Ostre zapalenie pęcherzyka żółciowego
Patofizjologia i mechanizm

Ostre zapalenie pęcherzyka żółciowego (OZPŻ) jest stanem zapalnym rozwijającym się w ciągu kilku godzin, najczęściej na tle niedrożności przewodu pęcherzykowego, głównie spowodowanej kamicą żółciową (90-95% przypadków). Patomechanizm obejmuje zatrzymanie żółci, wzrost ciśnienia wewnątrzpęcherzykowego, zaburzenia ukrwienia ściany pęcherzyka oraz uwolnienie fosfolipazy A, która przekształca lecytynę w toksyczną lizolecytynę. Proces zapalny jest podtrzymywany przez mediatory, takie jak prostaglandyny, prowadząc do obrzęku, martwicy i ropnego zapalenia. Niedokrwienie ściany pęcherzyka, szczególnie dna, skutkuje martwicą, a nieleczone OZPŻ może przejść w fazy obrzękową (2-4 dni), martwiczą (3-5 dni) i ropną (7-10 dni), z ryzykiem perforacji, ropni okołopęcherzykowych i przetok żółciowych.

Ostre zapalenie pęcherzyka żółciowego: Patogeneza i mechanizm

Ostre zapalenie pęcherzyka żółciowego (OZPŻ) to stan zapalny pęcherzyka żółciowego, który rozwija się w ciągu kilku godzin, najczęściej w wyniku niedrożności przewodu pęcherzykowego lub zaburzeń opróżniania pęcherzyka żółciowego. Patofizjologiczny mechanizm tego schorzenia jest złożony i wieloczynnikowy, lecz kluczowym elementem jest blokada odpływu żółci z pęcherzyka żółciowego.12

Niedrożność przewodu pęcherzykowego jako główny mechanizm patogenetyczny

Około 90-95% przypadków ostrego zapalenia pęcherzyka żółciowego jest związanych z kamicą żółciową (ostre zapalenie kamicze pęcherzyka żółciowego), a pozostałe 5-10% to przypadki bez obecności kamieni (ostre zapalenie bezkamicze pęcherzyka żółciowego).12 Podstawowym mechanizmem rozwoju zapalenia kamiczego jest zablokowanie przewodu pęcherzykowego przez kamień żółciowy, zwykle unieruchomiony w szyi pęcherzyka lub w samym przewodzie pęcherzykowym.12

Konsekwencje niedrożności przewodu pęcherzykowego obejmują:12

  • Zatrzymanie żółci w pęcherzyku żółciowym i zwiększenie ciśnienia wewnątrzświatłowego
  • Zaburzenie normalnego przepływu krwi i drenażu limfatycznego, prowadzące do przekrwienia żylnego, a następnie tętniczego
  • Rozciągnięcie i podrażnienie ściany pęcherzyka żółciowego
  • Rozwój stanu zapalnego i obrzęku

12

Im dłuższy czas i większy stopień niedrożności, tym poważniejszy przebieg choroby. Jeśli niedrożność jest częściowa i krótkotrwała, pacjent doświadcza kolki żółciowej. Natomiast przy całkowitej i długotrwałej niedrożności rozwija się pełnoobjawowe ostre zapalenie pęcherzyka żółciowego.12

Biochemiczne mechanizmy zapalne

Zastój żółci i uszkodzenie śluzówki pęcherzyka uruchamiają kaskadę reakcji zapalnych:1

  • Uwolnienie fosfolipazy A z uszkodzonej śluzówki – enzym ten przekształca lecytynę żółciową w lizolecytynę, która działa toksycznie na nabłonek pęcherzyka żółciowego
  • Zwiększone wydzielanie płynu do światła pęcherzyka przez uszkodzoną błonę śluzową
  • Uwolnienie mediatorów zapalnych (m.in. prostaglandyn), które nasilają uszkodzenie śluzówki i powodują niedokrwienie
  • Powstanie błędnego koła: wydzielanie płynu i zapalenie – prowadzące do dalszego rozciągnięcia pęcherzyka i zwiększenia ciśnienia wewnętrznego

12

Lizolecytyna odgrywa szczególną rolę w patogenezie zapalenia pęcherzyka. W modelach eksperymentalnych jest używana do wywoływania zapalenia, a jej obecność można wykryć w żółci pęcherzykowej pacjentów z ostrym zapaleniem pęcherzyka żółciowego. Proces zapalny jest podtrzymywany przez prostaglandyny, które wpływają na kurczliwość pęcherzyka i absorpcję płynów.1

Niedokrwienie i martwica

Podwyższone ciśnienie wewnątrzpęcherzykowe, w połączeniu ze stanem zapalnym, prowadzi do zaburzeń ukrwienia ściany pęcherzyka żółciowego:12

  • Zaburzenie przepływu krwi przez tętnicę pęcherzykową, która jako tętnica końcowa jest szczególnie podatna na niedokrwienie
  • Kompresja naczyń krwionośnych przez rozciągnięty pęcherzyk
  • Zmniejszenie perfuzji ściany pęcherzyka, prowadzące do niedotlenienia tkanek
  • Obumieranie komórek z powodu niedostatecznego zaopatrzenia w tlen

12

Dno pęcherzyka żółciowego, znajdujące się najdalej od dopływu krwi przez tętnicę pęcherzykową, jest najbardziej narażone na niedokrwienie i najczęstszą lokalizacją martwicy.1

Fazy zapalenia pęcherzyka

Ostre zapalenie pęcherzyka żółciowego rozwija się w sposób stopniowy, przechodząc przez następujące fazy:1

  • Faza obrzękowa (2-4 dni) – charakteryzuje się przekrwieniem i obrzękiem ściany pęcherzyka
  • Faza martwicza (3-5 dni) – pojawia się krwawienie i martwica tkanek
  • Faza ropna (7-10 dni) – dochodzi do ropnego zapalenia pęcherzyka żółciowego (cholecystitis suppurativa)
  • Przy braku leczenia choroba przechodzi w podostre zapalenie pęcherzyka, a ostatecznie w przewlekłe zapalenie pęcherzyka żółciowego

12

Nieleczone ostre zapalenie pęcherzyka żółciowego może prowadzić do poważnych powikłań, w tym do perforacji pęcherzyka żółciowego (zapalenie otrzewnej żółciowe) podczas fazy krwotoczno-martwiczej oraz do ropni okołopęcherzykowych i przetok żółciowych wewnętrznych podczas fazy ropnej.12

Infekcja bakteryjna

Zakażenie bakteryjne jest często wtórne do procesu zapalnego i występuje w około 20% przypadków ostrego zapalenia pęcherzyka żółciowego.12 Najczęstsze patogeny to bakterie Gram-ujemne pochodzenia jelitowego, takie jak:12

  • Escherichia coli
  • Klebsiella spp.
  • Enterococcus faecalis
  • Bacteroides spp.
  • Pseudomonas spp.
  • Proteus spp.

12

W przypadku zakażenia bakteriami wytwarzającymi gaz (np. E. coli, Klebsiella, Clostridium perfringens) może rozwinąć się ostre zapalenie pęcherzyka żółciowego z odmą (emphysematous cholecystitis), które jest szczególnie groźne i wiąże się z wysoką śmiertelnością.12

Patogeneza ostrego zapalenia bezkamiczego pęcherzyka żółciowego

Ostre bezkamicze zapalenie pęcherzyka żółciowego (acalculous cholecystitis) stanowi około 10% przypadków ostrego zapalenia pęcherzyka i występuje głównie u pacjentów w stanie krytycznym. Patogeneza jest wieloczynnikowa i obejmuje:12

  • Zastój żółci – spowodowany głodzeniem, brakiem stymulacji cholecystokininą (brak doustnego odżywiania), żywieniem pozajelitowym, niedrożnością przewodu pokarmowego
  • Niedokrwienie pęcherzyka – związane z hipoperfuzją w stanach hipotonii, wstrząsu, po dużych operacjach, urazach, oparzeniach lub przy stosowaniu leków wazopresyjnych
  • Reakcję zapalną – ogólnoustrojową lub miejscową, z uwalnianiem cytokin prozapalnych
  • Zwiększoną lepkość żółci – w wyniku odwodnienia, gorączki
  • Zakażenia wirusowe lub bakteryjne – szczególnie u pacjentów z obniżoną odpornością (np. cytomegalowirus, mikrosporydia, Cryptosporidium u pacjentów z AIDS)

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Rozciągnięcie pęcherzyka żółciowego zwiększa napięcie ściany, dodatkowo upośledzając perfuzję, a zastój żółci prowadzi do koncentracji detergentów żółciowych, które mogą uszkadzać ścianę pęcherzyka. Proces ten można porównać do niedrożności porażennej (paralitycznego zapalenia) pęcherzyka żółciowego.12

Czynniki wirulencji patogenów

W rozwoju zakażenia pęcherzyka żółciowego istotną rolę odgrywają czynniki wirulencji drobnoustrojów chorobotwórczych:1

  • Adhezyny bakteryjne – umożliwiające przyleganie do komórek nabłonka wyściełającego śluzówkę pęcherzyka
  • Toksyny – bezpośrednio uszkadzające i zaburzające błony komórkowe komórek nabłonka pęcherzyka żółciowego
  • Enzymy zewnątrzkomórkowe – rozkładające komponenty strukturalne komórek gospodarza i otaczającą macierz pozakomórkową
  • Adaptacje metaboliczne – pozwalające drobnoustrojom pozyskiwać niezbędne składniki odżywcze w środowisku pęcherzyka żółciowego

12

Odpowiedź immunologiczna

W odpowiedzi na zakażenie i zapalenie pęcherzyka żółciowego organizm uruchamia skoordynowaną odpowiedź immunologiczną wrodzoną i adaptacyjną:1

  • Aktywacja makrofagów rezydujących i komórek nabłonkowych do wydzielania cytokin prozapalnych, w tym IL-1, IL-6 i TNF-alfa
  • Nagromadzenie granulocytów obojętnochłonnych w ścianie pęcherzyka
  • Rozwój reakcji zapalnej mającej na celu eliminację patogenów i ograniczenie uszkodzeń tkanek

1

Czynniki predysponujące i modyfikujące

Na rozwój kamicy żółciowej i ostrego zapalenia pęcherzyka żółciowego wpływają różne czynniki:12

  • Skład kamieni żółciowych – mogą być cholesterolowe, barwnikowe lub wapniowe
  • Czynniki modyfikujące skład żółci – choroby hemolityczne (np. niedokrwistość sierpowatokrwinkowa) zwiększające ilość bilirubiny i tworzenie kamieni barwnikowych
  • Nadmiar wapnia (np. w nadczynności przytarczyc) sprzyjający tworzeniu kamieni wapniowych
  • Nadmiar cholesterolu sprzyjający tworzeniu kamieni cholesterolowych
  • Niedrożność dróg żółciowych (np. w nowotworach lub zwężeniach) prowadząca do zastoju żółci i tworzenia kamieni
  • Czynniki żywieniowe – wysoka podaż tłuszczów nasyconych i cukrów rafinowanych zwiększa ryzyko tworzenia kamieni
  • Odwodnienie – szczególnie w okresie letnim, może nasilać zastój żółci i zmniejszać opróżnianie pęcherzyka

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Powikłania

Nieleczone ostre zapalenie pęcherzyka żółciowego może prowadzić do szeregu poważnych powikłań:12

  • Zgorzel pęcherzyka żółciowego (20% przypadków) – martwica ściany pęcherzyka
  • Perforacja pęcherzyka żółciowego (20% przypadków) – przebicie ściany pęcherzyka z wyciekiem żółci do jamy otrzewnej
  • Ropień okołopęcherzykowy – zlokalizowane zbiorniki ropy wokół pęcherzyka
  • Przetoki żółciowe wewnętrzne – najczęściej pęcherzykowo-dwunastnicze (70%), pęcherzykowo-okrężnicze (10-20%) lub rzadziej pęcherzykowo-żołądkowe
  • Ropniak pęcherzyka żółciowego (empyema) – nagromadzenie ropy w pęcherzyku
  • Posocznica i wstrząs septyczny – ogólnoustrojowa reakcja na zakażenie
  • Zespół Mirizziego – ucisk na przewód wątrobowy wspólny lub przewód żółciowy wspólny przez kamień unieruchomiony w szyi pęcherzyka lub przewodzie pęcherzykowym

123

Raportowana ogólna śmiertelność w ostrym zapaleniu pęcherzyka żółciowego wynosi 2-3%, z wyższymi wskaźnikami (do 10%) u pacjentów powyżej 70 roku życia, głównie z powodu współistniejących chorób sercowo-naczyniowych i powikłań.1

Podsumowanie mechanizmów patogenetycznych

Ostre zapalenie pęcherzyka żółciowego to złożony proces, w którym kluczową rolę odgrywa:123

  1. Niedrożność przewodu pęcherzykowego – najczęściej przez kamień żółciowy
  2. Zastój żółci z rozciągnięciem pęcherzyka i wzrostem ciśnienia wewnątrzpęcherzykowego
  3. Reakcja chemiczna – uwolnienie fosfolipazy A i przekształcenie lecytyny w toksyczną lizolecytynę
  4. Reakcja zapalna – uwolnienie mediatorów zapalnych, m.in. prostaglandyn
  5. Zaburzenie ukrwienia ściany pęcherzyka prowadzące do niedokrwienia i martwicy
  6. Wtórne zakażenie bakteryjne – nasilające proces zapalny

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Zrozumienie złożonej patogenezy ostrego zapalenia pęcherzyka żółciowego ma kluczowe znaczenie dla właściwego rozpoznania i leczenia tego schorzenia, szczególnie że wczesna interwencja może zapobiec rozwojowi poważnych, zagrażających życiu powikłań.1

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  1. 16.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis is inflammation of the gallbladder that occurs due to occlusion of the cystic duct or impaired emptying of the gallbladder. […] The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death. […] Gallstones form from various materials such as bilirubinate or cholesterol. […] These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones.
  • #1 Acute Cholecystitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/171886-overview
    Ninety percent of cases of cholecystitis involve stones in the gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis. […] Acute calculous cholecystitis is caused by an obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis. […] Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder does not receive a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen. […] A study by Cullen et al demonstrated the ability of endotoxins to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxins also abolish the contractile response to CCK, leading to gallbladder stasis.
  • #1 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #1 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] Acute cholecystitis is the most common complication of cholelithiasis. In fact, 95% of patients with acute cholecystitis have cholelithiasis. When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation.
  • #1
    https://link.springer.com/article/10.1007/s00534-006-1152-y
    Acute cholecystitis is an acute inflammatory disease of the gallbladder. It is often attributable to gallstones, but many factors, such as ischemia; motility disorders; direct chemical injury; infections with microorganisms, protozoa, and parasites; collagen disease; and allergic reaction are involved. […] In the majority of patients, gallstones are the cause of acute cholecystitis. The process is one of physical obstruction of the gallbladder by a gallstone, at the neck or in the cystic duct. This obstruction results in increased pressure in the gallbladder. There are two factors which determine the progression to acute cholecystitis the degree of obstruction and the duration of the obstruction. If the obstruction is partial and of short duration the patient experiences biliary colic. If the obstruction is complete and of long duration the patient develops acute cholecystitis. If the patient does not receive early treatment, the disease becomes more serious and complications occur.
  • #1 Updates on Antibiotic Regimens in Acute Cholecystitis
    https://www.mdpi.com/1648-9144/60/7/1040
    Acute cholecystitis (AC) is usually caused by cystic duct obstruction and the irritating effects of stones on the gallbladder wall. Cystic duct obstruction alone, in fact, is not enough to explain the pathogenesis of gallbladder inflammation. […] In experimental models, lysolecithin, a product derived from lecithin and produced during gallbladder wall micro trauma, is used to induce gallbladder inflammation. This process is in vivo activated by phospholipase A, which is normally present within the mucosa and released when its integrity is disrupted (for example, due to the mechanical effects of stones). This molecule is, in fact, detectable in gallbladder bile in patients with AC. The propagation of the inflammation is sustained by inflammatory mediators, i.e., prostaglandins, which have a role in the contraction of the gallbladder and in the absorption of fluids. […] Besides the inflammatory process, in some cases, the situation is worsened by bile infection. Histologic changes in the gallbladder in AC can range from mild edema and acute inflammation to necrosis and gangrene.
  • #1 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Patients with excessive calcium such as in hyperparathyroidism can form calcium stones. […] Patients with excessive cholesterol can form cholesterol stones. […] Occlusion of the common bile duct such as in neoplasms or strictures can also lead to stasis of the bile flow causing gallstone formation. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. […] The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality.
  • #1 Cholecystitis | Abdominal Key
    https://abdominalkey.com/cholecystitis/
    The cause of acute cholecystitis is an impacted gallstone in the outlet of the gallbladder, either in the infundibulum or in the cystic duct (Sjodahl et al, 1978). The impacted gallstone results in gallbladder distension and edema with acute inflammation, which eventually can result in venous stasis and obstruction, followed by thrombosis of the cystic artery. Ultimately, ischemia and necrosis of the gallbladder occur. Because the fundus of the gallbladder is the greatest distance from the cystic arterial blood supply, it is more sensitive to ischemia and is the most common location for necrosis of the gallbladder. […] The acute inflammation of cholecystitis may be complicated by secondary biliary infection. Positive biliary cultures are found in about 20% of patients with acute cholecystitis (den Hoed et al, 1998), the most common of which are gram-negative bacteria of gastrointestinal origin, such as Klebsiella spp. and Escherichia coli.
  • #1 Pathophysiology and pathology of acute cholecystitis: A secondary publication of the Japanese version from 1992 – PubMed
    https://pubmed.ncbi.nlm.nih.gov/33570821/
    Acute cholecystitis is a progressive inflammation of the gallbladder usually caused by gallstones obstructing the cystic duct. Congestion and edema are evident symptoms during the first 2-4 days, also known as the phase of edematous cholecystitis. Necrotizing cholecystitis, a phase characterized by bleeding and necrosis, is seen at 3-5 days. From 7-10 days, the disease progresses to its purulent phase, also known as suppurative cholecystitis. If the disease is still left untreated at this point, it progresses to subacute cholecystitis and it eventually becomes chronic cholecystitis. Possible complications that affect the management of cholecystitis include perforation of the gallbladder (bile peritonitis) during the hemorrhagic and necrosis phase, and peri-gallbladder abscess and internal biliary fistula during the purulent phase. […] Roles of lithogenic bile and cystic duct occlusion in the pathogenesis of acute cholecystitis.
  • #1 Acute cholecystitis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Acute_cholecystitis_pathophysiology
    Gallbladder stasis is usually due to the lack of gallbladder stimulation and contractility. This leads to concentration of the bile salts with a build-up of pressure within the organ. An increased intraluminal pressure results in ischemia and necrosis of the gallbladder. The gallbladder stasis also facilitates the proliferation of the bacteria such as Escherichia coli, Klebsiella, Bacteroides, Proteus, Pseudomonas, and Enterococcus faecalis. This can also cause an inflammatory reaction in the gallbladder.
  • #1 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Once acalculous cholecystitis is established, secondary infection with enteric pathogens, including Escherichia coli, Enterococcus faecalis, Klebsiella spp, Pseudomonas spp, Proteus spp, and Bacteroides fragilis and related strains, is common. […] The majority of patients with acalculous cholecystitis have multiple risk factors. In some cases, specific primary infections with non-enteric organisms predispose to acalculous cholecystitis. As an example, acalculous cholecystitis occurring in patients with acquired immunodeficiency syndrome (AIDS) and other immunosuppressed patients may be due to opportunistic infections such as microsporidia, Cryptosporidium, or cytomegalovirus. More often, however, these infections cause a cholangiopathy without cholecystitis. There is also association of acalculous cholecystitis with COVID-19, though it is unclear whether disease results from primary infection of the biliary system or critical illness.
  • #1 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Acute acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis, occurring in the absence of gallstones. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates. […] The pathogenesis of acalculous cholecystitis is multifactorial and likely results from ischemia and cholestasis. The cystic artery, which supplies blood to the gallbladder, is a terminal artery and susceptible to ischemia. Ischemia and necrosis of the gallbladder wall can occur with hypoperfusion in cases of hypotension, vasoactive drug use, or major surgery and trauma. Cholestasis may be seen in prolonged fasting states, usage of total parental nutrition, and ileus or bowel obstruction. Cholestasis results in increased pressure within the gallbladder and distension, further decreasing perfusion to the gallbladder wall. Pathologically, ischemia and cholestasis result in local inflammatory response in the gallbladder wall, epithelial injury, and eventually necrosis of the gallbladder tissue.
  • #1 Acalculous Cholecystitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/187645-overview
    The main cause of this illness is thought to be bile stasis and increased lithogenicity of bile. […] Critically ill patients are more predisposed because of increased bile viscosity due to fever and dehydration and because of prolonged absence of oral feeding resulting in a decrease or absence of cholecystokinin-induced gallbladder contraction. […] Gallbladder wall ischemia that occurs because of a low-flow state due to fever, dehydration, or heart failure may also play a role in the pathogenesis of acalculous cholecystitis.
  • #1 Acalculous cholecystitis – EMCrit Project
    https://emcrit.org/ibcc/acalculous-cholecystitis/
    Acalculous cholecystitis is defined as cholecystitis that occurs without a gallstone. […] This typically occurs in critically ill patients due to a combination of factors (e.g. bile stasis and hypoperfusion). […] Pathogenesis may be summarized roughly as follows. In some ways, this may be conceptualized as a paralytic ileus of the gallbladder. […] (1) Lack of enteral nutrition and hypoperfusion create a hypotonic, dilated gallbladder. […] Distension of the gallbladder increases wall tension, further impairing perfusion of the gallbladder wall. […] Biliary stasis causes concentration of biliary detergents, which may damage the gallbladder wall. […] (2) Further complications ensue: […] Necrosis and perforation of the gallbladder may occur. […] Superinfection with enteric bacteria may occur (empyema of the gallbladder). Note that many cases of acalculous cholecystitis occur without bacterial infection.
  • #1 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Critical to the ability of bacteria, parasites, and fungi to establish infection of the gallbladder is their expression of specific virulence factors that enable adhesion to epithelial cells lining the gallbladder mucosa. […] In addition to adhesion, many pathogens produce toxins that directly damage and disrupt the epithelial cell membranes of the gallbladder. These pore-forming toxins represent another key virulence factor contributing to acute cholecystitis. […] Pathogenic microbes involved in acute cholecystitis produce a variety of extracellular enzymes that directly breakdown and destroy host cell structural components and the surrounding extracellular matrix. […] The production of virulence factors by bacteria, parasites, and fungi causing cholecystitis involves coordinated transcription and translation of the genes encoding these pathogenicity proteins.
  • #1 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    For microorganisms to proliferate and thrive within the nutrient-limited environment of the gallbladder, they must adapt their metabolism to obtain essential nutrients from host cells. […] The secretion of toxins and enzymes is a key virulence strategy used by diverse microbes to establish infection and cause damage to the gallbladder epithelium. […] The host responds to acute cholecystitis through a coordinated innate and adaptive immune response aimed at clearing the infectious pathogens and limiting tissue damage. […] Infection and obstruction of the gallbladder activate resident macrophages and epithelial cells to secrete pro-inflammatory cytokines including IL-1, IL-6, and TNF-alpha. […] The obstruction of bile drainage from the gallbladder that occurs in acute cholecystitis has two major detrimental effects-bile stasis within the gallbladder and jaundice due to the backup of bile constituents. […] The pathogenesis of acute cholecystitis is intimately linked to the development of gallstones, which obstruct bile drainage and initiate gallbladder inflammation. […] Further research into microbial toxins and their role in acute cholecystitis pathogenesis remains an impactful area of study.
  • #1 acute-cholecystitis | Calgary Guide
    https://calgaryguide.ucalgary.ca/acute-cholecystitis/acute-cholecystitis-2022/
    Acute Cholecystitis: Pathogenesis and clinical findings Gallstone blocks the cystic duct, backing up bile into the gallbladder […] Gallstones causing physical trauma to gallbladder wall […] Inflammatory mediator (i.e. prostaglandin) release by gallbladder and systemic inflammatory response […] Inflammation self-perpetuates […] Irritation of inner gallbladder wall/mucosa […] Gallbladder ischemia […] Local inflammation, loss of gallbladder mucosal integrity […] Bacterial invasion transmural inflammation of gallbladder […] Without treatment, prolonged ischemia and inflammation of the gallbladder […] Gallbladder gangrene (20%) […] Gallbladder perforation (20%)
  • #1 Aetiopathogenesis and management of calculus cholecystitis | PPT
    https://www.slideshare.net/slideshow/aetiopathogenesis-and-management-of-calculus-cholecystitis/45625880
    Cholecystitis is the inflammation of the gall bladder. Calculus cholecystitis results from obstruction by gall stone and is the commonest cause of cholecystitis. […] 90% of patient with acute cholecystitis is associated with calculus obstruction. […] When stone becomes impacted in the cystic duct the gall bladder becomes inflamed(chemical and bacterial inflammation). The mucous membrane is swollen and the wall thickened. […] stones obstruction to bile outflow inflammation of gall bladder wall due to phospholipases from the mucosa hydrolyzes biliary lecithin to lysolecithin (toxic to the mucosa) disrupt normal protective glycoprotein layer exposed the mucosal epithelium to the direct detergent action of bile salts Superimposed bacterial infection Distended gall bladder Prostaglandin released Mucosal and mural inflammation Increase intraluminal pressure Compromise mucosal blood flow. […] Overall reported mortality of acute cholecystitis is 2-3% with much higher figures (10%) in patient over 70. This is largely due to incidental cardiorespiratory disease and complication.
  • #1 The Diagnosis and Treatment of Acute Cholecystitis: A Comprehensive Narrative Review for a Practical Approach
    https://www.mdpi.com/2077-0383/13/9/2695
    Acute cholecystitis (AC), defined as acute inflammation of the gallbladder wall, is generally related to the presence of gallstones in the cystic duct or in the gallbladder neck. […] The key event underlying calculous AC is the obstruction of the cystic duct by stones or sludge. The resulting increase in gallbladder intraluminal pressure generates an acute inflammatory response of the gallbladder wall. […] In most patients, acalculous AC presents a multifactorial pathogenesis, resulting in stasis and ischemia of the gallbladder wall, with a subsequent local inflammatory response. […] Well-known risk factors for acalculous AC are sepsis, hypotension, cardiovascular disease, total parenteral nutrition, immunosuppression, major trauma, or burns, typically with a long stay in the intensive care unit. […] The importance of AC is related to its frequency and to its clinical impact, requiring adequate management.
  • #2 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] Acute cholecystitis is the most common complication of cholelithiasis. In fact, 95% of patients with acute cholecystitis have cholelithiasis. When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation.
  • #2 A Review of Cholelithiasis and Cholecystitis for Pharmacists
    https://www.uspharmacist.com/article/a-review-of-cholelithiasis-and-cholecystitis-for-pharmacists
    Patients with chronic gallstones may develop progressive fibrosis and loss of motor function of the gallbladder, resulting in cholecystitis, an inflammation of the gallbladder. Cholecystitis can be acute or chronic, with recurrent episodes of acute inflammation possibly leading to chronic cholecystitis, the most common complication associated with gallstones. Cholelithiasis is linked with 90% to 95% of chronic cholecystitis cases. […] Acute cholecystitis is a sudden inflammation of the gallbladder that develops over hours, typically because a gallstone impedes the cystic duct. Symptoms include right upper quadrant pain and tenderness; patients may also present with fever, chills, nausea, and vomiting. The majority of patients (95%) with acute cholecystitis have cholelithiasis. Risk factors for cholecystitis are considered to be analogous to the risk factors for cholelithiasis.
  • #2 Cholecystitis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/cholecystitis/symptoms-causes/syc-20364867
    Cholecystitis is when your gallbladder is inflamed. Gallbladder inflammation can be caused by: […] Most often, cholecystitis is the result of hard particles of bile that can form in the gallbladder, called gallstones. Gallstones can block the tube that carries bile when it leaves the gallbladder. The tube is called the cystic duct. Bile builds up in the gallbladder, causing swelling and irritation. […] A tumor may keep bile from draining out of the gallbladder as it should. This causes bile buildup that can lead to cholecystitis. […] Stones or thickened bile and tiny particles called sludge can block the bile duct and lead to cholecystitis. Kinking or scarring of the bile ducts also can cause blockage. […] Very serious illness can damage blood vessels and lessen blood flow to the gallbladder. This can lead to cholecystitis.
  • #2
    https://link.springer.com/article/10.1007/s00534-006-1152-y
    Acute cholecystitis is an acute inflammatory disease of the gallbladder. It is often attributable to gallstones, but many factors, such as ischemia; motility disorders; direct chemical injury; infections with microorganisms, protozoa, and parasites; collagen disease; and allergic reaction are involved. […] In the majority of patients, gallstones are the cause of acute cholecystitis. The process is one of physical obstruction of the gallbladder by a gallstone, at the neck or in the cystic duct. This obstruction results in increased pressure in the gallbladder. There are two factors which determine the progression to acute cholecystitis the degree of obstruction and the duration of the obstruction. If the obstruction is partial and of short duration the patient experiences biliary colic. If the obstruction is complete and of long duration the patient develops acute cholecystitis. If the patient does not receive early treatment, the disease becomes more serious and complications occur.
  • #2 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #2 Diagnosing Biliary Colic and Acute Cholecystitis | AAFP
    https://www.aafp.org/pubs/afp/issues/2000/0915/p1386.html
    Pain in the area of the gall bladder lasting more than three hours is characteristic of acute cholecystitis. The most common cause is cystic duct obstruction by gallstone(s), and the initial symptom may be epigastric pain. […] Acalculous cholecystitis is more common in older male patients with serious conditions. Bile statis is the proposed underlying mechanism. […] Leukocytosis with bandemia is a frequent finding in patients with acute cholecystitis, and mild elevations of serum aminotransferase levels may occur within a few hours of onset.
  • #2 Updates on Antibiotic Regimens in Acute Cholecystitis
    https://www.mdpi.com/1648-9144/60/7/1040
    Acute cholecystitis (AC) is usually caused by cystic duct obstruction and the irritating effects of stones on the gallbladder wall. Cystic duct obstruction alone, in fact, is not enough to explain the pathogenesis of gallbladder inflammation. […] In experimental models, lysolecithin, a product derived from lecithin and produced during gallbladder wall micro trauma, is used to induce gallbladder inflammation. This process is in vivo activated by phospholipase A, which is normally present within the mucosa and released when its integrity is disrupted (for example, due to the mechanical effects of stones). This molecule is, in fact, detectable in gallbladder bile in patients with AC. The propagation of the inflammation is sustained by inflammatory mediators, i.e., prostaglandins, which have a role in the contraction of the gallbladder and in the absorption of fluids. […] Besides the inflammatory process, in some cases, the situation is worsened by bile infection. Histologic changes in the gallbladder in AC can range from mild edema and acute inflammation to necrosis and gangrene.
  • #2 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Acute acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis, occurring in the absence of gallstones. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates. […] The pathogenesis of acalculous cholecystitis is multifactorial and likely results from ischemia and cholestasis. The cystic artery, which supplies blood to the gallbladder, is a terminal artery and susceptible to ischemia. Ischemia and necrosis of the gallbladder wall can occur with hypoperfusion in cases of hypotension, vasoactive drug use, or major surgery and trauma. Cholestasis may be seen in prolonged fasting states, usage of total parental nutrition, and ileus or bowel obstruction. Cholestasis results in increased pressure within the gallbladder and distension, further decreasing perfusion to the gallbladder wall. Pathologically, ischemia and cholestasis result in local inflammatory response in the gallbladder wall, epithelial injury, and eventually necrosis of the gallbladder tissue.
  • #2 acute-cholecystitis | Calgary Guide
    https://calgaryguide.ucalgary.ca/acute-cholecystitis/acute-cholecystitis-2022/
    Acute Cholecystitis: Pathogenesis and clinical findings Gallstone blocks the cystic duct, backing up bile into the gallbladder […] Gallstones causing physical trauma to gallbladder wall […] Inflammatory mediator (i.e. prostaglandin) release by gallbladder and systemic inflammatory response […] Inflammation self-perpetuates […] Irritation of inner gallbladder wall/mucosa […] Gallbladder ischemia […] Local inflammation, loss of gallbladder mucosal integrity […] Bacterial invasion transmural inflammation of gallbladder […] Without treatment, prolonged ischemia and inflammation of the gallbladder […] Gallbladder gangrene (20%) […] Gallbladder perforation (20%)
  • #2 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis is inflammation of the gallbladder that occurs due to occlusion of the cystic duct or impaired emptying of the gallbladder. […] The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death. […] Gallstones form from various materials such as bilirubinate or cholesterol. […] These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones.
  • #2 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis-2/
    Inflammation may be sparse in early disease […] Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol […] Trauma to mucosa releases phospholipase from lysosomes […] Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium […] Secondary bacterial infection with enteric organisms occurs in 20% of cases […] Overgrowth by gas-producing organisms leads to emphysematous cholecystitis.
  • #2 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp. […] Inflammatory bowel disease (IBD) is commonly associated with increased risk of cholelithiasis, particularly in patients with crohn’s disease (CD), the etiology is not clear.
  • #2 Acute Cholecystitis – Core EM
    https://coreem.net/core/acute-cholecystitis/
    Cystic duct obstruction is the proximate cause of cholecystitis. […] An inflammatory reaction occurs due to either mucosal ischemia from increased hydrostatic pressure or cytotoxic effects of bile degradation. […] The role of bacterial infection in the pathogenesis of cholecystitis is not completely understood. […] Likely caused by invasion of gas-producing pathogens (E. coli, Klebsiella, Clostridium perfringens).
  • #2 Acalculous cholecystitis – EMCrit Project
    https://emcrit.org/ibcc/acalculous-cholecystitis/
    Acalculous cholecystitis is defined as cholecystitis that occurs without a gallstone. […] This typically occurs in critically ill patients due to a combination of factors (e.g. bile stasis and hypoperfusion). […] Pathogenesis may be summarized roughly as follows. In some ways, this may be conceptualized as a paralytic ileus of the gallbladder. […] (1) Lack of enteral nutrition and hypoperfusion create a hypotonic, dilated gallbladder. […] Distension of the gallbladder increases wall tension, further impairing perfusion of the gallbladder wall. […] Biliary stasis causes concentration of biliary detergents, which may damage the gallbladder wall. […] (2) Further complications ensue: […] Necrosis and perforation of the gallbladder may occur. […] Superinfection with enteric bacteria may occur (empyema of the gallbladder). Note that many cases of acalculous cholecystitis occur without bacterial infection.
  • #2 Acalculous Cholecystitis | 5-Minute Clinical Consult
    https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688222/all/Acalculous_Cholecystitis
    Acalculous cholecystitis, also known as acute alithiasic cholecystitis (AAC), is an acute necroinflammatory disease of the gallbladder occurring in the absence of cholelithiasis with a multifactorial pathogenesis. […] The pathogenesis of AAC is multifactorial. Bile stasis and ischemia both likely contribute. Bile stasis can be caused by fasting, obstruction, procedural irritation, and/or ileus. This can lead to bile inspissation that is directly toxic to the gallbladder epithelium. Ischemia may occur as a result of systemic inflammation, iatrogenesis, or shock. Trauma, total parenteral nutrition, viral (hepatotropic virus) or bacterial (mostly gram-negative or anaerobic) infections are also associated with AAC.
  • #2 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    For microorganisms to proliferate and thrive within the nutrient-limited environment of the gallbladder, they must adapt their metabolism to obtain essential nutrients from host cells. […] The secretion of toxins and enzymes is a key virulence strategy used by diverse microbes to establish infection and cause damage to the gallbladder epithelium. […] The host responds to acute cholecystitis through a coordinated innate and adaptive immune response aimed at clearing the infectious pathogens and limiting tissue damage. […] Infection and obstruction of the gallbladder activate resident macrophages and epithelial cells to secrete pro-inflammatory cytokines including IL-1, IL-6, and TNF-alpha. […] The obstruction of bile drainage from the gallbladder that occurs in acute cholecystitis has two major detrimental effects-bile stasis within the gallbladder and jaundice due to the backup of bile constituents. […] The pathogenesis of acute cholecystitis is intimately linked to the development of gallstones, which obstruct bile drainage and initiate gallbladder inflammation. […] Further research into microbial toxins and their role in acute cholecystitis pathogenesis remains an impactful area of study.
  • #2 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Patients with excessive calcium such as in hyperparathyroidism can form calcium stones. […] Patients with excessive cholesterol can form cholesterol stones. […] Occlusion of the common bile duct such as in neoplasms or strictures can also lead to stasis of the bile flow causing gallstone formation. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. […] The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality.
  • #2 Biliary Colic and Cholecystitis – TeachMeSurgery
    https://teachmesurgery.com/hpb/gall-bladder/colic-and-cholecystitis/
    A gallbladder empyema is when the gallbladder becomes filled with pus. Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis. They are associated with significant morbidity and mortality. […] Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum).
  • #2 Acute Cholecystitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/171886-overview
    Ninety percent of cases of cholecystitis involve stones in the gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis. […] Acute calculous cholecystitis is caused by an obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis. […] Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder does not receive a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen. […] A study by Cullen et al demonstrated the ability of endotoxins to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxins also abolish the contractile response to CCK, leading to gallbladder stasis.
  • #3 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Once acalculous cholecystitis is established, secondary infection with enteric pathogens, including Escherichia coli, Enterococcus faecalis, Klebsiella spp, Pseudomonas spp, Proteus spp, and Bacteroides fragilis and related strains, is common. […] The majority of patients with acalculous cholecystitis have multiple risk factors. In some cases, specific primary infections with non-enteric organisms predispose to acalculous cholecystitis. As an example, acalculous cholecystitis occurring in patients with acquired immunodeficiency syndrome (AIDS) and other immunosuppressed patients may be due to opportunistic infections such as microsporidia, Cryptosporidium, or cytomegalovirus. More often, however, these infections cause a cholangiopathy without cholecystitis. There is also association of acalculous cholecystitis with COVID-19, though it is unclear whether disease results from primary infection of the biliary system or critical illness.
  • #3 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    As with many communicable and noncommunicable diseases the incidence of acute cholecystitis rises and falls in an annual seasonal pattern. […] Although the exact mechanism underlying the fluctuation of cholecystitis in a particular time of the year is still not clear, several researchers have suggested that the behavioural and environmental risk factors such as temperature, humidity, dietary habits, and hydration can trigger gallstone formation and subsequent acute cholecystitis. […] Dietary factors have been implicated in the pathogenesis of cholelithiasis. A high intake of saturated fat has been linked to an increased risk of gallstone formation. […] The ingestion of refined sugars has been shown to be associated with higher cholesterol synthesis in the liver secondary to increased insulin in response to high sugar consumption, whereas low fiber intakes have been associated with an increase in the risk of gallstone formation because of the resultant increase in secondary bile acid secretions due to decreased colonic motility.
  • #3 Management of Gallstones and Their Complications | AAFP
    https://www.aafp.org/pubs/afp/issues/2000/0315/p1673.html
    Gallstones are a major cause of morbidity worldwide, and cholecystectomy is the most commonly performed abdominal surgery in medicine. […] The most common cause of acute cholecystitis is obstruction of the cystic duct by gallstones, resulting in acute inflammation. Approximately 90 percent of cases of acute cholecystitis are associated with cholelithiasis. […] The pathogenesis may involve edema and inflammation secondary to the impacted stone in the cystic duct. This leads to the compression of the common hepatic duct or the common bile duct (Mirizzi’s syndrome). […] Acute cholecystitis may present as an acalculous disorder in 5 to 10 percent of patients. Acalculous cholecystitis typically affects critically ill, older men in the setting of major surgery, critical illness, total parenteral nutrition, extensive trauma or burn-related injury. The pathogenesis probably involves a combination of biliary stasis, chemical inflammation and ischemia. […] Rarely, infectious agents can cause acute cholecystitis. Cytomegalovirus and cryptosporidia can result in cholecystitis and cholangitis in immunocompromised persons. Salmonella can colonize the gallbladder epithelium without eliciting inflammation, creating a carrier state.
  • #3 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] Acute cholecystitis is the most common complication of cholelithiasis. In fact, 95% of patients with acute cholecystitis have cholelithiasis. When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation.
  • #4 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp. […] Inflammatory bowel disease (IBD) is commonly associated with increased risk of cholelithiasis, particularly in patients with crohn’s disease (CD), the etiology is not clear.
  • #4 Acute Acalculous Cholecystitis in Neurological Patients; Clinical Review, Risk Factors, and Possible Mechanism
    https://www.e-jnic.org/journal/view.php?number=33
    Acute cholecystitis is known to be caused by the pathologic mechanism of inflammation and ischemia in the gallbladder (GB) wall, stagnant pooling of bile juice, and the lithogenicity of bile juice in a complex manner. […] Hypoperfusion and bile stasis are the key pathogenesis of AAC, which could be aggravated by hypotension, dehydration, and the usage of vasoactive drugs. […] Bile stasis is caused by the use of opioids, fasting with total parenteral nutrition (TPN), and mechanical ventilation with positive end-expiratory pressure (PEEP). […] Gallbladder ischemia is pathogenesis of AAC. […] Intraluminal pressure is increased by bile stasis, which results in a decrease in gallbladder perfusion pressure. […] Another mechanism closely related to the pathogenesis of AAC is systemic inflammatory response. […] Systemic inflammatory response can cause cholestasis, gallbladder ischemia, therefore could affect the incidence of AAC in neurological patients.