[Comparison of traditional neuroleptanalgesia and neuroleptanalgesia with low-concentration isoflurane in patients undergoing general surgery].
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The objective of the study was to compare the influence of a fentanyl and droperidol mixture (neuroleptanalgesia) with morphine on the in-hospital instability, development of acute myocardial infarction (AMI), and mortality during a 30-day and 12-month follow-up in unstable angina patients. The study was performed in 112 unstable angina patients. In addition to standard therapy for unstable angina (aspirin, heparin, nitroglycerin, and oxygen), 53 patients (63.2 +/- 9.7 years; 32 males) were randomized to receive neuroleptanalgesia (0.025 mg fentanyl and 1.25 mg droperidol in a volume of 1 mL) and 59 patients (58.6 +/- 11.5 years; 41 males) to receive morphine. Neuroleptanalgesia was started i.v. with 2 mL and could be followed by 1 mL every 4 hours. Morphine was started i.v. with 10 mg and could be followed by 5 mg every 4 hours up to angina resolution during 24 hours of hospitalization. Another 1 mL of neuroleptanalgesia or 5 mg of morphine could be administered on demand if angina lasted or reappeared earlier than the next scheduled dose. Odds ratios with 95% confidence intervals (95% CI) adjusted for the age, sex, smoking, previous myocardial infarction, and hypertension were evaluated for all study outcomes. The odds ratios for clinical in-hospital instability (5.93, 95% CI: 2.49-14.15; P = 0.0001), 12-month AMI development (3.57, 95% CI: 1.51-8.45; P = 0.0038), and 12-month mortality (6.00, 95% CI: 1.63-22.09; P = 0.0070) were significantly increased in the neuroleptanalgesia group compared with the patients on morphine. It is concluded that neuroleptanalgesia negatively influences disease course, AMI development, and total mortality in unstable angina patients.
In 8 volume expanded dogs with an equilibrium between input and renal output of sodium and water neuroleptanalgesia of 6 hours duration with a total of 9 mg/kg of droperidol and 0.35 mg/kg of fentanyl was performed. Under anaesthesia GFR was increased by about 10% (p less than 0,02) compared with the conscious state, whilst renal sodium and water excretion was reduced by about 50%. From this we conclude that active tubular transport of sodium is augmented under neuroleptanalgesia. Due to decreased excretion, retention of sodium and water increased during anaesthesia changes of functional ECFV tending into the same direction. Plasma volume and intravascular protein did not change under neuroleptanalgesia compared with the conscious state. Urine osmolality and negative free water clearance (TcH2O) increased by about 60% under droperidol and fentanyl. In volume expanded dogs under neuroleptanalgesia intravenous application of 0.5-1.0 mg of atropine resulted in a temporary water diuresis.
In a group of 25 patients divided at random into subgroups anaesthetized by neuroleptoanalgesia or ataralgesia resp. on account of arthroscopy, the authors assessed the state of mental functions--perception, memory before, and after operation, emotional make-up, affectivity, cognitive functions and some personality parameters. By means of an algometer and the cuff of a manometer they assessed the threshold of pressure and ischemic pressure pain. They found that in no instance intraoperative experience appeared, the threshold of nociceptive pressure perception was considerably reduced after operation in both groups. The threshold of ischemic pressure pain was significantly reduced only in the group with Hb greater than 150 and Le greater than 8.0, anaesthetized by neuroleptanalgesia. A significant increase of the depressivity (5%) was recorded in the group with combined neuroleptoanalgesia. Dysphoria and emotional indifference increased (5%) in the group with neuroleptanalgesia. Within 2-4 hours after termination of anaesthesia significant consolidation of long-term memory occurred, whereby short-term memory did not display any changes in either group i.e. regardless of the type of anaesthesia. Attention was significantly improved after both types of anaesthesia, but more markedly after neuroleptanalgesia. In the group with combined neuroleptanalgesia sensory and neurasthenic complaints improved (5%). The degree of experienced fear and anxiety in conjunction with the operation as well other psychic parameters before operation were equal in both groups and the groups were thus equivalent. In relation to the plasma cortisol level (degree of preoperative stress) there was a close correlation between the emotional lability on the one hand and maladaptation on the other. The degree of preoperative stress created a close correlation between fear and maladaptation on the one hand and frightening experience on the other.
The literature concerning the value of the "small neuroleptanalgesia" for obstetrical pain-relieve is in dispute. Our experiences are based on the single application of 0.05 mg Fentanyl and 2.5 mg Droperidol on the presupposition of a well--proportionate labour activity with a cervix dilatation of at least 2-4 cm. Sporadically we reinject Fentanyl once more or exceptionally Droperidol, too. Among 308 primigravidae and 189 multigravidae with continuously directed application of Oxytocine the duration of the delivery was shortened distinctly compared with the control group without "small neuroleptanalgesia" but with the same tocergic treatment. After the application of the "small neuroleptanalgesia" the labour--intensity is unchanged, exceptionally a very short lessening in the immediate phase after injection. The method is innocuous for the mother, for the fetus and for the new-born. It is effective and practicable under all circumstances. The method of the "small neuroleptanalgesia" is recommended.
The influence of neuroleptanalgesia and halothane-N2O-anaesthesia on the activity of the sympathetic nervous system was studied continuously in the intra- and postoperative period in 2 groups of 10 patients undergoing abdominal operations. In the neuroleptanalgesia-group the noradrenaline level in plasma rose continuously during the course of the operation and this increase was highly significant. The adrenaline level in plasma increased as well, however this increase did not depend on the duration of the operation. In the halothane-N2O-group only a small increase of both adrenaline and noradrenaline in plasma could be demonstrated intraoperatively. One hour after the end of the operation the plasma levels of adrenaline and noradrenaline were elevated in both groups. The noradrenaline level was even higher after neuroleptanalgesia. Four hours after the end of surgery the levels of adrenaline and noradrenaline started to decrease, but were still above the preanaesthetic level. The increase of the concentration of catecholamines in plasma indicating an activation of the sympathetic nervous system was not associated with a corresponding increase in heart rate and blood pressure intra- as well as postoperatively in either group. Only in the neuroleptanalgesia-group was there a small, but insignificant increase of the systolic and diastolic pressure postoperatively.
Patients with chronic ischaemic heart disease and a history of myocardial infarction or who present with exertional or spontaneous angina suffer a decrease in left ventricular pump function during recovery from anaesthesia and in the period immediately after operation. This decrease is reflected in an increase in pulmonary capillary wedge pressure and in a decrease in stroke volume and cardiac output. Two groups of 10 such patients, clinically and haemodynamically comparable in the preoperative period, were studied: 10 patients received balanced anaesthesia, and 10 neuroleptanalgesia. The disturbance in left ventricular function was less pronounced with neuroleptanalgesia. A significant difference was noted between the groups with regard to pulmonary capillary wedge pressure during recovery from anaesthesia (balanced anaesthesia 15.8 +/- 4.4 mm Hg; neuroleptanalgesia 10.7 +/- 4.4 mm Hg; P less than 0.02). There was a relationship between type of anaesthesia and pulmonary capillary wedge pressure variations (P less than 0.01).
The serum activities of creatine kinase (CPK), aldolase (ALD) and alpha-hydroxybutyrate dehydrogenase (HBD) were determined in a group of Welsh Mountain ponies before and after a 30 minute period of neuroleptanalgesia induced by i.v. injection of Immobilon and terminated by i.v. injection of Revivon. There were slight but significant increases in the serum activities of CPK and HBD following neuroleptanalgesia, but no change in the serum activity of ALD. It is suggested that this form of neuroleptanalgesia may be associated, in ponies, with a degree of reversible myocardial hypoxic change, possibly as a result of coronary insufficiency.
Neuroleptanalgesia was induced in late pregnancy in guinea pigs with diazepam and fentanyl-fluanisone. Hypotension occurred, but the arterial acid-base status after 45-60 min was near normal. When repeated injections of fentanyl-fluanisone were given to maintain neuroleptanalgesia, the blood pressure fell further and severe metabolic acidosis developed. Placental blood flow determined with radioactive microspheres was much lower during maintained neuroleptanalgesia than in guinea pigs anaesthetized with diazepam and pentobarbitone.
In 66 patients who had to undergo radical abdominal hysterectomy because of cancer of the cervix uteri, the plasma concentrations of beta-endorphin were observed intra- and postoperatively. Two anaesthetic techniques were used: neuroleptanalgesia and thoracolumbar epidural analgesia with sedation and controlled inhalation of a mixture of oxygen and nitrous oxide. While the higher dosage of analgesics administered intraoperatively resulted in markedly lower plasma concentrations of beta-endorphin, there was no such effect in the postoperative phase. Patients with epidural analgesia who were absolutely painless postoperatively had, during that stage, higher concentrations of beta-endorphin in the plasma than those patients who had been given neuroleptanalgesia. They had received no analgetic treatment during the postoperative observation period. These differences are attributed to an increased adaptability of patients subsequent to neuroleptanalgesia. The neuronal block can result in a decrease in functional activity of the suprarenal medulla and impair adaptability. The stress-induced opioid analgesia can be suppressed by circulating enkephalin from the suprarenal medulla.
15 patients (12 women and 3 men) undergoing cholecystectomy were randomized into two groups. 8 patients were operated on under continuous thoracic epidural anaesthesia in combination with light general anaesthesia. Postoperatively they were kept painfree by continuous infusion of an 0.125% solution of bupivacaine via epidural catheter at a rate of 0.25-0.3 ml/kg X h over a period of four days. The 7 patients in the control group were operated on under neuroleptanalgesia. Piritramide was given for postoperative analgesia. All patients received 40 ml/kg X day of electrolyte solution during the period of investigation. Blood was collected at 8 am, 12 am, 4 pm, 8 pm, and 12 pm on the day of operation and on the third postoperative day, at 8 am on the first and second postoperative day, and at 8 am, 12 am, and 4 pm on the fourth postoperative day. Plasma glucose, ACTH, cortisol, T4, T3, and reverse T3 were measured. During the operation and for 12 h thereafter a mild hyperglycaemia was observed in the neuroleptanalgesia group but not in the epidural group. The differences were significant. A rise in ACTH was seen in both groups during and shortly after operation. The increase in cortisol concentration following this ACTH release was significant only in the neuroleptanalgesia, but not in the epidural group. From the first to the fourth postoperative day ACTH levels were low and cortisol concentrations within the normal range. On the third day it appeared that a diurnal variation in cortisol levels was again present. Cortisol suppression following the administration of 2 mg dexamethasone on the fourth postoperative day was detectable in both groups. Of the thyroid hormones, T4 remained unchanged and at a normal level during the investigation. T3 decreased and reverse T3 increased significantly, the maximum rise being observed on the second day. There were no differences between the groups. These changes are defined as low T3 syndrome, following caloric deprivation, injury, and stress. The metabolic and hormonal alterations caused by cholecystectomy are marked only during operation and shortly thereafter and only in this period are they influenced by epidural analgesia. From the first postoperative day onwards they are almost negligible so that a mitigation by using continuous epidural analgesia is not to be expected.
Application of 0.1 mg Fentanyl and 5 mg Droperidol iv. (obstetric neurolept-analgesia) causes an enduring pain relief. Labor is not influenced. The obstetric neuroleptanalgesia appears to accelerate labor indirectly. The condition of the fetus will be not affected by obstetric neuroleptanalgesia. In respect of this obstetric neuroleptanalgesia can be recommended as a method of analgesia during parturition.
Neuroleptanalgesia describes a state of sedated analgesia produced by the administration of the tranquilizer, droperidol, and the potent narcotic, fentanyl, in combination. This combination of drugs was administered intravenously to effect neuroleptanalgesia in the early treatment of eight patients with acute anterior transmural myocardial infarction. Criteria for inclusion in the study were (1) persistent ischemic pain, (2) ST segment elevation of 0.3 or more mV in at least two standard precordial leads, (3) a heart rate of 80 or more beats per minute, (4) a mean arterial pressure of 75 or more mm Hg, and (5) a cardiac index of 2.0 L/min/m(2). Within 30 minutes of the administration of the drugs, all patients were relieved of pain and emotional stress. The sum of ST segment elevation from leads V(1) through V(6) (sigmaST(6)) and the average ST elevation over the precordium (ST) decreased significantly by 57% and 56%, respectively. At the same time, there was a significant reduction in heart rate (from 112 +/- 17 to 86 +/- 8 beats per minute), mean arterial pressure (from 100 +/- 7 to 82 +/- 4 mm Hg), and pulmonary arterial wedge pressure (from 17 +/- 7 to 12 +/- 2 mm Hg). The cardiac index increased from 2.25 +/- 0.22 to 2.40 +/- 0.07 L/min/m(2). Two hours later the hemodynamic parameters had returned to control levels, but the beneficial effect on myocardial injury persisted. Thus neuroleptanalgesia in the early hours of myocardial infarction can reduce preload, afterload, oxygen demand, and eventually the infarct size without depressing myocardial function.
The use of neuroleptanalgesia in acute myocardial infarction offers the possibility of reducing pain and emotional stress. The influence of such treatment on hemodynamic parameters (heart rate, cardiac output, stroke volume, peripheral resistance, systemic blood pressure, and pulmonary pressure) and on the plasma level of adrenaline and noradrenaline has been studied in 6 patients with acute myocardial infarction. This results demonstrate that during neuroleptanalgesia the already elevated levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the patients with the highest initial levels of catecholamines. Since the peripheral resistance and systolic and diastolic blood pressures decrease concomitantly, it is concluded that the increase in levels of noradrenaline and adrenaline further increase. This increase was most pronounced in the plasma catecholamines is due to a reaction of the sympathetic nervous system to the alpha-adrenergic receptor blocking activity of droperidol causing vasodilation. The data indicate that pain, emotional stress, and anxiety in the acute phase of myocardial infarction do not play the expected essential role for the activation of the sympathetic nervous system generally observed in acute myocardial infarction. Additionally, the data demonstrate that drugs producing a vasodilation can have a deteriorating effect on the hemodynamic situation and that a reduction of the afterload by vasodilating drugs can result in a further increase in the release of catecholamines.
Women undergoing interval laparoscopic electrocoagulation sterilization were randomly assigned to one of three neuroleptanalgesia regimens. The 299 women received either morphine (10 mg)/droperidol (2.5 mg)/atropine (0.3 mg) or pethidine (100 mg)/droperidol (2.5 mg)/atropine (0.3 mg) or pethidine (100 mg)/droperidol (2.5 mg). A significantly higher proportion of anesthesia complications were recorded in the morphine group. The amount of pain experienced by the women was similar in the three groups, as were the rates of early follow-up complications and complaints. The neuroleptanalgesia regimen containing pethidine/droperidol/atropine appears to be the safest and most effective of the three considered here.
Flunitrazepam or diazepam with atropine and a combination of phenoperidine, droperidol and cyclizine (neuroleptanalgesia) were compared as premedication in three groups of 25 patients undergoing routine upper gastrointestinal endoscopy. Drug doses were titrated carefully against response and all three regimes were found to be similar in terms of safety, patient co-operation, relaxation and speed of recovery. Neuroleptanalgesia however produced a statistically significant rise in endtidal pCO2 and systolic blood pressure. The benzodiazepines, and in particular flunitrazepam, produced a significantly greater amnesia for the procedure, patients given these drugs being more willing to undergo repeat endoscopy.
In eight patients, following carotid angiography under neuroleptanalgesia, a radiopaque dye was instilled into the pharynx. The chest was x-rayed 15 min later. All eight patients were observed to have aspirated the dye. The technique of neuroleptanalgesia described should not be used without safeguarding the airway in patients liable to regurgitate and inhale gastric contents.
The aim of the present work was to determine the likelihood of lipid peroxidation in the lungs of rats subjected to neuroleptanalgesia and its components. In particular, the effect of fentanyl, droperidol, a nitrous oxide/oxygen mixture when used separately or in combination, on the lung level of lipid peroxidation was investigated. The in vitro antioxidant properties of fentanyl and droperidol were also tested. Lipid peroxidation was evidenced by the endogenously generated conjugated dienes and fluorescent products of lipid peroxidation and the decrease in lung vitamin E content. It was found that fentanyl and droperidol, used separately or in combination, did not induce lipid peroxidation in the rat lung, while the exposure of rats for 120 min to a nitrous oxide/oxygen mixture (2:1 v/v) led to well-expressed peroxidation. The (N2O + O2)-pro-oxidant action was significantly inhibited in rats previously injected with fentanyl and/or droperidol. The results show that the application of fentanyl, droperidol and (N2O + O2), as in neuroleptanalgesia, ensures minimal lipid peroxidation in the lung. In addition, we found that fentanyl and droperidol were able to inhibit the Fe(2+)-catalysed lipid peroxidation in lung homogenate. We speculate that the inhibitory effect of fentanyl and/or droperidol on the (N2O + O2)-induced lipid peroxidation in the rat lung may be caused directly by their antioxidant properties. However, another explanation seems to be possible. The free radicals that are produced during the metabolism of fentanyl and droperidol may react with the radicals generated during the one-electron reduction of nitrous oxide. Such reactions will obviously reduce the free radical concentration in the organism and, hence, the likelihood of initiating lipid peroxidation.