[Current aspects of anesthesia in neuromuscular diseases].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Wappler.
Explore the source record for details and available documents.
OBJECTIVE: The most frequently used drugs for premedication are benzodiazepines and alpha (2)-adrenoceptor agonists. In this study we examined midazolam and clonidine for premedication in combination with target controlled infusion anaesthesia (TCI) in patients undergoing orthopaedic shoulder surgery and analysed the effects on the peri- and postoperative course. METHODS: Forty-five Patients (ASA I-III) were included in this prospective randomized, double blind study. Sixty minutes prior to anaesthetic induction the patients received clonidine in a dosage of 2 microg x kg(-1) (group ND) or 5 microg x kg(-1) (group HD) or 0.1 mg x kg(-1) midazolam (group midazolam) per orally. Anaesthesia was performed as TCI with propofol (plasma concentration 2.0-4.0 microg x ml(-1)) und remifentanil (plasma concentration 0.2-0.4 microg x ml(-1) x min(-1)). 15 minutes before the operation was finished, all patients received a bolus dose of 0.1 mg x kg(-1) piritramid i.v., followed by administration of piritramid via a PCA pump (patient controlled analgesia) for a duration of 24 hours. During the time of the operation the influence of premedication on the anaesthetic course was determined by vital parameters and ranking scales. For statistic evaluation we used the Kruskal-Wallis test, ANOVA with Tukey as post hoc test and the test named after Fisher (p < 0.05). RESULTS: The effects of premedication on haemodynamic parameters and ranking scales for sedation as well as anaesthetic requirements were comparable in all three groups. In the postoperative period the incidence of postoperative nausea and vomiting (PONV) (ND: n = 8, HD: n = 2, midazolam: n = 6) and the use of pritramid were lower in the clonidine HD group (HD: 38.7 +/- 30.7 mg, ND: 51.7 +/- 25.1 mg, midazolam: 45.1 +/- 30.4 mg) than in the other groups. CONCLUSIONS: Premedication with the alpha(2)-adrenoceptor agonist clonidine is as good as with benzodiazepines in combination with TCI. Because of the lower incidence of PONV and the need of piritramid in the postoperative period patients premedicated with 5 microg x kg(-1) clonidine may benefit from this premedication.
BACKGROUND: Compound A, a degradation product of sevoflurane, has been demonstrated to induce sister chromatid exchanges (SCE) in Chinese hamster ovary cells in vitro as a marker for possible genotoxicity. We investigated the formation of SCE in mitogen-stimulated T-lymphocytes of 40 children undergoing sevoflurane anaesthesia for minor surgical procedures. METHODS: Anaesthesia was induced by inhalation of up to 8% sevoflurane and maintained at 2.5-3% in oxygen/nitrous oxide (65/35%) at a fresh gas flow of 3 litre min(-1). Soda lime (humidity 12-15%) was used as a carbon dioxide absorbent. Blood was drawn directly before induction and after termination of anaesthesia. Twenty-five second division metaphases of mitogen-stimulated T-lymphocytes per blood sample were screened for SCE rates using standard techniques. RESULTS: Average duration of anaesthesia was 49.6 (SD 24.0) min. Before anaesthesia induction, 7.93 (1.23) SCE per metaphase were determined. After sevoflurane anaesthesia [1.40 (0.77) MAC h] 7.92 (1.19) SCE per metaphase were observed. Additionally, no differences were evident between male or female children. CONCLUSION: Short-term administration of sevoflurane anaesthesia did not induce SCE in T-lymphocytes of children. No indication for a possible genotoxic effect has been observed.
Patients with Duchenne muscular dystrophy (DMD) are at high risk of perioperative complications. DMD may be accompanied by heart failure resulting from dystrophic involvement of the myocardium, which can be subclinical in the early stages of the disease. This case demonstrates that a normal preoperative ECG and echocardiograph cannot exclude the development of heart failure during anaesthesia in DMD patients undergoing major surgery.
BACKGROUND: The pathophysiology of the serotoninergic system in malignant hyperthermia (MH) is not completely understood. The serotonin-2 (5HT(2A)) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) induces typical MH symptoms, including skeletal muscle rigidity, an increase in body temperature, hyperventilation and acidosis in conscious MH-susceptible (MHS) pigs. Whether these symptoms are directly generated in skeletal muscle, result from central serotonergic overstimulation or from a porcine stress syndrome remains unresolved. In this study the in vivo effects of DOI on anaesthetized (and thus stress-protected) MHS and MH-normal (MHN) pigs were investigated. METHODS: and results. DOI 1 mg kg(-1) was administered three times at 40-min intervals to five MHS and five MHN anaesthetized pigs. Body temperature, heart rate, muscle tone, arterial carbon dioxide pressure (Pa(CO(2))), pH and creatine kinase concentrations were measured. The clinical occurrence of MH was defined by Pa(CO(2)) above 70 mm Hg and an increase in body temperature of more than 2 degrees C. Intragroup differences were analysed with the Friedman test as an overall non-parametric ANOVA and, in case of significance, with the Wilcoxon test. Intergroup comparisons were performed with the Mann-Whitney U-test (statistical significance P<0.05). MHS and MHN pigs developed muscle fasciculations, significant increases in body temperature and Pa(CO(2)) and a significant decrease in pH after the administration of DOI. These changes were comparable in both groups until the third dose of DOI, when in MHS pigs heart rate and Pa(CO(2)) rose significantly and pH fell significantly compared with MHN pigs. All MHS pigs fulfilled the MH criteria. Body temperature increased by more than 2 degrees C in all MHN pigs and Pa(CO(2)) exceeded 70 mm Hg in two. Thus, two MHN pigs fulfilled the criteria of MH. CONCLUSIONS: The comparability of the clinical presentation following DOI administration in MHS and MHN animals and the order of the development of MH-like symptoms favour the hypothesis of a central serotonergic overstimulation, leading to a serotonin syndrome.
Using the combined CLEO II and CLEO II.V data sets of 9.1 fb(-1) at the Upsilon(4S), we measure properties of psi mesons produced directly from decays of the B meson, where "B" denotes an admixture of B+, B-, B0, and B;(0), and "psi" denotes either J/psi(1S) or psi(2S). We report first measurements of psi polarization in B-->psi(direct)X: alpha(psi(1S))=-0.30(+0.07)(-0.06)+/-0.04 and alpha(psi(2S))=-0.45(+0.22)(-0.19)+/-0.04. We also report improved measurements of the momentum distributions of psi produced directly from B decays, correcting for measurement smearing. Finally, we report measurements of the inclusive branching fraction for B-->psiX and B-->chi(c1)X.
Using 13.53 fb(-1) of CLEO data, we have measured the ratios of the branching fractions R(+)(e),R(+)(mu) and the combined branching fraction ratio R(+)(l), defined by R(+)(l)=[B(D+-->K(*0)l(+)nu(l))]/[B(D+-->K-pi(+)pi(+))]. We find R(+)(e)=0.74+/-0.04+/-0.05, R(+)(mu)=0.72+/-0.10+/-0.05, and R(+)(l)=0.74+/-0.04+/-0.05, where the first and second errors are statistical and systematic, respectively. The known branching fraction B(D+-->K-pi(+)pi(+)) leads to B(D+-->K(*0)e(+)nu(e))=(6.7+/-0.4+/-0.5+/-0.4)%, B(D+-->K(*0)mu(+)nu(mu))=(6.5+/-0.9+/-0.5+/-0.4)%, and B(D+-->K(*0)l(+)nu(l))=(6.7+/-0.4+/-0.5+/-0.4)%, where the third error is due to the uncertainty in B(D+-->K-pi(+)pi(+)).
Using the CLEO detector at the Cornell Electron Storage Ring we have observed the Omega(0)(c) (css ground state) in the decay Omega(0)(c)-->Omega(-)e(+)nu(e). We find a signal of 11.4+/-3.8(stat) events. The probability that we have observed a background fluctuation is 7.6x10(-5). We measure B(Omega(0)(c)-->Omega(-)e(+)nu(e)).sigma(e(+)e(-)-->Omega(0)(c)X)=(42.2+/-14.1(stat)+/-5.7(syst)) fb and R=[Gamma(Omega(0)(c)-->Omega(-)pi(+))]/[Gamma(Omega(0)(c)-->Omega(-)enu(e))]=00.41+/-0.19(stat)+/-0.04(syst). This is the first statistically significant observation of an individual decay mode of the Omega(0)(c) in e(+)e(-) annihilation and the first example of a baryon decaying via beta emission, where no quarks from the first generation participate in the reaction.
We determine the weak coupling /V(cb)/ between the b and c quarks using a sample of 3 x 10(6) BB; events in the CLEO detector at the Cornell Electron Storage Ring. We determine the yield of reconstructed B-->D*l nu; decays as a function of w, the boost of the D* in the B rest frame, and from this we obtain the differential decay rate d Gamma/dw. By extrapolating d Gamma/dw to w=1, the kinematic end point at which the D* is at rest relative to the B, we extract the product /V(cb)/F(1), where F(1) is the form factor at w=1. Combined with theoretical results for F(1) we determine /V(cb)/=0.0469+/-0.0014(stat)+/-0.0020(syst)+/-0.0018(theor).
We report a new measurement of the Cabibbo-Kobayashi-Maskawa parameter Vub made with a sample of 9.7 x 10(6) BB- events collected with the CLEO II detector. Using heavy quark theory, we combine the observed yield of leptons from semileptonic B decay in the end-point momentum interval 2.2-2.6 GeV/c with recent CLEO II data on B-->X(s)gamma to find Vub = (4.08+/-0.34+/-0.44+/-0.16+/-0.24)x10(-3), where the first two uncertainties are experimental and the last two are from theory.
We search and find no evidence for CP violation in tau decays into the K(pi)nu(tau) final state. We provide limits on the imaginary part of the coupling constant Lambda describing a relative contribution of the CP violating processes with respect to the standard model to be -0.172<Im(Lambda)<0.067 at 90% C.L.
We report the first observation of the exclusive decays B-->D((*))K(*-), using 9.66 x 10(6) BB pairs collected at the Upsilon(4S) with the CLEO detector. We measure the following branching fractions: B(B--->D(0)K(*-)) = (6.1+/-1.6+/-1.7)x10(-4), B(B(0)-->D(+)K(*-)) = (3.7+/-1.5+/-1.0)x10(-4), B(B(0)-->D(*+)K(*-)) = (3.8+/-1.3+/-0.8)x10(-4), and B(B--->D(*0)K(*-)) = (7.7+/-2.2+/-2.6)x10(-4). The B-->D(*)K(*-) branching ratios are the averages of those corresponding to the 00 and 11 helicity states. The errors shown are statistical and systematic, respectively.
Explore the source record for details and available documents.
BACKGROUND AND OBJECTIVE: The in vitro contracture test with halothane and caffeine is the current gold standard for diagnosis of malignant hyperthermia. This test has a sensitivity of 99.0% but a specificity of only 93.6%. Therefore, an alternative drug is desirable which distinguishes between malignant hyperthermia-susceptible and malignant hyperthermia-normal subjects with a higher specificity and sensitivity. METHODS: 4-chloro-3-ethylphenol has recently been shown to trigger Ca2+-induced Ca2+-release in skeletal muscle terminal cisternae and to increase the myoplasmic free Ca2+ concentration in skeletal muscle fibres. The purpose of this study was to investigate the ability of 4-chloro-3-ethylphenol to distinguish between malignant hyperthermia-susceptible and malignant hyperthermia-normal porcine muscle specimen in the in vitro contracture test. Ten malignant hyperthermia-susceptible and 14 malignant hyperthermia-normal swine were anaesthetized and muscle biopsies were taken. For the in vitro contracture test muscle specimens were exposed to cumulative concentrations of 4-chloro-3-ethylphenol (12.5 to 200 micromol L(-1)). RESULTS: 4-chloro-3-ethylphenol produced contractures in a concentration-dependent manner in the malignant hyperthermia-susceptible muscle bundles. In contrast, cumulative 4-chloro-3-ethylphenol did not generate contractures in malignant hyperthermia-normal specimens. Contractures were significantly greater (P < 0.05) in the malignant hyperthermia-susceptible compared to the malignant hyperthermia-normal preparations in all 4-chloro-3-ethylphenol concentration steps from 50 micromol L(-1) to 200 micromol L(-1). There was no overlap between the two groups above a concentration of 75 micromol L(-1) in cumulative 4-chloro-3-ethylphenol in vitro contracture tests. CONCLUSIONS: It remains to be verified whether an in vitro contracture test with 4-chloro-3-ethylphenol can also discriminate between malignant hyperthermia-susceptible and malignant hyperthermia-normal humans. Since no prior tested agent revealed a clear differentiation in contracture development without overlap, the 4-chloro-3-ethylphenol test might be a promising new approach to the diagnosis of malignant hyperthermia.
We report on the general anesthesia in the case of an orthopedic surgery conducted on two brothers with sickle cell anemia. After concerted planning with a pediatric hematologist concerning the perioperative management an exchange transfusion was conducted ambulatorily before surgery. The following anesthesia under continuous fluid infusion, warming and regular hemoglobin and temperature control could be conducted without problems. One of the boys was treated with two heterologous red cell packs after an unexpected hemoglobin drop intraoperatively. The postoperative course was uneventful, especially concerning sickle cell relevant complications. The case reports are intended to show up the pathogenesis of patient-relevant sickle cell crises and critically evaluate central points of anesthesiological management, especially the choice of preoperative transfusion.
Explore the source record for details and available documents.
OBJECTIVE: The abuse of cocaine can cause serious medical complications like tachycardia, rhabdomyolysis, and hyperthermia. Because of the clinical similarities, it has been suggested that cocaine might be a trigger of malignant hyperthermia (MH). Therefore, aim of this study was to investigate the in-vitro effects of cocaine in skeletal muscle specimens of MH susceptible (MHS) and normal (MHN) patients. METHODS: 62 patients undergoing the in-vitro contracture test (IVCT) according to the protocol of the European MH Group (EMHG) for diagnosis of MH susceptibility were included in this study. In muscle specimens surplus to diagnostic requirements cocaine was added in order to achieve tissue bath concentrations of 0.01, 0.1 and 1.0 mM. The contracture development and twitch response have been registered. RESULTS: 21 patients were diagnosed as MHS and 36 patients as MHN. 5 patients tested as MH-equivocal (MHE) were excluded from the study. Following bolus administration of cocaine, no contracture development was observed in MHS, as well as MHN specimens. The muscle twitch decreased after cocaine administration significantly in both diagnostic groups. CONCLUSION: In contrast to the established MH trigger substances like volatile anaesthetics, cocaine produced no contracture development in MHS muscle specimens. Furthermore, cocaine produced a negative inotropic effect in all skeletal muscle preparations, which might be explained by local anaesthetic effects. Regarding these results, cocaine seems not to be a MH trigger agent.
Postoperative nausea and vomiting (PONV) are among the most common complications in operative medicine. Especially patients undergoing middle ear surgery or adenotonsillectomy are frequently associated with PONV (70 %). Furthermore, emesis carries the risk of severe postoperative complications and is associated with additional costs and distress in patient management. If the patient carries a high risk for postoperative emesis, the patient should receive a prophylactic antiemetic therapy. 5-HT 3 receptor antagonists are highly effective in prevention and management of PONV. This review will discuss pathophysiology, prophylaxis and treatment of postoperative nausea and vomiting after E.N.T. surgery.