Acute Acalculous Cholecystitis

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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

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 The ICU Book 1998; p531-2



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

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-opDx: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

• 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-

abdominal 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 bloodvessel thrombosis in the seromuscular layer of the

gallbladderOxford 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 demostrate stones

– intramural gas, pericholecystic fluid or

sloughed mucosa – no intrahepatic or extrahepatic ducts dilatation

– color doppler scan to r/o ischemia condition




Images studies-II• Evaluate sonographic abnormalities of gallbladder

other 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 walledema

– r/o other differential diagnosis

• PES and ERCP: – r/o other differential diagnosis




Images studies-IV

• Cholescintigraphy to the early diagnosis of acuteacalculous cholecystitis 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 Positive

predictive value

Negative

predictive valueUS 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

syndrome

• acute/chronicpancreatitis




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; 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 p’t during 1987~1997, retrospectively

– 6 p’ts had prolonged intraoperative hypotension

and increase blood transfusion

– s/s: developed fever, leukocytosis. LFT

elevation in a mean of 32 days after operation

– 5 p’ts underwent cholecystectomy, 2 p’ts hadplacement 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 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

from 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

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

cholecystitis

– 3 major finding under US: 25% sludge, 22% wallthickening, 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;3/58: 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

+imipenem• Immediate cholecystectomy: larparoscopic

or laparotomy

• percutaneous cholecystosotomy withexternal biliary drainage




Thanks for your attention!!

Acute Acalculous Cholecystitis

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