Medical documentation: the value of scoring systems and databases in intensive care medicine.
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Biomedical subjects
Publications and source records attributed to C K Spiss.
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Patients receiving anticonvulsant drugs chronically are relatively resistant to some non-depolarizing neuromuscular blocking drugs. We investigated the influence of chronic carbamazepine therapy on neuromuscular block induced by mivacurium in 20 otherwise healthy individuals undergoing neurosurgical operations, 10 of whom were receiving chronic treatment with carbamazepine and the other 10 served as controls. The median duration of carbamazepine therapy was 22 weeks (range 4-182 weeks). After premedication with oral diazepam, anaesthesia was induced with fentanyl and thiopentone and maintained with 0.5% isoflurane and nitrous oxide in oxygen. The ulnar nerve was stimulated and the evoked electromyogram recorded using a Datex NMT monitor. Mivacurium 0.15 mg kg-1 (2 x ED95) was given as a bolus i.v. Based on the response to the first of four stimuli, lag time, onset-time, times to recovery to 10%, 25%, 50% and 75% of baseline responses and recovery index (RI 25-75%) did not differ between the two groups. We conclude that mivacurium-induced neuromuscular block was not influenced by preceding chronic carbamazepine therapy.
We have evaluated the effects of a single bolus dose of rocuronium 0.6 mg kg-1 (group 1, n = 10) or vecuronium 0.1 mg kg-1 (group 2, n = 10) on intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and heart rate (HR) in 20 neurosurgical patients undergoing mechanical ventilation of the lungs during continuous sedation with sufentanil and midazolam. Before and after neuromuscular block using twice the ED90 of the blockers, ICP, MAP, CPP and HR were recorded continuously for 15 min. Treatment caused no significant changes in ICP, CPP or MAP and there was no evidence of histamine release. Mean maximum block in the rocuronium group was slightly less than that in the vecuronium group (95.9 (3.1)% vs 100%; ns) The difference between the two groups in onset time (rocuronium 142 (62) s, vecuronium 192 (64) s; P = 0.04) was significant. Patients in the rocuronium group showed a slight (7(4)%) but significant (P = 0.003) increase in heart rate.
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BACKGROUND: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction. METHODS: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold. RESULTS: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01). CONCLUSIONS: Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.
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We investigated the effect of clonidine in 19 patients having lumbar disc surgery under nitrous oxide/isoflurane/relaxant anaesthesia. The EEG, spinal and cortical somatosensory evoked potentials, and the brainstem auditory evoked potentials were recorded. After equilibration of the general anaesthetic, two successive infusions of clonidine (5 micrograms.kg-1) were given. After the second infusion of clonidine, the plasma concentration increased from 0.2(SEM 0.05) to 6.4(SEM 0.06) ng.ml-1 (p < 0.05). In the EEG, delta-activity was maintained, but the beta-fraction, and the 95% and 50% spectral frequencies were reduced. Total EEG power progressively decreased from 296(152-397) microV2 to 108(51-240) microV2. The somatosensory evoked spinal potential (N13) decreased in amplitude, (1.77(SEM 0.35) microV to 1.59(SEM 0.35) microV, p < 0.05) and increased in latency (14.37(SEM 0.29) ms to 14.69(SEM 0.31) ms, p < 0.05). The central conduction time increased from 6.47(SEM 0.16) ms to 6.92(SEM 0.25) ms, ns. There was no effect on the cortical somatosensory potentials, or the brainstem auditory evoked potentials. According to the EEG spectral indices, anaesthesia appeared to deepen despite a reduction in the end expiratory isoflurane concentration from 0.53(SEM 0.07) to 0.28(SEM 0.06) vol%, which indicated a reduction in anaesthetic requirements following clonidine.
Comparative measuring of epidural pressure using the Spiegelberg probe 1 and ventricular fluid pressure was carried out in 15 neurosurgical intensive-care patients. Deviations in both directions were established, with a trend toward overestimating ventricular pressure in epidural pressure measuring (r = 0.77). Individual pulsations, spontaneous wave courses and therapy-induced pressure changes were reflected without delays. There were no complications observed with probe implantation periods for up to 6 days. The system has been shown to be mechanically stable and easy to implant. We believe the device to be fit for trend monitoring of intracranial pressure. As with other epidural pressure monitoring systems, false assessments of ventricular pressure may lead to wrong decisions as to required therapy.
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Coeliac plexus block, an established method of treatment for pain associated with pancreatitis and cancer, was used in neurosurgical patients with gastrointestinal dysfunction. The study was performed in 16 patients whose gastric reflux volume exceeded 600 ml per day for 3 consecutive days. Patients were allocated to a block group (n = 8) or a control group (n = 8). Coeliac plexus block was accomplished with a modified Moore technique using 50 ml bupivacaine 0.25%. In the block group, gastric reflux volumes for 3 days preceding coeliac plexus block and 3 consecutive days following coeliac plexus block were analysed. In the control group, gastric reflux volumes were observed over a period of 6 days. Mean (SEM) gastric reflux volume decreased significantly following coeliac plexus block from 770 (50) ml to 60 (30) ml (p < 0.01). In the control group, gastric reflux remained unchanged over the corresponding periods (730 (60) ml c.f. 670 (50) ml). The response of gastric reflux volume to coeliac plexus block suggests that the mechanism is related to inhibition of sympathetic activity in patients whose sympathetic drive is increased due to the underlying neurological disease, and possibly due to sedation withdrawal symptoms.
The effects of tracheobronchial suction before and after neuromuscular blockade with vecuronium (0.12 mg.kg-1; ED95 x 2; group A) and atracurium (0.4 mg.kg-1; ED95 x 2; group B) on intracranial pressure were studied in 18 neurosurgical patients with a Glasgow Coma Scale < 7. Despite adequate sedation, moderate to severe diaphragmatic movements (bucking and coughing) in response to carinal stimulation with significant increases in intracranial pressure (A: 18 SD 7 to 24 SD 8 mmHg; B: 19 SD 7 to 27 SD 5 mmHg) and subsequent decreases in cerebral perfusion pressure (group A: 69 SD 11 to 63 SD 8 mmHg; group B: 63 SD 11 to 59 SD 17 mmHg) could be observed without muscle relaxation. After a bolus dose of vecuronium or atracurium, profound neuromuscular paralysis quantified by the post-tetanic count, was observed after an onset time of 253 SD 72 s (vecuronium) and 159 SD 54 s (atracurium). Slight diaphragmatic movements could be elicited in only two patients in group A and in two patients in group B during tracheal suction; intracranial pressure (group A: 20 SD 8 to 20 SD 8 mmHg; group B: 19 SD 7 to 19 SD 7 mmHg) and cerebral perfusion pressure (group A: 65 SD 13 to 65 SD 13 mmHg; group B: 66 SD 12 to 65 SD 11 mmHg) remained unchanged. When coordinating respiratory therapy in neurosurgical intensive care patients, profound neuromuscular block, quantified by a post-tetanic count of at least 5 for vecuronium and 1 for atracurium, it is necessary to rule out any impact of diaphragmatic movement on intracranial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
The hemodynamic effects of a propofol infusion adjusted to achieve and maintain a burst-suppression pattern [episodes of depressed background activity (electrical silence) more than 4 s alternating with a high-voltage slow activity], were studied in 10 patients without cardiorespiratory disease undergoing elective neurosurgical interventions. Propofol infusion was started after a bolus dose of 1 mg/kg at a rate of 20 mg.kg-1 x h-1, reduced after 30 min to 15 mg.kg-1 x h-1, and terminated after 60 min (1926 +/- 346 mg cumulative propofol dose, maximal serum concentration 9.2 +/- 2.9 micrograms/dL; mean +/- SD). Hemodynamic data and arterial blood samples were collected during a sedated, resting control period, and then every 15 min during drug infusion. Lactated Ringer's solution was infused at a rate sufficient to maintain pulmonary capillary wedge pressure at or above control levels (20-30 mL.kg-1 x h-1). Burst-suppression pattern in the electroencephalogram was achieved after 15.7 +/- 3.2 min and maintained until 10.9 +/- 2.6 min after the propofol infusion was terminated. Significant decreases (% of control, Friedman and Wilcoxon Wilcox test, P < 0.05) were found in heart rate (19%), mean arterial pressure (20%), cardiac index (23%), and left ventricular stroke work index (26%). No adverse consequences were caused by the propofol or crystalloid infusion. The results demonstrate that doses of propofol sufficient to silence the electroencephalogram are associated with venodilating and myocardial depressant properties. However, propofol can be administered with minimal hemodynamic risk in healthy patients when cardiac filling pressures are maintained by intravenous fluid administration.