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Biomedical subjects

T Ziegenfuss

Publications and source records attributed to T Ziegenfuss.

At least 19 recordsLinked to original sources
PubMed1999

[Rocuronium for anesthesia induction in elective procedures. Time course of muscular blockade and intubation after administration of 2-compartment ED95 (0.6 mg/kg) and dose reduction (0.4 mg/kg)].

BACKGROUND: Rocuronium is a non-depolarising neuromuscular blocking agent structurally related to vecuronium. The compound has a rapid onset and an intermediate duration of action. The rapid onset is of importance in patients at risk for pulmonary aspiration, for elective induction of anaesthesia slower onset properties generally are accepted. In this context, we asked whether the induction dose of rocuronium may be reduced to doses smaller than 2 x ED95 in situations in which slower onset properties may be acceptable. METHODS: The time course of neuromuscular block and intubating conditions of two different doses rocuronium, 2 x ED95 (0.6 mg/kg) and 1.3 x ED95 (0.4 mg/kg), were investigated in 90 patients. We first determined the time course of neuromuscular block using electromyography (EMG), n = 15 for each group. In the second part the intubating conditions 3 min after injection of either rocuronium 0.6 mg/kg or rocuronium 0.4 mg/kg were evaluated, n = 30 for each group. RESULTS: In the present study reduction of the dose of rocuronium led to a slower onset (148 +/- 32 s vs. 220 +/- 30 s; P < 0.05) and a shorter clinical duration (21 min +/- 4 vs. 36 +/- 7 min; P < 0.05). The recovery index was modified by the dose reduction: 11 +/- 3 min after 0.6 mg/kg rocuronium and 9 +/- 2 min after 0.4 mg/kg. After both doses of rocuronium the intubating conditions were good to excellent, no difference between both rocuronium groups were found. CONCLUSION: In the present study dose reduction from 0.6 mg/kg rocuronium to 0.4 mg/kg rocuronium led to a slower onset and reduced clinical duration. However, the intubating conditions, evaluated 3 min after injection of the muscle relaxant were comparable. This offers new possibilities for muscle relaxation for surgical or diagnostic procedures of short duration and may reduce costs.

Adult↗
PubMed1999

Mixed agonistic-antagonistic cytokine response in whole blood from patients undergoing abdominal aortic aneurysm repair.

OBJECTIVE: To characterize the impact of abdominal aortic aneurysm repair (AAAR) on spontaneous as well as lipopolysaccharide (LPS)-induced gene expression of pro- and anti-inflammatory cytokines. DESIGN: Prospective, controlled in vivo/ex vivo study. SETTING: University hospital. PATIENTS AND INTERVENTIONS: Whole blood from 14 consecutive patients undergoing AAAR withdrawn prior to surgery (T1), at the end of ischemia (T2), 90 min after declamping (T3) and on the first postoperative day (T4) was cultured in the absence or presence of LPS. Five patients undergoing elective inguinal hernia repair served as controls. MEASUREMENTS AND RESULTS: While tumor necrosis factor (TNF), Interleukin (IL)-1 and IL-10 plasma concentrations did not increase significantly, IL-6 was elevated at each time point, as compared with T1. Despite the spontaneous release of trace amounts of IL-6, the ability of cultured whole blood to mount a cytokine response in vitro to LPS was impaired for all cytokines studied at T2 (TNF-62%, IL-1-51%, IL-6 -20%, IL-10-51%). The stimulated IL-6 response was restored early after declamping (T3: +56 %) and enhanced 1 day after operation (T4: +144%). In contrast, stimulated TNF and IL-1 responses remained depressed at T3 (TNF -48%, IL-1-64%) and T4 (TNF-40%, IL-1-24%). A biphasic pattern was observed for IL-10 with initial depression at T3 (-51%) and restoration at T4 (+40%). Among the different cytokines monitored, only impaired TNF responsiveness at early reperfusion (T3) correlated with the postoperative course, as reflected by APACHE II. Cytokine response to LPS was maintained or even increased during and after surgery in the whole blood from patients undergoing hernia repair. CONCLUSIONS: Despite consistent development of clinical signs of systemic inflammatory response syndrome (SIRS) and spontaneous release of IL-6 abdominal aortic aneurysm repair produces a state of impaired pro-inflammatory cytokine response upon a subsequent in vitro Gram-negative stimulus. This early impairment of TNF responsiveness seems to correlate with an unfavorable postoperative course.

Aged↗
PubMed1999

Antagonism of vecuronium-induced neuromuscular block in patients pretreated with magnesium sulphate: dose-effect relationship of neostigmine.

We have investigated the dose-effect relationship of neostigmine in antagonizing vecuronium-induced neuromuscular block with and without magnesium sulphate (MgSO4) pretreatment. Neuromuscular block was assessed by electromyography with train-of-four (TOF) stimulation. First, we determined neostigmine-induced recovery in patients pretreated with MgSO4 (group A) or saline (group B) (n = 12 each). The height of T1, 5 min after neostigmine, was 43 (7)% in group A and 65 (6)% in group B (P < 0.01). Respective values after 10 min were 59 (7)% and 83 (5)% (P < 0.01). TOF ratio, 5 min after neostigmine, was 29 (6)% in group A and 29 (5)% in group B. Respective values after 10 min were 38 (11)% and 51 (7)% (P < 0.01). To gain insight into the mechanisms leading to delayed recovery after MgSO4, we calculated assisted recovery, defined as neostigmine-induced recovery minus mean spontaneous recovery. Spontaneous recovery was assessed in another 24 patients. Patients in group C received MgSO4/vecuronium and patients in group D vecuronium only (n = 12 each). Five minutes after neostigmine, assisted recovery was 22 (7)% in the MgSO4 pretreated patients and 28 (6)% in controls (P < 0.05). Ten minutes after neostigmine, values were 24 (7)% and 22 (6)%. Maximum assisted recovery was not influenced by MgSO4 pretreatment (27 (6)% in group A and 32 (6)% in group B) and time to maximum effect was comparable between groups: 6 (4-10) min and 7 (5-8) min, respectively. We conclude that neostigmine-induced recovery was attenuated in patients treated with MgSO4. This was mainly a result of slower spontaneous recovery and not decreased response to neostigmine.

Adult↗
PubMed1998

[Anesthesia and perioperative immune function].

Innate and acquired immunity plays a pivotal role in the host defense response. Pain, stress, necrotic tissue and invading microorganisms are known modulators of the complex immune response of patients undergoing major surgery. Anaesthesia itself or perioperative interventions of the anaesthesiologist may substantially alter the immune function with potential impact on the postoperative course. For instance, transfusion of allogenic blood and administration of dopamine or metoclopramide may interfere with immunity. Stress and pain are associated with immune tolerance, increased susceptibility to infection and tumor spreading in animal models. Thus, anaesthesia may--through modulation of the neurohumoral stress response--indirectly affect immunity of the surgical patient. In particular epidural anaesthesia and/or administration of epidural or spinal opioids seem to attenuate the stress response with beneficial effects on cellular and humoral immunity. In addition, anaesthetics, such as etomidate, propofol, or thiopentone and opioid analgesics may directly affect function of immune competent cells. However, these actions may only be apparent with high or supraclinical concentrations and/or long-term exposure. Regarding the latter, evidence suggests that long-term sedation using thiopentone in neurosurgical patients is paralleled by infectious complications in a dose-dependent manner. At present, no data are available regarding the significance of the observed alterations associated with various anaesthetic procedures of the incidence of postoperative complications associated with impaired immunity, such as infection or metastatic spreading in oncological surgery.

Anesthesia↗
PubMed1998

[The effect of gamma-hydroxybutyrate (GHB) on proinflammatory cytokine gene expression in coronary surgical procedures].

OBJECTIVE: To determine the influence of gamma-hydroxy-butyrate (GHB) on spontaneous and lipopolysaccharide (LPS)-stimulated release of tumour necrosis factor-alpha (TNF), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and interleukin-10 (IL-10) in whole blood from patients undergoing coronary artery bypass grafting (CABG) with extracorporeal circulation (ECC). In addition, the pharmacological modulation on lipopolysaccharide (LPS)-stimulated cytokine release by GHB (GHB-Na and GHB-ethanolamide) was characterized in a separate in vitro-assay. METHODS: In a prospective, randomized, double-blinded study, 12 patients undergoing elective CABG were assigned to receive either saline (control) or GHB-Na (25 mg/kg as loading dose followed by 25 mg/kg/h) intraoperatively. Blood samples were obtained (A) preoperatively, (B) 20 min after ECC and (C) 24 h after ECC. Plasma levels (spontaneous release) as well as LPS-stimulated cytokine secretion were measured in a whole blood culture system ex vivo and correlated with mRNA-expression in peripheral blood mononuclear cells (PBMC). In addition, the dose-response characteristics of modulation of the cytokine response by GHB was studied in vitro in the same assay. RESULTS: Plasma IL-6 and IL-10 levels were significantly elevated after CABG, while TNF and IL-1 beta were detectable only occasionally in both groups. Expression of all cytokines studied was significantly reduced upon ex vivo LPS-stimulation at time point B. Despite maintained expression of TNF and IL-1 beta mRNA-transcripts upon ex vivo LPS-stimulation in patients treated with GHB, release of the cytokines in the supernatant was decreased to a similar degree as in the control group. Cytokine response upon LPS-stimulation was restored 24 h after CABG for the group mean, however, with substantial individual heterogeneity. In vitro, pharmacological doses of GHB-Na (2 mg/ml) attenuated LPS-induced IL-1 beta release. However, application of the GHB-receptor antagonist NCS-382 caused a nearly complete cessation of IL-1 beta release in vitro (to 2.5% of control). GHB-ethanolamide (LK 544) did not influence the LPS-stimulated release of the cytokines studied. CONCLUSION: The results suggest a biphasic response of stimulated PBMC cytokine gene expression during CABG with an initial tolerance to LPS-stimulation shortly after termination of ECC. However, whether or not PBMC express functional GHB receptors remains unclear in light of contradictory effects of the different ligands. In spite of the ex vivo and in vitro results, application of GHB-Na in doses which are primarily based on its use as an anesthetic agent do not seem to modulate the release of the cytokines studied.

Adult↗
PubMed1998

Thiopental or etomidate for rapid sequence induction with rocuronium.

We have assessed the effect of the choice of i.v. induction agent on intubation conditions, 60 s after administration of rocuronium 0.6 mg kg-1. We studied 60 adult patients, allocated randomly to one of two groups. Anaesthesia was induced with alfentanil 10 micrograms kg-1 followed by thiopental 5 mg kg-1 (AT-R group; n = 30) or etomidate 0.3 mg kg-1 (AE-R group; n = 30). Both groups received rocuronium 0.6 mg kg-1. Laryngoscopy was started 60 s later and intubation conditions were evaluated according to a standard score, which considered ease of laryngoscopy, condition of the vocal cords and reaction to intubation. In the AT-R group, overall intubation conditions were scored as excellent in 20 patients, good in nine and fair in the remaining patient. In the AE-R group, overall intubating conditions were excellent in 24 and good in six patients. The difference between the two groups was not significant. Of the three components of the intubation score assessed, response to intubation stimulus was significantly less pronounced in group AE-R compared with group AT-R (P < 0.05): group AE-R, no reaction in 24 patients, slight diaphragmatic movement in five and mild coughing in one patient; group AT-R, no reaction in 13, slight diaphragmatic movement in 14, mild coughing in two and severe coughing in one patient. We conclude that etomidate as part of an induction regimen containing alfentanil and rocuronium attenuated the reaction to intubation to a greater extent than thiopental.

Adolescent↗
PubMed1998

Proinflammatory cytokine gene expression in whole blood from patients undergoing coronary artery bypass surgery and its modulation by pentoxifylline.

The influence of coronary artery bypass grafting (CABG) on spontaneous and lipopolysaccharide (LPS)-stimulated release of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10 as well as its modulation by pentoxifylline (PTF) were studied in a prospective, randomized, double-blinded study. 12 patients undergoing elective CABG were randomly assigned to receive either saline or PTF (1 mg/kg as a loading dose followed by 1 mg/kg/h) intraoperatively. Blood samples were obtained (A) preoperatively, (B) 20 min after CABG, and (C) 24 h after CABG. Cytokine plasma levels as well as LPS-stimulated cytokine secretion were measured in a whole blood culture system ex vivo and correlated with mRNA expression in peripheral blood mononuclear cells. In addition, the dose-response characteristics of modulation of the cytokine response by PTF were studied in cultured whole blood in vitro. Plasma IL-6 and IL-10-levels were significantly elevated after CABG, whereas neither TNF-alpha nor IL-1beta were detectable. In contrast to the spontaneous release of IL-6 and IL-10, the expression of all cytokines studied was significantly reduced upon ex vivo LPS stimulation early after CABG. Proinflammatory cytokine response upon LPS stimulation was restored 24 h after CABG for the group mean, however, with substantial interindividual heterogeneity. Therapeutic doses of PTF in vitro attenuated LPS-induced TNF-alpha (-50.5%) and most notably IL-10 (-83.9%) release, whereas IL-1beta was even increased (+45.7%). However, application of PTF during CABG neither inhibited the spontaneous production of IL-10 nor modulated cytokine production ex vivo. These results suggest a biphasic response of stimulated peripheral blood mononuclear cell cytokine gene expression during CABG with an initial tolerance to LPS stimulation. The application of PTF during CABG in doses that are primarily based on its use in occlusive arterial disease do not seem to modulate the release of the cytokines studied.

Adult↗
PubMed1996

[Emergency management of polytrauma patients].

Adequate prehospital care of the severely traumatised patient is important to prevent or attenuate early as well as late life threatening complications, such as tissue hypoxia, ischemia/reperfusion injury and finally multiple organ failure. A mismatch of oxygen supply and oxygen demand is a hallmark in the pathophysiology of multiple trauma. Oxygen supply may be diminished by the following factors: shock-related decrease of cardiac output, anemia and hypoxia. On the other hand, oxygen demand may be increased by pain, panic, and agitation. Hence, it is a central point in prehospital care to reduce this supply-demand imbalance by identification and prompt reversal of the underlying causes. Most often, shock is caused by hypovolaemia and tissue injury ("traumatic-hemorrhagic shock"). However, shock may also be a result of central nervous system injury (neurogenic shock as a special form of distributive shock) or circulatory obstruction, e.g tension pneumothorax or cardiac tamponade (obstructive shock). Volume resuscitation by means of crystalloid or colloid solutions is an essential part in the therapy of the traumatic-haemorrhagic shock. In addition, catecholamines may be necessary in order to achieve an adequate arterial pressure. However, if bleeding cannot be controlled in the prehospital setting, only moderate volume support and permissive hypotension as well as rapid transportation into the next hospital may be preferable. This may be the case in penetrating thoracic or abdominal injuries as well as in traumatic amputations of the proximal limb. On the contrary, in patients with severe head injury, hypotension must be avoided by all means. Obstructive shock has to be treated urgently by insertion of a chest drain or drainage of the pericardium, respectively. Under all circumstances, it is an essential part of prehospital therapy to provide sufficient analgesia as soon as possible. Prehospital anesthesia, combined with artificial ventilation may be necessary for optimal patient management. Furthermore, ventilatory support is indicated when respiratory failure, loss of consciousness, or severe shock are present. Additional oxygen should be given whenever possible, even in the absence of an overt hypoxic state. Important additional measures are cervical spine immobilisation and reposition as well as splinting of long bone fractures or luxations, in order to avoid secondary injury of the spinal cord or ongoing tissue and vascular damage.

Analgesia↗
PubMed1996

[Intensive care medicine aspects of polytrauma].

Multiple trauma often leads to systemic inflammatory reaction and multiple organ dysfunction. Modulation of this response may be promising. Several pharmacologic approaches, such as antioxidants (e.g. superoxidedismutase), calcium channel blockers (e.g. diltiazem), cytokines (e.g. interferone gamma), and modulators of intracellular signal transduction pathways (e.g. pentoxiphylline) have been shown to improve outcome in experimental models and/or in clinical pilot studies. However, up to now no definitive evidence has been provided in prospective, randomized, and blinded "intention to treat" trials that these agents are able to reduce mortality and morbidity of the traumatized patient. Hence, supportive care of failing organs, treatment of hypoxemia and maintenance of an appropriate systemic blood pressure remain the mainstay of critical care therapy. Widely accepted therapeutic measures are (i) immediate treatment of hypoxia by administration of oxygen and ventilatory support, if needed, to maintain an oxygen tension of 60 mmHg or higher (ii) maintenance of adequate oxygen content by transfusion of red packed cells in order to restore a hematocrit of 23-30% (iii) treatment of hypovolemia by infusion of crystalloids, colloids and blood products (iv) normoventilation and restoration of a normal or elevated blood pressure in patients with severe head injury (v) immobilisation and early administration of methylprednisolone in patients with spinal cord injury (vi) analgesia by administration of opioids, non-steroidal antiinflammatory drugs, or ketamine (vii) sedation with benzodiazepines, gamma-hydroxbutyrate or propofol (viii) early enteral nutrition (ix); antibiotic therapy of infections (x) pressure controlled ventilation in patients with acute lung injury (xi) continuous veno-venous hemofiltration in patients developing acute renal failure and (xii) early surgical interventions to control bleeding and/or to evacuate intracerebral hematomas.

Combined Modality Therapy↗
PubMed1996

[Perspectives of polytrauma management].

Despite a high standard of preclinical, clinical and rehabilitative trauma care, the number and degree of injuries will remain a social and medical challenge. Improvements of trauma care in the future may be possible in respect to social, economic, organisational, clinical and research issues. Prevention of trauma will be of major impact and improvements may be possible by preventive legislation and technical developments. Organisation of trauma care should integrate high level trauma centres early-on including a national, regional and local quality control system. The future preclinical and clinical individual care of multiple trauma patients should consider the complex pathophysiological mechanisms at all levels, while the understanding of these mechanisms is increasing continuously.

Cause of Death↗
PubMed1995

Attenuation of shock-induced hepatic microcirculatory disturbances by the use of a starch-deferoxamine conjugate for resuscitation.

OBJECTIVE: To determine the effects of a hydroxyethyl starch-deferoxamine conjugate on hepatic microcirculation in an isobaric, anesthetized rat model of hemorrhagic shock and asanguineous resuscitation. DESIGN: Prospective, randomized, controlled study. SETTING: Laboratory at a university hospital. SUBJECTS: Twenty-three female, inbred Lewis rats (190 to 215 g). INTERVENTIONS: After anesthesia (pentobarbital-sodium; 50 mg/kg), tracheotomy, and cannulation, animals were assigned to a hemorrhagic shock (mean arterial pressure at 40 +/- 3 mm Hg for 45 mins) or a time-matched sham protocol. Rats in the shock groups received either hydroxyethyl starch or a starch-deferoxamine conjugate for resuscitation. Liver microcirculation was assessed in vivo 60 mins after onset of volume therapy by epifluorescence microscopy. MEASUREMENTS AND MAIN RESULTS: Conventional resuscitation with the starch-vehicle failed to restore sinusoidal blood flow compared with either time-matched controls (71% of control value; p < .01) or the starch-deferoxamine-treated animals (89% of control value; p < .05 compared with starch-vehicle), although a comparable restoration of central hemodynamics was achieved with both starch preparations. Additionally, treatment with the starch-deferoxamine conjugate resulted in a significant attenuation of sinusoidal leukocyte margination (sham 72.4 +/- 11.0/mm2; starch-vehicle 194.5 +/- 19.0/mm2 [p < .01 compared with controls]; starch-deferoxamine conjugate 135.9 +/- 12.1/mm2 [p < .02 compared with sham and starch-vehicle]). CONCLUSIONS: Asanguineous resuscitation with conventional hydroxyethyl starch failed to restore hepatic microvascular blood flow, despite otherwise effective resuscitation. In contrast, the starch-deferoxamine conjugate improved volumetric blood flow and attenuated leukocyte margination in hepatic sinusoids compared with starch-vehicle, suggesting involvement of iron-dependent, oxygen-derived radicals in shock-induced hepatic microcirculatory disturbances.

Animals↗
PubMed1994

[Clinical aspects, analysis and follow-up of poisoning with the alkyl phosphate demeton-S-methylsulfoxide (Metasystox R)].

UNLABELLED: We report on a 52-year old woman who had taken an unknown dose of the organophosphate insecticide Metasystox R with suicidal intention. Ingestion was followed by cardio-respiratory failure. After successful cardio-pulmonary resuscitation, main therapeutic principles were the immediate application of atropine and decontamination procedures such as gastric lavage, induction of diarrhoea and instillation of carbon. A single combined haemoperfusion and haemodialysis treatment was performed as a secondary elimination technique. After rapid toxicological analysis, obidoxime was administered as a supplementary antidote. After 14 days of treatment, the patient could leave the ICU with a complete restitution. CONCLUSION: Our case report demonstrates the efficiency of immediate application of antidotal therapy (atropine), decontamination and elimination techniques even in case of cardio- respiratory failure after organophosphate poisoning. Toxicological analysis will be beneficial for diagnosis and the indication of further treatment with obidoxime.

Atropine↗
PubMed1993

[Septic-toxic heart failure as a result of a heparin-induced thrombocytopenia with "white-clot-syndrome"].

A patient is presented who developed pulmonary artery embolism and thrombocytopenia with various arterial clots several days after an ankle joint osteosynthesis, which finally caused the amputation of the right arm. Unfractionated heparin was applied for the prevention of postoperative thrombosis. Obviously as a consequence of the liberation of toxic metabolites from the gangrenous lower arm, the patient developed septic shock which was exacerbated by a severe pneumonia caused by methicillin-resistant S. aureus bacteria (MRSA). Laboratory investigations showed an antibody (IgG) induced thrombopenia mediated by all low molecular weight and unfractionated heparins. By eliminating heparin and further treatment with a low molecular weight heparinoid (ORG 10,172), platelet count rose sufficiently and thrombotic process ceased completely. Septic shock was successfully treated by fluid replacement, antibiotics and inotropic substances.

Adult↗
PubMed1993

[The effect of intermittent prone position on pulmonary gas exchange in acute lung failure].

In a clinical trial, the influence of repeated intermittent prone position on pulmonary gas exchange was investigated in 6 patients with severe ARDS. Despite various intra- and interindividual differences, oxygenation index (calculated by the paO2:FiO2 ratio) was improved significantly by change from supine to prone position in the first two days of treatment, whereas paCO2 remained unchanged. Later on, a significant improvement of oxygenation could not be verified. In patients with proven or presumed densities of dorsal lung regions, body position changes from supine to prone position in the early phase of treatment may improve arterial oxygenation and may be regarded as a therapeutic principle in conventional ARDS treatment.

Adult↗
PubMed1993

Comparative effects of crystalloid and small volume hypertonic hyperoncotic fluid resuscitation on hepatic microcirculation after hemorrhagic shock.

Hepatic microcirculation, leukocyte-endothelial interaction, and sinusoidal widths were studied by means of intravital microscopy in a non-heparinized fixed pressure hemorrhagic shock model in the rat. Asanguineous resuscitation was performed either with "adequate" amounts of lactated Ringer's solution (threefold shed volume/30 min) or 4 ml/kg/3 min 7.2% saline/10% Dextran 60 (HSDex) or 4 ml/kg/3 min 7.2% saline/10% hydroxyethylstarch 200/0.62 (HSHes). Hemorrhagic shock and resuscitation was paralleled by significant (P < 0.01) lumenal narrowing of sinusoids that remained largely uninfluenced by the type of fluid used for resuscitation (HSDex: 9.28 +/- 0.56; HSHes: 8.93 +/- 0.29, LR: 8.87 +/- 0.6 microns compared to 12.17 +/- 0.24 microns in controls). Whereas HSHes and LR-therapy resulted in comparably increased leukocyte adhesion to the sinusoidal wall, the dextran-containing solution led to a significant attenuation of leukocyte-endothelial interaction, suggesting involvement of dextran-binding adhesion molecules, e.g., selectins.

Animals↗