8 research outputs found

    Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

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    Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

    Islet composition and architecture in streptozotocin-induced diabetic rat following pancreatic duct ligation

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    Thesis (MScMedSc)--Stellenbosch University, 2015.ENGLISH ABSTRACT: Diabetes Mellitus is a metabolic disease characterized by the loss of beta cells from the islets, thereby disrupting islet composition and architecture which are important components that influence islet function. The experimental technique of pancreatic duct ligation (PDL), which is thought to induce the regeneration of beta cells within the adult pancreas, was investigated as a novel treatment strategy for diabetes. This study aimed at investigating the possibility that the PDL model may have the capacity to restore normal islet composition and architecture in diabetic animals, which could make it an effective approach to reverse diabetes. Male Wistar rats (n=55) were divided into three study groups: the normal control (NC) group, the diabetic control (DC) group consisting of five subgroups (day 0, 3, 5, 10 and 30) and the experimental (EX) group consisting of four subgroups (day 3, 5, 10 and 30). The experimental group was exposed to PDL. All pancreata were divided into a P1 portion (proximal to the point of ligature) and P2 portion (distal to the point of ligature) for histological assessment. Animals’ non-fasting blood glucose levels (BGLs) and body weights were monitored. The general morphology of the tissue was studied, while an immunohistochemical (IHC) study was performed to determine insulin, pancreatic polypeptide, glucagon and somatostatin protein expression in the P1 and P2 portions of the pancreas. From the IHC slides hormone fractions, staining intensity and distribution were determined as indication of islet composition and architecture. Despite apparent morphological recovery in the islet 30 days post-PDL, islet composition and architecture remained disrupted. Compared to diabetic animals, the proximal portion of the pancreas in experimental animals had a decreased beta cell fraction and increased delta cell fraction thirty days following PDL. These observed changes in islet composition in the part of the pancreas proximal to the ligature are novel findings. There was no change in the diabetic islet composition in the portion of the pancreas distal to the ligature thirty days following PDL. Furthermore, pancreatic duct ligation did not restore body weight or normoglycemia. We conclude that STZ disrupts islet composition and architecture and this could not be restored using PDL; we therefore suggest that a comparative study using a Type 2 diabetic model, where there is limited damage to pre-existing beta cells, may yield different results.AFRIKAANSE OPSOMMING: Diabetes Mellitus is ʼn metaboliese siekte wat deur die verlies van beta selle uit die eilande van Langerhans gekarakteriseer word. Hierdie verlies van beta selle ontwrig eiland komposisie en argitektuur, twee belangrike komponente van eiland funksie. Die eksperimentele tegnieke van pankreatiese buisafbinding (in Engels PDL), wat moontlik beta sel regenerasie in die volwasse pankreas kan induseer, is ondersoek as behandelings-strategie vir diabetes. Hierdie studie het ten doel gehad om die moontlikheid te ondersoek dat die PDL model die kapasiteit het om normale eiland komposisie en argitektuur te herstel in diabetiese diere, wat dit ʼn effektiewe benadering vir die omkeer van diabetes kan maak. Manlike Wistar rotte (n=55) was in 3 studie groepe verdeel: die normale kontrole (NC) groep, die diabetiese kontrole (DC) groep wat uit vyf subgroepe bestaan (dag 0, 3, 5, 10 en 30) en die eksperimentele (EX) groep wat uit vier subgroepe bestaan (dag 3, 5, 10 en 30). Die eksperimentele groep is aan PDL blootgestel. Alle pankreata is verdeel in ʼn P1 porsie (proksimaal tot die afbinding) en ʼn P2 porsie (distaal tot die afbinding) vir histologiese assessering. Die diere se nie-vastende bloed glukose vlakke en liggaamsgewig is gemonitor. Die algemene morfologie van die pankreas weefsel is bestudeer, terwyl ’n immunohistochemiese (IHC) studie gedoen is om insulien, pankreatiese polipeptied, glukagon en somatostatien proteïen uitdrukking in die P1 en P2 porsies van die pankreas te bepaal. Vanaf die IHC snitte is hormoon fraksie, kleur intensiteit en verspreiding bepaal as aanduidings van eiland komposisie en argitektuur. Ten spyte van ooglopende morfologiese herstel in die eilande op dag 30 na PDL, het eiland komposisie en argitektuur versteur gebly. In vergelyking met die diabetiese diere, het die proksimale deel van die pankreas van eksperimentele diere verlaagde beta sel fraksie en verhoogde delta sel fraksie getoon dertig dae na PDL. Die waarneming van veranderde komposisie in die deel van die pankreas proksimaal tot die afbinding is nuut. Daar was geen verandering in diabetiese eiland komposisie in die deel van die pankreas distaal tot die afbinding dertig dae na PDL nie. Verder het PDL nie liggaamsgewig of bloedsuiker genormaliseer nie. Ons gevolgtrekking is dat STZ eiland komposisie en argitektuur ontwrig en dat dit nie met PDL herstel kon word nie; daarom stel ons ʼn vergelykende studie in ʼn tipe 2 diabetes model voor, waar die skade aan reeds bestaande beta selle beperk is, wat ander resultate mag lewer

    Immunohistomorphology of pancreatic islet microvasculature and the immunophenotypic analysis of CEPC in adult diabetic rats

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    CITATION: Tchokonte-Nana, V. 2017. Immunohistomorphology of pancreatic islet microvasculature and the immunophenotypic analysis of CEPC in adult diabetic rats. International journal of morphology, 35(4):1560-1567.The original publication is available at http://www.intjmorphol.comENGLISH ABSTRACT: Hyperglycaemia is one of the main causes for the endothelial cell (EC) damage in diabetic patients. Even though circulating endothelial progenitor cells (CEPC) could be used as a prognosis for microvascular complications, there is very little information on the islet microvasculature. We analysed by immunohistochemistry and by flow cytometric immunophenotyping, the expression of CD34 on EC and the expressions of CD31, CD34, CD45 and CD133 on CEPC in Streptozotocin (STZ)-induced diabetic rats. Peripheral blood and tissue specimens were obtained from rats of different treatment regimens: STZ treatment, control saline (NS) and sodium citrate (CB) treatments. Blood cells were exposed to flow cytometric immunophenotyping for CD133, CD31, CD34, CD45 and CD133. While tissues from the pancreas, liver and kidney were routinely processed and stained immunohistochemically for CD34. There was a tendency of an increased in CD45-/CD133+/CD31+/CD34+ cells (0.04 ± 0.11 %) in diabetic rats compared to the controls (CB: 0.03 ± 0.04 %; Saline: 0.01 ± 0.03 %). But there was no significant statistical difference between them. The expression pattern of CD34 on the EC in the organs’ vascular beds including arterioles, venules, capillaries and sinusoids was extremely heterogeneous across and within treatment regimens. The ECs in the sinusoids of the liver presented similar CD34 expression patterns across different treatment regimens, while the expression of CD34 on the ECs of sinusoidal capillaries in the pancreas vary with the treatment regimen. We conclude that the degree of endothelial cell damage is not uniform across organs’ vascular beds in the rat, contrary to mice and humans. Furthermore, the sinusoids in the pancreas and the kidney may have the same degree of endothelial damage when exposed to the same deleterious causes.http://www.intjmorphol.com/abstract/?art_id=4601Publisher's versio

    Correction to: Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study (Intensive Care Medicine, (2021), 47, 2, (160-169), 10.1007/s00134-020-06234-9)

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    The original version of this article unfortunately contained a mistake. The members of the ESICM Trials Group Collaborators were not shown in the article but only in the ESM. The full list of collaborators is shown below. The original article has been corrected
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