Learn about possible causes of elevated liver enzymes, what it may mean for you, and what potential treatments are available.. Metabolic diseases, inherited: Also called inborn errors of metabolism, these are heritable (genetic) disorders of biochemistry. Acute pancreatitis (AP) is an inflammatory condition of the pancreas that can extend to extrapancreatic tissues.
Acute fluid collections can form in the peripancreatic areas and are not encapsulated by a fibrous wall.
When acute pancreatitis occurs on two or more occasions, it is classified as acute recurrent pancreatitis. The yearly incidence of AP in the United States is approximately 32-44 new cases per 100,000 popuation and has increased over the last decade. Gallstones and alcohol are the two most common causes of AP in Western countries, accounting for 80% of cases. Acute pancreatitis manifests with the sudden onset of epigastric pain radiating to the back. Physical examination often reveals systemic signs such as fever, tachycardia, and hypotension. Laboratory abnormalities encountered in AP include hyperglycemia, hypocalcemia, leukocytosis, and mild elevations of liver function test results.
Plain films of the chest and abdomen are appropriate for the initial radiographic assessment of AP.
Although transabdominal ultrasound is poorly reliable for imaging the pancreas itself, it is the best initial radiographic test for the evaluation of mild AP.
Contrast-enhanced computed tomography (CT) of the abdomen is the preferred test for detecting complications. Endoscopic ultrasound (EUS) and magnetic resonance cholangiopancreatography (MRCP) are emerging as potentially valuable tests in the evaluation of AP.
An important initial step in management is the assessment of severity by clinical and radiographic criteria. In addition to formal scoring systems, patients should be followed closely for other markers of increased severity, including signs of hemodynamic instability or organ failure. The primary goals of therapy in AP are meticulous supportive care and prevention of pancreatic necrosis, infection, and organ failure. The importance of vigorous hydration to optimize outcomes has been increasingly recognized.
Oral intake should be severely limited initially and then carefully advanced as pain subsides and hunger returns. The ACG guidelines advise nutritional support if NPO status is maintained for longer than 5 to 7 days. Although the ACG guidelines state that "patients with severe pancreatitis caused by gallstones should undergo urgent ERCP," there has been much recent debate over the benefit of early endoscopic removal of common bile duct stones in suspected gallstone pancreatitis. Invasive management of AP is indicated in two clinical settings: infected pancreatic necrosis and gallstone pancreatitis.
Management of infected pancreatic necrosis has evolved dramatically over the last few decades from primary open debridement early in the course of disease to a delayed minimally invasive approach, utilizing radiologic, laparoscopic or endoscopic techniques. MRCP is a useful first line test for detecting obstructive pathology of the pancreatic duct, such as ductal strictures, mucinous ductal ectasia, common bile duct stones, and pancreas divisum. The management of acute pancreatitis includes meticulous supportive care and aggressive but careful volume resuscitation.
Assessment of severity is an important initial step in the care of all patients with acute pancreatitis.
A contrast-enhanced pancreatic CT scan should be considered for patients with severe acute pancreatitis.
Endoscopic retrograde cholangiopancreatography should be performed in patients with gallstone pancreatitis and signs of ongoing biliary obstruction or cholangitis. Nutritional support should be administered to all patients with prolonged NPO status or severe acute pancreatitis. Surgical consultation and percutaneous aspiration of pancreatic necrosis should be considered for patients with clinical deterioration or multiorgan system failure. Liver enzymes (ast, alt, total bilirubin, albumin, prothrombin time, afp), elevated liver enzymes, when the liver is diseased, how liver works and other questions. Examples include albinism, cystinuria (a cause of kidney stones), phenylketonuria (PKU), and some forms of gout, sun sensitivity, and thyroid disease. These include acute peripancreatic fluid collection, acute pseudocyst, pancreatic necrosis and walled off pancreatic necrosis (WOPN). Acute pseudocysts are well-developed peripancreatic fluid collections of pancreatic juice encapsulated by a nonepithelialized wall of granulation tissue (Figure 1). In some cases, acute recurrent pancreatitis progresses to chronic pancreatitis, characterized by parenchymal fibrosis and loss of exocrine function. Gallstone (biliary) pancreatitis results from transient obstruction of the ampulla of Vater by small stones or crystals (microlithiasis). Causes of obstructive AP include ductal adenocarcinoma, ampullary tumors and polyps, neuroendocrine and cystic pancreatic tumors, and intraductal papillary mucinous tumors. Although different etiologies produce distinct inciting events, the final common pathway is premature activation of enzymes within the acinar cell.
An abdominal radiograph is helpful for excluding other causes of acute abdominal pain, such as obstruction and perforation.
Transabdominal US detects gallstones, sludge, and biliary dilation indicating a biliary source, and rules out acute cholecystitis. Both are helpful in detecting stones in the common bile duct and in directly assessing the pancreatic parenchyma. The Ranson score was developed for alcoholic AP and comprises five clinical criteria measured at admission and six clinical criteria measured at 48 hours (see Table 2).
Respiratory failure can occur through the development of large pleural effusions or acute respiratory distress syndrome. The ACG guidelines stress, "Patients with evidence of significant third-space losses require aggressive fluid resuscitation." Many patients sequester substantial amounts of fluid into the retroperitoneal space, producing very high fluid requirements.

Patients with severe AP should receive early nutritional support because of its inherently high level of stress and hypercatabolism. The ACG guidelines recommend that "in patients with necrotizing pancreatitis associated with organ failure, it is reasonable to initiate treatment with antibiotics with good spectrum of activity against aerobic and anaerobic bacteria." However, few randomized trials have shown a benefit for 'prophylactic' broad-spectrum antibiotics in necrotizing AP. This is because most stones pass spontaneously and ERCP can further exacerbate acute pancreatitis. Confirmation of infected pancreatic necrosis is important because an intervention to debride necrotic tissue or provide drainage to control sepsis is indicated.
In mild disease, an early cholecystectomy performed during the same hospitalization is favored.
Potential underlying causes include biliary microlithiasis, sphincter of Oddi dysfunction, and undiagnosed genetic defects.
Recurrent acute episodes can develop in the absence of gallstones on ultrasound, with or without elevated liver enzyme levels. Endsocopic ultrasound (EUS) is another sensitive structural test for detecting ampullary, biliary, and pancreatic causes of AP. Most clinicians do not favor extensive evaluation for the first episode of IAP, because it does not recur in most patients after the first episode; however, CT after resolution is probably reasonable for excluding pancreatic cancer.
It is now recognized that the most important determinants of mortality in acute pancreatitis are persistent organ failure and infected necrosis. Classification of acute pancreatitis--2012: Revision of the atlanta classification and definitions by international consensus. Blood urea nitrogen in the early assessment of acute pancreatitis: An international validation study.
Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Endoscopic transgastric vs surgical necrosectomy for infected necrotizing pancreatitis: A randomized trial.
A conservative and minimally invasive approach to necrotizing pancreatitis improves outcome.
Moderately severe acute pancreatitis: Prospective validation of this new subgroup of acute pancreatitis. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. These are only a very few of the hundreds of known inborn errors of metabolism. Advances in the diagnosis and treatment of inborn errors of metabolism have improved the outlook for many of these conditions so that early diagnosis, if possible in infancy, can be helpful.
Mild AP is often referred to as interstitial pancreatitis, based on its radiographic appearance. Acute pancreatitis is the most common cause of GI related hospitalizations, with more than 274,000 hospitalizations in 2012. Clinical features suggesting biliary pancreatitis include preceding biliary colic, the presence of cholelithiasis or biliary dilation on gallbladder ultrasound, and liver function test abnormalities. Therefore, triglyceride level should be routinely checked in patients presenting with AP within 24 hours of presentation. Congenital abnormalities such as pancreas divisum and annular pancreas can also result in obstructive AP.
Pancreatic enzyme levels are elevated because of leakage from pancreatic acinar cells into the interstitial space and subsequent absorption into the circulation. In AP, the abdominal radiograph is typically normal or may demonstrate a localized upper quadrant ileus. Contrast enhanced CT detects areas of pancreatic necrosis (Figure 2), which carries significant morbidity and increased mortality if infected or associated with organ failure.
Magnetic resonance imaging is similar or superior to contrast CT in its ability to stage AP and detect necrosis and complications, and it does not require intravenous contrast. Although in the original Atlanta classification definition of severe AP included those with acute pseudocyst and pancreatic necrosis, it is now recognized that sterile pancreatic necrosis or pseudocyst without organ failure, has a mortality rate comparable to interstitial AP. The criteria measured at admission reflect the local inflammatory effects of pancreatic enzymes; those measured at 48 hours represent the later systemic effects.
Patients should be given nothing by mouth, and intravenous fluids should be given with careful attention to volume status. Intravascular volume depletion can lead to tachycardia, hypotension, renal failure, elevated BUN, hemoconcentration, and generalized circulatory collapse. Intravenous narcotics by injection or by patient-controlled analgesia should be used liberally during the attack and tapered as the diet is advanced to enable prompt bowel recovery. Nasojejunal feeding past the ligament of Treitz does not stimulate the pancreas and is preferred over parenteral feeding in AP. Potential drawbacks of prophylactic antibiotics include the development of resistant organisms and fungal infections.
There is strong evidence to suggest a benefit for ERCP with papillotomy and stone extraction in the setting of stone impaction and cholangitis.7 However, randomized trials of early ERCP in the management of all patients with suspected gallstone pancreatitis have shown conflicting results.
Diagnosis of infected pancreatic necrosis may be suspected clinically or radiographically (e.g. Therefore, when possible, necrosectomy should be postponed for 3-4 weeks from symptom onset. In severe gallstone pancreatitis, cholecystectomy may be delayed until the patient has clinically improved. When ductal pathology is found, ERCP may be considered to provide therapy such as stone removal and dilation and stenting of strictures.
It is best to tailor the diagnostic approach individually based on patient characteristics.
Walled off pancreatic necrosis refers to a collection containing pancreatic and peripancreatic necrotic debri and liquefied dead tissues encased by a fibrous tissue wall. Biliary pancreatitis typically does not recur after cholecystectomy or endoscopic therapy (biliary sphincterotomy and stone extraction). Markedly elevated triglyceride levels may be encountered in the setting of diabetes, alcoholism, and inherited disorders of lipoprotein metabolism (Fredrickson types I, II, and V). Pancreatitis results when activation of pancreatic enzymes occurs early within the acinar cells, producing autodigestion of the pancreas and surrounding tissues.

Less-frequent findings signal complications, including Grey Turner's (flank ecchymosis) or Cullen's (umbilical ecchymosis) signs suggesting retroperitoneal hemorrhage, a palpable mass suggesting a pseudocyst, panniculitis suggesting subcutaneous fat necrosis, and dullness to percussion of lung fields suggesting pleural effusion. The amylase level becomes elevated within hours of the development of pain and can remain elevated for 3 to 5 days. A chest radiograph can detect pulmonary complications of AP such as atelectasis, pleural effusions (most commonly left-sided), or infiltrates suggesting acute respiratory distress syndrome.
Extra vigilance for these complications will result in more timely and aggressive management and improve patient outcomes. The ACG guidelines state, "all patients should receive close supportive care including pain control, fluid resuscitation, and nutritional support." A therapeutic algorithm closely based on the ACG guidelines is shown in (Figure 3). More than 6 L of fluid sequestration within the first 48 hours is considered a marker of increased severity, according to the Ranson criteria (Table 2). Carbohydrates are best for early refeeding because they do not stimulate the pancreas as much as fats and proteins.
The clinical benefits of enteral over parenteral feeding has been shown in multiple studies. If antibiotics are used, antibiotics with good pancreatic tissue penetration, such as imipenem (500 mg IV every 8 hours), cefuroxime (1.5 g IV every 8 hours), or ciprofloxacin (400 mg IV every 12 hours) are favored in this setting. Guidelines from the British Society of Gastroenterology advise that "severe gallstone pancreatitis in the presence of increasingly deranged liver function tests and signs of cholangitis (fever, rigors, and positive blood cultures) require an immediate and therapeutic ERCP." If there is only moderate suspicion of retained stones, EUS and MRCP are less risky alternatives to ERCP, with excellent sensitivity for the detection of common bile-duct stones. All patients with suspected or proven infected necrosis should receive broad-spectrum antibiotics Debridement involves resection of all devitalized pancreatic and surrounding tissue a€“ which can be achieved through open surgery, laparoscopically or endoscopically.
The finding of cholesterol monohydrate or calcium bilirubinate crystals on microscopic bile analysis strongly supports the diagnosis of microlithiasis; however, it is not completely sensitive. ERCP with sphincter of Oddi manometry and sphincterotomy may be considered when sphincter of Oddi dysfunction is strongly suspected.
One suggested approach to the patient with idiopathic recurrent acute pancreatitis is demonstrated in Figure 4.
Exposure of trypsinogen to lysosomal enzymes such as cathepsin B has been shown as a mechanism for early trypsin activation. The differential diagnosis of upper gastrointestinal bleeding in acute pancreatitis includes erosion of a pseudocyst into the splenic artery (hemosuccus pancreaticus) or bleeding from gastric varices that arise secondary to splenic vein thrombosis.
The differential diagnosis for hyperamylasemia includes intestinal obstruction, visceral perforation, tubo-ovarian abscess, renal failure, and salivary gland disease. Patients with evidence of hemoconcentration resulting from intravascular water loss appear to be at increased risk for the development of pancreatic necrosis and organ failure.
A recent Cochrane meta-analysis found a significantly reduced rate of multi-organ failure, systemic infection, need for operative intervention and mortality.6 Physiologic basis for such benefits include improved humoral and cellular immunity, decreased systemic inflammatory response, and decreased bacterial translocation for enteral feeding compared with parenteral nutrition. This procedure is safe and reliable, and it has been recommended for patients with CT criteria for pancreatic necrosis and evidence of sepsis or organ failure. Laparoscopic cholecystectomy prevents recurrence in patients with IAP and should be considered in all patients with acute recurrent pancreatitis of unclear cause. Hypercalcemia-associated AP can occur in the setting of primary and secondary hyperparathyroidism, malignancy, and metabolic bone disease.
However, occasional patients manage their symptoms at home by minimizing oral intake for a few days.
Macroamylasemia is a condition in which amylase is chronically elevated because of its binding to an abnormal serum protein, leading to delayed clearance. A CT is also appropriate 4 to 6 weeks after resolution of AP to exclude a tumor if the cause of the attack is unclear. Early recognition of severe pancreatitis improves outcomes by prompting aggressive fluid resuscitation and transfer of the patient to an intensive care unit. The calculation of APACHE scores helps predict severity from the day of admission and may be recalculated on a daily basis. In addition to maintenance fluid requirements, the amount sequestered should be monitored and replaced with isotonic fluids such as normal saline or lactated ringers. The presence of a severe intestinal ileus or delay in tube placement can limit the use of enteral feeding. Presence of gas within the pancreatic or peripancreatic collection is also considered strongly suggestive of infection. However, in some patients with infected necrosis, percutaneous or endoscopic drainage alone may postpone or even spare the need for necrosectomy.
Serum lipase has higher specificity for pancreatic disease, but its level may be elevated in other conditions as well. More recently, Bedside Index of Severity in Acute Pancreatitis (BISAP) was developed as a simpler and equally accurate prediction tool (see Table 3).5 This severity index comprises of five clinical variables that are routinely available on hospital admission and has been prospectively validated. Fluid therapy should be goal directed, with close monitoring of urine output and BUN levels.
Many patients with AP develop gastric and colonic ileus but maintain adequate small bowel motility for enteral feeding. Stone dissolution therapy is effective only for noncalcified, cholesterol monohydrate stones smaller than 1 cm in diameter.
The severity of pancreatitis does not correlate well with the magnitude of elevation of the serum amylase and lipase levels. A score of 3 or more was associated with significantly increased mortality with equal discrimination as APACHE.
Studies have shown that in patients with elevated BUN, failure to decrease over 24 hours was associated with significant mortality.
There is no value in following daily trends of serum amylase and lipase levels because they do not correlate with recovery or prognosis. Of course, the aggressiveness of fluid replacement must be tempered in the elderly and in the presence of underlying cardiac or renal disease.

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