[Acute Respiratory Failure after Silicone Injection]. / Akutes respiratorisches Versagen durch Silikon-Injektion.

A 35-year-old male patient presented to the emergency department with complains of fever, dyspnea and petechiae. The chest X-ray revealed signs of bipulmonary infiltration. 5 days ago, an illicit silicone injection was performed into the penis for cosmetic reasons. Due to progressive respiratory failure the patient required mechanical ventilation. Bronchoalveolar lavage revealed diffuse alveolar hemorrhage. Silicone pneumonitis with a severe acute respiratory failure based on silicone embolization syndrome was diagnosed. Prone positioning, lung-protective ventilation and corticosteroid therapy were initiated. The patient was discharged from ICU after 19 days. In an outpatient follow up, lung function was fully recovered. CONCLUSION: Silicone pneumonitis should be considered in case of fever, respiratory distress and alveolar hemorrhage linked to cosmetic procedures. High dose corticosteroid therapy and lung-protective ventilation strategies may help for complete recovery of lung function.

[Sepsis and septic shock : Overview after sepsis-3 and the requirements of the clinician regarding the autopsy of critically ill patients]. / Sepsis und septischer Schock : Übersicht nach Sepsis-3 und Ansprüche des Klinikers an die Autopsie des Intensivpatienten.

Sepsis and septic shock are frequent conditions of patients in the intensive care unit. Recent guidelines adjusted the diagnostic criteria for sepsis and septic shock as well as the recommendations for sepsis treatment, which together is important for the intensivist as well as for the pathologist. Patients who die from septic shock despite invasive and intense therapies display various pathological findings that have to be placed in a reasonable clinical context, which is challenging for the pathologist without close cooperation with the former caring clinician. This short review gives an overview of recent definitions, the pathophysiology and treatment recommendations for sepsis and septic shock and discusses the importance of interdisciplinary cooperation between the pathologist and intensivist in the autopsy of a patient.

[New Pathogenetic Concepts and Pharmacological Studies on Adjuvant Therapy in Severe Pneumonia]. / Neue pathogenetische Konzepte und pharmakologische Studien zur adjuvanten Therapie bei schwerer Pneumonie.

Acute lung injury secondary to pneumonia results from inadequate activation of the innate immune system with hyperinflammation and alveolar-capillary barrier dysfunction. To date, effective strategies for prevention or treatment of acute lung injury in pneumonia besides antibiotics are lacking. In preclinical studies, promising therapeutic targets have been identified and novel strategies demonstrated to protect against lung failure in pneumonia. This review highlights some adjuvant therapeutic strategies for modulation of inflammation and stabilization of lung barrier function in pneumonia.

Moxifloxacin is not anti-inflammatory in experimental pneumococcal pneumonia.

OBJECTIVES: Anti-inflammatory functions of antibiotics may counteract deleterious hyperinflammation in pneumonia. Moxifloxacin reportedly exhibits immunomodulatory properties, but experimental evidence in pneumonia is lacking. Therefore, we investigated moxifloxacin in comparison with ampicillin regarding pneumonia-associated pulmonary and systemic inflammation and lung injury. METHODS: Ex vivo infected human lung tissue and mice with pneumococcal pneumonia were examined regarding local inflammatory response and bacterial growth. In vivo, clinical course of the disease, leucocyte dynamics, pulmonary vascular permeability, lung pathology and systemic inflammation were investigated. In addition, transcellular electrical resistance of thrombin-stimulated endothelial cell monolayers was quantified. RESULTS: Moxifloxacin reduced cytokine production in TNF-α-stimulated, but not in pneumococci-infected, human lung tissue. In vivo, moxifloxacin treatment resulted in reduced bacterial load as compared with ampicillin, whereas inflammatory parameters and lung pathology were not different. Moxifloxacin-treated mice developed less pulmonary vascular permeability during pneumonia, but neither combination therapy with moxifloxacin and ampicillin in vivo nor examination of endothelial monolayer integrity in vitro supported direct barrier-stabilizing effects of moxifloxacin. CONCLUSIONS: The current experimental data do not support the hypothesis that moxifloxacin exhibits potent anti-inflammatory properties in pneumococcal pneumonia.

Microvesicles released from pneumolysin-stimulated lung epithelial cells carry mitochondrial cargo and suppress neutrophil oxidative burst.

Microvesicles (MVs) are cell-derived extracellular vesicles that have emerged as markers and mediators of acute lung injury (ALI). One of the most common pathogens in pneumonia-induced ALI is Streptococcus pneumoniae (Spn), but the role of MVs during Spn lung infection is largely unknown. In the first line of defense against Spn and its major virulence factor, pneumolysin (PLY), are the alveolar epithelial cells (AEC). In this study, we aim to characterize MVs shed from PLY-stimulated AEC and explore their contribution in mediating crosstalk with neutrophils. Using in vitro cell and ex vivo (human lung tissue) models, we demonstrated that Spn in a PLY-dependent manner stimulates AEC to release increased numbers of MVs. Spn infected mice also had higher levels of epithelial-derived MVs in their alveolar compartment compared to control. Furthermore, MVs released from PLY-stimulated AEC contain mitochondrial content and can be taken up by neutrophils. These MVs then suppress the ability of neutrophils to produce reactive oxygen species, a critical host-defense mechanism. Taken together, our results demonstrate that AEC in response to pneumococcal PLY release MVs that carry mitochondrial cargo and suggest that these MVs regulate innate immune responses during lung injury.