Acute Pancreatitis



ESSENTIALS OF DIAGNOSIS





ESSENTIALS OF DIAGNOSIS




  • Gallstone disease and alcohol are the most common causes of acute pancreatitis; other causes include hypertriglyceridemia, drugs, and specific disorders of the biliary tree and pancreas.



  • Diagnosis is usually made based on a history of acute abdominal pain; a threefold elevation in serum amylase or lipase, or both; or an abnormal abdominal computed tomography (CT) scan showing changes of acute pancreatitis.



  • Severe acute pancreatitis is characterized by persistent (>48 hours) organ failure (systemic blood pressure <90 mm Hg, PaO2 <60 mm Hg, creatinine >2.0 mg/dL) or pancreatic necrosis.



  • Diagnosis of necrotizing pancreatitis is confirmed by contrast-enhanced abdominal CT scan or MRI scan.







GENERAL CONSIDERATIONS





Acute pancreatitis is an acute inflammatory disorder of the pancreas that involves the pancreas and peripancreatic tissues but can sometimes affect other organ systems. The initial evaluation of patients with acute pancreatitis involves determining the cause and assessing the severity of disease since this guides subsequent management.



A. Incidence



Acute pancreatitis is the most common inpatient gastrointestinal diagnosis in the United States. There were 274,119 hospitalizations in 2012 for acute pancreatitis with a median length of stay of 4 days and median charges amounting to $11,402. The incidence rate of acute pancreatitis appears to be increasing without any changes in the short-term or long-term case fatality rates.



B. Causes and Risk Factors



The most common causes of acute pancreatitis in the United States are gallstones and alcohol abuse, accounting for 70–80% of cases. Table 26–1 lists other causes, including hypertriglyceridemia, drug reactions, iatrogenic causes (eg, postsurgical or endoscopic retrograde cholangiopancreatography [ERCP]), hereditary factors, and idiopathic causes.




Table 26–1.   Causes of acute pancreatitis. 



The first attack of alcohol-induced acute pancreatitis typically occurs after many (eg, 8–10) years of heavy alcohol consumption, and recurrent episodes can be anticipated if alcohol abuse continues. Gallstone-induced pancreatitis occurs in the setting of choledocholithiasis and is believed to be related to transient or complete obstruction of pancreatic ductal flow or reflux of bile into the pancreatic duct. Hypertriglyceridemia-associated acute pancreatitis does not typically occur unless the triglyceride level exceeds 1000 mg/dL and is often seen in patients with type I and V hyperlipidemia as well as in alcoholics. Because triglyceride levels fall by one-half in patients who have been fasting for 24 hours, levels are best assessed after an episode of acute pancreatitis with a fasting lipid profile in patients who are consuming a normal diet.



Although many drugs have been associated with acute pancreatitis, the strength of association between the use of a particular drug and the development of acute pancreatitis warrants careful scrutiny. Table 26–2 lists drugs that have a strong association with acute pancreatitis based on a recent review.




Table 26–2.   Drugs implicated in acute pancreatitis based on class. 



ERCP-induced acute pancreatitis is another cause of pancreatic injury. Acute pancreatitis is seen in 5–7% of ERCP cases and, despite extensive research into the medical and endoscopic prevention of post-ERCP pancreatitis, there has been little decline in the rates of occurrence. Recently, use of a prophylactic pancreatic duct stent placed after retrograde pancreatography has shown promise but requires further prospective evaluation. In addition, rectal indomethacin has been shown to decrease post-ERCP pancreatitis in a randomized clinical trial. Risk factors for post-ERCP pancreatitis based on a recent prospective study include minor papilla sphincterotomy, sphincter of Oddi dysfunction, prior history of post-ERCP pancreatitis, age younger than 60, more than two contrast injections into the pancreatic duct, and involvement of endoscopic trainees in the procedure.



In recent years, molecular genetic techniques have increased our understanding of acute pancreatitis. Hereditary pancreatitis is an autosomal-dominant disease most commonly associated with mutations in the cationic trypsinogen PRSS1 gene that leads to the inability to deactivate intracellular trypsin resulting in acinar cell autodigestion. Hereditary pancreatitis should be suspected in patients with early-onset (before 20 years of age) acute pancreatitis or those with a strong family history of idiopathic acute pancreatitis in first- or second-degree relatives. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene are increasingly being recognized as a cause of both acute and chronic pancreatitis. The mechanism of injury is not completely known but is most likely related to decreased pancreatic juice flow due to duct cell secretory dysfunction. Patients with a family history of cystic fibrosis or a history of recurrent pulmonary symptoms (eg, bronchitis, asthma), nasal polyps, or sterility among males should be considered for genetic testing.





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Jun 9, 2016 | Posted by in HEPATOPANCREATOBILIARY | Comments Off on Acute Pancreatitis

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