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Marcus Rowell Cueno, RN


• Pancreatitis - inflammatory process of the pancreas
o May be acute or chronic
o Severity depends on extent of inflammation and tissue destruction
o Range from edema and inflammation to necrotizing hemorrhagic
pancreatitis with fibrosis and tissue death

Acute Pancreatitis

• Major Pathophysiologic Processes Are:
o Lypolysis
o Proteolysis
o Necrosis of Blood Vessels
o Inflammation

Etiology of Pancreatitis

• Contributing factors may be alcoholism and biliary tract disease with
• Trauma, surgical minipulation, the Whipple procedure, and partial
• Viral infections, gactric or duodenal ulcers, tumors, cysts, abcesses,
• Drug toxicities and oral contraceptives


• Middle-aged males after heavy alcohol consumption
• Females after biliary tract disturbances
• Prognosis better if unrelated to alcohol
• 10% die, 60% if alcohol related

Nursing Care

• Assessment - History very important; ask re: abdominal pain, alcohol
consumption, high fat meals, family history, biliary or pancreatic problems,
abdominal surgery, other contributing causes previously listed

Physical Assessment/Clinical Manifestations

• Abdominal pain; mid or ULQ area; radiates to back, left flank or left shoulder
and aggravated by alcohol, fatty meal, lying in recumbent position; relieved
with fetal position or sitting upright and bending forward
• Weight loss, N&V, jaundice, gray-blue discoloration of abdomen (Cullen’s
sign) and the flanks (Turner’s sign)
• Bowel sounds absent or decreased (paralytic ileus), abdominal tenderness,
rigidity, and guarding (peritonitis); palpable mass
• Elevated temp, tachycardia, decreased BP, decreased or abnormal breath
sounds, dyspnea or orthopnea
• Changes in behavior and sensorium
Diagnostic Assessment

• Elevated serum amylase, lipase, glucose, bilirubin, alkaline phosphatase,
• Elevated urine amylase
• Decreased serum calcium
• CT
• Chest x-ray
• Ultrasound and MRI
• Bentiromide test to assess pancreatic functioning

Nursing Diagnoses (Analysis)

• Pain related to the effects of pancreatic inflammation and enzyme leakage
• Altered nutrition: Less than body requirements related to the effects of
pancreatic dysfunction, N&V, and anorexia AEB____
• Others???

Planning/Expected Outcomes

• The client will experience relief of abdominal pain by_____
• The client will have sufficient nutritional intake to maintain body weight
with a decrease in pancreatic stimulation by___

Non-Surgical Management

• Fasting to rest pancreas and reduce enzyme secretion
• IV fluids, NG tube (must have bowel sound before removed)
• Drug therapy and comfort measures

Drug Therapy

• Meperidine
• Nitroglycerine
• Antispasmodics
• Carbonic anhydrase inhibitor
• Antacids
• Histamine H2-receptor antagonists
• Calcium gluconate

• Adrenocortical steroids
• Aprotinin
• Glucagon
• Somatostatin
• Albumin (if shock present)
• Chronic Pancreatitis - Pancreatin and Insulin used

Comfort Measures

• Fetal position
• Oral hygiene -NG tube
• Lower anxiety level - explain procedures, diversional activities, encourage
visitors, encourage expression of emotions

Surgical Management

• Usually not indicated
• Complications such as cyst and abcess may necessitate surgical drainage
• General pre-op measures, NG- tube, IV fluids, teaching re: pancreatic
drainage tube and what to expect
• Drainage tubes may be connected to low suction (80mmHg or less)

Postoperative Care-Interventions

• `Monitor drainage tubes for patency, kinks, ordered suction pressure,
• Record intake and output, character of drainage
• Meticulous skin care and dressing changes

• Skin barriers -Stomahesive wafer, aluminum paste; ET nurse
• Begin with small frequent, moderate to high carbohydrate, high-protein,
low-fat meals; bland; no caffeine
• Ensure, Isocal to supplement diet, fat-soluable and other vitamin/mineral

Continuing Care

• Health teaching to avoid further episodes
• Acute pain, jaundice, clay-colored stools, dark urine call Dr.
• Limit physical activity
• Home visits, AA, family support (Al-Anon)


• Expected outcomes from nursing diagnoses should be evaluated as well as
nursing interventions.

Chronic Pancreatitis

• Chronic Calcifying Pancreatitis (CCP) - alcohol induced; protein plugs ducts
causing inflammation and fibrosis
• Chronic Obstructive Pancreatitis - develops from inflammation, spasm, and
obstruction of the sphincter of Oddi
• Review Patho notes for other changes!

Key Features of Chronic Pancreatitis

• Intense burning or gnawing abdominal pain
• Abdominal tenderness; ascites; LUQ mass (cyst or abscess)
• Respiratory compromise
• Steatorrhea; clay-colored stools
• Weight loss; jaundice; dark urine
• Polyuria, polydipsia, polyphagia (diabetes)

Nursing Care/Interventions

• Same as with acute
• Analgesia important for pain
• Enzyme replacement essential - give before or with meals, swallow without
chewing, mix with applesauce or fruit juice, not protein-containing foods,
wipe lips after taking meds, monitor serum uric acid levels for increase
(caused by pancrelipase)
Surgical Invervention

• Not a primary intervention
• Done for abscess, cyst, or underlying cause
• Pancreaticojejunostomy to relieve obstruction
• Whipple procedure for pancreatic cancer



• CHOLECYSTITIS - inflammation of the gallbladder
• Acute - usually associated with cholelithiasis (gallstones); may be caused by
bacteria in absence of stones
• Trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder
wall having a toxic effect

• Bile, impaired circulation, edema, and distention cause ischemia, resulting
in tissue sloughing with necrosis and gangrene
• Perforation may occur causing an abcess or peritonitis
• Interfere with bile for fat digestion

Chronic Cholecystitis

• Results with persistent inefficient emptying of bile by the gallbladder
• May be caused by or lead to the formation of gallstones
• Gallbladder becomes fibrotic and contracted which results in decreased
motility and deficient absorption
• Pancreatitis and cholangitis (inflammation of the common bile duct) can
occur as complications due to back up of bile

• Bile obstruction leads to jaundice which may be extrahepatic or intrahepatic
• Circulating levels of bilirubin are increased, and jaundice occurs if more
than 2 mg/dL

Cause of Cholecystitis

• Exact etiology unknown
• Formation of gallbladder calculi, trauma, decreased blood supply, prolonged
anesthesia/surgery, adhesions, edema, neoplasms, long-term fasting,
prolonged dehydration, prolonged immobility, excessive opioid use,
anatomic problems sedentary lifestyle, familial tendency, obesity, and


• Sedentary life style
• Familial tendancy
• Obesity
• Diabetes
• White women

Symptoms and Assessment

• Episodic or vague abdominal pain or discomfort that may radiate to right
• Pain after high fat or high volume meal
• Anorexia
• Nausea or vomiting

• Dyspepsia
• Eructation
• Flatulence
• Feeling of abdominal fullness
• Pruritis (itching) or burning sensation of skin
• Rebound tenderness (Blumberg’s sign)
• Fever
• Jaundice, clay-colored stools, dark urine, steatorrhea (most common with
chronic cholecystitis)

Diagnostic Assessment

• Elevated serum levels of alkaline phosphatase, aspartate aminotransferase
(AST), Lactate dehydrogenase (LDH), direct and indirect bilirubin, WBC, and
• Oral cholecystogram (OCG)
• Gallbladder (GB) radiographic series
• Upper GI radiographic series
• Technetium-labeled acetanilido iminodiacetic acid (99mTc HIDA)
• Ultrasonography of gallbladder (has replaced OCG)


• Non-surgical initially to rest inflammed gallbladder and relieve pain
• Diet Therapy - avoid high fat and high volume meals, NG tube to
decompress stomach, smaller more frequent meals
• Drug Therapy, - opioid analgesics (Demerol), antispasmodic agents, and

Surgical Management

• CHOLECYSTECTOMY - removal of the gallbladder
• Pre-op Care - teaching re: deep breathing, coughing, splinting, early
ambulation, NPO
• Operative Procedure - T-tube, Penrose or Jackson-Pratt drain for
serosanguineous, bile stained drainage.

Postoperative Nursing Care

• Incisional pain relief (PCA pump)
• Coughing and deep breathing
• Antiemetics
• Wound and T-tube care; drainage irritating
• NPO or NG tube
• 4-6 weeks recovery

Nursing Care: T-Tube

• Assess drainage; bloody, green-brown; report more than 1000ml/day
• Administer bile salts (Decholin)
• Inspect skin around T-tube insertion; keep dressing dry
• Keep drainage system below level of gallbladder

• Never clamp, irrigate, or aspirate a T-tube without a physician’s order
• Assess drainage system for kinks, pulling, or tangling of tubing
• When ordered, raise the drainage bag to level of abdomen (4th or 5th post-
op day) and assess client for feelings of fullness, nausea, or pain

• Clamp T-tube for 1-2 hours before and after meals as ordered; assess for
tolerance of food
• Observe stools for return of brown color 7-10 days post-op

Laparoscopic Cholecystectomy

• Treatment of choice since 1989
• 10 mm incision at umbilicus, abdominal cavity insufflated with 3-4L carbon
• Trocar catheter inserted and laparoscope is passed through it and attached
to a video camera so abdominal organs can be viewed on monitor; laser
used to dissect.

• Reduces risk of wound complications
• Early ambulation promotes absorption of carbon dioxide and decreased
"free air pain"
• Requires less pain med
• Return to usual activities, including work, much sooner (1-3 weeks)


• The presence of one or more gallstones in biliary tract; most common
• Contributing factors: excessive bile salt losses, decreased gallbladder-
emptying rates, supersaturation of bile with cholesterol, changes in bile
concentration or bile stasis within the gallbladder
• Causes cholecystitis

Composition of Gallstones

• Substances normally found in bile such as:
• Cholesterol
• Bilirubin
• Bile salts
• Calcium
• Proteins

Types of Gallstones

• Cholesterol Stones
• Result of metabolic imbalances of cholesterol and bile salts
• Most common type in U.S.

• Pigment Stones
• Result of metabolic imbalances of unconjugated bilirubin
• Small, brown or black
• Black stones composed of calcium bilirubinate; most common


• Familial tendency related to dietary habits, excessive cholesterol intake,
and sedentary lifestyles
• Seen more frequently in obese clients with impaired fat metabolism
• Low-calorie or liquid diets cause liberation of cholesterol from tissues and
excretion as crystals in bile

Women’s Health Considerations

• Incidence of gallbladder disease is higher in women, especially European
American women.
• By age 60, nearly one-third of obese women develop biliary disease
• Pregnancy tends to increase gallstone formation

• Pregnancy and estrogen cause delayed muscular contraction of gallbladder
which decrease rate of bile emptying
• Incidence of gallstones higher in women who have had multiple
• Cholelithiasis seen with hemolytic blood disorders, bowel disease, and after
jejunoileal bypass surgery for obesity, and diabetes

Incidence of Cholelithiasis

• Higher in women; males 50 and older
• Caucasians and Native Americans (Navajo and Pima tribes) have higher
• Prevalent in Asian-Americans and African-American
• More than 20 million diagnosed in U.S.
• One million cases reported yearly

Assessment and Symptoms

• Severity of pain and presentaion depend on mobility, size, location,
obstruction, and inflammation
• Initially a steady, mild ache in mid-epigastric area; may radiate to right
shoulder or back; RUQ pain of abdomen
• Biliary colic may include tachycardia, pallor, diaphoresis, and prostration; N


• Same lab tests as cholecystitis
• Abdominal x-ray
• Oral or IV cholecystogram
• Ultrasound (test of choice); 95% accurate
• Percutaneous transhepatic cholangiography

Nonsurgical Interventions

• Rest inflammed gallbladder
• Diet Therapy - low fat, vitamins A, D, E, K, bile salts
• Drug Therapy - same as before; Questran
• Bile acid therapy (Ursodiol - Actigall)
• Extracorporeal shock wave lithotripsy; 3 or fewer stones
• Percutaneous transhepatic biliary catheter insertion

Surgical Intervention

• Cholecystotomy - opening made and stones removed
• Choledocholithotomy - incision into common bile duct to remove stones

Nursing Care: Same as with Cholecystectomy and T-Tube
• The nurse also instructs the client to report symptoms of biliary tract
disease, including jaundice, darkened urine, light-colored stools, pain, fever,
or chills



• Associated with liver disorders
• Yellowish coloration visible when bilirubin levels in the blood 3x normal
• alteration in bilirubin metabolism or obstruction to flow of bile into the duct
• first seen in sclera and skin

Types of Jaundice

• Hemolytic - increased RBC breakdown, blood transfusion, sickle cell crisis,
hemolytic anemia
• Hepatocellular - Hepatic carcinoma or hepatitis; alteration in bilirubin
uptake, conjugation or excretion
• Obstructed - impeded flow of bile through liver; liver tumors, hepatitis or

Jaundice and Hyperbilirubinemia

• Refer to Patho notes for forms of bilirubin (unconjugated and conjugated)
• Excess production of bilirubin
• Impaired uptake of unconjugated bilirubin
• Impaired conjugation of bilirubin
• Decreased excretion of conjugated bilirubin


• Primarily viral in origin but can be caused by bacteria, drugs, and chemicals
• Viral Hepatitis - A,B,C,D,E; cytomegalovirus, Epstein-Barr herpes,
coxsackievirus, and rubella
• Many cases asymptomatic - undiagnosed

• Up to 50% of adults in U.S. have been infected with Type A virus
• Diagnosis based on presence of antigens and antibodies
• Infection with one type provides immunity to that type but not to others


• Occurs worldwide in children
• fecal-oral route, contaminated food or water
• Incubation of 15-50 days
• Found in feces before and after symptoms
• In blood only briefly

• Transmitted through exposure to blood/products, sexual & perinatal contact
• Incubation 45-180 days
• Complex DNA structure with 3 antigens


• Transmitted by exposure to blood/products, sexual contact
• Incubation 14-180 days
• RNA virus


• Delta virus always follows HBV
• Chronic carriers of HBV at risk
• Incubation period not known
• Routes of transmission same as HBV


• Fecal-oral transmission
• Mostly in underdeveloped countries with poor sanitation
• Incubation 15-64 days
• Based on diagnosis of exclusion - no serologic tests

Hepatitis and Liver Damage

• Inflammation causes liver tissue damage
• Bile flow may be interrupted & inflammation of the gall bladder may occur
• Without complications, liver cells will regenerate & normal function returns
• Systemic effects are: immune reactions (rash, angioedema, arthritis, fever,
malaise, glomerulonephritis, vasculitis; many asymptomatic, especially

Phases of Hepatitis

• Pre-icteric Phase: 1-2 days before onset of jaundice, anorexia, nausea,
vomiting, RUQ pain, constipation or diarrhea, malaise, headache, fever,
joint pain, urticaria, weight loss, liver and spleen enlargement

• Icteric Phase: 2-4 weeks, jaundice, pruritis, dark urine, bilirubinuria, light
stools, fatigue, liver enlargement, tenderness, and weight loss

• Post-icteric Phase: convalescent or recovery phase, lasts weeks to months,
fatigue, general malaise, spleen returns to normal before liver, relapses
may occur

• Hepatitis mortality rate low, high in elderly


• Can become chronic persistent with delayed convalescence
• Chronic active - idiopathic, may lead to cirrhosis, persistent
• Fulminant - severe necrosis, liver failure and death
Diagnosis of Hepatitis

• Liver studies, serologic tests, biopsy
• Liver tenderness, hepatomegaly, myalgia, splenomegaly, arthralgia,
abdominal pain, fever, irritability, lethargy, malaise, N&V

Nursing Diagnoses/Analysis

• Altered nutrition
• Activity intolerance
• Anxiety
• Pain
• Body image disturbance
• Fatigue
• Knowledge deficit


• Usually at home
• Rest
• Adequate diet, high protein and carbohydrate, vitamins
• Avoid alcohol and drugs (detoxified in liver), fatty foods
• Vaccine, gamma globulin, interferon

Nursing Care/Interventions

• Comfort measures
• Small frequent feedings; adequate fluid intake;, oral hygiene
• Antiemetics (Tigan, Dramamine)
• Monitor activities; weak, build strength
• Promote return of normal liver function

Other Types of Hepatitis

• Toxic and Drug-Induced: may occur after injection, ingestion, inhalation of
chemical substances, systemic poisons, drugs (acetaminophen), drug
sensitivity; liver necrosis occurs within days
• Idiopathic: Autoimmune form; usually affects women; treated with
corticosteroids and immunosuppressive agents


• Winningham, GI Disorders, Case Study 8: Hepatitis A
• Work in groups
• Critical thinking activity
• Be thorough!


• Chronic, progressive disease; long, tortuous
• Extensive cell destruction
• Disorganized regrowth with fibrous distortion of blood vessels and bile ducts
• Lobes become irregular in shape and size, impeding vascular flow
• Alcohol most common cause; men 40-60; high death rate; unpleasant
disease course

• Alcoholic (Laennec’s) -early changes reversible, fat accumulation; later scar
tissue forms and irreversible; alcohol or malnutrition cause
• Postnecrotic - complication of viral, toxic, idiopathic; scar tissue
• Cardiac - chronic right sided heart failure with cor pulmonale, constrictive
pericarditis, and tricuspid insufficiency
• Biliary - chronic biliary obstruction and infection; scar tissue

Early Manifestations

• GI disturbances, anorexia, flatulence, N&V, changes in bowel habits d/t
alterations in metabolism
• Abdominal pain, fever, lassitude, weight loss, liver and spleen enlargement

Late Manifestations

• Jaundice, peripheral edema, ascites, skin lesions, hematologic disorders,
endocrine disturbances, peripheral neuropathies; liver becomes small and
nodular; bile salts collect under the skin causing severe pruritus, anemia,
clotting disorders
• Every body system affected! (See picture in textbook.)

Complications of Cirrhosis

• Portal hypertension
• Ascites
• Bleeding esophageal varices
• Coagulation defects
• Jaundice
• Portal-systemic encephalopathy (PSE) with hepatic coma
• Hepatorenal syndrome


• Serum enzymes
• Bilirubin
• Serum Proteins
• Serum Ammonia
• Prothrombin time
• Serum protein & albumin decreased in chronic/severe liver disease
• Abdominal x-ray
• Upper GI series
• CT of abdomen
• Esophagogastroduode-noscopy(EGD)
• Injection sclerotherapy

Portal Hypertension & Esophageal Varices

• Compression and destruction of portal & hepatic veins cause obstruction to
blood flow causing portal hypertension
• Collateral circulation develops as a compensatory mechanism particularly in
esophageal area
• Varicosities also develop where systemic and collateral circulations join,
causing esophageal and gastric varices/hemorrhoids
• Collateral vessels are fragile, fairly non-distensible, so they don’t tolerate
high pressure; bleed easily
• The bigger and more tortuous the vessel, the more it will bleed; mortality
rate high
• Reoccurrence of bleeding high; precipitated by alcohol, coarse food,
straining, vomiting, sneezing, lifting

Peripheral Edema & Ascites

• Caused by change in osmotic pressure due to impaired synthesis of albumin
and increased portacaval pressure from PHT
• Edema at ankles and presacral areas
• Ascites: fluid collection in peritoneal cavity results in increased abdominal
girth and weight gain
• ADH, water & sodium retention cause K+ loss, decreased output &

• Decreased blood flow and other problems cause renal damage
• Increased levels of ammonia in blood cause hepatic encephalopathy,
lethargy, coma
• progressive disorientation, impaired judgement, and confusion occur
• Asterixis, liver flap etc.