1. Cirrhosis by: Ashley Anderton, RN, BSN
From the notes of: John Nation, RN, MSN
Charlene Morris, RN, MSN
Kelle Howard, MSN. RN, CNE

2. Cirrhosis Facts: Progressive, leads to liver failure
Insidious, prolonged course
9th leading cause of death in U.S.
Twice as common in men
Highest incidence between ages
40 and 60.

3. What is Cirrhosis? Extensive destruction of liver cells
Cells attempt to regenerate
Regenerative process is disorganized
Functional liver tissue is destroyed and scarring of liver occurs
Overgrowth of fibrous connective tissue, distorting liver structure; obstructing blood flow

4. Four Types of Cirrhosis:
Alcoholic
formerly called ________
Post-necrotic
Biliary/obstructive
Cardiac

5. Alcoholic cirrhosis: Usually associated with alcohol abuse
Most common cause of cirrhosis
Causes metabolic changes in liver
fat accumulates in liver (fatty liver)
Fatty liver potentially reversible
If alcohol abuse continues, widespread liver scar formation occurs

6. Post Necrotic cirrhosis:
Complication of:
viral infections
toxicity
autoimmune hepatitis
20% of patient’s with chronic hepatitis C will develop cirrhosis
Broad bands of scar tissue form within the liver

7. Biliary cirrhosis: Associated with chronic biliary obstruction and/or
infection
Primary sclerosing cholangitis?
Diffuse fibrosis of liver
Jaundice is main feature

8. Cardiac cirrhosis:
Develops from long-standing right sided heart failure
Results in patients with cor-pulmonale, constrictive pericarditis, and tricuspid insufficiency

9. Diagnostic Studies: Enzyme levels (AST, ALT)
initially elevated due to release from damaged liver cells
In end-stage liver disease
AST & ALT may be normal
Decrease:
total protein
albumin
Increase:
serum bilirubin
globulin levels
Prothrombin time prolonged

10. Early Signs of cirrhosis:
Nausea and vomiting
Anorexia
Diarrhea or constipation
Pain
Fever
Weight loss

11. Later Manifestations:
Jaundice
Skin Lesions/Spider angiomas
Palmer erythema
Thrombocytopenia, Leukopenia, Anemia
Coagulation disorders
Endocrine disturbance
Peripheral neuropathy & peripheral edema

12. Jaundice
Results from functional derangement of liver cells, compression of bile ducts
Liver’s decreased ability to excrete _________
+ Biliary obstruction, obstructive jaundice may occur accompanied by pruritus (accumulation of bile salts)

13. Skin Lesions WHY? Dilated blood vessels (spider angiomas)
Palmar erythema

14. Hematologic Problems Thrombocytopenia Leukopenia Anemia
Vitamin K deficiency

15. Endocrine Problems: Inactivation of adrenocortical hormones Men Women
Hyperaldosteronism

16. Peripheral Neuropathy
&
Peripheral Edema
Neuropathies due to:
Results in mixed nervous symptoms
Sensory symptoms are most common
Edema due to:

17. Complications: Portal Hypertension Esophageal & Gastric Varices
Peripheral Edema & Ascites
Hepatic Encephalopathy

18. Complications: Portal Hypertension
Compression and destruction of portal & hepatic veins
Increased venous pressure in portal circulation
Characterized by:
Collateral circulation develops

19. Esophageal & Gastric Varices:
Complications:
Esophageal & Gastric Varices:
Esophageal:
Complex of twisting veins at lower end of esophagus
enlarged & swollen
Gastric-
upper portion of stomach
may occur alone or in combination with esophageal
Tolerate high pressure poorly, bleeding easily with distention
Rupture in response to irritation
Most life threatening complication!!

20. Treatment for Varices:
Stop bleeding, manage airway, prevent aspiration of blood!!
Drug Therapy:
Propranolol, Sandostatin, Vasopressin, NTG
Band ligation of varices
Endoscopic sclerotherapy
thromboses and obliterates distended veins
Balloon tamponade-mechanical compresson of varices
Sengstaken-Blakesmore
Avoid:
alcohol & irritating foods
What common drugs should be avoided?

21. Sengstaken-Blakesmore
www. medical-dictionary.com

22. Sengstaken-Blakemore Tube
Three Lumens:
Esophageal balloon inflation
Gastric balloon inflation
Gastric aspiration

23. Acute Bleed Supportive Measures: FFP, PRBC’s, Vitamin K Antibiotics
Protonix, Zantac
Propanolol
Prevent factors that may increase intra-abdominal pressure
Higher incidence of recurrent bleeds, so continued therapy is necessary!!

24. Shunting Procedures: Used more after 2nd major bleeding episode TIPS
shunt is placed between systemic and portal venous systems
redirect’s portal blood flow
reduces portal venous pressure
decompresses varices
contraindicated in patient’s with hepatic encephalopathy

25. TIPS Transjugular intrahepatic portosystemic shunt

26. Ascites & Peripheral Edema
Complications:
Ascites & Peripheral Edema
Results from impaired liver synthesis of albumin = hypoalbuminemia
Occurs as ankle and presacral edema
Ascites
accumulation of serous fluid in periotoneal or abdominal cavity
Hyperaldosteronism

27. Four Factors Lead to Ascites
Hypoproteinemia
Increased Na+
&
H2O retention
Increased capillary
permeability
Portal Hypertension

29. Nursing Management of ASCITES:
Assess for respiratory distress
Fowler’s position helps ease work of breathing
Daily weights
Measure abdominal girth
Accurate I&O

30. Medical Management of Ascites:
Na+ and Fluid restriction
Albumin
Diuretic therapy:
Aldactone, HCTZ, Lasix
Paracentesis
needle puncture of abdominal cavity to remove ascitic fluid- temporary
have patient void before procedure

31. Management of Ascites:
Peritoneovenous Shunt
surgical procedure
provides continuous reinfusion of ascitic fluid into venous system
Not 1st line therapy due to high number of complications
Does not improve survival rates

32. Hepatic Encephalopathy:
Terminal complication of liver disease
Disorder of protein metabolism and excretion
Ammonia
enters the systemic circulation without liver detoxification
crosses blood-brain barrier, causing neurologic toxic manifestations
Four stages of manifestations

33. Where does ammonia come from?
A by-product of protein metabolism
Protein and amino acids are broken down by bacteria in GI tract, producing ammonia.
Liver converts this to urea which is eliminated in the urine

34. Hepatic Encephalopathy Stages 0-1st
Insomnia
Personality changes
Disturbances of awareness
Forgetfulness, irritability, & confusion
Trouble writing

35. Hepatic Encephalopathy Stages 2nd & 3rd
Lethargy, drowsiness
Inappropriate speech
Slurred speech
Disorientation
Asterixis
flapping tremors
Hiccups
Hyperactive reflexes
Violent behavior
Slow, deep respirations
Fetor hepaticus
musty sweet smell to breath

36. Hepatic Encephalopathy Stages 4th
+ Babinski
Possible seizures
Swelling of brain tissue

37. Hepatic Encephalopathy
Treatment
Hepatic Encephalopathy
Reduce ammonia formation
Lactulose
Control GI bleeding
Decreasing protein in intestine
Neomycin
Electrolyte replacement
Possible liver transplant
(depends on a number of factors)

38. Hepatorenal Syndrome:
Serious complication
Functional renal failure with advancing azotemia, oliguria, and ascites
Portal hypertension + liver decompensation = decreased arterial blood volume & renal vasoconstriction
May be reversed by liver transplantation

39. Nutritional Therapy: High calorie/High Carb diet Low protein diet
if Hepatic Encephalopathy present
Parenteral nutrition of tube feedings may be required
Low-sodium diet
if ascites and edema
Dietary education on reading labels at home

40. Overall Goals: Relief of discomfort Minimal to no complications
(ascites, varices, hepatic encephalopathy)
Return to normal as possible lifestyle

41. Liver Dialysis
Bridge to transplant
Dialyze 6 hours at a time

42. Donors: Live donor liver transplants are an excellent option.
Liver regenerates to appropriate size for their individual bodies.
Survival rates increase / shorter wait time
The donor - a blood relative, spouse, or friend, will have extensive medical and psychological evaluations to ensure the lowest possible risk.

44. Liver Transplantation
Blood type and body size are critical factors in determining who is an appropriate donor.
Potential donors evaluated for:
liver disease, alcohol or drug abuse, cancer, or infection.
hepatitis, AIDS, and other infections.
matched according to blood type and body size.
Age, race, and sex are not considered.
Cadaver donor have to wait