Pancreatitis

Question 1

Risk factors

Answer 1

• Typically history of alcoholism or biliary disease (80% of patients with acute pancreatitis have biliary tract disease e.g. gallstones).
• Bacterial or viral infections ie mumps virus
• Spasm and edema of the ampulla of Vater from duodenitis can produce pancreatitis.
• Blunt abdominal trauma, peptic ulcer disease, ischemic vascular disease, oral contraceptives have been associated with an increased incidence of pancreatitis.
• Acute may follow surgery on or near the pancreas or after exploratory instrumentation of the pancreatic duct e.g. ERCP.
• There is a small incidence of hereditary Pancreatitis.

Question 2

Pathophysiology

Answer 2

• Pancreatic digestive exocrine enzymes:
  
  • Trypsinogen, an inactive protease that is activated in the duodenum into trypsin.
  • This breaks down proteins to amino acids.
  • Lipase breaksdown triglycerides into fatty acids and glycerol.
  • Amylase breaks down CHO
• Pancreatitis is an inflammation and autodigestion of the pancreas by its own proteolytic enzymes, principally trypsinogen, causes acute pancreatitis.
• Hypersecretion of the exocrine enzymes of the pancreas – amylase (CHO), lipase (Fat), tripsin (Protein)- that aid digestion.
• The pancreatic duct becomes obstructe. Bile reflux and enzyme activation in the pancreatic duct causes inflammation, edema, vasodilation, increased vascular permeability, necrosis, erosion, interstitial hemorrhage which leads to pancreatitis.
• Pancreatic necrosis is a major cause of morbidity and mortality in patients with acute pancreatitis. The patient is at risk for hemorrhage, septic shock and multiple organ failure
• 80% of patients with acute pancreatitis have biliary tract disease
• 5% of patients with gallstones develop pancreatitis. Gallstones enter the CBD and lodge at the ampulla of Vater, obstruction the flow of pancreatic juice or causing a reflux of bile from the common bile duct into the pancreatic duct, activating the enzymes of the pancreas.

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Question 3

Chronic Pancretitis

Answer 3

• The major causes of chronic pancreatitis are alcohol (70% of cases) and malnutrition
• Is an inflammatory disorder characterized by progressive anatomic and functional destruction of the pancreas.
• Long term alcohol consumption causes hypersecretion of protein in pancreatic duct, resulting in protein plugs and calculi within the pancreatic ducts. Alcohol has a direct toxic effect on the pancreatic cells.
• As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure within the pancreas increases
• The end result is mechanical obstruction of the pancreatic and CBD
• There is atrophy of the epithelium of the ducts, inflammation, and destruction of the secreting cells of the pancreas

Question 4

Acute Pancretitis

Answer 4

• Medical emergency
• High risk for life-threatening complication and mortality.
• Mortality rate of acute Pancreatitis is high (10%) because of shock, anoxia(HYPOXIA), hypotension, or F&E imbalances.
• Attacks may result in complete recovery or may progress to chronic pancreatitis
• Ranges from a mild, self-limiting disorder to a severe, rapidly fatal disease.
• The patient who has survives an episode of acute pancreatitis is often weak and debilitated weeks or months after an acute episode of pancreatitis.
• After the acute attack has subsided, some patients may be inclined to return to their previous drinking habits – they must avoid alcohol
  
  • Mild acute Pancreatitis is:
    
    • Characterized by edema and inflammation confined to the pancreas.
    • Minimal pancreatic dysfunction and return to normal usually occurs within 6 months.
  • Severe acute Pancreatitis is:
    
    • More widespread and with complete enzymatic digestion of the pancreatic gland.
      
      • WHICH LEADS TO -
    • The tissue becomes necrotic, and the damage extends into the retroperitoneal tissues.
    • Systemic complications, such as acute respiratory distress syndrome, shock, fluid and electrolyte disturbances and sepsis and disseminated intravascular coagulopathy and pleural effusion can increase the mortality rate to 50% or higher.

Question 5

Diagnosis

Answer 5

• History of abdominal pain
• Presence of known risk factors
• WBC is usually elevated
• In 90% of the cases , serum amylase and lipase levels usually rise in excess of three times their normal upper limit within 24 hours
  
  • Serum amylase usually returns to normal within 48-72 hours. (normal 60-80 units/L)
  • Serum lipase levels may remain elevated for 7 to 14 days (normal 0-160 units /L)
• Urinary amylase levels become elevated
• Hypocalcemia is present and correlates well with the severity of pancreatitis
  
  • Inflamed pancreas causes release of fatty acids that bind to calcium. Fatty acids also cause increasing binding of calcium to albumin.
  • Occurs in approx. 25% of patients with acute pancreatitis. Assess for Trousseau’s sign and Chvostek’s
  • May require prompt treatment. Keep a supply of IV calcium gluconate readily available. Calcium may be prescribed to prevent of treat tetany.
• Transient hyperglycemia and glucosuria and elevated serum bilirubin levels
• X rays of the abdomen and chest to detect pleural effusions
• Ultrasound and contrast CT scan to identify pancreatic cysts, abscesses, or pseudocysts
• H&H are used to monitor the patient for bleeding
• Peritoneal fluid, obtained through paracentesis, may contain increase levels of pancreatic enzymes
• The stools of patients with pancreatic disease are often bulky, pale, and foul-smelling. Because lipase and bile are not getting into the duodenum. Fat content of stools varies between 50-90% in pancreatic disease. Normally the fat content is 20%.
• ERCP is rarely used in the diagnostic evaluation of acute pancreatitis because the patient is acutely ill, however it may be valuable in the treatment of gallstone pancreatitis**** (avoid perforation)
• 4 major complications : Pulmonary , Tetany , Hemorrhage -> necrotic, Billary obsturction.

Question 6

Acute pancretitis Treatment

Answer 6

The objectives of therapy are to relieve pain and decrease secretion of the enzymes of the pancreas that produces auto-digestion of the pancreas. Acute Pancreatitis generally subsides 3-7 days after the start of treatment.

• Intensive Care
• Bedrest and limit activities to reduce metabolic stress.
• Monitor for early signs of shock
• Nasogastric suction may be used to relieve nausea and vomiting, to decrease painful abdominal distention and paralytic ileus and to remove hydrochloric acid so that it does not enter the duodenum and stimulate the pancreas
• All oral (food and fluid) intake is withheld to inhibit pancreatic secretion of pancreatic enzymes.
• Assess the patient’s nutritional status
  
  • As acute symptoms (pain and organ dysfunction) subside, reintroduce oral feedings. Usually after 1-2 days clear fluids are resumed.
  • ​Between acuteattacks, a diethigh in CHO and low in fat and proteins.
  • Avoid heavy meals and alcohol
  • Parenteral nutrition is usually an important part of therapy, particularly in debilitated patients.
  • Post pancreatitis:
    
    • Provide high CHO, low protein and low fat when tolerated.
    • ​Caffeine (coffee), spicy foods and alcohol are ELIMINATED from the diet because they increase pancreatic and gastric secretions
  • Monitor serum glucose levels every 4-6 hours
• Histamine -2 (H2) antagonists and Proton Pump Inhibitors to decrease pancreatic activity by inhibiting HCL secretion.
• Monitor fluid status:
  
  • ​Correct of fluid, blood loss and low albumin levels to maintain fluid volume and prevent shock and renal failure. May need to administer 6-8 liters of fluid per day. Assess for overload.
  • Report decreased urine output, decreased BP
• ​​Monitor F&E disturbances due to N,V, movement of fluid from the vascular compartment to the peritoneal cavity (ascites – 3rd spacing)), diaphoresis, fever, and the use of gastric suction
• Pain management :
  
  • The pain of acute pancreatitis is often very severe, necessitating the liberal use of analgesic agents
  • If the patient experiences increasing severity of pain, the patient may be experiencing hemorrhage of the pancreas, or the dose of the analgesic may be inadequate. Symptoms of Hemorrhagic Pancreatitis are blue discoloration around the umbilicus (Cullen’s sign) and the flank area (Turner’s sign)
  • Anticholinergic medication reduce gastric and pancreatic secretion
  • Morphine and morphine derivatives are often avoided because they may cause spasm of the sphincter of Oddi
  • Hydromorphine , Fentanyl –can be prescribed prescribed because they are less likely to cause spasm of the sphincter.
  • Antiemetic agents may be prescribed to prevent vomiting
  • Bedrest to reduce metabolic rate and reduce the secretion of pancreatic and gastric enzymes.
• ​Stool softeners for constipation caused by immobility or opoids use
• Antibiotic MAY be prescribed if infection is present
• Insulin may be required if significant hyperglycemia occurs. Monitor serum glucose levels and administer insulin as prescribed
• Aggressive respiratory care is indicated because of elevation of the diaphragm, pulmonary infiltrates and effusion, and atelectasis (dullness at the bases, and abnormal tactile fremitus)​
  
  • O2 as prescribed to reduce metabolic demands on the body.
  • Maintain in a semi-fowlers position to decrease pressure on the diaphragm by a distended abdomen and to increase respiratory expansion
• Maintain biliary drainage
  
  • Placement of biliary drains (for external drainage) and stents (indwelling tubes) in the pancreatic duct by endoscopy to reestablish drainage of the pancreas.
• ​Surgical interventions
  
  • Often risky because patient is acutely ill – is a poor surgical risk
  • May be performed to diagnosis pancreatitis, to establish pancreatic drainage, or to resect or debride a necrotic pancreas.
• ​Post acute pain management :
  
  • Assess current nutritional status and increased metabolic requirements
  • ​Assess the stool characteristics return to normal

Question 7

Treatment of chronic pancreatitis

Answer 7

• Nonsurgical Management
  
  • Endoscopy to remove pancreatic duct stone and stent strictures to relieve obstruction and manage pain
  • Pain management:
  • Similar to acute pancreatitis but usually use nonopioid methods to manage pain
  • Diabetes mellitus resulting from dysfunction of the pancreatic islet cells is treated with diet , insulin, or oral antidiabetic agent
  • Pancreatic enzyme replacement is indicated in the patient with Malabsorption and steatorrhea.
• Surgical management :
  
  • To relieve abdominal pain and discomfort
  • Restore drainage of pancreatic secretion
  • Reduce frequency of acute attacks
  • Types:
    
    • Pancreaticojejunostomy (Roux-en-Y)
      
      • With a side-to-side anastomosis or joining of the pancreatic duct to the jejunum allows drainage of the pancreatic secretion into the jejunum
    • Revision of the Ampulla of Vater
    • Insertion of a stent
    • Wide resection or removal of the pancreas
    • Whipple resection (pancreaticoduodenectomy)
    • Autotransplantation or implantation of the patient’s pancreatic islet cells – experimental
    • Chronic pancreatitis from gallbladder disease- explore the CBD by dividing the sphincter of Oddi, a muscle located at the Ampulla of Vater.This surgical procedure is called a sphincterotomy via an ERCP
  • Even after these procedures, the patient is likely to continue to have pain and impaired digestion secondary to pancreatitis unless alcohol is avoided.

Question 8

Clinical manifestation of acute pancreatitis

Answer 8

• Acute severe pain in the upper midepigastrium abdomin that radiates to the back and flank area
  
  • Nausea
  • Vomiting that does not relieve the pain or nausea.
  • Pain may indicate pancreatic hemorrhage
  • Abdominal guarding is present
  • Pain is frequently acute and severe in onset, occurring 24-48 hours after meals or alcohol ingestion and is unrelieved by antacids or vomiting.
• A rigid or board-like abdomen may develop and is generally an ominous sign
  
  • Abdominal distention
  • Decreased peristalsis
• The stools become frequent, pale, bulky, frothy, and foul-smelling because of impaired fat digestion, which results in stools with a high fat content. This is steatorrhea. Fat content of stools varies between 50-90% in pancreatic disease. Normally the fat content is 20%
• Shock and multi organ failure may occur with acute pancreatitis.
• Hypovolemic shock may occur as a result of hypovolemia and sequestering of fluid in the peritoneal cavity (ascites) and pleural space (pleural effusion) - 3rd spacing - (fluid retention or sequestering of fluid in peritoneal cavity – can be > 6L). (Review symptoms of Hypovolemic shock)
• Hemorrhagic shock may occur with hemorrhagic pancreatitis.
• Septic shock may occur from the bacteria infection and toxins of a necrotic pancreas.
• Cardiac dysfunction may occur as a result of fluid and electrolyte disturbances, and acid-base imbalances.
• Bruising (Ecchymosis) over flank area (turner’s sign) or around the umbilicus (Cullen”s sign) may indicate severe pancreatitis
• Fever, jaundice, mental confusion and agitation may also appear.
• Respiratory distress and hypoxia - may develop diffuse pulmonary infiltrates. Acute pancreatitis produces retroperitoneal edema, elevation of the diaphragm, pleural effusion, and inadequate lung ventilation

Question 9

Clinical manifestation of chronic pancreatitis

Answer 9

• continuous severe upper midepigastrium abdominal and back pain or a dull nagging constant pain
  
  • vomiting
  • As the disease progresses, recurring attacks of pain are more severe, more frequent, and of longer duration
• The stools become frequent, pale, bulky, frothy, and foul-smelling because of impaired fat digestion, which results in stools with a high fat content. This is steatorrhea.
• More than 75% of patient experience significant weight loss, usually caused by decreased dietary intake secondary to anorexia or fear that eating will precipitate another attack.
  
  • Weight loss is a major problem in chronic pancreatitis
• Malabsorption occurs late in the disease and impaired digestion, especially of proteins and fats.