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

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

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

The original version of this article unfortunately contained a mistake

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

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

Bradykinin receptors in ischemic stroke

Moždani udar je u razvijenim zemljama treći po učestalosti uzrok smrti i vodeći uzrok invalidnosti. Svake godine približno 800 000 ljudi doživi moždani udar, bilo da je riječ o prvom ili o rekurentnom moždanom udaru. Jedina terapija koja se primijenjuje kod pacijenata s moždanim udarom je fibrinoliza, koja je opcija za ograničen broj pacijenata. U ishemijskom moždanom udaru je kalikrein-kinin sustav jedan od prvih upalnih puteva koji se aktivira nakon oštećenja tkiva. Tijekom ishemije značajno se povećava koncentracija bradikinina kao i izražaj bradikininskih receptora. Jedan od najvažnijih i najčešće zabilježenih učinaka bradikinina u ishemijskom moždanom udaru je učinak na permeabilnost krvno-moždane barijere. Bradikinin, povećavajući vaskularnu permeabilnost i vazodilataciju, povećava moždani edem i na taj način značajno pogoršava ishemijsko oštećenje. Mikroglija i astrociti su glija stanice koje imaju brojne ulogu u razvoju ishemijskog moždanog udara te u interakciji s bradikininom ostvaruju različite upalne, ali i protuupalne učinke. S jedne strane bradikinin potiče lučenje citokina i kemokina, djeluje kao kemoatraktant leukocita, potiče adheziju trombocita te pojačava oštećenje, dok s druge strane inhibira proizvodnju proupalnih citokina, potiče migraciju reparativnih stanica do mjesta ozljede te sudjeluje u popravku i regeneraciji nastalog ishemijskog oštećenja. Kalikrein, stvaranjem kinina, inducira angiogenezu, neovaskularizaciju te obnavlja poremećeni krvni moždani protok. Također, kalikrein smanjuje ishemijski induciranu apoptozu i oksidacijski stres. Zaključno možemo reći da aktivacija bradikininskih receptora u ishemijskom moždanom udaru uzrokuje različite štetne, ali i protektivne učinke ovisne o vremenu proteklom od nastanka ishemije i stupnju ishemije.Stroke is the third leading cause of death and the leading cause of disability in the Western world. Every year approximately 800,000 people experience stroke, whether it is the primary or recurrent stroke. Today, fibrinolysis is the only therapy applied in stroke patients, which is an option for a limited number of patients. In ischemic stroke, the kinin-kallikrein system is one of the first inflammatory pathways activated after ischemic tissue damage. Bradykinin concentrations as well bradykinin receptors expression significantly rise during stroke. One of the most important and most commonly reported effects of bradykinin in ischemic stroke is its effect on blood-brain barrier vascular permeability. Bradykinin expands the size of cerebral edema by increasing vascular permeability and vasodilation, significantly exacerbating the ischemic damage. Microglia and astrocytes play a significant role in the development of ischemic stroke. Their interaction with bradykinin cause various inflammatory and antiinflammatory effects. Bradykinin stimulates cytokine and chemokine secretion, acts as a leukocyte chemoattractant, promotes platelet adhesion and exacerbates inflammatory damage, but also inhibits the production of proinflammatory cytokines, stimulates migration of repair cells to the site of injury and participates in repair and regeneration of the ischemic damage. Kallikrein, forming kinins, induces angiogenesis, neovascularization and regenerates the disturbed blood flow. Moreover, kallikrein reduces ischemically induced apoptosis and oxidative stress. In conclusion, the activation of bradykinin receptors in ischemic stroke causes various deleterious but also neuroprotective effects, primarily depending on the time elapsed since the onset of ischemia and the degree of ischemia

Bradykinin receptors in ischemic stroke

Moždani udar je u razvijenim zemljama treći po učestalosti uzrok smrti i vodeći uzrok invalidnosti. Svake godine približno 800 000 ljudi doživi moždani udar, bilo da je riječ o prvom ili o rekurentnom moždanom udaru. Jedina terapija koja se primijenjuje kod pacijenata s moždanim udarom je fibrinoliza, koja je opcija za ograničen broj pacijenata. U ishemijskom moždanom udaru je kalikrein-kinin sustav jedan od prvih upalnih puteva koji se aktivira nakon oštećenja tkiva. Tijekom ishemije značajno se povećava koncentracija bradikinina kao i izražaj bradikininskih receptora. Jedan od najvažnijih i najčešće zabilježenih učinaka bradikinina u ishemijskom moždanom udaru je učinak na permeabilnost krvno-moždane barijere. Bradikinin, povećavajući vaskularnu permeabilnost i vazodilataciju, povećava moždani edem i na taj način značajno pogoršava ishemijsko oštećenje. Mikroglija i astrociti su glija stanice koje imaju brojne ulogu u razvoju ishemijskog moždanog udara te u interakciji s bradikininom ostvaruju različite upalne, ali i protuupalne učinke. S jedne strane bradikinin potiče lučenje citokina i kemokina, djeluje kao kemoatraktant leukocita, potiče adheziju trombocita te pojačava oštećenje, dok s druge strane inhibira proizvodnju proupalnih citokina, potiče migraciju reparativnih stanica do mjesta ozljede te sudjeluje u popravku i regeneraciji nastalog ishemijskog oštećenja. Kalikrein, stvaranjem kinina, inducira angiogenezu, neovaskularizaciju te obnavlja poremećeni krvni moždani protok. Također, kalikrein smanjuje ishemijski induciranu apoptozu i oksidacijski stres. Zaključno možemo reći da aktivacija bradikininskih receptora u ishemijskom moždanom udaru uzrokuje različite štetne, ali i protektivne učinke ovisne o vremenu proteklom od nastanka ishemije i stupnju ishemije.Stroke is the third leading cause of death and the leading cause of disability in the Western world. Every year approximately 800,000 people experience stroke, whether it is the primary or recurrent stroke. Today, fibrinolysis is the only therapy applied in stroke patients, which is an option for a limited number of patients. In ischemic stroke, the kinin-kallikrein system is one of the first inflammatory pathways activated after ischemic tissue damage. Bradykinin concentrations as well bradykinin receptors expression significantly rise during stroke. One of the most important and most commonly reported effects of bradykinin in ischemic stroke is its effect on blood-brain barrier vascular permeability. Bradykinin expands the size of cerebral edema by increasing vascular permeability and vasodilation, significantly exacerbating the ischemic damage. Microglia and astrocytes play a significant role in the development of ischemic stroke. Their interaction with bradykinin cause various inflammatory and antiinflammatory effects. Bradykinin stimulates cytokine and chemokine secretion, acts as a leukocyte chemoattractant, promotes platelet adhesion and exacerbates inflammatory damage, but also inhibits the production of proinflammatory cytokines, stimulates migration of repair cells to the site of injury and participates in repair and regeneration of the ischemic damage. Kallikrein, forming kinins, induces angiogenesis, neovascularization and regenerates the disturbed blood flow. Moreover, kallikrein reduces ischemically induced apoptosis and oxidative stress. In conclusion, the activation of bradykinin receptors in ischemic stroke causes various deleterious but also neuroprotective effects, primarily depending on the time elapsed since the onset of ischemia and the degree of ischemia

Bradykinin receptors in ischemic stroke

Moždani udar je u razvijenim zemljama treći po učestalosti uzrok smrti i vodeći uzrok invalidnosti. Svake godine približno 800 000 ljudi doživi moždani udar, bilo da je riječ o prvom ili o rekurentnom moždanom udaru. Jedina terapija koja se primijenjuje kod pacijenata s moždanim udarom je fibrinoliza, koja je opcija za ograničen broj pacijenata. U ishemijskom moždanom udaru je kalikrein-kinin sustav jedan od prvih upalnih puteva koji se aktivira nakon oštećenja tkiva. Tijekom ishemije značajno se povećava koncentracija bradikinina kao i izražaj bradikininskih receptora. Jedan od najvažnijih i najčešće zabilježenih učinaka bradikinina u ishemijskom moždanom udaru je učinak na permeabilnost krvno-moždane barijere. Bradikinin, povećavajući vaskularnu permeabilnost i vazodilataciju, povećava moždani edem i na taj način značajno pogoršava ishemijsko oštećenje. Mikroglija i astrociti su glija stanice koje imaju brojne ulogu u razvoju ishemijskog moždanog udara te u interakciji s bradikininom ostvaruju različite upalne, ali i protuupalne učinke. S jedne strane bradikinin potiče lučenje citokina i kemokina, djeluje kao kemoatraktant leukocita, potiče adheziju trombocita te pojačava oštećenje, dok s druge strane inhibira proizvodnju proupalnih citokina, potiče migraciju reparativnih stanica do mjesta ozljede te sudjeluje u popravku i regeneraciji nastalog ishemijskog oštećenja. Kalikrein, stvaranjem kinina, inducira angiogenezu, neovaskularizaciju te obnavlja poremećeni krvni moždani protok. Također, kalikrein smanjuje ishemijski induciranu apoptozu i oksidacijski stres. Zaključno možemo reći da aktivacija bradikininskih receptora u ishemijskom moždanom udaru uzrokuje različite štetne, ali i protektivne učinke ovisne o vremenu proteklom od nastanka ishemije i stupnju ishemije.Stroke is the third leading cause of death and the leading cause of disability in the Western world. Every year approximately 800,000 people experience stroke, whether it is the primary or recurrent stroke. Today, fibrinolysis is the only therapy applied in stroke patients, which is an option for a limited number of patients. In ischemic stroke, the kinin-kallikrein system is one of the first inflammatory pathways activated after ischemic tissue damage. Bradykinin concentrations as well bradykinin receptors expression significantly rise during stroke. One of the most important and most commonly reported effects of bradykinin in ischemic stroke is its effect on blood-brain barrier vascular permeability. Bradykinin expands the size of cerebral edema by increasing vascular permeability and vasodilation, significantly exacerbating the ischemic damage. Microglia and astrocytes play a significant role in the development of ischemic stroke. Their interaction with bradykinin cause various inflammatory and antiinflammatory effects. Bradykinin stimulates cytokine and chemokine secretion, acts as a leukocyte chemoattractant, promotes platelet adhesion and exacerbates inflammatory damage, but also inhibits the production of proinflammatory cytokines, stimulates migration of repair cells to the site of injury and participates in repair and regeneration of the ischemic damage. Kallikrein, forming kinins, induces angiogenesis, neovascularization and regenerates the disturbed blood flow. Moreover, kallikrein reduces ischemically induced apoptosis and oxidative stress. In conclusion, the activation of bradykinin receptors in ischemic stroke causes various deleterious but also neuroprotective effects, primarily depending on the time elapsed since the onset of ischemia and the degree of ischemia

A Reminder of Skin Cancer During the COVID-19 Pandemic

The year 2020 has been marked by the coronavirus disease 2019 (COVID-19) pandemic, caused by an RNA virus called SARS-COV2 (severe acute respiratory syndrome coronavirus). The fight against this epidemic has become the center of our daily clinical practice as well as of our private lives, in which avoiding infection has become one of our most important goals. Even though COVID-19 is a potentially lethal disease, especially for the elderly and people with chronic diseases, it did not cause all the other life-threatening diseases to vanish. On the contrary, many scheduled medical activities and procedures, especially preventive and non-urgent internal and surgical activities, had to be postponed due to COVID-19 crisis. This interruption in the health care system can negatively affect the diagnosis and management of our patients with other health issues, namely malignant skin tumors, of which melanoma is the most aggressiv

Nanočestice kao terapijski sustavi za primjenu lijeka u oko

Despite extensive research in the field, the major problem in ocular drug delivery is the attainment of an optimal drug concentration at the intended site of action for a sufficient period of time. The site of action maybe located on the eye surface or in the inner ocular structures. The important barriers that need to be overcome in order to reach the target site limits not only the number of medications available for the treatment of ocular diseases, but aIso the extent to which those available can be used without incurring undesirable systemic side effects. From the results described in this chapter, it is possible to conclude that nanoparticles offer great chances of solving these limitations, while still benefiting from their topical administration as eye drops. Indeed, nanoparticles, depending on their composition, are significantly retained on the ocular mucosa, and from this location, they deliver the associated drugs for extended periods of time. This situation normally results in an enhanced and prolonged therapeutic response, and also in a decrease in the side effects. The results reported so far have also evidenced that both the extent of interaction and the penetration depth of the colloidal systems with the cornea, can be modulated by the selection of an appropriate coating. In addition to these beneficial effects associated with the topical ocular administration, nanoparticles offer an interesting potential in terms of improving intraocular drug administration. This potential includes not only the prolongation of the residence time of drugs in the eye, but also their targeting to the retina! cells. Finally, significant efforts are currently underway to develop highly sophisticated nanoparticles functionalized with specific targeting ligands (i.e. lectins and antibodies). Advances in this area are expected to open new avenues for the diagnostic and therapy (including gene therapy) of ocular disorders