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E Pfenninger

Publications and source records attributed to E Pfenninger.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Clinical randomized controlled studies in anesthesiology according to quality guidelines of good clinical practice. 2: Principles of implementation, analysis, publication and evaluation].

This article was written to give researchers and clinicians a short synopsis of ethical and thorough design, conduct, analysis, publication, and interpretation of randomised controlled clinical trials according to the European quality standards of Good Clinical Practice (GCP). The paper consists of two parts. In the first part we introduce important elements of study design, especially study hypothesis, criteria of inclusion and study population, sample size calculation, validity considerations, bias and confounding, randomisation, stratification, and masking of treatment assignment. Different treatment allocation like multiple parallel groups, factorial experiment, cross-over, and sequential design are presented. Requirements of ethical standards according to the Declaration of Helsinki are discussed for their necessity in any experimentation in humans. Principles of informed consent are demonstrated with emphasis on special conditions in anaesthesia, emergency medicine, and intensive care research. In the second part of this article we explain issues of baseline assessment, experimental intervention, data recording, and data monitoring, particularly of negative or hazardous treatment effects. Topics of data analysis and reporting of trial results in publications are illustrated with regard to their influence on subsequent interpretation.

Anesthesiology↗
PubMed1994

[Do we need trauma scoring in emergency medicine?].

Trauma scores in emergency medicine quantitatively characterise the severity of trauma victims' injuries and physiologic derangements. They are used to detect and assess patients and have applications in guiding patient care and early therapeutic decisions. In the pre-clinical setting, an effective trauma index meets the following criteria: It is highly reliable with regard to identifying high- and low-risk patients. It has high face-validity. It has high inter- and intra-rater reliability. It is easy to use and allows rapid, accurate measurements. The most widely accepted injury severity index is probably the Injury Severity Score (ISS). It is calculated as the sum of the squares of the three most severely injured body regions, and was originally developed as a means to standardise the description of injuries sustained in motor vehicle accidents. The Trauma Score (TS) represents the gold standard of physiologic scoring of injury severity. It summarises the numerical assessments of the central nervous and cardiopulmonary system functions. The recently developed Mainz Emergency Evaluation Score (MEES) is based upon numerical specification of the vital signs, including a pain scale, and has been designed as a dynamic score. Nevertheless, limitations of the established trauma score systems have been described. Mortality and patient outcome do not strictly correlate with injury severity scoring. In addition, intubated or paralysed patients were excluded from outcome studies since the scoring systems lacked options for evaluation of pathophysiological conditions after therapeutic interventions. Thus, therapeutic efficacy could hardly be assessed, and subsequent scoring during time periods was impossible.(ABSTRACT TRUNCATED AT 250 WORDS)

Emergency Medicine↗
PubMed1994

[Psychometric changes as well as analgesic action and cardiovascular adverse effects of ketamine racemate versus s-(+)-ketamine in subanesthetic doses].

The intravenous anaesthetic ketamine is widely used in subanaesthetic doses as a potent analgesic in emergency and disaster medicine. At present, ketamine is commercially available only in its racemic form, although the S(+)-isomer has proved to be approximately three times as potent than the R(-)-isomer. In first clinical trials in Germany, S(+)-ketamine was reported to be markedly advantageous with regard to analgesia in anaesthetized patients. We therefore evaluated ketamine's analgesic and psychotropic effects in subanaesthetic doses given to healthy volunteers. MATERIALS AND METHODS. After institutional approval of the study by the university's Ethics Committee, 16 volunteers received ketamine racemate (1 mg/kg) and S(+)-ketamine (0.5 mg/kg) i.m. with 1-week intervals between injections in a randomized, double-blind fashion. Analgesia (electric pain stimulation of the median nerve), long-term memory, anterograde amnesia (recognition of simple pictures), motor coordination (Trieger test), immediate recall (short test of general intelligence) and concentration capacity (CI test: recognition of a preselected symbol among several symbols) were measured over a 60-min period and mean arterial pressure, heart rate, and ketamine plasma levels in venous blood samples were determined. Values were calculated as means and data were analysed by Wilcoxon's paired test for group comparison. RESULTS. Within 15 min, both agents induced a measurable degree of analgesia. After ketamine racemate, the level of pain tolerated increased from 38.8 +/- 14.0 to 57.0 +/- 13.7 mA and after S(+)-ketamine, from 36.9 +/- 10.5 to 53.3 +/- 15.2 mA. Ketamine racemate did not exert measurable effects on long-term memory, whereas anterograde amnesia was observed in 46% and 54% of the study subjects after 15 and 30 min, respectively. However, after S(+)-ketamine, only 8% of the volunteers demonstrated anterograde amnesia (P < 0.05). Immediate recall also declined in both groups (baseline: 5 points, after 15 min: 3.5 points for ketamine racemate, 4 points for S(+)-ketamine), whereas concentration capacity worsened from 14.5 +/- 3.8 s to 35.9 +/- 18.6 s after ketamine racemate and significantly less, from 14.8 +/- 2.5 s to 22.9 +/- 7.6 s, after S(+)-ketamine (P < 0.01). Furthermore, after 15 min, ketamine racemate induced an increase in heart rates from 73 +/- 15 b/min to 97 +/- 11 b/min, while S(+)-ketamine raised heart rates from 74 +/- 13 b/min to 89 +/- 11 b/min only (P < 0.05). Mean arterial pressure increased from 97 +/- 11 mmHg to 111 +/- 9 mmHg after ketamine racemate and from 92 +/- 11 mmHg to 110 +/- 13 mmHg after S(+)-ketamine (not significantly different). CONCLUSION. S(+)-Ketamine at half-dose of ketamine-racemate is as potent as ketamine-racemate in subanaesthetic doses with powerful analgesic properties. The (+)-isomer exerts less adverse effects on measurable cerebral functions and induces a significantly smaller increase in heart rate. Since states of impaired consciousness and disorientation are especially disturbing under emergency conditions, further investigations should be carried out to define S(+)-ketamine's position as a potent analgesic for therapeutic use in emergency and disaster medicine.

Adult↗
PubMed1993

[Management of the patient with craniocerebral injuries at the accident site and clinic admission].

Between January 1991 and December 1992, there were 686 rescue operations involving patients with craniocerebral trauma in the catchment area of Ulm. There were 376 patients who had to be graded as seriously injured according to the NACA classification. In 178 cases there was a severe craniocerebral trauma, and 131 of these patients were admitted to the traumatology department of the University of Ulm. The pattern of injuries was analysed; multiple injuries were found in 63 patients, with injuries to the extremities and the thorax being most-frequent. The primary preclinical treatment for patients with craniocerebral trauma is demonstrated; the indications for intubation and artificial respiration are discussed, and also the selection of drugs. Diagnostic procedures and immediate treatment must initially be directed at securing vital functions. Treatment of life-threatening haemorrhage has priority over neurosurgical diagnosis and therapy. The urgent indications for neurosurgical intervention are: space-occupying intracranial bleeding, open craniocerebral traumas, and space-occupying depressed fractures.

Brain Injuries↗
PubMed1991

The consequences of continuous haemofiltration on lung mechanics and extravascular lung water in a porcine endotoxic shock model.

Endotoxinaemia (E. coli endotoxin, 0.111.B4) and pulmonary hypertension were evoked in 20 swine, randomly assigned to receive either zero-balanced venovenous haemofiltration (HF) with an ultrafiltration and replacement rate of 600 ml/h (HF group, n = 10) or to undergo an uninfluenced spontaneous course (E group, n = 10) during a constant infusion of endotoxin until the end of the experiment. Endotoxin-induced pulmonary dysfunction was assessed on the basis of extravascular lung water (EVLW) using a thermo-dye technique via a fiberoptic intra-aortic probe, gas exchange and lung mechanics, the latter derived by a pressure-volume loop (P/V loop) of the respiratory system (super syringe, flow 30 ml/s, tidal volume 600 ml). A comparable increase in alveolo-arterial oxygen difference and a constant EVLW was observed in both groups. The progressive deterioration of hysteresis area and compliance parameters by endotoxinaemia was significantly blunted by HF. Independent of an impact on pulmonary oedema zero-balanced HF modifies endotoxin induced lung injury, probably by the convective transport of mediator substances.

Animals↗
PubMed1991

[Mechanical ventilation in an anesthetic circle system using the lowest tidal volume--studies of 3 anesthesia ventilators in a lung model and an animal experiment].

No anesthesia ventilator attached to a circle system is manufactured for use in neonates. However, a small bellows can be supplied for the following anesthesia ventilators: Spiromat NS 656 (NS), Ventilog 2 (V2) and AV1 (Draeger Co.) We investigated the minimal tidal volume delivered by each of the three ventilators. In addition, we tested the performance of the AV1 in neonatal piglets for manual and controlled ventilation, and in decreased lung compliance. MATERIALS AND METHODS. All circuits were equipped with one CO2 canister (750 ml) and the low-compliance tubes of the "Ulmer Kinder Set" (Ruesch Co.) The circuits were connected to a lung model consisting of a glass cylinder filled with copper wool with a compliance of 3.0 ml/mbar. By using calibrated glass syringes we created a pressure-volume correlation for the entire system, i.e., the lung model, the anesthesia circuit and the ventilator, which was linear for each of the three ventilators. The pressure was measured in the test lung. The pressure increase caused by the tidal volume therefore reflected the actual tidal volume delivered, which was calculated using the pressure-volume correlation. Tidal volumes were determined for varying the fresh gas flow (FGF), the respiratory rate (RR), which was varied between 20 and 60/min and the I:E ratio (IE), which was varied between 1:1 and 1:2. Six newborn piglets aged 2-12 h and with body weight 1000-1300 g were anesthetized, tracheotomized and ventilated with an oxygen-nitrous oxide mixture (FIO2 0.25). The manual ventilation lasted 30 min (period 1) and was followed by mechanical ventilation for 60 min (period 2). Thereafter, a left pneumothorax with constant pressure of 20 mbar and then 40 mbar for 15 min each was created (period 3). A fall in blood pressure was treated with 10 ml colloids in five of the six animals. During the experiment arterial blood pressure in the carotid artery, mean airway pressure at the distal end of the tracheal tube and end-tidal CO2 were continuously recorded. Arterial blood gases were analyzed at the end of each period. RESULTS. The tidal volumes delivered with an identical position of the bellows varied in ventilators NS and V2 with changes in FGF, RR and IE. Decrease in FGF, higher RR and longer expiration resulted in a decrease in the tidal volume. The "smallest" tidal volume delivered by NS varied from 50 ml (FGF 2 l/min, RR 60, IE 1:2) to 188 ml (FGF 4 l/min, RR 20, IE 1:1) and from 11 ml (FGF 2 l/min, RR 60, IE 1:2) to 110 (FGF 4 l/min, RR 20, IE 1:1) in the V2. The AV1 showed a minimal tidal volume of about 5 ml, and no changes in tidal volume attributable to alterations in FGF, RR or IE could be observed. No problems occurred during manual or mechanical ventilation in the piglets. With the experimental decrease in lung compliance no increase in airway pressure was noted, but an increase in arterial pCO2 by 8 mmHg (mean) reflects hypoventilation that was not corrected by the ventilator. DISCUSSION. We believe that the changes in tidal volume in ventilators NS and V2 are caused by adding FGF to the volume delivered by the below during inspiration. Because of the unpredictability of the tidal volumes, these ventilators are not suitable for the use in neonates. The AV1 has a very low systemic compliance which makes it suitable for use in neonatal anesthesia. However, a decrease in lung compliance is not compensated by an increase in airway pressure and leads to hypoventilation. When small tidal volumes are used in patients with low lung compliance, it does not act as expected of a volume-cycled ventilator.

Anesthesiology↗
PubMed1991

[Epinephrine and norepinephrine release immediately following acute cranio-cerebral trauma and the resulting metabolic changes].

Severe head injury leads to typical cardiocirculatory and metabolic changes by massive release of catecholamines. However, in the literature no data on these disturbances are available in humans in the preclinical phase. Therefore we measured in 34 head injured patients at the site of the accident and after hospital admission the degree of unconsciousness (Glasgow-Coma-Scale), blood pressure, heart rate, catecholamines, free fatty acids, electrolytes, lactate and blood sugar. Immediately after trauma a close correlation was found between the Glasgow-Coma-Score and the levels of adrenaline and noradrenaline, respectively (R = 0.64; R = 59). A closer relationship was found between Glasgow-Coma-Scale and the extent of hypopotassemia. However, no correlation existed between the degree of loss of consciousness and haemodynamic parameters, electrolytes, blood sugar and lactate. On hospital admission the extent of hypopotassemia showed a close relationship to the degree of excreted catecholamines at the site of accident. Patients intubated and ventilated at the scene showed remarkably lower catecholamine levels at the time of admission.

Acute Disease↗
PubMed1990

Binding of a Bolton-Hunter substituted homostatine analog to affinity-immobilized human renin.

The binding of a Bolton-Hunter reagent substituted homostatine analog, SDZ 213-776, to human renin was investigated at pH 6.5 and 7.4. At both pH values, SDZ 213-776 bound to human renin in a reversible and saturable manner. The binding characteristics conformed to a one-site binding model. The dissociation constant Kd, obtained at equilibrium, was four-fold lower at pH 6.5 that at pH 7.4 (0.94 nM vs 3.7 nM). Under non-equilibrium conditions, only the association kinetic constant k+1 was affected by pH. The results of the binding assay at pH 6.5 correlated well with those obtained in enzymatic assay at the same pH.

Antibodies, Monoclonal↗
PubMed1990

Influence of continuous haemofiltration on haemodynamics and central blood volume in experimental endotoxic shock.

In order to assess the influence of continuous haemofiltration (HF) on haemodynamics and central blood volume in endotoxic shock, endotoxinaemia was invoked in 20 swine (28-32 kg). 15 min after doubling the mean pulmonary pressure, the animals were randomly assigned to receive either a zero-balanced veno-venous HF with an ultrafiltration and replacement rate of 600 ml/h (HF group, n = 10) or to observe the spontaneous course (E group, n = 10) under a constant infusion of endotoxin for 4 h. A trend to a higher survival rate in the HF group (6/10 vs. 3/10; E group) during the observation period was evident, but not statistically significant. Early initiation of HF during endotoxic shock modifies the haemodynamic response, lowering the pulmonary artery pressure (PAP), PCWP, pulmonary (PVR) and systemic vascular resistance (SVR), compared to the spontaneous course, whereas the decrement of central blood volume was comparable in both groups. These changes cannot be explained by effects of the HF on the volume status, but supports and additional effect by the filtration of small and medium-sized molecules.

Animals↗
PubMed1990

[The bowel as an ischemic organ].

Due to the progress that has been made in intensive care, more and more patients survive shock. It is a clinical observation that their condition improves substantially with the restoration of intestinal function. Different experimental models have been developed to investigate the pathophysiology of the intestine in shock. As noxious periods, both the phase of ischemia and the phase of reperfusion have been identified. Since the experimental models are methodologically very different, the results of the various studies may only be compared with reservations. Nevertheless, it can be stated that reduced intestinal blood flow leads to ischemia and hypoxia of the villous tips. Reperfusion may lead to further mucosal injury. During this period oxygen free radicals and their derivates seem to play an essential role. Xanthine oxidase is thought to be the major source of these radicals in the small intestine. During ischemia ATP is catabolized to hypoxanthine, which is enzymatically transformed to xanthine, a process generating oxygen free radicals. Moreover oxygen free radicals seem to be produced by activated neutrophilic granulocytes. At present, only hypotheses exist concerning the interactions between granulocytes and these radicals. The mechanism of injury produced by oxygen free radicals is based on the peroxidation of the lipid components of the cellular membrane system. The small intestine represents a very vulnerable shock organ: apart from its very important nutritive functions, it provides the necessary barrier between the intestinal pool of endotoxin and the circulation. The loss of these vital functions due to ischemic lesions dramatically worsens the chances for the patient to survive. Therefore, it is necessary to develop therapeutic principles to maintain or restore intestinal function in shock.

Free Radicals↗