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Acute Cholecystitis Jane Chunwen Teng D.O. 12/5/12.

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Presentation on theme: "Acute Cholecystitis Jane Chunwen Teng D.O. 12/5/12."— Presentation transcript:

1 Acute Cholecystitis Jane Chunwen Teng D.O. 12/5/12

2 Acute Cholecystitis Acute Cholecystitis: symptoms of RUQ pain, fever, and leukocytosis associated with gallbladder inflammation that is usually related to gallstone disease. Acalculous Cholecystitis: Clinically identical to acute cholecystitis but is not associated with gallstones, and usually occurs in critically ill pts. It accounts for approximately 10 % of cases of acute cholecystitis and is associated with high morbidity and mortality.

3 Chronic Cholecystitis
Chronic inflammatory cell infiltration of the gallballdder seen on histopathology. Almost invariably associated with the presence of gallstones and is thought to be the result of mechanical irritation or recurrent attacks of acute cholecystitis leading to fibrosis and thickening of the gallbladder.

4 Pathogenesis In contrast to biliary colic, the development of acute cholecystitis is not fully explained by cystic duct obstruction alone. Studies in animals have demonstrates that ligation of the cystic duct does not result in acute cholecystitis. However, acute cholecystitis can be produced experimentally by blockade of the cystic duct followed by deliberate irritation of the gallbladder mucosa.

5 PAthogenesis Lysolecithin (normally absent in bile) maybe release following trauma of the gallbladder wall from an impacted gallstone. Inflammatory mediators (e.g. PGE2 and 6 keto PG F1 alpha) synthesized by inflamed human gallbladder microsomes increased four times above normal. Prolonged impaction of stones in the cystic duct can lead to hydrops.

6 Clinical Manifestation
RUQ or epigastrium abdominal pain, may radiate to the right shoulder or back. Pain is usually steady and sever. Nausea, vomiting, and anorexia. Hx of fatty food ingestion about one hour or more before the initial onset of pain.

7 Physical Exam Pt usually are ill appearing, febrile, tachycardic and lie still on the examining table because any movement can aggravate the pain. Abdominal exam usually demonstrates voluntary and involuntary guarding.

8 Physical Exam Positive “Murphy’s sign” While palpating the area of the gallbladder fossa just beneath the liver edge, the patient is asked to inspire deeply, causing the gallbladder to descend toward the examining fingers. Pt with acute cholecystitis commonly experience increased discomfort and may have associated inspiratory arrest. Using cholescintigraphy as the gold standard, the sensitivity and specificity of a positive Murphy’s sign were 97 and 48 %, respectively.

9 Complication Left untreated, symptoms of cholecystitis may abate within 7-10 days. Complication can occur at alarmingly high rate, including the development of gallbladder gangrene (up to 20%) and subsequent perforation (2%). Other complications include cholecystoenteric fistula, gallstone ileus, emphysematous cholecystitis.

10 Diagnosis Confirmation of the diagnosis must be based upon a combination of physical findings, laboratory studies, and imaging tests. The most accurate physical findings were a positive Murphy sign (positive likelihood ratio 2.8, 95% CI 0.8 to 8.6) and right upper quadrant tenderness (negative LR 0.4, 95% CI 0.2 to 1.1) Lab: CBC shows leukocytosis with a left shift.

11 Diagnosis Elevation in the serum total bilirubin and alkaline phosphatase concentrations are NOT common in uncomplicated cholecystitis, since biliary obstruction is limited to the gallbladder; if present, they should raise the concerns about complicating conditions such as cholangitis, choledocholithiasis, or the Mirizzi syndrome (a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct)

12 Diagnosis There have been reports of mild elevation of serum aminotransferase and amylase, along with hyperbilirubinemia and jaundice. These abnormalities maybe due to the passage of small stones, sludge, or pus.

13 Imaging Tests Ultrasonograpy is usually the first test obtained and can often establish the diagnosis. Nuclear cholescintigraphy may be useful in cases in which the diagnosis remains uncertain after ultrasounography.

14 Ultrasound Diagnosis Gallbladder wall thickening (>4-5 mm) or edema (double wall sign) A “sonographic Murphy’s sign”, which is similar to the Murphy’s sign elicited during abdominal palpation, except that the positive response is observed during palpation with the ultrasound transducer. A particularly informative systematic review summarized the results of 30 studies of ultrasonography for gallstones and acute cholecystitis. Adjusted sensitivity and specificity for diagnosis of acute cholecystitis were 88% and 80% respectively.


16 Cholescintigraphy (HIDA scan)
Indicated if the diagnosis remain uncertain following ultrasonography. Technetium labeled hepatic iminodiacetic acid (HIDA) is injected intravenously and is then taken up selectively by hepatocytes and excreted into bile. If the cystic duct is patent, this agent will enter the gallbladder, leading to its visualization without the need for concentration.

17 Cholescintigraphy (HIDA scaN)
HIDA scan is also useful demonstrating patency of the common bile duct and ampulla. Visualization of the contrast within the common bile duct, gallbladder, and small bowel occurs within 30 to 60 mins. The test is positive if the gallbladder does not visualize, which is invariably due to cystic duct obstruction, usually from edema associated with acute cholecystitis or an obstructing stone.

18 Cholescintigraphy (HIDA sCAN)
Cholescintigraphy has a sensitivity and specificity of approximately 97 and 90 %, respectively. Cystic duct obstruction with a stone or tumor in the absence of acute cholecystitis can cause a false positive test. Other conditions that can cause false positive results include: Severe liver disease, Fasting pt receiving TPN, Biliary sphincterotomy and Hyperbilirubinemia.


20 Morphine Cholescintigraphy
A modified version of the HIDA scan, in which pts are given IV morphine during the exam. Morphine increases sphincter of Oddi pressure, thereby causing a more favorable pressure gradient for the radioactive tracer to enter the cystic duct. This modification is thought to be particularly useful in critically ill pts, in whom standard HIDA scans may be associated with false positive results.

21 Magnetic Resonance Cholangiography (MR Cholangiography)
Noninvasive technique for evaluating the intrahepatic and extrahepatic bile ducts. In a series that included 35 pts with symptoms of acute cholecystitis who underwent both ultrasound and MR cholangiography prior to cholecystectomy. MR cholangiography was superior to ultrasound for detecting stones in the cystic duct (sensitivity 100 vs. 14 %) but was less sensitive than ultrasound for detecting gallbladder wall thickening (sensitivity 69 vs. 96 %)

22 CT Abdominal CT is usually unnecessary in the diagnosis of acute cholecystitis, although it can easily demonstrate gallbladder wall edema associated with acute cholecystitis. Other CT findings include pericholecystic stranding and fluid, and high-attenuation bile. However, CT may fail to detect gallstones because many stones are isodense with bile. CT can be useful when complications of acute cholecystitis are suspected or when other diagnosis are considered.

23 TreatMENT Pts diagnosed with acute cholecystitis required hospital admission for IV hydration, correction of electrolyte disorders, and pain control (IM ketorolac mg adjusted for age and renal function). Pts should be kept NPO and those who are vomiting may need NGT placement. The guidelines of the Infectious Diseases Society of America (IDSA) recommend that antimicrobial therapy be instituted if infection is suspected on the basis of lab (>12,5000 WBC) or clinical findings (temp ≥38.5 degree) , and radiographic findings .

24 Treatment Routine antibiotics are also recommended in pts of advanced age or who have diabetes or immunodeficiency, and for prophylaxis in patients undergoing cholecystectomy to reduce septic complications even when infection is not suspected. Empiric antibiotic therapy should induce activity against the most common pathogens.

25 Treatment In a study of 467 pts, including a control group of 42 pts, including a control group of 42 with normal biliary tress, positive bile cultures were found in 22 % pts with symptomatic gallstones and 46 & of pts with acute cholecystitis. The most frequent isolates from the gallbladder or common bile duct were E.Coli (12%), Klebsiella (11%) , and Enterobacter (9%).

26 Treatment Empiric antibiotic Treatment for gram negative and anaeronic bateria 1st choice: Monotherapy with a beta-lactam or beta-lactamase inhibitor (e.g. pipercillin tazobactam or 4.5 g IV q6hr or ticarcillin-clauvulanate 3.1 g q4hr) Or Combination of 3rd generation cephalosporin PLUS metronidazole (ceftriaxone 1g q 24 hr or 2g q 12 hr for CNS infection and metronidazole 500mg q8hr)

27 Treatmetn The duration of antibiotic therapy is tailored to clinical improvement. For pts requiring prompt surgical intervention, antibiotics may be warranted for 24 to 48 hours following cholecystectomy, although longer or shorter courses may be appropriate depending on individual circumstances. Pts for whom surgical intervention is initially deferred ay warrant antibiotic therapy over 48 to 72 hours pending resolution of clinical signs and symptoms.

28 TIMING FOR SURGERY Although there is consensus that incidentally discovered asymptomatic gallstones should not be treated. Once a pt develops symptoms or complications related to gallstones (such as biliary colics or acute cholecystis), treatment to eliminate the gallstones should be recommended, because the likelihood of subsequent symptoms or complications is high. The National Cooperative Gallstone Study, a trial of nonsurgical treatment with chenodiol for biliary tract pain, demonstrated that the risk for recurrent symptoms was approximately 70 % during the two yrs following initial presentation.

29 Timing for Surgery The selection of treatment and timing of definitive therapy for acute cholecystitis depends upon the severity of symptoms and the pts overall risk of surgery. The aim of definitive therapy is to eliminate the precipitating cause of acute cholecystitis (ie, gallstones in the case of calculous cholecystitis) to prevent recurrent attacks.

30 Treatment The benefit of prompt surgical intervention was also illustrated in a subsequent study of 29,818 Medicare pts with acute cholecystitis. Compared to pts who underwent cholecystectomy in the initial hospitalization, pts who were discharged without surgery were more likely to require readmission (38 vs. 4 %) and had higher mortality (hazard ratio 1.56, 95% CI, ) over the following two yrs.

31 TREATMENT Lows-risk pts - The physical status scale established by the American Society of Anesthesiologists (ASA) is commonly used to determine the risk of surgery. Although previously considered to be at higher risk, pts with DM who do not have substantial microvascular or macrovascular disease have an outcome after acute cholecystitis similar to the nondiabetic population.

32 Treatment The ASA physical status classification system is a system for assessing the fitness of patients before surgery . A normal healthy patient. A patient with mild systemic disease. A patient with severe systemic disease. A patient with severe systemic disease that is a constant threat to life. A moribund. patient who is not expected to survive without the surgery A declared brain-dead patient whose organs are being removed for donor purposes.

33 Treatment in low risk pts
Immediate Cholecystectomy is preferred for pts who are at low risk (ASA class I and II) Several studies have indicated that cholecystectomy performed for low surgical risk pts during the initial hospitalization can reduce morbidity and costs. Early Surgery is also easier to perform as local inflammation increases 72 hr past the initial onset of symptoms making dissection less precise, increasing the severity of surgical complications, and open conversion more likely.

34 Treatment in high risk pts
High-risk pts - Pts who are in ASA classes III, IV, or V have a surgical mortality ranging from 5-27%, and are considered high-risk for cholecystectomy. This category generally includes pts with severe chronic illnesses, such as cardiovascular or pulmonary disease, or advanced malignancy. High risk pts, or pts who present late in the course of their disease process(>3-5 days), who continue to have severe symptoms and show no appreciable improvement despite one to two days of medical management require further intervention.

35 Treatment in high risk pts
Gallbladder drainage by percutaneous cholecystostomy in conjunction of antibiotic is the initial treatment of choice for high risk pts. The goal of cholecystostomy is to drain purulent material from the obstructed gallbladder. Tube decompression of the gallbladder allows for resolution of edema which often “opens” up the obstructed cystic duct.

36 Treatment in high risk pts
Endoscopic transpapillary gallbladder drainage has also been reported in pts with acute cholecystitis in whom percutaneous approaches are contraindicated or anatomically impossible. A limitation of the technique is that it can be technically challenging to place a guidewire and drainage tube into the gallbladder. In addition, this procedures carries all the inherent complications of ERCP.

37 Treatment – Surgery When the acute cholecystits has resolved, pts who are surgical candidates should undergo cholecystectomy. Surgery may also be required when the pt does not improve following percutaneous drainage, which suggests that the gallbladder has already progressed to gangrene. Pts who are particularly unstable will benefit from open cholecystostomy tube drainage achieved through a limited lapratomy. This can be performed at the bedside in the ICU setting if necessary.

38 Nonsurgical Treatment
Pts who stabilize but continue to be at high risk for surgery can be considered for percutaneous gallstone extraction with or without mechanical lithotripsy.

39 Reference

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