Epidural analgesia for labour.
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Biomedical subjects
Publications and source records attributed to R Segstro.
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PURPOSE: Arteriovenous malformations (AVM) of the spinal cord are rare. We report the successful management of a patient with a cervical spinal cord AVM undergoing Caesarean section delivery, using a spinal anaesthetic. CLINICAL FEATURES: Based on previous radiological investigations, the patient was known to have an AVM at the third cervical level of her spinal cord. After application of monitors and intravenous administration of 1 L normal saline, a 25 g Whitacre needle was inserted into the subarachnoid space at the L3-4 interspace. Spinal anaesthesia was established with a solution consisting of hyperbaric spinal bupivacaine 12 mg, fentanyl 12.5 micrograms and epidural morphine 0.25 mg. There was no neurological deficit during hospital stay or after discharge. CONCLUSION: The safe outcome of spinal anaesthesia for our patient is encouraging. The presence of spinal cord AVM at the cervical region is not an absolute contraindication to spinal anaesthesia.
Intrathecal meperidine administration can provide surgical anaesthesia and postoperative analgesia for about two to six hours. We have observed two cases of respiratory depression associated with meperidine spinal anaesthesia. An 81-yr-old woman received 50 mg intrathecal meperidine for inguinal hernia repair. Supplemental oxygen was administered at 3 L.min-1 by nasal prongs. About 40 min later, the patient's oxygen saturation decreased from 97% to 87% and she was asked to take big breaths. She responded immediately and oxygen saturation returned to 97%. Two more similar episodes followed in the next five minutes. Naloxone 0.1 mg iv was administered and the oxygen saturation remained at 96-97% until completion of surgery about 15 min later. She had an uneventful recovery. A 24-yr-old healthy woman presented for tubal ligation eight hours after vaginal delivery of an infant. The surgical procedure was performed under spinal anaesthesia produced by 50 mg meperidine. During surgery, midazolam 2 mg iv was given for anxiolysis. About five minutes after admission to the postanaesthesia care unit, the patient's respiratory rate decreased to ten breaths per minute and oxygen saturation decreased to 89%. Supplemental oxygen at 3 L.min-1 was administered by nasal prongs. The patient was encouraged to take big breaths and the arterial oxygen saturation rapidly increased to 98-99%. Forty minutes later, nasal oxygen was discontinued. The patient maintained her oxygen saturation while breathing room air. She was then discharged to the ward and had an uneventful recovery course. We recommend that a patient's respiratory variables and oxygenation be closely monitored for at least one hour after intrathecal meperidine administration.
This prospective, randomized, double-blind trial evaluated the efficacy of rectal indomethacin as an adjunct to morphine for controlling postoperative pain. Fifty healthy patients undergoing elective hip arthroplasty were investigated. Group 1 (n = 25) received placebo suppositories, Group 2(n = 25) received indomethacin suppositories, 100 mg q8hr for five doses, starting at the end of the procedure. Both groups received morphine via a PCA pump, which recorded the amount of morphine delivered each hour. After a standardized general anaesthetic, PCA was begun in the recovery room. Pain was measured with a standard 100 mm VAS at 2, 6, 20, 28, 42 hr after surgery and the morphine consumption recorded. Over the 42-hr study period, patients in Group 2 required less morphine than those in Group 1 (34.8 +/- 21.8 mg vs 89.6 +/- 43.7, P less than 0.01). Pain scores were lower in Group 2 at 20, 28, 42 hr postoperatively. The incidence of side-effects did not differ between groups and no patient had excessive postoperative bleeding. The combination of indomethacin and morphine provided superior pain relief to morphine alone even though the control group had liberal access to morphine. This synergistic effect would make indomethacin a useful adjunct to intramuscular or epidural narcotics.
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Intravenous administration of hypotensive doses (30-200 micrograms/kg) of nifedipine to cats anesthetized with pentobarbital caused an increase in cardiac output accompanied by hepatic venoconstriction. The hepatic venoconstriction and the increase in cardiac output were abolished in animals in which the hepatic sympathetic nerves were cut, the adrenal glands were excluded, and the kidneys were removed. This contrasts with the indirect hepatic venoconstrictor action of isoproterenol which was shown previously not to be abolished by these procedures. Further experiments showed that the hepatic venoconstrictor effect of nifedipine was blocked by removal of the kidneys, but not by removal of the hepatic sympathetic nerves and adrenals. These results support the hypothesis that venoconstriction plays an important role when drugs produce increased cardiac output. In nephrectomized animals, nifedipine had no direct effects on hepatic blood volume and it did not alter the effects of infusions of norepinephrine on hepatic blood volume, which have previously been shown to be mediated through alpha 2-adrenoceptors. However, it did reduce the hepatic venous responses to hepatic sympathetic nerve stimulation by 30%.
Previous studies have suggested that sympathetic effects on hepatic blood volume may be mediated through alpha-2 adrenoceptors in anesthetized cats as prazosin did not block whereas phentolamine and phenoxybenzamine impaired these responses markedly. In this study we have shown that yohimbine blocks hepatic volume responses to both nerve stimulation and norepinephrine infusions. In comparison with norepinephrine, phenylephrine had much weaker effects on hepatic blood volume than on arterial and portal pressures. Clonidine produced a slow weak contraction of the hepatic venous bed which was blocked by yohimbine but not by prazosin. alpha-Methylnorepinephrine produced a norepinephrine-like contraction of the hepatic venous bed which was blocked by yohimbine but not by prazosin. Taken together, these data suggest that hepatic blood volume responses to both sympathetic nerve stimulation and infusions of catecholamines are mediated through alpha-2 adrenoceptors, whereas portal pressure responses are mediated through both alpha-1 and alpha-2 adrenoceptors.