syndrome.

Conclusions

Patients with high-grade bilateral ICA stenoses or a unilateral high-grade stenosis and a contralateral ICA occlusion are a high- risk group for post-CEA hyperperfusion syndrome. We suggest that CEA using routine shunting is a safe method and the use of a smaller shunt than the shunt that could be otherwise fitted to the ICA is surgical practice that can reduce the incidence of this syndrome.

Received on June 7, 2007; accepted for publication on October 10, 2007.

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C. N. BAKOYIANNIS, N. TSEKOURAS, S. GEORGOPOULOS, C. TSIGRIS, K. FILIS

I. SKRAPARI, E. BASTOUNIS

First Department of Surgery, Vascular Department

University of Athens Medical School, Laiko General Hospital, Athens, Greece

Address reprint requests to: C. N. Bakoyiannis, MD, 17, Agiou Thoma 11527 Goudi, Laiko Hospital, First Department of Surgery, Athens, Greece. E-mail: [email protected]

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