Int J Angiol 2014; 23(02): 125-130
DOI: 10.1055/s-0034-1376158
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Postendarterectomy Cerebral Hyperperfusion Syndrome: The Etiological Significance of “Cerebral Reserve”

George L. Hines
1   Department of Thoracic and Cardiovascular Surgery, Winthrop University Hospital, Mineola, New York
,
Donald DeCrosta
2   Department of Anesthesia, Winthrop University Hospital, Mineola, New York
,
Sarah Kantaria
3   School of Medicine, State University of New York at Stony Brook, Stony Brook, New York
,
Chris Cary III
3   School of Medicine, State University of New York at Stony Brook, Stony Brook, New York
,
Shahidul Islam
4   Department of Biostatistics, Winthrop University Hospital, Mineola, New York
› Author Affiliations
Further Information

Publication History

Publication Date:
09 June 2014 (online)

Abstract

Postoperative cerebral hyperperfusion syndrome (CHS) in patients undergoing carotid intervention is thought to be related to the absence of cerebral reserve. Although hyperperfusion syndrome is rare, severe postoperative headache is common and is considered to be a prodromal sign. Cerebral reserve is measured by studying the response of cerebral vessels to a vasodilator such as hypercarbia. We produced hypercarbia by holding respiration for 60 seconds during carotid endarterectomy. We attempted to evaluate the relationship between intraoperatively evaluated cerebral reserve and the development of postoperative headache which was severe enough to require the patient to take an over the counter analgesic (e.g., ibuprofen, acetaminophen, aspirin). Internal carotid artery flow 1 (F1), Pco 2, and blood pressure 1 (BP1) were recorded before and after (F2, Pco 2, and BP2) 60 seconds of apnea. An increase in flow of > 20% was considered indicative of adequate cerebral reserve. Patients were evaluated before discharge and with follow-up calls at 2 to 5 days postdischarge. Fisher exact test was used to evaluate categorical predictors. Unpaired t test was used to compare continuous variables. Results were considered significant when p < 0.05. A total of 30 nonconsecutive patients were evaluated prospectively. Of the 30 patients, 4 (Group I) developed severe postoperative headache; 26 did not (Group II). Demographics were similar in both the groups. Three patients in Group I and 16 patients in Group II had > 20% increase in flow (p = 0.6315). Pco 2 rose in both groups and BP2 was unchanged from BP1 in both groups. Lack of cerebral reserve does not appear to be related to the development of severe postoperative headache.

 
  • References

  • 1 Ferguson GG, Eliasziw M, Barr HW , et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke 1999; 30 (9) 1751-1758
  • 2 Pomposelli FB, Lamparello PJ, Riles TS, Craighead CC, Giangola G, Imparato AM. Intracranial hemorrhage after carotid endarterectomy. J Vasc Surg 1988; 7 (2) 248-255
  • 3 Bernstein M, Fleming JF, Deck JH. Cerebral hyperperfusion after carotid endarterectomy: a cause of cerebral hemorrhage. Neurosurgery 1984; 15 (1) 50-56
  • 4 Coutts SB, Hill MD, Hu WY. Hyperperfusion syndrome: toward a stricter definition. Neurosurgery 2003; 53 (5) 1053-1058 , discussion 1058–1060
  • 5 Sfyroeras GS, Karkos CD, Arsos G , et al. Cerebral hyperperfusion after carotid stenting: a transcranial doppler and SPECT study. Vasc Endovascular Surg 2009; 43 (2) 150-156
  • 6 Moulakakis KG, Mylonas SN, Sfyroeras GS, Andrikopoulos V. Hyperperfusion syndrome after carotid revascularization. J Vasc Surg 2009; 49 (4) 1060-1068
  • 7 Markus HS, Harrison MJ. Estimation of cerebrovascular reactivity using transcranial Doppler, including the use of breath-holding as the vasodilatory stimulus. Stroke 1992; 23 (5) 668-673
  • 8 Meyers PM, Higashida RT, Phatouros CC , et al. Cerebral hyperperfusion syndrome after percutaneous transluminal stenting of the craniocervical arteries. Neurosurgery 2000; 47 (2) 335-343 , discussion 343–345
  • 9 Piepgras DG, Morgan MK, Sundt Jr TM, Yanagihara T, Mussman LM. Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg 1988; 68 (4) 532-536
  • 10 Ogasawara K, Sakai N, Kuroiwa T , et al; Japanese Society for Treatment at Neck in Cerebrovascular Disease Study Group. Intracranial hemorrhage associated with cerebral hyperperfusion syndrome following carotid endarterectomy and carotid artery stenting: retrospective review of 4494 patients. J Neurosurg 2007; 107 (6) 1130-1136
  • 11 Fukuda T, Ogasawara K, Kobayashi M , et al. Prediction of cerebral hyperperfusion after carotid endarterectomy using cerebral blood volume measured by perfusion-weighted MR imaging compared with single-photon emission CT. AJNR Am J Neuroradiol 2007; 28 (4) 737-742
  • 12 Reigel MM, Hollier LH, Sundt Jr TM, Piepgras DG, Sharbrough FW, Cherry KJ. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. J Vasc Surg 1987; 5 (4) 628-634
  • 13 Ascher E, Markevich N, Schutzer RW, Kallakuri S, Jacob T, Hingorani AP. Cerebral hyperperfusion syndrome after carotid endarterectomy: predictive factors and hemodynamic changes. J Vasc Surg 2003; 37 (4) 769-777
  • 14 Pennekamp CW, Immink RV, den Ruijter HM , et al. Near-infrared spectroscopy can predict the onset of cerebral hyperperfusion syndrome after carotid endarterectomy. Cerebrovasc Dis 2012; 34 (4) 314-321
  • 15 Ringelstein EB, Van Eyck S, Mertens I. Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab 1992; 12 (1) 162-168
  • 16 Müller M, Voges M, Piepgras U, Schimrigk K. Assessment of cerebral vasomotor reactivity by transcranial Doppler ultrasound and breath-holding. A comparison with acetazolamide as vasodilatory stimulus. Stroke 1995; 26 (1) 96-100
  • 17 Kaku Y, Yoshimura S, Kokuzawa J. Factors predictive of cerebral hyperperfusion after carotid angioplasty and stent placement. AJNR Am J Neuroradiol 2004; 25 (8) 1403-1408
  • 18 Hines GL, Oleske A, Feuerman M. Post-carotid endarterectomy hyperperfusion syndrome-is it predictable by lack of cerebral reserve?. Ann Vasc Surg 2011; 25 (4) 502-507
  • 19 Stock MC, Downs JB, McDonald JS, Silver MJ, McSweeney TD, Fairley DS. The carbon dioxide rate of rise in awake apneic humans. J Clin Anesth 19 FI88; 1 (2) 96-103
  • 20 Stock MC, Schisler JQ, McSweeney TD. The PaCO2 rate of rise in anesthetized patients with airway obstruction. J Clin Anesth 1989; 1 (5) 328-332