NS3P1 Mod 2 Pancreatitis

• 1. Amylase digests starch to maltose.
• 2. Maltase reduces maltose to monosaccharideglucose
• 3. Lactase splits lactose into galactose and glucose.
• 4. Sucrase reduces sucrose to fructose and glucose.
• 5. Nucleases split nucleic acids to nucleotides.
• 6. Enterokinase activates trypsinogen to trypsin.

• => Actions:
• Trypsinogen: Protein digestion
• Chymotrypsin: protein digestion
• Amylase: starch to disaccharides
• Lipase: Fat digestions

A long slender gland lying ehind the stomach, and in front of the first and second lumbar vertebrae.

Consists of Head, body, and tail.

The pancreatic ducts extends along the gland and enters the duodenum through the common bile duct.

Has bone exocrine and endocrine functions.

• => Exocrine gland
• a. Secretes sodium bicarbonate to neutralize theacidity of the stomach contents that enterthe duodenum
• b. Pancreatic juices contain enzymes for digestingcarbohydrates, fats, and proteins.

• => Endocrine gland
• a. Secretes glucagon to raise blood glucose levels and secretes somatostatin to exert a hypoglycemic effect
• b. The islets of Langerhans secrete insulin:
• By Beta cells, Alpha cells: glucagon, Delta cells: somatostain, F cells: secrete pancreatic polypeptide
• c. Insulin is secreted into the bloodstream and is important for carbohydrate

• 1. Description
• a. This enzyme, produced by the pancreas andsalivary glands, aids in the digestion of complex carbohydrates and is excreted by thekidneys.
• b. In acute pancreatitis, the amylase level isgreatly increased; the level starts rising 3 to6 hours after the onset of pain, peaks atabout 24 hours, and returns to normal in2 to 3 days after the onset of pain.

2. Value: 25 to 151 units/L

• 3. Nursing considerations
• a. On the laboratory form, list the medicationsthat the client has taken during the previous24 hours before the test
• b. Note that many medications may cause falsepositiveor false-negative results.
• c. Results are invalidated if the specimen wasobtained less than 72 hours after cholecystographywith radiopaque dyes.

• a. This pancreatic enzyme converts fats and triglyceridesinto fatty acids and glycerol.
• b. Elevated lipase levels occur in pancreatic disorders;elevations may not occur until 24 to36 hours after the onset of illness and mayremain elevated for up to 14 days.

2. Value: 10 to 140 units/L

3. Nursing considerations: Endoscopic retrogradecholangiopancreatography (ERCP) may increaselipase activity.

• An acute inflammatory process of the pancreas
• Varies from mild edema to severe necrosis
• Most common in middle-aged persons and African Americans

panc pain: sharp pain, radiating through midback, usually increased by eating

key factors: obesity, smoking, alcohol

• => Notes:
• Acute pancreatitis is an acute inflammation of the pancreas. The degree of inflammation varies from mild edema to severe hemorrhagic necrosis. Can be hemmoragic or necrotic.

• Acute pancreatitis is most common in middle-aged men and women. It affects women and men equally.
• The rate of pancreatitis in African Americans is three times higher than in white persons.

• Gallbladder disease (women): cholelithaisis
• Chronic alcohol intake (men)
• Smoking
• Hypertriglyceridemia

• => In the United States, the most common cause is gallbladder disease (gallstones), which is more common in women. The second most common cause is chronic alcohol intake, which is more common in men.
• Smoking is an independent risk factor for acute pancreatitis. Biliary sludge or microlithiasis, which is a mixture of cholesterol crystals and calcium salts, is found in 20% to 40% of patients with acute pancreatitis.
• The formation of biliary sludge is seen in patients with bile stasis.
• Acute pancreatitis attacks are also associated with hypertriglyceridemia (serum levels >1000 mg/dL).

• => Less common causes
• Drugs
• Metabolic disorders
• Vascular diseases
• Surgery and endoscopic procedures: EGD puts pt at risk for possible panc b/c you go into intestiant tract and irritating sphicter of odio, and backing up of secretion of GI tract into panc tract.
• Idiopathic causes

=> Other less common causes include certain drugs (corticosteroids, thiazide diuretics, oral contraceptives, sulfonamides, NSAIDs), metabolic disorders (hyperparathyroidism, renal failure), and vascular diseases.Pancreatitis may occur after surgical procedures on the pancreas, stomach, duodenum, or biliary tract. Pancreatitis can also occur after endoscopic retrograde cholangiopancreatography (ERCP). In some cases, the cause is unknown (idiopathic).

• => Less common causes
• Trauma (postsurgical, abdominal)Viral infections Penetrating duodenal ulcer CystsAbscesses Cystic fibrosisKaposi sarcoma

-Other less common causes of acute pancreatitis include trauma (postsurgical, abdominal), viral infections (mumps, coxsackievirus B, HIV), penetrating duodenal ulcer, cysts, abscesses, cystic fibrosis, and Kaposi sarcoma.

• Caused by autodigestion of pancreas: That's why pain gets worse when we eat, the enzymes get activated.
• Key factors: alcohol, gall bladder stones, medications possible, and food--go NPO. you have to remove the factors. And let the pancrease rest! Even ice or gum chewing, because digestion starts in the mouth o:

Injury to pancreatic cells

Activation of pancreatic enzymes: becomes active and take effect on the pancrase. THey're SUPPOSED to be made in non-active form in panc, and get activated in the duodenum. Activation of trypsinogen to trypsin within the pancreas leads to bleeding

• Inflammation and swelling occur so damage occurs
• -shock: when enzymes act on BVs

=>The most common pathogenic mechanism is autodigestion of the pancreas. The etiologic factors cause injury to pancreatic cells or activation of the pancreatic enzymes in the pancreas rather than in the intestine.

This may be due to reflux of bile acids into the pancreatic ducts through an open or distended sphincter of Oddi.

• This reflux may be due to blockage created by gallstones. Obstruction of pancreatic ducts results in pancreatic ischemia.
• --Trypsinogen is an inactive proteolytic enzyme produced by the pancreas. It is released into the small intestine via the pancreatic duct. In the small intestine, it is activated to trypsin by enterokinase. Normally, trypsin inhibitors in the pancreas and plasma bind and inactivate any trypsin that is inadvertently produced.
• -In pancreatitis, activated trypsin is present in the pancreas. This enzyme can digest the pancreas and produce bleeding.

• => Other pancreatic enzymes:
• Trypsin, Elastase, Phopholipase A and lipase, Kallikrein
• -Audogigestive effects: edema, necrosis, hemorrhage-Kallikrein can cause shock, smooth muscle conttraction, and vascular permeability, edema

• => Mild: Edematous or interstitial
• See it on catscan

• => Severe pancreatitis
• Necrotizing :Depends on how much tissue is dying and the long term complications. Pt can develop diabetes and exocrine: lack enzymes that they need to digest food.
• Endocrine and exocrine dysfunction
• Necrosis, organ failure, sepsis

Rate of mortality: 25%

=The pathophysiologic involvement of acute pancreatitis is classified as either mild pancreatitis (also known as edematous or interstitial pancreatitis) or severe pancreatitis (also called necrotizing pancreatitis).

In severe pancreatitis, permanent decreases in endocrine and exocrine function occur in approximately half of affected patients. Patients with severe pancreatitis are also at high risk for developing pancreatic necrosis, organ failure, and septic complications, which result in a 25% mortality rate.

Flushing, Cyanosis, Dyspnea, n/v, Low grade feeer, Leuocytosis, Hypotension, tachycardia, Jaundice (cheolecystitis), Abd tenderenss, decreased BS, cracks, skin discoloration and shock (effect on enzymes on vessels: vasodilation), Electrolyte imbalances: Vomitting-HypoK and HypoC.

• => Abdominal pain predominant: KEY COMPLAINT
• Left upper quadrant or midepigastrium
• Radiates to the backSudden onset

=> Abdominal pain is the predominant manifestation of acute pancreatitis. The pain is due to distention of the pancreas, peritoneal irritation, and obstruction of the biliary tract.

The pain is usually located in the left upper quadrant, but it may be in the midepigastrium. It commonly radiates to the back because of the retroperitoneal location of the pancreas.

The pain has a sudden onset and is described as severe, deep, piercing, and continuous or steady. The pain is aggravated by eating, and frequently has its onset when the patient is recumbent. It is not relieved by vomiting; may be accompanied by flushing, cyanosis, and dyspnea. The patient may assume various positions involving flexion of the spine in an attempt to relieve the severe pain.

Other manifestations of acute pancreatitis include nausea and vomiting, low-grade fever, leukocytosis, hypotension, tachycardia, and jaundice. Abdominal tenderness with guarding

Decreased or absent bowel sounds: enzymes leaking into peritoneal cavities

=> Resp: Crackles, dyspnea (shallow breathing: panc enzymes can irritate the pleural lining so as a result, pt may develop carackles/atelectasis-don't take a deep breath b/c of the pain

• Abdominal skin discoloration: Grey Turner’s spots or sign, Cullen’s sign
• Shock

=> Abdominal tenderness with muscle guarding is common. Bowel sounds may be decreased or absent. Paralytic ileus may occur and causes marked abdominal distention.

The lungs are frequently involved, with crackles present. Intravascular damage from circulating trypsin may cause areas of cyanosis or greenish to yellow-brown discoloration of the abdominal wall.

Other areas of ecchymoses are the flanks (Grey Turner’s spots or sign, a bluish flank discoloration) and the periumbilical area (Cullen’s sign, a bluish periumbilical discoloration). These result from seepage of blood-stained exudate from the pancreas and may occur in severe cases. Prominent in severe or advaced

Shock may result from hemorrhage into the pancreas, toxemia from the activated pancreatic enzymes, or hypovolemia as a result of fluid shift into the retroperitoneal space (massive fluid shifts).

• => Pseudocyst: when all broken down tissues accumulates within capusule of pancreas, forming a pseudocyst.
• Fluid, enzyme, debris, and exudates surrounded by wall
• Abdominal pain, palpable mass, nausea/vomiting, anorexia
• Detected with imaging
• WORRY: Resolves spontaneously or may perforate and cause peritonitis--> Sepsis.
• Surgical or endoscopic drainage: may have to be drained, CT guided procedures, Drain if they can't aspirate all the fluid.

• => Pancreatic abscess (More worried: true infection)
• A pancreatic abscess is a collection of pus. It results from extensive necrosis in the pancreas. WBCs elevated and high fever! so you have to treat more aggressively!
• It may become infected or perforate into adjacent organs.
• Manifestations of an abscess include upper abdominal pain, abdominal mass, high fever, and leukocytosis. Pancreatic abscesses necessitate prompt surgical drainage to prevent sepsis.
• Regular uncomplicated is rarely treated with abx because it's caused by inflammation, BUT IF ABSCESS: then you need abx
• -If a mass is palpable: you have to differentiate if it's a pseudocyst or abscess. But if you palpate pancreeatitis abdoment: tender, bloated (hypoactive BS)

• => Two significant local complications of acute pancreatitis are pseudocyst and abscess.
• A pancreatic pseudocyst is an accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall.
• Manifestations of pseudocyst are abdominal pain, palpable epigastric mass, nausea, vomiting, and anorexia.
• The serum amylase level frequently remains elevated. CT, MRI, and endoscopic ultrasonography (EUS) may be used in the detection of a pseudocyst.
• The cysts usually resolve spontaneously within a few weeks but may perforate, causing peritonitis, or rupture into the stomach or duodenum.
• Treatment options include surgical drainage procedure, percutaneous catheter placement and drainage, and endoscopic drainage.

• Pleural effusion
• Atelectasis: painful to breathe
• Pneumonia
• ARDS
• Hypotension
• Hypocalcemia: tetany.

• => The main systemic complications of acute pancreatitis are pulmonary (pleural effusion, atelectasis, pneumonia, and acute respiratory distress syndrome [ARDS]) and cardiovascular (hypotension) complications and tetany caused by hypocalcemia. The pulmonary complications are probably due to the passage of exudate containing pancreatic enzymes from the peritoneal cavity through transdiaphragmatic lymph channels.
• When hypocalcemia occurs, it is a sign of severe disease. It is due in part to the combining of calcium and fatty acids during fat necrosis. The exact mechanisms of how or why hypocalcemia occurs are not well understood.

• Laboratory tests: Pancreatic enzymes
• 1. Serum amylase level
• 2. Serum lipase level
• Liver enzyme levels
• Triglyceride levels
• Glucose level: acute accuchecks.
• Bilirubin level: because gallbladder is second leading cause !
• Serum calcium level

=> The primary diagnostic tests for acute pancreatitis are serum amylase and lipase measurements.

The serum amylase level is usually elevated early and remains elevated for 24 to 72 hours.

Serum lipase level, which is also elevated in acute pancreatitis, is an important test because other disorders (e.g., mumps, cerebral trauma, renal transplantation) may increase serum amylase levels.

Other findings include an increase in liver enzymes, triglycerides, glucose, and bilirubin levels and a decrease in calcium level.

=> Abdominal ultrasonography:

=>X-ray

=>Contrast-enhanced CT scan

• =>Endoscopic retrograde cholangiopancreatography (ERCP)
• Diagnostic evaluation of acute pancreatitis is also directed at determining the cause.
• Abdominal ultrasonography, x-ray, or contrast-enhanced CT scanning can be used to identify pancreatic problems.
• CT scanning is the best imaging test for pancreatitis and related complications such as pseudocysts and abscesses.
• ERCP is can be used, although ERCP can cause acute pancreatitis in some cases.

=>Endoscopic ultrasonography (EUS): gall bladder stones, looking for duct occlusion

=>Magnetic resonance cholangiopancreatography (MRCP)

=>Angiography

=>Chest x-rays may show pulmonary changes, including atelectasis and pleural effusions.

• 1. Description
• a. Examination of the hepatobiliary system is performed via a flexible endoscope inserted into the esophagus to the descending duodenum; multiple positions are required during the procedure to pass the endoscope.

b. If medication is administered before the procedure, the client is monitored closely for signs of respiratory and central nervous systemdepression, hypotension, oversedation,and vomiting.

• 2. Preprocedure
• a. Client is NPO for several hours before the procedure.
• b. Sedation is administered before the procedure.

• 3. Postprocedure
• a. Monitor vital signs.
• b. Monitor for the return of the gag reflex: numming the throat locallyc. Monitor for signs of perforation (see Box 56-3) or peritonitis.

-Checks the sphincter of odi, which opens into common bile duct in duodenum, If they'res a occlusion of stone, they can remove the stone. They can do sphincterectomy to ease the pass of the stone.

Relief of pain: putting pt on NPO or even NG tube to remove stomach contents. Maintain their fluds and electrolytes

Prevention or alleviation of shock

↓ Pancreatic secretions

Correction of fluid/electrolyte imbalance

Prevention/treatment of infection: treat infection before removing gallbladder

Removal of the precipitating cause: education of med causes

=> Goals of collaborative care for acute pancreatitis include (1) relief of pain; (2) prevention or alleviation of shock; (3) reduction of pancreatic secretions; (4) correction of fluid and electrolyte imbalances; (5) prevention or treatment of infections; and (6) removal of the precipitating cause, if possible

• Aggressive hydration
• Pain management(IV morphine, antispasmodic agent)
• Management of metabolic complications (Oxygen, glucose levels)
• Minimizing pancreatic stimulation (NPO status, NG suction, decreased acid secretion, enteral nutrition if needed)
• Shock : Plasma or plasma volume expanders (dextran or albumin)
• Fluid/electrolyte imbalance: Lactated Ringer’s solution

• => If shock is present, blood volume replacements are used.
• Plasma or plasma volume expanders such as dextran or albumin may be given.
• Fluid and electrolyte imbalances are corrected with lactated Ringer’s solution or other electrolyte solutions.
• Central venous pressure readings may be used to assist in determining fluid replacement requirements.

• => Treatment is focused primarily on supportive care, including aggressive hydration, pain management, management of metabolic complications, and minimizing pancreatic stimulation.
• Treatment and control of pain are very important. IV morphine may be used. Pain medications may be combined with an antispasmodic agent. However, atropine and other anticholinergic drugs should be avoided when paralytic ileus is present because they can decrease GI mobility, thus contributing to the problem.

Other medications that relax smooth muscles (spasmolytics), such as nitroglycerin or papaverine, may be used. It is important to reduce or suppress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest.

This is accomplished in several ways. First, the patient is on NPO status. Second, NG suction may be used to reduce vomiting and gastric distention and to prevent gastric acidic contents from entering the duodenum.

• In addition, certain drugs may be used to suppress gastric acid secretion. With resolution of the pancreatitis, the patient will resume oral intake.
• For the patient with severe acute pancreatitis in whom oral intake is not resumed, enteral nutrition support may be initiated.

=> Ongoing hypotension: Vasoactive drugs: dopamine (Intropin)

• => Prevent infection
• Enteral nutrition
• Antibiotics: not as a standard of care though.
• Endoscopically or CT-guided percutaneous aspiration

• -Vasoactive drugs such as dopamine (Intropin) may be used to increase systemic vascular resistance in patients with ongoing hypotension.
• The inflamed and necrotic pancreatic tissue is a good medium for bacterial growth. In patients with acute necrotizing pancreatitis, infection is the leading cause of morbidity and mortality. Therefore, it is important to prevent infections.

Because many of the organisms come from the intestine, enteral feeding reduces the risk of necrotizing pancreatitis.

It is important to monitor the patient closely so that antibiotic therapy can be instituted early if necrosis and infection occur.

Endoscopically or CT-guided percutaneous aspiration with Gram stain and culture may be performed.

For gallstones, ERCP

Cholecystectomy

Uncertain diagnosis

Not responding to conservative therapy

Drainage of necrotic fluid collections

=> When the acute pancreatitis is related to the presence of gallstones, an urgent ERCP plus endoscopic sphincterotomy (severing of the muscle layers of the sphincter of Oddi) may be performed. This may be followed by laparoscopic cholecystectomy to reduce the potential for recurrence.

Surgical intervention may also be indicated when the diagnosis is uncertain and in patients who do not respond to conservative therapy.

Patients with severe acute pancreatitis may require drainage of necrotic fluid collections. This can be done either surgically, under CT guidance, or endoscopically. Percutaneous drainage of a pseudocyst can be performed, and a drainage tube is left in place.

=>Morphine: For pain relief

=>Antispasmodics (e.g., dicyclomine [Bentyl] ↓ Vagal stimulation, motility, pancreatic outflow (↓ volume and concentration of bicarbonate and enzyme secretion); contraindicated in paralytic ileus

=>Carbonic anhydrase inhibitor (acetazolamide [Diamox]) ↓ Volume and bicarbonate concentration of pancreatic secretion

=> Antacids: Neutralization of gastric hydrochloric (HCl) acid secretion; ↓ production and secretion of pancreatic enzymes and bicarbonate

=>Proton pump inhibitors (omeprazole [Prilosec]): ↓ HCl acid secretion (HCl acid stimulates pancreatic activity)

• NPO status initially (facility is more strict now: 48-72 hours: dietay consult must be made b/c nutrition is important for recovery)
• Only parenteral, you can't give NG b/c it's going through GI tract

-Especially if longer than 72 hours.

-Consider TPN before lipids (more complex for the body to breakdown)

Enteral versus parenteral nutrition

Monitor triglycerides if IV lipids given

• Small, frequent feedings when able
• High-carbohydrate

No alcohol

Supplemental fat-soluble vitamins

Pain is key symptom in addition to amylase and lipase on NPO status, that must be gone before you can advance the pt's diet (so they better not be taking pain meds!)

Decrease foods that stimulate pancrease: fats, spices. Extra nutrition from protein and carbs :)

->advancing meal: clear to full liq diet


=> Initially the patient with acute pancreatitis is on NPO status to reduce pancreatic secretion. Depending on the severity of the pancreatitis, enteral feedings via nasojejunal tube are initiated. Because of infection risk, parenteral nutrition is reserved for patients who cannot tolerate enteral nutrition. If IV lipids are ordered, blood triglyceride levels need to be monitored. When food is allowed, small, frequent feedings are given. The diet is usually high in carbohydrate content because that is the least stimulating to the exocrine portion of the pancreas.Suspect intolerance to oral foods when the patient reports pain, has increasing abdominal girth, or has elevations in serum amylase and lipase levels. The patient needs to abstain from alcohol. Supplemental fat-soluble vitamins may be given.

• => Subjective data
• Health history
• Biliary tract disease
• Alcohol use
• Abdominal trauma
• Duodenal ulcers
• Infection
• Metabolic disorders
• -Note: Past health history: biliary tract disease, alcohol use, abdominal trauma, duodenal ulcers, infection, metabolic disordersMedications: Thiazides, NSAIDsSurgery or other treatments: Pancreas, stomach, duodenum, biliary tract, ERCP (endoscopic retrograde cholangiopancreatography)

• => Functional health patterns
• Alcohol abuseFatigueNausea, vomiting, anorexiaDyspneaPainAlso obtain the following important health information related to pertinent functional health patterns:
• Health perception–health management: alcohol abuse; fatigue
• Nutritional-metabolic: nausea and vomiting; anorexia
• Activity-exercise: dyspnea
• Cognitive-perceptual: severe midepigastric or left upper quadrant pain that may radiate to the back, aggravated by food and alcohol intake and unrelieved by vomiting

• => Objective data
• Restlessness, anxiety, low-grade feverFlushing, diaphoresisDiscoloration of abdomen/flankCyanosisJaundiceDecreased skin turgorDry mucous membranesPerform a focused physical assessment for the following clinical manifestations:General: restlessness, anxiety, low-grade feverIntegumentary: flushing, diaphoresis, discoloration of abdomen and flanks, cyanosis, jaundice; decreased skin turgor, dry mucous membranesTachypneaBasilar cracklesTachycardiaHypotensionAbdominal distention/tendernessDiminished bowel sounds
• => Respiratory: tachypnea, basilar crackles
• Cardiovascular: tachycardia, hypotension
• Gastrointestinal: abdominal distention, tenderness, and muscle guarding; diminished bowel sounds

↑ Serum amylase/lipase levels

Leukocytosis

Hyperglycemia

Hypocalcemia

Abnormal findings on ultrasonography/CT scans

Abnormal findings on ERCP

• Nursing diagnoses for the patient with acute pancreatitis may include, but are not limited to, the following:
• • Acute pain related to distention of pancreas, peritoneal irritation, obstruction of biliary tract, and ineffective pain and comfort measures• Deficient fluid volume related to nausea, vomiting, restricted oral intake, and fluid shift into the retroperitoneal space
• • Imbalanced nutrition: less than body requirements related to anorexia, dietary restrictions, nausea, loss of nutrients from vomiting, and impaired digestion
• • Ineffective self–health management related to lack of knowledge of preventive measures, diet restrictions, alcohol restriction intake, and follow-up care

Hypocalcemia: s/s & therapies

• **Acute Pancreatitis Planning:
• Relief of pain, Normal fluid and electrolyte balance, Minimal to no complications, No recurrent attacks

• **Acute Pancreatitis Nursing Implementation Health promotion
• Assessment and early treatment of predisposing/etiologic factors
• Early diagnosis/treatment of biliary tract disease
• Elimination of alcohol intake
• -The major factors involved in health promotion are (1) assessment of the patient for predisposing and etiologic factors and (2) encouragement of early treatment of these factors to prevent occurrence of acute pancreatitis.

Encourage early diagnosis and treatment of biliary tract disease, such as cholelithiasis.

Encourage the patient to eliminate alcohol intake, especially if there have been any previous episodes of pancreatitis. Attacks of pancreatitis become milder or disappear with the discontinuance of alcohol use.

• During the acute phase, it is important to monitor vital signs. Hemodynamic stability may be compromised by hypotension, fever, and tachypnea.
• Respiratory failure may develop in the patient with severe acute pancreatitis. Assess respiratory function (e.g., lung sounds, oxygen saturation levels). If ARDS develops, the patient may require intubation and mechanical ventilatory support.
• Monitor the response to IV fluids.

=> Monitor fluid and electrolyte balance Chloride, sodium, and potassium

• Hypocalcemia : Tetany, Calcium gluconate to treat
• Hypomagnesemia

• => Closely monitor fluid and electrolyte balance.
• Frequent vomiting, along with gastric suction, may result in decreases in chloride, sodium, and potassium levels.
• Because hypocalcemia can also occur, observe for symptoms of tetany, such as jerking, irritability, and muscular twitching. Numbness or tingling around the lips and in the fingers is an early indicator of hypocalcemia.
• Assess the patient for positive Chvostek’s sign or Trousseau’s sign.
• Calcium gluconate (as ordered) should be given to treat symptomatic hypocalcemia.
• Hypomagnesemia may also develop, necessitating the monitoring of serum magnesium levels.

• => Pain assessment and management
• Because abdominal pain is a prominent symptom of pancreatitis, a major focus of your care is the relief of pain. Pain and restlessness can increase the metabolic rate and subsequent stimulation of pancreatic enzymes. In addition, acute pain can contribute to hemodynamic instability. Morphine may be used for pain relief. Assess and document the duration of pain relief. Measures such as comfortable positioning and frequent changes in position assist in reducing the restlessness that usually accompanies the pain. Assuming positions that flex the trunk and draw the knees up to the abdomen may decrease pain.
• A side-lying position with the head elevated 45 degrees decreases tension on the abdomen and may help ease the pain
• .For the patient who is on NPO status or has an NG tube, provide frequent oral and nasal care to relieve the dryness of the mouth and nose. Oral care is essential to prevent parotitis. If the patient is taking anticholinergics to decrease GI secretions, there will be additional dryness of the mouth.
• If the patient is taking antacids to neutralize gastric acid secretion, they should be sipped slowly or inserted in the NG tube.

• Observe for fever and other manifestations of infection in the patient with acute pancreatitis.
• Respiratory infections are common because the retroperitoneal fluid raises the diaphragm, which causes the patient to take shallow, guarded abdominal breaths.
• Measures to prevent respiratory infections include turning, coughing, and deep breathing (TCDB) and assuming a semi-Fowler’s position.
• Other important assessments are observation for signs of paralytic ileus, renal failure, and mental changes.
• Determine the blood glucose level to assess damage to the β-cells of the islets of Langerhans in the pancreas.
• After pancreatic surgery, the patient may require special wound care for an anastomotic leak or a fistula.
• To prevent skin irritation, use measures such as skin barriers (e.g., Stomahesive Paste, Karaya Paste, or Colly-Seel Disc), pouching, and drains. In addition to protecting the skin, pouching also enables a more accurate determination of fluid and electrolyte losses and increases patient comfort. Sterile pouching systems are available. Consult with a clinical specialist or an enterostomal therapy nurse, if available.

Because of loss of physical and muscle strength, physical therapy may be needed.

Because frequent doses of opioids may be required for this patient during the acute stage, follow-up for assessment of possible opioid addiction may be indicated. This problem is more likely to occur with chronic pancreatitis than with acute pancreatitis.

Counseling regarding abstinence from alcohol is important to prevent the patient from experiencing future attacks of acute pancreatitis and development of chronic pancreatitis. Because cigarettes can stimulate the pancreas, smoking should be avoided.

=> Dietary teaching should include restriction of fats because they stimulate the secretion of cholecystokinin, which then stimulates the pancreas. Carbohydrates are less stimulating to the pancreas and are encouraged. Instruct the patient to avoid crash dieting and bingeing because they can precipitate attacks.

=>Instruct the patient and the caregiver regarding the recognition and reporting of symptoms of infection, diabetes mellitus, or steatorrhea (foul-smelling, frothy stools). These changes indicate possible ongoing destruction of pancreatic tissue. Teach the patient and caregiver about the prescribed regimen, including the importance of taking the required medications and following the recommended diet.

Important: how to avoid future attacks, teach of signs because we're looking foir reccurence: risk for chronic. notes: Stetorrhea: fatty or floating stool: pancreas loses ability to produce endo enzymes

• => Expected outcomes
• Have adequate pain controlMaintain adequate fluid volumeBe knowledgeable about treatment regimenGet help for alcohol dependence ( if appropriate)

Continuous, prolonged inflammatory, and fibrosing process of the pancreas

One is obstructive and another isn't obstructive: most likely just inflimmation

• => Etiology:
• key: alc & gal
• lAlcohol, gallstones, tumor, pseudocysts, trauma, systemic disease
• Acute pancreatitis
• Idiopathic
• -Chronic pancreatitis is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas.

The pancreas becomes progressively destroyed as it is replaced with fibrotic tissue. Strictures and calcifications may also occur in the pancreas.

Chronic pancreatitis can result from alcohol abuse; obstruction due to cholelithiasis (gallstones), tumor, pseudocysts, or trauma; and systemic diseases (e.g., systemic lupus erythematosus), autoimmune pancreatitis, and cystic fibrosis. In some patients, there may not be an identifiable risk factor (idiopathic pancreatitis). Chronic pancreatitis may follow acute pancreatitis, but it may also occur in the absence of any history of an acute condition.

As a result: pt can develop type 1 diabetes if they lose ability to produce insulin, abnormal albumin, low H&H,

1. Chronic obstructive pancreatitis: Gallstones cause inflammation of sphincter of Oddi

2. Chronic nonobstructive pancreatitis: Inflammation and sclerosis n head of pancreas and around duct


The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi in association with cholelithiasis.

Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis.

In nonobstructive pancreatitis, there is inflammation and sclerosis, mainly in the head of the pancreas and around the pancreatic duct.

This type of chronic pancreatitis is the most common form.

In the United States, chronic pancreatitis is found almost exclusively in individuals who abuse alcohol.

There may be a genetic factor that predisposes a person who drinks to the direct toxic effect of the alcohol on the pancreas.

• => Abdominal pain
• Located in the same areas as in acute pancreatitis
• Heavy, gnawing feeling; burning and cramplike
• Malabsorption with weight loss
• Constipation, jaundice, icteric urine, steatorrhea, diabetes mellitus
• --The pain is located in the same areas as in acute pancreatitis, but it is usually described as a heavy, gnawing feeling or sometimes as burning and cramplike. The pain is not relieved with food or antacids.The patient may have episodes of acute pain, but it usually is chronic (recurrent attacks at intervals of months or years).The attacks may become more and more frequent until they are almost constant, or they may diminish as pancreatic fibrosis develops. Some abdominal tenderness may be present.

Other clinical manifestations include symptoms of pancreatic insufficiency, such as malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes mellitus.

The steatorrhea may become severe, with voluminous, foul-smelling, fatty stools. Urine and stool may be frothy.

• => Chronic Pancreatitis Complications
• Pseudocyst formation
• Bile duct or duodenal obstruction
• Pancreatic cancer
• Chronic pancreatitis is also associated with a variety of complications. These include pseudocyst formation, bile duct or duodenal obstruction, pancreatic ascites or pleural effusion, splenic vein thrombosis, pseudoaneurysms, and pancreatic cancer.

Confirming diagnosis can be challenging

Based on signs/symptoms, laboratory studies, and imaging

• => Laboratory tests
• Serum amylase/lipase levels: May be ↑ slightly or not at all

↑ Serum bilirubin level↑ Alkaline phosphatase level (more specific)

Mild leukocytosis

↑ Sedimentation rate (but elevated in a lot of chronic, autoimmune conditions)

• => Diagnostic Studies
• ERCP
• CT, MRI, MRCP, abdominal and/or endoscopic ultrasonography
• Stool samples for fat content: ↓ Fat-soluble vitamin and cobalamin levels
• Glucose intolerance/diabetes

NOTES: ERCP is used to visualize the pancreatic and common bile ducts. Imaging studies such as CT, MRI, MRCP, abdominal ultrasonography, and EUS are useful in patients with chronic pancreatitis. These procedures show a variety of changes, including calcifications, ductal dilation, pseudocysts, and pancreatic enlargement.Stool samples are examined for fecal fat content. Deficiencies of fat-soluble vitamins and cobalamin, glucose intolerance, and possible diabetes may also be found in patients with chronic pancreatitis. A secretin stimulation test may be used to assess the degree of pancreatic function.

Analgesics for pain relief (morphine or fentanyl transdermal patch [Duragesic])

• Diet : Bland, low-fat, Small, frequent meals
• But if diabetes, then carb control

No smoking

No alcohol or caffeine

Vitamins should be given with the meals, but if they'res nothing to digest, then pt shouldn't be getting it.

• => When the patient with chronic pancreatitis is experiencing an acute attack, the therapy is identical to that for acute pancreatitis. At other times, the focus is on prevention of further attacks, relief of pain, and control of pancreatic exocrine and endocrine insufficiency.
• It sometimes takes frequent doses of analgesics (morphine or fentanyl transdermal patch [Duragesic]) to relieve the pain if dietary measures and enzyme replacement are not effective.
• Diet, pancreatic enzyme replacement, and control of the diabetes are measures used to control the pancreatic insufficiency. The diet should be bland and low in fat.Small, frequent meals that are low in fat content are recommended to decrease pancreatic stimulation. Smoking is associated with accelerated progression of chronic pancreatitis. Teach the patient not to consume alcohol and caffeine beverages.

=>Pancreatic enzyme products (PEPs) such as pancrelipase (Creon, Zenpep, and Pancrease) contain amylase, lipase, and trypsin and are used to replace the deficient pancreatic enzymes.

=>They are usually enteric coated to prevent their breakdown or inactivation by gastric acid.

=>Bile salts are sometimes given to facilitate the absorption of the fat-soluble vitamins (A, D, E, and K) and prevent further fat loss. If diabetes develops, it is controlled with insulin or oral hypoglycemic agents.

=>Acid-neutralizing drugs (e.g., antacids) and acid-inhibiting drugs (e.g., H2-receptor blockers, proton pump inhibitors) may be given to decrease HCl acid secretion but have little overall effect on patient outcomes.

=> Antidepressants, such as nortriptyline (Aventyl), have been shown to reduce the neuropathic pain associated with chronic pancreatitis. For chronic, adjuct therapy

Not very common with Chronic Panc..Indicated when biliary disease is present or if obstruction or pseudocyst develops

Diverts bile flow or relieves ductal obstruction

Pancreatic drainage

ERCP with spincterotomy and/or stent placement

=> notes: When biliary disease is present or if obstruction or pseudocyst develops, surgery may be indicated. Surgical procedures can divert bile flow or relieve ductal obstruction.

A choledochojejunostomy diverts bile around the ampulla of Vater, where there may be spasm or hypertrophy of the sphincter. In this procedure, the common bile duct is anastomosed into the jejunum.

Another type of surgical diverting procedure is the Roux-en-Y pancreatojejunostomy, in which the pancreatic duct is opened and an anastomosis is made with the jejunum.

Focus is on chronic care and health promotion

• => Patient and family teaching
• Dietary control
• Pancreatic enzyme with meals/snack
• Observe for steatorrhea
• Monitor glucose levels
• Antacids after meals and at bedtime
• No alcohol

=> notes: Except during an acute episode, the focus of nursing management is on chronic care and health promotion. Instruct the patient to take measures to prevent further attacks. Dietary control, along with consistency of other treatment measures, such as taking pancreatic enzymes, is essential. These are usually taken with meals

• Description
• 1. Most pancreatic tumors are highly malignant,rapidly growing adenocarcinomas originatingfrom the epithelium of the ductal system.

2. Pancreatic cancer is associated with increasedage, a history of diabetes mellitus, alcohol use,history of previous pancreatitis, smoking, ingestionof a high-fat diet, and exposure to environmentalchemicals.

3. Symptoms usually do not occur until the tumoris large; therefore, the prognosis is poor.

4. Endoscopic retrograde cholangiopancreatographyfor visualization of the pancreatic ductand biliary system and collection of tissue andsecretions may be done.

• B. Assessment
• 1. Nausea and vomiting2. Jaundice3. Unexplained weight loss4. Clay-colored stools5. Glucose intolerance6. Abdominal pain

• C. Interventions
• 1. Radiation2. Chemotherapy3. Whipple procedure, which involves a pancreaticoduodenectomywith removal of the distal third of the stomach, pancreaticojejunostomy,gastrojejunostomy, and choledochojejunostomy(Fig. 52-4)4. Postoperative care measures and complications are similar to those for the care of a client with pancreatitis and the client following gastric surgery; monitor blood glucose levels for transient hyperglycemia or hypoglycemia resulting from surgical manipulation of the panc

This surgical procedure involves resection of the proximal pancreas, adjoining duodenum and distal portion of the stomach, and distal portion of the common bile duct. An anastomosis of the pancreatic ducct, common bile ducct, and stomach to the jejunum is done.