Zakrzepica jelitowa
Patofizjologia i mechanizm

Zakrzepica jelitowa, czyli niedokrwienie krezkowe, to stan charakteryzujący się nagłym lub przewlekłym ograniczeniem przepływu krwi przez naczynia krezkowe, prowadzącym do niedotlenienia, uszkodzenia komórkowego i martwicy jelit. Ostre niedokrwienie krezkowe (AMI) stanowi ponad 95% przypadków i dzieli się na okluzyjne (60-85%) – zatorowość tętnic krezkowych (40-50%) i zakrzepicę tętnic krezkowych (15-30%), oraz nieokluzyjne (NOMI, 15-30%) i zakrzepicę żył krezkowych (5-15%). Przewlekłe niedokrwienie krezkowe (CMI) to około 5% przypadków, najczęściej związane z miażdżycą. Jelito cienkie i prawa część okrężnicy są szczególnie narażone ze względu na wysokie zapotrzebowanie metaboliczne i unaczynienie przez tętnicę krezkową górną (SMA), która jest podatna na zatory. Patofizjologia obejmuje niedotlenienie, przerwanie bariery śluzówkowej, uwolnienie bakterii i mediatorów zapalnych, co prowadzi do sepsy, niewydolności wielonarządowej i wysokiej śmiertelności (60-80%).

Patogeneza zakrzepicy jelitowej (Mesenteric Ischemia)

Zakrzepica jelitowa (niedokrwienie krezkowe) jest schorzeniem powstającym w wyniku nagłego lub przewlekłego zmniejszenia przepływu krwi przez naczynia krezkowe, co prowadzi do niedotlenienia, uszkodzenia komórkowego, a w konsekwencji do martwicy jelit. Niedokrwienie krezkowe charakteryzuje się wysoką śmiertelnością, sięgającą 60-80%, głównie z powodu niespecyficznych objawów i szybkiego postępu choroby12.

Klasyfikacja niedokrwienia krezkowego

Niedokrwienie krezkowe można sklasyfikować jako ostre lub przewlekłe. Ostre niedokrwienie krezkowe (AMI) występuje w ponad 95% przypadków i może być dalej podzielone na12:

  • Okluzyjne niedokrwienie krezkowe tętnicze (60-85% przypadków)
    • Zatorowość tętnic krezkowych (40-50% przypadków)
    • Zakrzepica tętnic krezkowych (15-30% przypadków)
  • Nieokluzyjne niedokrwienie krezkowe (NOMI) (15-30% przypadków)
  • Zakrzepica żył krezkowych (MVT) (5-15% przypadków)

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Przewlekłe niedokrwienie krezkowe (CMI) stanowi około 5% przypadków i najczęściej jest związane z postępującą miażdżycą1.

Anatomia i fizjologia unaczynienia krezkowego

Jelita otrzymują ukrwienie głównie z trzech dużych naczyń tętniczych:

  • Tętnicy trzewnej (pień trzewny)
  • Tętnicy krezkowej górnej (SMA) – główne naczynie zaopatrujące jelito cienkie
  • Tętnicy krezkowej dolnej (IMA)

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Obszar jelita cienkiego i prawej części okrężnicy jest szczególnie podatny na niedokrwienie ze względu na jego wysokie zapotrzebowanie metaboliczne. Błona śluzowa jelita ma wysokie tempo metabolizmu i normalnie otrzymuje 20-25% pojemności minutowej serca, co czyni ją bardzo wrażliwą na niedokrwienie12.

SMA jest szczególnie podatna na zatory ze względu na ostry kąt odejścia od aorty i wyższy przepływ krwi1. Jelita są chronione przez rozległe krążenie oboczne, ale niedokrwienie rozwija się, gdy przepływ przez naczynia bezpośrednie lub oboczne jest niewystarczający1.

Mechanizmy ostrego niedokrwienia krezkowego

Zatorowość tętnic krezkowych

Zatory tętnic krezkowych stanowią około 40-50% przypadków ostrego niedokrwienia krezkowego. Najczęściej powstają w sercu i blokują tętnicę krezkową górną12. Główne czynniki ryzyka obejmują:

  • Migotanie przedsionków
  • Niewydolność serca
  • Niedawno przebyty zawał mięśnia sercowego
  • Kardiomiopatie
  • Tętniak komory
  • Zapalenie wsierdzia

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Mechanizm obejmuje tworzenie skrzepliny w sercu, która następnie przemieszcza się do naczyń krezkowych, powodując nagłe zablokowanie przepływu krwi. Doprowadza to do ostrego niedokrwienia i martwicy jelit, szczególnie w obszarach zaopatrywanych przez zablokowaną tętnicę1.

Zakrzepica tętnic krezkowych

Zakrzepica tętnic krezkowych stanowi około 15-30% przypadków AMI i wiąże się z najgorszym rokowaniem spośród wszystkich form niedokrwienia krezkowego1. Najczęściej występuje u pacjentów z wcześniej istniejącą chorobą miażdżycową1. Zakrzepica tętnic krezkowych zwykle pojawia się u ich ujścia, powodując rozległy zawał i często dotyczy co najmniej dwóch głównych naczyń trzewnych12.

Czynniki przyczyniające się do zakrzepicy tętnic krezkowych obejmują:

  • Miażdżycę (główna przyczyna)
  • Tętniak tętnicy krezkowej
  • Inne patologie naczyniowe, takie jak rozwarstwienie, uraz
  • Dysplazja włóknisto-mięśniowa
  • Zapalenie naczyń

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Zakrzepica zwykle prowadzi do ostrego pogorszenia już ograniczonego przepływu krwi w wyniku stopniowo postępującej miażdżycy. Pacjenci z zakrzepicą tętnic krezkowych często mają historię przewlekłego niedokrwienia krezkowego, objawiającego się jako bóle poposiłkowe, postępująca utrata wagi i inne objawy przewlekłego niedokrwienia jelit12.

Nieokluzyjne niedokrwienie krezkowe (NOMI)

NOMI stanowi około 15-30% przypadków niedokrwienia krezkowego i wiąże się z najwyższymi wskaźnikami śmiertelności wewnątrzszpitalnej1. NOMI występuje w wyniku hipoperfuzji przy braku okluzji naczyniowej1.

Główny mechanizm NOMI obejmuje skurcz naczyń krezkowych wtórny do ciężkiej i przedłużającej się hipoperfuzji. Najczęstsze czynniki inicjujące to12:

  • Wstrząs układowy z powodu:
    • Zmniejszonej pojemności minutowej po zawale mięśnia sercowego
    • Zastoinowej niewydolności serca
    • Wstrząsu septycznego
    • Hipowolemii
  • Leki powodujące skurcz naczyń:
    • Kokaina
    • Ergotaminy
    • Noradrenalina
    • Wazopresyna

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Patofizjologia NOMI jest związana z mechanizmem homeostatycznym, który utrzymuje przepływ krwi do serca i mózgu kosztem krążenia krezkowego i obwodowego. Wazopresyna i angiotensyna są prawdopodobnie mediatorami neurohormononalnymi tego zjawiska1.

W NOMI dochodzi do zmniejszenia perfuzji trzewnej z wyraźnym skurczem naczyń krezkowych, co prowadzi do niedokrwienia jelit. Jest to często spotykane u pacjentów w stanie krytycznym, po zatrzymaniu krążenia, i u osób z wieloma czynnikami ryzyka sercowo-naczyniowego12.

Zakrzepica żył krezkowych (MVT)

Zakrzepica żył krezkowych stanowi 5-15% przypadków ostrego niedokrwienia krezkowego i często jest związana z nadkrzepliwością12. MVT może być pierwotna (bez identyfikowalnego czynnika predysponującego) lub wtórna1.

Mechanizm niedokrwienia w MVT różni się od niedokrwienia tętniczego. Obejmuje on12:

  • Masowy napływ płynu do ściany jelita i światła, prowadzący do hipowolemii ogólnoustrojowej i hemokoncentracji
  • Obrzęk jelit i zmniejszony odpływ krwi z powodu zakrzepicy żylnej
  • Zahamowanie dopływu krwi tętniczej, prowadzące do niedokrwienia jelit

MVT często ma bardziej podstępny przebieg niż niedokrwienie tętnicze, z niejasnym bólem brzucha, który może utrzymywać się przez dłuższy czas, nawet miesiąc od początku objawów1.

Mechanizmy uszkodzenia tkanek w niedokrwieniu krezkowym

Kaskada niedokrwienia i odpowiedzi zapalnej

Niedokrwienie jelit inicjuje złożoną kaskadę wydarzeń, które prowadzą do uszkodzenia tkanek i ogólnoustrojowych powikłań1:

  • Niedokrwienie tętnicze zapoczątkowuje zmiany w tkankach poprzez blokowanie dopływu tlenu, uniemożliwiając w ten sposób tlenowy metabolizm energetyczny
  • Podczas procesu niedokrwienia, oprócz nieodpowiedniego zaopatrzenia w tlen z konsekwentnym upośledzeniem fosforylacji oksydacyjnej w mitochondriach, następuje gromadzenie się metabolitów, które bezpośrednio lub poprzez mediatory mogą powodować uszkodzenie komórek
  • Uszkodzenie postępuje w miarę trwania niedokrwienia, a bariera śluzówkowa ulega przerwaniu
  • Bakterie, toksyny i substancje wazoaktywne są uwalniane do krążenia ogólnoustrojowego

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Niedokrwienie przerywa barierę śluzówkową, umożliwiając uwolnienie bakterii, toksyn i mediatorów wazoaktywnych, co prowadzi do depresji mięśnia sercowego, zespołu ogólnoustrojowej odpowiedzi zapalnej, niewydolności wielonarządowej i śmierci1.

Progresja uszkodzenia tkanek w czasie

Uszkodzenie tkanek w niedokrwieniu krezkowym postępuje w przewidywalny sposób w zależności od czasu trwania niedokrwienia12:

  • W ciągu 3-4 godzin od początku niedokrwienia następuje martwica kosmków śluzówkowych
  • W ciągu 6 godzin można zaobserwować zawał przezmurowy, ścienny lub śluzówkowy
  • Przedłużone niedokrwienie prowadzi do postępującego skurczu naczyń krezkowych, co zwiększa w nich ciśnienie, prowadząc do zmniejszenia przepływu obocznego

Ciężkość uszkodzenia jest odwrotnie proporcjonalna do przepływu krwi krezkowej i zależy od liczby zaangażowanych naczyń, średniego ciśnienia tętniczego, czasu trwania niedokrwienia i krążenia obocznego1.

Uszkodzenie dotknięcej części jelita może wahać się od odwracalnego niedokrwienia do przezmurowego zawału z martwicą i perforacją12.

Uszkodzenie reperfuzyjne

Istotnym mechanizmem uszkodzenia w niedokrwieniu krezkowym jest uszkodzenie spowodowane reperfuzją, które występuje po przywróceniu przepływu krwi do obszaru niedokrwionego12:

  • W zależności od czasu i intensywności niedokrwienia, po ponownym wprowadzeniu tlenu do tkanek, uszkodzenie tkanek może się jeszcze bardziej nasilić (paradoks tlenowy)
  • Niedokrwienie/reperfuzja (I/R) może wywołać złożone interakcje między śródbłonkiem a różnymi typami komórek, prowadząc do urazu mikronaczyniowego, martwicy komórek i/lub apoptozy
  • Okluzja i reperfuzja tętnic trzewnych wywołuje wstrząs krążeniowy, który głównie poprzez zwiększenie przepuszczalności naczyń powoduje aktywację i adhezję neutrofilów wielojądrzastych (PMN), uwalnianie substancji prozapalnych i tworzenie wolnych rodników pochodnych zarówno azotu, jak i tlenu

Mechanizm uszkodzenia prawdopodobnie obejmuje wytwarzanie wolnych rodników tlenowych przez oksydazę ksantynową, co następnie powoduje głębokie lokalne uszkodzenie tkanek poprzez peroksydację lipidów, przerwanie błon i zwiększoną przepuszczalność mikronaczyń1.

Niedokrwiony śródbłonek rekrutuje PMN w sposób autokrynny i parakrynny, wydzielając chemotaktyczne cytokiny (czynnik martwicy nowotworów [TNF]-α, interleukina [IL]-1, płytkopochodny czynnik wzrostu [PDGF]), które nasilają dalsze uszkodzenia reperfuzowanej tkanki1.

Rola mediatorów i czynników bioaktywnych

Regulatory przepływu trzewnego

Krążenie trzewne odgrywa kluczową rolę w regulacji homeostazy sercowo-naczyniowej12. Szereg endogennych i egzogennych czynników humoralnych wpływa na krążenie trzewne1:

  • Czynniki powodujące skurcz naczyń krezkowych:
    • Noradrenalina i wysokie dawki adrenaliny
    • Wazopresyna
    • Fenylofryna
    • Digoksyna
  • Czynniki zwiększające przepływ krwi krezkowej:
    • Papaweryna
    • Adenozyna
    • Dobutamina
    • Fenoldopam
    • Nitroprusydek sodu
  • Naturalne neurotransmitery działające jako rozszerzacze naczyń trzewnych:
    • Acetylocholina
    • Histamina
    • Tlenek azotu
    • Leukotrieny
    • Analogi tromboksanu
    • Glukagon

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Niska dawka dopaminy powoduje rozszerzenie naczyń trzewnych, podczas gdy wyższe dawki prowadzą do skurczu naczyń poprzez stymulację receptorów adrenergicznych alfa1.

Mechanizmy adaptacyjne i autoregulacja

W odpowiedzi na niedokrwienie naczynia krezkowe przechodzą wewnętrzną autoregulację, która jest adaptacyjną odpowiedzią na niedokrwienie1:

  • W celu rekompensacji niedokrwienia następuje skurcz naczyń krezkowych, czego skutkiem jest zwiększona ekstraktacja tlenu z tkanek wraz z rozszerzeniem naczyń obocznych
  • Dzięki temu mechanizmowi jelito jest w stanie skompensować około 75% redukcji przepływu krwi

Rozbieżność między zapotrzebowaniem na tlen w tkankach a podażą podnosi stężenie lokalnych metabolitów, takich jak wodór, potas, dwutlenek węgla i adenozyna, prowadząc do rozszerzenia naczyń i przekrwienia1.

Ostre zmniejszenie ciśnienia perfuzji jest kompensowane przez zmniejszenie napięcia ściany tętniczek, utrzymując w ten sposób przepływ krwi trzewnej1.

Interakcje komórkowo-naczyniowe

Niedokrwienie i reperfuzja krezkowa wywołują złożone interakcje między komórkami i naczyniami12:

  • Aktywacja układu dopełniacza może prowadzić do translokacji NF-kB i zwiększenia transkrypcji iNOS
  • Aktywacja NF-kB prowadzi do skoordynowanej ekspresji wielu genów, które kodują białka zaangażowane w syntezę mediatorów oraz w amplifikację i utrzymanie odpowiedzi zapalnej
  • Nagromadzenie płytek krwi w pozawałowym mikrokrążeniu może znacząco przyczynić się do manifestacji uszkodzeń I/R
  • Serotonina jest aminą bioaktywną, która działa w kilku zjawiskach fizjologicznych, takich jak neurotransmisja, ruchy jelitowe, aktywacja płytek krwi i skurcz naczyń

Wykazano niedawno, że proteazy trzustkowe są zaangażowane w produkcję mediatorów zapalnych po jelitowym I/R, takich jak trypsyna i metaloproteinaza-9 (MMP-9)1.

Apoptoza i uszkodzenie komórek

Mechanizmy apoptozy w niedokrwieniu krezkowym

Nowsze badania wskazują, że apoptoza jest wyraźnie znaczącym, a być może głównym czynnikiem przyczyniającym się do śmierci komórek po uszkodzeniu I/R1:

  • Głównym wykonawcą „zaprogramowanej śmierci komórki” są cysteiny endoproteazy zwane kaspazami
  • Reaktywne cząsteczki chemiczne inicjują sekwencję zdarzeń, w tym aktywację neutrofilów i uwalnianie szkodliwych substancji, takich jak PAF i histamina

Apoptoza w niedokrwieniu krezkowym jest złożonym procesem, który przyczynia się do ogólnego uszkodzenia tkanek i może być celem interwencji terapeutycznych1.

Progresja do martwicy jelit

W miarę postępu niedokrwienia, dochodzi do uszkodzenia wszystkich warstw jelita, co prowadzi do martwicy i perforacji1:

  • W miarę postępu niedokrwienia od błony śluzowej do wszystkich warstw pod nią (przezmurowo), dochodzi do przerwania wyściółki nabłonkowej
  • Umożliwia to bakteriom w świetle jelita wniknięcie do jamy otrzewnej, powodując zapalenie otrzewnej
  • Jeśli bakterie wejdą do krwiobiegu, prowadzi to do zespołu ogólnoustrojowej odpowiedzi zapalnej, co ostatecznie skutkuje sepsą i wstrząsem septycznym

Bez odpowiedniego i terminowego leczenia, martwica jelita cienkiego i okrężnicy prowadzi do sepsy i potencjalnie do śmierci1.

Konsekwencje ogólnoustrojowe niedokrwienia krezkowego

Niewydolność wielonarządowa

Niewydolność wielonarządowa jest częstym powikłaniem po niedokrwieniu i reperfuzji jelit i obejmuje narządy takie jak wątroba, serce, nerki i płuca1.

Aktywacja endogennej kaskady zapalnej nie ogranicza się do uszkodzonego narządu i może również mieć szkodliwe skutki ogólnoustrojowe, z dysfunkcją układu sercowego, płucnego i innych układów narządowych1.

Sekwencja zdarzeń, które zachodzą w jelicie po zmniejszeniu przepływu krwi obejmuje uszkodzenie niedokrwienne, zmniejszoną dostawę tlenu i składników odżywczych, zakłócenie metabolizmu komórkowego, uszkodzenie tkanek z powodu hipoksji i reperfuzji, pełną grubość martwicy jelita i perforację ściany jelita1.

Zespół ogólnoustrojowej odpowiedzi zapalnej i sepsa

Okluzja naczyniowa prowadzi do1:

  • Przepływu krwi zapotrzebowania metabolicznego
  • Przerwania bariery śluzówkowej i translokacji bakterii do krążenia
  • Beztlenowej glikolizy w błonie śluzowej i produkcji mleczanów
  • Aktywacji czynników naczyniowych i humoralnych prowadzących do skurczu naczyń
  • Ogólnoustrojowej aktywacji odpowiedzi zapalnej
  • Kwasicy mleczanowej
  • Martwicy jelita
  • Niewydolności wielonarządowej

Hipowolemnia, niewydolność sercowa, endogenny skurcz naczyń i skurcz naczyń trzewnych prowadzą do hipoperfuzji błony śluzowej jelita, przywrócenia krwi przez rozszerzenie naczyń obocznych, przerwania bariery śluzówkowej jelita, uszkodzenia niedokrwienno-reperfuzyjnego oraz zwiększonej perfuzji błony śluzowej do toksyn bakteryjnych, aktywujących odpowiedź zapalną1.

Czynniki ryzyka i predyspozycje

Czynniki ryzyka dla różnych typów niedokrwienia krezkowego

Czynniki ryzyka niedokrwienia krezkowego różnią się w zależności od etiologii1:

  • Zatorowość tętnic krezkowych:
    • Migotanie przedsionków
    • Zapalenie wsierdzia
    • Skrzeplina w lewej komorze
    • Zaburzenia rytmu serca
  • Zakrzepica tętnic krezkowych:
    • Miażdżyca
    • Przewlekłe niedokrwienie krezkowe
    • Dyslipidemia
    • Palenie tytoniu
    • Nadciśnienie tętnicze
  • Nieokluzyjne niedokrwienie krezkowe:
    • Hipotensja
    • Wstrząs (septyczny, kardiogenny, hipowolemiczny)
    • Niewydolność serca
    • Leki naczynioaktywne (kokaina, noradrenalina)
  • Zakrzepica żył krezkowych:
    • Nadkrzepliwość
    • Choroby zapalne jelit
    • Zapalenie trzustki
    • Nadciśnienie wrotne
    • Uraz
    • Sepsa

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Ostra okluzyjne niedokrwienie krezkowe zwykle wynika z zjawisk zatorowych lub pęknięcia miażdżycy, więc czynniki ryzyka zwykle są rzeczami, które tworzą ruchome skrzepliny lub które poruszają miażdżycę1.

Predyspozycje anatomiczne

Niektóre obszary jelit są bardziej podatne na niedokrwienie ze względu na swoje unaczynienie1:

  • Obszary podatne na niedokrwienie obejmują zgięcie śledzionowe, połączenie odbytniczo-esicze i środkowy segment jelita czczego
  • SMA jest szczególnie podatna na zatory ze względu na ostry kąt jej wyjścia z aorty i wyższy wskaźnik przepływu krwi

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Rozwój niedokrwienia jelitowego z uszkodzenia okluzyjnego tętnic zależy od lokalizacji niedrożności, naczyń obocznych pacjenta, ostrości i stopnia niedrożności1.

Szczególne sytuacje kliniczne

Niedokrwienie krezkowe w ciężkich stanach klinicznych

Nieokluzyjne niedokrwienie krezkowe jest często spotykane u pacjentów w stanie krytycznym i wiąże się z wysoką śmiertelnością1:

  • NOMI należy podejrzewać u pacjentów w stanie krytycznym z bólem brzucha lub wzdęciem wymagającym wsparcia wazopresorem i z oznakami niewydolności wielonarządowej
  • Główną zasadą postępowania w NOMI jest leczenie podstawowej przyczyny wywołującej
  • Resuscytacja płynowa, optymalizacja rzutu serca i eliminacja wazopresorów pozostają ważnymi środkami pierwotnymi

Zespół przedziału brzusznego z bardzo wysokim ciśnieniem wewnątrzbrzusznym może powodować niedokrwienie jelit, które jest powikłane uszkodzeniem niedokrwienno-reperfuzyjnym po wykonaniu laparotomii dekompresyjnej1.

Niedokrwienie krezkowe w COVID-19

Niedokrwienie krezkowe opisano u pacjentów z COVID-19, prawdopodobnie związane z dużymi zdarzeniami zakrzepowo-zatorowymi, a także z zakrzepicą małych naczyń powiązaną z nadkrzepliwością i zamknięciem fibrynolizy1.

Ciężkie zakażenie COVID-19 i AMI mają złe rokowanie, opóźnienie w diagnozie i interwencji1.

Żywienie dojelitowe jako czynnik ryzyka

Kilka procesów patologicznych może przyczynić się do rozwoju NOMI u pacjentów otrzymujących żywienie dojelitowe12:

  • Absorpcja składników odżywczych przez metabolicznie zestresowane enterocyty zwiększa zapotrzebowanie energetyczne w świetle jelita, co z kolei może obniżyć próg niedokrwienia jelit u pacjentów z jednoczesną hipoperfuzją ogólnoustrojową
  • Preparaty dojelitowe są płynami o wysokiej osmolarności, które mogą powodować szybkie przesunięcie płynów z naczyń trzewnych do światła jelita, tworząc wzdęcie brzucha, które upośledza perfuzję jelitową
  • Żywienie dojelitowe sprzyja nadmiernemu namnażaniu bakterii z jednoczesnym wytwarzaniem gazu wewnątrzświatłowego, wzdęciem i gromadzeniem toksyn mikrobiologicznych

Wnioskiem dotyczącym żywienia dojelitowego może być konieczność wolniejszego zwiększania dawki żywienia ciągłego u pacjentów z wieloma czynnikami ryzyka NOMI1.

Implikacje dla diagnostyki i leczenia

Wczesna diagnostyka i znaczenie szybkiej interwencji

Kluczem do wczesnej diagnozy jest wysoki poziom podejrzenia klinicznego12:

  • Klasyczny scenariusz kliniczny pacjenta skarżącego się na przeszywający ból brzucha z nieujawniającym się badaniem brzucha jest typowy dla wczesnego AMI
  • Światowe Towarzystwo Chirurgii Ratunkowej sugeruje, że „ciężki ból brzucha nieproporcjonalny do wyników badania fizykalnego należy uznać za AMI, dopóki nie zostanie dowiedzione inaczej”

1

Ze względu na trudności w diagnozie i szybki postęp, niedokrwienie krezkowe jest stanem zagrożenia życia, jeśli nie zostanie wcześnie zidentyfikowane i leczone1.

Leczenie różnych typów niedokrwienia krezkowego

Leczenie ostrego niedokrwienia krezkowego zależy od jego typu12:

  • Okluzyjne niedokrwienie krezkowe:
    • Naprawa endowaskularna
    • Otwarta naprawa z lub bez bypassu naczyniowego
  • Nieokluzyjne niedokrwienie krezkowe:
    • Postępowanie w stanie wstrząsu, które koncentruje się na maksymalizacji przepływu krwi trzewnej
  • Niedokrwienie żylne krezkowe:
    • Antykoagulacja
    • Endowaskularne usunięcie skrzepliny

W przypadku wykrycia niedokrwienia krezkowego należy natychmiast rozpocząć resuscytację płynową, aby zwiększyć perfuzję trzewną. Należy natychmiast podać antybiotyki o szerokim spektrum działania1.

Chirurgia kontroli uszkodzeń jest ważnym uzupełnieniem dla pacjentów, którzy wymagają resekcji jelita ze względu na konieczność ponownej oceny żywotności jelit oraz u pacjentów z oporną sepsą1.

Perspektywy leczenia i podejścia terapeutyczne

Istnieje kilka endogennych mechanizmów hamujących uszkodzenia I/R, a wiele leków wykazało efekty ochronne1:

  • Podanie allopurinolu, inhibitora oksydazy ksantynowej, oraz zastosowanie czynnika wzrostu naskórka (EGF) oferowało ochronę po I/R w jelicie cienkim szczura
  • Mechanizmy ochronne hipotermii są wieloczynnikowe i muszą zostać zdefiniowane

Bezpośrednia infuzja leków rozszerzających naczynia, takich jak alkaloid opium – papaweryna, lek rozkurczowy lub prostaglandyna E1, do tętnicy krezkowej zwiększa perfuzję jelita cienkiego1.

Obecnie mechanizmy patofizjologiczne niedokrwienia krezkowego nadal nie są w pełni zrozumiane, co podkreśla potrzebę dalszych badań nad lepszymi metodami leczenia1.

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. 12.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Acute Mesenteric Ischemia – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431068/
    Acute mesenteric ischemia is caused by a sudden decline in blood flow through the mesenteric vessels. […] The condition progresses rapidly. […] The non-specific symptomatology in conjunction with rapid progression of acute mesenteric ischemia likely contribute to the high associated mortality rate of 60-80 percent. […] Acute mesenteric ischemia (AMI) is a condition due to a sudden decline in blood flow through the mesenteric vessels. Without appropriate and timely treatment, necrosis of the small and large intestine results, leading to sepsis and potentially death. […] Due to the difficulty of diagnosis and the rapid progression, the condition is life-threatening if not identified and treated early. […] AMI is classified as either occlusive or nonocclusive mesenteric ischemia (NOMI). Occlusive mesenteric arterial ischemia (OMI) is subdivided into acute thromboembolism and acute thrombosis.
  • #1 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4753178/
    Mesenteric ischemia (MI) is an uncommon medical condition with high mortality rates. includes inadequate blood supply, inflammatory injury and eventually necrosis of the bowel wall. The disease can be divided into acute and chronic MI (CMI), with the first being subdivided into four categories. Therefore, acute MI (AMI) can occur as a result of arterial embolism, arterial thrombosis, mesenteric venous thrombosis and non-occlusive causes. Bowel damage is in proportion to the mesenteric blood flow decrease and may vary from minimum lesions, due to reversible ischemia, to transmural injury, with subsequent necrosis and perforation. CMI is associated to diffuse atherosclerotic disease in more than 95% of cases, with all major mesenteric arteries presenting stenosis or occlusion. […] The thrombosis of mesenteric arteries typically occurs at their origin causing extensive infarction and often affects at least two of the major visceral vessels. It is mainly a complication of preexisting visceral atherosclerotic lesions and involves acute worsening of the already compromised blood flow. It may also be attributed to arterial aneurysm or other vascular pathologies, such as dissection, trauma, mesenteric aneurysm rupture, fibromuscular dysplasia or vasculitis.
  • #1 Diagnosis and Management of Acute Mesenteric Ischemia – Endovascular Today
    https://evtoday.com/articles/2021-jan/diagnosis-and-management-of-acute-mesenteric-ischemia
    Acute mesenteric ischemia is caused by one of four mechanisms: acute arterial embolism (40%-50%), acute arterial thrombosis (20%-30%), nonocclusive mesenteric ischemia (NOMI) (20%), and mesenteric venous thrombosis (5%-15%). […] Regardless of the etiology, the end result is diminished perfusion to the gastrointestinal mucosa, which rapidly leads to perforation, peritonitis, and death if not recognized in a timely fashion. […] The classic presentation of pain out of proportion to exam should trigger a workup focused on diagnosis of mesenteric ischemia. […] Patients who present with acute mesenteric ischemia and known atherosclerosis frequently have ischemia related to thrombosis. […] The degree of vascular compromise is also influenced by the presence of disease within the celiac and inferior mesenteric artery.
  • #1 Mesenteric ischemia | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/mesenteric-ischaemia?lang=us
    Mesenteric ischemia can be classified into broad groups according to etiology: acute mesenteric ischemia (95% cases), chronic mesenteric ischemia (5%). […] Although treatment will vary according to the severity and cause of the ischemia, in general the treatment is surgical. The bowel needs to be assessed for viability and if necrotic needs to be resected. In some instances, endovascular thrombolysis/thrombectomy may be beneficial. Mortality rate is high at ~60% (range 30-90%).
  • #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.
  • #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
    Acute mesenteric ischemia is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately infarction. […] 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. […] If diagnosis and treatment take place before infarction occurs, mortality is low; after intestinal infarction, mortality is high and varies depending on the etiology. For this reason, clinical diagnosis of mesenteric ischemia should supersede diagnostic tests, which may delay treatment.
  • #1 Mesenteric ischaemia | Deranged Physiology
    https://derangedphysiology.com/main/required-reading/gastrointestinal-intensive-care/Chapter-26/mesenteric-ischaemia
    The SMA is particularly susceptible to emboli due to the acute angle of its take-off from the aorta and its higher blood flow rate. […] There are several major ways this thing can happen: […] Acutely: […] Arterial embolism (40% of cases) […] Arterial thrombosis from ruptured atheroma (20-35% of cases) […] Non-occlusive mesenteric hypoperfusion (10-15% of cases) […] Venous infarction (5-15% of cases). […] Occlusive mesenteric ischaemia: […] This is in an acute occlusion of the vessels. […] Non-occlusive mesenteric ischaemia: […] Any increase in mesenteric vascular resistance can lead to mesenteric hypoperfusion. […] Venous mesenteric infarction: […] This is basically a DVT of the gut, with resulting oedema and diminished perfusion. […] Atherosclerosis of mesenteric vessels leads to chronically diminished flow through the mesenteric circulation.
  • #1 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. Obstruction of the venous mesenteric outflow occurs as a result of venous thrombosis of the superior (SMV) or inferior mesenteric veins (IMV). Lastly, chronic mesenteric ischemia most often arises in the setting of atherosclerosis of at least two of the three main visceral arteries (celiac artery, SMA, and inferior mesenteric artery) and is associated with insufficient mesenteric perfusion after meals and oral intake. The pain is thought to be due to an inability to meet the increased blood flow demands of the postprandial intestines.
  • #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 Mesenteric ischemia: what the radiologist needs to know – Olson – Cardiovascular Diagnosis and Therapy
    https://cdt.amegroups.org/article/view/21705/html
    Acute mesenteric ischemia (AMI) is a life-threatening condition that often presents with abdominal pain. […] Mesenteric ischemia is an umbrella term encompassing a broad array of disorders causing insufficient blood flow to the abdominal viscera and has both acute and chronic variations. […] Diagnosis is challenging secondary to the rarity of the disease, its nonspecific clinical presentation, and often subtle or non-specific imaging findings. […] Occlusive mesenteric ischemia can affect either arteries or veins. […] Embolic arterial obstruction is the most common cause of AMI, accounting for approximately 40-50% of cases. […] Thrombotic arterial mesenteric ischemia, responsible for 15-30% of cases, has the worst prognosis of any form of mesenteric ischemia. […] Non-occlusive mesenteric ischemia (NOMI) is caused by intestinal hypoperfusion in the absence of vascular occlusion.
  • #1 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://www.wjgnet.com/2150-5330/full/v7/i1/125.htm
    The thrombosis of mesenteric arteries typically occurs at their origin causing extensive infarction and often affects at least two of the major visceral vessels. It is mainly a complication of preexisting visceral atherosclerotic lesions and involves acute worsening of the already compromised blood flow. It may also be attributed to arterial aneurysm or other vascular pathologies, such as dissection, trauma, mesenteric aneurysm rupture, fibromuscular dysplasia or vasculitis. […] Current pathophysiologic understanding of visceral perfusion suggests a pivotal role for the visceral circulation in the cardiovascular homeostasis regulation. GI perfusion is usually impaired early in situations including critical illness, major surgery and exercise, all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery.
  • #1 Mesenteric ischemia: what the radiologist needs to know – Olson – Cardiovascular Diagnosis and Therapy
    https://cdt.amegroups.org/article/view/21705/html
    NOMI constitutes 5-15% of cases of mesenteric ischemia and is associated with the highest rates of in-hospital mortality. […] Mesenteric venous thrombosis accounts for 5-15% of cases and may be due to clotting diatheses. […] The most important prognostic factor in patients with AMI is intestinal viability. […] Revascularization methods include embolectomy, angioplasty, and bypass. […] Treatment of NOMI is predicated on correction of the underlying cause of reduced intestinal perfusion.
  • #1 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4753178/
    Current pathophysiologic understanding of visceral perfusion suggests a pivotal role for the visceral circulation in the cardiovascular homeostasis regulation. GI perfusion is usually impaired early in situations including critical illness, major surgery and exercise, all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery. […] Tissue damage results either from ischemic or reperfusion injury. Within 3-4 h after the onset of ischemia, there is necrosis of the mucosal villi and within 6 h, transmural, mural or mucosal infarction can be observed. […] Inflammatory vascular disease, smaller vessels are commonly affected. On the other hand, NOMI results from hypoperfusion with secondary severe and prolonged visceral vasoconstriction. The most common initiating conditions involve systemic shock due to decreased cardiac output following a myocardial infarction or congestive heart failure, septic shock or hypovolemia.
  • #1 Acute Mesenteric Ischemia: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/189146-overview
    Because the four types of AMI share similarities and a final common pathway (ie, bowel infarction and death, if not properly treated), they may usefully be discussed together. […] Insufficient blood perfusion of the small bowel and colon may result from embolic or thrombotic arterial occlusion (AMAE or AMAT), thrombotic venous occlusion (ie, MVT), or nonocclusive processes such as vasospasm or low cardiac output (NOMI). […] Whether the occlusion is arterial or venous, hemorrhagic infarction leading to perforation is the common pathologic pathway. […] Injury severity is inversely proportional to the mesenteric blood flow and is influenced by the number of vessels involved, systemic mean blood pressure, duration of ischemia, and collateral circulation. […] Damage to the affected bowel portion may range from reversible ischemia to transmural infarction with necrosis and perforation.
  • #1 Nonocclusive mesenteric ischemia – UpToDate
    https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia
    Acute mesenteric ischemia refers to the sudden onset of intestinal hypoperfusion, which can be due to a nonocclusive reduction of arterial blood flow. Nonocclusive mesenteric ischemia (NOMI) is most commonly due to primary mesenteric arterial vasoconstriction. […] The pathogenesis of NOMI is related to a homeostatic mechanism that maintains cardiac and cerebral blood flow at the expense of the mesenteric and peripheral circulation. […] Vasopressin and angiotensin are likely the neurohormonal mediators of this phenomenon. Spasm may also be triggered by other vasoactive and cardiotonic drugs.
  • #1 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). […] NOMI is considered to be associated with adverse neurological outcomes in CA patients. Therefore, NOMI should not only be regarded as a post-resuscitation complication but also as one of the prognostic markers in CA patients. This paper summarizes current knowledge on NOMI’s pathophysiology, diagnosis, treatment, and prognostic significance in CA patients. […] Currently, the exact pathophysiology of NOMI is still not fully understood. However, it is probably closely associated with the splanchnic blood flow reduction in shock conditions and the use of vasopressors. […] The mucosa of the intestinal wall is the layer most susceptible to the effects of ischemia. […] Ischemia damage starts from the mucosa and continues towards the serosa. Subsequent reperfusion of the intestine results in further damage to the mucosa.
  • #1 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4753178/
    Finally, MVT includes primary disorder with no identifiable predisposing factor and secondary MVT as well. The most common cause of secondary MVT is hypercoagulability. Additionally, in more than 95% of patients, diffuse atherosclerotic disease decreases the blood flow to the bowel and causes CMI. Other causes refer to fibromuscular dysplasia, vasculitis including Takayasu arteritis, giant cell arteritis, polyarteritis nodosa, systemic lupus erythematosus, thromboangiitis obliterans, malignancy and radiation. Subsequent complications conclude to thrombotic and embolic phenomena leading to manifestations of AMI.
  • #1 Diagnosis and Management of Acute Mesenteric Ischemia – Endovascular Today
    https://evtoday.com/articles/2021-jan/diagnosis-and-management-of-acute-mesenteric-ischemia
    NOMI can result from systemic or regional low flow states. […] These can be a result of shock (septic, cardiogenic, or hypovolemic), leading to activation of the renin-angiotensin-aldosterone pathway and subsequently causing splanchnic vasoconstriction. […] Mesenteric vein thrombosis may also lead to bowel infarction with a mortality rate of 13% to 50%. […] This outflow obstruction leads to bowel wall edema and an influx of intraluminal fluid. […] The massive pressurization of the bowel leads to obstruction of the capillaries as well, effectively inhibiting gas exchange and resulting in secondary arterial compromise.
  • #1 Improving the ED Diagnosis of Mesenteric Ischemia – emDocs
    https://www.emdocs.net/improving-the-ed-diagnosis-of-mesenteric-ischemia/
    Mesenteric ischemia remains a high mortality and easily missed diagnosis in emergency medicine. […] Mesenteric ischemia rises from various etiologies that involve thromboembolic occlusion or non-occlusive supply and demand mismatch. […] While all etiologies of mesenteric ischemia converge on the process of bowel ischemia, the underlying pathophysiology, and therefore, risk factors and presentation vary across four major categories. […] Arterial embolism accounts for the majority of cases of mesenteric ischemia with half occurring at the superior mesenteric artery (SMA) supplying the midgut. […] Nonocclusive arterial mesenteric ischemia results from inadequate supply of blood due to an underlying critical illness and most commonly affects the descending or sigmoid colon. […] Mesenteric vein thrombosis presents more insidiously with vague abdominal pain usually for greater than 24 hours and even one month from onset. […] Accurate and timely diagnosis significantly improves mortality in this deadly disease.
  • #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/
    Arterial ischemia initiates alterations in tissues by blocking the oxygen supply, thus impeding aerobic energetic metabolism. […] During the ischemia process, aside from the inadequate supply of oxygen, with the consequent compromise of oxidative phosphorylation in the mitochondria, there is an accumulation of metabolites, which, directly or through mediators, can cause cellular injury. […] 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.
  • #1 Acute Mesenteric Ischemia: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/189146-overview
    As the ischemia persists, the mucosal barrier becomes disrupted, and bacteria, toxins, and vasoactive substances are released into the systemic circulation. […] The mechanism responsible for ischemia in this setting is a massive influx of fluid into the bowel wall and lumen, which results in systemic hypovolemia and hemoconcentration. […] The consequent bowel edema and decreased outflow of blood secondary to venous thrombosis impede the inflow of arterial blood, and this leads to bowel ischemia.
  • #1 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://www.wjgnet.com/2150-5330/full/v7/i1/125.htm
    Tissue damage results either from ischemic or reperfusion injury. Within 3-4 h after the onset of ischemia, there is necrosis of the mucosal villi and within 6 h, transmural, mural or mucosal infarction can be observed. […] Inflammatory vascular disease, smaller vessels are commonly affected. On the other hand, NOMI results from hypoperfusion with secondary severe and prolonged visceral vasoconstriction. The most common initiating conditions involve systemic shock due to decreased cardiac output following a myocardial infarction or congestive heart failure, septic shock or hypovolemia. […] The aim of this review was to evaluate the results of surgical treatment for MI and to present the recent literature in order to provide an update on the current concepts of surgical management of the disease.
  • #1 Epidemiology and Pathophysiology of Mesenteric Vascular Disease | Thoracic Key
    https://thoracickey.com/epidemiology-and-pathophysiology-of-mesenteric-vascular-disease/
    Severe acute intestinal ischemia results from sudden symptomatic reduction in intestinal blood flow of sufficient magnitude to potentially result in intestinal infarction. […] Acute mesenteric ischemia, whether the underlying cause is embolic or thrombotic, may eventually lead to intestinal infarction. […] Hypoxia and hypercarbia that occur during flow interruption, and reperfusion injury once intestinal blood flow is restored, all contribute to tissue loss. […] Reperfusion injury is believed to be principally mediated by activation of the enzyme xanthine oxidase and recruitment and activation of circulating neutrophils (PMNs). […] The mechanism of injury likely involves production of oxygen-derived free radicals by xanthine oxidase that then causes profound local tissue injury through lipid peroxidation, membrane disruption, and increased microvascular permeability.
  • #1 Epidemiology and Pathophysiology of Mesenteric Vascular Disease | Thoracic Key
    https://thoracickey.com/epidemiology-and-pathophysiology-of-mesenteric-vascular-disease/
    The ischemic endothelium recruits PMNs in an autocrine and paracrine manner by secreting chemotactic cytokines (tumor necrosis factor [TNF]-, interleukin [IL]-1, platelet-derived growth factor [PDGF]) that perpetuate further damage to the reperfused tissue. […] Activation of this endogenous inflammatory cascade is not restricted to the injured organ and may also have deleterious systemic effects, with cardiac, pulmonary, and other organ system dysfunction. […] Nonocclusive mesenteric ischemia was first recognized in autopsies of patients with small-intestinal gangrene in the absence of arterial or venous occlusion. […] Investigation of the regulatory mechanisms of mesenteric circulation has demonstrated that the pathophysiology of NOMI is multifactorial. […] Mesenteric vasoconstriction, intestinal hypoxia, and ischemia-reperfusion injury all contribute to development of NOMI. […] Restoration of blood flow to the ischemic intestine may be complicated by reperfusion injury. […] The degree of reperfusion injury is thus related to the frequency and duration of the ischemic episodes.
  • #1 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    Numerous endogenous and exogenous humoral factors affect the splanchnic circulation. […] Norepinephrine and high doses of epinephrine produce intense vasoconstriction by stimulating the adrenergic receptors. […] Other pharmacologic compounds that decrease splanchnic blood flow include: Vasopressin, Phenylephrine, Digoxin. […] Low-dose dopamine causes splanchnic vasodilation, whereas higher doses lead to vasoconstriction by stimulating alpha adrenergic receptors. […] Exogenous agents that increase mesenteric blood flow include: Papaverine, Adenosine, Dobutamine, Fenoldopam, Sodium nitroprusside. […] In addition, numerous natural neurotransmitters can serve as splanchnic vasodilators, such as: Acetylcholine, Histamine, Nitric oxide, Leukotrienes, Thromboxane analogues, Glucagon. […] Areas prone to ischemia include the splenic flexure, rectosigmoid junction, and middle segment of jejunum.
  • #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 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    A discrepancy between tissue oxygen demand and supply raises the concentration of local metabolites such as hydrogen, potassium, carbon dioxide, and adenosine, resulting in vasodilation, and hyperemia. […] An acute decrease in perfusion pressure is compensated for by a reduction in arteriolar wall tension, thereby maintaining splanchnic blood flow. […] The extrinsic neural component of splanchnic circulatory regulation comprises the alpha-activated vasoconstrictor fibers. […] Intense activation of vasoconstrictor fibers through alpha-adrenergic stimulation results in vasoconstriction of small vessels and a decrease in mesenteric blood flow. […] After periods of prolonged alpha-adrenergic vasoconstriction, blood flow increases, presumably through beta-adrenergic stimulation, which acts as a protective response.
  • #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/
    Injury provoked by splanchnic I/R is characterized by intense infiltrated inflammations, found predominantly in the mucosae and submucosae, causing endothelial destruction. […] The process of translocation involves the initial contact of the bacteria with the intestine wall, which alone can precipitate the production of cytokines and a subsequent inflammatory response. […] The activation of NF-kB leads to the coordinated expression of many genes which codify proteins involved in mediator synthesis and in the amplification and maintenance of inflammatory response. […] The activation of the complement system can lead to the translocation of NF-kB and an increase in the transcription of iNOS. […] The depletion or inhibition of the complement could diminish many of the mediators of I/R injury.
  • #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 accumulation of platelets in the postischemic microvasculature could contribute significantly to the manifestation of I/R lesions. […] Serotonin is a bioactive amine, which acts, in several physiological phenomena like neurotransmission, intestinal movement, platelet activation and vasoconstriction. […] It has been demonstrated recently that pancreatic proteases are involved in the production of inflammatory mediators after intestinal I/R, such as trypsin and metalloproteinase-9 (MMP-9). […] More recent studies indicate that apoptosis is clearly a significant and, perhaps, the principal contributor to cellular death after I/R injury. […] The main executors of „programmed cell death” are the endoprotease cysteines called caspases. […] Reactive chemical species initiate a sequence of events including the activation of neutrophils and the release of harmful substances like PAF and histamine.
  • #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. […] Vasoactive and humoral factors control the regulation of vascular tone of mesenteric circulation in response to periods of stress such as systemic hypotension or postprandial state. […] Reduction in blood supply to the mesentery causes adaptive changes in the splanchnic circulation.
  • #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/
    Multiple organ failure is a frequent complication after intestinal I/R and involves organs like the liver, heart, kidneys and lungs. […] Several endogenous mechanisms exist to inhibit I/R lesions and many drugs have shown protective effects. […] The administration of allopurinol, a xanthine-oxidase inhibitor and the use of epidermal growth factor (EGF) offered protection after I/R in rat small-intestine. […] The protection mechanisms of hypothermia are multifactoral and have to be defined. […] 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 Mesenteric ischemia pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Mesenteric_ischemia_pathophysiology
    The sequence of events that take place in the small intestine subsequent to decreased blood flow includes ischemic insult, decreased delivery of oxygen and nutrients, disruption in cellular metabolism, tissue injury due to hypoxia and reperfusion, full thickness necrosis of the bowel, and perforation of the bowel wall. […] Vascular occlusion leads to blood flow metabolic demand, mucosal barrier disruption and bacterial translocation into the circulation, anaerobic glycolysis in mucosa and lactate production, activation of vascular and humoral factors leading to vasoconstriction, systemic activation of inflammatory response, lactic acidosis, intestinal necrosis, and multiorgan failure. […] Hypovolemia, cardiac failure, endogenous vasoconstriction, and splanchnic vasoconstriction lead to gut mucosal hypoperfusion, restoration of blood by vasodilation of collaterals, gut mucosal barrier disruption, ischemia-reperfusion injury, and increased mucosal perfusion to bacterial toxins, activating the inflammatory response.
  • #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. […] The most common universal presenting symptom is abdominal pain; for acute ischemia this is classically described as pain out of proportion to exam with an abdominal bruit on auscultation, although this is not present in all patients.
  • #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
    Mesenteric venous thrombosis (MVT) accounts for less than 10% of cases of mesenteric infarction. […] The additional components altering blood flow include portal hypertension, pancreatitis, inflammatory bowel disease, sepsis, and trauma. […] 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 exam is classic for early AMI. […] A careful history is important because distinct clinical scenarios are associated with the pathophysiological form of AMI. […] Patients with mesenteric arterial thrombosis often have a history of chronic postprandial abdominal pain, progressive weight loss, and previous revascularization procedures for mesenteric arterial occlusion. […] Patients with NOMI have pain that is generally more diffuse and episodic associated with poor cardiac performance.
  • #1 Mesenteric ischaemia | Deranged Physiology
    https://derangedphysiology.com/main/required-reading/gastrointestinal-intensive-care/Chapter-26/mesenteric-ischaemia
    The collateral circulation allows a major visceral arterial occlusion to be clinically silent, and to go virtually unnoticed. […] Occlusive acute mesenteric ischaemia tends to result from embolic phenomena or atheroma rupture, so the risk factors tend to be things which create mobile thrombi or which agitate atheromae. […] Non-occlusive acute mesenteric ischaemia is a phenomenon where an otherwise relatively normal mesenteric vascular bed is subjected to some sort of sudden increase in vascular resistance, or a sudden decrease in blood flow, or some combination of both. […] The World Society of Emergency Surgery suggest that „severe abdominal pain out of proportion to physical examination findings should be assumed to be AMI until disproven”. […] Specific management: […] Occlusive mesenteric ischaemia:
  • #1 Acute mesenteric ischaemia: a pictorial review | Insights into Imaging | Full Text
    https://insightsimaging.springeropen.com/articles/10.1007/s13244-018-0641-2
    The development of intestinal ischaemia from an arterially obstructing lesion depends upon the location of the obstruction, the patients collateral vasculature, acuity and degree of the obstruction. […] In the presence of obstructions involving all three major arteries (coeliac, SMA and IMA), the phrenic, lumbar and pelvic collateral arteries may dilate to provide accessory visceral blood flow. […] However, if the lesion is distal to the point of collateral flow, the collateral supply is ineffective and ischaemia is more likely to ensue. […] In the setting of non-occlusive causes such as septic, haemorrhagic or cardiogenic shock, a profound drop of systemic blood pressure results in a reflexive mesenteric arterial vasoconstriction with diversion of blood flow to the brain and heart. […] As a consequence, intestinal perfusion will decrease dramatically and nonocclusive bowel ischaemia may develop.
  • #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
    Severe COVID-19 infection and AMI have a poor prognosis, delay in diagnosis, and intervention. […] Non-occlusive mesenteric ischemia (NOMI) should be suspected in critically ill patients with abdominal pain or distension requiring vasopressor support and evidence of multiorgan dysfunction. […] The central principle of NOMI management is the treatment of the underlying precipitating cause. Fluid resuscitation, optimization of cardiac output, and elimination of vasopressors remain important primary measures.
  • #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
    Abdominal compartment syndrome with very high intraabdominal pressure may cause bowel ischemia that is complicated with ischemia-reperfusion injury when decompression laparotomy is performed. […] 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 classic presentation of AMI, i.e., severe, poorly localized abdominal pain that is out of proportion to the physical examination, is becoming less common, while the acute on chronic presentations of mesenteric ischemia are more typical, and probably underdiagnosed. […] Patients presenting with symptomatic chronic mesenteric ischemia are at high risk of developing in-hospital AMI.
  • #1 Enteral Feeding Induced Nonocclusive Mesenteric Ischemia | ACS
    https://www.facs.org/for-medical-professionals/news-publications/journals/case-reviews/issues/v3n7/ramey-nonocclusive-mesenteric/
    Nonocclusive mesenteric ischemia (NOMI) is caused by inadequate perfusion of the intestinal mucosa secondary to a nonocclusive reduction in arterial blood flow. […] NOMI encompasses all forms of mesenteric ischemia with patent mesenteric arteries. […] This condition is most commonly seen in patients older than 50. It is caused by decreased blood flow to mesenteric vessels secondary to impediments to blood flow, such as cardiovascular or renal disease, hypovolemia, sepsis, dialysis, and vasoconstricting medications. […] Roughly 20-30% of all cases of mesenteric ischemia are caused by NOMI, with a mortality rate ranging from 50% to 80%. […] Several underlying pathological processes may contribute to the development of NOMI. First, the absorption of nutrients by metabolically stressed enterocytes increases intraluminal energy demands, which, in turn, can decrease the threshold for bowel ischemia in patients with concomitant systemic hypoperfusion.
  • #1 Enteral Feeding Induced Nonocclusive Mesenteric Ischemia | ACS
    https://www.facs.org/for-medical-professionals/news-publications/journals/case-reviews/issues/v3n7/ramey-nonocclusive-mesenteric/
    Secondly, enteral formulas are high-osmolarity fluids that can cause a rapid fluid shift from splanchnic vessels into the intestinal lumen. […] This creates abdominal distension, which compromises intestinal perfusion. […] Finally, enteral nutrition supports bacterial overgrowth with concomitant intraluminal gas production, distension, and microbial toxin accumulation. […] The goal of treatment in patients with NOMI is promptly restoring adequate perfusion to the intestines. […] Direct infusion of vasodilators, such as the opium alkaloid antispasmodic medication Papaverine or prostaglandin E1, into the mesenteric artery increases small bowel perfusion. […] We conclude that our patients continuous feeds were advanced too quickly in the setting of multiple risk factors for NOMI.
  • #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
    When the diagnosis of AMI is made, fluid resuscitation should commence immediately to enhance visceral perfusion. […] Broad-spectrum antibiotics should be administered immediately. […] Damage control surgery is an important adjunct for patients who require intestinal resection due to the necessity to reassess bowel viability and in patients with refractory sepsis. […] Mesenteric venous thrombosis can often be successfully treated with a continuous infusion of unfractionated heparin. […] When NOMI is suspected, the focus is to correct the underlying cause wherever possible and to improve mesenteric perfusion. […] The finding of massive gut necrosis requires careful assessment of the patients underlying co-morbidities and advanced directives in order to judge whether comfort carries the best treatment.
  • #2 Acute Mesenteric Ischemia: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/189146-overview
    Acute mesenteric ischemia (AMI) is a syndrome caused by inadequate blood flow through the mesenteric vessels, resulting in ischemia and eventual gangrene of the bowel wall. […] Broadly, AMI may be classified as either arterial or venous. AMI as arterial disease may be subdivided into nonocclusive mesenteric ischemia (NOMI) and occlusive mesenteric arterial ischemia (OMAI); OMAI may be further subdivided into acute mesenteric arterial embolism (AMAE) and acute mesenteric arterial thrombosis (AMAT). AMI as venous disease takes the form of mesenteric venous thrombosis (MVT). […] The four types of AMI have somewhat different predisposing factors, clinical pictures, and prognoses. […] A secondary clinical entity of mesenteric ischemia occurs as a consequence of mechanical obstruction (eg, from internal hernia with strangulation, volvulus, or intussusception).
  • #2 Mesenteric ischemia | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/mesenteric-ischaemia?lang=us
    Mesenteric ischemia can be classified into broad groups according to etiology: acute mesenteric ischemia (95% cases), chronic mesenteric ischemia (5%). […] Although treatment will vary according to the severity and cause of the ischemia, in general the treatment is surgical. The bowel needs to be assessed for viability and if necrotic needs to be resected. In some instances, endovascular thrombolysis/thrombectomy may be beneficial. Mortality rate is high at ~60% (range 30-90%).
  • #2 Mesenteric artery ischemia Information | Mount Sinai – New York
    https://www.mountsinai.org/health-library/diseases-conditions/mesenteric-artery-ischemia
    Mesenteric artery ischemia occurs when there is a narrowing or blockage of one or more of the three major arteries that supply the small and large intestines. These are called the mesenteric arteries. […] Hardening of the arteries occurs when fat, cholesterol, and other substances build up in the walls of arteries. This is more common in smokers and in people with high blood pressure or high blood cholesterol. […] This narrows the blood vessels and reduces blood flow to the intestines. Like every other part of the body, blood brings oxygen to the intestines. When the oxygen supply is reduced, symptoms may occur. […] The blood supply to the intestines may be suddenly blocked by a blood clot (embolus). The clots most often come from the heart or aorta. These clots are more commonly seen in people with abnormal heart rhythm.
  • #2 Mesenteric ischemia – WikEM
    https://wikem.org/wiki/Mesenteric_ischemia
    Most commonly superior mesenteric artery (SMA), thus typically involves small bowel (especially jejunum) and right colon […] 4 distinct entities: Mesenteric arterial embolism (ex. Afib), Mesenteric arterial thrombosis (ex. Vasculopath), Nonocclusive mesenteric ischemia (ex. Hypovolemia from diuretics), Mesenteric venous thrombosis (ex. hypercoagulable state) […] Nonocclusive mesenteric ischemia is associated with a hypovolemic state, heart failure, myocardial infarction with decreased output, sepsis, and diuretic use […] Anticoagulation with heparin is usually appropriate in all patients with mesenteric ischemia, with exception of those with typical contraindications.
  • #2 Diagnosis and Management of Acute Mesenteric Ischemia – Endovascular Today
    https://evtoday.com/articles/2021-jan/diagnosis-and-management-of-acute-mesenteric-ischemia
    Acute mesenteric ischemia is caused by one of four mechanisms: acute arterial embolism (40%-50%), acute arterial thrombosis (20%-30%), nonocclusive mesenteric ischemia (NOMI) (20%), and mesenteric venous thrombosis (5%-15%). […] Regardless of the etiology, the end result is diminished perfusion to the gastrointestinal mucosa, which rapidly leads to perforation, peritonitis, and death if not recognized in a timely fashion. […] The classic presentation of pain out of proportion to exam should trigger a workup focused on diagnosis of mesenteric ischemia. […] Patients who present with acute mesenteric ischemia and known atherosclerosis frequently have ischemia related to thrombosis. […] The degree of vascular compromise is also influenced by the presence of disease within the celiac and inferior mesenteric artery.
  • #2 Acute mesenteric ischemia: A review of the main imaging techniques and signs | Radiología (English Edition)
    https://www.elsevier.es/en-revista-radiologia-english-edition–419-articulo-acute-mesenteric-ischemia-a-review-S2173510720300501?newsletter=true
    The most common cause of AMI is arterial, such as mesenteric artery embolism (MAE) and mesenteric artery thrombosis (MAT); other less common causes are venous, such as mesenteric vein thrombosis (MVT), and low-output states such as non-occlusive mesenteric ischaemia (NOMI). […] Arterial embolism is the most common cause of AMI and accounts for 40-50% of all cases. […] The main risk factors include atrial fibrillation, recent myocardial infarction, congestive heart failure, cardiomyopathies and embolisms due to aortic lesion or atherosclerosis. […] Arterial thrombosis accounts for approximately 25-30% of cases of AMI. […] MVT accounts for 5-10% of all cases of AMI. […] NOMI is often seen in patients of advanced age, and is responsible for approximately 20-30% of cases of AMI. […] This condition is characterised by high rates of morbidity and mortality, due to patients’ advanced age and diagnostic delay.
  • #2 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://www.wjgnet.com/2150-5330/full/v7/i1/125.htm
    The thrombosis of mesenteric arteries typically occurs at their origin causing extensive infarction and often affects at least two of the major visceral vessels. It is mainly a complication of preexisting visceral atherosclerotic lesions and involves acute worsening of the already compromised blood flow. It may also be attributed to arterial aneurysm or other vascular pathologies, such as dissection, trauma, mesenteric aneurysm rupture, fibromuscular dysplasia or vasculitis. […] Current pathophysiologic understanding of visceral perfusion suggests a pivotal role for the visceral circulation in the cardiovascular homeostasis regulation. GI perfusion is usually impaired early in situations including critical illness, major surgery and exercise, all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery.
  • #2 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4753178/
    Mesenteric ischemia (MI) is an uncommon medical condition with high mortality rates. includes inadequate blood supply, inflammatory injury and eventually necrosis of the bowel wall. The disease can be divided into acute and chronic MI (CMI), with the first being subdivided into four categories. Therefore, acute MI (AMI) can occur as a result of arterial embolism, arterial thrombosis, mesenteric venous thrombosis and non-occlusive causes. Bowel damage is in proportion to the mesenteric blood flow decrease and may vary from minimum lesions, due to reversible ischemia, to transmural injury, with subsequent necrosis and perforation. CMI is associated to diffuse atherosclerotic disease in more than 95% of cases, with all major mesenteric arteries presenting stenosis or occlusion. […] The thrombosis of mesenteric arteries typically occurs at their origin causing extensive infarction and often affects at least two of the major visceral vessels. It is mainly a complication of preexisting visceral atherosclerotic lesions and involves acute worsening of the already compromised blood flow. It may also be attributed to arterial aneurysm or other vascular pathologies, such as dissection, trauma, mesenteric aneurysm rupture, fibromuscular dysplasia or vasculitis.
  • #2 Mesenteric Ischemia
    https://errolozdalga.com/medicine/pages/mesentericischemia.cr.5.16.11.html
    They have bad preexisting atherosclerosis, and often have a history of Intestinal Angina representing chronic mesenteric ischemia where they have postprandial pain, nausea/vomiting, early satiety, and weight loss. […] Nonocclusive Ischemia: 20-30% of cases – Pathogenesis involves splanchnic hypoperfusion and vasoconstriction, often with vasospasm. […] This occurs in patients with bad atherosclerotic disease who are hypotensive (i.e. sepsis, CHF, etc), often on pressors, or other meds that cause decreased intestinal blood flow or vasoconstriction (Digoxin, Cocaine, Diuretics).
  • #2 Nonocclusive mesenteric ischemia – UpToDate
    https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia
    Acute mesenteric ischemia refers to the sudden onset of intestinal hypoperfusion, which can be due to a nonocclusive reduction of arterial blood flow. Nonocclusive mesenteric ischemia (NOMI) is most commonly due to primary mesenteric arterial vasoconstriction. […] The pathogenesis of NOMI is related to a homeostatic mechanism that maintains cardiac and cerebral blood flow at the expense of the mesenteric and peripheral circulation. […] Vasopressin and angiotensin are likely the neurohormonal mediators of this phenomenon. Spasm may also be triggered by other vasoactive and cardiotonic drugs.
  • #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 Enteral Feeding Induced Nonocclusive Mesenteric Ischemia | ACS
    https://www.facs.org/for-medical-professionals/news-publications/journals/case-reviews/issues/v3n7/ramey-nonocclusive-mesenteric/
    Nonocclusive mesenteric ischemia (NOMI) is caused by inadequate perfusion of the intestinal mucosa secondary to a nonocclusive reduction in arterial blood flow. […] NOMI encompasses all forms of mesenteric ischemia with patent mesenteric arteries. […] This condition is most commonly seen in patients older than 50. It is caused by decreased blood flow to mesenteric vessels secondary to impediments to blood flow, such as cardiovascular or renal disease, hypovolemia, sepsis, dialysis, and vasoconstricting medications. […] Roughly 20-30% of all cases of mesenteric ischemia are caused by NOMI, with a mortality rate ranging from 50% to 80%. […] Several underlying pathological processes may contribute to the development of NOMI. First, the absorption of nutrients by metabolically stressed enterocytes increases intraluminal energy demands, which, in turn, can decrease the threshold for bowel ischemia in patients with concomitant systemic hypoperfusion.
  • #2 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
    Mesenteric venous thrombosis (MVT) accounts for less than 10% of cases of mesenteric infarction. […] The additional components altering blood flow include portal hypertension, pancreatitis, inflammatory bowel disease, sepsis, and trauma. […] 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 exam is classic for early AMI. […] A careful history is important because distinct clinical scenarios are associated with the pathophysiological form of AMI. […] Patients with mesenteric arterial thrombosis often have a history of chronic postprandial abdominal pain, progressive weight loss, and previous revascularization procedures for mesenteric arterial occlusion. […] Patients with NOMI have pain that is generally more diffuse and episodic associated with poor cardiac performance.
  • #2 Acute Mesenteric Ischemia: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/189146-overview
    As the ischemia persists, the mucosal barrier becomes disrupted, and bacteria, toxins, and vasoactive substances are released into the systemic circulation. […] The mechanism responsible for ischemia in this setting is a massive influx of fluid into the bowel wall and lumen, which results in systemic hypovolemia and hemoconcentration. […] The consequent bowel edema and decreased outflow of blood secondary to venous thrombosis impede the inflow of arterial blood, and this leads to bowel ischemia.
  • #2 Acute Mesenteric Ischemia – Gastrointestinal Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/gastrointestinal-disorders/acute-abdomen-and-surgical-gastroenterology/acute-mesenteric-ischemia
    Acute mesenteric ischemia is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately infarction. […] 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. […] If diagnosis and treatment take place before infarction occurs, mortality is low; after intestinal infarction, mortality is high and varies depending on the etiology. For this reason, clinical diagnosis of mesenteric ischemia should supersede diagnostic tests, which may delay treatment.
  • #2 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4753178/
    Current pathophysiologic understanding of visceral perfusion suggests a pivotal role for the visceral circulation in the cardiovascular homeostasis regulation. GI perfusion is usually impaired early in situations including critical illness, major surgery and exercise, all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery. […] Tissue damage results either from ischemic or reperfusion injury. Within 3-4 h after the onset of ischemia, there is necrosis of the mucosal villi and within 6 h, transmural, mural or mucosal infarction can be observed. […] Inflammatory vascular disease, smaller vessels are commonly affected. On the other hand, NOMI results from hypoperfusion with secondary severe and prolonged visceral vasoconstriction. The most common initiating conditions involve systemic shock due to decreased cardiac output following a myocardial infarction or congestive heart failure, septic shock or hypovolemia.
  • #2 Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities
    https://www.wjgnet.com/2150-5330/full/v7/i1/125.htm
    Mesenteric ischemia (MI) is an uncommon medical condition with high mortality rates. includes inadequate blood supply, inflammatory injury and eventually necrosis of the bowel wall. The disease can be divided into acute and chronic MI (CMI), with the first being subdivided into four categories. Therefore, acute MI (AMI) can occur as a result of arterial embolism, arterial thrombosis, mesenteric venous thrombosis and non-occlusive causes. Bowel damage is in proportion to the mesenteric blood flow decrease and may vary from minimum lesions, due to reversible ischemia, to transmural injury, with subsequent necrosis and perforation. CMI is associated to diffuse atherosclerotic disease in more than 95% of cases, with all major mesenteric arteries presenting stenosis or occlusion. Because of a lack of specific signs or due to its sometime quiet presentation, this condition is frequently diagnosed only at an advanced stage.
  • #2 Epidemiology and Pathophysiology of Mesenteric Vascular Disease | Thoracic Key
    https://thoracickey.com/epidemiology-and-pathophysiology-of-mesenteric-vascular-disease/
    Severe acute intestinal ischemia results from sudden symptomatic reduction in intestinal blood flow of sufficient magnitude to potentially result in intestinal infarction. […] Acute mesenteric ischemia, whether the underlying cause is embolic or thrombotic, may eventually lead to intestinal infarction. […] Hypoxia and hypercarbia that occur during flow interruption, and reperfusion injury once intestinal blood flow is restored, all contribute to tissue loss. […] Reperfusion injury is believed to be principally mediated by activation of the enzyme xanthine oxidase and recruitment and activation of circulating neutrophils (PMNs). […] The mechanism of injury likely involves production of oxygen-derived free radicals by xanthine oxidase that then causes profound local tissue injury through lipid peroxidation, membrane disruption, and increased microvascular permeability.
  • #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 accumulation of platelets in the postischemic microvasculature could contribute significantly to the manifestation of I/R lesions. […] Serotonin is a bioactive amine, which acts, in several physiological phenomena like neurotransmission, intestinal movement, platelet activation and vasoconstriction. […] It has been demonstrated recently that pancreatic proteases are involved in the production of inflammatory mediators after intestinal I/R, such as trypsin and metalloproteinase-9 (MMP-9). […] More recent studies indicate that apoptosis is clearly a significant and, perhaps, the principal contributor to cellular death after I/R injury. […] The main executors of „programmed cell death” are the endoprotease cysteines called caspases. […] Reactive chemical species initiate a sequence of events including the activation of neutrophils and the release of harmful substances like PAF and histamine.
  • #2 Mesenteric ischemia: Types, symptoms, and more
    https://www.medicalnewstoday.com/articles/mesenteric-ischemia
    Mesenteric ischemia, or small bowel ischemia, involves a blockage of blood flow to the small intestine. […] Small bowel or mesenteric ischemia occurs when the blood vessels leading toward or away from the small intestine become fully or partly blocked. This is often due to a blood clot, but it can happen for other reasons. […] Both acute and chronic mesenteric ischemia can result from: a blood clot in the arteries that bring blood to the intestine, low blood pressure, atherosclerosis, scar tissue that develops after surgery, which can obstruct the bowel or blood vessels, a hernia. […] An acute blockage involves a sudden drop in blood pressure and can result from: a traumatic injury, a blood clot or scarring developing after surgery, a worsening of chronic mesenteric ischemia, low blood pressure due, for instance, to: trauma or recent cardiac or abdominal surgery, heart failure, dehydration, drugs that reduce blood flow, such as Vasopressin, sepsis.
  • #2 Enteral Feeding Induced Nonocclusive Mesenteric Ischemia | ACS
    https://www.facs.org/for-medical-professionals/news-publications/journals/case-reviews/issues/v3n7/ramey-nonocclusive-mesenteric/
    Secondly, enteral formulas are high-osmolarity fluids that can cause a rapid fluid shift from splanchnic vessels into the intestinal lumen. […] This creates abdominal distension, which compromises intestinal perfusion. […] Finally, enteral nutrition supports bacterial overgrowth with concomitant intraluminal gas production, distension, and microbial toxin accumulation. […] The goal of treatment in patients with NOMI is promptly restoring adequate perfusion to the intestines. […] Direct infusion of vasodilators, such as the opium alkaloid antispasmodic medication Papaverine or prostaglandin E1, into the mesenteric artery increases small bowel perfusion. […] We conclude that our patients continuous feeds were advanced too quickly in the setting of multiple risk factors for NOMI.
  • #2 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
    Abdominal compartment syndrome with very high intraabdominal pressure may cause bowel ischemia that is complicated with ischemia-reperfusion injury when decompression laparotomy is performed. […] 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 classic presentation of AMI, i.e., severe, poorly localized abdominal pain that is out of proportion to the physical examination, is becoming less common, while the acute on chronic presentations of mesenteric ischemia are more typical, and probably underdiagnosed. […] Patients presenting with symptomatic chronic mesenteric ischemia are at high risk of developing in-hospital AMI.
  • #2 Mesenteric ischaemia | Deranged Physiology
    https://derangedphysiology.com/main/required-reading/gastrointestinal-intensive-care/Chapter-26/mesenteric-ischaemia
    Endovascular repair […] Open repair with or without vascular bypass […] Non-occlusive mesenteric ischaemia: […] Management of the shock state which focuses on maximising splanchnic blood flow. […] Venous mesenteric ischaemia: […] Anticoagulation […] Endovascular clot retrieval. […] Like with everything in ICU, the prognosis of mesenteric ischaemia is mainly related to whatever else is going on.
  • #3 Mesenteric ischemia | Radiology Reference Article | Radiopaedia.org
    https://radiopaedia.org/articles/mesenteric-ischaemia?embed_domain=hackmd.io%2F%40yipuafecsl2jsu8smr5njq%2Fbnjhjgjghjghjghfavicon.ico&lang=us
    Mesenteric ischemia can be classified into broad groups according to etiology: acute mesenteric ischemia (95% cases), arterial occlusive mesenteric ischemia (60-85% cases), non-occlusive mesenteric ischemia (NOMI) (15-30% cases), veno-occlusive mesenteric ischemia / venous acute mesenteric ischemia (VAMI) (5-15% cases), mixed: e.g. strangulating bowel obstruction, chronic mesenteric ischemia (5%). […] Although treatment will vary according to the severity and cause of the ischemia, in general the treatment is surgical. The bowel needs to be assessed for viability and if necrotic needs to be resected. In some instances, endovascular thrombolysis/thrombectomy may be beneficial. Mortality rate is high at ~60% (range 30-90%).
  • #3
    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.
  • #3 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). […] NOMI is considered to be associated with adverse neurological outcomes in CA patients. Therefore, NOMI should not only be regarded as a post-resuscitation complication but also as one of the prognostic markers in CA patients. This paper summarizes current knowledge on NOMI’s pathophysiology, diagnosis, treatment, and prognostic significance in CA patients. […] Currently, the exact pathophysiology of NOMI is still not fully understood. However, it is probably closely associated with the splanchnic blood flow reduction in shock conditions and the use of vasopressors. […] The mucosa of the intestinal wall is the layer most susceptible to the effects of ischemia. […] Ischemia damage starts from the mucosa and continues towards the serosa. Subsequent reperfusion of the intestine results in further damage to the mucosa.