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Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation
ABSTRACTS James S. T. Yao, MD, Abstracts
Section Editor
Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation Powers AD, Smith RR. Neurosurgery 1990;26:56-60. The hyperperfirsion syndrome is known to occur after carotid thromboendarterectomy (TEA) ,and consists ofseizures, unilateral head, eye, and face pain, and delayed intracerebral hemorrhage. This syndrome was identified by transcranial Doppler (TCD) in two patients who demonstrated mild clinical symptoms after a TEA for severe critical carotid stenosis. Transcranial Doppler identified a substantial increase in middle cerebral artery (MCA) flow velocities associated with relatively low pulsatility indexes during the first 24 to 48 hours after operation. Preoperative TCD examination revealed marginal velocities and low pulsatility, suggesting reduced peripheral resistance. The MCA blood flow velocity was further reduced during cross-clamping, but immediate hyperemia occurred after clamp removal and restoration of flow. An increase of 100% to 400% of the ipsilateral MCA and anterior cerebral artery flow velocities occurred over the ensuing 48 hours. All velocities returned to normal during the next 3 days. Pulsatility, a reflection of vascular resistance, also increased proportionally, as flow velocity decreased to normal levels. A normotensive state was maintained in these patients throughout the postoperative period. A physiologic mechanism, the failure in cerebral blood flow autoregulation, was proposed as the cause for the hyperperfusion syndrome. Perioperative TCD findings imply that maximum dilation was present after the TEA. The intracranial vessels only constricted properly as autoregulation was reestablished. The exact mechanism of the interaction between multiple stimuli (i.e., extracellular pH, adenosine concentrations, the carotid sympathetic fiber network, and smooth muscle cell response to alterations of intraluminal pressure) on the autoregulatory mechanism remains ill defined. The two patients with hyperperfusion were contained in a group of 14 patients undergoing serial TCD monitoring before and after TEA. This 14% incidence of the syndrome is consistent with the literature. only IO% of this group with the hyperperfusion syndrome is reported to develop serious complications. Clinically, systemic blood pressure control would seem to be an important consideration after operation. Furthermore, antiplatelet agents or anticoagulants could possibly lead to increased complications in those patients experiencing the hypcrperfusion syndrome. An awareness of the presence of the syndrome is beneficial to the vascular surgeon. The TCD has provided further insight into the possible cause, although a much larger series will be required. S. Tim&y String, Mobile Infimury
354
ML3
Medical Center
Coeliac artery compression syndrome: the effect of decompression Geelkerken RH, van Bockel JH, de Roos WK, Hermans J. Br J Surg 1990;77:807-9. Most studies of decompression for celiac artery compression syndrome have shown poor results. However, a few recent studies, particularly those by Reilly (J VASC SURG 1985;2:79-91) and Thevenet (Chirurgie 1985; 111:85 l-6) have suggested good long-term benefit from this procedure. In an effort to partially resolve this controversy, 11 patients followed for up to 20 years after celiac axis decompression have been reviewed. The 11 patients included 9 women and 2 men, all who had chronic abdominal pain associated with 95% stenosis of the celiac artery by angiography. Weight loss was present in seven patients before surgery, and a 40 mm Hg gradient between the celiac artery and the aorta was found in the four patients in which this was measured. All patients were treated by division of the median arcuate ligament, but none underwent celiac artery reconstruction. In the immediate postoperative period symptoms were relieved in all 11 patients. However, by 3 months three patients had recurrent symptoms, and long-term (mean follow-up 6.8 years) all eight patients that were available for follow-up had return of symptoms. Five of these patients were subsequently reexplored without relief. This retrospective study suggests that though immediate symptom relief after celiac decompression for celiac compression syndrome may be good, long-term results are poor. Differences between the poor results of this study and the good results reported by the two papers mentioned above include the fact that celiac artery reconstruction (which was commonly done in the other two series) was not done in these patients and the longer follow-up in this study. Three of the 8 patients who failed in long-term follow-up failed at 14, 14, and 20 years, respectively. Thus the results of this study suggest that operation to relieve celiac artery compression should not be undertaken in patients with vague upper abdominal complaints even if compression of the celiac artery can be identified by arteriography. Although mesenteric ischemia caused by single vessel disease is possible, celiac artery decompression alone will likely not result in long-term symptom relief in this group of patients. James M.
Seeger, MD
University of Florida,
Collefle of Medicine
Section Editor
Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation Powers AD, Smith RR. Neurosurgery 1990;26:56-60. The hyperperfirsion syndrome is known to occur after carotid thromboendarterectomy (TEA) ,and consists ofseizures, unilateral head, eye, and face pain, and delayed intracerebral hemorrhage. This syndrome was identified by transcranial Doppler (TCD) in two patients who demonstrated mild clinical symptoms after a TEA for severe critical carotid stenosis. Transcranial Doppler identified a substantial increase in middle cerebral artery (MCA) flow velocities associated with relatively low pulsatility indexes during the first 24 to 48 hours after operation. Preoperative TCD examination revealed marginal velocities and low pulsatility, suggesting reduced peripheral resistance. The MCA blood flow velocity was further reduced during cross-clamping, but immediate hyperemia occurred after clamp removal and restoration of flow. An increase of 100% to 400% of the ipsilateral MCA and anterior cerebral artery flow velocities occurred over the ensuing 48 hours. All velocities returned to normal during the next 3 days. Pulsatility, a reflection of vascular resistance, also increased proportionally, as flow velocity decreased to normal levels. A normotensive state was maintained in these patients throughout the postoperative period. A physiologic mechanism, the failure in cerebral blood flow autoregulation, was proposed as the cause for the hyperperfusion syndrome. Perioperative TCD findings imply that maximum dilation was present after the TEA. The intracranial vessels only constricted properly as autoregulation was reestablished. The exact mechanism of the interaction between multiple stimuli (i.e., extracellular pH, adenosine concentrations, the carotid sympathetic fiber network, and smooth muscle cell response to alterations of intraluminal pressure) on the autoregulatory mechanism remains ill defined. The two patients with hyperperfusion were contained in a group of 14 patients undergoing serial TCD monitoring before and after TEA. This 14% incidence of the syndrome is consistent with the literature. only IO% of this group with the hyperperfusion syndrome is reported to develop serious complications. Clinically, systemic blood pressure control would seem to be an important consideration after operation. Furthermore, antiplatelet agents or anticoagulants could possibly lead to increased complications in those patients experiencing the hypcrperfusion syndrome. An awareness of the presence of the syndrome is beneficial to the vascular surgeon. The TCD has provided further insight into the possible cause, although a much larger series will be required. S. Tim&y String, Mobile Infimury
354
ML3
Medical Center
Coeliac artery compression syndrome: the effect of decompression Geelkerken RH, van Bockel JH, de Roos WK, Hermans J. Br J Surg 1990;77:807-9. Most studies of decompression for celiac artery compression syndrome have shown poor results. However, a few recent studies, particularly those by Reilly (J VASC SURG 1985;2:79-91) and Thevenet (Chirurgie 1985; 111:85 l-6) have suggested good long-term benefit from this procedure. In an effort to partially resolve this controversy, 11 patients followed for up to 20 years after celiac axis decompression have been reviewed. The 11 patients included 9 women and 2 men, all who had chronic abdominal pain associated with 95% stenosis of the celiac artery by angiography. Weight loss was present in seven patients before surgery, and a 40 mm Hg gradient between the celiac artery and the aorta was found in the four patients in which this was measured. All patients were treated by division of the median arcuate ligament, but none underwent celiac artery reconstruction. In the immediate postoperative period symptoms were relieved in all 11 patients. However, by 3 months three patients had recurrent symptoms, and long-term (mean follow-up 6.8 years) all eight patients that were available for follow-up had return of symptoms. Five of these patients were subsequently reexplored without relief. This retrospective study suggests that though immediate symptom relief after celiac decompression for celiac compression syndrome may be good, long-term results are poor. Differences between the poor results of this study and the good results reported by the two papers mentioned above include the fact that celiac artery reconstruction (which was commonly done in the other two series) was not done in these patients and the longer follow-up in this study. Three of the 8 patients who failed in long-term follow-up failed at 14, 14, and 20 years, respectively. Thus the results of this study suggest that operation to relieve celiac artery compression should not be undertaken in patients with vague upper abdominal complaints even if compression of the celiac artery can be identified by arteriography. Although mesenteric ischemia caused by single vessel disease is possible, celiac artery decompression alone will likely not result in long-term symptom relief in this group of patients. James M.
Seeger, MD
University of Florida,
Collefle of Medicine