[Cerebral hyperperfusion syndrome in carotid revascularisation surgery].
BACKGROUND
Cerebral hyperperfusion syndrome (CHS) is a serious complication of carotid revascularisation surgery associated with both carotid endarterectomy and carotid stenting.


OBJECTIVE
To review the literature published to date on CHS with the aim of updating the data available on its incidence, pathophysiology, clinical features, risk factors, diagnosis, management and treatment.


METHODS
Carotid revascularisation surgery entails a transient increase in cerebral blood flow, and if this increase is more than 100% of the pre-operative value, then hyperperfusion occurs. Two pathophysiological mechanisms are involved in increasing cerebral blood flow: alteration of the cerebrovascular autoregulation mechanisms and increased post-operative systolic arterial pressure. CHS consists in the clinical triad headache, convulsions and focal neurological deficit, associated with arterial hypertension and the absence of cerebral ischaemia. If left undiagnosed, as it progresses it will lead to brain oedema, brain or subarachnoid haemorrhage and, finally, death. The main risk factors for CHS are: diminished haemodynamic reserve, post-operative arterial hypertension and hyperperfusion, which remains for several hours after the carotid recanalisation. Diagnosis is based on clinical suspicion and complementary tests, such as trans-cranial Doppler ultrasonography or single-photon emission tomography, which confirm the suspected hyperperfusion. The keystone on which treatment is based is prevention by strict control of the arterial pressure with drugs such as labetalol and clonidine.


CONCLUSIONS
CHS is a serious, under-diagnosed complication of carotid revascularisation that the specialist must be aware of so that treatment can be established at an early stage, thereby reducing its high morbidity and mortality rate.
Servicio de Angiología, Cirugía Vascular y Endovascular, Hospital Universitario de León, Altos de Nava, s/n. E-24008 León, España. mballesterosp@telefonica.net
Marta
M
Ballesteros-Pomar
Gonzalo
G
Alonso-Argüeso
Javier
J
Tejada-García
Fernando
F
Vaquero-Morillo
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001929:Brain Edema / Q000209:etiology / Q000517:prevention & control; D016893:Carotid Stenosis / Q000601:surgery; D002543:Cerebral Hemorrhage / Q000209:etiology / Q000517:prevention & control; D002548:Cerebral Revascularization / Q000009:adverse effects*; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D003937:Diagnosis, Differential; D016894:Endarterectomy, Carotid / Q000009:adverse effects; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006261:Headache / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000209:etiology; D011183:Postoperative Complications / Q000209:etiology / Q000517:prevention & control; D012307:Risk Factors; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use; D012640:Seizures / Q000209:etiology; D015607:Stents; D013599:Systole; D015899:Tomography, Emission-Computed, Single-Photon; D017585:Ultrasonography, Doppler, Transcranial
D000305:Adrenal Cortex Hormones; D000959:Antihypertensive Agents; D016166:Free Radical Scavengers; D012462:Saline Solution, Hypertonic