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Original Article

Cerebral vascular reactivity response to anaesthetic induction with propofol in patients with intracranial space-occupying lesions and vascular malformations

Schmieder, K.*; Schregel, W.; Engelhardt, M.*; Harders, A.*; Cunitz, G.

Author Information
European Journal of Anaesthesiology: June 2003 - Volume 20 - Issue 6 - p 457-460

Abstract

It was shown a decade ago that with total intravenous anaesthesia (TIVA) using propofol, alfentanil and pancuronium, increases in arterial pressure during the induction of anaesthesia are less frequent than during balanced anaesthesia [1]. It was also shown that a reduction of flow velocity in the middle cerebral artery with a combined increase in pulsatility index reflected a reduction of the cerebral blood volume [2,3]. Animal studies in rats and baboons revealed that metabolic stimulation and cerebral blood flow increases are prevented by propofol and cerebral autoregulation is preserved [4,5]. In clinical trials, CO2 reactivity and autoregulation were preserved with propofol [1,6–8]. In patients with brain tumours, paradoxical increases of cerebral blood flow velocity during the induction of anaesthesia have been reported [9]. The aim of the present study was to evaluate the effects of propofol on cerebral blood flow velocity during the induction of anaesthesia in patients undergoing surgery for brain tumours, aneurysms and angiomas.

Methods

After approval of the local Ethics Committee, patients scheduled for resection of intracranial tumours, clipping of ruptured and non-ruptured intracranial aneurysms, and surgical treatment of angiomas were included in the study regardless of age, gender and co-existing diseases. Exclusion criteria were the absence of a temporal bone window for transcranial Doppler sonography and the inability to give informed consent.

Patient characteristics data were taken from the patient records. A neurological examination was performed in all patients using the Hunt and Hess classification in patients with aneurysms and angiomas [10]. The severity of subarachnoid haemorrhage was graded according to the Fisher scale using computed tomography (CT) scanning [11]. Since surgery in patients with ruptured aneurysms was performed within 3 days after the bleeding, the possible influence of cerebral vasospasm was minimized. In patients with tumours, three groups were made with regard to the overall size of the lesion on CT: summing up the net tumour mass, oedema, the mass effect, the uptake of contrast medium, the presence of cystic aspects and the midline shift.

In the induction room, patients were premedicated with midazolam 0.05–0.1 mg kg−1 intravenously (i.v.) and the bilateral 2 MHz transcranial Doppler probes were firmly attached to the head using a special fixation device. The mask was placed on the patient's face to make sure that no displacement of the Doppler probes would occur during the measurement process. Necessary adjustments were made before the start of measurements. An arterial cannula was placed, using local anaesthesia, in the patient's radial or femoral artery. Flow velocity in both middle cerebral arteries, the arterial pressure and the arterial tension of carbon dioxide (PaCO2) were recorded at that time. The end-tidal CO2 concentration was recorded to ensure stable CO2 concentrations during mask ventilation of the lungs with oxygen. Under stable conditions, propofol 1.5–2.5 mg kg−1 was slowly injected (over 30 s) via a peripheral venous cannula. Sixty seconds after injection, the bilateral flow velocity and mean arterial pressure were recorded. Any changes in mean arterial pressure and the middle cerebral artery flow velocity were analysed. PaCO2 was recorded again at that point to make sure that observed changes in blood flow velocity were due to the propofol administration. In patients with intracranial tumours, the side harbouring the tumour was compared with the opposite side and with the results of patients having lesions in the posterior fossa. Patients with aneurysms and angiomas were divided into two groups according to the side of the cerebrovascular lesion. Patients with anterior communicating aneurysms were assigned to the two groups as matched pairs with regard to age and the severity of the subarachnoid haemorrhage. This was possible because there was no side predominance of the aneurysm. The flow changes were evaluated with regard to the underlying diseases, searching for possible influences of the severity of the neurological impairment after subarachnoid haemorrhage or of the size of the tumour.

Non-parametric Wilcoxon's signed rank sum tests were used to assess statistical significance.

Results

Forty-seven patients (mean (range) age 50 (15–73) yr) with intracranial tumours and 22 patients (41 (21–67) yr) with aneurysms and angiomas were included in the study. The majority of tumours were located in the frontal lobe, with a comparable size distribution of large, medium and small lesions (Table 1). Twelve of the 17 patients with aneurysms had had subarachnoid haemorrhages and 3 of the 5 patients with angiomas had suffered a haemorrhage.

Table 1
Table 1:
Location and size of intracranial tumours.

The reduction of the mean arterial pressure was nearly identical in both groups of patients (Table 2). PaCO2 before the administration of propofol was 5.07 ± 0.48 kPa in patients with vascular malformations (n = 22) and 4.93 ± 0.39 kPa in patients with intracranial tumours (n = 47). After administration of propofol, PaCO2 was 5.3 ± 0.59 kPa in patients with vascular malformations and 5.47 ± 0.52 kPa in patients with intracranial tumours.

Table 2
Table 2:
Flow velocity (cm s−1) before and after propofol in patients with intracranial tumours, aneurysms and angiomas and lesions in the posterior fossa.

Mean flow velocity was higher on both sides in patients with aneurysms and angiomas compared with the tumour patients. The degree of reduction of flow velocity after propofol was statistically significant on both sides in tumour patients and in patients with aneurysms and angiomas (Table 2). The flow reduction on the side of the tumour was slightly less than on the healthy side, whereas in patients with cerebrovascular lesions there was no side difference.

In addition to this overall analysis, data were evaluated for abnormal responses to the administration of propofol. In two patients with tumours, the reduction of flow was only present on one side, whereas the side with the tumour showed a flow increase. In patients with vascular malformations, flow velocity was reduced on both sides after propofol except in one patient with a right middle cerebral aneurysm who showed an increase in flow on the side of the lesion. Statistical analysis of these observations did not provide supporting evidence to prove an abnormality of this response.

Discussion

Propofol was found to lower the mean arterial pressure [1]. Cerebral blood flow velocity was reduced in the majority of patients with intracranial tumours, aneurysms and angiomas [2,3,9]. In comparison with previous studies [9], the reduction of mean arterial pressure and of flow velocity was more pronounced, all values still ranging within the estimated autoregulatory capacity. Flow changes induced by propofol were also lower in this study [9] (Table 2). The observation that the response to the administration of propofol was normal in 93% of all study patients indicates intact cerebrovascular reactivity. One explanation for this is that there was no severe impairment of consciousness due to high intracranial pressure in either group of patients.

In 2 (4.2%) of 47 patients with tumours, an increase of flow velocity after propofol was found. Since no statistical proof was possible, this remains an observation; even more so since the observed perfusion patterns in tumours range from hypo- to hyperperfusion [12–14].

In the group of patients with aneurysms and angiomas in 3 (13.6%) of the 22 patients with angiomas, a less pronounced reduction to propofol was found. Since there was no statistical proof to this observation, further evaluation of patients with angiomas is necessary to verify this observation and see whether this reflects an impairment of the cerebrovascular reactivity in this group [15,16].

The idea that the reactivity to propofol due to the changes in arterial pressure may provide additional information on the integrity of cerebrovascular reactivity has no statistical evidence. The evaluation of cerebral autoregulation and CO2 reactivity to investigate the state of cerebrovascular reactivity are, even though more time consuming, not replaceable.

Conclusions

Further investigations in patients with angiomas and with tumours in a state of impaired consciousness are necessary to allow a proof of the observation that flow changes after propofol can provide any indication of the integrity of cerebrovascular reactivity.

References

1. Van Aken H, van Hemelrijck J, Merckx L, Mollhoff T, Mulier J, Lubbesmeyer HJ. Total intravenous anaesthesia using propofol and alfentanil in comparison with balanced anaesthesia in neurosurgery. Anästh Intensivther Notfallmed 1990; 25: 54-58.
2. Boishardy N, Chapotte C, Houi N, Poirier T, Granry JC, Delhumeau A. The effect of a combination of propofol and fentanyl on cerebral blood flow. A study using transcranial Doppler. Can Anaesth Soc J 1992; 40: 23-25.
3. Fischer M, Moskopp D, Nadstawek J, Ries F. Total intravenous anaesthesia using propofol and alfentanil as compared to combined inhalation anaesthesia reduces the flow velocity in the middle cerebral artery: a Doppler sonographic study. Anaesthesist 1992; 41: 15-20.
4. Van Hemelrijck J, Fitch W, Mattheussen M, Van Aken H, Plets C, Lauwers J. Effect of propofol on cerebral circulation and autoregulation in the baboon. Anesth Analg 1990; 71: 49-54.
5. Werner C, Hoffman WE, Kochs E, Schulte am Esch J, Albrecht RF. The effects of propofol on cerebral and spinal cord blood flow in rats. Anesth Analg 1993; 76: 971-975.
6. Akeson J, Messeter K, Rosen I, Bjorkman S. Cerebral haemodynamics and electrocortical CO2-reactivity in pigs anaesthetized with fentanyl, nitrous oxide and pancuronium. Acta Anaesthesiol Scand 1993; 37: 85-91.
7. Salord F, Naous H, Rizk T, et al. Cerebrovascular reactivity to CO2 during anesthesia maintained with either isoflurane-N2O or propofol N2O. A comparative study by transcranial Doppler velocimetry. Ann Fr Anesth Reanim 1995; 14: 166-171.
8. Strebel S, Lam AM, Matta B, Mayberg TS, Aaslid R, Newell DW. Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology 1995; 83: 66-76.
9. Schregel W, Geißler C, Winking M, Schaefermeyer H, Cunitz G. Transcranial Doppler monitoring during induction of anesthesia: effects of propofol, thiopental, and hyperventilation in patients with large malignant brain tumors. J Neurosurg Anesthesiol 1993; 5: 86-93.
10. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysm. J Neurosurg 1968; 28: 14-20.
11. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid haemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980; 6: 1-9.
12. Beaney RP, Brooks DJ, Leenders KL, Thomas DGT, Jones R, Halnan KE. Blood flow and oxygen utilization in the contralateral cerebral cortex of patients with untreated intracranial tumors as studied by positron emission tomography, with observation on the effect of decompressive surgery. J Neurol Neurosurg Psychiat 1985; 48: 331-335.
13. Kuroda K, Olsen TS, Lassen NA. Regional cerebral blood flow in various types of brain tumour. Acta Neurol Scand 1982; 66: 160-171.
14. Palvölgyi R. Regional cerebral blood flow in patients with intracranial tumors. J Neurosurg 1969; 31: 149-163.
15. Hassler W, Steinmetz H. Cerebral hemodynamics in angioma patients: in intraoperative study. J Neurosurg 1987; 67: 822-831.
16. De Salles AAF, Manchola I. CO2 reactivity in arteriovenous malformations of the brain: a transcranial Doppler ultrasound study. J Neurosurg 1994; 80: 624-630.
Keywords:

ANAESTHETICS; intravenous; propofol; MONITORING; Doppler sonography; SURGERY; neurological

© 2003 European Society of Anaesthesiology