Odleżyny
Patofizjologia i mechanizm

Odleżyny powstają w wyniku długotrwałego ucisku przekraczającego ciśnienie zamykające naczynia włosowate tętnicze (32 mm Hg) i żylne (8-12 mm Hg), co prowadzi do niedokrwienia, hipoksji i martwicy tkanek, zwłaszcza mięśni, które ulegają uszkodzeniu już po 4 godzinach ciągłego ucisku. Siły ścinające i tarcie nasilają uszkodzenia, szczególnie w warunkach zwiększonej wilgotności skóry, która powoduje macerację i osłabienie bariery naskórkowej. Patogeneza obejmuje także przewlekły stan zapalny z udziałem cytokin prozapalnych (IL-6, TNF-α), stres oksydacyjny oraz zaburzenia odpowiedzi immunologicznej, w tym zmniejszoną aktywację inflamasomu NLRP3 w starzejącej się skórze. Zaburzenia syntezy kolagenu i angiogenezy, a także dysregulacja szlaków sygnałowych (PI3K/AKT, p38-MAPK, NFκB) dodatkowo utrudniają gojenie ran. Czynniki ryzyka to m.in. unieruchomienie, choroby przewlekłe (cukrzyca, udar, demencja), niedożywienie, zaburzenia czucia, wiek podeszły oraz zaburzenia krążenia.

  1. Patogeneza odleżyn
    1. Mechanizm powstawania niedokrwienia
    2. Rola sił ścinających i tarcia
    3. Wpływ wilgotności
    4. Kaskada komórkowa i tkankowa
    5. Różnice w podatności tkanek
  2. Rola procesów zapalnych w patogenezie odleżyn
    1. Przewlekły stan zapalny
    2. Stres oksydacyjny
    3. Zaburzenia odpowiedzi immunologicznej
  3. Czynniki ryzyka i predysponujące do rozwoju odleżyn
    1. Czynniki wewnętrzne
    2. Czynniki zewnętrzne
  4. Zaawansowane mechanizmy komórkowe w patogenezie odleżyn
    1. Uszkodzenie niedokrwienno-reperfuzyjne
    2. Zaburzenia struktury i funkcji kolagenu
    3. Zaburzenia angiogenezy
    4. Zaburzenia odpowiedzi immunologicznej (przewlekłe)
  5. Specyficzne szlaki sygnałowe w patogenezie odleżyn
    1. Rola mikroRNA
    2. Rola białek SOCS
  6. Zaburzenia metaboliczne w odleżynach
    1. Niedokrwistość i zaburzenia białek surowicy
    2. Implikacje terapeutyczne
  7. Specyfika odleżyn u pacjentów z cukrzycą
    1. Neuropatia i powikłania naczyniowe
    2. Zaburzenia syntezy kolagenu
    3. Przewlekły stan zapalny w cukrzycy
    4. Zaburzenia angiogenezy w cukrzycy
  8. Odleżyny związane z COVID-19
  9. Podsumowanie mechanizmów patogenetycznych
    1. Kolejne rozdziały

Patogeneza odleżyn

Odleżyny, znane również jako rany odleżynowe lub owrzodzenia odleżynowe, są zlokalizowanymi obszarami uszkodzenia skóry i tkanek podskórnych, które powstają w wyniku długotrwałego ucisku, często w połączeniu z siłami ścinającymi i tarciem, zwykle nad wyniosłościami kostnymi. Rozwój odleżyn jest złożonym i wieloczynnikowym procesem, w którym zewnętrzne i wewnętrzne czynniki współwystępują, prowadząc do uszkodzenia tkanek.123

Mechanizm powstawania niedokrwienia

Podstawowym mechanizmem prowadzącym do powstania odleżyny jest przedłużony nacisk na tkanki, który powoduje okluzję naczyń włosowatych, zmniejszając przepływ krwi do obszaru poddanego uciskowi. Aby doszło do uszkodzenia tkanek, zewnętrzny nacisk musi przekroczyć ciśnienie zamykające naczyń włosowatych tętniczych (32 mm Hg), co zaburza dopływ krwi, oraz ciśnienie zamykające naczyń włosowatych żylnych (8-12 mm Hg), co upośledza odpływ krwi. Utrzymujący się nacisk powyżej tych wartości prowadzi do niedokrwienia tkanki i ostatecznie do martwicy.456

Należy podkreślić, że tkanki są w stanie wytrzymać znaczne naciski przez krótki czas, jednak przedłużona ekspozycja na ciśnienie nieznacznie przekraczające wartości kapilarnego przepływu krwi inicjuje spiralę uszkodzeń prowadzącą do martwicy tkanek i owrzodzenia. W badaniach wykazano, że nieodwracalne zmiany w tkankach mogą wystąpić już po 2 godzinach nieprzerwanego nacisku.789

Rola sił ścinających i tarcia

Oprócz ciśnienia bezpośredniego, w patogenezie odleżyn istotną rolę odgrywają również siły ścinające i tarcie:

  • Siły ścinające powstają, gdy kości i tkanki podskórne poruszają się względem skóry, która jest unieruchomiona przez siły tarcia (np. gdy pacjent siedzący zsuwa się na krześle lub gdy wezgłowie łóżka jest podniesione powyżej 30 stopni). W takich okolicznościach ciśnienie potrzebne do zamknięcia naczyń krwionośnych jest znacznie zmniejszone. Naczynia ulegają zagięciu i zakrzepicy, co przyczynia się do powstawania podminowanych krawędzi odleżyny.1011
  • Tarcie (pocieranie o odzież lub pościel) może przyczyniać się do powstawania owrzodzeń skóry poprzez powodowanie lokalnej erozji i uszkodzeń naskórka oraz powierzchownej skóry właściwej. Choć tarcie samo w sobie nie jest bezpośrednią przyczyną odleżyn, może znacząco osłabić integralność skóry, czyniąc ją bardziej podatną na uszkodzenia spowodowane ciśnieniem.1213

Wpływ wilgotności

Nadmierna wilgotność skóry, spowodowana np. poceniem się, nietrzymaniem moczu lub stolca, czy nadmiernym wysiękiem z rany, znacząco zwiększa szkodliwe działanie ciśnienia, tarcia i sił ścinających. Wilgotność prowadzi do maceracji skóry, co dodatkowo osłabia jej funkcję barierową. Badania wskazują, że efekty tarcia są do pięciu razy gorsze, jeśli obecna jest wilgoć.1415

Kaskada komórkowa i tkankowa

Na poziomie komórkowym i tkankowym, przedłużone działanie ciśnienia, sił ścinających i tarcia prowadzi do następującej sekwencji zdarzeń:

  1. Niedokrwienie – przedłużony ucisk powoduje zamknięcie naczyń włosowatych, ograniczając dopływ tlenu i składników odżywczych do tkanek.
  2. Hipoksja tkankowa – zmniejszony przepływ krwi prowadzi do niedotlenienia tkanek.
  3. Gromadzenie metabolitów toksycznych – w niedokrwionej tkance zaczynają gromadzić się toksyczne metabolity.
  4. Uszkodzenie błon komórkowych – przy wystarczająco wysokim ciśnieniu dochodzi do bezpośredniego uszkodzenia błon komórkowych komórek mięśniowych.
  5. Uraz reperfuzyjny – gdy nacisk zostaje zniesiony, reperfuzja może nasilić uszkodzenie tkanek poprzez uwolnienie wolnych rodników i mediatorów stanu zapalnego.
  6. Martwica tkanek – ostatecznie dochodzi do śmierci komórek i martwicy tkanek, co prowadzi do owrzodzenia.161718

Różnice w podatności tkanek

Warto zauważyć, że poszczególne tkanki wykazują różną podatność na uszkodzenia spowodowane uciskiem. Mięśnie są najbardziej wrażliwe i ulegają uszkodzeniu jako pierwsze, przed skórą i tkanką podskórną, prawdopodobnie ze względu na ich zwiększone zapotrzebowanie na tlen i wyższe wymagania metaboliczne. Badania wykazały, że martwica mięśni może wystąpić już po 4 godzinach ciągłego ucisku, podczas gdy skóra może wytrzymać do 12 godzin.192021

Ten fakt ma istotne znaczenie kliniczne, ponieważ w momencie gdy odleżyna staje się widoczna na poziomie skóry, znaczne uszkodzenie głębiej położonych mięśni mogło już nastąpić. Powoduje to, że całkowity kształt odleżyny przypomina odwrócony stożek, gdzie powierzchnia widoczna na skórze jest jedynie wierzchołkiem rozleglejszego uszkodzenia tkanek głębokich.22

Rola procesów zapalnych w patogenezie odleżyn

W patogenezie odleżyn istotne znaczenie mają także procesy zapalne, które mogą zarówno przyczyniać się do powstawania odleżyn, jak i utrudniać ich gojenie.23

Przewlekły stan zapalny

W przypadku odleżyn, normalny proces gojenia ran, który obejmuje fazę zapalną, proliferacyjną i remodelowania, zostaje zaburzony. Odleżyny często pozostają w przewlekłej fazie zapalnej, co uniemożliwia prawidłowe gojenie.2425

Cytokiny prozapalne, takie jak IL-6 i czynnik martwicy nowotworów alfa (TNFα), stymulują neutrofile i makrofagi do uwalniania kolejnych cytokin prozapalnych, co perpetuuje cykl zapalny. Przewlekły stan zapalny prowadzi do nadmiernej infiltracji neutrofilów w tkance ziarninowej, które produkują elastazę i kolagenazę, prowadząc do ciągłego rozpadu macierzy pozakomórkowej i upośledzenia gojenia ran.2627

Stres oksydacyjny

Istotną rolę w patogenezie odleżyn odgrywa również stres oksydacyjny, który nasila się podczas reperfuzji po okresie niedokrwienia. Procesy te prowadzą do produkcji reaktywnych form tlenu, które uszkadzają komórki i tkanki. Wiadomo, że stres oksydacyjny sprzyja rozwojowi fenotypu makrofagów M1 (prozapalnych) w ranach przewlekłych, takich jak odleżyny, co skutkuje podtrzymaniem sygnalizacji zapalnej i upośledzeniem gojenia ran.28

Zaburzenia odpowiedzi immunologicznej

Badania wskazują na zaburzenia odpowiedzi immunologicznej w patogenezie odleżyn. Szczególnie interesujące są odkrycia dotyczące białek inflamasomu NLRP3, których poziom spada w starzejącej się skórze. Zmniejszona aktywacja inflamasomu w odpowiedzi na uszkodzenie tkanek u osób starszych może przyczyniać się do większej podatności na rozwój odleżyn w tej grupie wiekowej. Sugeruje to, że osłabiona wrodzona odpowiedź zapalna w starzejącej się skórze może odgrywać rolę w patogenezie odleżyn.2930

Czynniki ryzyka i predysponujące do rozwoju odleżyn

Rozwój odleżyn jest uwarunkowany licznymi czynnikami ryzyka, które można podzielić na czynniki wewnętrzne (związane ze stanem pacjenta) i zewnętrzne (związane z warunkami środowiskowymi).31

Czynniki wewnętrzne

  • Unieruchomienie – ograniczona aktywność i mobilność są jednymi z najważniejszych czynników ryzyka; pacjenci, którzy nie mogą się poruszać lub zmieniać pozycji, są szczególnie narażeni.32
  • Choroby przewlekłe – cukrzyca, udar mózgu i zaawansowana demencja są najsilniej związane z rozwojem odleżyn. Choroby te wpływają na krążenie, odżywienie tkanek oraz zdolność pacjenta do poruszania się.33
  • Zaburzenia odżywiania – niedożywienie, niski poziom albumin i hemoglobiny, a także niski wskaźnik masy ciała (BMI) przyczyniają się do zwiększonego ryzyka odleżyn.3435
  • Zaburzenia czucia – osoby z zaburzeniami czucia, np. po urazie rdzenia kręgowego, nie odczuwają dyskomfortu związanego z przedłużonym uciskiem, co uniemożliwia im samodzielną zmianę pozycji.36
  • Podeszły wiek – skóra osób starszych jest cieńsza, mniej elastyczna i bardziej podatna na uszkodzenia mechaniczne. Ponadto, wraz z wiekiem zmniejsza się zdolność skóry do regeneracji.37
  • Zaburzenia krążenia – niewydolność krążenia, hipotensja, obniżony rzut serca oraz choroby naczyń obwodowych prowadzą do zmniejszonej perfuzji tkanek, co zwiększa ryzyko niedokrwienia i martwicy.38

Czynniki zewnętrzne

  • Przedłużony ucisk – długotrwały nacisk na tkanki, szczególnie nad wyniosłościami kostnymi, jest głównym czynnikiem prowadzącym do rozwoju odleżyn.39
  • Siły ścinające – powstają, gdy skóra pozostaje nieruchoma, a głębsze tkanki przesuwają się, np. gdy pacjent zsuwa się w łóżku lub fotelu.40
  • Tarcie – pojawia się, gdy skóra trze o pościel, odzież lub inne powierzchnie.41
  • Wilgotność – nadmierna wilgotność skóry prowadzi do maceracji i osłabienia jej funkcji barierowej.42
  • Urządzenia medyczne – ucisk wywierany przez sprzęt medyczny, taki jak rurki tlenowe, cewniki, kołnierze szyjne, gipsy czy urządzenia unieruchamiające, może również prowadzić do powstania odleżyn.43

Zaawansowane mechanizmy komórkowe w patogenezie odleżyn

Na poziomie komórkowym i molekularnym, patogeneza odleżyn obejmuje szereg złożonych procesów, które prowadzą do uszkodzenia tkanek i opóźnienia gojenia.44

Uszkodzenie niedokrwienno-reperfuzyjne

Jednym z kluczowych mechanizmów w patogenezie odleżyn jest cykliczne uszkodzenie niedokrwienno-reperfuzyjne. W przeciwieństwie do jednorazowego epizodu niedokrwienia z następującą reperfuzją, w przypadku odleżyn mamy do czynienia z powtarzającym się wzorcem uszkodzeń. Proces niedokrwienia prowadzi do zmniejszonej produkcji ATP i upośledzenia mitochondrialnej fosforylacji oksydacyjnej, zwiększonej aktywacji dopełniacza i leukocytów oraz podwyższonego poziomu stanu zapalnego.4546

Toksyczne metabolity, takie jak COX-2 i IL-6, stymulują neutrofile i makrofagi do uwalniania kolejnych cytokin prozapalnych, takich jak czynnik martwicy nowotworów alfa (TNFα) i IL-8, co perpetuuje cykl zapalny. Po zniesieniu ucisku, reperfuzja tkanek może paradoksalnie nasilić uszkodzenie poprzez dostarczenie wolnych rodników i mediatorów stanu zapalnego do uszkodzonego obszaru.47

Zaburzenia struktury i funkcji kolagenu

Przedłużony ucisk wpływa również na strukturę i orientację włókien kolagenowych w skórze i tkankach podskórnych. Badania wykazały, że obciążenie mechaniczne powoduje znaczące zmiany w orientacji włókien kolagenowych, co osłabia strukturalną integralność tkanek i zwiększa podatność na uszkodzenia. Zmiany te są szczególnie wyraźne w starzejącej się skórze, co może tłumaczyć zwiększoną częstość występowania odleżyn u osób starszych.48

Ponadto, w przypadku pacjentów z cukrzycą, przewlekła hiperglikemia zaburza syntezę i strukturę kolagenu, prowadząc do osłabienia tkanki łącznej i upośledzenia gojenia ran. Słabe tworzenie kolagenu zmniejsza wytrzymałość skóry na rozciąganie, czyniąc ją bardziej podatną na uszkodzenia pod wpływem ciśnienia.4950

Zaburzenia angiogenezy

W procesie gojenia ran kluczową rolę odgrywa angiogeneza, czyli tworzenie nowych naczyń krwionośnych. W przypadku odleżyn, proces ten jest często zaburzony, co utrudnia dostarczanie tlenu i składników odżywczych do łożyska rany. Zmniejszona gęstość naczyń włosowatych i upośledzona funkcja komórek śródbłonka zaburzają przepływ krwi do miejsca rany, kompromitując natlenienie tkanek i dostawę składników odżywczych, co opóźnia gojenie ran.51

Zaburzenia odpowiedzi immunologicznej (przewlekłe)

Jak wspomniano wcześniej, przewlekły stan zapalny jest charakterystyczną cechą odleżyn. Dysregulacja odpowiedzi immunologicznej prowadzi do utrzymującego się stanu zapalnego, który zamiast promować gojenie, przyczynia się do dalszego uszkodzenia tkanek. Szczególnie istotną rolę odgrywają tu inflamasomy, kompleksy białkowe związane z aktywacją wrodzonej odpowiedzi immunologicznej. Badania wykazały zmniejszoną ekspresję białek inflamasomu NLRP3 w starzejącej się skórze w odpowiedzi na obciążenie mechaniczne, co sugeruje osłabioną wrodzoną odpowiedź zapalną, która może przyczyniać się do patogenezy odleżyn.5253

Specyficzne szlaki sygnałowe w patogenezie odleżyn

Badania molekularne identyfikują coraz więcej specyficznych szlaków sygnałowych zaangażowanych w patogenezę odleżyn, co może prowadzić do nowych metod terapeutycznych.54

Rola mikroRNA

MikroRNA (miRNA) to małe, niekodujące cząsteczki RNA, które regulują ekspresję genów na poziomie potranskrypcyjnym. Odgrywają one istotną rolę w patogenezie i leczeniu ran przewlekłych, w tym odleżyn. Kluczowe szlaki sygnałowe regulowane przez miRNA w patofizjologii odleżyn obejmują PI3K/AKT, p38-MAPK, NFκB i MMP9.55

Rola białek SOCS

Białka SOCS (suppressors of cytokine signaling) są negatywnymi regulatorami sygnalizacji cytokinowej i odgrywają kluczową rolę w procesie gojenia ran. Badania wykazują, że białka SOCS regulują zachowanie komórek nabłonkowych i są istotne w procesie gojenia odleżyn:

  • SOCS-1 wchodzi w interakcje z IL-2, IL-4, IL-6, INF-γ i TNF-α, odgrywając ważną rolę w infiltracji fibroblastów, zwiększonym metabolizmie fibroblastów, angiogenezie, reepitelializacji, odkładaniu kolagenu i przebudowie tkanek.56
  • SOCS-3 wchodzi w interakcje z IL-1β, IL-2, IL-6, IL-10, INF-γ, TNF-α i innymi czynnikami wzrostu, uczestnicząc w procesach zapalnych, angiogenezie, reepitelializacji, odkładaniu kolagenu i przebudowie tkanek.57
  • SOCS-5 wchodzi w interakcje z receptorami IL-4, IL-6 i EGF, biorąc udział w procesach zapalnych, angiogenezie, reepitelializacji i przebudowie tkanek.58

Badania sugerują, że ko-transfekcja SOCS-1, -3 i -5, które są kluczowymi regulatorami w każdej fazie gojenia ran, może zwiększyć efekt gojenia owrzodzeń odleżynowych.59

Zaburzenia metaboliczne w odleżynach

Pacjenci z odleżynami cierpią na szereg zaburzeń metabolicznych, które mogą zarówno przyczyniać się do rozwoju odleżyn, jak i być ich konsekwencją.60

Niedokrwistość i zaburzenia białek surowicy

Badania wykazały, że pacjenci z odleżynami wykazują znaczące zmiany w parametrach hematologicznych i biochemicznych, takie jak:

  • Zmniejszona liczba czerwonych krwinek
  • Obniżony poziom hemoglobiny i hematokrytu
  • Zwiększona liczba białych krwinek
  • Podwyższony poziom ferrytyny i obniżony poziom transferryny
  • Hipoproteinemia i hipoalbuminemia
  • Zwiększony poziom alfa-1 i gamma globulin
  • Podwyższone OB i białko C-reaktywne61

Te zmiany są charakterystyczne dla zaburzeń metabolicznych występujących w przewlekłych schorzeniach i chorobach nowotworowych. Wynikają one z zmniejszonego wykorzystania zapasów żelaza w układzie siateczkowo-śródbłonkowym oraz zahamowania syntezy albuminy w wątrobie. Co istotne, badania wskazują, że zmiany te są ściśle związane z obecnością odleżyn, a nie są specyficzne dla samego urazu rdzenia kręgowego czy innych chorób podstawowych. Zanikają one wkrótce po chirurgicznym wygojeniu odleżyn, co wspiera hipotezę o ich powiązaniu przyczynowym.62

Implikacje terapeutyczne

Zrozumienie zaburzeń metabolicznych u pacjentów z odleżynami ma istotne implikacje terapeutyczne. Na przykład, pacjenci z odleżynami są często leczeni suplementami żelaza z powodu niedokrwistości. Jednak ponieważ niedokrwistość u tych pacjentów wynika z trudności w wykorzystaniu zapasów żelaza, a nie z jego niedoboru, terapia żelazem jest bezużyteczna, a nawet potencjalnie niebezpieczna ze względu na możliwość jatrogennnej hemochromatozy. Dane sugerują, że ten rodzaj leczenia powinien być unikany.63

Specyfika odleżyn u pacjentów z cukrzycą

Cukrzyca może znacząco zwiększać ryzyko rozwoju odleżyn ze względu na różne czynniki fizjologiczne i metaboliczne.64

Neuropatia i powikłania naczyniowe

Jednym z głównych czynników ryzyka jest wpływ cukrzycy na neuropatię obwodową i powikłania naczyniowe. Neuropatia, częsta u pacjentów z cukrzycą, zmniejsza czucie w kończynach, sprawiając, że osoby te są mniej świadome punktów nacisku i dyskomfortu, co zwiększa prawdopodobieństwo przedłużonego nacisku na określone obszary. Dodatkowo, cukrzyca może prowadzić do niewydolności naczyniowej, upośledzając przepływ krwi do tkanek i ograniczając dostawę tlenu i składników odżywczych niezbędnych do gojenia ran.65

Zaburzenia syntezy kolagenu

Cukrzyca zaburza syntezę i strukturę kolagenu, prowadząc do osłabienia tkanki łącznej i upośledzenia gojenia ran. Słabe tworzenie kolagenu zmniejsza wytrzymałość skóry na rozciąganie, czyniąc ją bardziej podatną na uszkodzenia pod wpływem ciśnienia.66

Przewlekły stan zapalny w cukrzycy

Przewlekła hiperglikemia u pacjentów z cukrzycą prowadzi do utrzymującego się stanu zapalnego w miejscu rany, charakteryzującego się nadmierną produkcją cytokin prozapalnych i upośledzonym rozwiązaniem stanu zapalnego.67

Zaburzenia angiogenezy w cukrzycy

Cukrzyca zaburza proces angiogenezy, który jest niezbędny do dostarczania tlenu i składników odżywczych do łożyska rany. Zmniejszona gęstość naczyń włosowatych i upośledzona funkcja komórek śródbłonka zaburzają przepływ krwi do miejsca rany, kompromitując natlenienie tkanek i dostawę składników odżywczych, co opóźnia gojenie ran.68

Co istotne, odleżyny u pacjentów z cukrzycą to głównie owrzodzenia stóp, które powstają z powodu neuropatii obwodowej, prowadzącej do długotrwałej niewrażliwości na ucisk, martwicy i niegojenia się uciśniętych obszarów. Obecne leczenie odleżyn u tych pacjentów obejmuje głównie opatrunki lecznicze i zewnętrzne środki dezynfekujące zawierające srebro i jod. W profilaktyce odleżyn u pacjentów z cukrzycą najważniejszą kwestią jest kontrola poziomu cukru we krwi.6970

Odleżyny związane z COVID-19

Badania wskazują na związek między patofizjologią COVID-19 a rozwojem odleżyn. Europejski Panel Doradczy ds. Odleżyn (EPUAP) podkreślił rolę cytokin prozapalnych interleukiny-6 i czynnika martwicy nowotworów alfa, które występują w dużych ilościach u pacjentów z COVID-19, jako czynników przyczyniających się do powstawania i utrzymywania się stanu zapalnego po śmierci komórek i formowaniu się odleżyny.7172

Mechanizm ten może tłumaczyć zwiększoną częstość występowania i ciężkość odleżyn u pacjentów hospitalizowanych z powodu COVID-19, szczególnie tych wymagających intensywnej terapii i wentylacji mechanicznej.

Podsumowanie mechanizmów patogenetycznych

Patogeneza odleżyn jest złożonym, wieloczynnikowym procesem, w którym kluczową rolę odgrywają:

  1. Przedłużony ucisk – przekraczający ciśnienie zamykające naczyń włosowatych (32 mm Hg dla tętniczych, 8-12 mm Hg dla żylnych)
  2. Siły ścinające i tarcie – nasilające efekty ucisku i przyczyniające się do uszkodzenia tkanek
  3. Wilgotność – prowadząca do maceracji skóry i osłabienia jej funkcji barierowej
  4. Niedokrwienie tkanek – skutkujące hipoksją i akumulacją toksycznych metabolitów
  5. Uraz reperfuzyjny – nasilający uszkodzenie poprzez dostarczenie wolnych rodników i mediatorów stanu zapalnego
  6. Przewlekły stan zapalny – uniemożliwiający prawidłowe gojenie rany
  7. Zaburzenia na poziomie komórkowym i molekularnym – obejmujące dysregulację szlaków sygnałowych, zaburzenia syntezy kolagenu i angiogenezy

Zrozumienie tych mechanizmów jest kluczowe dla opracowania skutecznych strategii profilaktyki i leczenia odleżyn, szczególnie u pacjentów z grup wysokiego ryzyka, takich jak osoby starsze, unieruchomione, niedożywione czy cierpiące na choroby przewlekłe.737475

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Pressure Ulcer – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK553107/
    Pressure injuries are localized skin and soft tissue injuries that develop due to prolonged pressure exerted over specific areas of the body, typically bony prominences. […] Pressure injuries, also termed bedsores, decubitus ulcers, or pressure ulcers, are localized skin and soft tissue injuries that form as a result of prolonged pressure and shear, usually exerted over bony prominences. […] The development of pressure injuries is complex and multifactorial. External and internal factors co-occur to form these ulcers. Externally, prolonged pressure, friction, shear force, and moisture can lead to tissue deformation and ischemia. Internal factors such as malnutrition, anemia, and endothelial dysfunction can speed up the process of tissue damage. […] Prolonged pressure on tissues can cause capillary bed occlusion, reducing oxygen levels in the area. Over time, the ischemic tissue begins to accumulate toxic metabolites. Subsequently, tissue ulceration and necrosis occur.
  • #2 Pressure ulcers
    https://pmc.ncbi.nlm.nih.gov/articles/PMC1382548/
    A pressure ulcer is defined by the European Pressure Ulcer Advisory Panel as an area of localised damage to the skin and underlying tissue caused by pressure, shear, or friction, or a combination of these. Pressure ulcers are caused by a local breakdown of soft tissue as a result of compression between a bony prominence and an external surface. […] The four main factors implicated are interface pressure, shear, friction, and moisture. […] When pressure of short duration is relieved, tissues demonstrate reactive hyperaemia, reflecting increased blood flow to the area. However, sustained high pressure leads to decreased capillary blood flow, occlusion of blood vessels and lymphatic vessels, and tissue ischaemia. […] These changes are ultimately responsible for necrosis of muscle, subcutaneous tissue, dermis and epidermis, and consequent formation of pressure ulcers. An external pressure of 50 mm Hg may rise to over 200 mm Hg at a bony prominence, leading, with time, to deep tissue destruction, which may not be evident on the surface of the skin. Regular relief from high pressures in the at-risk patient is essential to prevent pressure ulceration.
  • #3 Pressure ulcer – Wikipedia
    https://en.wikipedia.org/wiki/Pressure_ulcer
    Pressure ulcers, also known as pressure sores, bed sores or pressure injuries, are localised damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of usually long-term pressure, or pressure in combination with shear or friction. […] Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. […] There are four mechanisms that contribute to pressure ulcer development: External (interface) pressure applied over an area of the body, especially over the bony prominences can result in obstruction of the blood capillaries, which deprives tissues of oxygen and nutrients, causing ischemia, hypoxia, edema, inflammation, and, finally, necrosis and ulcer formation. […] Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. […] The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. […] This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.
  • #4 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomy
    https://emedicine.medscape.com/article/190115-overview
    In 1873, Sir James Paget described the production of pressure ulcers remarkably well, and his description is still quite accurate today. Many factors contribute to the development of pressure injuries, but pressure leading to ischemia and necrosis is the final common pathway. […] In this view, pressure injuries result from constant pressure sufficient to impair local blood flow to soft tissue for an extended period. This external pressure must be greater than the arterial capillary pressure (32 mm Hg) to impair inflow and greater than the venous capillary closing pressure (8-12 mm Hg) to impede the return of flow for an extended time. […] Tissues are capable withstanding enormous pressures for brief periods, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a downward spiral toward tissue necrosis and ulceration.
  • #5 Pressure Ulcer – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK553107/
    Decubitus ulcer formation is multifactorial, but these ulcers result in a common pathway to ischemia and necrosis. Tissues can sustain an abnormal amount of external pressure, but constant pressure exerted over a prolonged period is the main culprit. […] The pressure must be greater than the venous capillary closing pressure of 8 to 12 mm Hg to impair venous blood return. Sustaining pressure above these values leads to tissue ischemia and necrosis. […] In addition, the EPUAP emphasized the link between the pathophysiology of COVID-19 and the development of pressure ulcers. The panel attributed the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, abundant in COVID-19 patients, as a contributor to the onset and maintenance of inflammation following cell death and the formation of a pressure ulcer.
  • #6 Pressure Sores | PPT
    https://www.slideshare.net/slideshow/pressure-sores-55126646/55126646
    Pressure ulcers, also known as bedsores or decubitus ulcers, are areas of skin breakdown that occur when soft tissue is compressed between a bony prominence and an external surface. They develop primarily in elderly patients in healthcare settings. The four main forces that contribute to pressure ulcer development are pressure, friction, shear, and strain. […] Pressure Ulcers are localized areas of tissue necrosis that tend to occur when soft tissue is compressed between a bony prominence and an external surface for a prolonged period. […] Prolong weight bearing and mechanical shear forces act on areas of soft tissue overlying bony prominence when this pressure exceeds normal capillary perfusion pressure (32 mm Hg) occlusion tearing of small blood vessels reduced tissue perfusion ischaemic necrosis Pressure sore.
  • #7 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomy
    https://emedicine.medscape.com/article/190115-overview
    The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface. […] Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. […] Pressure, shear forces, and friction cause microcirculatory occlusion and consequent ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration. […] Of the various tissues at risk for death due to pressure, muscle tissue is damaged first, before skin and subcutaneous tissue, probably because of its increased need for oxygen and higher metabolic requirements. […] Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. […] By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone. […] Reperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing an ulcer to enlarge or become more chronic.
  • #8 Pressure Ulcer | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/20286
    Pressure injuries, also termed bedsores, decubitus ulcers, or pressure ulcers, are localized skin and soft tissue injuries that form as a result of prolonged pressure and shear, usually exerted over bony prominences. […] The development of pressure injuries is complex and multifactorial. External and internal factors co-occur to form these ulcers. Externally, prolonged pressure, friction, shear force, and moisture can lead to tissue deformation and ischemia. Internal factors such as malnutrition, anemia, and endothelial dysfunction can speed up the process of tissue damage. […] Prolonged pressure on tissues can cause capillary bed occlusion, reducing oxygen levels in the area. Over time, the ischemic tissue begins to accumulate toxic metabolites. Subsequently, tissue ulceration and necrosis occur. Immobility of only two hours in a bedridden patient or patient undergoing surgery is sufficient to form the foundation of a decubitus ulcer.
  • #9 Pressure Areas and Pressure Ulcers • LITFL • CCC
    https://litfl.com/pressure-areas-and-pressure-ulcers/
    A pressure ulcer is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear […] skin and subcutaneous tissues compressed or subjected to shear forces- decreased perfusion- tissue necrosis […] can develop within 2-6 hours.
  • #10 Pressure ulcers
    https://pmc.ncbi.nlm.nih.gov/articles/PMC1382548/
    Shear force is generated by the motion of bone and subcutaneous tissue relative to the skin, which is restrained from moving due to frictional forces (for example, when a seated patient slides down a chair or when the head of a bed is raised more than 30). In such circumstances the pressure needed to occlude the blood vessels is greatly reduced. […] An excessively moist environment caused, for example, by perspiration, urinary or faecal incontinence, or excessive wound drainage increases the deleterious effects of pressure, friction, and shear. It also causes maceration of the surrounding skin, which compounds these factors. Friction and moisture exert their greatest effects in areas of high pressure: the effects of friction are up to five times worse if moisture is present.
  • #11 Pressure Ulcers Pathogenesis and clinical findings | Calgary Guide
    https://calgaryguide.ucalgary.ca/pressure-ulcers-pathogenesis-and-clinical-findings/pressure-ulcers-pathogenesis-and-clinical-findings/
    Dermatology Wounds Pressure Ulcers: Pathogenesis and clinical findings […] Pressure Ulcers Pathogenesis and clinical findings […] External physical compression Involuntary muscle movement, passive repositioning of torso Shear forces (dermis/epidermis fixed through contact with a surface while deeper tissues are moved; vessels angulate and thrombose, creating undermining of ulcer) […] Unrelieved pressure greater than arterial capillary pressure (32 mmHg, with more rapid ulcer formation at higher pressures; normal range 12-32 mmHg) Disrupts blood supply and deprives tissues of oxygen and nutrients […] Pressure Ulcer (local injury to skin and/or underlying tissues, often over bony prominence) […] Risk factors: diabetes, peripheral arterial disease, immunodeficiency, steroid therapy, smoking, dementia, poor nutrition, sensory deficit, circulatory disturbance, prolonged immobility
  • #12 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/pressure-injury/pressure-injuries
    Friction: Friction (rubbing against clothing or bedding) can help trigger skin ulceration by causing local erosion and breaks in the epidermis and superficial dermis. […] Shearing forces: Shearing forces (eg, when a patient is placed on an inclined surface) stress and damage supporting tissues by causing forces of muscles and subcutaneous tissues that are drawn down by gravity to oppose the more superficial tissues that remain in contact with external surfaces. Shearing forces contribute to pressure injury but are not direct causes. […] Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen pressure injuries. […] Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie pressure injuries resulting from prolonged compression.
  • #13 Part 1. Causes of pressure ulcers | Nursing Times
    https://www.nursingtimes.net/archive/part-1-causes-of-pressure-ulcers-14-03-2002/
    The most serious pressure damage usually occurs as a result of the deformation in the deep tissues near the underlying bony prominence. […] Shearing of soft tissue occurs when forces moving in different directions are applied to the same tissue mass. […] Because shearing occludes flow more easily than compression, shear can be considered to be even more significant than pressure in the causation of pressure ulcers. […] Friction is not, therefore, a direct cause of pressure ulcers, although it is clearly possible that skin weakened by pressure ischaemia may be more susceptible to friction, and the two will act together to hasten skin breakdown. […] When the reactive hyperaemia cycle ceases to function adequately, a pressure ulcer will almost certainly develop unless preventive action is taken.
  • #14 Pressure ulcers
    https://pmc.ncbi.nlm.nih.gov/articles/PMC1382548/
    Shear force is generated by the motion of bone and subcutaneous tissue relative to the skin, which is restrained from moving due to frictional forces (for example, when a seated patient slides down a chair or when the head of a bed is raised more than 30). In such circumstances the pressure needed to occlude the blood vessels is greatly reduced. […] An excessively moist environment caused, for example, by perspiration, urinary or faecal incontinence, or excessive wound drainage increases the deleterious effects of pressure, friction, and shear. It also causes maceration of the surrounding skin, which compounds these factors. Friction and moisture exert their greatest effects in areas of high pressure: the effects of friction are up to five times worse if moisture is present.
  • #15 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/pressure-injury/pressure-injuries
    Friction: Friction (rubbing against clothing or bedding) can help trigger skin ulceration by causing local erosion and breaks in the epidermis and superficial dermis. […] Shearing forces: Shearing forces (eg, when a patient is placed on an inclined surface) stress and damage supporting tissues by causing forces of muscles and subcutaneous tissues that are drawn down by gravity to oppose the more superficial tissues that remain in contact with external surfaces. Shearing forces contribute to pressure injury but are not direct causes. […] Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen pressure injuries. […] Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie pressure injuries resulting from prolonged compression.
  • #16 Pressure Ulcer – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK553107/
    Pressure injuries are localized skin and soft tissue injuries that develop due to prolonged pressure exerted over specific areas of the body, typically bony prominences. […] Pressure injuries, also termed bedsores, decubitus ulcers, or pressure ulcers, are localized skin and soft tissue injuries that form as a result of prolonged pressure and shear, usually exerted over bony prominences. […] The development of pressure injuries is complex and multifactorial. External and internal factors co-occur to form these ulcers. Externally, prolonged pressure, friction, shear force, and moisture can lead to tissue deformation and ischemia. Internal factors such as malnutrition, anemia, and endothelial dysfunction can speed up the process of tissue damage. […] Prolonged pressure on tissues can cause capillary bed occlusion, reducing oxygen levels in the area. Over time, the ischemic tissue begins to accumulate toxic metabolites. Subsequently, tissue ulceration and necrosis occur.
  • #17 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomy
    https://emedicine.medscape.com/article/190115-overview
    The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface. […] Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. […] Pressure, shear forces, and friction cause microcirculatory occlusion and consequent ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration. […] Of the various tissues at risk for death due to pressure, muscle tissue is damaged first, before skin and subcutaneous tissue, probably because of its increased need for oxygen and higher metabolic requirements. […] Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. […] By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone. […] Reperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing an ulcer to enlarge or become more chronic.
  • #18 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion. […] The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation. […] Toxic metabolites such as COX-2 and IL-6 stimulate neutrophils and macrophages to release more pro-inflammatory cytokines such as tissue necrosis factor alpha (TNFα) and IL-8, which perpetuates the inflammatory cycle. […] Oxidative stress is known to promote an M1, pro-inflammatory, macrophage phenotype in chronic wounds such as pressure ulcers and diabetic wounds, resulting in sustained inflammatory signaling and impaired wound healing.
  • #19 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomy
    https://emedicine.medscape.com/article/190115-overview
    The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface. […] Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. […] Pressure, shear forces, and friction cause microcirculatory occlusion and consequent ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration. […] Of the various tissues at risk for death due to pressure, muscle tissue is damaged first, before skin and subcutaneous tissue, probably because of its increased need for oxygen and higher metabolic requirements. […] Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. […] By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone. […] Reperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing an ulcer to enlarge or become more chronic.
  • #20 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/pressure-injury/pressure-injuries
    Friction: Friction (rubbing against clothing or bedding) can help trigger skin ulceration by causing local erosion and breaks in the epidermis and superficial dermis. […] Shearing forces: Shearing forces (eg, when a patient is placed on an inclined surface) stress and damage supporting tissues by causing forces of muscles and subcutaneous tissues that are drawn down by gravity to oppose the more superficial tissues that remain in contact with external surfaces. Shearing forces contribute to pressure injury but are not direct causes. […] Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen pressure injuries. […] Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie pressure injuries resulting from prolonged compression.
  • #21 Pressure Ulcers- Pathology and Management | PPT
    https://www.slideshare.net/slideshow/pressure-ulcers-pathology-and-management/242339683
    Infection/sepsis decreases tissue perfusion. […] High degree of pressure can be tolerated when evenly distributed. […] Soft tissue compression (32mmHg) results in ischaemia – necrosis – ulceration. […] Muscles necrosis occur after 4 hours whereas skin after 12 hours. […] Hyperemia is observed within less than 30 minutes of pressure. […] Ischaemia occurs with continuous pressure for 2-6 hours. […] Necrosis occurs with unrelieved pressure within 6 hours. […] Ulceration occurs within 2 weeks following development of necrosis typically in bony prominences.
  • #22 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomy
    https://emedicine.medscape.com/article/190115-overview
    The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface. […] Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. […] Pressure, shear forces, and friction cause microcirculatory occlusion and consequent ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration. […] Of the various tissues at risk for death due to pressure, muscle tissue is damaged first, before skin and subcutaneous tissue, probably because of its increased need for oxygen and higher metabolic requirements. […] Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. […] By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone. […] Reperfusion has been suggested as a cause of additional damage to the ulcerated area, inducing an ulcer to enlarge or become more chronic.
  • #23 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Pressure ulcers are preventable, yet highly prevalent, chronic wounds that have significant patient morbidity and high healthcare costs. […] This review will highlight key biochemical pathways in the pathogenesis of pressure injury and how this signaling leads to impaired wound healing. […] Pressure ulcers, also known as bed sores and decubitus ulcers, are skin and soft tissue wounds that develop due to pressure injury. […] Major components of pressure ulcer pathogenesis include ischemia-reperfusion injury, poor lymphatic drainage, cellular deformation, and excess cellular apoptosis and extracellular matrix (ECM) breakdown resulting in a chronic inflammatory state and dysregulated healing. […] The mechanism of pressure injury has unique elements that require more specific preventative and therapeutic intervention.
  • #24 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    The pathways described below that are involved in the pathogenesis of pressure ulceration are depicted in Figure 1. […] The study of pressure ulcer pathophysiology in preclinical and clinical models is challenging, so correlations with other models of chronic wound healing are often used to guide future investigation. […] Chronic pressure ulcers have excessive neutrophil infiltration within granulation tissue, and these cell lines produce elastase and collagenase that lead to ongoing extracellular matrix breakdown and impaired wound healing. […] Dysregulated responses by specific immune cell lines have been implicated in chronic wound and pressure ulcer pathogenesis. […] Normal wound healing follows a three-phase immune response with an initial inflammatory phase followed by proliferative and remodeling phases.
  • #25 Bedsores (Pressure Ulcers) — DermNet
    https://dermnetnz.org/topics/pressure-ulcer
    Pressure ulcers are skin and soft tissue injuries sustained from prolonged pressure. Specifically, they involve a breakdown of the skin, subcutaneous tissues and sometimes even deeper structures (tendons, muscle, bone) caused by cumulative pressure and are often related to pre-existing health conditions or injuries. […] The most important cause of pressure ulcers is external pressure at a skin site for prolonged periods, although the exact mechanism is complex and poorly understood. […] A proposed mechanism involves a complex interplay of local tissue ischaemia, reperfusion injury, increased capillary permeability, increased autophagy, and cell senescence causing direct insult to skin cells. After the inciting external pressure is gone, patients have a delayed reperfusion time which increases the risk of ulcer formation. […] A prolonged inflammatory phase hypothesis has also been proposed, whereby pressure ulcers do not follow the normal trajectory of inflammation, remodelling, and maturation, but are instead arrested in the inflammatory phase of wound healing.
  • #26 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion. […] The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation. […] Toxic metabolites such as COX-2 and IL-6 stimulate neutrophils and macrophages to release more pro-inflammatory cytokines such as tissue necrosis factor alpha (TNFα) and IL-8, which perpetuates the inflammatory cycle. […] Oxidative stress is known to promote an M1, pro-inflammatory, macrophage phenotype in chronic wounds such as pressure ulcers and diabetic wounds, resulting in sustained inflammatory signaling and impaired wound healing.
  • #27 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    The pathways described below that are involved in the pathogenesis of pressure ulceration are depicted in Figure 1. […] The study of pressure ulcer pathophysiology in preclinical and clinical models is challenging, so correlations with other models of chronic wound healing are often used to guide future investigation. […] Chronic pressure ulcers have excessive neutrophil infiltration within granulation tissue, and these cell lines produce elastase and collagenase that lead to ongoing extracellular matrix breakdown and impaired wound healing. […] Dysregulated responses by specific immune cell lines have been implicated in chronic wound and pressure ulcer pathogenesis. […] Normal wound healing follows a three-phase immune response with an initial inflammatory phase followed by proliferative and remodeling phases.
  • #28 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion. […] The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation. […] Toxic metabolites such as COX-2 and IL-6 stimulate neutrophils and macrophages to release more pro-inflammatory cytokines such as tissue necrosis factor alpha (TNFα) and IL-8, which perpetuates the inflammatory cycle. […] Oxidative stress is known to promote an M1, pro-inflammatory, macrophage phenotype in chronic wounds such as pressure ulcers and diabetic wounds, resulting in sustained inflammatory signaling and impaired wound healing.
  • #29 Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069223
    The challenge in studying the development of PU results from lack of adequate experimental models that accurately resemble human disease. […] We found that the morphology of skin differed among young and aged individuals in response to load. […] We also report that young skin has significantly higher levels of inflammasome proteins than aged skin. […] Taken together, our findings support the idea that the effects of aging and load synergize to contribute to morphological changes that lead to development of DTI and further to PU. […] Aged skin showed changes as early as 2 hrs of loading, and changes in collagen alignment were only observed in aged skin. […] Interestingly, we found that loading induced significant alterations in NLRP3 inflammasome protein levels in young skin in a time-dependent manner.
  • #30 Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069223
    These findings suggest that compressive load further affects tissue collagen fiber orientation. […] Taken together, although external load/pressure is viewed as one of the key factors in the development of DTI/PU, observed decrease in NLRP3 inflammasome proteins in aged skin may indicate diminished innate immune response in skin due to aging, providing an explanation why PU develop more frequently in elderly.
  • #31 Journal of the Korean Medical Association
    https://jkma.org/m/journal/view.php?number=3188
    The development of a pressure ulcer is associated with external factors such as pressure, shear stress, and friction and internal factors such as age, general condition, skin condition, and nutritional status. […] This tissue damage is caused by continuous deformation of the tissue due to the pressure acting perpendicular to the tissue surface and shear stress acting parallel to the tissue, either alone or in combination. […] Limitation of activity and mobility, skin condition, blood circulation and oxygen saturation, nutrition, humidity, body temperature, age, low pain sensitivity, blood count, and general and mental conditions are the primary risk factors for pressure ulcers. […] A mattress and cushion that reduce pressure and an appropriate posture are necessary to prevent pressure ulcers. […] Sufficient nutrition may help prevent wounds in patients who are susceptible to pressure ulcers. […] Furthermore, early screening, individualized management of posture, and regular skin and nutrition monitoring are essential to prevent pressure ulcers.
  • #32 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Text
    https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
    Direct PU causal factors associated with comorbidities include immobility, skin/pressure ulcer status and poor perfusion. Indirect factors are moisture, sensory perception, diabetes, low albumin and poor nutrition. Other potential factors include old age, medication, pitting edema and other factors relating to general health status including infection, acute illness, raised body temperature and chronic wounds. […] Among chronic diseases, diabetes, stroke, and advanced dementia seem to be most strongly associated with PU development. Immobility patients with low BMI, low albumin and haemoglobin, high inflammatory markers (CRP and ESR) associated with these conditions and with hemodynamic instability (low cardiac output, hypotension) and chronic complications may be most likely to lead to unavoidable PU.
  • #33 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Text
    https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
    Direct PU causal factors associated with comorbidities include immobility, skin/pressure ulcer status and poor perfusion. Indirect factors are moisture, sensory perception, diabetes, low albumin and poor nutrition. Other potential factors include old age, medication, pitting edema and other factors relating to general health status including infection, acute illness, raised body temperature and chronic wounds. […] Among chronic diseases, diabetes, stroke, and advanced dementia seem to be most strongly associated with PU development. Immobility patients with low BMI, low albumin and haemoglobin, high inflammatory markers (CRP and ESR) associated with these conditions and with hemodynamic instability (low cardiac output, hypotension) and chronic complications may be most likely to lead to unavoidable PU.
  • #34 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Text
    https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
    Direct PU causal factors associated with comorbidities include immobility, skin/pressure ulcer status and poor perfusion. Indirect factors are moisture, sensory perception, diabetes, low albumin and poor nutrition. Other potential factors include old age, medication, pitting edema and other factors relating to general health status including infection, acute illness, raised body temperature and chronic wounds. […] Among chronic diseases, diabetes, stroke, and advanced dementia seem to be most strongly associated with PU development. Immobility patients with low BMI, low albumin and haemoglobin, high inflammatory markers (CRP and ESR) associated with these conditions and with hemodynamic instability (low cardiac output, hypotension) and chronic complications may be most likely to lead to unavoidable PU.
  • #35 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cord
    https://www.nature.com/articles/3101622
    Patients with pressure sore showed significant decreased red cells, decreased haemoglobin and haematocrit, increased white cells and ferritin and decreased transferrin and transferrin saturation; total hypoproteinemia and hypoalbuminemia with increased Alfa-1 and gamma globulins increased erythrocyte sedimentation rate and C-reactive protein were also present. […] Patients with pressure sores suffer from anaemia and serum protein alteration that fells within the range of metabolic alteration of chronic disorders and neoplastic diseases. […] The alterations depend on a decreased utilisation of iron stores in the reticuloendothelial system and on inhibition of the hepatic synthesis of albumin. […] Patients with pressure sores show mild to moderate anaemia and specific serum protein alterations.
  • #36
    https://www.crh.org/healthy-tomorrow/story/healthy-tomorrow/2016/10/25/what-causes-bed-sores-and-how-can-they-be-prevented
    Poor Skin Perfusion (or decreased blood flow): Any reduction in blood flow to the skin can cause hypoxia (decreased oxygen) in skin tissues causing decreased exposure time to develop a pressure ulcer. […] Sensory Loss: Poor sensation doesnt allow patients to feel when pressure is building up. […] Moisture: Increased Moisture over prolonged periods can lead to skin maceration and cause skin to be more prone to injury from pressure and other forces. […] Friction/Shear: Friction or shear-induced ulcers or skin tears can be another potential etiology for a bed sore and comes from moving skin over the surface of a fixed object.
  • #37 Pressure Ulcers Pathogenesis and clinical findings | Calgary Guide
    https://calgaryguide.ucalgary.ca/pressure-ulcers-pathogenesis-and-clinical-findings/pressure-ulcers-pathogenesis-and-clinical-findings/
    Dermatology Wounds Pressure Ulcers: Pathogenesis and clinical findings […] Pressure Ulcers Pathogenesis and clinical findings […] External physical compression Involuntary muscle movement, passive repositioning of torso Shear forces (dermis/epidermis fixed through contact with a surface while deeper tissues are moved; vessels angulate and thrombose, creating undermining of ulcer) […] Unrelieved pressure greater than arterial capillary pressure (32 mmHg, with more rapid ulcer formation at higher pressures; normal range 12-32 mmHg) Disrupts blood supply and deprives tissues of oxygen and nutrients […] Pressure Ulcer (local injury to skin and/or underlying tissues, often over bony prominence) […] Risk factors: diabetes, peripheral arterial disease, immunodeficiency, steroid therapy, smoking, dementia, poor nutrition, sensory deficit, circulatory disturbance, prolonged immobility
  • #38
    https://www.crh.org/healthy-tomorrow/story/healthy-tomorrow/2016/10/25/what-causes-bed-sores-and-how-can-they-be-prevented
    Poor Skin Perfusion (or decreased blood flow): Any reduction in blood flow to the skin can cause hypoxia (decreased oxygen) in skin tissues causing decreased exposure time to develop a pressure ulcer. […] Sensory Loss: Poor sensation doesnt allow patients to feel when pressure is building up. […] Moisture: Increased Moisture over prolonged periods can lead to skin maceration and cause skin to be more prone to injury from pressure and other forces. […] Friction/Shear: Friction or shear-induced ulcers or skin tears can be another potential etiology for a bed sore and comes from moving skin over the surface of a fixed object.
  • #39 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bed-sores/symptoms-causes/syc-20355893
    Bedsores are areas of damaged skin and tissue caused by sustained pressure that reduces blood flow to vulnerable areas of the body. This pressure may be caused from being in a bed or wheelchair for a long time. […] Bedsores are injuries to the skin and the tissue below the skin that are due to pressure on the skin for a long time. […] Pressure against the skin that limits blood flow to the skin causes bedsores. Limited movement can make skin prone to damage and cause bedsores. […] The three main things that lead to bedsores are: Pressure. Constant pressure on any part of the body can lessen the blood flow to tissues. Blood flow is essential to deliver oxygen and other nutrients to tissues. Without these key nutrients, skin and nearby tissues are damaged and might die over time. […] Friction occurs when the skin rubs against clothing or bedding. It can make fragile skin more vulnerable to injury, especially if the skin also is moist. […] Shear occurs when two surfaces move in the opposite direction. For example, when a bed is raised at the head, a person can slide down in bed. As the tailbone moves down, the skin over the bone might stay in place, pulling in the opposite direction.
  • #40 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bed-sores/symptoms-causes/syc-20355893
    Bedsores are areas of damaged skin and tissue caused by sustained pressure that reduces blood flow to vulnerable areas of the body. This pressure may be caused from being in a bed or wheelchair for a long time. […] Bedsores are injuries to the skin and the tissue below the skin that are due to pressure on the skin for a long time. […] Pressure against the skin that limits blood flow to the skin causes bedsores. Limited movement can make skin prone to damage and cause bedsores. […] The three main things that lead to bedsores are: Pressure. Constant pressure on any part of the body can lessen the blood flow to tissues. Blood flow is essential to deliver oxygen and other nutrients to tissues. Without these key nutrients, skin and nearby tissues are damaged and might die over time. […] Friction occurs when the skin rubs against clothing or bedding. It can make fragile skin more vulnerable to injury, especially if the skin also is moist. […] Shear occurs when two surfaces move in the opposite direction. For example, when a bed is raised at the head, a person can slide down in bed. As the tailbone moves down, the skin over the bone might stay in place, pulling in the opposite direction.
  • #41 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bed-sores/symptoms-causes/syc-20355893
    Bedsores are areas of damaged skin and tissue caused by sustained pressure that reduces blood flow to vulnerable areas of the body. This pressure may be caused from being in a bed or wheelchair for a long time. […] Bedsores are injuries to the skin and the tissue below the skin that are due to pressure on the skin for a long time. […] Pressure against the skin that limits blood flow to the skin causes bedsores. Limited movement can make skin prone to damage and cause bedsores. […] The three main things that lead to bedsores are: Pressure. Constant pressure on any part of the body can lessen the blood flow to tissues. Blood flow is essential to deliver oxygen and other nutrients to tissues. Without these key nutrients, skin and nearby tissues are damaged and might die over time. […] Friction occurs when the skin rubs against clothing or bedding. It can make fragile skin more vulnerable to injury, especially if the skin also is moist. […] Shear occurs when two surfaces move in the opposite direction. For example, when a bed is raised at the head, a person can slide down in bed. As the tailbone moves down, the skin over the bone might stay in place, pulling in the opposite direction.
  • #42 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/bed-sores/symptoms-causes/syc-20355893
    Bedsores are areas of damaged skin and tissue caused by sustained pressure that reduces blood flow to vulnerable areas of the body. This pressure may be caused from being in a bed or wheelchair for a long time. […] Bedsores are injuries to the skin and the tissue below the skin that are due to pressure on the skin for a long time. […] Pressure against the skin that limits blood flow to the skin causes bedsores. Limited movement can make skin prone to damage and cause bedsores. […] The three main things that lead to bedsores are: Pressure. Constant pressure on any part of the body can lessen the blood flow to tissues. Blood flow is essential to deliver oxygen and other nutrients to tissues. Without these key nutrients, skin and nearby tissues are damaged and might die over time. […] Friction occurs when the skin rubs against clothing or bedding. It can make fragile skin more vulnerable to injury, especially if the skin also is moist. […] Shear occurs when two surfaces move in the opposite direction. For example, when a bed is raised at the head, a person can slide down in bed. As the tailbone moves down, the skin over the bone might stay in place, pulling in the opposite direction.
  • #43 Pressure sores | Better Health Channel
    https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/pressure-sores
    Anyone confined to a bed or chair for a long time is at risk of developing a pressure sore. […] Pressure sores are areas of damage to the skin and the underlying tissue caused by constant pressure or friction. […] The lack of enough blood flow can cause the affected tissue to die if left untreated. […] A pressure sore is caused by constant pressure applied to the skin over a period of time. […] If you use a wheelchair you’re most likely to develop a pressure sore on the parts of the body where they rest against the chair. […] If you’re bedridden, pressure sores can occur in a number of areas, including: back or sides of the head, rims of the ears, shoulders or shoulder blades, hipbones, lower back or tailbone, backs or sides of the knees, heels, ankles and toes. […] Pressure injury monitoring devices that measure the skin moisture content, body motion and the pressure in-between may be used to prevent pressure sores and injuries. […] Pressure from medical devices such as oxygen tubing, catheters, cervical collars, casts and restraints should be minimised or removed. […] There are a variety of treatments available to manage pressure sores and promote healing, depending on the severity of the pressure sore.
  • #44 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Pressure ulcers are preventable, yet highly prevalent, chronic wounds that have significant patient morbidity and high healthcare costs. […] This review will highlight key biochemical pathways in the pathogenesis of pressure injury and how this signaling leads to impaired wound healing. […] Pressure ulcers, also known as bed sores and decubitus ulcers, are skin and soft tissue wounds that develop due to pressure injury. […] Major components of pressure ulcer pathogenesis include ischemia-reperfusion injury, poor lymphatic drainage, cellular deformation, and excess cellular apoptosis and extracellular matrix (ECM) breakdown resulting in a chronic inflammatory state and dysregulated healing. […] The mechanism of pressure injury has unique elements that require more specific preventative and therapeutic intervention.
  • #45 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion. […] The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation. […] Toxic metabolites such as COX-2 and IL-6 stimulate neutrophils and macrophages to release more pro-inflammatory cytokines such as tissue necrosis factor alpha (TNFα) and IL-8, which perpetuates the inflammatory cycle. […] Oxidative stress is known to promote an M1, pro-inflammatory, macrophage phenotype in chronic wounds such as pressure ulcers and diabetic wounds, resulting in sustained inflammatory signaling and impaired wound healing.
  • #46 A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model | Spinal Cord
    https://www.nature.com/articles/sc201661
    This model also demonstrates the ischemia/reperfusion mechanism of injury that is presumed to be a causative factor in pressure ulcer formation. […] Sustained pressure causes ischemia in the capillaries and microvasculature of the muscle tissue. Thus, subsequent reperfusion delivers free radicals, exacerbating damage done to the previously hypoxic tissue. […] We were able to show a statistically significant decrease in blood flow immediately following pressure application compared with blood flow assessment before the insult. Subsequent measurement of blood flow after 24h, however, showed a marked increase in blood flow to the region. […] This increased blood flow is expected to be due to reactive hyperemia followed by inflammatory vasodilation.
  • #47 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Ischemia-reperfusion events within chronic pressure ulcer pathogenesis typically follow a repetitive pattern of insults, rather than a single episode of ischemia followed by reperfusion. […] The process of ischemia results in reduced ATP generation and impaired mitochondrial oxidative phosphorylation, increased complement and leukocyte activation, and elevated levels of inflammation. […] Toxic metabolites such as COX-2 and IL-6 stimulate neutrophils and macrophages to release more pro-inflammatory cytokines such as tissue necrosis factor alpha (TNFα) and IL-8, which perpetuates the inflammatory cycle. […] Oxidative stress is known to promote an M1, pro-inflammatory, macrophage phenotype in chronic wounds such as pressure ulcers and diabetic wounds, resulting in sustained inflammatory signaling and impaired wound healing.
  • #48 Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069223
    These findings suggest that compressive load further affects tissue collagen fiber orientation. […] Taken together, although external load/pressure is viewed as one of the key factors in the development of DTI/PU, observed decrease in NLRP3 inflammasome proteins in aged skin may indicate diminished innate immune response in skin due to aging, providing an explanation why PU develop more frequently in elderly.
  • #49 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Diabetes compromises the immune system’s ability to combat infections and heal wounds. […] Chronic hyperglycemia impairs white blood cell function and cytokine production, prolonging inflammation and delaying tissue repair. […] Diabetes alters collagen synthesis and structure, leading to weakened connective tissues and impaired wound healing. […] Poor collagen formation reduces the skin’s tensile strength, making it more susceptible to breakdown under pressure. […] Chronic hyperglycemia in diabetic patients leads to persistent inflammation at the wound site, characterized by excessive production of pro-inflammatory cytokines and impaired resolution of inflammation. […] Diabetes disrupts the process of angiogenesis, which is essential for delivering oxygen and nutrients to the wound bed.
  • #50 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Reduced capillary density and impaired endothelial cell function impair blood flow to the wound site, compromising tissue oxygenation and nutrient supply, thereby delaying wound healing. […] Chronic hyperglycemia disrupts normal wound healing processes and compromises tissue viability, predisposing diabetic individuals to pressure ulcer formation. […] Diminished sensation increases the risk of unnoticed trauma, delayed wound detection, and inadequate wound care, further complicating the healing process. […] Chronic hyperglycemia disrupts the synthesis and cross-linking of collagen and elastin fibers, essential components of the skin’s structural integrity. […] Weakened collagen and elastin fibers make the skin less resilient to mechanical stress and shear forces, predisposing diabetic individuals to pressure ulcer formation even at relatively low-pressure levels.
  • #51 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Reduced capillary density and impaired endothelial cell function impair blood flow to the wound site, compromising tissue oxygenation and nutrient supply, thereby delaying wound healing. […] Chronic hyperglycemia disrupts normal wound healing processes and compromises tissue viability, predisposing diabetic individuals to pressure ulcer formation. […] Diminished sensation increases the risk of unnoticed trauma, delayed wound detection, and inadequate wound care, further complicating the healing process. […] Chronic hyperglycemia disrupts the synthesis and cross-linking of collagen and elastin fibers, essential components of the skin’s structural integrity. […] Weakened collagen and elastin fibers make the skin less resilient to mechanical stress and shear forces, predisposing diabetic individuals to pressure ulcer formation even at relatively low-pressure levels.
  • #52 Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069223
    The challenge in studying the development of PU results from lack of adequate experimental models that accurately resemble human disease. […] We found that the morphology of skin differed among young and aged individuals in response to load. […] We also report that young skin has significantly higher levels of inflammasome proteins than aged skin. […] Taken together, our findings support the idea that the effects of aging and load synergize to contribute to morphological changes that lead to development of DTI and further to PU. […] Aged skin showed changes as early as 2 hrs of loading, and changes in collagen alignment were only observed in aged skin. […] Interestingly, we found that loading induced significant alterations in NLRP3 inflammasome protein levels in young skin in a time-dependent manner.
  • #53 Deep Tissue Injury in Development of Pressure Ulcers: A Decrease of Inflammasome Activation and Changes in Human Skin Morphology in Response to Aging and Mechanical Load | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069223
    These findings suggest that compressive load further affects tissue collagen fiber orientation. […] Taken together, although external load/pressure is viewed as one of the key factors in the development of DTI/PU, observed decrease in NLRP3 inflammasome proteins in aged skin may indicate diminished innate immune response in skin due to aging, providing an explanation why PU develop more frequently in elderly.
  • #54 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Pressure injury has a significant physical, psychosocial, and economic burden on patient care. […] MicroRNAs have been described in the pathogenesis and treatment of chronic wounds, but their specific roles in the pathogenesis of pressure ulcers have not been reviewed previously. […] Critical pathways involved in miRNA regulation of pressure ulcer pathophysiology include PI3K/AKT, p38-MAPK, NFκB, and MMP9. […] MiRNAs offer potential regulatory targets to prevent the ongoing pressure injury and improve pressure ulcer resolution.
  • #55 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment
    https://www.mdpi.com/1422-0067/22/1/64
    Pressure injury has a significant physical, psychosocial, and economic burden on patient care. […] MicroRNAs have been described in the pathogenesis and treatment of chronic wounds, but their specific roles in the pathogenesis of pressure ulcers have not been reviewed previously. […] Critical pathways involved in miRNA regulation of pressure ulcer pathophysiology include PI3K/AKT, p38-MAPK, NFκB, and MMP9. […] MiRNAs offer potential regulatory targets to prevent the ongoing pressure injury and improve pressure ulcer resolution.
  • #56 Therapeutic Effects and Underlying Mechanism of SOCS-com Gene-Transfected ADMSCs in Pressure Ulcer Mouse Models
    https://www.mdpi.com/2073-4409/12/14/1840
    Pressure ulcers (PUs) refer to damage to the skin or underlying tissue from ischemic tissue necrosis caused by the obstruction of blood capillaries when pressure or pressure in combination with friction and shearing force is applied continuously and repeatedly to localized areas of the body. […] Pressure ulcer sores are classified based on their state and severity into conditions such as non-blanchable erythema and partial-thickness tissue loss. […] The suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine signaling. SOCS proteins are key components of the wound-healing process that regulate the behavior of epithelial cells. […] SOCS-1 interacts with IL-2, IL-4, IL-6, INF-γ, and TNF-α to play an important role in fibroblast infiltration, increased fibroblast metabolism, angiogenesis, re-epithelialization, collagen deposition, tissue remodeling, increased vascular permeability, homeostasis, and the provision of metabolic substrates during wound healing.
  • #57 Therapeutic Effects and Underlying Mechanism of SOCS-com Gene-Transfected ADMSCs in Pressure Ulcer Mouse Models
    https://www.mdpi.com/2073-4409/12/14/1840
    SOCS-3 interacts with IL-1β, IL-2, IL-6, IL-10, INF-γ, TNF-α, EGF, PDGF, HGF, and TGF-β during the wound-healing process and is involved in inflammation, angiogenesis, re-epithelialization, collagen deposition, tissue remodeling, keratinocyte chemotaxis, macrophage and neutrophil migration, and fibroblast proliferation and infiltration. […] SOCS-5 interacts with IL-4R, IL-6, EGF, and EGFR and is involved in inflammation, angiogenesis, re-epithelialization, collagen deposition, tissue remodeling, induction of fibroblast proliferation, and fibroblast collagen secretion. […] SOC-1, -3, and -5 play important roles in the wound-healing process. […] This study aimed to maximize the ulcer wound-healing effect of ADMSCs, which are non-invasive and can be produced in mass amounts by co-transfecting SOCS-1, -3, and -5, which act as key regulators in each stage of wound healing, to enhance the low healing rates of ulcers and confirm their potential as a high-performance ulcer treatment.
  • #58 Therapeutic Effects and Underlying Mechanism of SOCS-com Gene-Transfected ADMSCs in Pressure Ulcer Mouse Models
    https://www.mdpi.com/2073-4409/12/14/1840
    SOCS-3 interacts with IL-1β, IL-2, IL-6, IL-10, INF-γ, TNF-α, EGF, PDGF, HGF, and TGF-β during the wound-healing process and is involved in inflammation, angiogenesis, re-epithelialization, collagen deposition, tissue remodeling, keratinocyte chemotaxis, macrophage and neutrophil migration, and fibroblast proliferation and infiltration. […] SOCS-5 interacts with IL-4R, IL-6, EGF, and EGFR and is involved in inflammation, angiogenesis, re-epithelialization, collagen deposition, tissue remodeling, induction of fibroblast proliferation, and fibroblast collagen secretion. […] SOC-1, -3, and -5 play important roles in the wound-healing process. […] This study aimed to maximize the ulcer wound-healing effect of ADMSCs, which are non-invasive and can be produced in mass amounts by co-transfecting SOCS-1, -3, and -5, which act as key regulators in each stage of wound healing, to enhance the low healing rates of ulcers and confirm their potential as a high-performance ulcer treatment.
  • #59 Therapeutic Effects and Underlying Mechanism of SOCS-com Gene-Transfected ADMSCs in Pressure Ulcer Mouse Models
    https://www.mdpi.com/2073-4409/12/14/1840
    Overall, SOCS-com-transfected ADMSCs alleviated inflammatory reactions more effectively than the groups transfected with SOCS-1, -3, and -5 alone. […] These findings suggest that the co-transfection of ADMSCs with SOCS-1, -3, and -5 accelerates different phases of chronic wound healing. […] In conclusion, co-transfection of SOCS-com with SOCS-1, -3, and -5, which are key regulators of the complex and sophisticated processes of wound healing, effectively enhanced the wound-healing function of ADMSCs by increasing the expression of essential chemokines, CCL, and related genes.
  • #60 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cord
    https://www.nature.com/articles/3101622
    Patients with pressure sore showed significant decreased red cells, decreased haemoglobin and haematocrit, increased white cells and ferritin and decreased transferrin and transferrin saturation; total hypoproteinemia and hypoalbuminemia with increased Alfa-1 and gamma globulins increased erythrocyte sedimentation rate and C-reactive protein were also present. […] Patients with pressure sores suffer from anaemia and serum protein alteration that fells within the range of metabolic alteration of chronic disorders and neoplastic diseases. […] The alterations depend on a decreased utilisation of iron stores in the reticuloendothelial system and on inhibition of the hepatic synthesis of albumin. […] Patients with pressure sores show mild to moderate anaemia and specific serum protein alterations.
  • #61 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cord
    https://www.nature.com/articles/3101622
    Patients with pressure sore showed significant decreased red cells, decreased haemoglobin and haematocrit, increased white cells and ferritin and decreased transferrin and transferrin saturation; total hypoproteinemia and hypoalbuminemia with increased Alfa-1 and gamma globulins increased erythrocyte sedimentation rate and C-reactive protein were also present. […] Patients with pressure sores suffer from anaemia and serum protein alteration that fells within the range of metabolic alteration of chronic disorders and neoplastic diseases. […] The alterations depend on a decreased utilisation of iron stores in the reticuloendothelial system and on inhibition of the hepatic synthesis of albumin. […] Patients with pressure sores show mild to moderate anaemia and specific serum protein alterations.
  • #62 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cord
    https://www.nature.com/articles/3101622
    More importantly, our work demonstrates that these metabolic alterations are closely related to the presence of sores and are not specific for SCI. […] The disappearance of both anaemia and protein alterations soon after surgical healing of sores also supports our hypothesis. […] Chronic inflammatory status inhibits the use of iron stored in the reticuloendothelial system and the hepatic synthesis of albumin. […] The characteristics of anaemia and serum protein alteration, the coexistence of inflammatory status indexes, and the lack of correlation between metabolic alterations and pressure sore area do not permit us to attribute anaemia to a loss of plasma and blood from the sore or to protein hypercatabolism. […] The present work demonstrates the close relationship between surgical healing of sores and metabolic improvement.
  • #63 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cord
    https://www.nature.com/articles/3101622
    With regard to anaemia therapy, patients with pressure sores are often treated with iron therapy; since the anaemia of these patients is due to difficulty in using iron stores, iron treatment is useless, and might even be potentially dangerous because of the possibility of iatrogenic hemochromatosis. […] Our data suggest that this form of treatment should be avoided.
  • #64 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Diabetes can significantly increase the risk of developing pressure ulcers due to various physiological and metabolic factors. […] One primary reason is the impact of diabetes on peripheral neuropathy and vascular complications. […] Neuropathy, common in diabetic patients, diminishes sensation in the extremities, making individuals less aware of pressure points and discomfort, thus increasing the likelihood of prolonged pressure on specific areas. […] Additionally, diabetes can lead to vascular insufficiency, impairing blood flow to tissues and compromising the delivery of oxygen and nutrients essential for wound healing. […] Furthermore, diabetes-related alterations in collagen formation and immune function can hinder the body’s ability to repair damaged skin and fight off infections, further predisposing individuals to pressure ulcer formation.
  • #65 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Diabetes can significantly increase the risk of developing pressure ulcers due to various physiological and metabolic factors. […] One primary reason is the impact of diabetes on peripheral neuropathy and vascular complications. […] Neuropathy, common in diabetic patients, diminishes sensation in the extremities, making individuals less aware of pressure points and discomfort, thus increasing the likelihood of prolonged pressure on specific areas. […] Additionally, diabetes can lead to vascular insufficiency, impairing blood flow to tissues and compromising the delivery of oxygen and nutrients essential for wound healing. […] Furthermore, diabetes-related alterations in collagen formation and immune function can hinder the body’s ability to repair damaged skin and fight off infections, further predisposing individuals to pressure ulcer formation.
  • #66 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Diabetes compromises the immune system’s ability to combat infections and heal wounds. […] Chronic hyperglycemia impairs white blood cell function and cytokine production, prolonging inflammation and delaying tissue repair. […] Diabetes alters collagen synthesis and structure, leading to weakened connective tissues and impaired wound healing. […] Poor collagen formation reduces the skin’s tensile strength, making it more susceptible to breakdown under pressure. […] Chronic hyperglycemia in diabetic patients leads to persistent inflammation at the wound site, characterized by excessive production of pro-inflammatory cytokines and impaired resolution of inflammation. […] Diabetes disrupts the process of angiogenesis, which is essential for delivering oxygen and nutrients to the wound bed.
  • #67 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Diabetes compromises the immune system’s ability to combat infections and heal wounds. […] Chronic hyperglycemia impairs white blood cell function and cytokine production, prolonging inflammation and delaying tissue repair. […] Diabetes alters collagen synthesis and structure, leading to weakened connective tissues and impaired wound healing. […] Poor collagen formation reduces the skin’s tensile strength, making it more susceptible to breakdown under pressure. […] Chronic hyperglycemia in diabetic patients leads to persistent inflammation at the wound site, characterized by excessive production of pro-inflammatory cytokines and impaired resolution of inflammation. […] Diabetes disrupts the process of angiogenesis, which is essential for delivering oxygen and nutrients to the wound bed.
  • #68 Impact of Diabetes on Pressure Ulcers: Understanding the Intricate Relationship
    https://www.thewoundpros.com/post/impact-of-diabetes-on-pressure-ulcers-understanding-the-intricate-relationship
    Reduced capillary density and impaired endothelial cell function impair blood flow to the wound site, compromising tissue oxygenation and nutrient supply, thereby delaying wound healing. […] Chronic hyperglycemia disrupts normal wound healing processes and compromises tissue viability, predisposing diabetic individuals to pressure ulcer formation. […] Diminished sensation increases the risk of unnoticed trauma, delayed wound detection, and inadequate wound care, further complicating the healing process. […] Chronic hyperglycemia disrupts the synthesis and cross-linking of collagen and elastin fibers, essential components of the skin’s structural integrity. […] Weakened collagen and elastin fibers make the skin less resilient to mechanical stress and shear forces, predisposing diabetic individuals to pressure ulcer formation even at relatively low-pressure levels.
  • #69 Pressure ulcers in patients with diabetes: a bibliometrics analysis – Dong – Annals of Palliative Medicine
    https://apm.amegroups.org/article/view/82196/html
    Pressure ulcers (PU) refer to local tissue ulceration and necrosis caused by long-term compression and friction brought on by tissue ischemia and hypoxia. […] Diabetic wounds do not easily heal, and once a pressure ulceration occurs, it is difficult to deal with. […] PUs in diabetic patients are mainly foot ulcers and arise because of peripheral neuropathy, which leads to long-term insensitivity to compression, necrosis, and the nonhealing of the compressed areas. […] The mechanism of PUs involves the following: first, for a variety of reasons, the local soft tissues of the bone protrusion may be continuously compressed for a long time, which directly leads blockage in local blood supply, requiring the pressure to be effectively relieved. Second, shear and friction can damage the subcutaneous vascular bed and cause ischemia.
  • #70 Pressure ulcers in patients with diabetes: a bibliometrics analysis – Dong – Annals of Palliative Medicine
    https://apm.amegroups.org/article/view/82196/html
    Current treatment of PUs mainly includes medicinal dressings and external disinfectants containing silver and iodine. […] In the prevention of PUs in patients with diabetes, the most important issue is controlling blood sugar. […] The current research focuses lies on the management of the risk of PUs in patients with diabetes.
  • #71 Pressure Ulcer – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK553107/
    Decubitus ulcer formation is multifactorial, but these ulcers result in a common pathway to ischemia and necrosis. Tissues can sustain an abnormal amount of external pressure, but constant pressure exerted over a prolonged period is the main culprit. […] The pressure must be greater than the venous capillary closing pressure of 8 to 12 mm Hg to impair venous blood return. Sustaining pressure above these values leads to tissue ischemia and necrosis. […] In addition, the EPUAP emphasized the link between the pathophysiology of COVID-19 and the development of pressure ulcers. The panel attributed the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, abundant in COVID-19 patients, as a contributor to the onset and maintenance of inflammation following cell death and the formation of a pressure ulcer.
  • #72 Pressure Ulcer | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/20286
    Decubitus ulcer formation is multifactorial, but these ulcers result in a common pathway to ischemia and necrosis. Tissues can sustain an abnormal amount of external pressure, but constant pressure exerted over a prolonged period is the main culprit. External pressure must exceed the arterial capillary pressure of 32 mm Hg to impede blood flow. The pressure must be greater than the venous capillary closing pressure of 8 to 12 mm Hg to impair venous blood return. Sustaining pressure above these values leads to tissue ischemia and necrosis. […] In addition, the EPUAP emphasized the link between the pathophysiology of COVID-19 and the development of pressure ulcers. The panel attributed the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, abundant in COVID-19 patients, as a contributor to the onset and maintenance of inflammation following cell death and the formation of a pressure ulcer.
  • #73 Pressure Ulcer – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK553107/
    Pressure injuries are localized skin and soft tissue injuries that develop due to prolonged pressure exerted over specific areas of the body, typically bony prominences. […] Pressure injuries, also termed bedsores, decubitus ulcers, or pressure ulcers, are localized skin and soft tissue injuries that form as a result of prolonged pressure and shear, usually exerted over bony prominences. […] The development of pressure injuries is complex and multifactorial. External and internal factors co-occur to form these ulcers. Externally, prolonged pressure, friction, shear force, and moisture can lead to tissue deformation and ischemia. Internal factors such as malnutrition, anemia, and endothelial dysfunction can speed up the process of tissue damage. […] Prolonged pressure on tissues can cause capillary bed occlusion, reducing oxygen levels in the area. Over time, the ischemic tissue begins to accumulate toxic metabolites. Subsequently, tissue ulceration and necrosis occur.
  • #74
    https://link.springer.com/article/10.1007/s10237-021-01432-w
    Pressure ulcers are localized sites of tissue damage which form due to the continuous exposure of skin and underlying soft tissues to sustained mechanical loading, by bodyweight forces or because a body site is in prolonged contact with an interfacing object. […] Etiological research has established three key contributors to pressure ulcer formation, namely direct cell and tissue deformation, inflammatory edema and ischemic damage which are typically activated sequentially to fuel the injury spiral. […] We demonstrate the detrimental effects of exposure to high-level continuous external strains, which causes deformation-inflicted cell damage almost immediately. This in turn induces localized edema, which exacerbates the cell-scale mechanical loading state and thereby progresses cell damage further in a nonlinear, escalating pattern.
  • #75 Pressure ulcer – Wikipedia
    https://en.wikipedia.org/wiki/Pressure_ulcer
    Pressure ulcers, also known as pressure sores, bed sores or pressure injuries, are localised damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of usually long-term pressure, or pressure in combination with shear or friction. […] Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. […] There are four mechanisms that contribute to pressure ulcer development: External (interface) pressure applied over an area of the body, especially over the bony prominences can result in obstruction of the blood capillaries, which deprives tissues of oxygen and nutrients, causing ischemia, hypoxia, edema, inflammation, and, finally, necrosis and ulcer formation. […] Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. […] The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. […] This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.

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