For the purposes of this guideline, a diving accident is defined as an event that is either potentially life-threatening or hazardous to health as a result of a reduction in ambient pressure while diving or in other hyperbaric atmospheres with and without diving equipment. This national consensus-based guideline (development grade S2k) presents the current state of knowledge and recommendations on the diagnosis and treatment of diving accident victims. The treatment of a breath-hold diver as well as children and adolescents does not differ in principle. In this regard only unusual tiredness and itching without visible skin changes are mild symptoms. The key action statements: on-site 100% oxygen first aid treatment, immobilization/no unnecessary movement, fluid administration and telephone consultation with a diving medicine specialist are recommended. Hyperbaric oxygen therapy (HBOT) remains unchanged as the established treatment in severe cases, as there are no therapeutic alternatives. The basic treatment scheme recommended for diving accidents is hyperbaric oxygenation at 280 kPa.
Carbon monoxide (CO) can occur in numerous situations and ambient conditions, such as fire smoke, indoor fireplaces, silos containing large quantities of wood pellets, engine exhaust fumes, and when using hookahs.Symptoms of CO poisoning are nonspecific and can range from dizziness, headache, and angina pectoris to unconsciousness and death.This guideline presents the current state of knowledge and national recommendations on the diagnosis and treatment of patients with CO poisoning.The diagnosis of CO poisoning is based on clinical symptoms and proven or probable exposure to CO. Negative carboxyhemoglobin (COHb) levels should not rule out CO poisoning if the history and symptoms are consistent with this phenomenon. Reduced oxygen-carrying capacity, impairment of the cellular respiratory chain, and immunomodulatory processes may result in myocardial and central nervous tissue damage even after a reduction in COHb.If CO poisoning is suspected, 100% oxygen breathing should be immediately initiated in the prehospital setting.Clinical symptoms do not correlate with COHb elimination from the blood; therefore, COHb monitoring alone is unsuitable for treatment management. Especially in the absence of improvement despite treatment, a reevaluation for other possible differential diagnoses ought to be performed.Evidence regarding the benefit of hyperbaric oxygen therapy (HBOT) is scant and the subject of controversy due to the heterogeneity of studies.If required, HBOT should be initiated within 6 h.All patients with CO poisoning should be informed about the risk of delayed neurological sequelae (DNS).
Die Symptome einer akuten Kohlenmonoxid(CO-)Vergiftung sind unspezifisch und reichen von Kopfschmerzen bis zu Bewusstlosigkeit und Tod. Neben den Akutsymptomen können schwere neurologische Spätschäden auftreten. Die Zahl der in Deutschland amtlich registrierten Todesfälle aufgrund von CO-Vergiftung steigt an. Es liegen keine umfassenden Daten zur klinischen Symptomatik, zum Verlauf sowie zur Versorgungsqualität vor.
Knörr et al. präsentieren eine bisher nichtalltägliche Kasuistik aus der kinderärztlichen Notaufnahme. Die Darstellung der Diagnose und insbesondere der Therapie und des Verlaufs sollte allerdings diskutiert und ergänzt werden. Im Abschn. „Anamnese und Befund“ wird eine schwere Kohlenmonoxidintoxikation mit initialer Bewusstlosigkeit und fortgesetzt eingeschränkter Orientierung zur Situation sowie nachgewiesener Exposition mit Kohlenmonoxid beschrieben. InderBlutgasanalysewurde die Diagnose bestätigt. Folgerichtig ist die Behandlung mit einer Sauerstoffatmung über eine Reservoirmaske begonnen worden. Nach Absetzen der Sauerstoffgabe bestand allerdings weiterhin eine Bewusstseinsstörung. In dem beschriebenen Fall war nach 16h eine Elimination des Carboxyhämoglobins (CO-Hb) bei 100%iger Sauerstoffatmung zu erwarten und nachweisbar (. Abb. 1). Dennoch ist ausdrücklich zu betonen, dass CO-Hb nur als Surrogatparameter aufgrund seiner einfachen Messbarkeit zu bewerten ist. Die pleiotropen Effekte des CO bewirken u. a. eine Einschränkung der mitochondrialen Atmungskette, zellulären Energiegewinnung, Inflammation und Radikalbildung, insbesondere zerebral und kardial mit einem von demCOHbunabhängigenEliminationsverhalten [1]. Die klinischen Symptome der systemischen zellulären Hypoxie bei Kohlenmonoxidintoxikationen sind unspezifisch. Die häufigsten Symptome in
Lipid emulsions influence platelet aggregation and receptor expression. However, the effect on platelet function is not fully explained. Therefore, the aim of this study was to examine the influence of the lipids Lipofundin®, Lipidem® and ClinOleic® on surface expressions of P-selectin, GPIb and GPIIb/IIIa on platelets in vitro. Whole blood was incubated in two different concentrations (0.06 and 0.6 mg/ml) of LCT/MCT, n-3/LCT/MCT and LCT-MUFA for 30 min, followed by activation with TRAP-6 or ADP for flow-cytometric assay. Rates of P-selectin, GPIb and GPIIb/IIIa expression were analyzed. There was a significant increase in GPIIb/IIIa- and P-selectin-expression after incubation with LCT/MCT and n-3/LCT/MCT at the concentration of 0.6 mg/ml, without and after stimulation with TRAP-6 and ADP. GPIb was significantly decreased. Accordingly, LCT-MUFA had no effect on receptor expression of platelets in vitro. We demonstrated that LCT-MUFA did not activate receptor expression of platelets whereas LCT/MCT significantly increased platelet aggregation in vitro. This finding should be noted for parenteral nutrition of intensive care patients and, in the future, might provide further insight into the pathogenic pathways of acute thromboembolic events. However, prospectively designed clinical studies are needed to support our results.
We appreciate the concerns raised by Juttner et al.1 regarding our recent paper on first-aid oxygen delivery devices and flow rates.2 Our unexpected results with the use of the demand valve have been an area of much discussion both within our research group and at the SPUMS 2015 Annual Scientific Meeting. We agree this issue is complex and the lower than expected values we observed with demand valve ventilation may be attributable to several variables, however any leak caused by the nasal cannula should be minimal, and would not fully explain our findings.
Die überarbeitete „Leitlinie Tauchunfall 2014–2017“ wurde im April 2015 von der Gesellschaft für Tauch- und Überdruckmedizin (GTÜM) und der Schweizerischen Gesellschaft für Unterwasser- und Hyperbarmedizin (SUHMS) veröffentlicht. In Zusammenarbeit mit Vertretern der Deutschen Interdisziplinären Vereinigung für Intensiv- und Notfallmedizin (DIVI), Sektion Hyperbarmedizin, dem Verband Deutscher Sporttaucher e. V. (VDST), dem Schifffahrtmedizinischen Institut der Marine, der Berufsgenossenschaft der Bauwirtschaft (BG Bau), dem Verband Deutscher Druckkammerzentren (VDD) sowie der Deutschen Gesellschaft für Arbeitsmedizin und Umweltmedizin (DGAUM) wurde die Leitlinie auf der Basis einer strukturierten Konsensfindung aktualisiert (Entwicklungsstufe S2k). Das Leitlinienprojekt wurde von der Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften (AWMF) methodisch begleitet. Die „Leitlinie Tauchunfall 2014–2017“ soll Laien, medizinischem Assistenzpersonal und Ärzten in einem spezifischen Notfallbereich Informationen und Instruktionen über den aktuellen Stand der Diagnostik und der Behandlung von Tauchunfällen geben. Dieser Beitrag fasst Empfehlungen, Zielsetzungen und die wesentlichen Schlüsselempfehlungen der „Leitlinie Tauchunfall“ zusammen. Wesentliche Bedeutung bei der Versorgung von Tauchunfällen hat die frühzeitige Atmung von 100 %igem Sauerstoff. Weiterhin werden die Ruhiglagerung und eine moderate Flüssigkeitsgabe empfohlen. Die hyperbare Sauerstofftherapie (HBO) ist bei schweren Dekompressionsunfällen unverändert ohne therapeutische Alternative. Als Behandlungsschema wird grundsätzlich eine hyperbare Oxygenation bei 280 kPa empfohlen. Zukünftig sollte die Etablierung eines bundesweiten Registers von HBO-Notfallbehandlungen zur Qualitätssicherung angestrebt werden.
BACKGROUND:We report on a 62-year-old gentleman presenting at our urological department with an advanced renal cell cancer of the right kidney (10 cm in diameter), with an extensive caval vein thrombus (level IV) and bilateral pulmonary metastases. Another suspicious lesion at the left hemithorax was radiologically described.METHOD:A presurgical, neoadjuvant systemic therapy with sunitinib, a tyrosine kinase inhibitor, was initiated for 4 cycles in total (50 mg/day; 4 weeks on/2 weeks off). The cytoreductive nephrectomy was performed following the fourth cycle of sunitinib and after a 14-day break. Transesophageal echocardiography was used for intraoperative monitoring of the caval vein thrombus. Systemic treatment with sunitinib was continued 4 weeks after surgery.RESULTS:A significant reduction in tumor size, metastatic sites and down-staging of IVC from level IV to level III according to Novick classification was achieved.CONCLUSION:Significant down-staging of the tumor caval vein thrombus which initially reached the right atrium enabled us to perform surgery limited to the abdominal cavity without extracorporeal circulation nor hypothermia.
Eine bundesweite Erfassung der Versorgungsqualität in der Anästhesie existiert nicht. Bisher wurde die Darstellung der anästhesiologischen Ergebnisqualität mit routinemäßig verfügbaren Abrechnungsdaten nicht untersucht.
This example of a fatal diving accident shows how challenging such cases can be in pre-hospital and clinical care. There is no common mechanism in diving fatalities and more than one group of disorders coming along with decompression sickness. Diving medicine is not an element of medical education, which results in insecurity and hampers adequate therapy of diving incidents. This is aggravated by an insufficient availability of hyperbaric chambers in Germany.
Background Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of β1 or β2 agonists on adhesion molecule formation on endothelial cells has remained unclear. Methods Cultured human umbilical vein endothelial cells were stimulated with E. coli . Following bacterial stimulation the cells were incubated with either β2 receptor agonist terbutaline or β1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry. Results Administration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found. Conclusions Bacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules.
Background:It has been supposed that liver transplant recipients with hepatitis C virus infection have a higher incidence of infectious complications after transplantation. This study was designed to investigate whether neutrophil function is immediately affected by liver transplantation.Methods:Biochemical values, plasma levels of myeloperoxidase (MPO), hydrogen peroxide production of neutrophils and neutrophil-platelet complexes were analyzed in 32 patients who underwent liver transplantation and 20 healthy volunteers.Results:MPO levels were significantly increased 24 h after reperfusion. In post-hepatitic patients levels were significantly lower three d up to one wk post-transplant than in patients due to other liver diseases. One wk post-operatively the respiratory burst activity following N-formyl-methionyl-leucylphenylalanine (fMLP) or (tumor necrosis factor-alpha) TNF-alpha/fMLP stimulation was depressed in post-hepatitic recipients. Respiratory burst stimulated with phorbol 12-myristate 13-acetate in these patients was increased one wk after transplantation. One d after transplantation the neutrophil-platelet complexes decreased significantly throughout the post-operative period.Conclusions:The results of this study suggest a reduced post-operative neutrophil activation in liver transplant recipients suffering from post-hepatitic cirrhosis compared to cirrhosis due to other causes. We hypothesized that neutrophil dysfunction in those patients depends on the underlying disease with an increased susceptibility to bacterial or fungal infections.
Background: Rupture of a normal thyroid gland after blunt cervical trauma is a rare case of airway compression. This case report describes the case of a 79-year-old woman who developed severe respiratory distress after a bicycle crash. Case Report: Presenting about 2 h after the crash, the patient noted cervical swelling and increasing dyspnea. The diagnosis of thyroid gland rupture was made with a combination of computed tomography scan, cervical radiography, and bronchoscopy. Invasive airway management was required in the first few hours after the crash. The patient underwent a left hemithyroidectomy, and recovered without complications. Conclusion: This case report highlights the fact that thyroid gland rupture can be a threatening complication of blunt cervical trauma.
Background: Hemodialysis patients are in a state of oxidant stress. In renal transplantation reactive oxygen species (ROS) are considered to be important factors of ischemia-reperfusion injury. Neutrophils produce ROS as part of the host defense against invading bacteria. This study was designed to investigate whether neutrophil function in hemodialysis patients is immediately affected by renal transplantation. Methods: We evaluated the neutrophil respiratory burst and phagocytic activity in renal transplant patients with living-related donor (LRD) and cadaveric donor (CAD) grafts using flow cytometry techniques. Twenty patients (LRD = 6, CAD = 14) and 20 healthy volunteers were included in the study. Venous blood samples were drawn before anesthesia, 5 min before reperfusion, 1 h and 1, 3 and 7 days after reperfusion. Results: Before surgery, a significant increase in hydrogen peroxide production in neutrophils was seen for both renal transplantation groups compared to healthy subjects. Within 24 h after reperfusion hydrogen peroxide production almost decreased to normal values. The phagocytic capacity of neutrophils was continuously depressed. There were no differences between the CAD and LRD groups. Conclusions: We found that the enhanced respiratory burst activity of patients with chronic renal failure decreased to normal values within 1 day following renal transplantation. Our results suggest that reduced respiratory burst activity resulting in a diminished risk of tissue damage by the uncontrolled production of ROS.
Background: It is increasingly recognized that infectious complications in patients treated with total parenteral nutrition (TPN) may be caused by altered immune responses. Neutrophils and monocytes are the first line of defence against bacterial and fungal infection through superoxide anion production during the respiratory burst. To characterize the impact of three different types of lipid solutions that are applied as part of TPN formulations, we investigated the unstimulated respiratory burst activation of neutrophils and monocytes in whole blood.Methods: Whole blood samples were incubated with LCT ( Intralipid r), LCT/ MCT (Lipofundin r) and LCT- MUFA (ClinOleic (R)) in three concentrations (0.06, 0.3 and 0.6 mg ml- 1) for time periods up to one hour. Hydrogen peroxide production during the respiratory burst of neutrophils and monocytes was measured by flow cytometry.Results: LCT and LCT- MUFA induced a hydrogen peroxide production in neutrophils and monocytes without presence of a physiological stimulus in contrast to LCT/ MCT.Conclusion: We concluded that parenteral nutrition containing unsaturated oleic (C18: 1) and linoleic (C18: 2) acid can induce respiratory burst of neutrophils and monocytes, resulting in an elevated risk of tissue damage by the uncontrolled production of reactive oxygen species. Contradictory observations reported in previous studies may in part be the result of different methods used to determine hydrogen peroxide production.
Mit der subjektiven Bewertung durch die Patienten, den Operateur und den Anästhesisten werden Kriterien für die Auswahl des Narkoseverfahrens für geriatrische Patienten in der Ophthalmochirurgie evaluiert.