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AIM Although adverse effects on cerebral blood flow have been reported, intravenous anaesthetic and sedative agents are often used in neurosurgical patients. Monitoring of these effects by transcranial Doppler sonography remains a questionable procedure as long as the cross-sectional area of the insonated basal cerebral arteries is unknown. This study should evaluate the effects of thiopental, propofol, midazolam and alfentanil on flow velocities and "vessel cross-sectional area" (proportional to the reflected Doppler signal power) measured by transcranial Doppler sonography. METHOD 19 patients with severe cerebral lesions (Glasgow Coma Scale < 6) were investigated. They were hyperventilated and sedated with fentanyl and flunitrazepam. The Doppler probe was fixed to the temporal bone and focussed to the middle cerebral artery of the more severely lesioned side. Baseline values of flow velocities and vascular cross-sectional area were measured. If routine nursing procedures required a deeper degree of sedation, either thiopental 2.5 mg/kg, propofol 1 mg/kg, midazolam 0.075 mg/kg or alfentanil 0.025 mg/kg were injected intravenously over 30 s. Further measurements were made 60, 120 and 300 s after start of the injection. Mean +/- SD were calculated, statistical evaluation was performed by analysis of variance and paired t-tests using the Bonferroni correction (p < 0.05). RESULTS The injected agents induced significant decreases of the mean value of flow velocities; the "vessel cross-sectional area" remained unaltered. In some patients paradoxical increases of v were observed. CONCLUSION The results indicate that intravenous anaesthetic agents are not likely to influence the cross-sectional area of the major basal cerebral arteries. Therefore TCD seems to be a valid tool to monitor the effects of these agents on the cerebral circulation of neurosurgical patients. This is probably of prognostic and therapeutic value.

SummaryBackground and objective: In clinical trials, autoregulation and carbon dioxide reactivity are preserved during propofol anaesthesia. Paradoxical increases of blood flow velocity during induction of anaesthesia could be demonstrated in patients with brain tumours. This study evaluates the effects of propofol on cerebral blood flow velocity in patients undergoing surgery for brain tumours and vascular malformations.Methods: Changes in cerebral blood flow velocity after the administration of propofol were assessed using bilateral 2 MHz transcranial Doppler probes in 47 patients undergoing surgery for brain tumours and in 22 patients undergoing surgery for aneurysms and angiomas.Results: Flow reduction after propofol was slightly less pronounced on the side of the tumour; in patients with cerebrovascular lesions, no difference between the two sides was detectable. After the administration of propofol a flow increase was present on the side of the tumour in 2 patients. In 3 patients with angiomas, the flow decrease after the administration of propofol was less pronounced on the side of the angioma. Neither observation gave statistical proof of abnormality.Conclusions: The flow changes after propofol may give a hint of cerebrovascular reactivity. Further investigations should focus on combined measurements of cerebral autoregulation and carbon dioxide reactivity and should focus on patients with impaired consciousness to test for reliability.

OBJECTIVE Patients will be discharged from the postoperative recovery room mostly on subjective clinical assessment. In this study an approach to a more quantitative judgment of postoperative vigilance is made by recording the P300-latency and neuropsychological tests. METHODS 22 adult patients undergoing a disc operation were examined. For induction of anesthesia thiopental (4-5 mg/kg), fentanyl (0.1 mg) and a musclerelaxant (atracurium 0.4 mg/kg or succinylcholine 1-2 mg/kg after precurarisation with atracurium 5 mg) were given. Anesthesia was then continued with enflurance (1.0-1.2 MAC) in a mixture of 67% nitrous oxide in oxygen. If postoperative analgesia was needed, piritramid was injected in boli a 3-6 mg. The P300 was acoustically stimulated with an oddball-paradigm and recorded at Fz and Cz. Afterwards the latencies were measured and compared with a vigilance score composed of clinical parameters and neuropsychological tests. Recordings were done preoperatively and every 30 minutes up to 2 hours postoperatively. A correlation between P300-latencies and vigilance score was made with the coefficient of Spearman. Comparison of pre- and postoperative values was managed by using Wilcoxon test for matched pairs with Bonferroni-correction. RESULTS Immediately after operation, P300 was obtained only in 8 patients (36%). The latencies were delayed (394 +/- 35 ms versus 326 +/- 12 ms preoperatively). During follow-up patients recovered and 2 hours postoperatively only one patient had no P300. At the end of the examination period P300-latencies of most patients had not yet reached the preoperative levels. The vigilance score in parallel showed decreases immediately after the operation and increases later on. However there were discrepancies between P300 latencies and neuropsychological findings, in some cases possibly due to the sedative effects of postoperative analgetics. CONCLUSION Recording of P300-latencies showed remarkable cognitive deficits because of subclinical anesthesia hangover even 2 hours after a routine inhalational anesthesia. It is a good quantifiable method for assessment of postoperative vigilance. In some cases P300-latency is a more sensitive parameter for vigilance phenomena than clinical and neuropsychological scores.

Die Arbeit gibt einen Uberblick zur Handhabung von schwierig zu intubierenden erwachsenen Patienten. Die schwierige Intubation kommt bei 1–18% aller Intubationen vor. Der schwerwiegendste Fall, in dem weder intubiert noch mit Gesichtsmaske beatmet werden kann („cannot ventilate – cannot intubate“, ca. 2 bis 0,01 pro 10000 Narkosen), fuhrt haufig zu Hirnschaden oder Tod. Drei solche Situationen an unserem Haus werden vorgestellt. Besprochen werden offenkundige Intubationsprobleme und indirekte Hinweise bei Patienten mit auserlich „normaler“ Halsanatomie, die in 50–70% durch 3 praeoperative Untersuchungen erkennbar sind: Mallampati Klassifikation, reduzierte Grose des inframandibularen Raumes, und eingeschrankte Beweglichkeit im Atlanto-Occipital Gelenk. Das Vorgehen bei schwieriger Intubation, zusatzliche Intubationshilfen, sowie die Bestuckung eines tragbaren Behalters mit hausspezifischer Zusatzausrustung werden dargelegt, ebenso sichere Zeichen der endotrachealen Tubuslage (CO 2 et, SaO 2 , brochoskopische und direkte laryngoskopische Kontrolle). Als Alternativen zur endotrachealen Intubation werden Kehlkopfmaske, Jet ventilation und Minikoniotomie vorgestellt. Es wird empfohlen, das Ablaufschema der American Society of Anesthesiologists hausspezifisch zu modifizieren und zu trainieren. Mit besserer Voruntersuchung, klarer Vorgehensweise und Training von Spezialverfahren kann eine wesentliche Ursache der anasthesiebedingten Mortalitat reduziert werden.

Die Indikation fur eine kombinierte Pankreas-/Nierentransplantation ist ein Diabetes mellitus Typ I mit terminaler Niereninsuffizienz. Das anasthesiologische Management dieser Patienten muβ zum einen

Das Vorliegen eines schweren Schadel-Hirn-Traumas (SHT), sei es in isolierter Form oder im Rahmen einer Mehrfachverletzung, stellt eine Herausforderung fur die erstbehandelnden Arzte am Unfallort oder in der Klinik dar. Es ist von Vorteil, Grundbegriffe der neurologischen Beurteilung zu beherrschen, so das der Schweregrad der Verletzung eingeschatzt werden kann. Sehr viel benutzt wird hier die Glasgow-Coma Skala und die Einteilung in leichtes, mittelschweres und schweres SHT. Es ist sehr wichtig, Begleitverletzungen anderer Korperregionen zu erkennen, welche in etwa 40% vorkommen. Da gleichzeitig vorhandene Hypoxamien und systemische Blutdruckabfalle den Verlauf eines SHT durch Ausbildung eines sekundaren Hirnschadens negativ beeinflussen, ist die Wiederherstellung bzw. Sicherung der Vitalfunktionen zunachst das wichtigste therapeutische Anliegen. Bewustlose Patienten werden intubiert und beatmet. Forcierte Hyperventilationen scheinen eher ungunstig zu sein. Es werden Anasthetika und Adjuvanzien eingesetzt, die das intrakranielle Gefassystem nicht erweitern und damit den intrakraniellen Druck nicht erhohen, was fur alle i.v. Hypnotika, Sedativa und Opioide gilt, solange keine Atemdepression auftritt. Ketamin hat am Unfallort seit Jahren eine feste Indikation. Ein abgefallener Systemblutdruck wird angehoben. Ein nach dem Trauma angestiegender Blutdruck wird erst vorsichtig gesenkt, wenn er etwa 30% uber dem individuellen Normbereich liegt. Ein adaquater zerebraler Perfusionsdruck (BD minus ICD) wird angestrebt. Liegt ein Polytrauma vor, mus eine starke chirurgische Blutung, z.B. aus Leber oder Milz, zunachst operativ versorgt werden, bevor die Kraniotomie beginnt. Eine ubermasige Gabe von Ringerlaktatlosungen ist wegen der nicht auszuschliesenden Gefahr eines Hirnodems zu vermeiden. Die routinemasige Gabe von Osmodiuretika wie Mannit ist nicht indiziert. Eine gunstige klinische Wirkung von Kortikosteroiden konnte bisher bei Vorliegen eines SHT nicht gezeigt werden – anders als vielleicht bei spinalen Traumen. Neuere Therapieansatze wie Anhebung des zerebralen Perfusionsdrucks, Gabe von hypertonen-hyperonkotischen Losungen, von NMDA-/AMPA-Antagonisten und von z.B. 21-Aminosteroiden werden zwar erprobt, haben aber noch keinen generellen oder auch noch gar nicht Eingang in die Klinik bei der Therapie des SHT gefunden.

Cannulation of the axillary vein is claimed to be an effective and relatively safe access to the central venous (CV) system [2, 4, 5, 8]. However, anatomical landmarks recommended for venous location (Muskulus pectoralis minor, processus coracoideus) are probably hard to identify in the majority of intensive care (ICU) patients. This investigation evaluated unidirectional 8 MHz Doppler ultrasound (US) in locating the axillary vein. Success rates and complications of this CV access in ICU patients is analysed. METHODS. The experimental design was approved by the local ethical committee (RUB). In 50 patients from our ICU cannulation of the axillary vein was attempted; all were in need of a CV line. Other CV puncture sites (except for the subclavian vein) were associated with contraindications. Patients were placed in a 15 degrees Trendelenburg position (15 exceptions); the arm was abducted to 45 degrees [5, 8]. The course of the axillary vein was located by Doppler US and marked on the skin with a felt pen. Prior to puncture, US intensity was judged by a score ranging from 0 to 4. After skin desinfection, sterile draping, and local anaesthesia, puncture of the axillary vein was attempted. The puncture kit LeaderCath 11,515 (Vygon, Aachen, FRG) was used. When venous blood could be aspirated, the Seldinger guidewire was inserted and the definite catheter placed. The experimental design allowed up to ten punctures, slightly modified in angle and direction of the needle, if puncture of the axillary vein or guide-wire placement failed. The cannulation attempt was classified as unsuccessful in the following cases: malposition, axillary vein not encountered by the puncture needle, guide-wire placement unsuccessful, or if identification and cannulation of the vein lasted more than 20 min. The puncture attempts were evaluated in respect to success rate, time, relation of US intensity to puncture attempts and CV pressure, complications, and malposition. RESULTS. Of the 50 attempted CV catheters, 43 were placed successfully. In 2 cases the axillary vein could not be encountered by the puncture needle. Guide-wire placement did not succeed in 4 patients. One catheter was malpositioned in the ipsilateral internal jugular vein. Four inadvertent punctures of the axillary artery remained without sequelae after compression. No further puncture-related complications were observed. With high US intensity score the number of puncture attempts necessary for successful vein cannulation was lower. On the other hand, complications and puncture failure seemed to be more frequent in patients with lower US intensity scores. DISCUSSION. CV access via the axillary vein had a satisfying success rate (43/50) and proved to be a safe procedure in our ICU patients despite higher risk factors compared to a healthy population. Although ethical reasons did not allow a randomised comparison with the standard technique, location of the axillary vein by Doppler US is likely to improve cannulation results and reduce complications induced by "blind" needle probing. With a low US intensity score, the rate of successful punctures is lower and complication rates increase. In some patients, e.g., those with extended tumour operations involving the head and neck, CV access via the axillary vein may be of high clinical value.

The effects of the opioids alfentanil (A), fentanyl (F), and sufentanil (S) on cerebral blood flow (CBF) and intracranial pressure (ICP) have been discussed in several recent publications. The purpose of this review is to describe the results of studies in animals, healthy volunteers, and patients with and without intracranial diseases. Clinical relevance and mechanisms of the reported ICP and CBF increases are analysed. METHODS. Approximately 70 original articles and abstracts were retrieved by a systematic literature search using the key word list at the end of this abstract. The cited studies came from computerised database systems like Silver Platter and DIMDI, the SNACC reference list, and the bibliographies of pertinent articles and books. These studies were classified into three groups: significant increase of ICP and/or CBF; no significant or clinically relevant alterations; and significant decreases of ICP and/or CBF. RESULTS. The numerical relationship was 6:7:3 for A, 7:16:9 for F, and 5:11:8 for S. Increases of previously normal or only slightly elevated ICP were registered in some studies in connection with a decrease in mean arterial pressure (MAP). On the other hand, in patients with brain injury and elevated ICP opioids did not further increase ICP despite MAP decreases. In studies monitoring ICP and/or CBF continuously, transient and moderate increases of questionable clinical relevance became apparent a few minutes after bolus injection of opioids. Alterations of systemic and cerebral haemodynamics observed after bolus application were not registered during continuous infusion of A and S. DISCUSSION AND CONCLUSIONS. The cerebral effects of opioids are dependent on several factors, e.g., age, species, ventilation, anaesthesia before and during measurements, systemic haemodynamics, and underlying diseases. The probable mechanism of ICP increase during decreasing MAP is cerebral vasodilatation due to maintained autoregulation. With increasing severity of the cerebral lesion autoregulation is often disturbed. Therefore, ICP often remains unaltered despite MAP decreases. However, the resulting decrease in cerebral perfusion pressure makes such patients more susceptible to develop ischaemic neurological deficits. Induction of somatic rigidity or (with high doses) convulsions, exceeding the upper limit of autoregulation, histamine release, cerebral vasodilatation, increased cerebral oxygen consumption, or carbon dioxide accumulation during spontaneous breathing were discussed as mechanisms for transient ICP/CBF increases. It is concluded that opioids are often beneficial and not generally contraindicated for patients with cerebral diseases and compromised intracranial compliance. However, since negative side effects cannot be excluded, opioid effects and side effects should be monitored (MAP, ICP, cerebrovenous oxygen saturation, transcranial Doppler sonography) in patients at risk. It has to be stressed that opioids should be administered only to patients with stable haemodynamic situations and preferably in well-titrated, continuous infusions.

Magnetic stimulation of the cortex and recording of the motor-evoked potentials (MEPs) by electromyography (EMG) is a well proven method to assess the descending pathways of the spinal cord and detect neurological impairment. We have assessed, in 33 adult patients undergoing spinal surgery, the influence of four total i.v. anaesthesia regimens (TIVA) on this recording technique. In 20 patients, the effect of 50% nitrous oxide was also studied. MEP amplitudes, latencies and success rates of stimulation were obtained in the steady-state after induction of anaesthesia. Combinations of midazolam and ketamine, and alfentanil and etomidate had the least effect on MEPs. Propofol (in combination with alfentanil or ketamine) showed marked depression of the MEP amplitude and the lowest success rates of stimulation. The latencies did not change at all. The addition of nitrous oxide significantly depressed the registered MEPs and lowered the success rates.

Patients will be discharged from the postoperative recovery room mostly on subjective clinical assessment. In this study an approach to a more quantitative judgment of postoperative vigilance is made by recording the P300-latency and neuropsychological tests.22 adult patients undergoing a disc operation were examined. For induction of anesthesia thiopental (4-5 mg/kg), fentanyl (0.1 mg) and a musclerelaxant (atracurium 0.4 mg/kg or succinylcholine 1-2 mg/kg after precurarisation with atracurium 5 mg) were given. Anesthesia was then continued with enflurance (1.0-1.2 MAC) in a mixture of 67% nitrous oxide in oxygen. If postoperative analgesia was needed, piritramid was injected in boli à 3-6 mg. The P300 was acoustically stimulated with an oddball-paradigm and recorded at Fz and Cz. Afterwards the latencies were measured and compared with a vigilance score composed of clinical parameters and neuropsychological tests. Recordings were done preoperatively and every 30 minutes up to 2 hours postoperatively. A correlation between P300-latencies and vigilance score was made with the coefficient of Spearman. Comparison of pre- and postoperative values was managed by using Wilcoxon test for matched pairs with Bonferroni-correction.Immediately after operation, P300 was obtained only in 8 patients (36%). The latencies were delayed (394 +/- 35 ms versus 326 +/- 12 ms preoperatively). During follow-up patients recovered and 2 hours postoperatively only one patient had no P300. At the end of the examination period P300-latencies of most patients had not yet reached the preoperative levels. The vigilance score in parallel showed decreases immediately after the operation and increases later on. However there were discrepancies between P300 latencies and neuropsychological findings, in some cases possibly due to the sedative effects of postoperative analgetics.Recording of P300-latencies showed remarkable cognitive deficits because of subclinical anesthesia hangover even 2 hours after a routine inhalational anesthesia. It is a good quantifiable method for assessment of postoperative vigilance. In some cases P300-latency is a more sensitive parameter for vigilance phenomena than clinical and neuropsychological scores.

Patients with head injury need effective help. The restoration of disturbed ventilation and an impaired general circulation is important. Concomitant injuries, which occur in about 40% of cases, should be recognized. Priority must be given to treating large lesions of vital organs. Hypoxia and hypotension should be avoided because they produce secondary brain damage. Unconscious patients are intubated and ventilated. In a few cases a laryngeal mask could be applied. Intravenous hypnotics, narcotics and benzodiazepines are used. Inhalational anesthetics, among them N2O, are harmful and should be avoided in these cases. The patients are given normal volumes of colloid fluids or water electrolyte solutions. A long-lasting muscle relaxation will impede clinical assessment. Cerebral protection and effective drug treatment of the lesions is still under debate: Nimodepine in traumatic SAH and glucosteroids in local lesions with BBB rupture, however, seem to be effective.

GOAL OF THIS REVIEW: We review the recent literature and our experience in order to determine how one can recognize and handle patients with difficult endotracheal intubation."An intubation is called difficult if a normally trained anesthesiologist needs more than 3 attempts or more than 10 min for a successful endotracheal intubation." The incidence of difficult intubation depends on the degree of difficulty encountered showing a range of 1-18% of all intubations to about 2/10000-1/million for "cannot ventilate-cannot intubate" situations. Three "cannot ventilate-cannot intubate" situations are presented that occurred at our institution in the last 10 years out of about 85000 anaesthesias.Intubation will be overtly difficult in patients with a small mouth opening, protruding upper teeth, a stiff neck, engorgement of the tongue, cervical swelling after an operation for a face tumour, or in patients with an unstable cervical spine. In about 50-70%, a difficult intubation can be detected preoperatively in patients with grossly normal cervical anatomy by three indirect signs: if the soft palate cannot be visualized (Mallampati classification), if the inframandibular space is smaller than normal, and if the mobility of the atlanto-occipital joint is reduced to below 15 degrees. It is essential that these indirect parameters be tested preoperatively, especially in patients in whom general anaesthesial is planned for a caesarean section or if an ileus intubation is planned.General handling of difficult intubation, use of special material including a portable unit, and confirmation of the endotracheal position of an endotrachaeal tube are outlined (CO2 et, SaO2, fibreoptic bronchoscopy, direct visualization of the translaryngeal position of the tube). The laryngeal mask airway, transtracheal jet ventilation, and the mini-coniotomy are selectively presented as alternative airways. The American Society of Anesthesiologists' (ASA) difficult airway algorithm is presented.With better preoperative evaluation and clear guidelines and training for difficult intubation anaesthetic morbidity and mortality can be reduced.

The occurrence of severe head injury, isolated or in connection with polytrauma, is a challenge for all physicians working in emergency care at the scene of an accident or afterwards in hospital care. It is an advantage to have a basic knowledge of neurological assessment. The Glasgow Coma Scale is widely used in this context; we refer to mild, moderate, and severe injuries. It is very important to recognise concomitant injuries, which occur in about 40% of cases. As coexisting hypoxaemia and hypotension have an adverse effect on the time course of head injury by inducing secondary brain damage, it is essential in therapy to quickly restore the vital body functions. Unconscious patients are tracheally intubated and ventilated. Forced hyperventilation over a lengthy period seems to have an unfavourable effect on outcome. Anaesthetic drugs and adjuvant therapies are used that do not increase intracranial vessel diameter and consequently intracranial pressure (ICP). This applies to all i.v. anaesthetics, sedatives, and opioids, as long as no respiratory depression occurs. Ketamine has been useful for many years at the scene of an accident. An existing low blood pressure (BP) is raised while a significantly increased BP is moderately lowered. It is necessary to have adequate cerebral perfusion pressure (CPP), which is defined as mean BP minus ICP. In cases of polytrauma with heavy bleeding, e.g., from the liver or spleen, the blood loss must be stopped before the neurosurgeon begins. Excessive i.v. administration of Ringer's lactate should be avoided. Today, the routine use of osmodiuretics, e.g., mannitol, is not indicated. It has not yet been possible to show that using corticosteroids is definitely beneficial in human brain trauma; there may be a positive effect in connection with spinal trauma. New therapies are being investigated, such as increasing CPP, administering AMPA/NMDA-antagonists, 21-aminosteroids, or hypertonic-hyperoncotic solutions. However, they have not as yet been proven effective for general clinical use or clinical use et al.

Although adverse effects on cerebral blood flow have been reported, intravenous anaesthetic and sedative agents are often used in neurosurgical patients. Monitoring of these effects by transcranial Doppler sonography remains a questionable procedure as long as the cross-sectional area of the insonated basal cerebral arteries is unknown. This study should evaluate the effects of thiopental, propofol, midazolam and alfentanil on flow velocities and "vessel cross-sectional area" (proportional to the reflected Doppler signal power) measured by transcranial Doppler sonography.19 patients with severe cerebral lesions (Glasgow Coma Scale6) were investigated. They were hyperventilated and sedated with fentanyl and flunitrazepam. The Doppler probe was fixed to the temporal bone and focussed to the middle cerebral artery of the more severely lesioned side. Baseline values of flow velocities and vascular cross-sectional area were measured. If routine nursing procedures required a deeper degree of sedation, either thiopental 2.5 mg/kg, propofol 1 mg/kg, midazolam 0.075 mg/kg or alfentanil 0.025 mg/kg were injected intravenously over 30 s. Further measurements were made 60, 120 and 300 s after start of the injection. Mean +/- SD were calculated, statistical evaluation was performed by analysis of variance and paired t-tests using the Bonferroni correction (p0.05).The injected agents induced significant decreases of the mean value of flow velocities; the "vessel cross-sectional area" remained unaltered. In some patients paradoxical increases of v were observed.The results indicate that intravenous anaesthetic agents are not likely to influence the cross-sectional area of the major basal cerebral arteries. Therefore TCD seems to be a valid tool to monitor the effects of these agents on the cerebral circulation of neurosurgical patients. This is probably of prognostic and therapeutic value.

Cannulation of the axillary vein is claimed to be an effective and relatively safe access to the central venous (CV) system [2, 4, 5, 8]. However, anatomical landmarks recommended for venous location (Muskulus pectoralis minor, processus coracoideus) are probably hard to identify in the majority of intensive care (ICU) patients. This investigation evaluated unidirectional 8 MHz Doppler ultrasound (US) in locating the axillary vein. Success rates and complications of this CV access in ICU patients is analysed. METHODS. The experimental design was approved by the local ethical committee (RUB). In 50 patients from our ICU cannulation of the axillary vein was attempted; all were in need of a CV line. Other CV puncture sites (except for the subclavian vein) were associated with contraindications. Patients were placed in a 15 degrees Trendelenburg position (15 exceptions); the arm was abducted to 45 degrees [5, 8]. The course of the axillary vein was located by Doppler US and marked on the skin with a felt pen. Prior to puncture, US intensity was judged by a score ranging from 0 to 4. After skin desinfection, sterile draping, and local anaesthesia, puncture of the axillary vein was attempted. The puncture kit LeaderCath 11,515 (Vygon, Aachen, FRG) was used. When venous blood could be aspirated, the Seldinger guidewire was inserted and the definite catheter placed. The experimental design allowed up to ten punctures, slightly modified in angle and direction of the needle, if puncture of the axillary vein or guide-wire placement failed. The cannulation attempt was classified as unsuccessful in the following cases: malposition, axillary vein not encountered by the puncture needle, guide-wire placement unsuccessful, or if identification and cannulation of the vein lasted more than 20 min. The puncture attempts were evaluated in respect to success rate, time, relation of US intensity to puncture attempts and CV pressure, complications, and malposition. RESULTS. Of the 50 attempted CV catheters, 43 were placed successfully. In 2 cases the axillary vein could not be encountered by the puncture needle. Guide-wire placement did not succeed in 4 patients. One catheter was malpositioned in the ipsilateral internal jugular vein. Four inadvertent punctures of the axillary artery remained without sequelae after compression. No further puncture-related complications were observed. With high US intensity score the number of puncture attempts necessary for successful vein cannulation was lower. On the other hand, complications and puncture failure seemed to be more frequent in patients with lower US intensity scores. DISCUSSION. CV access via the axillary vein had a satisfying success rate (43/50) and proved to be a safe procedure in our ICU patients despite higher risk factors compared to a healthy population. Although ethical reasons did not allow a randomised comparison with the standard technique, location of the axillary vein by Doppler US is likely to improve cannulation results and reduce complications induced by "blind" needle probing. With a low US intensity score, the rate of successful punctures is lower and complication rates increase. In some patients, e.g., those with extended tumour operations involving the head and neck, CV access via the axillary vein may be of high clinical value.

The effects of the opioids alfentanil (A), fentanyl (F), and sufentanil (S) on cerebral blood flow (CBF) and intracranial pressure (ICP) have been discussed in several recent publications. The purpose of this review is to describe the results of studies in animals, healthy volunteers, and patients with and without intracranial diseases. Clinical relevance and mechanisms of the reported ICP and CBF increases are analysed. METHODS. Approximately 70 original articles and abstracts were retrieved by a systematic literature search using the key word list at the end of this abstract. The cited studies came from computerised database systems like Silver Platter and DIMDI, the SNACC reference list, and the bibliographies of pertinent articles and books. These studies were classified into three groups: significant increase of ICP and/or CBF; no significant or clinically relevant alterations; and significant decreases of ICP and/or CBF. RESULTS. The numerical relationship was 6:7:3 for A, 7:16:9 for F, and 5:11:8 for S. Increases of previously normal or only slightly elevated ICP were registered in some studies in connection with a decrease in mean arterial pressure (MAP). On the other hand, in patients with brain injury and elevated ICP opioids did not further increase ICP despite MAP decreases. In studies monitoring ICP and/or CBF continuously, transient and moderate increases of questionable clinical relevance became apparent a few minutes after bolus injection of opioids. Alterations of systemic and cerebral haemodynamics observed after bolus application were not registered during continuous infusion of A and S. DISCUSSION AND CONCLUSIONS. The cerebral effects of opioids are dependent on several factors, e.g., age, species, ventilation, anaesthesia before and during measurements, systemic haemodynamics, and underlying diseases. The probable mechanism of ICP increase during decreasing MAP is cerebral vasodilatation due to maintained autoregulation. With increasing severity of the cerebral lesion autoregulation is often disturbed. Therefore, ICP often remains unaltered despite MAP decreases. However, the resulting decrease in cerebral perfusion pressure makes such patients more susceptible to develop ischaemic neurological deficits. Induction of somatic rigidity or (with high doses) convulsions, exceeding the upper limit of autoregulation, histamine release, cerebral vasodilatation, increased cerebral oxygen consumption, or carbon dioxide accumulation during spontaneous breathing were discussed as mechanisms for transient ICP/CBF increases. It is concluded that opioids are often beneficial and not generally contraindicated for patients with cerebral diseases and compromised intracranial compliance. However, since negative side effects cannot be excluded, opioid effects and side effects should be monitored (MAP, ICP, cerebrovenous oxygen saturation, transcranial Doppler sonography) in patients at risk. It has to be stressed that opioids should be administered only to patients with stable haemodynamic situations and preferably in well-titrated, continuous infusions.

An infected fistula was observed in a woman (Age: 69 years, weight: 60 kg, height: 159 cm) 14 days after insertion and 8 days after removal of a peridural catheter inserted preoperatively for postoperative analgesia after nephrectomy (carcinoma). Due to haemodynamic problems in the early postoperative period no analgetic or local anaesthetic medication was applied via the peridural catheter. After unsuccessful antibiotic and surgical treatment the women was transferred to the Neurosurgical department five weeks after nephrectomy. Magnetic resonance imaging of the lumbar region showed a fistula (Segment L2/L3) reaching the epidural space but no epidural spreading or epidural abscess. Partial laminectomy L2/L3 was performed and the fistula excised under continuous antibiotic treatment with ofloxacin. Up until 21 months after the operation no recidivation occurred. Exact details of catheter insertion and catheter treatment in the postoperative period are not available; the fact, that no bactericide [9] local anaesthetic agents were applied, might have favoured the occurrence of this infection. Infectious complications have to be taken into consideration for the indication of peridural catheters in the perioperative period.

Transcranial Doppler sonography (TCD) has gained in relevance for noninvasive monitoring of the cerebral circulation during the perioperative period. As long as the diameters of the investigated vessels remain unknown, however, flow velocities alone are not really informative. Exact vessel diameter determination in humans under the influence of different anesthetic drugs has not yet been performed due to ethical and methodological restrictions. A new modification of TCD allows analysis of the reflected "Doppler power", which is proportional to the cross-sectional area of the insonated vessel. METHODS. Three groups of 15-16 patients each (ASA I) were investigated after informed consent. Anesthesia was induced with droperidol, alfentanil, thiopental, and vecuronium bromide. After intubation patients were normoventilated with N2O:O2 = 3:2 and additional doses of alfentanil were injected until the transcranial ultrasound probe was fixed to the temporal bone and focused on the middle cerebral artery. Baseline values of heart rate (HR), mean arterial pressure (MAP), expiratory minute volume (EMV), end-expiratory CO2 (FeCO2), and TCD were measured. Then 1.5 vol% halothane, 25-50 micrograms/kg alfentanil, or propofol (1.5 mg/kg iv., 10 mg/kg.min) was administered. Further measurements (HR, MAP, EMV, FeCO2 and TCD) were performed at 3, 6, 10, and 20 min after the start in the halothane and propofol groups and after 3 and 6 min in the alfentanil group. The following transcranial parameters were derived from the TCD device: mean maximal flow velocity (vmmax), pulsatility index, time-averaged mean velocity (vmmen), "vessel area (VA)", and "volume flow (VF)". The mean +/- standard deviation of each parameter was calculated. Statistical evaluation was performed by paired t-tests (level of significance P less than 0.05). RESULTS. HR showed a tendency to increase after halothane and to decline after alfentanil. Alfentanil induced a short-term decline in MAP. End-expiratory minute volume and FeCO2 showed only minor alterations in all three groups. The vmmax was nearly doubled by halothane. Alfentanil induced a transitory decline in vmmax while Propofol decreased it markedly. The pulsatility index showed a decrease after halothane; alfentanil caused a short-term increase. Propofol induced a strong increase after 3 min; in the following period a return to baseline values was observed. The vmmean was increased by halothane and reduced by 32% propofol. VA was found to be unaltered by alfentanil and propofol but was more than doubled by halothane. Accordingly, the relative value for VF increased by 148% under halothane. VF appeared to decline after propofol. DISCUSSION. The described method allows only the determination of relative values: it is not possible to quantify exactly how much the VA changed. Halothane caused significant increases of VA measured in the middle cerebral artery, whereas alfentanil and propofol did not influence this parameter. This is in accordance with previous experiments in dogs in which halothane decreased the resistance of large basal cerebral arteries (LAR). LAR remained unaltered after alfentanil administration. The site of action of some anesthetic agents on cerebral vessels does not seem to be restricted to cerebral arterioles: at least for halothane, a vasodilating effect on large cerebral arteries could be demonstrated. This should be kept in mind when transcranial Doppler is applied during the perioperative period.

Transcranial Doppler Sonography (TCD) can meet some requirements for an ideal measuring device of the cerebral circulation. TCD can measure non-invasively and repeatably blood flow velocities of basal cerebral arteries. Under the assumption of constant vessel diameters can altered flow velocities reflect alterations of cerebral blood flow. TCD-measurements have been used frequently for diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Furthermore TCD has been applied in cerebrovascular diseases, during operations with extracorporal circulation and in patients with increased intracranial pressure. Unchanged diameters of basal cerebral arteries have been proven only for carbon dioxide variations and some drugs; this cannot be presupposed during alterations of mean arterial or intracranial pressure. If conditions as ventilation, hemodynamics and drug therapy are kept constant, TCD may be valuable for short-term-trend-detection of cerebral blood flow and intracranial pressure.

In a prospective study on 78 patients the influence of the severity of an isolated head injury on the pulmonary gas exchange has been examined. Our results show that with increasing severity of the isolated cerebral trauma the quotient A -- aDO2/PAO2 increases as well (P less than 0.001). Patients with comparable degrees of head injury but nearly unchanged pulmonary function have a greater chance to survive (P less than 0.05), though with neurological defects, than patients with an additional disturbed pulmonary gas exchange. The overall survival rate amounts to 53.8 per cent.

The effects of a hyperventilation, positive negative pressure ventilation (PNPV) and ventilation using positive endexpiratory pressure (PEEP), on intracranial pressure (ICP) was measured in 24 patients suffering from different neurosurgical disorders. The patients were given a basic anaesthesia including muscle relaxation. The investigations showed, that hyperventilation, followed by a PCO2 of 26 and 30 torr, clearly lowered the intracranial pressure. The pressure drop was much more pronounced when the preexisting ICP was high than when it was low, due to the form of the compliance curve of the brain. PNPV also lowered intracranial pressure, but a harmful effect of this technique on lung function and structure is known. Its use is justified only for short periods and in addition to other measures for lowering ICP. The results also demonstrated that PNPV possesses limited beneficial properties with regard to the subject discussed here. Ventilation by PEEP significantly increased ICP. This technique is to be employed with caution in neurosurgery. Arterial pressure (radial artery) and central venous pressure (subclavian vein) were also recorded.

In a prospective study in 129 patients with isolated head injury the efficacy of respiratory treatment/controlled moderate hyperventilation on the neurological outcome is to be tested. Indications for mechanical ventilation are either a bad neurological behaviour (GCS less than or equal to 5) or neurogenic-induced disturbances of pulmonary gas exchange. Both oxygenation and neurological behaviour are worse in the ventilated group than in patients breathing spontaneously. Therefore a direct and quantitative comparison between these two groups of patients is not possible; however, conclusions can be drawn on the efficacy of the respiratory management. Survival rate of all patients on discharge from ICU amounts to 61.2%; of the patients breathing spontaneously 96.1% survive the cerebral trauma, while only 39.7% of the ventilated patients survive. The post-traumatic course of the GCS-values shows a transient but statistically and clinically significant decrease for the nonventilated survivors, while a continuous increase can be demonstrated for the patients being ventilated and surviving the cerebral trauma (n = 31). The survival rate for the most severely injured and ventilated group (n =59; GCS less than or equal to 5) amounts to 38.9% (23/59 patients). Out of these 23 patients with initial extensor spasm 15 reach greater than or equal to 10 points on GCS-scale (12.2 +/- 0.5 P.) on discharge from ICU. An additional neurogenic-initiated respiratory failure increases the rate of mortality to a statistically significant extent (P less than 0.025). It is concluded that respiratory treatment with moderate hyperventilation positively influences the quality of the neurological outcome in patients with severe head injury.

Der intrakranielle Druck (ICP) setzt sich aus den Komponenten Gehirngewebe, Blutgefase (einschlieslich Zerebralvolumen) und zerebrospinale Flussigkeit zusammen. Wenn eine dieser Komponenten ihr Volumen vergrosert, steigt der Druck innerhalb des Schadels an, nachdem nicht genugend Platz fur eine rasche Kompensation vorhanden ist.

Der Druck im Schadelinneren hangt von den intracraniellen Bestandteilen Hirnsubstanz, Liquor cerebrospinalis und Gefassystem mit Blutvolumen ab. Der intracranielle Druck kann vom Anaesthesisten in einer fur den Patienten gunstigen oder ungunstigen Weise beeinflus werden. Angriffspunkt ist das cerebrale Gefassystem, dessen Volumen etwa 3 – 5 % des gesamten intracraniellen Volumens ausmacht.

The ultrasound Doppler technique is a non-invasive method for the evaluation of arterial and venous blood flow. It can be useful in anaesthesia and in intensive medicine for different purposes, e.g. for more exact blood pressure determination in difficult cases, in cases of blood supply disorders or as a helpful guide for the puncture of arterial and venous vessels. This technique has also been used successfully as a screening method of cerebral death, for the evaluation of flow rates during arterio-venous hemofiltration and for the investigation of the effects of peridural anaesthesia on peripheral resistance.

Although many different approaches have been recommended for catheterization of the internal jugular vein, sometimes difficulties and serious complications may occur. The Ultrasound-Doppler-technique is a simple and non-invasive method for localizing and differentiating arterial and venous vessels, e.g. carotid artery and internal jugular vein. A method for puncture of the internal jugular vein with the help of the Ultrasound-technique will be described. In our investigation of 150 punctures this method proved to be superior to approaches recommended up until now.

Enflurane (Ethrane) was given before operation to 13 neurosurgical patients. 11 of them received halothane for comparison of effects on intracranial pressure (ventricular catheter), blood pressure and central venous pressure during controlled ventilation. Neuroleptanalgesia was used as basic anaesthesia. The results showed that enflurane, when initial pressure levels were between 0-20 mm Hg, had better properties with regard to intracranial pressure than halothane. The intracranial pressure of 6 patients under enflurane rose. Of the remaining patients pressure did not change or even fell. Under halothane, given in a comparable doses, there was always a marked increase of intracranial pressure. If intracranial pressure of one patient under enflurane rose, then the increase by halothane always was more pronounced. The results from 1 patient had to be excluded because of spontaneously occurring plateau waves. Blood pressure was lowered by both agents while central venous pressure remained unchanged.

Der Druck im Schadelinneren wird, anatomisch gesehen, durch das Gehirn selbst, den Liquor cerebrospinalis und das Gefassystem mit dem darin enthaltenen Blut bestimmt.

Intracranial pressure (ICP) is built up by the components brain tissue, blood-vessels (including cerebral volume), and cerebrospinal fluid. If one of them increases its volume, pressure within the skull will rise, for there is no room for rapid compensation. A pressure increase or decrease under the influence of anaesthetics is mainly caused by changes in cerebral blood flow, or rather blood volume. Recently it was shown that the brain tissue itself can in this context contribute to a pressure increase during anaesthesia. Modern inhalation anaesthetics, such as halothane, enflurane, or methoxyflurane, are well known to increase ICP. Since the investigations of McDowall et al. [6], Marx et al. [5], Jennett et al. [4], and others, we know that halothane increases ICP, that this effect is dosage-dependent, and that the increase will be greater the higher the pre-existing pressure level is.

Fur Patienten mit einem Schadel-Hirn-Trauma (SHT) kann in folgenden Situationen eine Allgemeinnarkose notwendig werden: 1. Bei der Bergung und Erstversorgung am Unfallort. 2. Bei der Primardiagnostik in der Klinik, z. B. fur Angiographien, Computertomographien, sonstige Rontgenuntersuchungen oder Lavagen. 3. Bei der operativen Versorgung einer epi-, sub- oder intrazerebralen Blutung oder einer offenen Hirnverletzung. 4. Bei einer dringlichen Operationsindikation aus nicht neurochirurgischen Grunden, z. B. bei intraabdominellen Blutungen, offenen Extremitatenfrakturen oder auch Augen- und Gesichtsschadelverletzungen.

Die Anasthesie in der Neurochirurgie ist zwar keine grundsatzlich andere als die, welche in den anderen operativen und diagnostischen Disziplinen praktiziert wird. Es sind jedoch von der Grunderkrankung her und aus operationstechnischer Sicht des ofteren besondere Techniken und Verfahren notwendig, die es rechtfertigen, sie in einer zusammenfassenden Darstellung abzuhandeln.

Die Uberwachung von Patienten mit einem schweren Schadel-Hirn-Trauma umfast selbstverstandlich zunachst einmal Masnahmen, die allgemein in der Intensivtherapie ublich sind und daruber hinaus spezielle Verfahren.

Investigations with small laboratory animals (rats) which have to be performed under controlled artificial ventilation can be done easier with a new respirator, developed by the authors, allowing simultaneous ventilation of four animals. The underlying design is that of a constant pressure generator with a mechanical interrupter for timing the ventilation cycle; the latter is constant (75/min). Each animal can be handled independently from the other, concerning respiratory pressure and, therefore, of ventilation volume. Rats have been ventilated successfully for 7 h by controlling pO2 pCO2 and pH of the blood. Longer times for controlled ventilation are possible.

In 60%-90% of cases head injury is a part of multisystem trauma and of very decisive importance for the post-traumatic prognosis. Hypoxia, hypercarbia, and hypotension increase the primary lesion and cause secondary brain damage. Therefore, emergency measures must be directed to the essentials of sustaining vital functions, i.e. intubation/ventilation/oxygenation and stabilization of the circulatory system. All trauma-specific measures should avoid additional increases in intracranial pressure or should decrease it if already elevated. Moderate hyperventilation not only causes cerebral vasoconstriction with a concomitant decrease in intracranial blood volume and intracranial pressure, but also partly restores the disturbed cerebral autoregulation, and is therefore an important part of the emergency care and anesthetic procedure in patients with severe head injuries. It is supplemented by analgesia and sedation to prevent intracranial pressure increases due to painful external stimuli. Elevation of the head and upper part of the body by 30 degrees causes a decrease in intracranial pressure by decreasing intracranial blood volume due to improved venous return from the brain; however, this measure is to be applied only in stable circulatory conditions. The head should be put in mid-position avoiding sideways rotation, flexion, and hyperextension. Osmotically active agents are only indicated in emergency situations when there are signs of clinical deterioration. High-dose barbiturate therapy is reserved as a "last resort", under intensive care conditions, for controlling an otherwise intractable intracranial pressure rise. Calcium antagonists have no indication in this context. Anesthesia in patients with severe head injury must involve only those techniques that do not further increase an already elevated intracranial pressure. As inhalational anesthetics, including nitrous oxide, elevate the intracranial pressure to varying extents due to cerebral vasodilation with a concomitant rise in intracranial blood volume, these substances have to be avoided whenever raised intracranial pressure cannot be excluded. Narcotics, benzodiazepines, small dosages of barbiturates, and long-lasting muscle relaxants can be regarded as useful.

Some of the important points of view of anesthesia in pediatric neurosurgery are: adequate alveolar exchange of oxygen and carbondioxide by means of artificial ventilation; stable cardiovascular function; fluid balance; monitoring, and attempts to keep intracranial pressure low. This last point is achieved by various anesthesiological procedures, e.g., hyperventilation, positive-negative pressure ventilation, rapid induction of anesthesia and choice of suitable anesthetics. Enflurane (Ethrane®) increases intracranial pressure less than halothane. The new intravenous anesthetic etomidate lowers intracranial pressure in a favorable manner quite similar to thiopental (Pentothal-Sodium®).

Transcranial Doppler Sonography (TCD) can meet some requirements for an ideal measuring device of the cerebral circulation. TCD can measure non-invasively and repeatably blood flow velocities of basal cerebral arteries. Under the assumption of constant vessel diameters can altered flow velocities reflect alterations of cerebral blood flow. TCD-measurements have been used frequently for diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Furthermore TCD has been applied in cerebrovascular diseases, during operations with extracorporal circulation and in patients with increased intracranial pressure. Unchanged diameters of basal cerebral arteries have been proven only for carbon dioxide variations and some drugs; this cannot be presupposed during alterations of mean arterial or intracranial pressure. If conditions as ventilation, hemodynamics and drug therapy are kept constant, TCD may be valuable for short-term-trend-detection of cerebral blood flow and intracranial pressure.

Zu den muskularen Erkrankungen gehort eine Vielzahl von Storungen unterschiedlichster Atiologie und Symptomatik. Die Verabreichung einer Kombinationsnarkose wird bei den meisten von ihnen keine besonderen Probleme aufwerfen, soweit allgemeine Grundsatze der Anasthesie wie wirkungsbezogene Dosierung und Berucksichtigung des klinischen Allgemeinzustandes befolgt werden. Narkotika, Analgetika und Muskelrelaxanzien konnen negative Auswirkungen auf die postanasthetische Symptomatologie des Krankheitsbildes haben. Hier ist besonders eine protrahierte Ateminsuffizienz zu furchten. Muskelrelaxanzien spielen in diesem Punkt zweifelsohne die groste Rolle, wobei ihr Wirkungsmodus - depolarisierend oder nichtdepolarisierend - und die angewandten Dosierungen in den anschliesenden Krankheitsverlauf eingehen konnen. Vom Anasthesisten werden relevante Muskelerkrankungen im allgemeinen Routinebetrieb relativ selten gesehen. Die Kenntnis dieser Storungen ist aber trotzdem wichtig, da ein solcher Patient jederzeit vor einer Operation angetroffen werden kann und dann die richtige Auswahl getroffen werden mus

Narkoseeinleitung und -verlauf bei supratentoriellen Eingriffen zeigen viele Gemeinsamkeiten mit den ublichen Verfahren der Anasthesie und dazu einige Besonderheiten.

Hormone der Achse Hypothalamus-Hypophysenvorderlappen-Nebennierenrinde und aus dem sympathischen Nervensystem freigesetzte Katecholamine sind an verschiedensten Gegenregulationen und Adaptationsmechanismen des Organismus beteiligt.