Epidural analgesia with sufentanil during labor and operative delivery.

BACKGROUND: It has been argued that by adding an opioid to the local anesthetic drug used for epidural analgesia during childbirth, one can reduce the risk of operative delivery. Objective. In a population-based observational study, to evaluate the effect of adding an opioid to a local anesthetic drug on the risk of instrumental delivery or cesarean section. DESIGN: Comparison of delivery units adding/not adding opioid to the local anesthetic for epidural analgesia in labor. SETTING: All deliveries using epidural analgesia in Sweden during 1992-96 were evaluated on the basis of information stored at the Medical Birth Registry, the National Board of Health and Welfare, Stockholm. METHOD: A questionnaire was sent to all delivery units (n=61), as well as to the Head of corresponding Anesthesiology Department in each hospital, requesting information regarding the period when opioids (sufentanil) were first added to the local epidural analgesic. Parturients given epidural analgesia were divided into three time-related groups: those delivered before the introduction of opioids (n=34,071), when opioids were first added (n=7,236), and since the introduction of opioids (n=44,384). Odds ratio (OR) with 95% confidence interval (CI) was used to assess the effect of sufentanil versus no sufentanil, on the risk of operative delivery. The parturients were stratified for year of delivery, age, and parity. Main outcome measures. Instrumental delivery, cesarean section, length of stay in hospital post partum. RESULTS: A significant reduction was observed in the incidence of instrumental delivery (OR 0.72; 95% CI 0.68-0.76). A similar though less pronounced effect was evident concerning the risk of cesarean section for nulliparae (OR 0.79; 95% CI 0.72-0.88) but not for multiparae (OR 0.93; 95% CI 0.80-1.07). Fewer women with an opioid added to the local anesthetic spent more than 4 (or more than 7) days in hospital post partum, compared with those given epidural analgesia without an opioid. CONCLUSION: When added to the local anesthetic used for epidural analgesia, as in Sweden during the last 5 years, opioids appear to reduce the incidence of instrumental delivery and cesarean section and also the post partum hospital stay.

[Risks and recommendations in Bechterew disease. Paraparesis after epidural anesthesia]. / Risker och rekommendationer vid Bechterews sjukdom. Parapares efter epidural bedövning.

We describe a case of paraparesis caused by an epidural haematoma in a 74-year-old man with advanced ankylosing spondylitis who received combined epidural and general anaesthesia for graft repair of an aneurysm of the abdominal aorta. Before the induction of general anaesthesia, an epidural catheter was inserted at the level of thoracic vertebrae 10-11 without difficulty or signs of bleeding. Total analgesia and paralysis of the legs in the early postoperative period raised suspicions of the presence of an epidural haematoma, which was confirmed by magnetic resonance tomography. Aspiration of the epidural catheter yielded 13 ml of blood. Despite early surgical decompression after transfer to a regional hospital, the patient remains paraparetic. We wish to highlight the risks of epidural anaesthesia in cases of ankylosing spondylitis, and to stress the need of routine control of motor function after epidural anaesthesia.

Neurological complications after anaesthesia. A follow-up of 18,000 spinal and epidural anaesthetics performed over three years.

17 733 consecutive central blocks (8501 spinal and 9232 epidural anaesthetics) performed during a three-year period were analyzed for alleged complications. Neurological complications related to anaesthesia were reported in 17 cases of which 13 patients had persisting lesions after three spinal and ten epidural blocks. In two patients given spinal anaesthesia, the technique was inadequate. In seven epidural blocks, the connection between neurological lesion and the anaesthetic technique could be argued. In five of these cases, polyneuropathy or nonspecific neurological symptoms were present. Three complications after epidural blocks were paraplegias caused by spinal haematomas in patients with deranged haemostatic capacity.

Local cerebral blood flow in spontaneously breathing rats subjected to graded isobaric hypoxia.

Local cerebral blood flow (l-CBF) was measured with an autoradiographic technique in spontaneously breathing rats exposed to air or gas mixtures of O2 and N2, giving inspired oxygen fractions (FiO2) ranging from 0.21 to 0.07. The arterial O2 tension (PaO2) changed from 10.9 +/- 0.3 (FiO2 0.21) to 3.9 kPa (FiO2 0.07) (82 +/- 2 to 29 mmHg). Hypoxia caused hyperventilation, and the arterial CO2 tension (PaCO2) fell from 5.21 +/- 0.05 kPa (FiO2 0.21) to 3.27 kPa (FiO2 0.07) (39.1 +/- 0.4 to 24.5 mmHg). The hyperventilatory response was markedly augmented when changing FiO2 from 0.13 to 0.11, causing a fall in PaCO2 of 0.75 kPa and a shift in arterial pH from 7.45 +/- 0.01 (FiO2 0.13) to 7.54 +/- 0.01 (FiO2 0.11). The l-CBF response to hypoxia was found to be biphasic for all the observed regions. At FiO2 0.13, l-CBF was measured about 75% above control but at FiO2 0.11, only 30% above control. A further reduction in FiO2 to 0.07 caused a marked increase in l-CBF, at least 240% of control; however, the applied CBF technique did not admit quantitation. These results suggest that the mechanisms controlling the cerebrovascular response to hypoxia and changes in arterial CO2 tensions are different. The results also indicate that hyperventilation might be harmful to the patient suffering from acute hypoxia.

Intravenous physostigmine treatment of Alzheimer's disease evaluated by psychometric testing, regional cerebral blood flow (rCBF) measurement, and EEG.

Ten patients with Alzheimer's disease were treated with intravenous infusion of physostigmine for 2 h. The acute effects on cognitive function, regional cerebral blood flow, and EEG were compared to placebo (isotonic glucose) using a double-blind cross-over design. Physostigmine causes a limited improvement of psychomotor performance and EEG and an increase of blood flow in the most severely affected cortical areas, predominantly in an early phase of Alzheimer's disease.

Adrenergic hyperactivity and epidural block in severe tetanus. A case report.

In a 69-year-old man with severe tetanus, sympatho-adrenal overactivity was successfully treated with a lumbar epidural block. Cardiovascular disturbances were reduced and fluctuations in plasma catecholamines were decreased. The duration of other manifestations of tetanus was, however, not influenced by the epidural block in this case.

Increased bleeding during liver resection after sympathetic block in normal rats.

The effect of sympathetic block on hemostasis after standardized liver resection was studied in the rat. Sympathetic block was undertaken by paravertebral block or surgical sympathectomy. Blood loss was significantly increased, but the bleeding time was not prolonged after paravertebral block. Surgical sympathectomy also increased blood loss as compared to controls, but there was no difference when compared with sham operation. Adenosine diphosphate and collagen induced platelet aggregation was not inhibited in all animals as compared to controls. The results indicate that primary hemostasis was not seriously affected, but that hepatic blood flow was augmented after sympathetic block.

The effect of indomethacin on the local cerebral blood flow increase induced by somato-sensory stimulation.

The local cerebral blood flow in cerebral cortical and subcortical regions of the rat brain was studied with the 14C-iodoantipyrine autoradiographic technique at rest and during strong non-noxious stimulation of the nose. Patterns of local blood flow changes evoked by stimulation with and without pretreatment of indomethacin, a potent cyclooxygenase inhibitor were determined. Stimulation produced a marked heterogeneous enhancement of CBF. Indomethacin did not prevent this effect although the absolute flow levels were considerably lower in indomethacin-treated animals. Indomethacin was especially effective in reducing the cerebral cortical blood flow response to stimulation whereas the subcortical response was much less affected.

Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model.

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.

Effect of diazepam on cerebral monoamine synthesis during hypoxia and hypercapnia in the rat.

In view of the fact that diazepam has been shown to prevent an increase in catecholamine synthesis and/or turnover rates in stressful situations, and to modify the cerebral metabolic (and circulatory) response to hypoxia and hypercapnia, the influence of the drug on synthesis rates of DOPA and 5-HTP in three regions of the rat brain were studied under normoxic-normocapnic conditions, as well as in hypoxia and hypercapnia. In order to exclude a modifying influence of variations in tissue pO2 during hypercapnia, cerebral venous pO2 was kept at control values by moderate arterial hypoxia. When compared to the control state (paralyzed animals maintained on 70% N2O) normoxic and normocapnic animals given diazepam (in the absence of N2O) showed a slightly enhanced DOPA synthesis in limbic structures and reduced 5-HTP synthesis in limbic structures and striatum. In hypoxia, the drug considerably curtailed DOPA synthesis in limbic structures and striatum but had no effect on synthesis rate in cortex. The drug also appeared to exaggerate the generalized reduction in 5-HTP synthesis observed under 70% N2O. In hypercapnia, diazepam reduced the enhanced rate of DOPA synthesis (observed under 70% N2O) in striatum but left that in the cortex unchanged. The drug prevented the hypercapnia-induced increase in 5-HTP synthesis, observed under 70% N2O. It is concluded that diazepam significantly alters dopamine and serotonin synthesis in hypoxia and hypercapnia. Probably an indirect action, perhaps related to the stress-alleviating effect of diazepam, is involved. The results suggest that the effect of the drug on cerebral metabolic rate and blood flow in hypoxia and hypercapnia is unrelated to changes in noradrenaline synthesis or turnover. Furthermore, although the results demonstrate that diazepam modulates dopamine metabolism in hypoxia and hypercapnia it seems questionable that this influence can explain the metabolic and circulatory effects of diazepam in these conditions.

Cerebral circulatory response to hypercapnia: effects of lesions of central dopaminergic and serotoninergic neuron systems.

The present study explores the possibility that the central dopaminergic and serotoninergic neuron systems influence CBF under normocapnic and hypercapnic conditions. In the first part of the study the effect of unilateral 6-hydroxydopamine lesion of the nigrostriatal dopamine pathway on local cerebral blood flow (1-CBF) was measured autoradiographically with [14C]iodoantipyrine as the diffusible tracer. The lesion caused no major effect on CBF under normocapnic or hypercapnic conditions. However, the circulatory response to hypercapnia was slightly enhanced (about 10%) in the denervated caudate-putamen. It is suggested that under hypercapnic conditions the pronounced increase in blood flow in the caudate-putamen is normally modulated by a slight vasoconstriction caused by dopamine release from the nigrostriatal system. In the second part of the study the effect of intraventricular 5,7-dihydroxytryptamine on cerebral metabolic rate for oxygen (CMRO2) and CBF was evaluated using a 133xenon modification of the Kety-Schmidt inert gas technique. The lesion, which removed about 90% of cortical 5-hydroxytryptamine, had no effect on the circulatory response to hypercapnia, not did it alter CMRO2. Under normocapnic conditions, though, the lesion seemed to induced a minor increase in CMRO2, which indicates that the serotoninergic system exerts a depressant resting tone on metabolic rate in the brain.

Cerebral blood flow and oxygen consumption in normocapnia and hypercapnia: modulating influence of paravertebral sympathetic blockade at the low thoracic level.

The objective of the present study was to explore whether the systemic consequences of sympathoadrenal activation influence the cerebral circulatory and metabolic effects of hypercapnia in the rat. To that end, a bilateral blockade of the sympathetic chain was performed at the low thoracic level by paravertebral injection of local anaesthetic. The injection was followed by a reduction in blood pressure and, in comparison to animals injected with local anaesthetic intramuscularly, those with paravertebral blockade showed lower blood and tissue concentrations of glucose and lactate. Overall ("cortical") CBF and CMRO2 were measured with a 133xenon modification of the Kety-Schmidt technique, and local CBF was estimated autoradiographically with 14C-iodoantipyrine as the diffusible tracer. Paravertebral blockade failed to modify the circulatory response to hypercapnia, nor did it prevent the increase in CMRO2d previously noted in this preparation. In animals maintained ventilated on 70% N2O, paravertebral blockade reduced overall CBF by 30% and local CBF by 30-40%, with a suggested but statistically nonsignificant reduction in CMRO2. In unparalysed, awake animals the blockade failed to affect local CBF. It is concluded, therefore, that blockade of the sympathetic chain causes a reduction of CBF only in the stressful conditions prevailing in paralysed and ventilated animals.

Treatment of stress response to laryngoscopy and intubation with fentanyl.

The cardiovascular response to laryngoscopy and intubation was investigated in lightly anaesthetised patients admitted to hospital for elective intracranial surgery. One group of patients was given fentanyl 5 microgram/kg body weight before induction with thiopentone and suxamethonium. The other group served as controls. Fentanyl treatment caused a significant attenuation of the blood pressure and pulse response to laryngoscopy and intubation. Different techniques for induction of anaesthesia are discussed in relation to the demands of neuroanaesthesia.

The effect of indomethacin on cerebral blood flow and oxygen consumption in the rat at normal and increased carbon dioxide tensions.

The effect of the fatty acid cyclo-oxygenase inhibitor indomethacin on cerebral blood flow (CBF) and the metabolic rate for oxygen (CMRO2) was studied in paralyzed and artificially ventilated rats. In normocapnic animals, the drug (10 mg.kg-1i.v.) reduced CBF to 50% of control without a measurable effect on CMRO2. During hypercapnia (PaCO2 70-80 mmHg) the increase in CBF was reduced by about 80% but CMRO2 remained unchanged. Autoradiographic evaluation of local CBF in 20 brain structures indicated that the reduction in CBF was relatively uniform throughout the brain. Dose response curves showed that an effect on CBF was evident already at an indomethacin dose of 1 mg.kg-1 and maximal effects were obtained with 3-5 mg.kg-1. Following i.v. injection of the drug reduction in CBF was observed already after 10 s and the full response occurred after 1-2 min. It is concluded that metabolites of arachidonic acid, possibly mainly prostacyclin, are powerful modulators of normal cerebrovascular tone, and help to mediate the CBF response to increased CO2 tensions. However, since indomethacin does not modify the circulatory response in other conditions with increased CBF these substances do not qualify as general coupling factors controlling CBF in physiological or pathological states.

Cerebral blood flow and oxygen consumption in the rat brain after lesions of the noradrenergic locus coeruleus system.

The effect of lesions of the locus coeruleus neuron system on cerebral metabolic rate for oxygen (CMRO2) and blood flow (CBF) was evaluated in paralyzed and mechanically ventilated rats, using a 133xenon modification of the Kety-Schmidt inert gas technique. Bilateral electrothermic lesions of its ascending bundle caused no significant change in CBF or CMRO2. The 6-hydroxydopamine lesions did not influence the CBF and CMRO2 responses to hypercapnia and hypoxia. It is concluded that the locus coeruleus does not exert any resting tone on CBF and CMRO2 and that no influence on the CBF and CMRO2 responses to hypercapnia and hypoxia is mediated via its ascending projections.

Effects of indomethacin on cerebral blood flow and oxygen consumption in barbiturate-anesthetized Normocapnic and hypercapnic rats.

Although results obtained in baboons and rats have demonstrated that the fatty acid cyclo-oxygenase inhibitor indomethacin reduces cerebral blood flow (CBF) under control conditions and markedly attenuates the CBF response to hypercapnia, nonconfirmatory results have been obtained in rabbits and cats. Since these latter studies were carried out under barbiturate anesthesia, we tested the effect of indomethacin (10 mg kg-1) on CBF and cerebral oxygen consumption in rats anesthetized with 150 mg kg-1 of phenobarbital. At normocapnia the barbiturate reduced CBF, measured with a 133Xe modification of the Kety-Schmidt technique, to about 50% of nitrous oxide control values as previously determined with a similar technique. At this CBF level, indomethacin induced a small, albeit highly significant decrease in CBF. We suggest that a reduction of this magnitude will escape detection with some CBF techniques in current use. Indomethacin induced a highly significant decrease in CBF during hypercapnia, demonstrating that the barbiturate does not eliminate the effect of indomethacin on CO2 responsiveness. The magnitude of the reduction in CO2 response was so large that is should be detected with most methods for measuring CBF. A comparison with previous data on animals under 70% N2O demonstrated that phenobarbital reduced the CO2 responsiveness. defined as the ratio deltaCBF/deltaPCO2, to 39% of that observed under nitrous oxide analgesia. With both types of anesthesia, indomethacin curtailed the CO2 responsiveness 4- to 5-fold.

Effect of indomethacin on local cerebral blood flow in awake, minimally restrained rats.

The effect of indomethacin (10 mg kg-1) on local CBF (1-CBF) was studied with autoradiographic techniques in awake, minimally restrained rats. When compared with uninjected awake control animals, those given indomethacin showed a reduction of 1-CBF by 25-45%. This reduction is somewhat less pronounced than that previously obtained in paralyzed animals maintained on 70% N2O (a reduction by 30-60%). An enhancement of the indomethacin response during nitrous oxide anesthesia was mainly observed in structures which show a maintained or increased CBF during anesthesia.