Lola Oyedele MSN, RN, CTN
Majuvy L. Sulse MSN, RN, CCRN
Liver Biliary
Pancreatic Problems
and
NRS 108
LIVER
Largest organ excluding skin located RUQ Lobule is functional unit Fat, CHO, Protein metabolism Clotting Drug metabolism & detoxification Liver enzymes
Alamine Aminotransferase ALT, SGPT-5-35U/L
Aspartate Aminotransferase AST, SGOT 0-35U/L
Alkaline Phosphatase ALP 20-90U/L
Liver Aminotransferases
Found in hepatocytes Markers of liver cell injury Detected within hours of injury to liver AST used in conjunction with ALT AST elevated in cardiac/skeletal muscle
Laboratory tests PT/PTT Se Albumin Se Ammonia Se Bilirubin
• Conjugated-Direct, post hepatic, glucoronic acid• Unconjugated- indirect, pre hepatic,albumin bound
Urobilinogen-sensitive test for hepatic damage
Liver Biopsy
Pre procedure Needle between 6-7 or 8-9th intercostals Check coagulation Type & X-match Baseline VS Sustained exhalations- prevent lung injury consent
Post procedure VS Lie on R side for 2 hours Flat 12-14 hours Watch for complications-shock, R pneumothorax, Biliary
peritonitis (rigid abdomen, high temp)
Jaundice
Yellowish discoloration from bilirubin & breakdown of Hgb Normal 2-3MG/DL (jaundice 3-4x normal value) Sclera & skin, palm of hands/feet Hemolytic
Increased RBC breakdown Increased unconjugated bilirubin Hemolytic anemia, ABO incompatibility
Hepatocellular Liver unable to take up bilirubin Conjugated & excreted Cirrhosis
Obstructive Impeded or obstructive Intrahepatic- swelling, fibrosis, tumors, cirrhosis, hepatitis Extrahepatic-CBD stones, Ca pancreas
CIRRHOSIS
DESCRIPTION A chronic, progressive disease of the liver, characterized by
diffuse damage to cells with fibrosis and nodular regeneration Repeated destruction of hepatic cells causes the formation of
scar tissue-nodular ASSESSMENT
Anorexia and weight loss Early morning nausea and vomiting (presence of blood in
vomitus) Dyspepsia Flatulence and changes in bowel habits Emaciation Fatigue
CIRRHOSIS ASSESSMENT
Jaundice Abdominal pain or
tenderness Ascites Peripheral edema Dry skin and rashes Petechiae or
ecchymosis Spider angiomas on
the nose, cheeks, upper thorax, and shoulders
•Hepatomegaly•Protruding umbilicus•Dilated abdominal veins•Fetor hepaticus; the fruity, musty breath odor of chronic liver disease•Asterixis (liver flap): A course tremor characterized by rapid, nonrhythmic extension and flexions in the wrist and fingers•Delirium
TYPES OF CIRRHOSIS
LAENNEC'S CIRRHOSIS Alcohol-induced, nutritional, or portal cirrhosis Cellular necrosis causes eventual widespread scar
tissue, with fibrotic infiltration of the liver POSTNECROTIC CIRRHOSIS
Occurs after massive liver necrosis Results as a complication of acute viral hepatitis or
exposure to hepatotoxins Scar tissue causes destruction of liver lobules and
entire lobes
TYPES OF CIRRHOSIS
BILIARY CIRRHOSIS Develops from chronic biliary obstruction (secondary),
bile stasis (Primary), and inflammation resulting in severe obstructive jaundice
CARDIAC CIRRHOSIS Associated with severe, right-sided congestive heart
failure (CHF) and results in an enlarged, edematous, congested liver
The liver becomes anoxic, resulting in liver cell necrosis and fibrosis
COMPLICATIONS OF CIRRHOSIS
PORTAL HYPERTENSION A persistent increase in pressure within the
portal vein that develops as a result of obstruction to flow of blood
Causes splenomegaly as blood backs up Also results in ascites, esophageal varices &
hemorrhoids
COMPLICATIONS OF CIRRHOSIS
ASCITES The accumulation of fluid (plasma)within the
peritoneal cavity that results in venous congestion of the hepatic capillaries
Increased hydrostatic pressure leads to plasma leaking directly from the liver surface and portal vein
Increased hepatic lymph formation present Renal vasoconstriction-triggers RAS-causes water &
Na reabsorption
ASCITES
Treatment Non surgical management
Diet Drug Comfort measures Paracentesis
Surgical management Shunt
• Peritoneovenous(LeVeen shunt)• Denver shunt
COMPLICATIONS OF CIRRHOSIS
BLEEDING ESOPHAGEAL VARICES Fragile, thin-walled, distended esophageal veins that
become irritated and rupture Caused by-chemical irritant, mechanical trauma,
increased pressure from esophagus & stomach Treatment-
Esophageal tamponadeGastric decompression & lavageVasopressinEndoscopic sclerotherapy or ligationTIPS
COMPLICATIONS OF CIRRHOSIS
JAUNDICE Occurs because the liver is unable to metabolize
bilirubin and because the edema, fibrosis, and scarring of the hepatic bile ducts interfere with normal bile and bilirubin secretion
PORTAL SYSTEMIC ENCEPHALOPATHY End stage hepatic failure and cirrhosis,
characterized by altered LOC, neurological symptoms, impaired thinking, and neuromuscular disturbances
Encephalopathy
Stages of encephalopathy Stage 1-
mild confusion, forgetfulness, mood changes, irritability, sleep disturbance
Stage 2 lethargy Aberrant behavior Liver flaps
Stage 3 Severe confusion-violent behavior Speech mumbling, asterixis hyperventilation
Stage 4 Comatose Abnormal posturing EEg abnormal
Management of Encephalopathy
Identify & treat cause GI bleed, systemic infection, drugs, alkalosis, dehydration
Eliminate or reduce generation of Ammonia toxins Control intake<0.5G/Kg/Day Calories 35-40KCAL/Kg/Day <Tyrosine/Phenylalanine,>
Leucine/Valine Vit A,D,E, K
Reduce amount of bacteria in bowel Stop Nitrogen containing drugs, give Neomycin, Lactulose,
Magnesium Citrate, fiber, stool softener, enemas
Hasten movement of ammonia in the bowel-3-5x stools/day
Lactulose
COMPLICATIONS OF CIRRHOSIS
HEPATORENAL SYNDROME Progressive renal failure associated with hepatic failure Characterized by a sudden decrease in urinary output,
elevated blood urea nitrogen (BUN) and creatinine, decreased urine sodium excretion, and increased urine osmolarity
COAGULATION DEFECTS Decreased synthesis of bile fats in the liver prevent the
absorption of fat-soluble vitamins Without vitamin K and clotting factors II, VII, IX, and X,
the client is prone to bleeding
CIRRHOSIS IMPLEMENTATION
Elevate the head of the bed to minimize shortness of breath
If ascites and edema is absent and the client does not exhibit signs of impending coma, a high-protein diet supplemented with vitamins is prescribed
Provide supplemental vitamins (B complex, vitamin A, C, and K, folic acid, and thiamine) as prescribed
Restrict sodium intake and fluid intake as prescribed Initiate enteral feedings or TPN as prescribed Administer diuretics as prescribed Monitor I&O and electrolyte balance Weigh client and measure abdominal girth daily Monitor LOC; assess for precoma state (tremors, delirium)
CIRRHOSIS
IMPLEMENTATION Monitor for asterixis Maintain gastric intubation to assess bleeding and/or
esophagogastric balloon tamponade to control bleeding varices if prescribed
Administer blood products as prescribed Monitor coagulation laboratory results; administer
vitamin K if prescribed Administer low-sodium antacids as prescribed Administer Lactulose (Chronulac), which
decreases the pH of the bowel, decreases production of ammonia by bacteria in the bowel, and facilitates the excretion of ammonia
CIRRHOSIS
Administer neomycin (Mycifradin) as prescribed to inhibit protein synthesis in bacteria and decrease the production of ammonia
Avoid medications such as narcotics, sedatives, and barbiturates, and any hepatotoxic medications or substances
Instruct the client about the restriction of alcohol intake
Prepare the client for paracentesis to remove abdominal fluid
Prepare the client for surgical shunting procedures if prescribed
Fatty Liver
Accumulations of triglycerides & fats in hepatic cells
Causes- alcoholism, malnutrition, DM, Obesity TPN, Pregnancy
S/S-RUQ pain, edema, hepatomegaly, jaundice
Dx-liver biopsyTx-dietary restrictions
Hepatic Abcess
Invasion of bacteria or protozoa-causing necrotic cavity filled with leukocytes & infective agents.
Causative agents- E Coli, Klebsiella, Salmonella, Enterococcus & Staph
Dx-liver scanLabs-blood culture to detect organism
LIVER Cancer
Hepatocellular carcinoma- most common primary liver Ca Metastatic Ca is more common than primary Ca Malignant cells cause liver to be enlarged and mishapen Difficult to diagnose Clinical manifestations similar to cirrhosis Tests used-CT, MRI, ERCP, liver biopsy, AFP (elevated in 70% of
hepatocellular Ca & helps to distinguish primary from metastatic cancer
Cryosurgery- cryoprobes directly in liver-liquid nitrogen used to freeze liver tissue
Radiofrequency-electrical energy to create heat in specific location PEI-percutaneous ethanol injection-guided US chemotherapy Liver transplantation
CHOLECYSTITIS
DESCRIPTION An inflammation of the gallbladder that may occur as an
acute or chronic process Acute inflammation is associated with gallstones
(cholelithiasis) Chronic cholecystitis results when inefficient bile
emptying and gallbladder muscle wall disease cause a fibrotic and contracted gallbladder
A calculus cholecystitis occurs in the absence of gallstones and is due to bacterial invasion via the lymphatic or vascular systems
CHOLECYSTITIS
ASSESSMENT Nausea and vomiting Indigestion, Belching, Flatulence Epigastric pain that radiates to the scapula 2 to 4 hours after
eating fatty foods and may persist for 4 to 6 hours
Pain localized in right upper quadrant Guarding, rigidity, and rebound tenderness Mass palpated in the right upper quadrant Murphy’s sign (cannot take a deep breath when the
examiner’s fingers are passed below the hepatic margin) Elevated temperature, Tachycardia Signs of dehydration Jaundice, pruritus, dark orange and foamy urine Steatorrhea and clay-colored feces
CHOLECYSTITIS IMPLEMENTATION
Maintain NPO status during nausea and vomiting episodes Maintain nasogastric decompression Administer antiemetics Administer analgesics as prescribed to relieve pain and
reduce spasm (morphine sulfate or codeine sulfate may cause spasm of the sphincter of Oddi and increase pain)
Administer antispasmodic (anticholinergics) as prescribed to relax smooth muscle
Instruct the client with chronic cholecystitis to eat low-fat meals more frequently in small amounts
Instruct the client to avoid gas-forming foods Prepare the client for nonsurgical and surgical procedures
as prescribed
CHOLECYSTITISNONSURGICAL IMPLEMENTATION
DISSOLUTION THERAPY To remove cholesterol stones Chenodeoxycholic acid (Chenodiol) or ursodiol
(Actigall) is administered PO to decrease the size of the stones or to dissolve small stones
Direct contact with repeated injections and aspirations of a dissolution agent via percutaneous catheter may be performed
CHOLECYSTITISNONSURGICAL IMPLEMENTATION
EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY Shock waves are
administered that disintegrate stones in the biliary system
Oral dissolution follows
CHOLECYSTITISSURGICAL IMPLEMENTATION
CHOLECYSTECTOMY Removal of the gallbladder
CHOLEDOCHOTOMY Incision into the common bile duct to remove
the stone
Surgical procedures may be performed by laparoscopy
CHOLECYSTITIS
POSTOPERATIVE IMPLEMENTATION Monitor for respiratory complications secondary to pain at
the incisional site Encourage coughing, deep breathing & early ambulation Splinting the abdomen to prevent discomfort during
coughing Administer antiemetics as prescribed for nausea and
vomiting Administer analgesics as prescribed for pain relief Maintain NPO status and NG tube suction as prescribed Advance diet from clear liquids to solids when prescribed
and as tolerated by the client Maintain and monitor drainage from the T-tube, if present
PANCREATITIS
DESCRIPTION An acute or chronic inflammation of the pancreas
with associated escape of pancreatic enzymes into surrounding tissue
Acute pancreatitis occurs suddenly as one attack or can be recurrent, but resolves
Chronic pancreatitis is a continual inflammation and destruction of the pancreas, with scar tissue replacing pancreatic tissue
Precipitating factors: trauma, alcohol, biliary tract disease, viral or
bacterial disease, hyperlipedemia, hypercalcemia, cholelithiasis, hyperparathyroidism, ischemic vascular disease, and peptic ulcer disease
ACUTE PANCREATITIS
ASSESSMENT Abdominal pain, including a sudden onset at the mid-
epigastric or left upper quadrant location with radiation to the back
Pain that is aggravated by a fatty meal, alcohol, or lying in a recumbent position
Abdominal tenderness and guarding Nausea and vomiting Weight loss Cullen’s sign (discoloration of the abdomen and
periumbilical area) Turner’s sign (bluish discoloration of the flanks) Absent or decreased bowel sounds Elevated WBC, glucose, bilirubin, alkaline
phosphatase, urinary amylase Elevated lipase and amylase
CULLEN’S SIGN VS TURNER’S SIGN
ACUTE PANCREATITIS
IMPLEMENTATION Maintain NPO status and maintain hydration with IV fluids as
prescribed Administer TPN for severe nutritional depletion Administer supplemental preparations and vitamins and minerals
to increase caloric intake if prescribed Maintain NG tube to decrease gastric distention and suppress
pancreatic secretion Administer meperidine hydrochloride (Demerol) as prescribed
for pain because it causes less incidence of smooth muscle spasm of the pancreatic ducts and sphincter of Oddi (avoid morphine sulfate or codeine sulfate, which may cause spasms)
Administer antacids as prescribed to neutralize gastric secretions
ACUTE PANCREATITIS
IMPLEMENTATION Administer histamine H2-receptor antagonists
as prescribed to decrease hydrochloric acid production and prevent activation of pancreatic enzymes
Administer anticholinergics as prescribed to decrease vagal stimulation, decrease GI motility, and inhibit pancreatic enzyme secretion
ACUTE PANCREATITIS
CLIENT EDUCATION The importance of avoiding alcohol The importance of follow-up visits with the
physician To notify the physician if acute abdominal pain,
jaundice, clay-colored stools, or dark urine develops
CHRONIC PANCREATITIS
ASSESSMENT Abdominal pain and tenderness Left upper quadrant mass Steatorrhea and foul-smelling stools that may
increase in volume as pancreatic insufficiency increases
Weight loss Muscle wasting Jaundice Signs and symptoms of diabetes mellitus
CHRONIC PANCREATITIS
IMPLEMENTATION Provide supplemental preparations and vitamins and
minerals to increase caloric intake Administer pancreatic enzymes as prescribed to aid in
the digestion and absorption of fat and protein Administer insulin or oral hypoglycemic medications as
prescribed to control diabetes mellitus, if present
CHRONIC PANCREATITIS
CLIENT EDUCATION The prescribed dietary measures (fat and/or protein
intake may be limited) Avoid heavy meals The importance of avoiding alcohol The use of pancreatic enzyme medications The treatment plan for glucose management To notify the physician if increased steatorrhea occurs
or if abdominal distention or cramping, and skin breakdown develops
The importance of follow-up visits
HEPATITIS
DESCRIPTION An inflammation of the liver caused by a virus,
bacteria, or exposure to medications or hepatotoxins
The goals of treatment include resting the inflammed liver to reduce metabolic demands and increasing the blood supply, thus promoting cellular regeneration and preventing complications
STAGES OF VIRAL HEPATITIS
PREICTERIC STAGE The first stage of hepatitis preceding the
appearance of jaundice Flu-like symptoms: malaise, fatigue Anorexia, nausea, vomiting, diarrhea Pain: headache, muscle aches, polyarthritis Serum bilirubin and enzyme levels are elevated
STAGES OF VIRAL HEPATITIS
ICTERIC STAGE The second stage of hepatitis, which includes the
appearance of jaundice and associated symptoms such as elevated bilirubin levels, dark or tea-colored urine, and clay-colored stools
Jaundice Pruritus Brown-colored urine Lighter-colored stools Decrease in preicteric phase symptoms
STAGES OF VIRAL HEPATITIS
POSTICTERIC STAGE The convalescent stage in which the jaundice
decreases and the color of the urine and stool return to normal
Energy levels increase Pain subsides GI symptoms are minimal to absent Serum bilirubin and enzyme levels return to
normal
VIRAL HEPATITISLABORATORY ASSESSMENT
ALANINE AMINOTRANSFERASE (ALT) Elevated to more than 1000 mU/ml and may rise to as high
as 4000 mU/ml Normal adult blood value: 6 to 24 U/L
ASPARTATE AMINOTRANSFERASE (AST) May rise to 1000 to 2000 mU/ml Normal adult blood value: 8 to 26 U/L
ALKALINE PHOSPHATASE LEVELS May be normal or mildly elevated Normal adult blood value: 4.5 to 13 King-Armstrong units/dl
SERUM TOTAL BILIRUBIN LEVELS Elevated to greater than 2.5 mg/dl Normal: less than 1.5 mg/dl Elevated levels of bilirubin in the urine
HEPATITIS A (HAV)
DESCRIPTION Formerly known as infectious hepatitis Commonly seen during the fall and early winter
INCREASED RISK INDIVIDUALS Commonly seen in young children Individuals in institutionalized settings Health care personnel
HEPATITIS A (HAV)
TRANSMISSION Fecal-oral route Person-to-person contact Parenteral Contaminated fruits, vegetables, or uncooked shellfish Contaminated water or milk Poorly washed utensils
INCUBATION PERIOD 2 to 6 weeks
INFECTIOUS PERIOD 2 to 3 weeks prior to, and 1 week after, developing
jaundice COMPLICATION
Fulminant hepatitis
HEPATITIS A (HAV)
PREVENTION Strict handwashing Stool and needle precautions Treatment of municipal water supplies Serologic screening of food handlers Hepatitis A vaccine (Havrix) Immune globulin (IG): For individuals exposed to HAV who
have never received the hepatitis A vaccine; administer during the period of incubation and within 2 weeks of exposure
IG is recommended for household members and sexual contacts of individuals with Hepatitis A
Pre-exposure prophylaxis with IG is recommended for individuals traveling to countries with poor or uncertain sanitation conditions
HEPATITIS B (HBV)
DESCRIPTION Is nonseasonal in nature All age groups are affected
INCREASED RISK INDIVIDUALS Drug addicts Clients undergoing long-term hemodialysis Health care personnel
HEPATITIS B (HBV)
TRANSMISSION Blood or body fluid contact Infected blood products Infected saliva or semen Contaminated needles Sexual contact Parenteral Perinatal period Blood or body fluids contact at birth
HEPATITIS B (HBV)
INCUBATION PERIOD 6 to 24 weeks
COMPLICATIONS Fulminant hepatitis Chronic liver disease Cirrhosis Primary hepatocellular carcinoma
HEPATITIS B (HBV)
TESTING Infection established by the presence of hepatitis B
antigen-antibody systems in the blood Presence of hepatitis B surface antigens (HBsAG) is the
serologic marker to establish the diagnosis of hepatitis B
Hepatitis B early antigen (HBeAG) is detected in the blood about 1 week after the appearance of HBsAG and its presence determines the infective state of the client
HEPATITIS B (HBV)
TESTING If the serologic marker (HBsAG) is present after
6 months, it indicates a carrier state or chronic hepatitis
Normally the serologic marker (HBsAG) level declines and disappears after the acute hepatitis B episode
The presence of antibodies to HBsAG (anti-HBS) indicates recovery and immunity to hepatitis B
HEPATITIS B (HBV)
PREVENTION Strict hand washing Screening blood donors Testing of all pregnant women Needle precautions Avoiding intimate sexual contact if hepatitis B
surface antigen (HBsAG) is positive Hepatitis B vaccine: Engerix-B, Recombivax HB Hepatitis B immune globulin (HBIG): For individuals
exposed to HBV either through sexual contact or through the percutaneous or transmucosal routes, who have never had hepatitis B and have never received hepatitis B vaccine
HEPATITIS C (HCV)
DESCRIPTION Occurs year-round Can occur in any age group Is common among drug abusers and is the
major cause of post-transfusion hepatitis Risk factors are similar as HBV since hepatitis
C is also parenterally transmitted INCREASED RISK INDIVIDUALS
Parenteral drug users Clients receiving frequent transfusions Health care personnel
HEPATITIS C (HCV)
TRANSMISSION Same as HBV; primarily through blood
INCUBATION PERIOD 5 to 10 weeks
COMPLICATIONS Chronic liver disease Cirrhosis Primary hepatocellular carcinoma
HEPATITIS C (HCV)
TESTING Anti-HCV is the antibody to HCV and is most
accurate in detecting chronic states of hepatitis C
PREVENTION Strict hand washing Needle precautions Screening of blood donors
HEPATITIS D (HDV)
DESCRIPTION Common in the Mediterranean and Middle Eastern
areas Seen with hepatitis B and may cause infection only in
the presence of active HBV infection Coinfection with the delta-agent intensifies the acute
symptoms of hepatitis B Transmission and risk of infection is the same as HBV,
via contact with blood and blood products Prevention of HBV infection with vaccine also prevents
HDV infection, since HDV is dependent on HBV for replication
HEPATITIS D (HDV)
HIGH RISK INDIVIDUALS Drug users Clients receiving hemodialysis Clients receiving frequent blood transfusions
TRANSMISSION Same as HBV
INCUBATION PERIOD 7 to 8 weeks
HEPATITIS D (HDV)
COMPLICATIONS Chronic liver disease Fulminant hepatitis
TESTING Serologic hepatitis delta virus (HDV) determination is
made by detection of the hepatitis D antigen (HDAg) early in the course of the infection and by detection of anti-HDV antibody in the later disease stages
PREVENTION Because hepatitis D must coexist with hepatitis B, the
precautions that help prevent hepatitis B are also useful in preventing delta hepatitis
HEPATITIS E (HEV)
DESCRIPTION A water-borne virus Prevalent in areas where sewage disposal is
inadequate or where communal bathing in contaminated rivers is practiced
Risk of infection is the same as HAV Presents as a mild disease except in infected
women in the third trimester of pregnancy, for whom the mortality rate is high
HEPATITIS E (HEV)
TRANSMISSION-Same as HAV INCUBATION PERIOD-2 to 9 weeks COMPLICATIONS
High mortality rate in pregnant women Fetal demise
TESTING Specific serologic tests for hepatitis E virus (HEV)
include detection of IgM and IgG antibodies to hepatitis E (anti-HEV)
PREVENTION Strict hand washing Treatment of water supplies and sanitation measures
HEPATITIS G (HGV)
DESCRIPTION Non-A, non-B, non-C hepatitis Autoantibodies are absent
RISK FACTORS Similar to those for hepatitis C Hepatitis G (HGV) has been found in some
blood donors, IV drug users, hemodialysis clients, and clients with hemophilia; however, HGV does not appear to cause significant liver disease
CLIENT AND FAMILY EDUCATION FOR
HEPATITIS Strict and frequent hand washingDo not share bathrooms unless the client
strictly adheres to personal hygiene measures
Individual washcloths, towels, drinking and eating utensils, as well as toothbrushes and razors, must be labeled and identified
The client must not prepare food for other family members
CLIENT AND FAMILY EDUCATION FOR HEPATITIS
The client should avoid alcohol and over-the-counter medications, particularly acetaminophen (Tylenol) and sedatives, because these medications are hepatotoxic
The client should increase activity gradually to prevent fatigue
The client should consume small, frequent, high-carbohydrate, low-fat foods
The client is not to donate blood
CLIENT AND FAMILY EDUCATION FOR HEPATITIS
The client may maintain normal contact with people as long as proper personal hygiene is maintained
Close personal contact such as kissing should be discouraged until HBsAg test results are negative
The client is to avoid sexual activity until hepatitis B surface antigen (HBsAg) results are negative