British journal of anaesthesia
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We have examined the time course of, and relationship between, primary and secondary hyperalgesia after thermal injury to the skin in humans. Burn injuries (15 x 25 mm rectangular thermode, 49 degrees C, 5 min) were produced in eight healthy, unmedicated male volunteers, on the medial side of the right calf, on two occasions at least 8 days apart. Heat pain detection thresholds (HPDT), heat pain tolerance (HPT), mechanical pain detection threshold (MPDT) and the intensity of burn-injury induced erythema (skin erythema index, SEI) were assessed inside the burn injury. ⋯ The time course of the intensity of primary hyperalgesia was related closely to that of changes in area of secondary hyperalgesia, and hyperalgesia outside the injury did not outlast hyperalgesia inside the injury in any volunteer. These findings suggest post-injury development of secondary hyperalgesia to be a dynamic process, closely related in time to a peripheral nociceptive input, with reversal to normal when the peripheral lesion disappears. These observations may be relevant to the concept of "pre-emptive" analgesia.
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We describe a new indicator dilution method of measuring cardiac output in man. A bolus injection of lithium chloride 0.6 mmol was given via a central venous catheter and arterial plasma [Li+] recorded using a specially developed sensor incorporating an Li(+)-selective electrode. Cardiac output was derived from the lithium dilution curve, with a correction for packed cell volume. ⋯ For each sensor, one LiDCO was measured immediately before and one immediately after three TD estimations and mean values of LiDCO and TD derived. The correlation coefficient, r, was 0.89; slope of the regression 0.84; y intercept 0.72; bias 0.3 (0.5) litre min-1 (mean (TD-LiDCO) (1 SD). LiDCO appeared to be a safe, simple and accurate technique which does not require insertion of a pulmonary artery catheter.
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Editorial Comment Review
Postdural puncture headache and extradural blood patch.
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Ten healthy patients and 25 patients with cirrhosis of the liver (10 Child's A, 10 Child's B and 5 Child's C) received a bolus dose of mivacurium chloride 150 micrograms kg-1. The electromyographic response was monitored throughout anaesthesia until recovery of the first twitch of the train-of-four (TOF) (T1/T0) to at least 85% and the TOF ratio (T4:T1) to at least 80%. There was no significant difference between the two groups in the onset of neuromuscular block, but recovery was prolonged in the cirrhotic group compared with the healthy patients (respective mean times to recovery of T1/T0: to 5% = 20.2 vs 11.2 min (P < 0.05); to 10% = 23.8 vs 13.4 min (P < 0.005); to 25% = 28.4 vs 16.6 min (P < 0.005); to 50% = 41.1 vs 20.1 min (P < 0.005); to 75% = 43.8 vs 24.9 min (P < 0.005). ⋯ Recovery was most prolonged in the Child's C patients. Mean plasma cholinesterase activity was less in the cirrhotic compared with the healthy group (mean 582 (SD 254) iu litre-1 vs 1125 (303) iu litre-1) (P < 0.001) and there was a significant negative correlation between plasma cholinesterase activity and all the indices of recovery (P < 0.001 for all except recovery index (P < 0.01)). We conclude that patients with hepatic cirrhosis may be sensitive to mivacurium, which could be explained, at least in part, by the lesser plasma cholinesterase activity.
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We have studied the effects of bolus doses of midazolam 0.15 mg kg-1 i.v. on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) in 12 patients with severe head injury (Glasgow Coma Scale score < or = 6). The study was performed in patients aged 17-44 yr who were sedated (phenoperidine 20 micrograms kg-1 h-1) and paralysed (vecuronium 2 mg h-1). Midazolam reduced MAP from 89.0 mmHg to 75.0 mmHg (P < 0.0001), while CPP decreased from 71.0 mmHg to 55.8 mmHg (P < 0.0001). ⋯ However, when control ICP was less than 18 mmHg (n = 7 patients), an increase in ICP was observed. The remaining five patients (control ICP > or = 18 mmHg) exhibited a slight decrease in ICP. These findings suggest that bolus administration of midazolam should be performed with great caution in patients with severe head injury, especially when ICP is less than 18 mmHg.