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We present a patient who developed a high central neural block after stellate-ganglion-blockade. The underlying pathophysiology was assessed via sonographic imaging. Stellate ganglion block was performed in a 19-year old patient according to the standard technique. Multiple aspiration tests were negative and a test dose of 3 ml bupivacaine 0.25% was injected. After a 3 min interval another 5 ml were injected. Two minutes after the local anaesthetic administration the patient reported nausea and sensations in the upper extremity. Spontaneous respiration efforts stopped, and the patient became unconscious. Tracheal intubation was performed, and the patient was ventilated in a controlled mode for two hours. Heart rate as well as blood pressure remained within the normal range. Neurologic recovery occurred rapidly and extubation was performed about two and a half hours after the event. Our sonographic studies demonstrated a local anaesthetic depot directly at the root of C 6, with a mean diameter of 10 mm and a length of 5 to 6 cm (about a third smaller than expected). Sonographic studies and clinical symptoms of our patient are most likely to occur with a subdural extra-arachnoidal block. Ultrasonographic guided puncture enhances the patient's safety by the opportunity to directly visualise transverse process, nerval root as well as local anaesthetic depot. In case of depot formation directly at the nerval root, injection may be stopped and the needle repositioned. Furthermore, direct visualisation of the great vessels (A. vertebralis) prevents intravascular injection and haematoma formation.

To analyze the characteristics of hemodynamic parameters and cerebral dynamics, the courses of intracranial pressure (ICP), cerebral perfusion pressure (CPP), mean arterial blood pressure (MAP) and PaCO2 were analyzed retrospectively in 29 patients with severe head injury, comparing periods before and after the ventilatory mode was changed from controlled mechanical ventilation to spontaneous breathing with continuous positive airway pressure. Measurements were done before and after changing of the ventilation. Patients were allocated either to group I (n = 22, ICP remained stable: 18 +/- 2 mm Hg in both periods of observation) or group II (n = 7, ICP increased from 25 +/- 3 mm Hg to 33 +/- 4 mm Hg, P < 0.05). While changes of MAP did not reach significant levels in either group, concomitant changes in CCP appeared in group II (67 +/- 2 mm Hg to 60 +/- 2 mm Hg). Based on the observation of relatively high incidence of ICP increases and deterioration of CPP during weaning from ventilator, it is recommended that continuous ICP monitoring should be continued.

The purpose of this prospective study was to verify the value of the supine chest radiograph with regard to the recognition and quantification of pleural effusions. The findings of supine chest radiographs were compared to those of chest sonography in a total of 320 pleural cavities. The correct identification and quantification of a pleural effusion was possible by supine chest radiograph alone in only 55% of cases (176/320). In 20% (64/320) supine chest x-ray was falsely negative and in 15% (48/320) falsely positive. In 10% an existing effusion was in fact recognised on supine chest x-ray; however the amount of effusion was wrongly estimated.

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.

Previous investigations have revealed that propofol has a beneficial effect on intracranial dynamics in patients undergoing elective neurosurgery. In the present study we evaluated the impact of propofol in patients with normal or compromised intracranial compliance. METHODS. Epidural ICP probes were implanted in 14 patients with head injury. The heart rate, mean arterial pressure (MAP), intracranial pressure (ICP) and end-tidal CO2 were recorded continuously, and propofol was given in doses of 0.5, 1.0 and 2.0 mg/kg; there were 15 min between each application. The data were evaluated 1, 2, 5 and 10 min after each application. The patients were allocated to group I (ICP less than 20 mmHg) or group II (ICP greater than 20 mmHg) according to their ICP baseline level. A statistical analysis was performed by one-way ANOVA. A P value of less than 0.05 was regarded as significant. RESULTS. In group I decreases in MAP at all measuring points were detected with 1.0 and 2.0 mg/kg propofol; ICP with 1.0 and 2.0 mg/kg and CPP with 2.0 mg/kg fell significantly. In group II MAP decreased with all doses studied, as did ICP with 1.0 and 2.0 mg/kg; however, CPP was not particularly influenced. CONCLUSION. Propofol decreased ICP in patients with normal and compromised intracranial compliance, particularly with 2.0 mg/kg. As the responses to the hypotensive effects of propofol were mild and almost similar in both groups, no inadvertent CPP drops were observed with any of the doses studied. Thus, propofol as a bolus can be used safely for the sedation of ICU patients with head injury and normal or compromised intracranial compliance.

Mortality of the septic syndrome is around 40-60% and can rise to 100% if multiple organ failure (MOF) develops. It is generally assumed that the high mortality of sepsis can only be reduced by early diagnosis and prevention of subsequent MOF. The aim of our study was to investigate the validity of routine TNF-alpha determination for the diagnosis of septicemia and, in combination with clinical scoring systems [MOF score and Acute Physiological and Therapeutic Intervention Score (APATIS)], to define a "therapeutic window" during which an anti-TNF-alpha agent could be applied with the greatest chance of success. METHODS. TNF-alpha serum levels were measured and APATIS and MOF scores were calculated daily in 87 ICU patients. TNF-alpha serum levels were determined by means of an immunoradiometric assay (TNF-alpha IRMA, Medgenix, Belgium). Sepsis was diagnosed in 24 patients according to clinical criteria. To quantify the severity of sepsis, we set up the APATIS. The MOF score was used to assess the severity of MOF. Data were analyzed using the SAS software package (SAS Institute, Cary, N.C.) and are expressed as mean +/- SEM. RESULTS. The mean values of all sequential TNF-alpha determinations were significantly higher in the septic patients compared to the nonseptic patients (73.2 +/- 4.3 vs 8.5 +/- 0.4 pg/ml; P less than 0.01). Similarly, the maximum TNF-alpha values were significantly higher in the septic group (156.9 +/- 26.5 vs 20.1 +/- 1.3 pg/ml; P less than 0.01). To differentiate between sepsis and nonsepsis we set the cut-off point at a TNF-alpha serum level of 40 pg/ml and calculated a sensitivity of 70.8%, a specificity of 98%, and a diagnostic accuracy of 91.3%. None of the patients with a maximum TNF-alpha level above 250 pg/ml survived. Mortality was 80% above a maximum TNF-alpha serum concentration of 200 pg/ml, whereas only 40% of patients with a TNF-alpha maximum below 150 pg/ml died. The mean APATIS and MOF scores were significantly higher for septic than for nonseptic patients (APATIS: 20.3 +/- 0.5 vs 8.1 +/- 0.2 and MOF: 9.8 +/- 0.1 vs 4.6 +/- 0.1). To differentiate between survival and nonsurvival, we set the cut-off point at 25 for APATIS and calculated a sensitivity of 79% and a specificity of 93%. At a MOF score of 8, the sensitivity was 89% and the specificity 82%. In our series cumulative mortality at a maximum MOF of less than 8 was 4% and at MOF greater than 10, 68%. We found an interval of 2.9 +/- 0.9 days between the time TNF-alpha serum levels first exceeded 40 pg/ml and the development of severe MOF (MOF greater than 10) in 13 patients. CONCLUSION. Sequential TNF-alpha serum level determinations are useful for the diagnosis and prognosis of septicemia. We found an interval of 3 days between rising TNF-alpha serum levels and the development of severe MOF. This latency may represent the "therapeutic window" during which an anti-TNF-alpha-agent, e.g., a monoclonal anti-TNF-alpha-antibody, could be applied as a therapeutic consequence.