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Cirrhosis
Jane E. Binetti DNP MSN RN
Objectives
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Describe the pathophysiological principles that occur with liver disease
Compare normal structure and function
Identify clinical decision making and pharmacological management
Discuss Collaborative interventions identified by the physician
Describe diagnostic tests and therapeutic interventions
Identify appropriate teaching/learning strategies
Utilize holism to assess, plan, implement and evaluate care
Cirrhosis - What is it?
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Chronic progressive disease of the liver
Chronic inflammation of hepatocytes destroys them
Cell necrosis causes fibrosis and then cirrhosis
Hepatocellular carcinoma (HCC) is a common cause of death in patients with
Cirrhosis
Cirrhosis - What happens?
• Inflamed liver cells try to regenerate but are ineffective, causing abnormality
in blood vessels and bile ducts
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Overgrowth of new tissue is fibrous, effecting the lobes and flow of blood
Cellular nutrition is diminished
Liver becomes irregular in shape
End result is impaired function of the liver
Demographics
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8th leading cause of death in the US
Cirrhosis is twice as common in men than in women
About 20% of people with Chronic HCV have Cirrhosis
About 10-20% with Chronic HBV have Cirrhosis
The most common causes in the US is chronic HCV and ETOH liver disease
Causes
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HCV and HBV
Alcoholism
Non Alcoholic Fatty Liver Disease (NAFLD)
Non Alcoholic Steatohepatitis (NASH)
Primary Biliary Cirrhosis (PBC)
Primary Sclerosing Cholangitis (PSC)
Cardiac Cirrhosis
Other Facts
• Protein malnutrition is a key problem with alcoholics
• Chronic hepatitis with alcohol intake accelerates liver damage
• Non ETOH related cirrhosis can also occur from obesity, malabsorption, and
extreme dieting
• Environmental factors, genetics can also cause Cirrhosis without diet or alcohol
influences
Diagnostics for Cirrhosis
• History & physical
• Liver function tests (LFT’s)
• Alkaline phosphatase, AST, ALT, GGT, LDH-5 are released with liver damage
• Creatinine, BUN, K, Na
• Protein, albumin, serum bilirubin and globulin
• Cholesterol
• Prothrombin time
More Diagnostics
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CT
MRI
Ultrasound
Liver Biopsy
• Check coags
• Risk of trauma to diaphragm or lung, and bleeding
• Post procedure VS q 15, pressure dressing, on R side
What do you see in early stages?
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Usually insidious symptoms, difficult to detect
Fatigue, loss of appetite, some weight loss, abdominal symptoms
May have normal liver function tests
Disease often not determined until a later, with more significant symptoms
What do you see in later stages?
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In late stages, the liver is nodular and shrinking with many complications
Jaundice, from liver failure
Skin lesions, blood disorders
Endocrine issues
Peripheral neuropathy
We will look at these one at a time
Jaundice
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Jaundice occurs when the liver is not working or when a bile duct is blocked
Damaged liver cells and tissue overgrowth cause bile duct compression
Liver has decreased ability to conjugate and excrete bilirubin
The skin and sclera become yellow, urine darkens, and stool lightens
Degree of jaundice with liver disease is dependent on its severity
Skin lesions
Telangiectasia and Palmar Erythema
Hematological Issues
• Thrombocytopenia and Leukopenia
• Portal HTN causes splenomegaly and increased removal of blood cells from circulation
• Anemia
• Decreased RBC production, poor diet, poor B12 & folic acid absorption, and bleeding varices
• Coagulation disorders
• Diseased liver cannot produce prothrombin; decreased Vit K absorption blocks synthesis of
clotting factors; also pts have existing thrombocytopenia:
• Epistaxis, purpura, petechiae, bruising, gingival bleeding, excess menstrual bleeding
Endocrine Issues
• Liver plays a functional role in adrenocortical hormones, testosterone and
estrogen so with cirrhosis you will see:
• Men: gynecomastia, loss of pubic and axillary hair, testicular atrophy and impotence
• Older women may have vaginal bleeding
• Young women will have amenorrhea
• Failure to metabolize aldosterone causes hyperaldosteronism and Na water
retention and K loss
Peripheral Neuropathy
• Common finding in Cirrhosis
• Thought to be from deficiency of thiamine, folic acid and cobalamin
• Sensory deficits in extremities are most common
Complications of Cirrhosis
• Liver disease without complications is referred to as “Compensated”
• “Uncompensated” has one or more of the following complications:
1. Portal Hypertension
2. Esophageal and or Gastric Varices
3. Peripheral Edema
4. Ascites
5. Hepatic Encephalopathy
6. Hepatorenal Syndrome
1. Portal Hypertension
• Changes to the liver with disease causes obstruction of blood flow
• Venous pressure increases in the portal circulation and causes splenomegaly
• Enlarged veins and collateral circulation develops to accommodate the
pressure but result in esophageal and gastric varices
• Caput medusa are varices around the umbilicus
• Hemorrhoids are common too
Caput Medusa
2. Esophageal and Gastric Varices
• Portal HTN causes pressure to build and vessels dilate and become tortuous in the
distal esophagus
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Gastric varices are in the fundus and bleed easily
Esophageal varices account for 80% of hemorrhages; Gastric about 20%
Bleeding esophageal varices are the most life threatening complication of Cirrhosis
Bleeds can be slow leaks or hemorrhages, successive bleeds increase mortality
Hematemesis or melena common
Varices
What do we do?
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Goal is to control bleeding, EGD for assessment
Avoid stimulus for bleeding: ASA, NSAIDS, ETOH
Beta Blockers to
portal HTN and reduce bleeding
Octreotide (Sandostatin), Vasopressin
Histamine blockers, Proton Pump Inhibitors
Mucosal Barriers, antacids
PRBc’s, FFP, Vitamin K
Interventions for Bleeding Varices
• The goal is to decrease bleeding
• Gastric lavage
• Sclerosing of vessels
• Ethamolin, Scleromate
• Endoscopic Variceal Ligation (EVL)
• Tamponade
Lavage or Sclerosing
Lavage
Sclerosing of Vessels
Ligation - Banding
Sengstaken-Blakemore Tube
Care of Tube
• If patient has a Blakemore:
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Make sure tube is patent and anchored properly and nasal pillow is in place
Frequent oral care and suctioning
Pressure is between 20-40-mm Hg by MD order
Assess for complications: erosion, regurgitation, aspiration, obstructed airway
If gastric balloon deflates or ruptures, esophageal balloon will migrate up and occlude
airway
• Keep scissors at the bedside!
3. Peripheral Edema
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Liver disease causes impaired synthesis of albumin
Low albumin causes low colloidal oncotic pressure
Edema can occur before ascites, or along with it
Usually seen in the ankles and feet or pre-sacral
Treatment for Edema
• Diuretics when used can lead to hypokalemia
• When assessing the patient, include
• Daily weights
• Measurement of circumference of extremities
• Note location of edema
• Provide good skin care
4. Ascites
• Accumulation of fluid in the peritoneal space
• Portal HTN increases blood flow resistance
• Hypoalbuminemia from impaired synthesis decreases colloidal oncotic pressure
• Proteins and fluids shift and leak through the Glisson capsule into the peritoneal space
• Hyperaldosteronism causes Na reabsorption, increase in water retention and loss in
potassium
Ascites Symptoms
• Abdominal distention with weight gain
• Abdominal striae, loss of appetite, dyspnea
• Pt looks dehydrated:
• Dry tongue, sunken eyes, muscle weakness, decreased urine output, low BP
• Hypokalemia from hyperaldosteronism
• Risk for subacute bacterial peritonitis (SBP) from altered immunity and
paracenteses
Ascites – Collaborative Care
• Ascites
• Sodium management, diuretics, fluid removal
• Albumin infusion to maintain intravascular volume and adequate urine output by raising
plasma colloid osmotic pressure
• Diuretics: Spironolactone (aldactone), Amiloride (Midamor), Furosemide (Lasix)
• Paracentesis – temporary
• TIPS; Peritoneovenous shunt is not often used
5. Hepatic Encephalopathy
• A neuropsychiatric complication of Liver Disease
• Normally amino acids are broken down to ammonia in the intestine and Ammonia
is converted to urea in the liver.
• If liver is failing it cannot convert Ammonia for excretion and Ammonia is toxic to
brain cells
• Symptoms range from
• Change in neuro functioning, inappropriate behavior, confusion
• Sleep disturbance, change in level of consciousness, coma
• Asterixis, apraxia and fetor hepaticus are often noted with encephalopathy
Encephalopathy – Collaborative Care
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Goal is to reduce ammonia levels
Lactulose traps ammonia in the GI system and has laxative effect
Given orally, via NGT or via enema
Antibiotics like Rifaximin (Xifaxin) and Neomycin are also used
Antibiotics are not laxatives, so be sure patient does not become constipated
More Collaborative Care
• Methods to shunt blood away from varices
• Transjugular Intrahepatic Portosystemic Shunt (TIPS) Procedure
• Track is made between systemic and portal venous systems to redirect flow and decrease
pressure on varices
• Usually done after second episode of bleeding, reduces portal pressure and decompresses
varices to control bleeds
• Can increase Hepatic encephalopathy, and stents can stenose
• Not used for severe HE, HCC, hepatorenal syndrome and portal vein thrombosis
• Portacaval and splenorenal shunts are also used but are surgical – see picture
TIPS
Transjugular Intrahepatic Portosystemic Shunt
• Catheter from the jugular through the vena cavas
to the hepatic vein
• Hepatic vein is punctured and a shunt placed
between it and the portal vein
• Reduces portal pressure and therefore pressure
on varices
• Increase in HE 24-48 hours after
• Portacaval and splenorenal shunt are possible
Portacaval Shunt and Splenorenal Shunt
6. Hepatorenal Syndrome
• Seen with decompensated Cirrhosis and structurally sound kidneys
• Renal failure with azotemia, oliguria and intractable ascites
• Portal HTN and decompensated liver function result in
• Splanchnic and system vasodilation
• Decreased arterial blood volume
• Renal vasoconstriction and renal failure
• With Cirrhosis, it follows diuretic therapy, GI bleed, and paracentesis
What do you do for Cirrhosis Patients?
• Assess your patient!!!
• Mentation and neuro functioning
• Respiratory status, VS
• Oral care for N, V, and D
• GI symptoms: anorexia, hematemesis, stool color
• Ascites, edema, urine color and output, electrolytes, coagulation
• Daily weights, abdominal girth measurements, peripheral edema, scrotal edema
Collaborative Standard Drug Therapy
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Vasopressin (Pitressin) - decreases bleeding by splanchnic constriction
Octreotide (Sandostatin) inhibitory hormone
Propranolol (Inderal)
Lactulose (Cephulac)
Rifaximin (Xifaxan), Neomycin sulfate
Collaborative Care - Nutrition
• Nutritional needs are important in Liver patients who have no energy
• Patients with compensated Cirrhosis requires >3000 cal/day in high CHO
and moderate/low protein
• Protein is restricted in patients with encephalopathy or acute flares
• Alcoholic Cirrhosis results in protein and calorie malnutrition and requires
parenteral or enteral nutrition
• Low sodium diets are necessary for patients with ascites
What else do you do?
• Assess for jaundice
• Degree of jaundice, provide skin care, air mattress
• Pruritus, Cholestyramine, hydroxyzine, Keri oil, tepid baths
• Paracentesis prep:
• Pts sit forward, high fowler’s if possible
• After, assess respiratory status, dressing and for hypovolemia and electrolyte imbalance
Still more to do…
• If on complete bedrest:
• Prevent complications:
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Turning, coughing and deep breathing
Incentive spirometry
Range of motion exercises
Good skin care
• Activity:
• Conserve strength, maintain tone, balance activity and rest
Patient Teaching
• Cirrhosis is a chronic condition. Teach patients the importance of:
• Continued follow up
• Maintenance of diet, rest and medications and compliance
• Encourage support groups
• Do NOT assume that Cirrhosis means your patient is an alcoholic!
• Signs and symptoms of complications: Portal HTN, Esophageal and Gastric varices,
peripheral edema, ascites, HE, Hepatorenal syndrome.
More Education
• Avoidance of hepatotoxic substances:
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ETOH, Tylenol, NSAIDS,
Thorazine (chlorpromazine), Compazine (prochlorperazine), Phenergan (promethazine)
Oral Contraceptives
Allopurinol (zyloprim), Tetracyclines (Sumycin
Valium (diazepam), Librium (chlordiazepoxide)
Anti-rejections: Tacrolimus(Prograf), Sirolimus (Rapamune), mycophenolate (Cellcept)
Monoclonal antibodies: Retuximab (Rituxin), Bevacizumab (Avastin)
Nursing Diagnoses
• Imbalanced nutrition: less than body requirements related to anorexia, nausea
and impaired utilization and storage of nutrients
• Impaired skin integrity related to peripheral edema, ascites and pruritus
• Excess fluid volume related to portal hypertension and hyperaldosteronism
• Ineffective self-health management related to ineffective coping and abuse of
alcohol.
Nursing Diagnoses continued
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Ineffective Breathing Pattern
Risk for aspiration
Risk for bleeding
Risk for injury
Risk for Infection