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.

Coordination of respiratory care with protection of the brain is critical in neurosurgical intensive care. Therefore, in addition to hyperventilation, adequate sedation and muscle relaxation are applied to mitigate the difficulties with control of intracranial pressure (ICP) during routine tracheobronchial suctioning (TBS). Although hypnotics have been shown to be effective in mitigating increases in ICP in response to endotracheal suctioning in paralyzed patients, brisk bucking and coughing with further increases in ICP may occur without muscle relaxation. Long-term neuromuscular (nm) paralysis may be undesirable in neurosurgical critical care because clinical evaluation with early detection of neurological deterioration will be impossible in the paralyzed patient. Therefore, the effects of TBS without and after nm blockade with an intermediate-acting nondepolarizing muscle relaxant on ICP were studied. Patients and Methods. Nine patients with moderate increases in mean ICP of 19.2 +/- 8 mmHg due to head injuries and spontaneous subarachnoid hemorrhage were investigated. All patients were on-line sedated with midazolam and sufentanil and controlled ventilation was adjusted to maintain a paCO2 of 30 +/- 2 mmHg. Respiratory and hemodynamic parameters and ICP (epidural probe) were continuously monitored and recorded on an integrated data bank. After a bolus dose of propofol, routine TBS was performed without the use of muscle relaxants. Before the next TBS, nm monitoring was initiated and train-of-four (TOF) stimulation was imposed at the ulnar nerve using supramaximal pulses. The response of the adductor pollicis muscle was recorded by accelerometry. After supramaximal stimulation had been achieved, a bolus dose of 2 times the ED95 of vecuronium (0.12 mg/kg) was given. Depth of nm blockade was quantified by the posttetanic count (PTC). ICP and CPP were measured before, during, and after TBS. Diaphragmatic movement, bucking, and coughing were registered by visual observation and graded as absent, slight, moderate, or severe. Statistics. Student's t-test and the Wilcoxon test for paired data (P < 0.05; values as xBAR +/- SD) were used. Results (see Table and Figure). Despite adequate sedation, moderate to severe diaphragmatic movements in response to carinal stimulation with significant increases in ICP (18.2 +/- 7 to 24 +/- 8 mmHg) and subsequent decreases in cerebral perfusion pressure (CPP) (68.9 +/- 2 to 62.4 +/- 8 mmHg) could be observed without muscle relaxation. After a bolus of vercuronium, profound nm paralysis quantified by a PTC of 5 was observed after an onset time of 4.2 +/- 1 min. ICP (20.2 +/- 8 vs. 20.1 +/- 8 mmHg) and CPP (64.9 +/-13 vs. 64.8 +/- 13 mmHg) remained unchanged. Slight diaphragmatic movements could be elicited in only two patients during TBS. Discussion. TBS is a potent trigger of diaphragmatic movement, bucking, and coughing by reflex activation of the phrenic nerve. A major determinant of the magnitude of ICP increase during TBS is the transmission of the cough-induced increase in intrathoracic pressure to the cerebral venous system. Vecuronium was utilized for nm blockade because of its proven lack of cerebral and cardiovascular side effects, its relatively short onset, and its intermediate duration of action. Despite the postulated faster onset of nm blockade in the diaphragm, suppression of thumb-twitch response to TOF stimulation does not necessarily predict absence of diaphragmatic movement elicited by excessive tracheal stimulation. As demonstrated, intense nm blockade quantified by a PTC of 5 is necessary to rule out any bucking and coughing, i.e., to ensure total diaphragmatic paralysis in response to tracheal stimulation. On-line neurological evaluation, one of the essentials in the approach to the neurosurgical patient, will not be prevented by the intermittent bolus regime utilized in this study.

Coordination of respiratory care with protection of the brain is critical in neurosurgical intensive care. Therefore, in addition to hyperventilation, adequate sedation and muscle relaxation are applied to mitigate the difficulties with control of intracranial pressure (ICP) during routine tracheobronchial suctioning (TBS). Although hypnotics have been shown to be effective in mitigating increases in ICP in response to endotracheal suctioning in paralyzed patients, brisk bucking and coughing with further increases in ICP may occur without muscle relaxation. Long-term neuromuscular (nm) paralysis may be undesirable in neurosurgical critical care because clinical evaluation with early detection of neurological deterioration will be impossible in the paralyzed patient. Therefore, the effects of TBS without and after nm blockade with an intermediate-acting nondepolarizing muscle relaxant on ICP were studied. PATIENTS AND METHODS. Nine patients with moderate increases in mean ICP of 19.2 +/- 8 mmHg due to head injuries and spontaneous subarachnoid hemorrhage were investigated. All patients were on-line sedated with midazolam and sufentanil and controlled ventilation was adjusted to maintain a paCO2 of 30 +/- 2 mmHg. Respiratory and hemodynamic parameters and ICP (epidural probe) were continuously monitored and recorded on an integrated data bank. After a bolus dose of propofol, routine TBS was performed without the use of muscle relaxants. Before the next TBS, nm monitoring was initiated and train-of-four (TOF) stimulation was imposed at the ulnar nerve using supramaximal pulses. The response of the adductor pollicis muscle was recorded by accelerometry. After supramaximal stimulation had been achieved, a bolus dose of 2 times the ED95 of vecuronium (0.12 mg/kg) was given. Depth of nm blockade was quantified by the posttetanic count (PTC). ICP and CPP were measured before, during, and after TBS. Diaphragmatic movement, bucking, and coughing were registered by visual observation and graded as absent, slight, moderate, or severe. STATISTICS. Student's t-test and the Wilcoxon test for paired data (P less than 0.05; values as mean +/- SD) were used. RESULTS. (see Table and Figure). Despite adequate sedation, moderate to severe diaphragmatic movements in response to carinal stimulation with significant increases in ICP (18.2 +/-7 to 24 +/- 8 mmHg) an d subsequent decreases in cerebral perfusion pressure (CPP) (68.9 +/- 2 to 62.4 +/- 8 mmHg) could be observed without muscle relaxation. After a bolus of vecuronium, profound nm paralysis quantified by a PTC of 5 was observed after an onset time of 4.2 +/- 1 min. ICP (20.2 +/- 8 vs. 20.1 +/- 8 mmHg) and CPP (64.0 +/- 13 vs. 64.8 +/- 13 mmHg) remained unchanged. Slight diaphragmatic movements could be elicited in only two patients during TBS. DISCUSSION. TBS is a potent trigger of diaphragmatic movement, bucking, and coughing by reflex activation of the phrenic nerve. A major determinant of the magnitude of ICP increase during TBS is the transmission of the cough-induced increase in intrathoracic pressure to the cerebral venous system. Vecuronium was utilized for nm blockade because of its proven lack of cerebral and cardiovascular side effects, its relatively short onset, and its intermediate duration of action. Despite the postulated faster onset of nm blockade in the diaphragm, suppression of thumb-twitch response to TOF stimulation does not necessarily predict absence of diaphragmatic movement elicited by excessive tracheal stimulation. As demonstrated, intense nm blockade quantified by a PTC of 5 is necessary to rule out any bucking and coughing, i.e., to ensure total diaphragmatic paralysis in response to tracheal stimulation. On-line neurological evaluation, one of the essentials in the approach to the neurosurgical patient, will not be prevented by the intermittent bolus regime utilized in this study.

Werba, A. M.D.; Weinstabl, C. M.D.; Plainer, B. M.D.; Petricek, W. M.D.; Spiss, C. K. M.D. Author Information

Although the pharmacokinetics of vecuronium are altered by the loss of kidney function, they do not differ significantly between patients with normal renal function and patients with renal failure. Therefore, the drug has become a preferred neuromuscular blocking agent in anuric patients. The author observed complete relaxation--verified by nerve stimulation--for more than 3 h following a single dose of 0.09 mg/kg vecuronium in a patient with chronic renal failure. Liver function was normal, and no drugs known to interact with vecuronium were used. The authors conclude that the altered pharmacokinetics of vecuronium in anuric patients might cause clinically significant effects in some patients.