Acute pulmonary non-cardiogenic edema after extubation with laryngospasm: a case report

Acute pulmonary edema post extubation due to negative pressure with laryngospasm in the early postoperative period has been reported and may occur at any time during anesthesia. The usual treatment consists of respiratory support and diuretics. We present the clinical case of a 15-year-old patient who underwent laparoscopic appendectomy, who presented acute non-cardiogenic pulmonary edema in the postoperative period. This complication can be presented in any surgical patient intubated, so it is important to know the pathophysiological basis to be able to diagnose and treat this pathology

Transfusion related acute lung injury: a case report

Transfusion Related Acute Lung Injury (TRALI) is one of the most serious complications of blood transfusion. All blood components have been implicated and most often those that contain plasma. The diagnosis is based fundamentally on the integration of clinical, radiological and gasometry elements, once the rest of the possible causes of acute lung injury have been ruled out. The differential diagnosis of a patient who develops a sudden pattern of respiratory failure after a transfusion of blood products must include hemodynamic overload, anaphylactic reaction, bacterial contamination of transfused blood products, haemolytic transfusion reaction and TRALI. Author presented the clinical case of a 33-year-old female patient with grade III hypovolemic shock due to a ruptured ectopic pregnancy, reanimated with crystalloid solutions, globular packages and fresh frozen plasma. The patient developed TRALI for what was managed with ventilatory and hemodynamic support in ICU

Transfusion related acute lung injury-TRALI: a review

Acute pulmonary damage caused by transfusion is characterized by the sudden onset of respiratory distress in newly transfused patients within 6 hours after the transfusion, bilateral infiltrative changes in chest X-ray, PaO2/FIO2 <300 mmHg, absence of other risk factors for acute lung injury and absence of signs suggesting cardiogenic origin of pulmonary edema. Being one of the most serious complications of blood transfusion, plasma is the most involved factor, although all blood components can cause it, and is caused by antigen reactions/leukocyte antibody and lipid activity with ability to modify the biological response on primitive leukocytes. The diagnosis is based on the integration of clinical, radiological and gasometric elements, ruling out the rest of the possible causes of acute lung injury. Its differential diagnosis should include hemodynamic overload, anaphylactic reaction, bacterial contamination of transfused blood products and transfusion hemolytic reaction. The treatment is supportive measures based on the needs and does not differ from the treatment of acute lung injury secondary to other etiologies, severe cases require endotracheal intubation and mechanical ventilation while the non-severe can be managed with oxygen therapy

Management of a ruptured epidural catheter, an anesthesiologist's dilemma: a case report

Epidural anesthesia is a widely used anesthetic technique in lower extremity surgeries although it is a relatively safe procedure, it can have complications, such as rupture of the epidural catheter. This is a 69-year-old male patient with a diagnosis of Wagner IV diabetic foot is presented, which was scheduled for left supracondylar amputation in which after epidural block, retention of the catheter tip in the epidural space at level L2-L3 was seen, so hemi laminectomy was performed in a second surgical stage in L2 and removal of the epidural catheter. Ideally a broken needle should be removed as soon as possible

Global hyperactivation of enhancers stabilizes human and mouse naïve pluripotency through inhibition of CDK8/19 Mediator kinases

Pluripotent stem cells (PSCs) transition between cell states in vitro and reflect developmental changes in the early embryo. PSCs can be stabilized in the naïve state by blocking extracellular differentiation stimuli, particularly FGF-MEK signaling. Here, we report that multiple features of the naïve state in human and mouse PSCs can be recapitulated without affecting FGF-MEK-signaling or global DNA methylation. Mechanistically, chemical inhibition of CDK8 and CDK19 kinases removes their ability to repress the Mediator complex at enhancers. Thus CDK8/19 inhibition increases Mediator-driven recruitment of RNA Pol II to promoters and enhancers. This efficiently stabilizes the naïve transcriptional program and confers resistance to enhancer perturbation by BRD4 inhibition. Moreover, naïve pluripotency during embryonic development coincides with a reduction in CDK8/19. We conclude that global hyperactivation of enhancers drives naïve pluripotency, and this can be achieved in vitro by inhibiting CDK8/19 kinase activity. These principles may apply to other contexts of cellular plasticity

Molecular Identification and Susceptibility Testing of Molds Isolated in a Prospective Surveillance of Triazole Resistance in Spain (FILPOP2 Study).

Antifungal resistance is increasing by the emergence of intrinsically resistant species and by the development of secondary resistance in susceptible species. A previous study performed in Spain revealed levels of azole resistance in molds of between 10 and 12.7%, but secondary resistance in Aspergillus fumigatus was not detected. We used itraconazole (ITZ)-supplemented medium to select resistant strains. A total of 500 plates supplemented with 2 mg/liter of ITZ were sent to 10 Spanish tertiary hospitals, and molecular identification and antifungal susceptibility testing were performed. In addition, the cyp51A gene in those A. fumigatus strains showing azole resistance was sequenced. A total of 493 isolates were included in the study. Sixteen strains were isolated from patients with an infection classified as proven, 104 were isolated from patients with an infection classified as probable, and 373 were isolated from patients with an infection classified as colonization. Aspergillus was the most frequent genus isolated, at 80.3%, followed by Scedosporium-Lomentospora (7.9%), Penicillium-Talaromyces (4.5%), Fusarium (2.6%), and the order Mucorales (1%). Antifungal resistance was detected in Scedosporium-Lomentospora species, Fusarium, Talaromyces, and Mucorales Three strains of A. fumigatus sensu stricto were resistant to azoles; two of them harbored the TR34+L98H mechanism of resistance, and the other one had no mutations in cyp51A The level of azole resistance in A. fumigatus remains low, but cryptic species represent over 10% of the isolates and have a broader but overall higher range of antifungal resistance.Gilead Sciences (IN-ES-131-1600) Fondo de Investigaciones Sanitarias (PI16CIII/00035, PI13/02783, FI14CIII/00025, PI13/02145)S

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field