Home » Pancreatico-Biliary

Category Archives: Pancreatico-Biliary

Diagnosis and Management of Asymptomatic Neoplastic Pancreatic Cysts

April 26, 2015 9:20 PM

The American Gastroenterological Association Institute Guideline on the Diagnosis and Management of Asymptomatic Neoplastic Pancreatic Cysts

 

Updated recommendations developed by the American Gastroenterological Association (AGA) on management of asymptomatic pancreatic neoplastic cysts call for a conservative approach in many cases as most such cysts are not cancerous. Approximately 15% of patients undergoing abdominal magnetic resonance imaging (MRI) for other indications harbor unsuspected pancreatic cysts. The incidence of pancreatic cysts in the US population increases with age and may be as common as 25% in those older than 70 years. The management of patients with an incidentally detected pancreatic cyst poses a significant challenge. In an effort to provide a strategy by which clinicians may identify the small minority of cysts with early invasive cancer or high-grade dysplasia – or those which will develop them in the near future – the AGA developeded 10 recommendations, although listed as “conditional” because of very low-quality evidence.

 

The AGA guidelines pertain only to asymptomatic pancreatic neoplastic cysts. The impact of symptoms on the management of cysts was not assessed, and this guideline does not consider some neoplastic lesions such as solid papillary neoplasms, cystic degeneration of adenocarcinomas, neuroendocrine tumors, and main duct intraductal papillary mucinous neoplasms (IPMNs) without side branch involvement, as identification of these neoplasms may be less challenging and the accepted approach is surgical resection if the patient is a suitable candidate.

 

 

The overall risk that an incidental pancreatic cyst is malignant is very low. The AGA estimates that a cyst seen incidentally on MRI has a 10 in 100,000 chance of being a mucinous invasive malignancy and a 17 in 100,000 chance of being a ductal cancer. MRI is the preferred surveillance imaging modality, because MRI does not expose the patient to radiation, and it is better able to demonstrate the structural relationship between the pancreatic duct and associated cyst than CT.

 

  • The AGA suggests that patients with pancreatic cysts less than 3 cm without a solid component or a dilated pancreatic duct undergo MRI for surveillance in 1 year and then every 2 years for a total of 5 years if there is no change in cyst size or characteristics.
  • The AGA suggests that pancreatic cysts with at least 2 high-risk features such as size ≥3 cm, a dilated main pancreatic duct, or the presence of an associated solid component, should be examined with endoscopic ultrasonography-guided fine-needle aspiration (EUS-FNA). The relative increase in risk of malignancy in the presence of high-risk features may be substantial but because the baseline risk is so low, the absolute effect of these features is modest.
  • The AGA suggests that patients without concerning EUS-FNA results should undergo MRI surveillance after 1 year and then every 2 years to ensure no change in risk of malignancy. The negative predictive value of unremarkable EUS-FNA results is very high and this in a setting with a very low risk of associated malignancy.
  • The AGA suggests that significant changes in the characteristics of the cyst including the development of a solid component, increasing size of the pancreatic duct, and/or diameter ≥3 cm, are indications for EUS-FNA.
  • The AGA suggests against continued surveillance of pancreatic cysts if there has been no significant change in the characteristics of the cyst after 5 years of surveillance or if the patient is no longer a surgical candidate.
  • The AGA suggests that patients with both a solid component and a dilated pancreatic duct and/or concerning features on EUS and FNA should undergo surgery to reduce the risk of mortality from carcinoma. Surgery is likely to be most beneficial in cases of cyst resection of high-grade dysplasia, thereby preventing malignancy. Since it is clear from other cancers that not all high-grade dysplasia progress, the proportion of patients who truly benefit from surgery is unclear even in this high-risk group.
  • The AGA recommends that if surgery is considered for a pancreatic cyst, patients are referred to a center with demonstrated expertise in pancreatic surgery.
  • The AGA suggests that patients with invasive cancer or dysplasia in a cyst that has been surgically resected should undergo MRI surveillance of any remaining pancreas every 2 years.
  • The AGA recommends against routine surveillance of pancreatic cysts without high-grade dysplasia or malignancy at surgical resection.
  • The AGA recommends that before starting any pancreatic cyst surveillance program, patients should have a clear understanding of programmatic risks and benefits.
Three commentaries in the April 2015 edition of Gastroenterology are worthwhile reading (April 2015, Volume 148, Issue 4, p669-862, e1-e16). One paper questions whether even small pancreatic cysts without concerning features have a high risk of malignancy. The clinician taking care of patients with pancreatic cysts is advised to be cautious in applying this new guideline.
In Summary – Issues Related to the Conduct of Surveillance
  1. The AGA recommends that before starting any pancreatic cyst surveillance program, patients should have a clear understanding of programmatic risks and benefits.
  2. The AGA suggests that patients with pancreatic cysts less than 3 cm without a solid component or a dilated pancreatic duct undergo MRI for surveillance in 1 year and then every 2 years for a total of 5 years if there is no change in size or characteristics.
  3. The AGA suggests that pancreatic cysts with at least 2 high-risk features, such as size ‡3 cm, a dilated main pancreatic duct, or the presence of an associated solid component, should be examined with EUS-FNA.
  4. The AGA suggests that patients without concerning EUS-FNA results should undergo MRI surveillance after 1 year and then every 2 years to ensure no change in risk of malignancy.
  5. The AGA suggests that significant changes in the characteristics of the cyst, including the development of a solid component, increasing size of the pancreatic duct, and/or diameter ‡3 cm, are indications for EUS-FNA.
  6. The AGA suggests against continued surveillance of pancreatic cysts if there has been no significant change in the characteristics of the cyst after 5 years of surveillance or if the patient is no longer a surgical candidate.
  7. The AGA suggests that patients with both a solid component and a dilated pancreatic duct and/or concerning features on EUS and FNA should undergo surgery to reduce the risk of mortality from carcinoma.
  8. The AGA recommends that if surgery is considered for a pancreatic cyst, patients are referred to a center with demonstrated expertise in pancreatic surgery.
  9. The AGA suggests that patients with invasive cancer or dysplasia in a cyst that has been surgically resected should undergo MRI surveillance of any remaining pancreas every 2 years.
  10. The AGA suggests against routine surveillance of pancreatic cysts without high-grade dysplasia or malignancy at surgical resection.
Abbreviations
EUS, endoscopic ultrasonography
FNA, fine-needle aspiration
HGD, high-grade dysplasia
IPMN, intraductal papillary mucinous neoplasm
MRI, magnetic resonance imaging

ACG Clinical Guideline: Primary Sclerosing Cholangitis

April 25, 2015 9:22 PM

Please review the excellent ACG Clinical Guideline on Primary sclerosing cholangitis (PSC).

 

PSC is a chronic cholestatic liver and biliary tract disease with a highly variable natural history. The pathogenesis of the disorder remains elusive. Complications of the disease are a direct result of fibrosis and strictures involving intra and extrahepatic bile ducts. PSC may be asymptomatic for long periods but may also have an aggressive course, leading to recurrent biliary tract obstruction, recurrent episodes of cholangitis, and progression to end-stage liver disease. The diagnosis is now most frequently established using magnetic resonance cholangiography (MRCP), although direct cholangiography may be more sensitive. The typical cholangiographic findings include focal stricturing and saccular dilatation of the bile ducts (“beaded”). The differential diagnosis of PSC includes several disorders that lead to biliary strictures such as bacterial cholangitis, intraarterial administration of floxuridine, prior biliary surgery, and AIDS- related cholangiopathy.

 

ACG Guideline Recommendation Summary:
  • Differential diagnosis of primary sclerosing cholangitis
    • Secondary sclerosing cholangitis
    • Cholangiocarcinoma
    • IgG4-associated cholangitis
    • Histiocytosis X
    • Autoimmune hepatitis
    • HIV syndrome
    • Bile duct strictures
    • Cholendocholithiasis
    • Primary biliary cirrhosis
    • Papillary tumors
  • Diagnosis
    • Endoscopic retrograde cholangiopancreatography (ERCP) has been the most common procedure in diagnosing PBS. However, magnetic resonance cholangiopancreatography (MRCP) is rapidly becoming the preferred method because it is noninvasive, cheaper and has no associated risk of pancreatitis. A liver biopsy is not needed unless a patient is suspected of having small duct PSC.
  • Therapy
    • There is currently no established treatment for PSC. However, clinicians are using doses of ursodeoxycholic acid at 20 mg/kg per day for treating PSC.
  • Endoscopic Management 
    • Endoscopic treatment of dominant strictures may improve prognosis, help to relieve the complications of pruritus and cholangitis, allow for early diagnosis of cholangiocarcinoma and may lead to improved survival. ERCP with balloon dilatation is recommended for relieving symptoms of dominant strictures of PSC patients. If a PSC patient undergoes ERCP, antibiotic prophylaxis should be taken to prevent post-ERCP cholangitis. Routine stenting after dilation is not recommended.
  • IBD and PSC
    • Up to 80% of patients with PSC have IBD. Undergoing annual colon surveillance is recommended in PSC patients with colitis at the time of PCS diagnosis. A colonoscopy with biopsies is recommended in PSC patients whether or not there are symptoms at PSC diagnosis. An exam every 3-5 years is also recommended for patients without prior evidence of colitis.
  • Hepatobiliary Malignancies and Gallbladder Disease
    • PSC patients are at risk for developing hepatobiliary malignancies. The risk for cholangiocarcinoma is several hundred times higher in patients with PSC vs. patients without PSC. Screening for cholangiocarcinoma with regular cross-sectional imaging with ultrasound or magnetic resonance and serial CA 19-9 is recommended every 6 to 12 months. Patients with PSC with gallbladder polyps more than 8 mm should also undergo cholecystectomy.
  • Special Situations
    • Every PSC patient is unique and some patients may develop autoimmune hepatitis and other infections. Testing for autoimmune hepatitis is recommended for patients with PSC under 25 years of age and for those patients with higher than expected aminotransferases. MRCP is recommended for PSC patients under 25 years of age with autoimmune hepatitis who have elevated alkaline phosphatase serum levels.
  • General Management
    • Patients with PSC should undergo bone mineral density screening at diagnosis using duel energy X-ray absorption repeated at 2- to 4-year intervals; patients with advanced liver disease should be checked and monitored for fat-soluble vitamin deficiencies; and patients with PSC and mild pruritus should undergo local skin treatment with antihistamines or emollients to reduce symptoms.

 

 

The ACG Guideline include 24 suggested recommendations on how to diagnose a patient, whether ursodeoxycholic acid should be used as a treatment, on endoscopic management, and how to treat patients who need a liver transplant or have inflammatory bowel disease (IBD), as well as general management issues.

 

DIAGNOSIS
  • MRCP is preferred over endoscopic retrograde cholangiopancreatography (ERCP) to establish a diagnosis of PSC.
  • Liver biopsy is not necessary to make a diagnosis in patients with suspected PSC based on diagnostic cholangiographic findings.
  • Liver biopsy is recommended to make a diagnosis in patients with suspected small duct PSC or to exclude other conditions such as suspected overlap with autoimmune hepatitis.
  • Antimitochondrial autoantibody testing can help exclude primary biliary cirrhosis.
  • Patients with PSC should be tested at least once for elevated serum immunogloblulin G4 (IgG4) levels.
MEDICAL TREATMENT
  • At this time, there is no established medical treatment for patients with PSC.
    • Ursodeoxycholic acid (UDCA) in doses >28 mg/kg/day should not be used for the management of patients with PSC.
  • Other treatments that have been tested without any obvious proven clinical benefit or improvement of liver biochemistries include:
    • Azathioprine
    • Budesonide
    • Docosahexaenoic acid
    • Methotrexate
    • Metronidazole
    • Minocycline
    • Mycophenolate mofetil
    • Nicotine
    • Pentoxifylline
    • Pirfenodone
    • Prednisolone
    • Tacrolimus
    • Vancomycin
ENDOSCOPIC MANAGEMENT
  • ERCP with balloon dilatation is recommended for PSC patients with dominant stricture and pruritus, and/or cholangitis, to relieve symptoms.
  • PSC with a dominant stricture seen on imaging should have an ERCP with cytology, biopsies, and fluorescence in-situ hybridization (FISH), to exclude diagnosis of cholangiocarcinoma.
  • PSC patients undergoing ERCP should have antibiotic prophylaxis to prevent post-ERCP cholangitis.
  • Routine stenting after dilation of a dominant stricture is not required, whereas short-term stenting may be required in patients with severe stricture.
PERCUTANEOUS MANAGEMENT
  • Percutaneous cholangiography for treatment of dominant strictures can be performed in PSC patients with altered anatomy that prevents successful ERCP, such as Roux-en-Y choledo-chojejunostomy or gastric bypass, or as a rescue therapy after failed endoscopic access. Percutaneous cholangiography is generally the second line of treatment after ERCP because of the risk of complications, including hepatic arterial injury, hemobilia, and cholangitis
LIVER TRANSPLANTATION
  • Liver transplantation, when possible, is recommended over medical therapy or surgical drainage in PSC patients with decompensated cirrhosis, to prolong survival.
  • Patients should be referred for liver transplantation when their Model for End-Stage Liver Disease (MELD) score exceeds 14.
  • In specific clinical circumstances, patients with PSC may be offered additional MELD points, to improve their priority for receiving a donor organ for liver transplantation. MELD exception points can be approved by the United Network for Organ Sharing Regional Review Board for the following indications:
    • Recurrent episodes of cholangitis, with >2 episodes of bacteremia or >1 episode of sepsis.
    • Cholangiocarcinoma less then 3 cm in diameter, without evidence of metastasis, undergoing treatment through an institutional review board-approved clinical trial.
    • Intractable pruritus.
  • Recurrence of PSC after liver transplantation is relatively common, affecting as many as 20% of patients at 5 years after transplantation.
PSC AND IBD
  • The risk of colorectal dysplasia and cancer is significantly higher (approximately four- to fivefold) among patients with PSC and IBD compared with those with IBD without PSC.
  • Annual colon surveillance preferably with chromoendoscopy is recommended in PSC patients with colitis beginning at the time of PSC diagnosis.
  • A full colonoscopy with biopsies is recommended in patients with PSC regardless of the presence of symptoms to assess for associated colitis at time of PSC diagnosis.
  • Some advocate repeating the exam every 3–5 years in those without prior evidence of colitis.
HEPATOBILIARY MALIGNANCIES AND GALLBLADDER DISEASE
  • Consider screening for cholangiocarcinoma with regular cross-sectional imaging with ultrasound or MR and serial CA 19-9 every 6–12 months.
  • Cholecystectomy should be performed for patients with PSC and gallbladder polyps >8 mm, to prevent the development of gallbladder adenocarcinoma.
SPECIAL SITUATIONS
  • PSC and autoimmune hepatitis may co-exist in the same patient and the prevalence of autoimmune hepatitis in patients with PSC is ~10%.
  • Further testing for autoimmune hepatitis is recommended for patients with PSC <25 years of age or those with higher- than-expected levels of aminotransferases usually 5× upper limit of normal.
  • MRCP is recommended for patients <25 years of age with autoimmune hepatitis, who have elevated serum ALP usually greater than 2× the upper limit of normal.
PSC IN CHILDREN
  • PSC appears to be much less common among children than adults, with an estimated prevalence 20% lower than in adults and is a rare indication for liver transplantation in this population. PSC in children is more often associated with higher serum aminotransferase levels and concomitant autommune hepatitis, and sclerosing cholangitis is a more common phenomenon, leading to the use of the term “autoimmune sclerosing cholangitis.” Serum ALP may be elevated in children due to bone growth; hence, suspected cholestasis should be confirmed by measurement of gamma-glutamyl transpeptidase levels. Cholangiocarcinoma appears to be rare in this population and surveillance for gallbladder cancer or cholangiocarcinoma is not recommended.
IMMUNOGLOBULIN G4-AASSOCIATED CHOLANGITIS
  • IgG4-associated pancreatitis and cholangitis is being increasingly recognized in patients who present with sclerosing cholangitis. IgG4-associated autoimmune pancreatitis is a clearly described entity characterized by strictures in the pancreatic duct, elevated IgG4 levels and response to immunosuppressive therapy. This condition may be associated with biliary strictures and elevated plasma IgG4 levels, and liver biopsy may reveal a lymphoplasmacytic infiltrate . In some cases, the biliary disease is predominant and features of autoimmune pancreatitis may or may not be present.
  • Measurement of IgG4 levels is reasonable in patients with PSC and consideration should be given to imaging for autoimmune pancreatitis and the presence of IgG4-associated cholangitis among those with markedly elevated IgG4 levels.
  • Liver biopsy should be considered to identify the classical lymphoplasmacytic infiltrate and consideration of immunosuppression therapy may be useful in such patients, especially if they have higher-than- expected elevations of serum aminotransferase levels.
GENERAL MANAGEMENT
  • Local skin treatment should be performed with emollients and/or antihistamines in patients with PSC and mild pruritus, to reduce symptoms.
  • Bile acid sequestrants such as cholestyramine should be taken (prescribed) in patients with PSC and moderate pruritus to reduce symptoms. Second-line treatment such as rifampin and naltrexone can be considered if cholestyramine is ineffective or poorly tolerated.
  • Recommend screening for varices in patients with signs of advanced disease with platelet counts <150×103/dl.
  • Patients with PSC should undergo bone mineral density (BMD) screening at diagnosis with dual energy X-ray absorption at diagnosis and repeated at 2- to 4-year intervals.
  • Patients with advanced liver disease should be screened and monitored for fat-soluble vitamin deficiencies.
SUMMARY OF RECOMMENDATIONS
  • MRCP is preferred over ERCP to establish a diagnosis of PSC.
  • Liver biopsy is not necessary to make a diagnosis in patients with suspected PSC based on diagnostic cholangiographics findings.
  • Liver biopsy is recommended to make a diagnosis in patients with suspected small duct PSC or to exclude other conditions such as suspected overlap with autoimmune hepatitis.
  • Antimitochondrial autoantibody testing can help exclude primary biliary cirrhosis.
  • Patients with PSC should be tested at least once for elevated serum IgG4 levels.
  • UDCA in doses >28 mg/kg/day should not be used for management of patients with PSC
  • ERCP with balloon dilatation is recommended for PSC patients with dominant stricture and pruritus, and/or cholangitis, to relieve symptoms.
  • PSC with a dominant stricture seen on imaging should have an ERCP with cytology, biopsies and FISH to exclude diagnosis of cholangiocarcinoma.
  • PSC patients undergoing ERCP should have antibiotic prophylaxis to prevent post-ERCP cholangitis.
  • Routine stenting after dilation of a dominant stricture is not required, whereas short-term stenting may be required in patients with severe stricture.
  • Liver transplantation, when possible, is recommended over medical therapy or surgical drainage in PSC patients with decompensated cirrhosis, to prolong survival
  • Patients should be referred for liver transplantation when their MELD score exceeds 14.
  • Annual colon surveillance preferably with chromoendoscopy is recommended in PSC patients with colitis beginning at the time of PSC diagnosis.
  • A full colonoscopy with biopsies is recommended in patients with PSC regardless of the presence of symptoms to assess for associated colitis at the time of PSC diagnosis.
  • Some advocate repeating the exam every 3–5 years in those without prior evidence of colitis.
  • Consider screening for cholangiocarcinoma with regular cross-sectional imaging with ultrasound or MR and serial CA 19-9 every 6–12 months.
  • Cholecystectomy should be performed for patients with PSC and gallbladder polyps >8 mm, to prevent the development of gallbladder adenocarcinoma.
  • Further testing for autoimmune hepatitis is recommended for patients <25 years of age with PSC or those with higher- than-expected levels of aminotransferases usually 5× upper limit of normal.
  • MRCP is recommended for patients <25 years of age with autoimmune hepatitis, who have elevated serum ALP usually >2× the upper limit of normal.
  • Local skin treatment should be performed with emollients and/or antihistamines in patients with PSC and mild pruritus, to reduce symptoms.
  • Bile acid sequestrants such as cholestyramine should be taken (prescribed) in patients with PSC and moderate pruritus, to reduce symptoms. Second-line treatment such as rifampin and naltrexone can be considered if cholestyramine is ineffective or poorly tolerated.
  • Recommend screening for varices in patients with signs of advanced disease with platelet counts <150×103/dl.
  • Patients with PSC should undergo BMD screening at diagnosis with dual energy X-ray absorption at diagnosis and repeated at 2- to 4-year intervals.
  • Patients with advanced liver disease should be screened and monitored for fat-soluble vitamin deficiencies.

The Diagnosis and Management of Focal Liver Lesions

February 16, 2015 4:34 PM

Please review the excellent ACG Clinical Guideline on “The Diagnosis and Management of Focal Liver Lesions“.
Focal liver lesions (FLL) have been a common reason for consultation faced by gastroenterologists and hepatologists. The increasing and widespread use of imaging studies has led to an increase in detection of incidental FLL. It is important to consider not only malignant liver lesions, but also benign solid and cystic liver lesions such as hemangioma, focal nodular hyperplasia, hepatocellular adenoma, and hepatic cysts, in the differential diagnosis.
      
Solid Focal Liver Lesions (FLL)
Suspected hepatocellular carcinoma
  • An MRI or triple-phase CT should be obtained in patients with cirrhosis with an ultrasound showing a lesion of >1cm.
  • Patients with chronic liver disease, especially with cirrhosis, who present with a solid FLL are at a very high risk for having HCC and must be considered to have HCC until otherwise proven.
  • A diagnosis of HCC can be made with CT or MRI if the typical characteristics are present: a solid FLL with enhancement in the arterial phase with washout in the delayed venous phase should be considered to have HCC until otherwise proven.
  • If an FLL in a patient with cirrhosis does not have typical characteristics of HCC, then a biopsy should be performed in order to make the diagnosis.
Suspected cholangiocarcinoma
  • MRI or CT should be obtained if CCA is suspected clinically or by ultrasound.
  • A liver biopsy should be obtained to establish the diagnosis of CCA if the patient is non operable.

Suspected hepatocellular adenoma

  • Oral contraceptives, hormone-containing IUDs, and anabolic steroids are to be avoided in patients with hepatocellular adenoma.
  • Obtaining a biopsy should be reserved for cases in which imaging is inconclusive and biopsy is deemed necessary to make treatment decisions.
  • Pregnancy is not generally contraindicated in cases of hepatocellular adenoma < 5 cm and an individualized approach is advocated for these patients.
  • In hepatocellular adenoma ≥ 5 cm, intervention through surgical or nonsurgical modalities is recommended, as there is a risk of rupture and malignancy.
  • If no therapeutic intervention is pursued, lesions suspected of being hepatocellular adenoma require follow-up CT or MRI at 6- to 12-month intervals. The duration of monitoring is based on the growth patterns and stability of the lesion over time.
  • Clinical variants of hepatocellular adenoma
    • Liver adenomatosis.
      • Multiple adenomas, defined as between > 3 and ≥ 10 lesions, are collectively referred to as liver adenomatosis. These multiple lesions have identical clinical, histological, and radiographic features as hepatocellular adenomas and are managed in the same manner.
    • Telangiectatic hepatocellular adenoma
      • Previously known as telangiectatic focal nodular hyperplasia, telangiectatic hepatocellular adenoma (THCA) has recently been reclassified as a subcategory of inflammatory hepatocellular adenoma. THCA should be managed as aggressively as hepatocellular adenomas as they are likely to be symptomatic, prone to hemorrhage, and may contain focal areas of necrosis. The high likelihood of hemorrhage combined with an unknown potential of transformation to HCC makes surgery the recommended treatment.

Suspected hemangioma

  • An MRI or CT scan should be obtained to confirm a diagnosis of hemangioma.
  • Liver biopsy should be avoided if the radiologic features of a hemangioma are present.
  • Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with a hemangioma.
  • Regardless of the size, no intervention is required for asymptomatic hepatic hemangiomas. Symptomatic patients with impaired quality of life can be referred for surgical or nonsurgical therapeutic modalities by an experienced team.

Suspected focal nodular hyperplasia

  • An MRI or CT scan should be obtained to confirm a diagnosis of FNH. A liver biopsy is not routinely indicated to confi rm the diagnosis.
  • Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with FNH.
  • Asymptomatic FNH does not require intervention.
  • Annual US for 2-3 years is prudent in women diagnosed with FNH who wish to continue OCP use. Individuals with a firm diagnosis of FNH who are not using OCP do not require follow-up imaging.
Suspected nodular regenerative hyperplasia
  • Liver biopsy is required to confirm the diagnosis of NRH.
  • Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with an NRH.
  • Asymptomatic NRH does not require intervention.
  • Management of NRH is based on diagnosing and managing any underlying predisposing disease processes.
       
Cystic Focal Liver Lesions (FLL)
Suspect simple hepatic cysts
  • A hepatic cyst identified on US with septations, fenestrations, calcifications, irregular walls, or daughter cysts should prompt further evaluation with a CT or MRI.
  • Asymptomatic simple hepatic cysts should be observed with expectant management.
  • Aspiration of asymptomatic, simple hepatic cysts is not recommended.
  • Symptomatic simple hepatic cysts may be managed with laparoscopic deroofing rather than aspiration and sclerotherapy, dictated based on availability of local expertise.
Suspected biliary cystadenoma (BC) or cystadenocarcinoma (BCA)
  • Routine fluid aspiration is not recommended when BCA is suspected because of limited sensitivity and the risk of malignant dissemination.
  • Imaging characteristics suggestive of BC or BCA, such as internal septations, fenestrations, calcifications, or irregular walls, should lead to referral for surgical excision.
  • Complete surgical excision, by an experienced team, is recommended if BC or BCA is suspected.
Suspected polycystic liver disease
  • Routine medical therapy with mammalian target of rapamycin inhibitors or somatostatin analogs is not recommended.
  • Aspiration, deroofing, resection of a dominant cyst(s) can be performed based on the patient’s clinical presentation and underlying hepatic reserve.
  • Liver transplantation with or without kidney transplantation can be considered in patients with refractory symptoms and significant cyst burden.
Suspected hydatid cysts
  • MRI is preferred over CT for concomitant evaluation of the biliary tree and cystic contents.
  • Monotherapy with antihelminthic drugs is not recommended in symptomatic patients who are surgical or percutaneous treatment candidates.
  • Adjunctive therapy with antihelminthic therapy is recommended in patients undergoing PAIR or surgery, and in those with peritoneal rupture or biliary rupture.
  • Percutaneous treatment with PAIR is recommended for patients with active hydatid cysts who are not surgical candidates, who decline surgery, or who relapse after surgery.
  • Surgery, either laparoscopic or open, based on available expertise, is recommended in complicated hydatid cysts with multiple vesicles, daughter cysts, fistulas, rupture, hemorrhage, or secondary infection.

 

Am J Gastroenterol advance online publication, 19 August 2014; doi: 10.1038/ajg.2014.213

Am J Gastroenterol advance online publication, 19 August 2014; doi: 10.1038/ajg.2014.213

Imaging characteristics of solid liver lesions
HCA (hepatocellular adenoma)
US:
  • Heterogeneous; hyperechoic if steatotic but anechoic center if hemorrhage
CT:
  • Well demarcated with peripheral enhancement; homogenous more often than heterogeneous; hypodense if steatotic, hyperdense if hemorrhagic
MRI:
  • HNF1 α : signal lost on chemical shift; moderate arterial enhancement without persistent enhancement during delayed phase
  • IHCA: markedly hyperintense on T2 with stronger signal peripherally; persistent enhancement in delayed phase
  • β – Catenin: inflammatory subtype has same appearance as IHCA; noninflammatory is heterogeneous with no signal dropout on chemical shift, isointense of T1 and T2 with strong arterial enhancement and delayed washout
THCA (telangiectatic hepatocellular adenoma)
US:
  • Variable appearance
CT:
  • Hypo- to isoattenuating
MRI:
  • T1: heterogeneous and well-defined iso- to hyperintense mass. Strongly hyperintense with persistent contrast enhancement in delayed phase
Hemangioma 
US:
  • Hyperechoic with well-defined rim and with few intranodular vessels
CT:
  • Discontinuous peripheral nodular enhancement isoattenuating to aorta with progressive centripetal fi ll-in
MRI:
  • T1: hypointense; discontinuous peripheral enhancement with centripetal fi ll-in
  • T2: hyperintense relative to spleen
FNH (focal nodular hyperplasia)
US:
  • Generally isoechoic
CT:
  • Central scar. Arterial phase shows homogenous hyperdense lesion; returns to pre contrast density during portal phase that is hypo- or isodense
MRI:
  • T1: isointense or slightly hypointense. Gadolinium produces early enhancement with central scar enhancement during delayed phase
  • T2: slightly hyperintense or isointense
NRH (nodular regenerative hyperplasia)
US:
  • Isoechoic / hyperechoic
CT:
  • Nonenhancing nodules, sometimes hypodense, with variable sizes (most sub-centimeter)
MRI:
  • T1: hyperintense
  • T2: varied intensity (hypo / iso / hyperintense)
Imaging characteristics of cystic liver lesions
Simple hepatic cysts (SHCs)
US:
  • Anechoic, homogeneous,fluid filled. Smooth margins
CT:
  • Well-demarcated, water-attenuated, smooth lesion without an internal structure. No enhancement with contrast
MRI:
  • Well-defined, homogeneous lesion. No enhancement with contrast.
  • T1: hypointense signal intensity
  • T2: hyperintense signal intensity
Biliary cystadenomas (BCs) 
US:
  • Irregular walls, internal septations forming loculi
CT:
  • Heterogeneous septations, internal septations, irregular papillary growths, thickened cyst walls
MRI:
  • May appear heterogeneous.
  • T1: Hypointense signal intensity
  • T2: Hyperintense signal intensity
Polycystic liver disease (PCLD)
US:
  • Multiple hepatic cysts, similar in characteristics to SHC US findings
CT:
  • Multiple hepatic cysts, similar in characteristics to SHC CT findings
MRI:
  • Multiple hepatic cysts, similar in characteristics to SHC MRI findings
Hydatid cysts (HCs) 
US:
  • May appear similar to SHC. Progress to develop thick, calcified walls, hyperechoic / hypoechoic contents. Daughter cysts in periphery.
CT:
  • Hypodense lesion with hypervascular pericyst wall, distinct endocyst wall. Calcified walls and septa easily detected. Daughter cysts seen peripherally within mother cyst.
MRI:
  • T1: Hypointense signal intensity of cyst contents.
  • T2: Hyperintense signal intensity of cyst contents.
  • Hypointense rim on T2.
  • Daughter cysts seen peripherally within mother cyst. Collapse parasitic membranes seen as floating linear structures within cyst.
BC, biliary cystadenoma;
BCA, biliary cystadenocarcinoma;
CCA, cholangiocarcinoma;
CT, computed tomography;
FLL, focal liver lesion;
FNH, focal nodular hyperplasia;
HCA, hepatocellular adenoma;
HCC, hepatocellular carcinoma;
HNF1 α, hepatocyte nuclear factor-1 α;
IHCA, inflammatory hepatocellular adenoma;
IUD, intrauterine device;
MRI, magnetic resonance imaging;
NRH, nodular regenerative hyperplasia;
OCP, oral contraceptive;
PAIR, puncture, aspiration, injection, and reaspiration;
THCA, telangiectatic hepatocellular adenoma;
US, ultrasonography.

Management of Acute Pancreatitis

September 21, 2013 9:57 PM

The current guidelines on the diagnosis and treatment of acute pancreatitis as published in the American Journal of Gastroenterology by the American College of Gastroenterology are summarized below.

IN SUMMARY:
During the past decade, there have been new understandings and developments in the diagnosis, etiology, and early and late management of the disease. As the diagnosis of AP is most often established by clinical symptoms and laboratory testing, contrast-enhanced computed tomography and/or magnetic resonance imaging of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically. Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed. Patients with organ failure and/or the systemic inflammatory response syndrome (SIRS) should be admitted to an intensive care unit or intermediary care setting whenever possible. Aggressive hydration should be provided to all patients, unless cardiovascular and/or renal comorbidites preclude it. Early aggressive intravenous hydration is most beneficial within the first 12-24 h, and may have little benefit beyond. Patients with AP and concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP) within 24 h of admission. Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients. Routine use of prophylactic antibiotics in patients with severe AP and/or sterile necrosis is not recommended. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis may be useful in delaying intervention, thus decreasing morbidity and mortality. In mild AP, oral feedings can be started immediately if there is no nausea and vomiting. In severe AP, enteral nutrition is recommended to prevent infectious complications, whereas parenteral nutrition should be avoided. Asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts do not warrant intervention regardless of size, location, and/or extension. In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed, preferably for 4 weeks, to allow the development of a wall around the necrosis.

 

DEFINITIONS OF SEVERITY IN ACUTE PANCREATITIS – Atlanta Revision (2013):
1. Mild acute pancreatitis

  • Absence of organ failure
  • Absence of local complications

2. Moderately severe acute pancreatitis

  • Local complications AND/OR
  • Transient organ failure (<48 h)

3. Severe acute pancreatitis

  • Persistent organ failure >48 hrs

 

CLINICAL FINDINGS ASSOCIATED WITH A SEVERE COURSE FOR INITIAL RISK ASSESSMENT:
1. Patient characteristics:

  • Age > 55 years
  • Obesity (BMI > 30 kg/m2)
  • Altered mental status
  • Comorbid disease

2. The systemic inflammatory response syndrome (SIRS) – Presence of >2 of the following criteria:

  • pulse >90 beats/min
  • REspirations >20/min or PaCO2 >32 mm Hg
  • temperature >38 ° C or <36 °C
  • WBC count >12,000 or <4,000 cells/mm3 or >10% immature neutrophils (bands)

3. Laboratory findings

  • BUN >20 mg/dl
  • Rising BUN
  • HCT > 44%
  • Rising HCT
  • Elevated creatinine

4. Radiology findings

  • Pleural effusions
  • Pulmonary infiltrates
  • Multiple or extensive extra-pancreatic collections

 

SUMMARY OF RECOMMENDATIONS:

1. DIAGNOSIS

  • The diagnosis of AP is most often established by the presence of two of the three following criteria:
    1. abdominal pain consistent with the disease
    2. serum amylase and/or lipase greater than three times the upper limit of normal, and/or
    3. characteristic findings from abdominal imaging
  • Contrast-enhanced computed tomographic and/or magnetic resonance imaging of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically within the first 48-72 h after hospital admission

2. ETIOLOGY

  • Transabdominal ultrasound should be performed in all patients with acute pancreatitis
  • In the absence of gallstones and/or history of significant history of alcohol use, a serum triglyceride should be obtained and considered the etiology if > 1,000 mg/dl
  • In a patient older than 40 years, a pancreatic tumor should be considered as a possible cause of acute pancreatitis
  • Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks and benefits of investigation in these patients are unclear
  • Patients with idiopathic pancreatitis should be referred to centers of expertise
  • Genetic testing may be considered in young patients (<30 years old) if no cause is evident and a family history of pancreatic disease is present

3. INITIAL ASSESSMENT AND RISK STRATIFICATION

  • Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed
  • Risk assessment should be performed to stratify patients into higher- and lower-risk categories to assist triage, such as admission to an intensive care setting
  • Patients with organ failure should be admitted to an intensive care unit or intermediary care setting whenever possible

4. INITIAL MANAGEMENT

  • Aggressive hydration, defined as 250-500 ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular and/or renal comorbidites exist. Early aggressive intravenous hydration is most beneficial the first 12-24 h, and may have little benefit beyond
  • In a patient with severe volume depletion, manifest as hypotension and tachycardia, more rapid repletion (bolus) may be needed
  • Lactated Ringer’s solution may be the preferred isotonic crystalloid replacement fluid
  • Fluid requirements should be reassessed at frequent intervals within 6 h of admission and for the next 24-48 h. The goal of aggressive hydration should be to decrease the blood urea nitrogen

5. ERCP IN ACUTE PANCREATITIS

  • Patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP within 24 h of admission
  • ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction
  • In the absence of cholangitis and/or jaundice, MRCP or endoscopic ultrasound (EUS) rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected
  • Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to prevent severe post-ERCP pancreatitis in high-risk patients

6. THE ROLE OF ANTIBIOTICS IN ACUTE PANCREATITIS

  • Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia
  • Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended
  • The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended
  • Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis who deteriorate or fail to improve after 7-10 days of hospitalization. In these patients, either
    1. initial CT-guided fine needle aspiration (FNA) for Gram stain and culture to guide use of appropriate antibiotics or
    2. empiric use of antibiotics without CT FNA should be given
  • In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole, may be useful in delaying or sometimes totally avoiding intervention, thus decreasing morbidity and mortality
  • Routine administration of antifungal agents along with prophylactic or therapeutic antibiotics is not recommended

7. NUTRITION IN ACUTE PANCREATITIS

  • In severe AP, enteral nutrition is recommended to prevent infectious complications. Parenteral nutrition should be avoided unless the enteral route is not available, not tolerated, or not meeting caloric requirements
  • Nasogastric delivery and nasojejunal delivery of enteral feeding appear comparable in efficacy and safety

8. THE ROLE OF SURGERY IN ACUTE PANCREATITIS

  • In patients with mild AP, found to have gallstones in the gallbladder, a cholecystectomy should be performed before discharge to prevent a recurrence of AP
  • In a patient with necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize
  • The presence of asymptomatic pseudocysts and pancreatic and/or extrapancreatic necrosis do not warrant intervention, regardless of size, location, and/or extension
  • In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed preferably for more than 4 weeks to allow liquefication of the contents and the development of a fibrous wall around the necrosis (walled-off necrosis)
  • In symptomatic patients with infected necrosis, minimally invasive methods of necrosectomy are preferred to open necrosectomy