Growth of Escherichia coli in propofol, lidocaine, and mixtures of propofol and lidocaine

BACKGROUND: Microorganisms grow rapidly in propofol. Extrinsic contamination of propofol is thought to be a source of postoperative sepsis and wound infection. We studied growth of a strain of Escherichia coli in thiopental, propofol, lidocaine, and mixtures of propofol and lidocaine. METHODS: The pathogen was exposed to 2.5% thiopental; 1.0% propofol; 1.0%, 2.0% and 4.0% preservative-free lidocaine; and propofol solutions containing 0.25%, 0.5%, 1.0%, 2.0%, or 4.0% lidocaine for 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, and 24 h at room temperature, respectively. The inocula from these suspensions were cultured for 48 h at 37 degrees C after the antimicrobial activity of the local anesthetics in the inocula was inactivated by a 1:1000 dilution with distilled water. RESULTS: No organisms grew after exposure to 2.5% thiopental. The exposure of E. coli to propofol increased the colony count to approximately 90 times the control count. The colony counts of E. coli after exposure to 1.0%, 2.0% and 4.0% lidocaine and 0.25%, 0.5%, 1.0%, 2.0% and 4.0% lidocaine in 1.0% propofol were lower than the counts after exposure to 1.0% propofol (P = 0.0048, 0.0027, 0.0003, 0.0503, 0.0188, 0.0080, 0.0044, and 0.0001, respectively). The growth rate of the microorganism was significantly higher in cultures exposed to 1.0% propofol than that in cultures exposed to lidocaine alone or lidocaine-propofol mixtures (P < 0.0001, respectively). CONCLUSION: Lidocaine possesses bacteriostatic activity against E. coli. Addition of lidocaine to propofol confers its bacteriostatic activity to the mixture and may decrease the hazard of infection associated with the extrinsic contamination of propofol.     

Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity

Study Objective: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (IV) lidocaine.

Design: Randomized, double-blind, placebo-controlled, cross-over study.

Setting: University-affiliated hospital.

Patients: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression.

Interventions: Patients received lidocaine 50 mg, 100 mg, 200 mg IV, or saline prior to induction of anesthesia via a standardized anesthetic technique.

Measurements and Main Results: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means ± SD) were 37 ± 13 sec and 64 ± 21 sec, 25 ± 11 sec and 52 ± 43 sec, 17 ± 12 sec and 32 ± 17 sec, 1 ± 3 sec and 18 ± 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups.

Conclusions: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity.     

Postoperative pain relief by topical lidocaine in the surgical wound of hysterectomized patients

Background: To improve postoperative analgesia, local anesthetics have been administered perioperatively as infiltration or as aerosol in the surgical area. A previous study showed good analgesic effects by topical lidocaine in the wound in minor extraabdominal surgery (herniorraphy), while the same treatment in minor lower laparotomies did not improve postoperative analgesia. The present study investigated the effect of topical wound anesthesia using lidocaine aerosol on postoperative pain following major lower abdominal surgery.
Methods: Postoperative pain and analgesic requirements were studied in a double-blind randomized trial including 30 hysterectomized patients. Patients were randomized to receive single wound treatment either with lidocaine aerosol 500 mg (100 mg/ml; Xylocain® aerosol, ASTRA, Sweden) (n=15) or placebo aerosol (n=15). Postoperative pain was evaluated by visual analogue scale (VAS). Requirements of opiate analgesics (buprenorphine) after surgery were monitored.
Results: Lidocaine aerosol induced a significantly ( P <0.001) better analgesia at rest (VAS) and a significant ( P <0.001) reduction in postoperative requirements of buprenorphine during the first 24 hours after surgery compared to placebo aerosol. Differences between the groups in pain scores (VAS) and buprenorphine requirements during the second postoperative day were not significant. Mean pain scores upon mobilization 24 h after surgery were significantly lower in the group receiving lidocaine aerosol ( P <0.05). The plasma lidocaine concentration 4 h after the administration of lidocaine was well below toxic level and plasma lidocaine was detectable 48 h postoperatively. No drug-related side effects were reported.
Conclsuion: A single dose of lidocaine aerosol topically administered in the surgical wound of hysterectomy patients improved analgesia during the first postoperative day with minimal risk of side effects.     

An assessment of prilocaine as a topical anaesthetic agent for fibreoptic bronchoscopy in comparison with lidocaine

We have evaluated prilocaine as a topical anaesthetic agent for fibreoptic bronchoscopy in comparison with lidocaine in terms of efficacy and safety. Forty patients were included in a randomised double-blind parallelgroup study. Efficacy was assessed using visual analogue scales, a patient ranking scale and the number of doses of local anaesthetic and intravenous sedative required. Measures of toxicity included peak plasma concentration of local anaesthetic, whether supplementary oxygen was needed and change in methaemoglobin concentration. For most of the outcome variables, the medians and quartiles were similar for the two local anaesthetics. However, the median peak plasma concentration of prilocaine (0.5 μg·ml^-1) was less than onethird that of lidocaine (1.76 μg·ml^-1). The merits and hazards of using multiple–regression modelling to improve the precision of the analysis of the results are considered. We conclude that prilocaine can be used successfully as a topical anaesthetic agent for fibreoptic bronchoscopy and is associated with a lower risk of toxicity.     

The effects of triazolam on cerebral blood flow and metabolism in the dog

The new benzodiazepine triazolam was given to six initially awake dogs maintained with spinal anaesthesia and mechanical ventilation. Both cerebral blood flow (CBF) and cerebral metabolic rate for O2 (CMRO2) were significantly reduced after the initial dose of 0.1 mg X kg-1 triazolam, and the EEG changed from an awake to a sleep pattern in less than 20 s. CMRO2 was gradually reduced with increasing doses of triazolam (0.3, 1.0, 10.0 and 30.0 mg X kg-1) to 76% of control after the final 30 mg X kg-1 dose. CBF did not decrease further after the initial dose, and the addition of N2O after the final dose did not cause any significant change in CBF or CMRO2. The dogs were hemodynamically stable during the study. Small increases in brain lactate and pyruvate levels, but not in the L/P ratio were the only significant changes in brain metabolite levels. Triazolam appears to be a safe and rapidly acting induction agent in the dog.     

The effects of prolonged isoflurane anaesthesia on cerebral blood flow and metabolism in the dog

To determine whether cerebral blood flow (CBF) changed with time under isoflurane anaesthesia, as has been reported for halothane, CBF and cerebral metabolic rate for oxygen (CMRO2) were studied in five dogs under prolonged isoflurane anaesthesia. CBF was measured with a modified sagittal sinus technique and CMRO2 was calculated as the product of CBF and the arteriovenous O2 difference. Maintaining this experimental dog model with 1% isoflurane in oxygen and nitrogen for 3 h in five dogs and for 4 h in three dogs did not cause any significant changes in CMRO2 or CBF. Cerebral metabolite levels were consistent with earlier reports from short-time studies and the EEG recordings showed a continuous sleep pattern with no pathological changes. It is concluded that there is no change in CBF or CMRO2 in our modified sagittal outflow model during 3-4 h of 1% isoflurane anaesthesia.     

Inhibition of brain cell excitability by lidocaine,QX314, and tetrodotoxin: a mechanism for analgesia from infused local anesthetics?

Local anesthetic infusions have been used to provide analgesia in a variety of painful conditions. The mechanism for this drug effect remains unknown. To better define the electrical effects of lidocaine concentrations comparable to those obtained during analgesic infusions, lidocaine (0.05-3 mmol l^-1), QX314 (an obligatorily charged, quaternary lidocaine derivative applied within the cells), and tetrodotoxin (10 nmoll^-1) were applied to rat hippocampal pyramidal cells. The three drugs, which inhibit Na⁺ currents by varying mechanisms, produced tonic increases in (firing) current threshold, and decreases in the amplitude of action potentials measured using an intracellular microelectrode technique. Lidocaine inhibited action potential spikes and increased current threshold in a concentration-dependent fashion. Lidocaine 50 and 100 μmol 1^-1 did not inhibit action potentials, but increased firing threshold by nearly 100%. Lidocaine 1–3 mmol l^-1 significantly inhibited action potential amplitude and increased threshold by as much as 800%. Similarly, QX314 and tetrodotoxin produced greater increases in current threshold than in action potential amplitude. QX314 produced phasic (or frequency-dependent) block during trains of stimuli at 1 Hz, even when almost no tonic block was present. Lidocaine produced less phasic block than QX314, and required both greater tonic block and more frequent stimulation to produce the phenomenon. Tetrodotoxin demonstrated no phasic block. Increases in current threshold occurred in lidocaine concentrations associated with analgesia and toxicity; inhibition of action potentials occurred scarcely at all at these concentrations. Thus, tonic increases in current threshold may underlie analgesia and supplementation of general anesthesia by intravenous lidocaine.     

A positron emission tomography study of cerebral blood flow and oxygen metabolism in healthy male volunteers anaesthetized with eltanolone

Background: The effects of eltanolone anaesthesia in humans on regional cerebral blood flow, regional cerebral metabolic rate of oxygen and oxygen extraction ratio were to be evaluated using positron emission tomography (PET).
Methods: Six healthy male volunteers were studied. Series of PET-measurements with ¹⁵O and H₂¹⁵O were carried out in the awake state (baseline) (n=6), during eltanolone anaesthesia (n= 5) and during early recovery (n=5), when the subjects were oriented with respect to person, place and time. Eltanolone was given as a programmed infusion.
Results: Cerebral blood flow (rCBF) was reduced in almost all cortex regions studied by 31216% (meanSD, P < 0.01). During recovery KBF increased to 10926% of pre-anaesthetic baseline levels ( P < 0.01). Eltanolone in the doses administered lowered oxygen metabolism (rCMRO₂) by 528% ( P < 0.01) in cortex regions. During recovery rCMRO₂ increased to 9013% of baseline ( P < 0.01). The oxygen extraction (OER) in cortical regions decreased by 32223% ( P < 0.01) during anaesthesia and returned to 82210% of baseline ( P < 0.01) during recovery. Less reduction in cortical blood flow during eltanolone anaesthesia was seen in the uncus ( P < 0.01), though no differences in the depression of oxygen metabolism were seen. Oxygen extraction remained homogeneous throughout the brain.
Conclusion: Eltanolone anaesthesia was shown to reduce cerebral oxygen metabolism and cerebral blood flow in healthy volunteers. There were no signs of ischaemic effects.     

Partial reversal of the cerebral effects of isoflurane in the dog by theophylline

The cerebral effects of adding theophylline to 1.4% isoflurane anaesthesia were studied in five dogs by a sagittal sinus outflow technique with direct measurement of the cerebral blood flow (CBF) and calculation of the cerebral metabolic rate for oxygen (CMRo2). Three 3 mg.kg-1 doses of theophylline were given with intervals of 10 min. Five min after the second and third dose, when the mean theophylline plasma concentration was 41 and 65 mumols.1(-1), respectively, CMRo2 had increased significantly with a mean value varying between 15% and 13%, and the EEG had changed from a sleep pattern to a more awake pattern in the four dogs with evaluable recordings. There were no significant changes in CBF or mean arterial blood pressure (MABP). It is concluded that the adenosine receptor antagonist theophylline in this study partially reversed the cerebral effects of isoflurane.     

Bupivacaine does not suppress cardiac sympathetic nerve activity during halothane anesthesia in the cat

Background: The finding that IV lidocaine suppresses cardiac sympathetic nerve activity during 1 MAC halothane, but not during 2 MAC or 3 MAC halothane, suggests that the neurally mediated circulatory effects of IV local anesthetics may vary with background autonomic activity. This study aimed to compare the effects of IV lidocaine and bupivacaine on cardiac sympathetic nerve activity (CSNA) during normal and high levels of CSNA.
Methods: Cats were anesthetized with halothane and allocated to three groups. In groups I-L and I-B, sympathetic hyperactivity was induced by electrical stimulation of the posterior hypothala-mus. CSNA, heart rate and mean arterial pressure were then measured before and after administration of lidocaine 2 mgkg BW^-l IV (Group I-L, n=7) or bupivacaine 0.5 mgkg BW^-1 IV (Group I-B, n=7) during 1% halothane anesthesia. In Group II (n=7), following administration of bupivacaine 0.5 mgkg BW^-1 IV, CSNA, sinus cycle length (SCL), and subintervals of atrio-ventricular conduction time (A-H, H-V, and H-S) at pacing were measured during O.8%, 1.6% and 2.4% halothane anesthesia without sympathetic hyperactivity.
Results: Lidocaine suppressed CSNA hyperactivity and tachycardia significantly in Group I-L, but bupivacaine did not do so in Group I-B. In Group 11, bupivacaine did not affect CSNA at any concentrations of halothane, but lengthened SCL, A-H, H-V and H-S intervals significantly at each concentration of halothane.
Conclusions: We conclude that IV bupivacaine, unlike IV lidocaine, does not suppress CSNA during either normal or high CSNA under halothane anesthesia although IV bupivacaine has stronger depressive effects on cardiac conduction than does IV lidocaine during deep halothane anesthesia.     

The effect of plain 0.5% 2–chloroprocaine on venous endothelium after intravenous regional anaesthesia in the rabbit

The possible venous endothelial toxicity of 0.5% 2–chloroprocaine without additives in intravenous regional anaesthesia (IVRA) was evaluated in rabbits. After exsanguination of a hind limb with an Esmarch's bandage a neonatal blood pressure cuff around the thigh was inflated (250 mmHg). For IVRA 4 ml of either plain 0.5% 2–chloroprocaine (pH 3.7), 0.9% NaCl (pH 6.0) or acidified NaCl (pH 3.7) was injected i.v. to the exsanguinated limb in a randomized, double–blind fashion. Each group comprised 15 rabbits. Eleven rabbits received 4 ml of 0.5 M or 1.0 M KC1, for the production of positive controls. Two hours after injection of the test solution the tourniquet was deflated and venous biopsies were taken one and 24 hours later for histological and immunocytochemical examination. Five to eight 24–hour samples from each group were also processed for electron microscopy. A macroscopic thrombus formation was observed in four rabbits after KC1 and in two after acidified NaCl administration. No inflammatory changes were observed at histologic and immunocytochemical examination of any of the vein samples. Electron microscopy revealed that KC1 had caused severe damage to the venous endothelium of four out of five samples and acidified NaCl had caused moderate damage to the endothelium of two out of seven samples. 2–chloroprocaine had caused moderate damage in four and severe damage in two of the vein samples; two samples were normal. No thrombus formation occurred. It is concluded that additive–free 2–chloroprocaine caused damage to the venous endothelium in rabbits when used for IVRA.     

Lidocaine-induced hemodynamic effects are enhanced by the inhibition of endothelium-derived relaxing factor in dogs

Background: Lidocaine has been shown to have direct vasoconstrictive effects at low concentrations. Since lidocaine inhibits endothelium-dependent vasodilation in vitro , the vasoconstrictor effect of lidocaine may be due to inhibition of endothelium-derived relaxing factor(EDRF/NO). Therefore, the current study was designed to determine the effects of N^G-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide synthase, on systemic and pulmonary hemodynamics during lidocaine infusion.
Methods: Systemic and pulmonary hemodynamic effects of lidocaine infusion, 1 mg kg^-1 min^-1, for 10 min were measured in dogs anesthetized with 1% halothane in oxygen. Dogs were studied twice with an interval of 1 week in a cross-over study, and were assigned to one of two groups that received saline or L-NNA intravenously in group 1 (n=8), or L-NNA or L-NNA+L-arginine which reverses the nitric oxide synthesis inhibitor effect of L-NNA, intravenously in group 2 (n=8) prior to lidocaine infusion. The free serum concentration of and protein-binding ratio for lidocaine were measured.
Results: With saline pretreatment in group 1, lidocaine infusion significantly decreased cardiac index (CI) and significantly in-
Conclusion: In contrast to in vitro study, vasoconstrictor effect of lidocaine is enhanced when a capacity for compensatory vasodilation including EDRF/NO pathway is exhausted in halo-thane-anesthetized dogs.     

Cerebral pharmacodynamics of anaesthetic and subanaesthetic doses of ketamine in the normoventilated pig

There are still divergent opinions regarding the pharmacodynamic effects of ketamine on the brain. In this study, the cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo₂) and electroencephalogra-phic (EEG) activity were sequentially assessed over 80 min in 17 normoventilated pigs following rapid i.v. infusions of anaesthetic (10.0 mg-kg^-1; n = 7) or subanaesthetic (2.0 mg-kg^-1; n = 7) doses of ketamine or of its major metabolite norketamine (10.0 mg-kg^-1; n = 3). The animals were continuously anaesthetized with fentanyl, nitrous oxide and pancuronium. CBF was determined by the intra-arterial mXe technique. Ketamine (10.0 mg-kg^-1) induced an instant, gradually reverting decrease in CBF, amounting to -26% (P<0.01) at 1 min and -13% (P<0.05) at 10 min, a delayed increase in CMRo₂ by 42% (P<0.01) at 10 min and a sustained rise in low- and intermediate-frequency EEG voltage by 87% at 1 and 97% at 10 min (P<0.0001). It is concluded that metabolically formed norketamine does not contribute to these effects. Considering the dissociation of CBF from CMRo₂ found 10–20 min after ketamine (10.0 mg-kg^-1) administration, it is suggested that ketamine should be used with caution for anaesthesia in patients with suspected cerebral ischaemia in order not to increase the vulnerability of brain tissue to hypoxic injury. Ketamine (2.0 mg-kg^-1) had no significant effects on CBF, CMRo₂ or EEG. It therefore seems that up to one fifth of the minimal anaesthetic i.v. dose can be used safely for analgesia, provided that normocapnaemia is preserved.     

Reversal of the cerebral effects of diazepam in the dog by the benzodiazepine antagonist 1015–1788

In six dogs initially anesthetized with halothane-N2O-O2 for surgery and maintained during the experiment with high spinal anesthesia and local infiltration, diazepam 3.0 mg X kg-1 converted the EEG from an awake to a sleep pattern. This was accompanied by a significant 21% reduction in cerebral metabolic rate for oxygen (CMRO2) and a 15% reduction in cerebral blood flow (CBF). Substituting nitrous oxide 70% for nitrogen had no additional cerebral effects. The benzodiazepine antagonist Ro15-1788, 2 mg, completely reversed the effects of diazepam on the EEG, CMRO2 and CBF. Cerebral biopsies taken at the end of the study revealed modest but significant decreases in ATP and the energy charge along with increases in AMP, lactate and lactate/pyruvate (L/P) ratio. These changes are unexplained and suggest a possible disturbance in oxidative phosphorylation produced by Ro15-1788 preceded by diazepam.     

Intravenous lidocaine, amantadine, and placebo in the treatment of sciatica: a double-blind, randomized, controlled study

BACKGROUND AND OBJECTIVES: Sciatica is a neuropathic pain syndrome caused by compression and/or inflammation of spinal nerve roots by herniated disc material, and its treatment is therefore usually aimed at reducing compression and inflammation. Studies have shown that both systemic local anesthetics and N-methyl-D-aspartate (NMDA) receptor antagonists may produce analgesia in a variety of neuropathic pain syndromes. The present study evaluated the analgesic efficacy of i.v. infusions of the local anesthetic lidocaine, the NMDA receptor antagonist amantadine, and a placebo in sciatica. METHODS: Thirty patients with sciatica, as confirmed by physical examination and imaging studies, were enrolled in a randomized, double-blind, three-arm crossover trial. Infusions of amantadine (2.5 mg/kg), lidocaine (5 mg/kg), and a placebo were administered over a 2-hour period, 2-7 days apart from each other. Spontaneous pain (visual analog scale) and evoked pain (straight leg raise) were measured every 30 minutes for 3 hours. RESULTS: Lidocaine reduced spontaneous pain as compared with amantadine and with the placebo for all measurements and at a significant level at the 30 (P < .05), 120, and 180 (P < .01) minute time points. Maximal pain reduction from the baseline was 62 +/- 7% for lidocaine, 43 +/- 7% for amantadine, and 47 +/- 7% for the placebo. Straight leg raise test also significantly improved with lidocaine (from 30 to 37 degrees; P < .05), as compared to amantadine (34-36 degrees) and to the placebo (32-34 degrees). All three treatments were relatively well tolerated. CONCLUSIONS: Intravenous lidocaine, rather than amantadine, reduces both spontaneous and evoked sciatic pain.     

Partial reversal of the cerebral effects of isoflurane in the dog by the benzodiazepine antagonist flumazenil

Six dogs initially anaesthetized with isoflurane-N2O-O2 for surgery with cannulation of the sinus sagittalis for direct measurement of cerebral blood flow (CBF) and maintained with 1% isoflurane-N2-O2 anaesthesia, were given two 2-mg doses of the benzodiazepine antagonist flumazenil with an interval of 10 min. This was accompanied by a significant increase in the cerebral metabolic rate for oxygen (CMRO2) 10 min after the first 2-mg dose, and 5, 10 and 15 min after the second 2-mg dose, the increase varying in mean value from 9% to 14%. EEG was recorded in five of the six dogs and administration of flumazenil converted the EEG from a sleep pattern to an awake pattern in two of them. There were no significant changes in the CBF or mean arterial blood pressure (MABP) values. In the brain biopsies taken at the end of the study there were no significant changes in the adenylate energy charge (EC) and the lactate/pyruvate ratio (L/P) when compared to five other dogs not given flumazenil. It is concluded that flumazenil in this study demonstrated a partial antagonism of the cerebral effects of isoflurane.     

Quantitative EEG changes associated with loss and return of consciousness in healthy adult volunteers anaesthetized with propofol or sevoflurane

Significant changes in topographic quantitative EEG (QEEG) featureswere documented during induction and emergence from anaesthesiainduced by the systematic administration of sevoflurane andpropofol in combination with remifentanil. The goal was to identifythose changes that were sensitive to alterations in the stateof consciousness but independent of anaesthetic protocol. Healthypaid volunteers were anaesthetized and reawakened using propofol/remifentaniland sevoflurane/remifentanil, administered in graded steps whilethe level of arousal was measured. Alterations in the levelof arousal were accompanied by significant QEEG changes, manyof which were consistent across anaesthetic protocols. Lightsedation was accompanied by decreased posterior alpha and increasedfrontal/central beta power. Frontal power predominance increasedwith deeper sedation, involving alpha and, to a lesser extent,delta and theta power. With loss of consciousness, delta andtheta power increased further in anterior regions and also spreadto posterior regions. These changes reversed with return toconsciousness. Br J Anaesth 2001; 87: 421–8     

The influence of midazolam on the plasma concentrations of bupivacaine and lidocaine after caudal injection of a mixture of the local anesthetics in children

Twenty children undergoing surgery received a caudal block using 1 ml per kg of a mixture of 50% lidocaine (1%) and 50% bupivacaine (0.25%). They were randomly allocated to two groups, one of which received midazolam 0.4 mg/kg rectally as premedication. Midazolam administration resulted in a significantly lower AUC value for lidocaine but did not influence the plasma concentrations of bupivacaine.     

The effects of tracheal tube cuffs filled with air,saline or alkalinised lidocaine on haemodynamic changes and laryngotracheal morbidity in children: a randomised,controlled trial

We studied the effects of tracheal tube cuffs filled with air, saline or alkalinised lidocaine on haemodynamic changes during tracheal extubation and postoperative laryngotracheal morbidity in children. We randomly allocated 164 children aged 3–13 years undergoing general anaesthesia to one of four groups; tracheal tube cuffs filled with air (n = 41); saline (n = 41); alkalinised lidocaine 0.5% (n = 41); or alkalinised lidocaine 1% (n = 41). Intracuff pressure was monitored and maintained below 20 cmH₂O. The mean (SD ) increases in systolic blood pressure after tracheal extubation compared with before extubation were 10.9 (10.8) mmHg, 7.3 (17.7) mmHg, 4.1 (10.5) mmHg and 1.9 (9.5) mmHg in the air, saline, 0.5% and 1% alkalinised lidocaine groups, respectively (p = 0.021). The mean (SD ) increases in diastolic blood pressure after tracheal extubation compared with before extubation were 3.9 (9.7) mmHg, 7.9 (14.6) mmHg, 0.7 (10.4) mmHg and 3.6 (6.9) mmHg in the air, saline, 0.5% and 1% alkalinised lidocaine groups, respectively (p = 0.019). The mean (SD ) increases in heart rate after tracheal extubation compared with before extubation were 14.2 (7.6) beats.min^?1, 15.5 (13.1) beats.min^?1, 5.2 (9.6) beats.min^?1 and 4.1 (6.6) beats.min^?1 in the air, saline, 0.5% and 1% alkalinised lidocaine groups, respectively (p < 0.001). The incidence of sore throat 8 h after tracheal extubation was 22.0% in the air‐filled group, 9.8% in the saline group, 4.9% in the 0.5% alkalinised lidocaine group and 2.4% in the 1% alkalinised lidocaine group, p = 0.015. We conclude that filling the tracheal tube cuff with alkalinised lidocaine‐filled reduces the haemodynamic response to tracheal extubation and postoperative laryngotracheal morbidity in children.