Cerebral Hyperperfusion Syndrome after Carotid Endarterectomy and Carotid Stenting



Cerebral Hyperperfusion Syndrome After Carotid Endarterectomy and Carotid Stenting



Thomas S. Riles and Caron B. Rockman


Cerebral hyperperfusion syndrome (CHS) and intracerebral hemorrhage are perhaps the most feared complications of carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS). Although relatively uncommon, such complications can have devastating and often fatal sequelae and remain a significant cause of neurologic morbidity after carotid interventions.


Intracerebral hemorrhage (ICH) after cerebral revascularization was recognized as early as 1964 by Wylie and colleagues and was found to be associated with patients who underwent CEA or carotid thrombectomy for an acute stroke. In these patients it was proposed that removal of an obstructing plaque or thrombus and subsequent cerebral reperfusion converted an ischemic infarct into a hemorrhagic one, most likely because of capillary and arteriolar damage caused by the original ischemic insult. In 1984, Bernstein and associates reported the first CEA patient with postoperative unilateral head, face, and eye pain, classic symptoms of CHS. This patient went on to have seizures and eventually died of a delayed ICH that occurred in the absence of other risk factors.



Pathophysiology


It is generally hypothesized that the cause of intracranial hemorrhage after CEA or CAS is postoperative hyperperfusion, that is, increased blood flow and/or increased pressure in the intracranial vessels. Schroeder and colleagues reported that even after uncomplicated CEA there is a pronounced increase in cerebral blood flow, as much as 37% in the ipsilateral and 33% in the contralateral hemisphere. The increase was most pronounced 2 to 4 days after surgery. After the initial rise, the blood flow gradually returned to normal.


Jansen and coworkers documented increased transcranial Doppler blood flow velocity measurements after CEA. The increases of peak blood flow velocities and pulsatility indices in patients who developed ICH were significantly higher than in patients who did not. Riegel and colleagues noted that when electroencephalography (EEG) was performed in patients with classic hyperperfusion syndrome, periodic lateralizing epileptiform discharges (PLEDs) were invariably noted ipsilateral to the endarterectomy site. These discharges denote an acute, localized cerebral focus of irritability.


Several groups have documented intracranial changes in the specimens of patients who died from ICH after CEA that closely resembled histologic changes seen in malignant hypertension. Interestingly, hemorrhage occasionally occurred within healthy brain tissue, not simply in areas of previous infarction.


Postoperative ICH appears to result from certain events. Patients with chronic severe carotid occlusive disease and relative cerebral hypoperfusion and ischemia experience maximal vascular dilatation as a protective measure, and this in turn likely causes paralysis of normal vascular autoregulatory mechanisms. When CEA or CAS is performed, this lack of autoregulation results in an increased perfusion pressure supplying an area in which vessels are fixed in dilation. This pathophysiologic mechanism is analogous to reperfusion injuries of ischemic limbs and other tissues. In less severe forms, hyperperfusion can result in mild cerebral edema, headache, and seizures. When an abnormal hyperperfused vessel ruptures, intracerebral hemorrhage results.



Incidence


The true incidence of CHS is difficult to ascertain because postoperative hypertension and headache are not uncommon after CEA. A review by Bouri and colleagues found the reported incidence in 36 studies to be approximately 1% of all cases; ICH, much easier to document, occurred in 0.5% of the reported cases they reviewed. In a review of data from the National Inpatient Sample by Timaran and associates, among 135,903 cases of carotid revascularization reported in 2005, the incidence of ICH among the CEA patients was 0.016%, and incidence among CAS patients was 0.15%. Because the data are based on discharge diagnosis and not postdischarge follow-up, it is likely these figures underestimate the actual incidence. The data do suggest, however, that the risk is higher with CAS than with CEA.


Although the cause of perioperative stroke in most large series of CEAs is less than 2%, ICH represents a significant component of those strokes. In a study by Ouriel and coworkers of 1471 CEAs, ICH accounted for 35% of the 31 perioperative neurologic events. Massive hemorrhage and death occurred in four of their patients. Others have reported a similarly high mortality for ICH. Considering the severe morbidity of this particular complication, it is important to recognize which patients are at increased risk.

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Cerebral Hyperperfusion Syndrome after Carotid Endarterectomy and Carotid Stenting

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