Coronavirus disease 2019 (COVID-19): update for anesthesiologists and intensivists March 2020.

The current outbreak of coronavirus disease (COVID-19) has reached Germany. The majority of people infected present with mild disease, but there are severe cases that need intensive care. Unlike other acute infectious diseases progressing to sepsis, the severe courses of COVID19 seemingly show prolonged progression from onset of first symptoms to life-threatening deterioration of (primarily) lung function. Diagnosis relies on PCR using specimens from the respiratory tract. Severe ARDS reflects the hallmark of a critical course of the disease. Preventing nosocomial infections (primarily by correct use of personal protective equipment) and maintenance of hospitals' operational capability are of utmost importance. Departments of Anaesthesia, Intensive Care and emergency medicine will envisage major challenges.

[Coronavirus disease 2019 (COVID-19): update for anesthesiologists and intensivists March 2020]. / "Coronavirus disease 2019" (COVID-19): update für Anästhesisten und Intensivmediziner März 2020.

The current outbreak of coronavirus disease (COVID-19) has reached Germany. The majority of people infected present with mild disease, but there are severe cases that need intensive care. Unlike other acute infectious diseases progressing to sepsis, the severe courses of COVID19 seemingly show prolonged progression from onset of first symptoms to life-threatening deterioration of (primarily) lung function. Diagnosis relies on PCR using specimens from the respiratory tract. Severe ARDS reflects the hallmark of a critical course of the disease. Preventing nosocomial infections (primarily by correct use of personal protective equipment) and maintenance of hospitals' operational capability are of utmost importance. Departments of Anaesthesia, Intensive Care and emergency medicine will envisage major challenges.

[Critical incidents in preclinical emergency airway management : Evaluation of the CIRS emergency medicine databank]. / Kritische Zwischenfälle im Atemwegsmanagement der präklinischen Notfallmedizin : Auswertung der Datenbank CIRS-Notfallmedizin.

BACKGROUND: Many patients are victims of disastrous incidents during medical interventions. One of the obligations of physicians is to identify these incidents and to subsequently develop preventive strategies in order to prevent future events. Airway management and prehospital emergency medicine are of particular interest as both categories frequently show very dynamic developments. Incidents in this particular area can lead to serious injury but at the same time it has never been analyzed what kind of incidents might harm patients during prehospital airway management. MATERIALS AND METHODS: The German website http://www.cirs-notfallmedizin.de (CIRS critical incident reporting systems) offers anonymous reporting of critical incidents in prehospital emergency medicine. All incidents reported between 2005 and 2012 were screened to identify those which were concerned with airway management and four experts in this field analyzed the incidents and performed a root cause analysis. RESULTS: The database contained 845 reports. The authors considered 144 reports to be airway management related and identified 10 root causes: indications for intubation but no intubation performed (n = 8), no indications for intubation but intubation attempt performed (n = 7), wrong medication (n = 25), insufficient practical skills (n = 46), no use of alternative airway management (n = 7), insufficient handling before or after intubation (n = 27), defect equipment (n = 28), lack of equipment (n = 31), others (n = 18) and factors that cannot be influenced (n = 12). CONCLUSIONS: The incidents that were reported via the website http://www.cirs-notfallmedizin.de and that occurred during airway management in prehospital emergency medicine are described. To improve practical airway management skills of emergency physicians are one of the most important tasks in order to prevent critical incidents and are discussed in the article.

Evidence against a role of physiological concentrations of estrogen in post-myocardial infarction remodeling.

OBJECTIVES: The purpose of this study was to examine whether endogenous estrogen deficiency induced by ovariectomy affects chronic left ventricular dysfunction post-myocardial infarction (MI). BACKGROUND: Epidemiologic findings suggest that mortality of postmenopausal women is increased after MI, but the underlying mechanisms are unknown. METHODS: Rats were either not ovariectomized (non-OVX), ovariectomized (OVX) or ovariectomized and treated with subcutaneous 17-beta-estradiol (E2) pellets (OVX + E2). Two weeks later, animals were sham-operated (Sham) or left coronary artery ligated (MI). Eight weeks later, in vivo echocardiographic and hemodynamic measurements were performed. Thereafter, hearts were isolated and perfused isovolumically. RESULTS: Mean infarct size was similar among the three MI groups. Ovariectomy decreased serum E2 levels (11 +/- 4 vs. 49 +/- 11 pg/ml in non-OVX, p < 0.01) and increased body weight. These changes were reversed by E2 replacement. The degree of cardiac hypertrophy was similar for all groups post-MI. Left ventricular diameters were increased post-MI (8.9 +/- 0.4 in non-OVX + MI vs. 6.7 +/- 0.2 mm in non-OVX + Sham hearts, p < 0.0001), but OVX or OVX + E2 replacement did not alter left ventricular diameters in post-MI and Sham hearts. Left ventricular fractional shortening was severely impaired post-MI (19 +/- 2% vs. 50 +/- 3 in non-OVX + Sham hearts, p < 0.0001) with no influence of hormonal status. Left ventricular end-diastolic pressure, measured in vivo, was increased in all MI groups without significant differences between groups. Pressure-volume curves, obtained in perfused hearts, demonstrated a right and downward shift with reduced maximum left ventricular developed pressure post-MI (75 +/- 6 vs. 108 +/- 3 mm Hg in non-OVX + Sham hearts, p < 0.001) and were also unaffected by either OVX or E2 replacement. CONCLUSIONS: Chronic endogenous estrogen deficiency does not have major effects on the development of cardiac hypertrophy, dysfunction and dilation post-MI.

Heparin and the nonanticoagulant N-acetyl heparin attenuate capillary no-reflow after normothermic ischemia of the lung.

BACKGROUND: Ischemia-reperfusion injury of the lung frequently occurs after cardiopulmonary bypass, after pulmonary thromboendarterectomy, and especially after lung transplantation. Heparin is known to be protective in ischemia-reperfusion injury, but the risk for bleeding disorders may restrict its use in a variety of diseased conditions. Therefore, we tested the efficiency of nonanticoagulant N-acetyl (NA) heparin to protect from postischemic reperfusion injury of the lung. METHODS: Pentobarbital-anesthetized, mechanically ventilated Lewis rats were heparinized (100 IU/kg) before insertion of catheters. Additionally, animals received either heparin (200 IU/kg; n = 7), NA heparin (1.1 mg/kg; n = 7), or saline (control, n = 7) before ischemia. After normothermic ischemia for 50 minutes, the left lung was reperfused for 120 minutes, or until the death of the animal. The nonischemic right lung was excluded after 10 minutes of reperfusion. RESULTS: Survival rate at 120 minutes of reperfusion was 7 of 7 and 6 of 7 in the heparin and the NA-heparin group, but 0 in 7 in the control group (p < 0.01). At 30 minutes of reperfusion, PaO2, blood flow through the ascending aorta and mean systemic blood pressure were also significantly higher in the heparin and the NA-heparin group when compared with the control group (p < 0.05). Pulmonary vascular resistance was significantly lower in the heparin and the NA-heparin groups, and histologic examination of the lungs from these groups confirmed reperfusion of nutritive alveolar capillaries by the presence of red blood cells. Lack of red blood cells in the alveolar capillaries of lung specimens from the control group indicated failure of capillary reperfusion. CONCLUSIONS: Heparin and NA heparin exert similar protection against capillary no-reflow after normothermic ischemia of the lung. This implies that the protective effect of heparin is mediated by properties different from its anticoagulant activity. Thus the nonanticoagulant N-acetyl heparin may pose a safe new therapeutic approach in lung ischemia-reperfusion injury without increasing the risk of hemorrhagic complications.

Model of chronic systolic and diastolic dysfunction after cryothermia-induced myocardial necrosis in rats.

BACKGROUND AND PURPOSE: Left ventricular dysfunction following myocardial infarction is the most important predictor of adverse prognosis. Novel treatment options in infarction require an appropriate experimental model with a standardized, hemodynamically relevant myocardial injury. We evaluated a cryoinjury model in rodents that allows quantitative analysis of systolic and diastolic dysfunction. METHODS: Anesthetized, orally intubated, and ventilated Lewis rats (n = 12) underwent sternotomy. Myocardial necrosis was induced by use of a standardized cryolesion to the obtuse margin of the left ventricle, freezing for 3 minutes to -160 degrees C. Left ventricular performance was analyzed at day 120 after cryoinjury. Sham-operated animals (n = 10) served as controls. RESULTS: Cryoinjured animals behaved normally and gained weight up to day 120. Average heart weight of cryoinjured animals significantly exceeded that of controls. Left ventricular systolic pressure and systolic, diastolic, and mean aortic pressures were lower 4 months after cryoinjury, whereas left ventricular end-diastolic pressure was significantly increased. Cryoinjured animals had reduced aortic blood flow, as well as impaired maximal left ventricular dP/dt during aortic occlusion and aortic occlusion-provoked peak systolic pressure. Analysis of maximal rates of isovolumic pressure decrease revealed significant reduction in peak negative dP/dt in cryoinjured animals. Finally, time constants of isovolumic pressure decline were significantly prolonged in cryoinjured animals. CONCLUSION: Standardized cryothermia induces a myocardial lesion that results in highly reproducible impairment of left ventricular performance 120 days after cryothermia. The model is ideally suited to test novel therapeutic strategies for myocardial dysfunction.

Molecular biology on the ICU. From understanding to treating sepsis.

Mounting evidence suggests that beside well established factors, such as virulence of pathogens or site of infection, individual differences in disease manifestation are a result of the genetic predisposition of the patient on an Intensive Care Unit (ICU). Specific genetic factors might not only predict the risk to acquire severe infections but also to develop organ dysfunction or ultimately to die. Thus, the advent of molecular techniques allowing screening for a wide variety of genetic factors, such as single nucleotide polymorphisms in genes controlling expression of important mediator systems in patients as well as their purposeful targeting in animal models of sepsis, are revolutionizing understanding of pathophysiology in the critically ill. Molecular tools are about to challenge ''state-of-the-art'' diagnostic tests such as blood culture as they not only increase sensitivity but dramatically reduce time requirements to identify pathogens and their resistance patterns. Similarly, knowledge of genetic factors might in the near future help to identify ''patients at risk'', i.e. those with a high likelihood to develop organ dysfunction or to guide therapeutic interventions in particular regarding resource-consuming and/or expensive therapies (''theragnostics''). While therapeutic options in molecular intensive care medicine, such as stem cells in the treatment of organ failure or therapeutic gene transfer are possible along the road and might become an option in the future, recombinant DNA technology has already a well defined role in the production of recombinant human proteins from insulin to activated protein C.

[When safety becomes a danger. Penetrating trauma by side impact protection]. / Wenn Sicherheit zur Gefahr wird. Penetrierendes Trauma durch Seitenaufprallschutz.

We report the case of a penetrating injury of the abdomen by an iron bar of a side impact protection after a traffic accident. The iron bar of the side impact protection entered the lateral thigh, penetrated the pelvis and retroperitoneum and left the body lateral of the spine at the L4 level. The patient was fixed by the iron bar to the car seat. The mechanism of the accident, the patient's symptoms and the initial treatment of the patient are described and discussed.

Single dose aztreonam in treating gonorrhoea.

Of 108 consecutive patients with urogenital gonorrhoea treated with a single 1 g intramuscular dose of aztreonam, 102 were suitable for evaluation. There was 100% cure at urogenital sites but treatment failed at three of 14 (21%) rectal or pharyngeal sites. In vitro resistance to aztreonam was not noted.

Clinically diagnosed nonocclusive mesenteric ischemia after cardiopulmonary bypass: retrospective study.

This retrospective study evaluates our experience with clinically diagnosed nonocclusive mesenteric ischemia after cardiopulmonary bypass. Twenty-three of 3,600 consecutive patients suffered from splanchnic malperfusion. Symptoms developed between day 2 and 6 postoperatively in 18 of 23 patients. Four of 23 patients had no abdominal symptoms. Laboratory evaluation revealed significantly higher serum lactate and creatine phosphokinase levels in the 18 symptomatic patients compared with those of a control group. Arteriography was performed in 20 cases and revealed nonocclusive splanchnic hypoperfusion. Risk factors for development of mesenteric ischemia include arrhythmias and low cardiac output. Patients with angiographically proven nonocclusive mesenteric ischemia were treated with intra-arterial bolus injection and subsequent intra-arterial infusion of tolazoline combined with heparin sodium. The overall mortality rate was 30% (7 of 23). Infusion therapy with tolazoline and heparin seems to be a successful treatment modality for clinically diagnosed mesenteric ischemia.