Oparzenia – Patofizjologia i mechanizm

Oparzenia
Patofizjologia i mechanizm

Oparzenia termiczne powodują koagulacyjną martwicę skóry i tkanek podskórnych, której głębokość zależy od temperatury (>44°C), czasu ekspozycji i energii urazu. Patofizjologia oparzeń obejmuje trzy strefy: koagulacji (martwicy), zastoju (stazy) i przekrwienia (hipermii), z których strefa zastoju może przejść w martwicę przy niewystarczającej resuscytacji. Uraz termiczny indukuje silną odpowiedź zapalną z udziałem mediatorów takich jak TNF-α, IL-1, IL-6, prostaglandyny, histamina i bradykinina, prowadząc do zwiększonej przepuszczalności naczyń, obrzęku i hipermetabolizmu. Występuje także wzrost produkcji reaktywnych form tlenu (ROS) i siarkowodoru (wzrost o 1,31-krotnie, P<0,01), co nasila uszkodzenia tkanek i ryzyko zespołu ogólnoustrojowej reakcji zapalnej (SIRS). Oparzenia obejmujące >30% TBSA wywołują wstrząs hipowolemiczny i wielonarządową dysfunkcję, a także długotrwały hipermetabolizm, który utrzymuje się nawet przez kilka lat, powodując katabolizm białek, insulinooporność i zaburzenia endokrynologiczne.

Oparzenia – Patogeneza

Strefy oparzenia według Jacksona
Lokalna reakcja na oparzenie
Mediatory zapalne w oparzeniach

Systemowe skutki oparzeń

Wstrząs oparzeniowy i zmiany w układzie krążenia
Hipermetabolizm i zaburzenia metaboliczne
Zaburzenia immunologiczne
Zespół ogólnoustrojowej reakcji zapalnej
Niewydolność wielonarządowa

Infekcje w oparzeniach
Neuropatofizjologia oparzeń
Powikłania ogólnoustrojowe

Powiązania z innymi narządami
Kolejne rozdziały

Oparzenia – Patogeneza

Oparzenie to złożony rodzaj urazu, który powoduje koagulacyjną martwicę różnych warstw skóry i tkanek podskórnych. Stopień uszkodzenia zależy od temperatury, energii przekazywanej przez czynnik wywołujący uraz oraz czasu ekspozycji ¹². Przy temperaturach przekraczających 44°C (111°F) białka komórkowe tracą swoją trójwymiarową strukturę i zaczynają się rozkładać, co prowadzi do uszkodzenia komórek i tkanek ³. Bezpośredni wpływ ciepła na tkankę powoduje koagulację białek komórkowych, co inicjuje reakcję organizmu wpływającą na krążenie w ranie i okolicznych obszarach ⁴.

Strefy oparzenia według Jacksona

Współczesne rozumienie ran oparzeniowych obejmuje trzy strefy urazu, co pomaga zrozumieć patofizjologię oparzenia ⁵⁶:

Strefa koagulacji (martwicy) – obszar maksymalnego uszkodzenia, gdzie bezpośredni wpływ ciepła spowodował nieodwracalną martwicę tkanek. Naczynia krwionośne zostają zniszczone, co powoduje niedokrwienie obszaru. Z powodu tego białka ulegają denaturacji, a komórki obumierają. Zakres tej strefy zależy głównie od temperatury źródła ciepła i czasu ekspozycji ⁷.
Strefa zastoju (stazy) – obszar otaczający centralną strefę martwicy. W tej strefie występuje zmniejszony przepływ krwi, który może prowadzić do niedokrwienia. Krążenie w skórze i tkance podskórnej jest zaburzone. Strefa ta może przekształcić się w pełną martwicę, jeśli niedokrwienie nie zostanie odwrócone. Jeśli resuscytacja jest niewystarczająca, niedokrwienie się pogłębi, a tym samym zwiększy się głębokość oparzenia ⁸. Transformacja strefy zastoju w strefę koagulacji wiąże się z wieloma czynnikami, w tym z postępującym niedokrwieniem skóry. Badania eksperymentalne wskazują na prostaglandyny, histaminę i bradykininę jako mediatory chemiczne tej postępującej okluzji naczyń ⁹.
Strefa przekrwienia (hipermii) – obszar otaczający strefę zastoju. W tej strefie wytwarzane są mediatory zapalne, takie jak histamina, serotonina, prostaglandyny i bradykinina. Te mediatory wpływają na integralność naczyń, zwiększając ich przepuszczalność, co prowadzi do powstawania obrzęku ¹⁰.

Lokalna reakcja na oparzenie

Gdy dochodzi do oparzenia, białka komórkowe w skórze ulegają denaturacji i koagulacji, a w naczyniach rozwija się zakrzepica ¹¹. Przepuszczalność naczyń zwiększa się, a zdenaturowane cząstki komórkowe zwiększają ciśnienie osmotyczne międzykomórkowe ¹². W następstwie urazu oparzeniowego, poziomy ATP w tkankach stopniowo spadają, a zwiększona ilość AMP jest przekształcana w hipoksantynę, dostarczając substrat dla oksydazy ksantynowej ¹³.

Podczas gojenia ran uwalniane są czynniki prozapalne, takie jak interleukina (IL)-1, IL-6 i czynnik martwicy nowotworów alfa (TNF-alfa), które sprzyjają przewlekłemu zapaleniu i tworzeniu różnych komórek zapalnych w uszkodzonej tkance ¹⁴. Czynnik martwicy nowotworów alfa i prostaglandyna E2 również odgrywają rolę w tworzeniu odpowiedzi zapalnej w procesie gojenia ran ¹⁵. TNF-α jest częściowo odpowiedzialny za indukcję apoptozy różnych elementów komórkowych ¹⁶.

Główną cytokina odpowiedzialną za tworzenie blizn jest wydzielanie transformującego czynnika wzrostu beta (TGF-β), który jest uwalniany z innych komórek zapalnych i miofibroblastów ¹⁷. Urazy termiczne występują w dwóch etapach. Najpierw rozwija się martwica typu koagulacyjnego w naskórku i tkankach ¹⁸.

Mediatory zapalne w oparzeniach

Jądrowy czynnik B (NF-B), białko aktywujące transkrypcję, jest aktywowany natychmiast po ciężkim urazie oparzeniowym (SBI) i uważa się, że reguluje indukcję kilku mediatorów zapalnych, w tym czynnika martwicy nowotworów (TNF-α) ¹⁹. Obrażenia termiczne również powodują przedłużony i głęboki hipermetabolizm, który obejmuje zwiększoną produkcję cytokin prozapalnych, a także tworzenie reaktywnych form tlenu (ROS) ²⁰.

Oparzenie powoduje również znaczący wzrost poziomu siarkowodoru w osoczu o 1,31-krotnie (P .01), co jest istotne ze względu na nowe dane potwierdzające prozapalną rolę siarkowodoru ²¹. Mediatory lipidowe, w tym eikozynoidy i niedawno odkryte wyspecjalizowane mediatory lipidowe proresolucyjne, są kluczowymi cząsteczkami sygnałowymi w rozwiązywaniu zapalenia, odgrywając kluczową rolę w regulowaniu profilu zapalnego i promowaniu powrotu do homeostazy po oparzeniu ²².

Oprócz związanej z oksydazą ksantynową generacji wolnych rodników w urazach oparzeniowych, aktywowane neutrofile adhezyjne wytwarzają dodatkowe wolne rodniki ²³. Jednak po oparzeniu dochodzi do ogromnej produkcji ROS, która jest szkodliwa i jest związana z zapaleniem, zespołem ogólnoustrojowej reakcji zapalnej, immunosupresją, infekcją i posocznicą, uszkodzeniem tkanek oraz niewydolnością wielonarządową ²⁴.

Systemowe skutki oparzeń

Ciężkie oparzenia wywołują odpowiedź, która wpływa na prawie każdy układ narządów ²⁵. Zapalenie, hipermetabolizm, zanik mięśni oraz oporność na insulinę są charakterystycznymi cechami patofizjologicznej odpowiedzi na ciężkie oparzenia, przy czym zmiany w metabolizmie mogą utrzymywać się przez kilka lat po urazie ²⁶.

Wstrząs oparzeniowy i zmiany w układzie krążenia

Oparzenia obejmujące ponad 30% całkowitej powierzchni ciała (TBSA) powodują znaczną hipowolemię w połączeniu z tworzeniem i uwalnianiem mediatorów zapalnych, prowadząc do efektu ogólnoustrojowego, mianowicie charakterystycznej dysfunkcji układu sercowo-naczyniowego znanej jako wstrząs oparzeniowy ²⁷²⁸. Jest to złożony proces upośledzenia krążenia i mikrokrążenia, powodujący obrzęk zarówno w tkankach oparzonych, jak i nieuszkodzonych ²⁹.

Wstrząs oparzeniowy rozwija się po oparzeniach i jest wstrząsem hipowolemicznym, proporcjonalnym do rozległości i ciężkości oparzeń ³⁰. Okres ten charakteryzuje się zwiększoną przepuszczalnością naczyń, przesunięciami płynów prowadzącymi do zmniejszenia objętości wewnątrznaczyniowej i tworzenia obrzęków ³¹. Głównym celem w tej fazie jest przywrócenie i zachowanie perfuzji tkanek, aby uniknąć niedokrwienia spowodowanego wstrząsem hipowolemicznym i komórkowym ³².

Hiperdynamiczna i hipermetaboliczna faza przepływu rozpoczyna się mniej więcej 24 do 72 godzin po urazie ³³. Faza ta charakteryzuje się zmniejszeniem przepuszczalności naczyń, zwiększeniem częstości akcji serca i zmniejszeniem oporu naczyń obwodowych, co prowadzi do zwiększenia pojemności minutowej serca ³⁴.

Jeden z mechanizmów związanej z oparzeniami dysfunkcji serca jest uważany za związany z mitochondriami ³⁵. Coraz więcej dowodów potwierdza rolę mediatorów zapalnych przyczyniających się do uszkodzenia serca po urazie oparzeniowym ³⁶.

Hipermetabolizm i zaburzenia metaboliczne

Ogromne zapotrzebowanie na energię, mierzone spoczynkowym wydatkiem energetycznym, jest typową cechą pacjentów z oparzeniami, przy czym wzrost metabolizmu (hipermetabolizm) zależy od wielkości oparzenia ³⁷³⁸. U podstaw odpowiedzi hipermetabolicznej po urazie termicznym leżą mechanizmy dysregulacji metabolicznej, hormonalnej i zapalnej. Jest to wysoce złożone zjawisko, wywołane utrzymującym się wzrostem wydzielania katecholamin, kortyzolu, glukagonu i dopaminy oraz podwyższonymi stężeniami interleukiny 1 (IL-1), interleukiny 6 (IL-6), czynnika martwicy tkanek (TNF), czynnika aktywującego płytki (PAF), kaskad dopełniacza, a także zwiększoną syntezą reaktywnych form tlenu (ROS) ³⁹⁴⁰.

Hipermetaboliczna odpowiedź organizmu ma szkodliwy wpływ na poziomie komórkowym i ogólnoustrojowym. Na poziomie ogólnoustrojowym dochodzi do zaburzeń struktury i funkcji głównych narządów (serca, wątroby, mięśni szkieletowych, skóry), układu odpornościowego i systemu transportu przez błony ⁴¹⁴². Gojenie ran jest upośledzone, co zwiększa ryzyko infekcji, utrudnia rehabilitację i opóźnia reintegrację pacjentów ze społeczeństwem ⁴³⁴⁴.

Zaburzenia endokrynologiczne, które występują po oparzeniu, zmieniają szlaki metaboliczne. Katecholaminy napędzają hipermetabolizm, podczas gdy wzrost wydzielania kortyzolu, adrenaliny i glukagonu (które są hormonami katabolicznymi), wraz ze wzrostem cytokin prozapalnych, hamuje syntezę białek i tłuszczów ⁴⁵. Badania wykazały, że zaburzenia metabolizmu glukozy mogą być widoczne nawet do trzech lat po urazie termicznym ⁴⁶⁴⁷.

W ciężkich oparzeniach hipermetabolizm i niedobór tlenu w komórkach prowadzą do beztlenowej glikolizy, gdzie glukoza jest przekształcana w kwas mlekowy ⁴⁸⁴⁹. Po urazie termicznym niezwykle ważne jest zapewnienie odpowiedniej podaży składników odżywczych, aby zaspokoić zwiększone wydatki energetyczne, które występują z powodu odpowiedzi hipermetabolicznej. Jednak proces trawienia jest upośledzony proporcjonalnie do wielkości oparzeń ⁵⁰⁵¹.

Uraz termiczny zaburza również funkcję wątroby. Badania wykazały, że uraz termiczny zmienia ekspresję w wątrobie i stężenie w surowicy białek ostrej fazy ⁵².

Zaburzenia immunologiczne

Oparzenie indukuje stan immunosupresji, który predysponuje pacjentów do sepsy i niewydolności wielonarządowej ⁵³. Odpowiedź endokrynna jest jedną z reakcji systemowych obserwowanych u ciężko poparzonych pacjentów i charakteryzuje się znacznymi zmianami funkcjonalnymi w osi podwzgórzowo-przysadkowej. Podczas wczesnej fazy po oparzeniu następuje wyraźny wzrost tzw. hormonów stresu, które obejmują katecholaminy, glukagon i kortyzol ⁵⁴.

W kontekście immunologicznym urazy termiczne mają znaczący wszechstronny wpływ na układ odpornościowy, szczególnie na komórkową odpowiedź immunologiczną ⁵⁵⁵⁶. Uważa się, że niedobór odporności u pacjentów z oparzeniami jest spowodowany upośledzeniem ekspresji receptorów czynnika stymulującego kolonie granulocytów (G-CSF) w szpiku kostnym ⁵⁷⁵⁸.

Podczas gdy utrata skóry i bariery mechanicznej ułatwia infekcję u pacjentów z oparzeniami, od dawna wiadomo, że upośledzone mechanizmy immunologiczne są kluczowymi czynnikami w infekcjach bakteryjnych, wirusowych i grzybiczych po urazie oparzeniowym ⁵⁹. Komórkowa i humoralna odpowiedź immunologiczna jest tłumiona proporcjonalnie do wielkości oparzenia ⁶⁰. Zwiększony katabolizm i wyciek z naczyń włosowatych prowadzą do zmniejszenia krążących IgG, IgA i IgM ⁶¹. Spadek IgG, szczególnie po urazach oparzeniowych, jest ściśle związany z powikłaniami septycznymi ⁶².

Oparzenia nie tylko zmieniają wrodzony immunologiczny charakter skóry, ale także inne elementy układu odpornościowego. Ogólnie, aktywność limfocytów T jest zmniejszona poprzez zwiększenie liczby regulatorowych komórek T i zmniejszenie liczby komórek pomocniczych ⁶³.

Zespół ogólnoustrojowej reakcji zapalnej

Pierwszą fazą jest dominujące zjawisko prozapalne znane jako zespół ogólnoustrojowej reakcji zapalnej ⁶⁴. Ponadto, uraz termiczny zwiększa produkcję tych mediatorów przez makrofagi ⁶⁵. Te wcześniej omówione mediatory zapalne wraz ze wzrostem hydrostatycznego ciśnienia naczyniowego spowodowanym rozszerzeniem naczyń są głównymi przyczynami ogólnoustrojowego wycieku z mikrokrążenia obserwowanego w oparzeniach ⁶⁶.

Gdy oparzenie przekracza 30% TBSA, dochodzi do ogólnoustrojowej reakcji zapalnej ⁶⁷. Występuje również szeroko rozpowszechniona reakcja zapalna w wyniku urazu oparzeniowego z uwolnieniem katecholamin, mediatorów wazoaktywnych i markerów zapalnych, które mogą wywołać zespół ogólnoustrojowej reakcji zapalnej (SIRS) prowadzący do zespołu niewydolności wielonarządowej (MODS) ⁶⁸.

SIRS przyczynia się również do immunosupresji, czyniąc pacjenta bardziej podatnym na infekcje bakteryjne i sepsę. Odpowiedź ogólnoustrojowa pogarsza początkowe uszkodzenie narządów spowodowane wstrząsem i zmniejsza zdolność organizmu do zwalczania infekcji; prowadzi to do zwiększonego ryzyka sepsy, która dalej wywołuje zapalenie, immunoparezę i infekcję ⁶⁹.

Niewydolność wielonarządowa

Zmiany patologiczne występują w układach metabolicznym, sercowo-naczyniowym, nerkowym, żołądkowo-jelitowym i krzepnięcia ⁷⁰. Jeśli obszar oparzenia przekracza 30% całkowitej powierzchni ciała, cytokiny uwolnione z obszaru oparzenia i inne mediatory zapalne osiągają poziomy, które wywołają odpowiedź ogólnoustrojową ⁷¹.

Ostra niewydolność nerek (AKI) związana z urazem termicznym najczęściej występuje w dwóch odrębnych momentach: wcześnie podczas resuscytacji lub późno wtórnie do sepsy ⁷². Patofizjologia późnego AKI różni się od patofizjologii wczesnego AKI i pozostaje poważnym problemem w oddziale intensywnej terapii oparzeń ⁷³.

Pacjenci z ogólnoustrojowymi oparzeniami często mają powiązane urazy inhalacyjne ⁷⁴. Uraz termiczny i przyleganie drażniących substancji do górnych dróg oddechowych prowadzi do uwolnienia mediatorów zapalnych i ROS, zwiększonej przepuszczalności naczyń i tworzenia obrzęków ⁷⁵. W przypadku ciężkich oparzeń może wystąpić niewydolność oddechowa, która zazwyczaj charakteryzuje się hipoksemią z ewolucją do ostrego urazu płuc lub zespołu ostrej niewydolności oddechowej (ARDS) ⁷⁶.

Niedotlenienie komórkowe prowadzi do wzrostu ciśnienia wewnątrzczaszkowego i tworzenia obrzęku mózgu ⁷⁷. Po głębokim urazie oparzeniowym dojdzie do regeneracji nerwów skórnych wraz z migracją nowych włókien nerwowych z łoża rany lub z pączkowania bocznego włókien nerwowych z sąsiedniego nieuszkodzonego obszaru ⁷⁸.

Stresindukowanya odpowiedź na oparzenie prowadzi do wydzielania endogennych katecholamin, które uważane są za główne mediatory hipermetabolizmu po ciężkich oparzeniach ⁷⁹.

Infekcje w oparzeniach

Infekcja pozostaje najczęstszą przyczyną zachorowalności i śmiertelności u pacjentów z oparzeniami ⁸⁰. Skóra zapewnia również podstawową ochronę przed infekcją, działając jako bariera fizyczna. Gdy ta bariera jest uszkodzona, patogeny mogą bezpośrednio infiltrować organizm, powodując infekcję ⁸¹. Oprócz natury i rozległości urazu termicznego wpływającego na infekcje, rodzaj i ilość mikroorganizmów kolonizujących ranę oparzeniową wydają się wpływać na ryzyko inwazyjnej infekcji rany ⁸².

Patogeny infekujące ranę to głównie bakterie gram-dodatnie, takie jak oporny na metycylinę Staphylococcus aureus (MRSA), oraz bakterie gram-ujemne, takie jak Acinetobacter baumannii-calcoaceticus complex, Pseudomonas aeruginosa i gatunki Klebsiella ⁸³.

Jednym z głównych problemów związanych z oparzeniami jest brak unaczynienia strupa, co uniemożliwia dostarczenie komórek odpornościowych i systemowo podawanych antybiotyków do miejsca infekcji ⁸⁴.

Bezpośrednio po oparzeniu termicznym powierzchnia rany oparzeniowej jest wolna od mikroorganizmów. Jednak głębokie struktury skóry, które przetrwały początkowy uraz oparzeniowy (np. gruczoły potowe, mieszki włosowe), często zawierają gronkowce, które kolonizują powierzchnię rany w ciągu kolejnych 48 godzin ⁸⁵. W modelach zwierzęcych oceniono progresję infekcji ran oparzeniowych i zaobserwowano następującą progresję: kolonizacja rany oparzeniowej, inwazja do sąsiadującej tkanki (w ciągu 5 dni), zniszczenie tkanki ziarninowej, zmiany krwiopochodne w narządach wewnętrznych, objawy wstrząsu septycznego i śmierć ⁸⁶.

Wczesne chirurgiczne oczyszczenie i przeszczep skóry, stosowanie miejscowych i ogólnoustrojowych środków przeciwdrobnoustrojowych oraz ulepszone praktyki kontroli zakażeń doprowadziły do zastąpienia paciorkowców beta-hemolizujących przez S. aureus i bakterie gram-ujemne, takie jak P. aeruginosa, Klebsiella pneumoniae i A. baumannii jako główne patogeny w zakażeniach ran oparzeniowych ⁸⁷. W oparzeniach starszych niż 7 dni biofilm może być wykryty w owrzodzonych obszarach ran ⁸⁸. Infekcje grzybicze często rozwijają się później, po podaniu antybiotyków o szerokim spektrum działania lub po opóźnieniu pielęgnacji rany ⁸⁹.

Neuropatofizjologia oparzeń

Po głębokim urazie oparzeniowym dojdzie do regeneracji nerwów skórnych wraz z migracją nowych włókien nerwowych z łoża rany lub z pączkowania bocznego włókien nerwowych z sąsiedniego nieuszkodzonego obszaru ⁹⁰.

Zniszczenie struktur somatosensorycznych w oparzeniu pełnej grubości prowadzi do ryzyka powtarzających się urazów z powodu zmienionej odpowiedzi na bodźce szkodliwe ⁹¹.

**Tabela 1: Patofizjologia oparzeń – główne mediatory i efekty**
Mediator/Czynnik	Funkcja/Efekt	Implikacje kliniczne
Czynnik martwicy nowotworów alfa (TNF-α)	Indukcja apoptozy, aktywacja zapalenia	Uszkodzenie komórek, nasilenie reakcji zapalnej
Interleukina-1 (IL-1)	Prozapalny mediator, aktywuje limfocyty	Nasilenie reakcji zapalnej, gorączka
Interleukina-6 (IL-6)	Prozapalny, indukuje białka ostrej fazy	Systemowa reakcja zapalna, hipermetabolizm
Reaktywne formy tlenu (ROS)	Uszkodzenie oksydacyjne komórek	Uszkodzenie tkanek, SIRS, niewydolność narządów
Katecholaminy	Stymulacja adrenergiczna, zwiększenie metabolizmu	Hipermetabolizm, hiperglikemia, katabolizm białek
Kortyzol	Hormon stresu, katabolizm, immunosupresja	Katabolizm białek, zaburzenia glikemii, osłabienie odporności
Prostaglandyny	Mediator zapalny, wazodilatacja	Rozszerzenie naczyń, ból, gorączka
Bradykinina	Zwiększona przepuszczalność naczyń	Obrzęk, przesięk do przestrzeni pozanaczyniowej
Histamina	Wazodilatacja, zwiększona przepuszczalność naczyń	Obrzęk, rumień
TGF-β	Regulacja proliferacji fibroblastów, synteza kolagenu	Bliznowacenie, zwłóknienie

Powikłania ogólnoustrojowe

Odpowiedź ogólnoustrojowa na oparzenia obejmuje wiele narządów i systemów ⁹². Systemowe zapalenie zwiększa przepuszczalność naczyń włosowatych, umożliwiając przesięk płynu do przestrzeni międzykomórkowej, pogarszając obrzęk obwodowy i nasilając hipotensję z powodu mniejszej objętości pozostającej w naczyniach i układzie krążenia ⁹³.

Szybka utrata płynu może prowadzić do wstrząsu oparzeniowego, opisywanego jako zmniejszona pojemność minutowa serca, zwiększony opór naczyniowy, hipowolemia i hipoperfuzja ⁹⁴. Przedłużona i ciężka reakcja zapalna może również prowadzić do niewydolności wielonarządowej z powodu zespołu ogólnoustrojowej reakcji zapalnej (SIRS), który charakteryzuje się szybką akcją serca, niskim ciśnieniem krwi, niską lub wysoką temperaturą ciała oraz niską lub wysoką liczbą białych krwinek ⁹⁵.

Po urazie oparzeniowym występuje stan hipermetaboliczny, w którym katabolizm wzrasta, a anabolizm maleje, co prowadzi do utraty mięśni i gęstości mineralnej kości ⁹⁶. Gojenie ran może również być dotknięte. Ten stan hipermetaboliczny utrzymuje się pomimo zamknięcia rany ⁹⁷. Rozpad białek trwa 6-9 miesięcy po początkowym oparzeniu, co sprawia, że wsparcie żywieniowe w celu utrzymania beztłuszczowej masy ciała i promowania gojenia ran ma kluczowe znaczenie ⁹⁸. Wzrost kości może być opóźniony do 2 lat po urazie oparzeniowym u dzieci ⁹⁹.

Nadmierna aktywacja dopełniacza prowadzi do przedłużonej odpowiedzi zapalnej ¹⁰⁰. W kontekście ran oparzeniowych, nadmierna aktywacja dopełniacza prowadzi do przedłużonej odpowiedzi zapalnej ¹⁰¹. Przedłużona i silna odpowiedź immunologiczna w dużych oparzeniach powoduje liczne efekty ogólnoustrojowe, uszkadzając naczynia krwionośne, serce, płuca, nerki i inne narządy ¹⁰².

Powiązania z innymi narządami

Choroba oparzeniowa wywołuje natychmiastową reakcję we wszystkich narządach i układach, które nie zawsze są w stanie utrzymać homeostazę i często ulegają uszkodzeniom patofizjologicznym i morfologicznym ¹⁰³. Pacjenci w każdym wieku, którzy doznali urazu oparzeniowego, mają zwiększone ogólne ryzyko rozwoju chorób żołądkowo-jelitowych, które obejmują patologię przełyku, żołądka i jelit, a także zmiany pęcherzyka żółciowego, dróg żółciowych i trzustki ¹⁰⁴.

Po ciężkich oparzeniach niedokrwienie jelit i hipoksja zaburzają barierę nabłonkową jelit i translokację bakterii jelitowych, prowadząc do poważnych powikłań, takich jak zespół ogólnoustrojowej reakcji zapalnej, sepsa i niewydolność wielonarządowa ¹⁰⁵. Ogólnie rzecz biorąc, dysfunkcja żołądkowo-jelitowa była częstsza u pacjentów z urazami inhalacyjnymi, wstrząsem oparzeniowym, dużymi obszarami oparzenia i wysokimi wymaganiami dotyczącymi środków przeciwbólowych ¹⁰⁶.

Pomimo wysokiej zachorowalności i śmiertelności wśród pacjentów z rozległymi oparzeniami skóry w oddziale intensywnej terapii z powodu rozwoju zespołu ostrej niewydolności oddechowej, skuteczne metody leczenia pozostają do ustalenia ¹⁰⁷. Badania wykazały, że oparzenia chemiczne skóry sprzyjają uszkodzeniu płuc z powodu ogólnoustrojowej aktywacji neutrofilów, w szczególności toksyczności zapośredniczonej przez rozwinięcie neutrofilowych pułapek zewnątrzkomórkowych (NETs) ¹⁰⁸.

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Materiały źródłowe

#1 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock. It is a complex process of circulatory and microcirculatory impairment, generating oedema in both burned and unaffected tissues. […] The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn.
#2 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Burns and their treatment are a significant medical problem. The loss of the physical barrier function of the skin opens the door to microbial invasion and can lead to infection. The repair process of the damage caused by the burn is impaired due to the enhanced loss of fluids and minerals through the burn wound, the onset of hypermetabolism with the concomitant disruption of nutrient supply, and derangements in the endocrine system. […] The publication discusses disorders occurring in patients after thermal injury and the methods used at various stages of treatment. […] Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock.
#3 Burn – Wikipedia
https://en.wikipedia.org/wiki/Burn
At temperatures greater than 44 C (111 F), proteins begin losing their three-dimensional shape and start breaking down. This results in cell and tissue damage. Many of the direct health effects of a burn are caused by failure of the skin to perform its normal functions, which include: protection from bacteria, skin sensation, body temperature regulation, and prevention of evaporation of the body’s water. Disruption of these functions can lead to infection, loss of skin sensation, hypothermia, and hypovolemic shock via dehydration (i.e. water in the body evaporated away). […] In large burns (over 30% of the total body surface area), there is a significant inflammatory response. This results in increased leakage of fluid from the capillaries, and subsequent tissue edema. This causes overall blood volume loss, with the remaining blood suffering significant plasma loss, making the blood more concentrated. Poor blood flow to organs like the kidneys and gastrointestinal tract may result in kidney failure and stomach ulcers. […] Increased levels of catecholamines and cortisol can cause a hypermetabolic state that can last for years. This is associated with increased cardiac output, metabolism, a fast heart rate, and poor immune function.
#4 Pathophysiology: What happens in burn injury? – Basics of Burn Carealign-left
https://basicsofburncare.org/pathophysiology/
It is important to understand what happens to the skin and the body after a burn in order to treat the injury properly. […] Burn injuries are complex wounds that most commonly affect the upper extremities (the arms, head and neck) and the trunk. There are two ways to look at the pathophysiology of these burns: […] The direct effect of heat on the tissue causes cellular proteins to coagulate. The body reacts to the burn, and this reaction influences the circulation in the wound and surrounding area. […] The zone of coagulation is the area of maximum damage. In this zone, the direct effect of the heat has resulted in irreversible tissue necrosis. Blood vessels are destroyed, which causes ischemia in the area. Because of this, proteins become denatured and cells die. The extent of this zone mostly depends on the temperature of the heat source and the duration of exposure.
#5 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
As a result of many years of research, the intricate cellular mechanisms of burn injury are slowly becoming clear. […] This review provides a discussion of the cellular mechanisms and pathways involved in burn injury, resultant systemic effects on organ systems, current management and treatment, and potential therapies that we may see implemented in the future. […] These statistics have driven a multitude of studies that have systematically began to uncover the intricate mechanisms involved in burn and the complex pathophysiology of burn injury. […] The current understanding of burn wounds includes three zones of injury: zone of coagulation, zone of stasis, and zone of hyperemia. […] Thermal injury induces an immunosuppressed state that predisposes patients to sepsis and multiple organ failure.
#6 Pathophysiology – RCEMLearning India
https://www.rcemlearning.org/modules/major-trauma-burns/lessons/pathophysiology-36/
Burn injuries result in both local and systemic responses […] Jacksons Burn wound model is made up of 3 zones. This helps us to understand the pathophysiology of a burn injury. […] The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 20-30% of total body surface area. […] Capillary permeability is increased, leading to loss of intravascular proteins and fluid into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased. These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end-organ hypoperfusion. […] Inflammatory mediators cause bronchoconstriction, and in severe burns, adult respiratory distress syndrome can occur.
#7 Pathophysiology: What happens in burn injury? – Basics of Burn Carealign-left
https://basicsofburncare.org/pathophysiology/
It is important to understand what happens to the skin and the body after a burn in order to treat the injury properly. […] Burn injuries are complex wounds that most commonly affect the upper extremities (the arms, head and neck) and the trunk. There are two ways to look at the pathophysiology of these burns: […] The direct effect of heat on the tissue causes cellular proteins to coagulate. The body reacts to the burn, and this reaction influences the circulation in the wound and surrounding area. […] The zone of coagulation is the area of maximum damage. In this zone, the direct effect of the heat has resulted in irreversible tissue necrosis. Blood vessels are destroyed, which causes ischemia in the area. Because of this, proteins become denatured and cells die. The extent of this zone mostly depends on the temperature of the heat source and the duration of exposure.
#8 Pathophysiology: What happens in burn injury? – Basics of Burn Carealign-left
https://basicsofburncare.org/pathophysiology/
The zone of stasis is the area surrounding the central zone of necrosis. In this zone, there is reduced blood flow that may lead to ischemia. The circulation of the skin and subcutaneous tissue is compromised. This zone may progress to full necrosis unless the ischemia is reversed. If resuscitation is inadequate, the ischemia will worsen and therefore the burn depth will increase. […] The zone of hyperemia is the area surrounding the Zone of Stasis. Inflammatory mediators such as histamine, serotonin, prostaglandins and bradykinin are produced in this zone. These mediators affect vascular integrity and thereby make the blood vessels more permeable, leading to edema. […] A burn injury affects these functions, which causes inflammatory mediators to be released and neurons to be stimulated.
#9 Thermal Burns: Overview, Pathophysiology, Quantifying Burn Severity
https://emedicine.medscape.com/article/1278244-overview
The ultimate outcome of a burn injury also is influenced by the depth of epidermal appendages in the burned tissue, which varies according to the age of the patient. Very young and old individuals have superficial appendages, which make both groups more susceptible to full-thickness burn injury. […] Transformation of the zone of stasis to coagulation occurs and has been related to many factors, including progressive dermal ischemia. Experimental studies have implicated prostaglandins, histamine, and bradykinin as the chemical mediators of this progressive vascular occlusion. […] In patients whose burns exceed 30% of TBSA, cytokines and other mediators are released into the systemic circulation, causing a systemic inflammatory response. Because vessels in burned tissue exhibit increased vascular permeability, an extravasation of fluids into the burned tissues occurs.
#10 Pathophysiology: What happens in burn injury? – Basics of Burn Carealign-left
https://basicsofburncare.org/pathophysiology/
The zone of stasis is the area surrounding the central zone of necrosis. In this zone, there is reduced blood flow that may lead to ischemia. The circulation of the skin and subcutaneous tissue is compromised. This zone may progress to full necrosis unless the ischemia is reversed. If resuscitation is inadequate, the ischemia will worsen and therefore the burn depth will increase. […] The zone of hyperemia is the area surrounding the Zone of Stasis. Inflammatory mediators such as histamine, serotonin, prostaglandins and bradykinin are produced in this zone. These mediators affect vascular integrity and thereby make the blood vessels more permeable, leading to edema. […] A burn injury affects these functions, which causes inflammatory mediators to be released and neurons to be stimulated.
#11 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
When burns occur, cell proteins in the skin denature and coagulate and thrombosis develops in the vessels. […] Vascular permeability increases and denatured cell particles increase intercellular osmotic pressure. […] Heat injuries occur in two stages. First, coagulative type necrosis develops in the epidermis and tissues. […] Burn injury causes both local and systemic changes. […] In severe burns, cytokines and other inflammatory mediators are released in excess both in the burn area and in the unburned areas. […] Pathological changes occur in metabolic, cardiovascular, renal, gastrointestinal, and coagulation systems. […] If the burn area exceeds 30% of the total body surface area, cytokines released from the burn area and other inflammatory mediators reach levels that will produce a systemic response.
#12 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
When burns occur, cell proteins in the skin denature and coagulate and thrombosis develops in the vessels. […] Vascular permeability increases and denatured cell particles increase intercellular osmotic pressure. […] Heat injuries occur in two stages. First, coagulative type necrosis develops in the epidermis and tissues. […] Burn injury causes both local and systemic changes. […] In severe burns, cytokines and other inflammatory mediators are released in excess both in the burn area and in the unburned areas. […] Pathological changes occur in metabolic, cardiovascular, renal, gastrointestinal, and coagulation systems. […] If the burn area exceeds 30% of the total body surface area, cytokines released from the burn area and other inflammatory mediators reach levels that will produce a systemic response.
#13 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
TNF- is responsible in part for inducing apoptosis of various cell elements. […] These previously discussed inflammatory mediators along with the increase of vascular hydrostatic pressure caused by vessel dilation are the major reasons for systemic microvascular leakage observed in burns. […] After thermal injury, tissue adenosine triphosphate levels gradually fall, and increased adenosine monophosphate is converted to hypoxanthine, providing substrate for xanthine oxidase. […] In addition to xanthine oxidase-related free radical generation in burn trauma, adherent-activated neutrophils produce additional free radicals. […] However following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage, and multiple organ failure.
#14 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
Burn pathophysiology can be broken into local and systemic response. […] The release of systemic inflammatory mediators and cytokines result in increased capillary permeability and wide scale extravasation of fluid and proteins from the intravascular to the extravascular space. […] During wound healing, proinflammatory factors, such as interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-alpha) are released. This promote chronic inflammation and various inflammatory cells are formed in the affected tissue. […] Tumor necrosis factor-alpha, prostaglandin E2 also play a role in the formation of inflammatory response in wound healing. […] The primary cytokine responsible for scar formation is transforming growth factor-beta (TGF-) secretion which is released from the other inflammatory cells and myofibroblasts.
#15 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
Burn pathophysiology can be broken into local and systemic response. […] The release of systemic inflammatory mediators and cytokines result in increased capillary permeability and wide scale extravasation of fluid and proteins from the intravascular to the extravascular space. […] During wound healing, proinflammatory factors, such as interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-alpha) are released. This promote chronic inflammation and various inflammatory cells are formed in the affected tissue. […] Tumor necrosis factor-alpha, prostaglandin E2 also play a role in the formation of inflammatory response in wound healing. […] The primary cytokine responsible for scar formation is transforming growth factor-beta (TGF-) secretion which is released from the other inflammatory cells and myofibroblasts.
#16 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
TNF- is responsible in part for inducing apoptosis of various cell elements. […] These previously discussed inflammatory mediators along with the increase of vascular hydrostatic pressure caused by vessel dilation are the major reasons for systemic microvascular leakage observed in burns. […] After thermal injury, tissue adenosine triphosphate levels gradually fall, and increased adenosine monophosphate is converted to hypoxanthine, providing substrate for xanthine oxidase. […] In addition to xanthine oxidase-related free radical generation in burn trauma, adherent-activated neutrophils produce additional free radicals. […] However following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage, and multiple organ failure.
#17 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
Burn pathophysiology can be broken into local and systemic response. […] The release of systemic inflammatory mediators and cytokines result in increased capillary permeability and wide scale extravasation of fluid and proteins from the intravascular to the extravascular space. […] During wound healing, proinflammatory factors, such as interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-alpha) are released. This promote chronic inflammation and various inflammatory cells are formed in the affected tissue. […] Tumor necrosis factor-alpha, prostaglandin E2 also play a role in the formation of inflammatory response in wound healing. […] The primary cytokine responsible for scar formation is transforming growth factor-beta (TGF-) secretion which is released from the other inflammatory cells and myofibroblasts.
#18 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
When burns occur, cell proteins in the skin denature and coagulate and thrombosis develops in the vessels. […] Vascular permeability increases and denatured cell particles increase intercellular osmotic pressure. […] Heat injuries occur in two stages. First, coagulative type necrosis develops in the epidermis and tissues. […] Burn injury causes both local and systemic changes. […] In severe burns, cytokines and other inflammatory mediators are released in excess both in the burn area and in the unburned areas. […] Pathological changes occur in metabolic, cardiovascular, renal, gastrointestinal, and coagulation systems. […] If the burn area exceeds 30% of the total body surface area, cytokines released from the burn area and other inflammatory mediators reach levels that will produce a systemic response.
#19 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
In assessing an approach to treat burn wounds, one must attempt to understand the numerous mechanisms behind the resulting microvascular dysfunction. […] Nuclear factor B (NF-B), a transcription activator protein, is activated immediately following severe burn injury (SBI) and is thought to regulate the induction of several inflammatory mediators, including tumor necrosis factor (TNF-). […] The first phase is the predominant proinflammatory phenomena known as systemic inflammatory response syndrome. […] Furthermore, thermal injury increases the production of these mediators by macrophages. […] Thermal injury also results in prolonged and profound hypermetabolism that involves increased production of proinflammatory cytokines, as well as the formation of reactive oxygen species (ROS).
#20 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
In assessing an approach to treat burn wounds, one must attempt to understand the numerous mechanisms behind the resulting microvascular dysfunction. […] Nuclear factor B (NF-B), a transcription activator protein, is activated immediately following severe burn injury (SBI) and is thought to regulate the induction of several inflammatory mediators, including tumor necrosis factor (TNF-). […] The first phase is the predominant proinflammatory phenomena known as systemic inflammatory response syndrome. […] Furthermore, thermal injury increases the production of these mediators by macrophages. […] Thermal injury also results in prolonged and profound hypermetabolism that involves increased production of proinflammatory cytokines, as well as the formation of reactive oxygen species (ROS).
#21 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
Burn injury has recently been shown to result in a significant increase of hydrogen sulfide level (P .01) by 1.31-fold in the plasma. […] This is significant due to new data supporting the proinflammatory role of hydrogen sulfide. […] Lipid mediators, including eicanosoids and recently discovered specialized proresolution lipid mediators, are key signaling molecules in the resolution of inflammation, playing a pivotal role in regulating the inflammatory profile and promoting return to homeostasis following burn. […] Severe burns induce response that affects almost every organ system. […] Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with changes in metabolism known to remain for several years following injury.
#22 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
Burn injury has recently been shown to result in a significant increase of hydrogen sulfide level (P .01) by 1.31-fold in the plasma. […] This is significant due to new data supporting the proinflammatory role of hydrogen sulfide. […] Lipid mediators, including eicanosoids and recently discovered specialized proresolution lipid mediators, are key signaling molecules in the resolution of inflammation, playing a pivotal role in regulating the inflammatory profile and promoting return to homeostasis following burn. […] Severe burns induce response that affects almost every organ system. […] Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with changes in metabolism known to remain for several years following injury.
#23 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
TNF- is responsible in part for inducing apoptosis of various cell elements. […] These previously discussed inflammatory mediators along with the increase of vascular hydrostatic pressure caused by vessel dilation are the major reasons for systemic microvascular leakage observed in burns. […] After thermal injury, tissue adenosine triphosphate levels gradually fall, and increased adenosine monophosphate is converted to hypoxanthine, providing substrate for xanthine oxidase. […] In addition to xanthine oxidase-related free radical generation in burn trauma, adherent-activated neutrophils produce additional free radicals. […] However following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage, and multiple organ failure.
#24 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
TNF- is responsible in part for inducing apoptosis of various cell elements. […] These previously discussed inflammatory mediators along with the increase of vascular hydrostatic pressure caused by vessel dilation are the major reasons for systemic microvascular leakage observed in burns. […] After thermal injury, tissue adenosine triphosphate levels gradually fall, and increased adenosine monophosphate is converted to hypoxanthine, providing substrate for xanthine oxidase. […] In addition to xanthine oxidase-related free radical generation in burn trauma, adherent-activated neutrophils produce additional free radicals. […] However following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage, and multiple organ failure.
#25 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
Burn injury has recently been shown to result in a significant increase of hydrogen sulfide level (P .01) by 1.31-fold in the plasma. […] This is significant due to new data supporting the proinflammatory role of hydrogen sulfide. […] Lipid mediators, including eicanosoids and recently discovered specialized proresolution lipid mediators, are key signaling molecules in the resolution of inflammation, playing a pivotal role in regulating the inflammatory profile and promoting return to homeostasis following burn. […] Severe burns induce response that affects almost every organ system. […] Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with changes in metabolism known to remain for several years following injury.
#26 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
Burn injury has recently been shown to result in a significant increase of hydrogen sulfide level (P .01) by 1.31-fold in the plasma. […] This is significant due to new data supporting the proinflammatory role of hydrogen sulfide. […] Lipid mediators, including eicanosoids and recently discovered specialized proresolution lipid mediators, are key signaling molecules in the resolution of inflammation, playing a pivotal role in regulating the inflammatory profile and promoting return to homeostasis following burn. […] Severe burns induce response that affects almost every organ system. […] Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with changes in metabolism known to remain for several years following injury.
#27 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock. It is a complex process of circulatory and microcirculatory impairment, generating oedema in both burned and unaffected tissues. […] The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn.
#28 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Burns and their treatment are a significant medical problem. The loss of the physical barrier function of the skin opens the door to microbial invasion and can lead to infection. The repair process of the damage caused by the burn is impaired due to the enhanced loss of fluids and minerals through the burn wound, the onset of hypermetabolism with the concomitant disruption of nutrient supply, and derangements in the endocrine system. […] The publication discusses disorders occurring in patients after thermal injury and the methods used at various stages of treatment. […] Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock.
#29 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock. It is a complex process of circulatory and microcirculatory impairment, generating oedema in both burned and unaffected tissues. […] The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn.
#30 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
An inflammatory reaction also occurs as a result of a minor thermal injury lasting for 2060 seconds and at a temperature of 5160C. […] Burn shock developed after burns is hypovolemic shock and is directly proportional to the extent and severity of burns. […] The cellular and humoral immune response is suppressed in direct proportion to the size of the burn. […] Increased catabolism and capillary leakage result in reduced circulating IgG, IgA, and IgM. […] The decrease in IgG, especially after burn injuries, is closely related to septic complications. […] With respect to the grade of the burn, T cell activation is impaired, creating a predisposing condition for viral and fungal infections.
#31 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#32 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#33 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#34 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#35 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#36 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#37 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Burn injuries cause coagulative necrosis of various layers of skin and underlying tissues. Because of its main function as a physiological barrier protecting underlying tissues, the skin usually limits the spread of damage to deeper layers, but the extent of damage is determined by the temperature, the energy transmitted by the causative agent, and the duration of exposure. […] Burns involving more than 30% of total body surface area (TBSA) result in considerable hypovolemia coupled with the formation and release of inflammatory mediators, leading to a subsequent systemic effect, namely a characteristic cardiovascular dysfunction known as burn shock. It is a complex process of circulatory and microcirculatory impairment, generating oedema in both burned and unaffected tissues. […] The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn.
#38 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn. […] Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The bodyâs hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society. […] The endocrine disruption that occurs after a burn alters metabolic pathways. Catecholamines drive hypermetabolism, while an increase in the secretions of cortisol, adrenaline and glucagon (which are catabolic hormones), together with an increase in pro-inflammatory cytokines, inhibits protein and fat synthesis.
#39 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The body’s hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society.
#40 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn. […] Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The bodyâs hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society. […] The endocrine disruption that occurs after a burn alters metabolic pathways. Catecholamines drive hypermetabolism, while an increase in the secretions of cortisol, adrenaline and glucagon (which are catabolic hormones), together with an increase in pro-inflammatory cytokines, inhibits protein and fat synthesis.
#41 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The body’s hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society.
#42 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn. […] Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The bodyâs hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society. […] The endocrine disruption that occurs after a burn alters metabolic pathways. Catecholamines drive hypermetabolism, while an increase in the secretions of cortisol, adrenaline and glucagon (which are catabolic hormones), together with an increase in pro-inflammatory cytokines, inhibits protein and fat synthesis.
#43 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The body’s hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society.
#44 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn. […] Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The bodyâs hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society. […] The endocrine disruption that occurs after a burn alters metabolic pathways. Catecholamines drive hypermetabolism, while an increase in the secretions of cortisol, adrenaline and glucagon (which are catabolic hormones), together with an increase in pro-inflammatory cytokines, inhibits protein and fat synthesis.
#45 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
The enormous energy demand, measured by resting energy expenditure, is a typical finding in burn patients, with the increase in metabolism (hypermetabolism) dependent on the size of burn. […] Underlying the hypermetabolic response following thermal injury are mechanisms of metabolic, hormonal and inflammatory dysregulation. This is a highly complex phenomenon, triggered by persistent increases in the secretion of catecholamine, cortisol, glucagon, and dopamine, and elevated concentrations of interleukin 1 (IL-1), interleukin 6 (IL-6), tissue necrosis factor (TNF), platelet-activating factor (PAF), complement cascades, as well as increased synthesis of reactive oxygen species (ROS). […] The bodyâs hypermetabolic response has detrimental effects at the cellular and systemic level. At the systemic level, the structure and function of major organs (heart, liver, skeletal muscle, skin), the immune system and the transmembrane transport system are compromised. Wound healing is impaired, which increases the risk of infection, hampers rehabilitation and delays the reintegration of patients back into society. […] The endocrine disruption that occurs after a burn alters metabolic pathways. Catecholamines drive hypermetabolism, while an increase in the secretions of cortisol, adrenaline and glucagon (which are catabolic hormones), together with an increase in pro-inflammatory cytokines, inhibits protein and fat synthesis.
#46 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] Thermal trauma also disrupts liver function. Research has shown that thermal injury alters hepatic expression and serum concentrations of acute phase proteins. […] Endocrine response is one of the systemic reactions observed in severely burned patients and is characterised by significant functional alterations in the hypothalamic-pituitary axis. During the early post-burn phase, there is a marked upsurge in so-called stress hormones, which include catecholamine, glucagon, and cortisol.
#47 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#48 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] Thermal trauma also disrupts liver function. Research has shown that thermal injury alters hepatic expression and serum concentrations of acute phase proteins. […] Endocrine response is one of the systemic reactions observed in severely burned patients and is characterised by significant functional alterations in the hypothalamic-pituitary axis. During the early post-burn phase, there is a marked upsurge in so-called stress hormones, which include catecholamine, glucagon, and cortisol.
#49 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#50 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] Thermal trauma also disrupts liver function. Research has shown that thermal injury alters hepatic expression and serum concentrations of acute phase proteins. […] Endocrine response is one of the systemic reactions observed in severely burned patients and is characterised by significant functional alterations in the hypothalamic-pituitary axis. During the early post-burn phase, there is a marked upsurge in so-called stress hormones, which include catecholamine, glucagon, and cortisol.
#51 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#52 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] Thermal trauma also disrupts liver function. Research has shown that thermal injury alters hepatic expression and serum concentrations of acute phase proteins. […] Endocrine response is one of the systemic reactions observed in severely burned patients and is characterised by significant functional alterations in the hypothalamic-pituitary axis. During the early post-burn phase, there is a marked upsurge in so-called stress hormones, which include catecholamine, glucagon, and cortisol.
#53 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
As a result of many years of research, the intricate cellular mechanisms of burn injury are slowly becoming clear. […] This review provides a discussion of the cellular mechanisms and pathways involved in burn injury, resultant systemic effects on organ systems, current management and treatment, and potential therapies that we may see implemented in the future. […] These statistics have driven a multitude of studies that have systematically began to uncover the intricate mechanisms involved in burn and the complex pathophysiology of burn injury. […] The current understanding of burn wounds includes three zones of injury: zone of coagulation, zone of stasis, and zone of hyperemia. […] Thermal injury induces an immunosuppressed state that predisposes patients to sepsis and multiple organ failure.
#54 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] Thermal trauma also disrupts liver function. Research has shown that thermal injury alters hepatic expression and serum concentrations of acute phase proteins. […] Endocrine response is one of the systemic reactions observed in severely burned patients and is characterised by significant functional alterations in the hypothalamic-pituitary axis. During the early post-burn phase, there is a marked upsurge in so-called stress hormones, which include catecholamine, glucagon, and cortisol.
#55 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors.
#56 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#57 Burns: Classification, Pathophysiology, and Treatment: A Review
https://pmc.ncbi.nlm.nih.gov/articles/PMC9959609/
In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors.
#58 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#59 Burns: Classification, Pathophysiology, and Treatment: A Review
https://www.mdpi.com/1422-0067/24/4/3749
Research has shown that impaired glucose metabolism can still be seen up to three years after thermal injury. In severe burns, hypermetabolism and oxygen deprivation in the cells lead to anaerobic glycolysis, where glucose is converted to lactic acid. […] Following thermal injury, it is critically important to provide for an adequate nutrient supply to meet the increased energy expenditure that occurs due to the hypermetabolic response. However, the digestive process is impaired in proportion to the magnitude of the burns. […] In the immunological context, thermal insults have a significant comprehensive impact on the immune system, particularly the cellular immune response. Immune deficiency in burn patients is thought to be caused by impaired expression of bone marrow granulocyte colony-stimulating factor (G-CSF) receptors. While the loss of skin and the mechanical barrier facilitates infection in patients with burn injuries, it has long been known that impaired immune mechanisms are key factors in bacterial, viral and fungal infections following burn injury.
#60 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
An inflammatory reaction also occurs as a result of a minor thermal injury lasting for 2060 seconds and at a temperature of 5160C. […] Burn shock developed after burns is hypovolemic shock and is directly proportional to the extent and severity of burns. […] The cellular and humoral immune response is suppressed in direct proportion to the size of the burn. […] Increased catabolism and capillary leakage result in reduced circulating IgG, IgA, and IgM. […] The decrease in IgG, especially after burn injuries, is closely related to septic complications. […] With respect to the grade of the burn, T cell activation is impaired, creating a predisposing condition for viral and fungal infections.
#61 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
An inflammatory reaction also occurs as a result of a minor thermal injury lasting for 2060 seconds and at a temperature of 5160C. […] Burn shock developed after burns is hypovolemic shock and is directly proportional to the extent and severity of burns. […] The cellular and humoral immune response is suppressed in direct proportion to the size of the burn. […] Increased catabolism and capillary leakage result in reduced circulating IgG, IgA, and IgM. […] The decrease in IgG, especially after burn injuries, is closely related to septic complications. […] With respect to the grade of the burn, T cell activation is impaired, creating a predisposing condition for viral and fungal infections.
#62 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
An inflammatory reaction also occurs as a result of a minor thermal injury lasting for 2060 seconds and at a temperature of 5160C. […] Burn shock developed after burns is hypovolemic shock and is directly proportional to the extent and severity of burns. […] The cellular and humoral immune response is suppressed in direct proportion to the size of the burn. […] Increased catabolism and capillary leakage result in reduced circulating IgG, IgA, and IgM. […] The decrease in IgG, especially after burn injuries, is closely related to septic complications. […] With respect to the grade of the burn, T cell activation is impaired, creating a predisposing condition for viral and fungal infections.
#63 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns not only alter the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of T regulatory cells and a decrease in the number of helper cells. […] One of the primary concerns associated with burn injuries is the avascularity of eschar, preventing immune cells and systemically administered antibiotics from being delivered to the infection site. […] Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. […] In animal models, the progression of burn wound infections has been assessed and the following progression observed: burn wound colonization, invasion into subjacent tissue (within 5 days), destruction of granulation tissue, visceral hematogenous lesions, manifestations of septic shock, and death.
#64 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
In assessing an approach to treat burn wounds, one must attempt to understand the numerous mechanisms behind the resulting microvascular dysfunction. […] Nuclear factor B (NF-B), a transcription activator protein, is activated immediately following severe burn injury (SBI) and is thought to regulate the induction of several inflammatory mediators, including tumor necrosis factor (TNF-). […] The first phase is the predominant proinflammatory phenomena known as systemic inflammatory response syndrome. […] Furthermore, thermal injury increases the production of these mediators by macrophages. […] Thermal injury also results in prolonged and profound hypermetabolism that involves increased production of proinflammatory cytokines, as well as the formation of reactive oxygen species (ROS).
#65 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
In assessing an approach to treat burn wounds, one must attempt to understand the numerous mechanisms behind the resulting microvascular dysfunction. […] Nuclear factor B (NF-B), a transcription activator protein, is activated immediately following severe burn injury (SBI) and is thought to regulate the induction of several inflammatory mediators, including tumor necrosis factor (TNF-). […] The first phase is the predominant proinflammatory phenomena known as systemic inflammatory response syndrome. […] Furthermore, thermal injury increases the production of these mediators by macrophages. […] Thermal injury also results in prolonged and profound hypermetabolism that involves increased production of proinflammatory cytokines, as well as the formation of reactive oxygen species (ROS).
#66 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
TNF- is responsible in part for inducing apoptosis of various cell elements. […] These previously discussed inflammatory mediators along with the increase of vascular hydrostatic pressure caused by vessel dilation are the major reasons for systemic microvascular leakage observed in burns. […] After thermal injury, tissue adenosine triphosphate levels gradually fall, and increased adenosine monophosphate is converted to hypoxanthine, providing substrate for xanthine oxidase. […] In addition to xanthine oxidase-related free radical generation in burn trauma, adherent-activated neutrophils produce additional free radicals. […] However following a burn, there is an enormous production of ROS which is harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression, infection and sepsis, tissue damage, and multiple organ failure.
#67 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#68 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#69 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#70 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
When burns occur, cell proteins in the skin denature and coagulate and thrombosis develops in the vessels. […] Vascular permeability increases and denatured cell particles increase intercellular osmotic pressure. […] Heat injuries occur in two stages. First, coagulative type necrosis develops in the epidermis and tissues. […] Burn injury causes both local and systemic changes. […] In severe burns, cytokines and other inflammatory mediators are released in excess both in the burn area and in the unburned areas. […] Pathological changes occur in metabolic, cardiovascular, renal, gastrointestinal, and coagulation systems. […] If the burn area exceeds 30% of the total body surface area, cytokines released from the burn area and other inflammatory mediators reach levels that will produce a systemic response.
#71 Burn Etiology and Pathogenesis | IntechOpen
https://www.intechopen.com/chapters/57336
When burns occur, cell proteins in the skin denature and coagulate and thrombosis develops in the vessels. […] Vascular permeability increases and denatured cell particles increase intercellular osmotic pressure. […] Heat injuries occur in two stages. First, coagulative type necrosis develops in the epidermis and tissues. […] Burn injury causes both local and systemic changes. […] In severe burns, cytokines and other inflammatory mediators are released in excess both in the burn area and in the unburned areas. […] Pathological changes occur in metabolic, cardiovascular, renal, gastrointestinal, and coagulation systems. […] If the burn area exceeds 30% of the total body surface area, cytokines released from the burn area and other inflammatory mediators reach levels that will produce a systemic response.
#72 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
This period is characterized by increased vascular permeability, fluid shifts resulting in intravascular volume depletion, and edema formation. […] The primary goal during this phase involves restoring and preserving tissue perfusion to avoid ischemia from hypovolemic and cellular shock. […] A hyperdynamic and hypermetabolic flow phase begins roughly 24 to 72 hours after injury. […] This phase is characterized by a decrease in vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in cardiac output. […] One mechanism of burn-related cardiac dysfunction is believed to involve mitochondria. […] Increasing evidence supports the role of inflammatory mediators contributing to cardiac damage following burn injury. […] AKI related to thermal injury is most likely to occur at two distinct time points: early during resuscitation or late secondary to sepsis.
#73 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#74 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#75 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#76 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#77 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#78 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#79 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The burn-induced stress response results in the secretion of endogenous catecholamines, which are thought to be the primary mediators of hyper metabolism after severe burns. […] The ability of MSCs to differentiate into multiple different cell lineages and produce important growth factors and cytokines has stimulated research into their use burn injuries.
#80 Burn wound infection and sepsis – UpToDate
https://www.uptodate.com/contents/burn-wound-infection-and-sepsis
Infection remains the most common cause of morbidity and mortality in burn patients. The diagnosis and management of burn wound infection remains challenging due to the many physiologic features unique to burn injury. A variety of factors increase the risk of developing burn wound infection, and individuals who sustain a severe burn have a particularly high risk for burn wound sepsis. […] Any rapid change in the burn wound appearance or the clinical condition of the burn patient may herald burn wound infection or sepsis. The different categories of burn wound infection are characterized based on clinical features and depth of invasion, which is determined through cultures and histopathology of tissue obtained by burn wound biopsy. A diagnosis of burn wound infection relies on the demonstration of >10^5 bacteria per gram tissue (or recovery of mold or yeast by culture). Specific criteria that include the presence of microbial invasion into adjacent normal tissue, among other criteria, have been suggested by the American Burn Association (ABA) to define burn wound sepsis.
#81 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns are wounds sustained through thermal injury. These injuries could be heat, chemical, electrical, radiation. […] Infection is the most common cause of morbidity and mortality in this population, with almost 61% of deaths being caused by infection. […] The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens can directly infiltrate the body, resulting in infection. […] In addition to the nature and extent of the thermal injury influencing infections, the type and quantity of microorganisms that colonize the burn wound appear to influence the risk of invasive wound infection. […] The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and gram-negative bacteria such as Acinetobacter baumannii-calcoaceticus complex, Pseudomonas aeruginosa, and Klebsiella species.
#82 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns are wounds sustained through thermal injury. These injuries could be heat, chemical, electrical, radiation. […] Infection is the most common cause of morbidity and mortality in this population, with almost 61% of deaths being caused by infection. […] The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens can directly infiltrate the body, resulting in infection. […] In addition to the nature and extent of the thermal injury influencing infections, the type and quantity of microorganisms that colonize the burn wound appear to influence the risk of invasive wound infection. […] The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and gram-negative bacteria such as Acinetobacter baumannii-calcoaceticus complex, Pseudomonas aeruginosa, and Klebsiella species.
#83 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns are wounds sustained through thermal injury. These injuries could be heat, chemical, electrical, radiation. […] Infection is the most common cause of morbidity and mortality in this population, with almost 61% of deaths being caused by infection. […] The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens can directly infiltrate the body, resulting in infection. […] In addition to the nature and extent of the thermal injury influencing infections, the type and quantity of microorganisms that colonize the burn wound appear to influence the risk of invasive wound infection. […] The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and gram-negative bacteria such as Acinetobacter baumannii-calcoaceticus complex, Pseudomonas aeruginosa, and Klebsiella species.
#84 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns not only alter the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of T regulatory cells and a decrease in the number of helper cells. […] One of the primary concerns associated with burn injuries is the avascularity of eschar, preventing immune cells and systemically administered antibiotics from being delivered to the infection site. […] Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. […] In animal models, the progression of burn wound infections has been assessed and the following progression observed: burn wound colonization, invasion into subjacent tissue (within 5 days), destruction of granulation tissue, visceral hematogenous lesions, manifestations of septic shock, and death.
#85 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns not only alter the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of T regulatory cells and a decrease in the number of helper cells. […] One of the primary concerns associated with burn injuries is the avascularity of eschar, preventing immune cells and systemically administered antibiotics from being delivered to the infection site. […] Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. […] In animal models, the progression of burn wound infections has been assessed and the following progression observed: burn wound colonization, invasion into subjacent tissue (within 5 days), destruction of granulation tissue, visceral hematogenous lesions, manifestations of septic shock, and death.
#86 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Burns not only alter the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of T regulatory cells and a decrease in the number of helper cells. […] One of the primary concerns associated with burn injuries is the avascularity of eschar, preventing immune cells and systemically administered antibiotics from being delivered to the infection site. […] Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. […] In animal models, the progression of burn wound infections has been assessed and the following progression observed: burn wound colonization, invasion into subjacent tissue (within 5 days), destruction of granulation tissue, visceral hematogenous lesions, manifestations of septic shock, and death.
#87 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Early surgical debridement and skin grafting, use of topical and systemic antimicrobials, and enhanced infection-control practices have led to the replacement of beta-hemolytic streptococci with S aureus and gram-negative bacteria such as P aeruginosa, Klebsiella pneumoniae, and A baumannii as major pathogens in burn wound infections. […] In burns older than 7 days, biofilm may be detected in the ulcerated areas of the wounds. […] Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed.
#88 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Early surgical debridement and skin grafting, use of topical and systemic antimicrobials, and enhanced infection-control practices have led to the replacement of beta-hemolytic streptococci with S aureus and gram-negative bacteria such as P aeruginosa, Klebsiella pneumoniae, and A baumannii as major pathogens in burn wound infections. […] In burns older than 7 days, biofilm may be detected in the ulcerated areas of the wounds. […] Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed.
#89 Burn Wound Infections: Background, Pathophysiology, Epidemiology
https://emedicine.medscape.com/article/213595-overview
Early surgical debridement and skin grafting, use of topical and systemic antimicrobials, and enhanced infection-control practices have led to the replacement of beta-hemolytic streptococci with S aureus and gram-negative bacteria such as P aeruginosa, Klebsiella pneumoniae, and A baumannii as major pathogens in burn wound infections. […] In burns older than 7 days, biofilm may be detected in the ulcerated areas of the wounds. […] Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed.
#90 Burns: Pathophysiology of Systemic Complications and Current Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC5214064/
The pathophysiology of late AKI is altered from that of early AKI, and remains a serious problem within the burn intensive care unit. […] Patients with systemic burn injuries often have associated smoke inhalation injury. […] Thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and ROS, increased vascular permeability, and edema formation. […] With severe burns, respiratory failure can occur and is generally characterized by hypoxemia with evolution to acute lung Injury or acute respiratory distress syndrome (ARDS). […] Cellular hypoxia leads to an increase in intracranial pressure and cerebral edema formation. […] After a deep burn injury, cutaneous nerve regeneration will occur with the migration of new nerve fibers from the wound bed or from the collateral sprouting of nerve fibers from adjacent uninjured area.
#91 Burns â Full Thickness â Pathogenesis and Clinical Findings | Calgary Guide
https://calgaryguide.ucalgary.ca/full-thickness-burns-pathogenesis-and-clinical-findings/burns-full-thickness-pathogenesis-and-clinical-findings-2023-2/
Full Thickness Burns: Pathogenesis and clinical findings Radiation Sunlight, x-ray, nuclear Emission/explosion can cause damage to keratinocytes […] Transfer of heat energy causes direct injury to keratinocytes […] Hypoxic injury (lack of oxygen) causes ischemia-related cell death leading to necrosis […] Non-uniform damage to the epidermal, dermal subcutaneous layers at varying widths depths due to unpredictable injury pattern […] Ulceration covered by eschar: a thick, dried, black (necrotic) layer […] Long-term risk of ulcers infections […] Vascular permeability in subcutaneous layers […] Edema Compression of surrounding muscles, nerves vessels Ischemia and/or necrosis […] Immunologic response due to impaired epidermal barrier function […] Microbial growth creating biofilm secretion of chemicals that inhibit natural protective process […] Risk of infection septic shock […] Destruction of somatosensory structures […] Risk of repeated injury due to response to noxious stimuli […] Destruction of cutaneous capillary beds […] Chronic wounds require surgical interventions […] Risk of contractures skin barrier weakness.
#92 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
Burns are diverse and complex injuries that not only have local effects but also serious systemic consequences through severe and prolonged inflammatory response. […] A prolonged and strong immune response makes major burns even worse by causing multiple systemic effects including damage to the heart, lungs, blood vessels, kidneys, and other organs. […] However, when it comes to severe burn injuries, the immune response is prolonged and strong, making the injury even worse by causing multiple systemic effects, and damaging several organs such as the heart, lungs, blood vessels, and kidneys. […] The purpose of this review is to describe the immune and cell responses to burn injury. […] The impact of burns may spread beyond the areas of direct injury. Indeed, severe burns, regardless of origin, trigger a systemic inflammatory response.
#93 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
Systemic inflammation increases the permeability of capillaries, allowing extravasation of fluid into the interstitium, worsening peripheral edema, and exacerbating hypotension due to less volume remaining within vessels and the circulatory system. […] The rapid loss of fluid may lead to burn shock, described as decreased cardiac output, increased vascular resistance, hypovolemia, and hypo-perfusion. […] A prolonged and severe inflammatory reaction can also lead to multiple organ failure due to systemic inflammatory response syndrome (SIRS) that is marked by fast heart rate, low blood pressure, low or high body temperature, and low or high white blood cell count. […] The innate immune system and its cells are the bodyâs first line of defense against invading pathogens following burn injury.
#94 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
Systemic inflammation increases the permeability of capillaries, allowing extravasation of fluid into the interstitium, worsening peripheral edema, and exacerbating hypotension due to less volume remaining within vessels and the circulatory system. […] The rapid loss of fluid may lead to burn shock, described as decreased cardiac output, increased vascular resistance, hypovolemia, and hypo-perfusion. […] A prolonged and severe inflammatory reaction can also lead to multiple organ failure due to systemic inflammatory response syndrome (SIRS) that is marked by fast heart rate, low blood pressure, low or high body temperature, and low or high white blood cell count. […] The innate immune system and its cells are the bodyâs first line of defense against invading pathogens following burn injury.
#95 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
Systemic inflammation increases the permeability of capillaries, allowing extravasation of fluid into the interstitium, worsening peripheral edema, and exacerbating hypotension due to less volume remaining within vessels and the circulatory system. […] The rapid loss of fluid may lead to burn shock, described as decreased cardiac output, increased vascular resistance, hypovolemia, and hypo-perfusion. […] A prolonged and severe inflammatory reaction can also lead to multiple organ failure due to systemic inflammatory response syndrome (SIRS) that is marked by fast heart rate, low blood pressure, low or high body temperature, and low or high white blood cell count. […] The innate immune system and its cells are the bodyâs first line of defense against invading pathogens following burn injury.
#96 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#97 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#98 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#99 Burns
https://www.rch.org.au/trauma-service/manual/Burns/
Once TBSA 30% a systemic inflammatory response will occur. […] A widespread inflammatory response also occurs as the result of a burn injury with release of catecholamines, vasoactive mediators and inflammatory markers which can trigger a systemic inflammatory response syndrome (SIRS) resulting in multiple organ dysfunction syndrome (MODS). […] SIRS also contributes to immunosuppression rendering a patient more susceptible to bacterial infection and sepsis. The systemic response worsens initial organ damage caused by shock and reduces the body’s ability to fight infection; this leads to an increased risk of sepsis which further triggers inflammation, immunoparesis and infection. […] Following a burn injury, a hypermetabolic state ensues where catabolism increases and anabolism decreases resulting in loss of muscle and bone mineral density. Wound healing may also be affected. This hypermetabolic state is sustained despite wound closure. Protein breakdown continues 6-9 months after the initial burn making nutritional support to sustain lean body mass and promote wound healing of crucial import. Bone growth can be delayed for 2 years after a burn injury in children.
#100 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
The cells of the innate immune system include neutrophils, monocytes and macrophages, natural killer cells, dendritic cells, and mast cells, which are collectively responsible for the acute inflammatory response to thermal injuries. […] Excessive complement activation results in a prolonged inflammatory response. […] In the context of burn wounds, excessive complement activation results in a prolonged inflammatory response. […] The prolonged and strong immune response in major burns causes multiple systemic effects, damaging blood vessels, the heart, lungs, kidneys, and other organs.
#101 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
The cells of the innate immune system include neutrophils, monocytes and macrophages, natural killer cells, dendritic cells, and mast cells, which are collectively responsible for the acute inflammatory response to thermal injuries. […] Excessive complement activation results in a prolonged inflammatory response. […] In the context of burn wounds, excessive complement activation results in a prolonged inflammatory response. […] The prolonged and strong immune response in major burns causes multiple systemic effects, damaging blood vessels, the heart, lungs, kidneys, and other organs.
#102 The Immune and Regenerative Response to Burn Injury
https://www.mdpi.com/2073-4409/11/19/3073
The cells of the innate immune system include neutrophils, monocytes and macrophages, natural killer cells, dendritic cells, and mast cells, which are collectively responsible for the acute inflammatory response to thermal injuries. […] Excessive complement activation results in a prolonged inflammatory response. […] In the context of burn wounds, excessive complement activation results in a prolonged inflammatory response. […] The prolonged and strong immune response in major burns causes multiple systemic effects, damaging blood vessels, the heart, lungs, kidneys, and other organs.
#103
http://generalsurgery.com.ua/article/view/308119
Burn disease produces an immediate reaction in all organs and systems, which are not always able to maintain homeostasis and frequently suffer pathophysiological and morphological damage. […] Patients of all ages who have experienced a burn injury have an increased overall risk of developing gastrointestinal diseases, which include pathology of the esophagus, stomach, and intestines, as well as lesions of the gallbladder, biliary tract, and pancreas. […] After severe burns, intestinal ischemia and hypoxia disrupt the intestinal epithelial barrier and enteric bacterial translocation, leading to serious complications such as systemic inflammatory response syndrome, sepsis, and multiple organ failure. […] In general, gastrointestinal dysfunction was more common in patients with inhalation injuries, burn shock, large burn areas, and high analgesic requirements.
#104
http://generalsurgery.com.ua/article/view/308119
Burn disease produces an immediate reaction in all organs and systems, which are not always able to maintain homeostasis and frequently suffer pathophysiological and morphological damage. […] Patients of all ages who have experienced a burn injury have an increased overall risk of developing gastrointestinal diseases, which include pathology of the esophagus, stomach, and intestines, as well as lesions of the gallbladder, biliary tract, and pancreas. […] After severe burns, intestinal ischemia and hypoxia disrupt the intestinal epithelial barrier and enteric bacterial translocation, leading to serious complications such as systemic inflammatory response syndrome, sepsis, and multiple organ failure. […] In general, gastrointestinal dysfunction was more common in patients with inhalation injuries, burn shock, large burn areas, and high analgesic requirements.
#105
http://generalsurgery.com.ua/article/view/308119
Burn disease produces an immediate reaction in all organs and systems, which are not always able to maintain homeostasis and frequently suffer pathophysiological and morphological damage. […] Patients of all ages who have experienced a burn injury have an increased overall risk of developing gastrointestinal diseases, which include pathology of the esophagus, stomach, and intestines, as well as lesions of the gallbladder, biliary tract, and pancreas. […] After severe burns, intestinal ischemia and hypoxia disrupt the intestinal epithelial barrier and enteric bacterial translocation, leading to serious complications such as systemic inflammatory response syndrome, sepsis, and multiple organ failure. […] In general, gastrointestinal dysfunction was more common in patients with inhalation injuries, burn shock, large burn areas, and high analgesic requirements.
#106
http://generalsurgery.com.ua/article/view/308119
Burn disease produces an immediate reaction in all organs and systems, which are not always able to maintain homeostasis and frequently suffer pathophysiological and morphological damage. […] Patients of all ages who have experienced a burn injury have an increased overall risk of developing gastrointestinal diseases, which include pathology of the esophagus, stomach, and intestines, as well as lesions of the gallbladder, biliary tract, and pancreas. […] After severe burns, intestinal ischemia and hypoxia disrupt the intestinal epithelial barrier and enteric bacterial translocation, leading to serious complications such as systemic inflammatory response syndrome, sepsis, and multiple organ failure. […] In general, gastrointestinal dysfunction was more common in patients with inhalation injuries, burn shock, large burn areas, and high analgesic requirements.
#107
https://insight.jci.org/articles/view/147564/figure/1
Despite the high morbidity and mortality among patients with extensive cutaneous burns in the intensive care unit due to the development of acute respiratory distress syndrome, effective therapeutics remain to be determined. […] We test the hypothesis that cutaneous chemical burns promote lung injury due to systemic activation of neutrophils, in particular, toxicity mediated by the deployment of neutrophil extracellular traps (NETs). […] Our data demonstrated that phenylarsine oxide (PAO) treatment of neutrophils caused increased intracellular Ca2+-associated PAD4 activity. A dermal chemical burn by lewisite or PAO resulted in PAD4 activation, NETosis, and ALI. […] NETs disrupted the barrier function of endothelial cells in human lung microvascular endothelial cell spheroids. […] Pharmacologic or genetic abrogation of PAD4 inhibited lung injury following cutaneous chemical burns. […] Cutaneous burns by lewisite and PAO caused ALI by PAD4-mediated NETosis. PAD4 inhibitors may have potential as countermeasures to suppress detrimental lung injury after chemical burns.
#108
https://insight.jci.org/articles/view/147564/figure/1
Despite the high morbidity and mortality among patients with extensive cutaneous burns in the intensive care unit due to the development of acute respiratory distress syndrome, effective therapeutics remain to be determined. […] We test the hypothesis that cutaneous chemical burns promote lung injury due to systemic activation of neutrophils, in particular, toxicity mediated by the deployment of neutrophil extracellular traps (NETs). […] Our data demonstrated that phenylarsine oxide (PAO) treatment of neutrophils caused increased intracellular Ca2+-associated PAD4 activity. A dermal chemical burn by lewisite or PAO resulted in PAD4 activation, NETosis, and ALI. […] NETs disrupted the barrier function of endothelial cells in human lung microvascular endothelial cell spheroids. […] Pharmacologic or genetic abrogation of PAD4 inhibited lung injury following cutaneous chemical burns. […] Cutaneous burns by lewisite and PAO caused ALI by PAD4-mediated NETosis. PAD4 inhibitors may have potential as countermeasures to suppress detrimental lung injury after chemical burns.