[Characteristics of the fetal and infant respiratory system : What the pediatric anesthetist should know]. / Besonderheiten des fetalen und kindlichen Atmungssystems : Was der/die (Kinder­)Anästhesist*in wissen sollte.

Respiratory complications are the most frequent incidents in pediatric anesthesia after cardiac events. The pediatric respiratory physiology and airway anatomy are responsible for the particular respiratory vulnerability in this stage of life. This article explains the aspects of pulmonary embryogenesis relevant for anesthesia and their impact on the respiration of preterm infants and neonates. The respiratory distress syndrome and bronchopulmonary dysplasia are highlighted as well as the predisposition to apnea of preterm infants and neonates. Due to the anatomical characteristics, the low size ratios and the significantly shorter apnea tolerance, airway management in children frequently represents a challenge. This article gives useful assistance and provides an overview of formulas for calculating the appropriate tube size and depth of insertion. Finally, the pathophysiology and adequate treatment of laryngospasm are explained.

[Fetal and pediatric cardiovascular physiology : Things you should know as an (pediatric) anesthesiologist]. / Fetale und kindliche Herz-Kreislauf-Physiologie : Was der/die (Kinder­)Anästhesist*in wissen sollte.

Immediately after birth the physiology of the cardiovascular system of the neonate undergoes some significant changes. The first breaths in life and the inflation of the lungs lead to a considerable drop in pulmonary arterial resistance. This results in the closure of the foramen ovale and ductus arteriosus; however, during the first weeks of life a sharp rise in pulmonary vascular resistance caused by hypoxia, hypercapnia and excessive positive pressure ventilation can lead to the reopening of the ductus arteriosus. This may result in subsequent strain of the left heart. In order to anticipate the reopening of the ductus arteriosus, it is recommended to measure the saturation of peripheral oxygen not only preductal (right hand), but also postductal (feet).An excessive volume therapy should be avoided as the neonatal myocardium is hallmarked by low cardiac compliance, reduced contractility and reduced ventricular filling.Until now there is still no uniform definition of hypotension in pediatric patients. Blood pressure values that are measured in awake children or are derived from the 50% age percentile values can thus only be used as approximate values. In all cases it is mandatory to recognize and consistently treat hypotension during pediatric anesthesia in order to prevent postoperative organ damage, particularly of the brain.The transcranial measurement of cerebral regional oxygen saturation (c­rSO2) by means of near-infrared spectroscopy (NIRS) provides valuable information about regional tissue oxygenation of the brain. This enables conclusions about the state of the multifactorial cerebral perfusion to be drawn. In this way monitoring of the hypoxia sensitive cerebral tissue can be accomplished and should be used in premature infants and neonates. When measuring a baseline in awake patients, a 20% drop of c­rSO2 from this baseline should be challenged and treated if necessary.

Monocyte phagocytosis of viable Staphylococcus aureus is impaired by barbiturates, but not by propofol.

BACKGROUND: Barbiturates and propofol are used for deep sedation of patients with elevated intracranial pressure refractory to standard therapeutic regimens. Such patients often suffer from bacterial infections, which are most commonly caused by Staphylococcus aureus. Various interactions of anesthetics with components of the host defense have been documented, but very little is known about the influence on monocytes, which are a first-line defense against bacterial invasion. Therefore, we studied the effects of thiopental, methohexital, and propofol on monocyte phagocytosis using an in vitro whole blood model of viable S. aureus. MATERIALS AND METHODS: Whole blood samples were preincubated with different concentrations of thiopental, methohexital, and propofol. Phagocytosis was stopped at different time points after addition of viable S. aureus. Monocytes then were stained with monoclonal antibodies for flow cytometric analysis of monocyte recruitment (ratio of ingesting monocytes). Furthermore, the fluorescence intensity of ingested bacteria served as semiquantitative measurement of phagocytosis activity. RESULTS: Both barbiturates inhibited monocyte recruitment and phagocytosis activity concentration-dependently, whereas propofol did not affect any of the investigated parameters. At concentrations of 7.6 x10(-3) M thiopental or 1.1 x 10(-3) M methohexital and greater, monocyte recruitment and phagocytosis activity were significantly inhibited. The calculated half-maximum inhibitory concentration (IC50) of thiopental was 8.4 x 10(-3) M for monocyte recruitment and 8.6 x 10(-3) M for phagocytosis activity. The corresponding values for methohexital were 4.1 x 10(-3) M and 1.1 x 10(-3) M, respectively. CONCLUSION: The two barbiturates induce concentration-dependent inhibition of monocyte phagocytosis, whereas propofol is without effect. In combination with previously described effects on granulocyte function, these findings suggest that defense against bacterial infection might be reduced by barbiturates.

Rhabdomyolysis in an obese patient after total knee arthroplasty.

We report the case of a morbidly obese patient who developed rhabdomyolysis with acute renal failure, hepatic dysfunction, and an increase of cardiac troponin-1 after total knee arthroplasty. Postoperative rhabdomyolysis has a wide range of triggers and differential diagnoses that should be considered by the anaesthesiologist and surgeons. We would like to emphasize that morbidly obese patients have an increased risk of developing postoperative rhabdomyolysis potentially leading to life-threatening disease. Intensified postoperative observation seem justified in these patients.

Remifentanil or sufentanil for coronary surgery: comparison of postoperative respiratory impairment.

BACKGROUND AND OBJECTIVE: High-dose opioid anaesthesia contributes to decreasing metabolic and hormonal stress responses in patients undergoing cardiac surgery. However, the increase in context-sensitive half-life of opioids given as a high-dose regimen can affect postoperative respiratory recovery. In contrast, remifentanil can be given in high doses without prolonging context-sensitive half-life due to its rapid metabolism. Therefore, we performed a prospective, randomized trial to compare anaesthesia consisting of propofol/remifentanil or propofol/sufentanil with regard to postoperative respiratory function and outcome. METHODS: Patients undergoing coronary artery bypass grafting were randomized to a propofol/remifentanil (0.5-1.0 microg kg(-1) min(-1)) or propofol/sufentanil (30-40 ng kg(-1) min(-1)) based anaesthetic. Carbon dioxide response, forced expiratory volume in one second, vital capacity, and functional residual capacity were measured 1 day prior to the operation, 1 h before extubation, 1, 24 and 72 h after extubation. In addition, the incidence of atelectasis, pulmonary infiltrates, intensive care unit and postoperative length of stay were compared. Patients and physicians were blinded to the treatment group. RESULTS: Twenty-five patients in each treatment group completed the study. There was no difference between patients of the treatment groups regarding demographics, risk- or pain scores. In all patients, carbon dioxide response, forced expiratory volume in one second, vital capacity and functional residual capacity were decreased postoperatively compared to baseline. Patients randomized to remifentanil had less depression of carbon dioxide response, less atelectasis and shorter postoperative length of stay (12 d vs. 10 d) than after sufentanil (P < 0.05). CONCLUSIONS: Intraoperative use of high-dose remifentanil for coronary artery bypass grafting may be associated with improved recovery of pulmonary function and shorter postoperative hospital length of stay than sufentanil.

[Effects of reduced shear stress on inflammatory reactions in vitro. Effects of pathological flow conditions on leukocyte-endothelial interactions and monocyte tissue factor expression in human cell cultures]. / Einfluss verminderter Scherkräfte auf Entzündungsreaktionen in vitro Effekte pathologischer Strömungsbedingungen auf Leukozyten-Endothel-Interaktionen und monozytäre "Tissue-factor-Expression" in humanen Zellkulturen.

BACKGROUND: During malperfusion and inflammation leukocyte adhesion is common. The purpose of this study was to examine the effects of reduced shear stress on leukocyte-endothelial interactions and subsequent inflammatory reactions such as up-regulation of tissue factor. METHODS: Isolated neutrophils and monocytes were co-incubated with human umbilical venous endothelium at 0-3 dynes/cm(2) in a flow chamber. Adhesion and tissue factor expression on adherent leukocytes were examined at various flow conditions. RESULTS: At 2-3 dynes/cm(2) adhesion occurred only on TNFalpha-activated endothelium. Below 1 dyne/cm(2) similarly increased adhesion was also observed on non-activated endothelium. As was observed for leukocyte adhesion, these shear stress-dependent cell interactions also resulted in an up-regulation of tissue factor on adherent monocytes from non-activated co-cultures. CONCLUSION: Apart from additional activators of inflammation, reduced shear forces may directly contribute to inflammation.

Release of S(+) enantiomers in breath samples after anaesthesia with isoflurane racemate.

BACKGROUND AND OBJECTIVE: Isoflurane is a chiral volatile anaesthetic, routinely administered as racemate. It has a low metabolic rate and is mostly eliminated via respiration. In blood samples, S(+) enantiomers are found in greater proportion in the days immediately after administration of isoflurane racemate whereas the ratio in breath samples is unknown. METHODS: Breath and blood samples were drawn immediately after recovery and daily up to 19 days after operation from patients undergoing anaesthesia with isoflurane racemate. The percentage of isoflurane enantiomer was determined by gas chromatography mass spectrometry in blood and thermodesorption gas chromatography mass spectrometry in breath samples. RESULTS: In breath samples, there were significant differences in S(+) enantiomers at all time points compared to the racemate. During the early postoperative phase, the percentage of S(+) enantiomers were significantly enhanced whereas 5 days after surgery predominantly R(-) enantiomers (50.41%) were detected in the breath samples. Also in blood samples a statistical significant accumulation of the S(+) enantiomer was noted between days 1 and 5 compared to isoflurane racemate blood control. S(+) enantiomers were significantly higher in blood compared to breath samples and was most evident on the third day after surgery (51.43%). CONCLUSIONS: During the first days after application of isoflurane racemate, the percentage of S(+) enantiomers are higher in breath and blood samples of patients. We suggest that resorption and/or redistribution of enantiomers are responsible for the different kinetics of isoflurane enantiomers.

[Aortocaval compression syndrome]. / Aortokavales Kompressionssyndrom.

Aortocaval compression syndrome (supine hypotensive syndrome) represents a common complication mainly of late pregnancy, although the syndrome has been described to occur as early as 16 weeks of gestation. The nature and severity of symptoms range from unspecific complaints to severe maternal hypotension, loss of consciousness, cardiovascular collapse, and consecutive fetal depression. Predominantly, the syndrome is provoked by placing the parturient supine. Since supine positioning is required for diverse diagnostic and therapeutic procedures in obstetrics, these involve increased risk of aortocaval compression. For the anesthetist, cesarean section is most relevant, because of the coincidence of several risk factors. The following article begins by reviewing the pathophysiology of the syndrome, known risk factors and anesthesiological procedures that predispose to the syndrome. The second part is concerned with prophylactic measures and therapeutic options, together with the discussion of a clinically practicable algorithm.

Endothelial accumulation of hydroxyethyl starch and functional consequences on leukocyte-endothelial interactions.

To date, accumulation of hydroxyethyl starch (HES) has been studied mainly in skin specimens, but there are no detailed reports available regarding starch accumulation in the endothelium. Because endothelial cells play an essential role during shock, we studied the accumulation of HES in human umbilical venous endothelial cells (HUVEC). HUVEC (n = 9) were incubated with a fluorescein-conjugated HES 200/0.5 (FITC-HES) at 0.5-20 mg/ml for 1-72 h. FITC-HES was internalized dose- and time-dependently by pinocytosis into secondary lysosomes. Asymptotic elimination curves showed that 50% of the formerly ingested molecules could not be eliminated. Despite accumulation, starch molecules did not attenuate the expression of E-selectin, ICAM-1 or VCAM-1 on TNF-alpha-activated HUVEC. However, apart from adhesion molecule expression, perfusion studies showed that HES reduced neutrophil adhesion by direct inhibition of integrin-mediated interactions.

Accumulation of S(+) enantiomer in human beings after general anaesthesia with isoflurane racemate.

BACKGROUND AND OBJECTIVE: Isoflurane is a chiral, volatile anaesthetic with low metabolic rate (0.17%) that is routinely administered in its racemic form. Knowledge about the distribution of the enantiomers in human beings may give some important information about the understanding of the mechanisms of volatile anaesthetics. METHODS: Blood samples were drawn immediately after tracheal extubation and daily up to 8 days postoperatively from patients undergoing general anaesthesia with isoflurane racemate. The enantiomer enrichment of isoflurane was determined by headspace gas chromatography-mass spectrometry. RESULTS: At all time points, there was a statistically significant accumulation of the S(+) enantiomer in blood, especially at days 2 (52.01%) and 7 (52.1%). Separate analysis of obese patients or in a small group of patients with co-existing lung disease did not show any difference to the total population. In addition, duration of anaesthesia did not influence the enantiomer concentrations. CONCLUSIONS: We suggest that a slower association and dissociation rate is responsible for the S(+) enrichment.

Inducible expression of inflammatory chemokines in respiratory syncytial virus-infected mice: role of MIP-1alpha in lung pathology.

Lower respiratory tract disease caused by respiratory syncytial virus (RSV) is characterized by profound airway mucosa inflammation, both in infants with naturally acquired infection and in experimentally inoculated animal models. Chemokines are central regulatory molecules in inflammatory, immune, and infectious processes of the lung. In this study, we demonstrate that intranasal infection of BALB/c mice with RSV A results in inducible expression of lung chemokines belonging to the CXC (MIP-2 and IP-10), CC (RANTES, eotaxin, MIP-1beta, MIP-1alpha, MCP-1, TCA-3) and C (lymphotactin) families. Chemokine mRNA expression occurred as early as 24 h following inoculation and persisted for at least 5 days in mice inoculated with the highest dose of virus (10(7) PFU). In general, levels of chemokine mRNA and protein were dependent on the dose of RSV inoculum and paralleled the intensity of lung cellular inflammation. Immunohisthochemical studies indicated that RSV-induced expression of MIP-1alpha, one of the most abundantly expressed chemokines, was primarily localized in epithelial cells of the alveoli and bronchioles, as well as in adjoining capillary endothelium. Genetically altered mice with a selective deletion of the MIP-1alpha gene (-/- mice) demonstrated a significant reduction in lung inflammation following RSV infection, compared to control littermates (+/+ mice). Despite the paucity of infiltrating cells, the peak RSV titer in the lung of -/- mice was not significantly different from that observed in +/+ mice. These results provide the first direct evidence that RSV infection may induce lung inflammation via the early production of inflammatory chemokines.