Acute pancreatitis (AP) is a sudden inflammation of the pancreas. Causes include a gallstone impacted in the common bile duct or the pancreatic duct, heavy alcohol use, systemic disease, trauma, elevated calcium levels, hypertriglyceridemia (with triglycerides usually being very elevated, over 1000 mg/dL), certain medications, hereditary causes and, in children, mumps. Acute pancreatitis may be a single event, it may be recurrent, or it may progress to chronic pancreatitis and/or pancreatic failure (the term pancreatic dysfunction includes cases of acute or chronic pancreatitis where the pancreas is measurably damaged, even if it has not failed).

In all cases of acute pancreatitis, early intravenous fluid hydration and early enteral (nutrition delivered to the gut, either by mouth or via a feeding tube) feeding are associated with lower mortality and complications. Mild cases are usually successfully treated with conservative measures such as hospitalization with intravenous fluid infusion, pain control, and early enteral feeding. If a person is not able to tolerate feeding by mouth, feeding via nasogastric or nasojejunal tubes are frequently used which provide nutrition directly to the stomach or intestines respectively. The abdominal pain is the most common symptom and it is usually described as being in the left upper quadrant, epigastric area or around the umbilicus, with radiation throughout the abdomen, or to the chest or back. The abdominal pain initially may worsen with eating or drinking but may become constant as the disease progresses.

Grey-Turner's sign (hemorrhagic discoloration of the flanks) or Cullen's sign (hemorrhagic discoloration of the umbilicus) are associated with severe disease. However both signs are rare (occurring in less than 1% of cases of acute pancreatitis) and are not specific nor sensitive for diagnosis of acute pancreatitis. Pleural effusions (fluid in the lung cavity) may occur in up to 34% of people with acute pancreatitis and are associated with a poor prognosis. The Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA)) is also associated with acute pancreatitis.

Complications

Complications of acute pancreatitis may occur. Necrotic pancreatitis occurs when inflammation of the pancreas progresses to cell death. Acute fluid collections may form adjacent to the pancreas or necrotic collections (discrete areas of dead tissue) may also form adjacent to or within the pancreas. These may progress to pancreatic pseudocysts and walled off areas of dead tissue which may persist for longer than 4 weeks. Both can become secondarily infected., multiple organ dysfunction syndrome, disseminated intravascular coagulation (DIC), hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), and malabsorption due to exocrine failure.

Tobacco use, recurrent episodes of acute pancreatitis, pancreatic tissue death, alcoholic pancreatitis are all risk factors for developing chronic pancreatitis.

Less common

  • Scorpion venom
  • Chinese liver fluke
  • Ischemia from bypass surgery
  • Heart valve surgery
  • Fat necrosis
  • Pregnancy
  • Infections other than mumps, including varicella zoster Additional labs may be used to identify organ failure for prognostic purposes or to guide fluid resuscitation rate. Serum lipase is more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis, and is the preferred test in the diagnosis.

Most, but not all individual studies support favor the diagnostic utility of lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase. Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.

Reduced lipase clearance due to kidney disease, gastrointestinal or hepatobiliary cancers, pancreatic enzyme hypersecretion, critical illness including due to neurosurgical causes have been shown to increase serum lipase and may complicate the diagnosis of acute pancreatitis.

Differential diagnosis

The differential diagnosis includes:

  • Perforated peptic ulcer
  • Biliary colic
  • Acute cholecystitis
  • Pneumonia
  • Pleuritic pain
  • Myocardial infarction

Computed tomography

thumb|Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas

Regarding the need for computed tomography, practice guidelines state:

CT is an important common initial assessment tool for acute pancreatitis. Imaging is indicated during the initial presentation if:

  • the diagnosis of acute pancreatitis is uncertain
  • there is abdominal distension and tenderness, fever >102 F (38,9 C), or leukocytosis
  • there is a Ranson score > 3 or APACHE score > 8
  • there is no improvement after 72 hours of conservative medical therapy
  • there has been an acute change in status: fever, pain, or shock

CT is recommended as a delayed assessment tool in the following situations:

  • acute change in status
  • to determine therapeutic response after surgery or interventional radiologic procedure
  • before discharge in patients with severe acute pancreatitis

Abdominal CT should not be performed before the first 12 hours of onset of symptoms as early CT (<12 hours) may result in equivocal or normal findings.

CT findings can be classified into the following categories for easy recall:

  • Intrapancreatic – diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
  • Peripancreatic / extrapancreatic – irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
  • Locoregional – Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus, etc.

The principal value of CT imaging to the treating clinician is the capacity to identify devitalized areas of the pancreas which have become necrotic due to ischaemia. Pancreatic necrosis can be reliably identified by intravenous contrast-enhanced CT imaging, and is of value if infection occurs and surgical or percutaneous debridement is indicated.

Magnetic resonance imaging

While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis, magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris. Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, and venous thrombosis.

Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP) sequences. MRCP provides useful information regarding the etiology of acute pancreatitis, i.e., the presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies.

Ultrasound

thumb|right|[[Abdominal ultrasonography of acute pancreatitis]]

Ultrasound is less preferred as a diagnostic test for acute pancreatitis, but it may be used in select cases. Abdominal ultrasonography may be obtained if there is concern of a gallstone blocking the pancreatic duct leading to pancreatitis.

Pain control

Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics.

Opioids are safe and effective at providing pain control in patients with acute pancreatitis. Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given both as a bolus as well as constant infusion.

Meperidine has been historically favored over morphine because of the belief that morphine caused an increase in sphincter of Oddi pressure. However, no clinical studies suggest that morphine can aggravate or cause pancreatitis or cholecystitis. In addition, meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite normeperidine, which causes neuromuscular side effects and, rarely, seizures.

Nutritional support

Acute pancreatitis is a catabolic state and with hemodynamic instability or fluid shifts or edema there may be reduced intravascular perfusion to the gut. This reduction in gut perfusion increases the risk of gut necrosis with bacterial translocation with the subsequent risk of sepsis or secondary infections. In patients with acute pancreatitis, the American Gastroenterological Association (AGA) recommends early oral nutrition, within 24 hours, rather than keeping the patient fasting (or nil by mouth). And in those unable to feed orally, the AGA recommends enteral nutrition (via a nasogastric or nasojejunal tube) rather than parenteral nutrition.

Antibiotics

Up to 20 percent of people with acute pancreatitis develop an infection outside the pancreas such as bloodstream infections, pneumonia, or urinary tract infections. These infections are associated with an increase in mortality. Fluid collections around the pancreas or areas within the pancreas that experience tissue death (necrosis) may also become secondarily infected requiring the use of antibiotics.

Endoscopic retrograde cholangiopancreatography

In 30% of those with acute pancreatitis, no cause is identified. Endoscopic retrograde cholangiopancreatography (ERCP) with empirical biliary sphincterotomy has an equal chance of causing complications and treating the underlying cause, therefore, is not recommended for treating acute pancreatitis. If a gallstone is detected, ERCP, performed within 24 to 72 hours of presentation with successful removal of the stone, is known to reduce morbidity and mortality. The indications for early ERCP are:

  • Clinical deterioration or lack of improvement after 24 hours
  • Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on abdominal CT

The risks of ERCP are that it may worsen pancreatitis, it may introduce an infection to otherwise sterile pancreatitis, and bleeding.

Surgery

In those with mild acute pancreatitis due to gallstones, cholecystectomy (removal of the gallbladder) is recommended in the hospital and is associated with a reduced risk of pancreatitis recurrence.

  • The use of octreotide has been shown not to improve outcomes.

Classification by severity: prognostic scoring systems

Acute pancreatitis patients recover in majority of cases. Some may develop abscess, pseudocyst or duodenal obstruction. About 20% of the acute pancreatitis are severe with a mortality of about 20%. but not all studies report that the Apache score may be more accurate. In the negative study of the APACHE-II, the APACHE-II 24-hour score was used rather than the 48-hour score. the Computed Tomography Severity Index (CTSI) is a grading system used to determine the severity of acute pancreatitis. The numerical CTSI has a maximum of ten points, and is the sum of the Balthazar grade points and pancreatic necrosis grade points:

Balthazar grade

{| class="wikitable"

|-

! Balthazar grade

! Appearance on CT

! CT grade points

|-

| Grade A

| Normal CT

| 0 points

|-

| Grade B

| Focal or diffuse enlargement of the pancreas

| 1 point

|-

| Grade C

| Pancreatic gland abnormalities and peripancreatic inflammation

| 2 points

|-

| Grade D

| Fluid collection in a single location

| 3 points

|-

| Grade E

| Two or more fluid collections and / or gas bubbles in or adjacent to pancreas

| 4 points

|}

Necrosis score

{| class="wikitable"

|-

! Necrosis percentage !! Points

|-

| No necrosis

| 0 points

|-

| 0 to 30% necrosis

| 2 points

|-

| 30 to 50% necrosis

| 4 points

|-

| Over 50% necrosis

| 6 points

|}

CTSI's staging of acute pancreatitis severity has been shown by a number of studies to provide more accurate assessment than APACHE II, Ranson, and C-reactive protein (CRP) level. However, a few studies indicate that CTSI is not significantly associated with the prognosis of hospitalization in patients with pancreatic necrosis, nor is it an accurate predictor of AP severity.

Glasgow score

The Glasgow score is valid for both gallstone and alcohol induced pancreatitis, whereas the Ranson score is only for alcohol induced pancreatitis. If a patient scores 3 or more it indicates severe pancreatitis and the patient should be considered for transfer to ITU. It is scored through the mnemonic, PANCREAS:

  • P – PaO2 <8kPa
  • A – Age >55-years-old
  • N – Neutrophilia: WCC >15x10(9)/L
  • C – Calcium <2&nbsp;mmol/L
  • R – Renal function: Urea >16&nbsp;mmol/L
  • E – Enzymes: LDH >600iu/L; AST >200iu/L
  • A – Albumin <32g/L (serum)
  • S – Sugar: blood glucose >10&nbsp;mmol/L

BISAP score

Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation.

  • BUN >25&nbsp;mg/dL (8.9&nbsp;mmol/L)
  • Abnormal mental status with a Glasgow coma score <15
  • Evidence of SIRS (systemic inflammatory response syndrome)
  • Patient age >60 years old
  • Imaging study reveals pleural effusion

Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test performance characteristics for predicting mortality as the APACHE II score. As is a problem with many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as length of hospital stay, need for ICU care, or need for intervention.

Epidemiology

The worldwide incidence of acute pancreatitis has increasing from 1961 to 2016 with an average annual percentage increase of 3%, the increased incidence was seen in North America and Europe. The incidence of acute pancreatitis in the United States is 110–140 cases per 100,000 people.