Hepatobilliar & Pancreas diseases

Hepatobilliar & Pancreas diseasesLiver abscessPyogenicAmubicPyogenic liver abscessmost common source of a pyogenic liver abscess is biliary tract obstruction, and the current treatment includes antibiotics, usually with a percutaneous drainage procedureAbscesses occur when normal hepatic clearance mechanisms fail or the system is overwhelmed. Parenchymal necrosis and hematoma secondary to trauma, obstructive biliary processes, ischemia, and malignancy also promote invasion of microorganisms.In order to appropriately treat the abscess, source control must be achieved. Six distinct categories have been identified as potential sources: (1) bile ducts, causing ascending cholangitis; (2) portal vein, causing pylephlebitis from appendicitis or diverticulitis; (3) direct extension from a contiguous disease; (4) trauma due to blunt or penetrating injuries; (5) hepatic artery, due to septicemia; and (6) cryptogenic3

Predisposing Factors

PathologyIn general, portal, traumatic, and cryptogenic hepatic abscesses are solitary and large, while biliary and arterial abscesses are multiple and small. Huang and associates4 reported that 63% of patients had abscesses involving the right lobe, 14% had abscesses involving the left lobe, and 22% had bilobar disease. The number of bilateral and multiple abscesses have increased as more patients present with a biliary etiology. Bilateral disease may be seen in 90% of patients with an arterial or biliary source. In contrast, those with intra-abdominal infections frequently present with right lobe abscesses due to preferential flow from the superior mesenteric vein. Fungal abscesses are usually multiple, bilateral, and miliary.5 EtiologyEscherichia coli, Klebsiella species, enterococci, and Pseudomonas species are the most common aerobic organisms cultured in recent series, whereas Bacteroides species, anaerobic streptococci, and Fusobacterium species are the most common anaerobes.Clinical findingsMost patients have fever (92%) and 50% have abdominal pain, but only half have pain in the right upper quadrant. Diarrhea occurs in less than 10% of patients. The liver may be tender (65%) and enlarged (48%), and the patient may appear jaundiced (54%). Other nonspecific complaints include malaise, anorexia, and nausea. If the diaphragm is involved, pleuritic chest pain, cough, or dyspnea may occur. If the abscess ruptures, peritonitis and sepsis may be presenting features Laboratory findingsLeukocytosis is present in 7090%, an elevated alkaline phosphatase in 80%, and an elevated bilirubin and transaminases in 5067% of patients. Anemia, hypoalbuminemia, and prolonged prothrombin time are seen in 6075% of patientsImaging Chest & Abdominal plain photoUSGCT scanTreatmentAntibioticNeedle aspiration/ surgical drainageClassic antibiotic regimens include an aminoglycoside, clindamycin, and either ampicillin or vancomycin. Fluoroquinolones can replace aminoglycosides, and metronidazole can be used instead of clindamycin, especially if an amebic source is suspected. Single-agent therapy with ticarcillin-clavulanate, imipenem-cilastatin or piperacillin-tazobactam is also acceptable.10 Treatment used to be given for 46 weeks; however, many studies now document success with only 2 weeks of antibiotic therapy

Amebic Liver abscessTwo species of ameba infect humans. E. dispar is associated with an asymptomatic carrier state and not with disease. E. histolytica is responsible for all forms of invasive disease. The life cycle involves cysts, invasive trophozoites, and fecally contaminated food or water to initiate the infection.18,19 Fecal-oral transmission occurs; the cyst passes through the stomach into the intestine unscathed, andthen pancreatic enzymes start to digest the outer cyst wall. The trophozoite is then released into the intestine and multiplies there. Normally, no invasion occurs, and the patient develops amebic dysentery alone or becomes an asymptomatic carrier. In a small number of cases, the trophozoite invades through the intestinal mucosa, travels through the mesenteric lymphatics and veins, and begins to accumulate in the hepatic parenchyma, forming an abscess cavity. Liquefied hepatic parenchyma with blood and debris gives a characteristic "anchovy paste" appearance to the abscessDiagnosisdefinitive diagnosis of amebic liver abscess is by E. histolytica trophozoites in the pus and by detection of serum antibodies to the ameba90% of amebic liver abscesses occur in young adult males. The presentation may be acute, with fever and right upper quadrant (RUQ) pain, or subacute, with weight loss and less frequent fever and abdominal pain. The usual case of amebic liver abscess does not present with concurrent colitis, but patients may have had dysentery within the last year. Alcohol abuse is common.22 Eighty percent of patients have symptoms that develop within 24 weeks, including fever, cough, and a dull aching pain in the RUQ or epigastrium. Diaphragmatic involvement causes right-sided pleural pain or pain referred to the shoulder. Gastrointestinal symptoms of nausea, vomiting, abdominal cramping, abdominal distention, diarrhea, and constipation occur in 1035%. Hepatomegaly with point tenderness over the liver or subcostal region is common. In contrast to pyogenic liver abscesses, amebic liver abscesses are more likely to occur in males under 50 years old who have immigrated or traveled to a country where the disease is endemic. The patient will also not be jaundiced or have biliary disease or diabetes mellitus

Laboratory findingsPatients may present with a mild to moderate elevation of the white blood cell count and anemia. Acutely, alkaline phosphatase will be normal and alanine aminotransferase levels will be elevated. The opposite is true of these values in patients with chronic disease.19 Jaundice is rare. Because amebic abscesses involve destruction of liver parenchyma and are often larger than pyogenic liver abscesses on presentation, patients may have an elevated prothrombin time.5

If colitis is present, wet mount preps of stool samples contain trophozoites 30% of the time in one sample and 70% if three samples are tested. Liver abscesses are associated with positive stool samples in 4050% of casesAntibioticMetronidazolePositive responses to metronidazole should be seen by the third day of treatment. At 5 days, an 85% cure rate is achieved, and this response may be increased to 95% by 10 days. Five to fifteen percent of patients with amebic liver abscess may be resistant to metronidazoleTherapeutic aspiration may occasionally be required as an adjunct to antiparasitic treatment. Drainage should be considered in patients that have no clinical response to drug therapy within 57 days or those with a high risk of abscess rupture defined as having a cavity >5 cm in diameter or by the presence of lesions in the left lobe.

CholelithiasisConditions predispose to the development of gallstones : obesity, pregnancy, dietary factors, Crohn's disease, terminal ileal resection, gastric surgery, hereditary spherocytosis, sickle cell disease, and thalassemia Women are three times more likely to develop gallstones than men, and first-degree relatives of patients with gallstones have a twofold greater prevalence.Schwartz's 2010Most patients will remain asymptomatic from their gallstones throughout life. For unknown reasons, some patients progress to a symptomatic stage, with biliary colic caused by a stone obstructing the cystic duct. Symptomatic gallstone disease may progress to complications related to the gallstones.26 Complications : acute cholecystitis, choledocholithiasis with or without cholangitis, gallstone pancreatitis, cholecystocholedochal fistula, cholecystoduodenal or cholecystoenteric fistula leading to gallstone ileus, and gallbladder carcinoma.Gall stoneCholesterolPigmentUSG

Choledocholithiasissecondary bile duct stones are cholesterol stones in 75% and black pigment stones in 25% of patients. Cholesterol stones are formed in the presence of cholesterol saturation, biliary stasis, and nucleating factors. Behavioral factors associated with cholesterol gallstones include nutrition, obesity, weight loss, and physical activity. Biologic factors linked to gallstones include increasing age, female sex and parity, serum lipid levels, and the Native American, Chilean, and Hispanic race.1 The formation of black pigment stones is associated with hemolytic disorders, cirrhosis, ileal resection, prolonged fasting, and total parenteral nutrition.2Primary bile duct stones, on the other hand, form within the bile ducts and usually are of the brown pigment variety. These tend to be lower in cholesterol content and higher in bilirubin content as compared with secondary stones. Unlike secondary stones, primary stones are associated with biliary stasis and bacteria.3 In fact, in the pathogenesis of brown pigment stones, bile infection appears to be the initial event leading to stone formation.Clinical findingsbiliary colic, bile duct obstruction, bilirubinuria (or tea-colored urine), pruritus, acholic stools, and jaundice. However, the biliary obstruction usually is incomplete. There may be nausea and vomiting with intermittent or constant epigastric or right upper quadrant pain.5 The clinical course may be complicated by acute gallstone pancreatitis, cholangitis, or rarely, hepatic abscess. Infected patients may present with back pain, fever, hypotension, and mental status changes.BiofilmCommon bile duct stones are covered by a bacterial biofilm of adherent quiescent bacteria residing in a hermetic environment. When stones cause obstruction of the ducts, cytokines released by epithelial cells activate these bacteria to the planktonic and virulent forms.1 Therefore, bile duct obstruction secondary to stones often is accompanied by bacterial sepsis resulting from activation of the bacterial biofilm on these stones. Sepsis is much less likely to occur in the context of malignant obstruction without choledocholithiasis.

ImagingUSGMRI : MRCP

TreatmentERCP