Summary

Background and objective: The optimal depth of insertion of left-sided double-lumen endobronchial tubes is strongly correlated with body height in average-sized adults. However, this relationship has not been studied in below average-sized adult patients. We investigated whether or not there is a clinically useful relationship in below average-sized adult patients. Methods: One hundred and ninety six consecutive adult patients undergoing thoracic surgery under one-lung anaesthesia (body height ≤ 155 cm) were included in this study. Left-sided double-lumen tubes were inserted under the guidance of a fibre-optic bronchoscope. Optimal depth was defined as the proximal surface of the bronchial cuff positioned just below the carina. Results: There was a statistically significant positive correlation between body height and the optimal depth of insertion (r = 0.61, P < 0.0001); however, the correlation coefficient was low. The actual optimal depth of insertion of one patient was even 4.5 cm shorter than that obtained from the equation. Conclusion: Although there was a statistically significant correlation between body height and the optimal depth of insertion of left sided double lumen tubes in adult patients of short stature (≤ 155 cm), clinical application of the equation is not warranted and these tubes should be inserted under direct vision with a fibre-optic bronchoscope.

Summary

Background and objective: To investigate and compare the performance of bispectral index (BIS) and auditory evoked response index (AAI) in detecting the transition from consciousness to unconsciousness during anaesthesia induction by propofol, alone and in combination with fentanyl.

Methods: Anaesthesia was induced with either an intravenous infusion of 30 mg kg−1 h−1 of propofol plus 2 μg kg−1 of fentanyl (Group PF, n = 20) or an intravenous infusion of 30 mg kg−1 h−1 of propofol plus normal saline (Group P, n = 20). BIS, AAI and the doses of propofol administered were recorded at the end-point of unresponsiveness to verbal commands. The propofol plasma concentration was also measured.

Results: The propofol dose and plasma propofol concentration required to achieve loss of consciousness were significantly lower in patients pretreated with fentanyl (P < 0.001). The mean BIS value at loss of consciousness was significantly different between the two groups (74.10 in Group PF vs. 60.80 in Group P) (P < 0.001). However, no difference in the AAI was seen between the two groups at loss of consciousness (32.90 in Group PF vs. 31.80 in Group P) (P > 0.05). In both groups, the regression analysis values (r-values) between BIS and plasma propofol concentrations at the onset of unconsciousness were higher than those between AAI and propofol concentrations (0.553 vs. 0.180 in Group P; 0.432 vs. 0.308 in Group PF).

Conclusions: These results show that a fentanyl bolus is effective in augmenting the hypnotic effect of propofol during anaesthesia induction. AAI appears to be able to measure the transition from consciousness to unconsciousness at similar values, regardless of whether or not fentanyl pretreatment is used whereas the BIS values were not independent of fentanyl pretreatment. This suggests that AAI may be a better indicator of conscious status during propofol/fentanyl anaesthesia, where it appears to be independent of the anaesthesia regimen.

In spite of the many tools available for monitoring the central nervous system, there are no clinical trials which prove that continuous monitoring of any single variable in the intensive care unit has had any significant impact on the outcome of patients. Even in the absence of robust evidence proving the efficacy of neuromonitoring tools, we believe it is time to re-examine the basic objectives of neuromonitoring. The main reasons for monitoring neurocritical patients could be summarized as follows: (1) to detect early neurological worsening before irreversible brain damage occurs; (2) to individualize patient care decisions; (3) to guide patient management; (4) to monitor therapeutic response of some interventions and to avoid any consequent adverse effects; (5) to allow clinicians to be able to understand the pathophysiology of complex disorders; (6) to design and implement management protocols; and (7) to improve neurological outcome and quality of life in survivors of severe brain injuries. To reach these goals, there is a need to overcome some obstacles, such as the learning curve needed for any monitor and establishing consensus among experts on how to interpret monitor readings. In this review, the obstacles confronted in running randomized clinical trials in this field are discussed. The lack of equipoise and the ethical concerns in conducting such trials are discussed. In addition, the reasons for failure to improve outcome through the use of some monitoring devices are discussed and potential solutions proposed.

Background and objective The aim of this study was to determine possible age-associated differences in human blood pressure regulation during an immunological challenge in healthy subjects.

Methods Eight healthy young volunteers (median age 24 yr) and nine healthy elderly volunteers (median age 66 yr) received an intravenous bolus injection of Eschericia coli endotoxin (2 ng kg−1). Blood pressure, heart rate and core temperature were monitored during the first 7 h. Plasma catecholamine concentrations were measured at hourly intervals.

Results The elderly showed a significantly more pronounced decrease in mean arterial pressure 4–7 h after endotoxin administration compared with the young controls (anova; age × time; P < 0.0005). This mainly reflected a decrease in the systolic blood pressure in the elderly. The heart rate of both groups increased without difference between groups. Increased plasma epinephrine concentrations were found 2–3 h after endotoxin administration in both groups. Five hours after the endotoxin challenge, the epinephrine concentration had returned to control values in the elderly group only, in spite of decreased blood pressure.

Conclusion In conclusion, healthy elderly subjects fail to maintain a constant mean arterial pressure in response to the immunological challenge of endotoxemia.

Summary

Background and objective: Arterial grafts are prone to vasospasm. Opioid analgesics are commonly used in the perioperative course of cardiac surgical procedures. Therefore, we investigated the direct effects of morphine, meperidine, fentanyl and remifentanil on the human radial artery. Methods: Radial artery segments, obtained from 20 patients, were precontracted with phenylephrine. Using the organ bath technique, the endothelium-independent vasodilatation was tested in vitro by addition of cumulative concentrations of morphine, meperidine, fentanyl and remifentanil in separate organ baths, in the presence or absence of naloxone. Indomethacin and NG-nitro-l-arginine methyl ester was added to all organ bath in order to determine the effects of prostaglandins and nitric oxide, respectively. Results: Morphine (10−8–10−4mol L−1), meperidine (10−10–10−6mol L−1), fentanyl (10−10–10−6mol L−1) and remifentanil (10−8–10−4mol L−1) caused a concentration-dependent vasorelaxation in the human being artery rings. The relaxations in the presence of naloxane did not change. The maximal relaxant effects of meperidine and fentanyl were significantly greater than those of morphine and remifentanil (P < 0.05). Conclusions: These findings indicate that morphine, meperidine, fentanyl and remifentanil produce concentration-dependent and endothelium-independent relaxations in human being radial artery rings. Meperidine and fentanyl are more potent relaxant agents than morphine and remifentanil in the human being radial artery in vitro.

Despite recent advances in intensive care medicine, acute lung injury and its more severe form, acute respiratory distress syndrome pose major therapeutic problems. While mechanical ventilation is integral to the care of these patients, its adverse consequences including ventilator-induced lung injury are determinants of disease progression and prognosis. Among several important ventilator parameters, the use of low tidal volumes is probably the most important feature of lung-protective mechanical ventilation. Intensivists should be trained to recognize acute lung injury and acute respiratory distress syndrome and encouraged to use low-tidal-volume ventilation in clinical practice. Alternative modes of ventilation such as high-frequency ventilation and prone position should be reserved for selected patients in whom conventional lung-protective ventilation strategies have failed.

Summary

We do not know how general anaesthetics cause their desired effects. Contrary to what has been thought until relatively recently, the clinical state of anaesthesia consists of multiple components that are mediated via interaction of the anaesthetic drugs with different targets on the molecular, the cellular, the network and the structural–anatomical levels. The mechanisms by which some of these drugs induce the different components of ‘anaesthesia’ may be rather specific: discrete mutations of single amino acids in specific proteins profoundly affect the ability of certain anaesthetics to achieve specific endpoints. Despite this potential specificity, inhalational anaesthetics are present in the body at very high concentrations during surgical anaesthesia. Due to their lipid solubility, general anaesthetics dissolve in every membrane, penetrate into organelles and interact with numerous cellular structures in multiple ways. A priori, it is therefore not unreasonable to assume that these drugs have the potential to cause insidious changes in the body other than those acute and readily apparent ones that we routinely monitor for. Some changes may wane within a short time after removal of the drug (e.g. the suppression of immune cell function). Others may persist after complete removal of the drug and even become self-propagating (e.g. spread of malignant cells, the β-oligomerization of proteins), still others may be irreversible (e.g. the induction of apoptosis in the central nervous system) but of unclear significance. This article will focus on evidence for anaesthetic toxicity in the central nervous system, which appears to be susceptible to anaesthetic neurotoxicity primarily at the extremes of ages but via different pathways: in the neonate, during the period of most intense synaptogenesis, anaesthetics can induce excessive apoptosis; in the aging brain subtle cognitive dysfunction can persist long after clearance of the drug and processes resembling neurodegenerative disorders may be accelerated. At all ages, anaesthetics affect gene expression regulating protein synthesis in poorly understood ways. While it seems reasonable to assume that the vast majority of our patients completely restore homeostasis after general anaesthesia, exposure to these drugs probably has more profound and longer-lasting effects on the brain than heretofore imagined.

Summary

Background and objective: The reasons for coagulopathy may be multiple and the identification of the underlying cause is often difficult. Recently, we identified two patients showing characteristics of heparin overdose during surgery. We hypothesised that filling a Shaldon dialysis catheter with heparin prior to closure, so-called heparin lock, might have triggered this coagulation disorder. Therefore, the aim of this in vitro study was to show whether this procedure can lead to an iatrogenic administration of heparin. Methods: A Shaldon catheter (GamCath®; Joka Kathetertechnik, Hechingen, Germany) was hung up in a container filled with NaCl solution 0.9% 5 mL and a heparin lock was simulated. Instead of using heparin solution we injected 1 mL of a KCl solution (1 mol L−1) into the Shaldon catheter, because the measurement of the potassium concentration is faster and more reliable than that of heparin. Ten measurements were taken after fast (0.5 s) and slow (3 s) injection speeds. Results: Although the catheter volume is specified as 1.07 mL, an amount up to 0.51 mL KCl solution on average was detectable in the solution after locking the catheter with 1 mL KCl solution. Conclusions: Following a heparin lock a considerable amount of the injected solution is accidentally administered to the patient. Only 49.1% of the injected volume may remain in the Shaldon catheter. This could lead to an increased risk of coagulopathy.

Improvement in surgical techniques, technology and perioperative assessment has dramatically simplified the anaesthetic care for elective liver resection. Patients with a non-tumorous healthy liver should only need the usual preoperative assessment. Patients with pre-existing parenchymal liver disease should be specifically assessed for gas exchange impairment, alcoholic or nutritional-associated cardiomyopathy, infection, cirrhosis decompensation, acute alcoholic hepatitis, and kidney impairment. The type of anaesthetic management does not influence the intra- and postoperative courses. Intermittent clamping of the portal vascular triad is better tolerated than prolonged continuous periods of ischaemia—especially in patients with abnormal liver parenchyma. Intraoperative antibiotic prophylaxis must be administered to prevent translocation of intestinal enterobacteria to the systemic circulation in patients with both healthy and diseased livers. Blood-salvage techniques have limited indications in liver resection. Systematic invasive haemodynamic monitoring is no longer warranted. An arterial cannula should only be considered in procedures of long duration and in selected situations likely to cause anticipated circulatory impairment: total liver vascular occlusion, repeat surgery, combined organ resection, and surgery conducted on tumours >10 cm in size or in connection with the vena cava. In a recent large series of liver resections, 60% of patients did not need a blood transfusion, only 2% of transfused patients received >10 units of blood and cirrhosis was not predictive of increased intraoperative bleeding. Postoperative ascites, which always develops at the expense of circulating fluid, is a frequent occurrence in patients with healthy or diseased livers. Intra- and postoperative fluid limitation does not prevent postoperative ascites. Volume expansion, diuretics and vasopressor therapy should be initiated early to prevent kidney failure.

Muscle relaxants are given as part of a rapid-sequence induction to facilitate tracheal intubation. Among all the muscle relaxants available, succinylcholine is the only one with a fast (≅1 min) onset and a fast recovery. Therefore it is still the most frequently used muscle relaxant for rapid-sequence induction despite its well-known side-effects. The short duration of action of succinylcholine is, however, no substitute for aggressive airway management in the case of an unexpectedly difficult intubation in order to prevent life-threatening hypoxia. A preoperative assessment of the airway is mandatory in any patient and may indicate the need for using intubation techniques without a muscle relaxant. Rocuronium in large doses (i.e. ≥1 mg kg−1) is an alternative to succinylcholine in a classical rapid-sequence setting under relatively light anaesthesia. With respect to rapid tracheal intubation, the timing and priming principles offer little advantage over the use of rocuronium in doses of 0.6 mg kg−1 in combination with an appropriate induction technique (i.e. including an opioid) or over the use of larger doses of rocuronium (≥1.0 mg kg−1) under relatively light anaesthesia, and may even be potentially harmful.

In contrast to rocuronium, the use of rapacuronium in a rapid-sequence setting has been associated with dose-dependent respiratory side-effects that limit its usefulness in doses higher than 1.5 mg kg−1 for this indication.

Summary

Background and objective: The clinical practice of spinal morphine administration for pain relief is based on observations in animals that opioid receptors exist in the spinal cord and intrathecal injections of opioids in those species (mostly rats) lead to antinociceptive effects. Clinicians are well aware that administration of spinal opioids is associated with side-effects, such as nausea and respiratory depression, that indicate supraspinal spread of the drug administered. Those observations call into question how much of the observed pain relief is due to action of the drug in the brain. This study investigated the spinal cord actions of morphine given intrathecally to rats in a model that allows investigation of drug–receptor interaction at the spinal cord level. Experiments were performed on male Wistar rats with chronically implanted lumbar subarachnoid catheters.

Methods: Nociceptive thresholds were measured in rats given morphine intrathecally alone and in combination with intrathecal injections of selective opioid receptor antagonists: β-funaltrexamine (μ), naltrindole (δ) and nor-binaltorphimine (κ).

Results: Intrathecal morphine caused dose-related antinociceptive effects that were reversed totally by naloxone. Intrathecal β-funaltrexamine and naltrindole did not reverse the effects of intrathecal morphine. However, intrathecal nor-binaltorphimine did reverse the electrical current threshold effects of morphine but not tail flick latency.

Conclusions: Antinociception following intrathecal morphine involves spinal and supraspinal opioid receptors. The tail flick effect described in rat experiments involves actions at opioid receptors in the brain that override any action that may be caused by combination of morphine with μ-opioid receptors in the spinal cord.

Summary

Background and objective: The aim of this study was to compare cardiac output (CO) measurements by arterial trans-cardiopulmonary thermodilution (ATD) and pulmonary arterial thermodilution (PATD) with CO estimated on the basis of the Fick calculation via a metabolic monitor in septic shock.

Methods: In a prospective animal study 20 anaesthetized, ventilated pigs (20.9 ± 1.9 kg) were investigated. Septic shock was induced with faecal peritonitis. A pulmonary artery catheter was used for conventional measurement of CO. Simultaneously ATD was measured with a thermistor tipped catheter inserted into right carotid artery. Whole body oxygen consumption was measured by indirect calorimetry. Eighty data pairs of simultaneous CO measurements were analysed.

Results: CO measured with Fick and that measured with PATD were significantly correlated (r = 0.94, r2 = 0.87, P < 0.001). Mean CO measured by PATD was 94.3 ± 40.1 mL min−1 kg−1. Bias was 10.1 mL min−1 kg−1 (95% confidence interval (CI): 6.0–14.2 mL min−1 kg−1) with limits of agreement of −26.8 to 47.0 mL min−1 kg−1 . Correlation between Fick derived CO estimation and ATD CO was similar (r = 0.91, r2 = 0.83, P < 0.001). Mean CO measured by trans-cardiopulmonary thermodilution was 104.3 ± 43.2 mL min−1 kg−1 . Bias was 0.75 mL min−1 kg−1 (95% CI: −3.8 to 5.3 mL min−1 kg−1) with limits of agreement of −39.7 to 41.2 mL min−1 kg−1.

Conclusions: Even during haemodynamic instability in septic shock the correlation of arterial trans-cardiopulmonary thermodilution and PATD derived CO with direct Fick was good. As arterial trans-cardiopulmonary thermodilution is less invasive than PATD, the former may offer practical advantages.

Nausea and vomiting are common side effects of opioids administered for pain control. This double-blind, randomized, parallel-group study evaluated the anti-emetic efficacy and tolerability of single intravenous (i.v.) doses of ondansetron 8 mg, ondansetron 16 mg and metoclopramide 10 mg in the treatment of opioid-induced emesis. Adult patients undergoing low emetogenic surgical procedures, using a standardized anaesthesia regimen were assessed for 24 h following administration of study anti-emetic to treat established post-surgical opioid-induced emesis. A total of 4511 patients were enrolled of whom 1366 experienced opioid-induced emesis and received randomized study medication. Ondansetron 8 mg and 16 mg were significantly better than metoclopramide 10 mg (P < 0.05) for both complete control of emesis, complete control of nausea and other efficacy measures. There were no significant differences between the two ondansetron groups. All three treatments were well tolerated. In conclusion, this large, multicentre study demonstrates that ondansetron is more effective than metoclopramide in the treatment of opioid-induced emesis following administration of post-surgical opioids to control pain.

A prospective observational study of 101 women having breast surgery under general anaesthesia was performed to assess the extent of postoperative nausea and vomiting in this group of women. The overall rate of postoperative nausea and vomiting was high, 56% and 41%, respectively, and was significantly associated with length of surgical procedure and morphine use. Techniques to reduce morphine requirement should be evaluated to try and reduce this cause ofmorbidity.