Caring for Patients with Liver, Gallbladder, and Pancreatic Conditions
Caring for Patients with Liver, Gallbladder, and Pancreatic Conditions
Liver Anatomy
Location:
Right, center of the abdominal cavity beneath the ribs.
Cannot normally be palpated in healthy individuals.
Characteristics:
Reddish-brown, soft, smooth.
Well-supplied with blood.
Liver Blood Supply
Dual blood supply with two major vessels:
Hepatic artery: Supplies 1/3 of the blood.
Portal vein: Supplies 2/3 of the blood, carrying blood that drains from the gut.
Blood Flow:
Huge volume of blood carried every minute through the blood vessel network of the liver which permits regulation of blood; returns to the inferior vena cava.
Liver Cells
Hepatocytes:
Comprises 60% of liver cells; secrete bile continuously.
Kupffer Cells:
Detoxifies blood and produces antibodies.
Capable of removing and destroying old RBCs, bacteria, and foreign material (phagocytic).
Composition of Bile
Mainly Water:
Excretory Function:
Carries excess bilirubin, urea, cholesterol for elimination in feces.
Bile Salts:
Emulsify fats and are essential for digestion and absorption of fats.
Practice Question
Which cells are important for the liver's antibody and immunity function?
A. Hepatocytes
B. Kupffer cells
C. Bile-producing cells
D. Exocrine cells
Hepatobiliary Tree
Bile leaves liver via hepatic ducts.
Connection to Gallbladder:
Hepatic duct joins cystic duct of gallbladder, forming the common bile duct (CBD).
Pathway to Duodenum:
Leads to the duodenum where it is joined by the pancreatic duct at the hepatopancreatic ampulla (Ampulla of Vater).
Regulation of Bile Flow:
Flow of bile into the duodenum is regulated by the Sphincter of Oddi.
Functions of Liver
Metabolism:
Receives nutrients, converts them, or re-packages them in usable forms.
Manufactures bile.
Detoxification:
Antibody production.
Regulation:
Blood clotting and recycling of hemoglobin.
Metabolism Function
Produces bile for fat digestion:
Produces about 500 ml of bile per day.
Emulsifies fats for digestion.
Excretes drugs, waste, bilirubin, and excess cholesterol.
Storage Functions:
Stores iron, vitamins (A, D, E, K, and B-12).
Stores excess glucose as glycogen.
Synthesizes, recycles, and eliminates cholesterol.
Protein Metabolism
Bacterial action in intestines during protein digestion creates a byproduct: ammonia.
Ammonia is transported in blood (hepatic-portal circulation) to the liver where it is detoxified by converting it to urea, which is then excreted by the kidneys in urine.
Importance of Ammonia Levels:
Ammonia is toxic to body cells, particularly neurons.
Normal ammonia levels: 10-80 mcg/dL.
Detoxification Function
Filtration of Blood:
Removes drugs, alcohol, chemicals, and bacteria from blood.
Changes harmful substances to less harmful ones.
Produces immune complexes and antibodies.
Regulation Function
Synthesis of Clotting Factors:
Prothrombin and fibrinogen are synthesized.
Synthesizes specific proteins: albumin which helps maintain blood volume by pulling tissue fluid into capillary circulation.
Regulates blood composition by removing old RBCs.
Excretes bilirubin into bile for elimination in feces.
Practice Question
If a lab report indicates a client’s albumin level is low, what physiological effect should a nurse check for?
A. Cerebral edema
B. Peripheral edema
C. Increased total protein level
D. Decreased clotting ability
Bilirubin
Characteristics:
Inert pigment; a breakdown product of hemoglobin.
Must be converted by the liver into a water-soluble compound that can be excreted in bile.
Bilirubin in Small Intestine:
Converted in the intestine to urobilinogen which colors feces.
A small amount is re-absorbed into blood, filtered, and excreted in the kidneys.
Blood Values:
Only a small amount of bilirubin should be in the blood.
Total serum bilirubin: 0.1 - 1.2 mg/dL.
Elevated levels can cause deposits of the pigment in body tissues, leading to jaundice.
Jaundice/Icterus
Description:
Abnormally high accumulation of bilirubin in blood results in pigment deposits in body tissues.
May first be noted in the sclera of the eye and palate.
Skin color changes range from pale yellow to golden orange.
Urine becomes dark as excess bilirubin is excreted.
Data Collection for Jaundice:
Inspection of the palate, mucous membranes, sclera, skin.
Check palms of hands and soles of feet.
In dark-skinned persons: inspect sclera, buccal membranes, palms, and soles.
Types of Jaundice
Hemolytic:
Excessive destruction of RBCs.
Liver cannot remove bilirubin fast enough.
Intrahepatic:
Liver disease interferes with the liver’s ability to remove bilirubin from blood or change it into a water-soluble form for elimination.
Obstructive:
Bile flow is obstructed between the liver and duodenum, leading to clay-colored stools.
Practice Question
A patient has hemolytic jaundice. Which lab test result is expected?
A. Elevated serum bilirubin level
B. Decreased serum protein
C. Elevated hemoglobin and RBC count
D. Elevated white blood cell count
Follow-Up:
If a patient presents with dark colored urine, jaundice, and clay-colored stools, which type of jaundice is this?
A. Hemolytic
B. Obstructive
C. Intrahepatic
Management of Jaundice
Definition:
Jaundice is an impairment of bilirubin breakdown.
Excess bile salts in skin cause pruritis.
Management Strategies:
Recommendations include wearing cool, loose clothing, taking tepid water baths, and using bile acid sequestrants (e.g., cholestyramine/Questran) to treat itching associated with biliary disease.
These medications bind with bile salts and are excreted in feces.
If obstructive jaundice is diagnosed, surgery may be required.
Practice Question
Oatmeal baths are ordered for a patient with jaundice. What is the chief reason for this?
A. Relief of paralytic ileus
B. Relief of bloating
C. Alleviation of pruritis associated with jaundice
D. Reducing the fever associated with jaundice
Practice Question
A nurse identifies yellow skin in a liver cancer patient. What is the cause?
A. Abnormally high concentrations of bilirubin in blood
B. Excessive production of RBCs
C. Excess production of albumin
D. Destruction of platelets in the blood
Diagnostic Tests
Common Diagnostic Procedures:
Ultrasound: Used to visualize structures.
Scans: CT and MRI, Radioisotope, Angiography.
Liver Biopsy:
Percutaneous with ultrasound or CT guidance.
Transvenous or Laparoscopic.
Nursing Responsibilities for Liver Biopsy:
No ASA/NSAIDs one week prior.
Check coagulation and CBC beforehand.
Patient should be in supine or left lateral position.
NPO for 6-8 hours prior; likely to receive sedation.
After a percutaneous biopsy, the patient should lie on right side for 2-6 hours and be monitored for bleeding.
Transvenous Liver Biopsy
Procedure:
Conducted via the jugular, antecubital, or femoral vein.
Practice Question
After a percutaneous liver biopsy, the nurse reinforces instructions to:
A. Avoid alcohol for 8 hours
B. Remain NPO for 24 hours
C. Lie on the right side for 2 hours
D. Save all stools to check for blood
Practice Question
What is the primary reason to have a patient lie on their side following a liver biopsy?
A. To immobilize the diaphragm
B. To facilitate full chest expansion
C. To reduce the likelihood of bleeding
D. To minimize danger of aspiration
Practice Question
Which finding in the first 24 hours after a liver biopsy indicates a complication from the procedure?
A. Anorexia, nausea, and vomiting
B. Abdominal distention
C. Pulse 112, blood pressure 100/60
D. Pain at the biopsy site
Blood Studies of Liver
Liver Function Tests (LFTs):
ALT: Liver specific
AST: Aspartate aminotransferase
LDH: Lactate dehydrogenase
Bilirubin: Total and direct levels assessed.
Albumin: Normal levels: 3.5-5 g/dL.
Prothrombin time: Measures clotting ability which indicates liver function.
Fibrinogen level: Another indicator of hepatic function.
GGT: Gamma-glutamyl transferase, shows damage to liver, helpful in diagnosing alcohol abuse.
Practice Question
If a patient has liver disease, which lab result places them at the most risk for bleeding?
A. Elevated liver enzymes
B. Low albumin
C. Low vitamin K
D. Elevated bilirubin
Cirrhosis
Definition:
Chronic, repeated inflammation causing widespread liver cell destruction, fibrosis, scarring, and ultimately, loss of function.
Characteristics:
Liver becomes hardened, nodular, lumpy, and eventually atrophies, impairing blood and lymph flow; leads to permanent damage.
Predisposing Factors/Causes
Chronic, excessive alcohol ingestion (Laennec’s Cirrhosis).
Chronic Hepatitis (B, C).
Exposure to toxins.
Biliary obstructions.
Severe right-sided heart failure.
Data Collection: Cirrhosis
Early Stages:
Symptoms include dull, aching RUQ pain, malaise, fatigue, anorexia, change in bowel habits, nausea.
Later Stages:
Symptoms include jaundice, protruding abdomen with dilated abdominal veins and protruding umbilicus (ascites), shortness of breath, peripheral edema, bleeding tendencies, spider angiomas, and increased infections.
Complications of Cirrhosis
Portal Hypertension:
Ascites.
Esophageal Varices.
Encephalopathy:
Hepatic Coma.
Hepatorenal Syndrome.
Blood Clotting Defects.
Portal Hypertension
Definition:
Persistent elevated pressure in the portal vein.
Effects:
Blood flow from gut meets increasing resistance in the scarred tissue of the liver.
Complications Related to Delayed Blood Flow
Swelling in the legs and abdomen (ascites) and pleural effusions.
Lack of albumin (hypoalbuminemia) causes fluid shift.
Enlargement of the spleen (splenomegaly).
Decreased white blood cells and platelets.
Can cause bleeding/ congestion of blood leading to dilated collateral veins.
Prominent abdominal veins.
Spider angiomas.
Rectal varices.
Management of Portal Hypertension
Antihypertensives:
E.g., beta-blockers.
Dietary Modifications:
Sodium and fluid restrictions.
Diuretics:
To decrease fluid retention, e.g., spironolactone/Aldactone (K-sparing diuretic).
Esophageal Varices
Definition:
Dilated, over-distended esophageal veins.
Thin-walled, fragile, blood-filled veins that are easily traumatized.
Asymptomatic but subject to rupture, which poses the danger of massive, life-threatening hemorrhage.
Risks for Hemorrhage
Vomiting.
Reflux of stomach acid.
Swallowing large, poorly chewed pieces of food or rough foods.
Valsalva maneuver: lifting, straining, coughing, sneezing.
Treatment of Varices
Prevention of Initial Hemorrhage:
Soft diet.
Use of antihypertensives.
Avoiding the Valsalva maneuver.
Limiting strenuous activity.
Management of Acute or Recurrent Hemorrhage:
Endoscopic injection sclerotherapy.
Ligation/banding of vessels.
Use of vasopressors.
Shunts:
TIPS (Transjugular Intrahepatic Portosystemic Shunt) diverting blood flow from distended channels, bypassing the liver to alleviate pressure on esophageal veins and prevent further bleeding episodes.
Balloon Tamponade
Emergency Treatment for Bleeding Varices:
Direct pressure on bleeding veins using devices such as the Sengstaken-Blakemore tube or Minnesota tube.
Nursing Considerations:
Elevate the head of bed (HOB).
Protect airway—do not leave patient alone.
Must periodically deflate esophageal balloon to prevent necrosis.
Practice Questions
Q1: A client with bleeding varices has balloon tamponade. The most important nursing action is:
A. Monitor IV fluids
B. Check that a clamp is at the bedside.
C. Regularly observe respiratory status.
D. Check that balloon is deflated on regular basis.
Q2: Following a Sengstaken-Blakemore tube insertion in a client with bleeding varices, the appropriate nursing action is:
A. Observe the gag reflex frequently.
B. Stay with the client at all times.
C. Administer fluids via the tube.
D. Monitor the bilirubin level.
Ascites
Definition:
Increase in fluid in the abdominal cavity caused by:
a. portal hypertension.
b. low serum albumin.
Mechanism:
Congestion of blood in the portal system pushes fluid out of blood vessels and the surface of the liver into the peritoneal space.
Lack of albumin allows seepage from the intravascular space.
Data:
Abdominal distention.
Dyspnea.
Management of Ascites
Treatment of Fluid Excess:
Sodium and fluid restrictions.
Diuretics.
Frequent measurement of abdominal girths and daily weights.
Elevate head of bed (HOB) to ease breathing.
Paracentesis:
Allows removal of fluid (up to 6-8 liters).
Administer IV albumin.
Ensure the bladder is empty prior to the procedure.
Peritoneal-Venous Shunt:
Bypasses portal circulation and reinfuses ascitic fluid back into the superior vena cava (venous circulation).
Practice Questions
Q1: What patient development necessitates a paracentesis procedure?
A. Dyspnea
B. A falling blood pressure
C. An inability to empty the bladder
D. A weight gain of more than 2 pounds
Q2: Before a paracentesis, which activity is essential?
A. Administer an enema
B. Ask the client to empty bladder.
C. Insert a nasogastric tube.
D. Check to see when the last bowel movement occurred.
Q3: After the paracentesis, which question is most important for the nurse to ask?
A. “Do your clothes still feel tight?”
B. “Do you need to void?”
C. “Are you feeling dizzy?”
D. “Do you have any pain?”
Hepatic Encephalopathy
Definition:
Liver’s inability to handle byproducts of protein digestion.
Unable to convert ammonia to urea for excretion.
Increased ammonia in blood interferes with brain functioning; progresses to hepatic coma if toxic levels are not decreased or managed.
Mortality Rate: 90% once coma begins.
Data Collection: Hepatic Encephalopathy
Symptoms:
Impaired mental status; level of consciousness changes (irritability, drowsiness).
Disorientation and confusion.
Disruption in sleep cycle.
Neuromuscular functioning changes (fatigue, asterixis: “Liver flap”).
Gradually lose consciousness leading to hepatic coma.
Medical Management of Encephalopathy
Treatment Goals:
Abstain from all alcohol.
Maintain normal dietary protein levels.
Ammonia Reduction Agents:
Non-absorbable disaccharides (e.g., lactulose/Cholac): Act as laxatives and reduce ammonia levels by pulling it into the bowel to be excreted in feces.
Antibiotics:
Neomycin/Mycifradin, rifaximin/Xifaxan: Reduce the number of colonic bacteria present that typically produce ammonia.
Nursing Management Goals:
Safety; observe for mental status changes (early sign); reorient as necessary.
Ensure proper ambulation with help only.
Promote rest, comfort, and sleep.
Alcohol Withdrawal
Definition:
Substance Use Disorder: Alcohol is a CNS depressant.
Sudden withdrawal increases brain hyperactivity.
Data Collection: Alcohol Withdrawal
Symptoms:
Some experience mild symptoms; others severe, even life-threatening.
Early Symptoms:
Anxiety, insomnia, irritability/nervousness, tremors, diaphoresis, tachycardia, nausea.
Later Symptoms:
Disorientation, hallucinations, changes in pulse and blood pressure (Pulse > 110, BP > 150/90), seizures (10%).
Severe Alcohol Withdrawal Syndrome (SAWS):
Untreated or undertreated withdrawal can lead to intense autonomic and psychological symptoms: delirium tremens (DTs).
Occurs 48-72 hours after cessation, with a mortality rate of 10-20%.
Symptoms: progressively severe confusion, hallucinations, and seizures.
Management of Alcohol Withdrawal
Clinical Assessment:
Use CIWA scale to determine the need for pharmacology.
Medications:
Benzodiazepines: relieve withdrawal symptoms, prevent progression to delirium tremens, and reduce seizure risks.
Examples: lorazepam/Ativan, diazepam/Valium, chlordiazepoxide/Librium.
Supportive Medications:
Beta-blockers to slow the heart rate and reduce tremors.
Antiseizure medications.
Medications for nausea and cramps (anticholinergics).
Vitamins: Thiamine, folic acid.
Care Considerations:
Maintain minimal stimuli.
Monitor vital signs frequently.
Orient client frequently to reduce anxiety.
How Body Responds to Alcohol
Mechanism of Action:
Alcohol primarily acts on nerve cells of the brain, affecting levels of neurotransmitters and causing physiological slowdown.
Absorption Process:
After absorption, alcohol enters the bloodstream, dissolves in the water of the blood, and then in the water of tissues.
Blood Alcohol Concentration (BAC):
Increases when the body absorbs alcohol faster than it can eliminate it.
Excretion pathways: 5% in kidney, 5-10% in lungs, and 80-90% in liver.
It takes approximately 1-1.5 hours to detoxify one standard drink.
Metabolism of Alcohol
By-products:
Acetaldehyde, which is very toxic to cells.
Consecutives Damages:
The liver can become inflamed, fatty, and enlarged, leading to eventual fibrosis and necrosis.
Continued Damage:
Processes that damage liver cells can persist even after alcohol ingestion has stopped.
NAFLD: Non-alcoholic Fatty Liver Disease
Definition:
A group of conditions characterized by the accumulation of excess fat in livers of individuals who drink little or no alcohol.
Associated Conditions:
Linked with obesity, high cholesterol, and insulin resistance.
Treatment:
Weight loss and possibly insulin sensitizing agents.
Stages:
Fatty liver: Non-serious fat accumulation in the liver, likely not causing noticeable damage.
NASH: Non-alcoholic steatohepatitis, fat accumulation associated with inflammation and some scarring, potentially leading to cirrhosis.
Summary: Stages of Liver Disease
Nutritional Management:
Adequate calories, potentially increased carbohydrates.
Vitamin supplementation: Thiamine.
Fluid and sodium restrictions are likely.
Restricted protein diet is not recommended as it may worsen malnutrition and muscle wasting.
If steatorrhea is present, fat restriction is indicated.
Nursing Interventions for Cirrhosis
Assessment of Fluid Status:
Daily weights, abdominal girth, and monitoring of peripheral edema, and supporting fluid restrictions.
Elevation:
Elevate HOB to ease breathing.
Itching Relief:
Measures to relieve itching.
Monitoring:
Monitor coagulation studies.
Monitor vital signs (during alcohol withdrawal).
Practice Questions: Cirrhosis
Q1: The patient with cirrhosis has bleeding tendencies because the liver cannot:
A. Produce RBCs and vitamin K
B. Produce prothrombin and other clotting factors.
C. Manufacture vitamins A and K
D. Make adequate amounts of albumin
Q2: Which new observation is most indicative of a serious development in a patient with cirrhosis?
A. Generalized pruritis
B. Patient is confused
C. Patient is jaundiced
D. There are numerous ecchymotic areas on the arms.
Q3: Which condition contributed to the diagnosis of esophageal varices?
A. Decreased prothrombin formation
B. Decreased albumin formation by the liver
C. Portal hypertension.
D. Increased central venous pressure
Q4: Which snack is best for a patient with cirrhosis?
A. Cheese and saltine crackers
B. A banana
C. Peanut butter and jelly sandwich.
D. Milk and cookies
Additional Nutritional Questions
Q5: A client with cirrhosis has ascites. Which treatment most effectively reduces ascites?
A. Administer albumin to the client.
B. Restrict dietary protein.
C. Administer diuretics.
D. Maintain the client on bedrest.
Practice Question
Q6: A patient with altered thought processes related to liver failure is likely to have which laboratory findings?
A. Low bilirubin
B. High albumin
C. Elevated troponin levels
D. High ammonia.
Practice Question
Q7: A 10-pound weight gain in a week, distended abdomen, and difficulty breathing indicate which nursing diagnosis formulated for this client?
A. Excess fluid volume.
B. Disturbed body image
C. Imbalanced nutrition; more than body requirements
D. Impaired gas exchange
Hepatitis
Definition:
Inflammation of liver cells.
Hepatocyte structure is altered; cells become inflamed and dysfunctional, resulting in disturbances in bilirubin excretion.
Hepatic cells usually regenerate with little residual damage, can be acute or chronic.
Etiology of Hepatitis
Causes:
Invasion by a virus (most common cause).
Exposure to toxic chemicals/drugs.
Lengthy alcohol abuse.
Common Hepatotoxic Substances
Alcohol.
Acetaminophen/Tylenol.
Diazepam/Valium.
Isoniazid/INH.
Phenytoin/Dilantin.
Tranquilizers.
Industrial chemicals (e.g., carbon tetrachloride, trichlorethylene, toluene).
Stages of Hepatitis
Viral Replication:
No symptoms.
Pre-icteric (Prodromal):
Lasts about one week; symptoms include fever, upper abdominal pain, fatigue, nausea.
Icteric:
Lasts 2-4 weeks; symptoms include jaundice, severe fatigue, pruritis, photophobia, dark urine.
Post-icteric (Convalescent):
Lasts 2-4 months; symptoms include fatigue, enlarged liver, elevated enzymes.
Diagnosis of Hepatitis
Liver Function Tests (LFTs):
Elevated ALT, AST, and elevated WBC; decreased albumin.
Virology Blood Exam:
For viral antigens to determine specific virus causing hepatitis.
Liver Biopsy:
For chronic hepatitis evaluation.
Management of Hepatitis
Rest:
Bedrest recommended.
Diet Modifications:
Restrict fat to reduce bile requirements, as anorexia is common—small, frequent, high-calorie meals recommended.
Avoid Harmful Substances:
Includes alcohol and hepatotoxic medications.
Complications of Hepatitis
Can lead to liver failure.
Some types (e.g., B, C, D) can lead to asymptomatic carrier status where the individual can infect others.
Once a carrier, the person is at risk of developing chronic hepatitis associated with hepatocellular carcinoma, cirrhosis, or liver failure.
Types of Viral Hepatitis
Hepatitis A (HAV):
Known as “Infectious hepatitis.”
Transmission: Contact with food or fecal material containing the virus (fecal-oral), contaminated water, uncooked shellfish.
Incubation: 6 weeks to 6 months.
Symptoms: Acute onset of gastroenteritis symptoms; rarely fatal; no carrier state.
Vaccine: Two doses recommended for children at age 1 (6 months apart); standard immune globulin (IG) for post-exposure management.
Hepatitis B (HBV):
Transmission: Direct contact with blood, including body fluids (sexual contact), or through birth; equipment contaminated by blood.
Incubation: 60-150 days.
Some have no symptoms; can become chronic carrier.
Vaccine: Available in three doses.
Risk of chronic infection is greater among young children—90% for infants and 25%-50% for children aged 1-5 years.
Hepatitis C (HCV):
Transmission: Parenteral exposure to blood (e.g., unregulated tattooing/piercing, body fluids contaminated with blood, injection drug use, needlestick injuries).
Incubation: 6-7 weeks.
Most do not show symptoms; 75-85% become chronic carriers; no vaccine available.
Hepatitis D (HDV):
Co-infection with Hepatitis B and requires HBV to replicate.
Incubation: 15-64 days; frequently leads to chronic active hepatitis or liver failure.
Immunity to HBV is immunity to HDV.
Hepatitis E (HEV):
Transmission: Fecal-oral route; most common source is fecally contaminated drinking water.
Incubation: 14-60 days; not common in the U.S.; no carrier state.
Who’s At Risk?
Hepatitis A: Individuals in daycare, military service, international travelers.
Hepatitis B: IV drug users, healthcare workers, transplant and hemodialysis patients, anal sex, unprotected sex, being born to a carrier.
Hepatitis C: IV drug abusers; those receiving blood transfusions before 1992.
Hepatitis E: Travelers to endemic areas.
Specific Prevention
Type A:
Use gloves in contact with secretions or feces; maintain cleanliness after toileting; avoid preparing food for others while infectious; avoid raw seafood; drink bottled water in underdeveloped areas.
Type B:
Adhere to Standard Precautions; dispose of sharps properly; receive vaccinations; practice safe sex; avoid sharing personal items; carriers should not donate blood.
Health Care Workers:
Occupational hazard due to patient contact or contact with equipment; observe Standard Precautions at all times; obtain Hepatitis B vaccine.
Rules for HBV Carriers
Cover any open cuts or sores with a bandage.
Discard used personal items (e.g., tampons, bandages) in a paper bag.
Clean up blood spills with bleach.
Use condoms.
Always inform medical personnel about carrier status.
Medication Therapy for Hepatitis
Antivirals focus on achieving sustained virologic response (SVR) or curing chronic hepatitis C:
For Hepatitis B: lamivudine/Epivir.
For Hepatitis C: ledipasvir-sofosbuvir/Harvoni, glecaprevir and pibrentasvir/Mavyret.
If Liver Transplant: Necessary in advanced liver damage cases.
Practice Question
A client asks how he contracted hepatitis A. Which is the most likely reason?
A. He ate home-canned corn.
B. He donated blood before he got sick.
C. He ate oysters brought home from a fishing trip.
D. He stepped on a nail two weeks ago.
Anatomy Review: Pancreas
Exocrine Functions:
Pancreatic juice flows into the duodenum via the Ampulla of Vater.
Enzymes are secreted in inactive form, becoming active in the duodenum: trypsin/protease, amylase, lipase.
Endocrine Functions:
Secretion of hormones: insulin and glucagon.
Pancreatitis
Definition:
Inflammation of the pancreas that can be mild or severe.
Duct obstruction due to stones, edema, sphincter spasms, or scar tissue leads to enzyme build-up and possible auto-digestion of pancreatic tissue.
Causes of Pancreatitis
History of alcohol abuse, excessive alcohol consumption.
Obstruction of ducts (e.g., gallstones).
Biliary tree disease or inflammation.
Abdominal surgical trauma.
Hypertriglyceridemia.
Data Collection: Acute Pancreatitis
Symptoms:
Nausea and vomiting.
Pain: Sudden onset, worse after eating, severe upper abdominal/epigastric pain radiating to back with distention and tenderness.
Pain may be relieved by sitting up, leaning forward, or using fetal position or knee-chest position.
Signs of Complications: Hemorrhage
Cullen's Sign: Periumbilical discoloration.
Grey-Turner's Sign: Bluish discoloration of flanks from retroperitoneal hemorrhage.
Diagnosis of Pancreatitis
Criteria:
Must present with two out of three signs, which include:
Characteristic abdominal pain.
Elevated lipase or amylase 2x more than normal (Normal levels:
Amylase: 25-125 units/liter.
Lipase: < 160 units/liter).
Imaging (CT) indicating inflammation or other complications.
Management of Acute Pancreatitis
Initial Care:
Bedrest to reduce pancreatic stimulation and secretions; NPO until nausea and pain controlled; possible NG tube.
Restore fluid losses via IV; nasojejunal enteral feedings as needed.
Pain Management:
Adequate pain relief with opioids while avoiding morphine & codeine to prevent sphincter of Oddi spasms.
Pancreatitis Diet
NPO initially.
As pain subsides and hunger returns, introduce:
Clear liquids.
Low-fat, high-carbohydrate diet in small feedings; avoid caffeine and alcohol.
If prolonged bouts occur, enteral feedings may be necessary.
Nursing Management of Acute Pancreatitis
Pharmacology:
Analgesics (opioids), antiemetics, anticholinergics, PPIs.
Observation:
Monitor for sudden pain return; patient should remain in a comfortable position (sitting upright or leaning forward).
Fluid Replacement:
Ensure IV fluid replacement and NG tube suctioning.
Consider Alcohol Withdrawal:
Observe for potential signs of withdrawal.
Respiratory Status:
Careful monitoring due to potential respiratory complications.
Complications of Pancreatitis
Pseudocyst:
Fibrous inflamed capsules filled with pancreatic juices; may resolve spontaneously or require surgery.
Abscesses:
Necrotic tissue that can erode into bowel/pelvic cavity.
Most Serious Complication:
Require intervention (surgery to drain and debride); observe for signs of peritonitis, an indication of abscess.
Practice Questions: Pancreatitis
Q1: What is the nurse’s initial focus in the acute pancreatitis patient?
A. Dietary management
B. Prevention of skin breakdown
C. Management of hypoglycemia
D. Pain control.
Q2: The rationale for keeping the acute pancreatitis patient on bedrest is:
A. Reduce pancreatic and gastric secretions.
B. Minimize effects of hypoglycemia
C. Reduce risk of DVT
D. Reduce likelihood of orthostatic hypotension
Q3: An important goal of nursing care for an acute pancreatitis patient is:
A. Providing supplemental oxygen
B. Daily weights
C. Monitoring the urine for albumin
D. Controlling nausea and vomiting.
Q4: A patient with pancreatitis tells the nurse that he dreads nighttime due to pain. Best explanation?
A. Pain is aggravated in the recumbent position.
B. The mattress is uncomfortable.
C. Pain increases with less activity.
D. There are fewer distractions at night.
Q5: Before discharging the acute pancreatitis patient, which information is essential?
A. The client must never donate blood.
B. The client should abstain from alcohol.
C. The client should take laxatives regularly.
D. The client should not perform any heavy lifting.
Chronic Pancreatitis
Definition:
Continuing pancreatic cell damage resulting in fibrotic scarring, ulcer formation, and decreased enzymatic functioning due to recurring inflammation.
Symptoms:
Intermittent attacks of abdominal or epigastric pain; pain may be daily or occasional.
Function Loss:
Loss of exocrine and endocrine function.
Causes of Chronic Pancreatitis
Excessive alcohol ingestion, repeated attacks of acute pancreatitis.
Chronic obstructive disease; persistent inflammation of pancreatic ducts.
Prolonged malnutrition can aggravate condition.
Cancer of the pancreas may be related.
Data Collection: Chronic Pancreatitis
Symptoms:
Recurring, consistent abdominal or epigastric pain.
Weight loss and anorexia.
Steatorrhea (fatty stools).
Jaundice may develop.
Consideration for the development of diabetes.
Complications of Chronic Pancreatitis
Acute Hemorrhagic Pancreatitis:
Can lead to shock.
Paralytic Ileus:
Pneumonia and Pleural Effusions:
Diabetes Mellitus:
Malnutrition:
Abscesses/Pseudocysts:
Nursing Intervention for Chronic Pancreatitis
Observation of Pain:
Implement measures for pain relief; be concerned for potential analgesic drug dependence.
Patient Education:
Avoid alcohol and report signs of weight loss or fatty stools.
Recognize signs of pancreatic cysts or abscesses (radiating pain and dyspnea).
Nutritional Support:
Prescribe pancreatic enzymes as necessary.
Practice Question: Which development might indicate an alcoholic patient has chronic pancreatitis?
A. Excessive hunger
B. Fatty stools (steatorrhea).
C. Steady weight gain
D. Attack of unrelenting abdominal pain
Critical Component of Care Plan:
A. Measuring abdominal girth
B. Performing glucometer readings
C. Adhering to fluid restrictions
D. Performing Homan’s sign
Gallbladder
Function:
Stores and concentrates bile produced in the liver and releases bile through cystic duct and common bile duct into the duodenum after a meal.
Gallbladder Anatomy and Disorders
Disorders Include:
Cholelithiasis: Presence of stones in the gallbladder.
Acute Cholecystitis: Inflammation of the gallbladder, often due to stones.
Chronic Cholecystitis: Thickened and fibrotic gallbladder that does not empty easily due to chronic irritation.
Causes and Risks for Cholelithiasis
Imbalance among cholesterol, bile salts, and calcium causing stone formation.
Bile stasis or pooling in the gallbladder.
Low-fat diet, sudden weight loss, and starvation that may increase cholesterol excretion/concentration in the bile.
Risk Factors:
Females are 3x more likely than males under age 50; being over 40, having multiple pregnancies, taking oral contraceptives, post-gastric bypass, and obesity.
90% of acute cholecystitis cases are due to cholelithiasis.
Acute Cholecystitis
Definition:
Inflammation and edema of the gallbladder in response to obstruction.
The gallbladder continues to contract to deliver bile, resulting in pain.
Trapped bile can irritate the gallbladder wall causing edema and vascular swelling leading to ischemia; bile may become infected.
Data Collection: Cholecystitis
Symptoms:
Biliary colic: intense, sudden RUQ pain, particularly after a fatty meal that radiates to the back or right shoulder blade.
Nausea and vomiting, fever.
Pain typically lasts 2-6 hours; jaundice or diarrhea may present if CBD is obstructed.
Diagnosis of Cholecystitis
Criteria:
Elevated WBC, ultrasound or CT scan.
Cholescintigraphy/HIDA scan shows abnormal contraction of the gallbladder.
Management of Cholecystitis
Non-Surgical Management:
Pain control utilizing analgesics and antiemetics.
After nausea subsides, low-fat diet in small amounts.
Dissolving Agents:
Unpleasant side effects may occur, and treatment may take months to years with a high chance of stone recurrence (e.g., chenodeoxycholic/Chenodiol; ursodiol/Actigall).
Surgical Approaches:
Laparoscopic Cholecystectomy:
Involves four small incisions, ambulation, and discharge the same day with a return to normal activities in 2 weeks.
Open Cholecystectomy:
Larger incisional discomfort may inhibit turning and coughing; may necessitate a biliary drainage tube (T tube) with a longer hospital stay.
Post Operative Diet and Nursing Concerns
Diet:
NPO until advancing diet; low-fat for 5-6 weeks.
Normal diet with no fat restriction thereafter; some may experience lingering problems with fat digestion.
Nursing Concerns:
Management of pain post-surgery, particularly in open procedures.
Monitor for risks related to fluid volume deficit from nausea, vomiting, or excessive tube drainage.
Observe for ineffective breathing patterns related to surgical incisions.
Reinforcement of diet guidelines post-cholecystectomy.
Practice Questions
Q1: People post-laparoscopic cholecystectomy report mild shoulder pain. Why?
A. Spasm of the ampulla of Vater
B. Reaction to narcotics irritates the muscles
C. Diaphragmatic irritation from residual CO2 instilled during surgery.
D. Development of paralytic ileus
Q2: Following a cholecystectomy, special nursing care prevents which complication?
A. Hypostatic pneumonia
B. Hemorrhage
C. Paralytic ileus.
D. Deep vein thrombosis
Q3: Four hours post-cholecystectomy, which data requires immediate nursing attention?
A. Absent bowel sounds in all quadrants
B. Urine output of 100 cc in two hours
C. NG tube draining greenish-brown fluid
D. Refusal to turn, cough, deep breathe.
Bile Duct Obstruction
Definition:
Gallstones or fragments of stones lodged in the common bile duct.
Serious and potentially life-threatening, causing episodic upper abdominal pain and jaundice; can lead to clay-colored stools, sepsis, or shock from bacteria leaking into the blood.
Treatment of Bile Duct Obstruction
Initial Surgery:
Gallbladder removal if not yet performed.
Consider Endoscopic Retrograde Cholangiopancreatography (ERCP):
Procedure to address the obstruction in the bile duct.
Practice Question
In a patient with cholelithiasis, which new finding indicates a stone may be blocking the common bile duct?
A. Jaundice.
B. Nausea
C. Right upper quadrant pain
D. Elevated cholesterol level
After ERCP:
Which intervention is part of the plan of care?
A. Monitor for return of gag reflex.
B. Instruct the client to cough.
C. Encourage early ambulation.
D. Increase fluid intake.
T Tube Function
Purpose:
To decrease abdominal distention and keep the common bile duct open until edema resolves, allowing bile drainage.
Practice Question
When will the T tube be removed?
A. When stool returns to normal brown color.
B. At the same time as stitches.
C. When it stops draining.
D. Usually removed the day after surgery.
Pharmacology Supplement for Liver/GB/Pancreatic Conditions
Antiemetics:
For nausea and vomiting related to pancreatitis and cholecystitis.
Serotonin (5-HT3) antagonists: ondansetron/Zofran, dolasetron/Anzemet.
Adjuncts:
Dexamethasone/Decadron.
Antispasmodics/Anticholinergics:
Relax smooth muscle of GI tract; used in pancreatitis and cholecystitis to relieve pain.
Side effects: Constipation, dizziness, drowsiness, headache, dry mouth; e.g., dicyclomine hydrochloride/Bentyl (short-term use only).
Medications to Treat Portal Hypertension:
Antihypertensives to lower BP; Diuretics to reduce fluid retention e.g. spironolactone/Aldactone (K-sparing).
Albumin: Used to pull fluid back into the blood, may be administered IV.
Medications to Treat Hepatic Encephalopathy:
Reduce ammonia levels.
Lactulose/Cholac: acidifies bowel and helps excrete ammonia in feces.
Neomycin/Mycifradin or rifaximin/Xifaxan: reduces colonic bacteria to lower ammonia production; administered orally or via NG tube.
Medications for Alcohol Withdrawal:
Benzodiazepines: oxazepam/Serax, lorazepam/Ativan; widely used to treat anxiety, insomnia, seizures, and alcohol withdrawal.
All options appear equally effective.
Medications for Cholelithiasis:
Inhibit intestinal absorption of cholesterol or reduce cholesterol production; dissolution takes significant time and may cause side effects (e.g., chenodiol/Chenix, ursodiol/Actigall).
Pancreatic Enzyme Replacements:
Supplement or replace pancreatic enzymes, taken with food; side effects include cramping, nausea, diarrhea (e.g., pancreatin/Creon, pancrelipase/Cotazym, Pancrease, Viokase).
Lab Values:
Ammonia: 10-80.
Amylase: 25-125.
Albumin: 3.5-5.
Bilirubin: 0.1-1.2.