1. Genetics
2. Viruses
3. Unhealthy life choces

When healthy liver tissue is replaced by:
Fibrotic Tissue (called cirrhosis)

Fatty Tissue (called Fatty Liver Disease) 

Chronic, progressive disease

Characterized by severe alteration in structure &
function of the liver cells 

Cirrhosis is characterized by inflammation & necrosis of the liver cells.

This results in hardening of liver tissue.

This results in enlarged liver cells compressing the liver lobule--leading to increased resistance to blood flow.

This interference with blood flow may result in portal hypertension. 

What causes chronic liver dysfunction 

in Cirrhosis?

Previously called Laennec's

Metabolite of alcohol causes liver necrosis.

Women are more prone to damage from alcohol 

• GI s/s: anorexia, dyspepsia, flatulence, N/V, bowel habit changes
• Fever
• Weakness
• Weight loss
• abdominal discomfort (RUQ or epigastric)

• Jaundice
• Peripheral edema
• Ascites
• Skin lesions
• Hematologic disorders
• Endocrine disturbances
• Peripheral neuropathies

1. Portal Hypertension
2. Reduced Liver Metabolic Processes
3. Impaired Bile Formation & Flow

Portal system of veins normally drains from the spleen, stomach, esophagus, intestines, pancreas and gallbladder

Instead of emptying directly into inferior vena cava, they empy into the portal vein and detour through the liver

• Ascites
• Esophageal & Gastric Varices

1. Altered carbohydrate metabolism
2. Altered fat metabolism
3. Altered protein metabolism

Manifests as fatigue & activity intolerance

Bile salts are not adquately produced, leading to an inability to metabolize fat.

Vitamin K is a fat soluble vitamin.  If fat is not metabolized, then there is a decreased supply.

Vitamin K is important for clotting--
manifests as prolonged PT & bleeding. 

1. Decreased synthesis of Albumin: leads to low serum albumin.  Albumin is needed to maintain colloidal osmotic pressure.  This pressure holds fluid into the intravascular space.  Low serum albumin is associated with the development of ascites & edema.
    
2. Decreased synthesis of Globulin: Globulin is essential for immune responses in the body.
    
3. Decreased synthesis of fibrinogen: fibrinogen is needed for clotting cascade, predisposing a patient to bleeding at low levels. PT is increased, PTT is increased. This manifests as bruising, epitaxis, gingival bleeding; can cause frank bleeding from esophageal and gastric varices. 

Fluid leaves the intravascular space and enters the peritoneal cavity (ascites) during portal htn.

This results in decreased plasma volume.

This activates a compensatory mechanism: ADH & Aldosterone are released.

The release of ADH & aldosterone causes sodium and water retention, making the ascites worse.

The Renin-Angiotensin system is also activated.
This causes systemic vasoconstriction.

Urine output decreases as a result of impaired perfusion. 

Both men & women may experience sexual dysfunction & spider angiomas.

Men: gynecomastia, loss of axillary & pubic hair, testicular atrophy, impotence

Women: amenorrhea, abnormal vaginal bleeding (older women)

Leads to an increase in serum bilirubin.

This leads to jaundice.

A symptom, not a disease.

Yellowing of the skin, sclera, & mucous membranes caused by elevated serum bilirubin.

Occurs when serum bilirubin levels are approximately 3x the normal value. 

It is formed from the breakdown of hemoglobin. 

The uncongugated bilirubin is released into circulation & binds to albumin. It is not water soluble and cannot be filtered or excreted in urine.

The unconjugated bilirubin is combined with glucouronic acid in the liver and converted to conjugated bilirubin.

Conjugated bilirubin is water soluble and is secreted by the hepatocytes into bile and released through the hepatic and biliary duct system into the small intestines.  

The conjugated bilirubin is converted, by bacterial action, into urobilinogen.

The urobilinogen is partly:

1. excreted in feces (gives color to stool)

2. Reabsorbed back into portal bloodstream through the intestinal mucosa

3. excreted by the kidneys, in very small amounts in the urine 

1. Hemolytic (prehepatic) Jaundice

2. Hepatocellular (hepatic) Jaundice

3. Obstructive (post-hepatic) Jaundice

Describe Hemolytic Jaundice.

What causes it?

What is the result? 

Hemoglobin that is released when cells die is converted into bilirubin. An increase in RBC lysis increases hemoglobin breakdown into bilirubin at a faster rate.  This causes accumulation of bilirubin in the blood and can cause jaundice. 

*Increased breakdown of RBC's produces an increased amount of unconjugated bilirubin*

Caused by incompatible blood transfusion reactions, sickle cell crisis, or malaria

Results in elevated unconjugated bilirubin

Hepatocytes are damaged and leak bilirubin into the bloodstream.  This increases levels of conjugated bilirubin.  Severe cases may have both increased unconjugated and increased conjugated bilirubin from the inability of the hepatocytes to conjugate the bilirubin and the continuous leakage of conjugated bilirubin into the bloodstream

Causes are hepatitis, cirrhosis, and hepatic carcinoma

Results in elevated conjugated & unconjugated bilirubin levels

Describe Obstructive Jaundice.

What causes it?

What results from it?

Failure of soluble bilirubin (conjugated) to reach the intestines after it has left the liver.

Causes: hepatitis, cirrhosis, gallbladder stones, bile duct stones, biliary strictures, pancreatic cancer

Complete obstruction results in: clay colored stools, because bilirubin does not enter intestines

Bilirubin overflows into the bloodstream and urine becomes a deep orange color & foams when shaken.

Results in elevated conjugated bilirubin 

• Sclera--in light skinned people, first site of yellow discoloration
• Hard palate--in dark skinned, best site to identify the yellowing
• Skin--light yellow to bronze in color
• Urine--tea colored to dark orange
• Stools--clay colored
• Bruising & Bleeding
• GI--indigestion, N/V
• Pruritus--worsened if body tissues lack O2; aggrivated by perspiration

• Decrease patient activity & well-ventilated room (due to pruritus)
• maintain dry linens--laundering without starch and harsh soaps is the best
• Keep fingernails short & discourage scratching
• Avoid harsh soaps, sponging with tepid water may be enough or use alkaline soaps & emollients--Oatmeal baths may help
• Body Image Changes
• Meds: Questran (binds with bile acids), Benadryl

Low protein-- due to waste buildup/altered metabolism

High Carb--need energy source, liver not adequately storing glycogen for conversion to glucose

Low salt--due to water retention already occuring 

• Severe thrombocytopenia
• Local infection of the lung base
• Prolonged PT
• Peritonitis
• Obstructive Jaundice

• NPO for at least 6 hours
• No ASA, Ibuprofin, or anticoagulants x 1-2 weeks if possible
• Review PT, clotting, or bleeding times
• Baseline vital signs
• Informed Consent

• Carefully monitor vital signs for first 6-8 hours
• Assess for hemorrhage, increased HR, decreased BP, or restlessness
• Observe for bile leakage: pain in RUQ or R shoulder pain
• Maintain bedrest in flat position for 12-14 hours
• First two hours lay on right side to splint the puncture site

• hemorrhage
• Puncture of adjacent organs
• Peritonitis
• Pneumothorax

Catheter is inserted into neck vein (usually Jugular) and threaded to the liver where biopsy needle obtains a sample.

Used in patients with blood-clotting problems or massive ascites

Used for dx & tx of problems with liver, gallbladder, bile ducts, and pancreas

Endoscope is guided through the mouth & throat and into the esophagus, stomach, duodenum

Can examine the biliary pancreatic ducts

These areas can be visualized, biopsies taken, and certain procedure performed.

Define Ascites.

What causes it?

What problems ensue with it? 

Ascites--an accumulation of free fluid containing almost pure plasma in the peritoneal cavity

Caused by increased hydrostatic pressure from portal hypertension, causing plasma to leak directly from the liver surface and portal vein.  Also caused by decreased levels of albumin.

Problem: fluid pushes up on diaphragm and impairs breathing mechanisms

• Assess respiratory status (may need intubation)
• Monitor abdominal girth at level of umbilicus; mark abdomen for measuring; kneeling position is most accurate method
• I&O, daily weight
• Semi-fowler's postioning
• CTDB

• Initially, bedrest
• Focused on sodium restriction, diuretics, and fluid removal
• Sodium restriction is 1st step, then diuretics
  1st line: Aldactone, 2nd line: Lasix
• Monitor BUN, Creatinine, Na, & K+
• Salt Poor Albumin may be administered temporarily to increase colloidal osmotic pressure and decrease fluid loss into the peritoneal cavity
• Paracentesis procedure 

• Have patient void prior to procedure
• Take pre and post abdominal girth measurements
• Monitor VS, especially as fluid is being withdrawn; sudden drop in BP & tachycardia is a major complication
• Document amount, color, character--send to lab
• Check dressing for bleeding & leakage

Distal end goes into peritoneum

Tunneled under skin into jugular vein or superior vena cava.

One-way valve triggered by breathing (breathing increases intrabdominal pressure, causing it to be higher than the venous pressure)
 

Provides continuous reinfusion of ascetic fluid into the venous system.

Drainage catheter placed in abdomen below the umbilicus

Allows repeated, intermittent drainage

Enables home drainage with ostomy bag

Frequent infections are common
DIC (bleeding disorder) may occur

Frequent leakage 

Indicated for both drug instillation and ascites management

Nothing external when site is not accessed

Need skilled nursing to access the site

Pain associated with repeated port access

Indicated for intermittent, long-term drainage of ascites

Superior location

Less Leakage

Allows for home use and easy use for patient

Abnormal ammonia metabolism

Since the liver cannot convert ammonia to urea if it is failing, serum ammonia levels increase.

Increased serum ammonia levels causes an altered level of consciousness that ranges from confusion to coma. 

Early: computation skills altered
(trouble balancing checkbook)

  euphoria, depression, apathy, irritability, memory loss, yawning, confusion, drowsiness, insomnia, agitation

Slow, slurred speech

Hiccups

Slow, deep respirations

Hyperactive reflexes

Positive Babinski reflex

Characteristic symptom: asterixis (flapping tremors) most commonly involving the arms and hands

• Fluid & electrolyte and acid base disturbances
• Increased protein intake
• infection
• Diarrhea
• GI bleeding
• Constipation

• Diuretics, analgesics, narcotics, sedatives
• Acetaminophen
• Phenobarbitol
• Thorazine
• Compazine
• Morphine
• Alcohol
• Codeine

Stage I: tremors, impaired decisions, personality change

Stage II: Drowsiness, loss of sphincter control, asterixis (best seen when pt stretches out their arms and dorsiflexes their wrists)

Stage III: Marked confusion, incomprehensible speech

Stage IV: Profound coma--unresponsive to pain

Bedrest--decreases metabolic workload on liver, which decreases the amount of ammonia that needs to be converted to urea

Aim is to decrease ammonia production

Lactulose (Chronulac): creates acidic environment in the bowel, causes ammonia to leave the bloodstream and enter the colon; the laxative effect of lactulose promotes elimination of ammonia.

Neomycin: destroys normal bacteria in bowel (some ammonia is formed in GI tract through action of intestinal bacteria on protein) Given PO.

Restrict Meds that are toxic to the liver.

Protect the patient from harm. 

Given PO 30mL qday or BID

& Increased until patient has 2-4 loose stools/day

Higher doses may be given via NG or rectal tubes

Lactulose enemas may also be given

MAY CAUSE SEVERE DIARRHEA & 
FLUID & ELECTROLYTE LOSS 

Describe how Neomycin is used to treat
Hepatic Encephalopathy. 

How is it given?

What are nursing considerations? 

It destroys the normal bacteria in the bowel.

Destroying the bacteria decreases protein breakdown and ammonia production.

Given q6 hours

Toxic to kidneys; monitor renal function

may cause hearing impairments

Other antibiotics may be used instead:
Flagyl, Vancomycin, Levaquin, Rifampin 

Where are the common areas in which collateral channels develop?

Why do they develop?

Commonly in the lower esophagus, upper stomach, periumbilical area, and anus (hemorrhoids)

Develop in an attempt to reduce the high portal pressures caused by portal hypertension

• Alcohol ingestion
• Inadequately chewed food
• GERD
• increased intraabdominal pressure secondary to N/V, coughing, sneezing, straining with defecation, and lifting heavy objects

• Assess severity of blood loss
• Vital signs q15 min or more often
• Assess for s/s of shock
• Bowel sounds usually hyperactive due to sensitivity of bowel to blood
• Systolic BP <100 or postural drop greater than 10 reflects a significant blood loss
• Hx: hx of bleeding, current illnesses that may lead to GI bleed (cancer, liver disease, coagulopathies)

Hematocrit does not change dramatically during first few hours after acute GI bleeds

Hct decreases when extravascular fluid enters the vascular space to restore volume

1. Patent Airway

2. Hemodynamic Stabilization

1. Sandostatin/Octreotide: natural hormone derivative used to control bleeding by decreasing portal pressure. Safe for heart patients and has few serious side effects.

2. Vasopressin: synthetic ADH that acts as a vasoconstritor, decreasing blood flow to area
-Need to be on cardiac monitor because 
Vasopressin is coronary vasoconstrictor;
decreases HR & increases BP

 -IV Nitroglycerine is often given with Vasopressin; can decrease side effects (tissue ischemia) while enhancing beneficial effects.

-Monitor for abdominal cramping--increased vessels within the liver and vasoconstriction causes increased cramping. 

• Gastric balloon is inflated and clamped first
• Pulled back until feel resistance to place pressure on Gastroesophageal junction
• Use traction with external force
• Balloon remains inflated for up to 48 hours
• X-ray confirmation that balloon is below GJ.
• Deflate balloon q 8-12 hours
• Must deflate esophageal balloon prior to gastric or entire tube will displace upward and can occlude the airway.

• Decompresses only the varices
• Selective distal splenorectal shunt
  - causes minimal disruption of
  normal hepatic blood flow 
  - has a lower incidence of
  Hepatic encephalopathy
  - Distal end of splenic vein is
  anastamosed to side of L
  renal vein; blood is diverted
  from high pressure varices
  to the low pressure renal vein 

• Decompresses entire portovenous system:
• Portal Caval Shunt
  -creates an anastamosis between the
  portal vein and the inferior vena cava  
  -results in total loss of portal blood flow to liver
  - associated with increased incidence of hepatic encephalopathy (diversion  of ammonia past liver into systemic circ.)
  - used in emergency situations only
  when all otehr non-surgical tx failed 

What is the preferred method for permanent diversion of blood around a blocked portal system?

Describe it.

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Nonsurgical procedure in which a tract (shunt) between the systemic and portal venous system is created to redirect blood flow.

Catheter placed into jugular vein and threaded to hepatic vein and portal vein. Stents are positioned. 

Reduces portal venous pressure and decompresses the varices, thus controlling bleeding. 

1. Beta blockers: typically Inderal and nadolol (corgard); reduces HR and lowers portal vein pressure, reducing variceal bleeding
Used as primary prevention of recurrent bleeds.
Avoid use in patients with Type I diabetes, COPD

2. Isosorbide mononitrate (Imdur): given for patients who cannot tolerate beta-blockers

3.  Antiotensin I receptor agonists--Cozaar: lowers portal pressure

What is hepatorenal syndrome associated with?

What is the aim with it?

End stage cirrhosis

Ascites

Decreased Albumin

Portal Hypertension

Aim is to improve liver function while supporting renal function: fluids and diuretics to increase urine output, and avoiding renal toxic drugs

Clinical syndrome characterized by severe impairment of liver function associated with hepatic encephalopathy

Most common cause is drugs, usually acetaminophen in combination with ETOH

Other causes include: INH, Fluothane (anesthetic), sulfa-containing drugs, and NSAIDs

Runs course over 8 weeks, but can last up to 26 weeks

Liver transplant increases survival rates.

• Absence/Resolution of bleeding
• H&H returns to baseline
• Coagulation studies WNL
• Sufficient protein intake to promote liver regeneration but not enough to increase ammonia levels
• Serum albumin/protein WNL
• Absence of ascites
• Stable weight
• Adequate oxygenation and ventilation
• Resolution of encephalopathy
• BUN & Creatinine stable

• Well balanced
• Low fat 
• High carb, high calorie (2500-3000 caloreis)
• at least 1 gram of protein/kg to promote hepatocyte regeneration
• Vitamin replacement
• Vitamin K
• Folic Acid
• Thiamin
• Vitamin B-6
• With ascites--sodium restriction