Acta Anaesthesiologica Scandinavica

Background:  The aim of this study was to investigate the effects of pre‐operative dexmedetomidine infusion on hemodynamics in patients with pulmonary hypertension undergoing mitral valve replacement surgery.

Methods:  Patients were randomly divided into placebo (group P, n= 16) and dexmedetomidine (group D, n= 16) groups. In group D, a 1 μg/kg bolus dose of dexmedetomidine was administered 10 min before the induction of anesthesia, followed by a 0.4 μg/kg/h infusion until the surgical incision. Anesthesia was induced with lidocaine (1 mg/kg), midazolam (0.2 mg/kg) and fentanyl (5 μg/kg) in both groups. Anesthesia was maintained with 0.5% isoflurane and fentanyl depending on the hemodynamic situation. The hemodynamic values during the investigation were obtained.

Results:  In group D, the mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP) and pulmonary capillary wedge pressure (PCWP) were decreased effectively in comparison with the values in the placebo group (P < 0.05), and there was an attenuation in the increase in the systemic vascular resistance index (SVRI) and pulmonary vascular resistance index (PVRI) at the post‐sternotomy period.

Conclusions:  The pre‐operative administration of the α₂‐agonist dexmedetomidine decreases the fentanyl requirement and attenuates the increase in SVRI and PVRI at the post‐sternotomy period relative to the baseline levels, and decreases effectively MAP, MPAP and PCWP in comparison with the values in the placebo group, in patients with pulmonary hypertension undergoing mitral valve replacement surgery.

The effect of thoracic (T_7–8) epidural etidocaine 1.5%, 9 ml, and continuous per‐ and postoperative epidural infusion of etidocaine 1.5%, 4 ml/h, on early (?<500 ms) somatosensory evoked potentials (SEPs), and cortisol and glucose in plasma during cholecystectomy, was examined in ten patients. Spread of analgesia (pin‐prick) was T₃ (T₁–T₃) to L₂ (T₁₁–L₃) 35 min after injection of etidocaine, and T₃ (T₂–T₄) to T₁₂ (T₈–L₄) 3 h after surgical incision (median (range)). Before operation, epidural etidocaine had no significant effects on peak‐to‐peak amplitude of SEPs to electrical stimulation at the L₁ T₁₀ or T₆ dermatomal level (P>0.09). SEPs were abolished in only two patients at T₆, and no patient had SEPs abolished at T₁₀ or L₁. The plasma concentrations of cortisol and glucose were significantly increased 20 min after surgical incision and remained increased throughout the study. No correlation was found between the block‐induced decrease in the peak‐to‐peak amplitude at T₆ or T₁₀ and increase in plasma cortisol, except for a negative correlation at T₁₀ and the initial increase in cortisol (Rs = 0.72, P = 0.03). In conclusion, thoracic epidural administration of 9 ml of etidocaine 1.5% does not provide total afferent somatic blockade assessed by SEP and the stress response to cholecystectomy.

Background:  Mild perioperative hypothermia produces morbid cardiac outcomes that may result from sympathetically induced hypertension. However, volatile anesthetics produce vasodilatation that may reduce the hemodynamic response to hypothermia. We tested the hypothesis that the volatile anesthetics isoflurane and desflurane blunt the normal cold‐induced hypertensive response.

Methods:  We analyzed prospective data from three analogous studies: 1) 10 volunteers given desflurane (2.6 Volume percentage) maintained in left‐lateral position; 2) nine volunteers without anesthesia or anesthetized with various doses of desflurane; and 3) eight volunteers given various concentrations of isoflurane. Mean skin temperature was reduced to 31 C, which decreased core body temperature and triggered thermoregulatory vasoconstriction. Mean arterial pressures were determined before and after hypothermia provoked intense thermoregulatory vasoconstriction.

Results:  The hemodynamic responses to thermoregulatory vasoconstriction were similar without anesthesia and at all concentrations of desflurane and isoflurane. On average, mean arterial pressure increased 14 (SD = 5) mmHg with and without anesthesia.

Conclusion:  We conclude that thermoregulatory vasoconstriction significantly increases arterial pressure with or without isoflurane or desflurane anesthesia.

Background: We investigated the incidence and severity of post‐injury morbidity and mortality in intensive care unit (ICU)‐treated trauma patients. We also identified risk factors in the early phase after injury that predicted the later development of complications.

Methods: A prospective observational cohort study design was used. One hundred and sixty‐four adult patients admitted to the ICU for more than 24 h were included during a 21‐month period. The incidence and severity of morbidity such as multiple organ failure (MOF), acute lung injury (ALI), severe sepsis and 30‐day post‐injury mortality were calculated and risk factors were analyzed with uni‐ and multivariable logistic regression analysis.

Results: The median age was 40 years, the injury severity score was 24, the new injury severity score was 29, the acute physiology and chronic health evaluation II score was 15, sequential organ failure assessment maximum was 7 and ICU length of stay was 3.1 days. The incidences of post‐injury MOF were 40.2%, ALI 25.6%, severe sepsis 31.1% and 30‐day mortality 10.4%. The independent risk factors differed to some extent between the outcome parameters. Age, severity of injury, significant head injury and massive transfusion were independent risk factors for several outcome parameters. Positive blood alcohol was only a predictor of MOF, whereas prolonged rescue time only predicted death. Unexpectedly, injury severity was not an independent risk factor for mortality.

Conclusions: Although the incidence of morbidity was considerable, mortality was relatively low. Early post‐injury risk factors that predicted later development of complications differed between morbidity and mortality.

Background:  We wished to assess the development in number and impact of publications in anaesthesiology and intensive care medicine from 1981 to 2000 in the four Scandinavian countries: Sweden, Norway, Finland, and Denmark. For comparison, we also analyzed data from the UK and the Netherlands.

Methods:  Publication and citation data from 1981 to 2000 were gathered from National Science Indicators (2001), covering 33 journals indexed in Current Contents. Data were analyzed in running 5‐year periods. The following informetric indicators were used: absolute number of publications; absolute number of citations; absolute citation impact (average number of citations per publication per 5‐year period); citation impact relative to the European Union and the world; and the percentage of cited papers from each country.

Results:  The annual number of publications from Denmark was stable over the 20‐year period. Sweden increased its production by 35%, while the remaining four countries showed increases from 100% to 146%. Thus, Sweden and Denmark lost visibility within the European Union (EU) and in world context. The EU and world citation shares of Finland and Norway increased slightly, whereas those of Sweden, Denmark, the UK, and the Netherlands all declined significantly. The absolute citation impact (ACI) increased for all the four Scandinavian countries. The ACI of the Netherlands did not change and was surpassed by all the Scandinavian countries by 1994–98, while the UK finished below the other five countries.

Conclusions:  (1) The annual number of publications from Sweden, Norway, Finland, the UK, and the Netherlands increased after the late eighties, whereas the net publication output from Denmark was stagnant over the 20‐year period investigated; (2) the international publication and citation visibility of Finland and Norway increased slightly, as opposed to the significant decrease seen by the other four countries; (3) judging from the increase in absolute and relative citation impact and in the percentage of cited papers, the recognition of publications from the four Scandinavian countries increased over the past 20 years.

Background: The number of citations an article receives reflects its scientific impact. The introduction of internet‐based resources to search and access articles has made it possible to review even whole scientific areas. This study identifies the top 50 most‐cited articles over the last 25 years in speciality journals dedicated to anaesthesia and pain, respectively.

Methods: Twenty‐two journals listed in The Science Citation Index Expanded™ in the field of anaesthesiology and nine major medical journals were screened using the cited reference option to identify articles cited more than 100 times between 1986 and 2002. The top 50 articles in speciality journals and the top 10 articles in major medical journals concerning anaesthesia and pain were retrieved for further analysis.

Results:  The most‐cited articles in speciality journals were published from 1986 to 1997 and received a mean of 222 (anaesthesia) and 279 (pain) citations. Sixty‐seven institutions produced the most‐cited articles and of those 28 were located outside North America. The articles were published in six journals led by the Journal of Pain (50 articles) and Journal of Anaesthesiology (39 articles). Forty‐seven articles were classified as related to clinical experience, 33 were review articles, and 20 discussed basic science.

Conclusion:  To make an article a possible ‘citation classic’ in anaesthesiology, it should be published in one of six leading journals and originate from an established institute in North America. Internet resources to publish and cite the literature have to date not advanced any article published in the last 5 years to the top 100 list.

Background: We sometimes encounter impairment of learning and memory after general anesthesia in elderly patients. The aim of this study was to examine age‐related modifications of the effects of ketamine and propofol on rat hippocampal acetylcholine (ACh) release because hippocampal cholinergic neurons are supposed to be involved in learning and memory.

Methods: The experiments were performed on male Wistar young rats (2 months old) and old rats (18 months old), using in vivo brain microdialysis technique under freely moving condition. After initial sampling of three collections, test drugs were administered. The ACh release was determined by the HPLC‐ECD method.

Results: In old rats, the hippocampal basal ACh release was significantly lower than in young rats. Ketamine (25 and 50 mg kg⁻¹ i.p.) increased and propofol (25 and 50 mg kg⁻¹ i.p.) decreased the hippocampal ACh release in both young and old rats. Furthermore, ketamine 50 mg kg⁻¹ i.p. (anesthetic dose) produced facilitatory effects on the hippocampal ACh release in young rats (193% of the basal release), while in old rats the same dose of ketamine i.p. produced more pronounced facilitatory effects on the hippocampal ACh release (317% of the basal release). On the other hand, propofol 50 mg kg⁻¹ i.p. (anesthetic dose) produced inhibitory effects on the hippocampal ACh release in young rats (56% of control) and in old rats (77% of control). Although the maximal inhibitory peak effects of propofol 50 mg kg⁻¹ i.p. did not differ significantly between young rats and old rats, decrease of the hippocampal ACh release in old rats persisted longer than in young rats.

Conclusion: Ketamine produced more pronounced facilitatory effects on the hippocampal ACh release in old rats, as compared with young rats. On the other hand, propofol has inhibitory effects on the hippocampal ACh release in young and old rats. The aging process may suppress the ability to recover from the inhibitory anesthetic state induced by propofol.

Bradycardia and hypotension were the first major signs of toxicity from a 250 mg bupivacaine axillary brachial plexus block experienced by a patient with chronic renal failure, who had an anion gap acidosis and hyperkalemia. Without these metabolic abnormalities, this patient received four similar blocks: three were without incident and one was complicated by seizure. Acidosis and/or hyperkalemia in man appears to increase the myocardial susceptibility to bupivacaine toxicity into the range of arterial concentrations of the drug normally produced by plexus blocks, even in the absence of drug‐induced cerebral toxicity, seizures and hypoxia.