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Etiology
Etiology:
Western: 10~15 % of acute cholecystitis
eMedicine journal, Jan 7 2002 vol 3,No.1
China: 58/258--22.48% 1998 Japanese series: 0.64% after gastrectomy post-operation: fifth to seventh decade, female dominant trauma or burn: second to fourth decades, male dominant Oxford textbook of Surgery
Predisposing factor
Most seen in ICU patients with severe illness
multiple trauma extensive burn major surgery sepsis TPN use opiates analgesia anesthesia HIV infection
Pathophysiology-I
depressed motility and starvation: trauma, burns, surgery, TPN, anesthesia, narcotics
2~14% after major trauma or burn
J. Burn Care and Reha. 18(2):141-6, 1997 May-Apr
decrease blood flow through cystic artery: CHF, arteriosclerosis, polyarteritis nodosa, SLE, diabetes, shock obstruction of cystic duct by extrinsic inflammation, lymphadenopathy, metastasis infection: Salmonella, cholera, ascaris, CMV Kawasakis disease Am Sur. 1983 May, 49(5):175-7
Pathophysiology-II
57 pts AAC treated over a 9-years periods
type I (trauma or critical illness, N=24): 45.8% mortality, 66.7% acute ischemic cholecystitis, pre-op Dx:50% type II (s/s of acute cholecystitis N=20): 5% mortality, 50% acute on chronic cholecystitis, pre-op Dx: 90% type III (non-calculous gallbladder outflow obstruction, N=13): 23.1% mortality, obstructive pathology, pre-op Dx:15.4%
AAC distinct clinical-pathological variant of the disease S Afr J Surg 1999 Nov;37(4):99-104
Pathophysiology-III
Impaired smooth muscle contractility-->the pathophysiology of acalculous cholecystitis
in common bile duct ligation(CBDL) guinea pigs , electric stimulation to activate intrinsic muscle H&E stained of muscle strips a. progressive increase the inflammation and decrease the muscle contractility to Ach b. nitric oxide synthase inhibitor increase
Pathophysiology-IV
Acaculous cholecystitis induced by intraabdominal sepsis
ligation and prick of the cecum in 25 animals varies degree of cholecystitis bile culture in 15 alive animals: 10 negative, 5 positive Streptococcus Fracalis and Streptococcus Sp.
AAC in early stage induced by inflammatory process, and infection of the bile represent a late event
Acta Biomed Ateneo Parmense 1996;67(1-2):61-7
Histopathology
gall bladder edema of the serosa and muscular layer, with patchy thrombosis of arterioles and venules area of necrosis develop and affect the underlying mucosa
may due to factor VII activation lead to blood vessel thrombosis in the seromuscular layer of the gallbladder
Oxford textbook of Surgery
Clinical presentation-I:
Symptoms:
fever (70~95%) RUQ pain with tenderness (60~100%) nausea and vomiting (35~65%) abdominal pain (60~90%)
Clinical presentation-II:
Laboratory finding:
ALT/AST: mildly raised alkaline phosphate: mildly elevated bilirubin: variable, may rise to 85 mol/l CBC/DC: elevated due to acute inflammation
Images studies-I
Ultrasound: the most useful diagnosis tool
gallbladder wall thickness>4 mm with an increase in its volume (vesicular hydrop) sonographic Murphys sign biliary sludge in a tender thickened gallbladder but fail to demostrate stones intramural gas, pericholecystic fluid or sloughed mucosa no intrahepatic or extrahepatic ducts dilatation color doppler scan to r/o ischemia condition
eMedicine J.Jan 7 2002, Vol 3 No.1
Images studies-II
Evaluate sonographic abnormalities of gallbladder other than acalculous cholecystitis
55 pt in ICU, US/every 2 weeks, calculi exclude (11/55) sonographic features of acalculous cholecystitis:
a. gallbladder wall thickening b. gallbladder distension c. intramural gallbladder lucencies d. pericholecystic fluid e. gallbladder sludge f. Murphys sign
correlated with clinical and laboratory finding echo result: 30/44 (84%): at least one; 25/44 (57%): 2~3; 6/44 (14%): 4~5
gallbladder abnormalities are frequently seen on US in ICU patient Am L Roentgenol 2000 Apr;174(4):973-7
Images studies-III
Images studies-IV
Cholescintigraphy to the early diagnosis of acute acalculous cholecystitis in ICU patients
32 pt (78% with TPN)--suspected AAC underwent Tc-99m mebrofenin cholescitigraphy, morphine sulphate administered if GB was not viualised after1 hr(16pt) final Dx: clinical improvement, another etiology for symptom presented or histopathology following cholecystectomy finding:
I: non-visualization of gallbladder during the first 60 II: persistent non-visualization 30 following morphine administration III: non-visualization of the small bowel for at least 90
79% sensitivity and 100% specificity using the criteria I and II or III Eur J Nucl Med 1999 Oct;26(10):1317-25
Images studies-V
Assess the respective value of ultrasonography (US) and morphine cholescintigraphy (MC) 28 pt clinically and biologically suspected AAC US(+): wall thickness>4mm, hydrops, sludge MC(+): the GB could not be visualized final Dx: cholecystectomy
sensitivity specificity US MC Positive predictive value Negative predictive value
50% 67%
94% 100%
86% 100%
71% 80%
Differential diagnosis
Bile duct stricture biliary colic biliary disease biliary obstruction choledocholithiasis cholelithiasis duodenal ulcer gallbladder cancer Gastric ulcer gastritis viral hepatitis irritable bowel syndrome acute/chronic pancreatitis
eMedicine J.Jan 7 2002, Vol 3 No.1
Clinical events-I
28 pts with contusion severe trauma US every 5~7 days for early detection 7 pts developed sono change starting 9th days 4 proved histologically, 3 underwent cholecystectomy; the other died due to hypovolemia
US easily detect the GB morphological change no morbidity or mortality due to cholecystectomy Rev Gastroenterol Mex 1996 Oct-Dec;61(4):348-55
Clinical events-II
AAC after aortic reconstruction
7/996 pt during 1987~1997, retrospectively 6 pts had prolonged intraoperative hypotension and increase blood transfusion s/s: developed fever, leukocytosis. LFT elevation in a mean of 32 days after operation 5 pts underwent cholecystectomy, 2 pts had placement of cholecystostomy tubes gangrene or perforation was evident overall mortality: 71% J Am Coll Surg 1997 Mar;184(3):245-8
Clinical events-III
AAC in patients with surgical acute renal failure
11/143 pts with surgical acute renal failure Dx: clinical, US, lab finding received Abx at the time of diagnosis 5 pts treated conservatively, 6 pts underwent cholecystectomy mortality rate: 45.5%, no significant different from ARF without AAC
Acta Med Croatica 2000;54(1):15-20
Clinical events-IV
GB abnormalities in MICU: ultrasound study
30 pts estimate US in the first 2 days, 2 exclude due to previous cholecystectomy 61%(17/28) considering acute acalculous cholecystitis 3 major finding under US: 25% sludge, 22% wall thickening, 11% hydrops none of these pts needed a surgical procedure
Intensive Care Med 1996 Apr;22(4):356-8
Clinical events-V
AAC in China
58/258 in acute cholecystitis Dx: 1.symptoms, 2. Signs, 3.Lab, 4. Image M:F:1.07:1; <60 y/o: 70.69%; less systemic disease no shock, no heart failure, no mortality all medical treatment etiology: 13/58: gastropathy; 5/58: HTN or angina; 3/58: GB polyp; 1/58: ascaris; 1/58:GB ca; 7/58:Hx of op; 3/58: pancreatic disease 1998
Clinical events-VI
AAC: incidence, risk factor, diagnosis, and outcome
53 m/o, 27 cases(M:17, F:10) 14(52%) in critical ill pts, 17(63%) from non-biliary tract operation, 0.19% in SICU pts image: MC (90% sensitivity), CT (67%), US(29%) AAC associate complication: gangrene(63%), perforation(15%), abscess(4%) total mortality: 41% To improve outcome, a high index of suspision with early radiologic evaluation and multiple studies is necessary.
Am Surg 1998 May;64(5):471-5
Treatment
medical treatment: no effective? initially antibiotic given: vancomycin +imipenem Immediate cholecystectomy: larparoscopic or laparotomy percutaneous cholecystosotomy with external biliary drainage
eMedicine J.Jan 7 2002, Vol 3 No.1