Acute pancreatitis is the third leading gastrointestinal disorder requiring hospitalization in the US.

Acute pancreatitis causes more than 275, 000 hospitalizations annually in the US.

Acute pancreatitis is the most common pancreatic disorder worldwide.

Moderately severe or severe disease develops in approximately 35% of patients with acute pancreatitis, a situation that is associated with worse outcomes.

Annual cost for care of patients with acute pancreatitis exceeds $2 billion per year.

The most common causes of acute pancreatitis is obstruction of the pancreatobiliary tree.

40%-50% of episodes of acute pancreatitis in adults are caused by gallstones.

Most cases attributable to gallstone disease or to excess alcohol consumption.

At least 50% of all cases of acute pancreatitis are due to the passage of small gallstones, usually 5 mm or less in diameter.

Gallstones have been recovered in the stool of 85-95% of patients with acute pancreatitis, and there is a 10% recovery rate among patients who have symptomatic cholelithiasis without pancreatitis (Acosta JM).

In 20% of cases the etiology of acute pancreatitis is unknown.

Drug induced acute pancreatitis is probably the third most common cause of acute pancreatitis, accounting for 3-5% of cases.

Serum lipase level is a better marker than amylase level.

Serum lipase has a sensitivity nearing 100% and a specificity of 83-98% and is the test of choice in making the diagnosis.

In the U.S. alcohol abuse is the leading cause, while gallbladder disease is the leading cause worldwide.

Smoking is associated with an increased risk of acute pancreatitis , independent of alcohol use and gallstones.

Phospholipase A2, cyclooxygenase and neutrophil-endothelial interactions play a role in the development of acute pancreatitis.

Acute pancreatitis much less common in children and adolescents than in adults.

Pancreatitis developed in only 4% of 382 children with gallstones (Urushihara N et al).

Acute pancreatitis per incident mortality rate approximately 5%.

In approximately 10-20% of patients with acute pancreatitis the disease progresses into a potentially life-threatening process, associated with multiple organ failure or death.

Approximately half of deaths occur within first 14 days of onset.

Deaths that occur within the first two weeks are usually due to systemic inflammatory response syndrome, and multisystem organ failure, whereas deaths that occur later typically related to necrotizing pancreatitis.

Necrotizing pancreatitis develops in approximately 20-30% of patients with acute pancreatitis.
Pancreatic and peripancreatic necrosis that becomes infected nearly always leads to invasive intervention.
The standard approach for infected necrotizing pancreatitis is a minimally invasive approach with catheter drainage as the first step.
Guidelines suggest cast of the drainage and administration of  antibiotics be postponed until the infected pancreatic and pancreatic necrosis has become encapsulated colon usually taking four weeks.

A randomized trial did not show superiority of immediate drainage over postponed drainage with regard to complications in patients with infected necrotizing pancreatitis.

Patients with acute pancreatitis and progressive multisystem organ dysfunction are at higher risk for mortality, which can be higher than 50%.

Baseline rates may be as high as 3 times higher for patients with diabetes in patients without diabetes (Noel) R.

Acute pancreatitis drug induced in approximately 2% of cases with higher likelihood in HIV populations.

CT scan of the abdomen should be used when the diagnosis is uncertain, the pancreatitis is expected to be severe, or the disorder worsens or fails to resolve.

Antibiotics indicated for patients with predicted severe acute pancreatitis.

Mortality rate for acute pancreatitis should be lower than 10 percent overall and less than 30% in patients diagnosed with severe disease.

Criteria for acute pancreatitis risk relies on 5 admission parameters and six 48 hour parameters.

Repeat episodes of acute pancreatitis is referred to as recurrent acute pancreatitis.

Recurrent acute pancreatitis may result in injury to the pancreatic duct with progressive inflammation and scarring that can lead to chronic pancreatitis.

Failure to respond to broad spectrum antibiotics is and indication for urgent surgery.

Observational studies found that hemoconcentration, a marker for systemic hypovolemia, is associated with pancreatic necrosis and fluid resuscitation during the first 24 hours of care is required: aggressive fluid resuscitation however results in fluid overload without improvement in clinical outcomes.

Contrast-enhanced testing is sensitive and specific for acute pancreatitis and pancreatic necrosis.

Patients with biliary obstruction should undergo urgent ERCP for biliary decompression.

Acute pancreatitis is most common major complication of ERCP.

Temporary pancreatic stents have prophylactic benefit for post-ERCP pancreatitis.

Rectal indomethacin in patients at high-risk of for post-ERCP pancreatitis significantly reduces the process, 9.2% vs. 16.9% in the placebo group (Elmunzer BJ et al).

In the absence of cholangitis or billiary obstruction, ERCP within 24 to 72 hours does not lead to reduction in mortality or local or systemic complications.

ERCP should be performed in patients with biliary obstruction or cholangitis.

Caused by transient biliary obstruction should undergo laparoscopic cholecystectomy without preoperative ERCP.

At time of cholecystectomy and intraoperative cholangiogram should be done.

80% of cases are mild and termed edematous or interstitial pancreatitis.

The prognosis of patients with acute pancreatitis depends on the severity of the disease.

Most patients with gallstone pancreatitis have mild disease and a benign clinical course.

Patients with gallbladder pancreatitis usually recover quickly with a response to conservative management.

Most patients with biliary induced pancreatitis, regardless of the predicted severity, do not benefit from the ERCP, with or without sphincterotomy.

Severe pancreatitis is associated with clinically significant complications.

20% of cases are severe associated with glandular necrosis and termed necrotizing pancreatitis.

Necrotizing pancreatitis develpos in approximately 20% of patients with acute pancreatitis.

Necrotizing pancreatitis associated with complications including: pancreatic pseudocyst, pancreatic abscess and organizing peripancreatic necrosis.

Necrotizing pancreatitis with infected necrotic tissue is associated with high rate of complications and death.

Necrotizing pancreatitis associated with a 8-39% death rate.

Necrotizing pancreatitis major cause of death is organ failure.

Necrotizing pancreatitis second most common cause of death is infection of pancreatic or peripancreatic necrotic tissue which leads to sepsis and multiple organ failure.

Necrotizing pancreatitis with secondary infection of necrotic tissue is an indication for surgical intervention.

Open necrosectomy for infected necrotic pancreatic tissue is associated with high complication rate of 34-95% and death rate of 11-39%, and a risk for long-term pancreatic insufficiency.

In a multicenter randomized study of 88 patients with necrotizing pancreatitis with suspected or proven necrosis underwent an open primary necrosectomy or stepwise approach using a percutaneous drainage procedure, followed, if necessary, by a minimally invasive retroperitoneal necrosectomy: the latter procedure was associated with fewer complications and death (Dutch Pancreatitis Study Group)

Cullen’s or Turner’s sign occur in approximately 3% of patients, reflecting hemorrhagic pancreatitis, and is associated with a 37% mortality.

Commonly causes hypocalcemia with formation of calcium free fatty acid soaps.

Hypocalcemia reversed by calcium infusion and terminates when inflammation subsides.

Hypocalcemia is a poor prognostic sign.

Hypocalcemia can be caused by hypoalbuminemia, hypomagnesemia, and vitamin D deficiency along with pancreatitis and need to be excluded.

Enteral nutrition compared to parenteral nutrition results in a statistically reduced risk for infectious complications, pancreatic infections and mortality (Petrov).

It is recommended that patients be given food within 24 hours of diagnosis to prevent complications, such as infected peripancreatic necrosis by reducing bacterial translocation: this is contrary to previous practice that encouraged bowel rest to prevent stimulating and inflamed pancreas.

Randomized controlled trials revealed no difference in mortality or risk of severe complications, including necrotizing pancreatitis between early and delayed feeding.

The above findings used a variety of diet types, therefore starting with a clear liquid diet is not required.

Patients unable to tolerate oral feeding should have enteral rather than parenteral nutrition.
In patients with mild or moderate acute biliary pancreatitis is recommended that cholecystectomy be carried out during an initial admission.
In patients with severe acute pancreatitis and necrotizing pancreatitis, guidelines recommend against prophylactic antibiotics.
A rare cause of chronic pancreatic inflammation is the hereditary/familial pancreatitis syndrome which often starts during childhood with recurrent episodes of acute pancreatitis.
The long-standing inflammation in familial pancreatitis syndrome predisposes to carcinogenesis.
Familial pancreatitis associated with a number of gene abnormalities and an increased risk of developing pancreatic duct adenocarcinoma between 26 and 87 fold.

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