Niedokrwienie jelit
Patofizjologia i mechanizm

Niedokrwienie jelitowe definiuje się jako ograniczenie przepływu krwi przez główne naczynia krezkowe o co najmniej 75% przez ponad 12 godzin, co prowadzi do niedotlenienia i uszkodzenia komórek jelita. Patofizjologia obejmuje mechanizmy takie jak zator tętniczy (50% przypadków ostrego niedokrwienia krezkowego, często pochodzenia sercowego), zakrzepicę tętniczą (15-25%), zakrzepicę żylną (5-15%) oraz niedokrwienie bez niedrożności naczyń (NOMI, 20-30%). Uszkodzenie jelita rozwija się etapowo: od złuszczania kosmków jelitowych po pełnościenną martwicę i perforację, co może prowadzić do zapalenia otrzewnej, sepsy i niewydolności wielonarządowej. Reperfuzja niedokrwionego jelita nasila uszkodzenia poprzez generację reaktywnych form tlenu (ROS) i aktywację neutrofilów, co potęguje stres oksydacyjny i stan zapalny. Na poziomie komórkowym obserwuje się różne formy śmierci komórkowej, w tym apoptozę, piroptozę, ferroptozę oraz martwicę, które przyczyniają się do dysfunkcji bariery jelitowej i rozwoju zespołu niewydolności wielonarządowej.

Patogeneza niedokrwienia jelit

Niedokrwienie jelit, określane również jako niedokrwienie jelitowe, występuje, gdy przepływ krwi przez duże naczynia krwionośne dostarczające krew do i z jelit zostaje ograniczony lub całkowicie ustaje. Niedokrwienie jelitowe rozwija się, gdy dochodzi do redukcji przepływu krwi jelitowej o co najmniej 75% przez okres dłuższy niż 12 godzin. W takim przypadku niewystarczający przepływ krwi nie może zaspokoić metabolicznych potrzeb tkanki jelitowej, prowadząc do niedotlenienia i uszkodzenia komórek.123

Jelita są głównie zaopatrywane przez dwie duże tętnice: tętnicę krezkową górną (SMA) oraz tętnicę krezkową dolną (IMA). Uszkodzenie ściany jelita zależy od nasilenia i czasu trwania zaburzeń perfuzji. Uszkodzenie błony śluzowej jelita może wystąpić już po 20 minutach niedokrwienia, podczas gdy zawał pełnościenny i zgorzel pojawiają się po 8-16 godzinach niedokrwienia.12

Mechanizmy powstawania niedokrwienia jelit

Niedokrwienie jelitowe może być spowodowane różnymi mechanizmami, które ograniczają przepływ krwi do jelit. Wyróżnia się cztery główne mechanizmy:12

  • Zator pochodzący z innego miejsca, który zatyka tętnicę (najczęściej tętnicę krezkową górną)
  • Powstanie nowego zakrzepu w tętnicy (najczęściej na podłożu miażdżycy)
  • Powstanie zakrzepu w żyle krezkowej górnej
  • Niewystarczający przepływ krwi spowodowany niskim ciśnieniem krwi lub skurczem tętnic

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Ostre niedokrwienie krezkowe najczęściej spowodowane jest zatorem w głównej tętnicy krezkowej, podczas gdy przewlekłe niedokrwienie krezkowe zazwyczaj wynika z miażdżycy. Zator wtórny do migotania przedsionków, zawału mięśnia sercowego lub choroby zastawkowej odpowiada za około 50% przypadków ostrego niedokrwienia krezkowego.12

Patofizjologia uszkodzenia niedokrwiennego

Patofizjologia niedokrwienia jelit jest złożona i wieloczynnikowa. Ostra niewydolność naczyniowa jelit prowadzi do aktywacji układu renina-angiotensyna, stymulacji współczulnej, skurczu naczyń, a w konsekwencji do hipoksji. Utrzymywanie się niedokrwienia może prowadzić do zawału pełnościennego, nieodwracalnego uszkodzenia i martwicy, perforacji jelita oraz uwolnienia bakterii i toksyn do krążenia systemowego.12

Uszkodzenie niedokrwienne rozpoczyna się od małych naczyń w pobliżu powierzchni kosmków jelitowych. Początkowo dochodzi do złuszczania się kosmków i infiltracji neutrofilowej. Wywołany przez zapalenie obrzęk może utrudniać drenaż żylny i dalej nasilać niedokrwienie. Początkowo oszczędzone są krypty jelitowe, ale ulegają uszkodzeniu wraz z postępem niedokrwienia. Końcowym rezultatem jest martwica jelita, plamiste krwawienia śluzówkowe i naciek neutrofilowy jako odpowiedź na zapalenie.12

W miarę postępu niedokrwienia, uszkodzenie przesuwa się od błony śluzowej do wszystkich warstw poniżej (pełnościennie), co prowadzi do przerwania ciągłości nabłonka. Umożliwia to bakteriom znajdującym się w świetle jelita przedostanie się do jamy otrzewnej, powodując zapalenie otrzewnej. Jeśli bakterie przedostaną się do krwiobiegu, może dojść do rozwoju zespołu ogólnoustrojowej reakcji zapalnej, który ostatecznie prowadzi do sepsy i wstrząsu septycznego.12

Rodzaje niedokrwienia jelitowego

Niedokrwienie jelitowe można podzielić na kilka kategorii w zależności od czasu trwania, lokalizacji i przyczyny. Wyróżnia się dwa główne typy: niedokrwienie jelit cienkich (zwane niedokrwieniem krezkowym) oraz niedokrwienie jelita grubego (zwane niedokrwieniem okrężnicy).12

Ostre niedokrwienie krezkowe

Ostre niedokrwienie krezkowe jest nagłym zmniejszeniem przepływu krwi do jelita cienkiego. Może być spowodowane:12

  • Zatorem tętniczym (50% przypadków) – najczęściej pochodzenia sercowego, głównie z powodu migotania przedsionków, niewydolności serca, zawału mięśnia sercowego, kardiomiopatii lub tętniaka komory
  • Zakrzepicą tętniczą (15-25% przypadków) – zwykle na podłożu istniejącej wcześniej miażdżycy
  • Zakrzepicą żylną (5-15% przypadków) – gdy krew nie może opuścić jelita cienkiego z powodu zakrzepu w żyle odprowadzającej krew z jelit
  • Niedokrwieniem bez niedrożności naczyń (NOMI, 20-30% przypadków) – spowodowanym skurczem naczyń krezkowych w przebiegu wstrząsu, hipoksemii obwodowej lub uszkodzenia reperfuzyjnego

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W rzadkich przypadkach leki obkurczające naczynia (np. kokaina i noradrenalina) oraz ergotaminy mogą powodować NOMI. Te substancje wywołują skurcz naczyń i zmniejszony przepływ krwi w krezce, co może prowadzić do niedokrwienia jelita.12

Przewlekłe niedokrwienie krezkowe

Przewlekłe niedokrwienie krezkowe występuje wtórnie do uogólnionej choroby miażdżycowej (95% przypadków) i objawia się jako dławica jelitowa z poposiłkowym bólem brzucha, niechęcią do jedzenia i utratą masy ciała. W przewlekłym niedokrwieniu krezkowym zwykle występuje zwężenie lub niedrożność co najmniej dwóch z trzech głównych naczyń trzewnych.123

Powstawanie zakrzepu dodatkowo do zwężenia może prowadzić do ostrego na przewlekłe niedokrwienie krezkowe, które przechodzi w ostre niedokrwienie krezkowe.123

Niedokrwienie okrężnicy

Niedokrwienie okrężnicy (jelita grubego) zazwyczaj występuje w okrężnicy i jest spowodowane hipoperfuzją naczyń jelitowych, co może wystąpić w przypadkach hipowolemii, wstrząsu septycznego i wstrząsu kardiogennego.12

Dwa główne obszary okrężnicy, w tym zgięcie śledzionowe (punkt Griffithsa) i połączenie odbytniczo-esicze (punkt Sudka), są szczególnie podatne na niedokrwienie. Są to tzw. obszary „watershed”, czyli rejony w okrężnicy między dwiema głównymi tętnicami zaopatrującymi okrężnicę. Obszary te są szczególnie narażone na niedokrwienie ze względu na ograniczony przepływ krwi kolateralnej.12

Mechanizm uszkodzenia niedokrwienno-reperfuzyjnego

Uszkodzenie jelita występuje zarówno z powodu niskiej perfuzji, jak i reperfuzji tkanek jelitowych. Niska perfuzja może spowodować uszkodzenie jelita, gdy ciśnienie perfuzji krezkowej spada o około 30 mmHg lub dochodzi do redukcji o 45 mmHg w średnim ciśnieniu tętniczym krezkowym.12

Uszkodzenie niedokrwienne

Fizjologicznie, jelito może skompensować około 75% redukcję przepływu krwi w naczyniach krezkowych przez 12 godzin bez znaczącego uszkodzenia dzięki rozszerzeniu krążenia obocznego i zwiększonemu wydobyciu tlenu. Jednak po przedłużeniu niskiej perfuzji lub hipoksemii, postępujący skurcz naczyń prowadzi do zmniejszenia przepływu obocznego, a następnie do pełnościennej martwicy ściany jelita i perforacji.123

Uszkodzenie niedokrwienne jelita przebiega etapowo:12

  • Stadium I (wczesne) – charakteryzuje się obrzękiem i krwawieniem do błony śluzowej
  • Stadium II (pośrednie) – występują specyficzne zmiany patologiczne (obrzęk, erozja, krwotok i martwica) w błonie podśluzowej i mięśniowej właściwej
  • Stadium III (późne) – pełnościenna martwica jelita, rozwijająca się gdy przepływ krwi nie zostaje przywrócony

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Uszkodzenie reperfuzyjne

Uszkodzenie reperfuzyjne po niedokrwieniu może być obserwowane z powodu uwolnienia toksycznych produktów ubocznych uszkodzenia niedokrwiennego, wolnych rodników tlenowych i aktywacji neutrofilów.12

Reperfuzja niedokrwionego jelita wiąże się z bardziej nasilonym uszkodzeniem, które zostało powiązane z wytwarzaniem reaktywnych form tlenu pochodzących z enzymu oksydazy ksantynowej. Gromadzenie się tych reaktywnych form w momencie reperfuzji, w połączeniu z inaktywacją tlenku azotu, tworzy fenotyp zapalny w naczyniach i błonie śluzowej.1

Wynikająca z tego rekrutacja leukocytów i płytek krwi oraz aktywacja rezydujących komórek zapalnych, które normalnie znajdują się w przestrzeni okołonaczyniowej (komórki tuczne, makrofagi), prowadzą do dalszego stresu oksydacyjnego i bardziej intensywnego stanu zapalnego, ostatecznie skutkując niewydolnością naczyń włosowatych i błony śluzowej oraz dysfunkcją narządów.12

Warto zauważyć, że niedokrwienie jelit połączone z uszkodzeniem reperfuzyjnym może prowadzić do przerwania bariery śluzówkowej, a następnie inwazji bakteryjnej, wstrząsu septycznego i niewydolności wielonarządowej, co może spowodować śmierć bez martwicy pełnościennej.1

Szczegółowe mechanizmy komórkowe

Rola reaktywnych form tlenu

W czasie niedokrwienia jelita, niedotlenienie prowadzi do wyczerpania ATP i zmiany metabolizmu komórkowego. Podczas reperfuzji, nagły napływ tlenu prowadzi do produkcji dużych ilości reaktywnych form tlenu (ROS), które mogą uszkodzić błony komórkowe, białka i DNA.12

Potężnym źródłem rodników tlenowych w niedokrwionej, reperfundowanej tkance jest enzym oksydaza ksantynowa (XO), enzym ograniczający szybkość degradacji kwasów nukleinowych. Neutrofile są kolejnym źródłem reaktywnych metabolitów tlenowych.1

Jony nadtlenkowe reagują z tlenkiem azotu (NO), tworząc nadtlenoazotyn, który następnie powoduje nasiloną peroksydację lipidów, modyfikacje białkowe i DNA, prowadząc do uszkodzenia komórek.1

Mechanizmy śmierci komórkowej

Niedokrwienie jelitowe i reperfuzja mogą inicjować różne mechanizmy śmierci komórkowej, w tym apoptozę, autofagię, piroptozę, ferroptyzę i martwicę. Mechanizmy leżące u podstaw śmierci komórek związanej z uszkodzeniem niedokrwienno-reperfuzyjnym jelita można podzielić na programowane i nieprogramowane formy.1

  • Śmierć komórkowa programowana obejmuje apoptozę, autofagię, piroptozę i ferroptyzę
  • Śmierć komórkowa nieprogramowana odnosi się głównie do martwicy

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U osób z niedokrwieniem jelit, dotknięte komórki doświadczają niewystarczającego dopływu tlenu i składników odżywczych, co prowadzi do zakłóceń metabolizmu energetycznego i niestabilnego środowiska wewnątrzkomórkowego. Te zmiany sprzyjają programowanej śmierci komórkowej.1

Podczas reperfuzji po niedokrwieniu, stymulacja i uszkodzenie jelita zwiększają się, głównie ze względu na nagromadzenie metabolitów wytworzonych podczas niedokrwienia i uwolnienie wolnych rodników tlenowych. W takich warunkach, jelito ulega nieprogramowanej śmierci komórkowej.1

Aktywacja wielu szlaków sygnałowych prowadzi do inicjacji różnych mechanizmów śmierci komórkowej. Uszkodzenie niedokrwienno-reperfuzyjne jelita indukuje apoptozę i martwicę w komórkach nabłonka jelitowego, co skutkuje upośledzeniem funkcji bariery jelitowej i ostatecznie prowadzi do zespołu niewydolności wielonarządowej.12

Rola zapalenia

Odpowiedź zapalna napędza wystąpienie apoptozy i martwicy. Wystąpienie piroptosis w uszkodzeniu niedokrwienno-reperfuzyjnym jelita zostało potwierdzone przez wyniki histopatologiczne i wskaźniki bariery jelitowej, w tym opór elektryczny nabłonka (TER), białka połączeń ścisłych i biomarkery surowicze.1

Główne czynniki przyczyniające się do ferroptozy w uszkodzeniu niedokrwienno-reperfuzyjnym jelita obejmują stres oksydacyjny, uwalnianie jonów żelaza, peroksydację lipidów i zależność od żelaza.1

Uważa się, że autofagia może być indukowana podczas uszkodzenia niedokrwienno-reperfuzyjnego jelita w celu eliminacji uszkodzonych składników komórkowych i utrzymania żywotności komórek. Jednak stwierdzono, że przepływ autofagii jest upośledzony podczas całego procesu uszkodzenia niedokrwienno-reperfuzyjnego jelita.1

Odkrycia z powyższych badań wskazują, że składanie i aktywacja inflammasomu NLRP3 silnie wpływają na inicjację piroptosis, niezależnie od zmian w genach docelowych lub szlakach regulujących ten proces.1

Czynniki wpływające na rozwój niedokrwienia jelit

Układ regulacyjny przepływu krwi jelitowej

Czynniki regulujące przepływ krwi w jelitach odgrywają kluczową rolę w rozwoju niedokrwienia krezkowego. Krążenie trzewne zmienia się w zależności od stanu karmienia lub głodzenia. Pomimo wysokiego unaczynienia jelitowego, ekstrakcja tlenu z tętnic jelitowych jest niska.12

Układ współczulny, głównie poprzez receptory α-adrenergiczne, ma podstawowe znaczenie w utrzymaniu spoczynkowego napięcia tętniczek trzewnych. Inne substancje wazoaktywne, w tym angiotensyna II, wazopresyna i prostaglandyny, również zostały wskazane w patogenezie uszkodzenia niedokrwiennego.1

W odpowiedzi na obniżenie ciśnienia systemowego, dochodzi do aktywacji układu renina-angiotensyna, stymulacji współczulnej i skurczu naczyń krezkowych. Mechanizm ten może być reakcją obronną, mającą na celu przekierowanie zmniejszonego przepływu krwi do bardziej istotnych narządów, takich jak mózg i serce.12

Czynniki ryzyka i choroby współistniejące

Niedokrwienie krezkowe występuje, gdy przepływ krwi jelitowej jest upośledzony o ponad 50% pierwotnego przepływu krwi bez aktywacji odpowiedzi adaptacyjnych. Może to prowadzić do przerwania bariery śluzówkowej, umożliwiając uwolnienie toksyn bakteryjnych (obecnych w świetle jelita) i mediatorów wazoaktywnych, które ostatecznie prowadzą do całkowitej martwicy (śmierci komórkowej) błony śluzowej jelita.1

Czynniki ryzyka rozwoju niedokrwienia krezkowego różnią się w zależności od etiologii, ale obejmują każdy proces, który powoduje hipoperfuzję krezkową lub zwiększa prawdopodobieństwo zatoru jelitowego, zakrzepicy lub skurczu naczyń.1

Częstość występowania niedokrwienia krezkowego rośnie wykładniczo z wiekiem. U pacjentów w wieku 75 lat lub starszych, niedokrwienie krezkowe jest częstszą przyczyną ostrego brzucha niż zapalenie wyrostka robaczkowego. Częstość występowania niedokrwienia krezkowego u 80-latka jest około dziesięciokrotnie wyższa niż u 60-letniego pacjenta.1

Niedokrwienie krezkowe opisano również u pacjentów z chorobą koronawirusową (COVID-19), prawdopodobnie związane z dużymi zdarzeniami zakrzepowo-zatorowymi, jak również z zakrzepicą małych naczyń związaną z nadkrzepliwością i zatrzymaniem fibrynolizy.12

Konsekwencje niedokrwienia jelit

Konsekwencje niedokrwienia jelit mogą być poważne i potencjalnie zagrażające życiu. Mniejszy przepływ krwi oznacza, że do komórek w układzie trawiennym dociera zbyt mało tlenu. Niedokrwienie jelit jest poważnym stanem, który może powodować ból i utrudniać prawidłowe funkcjonowanie jelit.1

Konsekwencje lokalne

W ciężkich przypadkach, utrata przepływu krwi do jelit może spowodować trwałe uszkodzenie jelit. Bez wystarczającego przepływu krwi, dotknięte narządy i tkanki nie mają wystarczającej ilości tlenu i nie mogą funkcjonować prawidłowo. Jeśli blokada jest wystarczająco poważna, dotknięte narządy i tkanki mogą zacząć obumierać.12

Niedokrwienie przerywa barierę śluzówkową, umożliwiając uwolnienie bakterii, toksyn i mediatorów wazoaktywnych, co z kolei prowadzi do depresji mięśnia sercowego, zespołu ogólnoustrojowej odpowiedzi zapalnej, niewydolności wielonarządowej i śmierci. Uwolnienie mediatorów może wystąpić nawet przed kompletnym zawałem.1

Konsekwencje systemowe

Niedokrwienie i reperfuzja niedokrwionego jelita mogą prowadzić do znaczącego uszkodzenia tkanek, które objawia się dysfunkcją naczyniową i niewydolnością bariery śluzówkowej. Odpowiedź na uszkodzenie wynikająca z samego niedokrwienia może być przypisana hipoksji i zmianom komórkowym wywołanym przez ten stan.1

Niedokrwienie jelit może prowadzić do powikłań, takich jak:1

  • Perforacja: W ścianie jelita może utworzyć się otwór, powodując wyciek zawartości jelita do jamy brzusznej
  • Martwica: Tkanka jelitowa może obumrzeć z powodu braku tlenu
  • Sepsa: Bakterie z jelita mogą przedostać się do krwiobiegu, powodując potencjalnie śmiertelną infekcję
  • Niewydolność wielonarządowa: W zaawansowanych przypadkach, niedokrwienie jelit może prowadzić do niewydolności innych narządów

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Niewydolność wielonarządowa jest częstym powikłaniem po niedokrwieniu i reperfuzji jelita i dotyczy narządów takich jak wątroba, serce, nerki i płuca.1

Biomarkery niedokrwienia jelit

Mimo intensywnych badań w tej dziedzinie, wczesne, czułe i swoiste biomarkery ostrego niedokrwienia jelit nie zostały dotychczas zidentyfikowane. Oto przegląd tradycyjnych i potencjalnie użytecznych biomarkerów:12

Tradycyjne biomarkery

D-mleczan jest normalnie produkowany w bardzo niskich stężeniach u ludzi. Zmiana integralności błony śluzowej spowodowana niedokrwieniem jelita może być uzasadnioną przyczyną zwiększonego stężenia D-mleczanu we krwi. Chociaż D-mleczan wydaje się działać lepiej niż L-mleczan ze względu na jego wyłącznie jelitowe źródło, wyniki uzyskane w różnych badaniach są przeważnie niespójne.12

Dodatkowe biomarkery zapalne, takie jak białko C-reaktywne (CRP) lub interleukina-6 (IL-6), zostały zbadane w diagnostyce niedokrwienia jelita.1

Obiecujące biomarkery

IMA (albumina modyfikowana niedokrwieniem) jest markerem biologicznym, który można łatwo i niedrogo zmierzyć w laboratoriach klinicznych. Pierwsze wstępne badanie u pacjentów z niedokrwieniem jelita zostało opublikowane w 2008 roku i wykazało, że wartości IMA były znacząco wyższe u siedmiu pacjentów z ostrym niedokrwieniem krezkowym w porównaniu do siedmiu zdrowych osób. Szczególną cechą kinetyki IMA jest wczesny wzrost równolegle z początkiem niedokrwienia, a następnie dalszy wzrost wartości przez kolejne godziny.12

-GST jest kolejnym biomarkerem stresu oksydacyjnego potencjalnie przydatnym w diagnostyce niedokrwienia jelita. Prokalcytonina (PCT) może być postrzegana jako cenna pomoc w diagnostyce lub monitorowaniu niedokrwienia jelita. D-dimer wykazał dobrą wydajność diagnostyczną w przypadku niedrożności zakrzepowo-zatorowej tętnicy krezkowej górnej, ale jego skuteczność diagnostyczna wydaje się ogólnie mniej zadowalająca w niewysiłkowym ostrym niedokrwieniu jelita.1

Cytrulina jest niebiałkowym aminokwasem syntetyzowanym z glutaminy przez enterocyty jelita cienkiego i jest prekursorem do syntezy de novo argininy. Stopniowo zmniejszająca się perfuzja jelitowa i utrata integralności błony komórkowej enterocytów przyczyniają się do szybkiego uwalniania I-FABP (jelitowego białka wiążącego kwasy tłuszczowe) do krążenia i dalszej eliminacji przez nerki.12

Podsumowanie patogenezy niedokrwienia jelit

Niedokrwienie jelit jest złożonym procesem patofizjologicznym, który może prowadzić do poważnych konsekwencji zdrowotnych, włącznie ze śmiercią. Niedokrwienie jelitowe występuje, gdy przepływ krwi przez główne naczynia krezkowe zostaje ograniczony o co najmniej 75% przez ponad 12 godzin, co prowadzi do niewystarczającego dostarczania tlenu i składników odżywczych do komórek jelita.12

Główne mechanizmy leżące u podstaw niedokrwienia jelit obejmują zatorowość, zakrzepicę, niedokrwienie bez niedrożności naczyń oraz zakrzepicę żylną. Początkowe uszkodzenie niedokrwienne może być następnie nasilone przez uszkodzenie reperfuzyjne, gdy przepływ krwi zostaje przywrócony.12

Na poziomie komórkowym, niedokrwienie jelitowe prowadzi do produkcji reaktywnych form tlenu, aktywacji procesów zapalnych i uruchomienia różnych mechanizmów śmierci komórkowej, w tym apoptozy, autofagii, piroptosis, ferroptozy i martwicy.12

Konsekwencje niedokrwienia jelit mogą być poważne, od lokalnego uszkodzenia ściany jelita, przez przerwanie bariery śluzówkowej i uwolnienie bakterii i toksyn do krążenia systemowego, po rozwój sepsy i niewydolności wielonarządowej.12

Wczesne rozpoznanie i interwencja są kluczowe dla poprawy rokowania pacjentów z niedokrwieniem jelit. Mimo postępów w diagnostyce i leczeniu, niedokrwienie jelit pozostaje stanem o wysokiej śmiertelności, sięgającej 50-80% w przypadkach ostrego niedokrwienia krezkowego.12

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

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

  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    Bowel ischemia can classify as small intestine ischemia, which is commonly known as mesenteric ischemia and large intestine ischemia, which generally referred to as colonic ischemia. Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. […] The intestine is mainly supplied by 2 major arteries, which include the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA). […] Two main areas in the colon, including splenic flexure (Griffiths point) and rectosigmoid junction (Sudek’s point), are prone to ischemia. These are also known as the 'watershed’ areas, which mean the regions in the colon between 2 major arteries that supplying colon. […] An acute decrease in mesenteric arterial blood flow accounts for 60% to 70% of patients with mesenteric ischemia.
  • #1 Intestinal ischemia – Wikipedia
    https://en.wikipedia.org/wiki/Intestinal_ischemia
    Intestinal ischemia is a medical condition in which injury to the large or small intestine occurs due to not enough blood supply. […] There are four mechanisms by which poor blood flow occurs: a blood clot from elsewhere getting lodged in an artery, a new blood clot forming in an artery, a blood clot forming in the superior mesenteric vein, and insufficient blood flow due to low blood pressure or spasms of arteries. […] Treatment of acute ischemia may include stenting or medications to break down the clot provided at the site of obstruction by interventional radiology. […] Surgical revascularisation remains the treatment of choice for intestinal ischaemia related to an occlusion of the vessels supplying the bowel, but thrombolytic medical treatment and vascular interventional radiological techniques have a growing role. […] The prognosis depends on prompt diagnosis (less than 12-24 hours and before gangrene) and the underlying cause.
  • #1
    https://step1.medbullets.com/gastrointestinal/109050/mesenteric-ischemia
    can be due to a variety of processes […] acute mesenteric ischemia is most commonly caused by an embolism in the main mesenteric artery […] chronic mesenteric ischemia is most commonly caused by atherosclerosis […] embolism secondary to atrial fibrillation, myocardial infarction, or valvular disease […] thrombosis secondary to artherosclerosis […] splanchnic vasoconstriction […] hypoperfusion due to hypotension […] venous thrombosis.
  • #1 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/20750
    Acute intestinal ischemia is a relative rare abdominal emergency, associated with considerably high morbidity and mortality rates. […] The pathophysiology is complex and multifaceted. The intestinal acute vascular insufficiency leads to renin-angiotensin activation, sympathic stimulation, vasospasm and consequently hypoxia. […] The persistence of ischemia may then lead to an evolvement of transmural infarction towards irreversible injury and necrosis, intestinal perforation and release of bacteria and toxins into the systemic circulation. […] Despite ample research in this field, early, sensitive and specific biomarkers of acute intestinal ischemia have not been identified so far. […] The aim of this narrative review is hence to provide an overview on traditional laboratory biomarkers of acute intestinal ischemia and summarize current evidence regarding some emerging and potentially useful biomarkers.
  • #1 Intestinal Ischemia & Angiodysplasia – Free Sketchy Medical Lesson
    https://www.sketchy.com/medical-lessons/intestinal-ischemia-angiodysplasia
    Ischemia initially affects the small vessels near the luminal surface of the villi in the bowel, leading to their sloughing. This triggers edema in the bowel wall, which increases pressure and obstructs venous drainage, exacerbating the ischemia. Initially, the crypts of the bowel are spared, but become involved as ischemia progresses. The end result is intestinal necrosis, patchy mucosal hemorrhage, and a neutrophilic infiltrate as a response to inflammation.
  • #1 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    Immune cells remove dead and damaged cells releasing cytokines such as TNF-alpha. […] Blood vessels become more permeable leading to edema of the small intestine. […] As the ischemia progresses from mucosa to all the layers beneath (transmural), it leads to breaks in the epithelial lining. […] This allows bacteria in the intestinal lumen to enter into the peritoneal cavity causing peritonitis. […] If bacteria enter into the blood stream, it results in systemic inflammatory response syndrome, which ultimately results in sepsis and septic shock.
  • #1 Intestinal ischemia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/intestinal-ischemia/symptoms-causes/syc-20373946
    Intestinal ischemia often is split into groups. Colon ischemia, also called ischemic colitis, affects the large intestine. Other types of ischemia affect the small intestine. These are acute mesenteric ischemia, chronic mesenteric ischemia and ischemia due to mesenteric venous thrombosis. […] Acute mesenteric ischemia is the result of a sudden loss of blood flow to the small intestine. It may be due to: A blood clot, also called an embolus, that comes loose in the heart and travels through the blood to block an artery. It most often blocks the superior mesenteric artery, which sends oxygen-rich blood to the intestines. […] Chronic mesenteric ischemia is due to the buildup of fatty deposits on an artery wall, called atherosclerosis. The disease process most often is slow. It’s also called intestinal angina because it’s due to less blood flow to the intestines after eating.
  • #1 Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery | World Journal of Emergency Surgery | Full Text
    https://wjes.biomedcentral.com/articles/10.1186/s13017-022-00443-x
    NOMI occurs in approximately 20% of cases, and is usually a consequence of SMA vasoconstriction associated with low splanchnic blood flow. The compromised SMA blood flow also affects the proximal colon due to involvement of the ileocolic artery. Patients with NOMI typically suffer from severe coexisting illness, commonly cardiac failure which may be precipitated by sepsis. […] Mesenteric venous thrombosis (MVT) accounts for less than 10% of cases of mesenteric infarction. Thrombosis is attributed to a combination of Virchow’s triad; stagnant blood flow, hypercoagulability, and endothelial damage. An inflammatory process around the superior mesenteric vein (SMV) due to acute pancreatitis or inflammatory bowel disease may cause thrombosis. […] The prevalence of AMI has changed in recent decades. The prevalence of acute mesenteric occlusion among patients with an acute abdomen may vary from 17.7% in emergency laparotomy and 31.0% in laparotomy for elderly non-trauma patients. Mesenteric arterial embolism decreased to 25% of cases. Mesenteric arterial thrombosis was the second most common cause of mesenteric ischemia, which historically accounted for 20-35% and recently increased to 40%. NOMI accounts for 25% of cases, which is also increasing, compared to the historical cohort, because of increased number of critically ill patients and overall improvement of intensive care.
  • #1 Acute Mesenteric Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431068/
    An acute mesenteric arterial embolism is often cardiogenic in origin and primarily affects the superior mesenteric artery (SMA). Preceding events include atrial tachyarrhythmia, congestive heart failure, myocardial ischemia or infarction, cardiomyopathy, and ventricular aneurysm, which results in thrombus formation that later embolizes to cause ischemia. […] Patients with acute mesenteric arterial thrombosis commonly have a pre-existing atherosclerotic disease. Vasospasm in the SMA often accompanies NOMI secondary to cardiac failure, peripheral hypoxemia, or reperfusion injury. […] In rare instances, vasopressors (e.g., cocaine and norepinephrine) and ergotamines may cause NOMI. These agents cause vasoconstriction and reduced blood flow in the mesentery, which may result in ischemia of the bowel.
  • #1 Intestinal Ischemia & Angiodysplasia – Free Sketchy Medical Lesson
    https://www.sketchy.com/medical-lessons/intestinal-ischemia-angiodysplasia
    Non-occlusive acute mesenteric ischemia usually occurs in the colon and is caused by hypoperfusion of intestinal vessels, which can occur in cases of hypovolemia, septic shock, and cardiogenic shock. […] Chronic mesenteric ischemia occurs secondary to generalized atherosclerotic disease and manifests as intestinal angina with postprandial abdominal pain, aversion to eating, and weight loss. […] Intestinal ischemia occurs due to inadequate perfusion of the bowel due to occlusive and non-occlusive etiologies. The primary occlusive cause is acute mesenteric artery occlusion, most commonly seen in the superior mesenteric artery (SMA) and often from an embolus or a thrombus formed from ruptured atherosclerotic plaques. Non-occlusive acute mesenteric ischemia occurs due to hypoperfusion of intestinal vessels.
  • #1 Intestinal ischemia – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/intestinal-ischemia/
    Sudden interruption of blood flow to small bowel; intestinal hypoxia hemorrhagic infarction and necrosis disruption of the mucosal barrier and perforation release of bacteria, toxins, and vasoactive substances life-threatening sepsis. […] Thrombus formation in addition to stenosis can lead to acute-on-chronic mesenteric ischemia, which leads to AMI.
  • #1 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. […] Generally, mesenteric ischemia (MI) can be divided based on the timing of onset into acute and chronic. […] Collateral circulation of the gastrointestinal tract can compensate for a 75% acute reduction in mesenteric perfusion for up to 12 hours without significant injury. […] The splanchnic circulation varies based on the feeding or fasting state. Despite high intestinal vasculature, oxygen extraction is low from the intestinal arteries. […] Intestinal ischemia happens when inadequate oxygen delivered to the intestine. However, intestinal injury occurs by low perfusion and reperfusion of intestinal tissues. […] Low perfusion can cause intestinal injury when mesenteric perfusion pressure decreases about 30 mmHg or reduction of 45 mmHg in mean mesenteric arterial pressure.
  • #1 Many faces of acute bowel ischemia: overview of radiologic staging | Insights into Imaging | Full Text
    https://insightsimaging.springeropen.com/articles/10.1186/s13244-021-00985-9
    Acute bowel ischemia (ABI) can be life threatening with high mortality rate. […] ABI is potentially reversible with prompt diagnosis. […] While ABI has been traditionally categorized based on the etiology with a wide spectrum of imaging findings overlapped with each other, the final decision for patients management is usually made on the stage of the ABI with respect to the underlying pathophysiology. […] Understanding the pathologic basis of ABI can help to estimate the probability of reversibility and choose the optimal treatment option. […] ABI is categorized into 3 stages based on the involvement of each layer. […] The early stage of ischemia is typically followed by the release of certain mediators (cytokines, platelet-activating factor and tumor necrosis factor), which leads to an inflammatory response, resulting in further damage of the intestinal wall.
  • #1 Many faces of acute bowel ischemia: overview of radiologic staging | Insights into Imaging | Full Text
    https://insightsimaging.springeropen.com/articles/10.1186/s13244-021-00985-9
    Stage II or the intermediate stage is described as presence of specific pathologic changes (edema, erosion, hemorrhage and necrosis) in submucosa and muscularis propria. […] Stage III, the late stage, is manifested by transmural bowel necrosis and is developed if blood supply is not eventually restored. […] It should be noted that bowel ischemia accompanied by reperfusion injury may lead to the disruption of mucosal barrier followed by bacterial invasion, septic shock and multiorgan failure, which may cause death without transmural necrosis. […] Understanding the pathophysiology of ABI can help for better management. […] Management should be based on the latest stage identified. […] The main goal of management is to achieve a prompt diagnosis, specify the best treatment option and reduce mortality in these patients.
  • #1 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    However, after a prolongation of low perfusion or hypoxemia, progressive vasoconstriction leads to reducing collateral flow and subsequently full-thickness necrosis of the intestinal wall and perforation. […] Reperfusion injury after ischemia can be observed due to the release of toxic byproducts of ischemic injury, free oxygen radicals, and neutrophil activation.
  • #1 Intestinal Ischemia and Reperfusion: Consequences and Mechanisms | SpringerLink
    https://link.springer.com/10.1007/978-3-642-37078-6_240
    Ischemia and reperfusion of the ischemic intestine can result in significant tissue injury that is manifested as vascular dysfunction and mucosal barrier failure. […] The injury response to ischemia per se can be attributed to hypoxia and the cellular alterations brought about by this condition. […] Reperfusion of the ischemic intestine is accompanied by a more profound injury response that has been linked to the generation of reactive oxygen species that are derived from the enzyme xanthine oxidase. […] The accumulation of these reactive species at the time of reperfusion, coupled with the inactivation of nitric oxide, creates an inflammatory phenotype within the vasculature and mucosal membrane. […] The resulting recruitment of leukocytes and platelets and the activation of resident inflammatory cells that normally reside in the perivascular space (mast cells, macrophages) lead to further oxidative stress and a more intense inflammatory condition, ultimately resulting in capillary and mucosal membrane failure and organ dysfunction.
  • #1 Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-01891-x
    The main factors contributing to ferroptosis in intestinal I/R injury include oxidative stress, the release of iron ions, lipid peroxidation, and iron dependence. […] Intestinal I/R injury induces oxidative stress, characterized by the excessive accumulation of reactive oxygen species generated intracellularly. […] Autophagy may be induced during intestinal I/R to eliminate impaired cellular constituents and maintain cell viability. […] Autophagy flux was found to be impaired throughout the intestinal I/R procedure. […] The findings of the above-mentioned studies indicated that the assembly and activation of the NLRP3 inflammasome strongly influence the initiation of pyroptosis, irrespective of alterations in the target genes or pathways governing pyroptosis.
  • #1 Intestinal Ischemia | Abdominal Key
    https://abdominalkey.com/intestinal-ischemia/
    The sympathetic nervous system, mainly via -adrenergic receptors, is of primary importance in maintaining resting splanchnic arteriolar tone; other vasoactive substances, including angiotensin II, vasopressin, and prostaglandins, also have been implicated in the pathogenesis of ischemic injury. […] Ischemic damage results both from hypoxia during the period of ischemia and reperfusion injury when blood flow is re-established. […] A potent source of oxygen radicals in ischemic, reperfused tissue is the enzyme xanthine oxidase (XO), the rate-limiting enzyme in nucleic acid degradation. […] Neutrophils are another source of reactive oxygen metabolites. […] The cornerstones of our approach, therefore, are the earlier and more liberal use of angiography and the incorporation of intra-arterial papaverine in the treatment of both occlusive AMI and NOMI. […] Diagnosis before intestinal infarction occurs is the most important factor in improving survival of patients with AMI.
  • #1 SciELO Brazil – Pathophysiology of mesenteric ischemia/reperfusion: a review Pathophysiology of mesenteric ischemia/reperfusion: a review
    https://www.scielo.br/j/acb/a/nsvfz8j9KBgNvs5GKQ7CznN/
    The superoxide ions react with nitric oxide (NO) to produce peroxynitrite, which then causes accentuated lipid peroxidation, proteic and DNA modifications resulting in cellular damage. […] The activation of the complement system can lead to the translocation of NF-kB and an increase in the transcription of iNOS. […] The activation of neutrophils was also complement-dependent during intestinal I/R. […] The depletion or inhibition of the complement could diminish many of the mediators of I/R injury. […] The accumulation of platelets in the postischemic microvasculature could contribute significantly to the manifestation of I/R lesions. […] Serotonin together with other bioactive substances could perform an important function in the pathogenesis of intestinal I/R. […] It has been demonstrated recently that pancreatic proteases are involved in the production of inflammatory mediators after intestinal I/R.
  • #1 Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-01891-x
    Intestinal ischemia-reperfusion (I/R) is a multifaceted pathological process, and there is a lack of clear treatment for intestinal I/R injury. During intestinal I/R, oxidative stress and inflammation triggered by cells can trigger a variety of cell death mechanisms, including apoptosis, autophagy, pyroptosis, ferroptosis, and necrosis. […] The mechanisms underlying cell death related to intestinal I/R injury can be categorized primarily into programmed and non-programmed forms. Programmed cell death includes apoptosis, autophagy, pyroptosis, and ferroptosis, whereas non-programmed cell death primarily refers to necrosis. […] In individuals with intestinal ischemia, affected cells experience inadequate oxygen and nutrient supplies, leading to energy metabolism disturbances and an unstable intracellular milieu. These changes promote programmed cell death.
  • #1 Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-01891-x
    During post-ischemic reperfusion, stimulation and damage to the intestine increase, primarily due to the buildup of metabolites generated during ischemia and the release of oxygen free radicals. Under such conditions, the gut undergoes non-programmed cell death. […] The activation of multiple signaling pathways leads to the initiation of various mechanisms of cell death. […] Intestinal I/R injury induces apoptosis and necrosis in the intestinal epithelial cells, which results in impaired intestinal barrier function and ultimately leads to multiple organ dysfunction syndrome. […] The inflammatory response drives the occurrence of apoptosis and necrosis. […] The occurrence of pyroptosis in intestinal I/R injury was confirmed by histopathological findings and intestinal barrier indices, including transepithelial electrical resistance (TER), tight-junction protein, and serum biomarkers.
  • #1 Ischemic Colitis: Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/24513-ischemic-colitis
    Ischemic colitis is inflammation in your colon thats caused by ischemia, which means reduced blood flow. Blood supplies oxygen to the tissues in your body. If something interrupts or diminishes the blood supply to certain tissues, they suffer damage from the lack of oxygen. Inflammation is your bodys response to this injury. It causes discomfort, swelling and bleeding, but it means your tissues are trying to repair themselves. Ischemic colitis mainly affects the inner lining of your colon (mucosa), usually in one section of it. But ischemia thats more severe or lasts longer may do deeper damage to your colon. […] Reduced blood flow in the arteries that supply blood to your colon causes inflammation in the tissues as a secondary effect. […] The arteries that supply your colon your superior and inferior mesenteric arteries are extra sensitive to anything that causes your blood vessels to constrict (vasoconstriction). This includes physical triggers like colds, medical conditions that cause low blood pressure and certain drugs (vasoconstrictors). These arteries respond to low blood pressure by constricting vigorously. Scientists believe this may be a survival mechanism designed to direct reduced blood flow to your more vital organs, like your brain and heart. As a result, your colon may be deprived of blood flow while this stress response is activated.
  • #1 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. […] Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. […] Intestinal mucosal damage occurs in response to ischemic insult. […] In response to providing protection from ischemia, mesenteric vessels undergo intrinsic autoregulation, which is an adaptive response to ischemia. […] In order to compensate for the ischemia, there is vasoconstriction of mesenteric vessels resulting in increased tissue oxygen extraction along with vasodilation of the collateral vessels. Owing to this mechanism, intestine is able to compensate for around 75% reduction in blood flow.
  • #1 Delayed Diagnosis of Mesenteric Ischemia | PSNet
    https://psnet.ahrq.gov/web-mm/delayed-diagnosis-mesenteric-ischemia
    The frequency of these major causes of mesenteric ischemia among all patients is estimated as: 50% mesenteric arterial embolism, 15-25% mesenteric arterial thrombosis, 5% mesenteric venous thrombosis, and 20-30% nonocclusive mesenteric ischemia. […] Risk factors for developing mesenteric ischemia vary by etiology but include any process that results in mesenteric hypoperfusion or increases the likelihood of intestinal embolism, thrombosis, or vasoconstriction. […] Given the potential for devastating outcomes when not diagnosed in a timely fashion, as in the presented case, mesenteric ischemia is an important diagnosis to consider in all patients with severe abdominal pain. […] Symptoms of weight loss and dietary changes in the setting of atherosclerosis should increase suspicion for chronic mesenteric ischemia until proven otherwise.
  • #1 Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery | World Journal of Emergency Surgery | Full Text
    https://wjes.biomedcentral.com/articles/10.1186/s13017-022-00443-x
    The incidence of AMI increases exponentially with age. In patients aged 75 years or older, AMI is a more prevalent cause of acute abdomen than appendicitis. The incidence of AMI in an 80-year-old is roughly tenfold that of a 60-year-old patient. […] AMI has been described in patients with coronavirus disease (COVID-19), probably related to large vessel thromboembolic events as well as to small vessel thrombosis linked to hypercoagulability and fibrinolysis shutdown. […] The key to early diagnosis is a high level of clinical suspicion. The clinical scenario of a patient complaining of excruciating abdominal pain with an unrevealing abdominal examination is classic for early AMI. The reason for the pain being disproportionate to the clinical findings is that ischemia starts from the mucosa toward the serosa.
  • #1 Intestinal ischemia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/intestinal-ischemia/symptoms-causes/syc-20373946
    Intestinal ischemia (is-KEE-me-uh) refers to a range of conditions that happen when blood flow to the intestines slows or stops. Ischemia can be due to a fully or partly blocked blood vessel, most often an artery. Or low blood pressure may lead to less blood flow. Intestinal ischemia can affect the small intestine, the large intestine or both. […] Less blood flow means that too little oxygen goes to the cells in the system through which food travels, called the digestive system. Intestinal ischemia is a serious condition that can cause pain. It can make it hard for the intestines to work well. […] In severe cases, loss of blood flow to the intestines can cause lifelong damage to the intestines. And it may lead to death. […] Intestinal ischemia happens when the blood flow through the major blood vessels that send blood to and from the intestines slows or stops. The condition has many possible causes.
  • #1 Acute Mesenteric Ischemia – Gastrointestinal Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/gastrointestinal-disorders/acute-abdomen-and-surgical-gastroenterology/acute-mesenteric-ischemia
    The intestinal mucosa has a high metabolic rate and, accordingly, a high blood flow requirement (normally receiving 20 to 25% of cardiac output), making it very sensitive to the effects of decreased perfusion. Ischemia disrupts the mucosal barrier, allowing release of bacteria, toxins, and vasoactive mediators, which in turn leads to myocardial depression, systemic inflammatory response syndrome, multisystem organ failure, and death. Mediator release may occur even before complete infarction. […] Mesenteric blood flow may be disrupted on either the venous or arterial sides. […] Early diagnosis of mesenteric ischemia is particularly important because mortality increases significantly once intestinal infarction has occurred. […] If diagnosis and treatment take place before infarction occurs, mortality is low; after intestinal infarction, mortality is high and varies depending on the etiology.
  • #1 Small Bowel Ischemia – American College of Gastroenterology
    https://gi.org/topics/small-bowel-ischemia/
    The goals of treatment are to restore blood supply to the intestines and maintain proper function in the digestive tract. Treatment options for intestinal ischemia vary depending on the cause of the condition and the severity of damage in the intestines. […] If you have small bowel ischemia but no damage to intestinal tissue, medications may be enough to manage the condition. Your doctor may recommend one or more medications, such as: Clot-busting medications to break up blood clots. […] Depending on your specific case, surgery might be the best treatment option. Typical surgical procedures include: Laparoscopy: The surgeon makes a few tiny incisions and uses small instruments to restore blood flow to the small bowel. […] Small bowel ischemia can lead to complications such as: Rupture: A hole in the intestinal wall can form, causing the contents of the intestine to leak into the abdominal cavity.
  • #1 SciELO Brazil – Pathophysiology of mesenteric ischemia/reperfusion: a review Pathophysiology of mesenteric ischemia/reperfusion: a review
    https://www.scielo.br/j/acb/a/nsvfz8j9KBgNvs5GKQ7CznN/
    More recent studies indicate that apoptosis is clearly a significant and, perhaps, the principal contributor to cellular death after I/R injury. […] Apoptosis inhibitors in injured tissue can preserve functional and morphological integrity in organs submitted to I/R. […] Reactive chemical species initiate a sequence of events including the activation of neutrophils and the release of harmful substances like PAF and histamine. […] Multiple organ failure is a frequent complication after intestinal I/R and involves organs like the liver, heart, kidneys and lungs. […] The events which occur during I/R are complex and well studied, although, there still remain many doubts as to their pathophysiology and therapeutics, revealing the need for new research to obtain a more complete understanding and in the search for improved treatments.
  • #1 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/html
    Acute intestinal ischemia is a relative rare abdominal emergency, associated with considerably high morbidity and mortality rates. […] The pathophysiology is complex and multifaceted. The intestinal acute vascular insufficiency leads to renin-angiotensin activation, sympathic stimulation, vasospasm and consequently hypoxia. […] The persistence of ischemia may then lead to an evolvement of transmural infarction towards irreversible injury and necrosis, intestinal perforation and release of bacteria and toxins into the systemic circulation. […] Despite ample research in this field, early, sensitive and specific biomarkers of acute intestinal ischemia have not been identified so far. […] The aim of this narrative review is hence to provide an overview on traditional laboratory biomarkers of acute intestinal ischemia and summarize current evidence regarding some emerging and potentially useful biomarkers.
  • #1 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/html
    D-lactate is normally produced at very low concentrations in humans. […] An alteration of mucosal integrity due to intestinal ischemia may be a reasonable cause of increased D-lactate concentration in blood. […] Although D-lactate seems hence to perform better than L-lactate because of its exclusively intestinal source, the results obtained in different studies are mostly inconsistent. […] IMA is a biologic marker that can be easily and inexpensively measured in clinical laboratories. […] The first preliminary investigation in patients with intestinal ischemia was published in 2008, and showed that IMA values were significantly higher in seven patients with acute mesenteric ischemia compared to seven healthy subjects. […] Notably, the peculiar IMA kinetics is characterized by an early increase in parallel with the onset of ischemia, with values then further increase for hours afterwards.
  • #1 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/html
    -GST is another biomarker of oxidative stress potentially useful for diagnosing intestinal ischemia. […] Additional inflammatory biomarkers, such as C-reactive protein (CRP) or interleukin-6 (IL-6), have been investigated in intestinal ischemia diagnostics. […] Procalcitonin (PCT) may be seen as a valuable aid for diagnosing or monitoring intestinal ischemia. […] D-dimer was shown to display good diagnostic performance in thrombo-embolic occlusion of the superior mesenteric artery, but its diagnostic efficiency seems overall less satisfactory in nonvascular acute intestinal ischemia. […] Citrulline is a non-proteinogenic amino acid synthesized from glutamine by the small bowel enterocytes and is a precursor for de novo synthesis of arginine. […] A progressively decreasing intestinal perfusion and a loss of integrity of the enterocyte cell membrane both contribute the rapid release of I-FABP into circulation and further elimination by the kidneys. […] Although acute intestinal ischemia remains a relative rare condition, a timely and accurate diagnosis is needed to prevent the development of serious complications, up to death.
  • #1 Acute mesenteric ischemia: guidelines of the World Society of Emergency Surgery | World Journal of Emergency Surgery | Full Text
    https://wjes.biomedcentral.com/articles/10.1186/s13017-017-0150-5
    Acute mesenteric ischemia (AMI) may be defined as a sudden interruption of the blood supply to a segment of the small intestine, leading to ischemia, cellular damage, intestinal necrosis, and eventually patient death if untreated. […] The overall incidence is low (0.09 to 0.2% of all acute admissions to emergency departments), representing an uncommon cause of abdominal pain. […] Prompt diagnostic and intervention are essential to reduce the high mortality rates (50 to 80%). […] Roughly, 50% of all cases of AMI are due to acute mesenteric embolism. […] Thrombosis of the SMA (approximately 25% of cases) is usually associated with pre-existing chronic atherosclerotic disease leading to stenosis. […] NOMI occurs in approximately 20% of cases and is usually a consequence of SMA vasoconstriction associated with low splanchnic blood flow.
  • #2 Intestinal ischemia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/intestinal-ischemia/symptoms-causes/syc-20373946
    Intestinal ischemia (is-KEE-me-uh) refers to a range of conditions that happen when blood flow to the intestines slows or stops. Ischemia can be due to a fully or partly blocked blood vessel, most often an artery. Or low blood pressure may lead to less blood flow. Intestinal ischemia can affect the small intestine, the large intestine or both. […] Less blood flow means that too little oxygen goes to the cells in the system through which food travels, called the digestive system. Intestinal ischemia is a serious condition that can cause pain. It can make it hard for the intestines to work well. […] In severe cases, loss of blood flow to the intestines can cause lifelong damage to the intestines. And it may lead to death. […] Intestinal ischemia happens when the blood flow through the major blood vessels that send blood to and from the intestines slows or stops. The condition has many possible causes.
  • #2 Intestinal ischemia – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/intestinal-ischemia/
    Intestinal ischemia occurs if bowel perfusion cannot meet the metabolic demands of the intestine. This relative hypoperfusion may be the result of atherosclerosis, thromboembolic disease, or severe systemic hypotension. […] Intestinal blood flow of the superior mesenteric artery (SMA) and/or inferior mesenteric artery (IMA) is acutely compromised intestinal hypoxia intestinal wall damage mucosal inflammation and possibly bleeding possible progression to infarction and necrosis (gangrenous colon ischemia) disruption of the mucosal barrier and perforation release of bacteria, toxins, and vasoactive substances life-threatening sepsis. […] Tissue damage depends on the severity and duration of perfusion disruption. […] Injury to the intestinal mucosa can occur after just 20 minutes of ischemia; transmural infarction and gangrene occur after 816 hours of ischemia.
  • #2
    https://step1.medbullets.com/gastrointestinal/109050/mesenteric-ischemia
    can be due to a variety of processes […] acute mesenteric ischemia is most commonly caused by an embolism in the main mesenteric artery […] chronic mesenteric ischemia is most commonly caused by atherosclerosis […] embolism secondary to atrial fibrillation, myocardial infarction, or valvular disease […] thrombosis secondary to artherosclerosis […] splanchnic vasoconstriction […] hypoperfusion due to hypotension […] venous thrombosis.
  • #2 Delayed Diagnosis of Mesenteric Ischemia | PSNet
    https://psnet.ahrq.gov/web-mm/delayed-diagnosis-mesenteric-ischemia
    Mesenteric ischemia occurs when there is reduced blood flow to the small or large intestines from multiple potential etiologies involving interruptions of either the arterial or venous systems. […] Acute mesenteric, or intestinal, ischemia occurs when perfusion abruptly decreases, with or without vascular occlusion. In general, the intestines are protected by an extensive collateral vasculature; as such, an ischemic insult develops when there is inadequate flow through either direct or collateral vessels. […] A sudden occlusive arterial obstruction is often due to thromboembolism frequently from a cardiac source that blocks the superior mesenteric artery (SMA), but it can also occur from thrombosis of an atherosclerotic plaque of the SMA. Nonocclusive mesenteric ischemia is the result of a low flow state often due to vasoconstriction in the setting of hypovolemia, vasopressor use, or poor cardiac output.
  • #2 Delayed Diagnosis of Mesenteric Ischemia | PSNet
    https://psnet.ahrq.gov/web-mm/delayed-diagnosis-mesenteric-ischemia
    The frequency of these major causes of mesenteric ischemia among all patients is estimated as: 50% mesenteric arterial embolism, 15-25% mesenteric arterial thrombosis, 5% mesenteric venous thrombosis, and 20-30% nonocclusive mesenteric ischemia. […] Risk factors for developing mesenteric ischemia vary by etiology but include any process that results in mesenteric hypoperfusion or increases the likelihood of intestinal embolism, thrombosis, or vasoconstriction. […] Given the potential for devastating outcomes when not diagnosed in a timely fashion, as in the presented case, mesenteric ischemia is an important diagnosis to consider in all patients with severe abdominal pain. […] Symptoms of weight loss and dietary changes in the setting of atherosclerosis should increase suspicion for chronic mesenteric ischemia until proven otherwise.
  • #2 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/html
    Acute intestinal ischemia is a relative rare abdominal emergency, associated with considerably high morbidity and mortality rates. […] The pathophysiology is complex and multifaceted. The intestinal acute vascular insufficiency leads to renin-angiotensin activation, sympathic stimulation, vasospasm and consequently hypoxia. […] The persistence of ischemia may then lead to an evolvement of transmural infarction towards irreversible injury and necrosis, intestinal perforation and release of bacteria and toxins into the systemic circulation. […] Despite ample research in this field, early, sensitive and specific biomarkers of acute intestinal ischemia have not been identified so far. […] The aim of this narrative review is hence to provide an overview on traditional laboratory biomarkers of acute intestinal ischemia and summarize current evidence regarding some emerging and potentially useful biomarkers.
  • #2 Acute mesenteric ischaemia: a pictorial review | Insights into Imaging | Full Text
    https://insightsimaging.springeropen.com/articles/10.1007/s13244-018-0641-2
    Intestinal ischaemia refers to insufficient blood flow within the mesenteric circulation to meet the metabolic demands in the bowel. […] The initial ischaemic damage to the intestinal wall may then range from only mild and superficial necrosis limited to the mucosa (stage I), or damage extending to the submucosal and muscularis propria layers (stage II), to dangerous and life-threatening continuous necrosis of all bowel wall layers (transmural bowel infarction) (stage III). […] From the pathophysiological point of view, the initial purely ischaemic lesions of the intestine are typically followed by the release of certain mediators such as cytokines, platelet-activating factor and tumour necrosis factor, which will lead to an inflammatory response and additionally damage the bowel wall.
  • #2 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    Bowel ischemia can classify as small intestine ischemia, which is commonly known as mesenteric ischemia and large intestine ischemia, which generally referred to as colonic ischemia. Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. […] The intestine is mainly supplied by 2 major arteries, which include the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA). […] Two main areas in the colon, including splenic flexure (Griffiths point) and rectosigmoid junction (Sudek’s point), are prone to ischemia. These are also known as the 'watershed’ areas, which mean the regions in the colon between 2 major arteries that supplying colon. […] An acute decrease in mesenteric arterial blood flow accounts for 60% to 70% of patients with mesenteric ischemia.
  • #2 Acute Mesenteric Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431068/
    An acute mesenteric arterial embolism is often cardiogenic in origin and primarily affects the superior mesenteric artery (SMA). Preceding events include atrial tachyarrhythmia, congestive heart failure, myocardial ischemia or infarction, cardiomyopathy, and ventricular aneurysm, which results in thrombus formation that later embolizes to cause ischemia. […] Patients with acute mesenteric arterial thrombosis commonly have a pre-existing atherosclerotic disease. Vasospasm in the SMA often accompanies NOMI secondary to cardiac failure, peripheral hypoxemia, or reperfusion injury. […] In rare instances, vasopressors (e.g., cocaine and norepinephrine) and ergotamines may cause NOMI. These agents cause vasoconstriction and reduced blood flow in the mesentery, which may result in ischemia of the bowel.
  • #2 Bowel Ischemia | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/18478
    Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. […] Bowel ischemia can be classified as small intestine ischemia, which is commonly known as mesenteric ischemia and large intestine ischemia, which generally referred to as colonic ischemia. […] Generally, mesenteric ischemia (MI) can be divided based on the timing of onset into acute and chronic. […] Collateral circulation of the gastrointestinal tract can compensate for a 75% acute reduction in mesenteric perfusion for up to 12 hours without significant injury. […] Etiologies of acute intestinal ischemia can categorize as mesenteric arterial embolism (50%), intestinal hypoperfusion or nonocclusive mesenteric ischemia (NOMI) (20% to 30%), mesenteric arterial thrombosis (15% to 25%) and mesenteric venous thrombosis (MVT)(5%).
  • #2 Non-Occlusive Mesenteric Ischemia in Cardiac Arrest Patients
    https://www.imrpress.com/journal/RCM/24/9/10.31083/j.rcm2409262/htm
    Non-occlusive mesenteric ischemia (NOMI) is a severe complication in patients after cardiac arrest (CA). […] The cause of this condition is mostly related to hypoperfusion of the intestine due to low cardiac output, spasm of mesenteric vessels, hypovolemia, or use of vasoconstrictive agents, which can significantly reduce the perfusion of the intestine and may result in transmural necrosis. […] The enterocytes are very sensitive to ischemia-reperfusion injury. […] Thus, depending on the duration of CA, especially in patients with prolonged CA, this process can aggravate a systemic inflammatory reaction with increased production of pro-inflammatory cytokines. […] Regarding the hypoperfusion and reperfusion that occur during cardiac arrest, NOMI is not only a severe complication of a critical state, but its incidence and severity are considered to be prognostic markers of CA outcome.
  • #2 Chronic Mesenteric Ischemia: Background, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/183683-overview
    Chronic mesenteric ischemia (CMI) usually results from long-standing atherosclerotic disease of two or more mesenteric vessels. […] It is also a manifestation of peripheral vascular disease in which the metabolic demands of visceral organs are not being met by the blood supply. […] Symptoms are caused by the gradual reduction in blood flow to the intestine. […] In more than 95% of patients, the process driving mesenteric ischemia is diffuse atherosclerotic disease, which decreases the flow of blood to the bowel and is characterized by postprandial abdominal pain. […] As the atherosclerotic disease progresses, symptoms worsen. […] The interconnections between the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA) often permit easy compensation if stenotic lesions develop in 1 of these 3 vessels.
  • #2 Intestinal Ischemia | Concise Medical Knowledge
    https://www.lecturio.com/concepts/intestinal-ischemia/
    Superior mesenteric vein: drains blood from the small intestine Small intestine The small intestine is the longest part of the GI tract, extending from the pyloric orifice of the stomach to the ileocecal junction. The small intestine is the major organ responsible for chemical digestion and absorption of nutrients. It is divided into 3 segments: the duodenum, the jejunum, and the ileum. Small Intestine: Anatomy. […] Sudden thrombus formation in addition to stenosis Stenosis Hypoplastic Left Heart Syndrome (HLHS) can lead to acute-on-chronic mesenteric ischemia Ischemia A hypoperfusion of the blood through an organ or tissue caused by a pathologic constriction or obstruction of its blood vessels, or an absence of blood circulation. Ischemic Cell Damage.
  • #2 Intestinal Ischemia | AMBOSS Rotation Prep
    https://resident360.amboss.com/adult-medicine/gastroenterology/intestinal-ischemia/intestinal-ischemia.html
    Although laboratory studies are nonspecific, lactic acidosis, leukocytosis, and an elevated D-dimer level may be seen in patients with suspected mesenteric ischemia. […] Immediate initiation of broad-spectrum antibiotics is recommended due to the high risk of infection associated with acute mesenteric ischemia. […] Once a diagnosis is made, definitive treatment involves a range of interventions, including endovascular or surgical repair. […] Colonic ischemia is the most frequent form of intestinal ischemia, and in contrast with mesenteric ischemia, generally results from nonocclusive causes such as small-vessel disease, systemic hypotension, decreased cardiac output, or aortic surgery. However, a specific inciting factor cannot be identified in most patients. […] Evaluation and diagnosis of colonic ischemia is similar to that of mesenteric ischemia except that large-vessel thrombus or embolus are seldom the cause of colonic ischemia. […] Most cases resolve spontaneously and thus treatment is generally supportive, with aggressive hydration, bowel rest, and occasionally antibiotics in moderate or severe disease due to risk for infection.
  • #2 Colonic Ischemia – Intestinal Ischemia – Intestinal Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.4.19.3.
    Segments of the intestine that are particularly vulnerable to ischemia include the region of the splenic flexure (ie, Griffiths point, where the IMA and SMA circulations meet and rely on collateral blood flow) and rectosigmoid junction (ie, Sudeck point, where blood flow is dependent on the terminal branches of the IMA). […] The right colon is less frequently involved in ischemic colitis but is vulnerable to low-flow states and embolic occlusion of the SMA because the ileocolic artery is the terminal branch of the SMA. […] The rectum is relatively unaffected due to its robust blood supply from both the mesenteric and iliac arteries.
  • #2 Bowel Ischemia | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/18478
    In chronic mesenteric ischemia, the diffuse atherosclerotic disease is an account for 95% of cases. […] The splanchnic circulation varies based on the feeding or fasting state. […] Intestinal ischemia happens when inadequate oxygen delivered to the intestine. […] However, intestinal injury occurs by low perfusion and reperfusion of intestinal tissues. […] Low perfusion can cause intestinal injury when mesenteric perfusion pressure decreases about 30 mmHg or reduction of 45 mmHg in mean mesenteric arterial pressure. […] Physiologically, the intestine can compensate for about 75% of the reduction in mesentery blood flow for 12 hours without significant injury due to vasodilation of collateral circulation and increased oxygen extraction. […] However, after a prolongation of low perfusion or hypoxemia, progressive vasoconstriction leads to reducing collateral flow and subsequently full-thickness necrosis of the intestinal wall and perforation. […] Reperfusion injury after ischemia can be observed due to the release of toxic byproducts of ischemic injury, free oxygen radicals, and neutrophil activation.
  • #2 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    However, after a prolongation of low perfusion or hypoxemia, progressive vasoconstriction leads to reducing collateral flow and subsequently full-thickness necrosis of the intestinal wall and perforation. […] Reperfusion injury after ischemia can be observed due to the release of toxic byproducts of ischemic injury, free oxygen radicals, and neutrophil activation.
  • #2 Many faces of acute bowel ischemia: overview of radiologic staging | Insights into Imaging | Full Text
    https://insightsimaging.springeropen.com/articles/10.1186/s13244-021-00985-9
    Stage II or the intermediate stage is described as presence of specific pathologic changes (edema, erosion, hemorrhage and necrosis) in submucosa and muscularis propria. […] Stage III, the late stage, is manifested by transmural bowel necrosis and is developed if blood supply is not eventually restored. […] It should be noted that bowel ischemia accompanied by reperfusion injury may lead to the disruption of mucosal barrier followed by bacterial invasion, septic shock and multiorgan failure, which may cause death without transmural necrosis. […] Understanding the pathophysiology of ABI can help for better management. […] Management should be based on the latest stage identified. […] The main goal of management is to achieve a prompt diagnosis, specify the best treatment option and reduce mortality in these patients.
  • #2 Intestinal Ischemia and Reperfusion: Consequences and Mechanisms | SpringerLink
    https://link.springer.com/10.1007/978-3-642-37078-6_240
    Ischemia and reperfusion of the ischemic intestine can result in significant tissue injury that is manifested as vascular dysfunction and mucosal barrier failure. […] The injury response to ischemia per se can be attributed to hypoxia and the cellular alterations brought about by this condition. […] Reperfusion of the ischemic intestine is accompanied by a more profound injury response that has been linked to the generation of reactive oxygen species that are derived from the enzyme xanthine oxidase. […] The accumulation of these reactive species at the time of reperfusion, coupled with the inactivation of nitric oxide, creates an inflammatory phenotype within the vasculature and mucosal membrane. […] The resulting recruitment of leukocytes and platelets and the activation of resident inflammatory cells that normally reside in the perivascular space (mast cells, macrophages) lead to further oxidative stress and a more intense inflammatory condition, ultimately resulting in capillary and mucosal membrane failure and organ dysfunction.
  • #2 SciELO Brazil – Pathophysiology of mesenteric ischemia/reperfusion: a review Pathophysiology of mesenteric ischemia/reperfusion: a review
    https://www.scielo.br/j/acb/a/nsvfz8j9KBgNvs5GKQ7CznN/
    However, when the process which initiates ischemia is corrected before irreversible alterations can occur, oxygen return allows for the reestablishment of energetic metabolism, the removal of toxic products and the progressive return of normal cell functions. […] Depending on the time and intensity of the ischemia, when oxygen is reintroduced to the tissues, tissue injury can be further exacerbated (oxygen paradox). […] I/R can provoke complex interactions between the endothelium and different cell types, leading to microvascular injury, cellular necrosis and/or apoptosis. […] Occlusion and reperfusion of the splanchnic arteries precipitate circulatory shock, which, principally through an increase in vascular permeability, causes the activation and adhesion of polymorphonuclear neutrophils (PMNs), the release of proinflammatory substances and the formation of both nitrogen-derived and oxygen-derived free radicals.
  • #2 SciELO Brazil – Pathophysiology of mesenteric ischemia/reperfusion: a review Pathophysiology of mesenteric ischemia/reperfusion: a review
    https://www.scielo.br/j/acb/a/nsvfz8j9KBgNvs5GKQ7CznN/
    The superoxide ions react with nitric oxide (NO) to produce peroxynitrite, which then causes accentuated lipid peroxidation, proteic and DNA modifications resulting in cellular damage. […] The activation of the complement system can lead to the translocation of NF-kB and an increase in the transcription of iNOS. […] The activation of neutrophils was also complement-dependent during intestinal I/R. […] The depletion or inhibition of the complement could diminish many of the mediators of I/R injury. […] The accumulation of platelets in the postischemic microvasculature could contribute significantly to the manifestation of I/R lesions. […] Serotonin together with other bioactive substances could perform an important function in the pathogenesis of intestinal I/R. […] It has been demonstrated recently that pancreatic proteases are involved in the production of inflammatory mediators after intestinal I/R.
  • #2 MicroRNA-378 protects against intestinal ischemia/reperfusion injury via a mechanism involving the inhibition of intestinal mucosal cell apoptosis | Cell Death & Disease
    https://www.nature.com/articles/cddis2017508
    Intestinal ischemia/reperfusion (I/R) injury remains a major clinical event and contributes to high morbidity and mortality rates, but the underlying mechanisms remain elusive. […] The factors contributing to intestinal I/R injury were complex, including microvascular dysfunction, reactive oxygen species over-production, inflammation and even intestinal epithelial cell death. […] Many evidence reveals that apoptosis is a major mode of cell death caused by intestinal I/R, which is a complex biological process that can be triggered by the death receptor and mitochondrial death signaling pathways. […] Previous studies have documented that apoptosis is the main mode of intestinal mucosal cell death after intestinal I/R, and the exploration of the mechanisms of apoptosis might lead to effective therapy for organ I/R injury.
  • #2 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. […] Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. […] Intestinal mucosal damage occurs in response to ischemic insult. […] In response to providing protection from ischemia, mesenteric vessels undergo intrinsic autoregulation, which is an adaptive response to ischemia. […] In order to compensate for the ischemia, there is vasoconstriction of mesenteric vessels resulting in increased tissue oxygen extraction along with vasodilation of the collateral vessels. Owing to this mechanism, intestine is able to compensate for around 75% reduction in blood flow.
  • #2 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/20750
    Acute intestinal ischemia is a relative rare abdominal emergency, associated with considerably high morbidity and mortality rates. […] The pathophysiology is complex and multifaceted. The intestinal acute vascular insufficiency leads to renin-angiotensin activation, sympathic stimulation, vasospasm and consequently hypoxia. […] The persistence of ischemia may then lead to an evolvement of transmural infarction towards irreversible injury and necrosis, intestinal perforation and release of bacteria and toxins into the systemic circulation. […] Despite ample research in this field, early, sensitive and specific biomarkers of acute intestinal ischemia have not been identified so far. […] The aim of this narrative review is hence to provide an overview on traditional laboratory biomarkers of acute intestinal ischemia and summarize current evidence regarding some emerging and potentially useful biomarkers.
  • #2 Intestinal Ischemia: Unusual but Fearsome Complication of COVID-19 Infection
    https://www.mdpi.com/2227-9059/10/5/1010
    The pathophysiology of gastrointestinal damage in coronavirus disease (COVID-19) is probably multifactorial. It is not clear whether the etiology of intestinal ischemia may be directly related to viral replication or may result from hyper-coagulability following SARS-CoV-2 infection. […] Microvascular injury (ischemic enteritis, patchy bowel necrosis, presence of thrombi, and perivascular inflammation) was observed in the submucosal arterioles of the small intestine from patients with COVID-19. […] SARS-CoV-2 can cause direct injury of the gastrointestinal mucosa through its attachment to the angiotensin-converting enzyme receptor (ACE2), which is abundantly expressed on enterocytes, or by disruption of the normal colonic gut flora or by bowel ischemia resulting from thromboembolic complications.
  • #2 Mesenteric Ischemia: Causes, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/23246-mesenteric-ischemia
    Narrowed and blocked arteries in the mesentery can cause ischemia, depriving your digestive tract of vital blood and oxygen. […] Without enough blood flow, the affected organs and tissues dont have enough oxygen and cant function correctly. If the blockage is severe enough, the affected organs and tissues may start to die. […] Chronic mesenteric ischemia often happens because of circulatory diseases that cause blood vessels to narrow. This narrowing, known as stenosis, means that blood flow to your mesentery drops over time. […] Non-occlusive mesenteric ischemia (NOMI), which happens without a blockage, makes up about 20% of all cases of acute mesenteric ischemia. Acute NOMI happens when blood vessels constrict, or there are spasms in the muscles lining those vessels. […] Chronic mesenteric ischemia may need some different treatments, depending on why it happens. But many of the possible treatments are the same as with acute mesenteric ischemia.
  • #2 SciELO Brazil – Pathophysiology of mesenteric ischemia/reperfusion: a review Pathophysiology of mesenteric ischemia/reperfusion: a review
    https://www.scielo.br/j/acb/a/nsvfz8j9KBgNvs5GKQ7CznN/
    More recent studies indicate that apoptosis is clearly a significant and, perhaps, the principal contributor to cellular death after I/R injury. […] Apoptosis inhibitors in injured tissue can preserve functional and morphological integrity in organs submitted to I/R. […] Reactive chemical species initiate a sequence of events including the activation of neutrophils and the release of harmful substances like PAF and histamine. […] Multiple organ failure is a frequent complication after intestinal I/R and involves organs like the liver, heart, kidneys and lungs. […] The events which occur during I/R are complex and well studied, although, there still remain many doubts as to their pathophysiology and therapeutics, revealing the need for new research to obtain a more complete understanding and in the search for improved treatments.
  • #2 Biochemical markers of acute intestinal ischemia: possibilities and limitations
    https://atm.amegroups.org/article/view/20595/20750
    Although D-lactate seems hence to perform better than L-lactate because of its exclusively intestinal source, the results obtained in different studies are mostly inconsistent. […] IMA is a biologic marker that can be easily and inexpensively measured in clinical laboratories by using the albumin cobalt binding (ACB) assay or with an enzyme-linked immunosorbent assay (ELISA). […] A progressively decreasing intestinal perfusion and a loss of integrity of the enterocyte cell membrane both contribute the rapid release of I-FABP into circulation and further elimination by the kidneys. […] Although acute intestinal ischemia remains a relative rare condition, a timely and accurate diagnosis is needed to prevent the development of serious complications, up to death.
  • #2 Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-01891-x
    During post-ischemic reperfusion, stimulation and damage to the intestine increase, primarily due to the buildup of metabolites generated during ischemia and the release of oxygen free radicals. Under such conditions, the gut undergoes non-programmed cell death. […] The activation of multiple signaling pathways leads to the initiation of various mechanisms of cell death. […] Intestinal I/R injury induces apoptosis and necrosis in the intestinal epithelial cells, which results in impaired intestinal barrier function and ultimately leads to multiple organ dysfunction syndrome. […] The inflammatory response drives the occurrence of apoptosis and necrosis. […] The occurrence of pyroptosis in intestinal I/R injury was confirmed by histopathological findings and intestinal barrier indices, including transepithelial electrical resistance (TER), tight-junction protein, and serum biomarkers.
  • #2 Delayed Diagnosis of Mesenteric Ischemia | PSNet
    https://psnet.ahrq.gov/web-mm/delayed-diagnosis-mesenteric-ischemia
    A definitive diagnosis for acute ischemia requires either exploration in the operating room or, more commonly, computed tomographic (CT) angiography of the abdomen to evaluate the mesenteric vessels and bowel viability. […] Once diagnosed, initial management consists of fluid resuscitation, broad spectrum antibiotics, anticoagulation in most cases, and urgent surgical consultation to General Surgery and Vascular Surgery for abdominal exploration. […] Outcomes of this disease process depend on the etiology, with higher mortality in arterial (50-70%) compared to venous ischemia (30%). […] Unfortunately, mortality rates exceed 60% in acute mesenteric ischemia and these high mortality rates have been unchanged in recent series.
  • #3 Bowel Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK554527/
    Intestinal ischemia occurs when at least a 75% reduction in intestinal blood flow for more than 12 hours. […] Generally, mesenteric ischemia (MI) can be divided based on the timing of onset into acute and chronic. […] Collateral circulation of the gastrointestinal tract can compensate for a 75% acute reduction in mesenteric perfusion for up to 12 hours without significant injury. […] The splanchnic circulation varies based on the feeding or fasting state. Despite high intestinal vasculature, oxygen extraction is low from the intestinal arteries. […] Intestinal ischemia happens when inadequate oxygen delivered to the intestine. However, intestinal injury occurs by low perfusion and reperfusion of intestinal tissues. […] Low perfusion can cause intestinal injury when mesenteric perfusion pressure decreases about 30 mmHg or reduction of 45 mmHg in mean mesenteric arterial pressure.
  • #3 Intestinal ischemia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/intestinal-ischemia/symptoms-causes/syc-20373946
    Intestinal ischemia often is split into groups. Colon ischemia, also called ischemic colitis, affects the large intestine. Other types of ischemia affect the small intestine. These are acute mesenteric ischemia, chronic mesenteric ischemia and ischemia due to mesenteric venous thrombosis. […] Acute mesenteric ischemia is the result of a sudden loss of blood flow to the small intestine. It may be due to: A blood clot, also called an embolus, that comes loose in the heart and travels through the blood to block an artery. It most often blocks the superior mesenteric artery, which sends oxygen-rich blood to the intestines. […] Chronic mesenteric ischemia is due to the buildup of fatty deposits on an artery wall, called atherosclerosis. The disease process most often is slow. It’s also called intestinal angina because it’s due to less blood flow to the intestines after eating.
  • #3 Chronic Mesenteric Ischemia: Background, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/183683-overview
    Usually, therefore, at least 2 of the 3 major visceral vessels must be occluded or narrowed for chronic mesenteric ischemia (CMI) to develop. […] CMI with intestinal hypoperfusion is rarely seen in clinical practice, but when it does occur, it represents a serious and complex vascular disorder. […] Although the pathophysiologic mechanism by which ischemia produces pain is still not completely understood, current physiologic understanding of splanchnic perfusion suggests a key role for the splanchnic circulation in the regulation of cardiovascular homeostasis. […] Conditions less frequently involved in the pathogenesis of CMI are celiac artery compression syndrome (CACS; also known as median arcuate ligament syndrome [MALS]) and fibromuscular dysplasia (FMD).
  • #3 Mesenteric ischemia – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/mesenteric-ischemia/symptoms-causes/syc-20374989
    In mesenteric ischemia, a blockage in an artery cuts off blood flow to a portion of the intestine. […] Mesenteric ischemia is a condition that happens when narrowed or blocked arteries restrict blood flow to your small intestine. Decreased blood flow can permanently damage the small intestine. […] Acute mesenteric ischemia is most commonly caused by a blood clot in the main mesenteric artery. The blood clot often starts in the heart. The chronic form is most commonly caused by a buildup of fatty deposits, called plaque, that narrows the arteries. […] If not treated promptly, acute mesenteric ischemia can lead to irreversible bowel damage. Not getting enough blood flow to the bowel can cause parts of the bowel to die. […] People with chronic mesenteric ischemia can develop acute-on-chronic mesenteric ischemia. Symptoms of chronic mesenteric ischemia can get worse, leading to the acute form of the condition.
  • #3 Bowel Ischemia | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/18478
    In chronic mesenteric ischemia, the diffuse atherosclerotic disease is an account for 95% of cases. […] The splanchnic circulation varies based on the feeding or fasting state. […] Intestinal ischemia happens when inadequate oxygen delivered to the intestine. […] However, intestinal injury occurs by low perfusion and reperfusion of intestinal tissues. […] Low perfusion can cause intestinal injury when mesenteric perfusion pressure decreases about 30 mmHg or reduction of 45 mmHg in mean mesenteric arterial pressure. […] Physiologically, the intestine can compensate for about 75% of the reduction in mesentery blood flow for 12 hours without significant injury due to vasodilation of collateral circulation and increased oxygen extraction. […] However, after a prolongation of low perfusion or hypoxemia, progressive vasoconstriction leads to reducing collateral flow and subsequently full-thickness necrosis of the intestinal wall and perforation. […] Reperfusion injury after ischemia can be observed due to the release of toxic byproducts of ischemic injury, free oxygen radicals, and neutrophil activation.