Multi-centred studies in patients who remain comatose after cardiac arrest and also in newborn babies with perinatal asphyxia have clearly demonstrated that mild hypothermia (32–34°C) can improve neurological outcome after post-anoxic injury. This represents a highly promising development in the field of neurocritical care. This review discusses the place of mild therapeutic hypothermia in the overall therapeutic strategy for cardiac arrest patients. Cooling should not be viewed in isolation but in the context of a ‘treatment bundle,’ which together can significantly improve outcome after cardiac arrest. Favourable outcomes of 50–60% are now routinely achieved in many centres in patients with witnessed arrest and an initial rhythm of ventricular fibrillation or ventricular tachycardia. These results have been achieved by combining a number of therapeutic strategies, including early and effective resuscitation with greater emphasis on continuing chest compressions throughout various procedures (including resumption of compressions immediately after defibrillation even if rhythm has been restored) as well as prevention of hypoxia and hypotension in all stages following restoration of spontaneous circulation. Regarding the use of hypothermia, early induction and proper management of side-effects are the key elements of successful implementation. Treatment should include the rapid infusion of 1500–3000 mL of cold fluids to induce hypothermia and prevent hypovolaemia and hypotension. Educational activities to increase awareness and acceptance of new therapeutic options and European Resuscitation Council guidelines are urgently required.

Summary

Cardiac complications are the major cause of perioperative morbidity and mortality of patients undergoing non-cardiac surgery. This is related to the frequent presence of underlying coronary artery disease. In the last few decades, attention has focused on preoperative cardiac risk assessment that may help to identify patients at increased cardiac risk for whom cardioprotective medication and, when indicated, coronary revascularization may improve perioperative outcome. On the other hand, less attention was given to the role of anaesthesia and monitoring techniques in the cardiac risk management of high-risk patients undergoing non-cardiac surgery. The aim of this review was to summarize the current evidence from published studies on the effect of the type of anaesthesia and monitoring techniques on perioperative cardiac outcome in non-cardiac surgery.

We describe a case of transient neurological deficit that occurred after unilateral spinal anaesthesia with 8 mg of 1% hyperbaric bupivacaine slowly injected through a 25-gauge pencil-point spinal needle. The surgery and anaesthesia were uneventful, but 3 days after surgery, the patient reported an area of hypoaesthesia over L3–L4 dermatomes of the leg which had been operated on (loss of pinprick sensation) without reduction in muscular strength. Sensation in this area returned to normal over the following 2 weeks. Prospective multicentre studies with a large population and a long follow-up should be performed in order to evaluate the incidence of this unusual side effect. However, we suggest that a low solution concentration should be preferred for unilateral spinal anaesthesia with a hyperbaric anaesthetic solution (if pencil-point needle and slow injection rate are employed), in order to minimize the risk of a localized high peak anaesthetic concentration, which might lead to a transient neurological deficit.

Background and objective: Monitoring of neuromuscular blockade still often relies on clinical judgement. Moreover, there are substantial national differences in the use of agents to 'reverse' their effects. We investigated the recovery characteristics and incidence of postoperative residual curarization after cisatracurium and rocuronium infusions for long duration interventions without systematic antagonism.

Methods: In 30 patients undergoing major surgery, we measured infusion dose requirements for rocuronium and cisatracurium during propofol anaesthesia. Infusions were discontinued at the beginning of surgical closure; spontaneous recovery of neuromuscular function was awaited in both groups. Neostigmine (50 μg kg−1) was administered only when a patient started to wake without a train-of-four ratio (TOF) of 0.9.

Results: In the cisatracurium and rocuronium groups, four (27%) and one (7%) patients, respectively, had a TOF ratio ≥0.9 at the end of surgery. The TOF ratio in each group at that time was 51 ± 32% for cisatracurium and 47 ± 31% for rocuronium (P = 0.78). Six patients (40%) in the cisatracurium group and seven (47%) in the rocuronium group required neostigmine. The TOF ratio at the time of reversal was 63 ± 7% for cisatracurium and 40 ± 19% for rocuronium (P = 0.01). The time interval between the end of surgery and a TOF ratio of 0.9 was 10 ± 9 min for cisatracurium and 18 ± 13 min for rocuronium (P = n.s.).

Conclusions: Patients receiving a cisatracurium or rocuronium infusion have a high incidence of postoperative residual curarization when the block is not antagonized. When ‘reversal’ is not attempted, cisatracurium seems to be safer than rocuronium.

The molecular mechanism of volatile anaesthetic action on presynaptic glutamate release is not clear. An inhibitory effect on voltage-gated calcium channels has been proposed. The present study examines the effect of isoflurane on cytosolic free calcium and synaptic glutamate release from isolated nerve terminals. Synaptosomes from rat cerebral cortex were used. Glutamate was measured with a continuous fluorometric measurement in a spectrophotometer as the fluorescence of NADPH and calcium as the fluorescence of fura-2. Isoflurane reduced the calcium-dependent glutamate release evoked by membrane depolarization with 4-aminopyridine in an inversely dose-dependent manner. The glutamate release was reduced by 56, 43 and 36% in response to isoflurane 0.5, 1.5 and 3.0%, respectively (for all: P<0.05). Membrane depolarization evoked a rise in cytosolic free calcium of ≈34%. Addition of isoflurane (0.5, 1.5 and 3.0%) produced no significant change in cytosolic free calcium. These results indicate that the isoflurane-induced reduction in presynaptic glutamate release is caused by other mechanisms than blocking voltage-gated calcium channels. As the release is inversely dose-dependent, two or more mechanisms could be involved.

Stellate ganglion block is a selective sympathetic block that affects the ipsilateral head, neck, upper extremity and upper part of the thorax. Convulsions are a recognized complication of intra-arterial injection during stellate ganglion block. As central nervous system toxicity depends ultimately on the concentration of the local anaesthetics presented to the brain, the likely causative factors are discussed as well as the types of toxic symptoms and their onset times. The paper considers the aetiological factors of such convulsions resulting from stellate ganglion block in two patients.

Summary

Background and objective: The effects of intra-aortic balloon pumping (IABP) on cerebral perfusion are still a matter of debate. End-diastolic reversal of blood flow in cerebral arteries has been observed in a small number of patients. We prospectively investigated the incidence and the amount of transient cerebral artery blood flow reversal during balloon pumping in patients recovering from cardiac surgery.

Methods: In 23 patients receiving IABP support, blood flow velocities in the right middle cerebral artery were assessed by transcranial Doppler-sonography. Additionally, systemic haemodynamics were monitored. In each patient, measurements were performed at three different pump settings: without support, assist ratio 1 : 1 and assist ratio 1 : 2.

Results: In 8 of 23 patients, balloon pumping caused a transient diastolic reversal of blood flow in the middle cerebral artery during balloon deflation. Antegrade mean flow velocity in the middle cerebral artery significantly increased from 57 ± 27 to 61 ± 26 (assist ratio 1 : 1) and 61 ± 29 cm s−1 (assist ratio 1 : 2) (P < 0.05). Taking transient blood flow reversal into account, net mean flow velocity did not increase with balloon pump support. Systemic haemodynamic parameters remained unchanged.

Conclusion: Left ventricular support with IABP significantly changed flow patterns in basal cerebral arteries of our patients. In 35% of patients, support resulted in a transient reversal of intracranial blood flow which counterbalanced a slight increase in mean antegrade flow.

We present a case of pulmonary embolism that occurred during the injection of lipiodol during transcatheter arterial chemoembolization under general anaesthesia. A 7-year-old child suffering from a large hepatoblastoma was admitted for arterial chemoembolization and carcinostatic administration. Pulmonary embolism due to lipiodol during arterial chemoembolization was evident by a sudden fall in oxyhaemoglobin saturation from 100 to 90%. This was associated with a spread of lipiodol into both lungs, particularly the middle lung zones and detected by chest fluoroscopy. Arterial blood gases returned to normal values 1 day later but pulmonary infiltration persisted for 7 days before final clearance. Pulmonary embolism caused by lipiodol during arterial chemoembolization is infrequent, but such a complication could prove fatal. Understanding the risk of pulmonary embolism in patients receiving lipiodol, during and after arterial chemoembolization, and late onset pulmonary injury is important and a close follow-up for several days after arterial chemoembolization is advisable.

Sixty children undergoing inguinal or urogenital surgery were allocated randomly to three groups to receive a caudal injection of either 0.125% bupivacaine 0.75 mL kg−1 with 0.5% midazolam 50 μg kg−1 (n=20) or with 1% morphine chlorhydrate 0.05mg kg−1 (n=20), or bupivacaine alone (n=20) after surgery under general anaesthesia. There were no significant changes in heart rate, blood pressure, respiratory rate or oxygen haemoglobin saturation values in all groups, and there were no significant differences in the incidence of vomiting and pruritus between the groups (P>0.05). Sedation scores were higher in the bupivacaine-midazolam and the bupivacaine-morphine groups than in the bupivacaine group at 8–12 h post-operatively (P<0.01). The durations of analgesia were 21.15±1.2 h in the bupivacaine-midazolam group, 14.50±1.6 h in the bupivacaine-morphine group and 8.15±1.3 h in the bupivacaine group. Differences between the bupivacaine-midazolam group and the bupivacaine group (P<0.001), the bupivacaine-midazolam group and the bupivacaine-morphine group (P<0.01), and the bupivacaine-morphine group and the bupivacaine group (P<0.01) were significant. It is suggested that caudal administration of a bupivacaine-midazolam mixture produces a longer duration of post-operative analgesia than a bupivacaine-morphine mixture and bupivacaine alone with sedation for 8–12 h post-operatively.

Background and objective Laparoscopic and open surgery have been compared with conflicting results regarding their systemic responses. The sensitivity of biochemical markers that are used to discriminate between the stress responses to different types of surgery varies from study to study. We wanted to evaluate the stress response and the sensitivity of clinical and biochemical stress markers in patients undergoing laparoscopically assisted vaginal or abdominal hysterectomy.

Methods We performed a case-control study with patients undergoing laparoscopically assisted vaginal hysterectomy (n=20) or abdominal hysterectomy (n=20). Pain scores were assessed at rest and during coughing, and active leg elevation and fatigue scores using a visual analogue scale. In 10 patients of each group, haematocrit, white cell count, C-reactive protein, glucose, cortisol, adrenocorticotrophic hormone, β-endorphin immunoreactivity, interleukin-6 and urine excretion of epinephrine and norepinephrine were measured preoperatively and during the first 44 postoperative hours.

Results The most sensitive symptoms and markers of the systemic response were pain scores during mobilization, fatigue scores, C-reactive protein and interleukin-6 (P < 0.01 in all comparisons). Pain scores at rest, and all other laboratory markers of the systemic response, did not discriminate between the two types of surgery.

Conclusion Follow-up of postoperative pain scores during mobilization and fatigue levels might be an easy tool for the evaluation of postoperative recovery. Using an identical anaesthetic technique, the neuroendocrine response was of the same magnitude after both types of surgery.

Bone injury while undergoing electro-convulsive therapy is thought to be rare. We report a case of hip fracture during treatment which was associated with osteoporosis. Patients at increased risk could be identified.

Summary

Objective: Intensive insulin therapy reduced mortality in patients admitted to an intensive care unit following mainly cardiac surgery. The aim of this prospective study was to evaluate, if intensive insulin therapy could reduce mortality in medical and non-cardiac surgical patients admitted to a multidisciplinary intensive care unit. Patients and methods: For 6 months all adult patients, admitted to the intensive care unit, were included. Insulin was administered, if blood glucose 12 mmol L−1. For the next 6 months blood glucose level was reduced with intensive insulin therapy (aim 4.4 < BG < 6.1 mmol L−1); 271 patients were included. Patient characteristics data, APACHE II score, morbidity and mortality were recorded. Results: At admission the two groups were comparable. The overall relative mortality was reduced 20% in the intensive insulin treated group (n.s.). In the intensive insulin treated group mortality was 13.1% in the medical patients and 11.2% in the surgical patients compared to 15.8% and 14.4%, respectively, in the conventional treated group (n.s.). The frequency of secondary infections was 21.5% in the intensive insulin treated group and 16.0% in the conventional treated group (n.s.). The proportion of hypoglycaemia increased from 4% to 14% (P < 0.05). Conclusions: Following intensive insulin therapy there was a trend towards reduced mortality in medical and non-cardiac surgical patients but less pronounced as in cardiac surgical patients. Intensive insulin therapy increased the frequency of hypoglycaemia. Around 4400 patients would have to be included in any future randomized study to reach significance.

Summary

Background and objective: Measurement of central blood volumes (CBV), such as global end-diastolic volume (GEDV) and right ventricular end-diastolic volume (RVEDV) are considered appropriate estimates of intravascular volume status. However, to apply those parameters for preload assessment in mechanically ventilated patients, the influence of tidal volume (TV) and positive endexpiratory airway pressure (PEEP) on those parameters must be known. Methods: In 13 mechanically ventilated piglets, the effect of low (10 mL kg−1) and high (20 mL kg−1) TVs on CBV was investigated in absence and presence of PEEP (0 and 15 cmH2O). GEDV, RVEDV, right heart (RHEDV) and left heart end-diastolic volume (LHEDV) were measured by thermodilution. Blood flow on the descending thoracic aorta measured with an ultrasonic flow-probe served to determine stroke volume (SV). Measurements were performed during baseline conditions, after volume loading with previously extracted haemodilution blood (20 mL kg−1) and following haemorrhage (30 mL kg−1). Results: Application of PEEP decreased GEDV and SV significantly (P < 0.05). Augmenting TV did not reduce GEDV systematically, but significantly reduced SV (P < 0.05). Changes in ventilator settings only influenced RVEDV following volume loading (P < 0.05). RHEDV and LHEDV decreased following application of PEEP, but only RHEDV decreased after augmenting TV at baseline and following volume loading. Correlation of SV with parameters of CBV was r = 0.487 (P < 0.01) for GEDV, r = 0.553 (P < 0.01) for RVEDV, r = 0.596 (P < 0.01) for RHEDV and r = 0.303 (P < 0.01) for LHEDV. Conclusion: Application of PEEP decreases CBV and SV. Augmenting TV reduces SV but not CBV. There is a moderate correlation between parameters of CBV and cardiac performance.