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

Cirrhosisby: Ashley Anderton, RN, BSN

From the notes of:John Nation, RN, MSNCharlene Morris, RN, MSNKelle Howard, MSN. RN, CNE

Cirrhosis Facts:

Progressive, leads to liver failureInsidious, prolonged course9th leading cause of death in U.S.Twice as common in menHighest incidence between ages 40 and 60.

What is Cirrhosis?

Extensive destruction of liver cellsCells attempt to regenerateRegenerative process is disorganizedFunctional liver tissue is destroyed and

scarring of liver occursOvergrowth of fibrous connective

tissue, distorting liver structure; obstructing blood flow

Four Types of Cirrhosis:

Alcoholic formerly called ________

Post-necrotic Biliary/obstructive Cardiac

Alcoholic cirrhosis:Usually associated with alcohol abuseMost common cause of cirrhosisCauses metabolic changes in liver

fat accumulates in liver (fatty liver)Fatty liver potentially reversibleIf alcohol abuse continues, widespread

liver scar formation occurs

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

Biliary cirrhosis:

Associated with chronic biliary obstruction and/or

infectionPrimary sclerosing cholangitis?

Diffuse fibrosis of liver

Jaundice is main feature

www.humanillnesses.com

Cardiac cirrhosis:

Develops from long-standing right sided heart failure

Results in patients with cor-pulmonale, constrictive pericarditis, and tricuspid insufficiency

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

Early Signs of cirrhosis:

Nausea and vomiting Anorexia Diarrhea or constipation Pain Fever Weight loss

Later Manifestations:

JaundiceSkin Lesions/Spider angiomasPalmer erythemaThrombocytopenia, Leukopenia, Anemia Coagulation disordersEndocrine disturbancePeripheral neuropathy & peripheral edema

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)

Skin Lesions

• WHY?

• Dilated blood vessels (spider angiomas)

• Palmar erythema

Hematologic Problems

Thrombocytopenia Leukopenia Anemia Vitamin K deficiency

www.elements4health.com

Endocrine Problems: Inactivation of adrenocortical

hormones Men Women Hyperaldosteronism

Peripheral Neuropathy&

Peripheral Edema Neuropathies due

to: Results in mixed

nervous symptoms Sensory symptoms

are most common Edema due to:

http://www.jhu.edu

Complications:

Portal Hypertension

Esophageal & Gastric Varices

Peripheral Edema & Ascites

Hepatic Encephalopathy

Complications:Portal Hypertension

• Compression and destruction of portal & hepatic veins

• Increased venous pressure in portal circulation

• Characterized by:• Collateral circulation develops

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!!

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?

Sengstaken-Blakesmore

www. medical-dictionary.com

Sengstaken-Blakemore Tube

Three Lumens:Esophageal balloon

inflationGastric balloon

inflationGastric aspiration

Acute BleedSupportive 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!!

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

TIPS Transjugular intrahepatic

portosystemic shunt

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

Increased capillary

permeability

Increased Na+

&H2O retention

Portal Hypertension

HypoproteinemiaFour Factors Lead to Ascites

www.patient.co.uk

Nursing Management of ASCITES:

Assess for respiratory distress Fowler’s position helps ease

work of breathing

Daily weightsMeasure abdominal girthAccurate I&O

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

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

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 manifestationshttp://chemistry.about.com

Where does ammonia come from?

A by-product of protein metabolismProtein and amino acids are broken

down by bacteria in GI tract, producing ammonia.

Liver converts this to urea which is eliminated in the urine

Hepatic Encephalopathy Stages

0-1st InsomniaPersonality

changesDisturbances of

awarenessForgetfulness,

irritability, & confusion

Trouble writing

http://lukeromyn.com/blog


2nd & 3rdLethargy, drowsinessInappropriate speech

Slurred speech

DisorientationAsterixis

flapping tremors

HiccupsHyperactive reflexesViolent behavior Slow, deep respirationsFetor hepaticus

musty sweet smell to breath


4th + Babinski

Possible seizures

Swelling of brain tissue

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)

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

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

www.reneerogers.com/nutrition

Overall Goals:

Relief of discomfort Minimal to no complications

(ascites, varices, hepatic encephalopathy)

Return to normal as possible lifestyle

http://www.fontana.org/index

Liver Dialysis

Bridge to transplantDialyze 6 hours at a time

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.

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

http://www.murketing.com/journal