Cholangitis and Cholecystitis (Dr.dr. Hery Djagat Purnomo,SpPD-KGEH)
Content
Cholangitis and Cholecystitis Dr.dr Dr .dr.Hery .Hery Djagat Purnomo, SpPDS pPDKGEH Divisi Gastroe Gastroenterohepatology nterohepatology Departement o !nternal "edicine Dr Kariadi Hospital Diponegoro #niversity Semarang
Anatomy
Anatomy
!ntroductions •
$he %rst report on acute &iliary inection 'as Charcot(s )$he symptoms o hepatic ever* in +.
Defnition •
cute cholangitis is a mor&id condition 'ith acute in/ ammation and inection in the &ile duct.
•
Hepatic ever. ever. “Hepatic ever” !ntermittent !ntermittent ever accompanied &y chills, right upper 0uadrant pain, and jaundice &ecame 1no'n as Charcot(s triad.
2eynolds and Dargan classi%ed acute micro&ial cholangitis 3 +. cute cholangitis developing rom acute cholecystitis 4. cute non-suppurative cholangitis 5. cute suppurative cholangitis 6. cute o&structive suppurative cholangitis 7. cute suppurative cholangitis accompanied &y hepatic a&scess
•
Acute obstructive cholangitis. Acute obstructive cholangitis 'as de%ned &y 2eynolds and Dargan, in +878 as a syndrome consisting o lethargy or mental conusion and shoc1, as 'ell as ever, jaundice, and a&dominal pain, caused &y &iliary o&struction.
Etiology cute cholangitis re0uires the presence o t'o actors3 9+: &iliary o&struction and 94: &acterial gro'th in &ile 9&ile inection:. ;re0uent causes o &iliary o&struction are choledocholithiasis, &enign &iliary stenosis, stricture o a &iliary anastomosis, and stenosis caused &y malignant disease
$a&le o etiology acute cholangitis
2is1 actors The bile o healthy subjects is generally aseptic. Ho'ever, &ile culture is positive or microorganisms in +<= o patients undergoing a non-&iliary operation, in 4= o acute cholangitis patients, in 66= o chronic cholangitis patients, and in 7>= o those 'ith &iliary o&struction. ?acteria in &ile are identi%ed in 8>= o patients 'ith choledocholithiasis accompanied &y jaundice.
•
•
•
Post-enoscopic retrograe cholangiopancreatography !E"#P$ inectious co%plications. &ther etiologies o acute cholangitis ' "iri@@i syndrome and lemmel syndrome. "iri@@i syndrome is a mor&id condition 'ith stenosis o the common &ile duct caused &y mechanical pressure andAor in/ ammatory changes caused &y the presence o stones in the gall&ladder nec1 and cystic ducts.
•
Bemmel syndrome is a series o mor&id conditions in 'hich the duodenal parapapillary diverticulum compresses or displaces the opening o the &ile duct or pancreatic duct and o&structs the passage o &ile in the &ile duct or hepatic duct, there&y causing cholestasis, jaundice, gallstone, cholangitis, and pancreatitis.
Causes o acute cholangitis 9=:
Pathophysiology •
•
$he onset o acute cholangitis involves t'o actors3 9i: increased &acteria in the &ile duct, and 9ii: elevated intraductal pressure in the &ile duct that allo's translocation o &acteria or endotoins into the vascular system 9cholangio-venous re/u:. $his process results in serious inections that can &e atal, such as hepatic a&scess and sepsis.
Prognosis •
•
$he reported mortality o acute cholangitis varies 4.7= - <7=. $he mortality rate &eore +8> 'as 7>=, and ater +8> it 'as +>= 5>=. Such dierences in mortality are pro&a&ly attri&uta&le to dierences in early diagnosis and improved supportive treatment.
•
•
$he major cause o death is multiple organ ailure 'ith irreversi&le shoc1, and mortality rates have not signi%cantly improved over the years. Causes o death in patients 'ho survive the acute stage o cholangitis include multiple organ ailure, heart ailure, and pneumonia.
•
Cholangitis –
!nection 'ithin &ile ducts due to o&struction o C?D.
–
!nection o the &ile ducts due to C?D o&struction secondary to stones, strictures
–
"ay lead to lie-threatening sepsis and septic shoc1
–
!t may present as t'o orms3 •
Suppurative
•
Fon-suppurative
•
Fon suppurative3 –
Persistent 2# pain ever jaundice, 9#harcot(s tria: IJ?C, IB;$,
•
Suppurative3 –
–
Persistent 2# pain ever jaundice, IJ?C, IB;$, Hepatic encephalopathy or hypotension may ensue 92eynold(s pentad:
"2CP E2CP
Acute cholecystitis Defnition cute cholecystitis is an acute in/ ammatory disease o the gall&ladder. !t is oten attri&uta&le to gallstones, &ut many actors, such as ischemiaL motility disordersL direct chemical injuryL inections 'ith microorganisms, proto@oa, and parasitesL collagen diseaseL and allergic reaction are involved.
incidence •
•
cute cholecystitis cases account or 5=+>= o all patients 'ith a&dominal pain. $he percentage o acute cholecystitis cases in patients under 7> years old 'ith a&dominal pain 9n ) *+,$ as lo/ at *.+0/ 'hereas that in patients aged 7> and over 9n ) 123*$ 'as high, at 4>.8= 9average, +>=:6
Etiology •
Cholecystolithiasis accounts or 8>= 87= o all causes o acute cholecystitis, 'hile acalculous cholecystitis accounts or the remaining 7=+>=
"is4 actors #holelithiasis A5D6 ?iliary disease may occur &y t'o mechanisms in !DS patients3 via !DS cholangiopathy 9'hich is more re0uent and via acute acalculous cholecystitisL !DS patients 'ith sclerosing cholangitis are also seen. Drugs as etiologic agents •
Gall bladder ultrasound •
•
Sho's gallstones the acoustic shado' due to a&sence o re/ected sound 'aves &ehind the gallstone
M M
►
Etiological mechanisms o gall&ladder diseases
•
•
•
Ascaris Complications in the &iliary tract include3 9+: cholelithiasis 'ith the ascarid as a nidus or stone ormation, 94: acalculous cholecystitis 95:, acute cholangitis 96:, acute pancreatitis, and 97: hepatic a&scess Pregnancy Acute cholecystitis an our !or f ve$ “7s” 9;air, at, emale, ertile, orty:
How would you like to stick the US probe on a pt and see HIM waving back at you!!! scaris lum&ricoides o the G?
Pathophysiology •
•
•
•
!n the majority o patients, gallstones are the cause o acute cholecystitis. $here are t'o actors 'hich determine the progression to acute cholecystitis N the degree o o&struction and the duration o the o&struction. ! the o&struction is partial and o short duration the patient eperiences &iliary colic. ! the o&struction is complete and o long duration the patient develops acute cholecystitis. ! the patient does not receive early treatment, the disease &ecomes more serious and complications occur.
Pathological classifcation •
•
•
•
Ee%atous cholecystitis' frst stage !182 ays$. 9ecroti:ing cholecystitis' secon stage !+8; ays$ 6uppurative cholecystitis' thir stage !8,3 ays$. #hronic cholecystitis
•
6pecif c or%s o acute cholecystitis. 9+: acalculous cholecystitis, 'hich is acute cholecystitis 'ithout cholecystolithiasisL 94: anthogranulomatous cholecystitis, 'hich is characteri@ed &y the anthogranulomatous thic1eningo the gall&ladder 'all and elevated intragall&ladder pressure due to stones, 'ith rupture o the the 2o1itans1y-cho sinuses.
•
•
95: emphysematous cholecystitis, in 'hich air appears in the gall&ladder 'all due to inection 'ith gas-orming anaero&es, including Clostridium perringens. $his orm is li1ely to progress to sepsis and gangrenous cholecystitisL it is oten seen in dia&etic patients. 96: $orsion o the gall&ladder.
Types o co%plications •
Peroration o the gall&ladder
•
?iliary peritonitis
•
•
Pericholecystic a&scess ?iliary % stula
Contrast C$ scan sho'ing emphysematous cholecystitis 'ith gall&ladder 'all disruption 9arro':, gas ormation 9arro'head:, and a &iloma
Contrast C$ scan sho'ing gallstones 9arro': 'ith gall&ladder rupture and /uid locali@ed at the gall&ladder ossa 9arro'head:
alse-positive case, 'ith poor enhancement o the mucosa o the ventral portion o the gall&ladder and suspected gall&ladder disruption. Gallstones 'ith acute cholecystitis and gall&ladder 'all gangrene 9arro': 'ere ound during surgery. Fo disruption o the gall&ladder 'all 'as noted. alse-positive case3 gall&ladder rupture 'ith liver penetration suspected &eore surgery. ctually, only chronic cholecystitis and a separated liver a&scess 9arro': 'ere ound during surgery.
&dominal radiograph o acalculous emphysematous cholecystitis demonstrating curvilinear air pattern conorming to the shape o the gall&ladder 'all
C$ images o emphysematous cholecystitis - same patient
#ltrasound %ndings o acalculous cholecystitis include mar1ed gall&ladder 'all thic1ening and pericholecystic /uid.
$ransverse ultrasound demonstrates mar1ed gall&ladder 'all thic1ening and pericholecystic /uid collection in a patient 'ith !DS 'ho 'as managed conservatively
treatment disposition cont. •
•
•
•
•
•
•
ntispasmodic agents 9glycopyrrolate: Opiate analgesics 9meperidine: ntiemetics 9prometha@ine: FS!DS 91etorolac: FG$ 9i protracted vomiting: !;(s 9once hydrated, can try PO /uids: ! sta&le and pain controlled, can arrange or outpt. surgical ollo'-up
Prognosis •
•
$he mortality in patients 'ith acute cholecystitis is >+>=, 'hereas the mortality in patients 'ith postoperative cholecystitis and acalculous cholecystitis is as high as 45=6>=. Elderly , mortality higher
"ecurrence rate o acute cholecystitis ater conservative treat%ent •
"ost patients 'ith acute cholecystitis are treated 'ith a cholecystectomy, and it is diQ cult to anticipate 'hether the outcome 'ill sho' recurrence
Presentasi clinic •
•
•
•
Clinical % ndings associated 'ith acute cholangitis include a&dominal pain, jaundice, ever 9Charcot(s triad:, and rigor. &out 7>=>= o patients 'ith acute cholangitis develop all three symptoms. 2eynolds( pentad 9Charcot(s triad plus shoc1 and a decreased level o consciousness: 'as presented in +878, 'hen 2eynolds and Dargan de% ned acute o&structive cholangitis. $he pentad is oten used to indicate severe 9grade !!!: cholangitis, &ut shoc1 and a decreased level o consciousness are o&served in only 5>= or e'er patients 'ith acute cholangitis . history o &iliary disease, such as gallstones, previous &iliary procedures, or the placement o a &iliary stent are actors that are very helpul to suggest a diagnosis o acute cholangitis
•
•
•
Clinical symptoms o acute cholecystitis include a&dominal pain 9right upper a&dominal pain:, nausea, vomiting, and ever. $he most typical symptom is right epigastric pain. $enderness in the right upper a&domen, a palpa&le gall&ladder, and "urphy(s sign are the characteristic % ndings o acute cholecystitis. positive "urphy(s sign has a speci% city o 8=8<= or acute cholecystitis
<loo tests •
•
•
•
•
Jhite &lood cell countL C-reactive protein liver unction tests, including al1aline phosphatase, gamma glutamyltranspeptidase 9GG$:, aspartate aminotranserase 9S$:, alanine aminotranserase 9B$:, and &iliru&in. ssessment o the severity 3 platelet count, &lood, urea nitrogen, creatinine, and prothrom&in time 9P$:. ?lood cultures are also helpul or severity assessment, Hyperamylasemia is a useul parameter to identiy complications such as choledocholithiasis causing &iliary pancreatitis
•
•
$here is no speci%c &lood test or acute cholecystitisL ho'ever, the 'hite &lood cell count and the measurement o Creactive protein is very useul in con%rming an in/ ammatory process. ?iliru&in, &lood urea nitrogen, creatinine, and P$ are very useul in assessing the disease severity status o the patient
Diagnostic i%aging •
•
&dominal ultrasound 9#S: and a&dominal computeri@ed tomography 9C$: 'ith intravenous contrast are very helpul studies in evaluating patients 'ith acute &iliary tract disease sses 3 &iliary o&struction, the level o the o&struction, and the cause o the o&struction,
•
•
characteristic % nding o acute cholecystitis include an enlarged gall&ladder, thic1ened gall&ladder 'all, gall&ladder stones andAor de&ris in the gall&ladder, sonographic "urphy(s sign, pericholecystic /uid, and pericholecystic a&scess. Sonographic "urphy(s sign is a very relia&le %nding o acute cholecystitis, 'ith a speci% city eceeding 8>= . C$ scan or even plain R-ray may demonstrate ree air, pneumo&ilia, and ileus.
;lo'chart sho'ing general guidance or the management o acute &iliary inection
;lo'chart or the management o acute cholangitis
;lo'chart cute cholecystitis
Anatomy
Anatomy
!ntroductions •
$he %rst report on acute &iliary inection 'as Charcot(s )$he symptoms o hepatic ever* in +.
Defnition •
cute cholangitis is a mor&id condition 'ith acute in/ ammation and inection in the &ile duct.
•
Hepatic ever. ever. “Hepatic ever” !ntermittent !ntermittent ever accompanied &y chills, right upper 0uadrant pain, and jaundice &ecame 1no'n as Charcot(s triad.
2eynolds and Dargan classi%ed acute micro&ial cholangitis 3 +. cute cholangitis developing rom acute cholecystitis 4. cute non-suppurative cholangitis 5. cute suppurative cholangitis 6. cute o&structive suppurative cholangitis 7. cute suppurative cholangitis accompanied &y hepatic a&scess
•
Acute obstructive cholangitis. Acute obstructive cholangitis 'as de%ned &y 2eynolds and Dargan, in +878 as a syndrome consisting o lethargy or mental conusion and shoc1, as 'ell as ever, jaundice, and a&dominal pain, caused &y &iliary o&struction.
Etiology cute cholangitis re0uires the presence o t'o actors3 9+: &iliary o&struction and 94: &acterial gro'th in &ile 9&ile inection:. ;re0uent causes o &iliary o&struction are choledocholithiasis, &enign &iliary stenosis, stricture o a &iliary anastomosis, and stenosis caused &y malignant disease
$a&le o etiology acute cholangitis
2is1 actors The bile o healthy subjects is generally aseptic. Ho'ever, &ile culture is positive or microorganisms in +<= o patients undergoing a non-&iliary operation, in 4= o acute cholangitis patients, in 66= o chronic cholangitis patients, and in 7>= o those 'ith &iliary o&struction. ?acteria in &ile are identi%ed in 8>= o patients 'ith choledocholithiasis accompanied &y jaundice.
•
•
•
Post-enoscopic retrograe cholangiopancreatography !E"#P$ inectious co%plications. &ther etiologies o acute cholangitis ' "iri@@i syndrome and lemmel syndrome. "iri@@i syndrome is a mor&id condition 'ith stenosis o the common &ile duct caused &y mechanical pressure andAor in/ ammatory changes caused &y the presence o stones in the gall&ladder nec1 and cystic ducts.
•
Bemmel syndrome is a series o mor&id conditions in 'hich the duodenal parapapillary diverticulum compresses or displaces the opening o the &ile duct or pancreatic duct and o&structs the passage o &ile in the &ile duct or hepatic duct, there&y causing cholestasis, jaundice, gallstone, cholangitis, and pancreatitis.
Causes o acute cholangitis 9=:
Pathophysiology •
•
$he onset o acute cholangitis involves t'o actors3 9i: increased &acteria in the &ile duct, and 9ii: elevated intraductal pressure in the &ile duct that allo's translocation o &acteria or endotoins into the vascular system 9cholangio-venous re/u:. $his process results in serious inections that can &e atal, such as hepatic a&scess and sepsis.
Prognosis •
•
$he reported mortality o acute cholangitis varies 4.7= - <7=. $he mortality rate &eore +8> 'as 7>=, and ater +8> it 'as +>= 5>=. Such dierences in mortality are pro&a&ly attri&uta&le to dierences in early diagnosis and improved supportive treatment.
•
•
$he major cause o death is multiple organ ailure 'ith irreversi&le shoc1, and mortality rates have not signi%cantly improved over the years. Causes o death in patients 'ho survive the acute stage o cholangitis include multiple organ ailure, heart ailure, and pneumonia.
•
Cholangitis –
!nection 'ithin &ile ducts due to o&struction o C?D.
–
!nection o the &ile ducts due to C?D o&struction secondary to stones, strictures
–
"ay lead to lie-threatening sepsis and septic shoc1
–
!t may present as t'o orms3 •
Suppurative
•
Fon-suppurative
•
Fon suppurative3 –
Persistent 2# pain ever jaundice, 9#harcot(s tria: IJ?C, IB;$,
•
Suppurative3 –
–
Persistent 2# pain ever jaundice, IJ?C, IB;$, Hepatic encephalopathy or hypotension may ensue 92eynold(s pentad:
"2CP E2CP
Acute cholecystitis Defnition cute cholecystitis is an acute in/ ammatory disease o the gall&ladder. !t is oten attri&uta&le to gallstones, &ut many actors, such as ischemiaL motility disordersL direct chemical injuryL inections 'ith microorganisms, proto@oa, and parasitesL collagen diseaseL and allergic reaction are involved.
incidence •
•
cute cholecystitis cases account or 5=+>= o all patients 'ith a&dominal pain. $he percentage o acute cholecystitis cases in patients under 7> years old 'ith a&dominal pain 9n ) *+,$ as lo/ at *.+0/ 'hereas that in patients aged 7> and over 9n ) 123*$ 'as high, at 4>.8= 9average, +>=:6
Etiology •
Cholecystolithiasis accounts or 8>= 87= o all causes o acute cholecystitis, 'hile acalculous cholecystitis accounts or the remaining 7=+>=
"is4 actors #holelithiasis A5D6 ?iliary disease may occur &y t'o mechanisms in !DS patients3 via !DS cholangiopathy 9'hich is more re0uent and via acute acalculous cholecystitisL !DS patients 'ith sclerosing cholangitis are also seen. Drugs as etiologic agents •
Gall bladder ultrasound •
•
Sho's gallstones the acoustic shado' due to a&sence o re/ected sound 'aves &ehind the gallstone
M M
►
Etiological mechanisms o gall&ladder diseases
•
•
•
Ascaris Complications in the &iliary tract include3 9+: cholelithiasis 'ith the ascarid as a nidus or stone ormation, 94: acalculous cholecystitis 95:, acute cholangitis 96:, acute pancreatitis, and 97: hepatic a&scess Pregnancy Acute cholecystitis an our !or f ve$ “7s” 9;air, at, emale, ertile, orty:
How would you like to stick the US probe on a pt and see HIM waving back at you!!! scaris lum&ricoides o the G?
Pathophysiology •
•
•
•
!n the majority o patients, gallstones are the cause o acute cholecystitis. $here are t'o actors 'hich determine the progression to acute cholecystitis N the degree o o&struction and the duration o the o&struction. ! the o&struction is partial and o short duration the patient eperiences &iliary colic. ! the o&struction is complete and o long duration the patient develops acute cholecystitis. ! the patient does not receive early treatment, the disease &ecomes more serious and complications occur.
Pathological classifcation •
•
•
•
Ee%atous cholecystitis' frst stage !182 ays$. 9ecroti:ing cholecystitis' secon stage !+8; ays$ 6uppurative cholecystitis' thir stage !8,3 ays$. #hronic cholecystitis
•
6pecif c or%s o acute cholecystitis. 9+: acalculous cholecystitis, 'hich is acute cholecystitis 'ithout cholecystolithiasisL 94: anthogranulomatous cholecystitis, 'hich is characteri@ed &y the anthogranulomatous thic1eningo the gall&ladder 'all and elevated intragall&ladder pressure due to stones, 'ith rupture o the the 2o1itans1y-cho sinuses.
•
•
95: emphysematous cholecystitis, in 'hich air appears in the gall&ladder 'all due to inection 'ith gas-orming anaero&es, including Clostridium perringens. $his orm is li1ely to progress to sepsis and gangrenous cholecystitisL it is oten seen in dia&etic patients. 96: $orsion o the gall&ladder.
Types o co%plications •
Peroration o the gall&ladder
•
?iliary peritonitis
•
•
Pericholecystic a&scess ?iliary % stula
Contrast C$ scan sho'ing emphysematous cholecystitis 'ith gall&ladder 'all disruption 9arro':, gas ormation 9arro'head:, and a &iloma
Contrast C$ scan sho'ing gallstones 9arro': 'ith gall&ladder rupture and /uid locali@ed at the gall&ladder ossa 9arro'head:
alse-positive case, 'ith poor enhancement o the mucosa o the ventral portion o the gall&ladder and suspected gall&ladder disruption. Gallstones 'ith acute cholecystitis and gall&ladder 'all gangrene 9arro': 'ere ound during surgery. Fo disruption o the gall&ladder 'all 'as noted. alse-positive case3 gall&ladder rupture 'ith liver penetration suspected &eore surgery. ctually, only chronic cholecystitis and a separated liver a&scess 9arro': 'ere ound during surgery.
&dominal radiograph o acalculous emphysematous cholecystitis demonstrating curvilinear air pattern conorming to the shape o the gall&ladder 'all
C$ images o emphysematous cholecystitis - same patient
#ltrasound %ndings o acalculous cholecystitis include mar1ed gall&ladder 'all thic1ening and pericholecystic /uid.
$ransverse ultrasound demonstrates mar1ed gall&ladder 'all thic1ening and pericholecystic /uid collection in a patient 'ith !DS 'ho 'as managed conservatively
treatment disposition cont. •
•
•
•
•
•
•
ntispasmodic agents 9glycopyrrolate: Opiate analgesics 9meperidine: ntiemetics 9prometha@ine: FS!DS 91etorolac: FG$ 9i protracted vomiting: !;(s 9once hydrated, can try PO /uids: ! sta&le and pain controlled, can arrange or outpt. surgical ollo'-up
Prognosis •
•
$he mortality in patients 'ith acute cholecystitis is >+>=, 'hereas the mortality in patients 'ith postoperative cholecystitis and acalculous cholecystitis is as high as 45=6>=. Elderly , mortality higher
"ecurrence rate o acute cholecystitis ater conservative treat%ent •
"ost patients 'ith acute cholecystitis are treated 'ith a cholecystectomy, and it is diQ cult to anticipate 'hether the outcome 'ill sho' recurrence
Presentasi clinic •
•
•
•
Clinical % ndings associated 'ith acute cholangitis include a&dominal pain, jaundice, ever 9Charcot(s triad:, and rigor. &out 7>=>= o patients 'ith acute cholangitis develop all three symptoms. 2eynolds( pentad 9Charcot(s triad plus shoc1 and a decreased level o consciousness: 'as presented in +878, 'hen 2eynolds and Dargan de% ned acute o&structive cholangitis. $he pentad is oten used to indicate severe 9grade !!!: cholangitis, &ut shoc1 and a decreased level o consciousness are o&served in only 5>= or e'er patients 'ith acute cholangitis . history o &iliary disease, such as gallstones, previous &iliary procedures, or the placement o a &iliary stent are actors that are very helpul to suggest a diagnosis o acute cholangitis
•
•
•
Clinical symptoms o acute cholecystitis include a&dominal pain 9right upper a&dominal pain:, nausea, vomiting, and ever. $he most typical symptom is right epigastric pain. $enderness in the right upper a&domen, a palpa&le gall&ladder, and "urphy(s sign are the characteristic % ndings o acute cholecystitis. positive "urphy(s sign has a speci% city o 8=8<= or acute cholecystitis
<loo tests •
•
•
•
•
Jhite &lood cell countL C-reactive protein liver unction tests, including al1aline phosphatase, gamma glutamyltranspeptidase 9GG$:, aspartate aminotranserase 9S$:, alanine aminotranserase 9B$:, and &iliru&in. ssessment o the severity 3 platelet count, &lood, urea nitrogen, creatinine, and prothrom&in time 9P$:. ?lood cultures are also helpul or severity assessment, Hyperamylasemia is a useul parameter to identiy complications such as choledocholithiasis causing &iliary pancreatitis
•
•
$here is no speci%c &lood test or acute cholecystitisL ho'ever, the 'hite &lood cell count and the measurement o Creactive protein is very useul in con%rming an in/ ammatory process. ?iliru&in, &lood urea nitrogen, creatinine, and P$ are very useul in assessing the disease severity status o the patient
Diagnostic i%aging •
•
&dominal ultrasound 9#S: and a&dominal computeri@ed tomography 9C$: 'ith intravenous contrast are very helpul studies in evaluating patients 'ith acute &iliary tract disease sses 3 &iliary o&struction, the level o the o&struction, and the cause o the o&struction,
•
•
characteristic % nding o acute cholecystitis include an enlarged gall&ladder, thic1ened gall&ladder 'all, gall&ladder stones andAor de&ris in the gall&ladder, sonographic "urphy(s sign, pericholecystic /uid, and pericholecystic a&scess. Sonographic "urphy(s sign is a very relia&le %nding o acute cholecystitis, 'ith a speci% city eceeding 8>= . C$ scan or even plain R-ray may demonstrate ree air, pneumo&ilia, and ileus.
;lo'chart sho'ing general guidance or the management o acute &iliary inection
;lo'chart or the management o acute cholangitis
;lo'chart cute cholecystitis
