Review of Acute Pancreatitis (3 CE’s)

Author: Brooke Baldwin-Rodriguez, RN, MSN

Written: February 18th, 2008

Updated: September 11, 2009

Course Description

Acute pancreatitis can range from mild to severe. Patients with severe acute pancreatitis require intensive care due to the high mortality rate related to sepsis and multiple organ dysfunction. Sepsis and multiple organ dysfunction are secondary to infected pancreatic necrosis. This course will review the etiology and pathophysiology of acute pancreatitis.  Signs and symptoms will be reviewed and the identification of early signs and symptoms stressed so that the nurse is able to assist in early identification. Current guidelines for treatment will be reviewed with an emphasis on early fluid resuscitation and optimal care focuses on minimizing complications. The final part of this course will review important aspects of discharge teaching that the nurse must address with the patient and family.

Course Objectives

Describe the function of the pancreas

Describe the cause of pancreatitis

Distinguish acute and severe acute pancreatitis

State the mortality rates associated with severe acute pancreatitis

Identify common causes of acute pancreatitis

Identify the most common cause of pancreatitis

Describe the pathophysiologic cascade of severe acute pancreatitis

State the enzyme that prompts the pathophysiologic cascade

Identify the universal symptom of acute pancreatitis

Identify common symptoms associated with acute pancreatitis

Differentiate Cullen’s sign from Grey-Turner’s sign

Identify laboratory values that aide in the diagnosis of acute pancreatitis

Describe Ranson’s Criteria

Outline treatment priorities of severe acute pancreatitis

Identify monitoring parameters for symptom management in acute pancreatitis

Identify indications for surgical intervention

Describe components of discharge teaching

Function of the Pancreas

The pancreas is a gland with endocrine and exocrine functions and is made up of two major tissues: the acini and the islets of Langerhans. Endocrine functions include production and secretion of the following substances:

·          Insulin from the beta cells. Insulin converts glucose into glycogen and lowers blood glucose levels.

·          Glucagon from the alpha cells. Glucagon converts glycogen to glucose when the body needs to raise blood glucose levels.

·          Somatostatin from the delta cells. Somatostatin inhibits the release of hormones such as growth hormone, corticotrophin, insulin, and gastrin.

Exocrine functions include production and secretion of digestive enzymes from acinar cells. Trypsin breaks down protein, amylase breaks down carbohydrates, and lipase breaks down fats. These enzymes are typically activated when they reach the intestines.

What causes Pancreatitis?

Pancreatitis is inflammation of the pancreas and can be either acute or chronic.  Activated pancreatic proteases begin to digest the pancreatic tissue itself which results in an inflammatory process. Acute pancreatitis has a spectrum of severity from mild acute to severe acute and is defined as a single episode where elevated enzymes levels return to normal after resolution of the episode. Mild acute pancreatitis usually has a self-limiting course and severe acute pancreatitis is a serious form of acute pancreatitis. Patients with severe acute pancreatitis usually require intensive care unit admission because of impaired pancreatic function and systemic complications that delay recovery. Severe acute pancreatitis develops in about 25% of patients with acute pancreatitis. Mortality rates for these patient’s ranges from 30% to 50%. High mortality rates are related to the development of systemic inflammatory response syndrome (SIRS) which can lead to multiple organ dysfunction.

The common causes of acute pancreatitis include:

• Gallstones

• Alcohol

• Infection

• Pancreatic tumor

• Drugs (which include; corticosteroids, ACE inhibitors and histamine H2 receptor blockers).

• Hyperlipidemia

• Abdominal trauma

• Hereditary pancreatitis

• Toxins

• Idiopathic

Approximately 40% to 60% of cases of acute pancreatitis are related to gallstones, with the second leading cause being alcohol abuse. Gallstones obstruct the bile duct, the pancreatic duct, or both. Increased ductal pressure leads to unregulated activation of the digestive enzymes. Early identification and treatment is of the utmost importance since approximately one-third to one-half of all deaths related to acute pancreatitis occurs in the first week. The three forms of acute pancreatitis include:

1.      Mild, edematous (interstitial pancreatitis)

2.      Severe, hemorrhagic (necrotizing pancreatitis)

3.      Extensive peripancreatic tissue necrosis and hemorrhage

Mild, edematous: Accounts for 95% of cases; mortality rate is 5%; Minimal or no necrotic damage.

Severe, hemorrhagic (necrotizing pancreatitis): Accounts for 5% of cases; mortality rate is 50%.

Extensive peripancreatic tissue necrosis and hemorrhage: There is necrosis or fat throughout the abdomen. Retroperitoneal hemorrhage caused by tissue necrosis or erosion of a pseudocysts into the vascular structure, vascular inflammation, and thrombus may occur.

Pathophysiology of Acute Pancreatitis

Independent of the initiating cause, all types of acute pancreatitis lead to the inappropriate or early activation, of pancreatic proenzymes to their active form. The activation of pancreatic proenzymes results in pancreatic autodigestion. Obstruction of the pancreas and pancreatic duct leads to pancreatic ischemia. Trypsin activation initiates the cascade of pancreatitis. Trypsin is an enzyme secreted by the small intestines for digestion of proteins. Generally, the pancreas has its own protective mechanisms to prevent overproduction of trypsin. The protective mechanisms that help reduce the risk of trypsin overproduction include: synthesis of the inactive enzyme trypsinogen, autolysis of activated trypsin, synthesis of specific trypsin inhibitors like serine protease inhibitors, and low intracellular ionized calcium concentrations. When trypsin is secreted in the acinar cells and is unregulated, other enzymes in the pancreas are signaled for release as well. The inappropriate release of enzymes by the pancreas leads to autodigestion of the gland and local inflammation.  The local inflammatory response leads to the release of proinflammatory cytokines such as interleukin 1, interleukin 6, interleukin 8, and tumor necrosis factor. As the area receives less and less flow of oxygen, oxygen-free radicals are released and leads to further injury. As the process continues, the acinus cells necrose which leads to further release of proinflammatory cytokines. Systemic inflammatory response syndrome is a result of the release of the systemic inflammatory mediators. A significant effect is exerted on the other organ systems due to the increased vascular permeability, vasodilation, vascular stasis, and microthrombosis.

As the inflammatory mediators travel through the blood, the lungs become susceptible to injury from the mediators as well. Gut barrier failure also occurs in acute pancreatitis as the bacterial endotoxins from the gut increase the intestinal capillary permeability. Translocation of bacterial endotoxins from the gut likely contributes to the local infection and multiple organ failure associated with severe acute pancreatitis. Multiple organ failure results from severe acute pancreatitis because of a suppression of the immune system and the increased circulation of cytokines.

Clinical Signs and Symptoms

A universal sign of acute pancreatitis is abdominal pain in the epigastric area (right upper quadrant) that radiates to the midback. This pain is found in about 95% of patients with pancreatitis. The pain might last for several days and may be associated with nausea and vomiting. The pain is usually worse in the supine position.

The signs and symptoms of acute pancreatitis are variable and range from:

• Acute epigastric pain

• Nausea and vomiting

• Abdominal distension associate with a small bowel ileus or pseudocyst with decreased or absent bowel sounds

• Low grade fever

• Increased pulse rate and decreased blood pressure (shock)

•Retroperitoneal hemorrhage (usually in severe cases only). Assess for the presence of

 Grey-Turners (bruising over flank) or Cullen’s sign (bruising around umbilicus).

• Diaphoresis

• Dehydration

• Abdominal distension

• Jaundice; dark, foamy urine

• Steatorrhea: bulky, pale, foul-smelling stools

Diagnostic Criteria

Clinical features and increased plasma levels of pancreatic enzymes are the primary diagnostic criteria. Ultrasonography may assist with the visualization of the dilated pancreatic ducts, ascites or the presence of gallstones (if the cause is biliary-induced pancreatitis). Ultrasonography may not be the best diagnostic tool, because of the difficulty with visualizing the pancreas. Contrast computed tomography (CT) may be used to monitor for complications such as fluid collections and necrosis.

Serum amylase is the most rapid way to diagnosis pancreatitis. However, amylase has low sensitivity in the diagnosis because it is rapidly excreted by the kidneys. Peak levels may decrease rapidly in 3 to 4 days. Urinary amylase may be increased to three times the normal value in acute pancreatitis and remains elevated for 10 to 14 days in patients with normal renal function.

Serum lipase is considered to be the most sensitive marker and persists after the onset of the acute episode. Serum lipase concentrations rise within 4 to 8 hours after an episode of acute pancreatitis, peak at 24 hours and then return to normal after 8 to 14 days. Levels are normally elevated three times the upper limit.

Other laboratory tests used to monitor for clinical progression and monitoring for complications include complete blood count, liver function tests, urea and electrolytes, coagulation screen, triglycerides, blood glucose, arterial blood gases, and C-reactive protein (CRP). If nausea and vomiting are present, imbalances in calcium, magnesium, phosphate and potassium should be monitored.

Scoring systems have been developed to predict the severity of pancreatitis. Ranson’s criteria is used to predict severity of the disease:

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