lola oyedele msn, rn, ctn majuvy l. sulse msn, rn, ccrn liver biliary pancreatic problems and nrs...

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


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


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


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


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


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


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


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


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)


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


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


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

lola oyedele msn, rn, ctn majuvy l. sulse msn, rn, ccrn liver biliary pancreatic problems and nrs...

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