Post-carotid endarterectomy hyperperfusion syndrome-is it predictable by lack of cerebral reserve?

Cerebral hyperperfusion syndrome (HS) is presumed to be because of an increase in postendarterectomy flow in patients with fixed cerebral vascular reserve. Severe headache is thought to be an early sign of possible HS. An increase in partial pressure CO₂ (pCO₂) is known to cause cerebral vasodilatation and is used to evaluate the presence of cerebral reserve.

A total of 45 patients undergoing carotid endarterectomy had internal carotid artery flow measured with a transonic flow probe as follows: F1, immediately after full dissection of the internal carotid artery; F2, after 30 seconds of breath holding; and F3, after restoration of flow. ΔF2-F1 and ΔF3-F2 were also evaluated. A 10% increase between F2 and F1 indicated normal cerebral reserve and between F3 and F2 indicated increased postoperative flow. Age, gender, medical comorbidities, indication for carotid endarterectomy, intraoperative cerebral oximetry values, and percentage of bilateral carotid stenosis were recorded. All patients were contacted after discharge about the presence of postoperative headache or other suggestions of HS. Fisher's exact test was used for categorical predictors and the rank-sum test for continuous predictors.

Seven (16%) patients (group A) developed postoperative headache and 38 (group B) did not. No patient developed HS. No variables were associated with postoperative headache except for female gender (p = 0.005). There were no statistically significant differences in F1, F2, F3, and ΔF (F2-F1 or F3-F2) between groups A and B (there was no descriptively significant ΔF2-F1 in 17 patients). Only one of the nine patients who had no change between F2 and F1, who had a significant increase in F3, and who was thought to be at higher risk for HS developed a postoperative headache.

Lack of cerebral reserve is common in patients undergoing endarterectomy. If headache is an early sign of hyperperfusion, it does not seem to be predicted by lack of cerebral reserve and an increase in postendarterectomy flow.