[Terminology in the context of anesthesia for preterm and term newborns and infants]. / Terminologie bei der Anästhesie von frühgeborenen und reifen Neugeborenen.

An acceptable, standardized and mandatory terminology is important for the planning and implementation of anesthetic procedures on term and preterm newborns and infants. Contradictory use of perinatal terminology poses a problem in current medical practice. This article provides an overview of conventional definitions and technical terms. It also puts forward terminological principles for a model of risk stratification of anesthesia in the newborn period and infancy.

Corresponding minimum alveolar concentrations of isoflurane and isoflurane/nitrous oxide have divergent effects on thalamic nociceptive signalling.

BACKGROUND: Suppression of nociceptive signalling in the thalamus is considered to contribute significantly to the anaesthetic state. Assuming additivity of anaesthetic mixtures, our study assessed the effects of corresponding minimum alveolar concentrations (MACs) of isoflurane and isoflurane/nitrous oxide on thalamic nociceptive signalling. METHODS: Nociceptive response activity (elicited by controlled radiant heat stimuli applied to cutaneous receptive fields) of single thalamic neurons was compared in rats anaesthetized at approximately 1.1 and approximately 1.4 MAC isoflurane with that at approximately 1.1 and approximately 1.4 MAC isoflurane/nitrous oxide. RESULTS: Under baseline anaesthesia ( approximately 0.9 MAC isoflurane), noxious stimulation elicited excitatory responses in all neurons (n = 19). These responses were uniformly suppressed at approximately 1.1 and approximately 1.4 MAC isoflurane. In contrast, at approximately 1.1 and approximately 1.4 MAC isoflurane/nitrous oxide, excitatory responses no different to baseline were still present in 64 and 37% of the neurons, respectively. CONCLUSIONS: These data demonstrate a pronounced nitrous oxide-induced response variability. It appears that, with respect to thalamic transfer of nociceptive information, the interaction of isoflurane and nitrous oxide may not be compatible with the concept of additivity and that the antinociceptive potency of nitrous oxide is considerably less than previously reported.

Early recovery after remifentanil-pronounced compared with propofol-pronounced total intravenous anaesthesia for short painful procedures.

BACKGROUND: We compared recovery from high-dose propofol/low-dose remifentanil ('propofol-pronounced') compared with high-dose remifentanil/low-dose propofol ('remifentanil-pronounced') anaesthesia. METHODS: Adult patients having panendoscopy, microlaryngoscopy, or tonsillectomy were randomly assigned to receive either propofol-pronounced (propofol 100 microg x kg(-1) min(-1); remifentanil 0.15 microg x kg(-1) min(-1)) or remifentanil-pronounced (propofol 50 microg x kg(-1) min(-1); remifentanil 0.45 microg x kg(-1) min(-1)) anaesthesia. In both groups, the procedure was started with remifentanil 0.4 microg x kg(-1), propofol 2 mg x kg(-1), and mivacurium 0.2 mg x kg(-1). Cardiovascular measurements and EEG bispectral index (BIS) were recorded. To maintain comparable anaesthetic depth, additional propofol (0.5 mg x kg(-1)) was given if BIS values were greater than 55 and remifentanil (0.4 microg x kg(-1)) if heart rate or arterial pressure was greater than 110% of pre-anaesthetic values. RESULTS: Patient and surgical characteristics, cardiovascular measurements, and BIS values were similar in both groups. There were no differences in recovery times between the groups (time to extubation: 12.7 (4.5) vs 12.0 (3.6) min, readiness for transfer to the recovery ward: 14.4 (4.4) vs. 13.7 (3.6) min, mean (SD)). CONCLUSIONS: In patients having short painful surgery, less propofol does not give faster recovery as long as the same anaesthetic level (as indicated by BIS and clinical signs) is maintained by more remifentanil. However, recovery times were less variable following remifentanil-pronounced anaesthesia suggesting a more predictable recovery.

Differential effects of isoflurane on excitatory and inhibitory synaptic inputs to thalamic neurones in vivo.

BACKGROUND: Mechanosensory thalamocortical relay neurones (TCNs) receive glutamatergic excitatory input and are subjected to gamma-aminobutyric acid (GABA)Aergic inhibitory input. This study assessed the effects of an increase in concentration of isoflurane on thalamic excitatory and inhibitory mechanisms. METHODS: TCNs (n = 15) of the thalamic ventral posteromedial nucleus responding to mechanical stimulation of whiskers were investigated in rats anaesthetized with end-tidal concentrations of isoflurane of approximately 0.9% (ISOlow, baseline) and approximately 1.9% (ISOhigh). Response activity induced by controlled vibratory movement of single whiskers was recorded before, during and after iontophoretic administration of the GABAA receptor antagonist bicuculline to the vicinity of the recorded neurone. RESULTS: The increase in concentration of isoflurane induced a suppression of vibratory responses to 14 (4)% [mean (SEM)] of baseline activity. Blockade of GABAA receptors by bicuculline during ISOlow and ISOhigh caused increases in response activity to 259 (32)% and 116 (25)% of baseline activity, respectively. The increase in isoflurane concentration enhanced overall inhibitory inputs by 102 (38)%, whilst overall excitatory inputs were reduced by 54 (7)%. CONCLUSIONS: These data suggest that doubling the concentration of isoflurane doubles the strength of GABAAergic inhibition and decreases the excitatory drive of TCNs by approximately 50%. The isoflurane-induced enhancement of GABAAergic inhibition led to a blockade of thalamocortical information transfer which was not accomplished by the effects of isoflurane on glutamatergic synaptic transmission alone. Thus, it appears that, with respect to transmission of information in the thalamus, the most prominent action of isoflurane is an enhancement of GABAAergic synpatic inhibition, and that effects on glutamatergic neurotransmission may contribute to a lesser extent.

Local GABA(A) receptor blockade reverses isoflurane's suppressive effects on thalamic neurons in vivo.

Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the gamma-aminobutyric acid-A (GABA(A)) receptor antagonist bicuculline in the thalamic ventral posteromedial nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% +/- 0.01%, mean +/- SEM) were suppressed under large concentrations (1.44% +/- 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABA(A) receptor-mediated inhibition.

Increasing isoflurane concentration may cause paradoxical increases in the EEG bispectral index in surgical patients.

We have studied the effects of increases in isoflurane concentration on the EEG bispectral index (BIS) in 70 patients anaesthetized with isoflurane-nitrous oxide-sufentanil for major abdominal surgery. During surgery, baseline BIS was recorded at 0.8% end-tidal isoflurane with nitrous oxide in oxygen (FIO2 0.35). After this, end-tidal isoflurane was increased to 1.6% for 15 min and decreased subsequently to 0.8% for 20 min to assess recovery. In 20 patients, BIS decreased from a mean value of 40 (SD 9) during baseline to 25 (10) at 1.6% isoflurane. In contrast, BIS did not change in 23 patients and increased in 27 patients from 35 (6) to 46 (8) as isoflurane was increased to 1.6%. In all patients, BIS recovered to baseline values at 0.8% isoflurane. The changes in BIS with increasing isoflurane concentration were not related to drugs or differences in physiological variables, which did not differ between groups. Patients with a decrease in BIS were significantly younger (38 (range 18-68) yr) than those with unchanged (55 (26-70) yr) or increased (60 (40-70) yr) BIS values (P < 0.001). It is possible that the paradoxical increase in BIS is related to continuous pre-burst EEG patterns consisting of high-frequency activity. This suggests that the use of BIS as a guide for isoflurane administration may be misleading in some patients undergoing surgical procedures.

Isoflurane induces dose-dependent changes of thalamic somatosensory information transfer.

In spite of several reports about suppressive effects of volatile anesthetics on somatosensation, their neuronal mechanisms are largely unknown. The present study investigates somatosensory impulse transmission at the thalamic level in rats under varied concentrations of isoflurane by recordings of neuronal responses to mechanical stimulation of the body surface. Single-unit recordings of thalamo-cortical relay neurons (TCNs, third order neurons; n=28) and presumed trigemino-thalamic fibers (TTFs, second order neurons; n=7) were performed in the ventral posteromedial nucleus. Functional response characteristics were quantified following defined tactile stimulation (trapezoidal or vibratory deflection of sinus hairs or fur) applied to the neuronal receptive fields. End-tidal isoflurane concentration was increased in steps of 0.2% between 0.6% (baseline) and 2.0%. The response activity in all TCNs studied was suppressed in a dose-dependent manner (2.0% isoflurane decreased responses to 3. 5+/-1.1% of baseline; mean+/-S.E.M.); the response activity in TTFs was much less affected (decrease to 55.0+/-8.2%). Suppression of ongoing activity, however, was similar for both, TCNs and TTFs. Furthermore, in TCNs, the response characteristics changed with increasing isoflurane between 1.0% and 1.8%: tonic and sustained responses were converted to phasic on-responses. In contrast, the tonic and sustained response characteristics of TTFs were preserved even at higher isoflurane concentrations. The results indicate that isoflurane attenuates the output of somatosensory signals in the specific nucleus of the rat's thalamus, while its input is only marginally affected. The observed changes of thalamic neuronal response characteristics, at least in part, may cause the loss in sensory discrimination observed during general anesthesia.

Cerebral blood flow velocity and carbon dioxide vasoreactivity during gamma-hydroxybutyrate/fentanyl anaesthesia in non-neurosurgical patients.

In this study the effects of gamma-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with gamma-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg-1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect Vmean [awake: 57 +/- 12 cm s-1 (mean +/- SD); 22.5 min: 62 +/- 15 cm s-1, NS difference] or mean arterial blood pressure (MAP) (awake: 97 +/- 12 mmHg; 22.5 min: 89 +/- 10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal PCO2 of 4.6 +/- 0.4 kPa (30 min). At 30 min after the start of the GHB infusion, Vmean and MAP decreased to 38 +/- 10 cm s-1 and 76 +/- 12 mmHg (both P < 0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal PCO2 3.5 +/- 0.2 mmHg), Vmean decreased to 29 +/- 7 cm s-1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in Vmean/0.133 kPa change in the end-tidal PCO2 from normocapnia to hypocapnia) to be estimated as 2.7 +/- 1.6% 0.133 kPa-1. This suggests that cerebrovascular response to CO2 during gamma-hydroxybutyrate/fentanyl anaesthesia is maintained.

Topographical analysis of the EEG effects of a subconvulsive dose of lidocaine in healthy volunteers.

BACKGROUND: The purpose of the present study was to assess the effects of intravenous lidocaine on spatial changes of electroencephalographic power and on psychomotoric status in conscious volunteers. METHODS: In 11 healthy volunteers lidocaine (2-min bolus, 100 mg; 15 min infusion, 40 micrograms.kg-1.min-1) or placebo were given intravenously in a randomized, single-blinded, two-way crossover study. Haemodynamics and lidocaine plasma concentrations were measured at baseline and within a period of 30 min following bolus injection. Vigilance and emotional status were tested using visual analogue scales (VAS). Toxic CNS effects were evaluated by a questionnaire. The raw EEG (17 leads, reference Cz) and computed power spectra were continuously recorded. RESULTS: The chosen lidocaine dosage led to nearly constant plasma concentrations (unbound lidocaine 2.5 min and 15 min after bolus 0.36 +/- 0.14 microgram/ml and 0.30 +/- 0.06 microgram/ml, respectively [mean +/- SD]). The placebo caused no symptoms, changes in VAS-scores or EEG-parameters. Lidocaine induced pronounced subjective symptoms and significant increases in delta activity for 15 min, most dominant at the frontotemporal and occipital leads (max. +219% O1). Frontal and occipital beta 1 and beta 2 power (max. +131% and +124% at O1, respectively) was immediately increased after the bolus injection. No EEG changes occurred at central region Cz, and no interhemispheric EEG differences were noted. Theta, alpha 1, and alpha 2 power remained unchanged. CONCLUSION: The current data demonstrate simultaneous changes in psychomotoric status as well as delta and beta spectral power during lidocaine infusion. These data could be an indication that the pronounced frontotemporal and occipital EEG changes are the electroencephalographic expression of subjective sensations.

[Effects of ketamine on CNS-function]. / Effekte von Ketamin auf die ZNS-Funktion.

The present review summarises the main actions of racemic ketamine and ketamine enantiomers on central nervous system receptors. The primary CNS action of ketamine appears to be a non-competitive block of N-methyl-D-aspartate receptors. Although numerous other receptors (e.g., GABA, nicotinic acetylcholine, opiate, voltage-operated channels) have been reported to interact with ketamine, their role in inducing dissociative anaesthesia is still under discussion. In humans, characteristic electroencephalographic (EEG) changes after administration of ketamine are dose-dependent increases in delta, theta, and beta power. In equipotent doses S-(+)-ketamine induces similar EEG changes. However, in comparison to racemic ketamine and S-(+)-ketamine, R-(-)-ketamine does not suppress the EEG to the same extent. Former studies suggested that ketamine is a proconvulsive agent; however, recent studies have demonstrated anticonvulsive and even neuroprotective properties. In humans, low-dose ketamine has no influence on early cortical peaks of somatosensory evoked potentials (SEP). Larger doses induce increases in SEP amplitude while latencies are unchanged. Recent data indicate that analgesia induced by low-dose ketamine may be quantitated by specific pain-related SEP. Significant reductions of pain-induced cortical potentials may be correlated with subjective pain ratings. Brain-stem auditory evoked potentials (AEP) are not influenced by ketamine. Interestingly, in contrast to many other anaesthetics, middle-latency AEP were not altered by racemic and S-(+)-ketamine. This observation may indicate insufficient suppression of auditory stimulus processing during ketamine anaesthesia. Motor evoked responses to transcranial electrical or magnetic stimulation in humans are not markedly suppressed by ketamine.

[Does anesthesia always involve analgesia?]. / Bedeutet Anästhesie immer auch Analgesie?

The primary aim of anesthesia is the prevention of pain perception (analgesia), intraoperative awareness (hypnosis), and postoperative recall (amnesia) (anesthetic trade). Analgesia would be a component of the anesthetic state. Pain is the conscious perception of a noxious stimulus and analgesia is the abolished perception of pain in an otherwise conscious patient. During general anesthesia pain can not be experienced, since the patient is unconscious. However, there is no certainty that during anesthesia a blockade of the nociceptive system is reliably provided in all circumstances. The impact of insufficient blockade of nociceptive pathways during anesthesia on mental status and implicit memory are largely unknown. Therefore, the anesthetic trade should consist of hypnosis, amnesia and antinociception.

[Perfusion changes in hemodilution. The effect of extensive isovolemic hemodilution with gelatin and hydroxyethylstarch solutions on cerebral blood flow velocity and cutaneous microcirculation in humans]. / Perfusionsveränderungen bei Hämodilution. Einfluss einer ausgedehnten isovolämischen Hämodilution mit Gelatine- und Hydroxyethylstärkelösungen auf die zerebrale Blutflussgeschwindigkeit und die kutane Mikrozirkulation beim Menschen.

OBJECTIVE: Quantifying the influence of extreme isovolemic hemodilution (NH) with different colloids on cerebral blood flow velocities (transcranial Doppler sonography) and cutaneous microcirculatory blood flow (laser Doppler flowmetry) in healthy, non-premedicated volunteers was the aim of this study. METHODS: In seven volunteers (randomized cross-over design) 20 ml/kg blood was withdrawn within 30 min and simultaneously replaced with 6% hydroxyethyl starch (200,000/0.5, HES) or 3% gelatin (GEL). Thirty minutes later, the autologous blood was retransfused (RT) within 30 min. Due to a severe allergic reaction to gelatin in one volunteer, only 6 GEL-NH were evaluated. Recorded parameters were: mean blood flow velocities (Vm-MCA) as well as the pulsatility index (PI) and the resistance index (RI) over the middle cerebral artery. In addition laser Doppler flux (FLUX), cell velocity (SPEED), mean arterial pressure (MAP), heart rate (HR), hemoglobin (Hb) and hematocrit (Hc) were monitored. RESULTS: NH resulted in a withdrawal volume of 1498 +/- 85 ml (HES) and 1493 +/- 95 ml (GEL), (mean +/- SD) and induced a decrease in hemoglobin from 40.9 to 29.0% (HES) and from 39.8 to 30.0% (GEL). RT increased Hc to 34.2% (HES) and 34.5% (GEL). MAP and HR showed no significant alterations in both groups. Following NH, Vm-MCA rose almost the same way in either case (26% HES), 21% (GEL), but decreased continuously again during RT. After completing RT, only in the HES group Vm-MCA still remained higher than baseline values (14% HES, only 3% GEL). Similar inverse regression lines were found for the two groups between Hc and Vm-MCA: [Vm-MCAHES (cm/s) = -1.27 x Hc + 110.9; r = 0.98, P < 0.001 and Vm-MCAGEL (cm/s) = -1.32 x Hc + 110.9; r = 0.91, P < 0.001]. Furthermore, as a result of NH, FLUX and SPEED increased about 61% and 38% in the HES group and remained on higher values in comparison with starting positions (21% FLUX, 13% SPEED). However, the results in the GEL group were of a different kind: FLUX and SPEED increased stupendously to 291% and 114% combined with NH, but both were reduced by RT on a large scale (39 and 27% below baseline values). Whereas RI showed no group differences, there was a remarkable drop in PI during RT (17% HES, 12% GEL). CONCLUSION: The two plasma expanders studied show a close inverse correlation between the alterations of blood flow velocities in the middle cerebral artery and systemic hemoglobin and hematocrit values. In both groups the change in blood flow velocities is comparable. For the first time the results of relative changes in blood flow velocities following hemodilution and retransfusion in healthy volunteers are described that correspond closely by relative cerebral blood flow alterations found in animal studies as well. Moreover, a non-linear correlation of cutaneous microcirculation was shown by means of HES, but also by GEL. Obviously, there was the GEL group to be responsible for pronounced differences in cutaneous circulation.

Volume replacement with gelatin or hydroxyethylstarch solutions does not impair somatosensory evoked potential monitoring: a haemodilution study in conscious volunteers.

The influence of haemodilution with colloids on somatosensory evoked potentials in non-premedicated volunteers is reported. In seven volunteers (randomized crossover design), blood (20 mL kg-1 within 30 min) was removed and simultaneously replaced by gelatin 3% or hydroxyethylstarch 6%. After 30 min, blood was retransfused within 30 min. Median and posterior tibial nerve somatosensory evoked potentials were recorded from the cortex, second cervical vertebra, Erb's point and 1st lumbar vertebra, respectively. One volunteer experienced a severe allergic reaction to gelatin, therefore only six gelatin trials were evaluated. Haemodilution decreased the haematocrit from 39.8 +/- 1.6% (mean +/- SD) to 31.1 +/- 2.0% (gelatin) and from 40.7 +/- 1.7% to 29.8 +/- 1.5 % (hydroxyethylstarch), respectively. Retransfusion increased haematocrit to 34.4 +/- 0.9% (gelatin) and to 34.2 +/- 1.3% (hydroxyethylstarch). Neither haemodilution with gelatin nor haemodilution with hydroxyethylstarch or retransfusion influenced evoked potentials. In conclusion, the treatment of blood loss up to 30% of estimated blood volume with gelatin or hydroxyethylstarch will not affect somatosensory evoked potential monitoring provided normovolaemic conditions are maintained.

Isovolaemic haemodilution with hydroxyethylstarch has no effect on somatosensory evoked potentials in healthy volunteers.

BACKGROUND: An animal study in anaesthetized baboons demonstrated that somatosensory evoked potentials (SSEP) can be affected by extreme haemodilution. This might lead to misinterpretation and reduce the value of intraoperative SSEP monitoring when colloids are administered. In the present study, the effect of haemodilution (HD) and subsequent retransfusion of autologous blood on SSEP was determined in healthy non-premedicated volunteers. METHOD: Acute isovolaemic HD served as a model for blood loss immediately replaced with colloids. In 12 volunteers, 20 ml/kg.bw blood was withdrawn within 30 minutes and simultaneously multaneously replaced with 6% hydroxyethylstarch (HES). 30 minutes later, the autologous blood was retransfused within 30 minutes. Recording sites and parameters were: 1. Median nerve SSEP: cortical, cervical (C2), Erb's point; 2. Posterior tibial nerve SSEP: cortical, cervical (C2), lumbar (L1). In addition to SSEP latency and amplitude, median and tibial nerve central conduction times, spinal conduction time and nerve conduction velocity were determined. Serial SSEP measurements were made before, during and after HD and retransfusion every 15 minutes. RESULTS: HD consisting of a withdrawal volume of 1550 +/- 155 ml (mean +/- SD) induced a decrease in haematocrit from 42.0 +/- 3.1% to 29.6 +/- 1.6% (P < 0.001). Following retransfusion, haematocrit increased to 35.0 +/- 2.1% (P < 0.001). Neither HD nor retransfusion influenced SSEP parameters. CONCLUSION: We conclude from our data that the therapy of blood loss up to 30% of estimated blood volume with HES does not affect SSEP monitoring as long as normovolaemia is maintained.

[The in vitro effect of alpha-2 agonists on thrombocyte function and density of thrombocyte alpha-2 receptors]. / Untersuchung über den in vitro Einfluss von alpha 2-Agonisten auf die Thrombozytenfunktion und Dichte thrombozytärer alpha 2-Rezeptoren.

UNLABELLED: alpha 2-Agonists are being used increasingly in anaesthesia and intensive care medicine because of their antihypertensive, analgesic and sedative properties. Platelets bear alpha 2-receptors on the cell surface. Stimulation of these receptors by agonists induces platelet aggregation. The present study examined whether in vitro incubation of blood with the alpha 2-agonists clonidine and dexmedetomidine decreases alpha 2-receptor density and hereby influences platelet aggregation. METHODS: Whole blood of 20 healthy volunteers was incubated over 24 h at 37 degrees C with 1 ng/ml clonidine or 1 or 10 ng/ml dexmedetomidine. Induced platelet aggregation was determined by means of turbidometry. Epinephrine (22 mumol/l) or collagen (20 mg/l) served as inductors. The density of alpha 2-receptors was measured in radioligand assays with 3H-Yohimbine. Phentolamine was used to assess unspecific binding. The data were analyzed with an analysis of variance. RESULTS: Neither 1 ng/ml clonidine nor 1 ng/ml dexmedetomidine altered platelet aggregation or alpha 2-receptor density in comparison with the control sample. As a major result we found that 10 ng/ml dexmedetomidine caused a significant (P < 0.05) reduction in epinephrine-induced platelet aggregation (16.0 +/- 5.4%, n = 20, mean +/- SEM) compared with the control (46.0 +/- 1.3%, n = 20). alpha 2-Receptor density was not any different from the control. CONCLUSIONS: This in vitro study showed that clinically relevant concentrations of 1 ng/ml clonidine or dexmedetomidine did not alter platelet aggregation or alpha 2-receptor density, even after 24 h exposure. However, 10 ng/ml dexmedetomidine was found to diminish significantly epinephrine-induced platelet aggregation, but did not change alpha 2-receptor density. This result showed that desensitization of platelet aggregation can occur without quantitative changes in alpha 2-receptors.

Increase of interleukin-6 plasma levels after elective craniotomy: influence of interleukin-10 and catecholamines.

Accidental and operative trauma are able to induce a systemic reaction of the organism characterized by fever, leukocytosis, catabolism, and an activation of the coagulation system. Interleukin-6 (IL-6) has been found to be an important mediator of this acute-phase response. In this study the influence of elective craniotomy on IL-6 plasma levels was evaluated. Blood samples were obtained from 20 patients undergoing elective craniotomy for vascular or tumorous diseases of the brain. IL-6 increased significantly (p < 0.05) from the pre-operative (0(0-5.4) pg/ml) to the intraoperative (180 min after beginning of surgery) time-point (10.6 (0-18.5) pg/ml). The maximum was reached on the first postoperative morning (13.9(4.3-45.0) pg/ml). Interleukin-10 (IL-10) is an anti-inflammatory cytokine which suppresses IL-6 synthesis in vitro in various cell lines. IL-10 plasma concentrations showed no alterations throughout the study period. Epinephrine plasma concentrations increased significantly from pre-operative values (15 (0-74) pg/ml) to the postoperative time-point (57(9-459) pg/ml). A 4.5-fold increase (p < 0.05) of norepinephrine plasma concentrations was found when comparing the data obtained 60 min after beginning of surgery with the data of the first postoperative morning. In monocytes, which are a major source of plasma IL-6, an elevation of intracellular cAMP stimulates the IL-6 synthesis. The postoperative maximum of IL-6 in plasma could be due to a release of catecholamines. In conclusion this study demonstrated an elevation of IL-6 plasma concentrations during and after elective craniotomy. Increased plasma catecholamine concentrations as well as a damage in the blood-brain barrier due to the surgical trauma with a spill-over of IL-6 from brain tissue into plasma could have contributed to this result.

The effects of epidural and intravenous lidocaine on somatosensory evoked potentials after stimulation of the posterior tibial nerve.

The measurement of somatosensory evoked potentials (SEPs) after stimulation of the posterior tibial nerve (PTN-SEPs) has been proposed as an objective indicator of the quality of lumbar epidural block. It is unclear whether peak latency increases after epidural application of local anesthetics may be due in part to systemic effects of the drug absorbed from the epidural space. In this clinical study, we compared PTN-SEPs after intravenous and epidural administration of lidocaine to those of a control group who did not receive lidocaine. Plasma concentrations of lidocaine remained within expected ranges for epidural and intravenous administration. No subjects developed signs for overdose or toxicity. After epidural application of 2% lidocaine, mean latencies of peaks P1, N1, and P2 increased significantly in comparison to baseline values. In 3 of 10 patients, latency changes were not observed. Intravenous lidocaine did not produce statistically significant changes in latencies, although a trend toward increasing latencies appeared to be present. In the control group without lidocaine, no statistically significant changes occurred during the 1-h study period. No correlation was found between peak latency changes and plasma concentrations of lidocaine. We conclude that latency increases observed after epidural application of lidocaine are due primarily to local, not systemic, effects of the local anesthetic.