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Background A paucity of literature exists specifically examining self-inflicted (SI) gunshot wounds (GSWs) to the hand and wrist, which impart greater energy and have a higher risk of adverse events than non–self-inflicted (NSI) GSWs. Methods We retrospectively reviewed records of patients who presented to our plastic surgery service after sustaining acute GSWs involving the hand and wrist between 2016 and 2018. Results We identified 60 patients who sustained GSWs involving the hand and wrist; 17 (28%) were SI, and 43 (72%) were NSI. Within the SI group, 100% of patients were Caucasian, with an average age of 54 years. Within the NSI cohort, 77% of patients were Black, 19% were Caucasian, and 4% identified as other. While not statistically significant, we noted a substantial increase in patients requiring operative intervention in the SI cohort (65% SI vs 37% NSI, P = .08). There was a statistically significant increase in patients requiring more than 1 operation in SI patients (24% SI vs 5% NSI, P = .04). Patients who sustained SI injuries were also more likely to present with acute carpal tunnel syndrome requiring urgent surgical release and to develop wound infections (12% vs 0%, P = .08). Conclusions Self-inflicted GSWs involving the hand and wrist are associated with greater morbidity than their low-energy NSI counterparts. Individuals presenting with SI GSWs are more likely to be older, to require multiple operations, to develop infections, and to present with acute carpal tunnel syndrome requiring urgent surgical decompression.

Obwohl die Berlin Definition des akuten Lungenversagens (ARDS) allgemein anerkannt ist, bleibt die Unterscheidung von anderen Erkrankungen mit schwerer Gasaustauschstorung in der klinischen Praxis oft schwierig. Insbesondere die Beurteilung der radiologischen Befunde und die Identifizierung des primar nichtkardiogenen Lungenodems bereiten Probleme. Beim ARDS finden sich typische inflammatorische Prozesse, in deren Mittelpunkt die Aktivierung neutrophiler Granulozyten steht. Antiinflammatorische Therapiestrategien waren nicht erfolgreich. Als evidenzbasierte Therapie sind nur die lungenprotektive Beatmung und die Lagerungstherapie anzusehen. Moglicherweise bietet die Phanotypisierung des ARDS entsprechend der Atiologie oder des Krankheitsverlaufes die Moglichkeit der gezielten, individualisierten Therapie. Die Kontrolle verschiedener Biomarker zu Beurteilung und Therapie steht im Mittelpunkt des wissenschaftlichen Interesses. Die Ergebnisse entsprechender Studien bleiben abzuwarten.

Although the Berlin definition of the acute respiratory distress syndrome (ARDS) is generally recognized, the differentiation from other diseases with severe gas exchange disturbances is often difficult in clinical practice. In particular, the assessment of radiological findings and identification of primary noncardiogenic lung edema pose problems. In ARDS typical inflammatory processes can be found with involvement of activated neutrophilic granulocytes. Anti-inflammatory treatment strategies were unsuccessful. Lung protective ventilation strategies and prone positioning are the only evidence-based treatment options. Identifying ARDS phenotypes according to the etiology or disease progression can possibly provide a targeted individualized treatment option. The control of various biomarkers for assessment and treatment is the main focus of scientific interest. The results of appropriate studies remain to be seen.

Die Beatmung von Patienten mit akutem Lungenversagen ist eine Herausforderung fur den behandelnden Arzt. In den letzten Jahren hat sich die Behandlung dieser Patienten grundlegend geandert. Neben dem Einsatz niedriger Tidalvolumina stand die Hohe des positiven endexspiratorischen Drucks („positive end-expiratory pressure“, PEEP) im Fokus der Forschung. Die Ergebnisse legen heute die Anpassung des PEEP-Levels je nach Schweregrad der Gasaustauschsstorung nahe. Zusatzlich ermoglichen die Erfassung des Rekrutierungspotenzials mithilfe der Computertomographie und die Verbesserung bettseitiger Methoden eine weitere Modifikation des PEEP. Dieser Ubersichtsbeitrag gibt einen Uberblick uber die Moglichkeiten der PEEP-Einstellung unter Berucksichtigung neuer Forschungsergebnisse. Zusatzlich werden die grundlegenden pathophysiologischen Vorgange von hypoxischem und hyperkapnischem akutem Lungenversagen als Basis der „optimalen“ PEEP-Einstellung dargestellt.

Acute lung injury (ALI) is of paramount importance for modern intensive care since it is one of the most frequent conditions necessitating admission to an ICU. ALI is characterised by severe life threatening hypoxemia which is based on ventilation perfusion mismatching within the lung. This is mostly resulting from atelectasis formation due to primary or secondary inflammation of lung tissue. Many studies showed that this inflammatory process is not restricted to the respiratory system but might result in non pulmonary organ failure and hemodynamic compromise as well. Mechanical ventilation is considered the hallmark treatment for ALI patients aimed to recruit lung tissue and thereby reverse hypoxemia without causing additional lung injury potentially resulting from overdistention or cycling collapse during expiration. Scientific evidence shows us that prevention of ventilator induced lung injury by protective ventilation with reduced tidal volumes is resulting in better clinical outcomes. Moreover, different technologies and adjunctive therapies have been suggested based on their pathophysiology. All these treatment options will be summarized in this article. Given the clear evidence for protective ventilation and bearing in mind that clinical application of this easy concept is still not widespread we will focus on this aspect.

Eine pulmonale Hypertonie kann bei akuter kardiopulmonaler Dekompensation auftreten oder entwickelt sich als chronisch progressive Erkrankung im Rahmen von Kollagenosen, Infektionen, Stoffwechselerkrankungen oder als idiopathische pulmonale Hypertonie. Regulationsstorungen endogener Vasodilatatoren und -konstriktoren, Wachstumsinhibitoren und -aktivatoren sowie anti- und prothrombotischer Faktoren fuhren zur pulmonalarteriellen Vasokonstriktion, Proliferation von Gefasmuskel- und Epithelzellen und thrombotischen Gefasverschlussen mit dem Resultat einer chronischen Rechtsherzbelastung. Eine kurative Therapie ist nicht moglich, Ziel der Palliativbehandlung ist die Reduktion des pulmonalarteriellen Drucks zur Rechtsherzentlastung mit Hilfe pulmonaler Vasodilatatoren. Je nach Schwere der Erkrankung ist die perioperative Letalitat hoch, deshalb ist praoperativ eine optimale medikamentose Einstellung der Patienten zu fordern. Perioperativ mussen Umstande, die zu einer Aggravierung der pulmonalen Hypertonie fuhren konnen, vermieden bzw. fruhzeitig erkannt und behandelt werden. Bei intraoperativ drohendem Rechtsherzversagen werden Masnahmen zur Optimierung der rechtsventrikularen Kontraktilitat und zur Reduktion der rechtsventrikularen Nachlast ergriffen. Postoperativ sind Uberwachung und Optimierung der kardiopulmonalen Situation, adaquate Analgosedierung und suffiziente Antikoagulation erforderlich.

Ventilation of patients suffering from acute respiratory distress syndrome (ARDS) with protective ventilator settings is the standard in patient care. Besides the reduction of tidal volumes, the adjustment of a case-related positive end-expiratory pressure and preservation of spontaneous breathing activity at least 48 h after onset is part of this strategy. Bedside techniques have been developed to adapt ventilatory settings to the individual patient and the different stages of ARDS. This article reviews the pathophysiology of ARDS and ventilator-induced lung injury and presents current evidence-based strategies for ventilator settings in ARDS.

Treatment of patients suffering from acute lung injury is a challenge for the treating physician. In recent years ventilation of patients with acute hypoxic lung injury has changed fundamentally. Besides the use of low tidal volumes, the most beneficial setting of positive end-expiratory pressure (PEEP) has been in the focus of researchers. The findings allow adaption of treatment to milder forms of acute lung injury and severe forms. Additionally computed tomography techniques to assess the pulmonary situation and recruitment potential as well as bed-side techniques to adjust PEEP on the ward have been modified and improved. This review gives an outline of recent developments in PEEP adjustment for patients suffering from acute hypoxic and hypercapnic lung injury and explains the fundamental pathophysiology necessary as a basis for correct treatment.

Early tracheostomy has been advocated for a number of reasons. Especially in association with weaning from mechanical ventilation, it is known that an early timepoint can help patients being weaned more rapidly from the ventilator. However, timing of tracheostomy is still unknown and evidence is lacking. The effects of early tracheostomy compared with intermediate and late tracheostomy were assessed in critically ill patients.Data collected from January 2005 to December 2007 were conducted for retrospective analysis. All patients needing tracheostomy due to extubation failure and/or weaning failure were included (N.=296). Early tracheostomy (ET) was defined as ≤4 days, intermediate tracheostomy (IT) as tracheostomy within 5-9 days, and late tracheostomy (LT) was defined as ≥10 days after endotracheal intubation. After proving normal distribution, significant changes between the three groups were tested by ANOVA followed by post hoc tests for multiple comparisons (Bonferroni's test).Intensive care unit (ICU) mortality was significantly higher in the LT group when being compared with the ET but not when being compared with the IT group (40.7% vs. 24.8% vs. 17.1%). Further, a significantly reduced incidence of VAP and sepsis, a smaller amount of ventilator days and a shorter ICU length of stay could be observed for the ET group. Length of weaning was not significantly different between the groups.The length of weaning after tracheostomy is not affected by the timing. It seems beneficial to favour early tracheostomy in order to reduce the time of mechanical ventilation and its associated risks.

In order to provide early achievement of practical experience during medical education, the medical faculty of the university Aachen has developed a new medical school curriculum which was offered in 2003 for the first time. In this curriculum anaesthesiology became a compulsory subject with practical training both in the operation theatre and in emergency medicine. Accordingly, a practical course in the field of intensive care medicine has also been designed with respect to the planned schedule and personnel resources. This course was evaluated by both students and teaching staff in a written, anonymous form as a quality control.A dedicated course was developed for medical students of the 8th and 9th semesters. In this course comprised of 6 students and lasting 1 week, practical training is provided by intensive care physicians and accompanied by theoretical lessons focusing on the definition, diagnosis, therapy and prophylaxis of sepsis, essentials of mechanical ventilation and patient presentation at the bedside during daily rounds. On the last day of training students were required to present patients by themselves thereby recapitulating the acquired knowledge. In the summer semester 2007 this intensive care training course was offered for the first time. All participating 83 students and 23 physicians involved in teaching evaluated the course with marks from 1 to 6 according to the standard German school grading system using an online questionnaire.Students rated the course with 1.6+/-0.7 (mean +/- SD) for comprehensibility, with 1.6+/-0.7 for structural design, and with 1.7+/-0.7 for agreement between teachers. They graded their personal learning success with 1.7+/-0.7. With a cumulative mark of 1.7+/-0.6, the course was ranked as 1 of the top 3 courses of the medical faculty from the very beginning. The majority of the teaching staff (80%) appreciated the focus on few selected teaching subjects. However, comprehensibility, structural design, agreement between teachers and personal learning success were graded one mark worse than by the students.According to the results, efficiency and acceptance of intensive care training courses were high. Major criteria for the high grading were a limited number of participants, the focus on few subjects, and a clear structural design. However, according to several personal notes from the students, simulation-based sessions and written teaching material might further improve success of this course.

Ventilator-associated pneumonia (VAP) is the most common nosocomial infection in critical care medicine and has been shown to be an independent risk factor for mortality. However, ventilator induced lung injury itself is probably only a minor factor predisposing to VAP. In contrast, invasive ventilation using an endotracheal tube is obviously a more important measure. Thus, microaspiration of potentially infectious secretion from the oropharynx into the trachea along the tube has been suggested to be the most critical pathophysiological event in the process of VAP development. Accordingly, non-invasive ventilation provides a decreased risk of VAP. Therefore, all measures aimed at averting microaspiration or shorten the duration of mechanical ventilation are appropriate to prevent VAP. Moreover, oropharyngeal decontamination may be helpful by reducing bacterial colonisation. Effectiveness of therapy depends on early treatment and therefore requires early diagnosis. With this aim combined clinical, radiologic, and microbiological parameters should be taken into account. Adequate antimicrobial therapy in due consideration for individual risk factors and local antibiotic resistance is the most important therapeutic measure.

Acute lung injury (ALI) is of paramount importance for modern intensive care since it is one of the most frequent conditions necessitating admission to an ICU. ALI is characterised by severe life threatening hypoxemia which is based on ventilation perfusion mismatching within the lung. This is mostly resulting from atelectasis formation due to primary or secondary inflammation of lung tissue. Many studies showed that this inflammatory process is not restricted to the respiratory system but might result in non pulmonary organ failure and hemodynamic compromise as well. Mechanical ventilation is considered the hallmark treatment for ALI patients aimed to recruit lung tissue and thereby reverse hypoxemia without causing additional lung injury potentially resulting from overdistention or cycling collapse during expiration. Scientific evidence shows us that prevention of ventilator induced lung injury by protective ventilation with reduced tidal volumes is resulting in better clinical outcomes. Moreover, different technologies and adjunctive therapies have been suggested based on their pathophysiology. All these treatment options will be summarized in this article. Given the clear evidence for protective ventilation and bearing in mind that clinical application of this easy concept is still not widespread we will focus on this aspect.

For patients with most severe acute respiratory distress syndrome (ARDS) conservative treatment with lung protective ventilation is often not sufficient to prevent life-threatening hypoxemia and additional strategies are necessary. Extracorporeal lung assist (ECLA) or extracorporeal membrane oxygenation (ECMO) using capillary membrane oxygenators can provide sufficient gas exchange and lung rest. In 2 randomized trials mortality was unchanged for ECMO. Today an technically enhanced ECMO is used for most severe ARDS using clinical algorithm and different case studies demonstrated a survival rate about 56%. Today miniaturized ECMO with optimized blood pumps and oxygenators are available and could enhance safety and clinical management. Another approach is an arterio-venous pumpless interventional lung assist (ILA) with a low resistance oxygenator. Advantages seem a simplified clinical management and less blood trauma. At present new devices are developed for chronic respiratory failure or bridge to lung transplant. Oxygenators with even less flow resistance could be implanted paracorporeal using the right ventricle as driving force. An intravascular oxygenator has been developed using the combination of a miniaturized blood pump and an oxygenator for implantation in the vena cava. Well designed clinical trials are necessary to demonstrate a clinical benefit for these experimental devices.

Over the last years, several observational studies have suggested that extracorporeal lung assist (ECLA) may be an important contribution to clinical algorithms for the treatment of most severe acute respiratory distress syndrome (ARDS). Today ECLA is used only as a rescue therapy in life threatening gas exchange disorders if maximal conventional therapy fails to prevent from hypoxemia. With subsequent reduction of complications and improvement of biocompability, extracorporeal membrane oxygentation (ECMO) indications may be extendend to treat patients earlier and not only in rescue situations along the original idea to buy the lung some time to heal by avoiding further ventilator associated lung injury. Veno-venous ECMO therapy at present is an important therapeutic option in severe ARDS with persisiting life threatening gas exchange disorder as a rescue therapy. The development of smaller, less complex and more secure ECMO or pumpless veno-arterial ECLA systems has the potential to perform controlled studies of its use in ARDS and potentially expand indications.

Mortality rates remain high for the acute respiratory distress syndrome (ARDS) despite standardised treatment algorithms. Little is known about prognostic factors and exclusion criteria for advanced treatment including extracorporeal membrane oxygenation (ECMO).In an observational study design a cohort of 93 patients with severe ARDS admitted to a referral centre were analysed according to ventilatory and vital parameters.Overall survival rate was 70% and in patients who received ECMO treatment it was 67%. In patients exhibiting relevant co-morbidity the odds ratio for fatal outcome increased to 4.7 (95% CI: 3.3-24.9), and patients with multiple organ failure had a 7.5-fold increase (95% CI: 2.3-25.2) for risk of death. Survivors demonstrated a more pronounced improvement in oxygenation ( p0.05) and CO(2) removal ( p0.05) than non-survivors.Advanced treatment of ARDS including ECMO represents a therapeutic option if none of the currently considered contraindications are present. An improvement in gas exchange parameters, but not a defined value per se may be useful as a prognostic factor for favourable outcome.

After various observational studies demonstrated a benefit of extracorporeal membrane oxygenation (ECMO) in the therapy of severe acute respiratory distress syndrome (ARDS), ECMO now represents an important contribution for ARDS therapy using clinical algorithms despite a lack of positive controlled studies. In specialized centers patients with severe ARDS and imminent hypoxia despite intensive conventional therapy, are treated with ECMO using blood pumps and artificial membrane lungs (oxygenators) for extracorporeal lung assist. The development of new surface modifications, optimized oxygenators and miniaturized blood pumps should increase hemocompatibility and lead to simplified treatment as well as less complications. New oxygenators with significantly decreased blood resistance allow the clinical application of pumpless arteriovenous extracorporeal lung assist (ECLA). After these new developments indications for ECMO could be extended from use not only as ultimate ratio but to less severe ARDS to enable lung protective, less invasive mechanical ventilation.

Storungen des pulmonalen Gasaustauschs unter Narkose werden auch bei Patienten ohne vorbestehende Lungenerkrankungen beobachtet und zahlen zu den haufigsten Ursachen der perioperativen Morbiditat. Die Einleitung einer Allgemeinanasthesie fuhrt regelmasig durch eine Tonusanderung der inspiratorischen Muskulatur und eine Verlagerung des Zwerchfells nach kranial zu einer Reduktion der funktionellen Residualkapazitat (FRC). Dies hat eine Abnahme der Compliance des respiratorischen Systems sowie eine Minderventilation der abhangigen Lungenbezirke zur Folge, so dass es in diesen Bezirken zur Ausbildung von Kompressionsatelektasen und einer Storung des Gasaustauschs durch Zunahme des intrapulmonalen Shunts kommt, die manchmal auch noch Stunden nach Beendigung der Narkose nachweisbar ist. Die genannten Veranderungen finden sich haufiger und ausgepragter bei alteren und ubergewichtigen Patienten, sind aber mit Ausnahme von Ketamin unabhangig von den eingesetzten Medikamenten und Narkoseverfahren (TIVA, Inhalationsanasthesie) und treten bei spontanatmenden Patienten und unter kontrollierter Beatmung gleichermasen auf. Die Anwendung von PEEP kann zu einer Wiedereroffnung der atelektatischen Bereiche fuhren, geht jedoch bei normgewichtigen Individuen nicht mit einer Verbesserung des pulmonalen Gasaustauschs einher. Die Ursachen fur die Entwicklung dieser Veranderungen sind noch nicht abschliesend geklart und Wechselwirkungen sowie eine gegenseitige Beeinflussung der Mechanismen bei der Entwicklung der Einschrankungen des pulmonalen Gasaustauschs sind wahrscheinlich. Der folgende Beitrag gibt einen Uberblick uber verschiedene Aspekte der pulmonalen Gasaustauschstorung unter Allgemeinanasthesie, uber deren klinische Relevanz sowie uber mogliche Strategien zu ihrer Vermeidung und Therapie.

Partial liquid ventilation, positive end-expiratory pressure (PEEP) and inhaled nitric oxide (NO) can improve ventilation/perfusion mismatch in acute lung injury (ALI). The aim of the present study was to compare gas exchange and hemodynamics in experimental ALI during gaseous and partial liquid ventilation at two different levels of PEEP, with and without the inhalation of nitric oxide.Seven pigs (24+/-2 kg BW) were surfactant-depleted by repeated lung lavage with saline. Gas exchange and hemodynamic parameters were assessed in all animals during gaseous and subsequent partial liquid ventilation at two levels of PEEP (5 and 15 cmH2O) and intermittent inhalation of 10 ppm NO.Arterial oxygenation increased significantly with a simultaneous decrease in cardiac output when PEEP 15 cmH2O was applied during gaseous and partial liquid ventilation. All other hemodynamic parameters revealed no relevant changes. Inhalation of NO and instillation of perfluorocarbon had no additive effects on pulmonary gas exchange when compared to PEEP 15 cmH2O alone.In experimental lung injury, improvements in gas exchange are most distinct during mechanical ventilation with PEEP 15 cmH2O without significantly impairing hemodynamics. Partial liquid ventilation and inhaled NO did not cause an additive increase of PaO2.

Wild-type Salmonella typhimurium can use carnosine (beta-alanyl-L-histidine) as a source of histidine, but carnosine utilization is blocked in particular mutants defective in the constitutive enzyme peptidase D, the product of the pepD gene. Biochemical evidence for assigning carnosinase activity to peptidase D (a broad-specificity dipeptidase) includes: (i) coelution of carnosinase and dipeptidase activity from diethylaminoethyl-cellulose and Bio-Gel P-300 columns; (ii) coelectrophoresis of carnosinase and dipeptidase on polyacrylamide gels; and (iii) inactivation of carnosinase and dipeptidase activities at identical rates at both 4 and 42 degrees C. Genetic evidence indicates that mutations leading to loss of carnosinase activity map at pepD. Several independent pepD mutants have been isolated by different selection procedures, and the patterns of peptide utilization of strains carrying various pepD alleles have been studied. Many pepD mutations lead to the production of partially active peptidase D enzymes with substrate specificities that differ strikingly from those of the wild-type enzyme. The growth yields of carnosinase-deficient strains growing in Difco nutrient broth indicate that carnosine is the major utilizable source of histidine in this medium.

The DNA of bacteriophage T3 was characterized by cleavage with seven restriction endonucleases. AvaI, XbaI, BglII, and HindIII each cut T3 DNA at 1 site, KpnI cleaved it at 2 sites, MboI cleaved it at 9 sites, and HpaI cleaved it at 17 sites. The sizes of the fragments produced by digestion with these enzymes were determined by using restriction fragments of T7 DNA as molecular weight standards. As a result of this analysis, the size of T3 DNA was estimated to be 38.74 kilobases. The fragments were ordered with respect to each other and to the genetic map to produce a restriction map of T3 DNA. The location and occurrence of the restriction sites in T3 DNA are compared with those in the DNA of the closely related bacteriophage T7.

The RNA polymerases encoded by bacteriophages T3 and T7 have similar structures, but exhibit nearly exclusive template specificities. We have determined the nucleotide sequence of the region of T3 DNA that encodes the T3 RNA polymerase (the gene 1.0 region), and have compared this sequence with the corresponding region of T7 DNA. The predicted amino acid sequence of the T3 RNA polymerase exhibits very few changes when compared to the T7 enzyme (82% of the residues are identical). Significant differences appear to cluster in three distinct regions in the amino-terminal half of the protein. Analysis of the data from both enzymes suggests features that may be important for polymerase function. In particular, a region that differs between the T3 and T7 enzymes exhibits significant homology to the bi-helical domain that is common to many sequence-specific DNA binding proteins. The region that flanks the structural gene contains a number of regulatory elements including: a promoter for the E. coli RNA polymerase, a potential processing site for RNase III and a promoter for the T3 polymerase. The promoter for the T3 RNA polymerase is located only 12 base pairs distal to the stop codon for the structural gene.

1. The ganglion blocking agents, chlorisondamine, pentamethonium, mecamylamine, decamethonium and hexamethonium all block nicotine extensor convulsions when administered intraventricularly in mice. Tetraethylammonium was inactive. 2. For the intraventricular route, there is a relationship between ganglionic blocking potency and blocking of nicotine extensor convulsions. Indirect evidence suggests that the site(s) of action of nicotine extensor convulsions and lethality is central in origin and associated with brain areas near the ventricles. 3. When ganglion blocking agents are given orally, subcutaneously or intravenously varying degrees of protection can be observed probably depending on factors such as whether or not the drugs cross the blood-brain barrier, absorption, etc., and the effectiveness in protecting mice from nicotine is not related to ganglionic blocking potency. 4. Atropine and morphine given intraventricularly or subcutaneously did not protect mice from the LD95 of nicotine. Chlorpromazine gave very erratic results and phenobarbitone was effective subcutaneously and to a lesser extent intraventricularly.

To the Editor.— Briggs ( 217 :1705, 1971) commented on the "You know syndrome." The dangers inherent in this syndrome are insidious; communication seems to reach a standstill, although your attention is compelled by the constant referral to "you" and the hidden compliment that you are aware. I have been left bewildered after talking with people of different ages. While hearing and agreeing, I admittedly did not understand completely! To interject "No, I really don't know or understand" may have broken a train of thought. But now I find it to be an almost necessary inquiry when an exchange of ideas is involved. The frequency of this subtle "you know" habit or pitfall may be increasingly noted in conversations and general television viewing. A syndrome, easily cured by a healthy "I don't know, please explain," would bring about a greater understanding of ideas for all ages.