1. NURSING MANAGEMENT OF ADULTS WITH DISORDERS OF THE LIVER
Spring 2009 1

2. TOPICS TO BE REVIEWED HEPATITIS CIRRHOSIS
STEATOHEPATITIS (FATTY LIVER)
HEPATIC ABSCESS
LIVER TRAUMA
CANCER OF LIVER
LIVER TRANSPLANT 2

3. NORMAL FUNCTION OF LIVER
MAIN FUNCTIONS OF THE LIVER: storage, protection, metabolism
Maintains normal serum glucose levels
Ammonia conversion
Protein metabolism
Fat metabolism
Vitamin and Iron storage
Drug metabolism and detoxification 3

4. LIVER FUNCTION: GLUCOSE METABOLISM
What happens to glucose in the liver?
Where is it stored?
When is it released?
What is gluconeogenesis?
When does it take place? 4

5. LIVER FUNCTION: AMMONIA CONVERSION
When gluconeogenesis takes place what is the byproduct of the process?
What happens to the byproduct?
What do the bacteria in the intestines produce as a byproduct?
How is this byproduct removed? 5

6. LIVER FUNCTION: PROTEIN METABOLISM
What is the liver’s job in terms of synthesizing plasma proteins?
What does the liver need to complete it’s job? 6

7. LIVER FUNCTION: FAT METABOLISM
What is the liver’s job in terms of fat metabolism?
When does the liver do this?
What are the results of this metabolism used for? 7

8. LIVER FUNCTION: VITAMIN & IRON STORAGE
Stores which fat soluble vitamins?
What other vitamins are stored in the liver?
What are these vitamins responsible for?
Which minerals are stored in the liver? 8

9. LIVER FUNCTION: DRUG METABOLISM and DETOXIFICATION
THE FOLLOWING CLASSIFICATION OF DRUGS ARE METABOLIZED BY THE LIVER?
What else is metabolized by the liver?
What does the liver do in terms of detoxification? 9

10. NORMAL FUNCTION: bile secretion
What is the liver’s job with Bile?
When is bile secreted?
Where is Bile collected and stored?
How is this related to Billirubin?
When do Billirubin levels increase? 10

11. LIVER FUNCTION: PROTECTION
What does the liver’s protection function involve?
What do the cells do?

12. LIVER FUNCTION CONTINUED
Inactivates Hormones
Estrogen
Testoterone
Progesterone
Aldosterone
cortisol
Sinusoids store blood (about cc) 12

13. DISORDER OF THE LIVER
HEPATITIS 13

14. Hepatitis Widespread viral inflammation of liver cells
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)
Hepatitis F and G are uncommon (HFV, HGV)
DRUG INDUCED HEPATITIS
Occurs as a secondary infection 14

15. Hepatitis A (HAV)
Similar to that of a typical viral syndrome; often goes unrecognized
Spread via the fecal-oral route by oral ingestion of fecal contaminants
Contaminated water, shellfish from contaminated water, food contaminated by handlers infected with hepatitis A
Also spread by oral-anal sexual activity
(Continued) 15

16. Hepatitis A (HAV)(Continued)
Incubation period for hepatitis A is 15 to 50 days.
Disease is usually not life threatening.
Disease may be more severe in individuals older than 40 years of age.
Many people who have hepatitis A don’t know it; symptoms are similar to a gastrointestinal illness. 16

17. Hepatitis B (HBV)
Spread is via unprotected sexual intercourse with an infected partner, sharing needles, accidental needle sticks, blood transfusions, hemodialysis, maternal-fetal route.
Symptoms occur in 25 to 180 days after exposure; symptoms include anorexia, nausea and vomiting, fever, fatigue, right upper quadrant pain, dark urine, light stool, joint pain, and jaundice.
(Continued)
S&P 17

18. Hepatitis B (HBV) (Continued)
Hepatitis carriers can infect others, even if they are without symptoms. 18

19. Hepatitis C (HCV)
Spread is by sharing needles, blood, blood products, or organ transplants (prior to 1992), needle stick injury, tattoos, intranasal cocaine use.
Incubation period is 21 to 140 days.
Most individuals are asymptomatic; damage occurs over decades.
Hepatitis C is the leading indication for liver transplantation in the U.S.
NOT TRANSMITTED BY CAUSUAL OR INTIMATE HOUSEHOLD CONTACT
S&P 19

20. Hepatitis D (HDV) Transmitted primarily by parenteral routes
Incubation period 14 to 56 days
HDV coinfects with HBV and needs it presence to replicate
S&P 20

21. Hepatitis E (HEV)
Present in endemic areas where waterborne epidemics occur and in travelers to those areas (India, Asia, Africa, Middle East, Mexico, Central America & South America)
Also seen in travellers coming from these areas
Transmitted via fecal-oral route
Resembles hepatitis A
Incubation period 15 to 64 days
S&P 21

22. Clinical Manifestations of all Hepatitis
Abdominal pain
Changes in skin or eye color
Arthralgia (joint pain)
Myalgia (muscle pain)
Diarrhea/constipation
Wgt loss
Hepatomegaly
Fever
Lethargy/Malaise
Nausea/vomiting
Intolerance to fats/dyspepsia
Pruritus
CHANGES IN COLOR OF URINE AND STOOL 22

23. ASSESSMENT HEALTH HISTORY Suspected exposure Medical history
SIGNS/SYMPTOMS
Pre-icteric stage
Icteric stage
Post-icteric stage
HEALTH HISTORY
Suspected exposure
Medical history 23

24. SIGNS/SYMPTOMS
PRE-ICTERIC STAGE
Lasts about 1 week 24

25. SIGNS AND SYMPTOMS ICTERIC STAGE Lasts 2-6 weeks Jaundice appears
Yellow skin, sclera, mucous membranes
Dark amber urine
Clay colored stools 25

26. SIGNS AND SYMPTOMS POST-ICTERIC STAGE Lasts 2-6 weeks
Jaundice subsides
Liver decreases in size
Good appetite 26

27. LABORATORY TESTS FOR HEPATITIS
There will be an increase of liver enzymes and serologic markers INDICATING A PRESENCE OF HEPATITIS A, B, C 27

28. LABORATORY TESTS FOR HEPATITIS A (HAV)
Presence of hepatitis A in client: when hepatitis A (HAV) antibodies (anti-HAV) are found in the blood
Presence of immunoglobulin M(IgM) antibodies means that ongoing inflammation of liver present (persisits for 4-6 wks)
Previous infection indicated by presence of immunoglbulin G (IgG) antibodies which provides permanent immunity to disease 28

29. LABORATORY TESTS FOR HEPATITIS B (HBV)
Serologic markers which indicate client has Hepatitis B (HBV) are:
HBsAg (Hepatitis B surface Antigen)
Anti-HBc IgM (IgM antibodies to hepatitis B core antigen)
If these levels are elevated after 6 months: chronic or carrier state
Presence of antibodies to HBsAb (hepatitis B surface antibody): indicates recovery and immunity to hepatitis B
Someone immunized will have a positive HBsAb 29

30. LABORATORY TESTS FOR HEPATITIS C (HCV)
ELISA (enzyme linked immunosorbent assay ) SCREENS INITIALLY & for HCV antibodies (anti-HCV): can detect antibodies in 4 wks
RIBA: (recumbent immunoblot assay): used to confirm that client has been exposed and has developed antibody
HCV PCR (HCV polymerase chain reaction test): confirms presence of circulating active virus 30

31. LABORATORY TEST FOR HEPATITIS D (HDV)
Presence of virus confirmed by identification of intrahepatic delta antigen
Also by rise in hepatitis D virus antibodies (anti-HDV) titer
Found within a few days of infection 31

32. LBORATORY TESTS FOR HEPATITIS E (HEV)
VIRUS CANNOT BE DETECTED
Presence of hepatitis E antibodies (anti-HEV) is found in people infected with virus 32

33. LABORATORY TESTS CONTINUED
A person having a previous infection is indicated by immunoglobulin G (IgG) antibodies. They persist in blood and provide permanent immunity to HAV 33

34. LABORATORY TESTS INDICATING HEPATITIS
TESTS WHICH ARE LOWERED:
Leukocytes (leukopenia)
Serum albumin
Serum glucose (hypoglycemia)
PT (prolonged)
TESTS WHICH ARE
ELEVATED:
serum bilirubin
Bilirubin in urine
ALT
AST
Alkaline phosphatase elevated or may be normal 34

35. Nonsurgical Management
Physical rest
Psychological rest
Drug therapy includes:
Antiemetics
Antiviral medications
Immunomodulators
Corticosteroids
DECREASE # MEDS TO ALLOW LIVER TO REST 35

36. DRUGS
ANTIVIRALS:
Lamivudine (Epivir-HBV)
Adefovir dipivoxil (Hepsera)
USED: to destroy Hepatitis B virus in chronic disease
SIDE EFFECTS: alters renal function; granulocytopenia 36

37. DRUGS IMMUNOMODULATING DRUGS:
Interferon(peginterferon alfa-2a) (Pegasys)
Oral ribavirin (Virazole) 37

38. NURSING CARE Diet therapy Hydration No alcohol
Low fat, moderate protein, high CHO diet, high calorie
Small frequent meals
Vit B, C, K 38

39. PATIENT EDUCATION Hepatitis A Vaccine Hepatitis B vaccine
Prevention to health care professionals
Knowledge of transmission routes
Proper personal hygiene and good sanitation
Gamma Globulin
Avoid sex until antibody results (negative)
Hepatitis A Vaccine
Hepatitis B vaccine
No vaccine for Hepatitis E
Hepatitis C mainly spread through blood transfusions: (screen blood products) 39

40. CIRRHOSIS DEFINED Chronic Degenerative Causes liver enlargement
Causes loss of normal liver function 40

41. PATHOPHYSIOLOGY
Fibrotic bands of connective tissue change the structure of the liver
Inflammation causes degeneration and destruction of liver cells
Tissue becomes nodular
Nodules block bile ducts and normal blood flow throughout the liver
Blood flow changes occur from compression by the fibrous tissue 41

42. TYPES OF CIRRHOSIS
Laennec’s cirrhosis: chronic ETOH, nutritional deficiencies
Biliary
Postnecrotic cirrhosis: hepatic necrosis
Cardiac: congestion and tissue damage due to heart failure 42

43. ETIOLOGY Known causes of liver disease include: Alcohol
Viral hepatitis
Autoimmune hepatitis
Steatohepatitis
Drugs and toxins
Biliary disease
(Continued) 43

44. ETIOLOGY CONTINUED
Metabolic/genetic causes
Cardiovascular disease 44

45. EARLY SIGNS AND SYMPTOMS CIRRHOSIS
Same for all types regardless of the cause
Start out vague, like flu
General weakness, Fatigue
Anorexia, Indigestion
Abnormal bowel function (constipation, or diarrhea)
Abdominal pain/liver tenderness 45

46. LATE S & S
Jaundice, pruritus, dry skin, warm bright red palms of hands (palmar erythema), rashes
Edema, ascites, significant wgt change, peripheral dependent edema extremities and sacrum
Bleeding tendencies/Anemia/petecchiae, echymosis
Infections
Menstrual irreg/gynecomastia/impotence
Renal failure/dark amber urine
Clay colored stools 46

47. ASSESSMENT INSPECTION: Jaundice Caput medusae: dilated abd veins,
striae,
spider angiomas
Contour of abdomen: Distension: massive ascites
Everted umbilicus (umbilicus protrusion)
HEPATOMEGALY, SPLENOMEGALY 47

48. Other Physical Assessments
Assess nasogastric drainage, vomitus, and stool for presence of blood
Fetor hepaticus (breath odor)
Amenorrhea
Gynecomastia, testicular atrophy, impotence
Neurologic changes: changes in LOC, leading to coma, Asterixis 48

49. HOW TO ELICIT ASTERIXIS
Have client extend the arm,
dorsiflex the wrist
Extend the fingers
OBSERVE rapid non-rhythmic extensions and flexions 49

50. Laboratory Assessment
AST: Aminotransferase serum levels and LDH: lactate dehydrogenase may be elevated from hepatic cell destruction.
Alkaline phosphatase levels may increase from obstructive jaundice.
Total serum bilirubin from hepatic disease and urobilinogen levels may rise from hepatocellular obstruction or liver disease.
decrease.
(Continued) 50

51. Laboratory Assessment (Continued)
Fecal urobilinogen is decreased due to obstructive liver disease
Total serum protein and albumin levels decreased
Prothrombin time prolonged; platelet count low
Decreased hemoglobin and hematocrit values due to anemia and white blood cell count
S&P 51

52. LABORATORY ASSESSMENT CONTINUED
Elevated ammonia levels: liver cannot excrete ammonia
BUN and Serum creatinine level possibly elevated due to decreased renal function 52

53. COMPLICATIONS: PORTAL HYPERTENSION
Increase pressure in portal vein
Comes from obstruction of blood flow from pressure by CT bands (see patho)
New channels looked for
Blood flows back to spleen (splenomegaly)
Veins become dilated (esophagus, stomach, intestines, abdomen, rectum) 53

54. PORTAL HYPERTENSION (CONTINUED)
Results in:
Ascites
Esophageal varices
Prominent abdominal veins (caput medusae)
hemorroids 54

55. COMPLICATION: ASCITES
DEFINED AS:
Accumulation of free fluid within the peritoneal cavity
With increased hydrostatic pressure from portal hypertension fluid leaks into peritoneal cavity
Albumin in fluid hypoalbuminemia 55

56. ASCITES CONTINUED Hypovolemia renal vasoconstriction
Renin-angiotensin system triggered
Sodium and water retention
Leads to increased hydrostatic pressure
Perpetuates the cycle of ASCITES 56

57. COMPLICATIONS ASCITES:
Bed rest, HOB up 30 degrees or higher; or sitting in chair
Abdominal girth measurements
bid wgts standing
Strict fluid restriction; strict I & O, vitamin supplements
Salt free diet/diuretics/electrolyte replacement 57

58. Excess Fluid Volume (Continued)
Paracentesis is insertion of trocar catheter into abdomen to remove & drain fluid from the peritoneal cavity.
Observe for possibility of impending shock, electrolyte imbalances: albumin IV. 58

59. EXCESS FLUID SURGICAL MANAGEMENT CONTINUED
LAVEEN SHUNT (peritoneovenous shunt): surgical procedure, tube placed in peritoneal cavity, drain fluid into superior vena cava
PORTACAVAL SHUNT: (See p 1378
fig 62.4) surgical shunting diverts portal venous blood flow from the liver
TIPS (transjugular intrahepatic portalsystemic shunt): non surgical procedure creating a connection within the liver between the portal and systemic circulation to reduce portal pressure 59

60. COMPLICATION: BLEEDING ESOPHAGEAL VARICES
DEFINED: fragile thin walled esophageal veins become distended from pressure
Portal hypertension blood backs up from liver to esophageal and gastric vessels 60

61. COMPLICATIONS ESOPHAGEAL VARICES MEDICAL EMERGENCY LIFE THREATENING
S&S: hematemesis, melena, shock
Can occur spontaneously
Can be caused by any activity that
Abdominal pressure 61

62. TREATMENT OF BLEEDING ESOPHAGEAL VARICES
IV fluids/electrolytes/volume expander/ transfuse
ESOPHAGOGASTRIC BALLOON TAMPONADE: via Sengstaken-Blakemore tube
Compressing bleeding vessels with this tube 62

63. SENGSTAKEN-BLAKEMORE TUBE
Used to control bleeding
Esophageal balloon
Gastric balloon
3 lumens
1 for gastric lavage
1 for inflating the esophageal balloon
1 for inflating the gastric balloon 63

64. SENGSTAKEN-BLAKEMORE TUBE: NRSG CARE
MD inserts tube with HOB degrees
MOST SERIOUS COMPLICATION: ASPIRATION AND AIRWAY OCCLUSION
SURGICAL SCISSORS AT BEDSIDE
Monitor for respiratory distress
Suction saliva from upper esophagus, nasopharynx
Check nostrils frequently, cleanse and lubricate to prevent ulceration
Removed after bldg controlled 64

65. RUPTURE OF ESOPHAGEAL VARICIES
Vasopressin: constriction arterial bed
Somatostatin: decreases bldg without vasoconstrictive effects of Vasopressin
Propranolol: beta blocker to decrease portal pressure 65

66. COMPLICATION: COAGULATION DEFECTS
synthesis of bile in liver
Prevents absorption of fat soluble vitamins (vit K)
Without vit K clotting factors are not produced
susceptible to bleeding
Abnormal PT (prolonged or ) 66

67. COMPLICATION: SPLENOMEGALY
Backup of blood into spleen
Spleen destroys platelets
thrombocytopenia (first sign of liver dysfunction) 67

68. COMPLICATION: JAUNDICE
Liver cells cannot excrete bilirubin
circulating bilirubin levels
LABORATORY TESTS: changes with hepatocellular jaundice
Serum bilirubin (indirect and direct)
Urine bilirubin
Urobilinogen stool: normal to
Urobilinogen urine: normal to 68

69. COMPLICATIONS: PORTAL SYSTEMIC ENCEPHALOPATHY (PSE)
Also called HEPATIC ENCEPHALOPATHY AND HEPATIC COMA
SEE: neurologic symptoms
Impaired LOC
Impaired thinking
Impaired neuromuscular disturbances
ACUTE AND REVERSIBLE with early intervention
CAUSED BY: elevated ammonia levels 69

70. NURSING DIAGNOSIS Activity intolerance Fluid volume deficit
Fluid volume excess
Ineffective breathing patterns
Risk for hemorrhage
Risk for infection
Altered nutrition
Pain
Sexual dysfunction 70

71. NURSING DIAGNOSIS CONTINUED
Altered thought processes
Risk for violence 71

72. NURSING CARE Bed rest with controlled activity, prevent clots
Prevent infection (pneumonia)
Assess for bleeding
Treat dry itching skin: no soap, soft linens, lotions, antihistamines
Assess F & E status, bid wgts, abd girth once shift, I&O, fluid restriction, amt of dietary protein
Assess neuro status q 2 hr
Psychological support/abstinence of alcohol 72

73. Fatty Liver (Steatohepatitis)
Fatty liver is caused by the accumulation of fats in and around the hepatic cells.
Causes include:
Diabetes mellitus
Obesity
Elevated lipid profile
Many clients are asymptomatic. 73

74. Hepatic Abscess Liver invaded by bacteria or protozoa causing abscess
Pyrogenic liver abscess; amebic hepatic abscess
Treatment usually involves:
Drainage with ultrasound guidance
Antibiotic therapy
S&P 74

75. Liver Trauma
The liver is the most common organ injured in clients with penetrating trauma of the abdomen, such as gunshot wounds and stab wounds.
Clinical manifestations include abdominal tenderness, distention, guarding, rigidity.
Treatment involves surgery, multiple blood products. 75

76. Cancer of the Liver One of the most common tumors in the world
LIVER BX: done in same day surgery, local anesthetic, done through skin. CRITICAL THAT COAGULATION TESTING BE DONE. MAJOR SE: hemorrhage
Most common c/o: abd discomfort
Tx includes: Chemotherapy/Surgery
S&P 76

77. Liver Transplantation
Used in the treatment of end-stage liver disease, primary malignant neoplasm of the liver
Donor livers obtained primarily from trauma victims who have not had liver damage
Donor liver transported to the surgery center in a cooled saline solution that preserves the organ for up to 8 hours
S&P 77

78. Complications Acute, chronic graft rejection Infection Hemorrhage
Hepatic artery thrombosis
Fluid and electrolyte imbalances
Pulmonary atelectasis
Acute renal failure
Psychological maladjustment 78