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Effect of pipecuronium and pancuronium on intracranial pressure and cardiovascular parameters in patients with supratentorial tumours.
Correspondence Address:
A prospective, randomised, single blind study was conducted to evaluate and compare the intracranial pressure (ICP) and cardiovascular effects of pipecuronium (PPC) and pancuronium (PNC) in 20 patients undergoing supratentorial surgery. Patients were randomly divided into two groups. Patients in Group I (n = 10) received pancuronium (0.1 mg kg(-1)) and in Group II (n = 10) pipecuronium (0.07 mg kg(-1)) for intubation. Intracranial pressure (ICP), heart rate (HR), systolic, diastolic and mean arterial pressures (SAP, DAP, MAP), central venous pressure (CVP), nasopharyngeal temperature and arterial blood gases (ABG) were monitored at the following time periods: before induction (0 minutes); 3 minutes after thiopentone and muscle relaxant; immediately after intubation; and 4, 6, 8, 10, 20 and 30 minutes following intubation. The rise in intracranial pressure at intubation was significantly greater in group I (21.10+/-3.97 torr, 122.59%) when compared to group II patients (1.80+/-0.70 torr, 10.04%) (p<0.0 1). Cardiovascular parameters also showed a significantly greater degree of rise in group I when compared to group II patients. Heart rate increased by 29+/-6.32 beats min(-1) (33.52%) and systolic arterial pressure by 11.60+/-7.37 torr (9.47%) in group I. These parameters did not change significantly in group II. No significant alterations were observed in the other measured parameters in either of the two groups.
Maintenance of steady intracranial pressure (ICP) is one of the primary goals in neuro-anaesthesia. The time honoured technique of using succinylcholine is associated with sudden accentuation of ICP.[1] The advent of non-depolarising muscle relaxants has heralded a new era of tracheal intubation without detrimental effects on ICP. Each of these relaxants has its own disadvantages. Pancuronium causes tachycardia and hypertension.[2] Vecuronium and atracurium are intermediate acting relaxants with no adverse effects on ICP and cerebral perfusion pressure (CPP)[3],[4],[5], but require supplementation by repeated incremental doses. Pipecuronium (PPC) is a long acting, cardiostable, non-depolarising muscle relaxant. Various studies have reported its cardiovascular effects[6],[7],[8] but there is only one isolated study evaluating its effects on ICP,[9] where the drug was administered to pre-intubated patients. PPC has never been used for intubation in the neurosurgical patients. We, therefore, decided to evaluate its efficacy as an intubating agent with special reference to its effect on ICP and cardiovascular parameters. At the same time, we planned to compare these effects with those of pancuronium (PNC), following a similar anaesthetic technique under similar surgical conditions. Methods This prospective, single blind, randomised study was undertaken after obtaining the approval of Institute's ethical committee and informed consent from patients. Twenty patients of ASA-I and II, aged 15-55 years, of either sex, with or without the clinical features of raised ICP, scheduled for elective surgery of supratentorial space occupying lesion were included in the study. Exclusion criteria included morbid obesity[6] and evidence of any major systemic illness. All patients received tablet diazepam 5-10 mg orally, the night before the surgery. Injection morphine (0.1 mg kg-1 and promethazine (0.4 mg kg-1 were given 45 minutes before the expected time of surgery. Peripheral venous, radial arterial and central venous cannulations were performed in the operation theatre under local anaesthesia. A subarachnoid pressure bolt (codman's screw No.80-1995-93) was inserted 2 cm anterior to the coronal suture, 3 cm away from the midline, under local anaesthesia by the surgeon. Invasive BP, CVP and ICP were continuously transduced and monitored (multichannel Horizon-2000 monitor). The subjects were anaesthetised with the sleep dose of thiopentone sodium, followed by an equipotent dose of either of the muscle relaxants i.e. ncuronium (PNC) 0.1 mg kg-1 in group I and pipecuronium (PPC) 0.07 mg kg-1 in group II. Endotracheal intubation was facilitated at the end of 3 minutes after confirming the adequacy of muscle relaxation. Morphine (0.1 mg kg-1 was given to all patients. Anaesthesia was maintained with 66% N2O in O2, intermittent halothane (0.5-1.0%) and ventilation was adjusted to maintain normocapnia. ICP, HR, BP (SAP, DAP, MAP), CVP, ABG and nasopharyngeal temperature were monitored before induction (0 minute), 3 minutes after thiopentone and muscle relaxant, immediately after intubation and 4, 6, 8, 10, 20 and 30 minutes following intubation. The data obtained was analysed and statistically compared using 2 way analysis of variance (ANOVA) and student's 't' test.
Patients were well matched with regards to the baseline variables and demographic data [Table I]. Three patients in group I and two patients in group II had normal ICP. Intracranial pressure: Elevation in ICP was observed in both the groups following intubation, the rise being significantly higher in group I (21.0+3.97 torr, 122.59%; p<0.01) as compared to that in group II (1.80+0.70 torr, 10.04%; p>0.05) [Table II]. The rise in ICP in group I was statistically significant within the group upto 10 minutes (4.40+0.97 torr, 25.58%; p<0.05) and between the groups upto 8 minutes (p<0.05) following intubation. On the contrary, no significant rise in ICP was observed in group II throughout the study period (p>0.05). Cardiovascular parameters: HR remained higher than the basal value throughout the study period in group I. The maximum rise in mean HR was 29+6.32 beats min-1 (33.52%) and was observed at the time of intubation. This was highly significant as compared to the basal value (p<0.01) [Table III]. On the contrary, only a marginal rise in HR of 11.10+5.18 beats min-1 (12.71%) was observed in group II at the time of intubation (p>0.05). A significant rise in SAP (11.60+7.37 torr, 9.47%) was observed in response to intubation in group I (p<0.05). Also, following intubation, SAP remained higher than the basal value throughout the study period in group I. However, it was not statistically significant (p>0.05) [Table IV]. SAP showed a nonsignificant fall in group II patients at the time of intubation (8.30+19.63 torr, 6.32%; p>0.05). No change in DAP, MAP, CVP and ABG was observed in either of the groups. Body temperature ranged between 37o-38oC and Pa Co2 was maintained between 25-30 torr throughout the study period in both the groups.
Anaesthesia for intracranial surgery involves a constant awareness of ICP and the need to maintain it well within the normal range throughout the surgery. The commonest clinical problem encountered by the neuro-anaesthetist and neurosurgeon is that of elevated ICP. Anaesthetic drugs can cause catastrophic changes in the CSF pressure and might even threaten the viability of the brain. Drug selection, therefore, assumes an added importance in patients having intracranial hypertension. In neuro-anaesthetic practice, non-depolarising muscle relaxants are preferred for intubation. We have studied the effect of PNC and PPC on ICP and cardiovascular parameters, as intubating agent. Therefore, changes seen in different parameters are the combined response of muscle relaxant and pressor response to intubation. However, we have taken measures to minimise the laryngoscopic stimulus by allowing the same doctor to intubate all patients in both the groups. Further, to minimise the individual variation of laryngoscopic responses, we have taken the mean increase in a particular parameter in each group. A neuromuscular blocking agent should optimally be devoid of direct intracranial or significant cardivascular effects in doses required for intubation. PNC does not increase ICP,[10] but produces cardiovascular stimulation,[2] which makes it undesirable for patients with derranged cerebral autoregulation and intracranial vascular lesions. PPC is a longer acting, cardiostable, non-depolarising muscle relaxant.[6],[7],[8] There is only one study by Guigno et al, evaluating its effect on ICP.[9] These authors have noted 2.89% rise in ICP with PPC, while the drug was administered to the pre-intubated patients. On the other hand, we have recorded a rise in ICP by 10.04% with PPC as an intubating agent. The results noticed by Guigno et al[9] are the true reflection of the effect of PPC on ICP, as there were no confounding factors to elevate ICP i.e. the pressor response to laryngoscopy and intubation. On the contrary, these factors could have contributed to a higher degree of rise in ICP in our study. A highly significant rise in ICP (122.59%), as seen in our study in group I with PNC, could be attributed to its vagolytic action, as PNC by itself does not increase ICP.[10] Vagolytic action of PNC results in tachycardia and hypertension. An elevation in ICP is expected, when there is an abrupt increase in MAP and/or when CBF autoregulation has been modified by the disease process. Mclesky et al[11] reported a rise in ICP of 22.5% with PNC as the intubating agent. This discrepancy in the percentage of rise in ICP could be due to the additional dose of thiopentone (50100 mg) given prior to intubation in their study. Lanier et al[10] observed no significant effect of PNC on ICP, while studying the cerebral effects of PNC in dogs anaesthetised with halothane. No positive correlation was observed between the tumour size (maximum diameter) on pre-operative CT scan and intraoperative rise in ICP, a finding earlier reported by Beford et al.[12] A significant rise in HR (33.52%) at the time of intubation in group I patients, noticed in our study could also be explained by the vagolytic effects of PNC. Our finding is consistent with other reports.[13],[14],[15] However, in contrast to our study, Foldes et el[16] reported only 20% rise in HR with intubating dose of PNC (0.1mg kg-1 under balanced anaesthesia. The lesser degree of rise in HR in their study, despite the use of meperidine hydrochloride, 60-90 minutes prior to surgery could be due to addition of fentanyl and droperidol to thiopentone during induction and maintenance of anaesthesia. We have noticed only a marginal rise in HR at the time of intubation in group II patients (12.7%, p>0.05). Similar results are also reported by Guigno et al.[9] These findings are attributed to the cardiostable properties of PPC. Structurally it is similar to PNC in having a steroid nucleus,[6] but differs in the side chain attached to it. PPC has a piperazine ring attached at 2 and 16 positions of steroid nucleus, whereas PNC has piperidine ringS[6]. This structural modification improves the specificity of action of PPC while reducing its nicotinic side effects, and is responsible for the cardiostability of this drug. Tassoyni et al[15] have reported that haemodynamic variables are not altered following doses of PPC as large as 3xED95, in patients undergoing CABG (coronary artery bypass grafting). On the contrary, Larijani et at[6] observed a significant fall in HR following administration of PPC. This effect could be due to the usage of both thiopentone and fentanyl for induction. In their study, PPC did not oppose opiate induced bradycardia[17] due to the lack of autonomic or vagolytic actions. Our results have demonstrated a significant rise (9.47%) in SAP at the time of induction with PNC (p<0.05), an effect attributed to its vagolytic action. Similar results have been reported earlier by Coleman et al[18] and Gregoretti et al.[14] Foldes et a1[16] have reported a non-significant rise in SAP with administration of PNC (0.1mg kg-1 under balanced anaesthesia. Additional fentanyl could explain this difference in rise of SAP. No significant change in SAP was observed in group II patients. Cardiostability of PPC has also been explained by the difference in its effect on the evoked release of norepinephrine from an isolated right atrium and on the force of contraction of the electrically stimulated atria. PNC increases the evoked release of norepinephrine and the force of contraction of the electrically stimulated right atria, because of its inhibitory effect on the muscarinic receptors located on the nonadrenergic nerve terminals and pacemaker cells of right atrium.[19] These effects of PNC cause acceleration of heart rate and elevation of blood pessure. On the contrary, pipecuronium has little or no inhibitory effect on these muscarinic receptors, and consequently, causes no alteration in heart rate and blood pressure.[20] The unaltered DAP, MAP and CVP in both the groups, similar to our study, has earlier been reported.[9],[15],[16] The results of our study conclude that PPC provides significantly greater cardiovascular stability and lesser rise in ICP at the time of intubation and during the first 30 minutes thereafter, as compared to PNC, when used as an intubating agent in patients with supratentorial tumours under standard anaesthetic technique.
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