NURS 2003H Chapter Notes - Chapter 46: Duodenum, Pain Management, Papaverine
26 Jun 2018
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Acute Pancreatitis CH 46 p.1248-52
- An acute inflammatory process of the pancreas
- Degree of inflammation varies from mild edema to severe hemorrhagic necrosis
- Most common in middle-aged men and women
- Severity varies based on the extent of pancreatic destruction
- Some recover completely, others have reoccurring attacks (chronic pancreatitis)
- Can be life-threatening
Etiology and Pathophysiology
-Causes: alcoholism, gallbladder disease (gallstones), hypertriglyceridemia, trauma, viral
infections, penetrating duodenal ulcers, cysts, abscesses, cystic fibrosis, certain drugs
(corticosteroids, estrogens, HIV meds, anti-inflammatory drugs), metabolic disorders
(renal failure or hypothyroidism), and vascular disease.
- Can also occur after abdominal surgery of any kind and after endoscopic retrograde
cholangiopancreatography (ERCP).
- Sometimes the cause is unknown (idiopathic)
- Most common pathogenic mechanism: auto digestion of the pancreas.
oInjury to the pancreatic cells or activation of the pancreatic enzymes is caused in
the pancreas rather than in the intestines (it is not clear how the enzymes are
activated)
Possible cause: the reflux of bile acids into the pancreatic ducts through an
open or distended sphincter of Oddi. This reflux may result from blockage
created by gallstones. Obstruction of a pancreatic duct results in pancreatic
ischemia.
oTrypsinogen is an inactive proteolytic enzyme produced by the pancreas.
Normally, it is released into the small intestine via the pancreatic duct. It is
activated to trypsin by enterokinase in the intestine. Normally trypsin inhibitors in
the pancreas and the plasma bind and inactivate any trypsin that is produced. In
pancreatitis, activated trypsin is present in the pancreas. This enzyme digests the
pancreas and can activate other proteolytic enzymes such as elastase and
phospholipase A.
oAuto digestion: Elastase and phospholipase A play a major role
Elastase causes hemorrhage by producing dissolution of the elastic fibers
of blood vessels
Phos. A is most likely activated by trypsin and bile acids and causes fat
necrosis.
- It is not clear how alcohol use causes acute pancreatitis. Maybe alcohol increases the
production of digestive enzymes in the pancreas. Environment (high-fat diet, smoking)
and genetics may also contribute as only 5-10% of alcoholics develop acute pancreatitis.
-Mild pancreatitis: The functions of the gland return to normal upon recovery.
-Severe pancreatitis: half of patient’s endocrine and exocrine function decrease
permanently. Also at risk of developing pancreatic necrosis, organ failure, septic
complications.
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Clinical Manifestations
- Abdominal pain is the main symptom (left upper quadrant, midepigastric)
oCommonly radiates to the back due to the retroperitoneal location of the pancreas
oSudden onset, severe, deep, piercing, and continuous or steady, aggravated by
eating, and frequently occurs when the patient is recumbent (lying down).
oNot relieved by vomiting, can be accompanied by flushing, cyanosis, dyspnea
oFlexion of the spine in an attempt to relieve the pain
oPain is caused by distention of the pancreas, peritoneal irritation, and obstruction
of the biliary duct.
- Nausea and vomiting, low grade fever, leukocytosis, hypotension, tachycardia, and
jaundice
- Abdominal tenderness with muscle guarding
- Bowel sounds may be decreased or absent
- Ileus may occur and causes marked abdominal distention
- The lungs may have crackles
- Intravascular damage from circulatory trypsin may cause areas of cyanosis or greenish or
yellow-brown discoloration of the abdominal wall.
- Ecchymosis (bruise) in the flanks-area between ribs and hip- (Grey Turner’s spots or
sign, a bluish flank discoloration) and the periumbilical area (Cullen’s sign, a bluish
periumbilical discoloration)
oResult from seepage of blood-stained exudate from the pancreas and may occur in
severe cases
- Shock may occur as a result of hemorrhage into the pancreas, toxemia from activated
pancreatic enzymes, or hypovolemia as a result of massive shift of exudates (any fluid
that filters from the circulatory system) of blood and plasma proteins into the
retroperitoneal space.
Complications
- Pancreatic pseudocyst: a cavity continuous with or surrounding the outside of the
pancreas.
oFilled with necrotic products and liquid secretions, such as plasma, pancreatic
enzymes, and inflammatory exudates.
oAs enzymes escape from the pseudocyst, the serosal surfaces next to the pancreas
become inflamed; granulation tissue subsequently forms, encapsulating the
exudate.
oAbdominal pain, palpable epigastric mass, nausea, vomiting, anorexia
oSerum amylase level remains raised
oUsually resolves within a few weeks
May perforate, causing peritonitis, or they may rupture into the stomach or
duodenum.
oTreatment: internal drainage procedure with an anastomosis between the
pancreatic duct and the jejunum.
- Pancreatic abscess: large fluid-filled containing cavity within the pancreas.
oResults from extensive necrosis in the pancreas
oMay become infected or perforate into adjacent organs
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Document Summary
An acute inflammatory process of the pancreas. Degree of inflammation varies from mild edema to severe hemorrhagic necrosis. Most common in middle-aged men and women. Severity varies based on the extent of pancreatic destruction. Some recover completely, others have reoccurring attacks (chronic pancreatitis) Causes: alcoholism, gallbladder disease (gallstones), hypertriglyceridemia, trauma, viral infections, penetrating duodenal ulcers, cysts, abscesses, cystic fibrosis, certain drugs (corticosteroids, estrogens, hiv meds, anti-inflammatory drugs), metabolic disorders (renal failure or hypothyroidism), and vascular disease. Can also occur after abdominal surgery of any kind and after endoscopic retrograde cholangiopancreatography (ercp). Possible cause: the reflux of bile acids into the pancreatic ducts through an open or distended sphincter of oddi. This reflux may result from blockage created by gallstones. Obstruction of a pancreatic duct results in pancreatic ischemia: trypsinogen is an inactive proteolytic enzyme produced by the pancreas. Normally, it is released into the small intestine via the pancreatic duct. It is activated to trypsin by enterokinase in the intestine.
