Unit 3: Cirrhosis Flashcards
What is the leading cause of cirrhosis?
Hepatitis C
Risk Factors for Developing Cirrhosis
- chronic infection with hepatitis A, B, or C
- chronic alcoholism
- biliary disease
- accumulation of fat in the liver
- autoimmune diseases
How to prevent cirrhosis
- improving health habits
- refraining from risky behaviors (needle sharing, unprotected sex)
- refraining from consumption of alcohol
- receiving vaccination for hepatitis
Laennec’s Cirrhosis
- alcohol-induced cirrhosis
- results from chronic alcoholism and malnutrition
- fibrosis occurs around central veins and portal areas
- may develop vascular or arterial spider angiomas on the abdomen; look like spider legs
- may develop reddened palms (palmar edema)
Post-necrotic or Micronodular Cirrhosis
-involves bands of scar tissue in the liver d/t previous acute viral hepatitis or exposure to hepatotoxins
Biliary Cirrhosis
- scarring of the liver tissue around the bile ducts and lobes of the liver b/c of chronic biliary obstruction and infection or cholangitis (inflammation of common bile duct)
- develop severe itching (pruritis) b/c of retention of bile salts
Nonalcoholic Steatohepatitis (NASH)
- cause of cirrhosis
- found in obese patients
- caused by accumulation of fat in liver cells, which leads to inflammation of the liver cells and over time results in cirrhosis
- NASH diagnosed by liver biopsy
Genetic causes of Cirrhosis
- Wilson’s disease
- Hemochromatosis (iron overload)
Wilson’s Disease
- cause of cirrhosis
- there is an abnormality of a protein that causes excessive accumulation of copper in the liver leading to chronic inflammation
- treatment: decrease levels of copper
Hemochromatosis
- causes cirrhosis
- iron overload
- there is an abnormally high accumulation of iron, which leads to chronic liver inflammation and cirrhosis
- Treatment: decrease levels of iron
Causes of Cirrhosis
- alcohol-induced (Laennec’s cirrhosis)
- post-necrotic or micronodular cirrhosis
- biliary cirrhosis
- nonalcoholic steatohepatitis (NASH)
- Wilson’s disease (copper overload)
- hemochromatosis (iron overload)
- autoimmune diagnosis
- hepatotoxins
- medications
- parasites
- cardiac dysfunction; cardiac cirrhosis (causes decreased oxygenation of liver cells, leading to liver cell death)
Cirrhosis of the Liver
causes cell destruction and fibrosis or scarring of hepatic tissues
Pathophysiology of Cirrhosis of the Liver
- Functional liver cells die, and damaged liver cells regenerate into nodules of liver cells that are surrounded by fibrous tissue
- bloody supply to this area is abnormal and occurs through a thick capillary network surrounding these nodules
- this irreversible chronic injury to functional liver cells result in liver cell necrosis, altered liver structure and function, and leads to alterations in blood and lymph flow resulting in hepatic insufficiency and hypertension in the portal vein
Portal Hypertension
- d/t alteration of blood flow to the liver
- an increase in the pressure in the veins that carry blood through the liver
Portal Hypertension
- d/t alteration of blood flow to the liver
- an increase in the pressure in the veins that carry blood through the liver
Alterations of blood flow to the liver results in?
> Portal hypertension
Shunting of blood around the liver, bypassing the liver cells
-while the blood reaches the liver from the stomach, intestines, spleen, and pancreas, it travels through the portal vein branching into the liver
-b/c these vessels are blocked by the scarring of the liver, blood cannot flow freely and blood backs up, causing an increase in pressure that leads to the enlargement of the veins in the esophagus, skin of abdomen, and veins in rectum and anus (hemorrhoids)
-this shunting of blood around the liver causes increased pressure in the surrounding vessels resulting in esophageal varices and gastric varices (abnormally dilated and weak veins), which may result in upper GI bleeding
Ascites
accumulation of protein-rich fluid in the abdominal cavity
- associated w/ poor quality of life, increased risk of infection, and poor long-term outcome
- may develop pleural effusions b/c of the exchange of fluid across the diaphragm to the pleural space surrounding the lungs
Coagulopathy
- B/c the liver synthesizes most of the coagulation cascade factors and fibrinolytic proteins, liver disease impacts the synthesis of clotting factors and coagulation mechanisms, leading to prolonged or excessive bleeding
- patients w/ liver disease are thrombocytopenic and have a prolonged PT
- some pts may exhibit bleeding, leading to disseminated intravascular coagulation (DIC)
Disseminated Intravascular Coagulation (DIC)
small blood clots form inside blood vessels, which in turn disrupt blood flow to organs and disrupt normal coagulation leading to excessive bleeding from the GI tract, pulmonary system, wounds, and any skin puncture sites such as IV sites
Hepatic Encephalopathy
- disturbance in central nervous system
- changes in motor function, changes in level of consciousness ranging from restlessness and confusion to seizures and coma
- staged based on severity of clinical presentation
- main cause: accumulation of ammonia and toxins in the blood that are normally detoxified by the liver; accumulations lead to altered neurological status
- other causes: dehydration, excessive diuresis, infection, surgery, fever, and exposure to sedatives or antianxiety medications
Stages of Hepatic Encephalopathy
> 1: slurred speech, tremors, lethargy and euphoria, reversal of day and night sleep patterns; asterixis, impaired writing, impaired decision making, poor coordination
2: increased drowsiness, disorientation, inappropriate behavior, mood swings, agitation; asterixis, fetor hepaticus (sweet fecal smell of breath)
3: severe confusion, difficult to awaken, slurred speech; asterixis, increased deep tendon reflexes, rigid extremities
4: coma, nonresponsive to painful stimulus
Clinical Manifestations of Cirrhosis
based on the degree of liver involvement; progressively more pronounced as liver dysfunction worsens
- SOB
- Jaundice
- Increased abdominal girth
- Abdominal pain and bloating
- Enlarged spleen
- Elevated Liver enzymes
- Increased risk of bleeding
- Thrombocytopenia (low platelets)
- Prolonged PT
- Hemorrhoids
- Elevated serum ammonia levels
- Changes in LOC
- Changes in motor function
- Hyponatremia
- Asterixis (flapping tremor of the hand when wrist extended)
Clinical Manifestations of Cirrhosis
based on the degree of liver involvement; progressively more pronounced as liver dysfunction worsens
- SOB
- Jaundice
- Increased abdominal girth
- Abdominal pain and bloating
- Enlarged spleen
- Elevated Liver enzymes
- Increased risk of bleeding
- Thrombocytopenia (low platelets)
- Prolonged PT
- Hemorrhoids
- Elevated serum ammonia levels
- Changes in LOC
- Changes in motor function
- Hyponatremia
- Asterixis (flapping tremor of the hand when wrist extended)
Lab Values to Assess with Liver disease
- ALT
- AST
- Alkaline Phosphate (total)
- Alkaline phosphate (liver fraction)
- Bilirubin (total, direct)
- Albumin
- Ammonia
- Coagulation Tests (PT, aPTT)
- Platelets
ALT
Males: 13 to 40 units/L
Females: 24-36 units/L
-Result of liver disease: Elevated
AST
Males: 20-40 units/L
Females: 15-35 units/L
-Result of liver disease: Elevated
Alkaline Phosphate (Total)
Males: 35-142 units/L
Females: 25-125 units/L
-Result of liver disease: Elevated
Alkaline Phosphate (Liver Fraction)
0-93 units/L
Bilirubin: Total
- 3 to 1 mg/dL
- Result of liver disease: Elevated
Bilirubin: Direct
- 1 to o.3 mg/dL
- Result of liver disease: Elevated
Albumin
- 4 to 5.1 g/dL
- Result of liver disease: decreased
Ammonia
-Result of liver disease: Elevated
Prothrombin Time (PT)
10 to 13 seconds
-Result of liver disease: prolonged
Partial thromboplastin time (aPTT)
25 to 35 seconds
-Result of liver disease: prolonged
Platelets
150,000 to 450,000 mm3
-Result of liver disease: decreased; thrombocytopenia
Diagnostic Studies To determine Severity of Liver Failure
- Diagnostic ultrasound and computed tomography (CT)
- Esophagogastroduodenoscopy (EGD)
- Percutaneous transhepatic portal angiography
- Percutaneous transhepatic cholangiography
- Liver biopsy
Diagnostic Ultrasound and Computed Tomography (CT) Scans
- noninvasive
- used to determine abnormalities of the liver
Esophagogastroduodenoscopy (EGD)
- minimally invasive
- uses endoscope to visualize GI tract from the esophagus to the duodenum to evaluate for esophageal varices or bleeding
Percutaneous transhepatic portal angiography
-used to visualize the portal venous system and liver biopsy
Endoscopic retrograde cholangiopancreatography (ERCP)
technique that combines endoscopy and fluoroscopy to visualize the biliary system to diagnose and treat causes of obstruction in the biliary tree
Percutaneous transhepatic cholangiography
- radiological test
- uses contrast medium injected into the bile duct of the liver to visualize the biliary tract and identify obstruction, that, if identified, can be treated w/ the insertion of drains or stents
Liver Biopsy
- invasive
- done to collect a sample of liver tissue to determine severity of liver disease
- done percutaneously, transvenously, or directly in the OR thorough the abdomen
- usually maintained on bedrest for several hours post-op; sometimes with a 5-10 lb. sandbag over the site
- careful monitoring b/c of risk of hypotension and bleeding
Safety Alert: Liver Biopsy
change in LOC or a decrease in blood pressure and increase in heart rate after a liver biopsy may = severe bleeding
-notify provider immediately
Treatment of Ascites
- restriction of sodium intake to less than 2 g /day
- administration of diuretics to increase salt and water excretion
- combo of diuretics (spironolactone and furosemide)
- w/ end-stage liver disease, secondary to cirrhosis, necessary to perform routine paracentesis for ascites that requires removal of several liters of fluid to relieve clinical manifestations of abdominal bloating, pain, and SOB
- w/ removal of fluid, may develop hypotension requiring close monitoring
Paracentesis
removal of several liters of fluid
- used to relieve clinical manifestations of abdominal bloating, pain, and SOB (from ascites); ease symptoms
- may become hypotensive; close monitoring
- used for lab analysis
Treatment of Portal Hypertension
- symptom management and controlling complications of bleeding
- endoscopic procedures such as banding or sclerotherapy
- beta blockers to lower systemic BP
Banding
involves placing bands around the varices to block the bleeding
Sclerotherapy
- procedure used to shrink veins
- involves injection of a solution into the bleeding varices to make them shrink to stop bleeding
Sengstaken- Blakemore Tube
- inserted into the GI tract through the nose to provide compression and traction in the esophagus and stomach to stop hemorrhage
- rarely used
Safety Alert: Sengstaken-Blakemore Tube
- temporary
- not be left in place for more than 24 hours
- can cause mucosal ulcerations, and the tube can migrate up out of the stomach and cause airway obstruction
- scissors kept at bedside for emergency use
Management w/ patients w/ Hepatic Encephalopathy
- avoid protein overload
- decreasing bacterial production of ammonia
- correcting fluid and electrolyte imbalances
- eat small, frequent meals to prevent protein loading
- receive neomycin and lactulose to reduce bacterial production of ammonia
- receive vitamins A, B, C, and K and folic acid to correct abnormalities
Neomycin
- for hepatic encephalopathy
- broad-spectrum antibiotic
- destroys bacteria normally present in GI tract, decreasing protein breakdown and production of ammonia
- can cause diarrhea and altered fluid and electrolytes
Lactulose
- promotes the excretion of ammonia in the stool
- orally or via rectal enema
- may cause diarrhea and altered fluid and electrolytes
Surgical Management for Ascites
patients w/ ascites require surgical intervention that includes the placement of a shunt between the portal venous system and the systemic venous system to reduce portal pressure to reduce fluid accumulation
-Transjugular intrahepatic portosystemic shunt (TIPS)
Surgical Management for Cirrhosis
- Liver transplant
- If ascites, Transjugular intrahepatic portosystemic shunt (TIPS)
Complications w/ cirrhosis
- risk for hyponatremia
- hepatorenal syndrome
- spontaneous bacterial peritonitis
- changes in liver function secondary to cirrhosis often results in liver failure
Complication: Hyponatremia
- low sodium
- seen with advanced cirrhosis
- associated w/ an impairment in the kidneys to excrete free water; resulting in retention of water that is disproportionate to retention of sodium
- demonstrate hyponatremia and decreased serum osmolality
Complications: Hepatorenal Syndrome (HRS)
rapid deterioration of kidney function as a result of altered blood flow to the kidneys
- long-term treatment: liver transplantation
- may have normal urine output or oliguria (small amounts)
- diagnosed by abnormal lab values (elevated creatinine and BUN)
Complications: Spontaneous Bacterial Peritonitis (SBP)
development of peritonitis in the abdomen that can occur in patients with chronic cirrhosis
- Manifestations: fever, abdominal pain, encephalopathy, or acute hemodynamic decompensation
- Diagnosis of SBP: confirmed with diagnostic paracentesis and culture of ascitic fluid
- culture usually positive for E.coli, Streptococcus species, or Klebsiella pneumoniae
- Treated w/ short course of antibiotic therapy; some treated for prolonged periods of time prophylactically
Nursing Management: Assessment and Analysis
clinical manifestations w/ cirrhosis are directly associated w/ the inability of the liver to perform its normal functions -SOB -Decreased Blood Pressure -Petechiae, bruising, and bleeding -Altered mental status -Asterixis -Elevated liver enzymes -Jaundice -Dark amber urine -Increased abdominal girth and bloating -Decreased serum albumin levels -Spider angiomas -Palmer erythema -Pruritis (secondary to accumulation of Bile Salts) >Other: acid-base disorders (respiratory alkalosis and metabolic alkalosis); elevated serum ammonia, hyperventilation, and hypoxemia d/t ascites or bacterial infection contribute respiratory alkalosis while the patient exhales more carbon dioxide -metabolic alkalosis can occur b/c of vomiting, fluid loss, diarrhea, and use of diuretics
Nursing Diagnoses
- Fluid volume excess associated w/ water and sodium retention secondary to decreased plasma protein (albumin)
- Fluid volume deficit associated w/ third spacing of peritoneal fluid (ascites), coagulation abnormalities, variceal bleed
- Altered nutrition, less than body requirements associated with altered liver metabolism of nutrients, impaired absorption of fat-soluble vitamins, B vitamins, insufficient intake
- Impaired skin integrity associated w/ compromised nutrition, edema, decreased immune status, and accumulation of bile salts (causes itching)
- Risk for injury: Bleeding associated w/ coagulopathy
Nursing Assessments
- Respiratory Status, SOB
- Vital Signs
- Peripheral edema secondary to fluid retention
- Abdominal girth
- Bleeding gums, ecchymosis (bruising), epistaxis (nosebleed), and petechiae (small, round spots on the skin as a result of bleeding)
- Skin, sclera, urine, and stool color
- Mental Status
- Intake and Output
- Daily weight
- Acid-base disorders
- Signs of organ rejection
Assessment: Respiratory status, SOB
adventitious breath sounds, decreased breath sounds, and increased respiration rate may = pulmonary fluid overload or inability to lower the diaphragm b/c of ascites
Assessment: Vital Signs
- blood pressure may be elevated b/c of fluid volume excess
- blood pressure may be low b/c of fluid shift out of the vascular space secondary to decreased oncotic pressure d/t low serum albumin
Assessment: Peripheral Edema secondary to fluid retention
fluid shift into tissues associated w/ retention of sodium and water; decreased albumin
Assessment: Abdominal Girth
increased girth d/t accumulation of fluid (ascites) in the peritoneal cavity secondary to fluid shifts caused by loss of intravascular plasma proteins
Assessment: Bleeding gums, ecchymosis (bruising), epistaxis (nosebleed), and petechiae
complications of decreased clotting factors and vitamin K+ deficiency
Assessment: Skin, Sclera, Urine, and Stool color
signs of jaundice along w/ dark urine and clay-colored stools are associated w/ increased Bilirubin levels d/t inability of the liver to produce bile or because flow is blocked
Assessment: Mental status
signs of anxiety, behavioral or personality changes, lethargy, stupor, asterixis = hepatic encephalopathy secondary to elevated ammonia levels
Assessment: Intake and output
fluid status requires monitoring d/t risk of fluid retention secondary to ascites, diarrhea, and potential fluid loss
Assessment: Daily weight
increased = fluid retention
Assessment: Acid-base disorders
- elevated serum ammonia, hyperventilation, and hypoxemia contribute to respiratory alkalosis
- metabolic alkalosis can occur b/c of vomiting and fluid loss, diarrhea, and use of diuretics
Assessment: Signs of Organ Rejection
- pts who undergo transplantation for cirrhosis, organ rejection may occur within first 10 days after procedure
- RUQ pain, changes in bile drainage, fever, tachycardia, and jaundice
Nursing Actions
- Administer diuretics
- Administer Electrolyte replacements (potassium)
- Administer magnesium as needed
- Administer Phosphate as needed
- Restrict Protein Intake
- Restrict Sodium and fluid intake as ordered
- Head of Bed elevation and Leg elevation
- Administer vitamin K+, Blood Products, and fresh frozen plasma as ordered
- Promote rest periods between activities; sit down while bathing, dressing
Actions: Administer Diuretics
help decrease fluid overload and edema
Actions: Administer electrolyte replacements (Potassium)
- maintains electrolytes within normal range
- potassium levels may be low associated w/ vomiting, diarrhea secondary to treatment for elevated ammonia levels, use of diuretics, or low-dietary intake of potassium-rich foods
Actions: Administer Magnesium as needed
hypomagnesemia in pts w/ a hx of alcohol abuse is a result of poor nutrition and diarrhea
Administer Phosphate as needed
hypophosphatemia (low phosphate levels), due to alcohol abuse, poor nutrition, and use of diuretics
Actions: Restrict sodium and fluid intake as ordered
prevents fluid accumulation and edema
Actions: Restrict protein intake
elevated amounts of protein in the diet can raise ammonia levels and lead to hepatic encephalopathy
Actions: HOB elevated and Leg elevation
helps respiratory status by decreasing pressure on the diaphragm secondary to ascites and minimizes dependent edema
Actions: Administer vitamin K+, blood products, and fresh frozen plasma as ordered
corrects coagulation disorders secondary to liver’s inability to synthesize clotting factors
Actions: Promote rest periods between activities; sit down while bathing, dressing
decreases metabolic demand on liver; decreases oxygen demand, and prevents fatigue
Nursing Teaching
- Overview of disease process and dietary restrictions (protein, sodium, fluid)
- Lifestyle changes: no alcohol intake
- Educate about medications that are metabolized in the liver (acetaminophen) and OTC herbs and supplements; can further liver damage
- Seek routine care for liver disease
- Consume adequate calories to minimize weight loss, eating a well-balanced diet w/ plenty of fruits, vegetables, and whole grains
- Need for care with hygiene, soft toothbrushes, careful flossing, electric razors; minimize risk of bleeding
Evaluating Care Outcomes
- Cirrhosis is a manageable disease when patients have a good understanding of the disease and are compliant with interventions and therapies
- Expected outcomes: stable vital signs, stable weight, decreased abdominal girth, and absence of bleeding tendencies
- Lifestyle activities that contribute to liver disease need to be altered or eliminated to slow progression of disease
- Knowledge of diet, nutritional intake, activity tolerance, and compliance w/ medical interventions
- Require routine follow-up and monitoring of symptoms
- Take proactive role in self-care
- if the disease progresses to end-stage symptoms and patient requires hospitalization at the end-of-life, education and interventions associated w/ the need for ICU management, potential transplantation, and/or palliative care can be explored
Connection Check: Elevated ammonia levels can lead to hepatic encephalopathy. Which provider order best reduces this risk in patient’s with cirrhosis?
A. Administer furosemide and spironolactone
B. Administer antibiotics
C. Restrict protein intake
D. Restrict caloric intake
C. Restrict Protein Intake
Connection Check: In a patient w/ cirrhosis, the nursing diagnosis "Risk for injury and bleeding associated with prolonged clotting factors" is most appropriate associated with which disorder? A. Pruritis B. Vitamin K deficiency C. Hyponatremia D. Ascites
B. Vitamin K+ Deficiency
