Acute Pancreatitis

last authored: Aug 2009, David LaPierre
last reviewed:

 

 

Introduction

Acute pancreatitis is an inflammatory process of the exocrine pancreas that can be very serious. It often leads to multi-organ involvement and failure and has a mortality rate of 5-10%. However, it is usually self-limiting, and patients often make a complete recovery.

Chronic pancreatitis is differentiated by:

 

 

The Case of Mrs Lagir

Mrs Lagir is a 45 year-old who comes to the emergency department with a two day history of severe abdominal pain. The physician, suspecting pancreatitis, orders a number of tests which come back suggesting pancreatitis.

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Causes and Risk Factors

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Pathophysiology

The etiology of pancreatitis is varied. Gallstones, the most common cause, are thought to cause obstruction potentially by bile influx. It is unclear as to how ethanol causes pancreatitis.

 

Acute pancreatitis appears to evolve in multiple stages. The first involves co-localization of pre-proteolytic enzymes cathepsin B and trypsinogen, which become inappropriately active and lead to acinar cell injury via auto digestion.

 

Next, an intrapancreatic inflammatory response is triggered by chemokines and cytokines, with inflammatory cell infiltration and increased vascular permeability and SIRS (systemic inflammatory response syndrome). With further progression, pancreatic injury can worsen and systemic inflammation can arise.

 

Mild pancreatitis leads to peripancreatic fat necrosis and interstitial edema due to inflammation. This can lead to hypovolemia (third spacing). Hypovolemic shock can, in turn, lead to renal failure via acute tubular necrosis (ATN).

 

Hypoxia can occur due to SIRS, pulmonary edema/ARDS, and raised diaphragm due to peritoneal fluid.

 

Necrosis results from pancreatic hypoperfusion and hypoxia caused by sludging in the vasculature.

 

Severe necrosis and hemorrhage can lead to infection and infarction. The release of toxic factors into the systemic circulation and peritoneum can lead to multi-organ failure.

 

Hypovolemia often warrants IV fluids. This, along with systemic inflammation, can lead to pulmonary edema and ARDS.

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Signs and Symptoms

  • history
  • physical exam

History

Abdominal pain is virtually always present, and may be severe and unresponsive to analgesics.

  • epigastric
  • abrupt onset
  • constant
  • radiation to the back
  • nausea, vomiting, and fever can occur.
  • may improve when leaning forward and is usually worse when supine

Physical Exam

Hypotension and tachycardia can reflect hypovolemia.

  • shallow breathing, decreased air entry
  • decreased oxygen saturation
  • low JVP

Abdominal exam

  • tenderness, with or without guarding

Flank or periumbilical brusing can be present with hemorrhagic pancreatitis.

Jaundice can follow blockage of the bile duct.

Tetany can follow transient hypocalcemia.

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Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

Diagnosis is made by elevations of serum amylase and lipase in excess of 3x the normal limit. The magnitude of levels does not correlate with disease severity. Increased amylase is sensitive, but not specific. It can be falsely negative if diagnosis is delayed, in the presence of hyperlipidemia, or if the pancreas is burned out.

  • CBC (elevated WBC and hematocrit)
  • electrolytes (dehydration)
  • liver enzymes (obstruction of the common bile duct)
  • BUN, creatinine (pre-renal azotemia)
  • calcium
  • glucose

Lipase has a higher sensitivty and specificity, and also stays elevated longer.

 

Metabolic problems often seen include hypocalcemia (caused by concomitant hypoalbuminemia), hyperglycemia, and acidosis.

 

DIC can result from systemic activation of prothrombin and thrombin by trypsin.

Diagnostic Imaging

Ultrasound is effective for identifying biliary tree dilation due to gallstones, with 70% sensitivity and 100% specificity, and is quick and readily available. It does not provide effective views of the pancreas.

 

Abdominal X ray can reveal 'sentinel loop' of dilated proximal jejeunum. Calcification and colonic spasm may also be present.

 

CT, with contrast, can be used to identify pancreatic enlargement, inflammatory changes, and extrapancreatic fluid collection. Only viable tissue will take up contrast; non-viable tissue can be biopsied to assess for infection. However, the need for contrast can be problematic if creatinine is elevated.

 

Choledocolethiasis - duct is greater than 1 cm, ALT/AST is up.

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Differential Diagnosis

Other conditions to consider include:

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Treatments

Supportive therapy is effective in 75% of cases.

Resuscitation is critical. Aggressive hydration is needed to correct hypovolemia, with up to 12 litres required. Fluid resucitation (250-300 cc/hour) is important, if cardiac status permits. Crysalloid or colloid can be used to expand volume. Follow the hematocrit. Foley catheter to monitor hydration.

 

Antibiotics are controversial, except where infection has been proven. Routine prophylaxis is not globally recommended. In cases of severe pancreatitis, emperic use of fluoroquinolones or imipenem should be used, as these drugs penetrate the pancreas.

 

Pain management often requires narcotics. There is some risk of opioids causing spasm of the

 

Nutrition in acute pancreatitis is complicated. Patients are fasted, though malnutrition decreases healing. Enteral feeding is given to patients with severe pancreatitis; in order to bypass the stomach (and further pancreatic enzyme release), a naso-jejeunal tube is used. NJ feeds also protect the gut mucosa from bacterial invasion.

TPN can be given if patients cannot tolerate other means. NG tubes shouldn't be used unless the patient is vomiting substantially or their airway is threatened.

 

Benzodiazepines and vitamins should be used to manage alcohol withdrawal if this is suspected to be the cause.

 

ERCP can be done to remove impacted gallstones, followed by elective cholecystectomy to prevent further events.

 

Surgery for infected, necrotic tissue should wait at least two weeks to allow discrimination between viable and necrotic tissue.

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Consequences and Course

Ranson's Criteria for prognosis

pancreatitis not due to gallstones

 

Difficult course if +2 are present

High mortality if +3 are present

 

At admission:

  • blood glucose >11 mmol/L
    (with no history of hyperglycemia)
  • age >55
  • LDH >350 IU/L
  • AST >250 IU/L
  • WBC >10 x109/L

During first 48 hours:

  • calcium <2 mmol/L
  • hematocrit drop >10%
  • PO2 <60 mmHg
  • base deficit >4 mmol/L
  • BUN rise >1.8 mmol/L
  • albumin drop
  • fluid sequestration >6 L

* no correlation with serum amylase/lipase

Most people recover from acute pancreatitis and have restoration of normal pancreatic function and architecture. However, 5-10% of people die, usually from multisystem organ failure due to SIRS or from local or systemic infection. Risks correlate with extent of pancreatic necrosis.

Complications include:

Systemic necrosis and organ damage can lead to shock, and multi-organ failure:

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The Case of Mr. Verm

Mr. Verm is a 35 year-old previously healthy man who goes to his family doctor for increasingly severe pain. CT shows an inflamed pancreas. He traveled recently to Africa. What could be causing his condition?

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Resources and References

 

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Topic Development

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