Acute acalculous cholecystitis

Presented by Ri 郎正麟

Etiology• Etiology:

– Western: 10~15 % of acute cholecystitis

eMedicine journal, Jan 7 2002 vol 3,No.1 – China: 58/258--22.48% 湖北醫科大學研究 1998

– Japanese series: 0.64% after gastrectomy– post-operation: fifth to seventh decade, female domi

nant– trauma or burn: second to fourth decades, male domi

nant 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 The ICU Book 1998; p531-2

Pathophysiology-I• depressed motility and starvation: trauma, burns, surge

ry, 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 Kawasaki’s disease Am Sur. 1983 May, 49(5):175-7

Pathophysiology-II• 57 p’ts 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 a

calculous cholecystitis– in common bile duct ligation(CBDL) guinea pigs , electric stimulation to activate intrins

ic 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

• CBDL affects the gallbladder contractility by two mechanism:– 1. Decrease smooth muscle contractility

– 2. Decrease neurally mediated contractions--• dysfunction of cholinergic excitory nerves

• upregulation of NO-mediated inhibition of smooth m. contractility

J Surg Res 2000 Feb;88(2):186-192

Pathophysiology-IV• Acaculous cholecystitis induced by intra-abdomin

al sepsis– ligation and prick of the cecum in 25 animals– varies degree of cholecystitis– bile culture in 15 alive animals: 10 negative, 5 positiv

e– 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 muscula

r 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%) The ICU Book 1998; p531-2

• Physical exam: vary with the severity– right hypochondrial tenderness

– muscle guarding, rigidity, rebound tenderness

– some degree of fever

– tachycardia– Murphy’s sign: variable eMedicine J.Jan 7 2002, Vol 3 No.1

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

eMedicine J.Jan 7 2002, Vol 3 No.1

Images studies-I• Ultrasound: the most useful diagnosis tool

– gallbladder wall thickness>4 mm with an increase in its volume (vesicular hydrop)

– sonographic Murphy’s sign– biliary sludge in a tender thickened gallbladder but fail to d

emostrate 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 ot

her than acalculous cholecystitis– 55 p’t in ICU, US/every 2 weeks, calculi exclude (11/55)

– sonographic features of acalculous cholecystitis:• a. gallbladder wall thickening d. pericholecystic fluid

• b. gallbladder distension e. gallbladder sludge

• c. intramural gallbladder lucencies f. Murphy’s 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• morphine cholescintigraphy :

– highly sensitive (95%) but poor specific (38%)

• CT scan:– periportal inflammation and gall bladder wall edema

– r/o other differential diagnosis

• PES and ERCP: – r/o other differential diagnosis eMedicine J.Jan 7 2002, Vol 3 No.1

Images studies-IV• Cholescintigraphy to the early diagnosis of acute acalculous cholec

ystitis in ICU patients• 32 p’t (78% with TPN)--suspected AAC

• underwent Tc-99m mebrofenin cholescitigraphy, morphine sulphate administered if GB was not viualised after1 hr(16p’t)

• 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 p’t clinically and biologically suspected AAC• US(+): wall thickness>4mm, hydrops, sludge

MC(+): the GB could not be visualized• final Dx: cholecystectomy

• MC is superior to US for confirming AAC Intensive Care Med 2000 Nov;26(11):1658-63

sensitivity specificity Positivepredictive value

Negativepredictive value

US 50% 94% 86% 71%MC 67% 100% 100% 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 syndro

me• acute/chronic pancreat

itis

eMedicine J.Jan 7 2002, Vol 3 No.1

Clinical events-I• AAC in p’ts with severe trauma

– 28 p’ts with contusion severe trauma– US every 5~7 days for early detection– 7 p’ts developed sono change starting 9th days– 4 proved histologically, 3 underwent cholecystectomy; th

e 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 p’t during 1987~1997, retrospectively– 6 p’ts had prolonged intraoperative hypotension and incr

ease blood transfusion– s/s: developed fever, leukocytosis. LFT elevation in a me

an of 32 days after operation– 5 p’ts underwent cholecystectomy, 2 p’ts 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 fa

ilure– 11/143 p’ts with surgical acute renal failure– Dx: clinical, US, lab finding– received Abx at the time of diagnosis– 5 p’ts treated conservatively, 6 p’ts underwent

cholecystectomy– mortality rate: 45.5%, no significant different f

rom ARF without AAC Acta Med Croatica 2000;54(1):15-20

Clinical events-IV

• GB abnormalities in MICU: ultrasound study– 30 p’ts estimate US in the first 2 days, 2 exclude du

e to previous cholecystectomy– 61%(17/28) considering acute acalculous cholecysti

tis– 3 major finding under US: 25% sludge, 22% wall t

hickening, 11% hydrops– none of these p’ts 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; 3/5

8: GB polyp; 1/58: ascaris; 1/58:GB ca; 7/58:Hx of op; 3/58: pancreatic disease 湖北醫科大學研究 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 p’ts, 17(63%) from non-biliary tract operation, 0.19% in SICU p’ts

• 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 +imip

enem • Immediate cholecystectomy: larparoscopic

or laparotomy • percutaneous cholecystosotomy with extern

al biliary drainage eMedicine J.Jan 7 2002, Vol 3 No.1

Thanks for your attention!!