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Liver Disorders John Nation, RN, MSN Fall 2011 From the notes of

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1 Liver Disorders John Nation, RN, MSN Fall 2011 From the notes of
Charlene Morris, RN, MSN Austin Community College

2 Overview of Today’s Lecture
A & P Review Hepatitis A Hepatitis B Hepatitis C Cirrhosis Portal Hypertension Esophageal Varices Hepatic Encephalopathy Hepatorenal Syndrome Liver Transplant

3 A and P Review

4 A and P Review Largest internal organ-weighs around 3 lbs!

5 A Liver B Hepatic vein C Hepatic artery D Portal vein E Common bile duct F Stomach G Cystic duct H Gallbladder

6 Blood Supply – 2 sources Hepatic artery: Portal vein – 1000ml/min
500ml/min of oxygenated blood. 30% of Cardiac output goes to the liver Portal vein – 1000ml/min partly oxygenated blood supplies % O2 plus rich supply of nutrients, toxins, drugs from stomach, small and large intestines, pancreas and spleen

7 Hepatic Blood Supply (Cont’d)
Both empty into capillaries/sinusoids Liver filters the blood Hepatic vein to inferior vena cava

8

9 Lobule – Functional unit of the liver Capillaries

10 Metabolic Functions of the liver
“Body’s Refinery” Over 400 functions Primary role in anabolism and catabolism Prompt: who remembers anabolism? And catabolism? Anabolism- simple to complex (ie glucose to glycogen) Catabolism- complext to simple (ie glycogen to glucose)

11 Metabolic Functions of the Liver
1. Metabolism of Glucose 2. Protein Storage 3. Fatty acids 4. Cholesterol Glucagon- from pancreas, causes liver to break glycogen back down to glucose into bloodstream. However, also stimulates insulin so that the glucose can be used by body’s cells

12 Other functions Immunologic Blood storage Plasma protein synthesis
Clotting Waste products of hemoglobin Formation and secretion of bile Steroids and hormones Ammonia Drugs, alcohol and toxins metabolism

13 To Summarize…. The liver: changes food into energy
removes alcohol and poisons from the blood makes bile, a yellowish-green liquid that helps with digestion

14 Hepatitis Simply means inflammation of the liver Viral hepatitis
“itis” means inflammation, “hepa” means liver. Viral hepatitis Most common cause Viral types include A, B, C, D, E, and G

15 Hepatitis Other possible causes Drugs (alcohol) Chemicals
Autoimmune liver disease Bacteria (rarely)

16 Hepatitis Etiology Causes A, B, C, D, E, and G virus Cytomegalovirus
Epstein-Barr virus Herpes virus Coxsackie virus Rubella virus

17 Hepatitis A Hepatitis A virus (HAV) RNA virus
Transmitted fecal–oral route, parenteral (rarely) Frequently occurs in small outbreaks

18 Hepatitis A 61,000 cases of hepatitis A occur annually in the United States 10 million cases of hepatitis A occur worldwide Nearly universal during childhood in developing countries

19 Hepatitis A Hepatitis A virus (HAV)
Found in feces 2 or more weeks before the onset of symptoms and up to 1 week after the onset of jaundice Present in blood briefly No chronic carrier state

20 Hepatitis A: Incubation Period
2-6 weeks Acute onset Mild flu-like manifestations Symptoms last up to 2 months Liver usually repairs itself, so no permanent effects

21 Hepatitis A Hepatitis A virus (HAV) Anti-HAV immunoglobulin M (IgM)
Appears in the serum as the stool becomes negative for the virus Detection of IgM anti-HAV indicates acute hepatitis

22 Hepatitis A Hepatitis A virus (HAV) Anti-HAV immunoglobulin G (IgG)
IgG anti-HAV: Indicator of past infection Presence of IgG antibody provides lifelong immunity

23 Hepatitis A: Mode of Transmission
Mainly by ingestion of food or liquid infected with the virus Poor hygiene, improper handling of food, crowding housing, poor sanitation conditions are all factors related to Hepatitis A

24 Hepatitis A: Mode of Transmission (Cont’d)
Occurs more frequently in underdeveloped countries Contaminated waters Drinking water, contaminated seafood Food-borne Hepatitis A outbreaks usually due to infected food handler Contamination of food during preparation

25

26 Hepatitis A: Vaccine 2 doses IM Initial dose Booster in 6 to 12 months

27 Post-exposure Prophylaxis
Standard IG-immune globulin Given IM within 2 weeks of exposure Hepatitis A Vaccine IG is recommended for persons who do not have anti-HAV antibodies and have had food borne exposure or close contact with HAV-infected person

28 Remember 2/2/2/2 Rule 2 doses IM for vaccination
Signs & symptoms last 2 months Contagious 2 weeks before signs & symptoms Post-exposure dose given IM within 2 weeks of exposure Must report within one day

29 Hepatitis B Nearly 400 million people infected with Hepatitis B
50% to 75% active viral replication 73,000 new cases of Hepatitis B annually in United States Incidence decreased due to HBV vaccine 29

30 Hepatitis B Hepatitis B virus (HBV) DNA virus Transmission of HBV
Perinatally by mothers infected Percutaneously (IV drug use) Mucosal exposure to infectious blood, blood products, or other body fluids

31 Hepatitis B Hepatitis B virus (HBV)
Transmission occurs when infected blood or other body fluids enter the body of a person who is not immune to the virus

32 Hepatitis B Hepatitis B virus (HBV) Sexually transmitted disease
Can live on a dry surface for 7 days More infectious than HIV

33 Hepatitis B- Precautions Source: Uptodate
PREVENT INFECTION OF FAMILY — Acute and chronic hepatitis B are contagious. Thus, people with hepatitis B should discuss measures to reduce the risk of infecting close contacts. This includes the following: Discuss the infection with any sexual partners and use a latex condom with every sexual encounter. Do not share razors, toothbrushes, or anything that has blood on it. Cover open sores and cuts with a bandage. Do not donate blood, body organs, other tissues, or sperm.

34 Hepatitis B- Precautions Source: Uptodate
Immediate family and household members should have testing for hepatitis B. Anyone who is at risk of hepatitis B infection should be vaccinated, if not done previously. (See "Patient information: Adult immunizations".) Do not share any injection drug equipment (needles, syringes). Clean blood spills with a mixture of 1 part household bleach to 9 parts water.

35 Hepatitis B- Prevention
Hepatitis B cannot be spread by: Hugging or kissing* (some disagreement) Sharing eating utensils or cups Sneezing or coughing Breastfeeding Source: Uptodate

36 Hep B Incubation Period
6-24 weeks Prevention Vaccine-3 doses Initial dose Dose at 4 weeks Dose 5 months later

37 Post-exposure Hep B Hepatitis B Immune globulin IM in 2 doses
First dose within 24 hours to 7 days of exposure Second dose 20 to 30 days post-exposure Provides short-term immunity Give HBV vaccine concurrently- vaccine can be beneficial post- exposure

38 Hepatitis B Hepatitis B virus (HBV)
Complex structure with three antigens Surface antigen (HBsAg) Core antigen (HBcAg) E antigen (HBeAg) Each antigen—a corresponding antibody may develop in response to acute viral Hepatitis B

39 Hepatitis B Virus Presence of Hepatitis B Surface Antibodies
Indicates immunity from HBV vaccine Past HBV infection With chronic infection, liver enzyme values may be normal or ↑ 15% to 25% of chronically infected persons die from chronic liver disease

40 Hepatitis C Approximately 170 million people are infected with the hepatitis C virus (HCV) Estimated 30,000 new cases diagnosed annually 40

41 Hepatitis C 8000 to 10,000 people in the United States die each year from complications of end-stage liver disease secondary to HCV Approximately 30% to 40% of HIV-infected patients also have HCV 41

42 Hepatitis C Hepatitis C virus (HCV)
Transmitted primarily percutaneously Risk factors IV drug use Most common mode of transmission in United States and Canada Blood transfusions

43 Hepatitis C Hepatitis C virus (HCV) Risk factors (cont’d) Hemodialysis
High-risk sexual behavior Hemodialysis Occupational exposure Perinatal transmission

44 Hepatitis C: Transmission
Hepatitis C virus (HCV) Up to 10% of patients with HCV cannot identify a source Risk of body piercings, tattooing, and intranasal drug use in transmission of HCV

45 Hepatitis C Diagnostic Studies
Anti-HCV antibody HCV RNA 45

46

47 Hepatitis C Interventions
Harm Reduction - Austin Harm Reduction Coalition

48 Hepatitis D Hepatitis D virus (HDV) Also called delta virus
Defective single-stranded RNA virus Cannot survive on its own Requires the helper function of HBV to replicate

49 Hepatitis D Hepatitis D virus (HDV) (cont’d) HBV-HDV co-infection
↑ Risk of fulminant hepatitis More severe acute disease

50 Hepatitis E Hepatitis E virus (HEV) RNA virus
Transmitted fecal–oral route Most common mode of transmission is drinking contaminated water Occurs primarily in developing countries

51 Hepatitis G Hepatitis G virus (HGV) RNA virus
Poorly characterized parenterally and sexually transmitted virus Found in some blood donors Can be transmitted by blood transfusion

52 Hepatitis G virus (HGV) (cont’d)
Coexists with other hepatitis viruses and HIV Does not appear to cause liver damage

53 Pathophysiology of Hepatitis
Acute infection- widespread inflammation of liver tissue Liver damage mediated by Cytotoxic cytokines Natural killer cells Liver cell damage results in hepatic cell necrosis

54 Common Manifestations of Acute Hepatitis
Predictable course among all the viruses Incubation Phase: after exposure to virus, no symptoms

55 Preicteric Phase of Hepatitis
Flu-like symptoms General malaise Fatigue Body aches, headache GI symptoms- nausea/vomiting, diarrhea, abdominal discomfort Chills, low grade fever

56 Icteric or Jaundice Phase
Usually 5-10 days after pre-icteric symptoms Jaundice results when bilirubin diffuses into tissues Sclera jaundiced Urine darkens due to excess bilirubin being excreted If bilirubin cannot flow out of liver, stool will be light or clay-colored

57 Severe Jaundice

58 Hepatitis Clinical Manifestations
Pruritus can accompany jaundice Accumulation of bile salts beneath the skin When jaundice occurs, fever subsides Liver usually enlarged and tender

59 Convalescent Phase Healing generally within 3-16 weeks
Begins as jaundice is disappearing GI symptoms minimal

60 Hepatitis Liver cells can regenerate with time and if no complications occur, resume their normal appearance and function

61 Hepatitis Complications
Fulminant Hepatic Failure Chronic Hepatitis Cirrhosis Hepatocellular Carcinoma

62 Fulminant Hepatitis Results in severe impairment or necrosis of liver cells and potential liver failure Develops in small percentage of patients Occurs because of Complications of Hepatitis B Toxic reactions to drugs and congenital metabolic disorders

63 Diagnostic tests Liver function studies
ALT (Alanine aminotransferase) – elevates: enzyme in liver cells released into bloodstream with injury or disease (0 – 50) normal AST (Aspartate aminotransferase) – elevates: enzyme in liver & heart cells released into bloodstream (0 -41) GGT – gamma glutamyltransferase: present in all cell membranes, inj or disease = elevates in cell lysis, (8 – 55). increases when bile ducts are blocked & hepatitis. Elevated until function returns.

64 Diagnostic tests Alkaline phosphatase – present in liver & bone cells. Elevated in hepatitis.( IU/L) CBC – low RBC, Hct, Hgb related to anemia, RBC destruction, bleeding, folic acid and vitamin deficiencies. Low WBC and Platelets Increased blood flow to spleen – cells destroyed faster than needed AFP- alpha fetoprotein– liver cancer marker Lactic dehydrogenase LDH5 specific for liver damage

65 Diagnostic tests Bilurubin – direct/conjugated (0-4 umol/L)
Coagulation – prolonged prothrombin time due to poor production of prothombin by liver and decreased Vitamin K absorption (Normal PT seconds, INR 0.8 to 1.2) Hyponatremia –hemodilution Hypokalemia, hypophosphatemia, hypomagnesemia –malnutrition & renal loss Bilirubin – Total (2-14 umol/L) Bilurubin – direct/conjugated (0-4 umol/L) Changed this slide- prothombin! (not PT/INR)

66 Diagnostic tests Serum albumin – low due to impaired liver production (3.3 – 5) Serum ammonia – high (0 – 150)(10 to 80 ug/l) Glucose and cholesterol –abnormal due to impaired liver function Abd. Ultrasound – liver size, ascites, or nodules Esophagascopy – look for varices Liver biopsy CT, MRI

67 Rx Impacting Liver A host of medications can cause abnormal liver enzymes levels. Examples include: Pain relief medications such as aspirin, acetaminophen (Tylenol), ibuprofen (Advil, Motrin), naproxen (Narosyn), diclofenac (Voltaren), and phenylbutazone (Butazolidine) Anti-seizure medications such as phenytoin (Dilantin), valproic acid, carbamazepine (Tegretol), and phenobarbital Antibiotics such as the tetracyclines, sulfonamides, isoniazid (INH), sulfamethoxazole, trimethoprim, nitrofurantoin, etc.

68 Rx Impacting Liver Cholesterol lowering drugs such as the "statins" (Mevacor, Pravachol, Lipitor, etc.) and niacin Cardiovascular drugs such as amiodarone (Cordarone), hydralazine, quinidine, etc. Anti-depressant drugs of the tricyclic type (ie elavil) With drug-induced liver enzyme abnormalities, the enzymes usually normalize weeks to months after stopping the medications.

69 Liver Biopsy Needle biopsy Laparoscopic biopsy: Most common in past
Used to remove tissue from specific parts of the liver.

70 Liver Biopsy (Cont’d) Transvenous biopsy
Catheter into a vein in the neck and guiding it to the liver. A biopsy needle is placed into the catheter and advanced into the liver. Used for patients with blood-clotting problems or excess fluid

71

72

73 Liver Biopsy Adequacy of clotting- PT/ INR, Platelets (Vit. K?)
Type and cross match for blood Usually hold aspirin, ibuprofen, and anticoagulants Chest x-ray Consent form & NPO 4 to 8 hr.

74 Liver Biopsy (Cont’d) Consent form & NPO 4 to 8 hr.
Vital signs & Empty bladder Supine position, R arm above head Hold breath after expiration when needle inserted Be very still during procedure – 20 minutes

75 Liver Biopsy Video

76

77 Complications are: Puncture of lung or gallbladder, infection, bleeding, and pain.

78 After Needle Liver Biopsy
Pressure to site, place pt on Rt side to maintain site pressure minimum of 2 hrs. & flat hrs. Vital signs & check for bleeding NPO X 2H after Assess for peritonitis, shock, & pneumothorax Rt. shoulder pain common caused by irritation of the diaphragm muscle usually radiates to the shoulder for a few hours or days.

79 After Needle Biopsy (Cont’d)
Soreness at the incision site Avoid aspirin or ibuprofen for pain control for the first week because they decrease blood clotting, which is crucial for healing. CONSULT HEALTHCARE PROVIDER! Avoid coughing, straining, lifting x 1-2 weeks

80 Hepatitis Care Rest is a priority!
Diet –High calorie & protein, Low fat Vitamin supplement – B complex & K Avoid alcohol & drugs detoxed in liver Life style changes

81 Meds for Chronic Hepatitis
Chronic HBV Pegylated a-interferon (Pegasys, PEG-Intron) Lamivudine (Epivir) Adefovir (Hepsera) Entecavir (Baraclude) Telbivudine (Tyzeka) Chronic HCV Ribavirin (Rebetol, Copegus)

82 Hepatitis Nursing Management
Nursing assessment Past health history Hemophilia Exposure to infected persons Ingestion of contaminated food or water Past blood transfusion (before 1992)

83 Hepatitis Nursing Management
Nursing assessment Medications (use and misuse) Acetaminophen Phenytoin Halothane Methyldopa

84 Hepatitis Nursing Management
Nursing assessment IV drug and alcohol abuse Weight loss Dark urine Fatigue Right upper quadrant pain Pruritus

85 Hepatitis Nursing Management
Nursing assessment Low-grade fever Jaundice Abnormal laboratory values

86 Hepatitis Nursing Management
Nursing diagnoses Imbalanced nutrition: Less than body requirements Activity intolerance Ineffective therapeutic regimen management

87 Hepatitis Nursing Management
Overall goals: Planning Relief of discomfort Resumption of normal activities Return to normal liver function without complications

88 Hepatitis Nursing Management
Nursing implementation Health promotion Hepatitis A Education Vaccination Good hygiene practices

89 Hepatitis Nursing Management
Nursing implementation Health Promotion Hepatitis B Vaccination Education Workplace safety

90 Hepatitis Nursing Management
Nursing implementation Health promotion Hepatitis C Education Infection control precautions Modification of high-risk behavior

91 Hepatitis Nursing Management
Nursing implementation Acute intervention Rest Jaundice Assess degree of jaundice Small, frequent meals

92 Hepatitis Nursing Management
Nursing implementation Ambulatory and home care Dietary teaching Assessment for complications Regular follow-up for at least 1 year after diagnosis

93 Hepatitis Nursing Management
Nursing implementation Ambulatory and home care Avoid alcohol

94 Hepatitis Nursing Management
Evaluation Expected outcomes Adequate nutritional intake Increased tolerance for activity Verbalization of understanding of follow-up care

95 Hepatitis Nursing Management
Evaluation Expected outcomes Able to explain methods of transmission and methods of preventing transmission to others

96 Hepatitis Reporting

97 Break!

98 Cirrhosis

99 Cirrhosis Pathophysiology
Cirrhosis is the end stage of chronic liver disease Progressive, leads to liver failure Insidious, prolonged course Ninth leading cause of death in United States Twice as common in men

100 Cirrhosis Pathophysiology
Hepatocytes are destroyed and portal hypertension develops Liver cells attempt to regenerate Regenerative process is disorganized Functional liver tissue is destroyed and scarring of liver occurs New fibrous connective tissue distorts liver’s normal structure, with impeded blood flow

101 Four Types of Cirrhosis
Alcoholic Cirrhosis – formerly called Laennec’s Post necrotic Cirrhosis Biliary/obstructive - bile flow obstructed causing damage to liver Cardiac- from right side heart failure

102 Alcoholic or Nutritional Cirrhosis (formerly called Laennec’s)
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 consumption ceases Same person came up with the stethescope French doctor.

103 Post Necrotic Cirrhosis
Results from complication of viral infections, Hepatitis, or exposure to toxins Liver shrinks because lobules destroyed, broad bands of scar tissue form within the liver

104 Biliary Cirrhosis Associated with chronic biliary obstruction and infection Retained bile damages and destroys liver cells, causing fibrosis of liver

105 Cardiac Cirrhosis Results from long-standing severe right sided heart failure Elevated central venous pressures cause stasis of blood in veins of liver, which leads to fibrosis

106 Early Signs of Cirrhosis Complications and Common Manifestations
Hepatomegaly and RUQ pain Weight loss Weakness Anorexia Diarrhea and constipation

107 Cirrhosis Interventions- Drugs
Diuretics- Aldactone (spironolactone): decreases aldosterone levels, K+ sparing Lasix (furosemide) Salt-poor albumin Neomycin – decrease ammonia forming organisms. Typically only recommended when unable to tolerate lactulose Lactulose – decreases ammonia forming organisms and inc. acidity of bowel. Goal is 2-3 loose stools per day. Ferrous sulfate and folic acid – to treat anemia/ vitamin deficiency

108 Cirrhosis Interventions- Drugs (Cont’d)
Beta blocker: propranolol (Inderal), nadolol- to prevent bleeding of E varices in conjunction with isosorbide mononitrate (Imdur) lowers hepatic venous pressure Proton Pump Inhibitors, H2 Receptor Blockers– decrease irritation of varices Serax (oxazepam) – benzodiazepine for alcohol withdrawal, sedation, sleep. Is metabolized in the liver – use cautiously.

109 Nursing Diagnoses - Cirrhosis
Fluid Volume deficit Ineffective protection: bleeding Disturbed thought process Ineffective breathing pattern Impaired skin integrity Imbalanced nutrition: less than body requirements

110 Cirrhosis Interventions- Diet and fluids
Low protein (sometimes), high carbohydrate, high calorie-if signs of acute hepatic encephalopathy With cirrhosis and no hepatic encephalopathy, high carbohydrate, high protein, low salt Low sodium-500 mg-2gms At first sign of encephalopathy or ammonia level increasing- decrease protein intake (sometimes) Early stage for liver regeneration- need high protein-(75-100gms)

111 Later Manifestations of Cirrhosis Jaundice
Jaundice occurs as a result of the decreased ability to conjugate and excrete bilirubin In the late stages of cirrhosis, patient is usually jaundiced

112

113 JAUNDICE Hepatocellular Obstructive Hemolytic

114 Cirrhosis- Hepatocellular or intrahepatic jaundice
Diseased liver cells can’t clear normal amounts of bilirubin from the blood.

115 Obstructive or Extrahepatic Jaundice
Due to the interference with the flow of bile in the hepatic duct. Liver is conjugating bilirubin but it cannot reach small intestines so is released into blood stream

116 Due to excessive destruction of RBC’s.
Hemolytic Jaundice Due to excessive destruction of RBC’s. transfusion reaction Faulty hemoglobin – sickle cell Autoimmune destruction of RBC’s

117 Major Complications of Cirrhosis
Portal hypertension Variceal bleeding Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Hepatic encephalopathy

118 Break!

119 Portal Hypertension The portal vein carries about 1500 ml/min of blood from the small and large bowel, spleen, and stomach to the liver. Any obstruction or increased resistance to flow or, rarely, pathological increases in portal blood flow may lead to portal hypertension with portal pressures over 12 mm Hg. alcoholic and viral cirrhosis are the leading causes of portal hypertension in Western countries.

120 Portal Hypertention (Cont’d)
Increases in portal pressure cause development of a portosystemic collateral circulation with resultant compensatory portosystemic shunting and disturbed intrahepatic circulation. These factors are partly responsible for the important complications of chronic liver disease, including variceal bleeding, hepatic encephalopathy, ascites, hepatorenal syndrome, recurrent infection, and abnormalities in coagulation. Variceal bleeding is the most serious complication and is an important cause of death in patients with cirrhotic liver disease.

121

122 PORTAL HYPERTENSION normal 3 mmHg 12 mmHg = esophageal rupture
Resistance to blood flow = Increase in pressure in portal venous system. Swelling, inflammation, fibrosis, scarring of liver Thrombus Resistance in Inferior vena cava: Rt.CHF, myopathy Blood takes collateral channels - esophagus, stomach, spleen etc, veins, hemorrhoids May need shunts or TIPS Transjugular Intrahepatic Portosystemic Shunt to decrease pressure, beta blockers also help

123

124 Portal Hypertension Arteriovenous shunting Esophageal Varices
Hypersplenism Moderate anemia Neutropenia Thrombocytopenia Marked ascites Caput medusae (dilated abd. veins) Hemorrhoids

125 Ascites &Caput medusae

126 Spider angiomas

127

128

129 Treatment of esophageal varices
Active bleeding Central line & pulmonary artery pressures Blood transfusions & fresh frozen plasma for clotting factors Somatostatin or Vasopressin – constrict gut vessels Nitroglycerin- to counter negative affects of vasopressin Airway/trach Later prevention of re-bleeding Beta-blockers Long-acting nitrates Soft food, chew well, avoid intra-abdominal pressure Protonix (pantoprazole)

130 Rapid Endoscopy!

131 Sclerotherapy: A sclerosant solution (ethanolamine oleate or sodium tetradecyl sulphate) is injected into the bleeding varix or the overlying submucosa Complications can include fever, dysphagia and chest pain, ulceration, stricture, and (rarely) perforation.

132 Band ligation: Band ligation is achieved by a banding device attached to the tip of the endoscope

133 Band Ligation

134 Balloon Tube Tamponade:
The balloon tube tamponade may be life saving in patients with active variceal bleeding if emergency sclerotherapy or banding is unavailable The main complications are gastric and esophageal ulceration, aspiration pneumonia, and esophageal perforation.

135 Minnesota Tube- Four lumens: one for gastric aspiration
two to inflate the gastric and esophageal balloons one above the esophageal balloon for suction of secretions to prevent aspiration

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

137 Long term Management of Esophageal Varices
Repeated endoscopic treatment Repeated endoscopic treatment eradicates esophageal varices in most patients, recurrent variceal bleeding is uncommon. Because portal hypertension persists, patients at risk for recurrent varices Long term drug treatment The use of beta-blockers after variceal bleeding has been shown to reduce portal blood pressures and lower the risk of further variceal bleeding. Prophylactic management Most patients with portal hypertension never bleed, and it is difficult to predict who will. Beta blockers have been shown to reduce the risk of bleeding.

138 Transjugular Intrahepatic Portosystemic Shunt
Special procedures – fistula created with portal vein and hepatic vein and then stents placed to keep it open. Bypasses the liver by returning blood to hepatic vein to inferior vena cava

139

140 TIPS Transjugular intrahepatic portosystemic shunt

141 TIPS POST

142 TIPS: Shunted blood contains high ammonia Can lead to: hepatic encephalopathy

143 Splenomegaly due to Portal hypertension
The spleen enlarges as blood is shunted to splenic vein This increases rate of destruction of RBCs, WBCs, and platelets Decreases storage capacity of spleen Causes anemia, leukopenia and thrombocytopenia

144 Ascites – Complication of Cirrhosis
Blood flow diverted to mesenteric vessels Increased capillary pressure leads to fluid leaving vessels out into peritoneal cavity High pressure in liver causes fluid to leave liver into peritoneal cavity This fluid is plasma filtrate with high concentration of albumin Minerals- Ca++ is attached to albumin decreases so phosphorus increases. K+ is low due to aldosterone

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

146 Responses to third spacing
Loss of albumin to ascites leads to hypoproteinemia, depletion of plasma proteins Loss of blood volume = lowered BP Reflexes aimed at returning blood pressure to normal include release of aldosterone Increases reabsorption of NA+ back into blood and H2O follows, thus increasing blood volume

147

148

149 accumulation of high protein fluid in the abdomen - 3rd spacing
ASCITES

150 Nursing Management ASCITES
Assess for Respiratory Distress- Fowler’s position helps ease work of breathing in ascites Measure Abdominal Girth Accurate I&O

151 MEDICAL TREATMENT Na+ restriction- 500 mg –2 gms Fluids-1500 ml/day Diuretics-Aldactone Albumin - NaCl poor

152 Paracentesis To treat respiratory distress
Pt will loose grams of protein Pt in sitting position Empty bladder first Post--watch for hypotension, bleeding, shock & infection

153 Additional Complications Liver Failure

154 Liver Failure Complex syndrome characterized by impairment of many organs and body functions Two conditions: Hepatic Encephalopathy Hepatorenal Syndrome

155 Hepatic encephalopathy: Alteration in neuro status due to accumulation of ammonia Build-up of other substances such as hormones, GI toxins, drugs also contribute

156 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

157 Precipitating Factors – all place demands on liver
Bleeding esophageal varices Ingestion of narcotics or barbiturates, anesthetics Excessive protein intake Electrolyte imbalance Hemodynamic alterations Diuretics Severe infection Blood transfusions

158 Stages of Hepatic Encephalopathy

159 Hepatic Encephalopathy - Onset Phase
Personality changes, disturbances of awareness, forgetfulness, irritability, & confusion

160 Hepatic Encephalopathy - Second Phase
Hyperreflexia Asterixis or flapping Altered hand writing Violent, abusive behavior

161 Hepatic Encephalopathy - Coma
+ Babinski hyperactive reflexes obtained with reflex hammer

162 Babinski Video

163 Medical Management Hepatic Encephalopathy
Neomycin Lactulose Protein reduction

164 Hepatorenal syndrome Complication of Hepatic Failure

165 Hepatorenal syndrome Complication of Hepatic Failure
kidneys may appear normal physically but functioning impaired. Usually sudden decrease Urine production, increase BUN & Creatinine, jaundice and signs of liver failure Poor prognosis- most die within 3 wks without transplant Think due to decreased perfusion &/or toxins from failure of liver

166 Liver Dialysis Bridge to transplant Dialyze 6 hours at a time

167 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.

168

169 Potential donors evaluated for:
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

170 Liver Transplant Video

171 Liver transplant complications
Rejection. About 70% of all liver-transplant patients have some degree of organ rejection prior to discharge. Anti-rejection medications are given to ward off the immune attack. Infection Most infections can be treated successfully as they occur. Cancer

172 Review Pathophysiology Cirrhosis Portal hypertension Liver failure
Encephalopathy Hepato-renal syndrome Signs & Symptoms Treatment Nsg. Care Complications

173 The End


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