Invasive Ventilatory Support in Patients With Pediatric Acute Respiratory Distress Syndrome: From the Second Pediatric Acute Lung Injury Consensus Conference.

OBJECTIVE: To provide evidence for the Second Pediatric Acute Lung Injury Consensus Conference updated recommendations and consensus statements for clinical practice and future research on invasive mechanical ventilation support of patients with pediatric acute respiratory distress syndrome (PARDS). DATA SOURCES: MEDLINE (Ovid), Embase (Elsevier), and CINAHL Complete (EBSCOhost). STUDY SELECTION: We included clinical studies of critically ill patients undergoing invasive mechanical ventilation for PARDS, January 2013 to April 2022. In addition, meta-analyses and systematic reviews focused on the adult acute respiratory distress syndrome population were included to explore new relevant concepts (e.g., mechanical power, driving pressure, etc.) still underrepresented in the contemporary pediatric literature. DATA EXTRACTION: Title/abstract review, full text review, and data extraction using a standardized data collection form. DATA SYNTHESIS: The Grading of Recommendations Assessment, Development and Evaluation approach was used to identify and summarize relevant evidence and develop recommendations, good practice statements and research statements. We identified 26 pediatric studies for inclusion and 36 meta-analyses or systematic reviews in adults. We generated 12 recommendations, two research statements, and five good practice statements related to modes of ventilation, tidal volume, ventilation pressures, lung-protective ventilation bundles, driving pressure, mechanical power, recruitment maneuvers, prone positioning, and high-frequency ventilation. Only one recommendation, related to use of positive end-expiratory pressure, is classified as strong, with moderate certainty of evidence. CONCLUSIONS: Limited pediatric data exist to make definitive recommendations for the management of invasive mechanical ventilation for patients with PARDS. Ongoing research is needed to better understand how to guide best practices and improve outcomes for patients with PARDS requiring invasive mechanical ventilation.

Does the widely distributed rodent Calomys tener (Cricetidae: Sigmodontinae) constitute a single evolutionary unit?

The nominal species Calomys tener (Winge, 1887) ranges broadly in open lands of the Caatinga, Cerrado, Pantanal and Mata Atlântica of Brazil, and was recently reported from the Pampas of southern Brazil, and in the Selva Paranaense of eastern Paraguay and northeastern Argentina. This rodent can be infected with the pathogenic Araraquara hantavirus in Brazil. Given that most epidemiological studies have not taken into account updated taxonomic findings of their rodent hosts, in this study, we obtained sequence data of the Cyt-b and COI genes of specimens of C. tener from 22 different geographical localities from throughout the currently known distribution of the species (including individuals from Argentina, Paraguay, Bolivia, and Brazil) to test if it constitutes a single genetic unit or if it presents genetic discontinuities that may represent different evolutionary lineages. Phylogenetic analyses including several species of Calomys recovered several clades with strong support. Regarding C. tener, it is recovered as sister to the node that cluster C. laucha (Fischer, 1814) sensu lato, C. expulsus (Lund, 1841) and species in the C. callosus (Rengger, 1830) species complex. At the intraspecific level there are no genetic gaps among haplotypes of C. tener that could suggest more than one species. The recent captures in the Pampas of southern Brazil and in the Selva Paranaense suggest that the species may be colonizing new geographic areas.(AU)

Does the widely distributed rodent Calomys tener (Cricetidae: Sigmodontinae) constitute a single evolutionary unit?

The nominal species Calomys tener (Winge, 1887) ranges broadly in open lands of the Caatinga, Cerrado, Pantanal and Mata Atlântica of Brazil, and was recently reported from the Pampas of southern Brazil, and in the Selva Paranaense of eastern Paraguay and northeastern Argentina. This rodent can be infected with the pathogenic Araraquara hantavirus in Brazil. Given that most epidemiological studies have not taken into account updated taxonomic findings of their rodent hosts, in this study, we obtained sequence data of the Cyt-b and COI genes of specimens of C. tener from 22 different geographical localities from throughout the currently known distribution of the species (including individuals from Argentina, Paraguay, Bolivia, and Brazil) to test if it constitutes a single genetic unit or if it presents genetic discontinuities that may represent different evolutionary lineages. Phylogenetic analyses including several species of Calomys recovered several clades with strong support. Regarding C. tener, it is recovered as sister to the node that cluster C. laucha (Fischer, 1814) sensu lato, C. expulsus (Lund, 1841) and species in the C. callosus (Rengger, 1830) species complex. At the intraspecific level there are no genetic gaps among haplotypes of C. tener that could suggest more than one species. The recent captures in the Pampas of southern Brazil and in the Selva Paranaense suggest that the species may be colonizing new geographic areas.

Musculoskeletal problems in persons with inhibitors: how do we treat?

Inhibitors are a serious complication, considerably increasing the morbidity, mortality and cost of treatment in this patient group. The challenge of treating people with haemophilia (PWH) with inhibitors can be met by a well-coordinated multidisciplinary team specialized in haemophilia. Each treatment centre must run a screening programme to detect inhibitors within their population and develop protocols to treat these patients. The treatment centre in Buenos Aires developed a screening programme that tests all our patients twice a year, ensuring early detection of inhibitors and early treatment of complications. In 2006, we analysed the quality of life (QOL) of non-inhibitor patients and compared it with inhibitor patients detected by this programme and found no differences in QOL measured by the SF36 questionnaire and no differences in school absenteeism. When diagnosis of the inhibitor does not come from a screening programme, its presence is suspected upon a lack of response to conventional replacement therapy for musculoskeletal bleeding, losing the 'golden moment' of treatment. This complication is much more serious when facing a traumatic bleed. In this situation, the lack of early diagnosis can lead to permanent damage or even death. Due to the cost of bypassing factors and the lack of experience of the medical team in the treatment of patients with inhibitors, many treatments that would improve the QOL of patients are instituted in an insufficient manner. Therefore, patients with haemophilia and inhibitors are often untreated or undertreated in their community. Orthopaedic surgeons and physiotherapists play a key role in the treatment of these patients and should be included in therapeutic decision making and most specifically in the postoperative treatment of patients with haemophilia and inhibitors. It is important that these patients have quick access to a trained therapeutic team in order to obtain an early diagnosis and treatment plan to prevent the evolution of the pathological process. Early treatment is cost-effective in maintaining and improving the QOL of patients. Experience in patients with haemophilia and inhibitors is not very extensive. Today, this situation is changing, with several treatment centres beginning to perform surgeries in these most complex patients, giving them a chance to improve their QOL. This article presents the experience of experts from various fields involved in treating patients with inhibitors from a developed and developing world perspective.

Ploidy status correlates with outcome in stage B prostate adenocarcinoma.

1. While there are extensive data showing that aneuploidy is associated with adverse outcome in stage D prostate cancer, the utility of ploidy analysis in stage B disease is unclear. We determined ploidy in radical prostatectomy specimens from 28 patients with clinical stage B prostate cancer, and with a mean follow-up of 4.1 years (2-10 years). Patients who had no recurrences had a minimum 5 years of follow-up. Patients who had only 2 years of follow-up were included if they had developed bone metastases during this period. 2. Ploidy determinations were done on Feulgen-stained 5-microns paraffin-embedded sections using a CAS 200 image analyzer. At least 400 tumor cells were counted in every case. Tumors with at least 70% diploid cells were classified as diploid, while those with less than 70% diploid cells were classified as aneuploid. The mean percentage of diploid cells in tumors classified as diploid was 90.6 +/- 7.4, while the mean percentage of diploid cells in tumors classified as aneuploid was 36 +/- 21.9. 3. Ploidy status correlated with disease progression: seven of the 10 patients (70%) with disease recurrence had aneuploid tumors, while 13 of 18 patients (72%) who remained disease-free had diploid tumors (P = 0.03, Chi-square test). 4. These data show that patients with stage B disease with aneuploid tumors at the time of prostatectomy are more likely to have recurrent disease within a mean of 3 years (2-6 years) compared to patients with diploid tumors.(ABSTRACT TRUNCATED AT 250 WORDS)

Ploidy status correlates with outcome in stage B prostate adenocarcinoma

1. While there are extensive data showing that aneuploidy is associated with adverse outcome in stage D prostate cancer, the utility of ploidy analysis in stage B disease in unclear. We determined ploidy in radical prostatectomy specimens from 28 patients with clinical stage B prostate cancer, and with a mean follow-up of 4.1 years (2-10 years). Patients who had no recurrences had a minimum 5 years of follow-up. Patients who had only 2 years of follow-up were included if they had developed bone metastases during this period. 2. Ploidy determinations were done on Feugen-stained 5-µm paraffin-embedded sections using a CAS 200 image analyzer. At least 400 tumor cells were counted in every case. Tumors with at least 70 percent diploid cells were classified as diploid, while those with less than 70 percent diploid cells were classified as aneuploid. The mean percentage of diploid cells in tumors classified as diploid was 90.6 ñ 7.4, while the mean percentage of diploid cells in tumors classified as aneuploid was 36 ñ 21.9. 3. Ploidy status correlated with disease progression: seven of the 10 patients (70 percent) with disease recurrence had aneuploid tumors, while 13 of 18 patients (72 percent) who remained disease-free had diploid tumors (P= 0.03, Chi-square test). 4. These data show that patients with stage B disease with aneuploid tumors at the time of prostatectomy are more likely to have recurrent disease within a mean of 3 years (2-6 years) compared to patients with diploid tumors. Ploidy determination done at the time of surgery may offer useful prognostic information