Intrathecal diamorphine for postoperative analgesia after caesarean section.
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Biomedical subjects
Publications and source records attributed to D M Levy.
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BACKGROUND: Hypoventilation may occur following induction of anaesthesia with propofol and is potentiated by concurrent use of opioid drugs. This effect is undesirable in patients who will continue to maintain spontaneous respiration during anaesthesia and surgery. The analeptic drug doxapram is known to have selective respiratory stimulatory effects but its action during induction of anaesthesia has been inconsistent. METHOD: In a double-blind, placebo-controlled study, the influence of alfentanil pre-treatment on the ventilatory effects of doxapram given during induction of anaesthesia with propofol was studied in 40 patients. Four groups of ten patients (two groups pre-treated with 7 micrograms.kg-1 of alfentanil and two groups with saline) were randomly allocated to receive either 0.5 mg.kg-1 doxapram or saline following infusion of propofol to loss of verbal contact. RESULTS: In the groups that received doxapram, minute volumes were significantly increased and end-tidal carbon dioxide concentrations were significantly reduced compared to control groups, although the duration and extent of these effects were less in the group that received alfentanil. Doxapram also reversed an alfentanil-induced reduction in respiratory rate. No adverse cardiovascular or neurological stimulatory effects of doxapram were evident at any time. CONCLUSION: We conclude that doxapram 0.5 mg.kg-1 is effective in augmenting ventilation that has been obtunded following induction of anaesthesia with propofol in patients pre-treated with alfentanil.
Vasoactive intestinal polypeptide (VIP) and substance P (SP) immunoreactivity are reduced in the cutaneous nerves of diabetic patients with peripheral neuropathy. The functional significance of this finding was studied by measuring the forearm sweat response to intradermal methacholine and the effect of coadministration of VIP and SP in six normal subjects, and in six diabetic patients with neuropathy and eight without. Flare responses to the two peptides were also measured. Methacholine-induced sweat output was significantly greater in neuropathic patients compared with the other groups (p < 0.05), suggesting upper limb denervation supersensitivity. VIP and SP alone did not evoke sweating in any subject. Injection of VIP or SP reduced methacholine-induced sweating to a similar degree in all groups, except that the reduction was smaller in the non-neuropathic group than in the others (p = 0.028 versus normal subjects, p = 0.014 versus neuropathic diabetic patients). Flare responses to the peptides were markedly reduced in the neuropathic patients compared with the other groups (p < 0.01). In neuropathic patients, increased sweat responses and decreased flare coexist with diminished neurophysiological measurements; cutaneous sweating and flare responses provide valuable additional information to conventional methods of neurological assessment in diabetic neuropathy.
Anaesthesia was induced in 30 ASA I patients by propofol titrated at 100 mg min-1 to loss of verbal contact, and maintained by infusion of propofol at 10 mg kg-1 h-1 with 100% oxygen. According to randomization, either alfentanil 30 micrograms kg-1 ketamine 1.5 mg kg-1, or 0.9% sodium chloride was injected over 20 s, followed 1 min later by vecuronium 0.08 mg kg-1. Mean arterial pressure and heart rate were measured before and after induction, and 1 and 2 min after analgesic or saline. Onset of neuromuscular block was measured by the evoked hypothenar electromyographic response to train-of-four supra-maximal stimuli at 0.1 Hz. There were significant haemodynamic differences between groups, but mean (SD) times to reduction of T1/control ratios below 95% were 114 (28.0), 106 (19.0) and 128 (34.3) s (P = 0.2, ANOVA). Supplementation of propofol anaesthesia with alfentanil or ketamine does not appear to influence the onset time of vecuronium.
The purpose of this report is to describe a new complication of epidural blood patch for inadvertent dural puncture. A dural tap in an obstetric patient was managed initially with a prophylactic blood patch via the epidural catheter. Despite this, 48 hr later, she developed post-dural puncture headache, neck, and shoulder pain, and was given a second epidural blood patch. This was followed by an immediate and severe exacerbation of her symptoms, which later resolved after the administration of diclofenac. There were no further sequelae. Although severe complications of epidural blood patch are rare, they are alarming. Exacerbation of the original symptoms of post-dural puncture headache caused by, or following, epidural blood patching has not previously been reported.
Gastric emptying was studied indirectly by paracetamol absorption in 20 patients at 8-12 weeks' gestation and also in 20 non-pregnant controls. Subjects received paracetamol 1.5 g in a tablet with 50 ml of water and remained semi-recumbent for 2 h while venous blood samples were obtained at 15-min intervals. The maximum concentration of paracetamol was significantly lower and the time to maximum concentration significantly greater in pregnant patients. In addition, the areas under the time-concentration curves at 60 and 120 min were significantly smaller in the pregnant group. These changes are indicative of a delay in gastric emptying at 8-12 weeks' gestation.
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Image-analysis was used to measure nerves immunoreactive to the general neuronal marker protein gene product 9.5 (PGP 9.5-IR) and the neuropeptides calcitonin gene-related peptide and vasoactive intestinal polypeptide in standardised leg skin biopsies of three age-matched groups of young subjects: non-diabetic (n = 14), diabetic patients with normal small fibre function ("non-neuropathic", (n = 11) and diabetic patients with abnormal small fibre function ("neuropathic", n = 11). Depletion of nerves and neuropeptides was most marked in the epidermis, where calcitonin gene-related peptide-immunoreactivity was more frequently absent than PGP 9.5-IR in diabetic patients. Epidermal PGP 9.5-IR nerve area and counts were reduced in neuropathic compared with normal subjects (p less than 0.001), as were epidermal calcitonin gene-related peptide nerve counts (p = 0.003). Sweat gland PGP 9.5 and vasoactive intestinal polypeptide, which may be involved in sweat production, showed no diminution in diabetic patients (area: p = 0.160, p = 0.372 by ANOVA). Two diabetic patients showed elevated sweat gland PGP 9.5-IR and three had increased sweat gland vasoactive intestinal polypeptide; this may represent nerve proliferation. In local sweat tests, acetylcholine-stimulated sweat output was associated with increased immunoreactivity, while the sympathetic skin response showed inverse correlations with immunoreactivity. There were no consistent changes with other commonly-used neurophysiological tests. HbA1 correlated negatively with immunohistochemical measurements. Neuropeptide changes were seen in the absence of macro- and microvascular disease, and epidermal nerve depletion occurred in patients with normal thermal thresholds and cardiac autonomic function.(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between dynamic pupillary function and peripheral nerve function was studied in 85 randomly-selected diabetic patients and 67 age-matched normals using a portable infrared pupillometer (Pupilscan Version 5). Seven measurements were chosen to represent different components of the pupillary constriction-redilatation curve after a standardized light stimulus. Constriction latency was significantly prolonged in diabetic patients (p = 0.05), as was time to 63% redilatation (p = 0.001). Thermal thresholds at the feet weakly correlated with relative reflex amplitude (warm: r = -0.22, p = 0.05; cool: r = -0.23, p = 0.05), but vibration perception thresholds were more strongly associated with constriction and redilatation velocity (r = -0.42, p = 0.001; r = -0.28, p = 0.03). Among the cardiovascular autonomic function tests, only respiratory R-R variation correlated with constriction velocity (r = 0.47, p < 0.001), and Valsalva ratio with redilatation velocity (r = 0.25, p = 0.04), but postural systolic blood pressure change was also correlated with reflex amplitude and latency time (r = -0.42, p < 0.001; r = 0.41, p = 0.001). There were no significant associations with three measures of sweating function in the feet. Pupil measurements were abnormal in 4-11% of diabetic patients, while other neurological tests were abnormal in 8-35%, consistent with the length-dependence of diabetic neuropathy. Median coefficients of variation were 2.0-7.2% in diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The sympathetic skin response (SSR) at the foot to a deep inspiration was measured in 68 randomly selected diabetic patients and 46 age matched normal subjects and compared with other quantitative measures of neurological and sudomotor function. SSR was obtained in all but three diabetic patients. The upper limit of normal for the onset latency was 2202 ms and the lower limit for the amplitude of the first wave 92 microV. Ten diabetic patients had measurable but prolonged latencies, and 11 had measurable but low amplitudes. There were no significant associations between latency, height, and age, but in insulin dependent patients there was a significant diminution of response amplitude with increasing duration of diabetes. Latency was weakly associated with Marstock thermal thresholds, respiratory RR variation, and common peroneal nerve conduction velocity. SSR amplitude was associated with the density of pilocarpine activatable sweatspots in the same region of the foot. Patients with abnormal latencies were significantly older and had reduced thermal sensation than those with normal latencies. Median coefficients of variation for repeat testing in diabetic patients were 9% for latency and 13% for amplitude. The test is objective and reproducible, but latency measurements reflect conduction in a long multineuronal pathway and are not purely a measure of peripheral C fibre function; amplitude measurements reflect the density of spontaneously activable sweat glands and are therefore a valid measure of peripheral sympathetic activity, though they depend more on temperature than do latencies (mean change over the range 32-34 degrees C; 8.5% degrees C for amplitude, -2.5%/degrees C for latency).
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Peripheral small-fibre denervation has been reported to result in decreased activation of eccrine sweat glands to muscarinic cholinergic agents. Using computerised image-analysis of pilocarpine-activated sweatspot prints of a 4 cm2 area of the dorsum of the foot in 79 randomly selected diabetic patients we have identified a group of neuropathic patients (18%) with decreased sweatspot activation (less than 20/cm2), and a smaller group (6%) of younger patients with less marked neuropathy who had increased activation (greater than 132/cm2), probably resulting from denervation supersensitivity. The associations between sweatspot density and other conventional tests of peripheral nerve function were weak. The prevalence of abnormal sweatspot density, 24%, was similar to that of other tests, except thermal thresholds at the feet (35-37%), which were not correlated with sweatspot activation, suggesting that diabetic neuropathy has differing effects on afferent and efferent small fibres. The method is rapid and reproducible (median coefficient of variation 14%) and its ability to identify patients with increased, as well as decreased, peripheral nerve function may be of value in the characterisation and longitudinal follow-up of small-fibre abnormalities in diabetes.