Odleżyny
Patofizjologia i mechanizm
Odleżyny to zlokalizowane uszkodzenia skóry i tkanek miękkich powstające na skutek długotrwałego ucisku przekraczającego ciśnienie kapilarne (32 mmHg), prowadzącego do niedokrwienia, niedotlenienia i martwicy tkanek. Krytyczny czas niedokrwienia wynosi od 30 do 240 minut, a nieodwracalne zmiany mogą pojawić się już po 2 godzinach. Patogeneza obejmuje także siły ścinające, tarcie i wilgotność, które nasilają uszkodzenia. Kluczową rolę odgrywa uszkodzenie reperfuzyjne, związane z uwalnianiem wolnych rodników tlenowych i cytokin prozapalnych (np. TNFα, IL-6, IL-8), co prowadzi do przewlekłego stanu zapalnego i zaburzeń gojenia. Tkanka mięśniowa ulega uszkodzeniu jako pierwsza, a proces gojenia jest często zatrzymany w fazie zapalnej, z nadmierną infiltracją neutrofilów i degradacją macierzy pozakomórkowej. W patogenezie istotne są także czynniki wewnętrzne, takie jak niedożywienie (hipoalbuminemia, niedokrwistość), dysfunkcja śródbłonka, wiek, choroby współistniejące (cukrzyca, choroby naczyń obwodowych) oraz unieruchomienie i zaburzenia funkcji poznawczych.
- Patogeneza odleżyn (bedsores/pressure ulcers)
- Podstawowy mechanizm powstawania odleżyn
- Czynniki fizyczne w powstawaniu odleżyn
- Kaskada patofizjologiczna
- Uszkodzenie reperfuzyjne jako kluczowy element patogenezy
- Zróżnicowana podatność tkanek na uszkodzenie ciśnieniowe
- Rola przewlekłego stanu zapalnego
- Rola zaburzeń limfatycznych i deformacji komórkowej
- Znaczenie czynników metabolicznych i stanu odżywienia
- Klasyfikacja kliniczna odleżyn
- Czynniki ryzyka w patogenezie odleżyn
- Czynniki wewnętrzne
- Choroby współistniejące a ryzyko odleżyn
- Unieruchomienie jako główny czynnik ryzyka
- Specyficzne aspekty patogenezy odleżyn
Patogeneza odleżyn (bedsores/pressure ulcers)
Odleżyny (łac. decubitus ulcers, ang. pressure ulcers, bedsores) to zlokalizowane uszkodzenia skóry i tkanek miękkich leżących poniżej, powstające w wyniku długotrwałego ucisku i sił ścinających, najczęściej występujące nad wyniosłościami kostnymi. Rozwój odleżyn jest procesem złożonym i wieloczynnikowym, angażującym zarówno mechanizmy zewnętrzne, jak i wewnętrzne.123
Podstawowy mechanizm powstawania odleżyn
Głównym czynnikiem patogenetycznym w powstawaniu odleżyn jest ucisk zewnętrzny wywierany na tkanki przez zbyt długi czas. Gdy ucisk przekracza ciśnienie w kapilarach tętniczych (32 mmHg), dochodzi do zaburzenia przepływu krwi, co prowadzi do niedokrwienia, niedotlenienia i ostatecznie do martwicy tkanek.123 Tkanki są w stanie wytrzymać ogromne ciśnienia przez krótki czas, jednak przedłużona ekspozycja nawet na ciśnienie nieznacznie przekraczające ciśnienie wypełniania włośniczek inicjuje proces prowadzący do martwicy tkanek i owrzodzenia.4
Krytyczny czas trwania niedokrwienia mogący spowodować uszkodzenie ciśnieniowe znacznie różni się między pacjentami, ale jako orientacyjny przedział czasowy przyjmuje się 30-240 minut. Nieodwracalne zmiany mogą pojawić się już po 2 godzinach nieprzerwanego ucisku, podczas gdy skóra może wytrzymać niedokrwienie wywołane bezpośrednim uciskiem do 12 godzin.567
Czynniki fizyczne w powstawaniu odleżyn
Oprócz ucisku, w patogenezie odleżyn istotną rolę odgrywają:8910
- Siły ścinające (shear forces) – powstają, gdy dwie powierzchnie poruszają się w przeciwnych kierunkach. Na przykład, gdy głowa łóżka jest uniesiona, pacjent może zsuwać się w dół, powodując, że skóra nad kością ogonową pozostaje w miejscu, pociągając w przeciwnym kierunku. Prowadzi to do ścinania naczyń krwionośnych, ich zagięcia i zakrzepicy, co powoduje podminowanie owrzodzenia.1112
- Tarcie (friction) – pojawia się, gdy skóra ociera się o ubranie lub pościel. To osłabia delikatną skórę i czyni ją bardziej podatną na uszkodzenia, szczególnie jeśli jest wilgotna.1314
- Wilgotność (moisture) – pot, mocz lub inne wydzieliny prowadzą do maceracji tkanek i ich rozpadu, co inicjuje lub pogarsza stan odleżyn.1516
Kaskada patofizjologiczna
Kaskada zdarzeń patofizjologicznych w odleżynach obejmuje:1718
- Ucisk i okluzja naczyń – długotrwały ucisk powoduje zamknięcie łożyska włośniczkowego, ograniczając dopływ tlenu do obszaru.
- Niedokrwienie i niedotlenienie – niewystarczający przepływ krwi prowadzi do niedotlenienia tkanek.
- Gromadzenie toksycznych metabolitów – w tkance niedokrwionej gromadzą się toksyczne produkty przemiany materii.
- Stan zapalny i uszkodzenie reperfuzyjne – po uwolnieniu ucisku może dojść do uszkodzenia reperfuzyjnego, gdy krew powraca do niedokrwionych tkanek, powodując dalsze uszkodzenia przez wolne rodniki i odpowiedź zapalną.
- Martwica i owrzodzenie – ostatecznie dochodzi do owrzodzenia i martwicy tkanek.
Uszkodzenie reperfuzyjne jako kluczowy element patogenezy
W patogenezie odleżyn coraz większą uwagę zwraca się na uszkodzenie reperfuzyjne. Epizody niedokrwienia-reperfuzji (nieadekwatny przepływ krwi, a następnie jego przywrócenie) stanowią ważny mechanizm w rozwoju odleżyn. W procesie reperfuzji dochodzi do uwolnienia wolnych rodników tlenowych, które uszkadzają komórki, oraz aktywacji układu dopełniacza i leukocytów.19202122
Proces niedokrwienia skutkuje zmniejszoną produkcją ATP, upośledzeniem mitochondrialnej fosforylacji oksydacyjnej, zwiększoną aktywacją dopełniacza i leukocytów oraz podwyższonym poziomem stanu zapalnego. Toksyczne metabolity, takie jak COX-2 i IL-6, stymulują neutrofile i makrofagi do uwalniania większej ilości cytokin prozapalnych, takich jak TNFα i IL-8, co utrwala cykl zapalny.23
Zróżnicowana podatność tkanek na uszkodzenie ciśnieniowe
Spośród różnych tkanek narażonych na uszkodzenie z powodu ucisku, tkanka mięśniowa ulega uszkodzeniu jako pierwsza, przed skórą i tkanką podskórną. Jest to prawdopodobnie związane z jej zwiększonym zapotrzebowaniem na tlen i wyższymi wymaganiami metabolicznymi.242526
Badania histologiczne odleżyn ujawniają dynamiczny proces, obejmujący rumień blednący i nieblednący, zapalenie skóry z odleżyną, owrzodzenie odleżynowe i czarny strup/zgorzel. Początkowa zmiana występuje w naczyniach brodawek skóry właściwej, a następnie dochodzi do martwicy struktur skóry.27
Gdy odleżyna jest już widoczna na poziomie skóry, znaczne uszkodzenie leżących poniżej mięśni mogło już nastąpić, co nadaje ogólnemu kształtowi odleżyny formę odwróconego stożka.28
Rola przewlekłego stanu zapalnego
Zaproponowano hipotezę przedłużonej fazy zapalnej, zgodnie z którą odleżyny nie podążają normalną trajektorią zapalenia, przebudowy i dojrzewania, ale są zatrzymane w fazie zapalnej gojenia się ran.29
Stres oksydacyjny promuje fenotyp makrofagów M1 (prozapalny) w przewlekłych ranach, takich jak odleżyny i rany cukrzycowe, powodując trwałą sygnalizację zapalną i upośledzenie gojenia się ran. Przewlekłe odleżyny charakteryzują się nadmierną infiltracją neutrofilów w tkance ziarninowej, a te linie komórkowe wytwarzają elastazę i kolagenazę, które prowadzą do ciągłego rozkładu macierzy pozakomórkowej i zaburzają gojenie się ran.3031
Panel EPUAP podkreślił związek między patofizjologią COVID-19 a rozwojem odleżyn. Panel przypisał prozapalne cytokiny interleukinę-6 i czynnik martwicy nowotworów alfa, obficie występujące u pacjentów z COVID-19, jako czynnik przyczyniający się do wystąpienia i utrzymywania się stanu zapalnego po śmierci komórek i powstawaniu odleżyny.32
Rola zaburzeń limfatycznych i deformacji komórkowej
Mechaniczna deformacja prowadzi do ucisku naczyń krwionośnych, ale także do trwałego zapadnięcia się kanałów limfatycznych. Upośledzenie odpływu limfatycznego, wraz z opisanym powyżej upośledzeniem drenażu żylnego, prowadzi do utrzymywania się wysokiego nacieku leukocytów przy słabym klirensie reaktywnych form tlenu (ROS) i cytokin.33
Długotrwała deformacja komórkowa, obserwowana w odleżynach, prowadzi do uszkodzenia cytoszkieletu i śmierci komórek.34
Znaczenie czynników metabolicznych i stanu odżywienia
Stan odżywienia odgrywa kluczową rolę w patogenezie odleżyn. Hipoalbuminemia i niedokrwistość są związane z powstawaniem odleżyn i zwiększoną śmiertelnością.3536
Pacjenci z odleżynami cierpią na anemię i zmiany w białkach surowicy, które mieszczą się w zakresie zmian metabolicznych charakterystycznych dla przewlekłych zaburzeń i chorób nowotworowych. Zmiany te zależą od zmniejszonego wykorzystania zasobów żelaza w układzie siateczkowo-śródbłonkowym i zahamowania wątrobowej syntezy albuminy.37
Badania wykazały, że obwód środkowy ramienia (p = 0,04; beta = 0,89), obwód mięśnia środkowego ramienia (p = 0,050; beta = 1,29), hemoglobina (p = 0,04, beta 1,1) i albumina (p = 0,04, beta 7,91) są odwrotnie skorelowane z występowaniem odleżyn.38
Przewlekły stan zapalny hamuje wykorzystanie żelaza zmagazynowanego w układzie siateczkowo-śródbłonkowym i wątrobową syntezę albuminy. Związek między odleżynami a wskaźnikami MAC (obwód środkowy ramienia) i MACM (obwód mięśnia środkowego ramienia) może potwierdzać powiązanie między odleżynami a kacheksją.39
Klasyfikacja kliniczna odleżyn
Klasyfikacja kliniczna odleżyn obejmuje cztery podstawowe stopnie:4041
- Stopień 1: Skóra jest zaczerwieniona lub różowa, nie ma otwartej rany. Rumień nie blednie po ucisku.
- Stopień 2: Powstaje płytka rana z różową lub czerwoną podstawą. Uszkodzenie obejmuje naskórek i część skóry właściwej.
- Stopień 3: Widoczna rana może sięgać warstwy tłuszczowej skóry (hipodermis). Uszkodzenie obejmuje pełną grubość skóry.
- Stopień 4: Rana penetruje wszystkie trzy warstwy skóry, odsłaniając mięśnie, ścięgna i kości w układzie mięśniowo-szkieletowym.
Czynniki ryzyka w patogenezie odleżyn
W patogenezie odleżyn kluczową rolę odgrywają zarówno czynniki zewnętrzne, jak i wewnętrzne, które działają synergistycznie, prowadząc do uszkodzenia tkanek.42
Czynniki wewnętrzne
Czynniki wewnętrzne wpływające na patogenezę odleżyn obejmują:434445
- Niedożywienie – przyczynia się do zmniejszenia masy mięśniowej, obniżenia odporności i pogorszenia gojenia ran
- Niedokrwistość – ogranicza transport tlenu do tkanek
- Dysfunkcja śródbłonka – wpływa na mikronaczynia i regulację przepływu krwi
- Wiek – skóra osób starszych jest cieńsza, delikatniejsza i mniej elastyczna
- Choroby współistniejące – w szczególności cukrzyca, choroby naczyń obwodowych, niedobory immunologiczne
- Niska wrażliwość na ból – ogranicza naturalny odruch zmiany pozycji ciała
- Stan ogólny i psychiczny pacjenta – wpływa na mobilność i świadomość zagrożenia
Choroby współistniejące a ryzyko odleżyn
Bezpośrednie czynniki przyczynowe odleżyn związane z chorobami współistniejącymi obejmują unieruchomienie, stan skóry/odleżyn i słabą perfuzję. Czynniki pośrednie to wilgotność, percepcja sensoryczna, cukrzyca, niski poziom albuminy i niedożywienie. Inne potencjalne czynniki obejmują podeszły wiek, leki, obrzęki wgłębione i inne czynniki związane z ogólnym stanem zdrowia, w tym infekcje, ostre choroby, podwyższona temperatura ciała i przewlekłe rany.46
- Wszystkie choroby ograniczające niezależną mobilność, które zwiększają ryzyko
- Zaburzenia funkcji poznawczych, które mogą utrudniać działania profilaktyczne
- Zaburzenia perfuzji, które zwiększają ryzyko odleżyn
Unieruchomienie jako główny czynnik ryzyka
Unieruchomienie jest głównym czynnikiem ryzyka odleżyn ze względu na ich patofizjologię. Zdrowy człowiek jest osobą dynamiczną, która nie rozwija odleżyn czy ran odleżynowych. Odleżyny u ludzi są objawem unieruchomienia spowodowanego znieczuleniem lub sedacją, chorobą lub urazem, co skutkuje zmniejszonym odczuwaniem bólu i/lub zmniejszoną aktywnością mięśniowo-szkieletową.4950
Specyficzne aspekty patogenezy odleżyn
Rola mikroRNA w patogenezie odleżyn
MikroRNA odgrywają rolę w patogenezie i leczeniu ran przewlekłych, ale ich szczególna rola w patogenezie odleżyn nie została jeszcze dokładnie zbadana. Regulacja poziomów ekspresji miRNA w obrębie odleżyn nie była szeroko badana w modelach klinicznych, ale oferuje potencjalną drogę do lepszej profilaktyki i strategii terapeutycznych.51
Odleżyny związane z urządzeniami medycznymi
Coraz większą uwagę zwraca się na odleżyny związane z urządzeniami medycznymi. Ucisk z urządzeń medycznych, takich jak rurki tlenowe, cewniki, kołnierze szyjne, gipsy i opaski unieruchamiające, powinien być minimalizowany lub usuwany, ponieważ może prowadzić do odleżyn specyficznych dla tych urządzeń.5253
Prognozy i efektywność leczenia
Rokowanie dla pacjentów z odleżynami różni się w zależności od lokalizacji anatomicznej, stopnia uszkodzenia i schematu leczenia. Większość wyników badań porównuje skuteczność leczenia, mierząc zmniejszenie częstości występowania odleżyn w określonej placówce jako środek zapobiegawczy, zamiast wskaźnika gojenia po rozpoczęciu leczenia.54
Odleżyny zwiększają ryzyko potencjalnie zagrażających życiu zakażeń bakteryjnych, takich jak zapalenie tkanki łącznej i posocznica. Może rozwinąć się sepsa lub może być konieczna amputacja. Na całym świecie odleżyny prowadzą do śmierci ponad 24 000 osób rocznie.55
Nie wszystkie odleżyny można zapobiec lub wyleczyć, co podkreśla znaczenie wczesnej identyfikacji ryzyka i wdrożenia skutecznych strategii profilaktycznych.56
Identyfikacja pacjentów z grupy ryzyka
Znajomość czynników przyczyniających się do patogenezy odleżyn pozwala na identyfikację pacjentów zagrożonych rozwojem owrzodzeń, tak aby działania zapobiegawcze mogły być ukierunkowane na tych konkretnych pacjentów.57
Zrozumienie drogi prowadzącej do unieruchomienia, niedokrwienia tkanek i niedożywienia w rozwoju odleżyn ma kluczowe znaczenie dla skutecznego zapobiegania i leczenia.58
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Materiały źródłowe
- #1 Pressure Ulcer – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK553107/
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 Bedsores (Pressure Ulcers) â DermNethttps://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.
- #2 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://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.
- #3 Pressure ulcer – Wikipediahttps://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 (deficiency of blood in a particular area), hypoxia (inadequate amount of oxygen available to the cells), edema, inflammation, and, finally, necrosis and ulcer formation.
- #3 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/dermatologic-disorders/pressure-injury/pressure-injuries
Pressure injuries are areas of necrosis and often ulceration (also called pressure ulcers) where soft tissues are compressed between bony prominences and external hard surfaces. They are caused by unrelieved mechanical pressure in combination with friction, shearing forces, and moisture. […] The main factors contributing to pressure injuries are Pressure: When soft tissues are compressed for prolonged periods between bony prominences and external surfaces, microvascular occlusion with tissue ischemia and hypoxia occurs. Pressures exceeding normal capillary pressure (range is 12 to 32mm Hg) result in reduced oxygenation and compromise the microcirculation of the affected tissue. If compression is not relieved, a pressure injury can develop in 3 to 4 hours. This most commonly occurs over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, but pressure injuries can develop anywhere.
- #4 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://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 Decubitus Ulcers: Pathophysiology and Primary Preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC2883282/
Pressure sores are a serious complication of multimorbidity and lack of mobility. […] Decubitus ulcers are not always preventable or curable. […] Impaired perfusion, among other factors, increases the risk of decubitus ulcers, and cognitive disturbances can make prophylactic measures more difficult. […] The most important cause of pressure ulcers is pressure exerted for an excessive period of time. […] Immobility is the main risk factor for decubitus ulcers because of their pathophysiology. […] All diseases that restrict independent mobility elevate this risk. […] The critical duration of ischemia that can cause pressure injury varies greatly among individuals; as a rule of thumb, it lies somewhere between 30 and 240 minutes. […] The most important cause of decubitus ulcers is externally applied pressure for an excessive period of time. […] Other physical influences that can damage the skin include friction at the skin surface, shearing forces, and moisture. […] Risk factors promoting the development of decubitus ulcers should be reduced as far as possible.
- #6 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://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. Skin can withstand ischemia from direct pressure for up to 12 hours.
- #7 Bedsores (Pressure Ulcers): Symptoms, Staging & Treatmenthttps://my.clevelandclinic.org/health/diseases/17823-bedsores-pressure-injuries
Bedsores are wounds that occur from prolonged pressure on your skin. People who are immobile for long periods, such as those who are bedridden or use a wheelchair, are most at risk for bedsores. These painful wounds, or pressure ulcers, can grow large and lead to infections. In some instances, bedsores can be life-threatening. […] Bedsores occur when pressure reduces or cuts off blood flow to your skin. This lack of blood flow can cause a pressure wound injury to develop in as little as two hours. Skin cells on your epidermis (your skins outer layer) start to die. As the dead cells break down, a pressure ulcer injury forms. […] Bedsores increase your risk of potentially life-threatening bacterial infections like cellulitis and septicemia. You may develop sepsis or require an amputation. Worldwide, bedsores lead to the deaths of more than 24,000 people each year.
- #8 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinichttps://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. […] 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. Limited movement can make skin prone to the damage that the pressure causes. […] 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.
- #9 Decubitus Ulcers: Pathophysiology and Primary Preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC2883282/
Pressure sores are a serious complication of multimorbidity and lack of mobility. […] Decubitus ulcers are not always preventable or curable. […] Impaired perfusion, among other factors, increases the risk of decubitus ulcers, and cognitive disturbances can make prophylactic measures more difficult. […] The most important cause of pressure ulcers is pressure exerted for an excessive period of time. […] Immobility is the main risk factor for decubitus ulcers because of their pathophysiology. […] All diseases that restrict independent mobility elevate this risk. […] The critical duration of ischemia that can cause pressure injury varies greatly among individuals; as a rule of thumb, it lies somewhere between 30 and 240 minutes. […] The most important cause of decubitus ulcers is externally applied pressure for an excessive period of time. […] Other physical influences that can damage the skin include friction at the skin surface, shearing forces, and moisture. […] Risk factors promoting the development of decubitus ulcers should be reduced as far as possible.
- #10 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://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.
- #11 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinichttps://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. […] 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. Limited movement can make skin prone to the damage that the pressure causes. […] 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.
- #12 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://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 Bedsores (pressure ulcers) – Symptoms and causes – Mayo Clinichttps://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. […] 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. Limited movement can make skin prone to the damage that the pressure causes. […] 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.
- #14 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://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.
- #15 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://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.
- #16https://step2.medbullets.com/dermatology/120253/wounds
ulcer resulting from vertical pressure […] Pathogenesis […] enough pressure can prevent delivery of important nutrients and oxygen to tissue, resulting in accumulation of waste products and free radicals […] muscles are most susceptible to damage, followed by subcutaneous fat and then dermis […] moisture from sweat or urine can cause skin maceration and predispose the area to ulceration.
- #17 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://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. Skin can withstand ischemia from direct pressure for up to 12 hours.
- #18 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://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, Anatomyhttps://emedicine.medscape.com/article/190115-overview
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 ulcer – Wikipediahttps://en.wikipedia.org/wiki/Pressure_ulcer
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. The muscle cells die as a result and skin fed through blood vessels coming through the muscle die. This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.
- #21 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://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.
- #22 SmartDerm: Using Technology to Prevent Bedsores | Surgical Innovationshttps://surgicalinnovations.ucsf.edu/smartderm-using-technology-prevent-bedsores
Now, one of his latest projects seeks to prevent a very common condition: pressure ulcers, also known as bedsores, which can develop in as little as two hours when constant pressure on the skin reduces blood flow and causes tissue death. […] While continuous pressure buildup can lead to a pressure ulcer, studies have demonstrated that cycles of ischemia and reperfusion inadequate blood flow followed by restoration of blood flow are an important mechanism in the development of pressure ulcers. […] This highlights the complicated nature of pressure ulcer formation and underlies the usefulness of the machine learning approach. We dont know what exactly leads to these pressure ulcers, but with our device we can exactly see the change in a patients pressure profile before the ulcer occurs, and with enough data, machine learning will enable us to identify the specific patterns in pressure profile changes that correlate with ulcer formation, said Rangarajan.
- #23 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://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.
- #24 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://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. Skin can withstand ischemia from direct pressure for up to 12 hours.
- #25 Pressure Injuries – Dermatologic Disorders – Merck Manual Professional Editionhttps://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.
- #26https://step2.medbullets.com/dermatology/120253/wounds
ulcer resulting from vertical pressure […] Pathogenesis […] enough pressure can prevent delivery of important nutrients and oxygen to tissue, resulting in accumulation of waste products and free radicals […] muscles are most susceptible to damage, followed by subcutaneous fat and then dermis […] moisture from sweat or urine can cause skin maceration and predispose the area to ulceration.
- #27 Pressure Ulcer – StatPearls – NCBI Bookshelfhttps://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. External pressure must exceed the arterial capillary pressure of 32 mm Hg to impede blood flow. […] 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. […] Histological studies of pressure ulcers reveal a dynamic process, including blanchable and non-blanchable erythema, decubitus dermatitis, decubitus ulcer, and black scab/gangrene. The initial change occurs in the vessels of the papillary dermis, followed by the necrosis of skin structures.
- #28 Pressure Injuries (Pressure Ulcers) and Wound Care: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/190115-overview
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.
- #29 Bedsores (Pressure Ulcers) â DermNethttps://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.
- #30 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://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.
- #31 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://www.mdpi.com/1422-0067/22/1/64
Mechanical deformation leads to compression of blood vessels, but also to the sustained collapse of lymphatic channels. […] The impairment of lymphatic clearance, along with impaired venous drainage described above, leads to the maintenance of high leukocyte infiltrate with poor ROS and cytokine clearance. […] Sustained cellular deformation, as seen in pressure ulcers, leads to cytoskeletal damage and cell death. […] 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. […] The regulation of miRNA expression levels within pressure ulcers has not been widely studied in clinical models, but offers a potential avenue for improved prevention and therapeutic strategies. […] 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.
- #32 Pressure Ulcer – StatPearls – NCBI Bookshelfhttps://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. External pressure must exceed the arterial capillary pressure of 32 mm Hg to impede blood flow. […] 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. […] Histological studies of pressure ulcers reveal a dynamic process, including blanchable and non-blanchable erythema, decubitus dermatitis, decubitus ulcer, and black scab/gangrene. The initial change occurs in the vessels of the papillary dermis, followed by the necrosis of skin structures.
- #33 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://www.mdpi.com/1422-0067/22/1/64
Mechanical deformation leads to compression of blood vessels, but also to the sustained collapse of lymphatic channels. […] The impairment of lymphatic clearance, along with impaired venous drainage described above, leads to the maintenance of high leukocyte infiltrate with poor ROS and cytokine clearance. […] Sustained cellular deformation, as seen in pressure ulcers, leads to cytoskeletal damage and cell death. […] 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. […] The regulation of miRNA expression levels within pressure ulcers has not been widely studied in clinical models, but offers a potential avenue for improved prevention and therapeutic strategies. […] 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.
- #34 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://www.mdpi.com/1422-0067/22/1/64
Mechanical deformation leads to compression of blood vessels, but also to the sustained collapse of lymphatic channels. […] The impairment of lymphatic clearance, along with impaired venous drainage described above, leads to the maintenance of high leukocyte infiltrate with poor ROS and cytokine clearance. […] Sustained cellular deformation, as seen in pressure ulcers, leads to cytoskeletal damage and cell death. […] 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. […] The regulation of miRNA expression levels within pressure ulcers has not been widely studied in clinical models, but offers a potential avenue for improved prevention and therapeutic strategies. […] 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.
- #35 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cordhttps://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 Nutritional parameters predicting pressure ulcers and short-term mortality in patients with minimal conscious state as a result of traumatic and non-traumatic acquired brain injury | Journal of Translational Medicine | Full Texthttps://translational-medicine.biomedcentral.com/articles/10.1186/s12967-015-0660-4
The association between malnutrition and worse outcomes as pressure ulcers and mortality is well established in a variety of setting. […] The aim of this study was to investigate the association between various nutritional status parameters (in particular albumin) and pressure ulcers formation and short-term mortality in minimal conscious state patients. […] At univariate and logistic regression analysis, mid-arm circumference (p = 0.04; beta = 0.89), mid-arm muscle circumference (p = 0.050; beta = 1.29), hemoglobin (p = 0.04, beta 1.1) and albumin (p = 0.04, beta 7.91) were inversely associated with pressure ulcers. […] Albumin, haemoglobin and mid-arm circumference are inversely associated with pressure ulcers. […] This association suggests to optimize nutrition and investigate on other mechanism leading to mortality and pressure ulcers.
- #37 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cordhttps://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.
- #38 Nutritional parameters predicting pressure ulcers and short-term mortality in patients with minimal conscious state as a result of traumatic and non-traumatic acquired brain injury | Journal of Translational Medicine | Full Texthttps://translational-medicine.biomedcentral.com/articles/10.1186/s12967-015-0660-4
The association between malnutrition and worse outcomes as pressure ulcers and mortality is well established in a variety of setting. […] The aim of this study was to investigate the association between various nutritional status parameters (in particular albumin) and pressure ulcers formation and short-term mortality in minimal conscious state patients. […] At univariate and logistic regression analysis, mid-arm circumference (p = 0.04; beta = 0.89), mid-arm muscle circumference (p = 0.050; beta = 1.29), hemoglobin (p = 0.04, beta 1.1) and albumin (p = 0.04, beta 7.91) were inversely associated with pressure ulcers. […] Albumin, haemoglobin and mid-arm circumference are inversely associated with pressure ulcers. […] This association suggests to optimize nutrition and investigate on other mechanism leading to mortality and pressure ulcers.
- #39 Pressure sores and blood and serum dysmetabolism in spinal cord injury patients | Spinal Cordhttps://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.
- #40 Bedsores (Pressure Ulcers): Symptoms, Staging & Treatmenthttps://my.clevelandclinic.org/health/diseases/17823-bedsores-pressure-injuries
Healthcare providers use a staging system to determine the severity of a pressure ulcer. […] Stages of bedsores or pressure ulcers include: […] Stage 1: Your skin looks red or pink, but there isnt an open wound. […] Stage 2: A shallow wound with a pink or red base develops. […] Stage 3: A noticeable wound may go into your skins fatty layer (the hypodermis). […] Stage 4: The wound penetrates all three layers of skin, exposing muscles, tendons and bones in your musculoskeletal system.
- #41 Bedsores (Pressure Ulcers) Condition, Treatments and Pictures for Adults – Skinsighthttps://skinsight.com/skin-conditions/pressure-ulcer-decubitus-ulcer/
Bedsores occur at areas of abnormal pressure on the body: […] The pain level associated with bedsores depends on whether or not there is feeling in the area. […] Bedsores occur in stages: […] Stage 1 has unbroken but pink or ashen (in darker skin colors) discoloration with perhaps slight discomfort or tenderness. […] Stage 2 has red, swollen skin with a blister or open area(s). […] Stage 3 has a crater-like ulcer extending deeper into the skin. […] Stage 4 extends to deep fat, muscle, or bone and may have a thick black scab (eschar). […] In the early stages (1 and 2) of bedsores, the area may heal with relief of pressure and by applying effective skin care (see below) to the affected skin. […] A good diet will aid skin healing, especially by taking in enough vitamin C and zinc, which are available as supplements.
- #42 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Texthttps://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
The prevalence of pressure ulcers particularly in the frail older adult population continues to be high and very costly especially in those suffering from chronic diseases and has brought a higher awareness to comprehensive, preventive and therapeutic measures for treatment of pressure ulcers. Internal risk factors highlighted by comorbidities play a crucial role in the pathogenesis of pressure ulcers. […] Multiple factors act together synergistically to cause PU in the functionally impaired frail older population. The pathogenesis of PU is a multifactorial process involving inflammatory factors, hormonal changes, reduced immune protection, impaired blood perfusion and degenerative changes. […] The etiological mechanisms by which stress and internal strain interact with damaged skin and subcutaneous tissue resulting in pressure ulcer development include localized ischaemia, reperfusion injury, impaired lymphatic drainage and sustained cell deformation.
- #43 Pressure Ulcer – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK553107/
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.
- #44 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Texthttps://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
The significance of comorbidity risk factors in the pathogenesis of PU requires further investigation, recognizing the insolvability of PU prevention solely with external relief devices. […] 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. […] Understanding the pathway to immobility, tissue ischemia and undernutrition to develop PU is crucial.
- #45 Journal of the Korean Medical Associationhttps://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. […] Furthermore, early screening, individualized management of posture, and regular skin and nutrition monitoring are essential to prevent pressure ulcers.
- #46 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Texthttps://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
The significance of comorbidity risk factors in the pathogenesis of PU requires further investigation, recognizing the insolvability of PU prevention solely with external relief devices. […] 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. […] Understanding the pathway to immobility, tissue ischemia and undernutrition to develop PU is crucial.
- #47 Decubitus Ulcers: Pathophysiology and Primary Preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC2883282/
Pressure sores are a serious complication of multimorbidity and lack of mobility. […] Decubitus ulcers are not always preventable or curable. […] Impaired perfusion, among other factors, increases the risk of decubitus ulcers, and cognitive disturbances can make prophylactic measures more difficult. […] The most important cause of pressure ulcers is pressure exerted for an excessive period of time. […] Immobility is the main risk factor for decubitus ulcers because of their pathophysiology. […] All diseases that restrict independent mobility elevate this risk. […] The critical duration of ischemia that can cause pressure injury varies greatly among individuals; as a rule of thumb, it lies somewhere between 30 and 240 minutes. […] The most important cause of decubitus ulcers is externally applied pressure for an excessive period of time. […] Other physical influences that can damage the skin include friction at the skin surface, shearing forces, and moisture. […] Risk factors promoting the development of decubitus ulcers should be reduced as far as possible.
- #48 Journal of the Korean Medical Associationhttps://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. […] Furthermore, early screening, individualized management of posture, and regular skin and nutrition monitoring are essential to prevent pressure ulcers.
- #49 Decubitus Ulcers: Pathophysiology and Primary Preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC2883282/
Pressure sores are a serious complication of multimorbidity and lack of mobility. […] Decubitus ulcers are not always preventable or curable. […] Impaired perfusion, among other factors, increases the risk of decubitus ulcers, and cognitive disturbances can make prophylactic measures more difficult. […] The most important cause of pressure ulcers is pressure exerted for an excessive period of time. […] Immobility is the main risk factor for decubitus ulcers because of their pathophysiology. […] All diseases that restrict independent mobility elevate this risk. […] The critical duration of ischemia that can cause pressure injury varies greatly among individuals; as a rule of thumb, it lies somewhere between 30 and 240 minutes. […] The most important cause of decubitus ulcers is externally applied pressure for an excessive period of time. […] Other physical influences that can damage the skin include friction at the skin surface, shearing forces, and moisture. […] Risk factors promoting the development of decubitus ulcers should be reduced as far as possible.
- #50 Pathogenesis of Pressure Sores | SpringerLinkhttps://link.springer.com/chapter/10.1007/978-1-349-10128-3_2
Healthy man is a dynamic person who does not develop decubitus ulcers or bed sores. […] Human pressure sores are a manifestation of immobility due to anaesthesia or sedation, disease or injury, resulting in diminished pain sensation and/or diminished musculoskeletal activity. […] Krouskop, T. A., Reddy, N. P., Spencer, W. A. and Secor, J. W. (1978). Mechanisms of decubitus ulcer formation – an hypothesis. […] Reddy, N. P., Cochran, G. van B. and Krouskop, T. A. (1981). Interstitial fluid flow as a factor in decubitus ulcer formation.
- #51 Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatmenthttps://www.mdpi.com/1422-0067/22/1/64
Mechanical deformation leads to compression of blood vessels, but also to the sustained collapse of lymphatic channels. […] The impairment of lymphatic clearance, along with impaired venous drainage described above, leads to the maintenance of high leukocyte infiltrate with poor ROS and cytokine clearance. […] Sustained cellular deformation, as seen in pressure ulcers, leads to cytoskeletal damage and cell death. […] 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. […] The regulation of miRNA expression levels within pressure ulcers has not been widely studied in clinical models, but offers a potential avenue for improved prevention and therapeutic strategies. […] 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.
- #52 Pressure sores | Better Health Channelhttps://www.betterhealth.vic.gov.au/health/conditionsandtreatments/pressure-sores
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. […] The skin of older people tends to be thinner and more delicate, which means an older person has an increased risk of developing a pressure sore during a prolonged stay in bed. […] 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.
- #53 Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury – UpToDatehttps://www.uptodate.com/contents/epidemiology-pathogenesis-and-risk-assessment-of-pressure-induced-skin-and-soft-tissue-injury
Pressure-induced skin and soft tissue injuries are lesions caused by unrelieved pressure that results in damage to the underlying tissue. Generally, these are the result of soft tissue compression between a bony prominence and an external surface for a prolonged time, although increasing attention is being paid to medical device-related pressure injury. The consequences of pressure-induced skin and soft tissue injury range from nonblanchable erythema of intact skin to deep ulcers extending to the bone. […] Knowledge of factors contributing to the pathogenesis of pressure-induced skin and soft tissue injury allows the identification of patients at risk for ulcer development such that preventive measures may then be targeted to those specific patients. […] The epidemiology, pathogenesis, risk factors, and risk assessment of pressure-induced skin and soft tissue injury will be reviewed here.
- #54 Pressure Ulcer – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK553107/
The prognosis for patients with pressure ulcers varies depending on the anatomic location, stage of injury, and treatment regimen. Most study results compare treatment efficacy by measuring the reduction in the incidence of pressure ulcers in a determined facility as a preventive measurement instead of the healing rate after treatment initiation.
- #55 Bedsores (Pressure Ulcers): Symptoms, Staging & Treatmenthttps://my.clevelandclinic.org/health/diseases/17823-bedsores-pressure-injuries
Bedsores are wounds that occur from prolonged pressure on your skin. People who are immobile for long periods, such as those who are bedridden or use a wheelchair, are most at risk for bedsores. These painful wounds, or pressure ulcers, can grow large and lead to infections. In some instances, bedsores can be life-threatening. […] Bedsores occur when pressure reduces or cuts off blood flow to your skin. This lack of blood flow can cause a pressure wound injury to develop in as little as two hours. Skin cells on your epidermis (your skins outer layer) start to die. As the dead cells break down, a pressure ulcer injury forms. […] Bedsores increase your risk of potentially life-threatening bacterial infections like cellulitis and septicemia. You may develop sepsis or require an amputation. Worldwide, bedsores lead to the deaths of more than 24,000 people each year.
- #56 Decubitus Ulcers: Pathophysiology and Primary Preventionhttps://pmc.ncbi.nlm.nih.gov/articles/PMC2883282/
Pressure sores are a serious complication of multimorbidity and lack of mobility. […] Decubitus ulcers are not always preventable or curable. […] Impaired perfusion, among other factors, increases the risk of decubitus ulcers, and cognitive disturbances can make prophylactic measures more difficult. […] The most important cause of pressure ulcers is pressure exerted for an excessive period of time. […] Immobility is the main risk factor for decubitus ulcers because of their pathophysiology. […] All diseases that restrict independent mobility elevate this risk. […] The critical duration of ischemia that can cause pressure injury varies greatly among individuals; as a rule of thumb, it lies somewhere between 30 and 240 minutes. […] The most important cause of decubitus ulcers is externally applied pressure for an excessive period of time. […] Other physical influences that can damage the skin include friction at the skin surface, shearing forces, and moisture. […] Risk factors promoting the development of decubitus ulcers should be reduced as far as possible.
- #57 Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury – UpToDatehttps://www.uptodate.com/contents/epidemiology-pathogenesis-and-risk-assessment-of-pressure-induced-skin-and-soft-tissue-injury
Pressure-induced skin and soft tissue injuries are lesions caused by unrelieved pressure that results in damage to the underlying tissue. Generally, these are the result of soft tissue compression between a bony prominence and an external surface for a prolonged time, although increasing attention is being paid to medical device-related pressure injury. The consequences of pressure-induced skin and soft tissue injury range from nonblanchable erythema of intact skin to deep ulcers extending to the bone. […] Knowledge of factors contributing to the pathogenesis of pressure-induced skin and soft tissue injury allows the identification of patients at risk for ulcer development such that preventive measures may then be targeted to those specific patients. […] The epidemiology, pathogenesis, risk factors, and risk assessment of pressure-induced skin and soft tissue injury will be reviewed here.
- #58 An overview of co-morbidities and the development of pressure ulcers among older adults | BMC Geriatrics | Full Texthttps://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-018-0997-7
The significance of comorbidity risk factors in the pathogenesis of PU requires further investigation, recognizing the insolvability of PU prevention solely with external relief devices. […] 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. […] Understanding the pathway to immobility, tissue ischemia and undernutrition to develop PU is crucial.