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Intracranial pressure changes with different doses of lignocaine under general anaesthesia.
Correspondence Address:
The effect of intravenous lignocaine on intracranial pressure (ICP) was studied on thirty patients of either sex, aged above 5 years and scheduled for elective ventriculoperitoneal shunt surgery. The patients were randomly divided into 3 groups, which received intravenous lignocaine in the dose of 1 mg, 1.5 mg and 2 mg/kg body weight respectively. Intracranial pressure, heart rate, ECG, arterial pressure and arterial blood gases were monitored at various intervals for a period of 30 minutes. Maximum decrease in ICP was seen at 2 minutes after IV lignocaine in all the three groups (p<0. 001). The fall in ICP was significantly more in group II and group III (35.65% and 37.5% respectively) as compared to group I (17.47%) (p<0.001). This fall in ICP in all the three groups persisted below the basal level, throughout the study period. None of the groups showed any significant change in the heart rate, but a statistically significant fall in arterial pressure was observed in group III (p<0. 05). In conclusion intravenous lignocaine, in a dose of 1.5 mg/kg, causes significant fall in ICP without causing any untoward cardiovascular effects and is recommended for routine clinical use.
Prevention and treatment of acute intracranial hypertension is one of the primary goals in the neuroanaesthetic care of patients with space occupying intracranial lesions. Various methods such as hyperventilation,[1],[2] CSF drainage,[3] hyperosmolar agents[4], distal loop diuretics[5] and barbiturates[6] have been advocated for lowering intracranial pressure (ICP). Each has its inherent advantages and disadvantages. Intravenous lignocaine used during the management of various cardiac arrhythmias was observed to lower ICP.[7] Since then it has been used by various workers to prevent the rise in ICP.[8],[9],[10] Although, Bedford et al have advocated a dose of 1.5 mg/kg body weight,[7] no worker has studied the optimum dosage and duration of action of lignocaine in decreasing ICP. The present study was therefore designed to observe ICP changes following intravenous administration of lignocaine in three different doses.
The present study was carried out on 30 patients of either sex, aged above five years, with clinical features of raised intracranial pressure, who were undergoing ventriculoperitoneal shunt surgery. Patients with cardiovascular, hepatic, renal or endocrinal diseases were excluded from the study. An informed consent was obtained. Hypersensitivity to lignocaine was tested in each patient prior to surgery. The patients were randomly divided into 3 groups with the help of randomisation chart. Group I : Lignocaine 1 mg/kg body weight. Group II : Lignocaine 1.5 mg/kg body weight. Group III : Lignocaine 2 mg/kg body weight. All the patients were premedicated with intramuscular morphine 0.1 mg/kg and promethazine 0.4 mg/kg body weight, administered 60 minutes prior to anaesthesia. Anaesthesia was induced with a sleep dose of thiopentone (4-6 mg/kg), as tested with loss of eye lash reflex and suxamethonium 1.5 mg/kg body weight. Once the patient was fully paralysed, trachea was intubated with a suitable sized endotracheal tube. Anaesthesia was maintained with 66% nitrous oxide in oxygen, pancuronium 0.1 mg/kg and morphine 0.15 mg/kg. Lungs were ventilated so as to maintain a PaCO2 between 30-35 mmHg. Lignocaine was administered after recording baseline ICP, as a single bolus dose (total solution amounting to 10 ml) over a period of one minute. Baseline ICP was recorded once steady state was achieved, i.e. after heart rate and arterial pressure reached between ñ10% of preoperative values. At the end of surgery residual effect of pancuronium was reversed with a mixture of atropine 0.02 mg/kg and neostigmine 0.05 mg/kg and trachea was extubated. ICP, ECG, heart rate and arterial blood pressure (non-invasive) were monitored prior to and at 2, 3, 5, 8, 15, 20 and 30 minutes after administration of lignocaine. Blood gas analysis was carried out prior to, and at 15 and 30 minutes after administration of lignocaine. A ventricular catheter (6 FG umbilical cannula) was placed in the lateral ventricle through the burr hole made for shunt surgery and was connected to a transducer (spectramed, statham, PXL, USA) through a high pressure tubing filled with normal saline. Adequate precautions were taken during connection of the set to avoid any loss of CSF. A continuous display of ICP was obtained by connecting the transducer to a pressure module using Horizon 2000 monitor. The level of the external auditory meatus was taken as the zero reference point. At the completion of the study, the data was statistically analysed and compared using analysis of variance (ANOVA) between the groups and paired `t' test within the groups.
Preoperative patient data was comparable in all the three groups [Table I]. Lignocaine caused a statistically significant fall in ICP at 2 minutes after administration in the three groups (p<0.001), the maximum fall being observed in group III (37.5%) and minimum fall in group I (17.47%). The ICP continued to remain lower than basal value throughout the study period, in group I (p<0.01) as well as group II and group III (p<0.001) [Table II]. On comparing group I with group II and group III, the fall in ICP was significant throughout the study period (p<0.01), but no statistically significant difference was observed between group II and group III (p>0.05) [Figure 1]. There was no statistically significant change in heart rate in each of the three groups [Table II]. Even between the groups there was no statistically significant difference. There was no statistically significant fall in systolic arterial pressure (SAP) in group I and II, but in group III there was a statistically significant fall from basal value at 2, 3 and 5 minutes (p<0.05) [Table II]. On comparing groups I and III there was a statistically significant fall of SAP in group III at 2, 3, (p<0.05) and 5 minutes (p<0.01). Diastolic and mean arterial pressures did not show any significant alterations except that a statistically significant fall was observed at 3 minutes following lignocaine in group III (p<0.05). PaCO2 was maintained between 30-35 mmHg in all the three groups throughout the study period.
Although conflicting reports exist in literature regarding effect of intravenous lignocaine on ICP,[7],[8],[10] our results clearly demonstrate that lignocaine causes maximum fall in ICP at 2 minute following intravenos administration. This fall persists for 30 minutes thereafter. Lignocaine has been known to lower ICP by reducing cerebral blood volume, cerebral metabolism11 as well as cerebral vascular resistance.[12] Lignocaine in a dose of 1 mg/kg caused less fall in ICP (mean 11.82% of basal) as compared to fall caused by 1.5 mg/kg and 2 mg/kg body weight (mean 27.26% and 30.36% of basal). However, the fall in ICP caused by later two doses of lignocaine was statistically comparable (p>0.05). Bedford et al observed a nearly 50% (15.3 mmHg) fall in ICP with a dose of 1.5 mg/kg of lignocaine,[7] whereas Yano et al reported no fall in ICP with the same dose, though they reported suppression of ICP response to endotracheal suctioning.[10] The mean ICP fall of 6.60 mmHg (maximum 8.20 mmHg and minimum 5.00 mmHg) observed over half an hour with lignocaine 1.5 mg/kg body weight falls in between these two extreme values. Bedford et al made basal ICP measurement after application of pin holder or scalp incision, thus these values may be higher than actual.[7] The observations made by Yano et al[10] are difficult to explain, as significant drop in ICP following intravenous lignocaine has been reported by other authors as well.[8],[13] We could not find any report in literature which studied the effects of 1 mg/kg and 2 mg/kg body weight lignocaine on ICP. In our study, after the maximum fall at 2 minutes, the ICP started increasing gradually. This increase started at 3 minutes after lignocaine administration in group I (p<0.01) and at 8 minutes in group II (p<0.001) and group III (p<0.01). Hence, it can be concluded that the peak fall in ICP persists for a longer duration with increased doses of lignocaine. There was no statistically significant fall in heart rate in either of the three groups (p>0.05). This correlates well with the earlier studies.[7],[8] Sinoatrial block, sinus bradycardia and even sinus arrest have been reported with intravenous lignocaine[12],[14],[15] but we did not find any such complication in any of our patients. However, the heart rate did drop from 100 to 70 beats/minute and 91 to 74 beats/minute in 2 patients in group III. There was no statistically significant change in SAP in group I and II, but in group III there was a statistically significant fall in SAP (p<0.05). The observations made in this study in group I and group II correlate well with the earlier studies which showed no haemodynamic changes with 1.5 mg/kg body weight intravenous lignocaine.[7],[8],[10],[13] Grover et al[16] reported a significant fall in SAP with 2 mg/kg intravenous lignocaine which corresponds with the present study. No definite correlation could be established between mean ICP changes, mean heart rate and mean SAP changes in any of the three groups. Thus in the present study, lignocaine in the dose of 1.5 mg/kg and 2 mg/kg body weight produced significantly more fall in ICP as compared to the dose of 1 mg/kg. However, a dose of 2 mg/kg caused cardiovascular instability. Hence we recommend a dose of 1.5 mg/kg body weight for routine clinical work.
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