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 domin
ant
– trauma or burn: second to fourth decades, male domin
ant 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, surger
y, 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, arterio

sclerosis, polyarteritis nodosa, SLE, diabetes, shock
• obstruction of cystic duct by extrinsic inflammation, ly
mphadenopathy, 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 th
e disease S Afr J Surg 1999 Nov;37(4):99-104
 Pathophysiology-III
• Impaired smooth muscle contractility-->the pathophysiology of ac
alculous 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 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 underlyi
ng mucosa
may due to factor VII activation lead to blood vesse
l thrombosis in the seromuscular layer of the gallblad
der
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 vol
ume (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 oth
er 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 cholecy
stitis in ICU patients
• 32 p’t (78% with TPN)--suspected AAC
• underwent Tc-99m mebrofenin cholescitigraphy, morphine sulphate administere
d if GB was not viualised after1 hr(16p’t)
• final Dx: clinical improvement, another etiology for symptom presented or histo
pathology 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

sensitivity specificity Positive Negative

predictive value predictive value
US 50% 94% 86% 71%
• MC is67%
MC superior100%
to US for confirming
100% AAC 80%
Intensive Care Med 2000 Nov;26(11):1658-63
 Differential diagnosis
• Bile duct stricture • Gastric ulcer
• biliary colic • gastritis
• biliary disease • viral hepatitis
• biliary obstruction • irritable bowel syndro
• choledocholithiasis me
• cholelithiasis • acute/chronic pancreatit
is
• duodenal ulcer
• gallbladder cancer 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; the
other died due to hypovolemia
• US easily detect the GB morphological change
• no morbidity or mortality due to cholecystectomy R
ev 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 increa
se blood transfusion
– s/s: developed fever, leukocytosis. LFT elevation in a mea
n 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 fail
ure
– 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 ch
olecystectomy
– mortality rate: 45.5%, no significant different fro
m 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 t
o previous cholecystectomy
– 61%(17/28) considering acute acalculous cholecystitis
– 3 major finding under US: 25% sludge, 22% wall thic
kening, 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 op
eration, 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 radiol
ogic 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!!