Hepatic Disorders PDF - Overview of Hepatitis & Treatments

HEPATIC DISORDERS  HEPATITIS inflammation of the liver Causes: – Virus infection is the most common cause of hepatitis – Alcohol, drugs, toxins, and autoimmune disorders  Three Phases of Hepatitis Preicteric (prodromal) phase = from the time of infection unt...

HEPATIC DISORDERS  HEPATITIS inflammation of the liver Causes: – Virus infection is the most common cause of hepatitis – Alcohol, drugs, toxins, and autoimmune disorders  Three Phases of Hepatitis Preicteric (prodromal) phase = from the time of infection until the start of signs and symptoms, such as malaise, fever, nausea, and vomiting. Icteric phase = when jaundice sets in; urine can be dark from increased bilirubin; cholestasis may develop. Posticteric phase = the recovery phase when jaundice resolves and the liver starts to repair itself.  Types of Hepatitis Acute Hepatitis → occurs in the initial period after infection and symptoms are clinically similar for all viral types. Chronic Hepatitis → lasts greater than six months – caused by hepatitis B, C, and D viruses – caused by alcohol, hepatotoxic substances (carbon tetrachloride) and drug-induced, and some hereditary conditions  Types Virus Name / Type of Virus Hepatitis A RNA virus (picornavirus) of the enterovirus family Serum hepatitis double-shelled DNA virus – Hepatitis B contains core antigen (HBcAg) and a surface antigen (HBsAg) Hepatitis C RNA virus RNA virus – needs the helper function of HBV to Hepatitis D infect and replicate Hepatitis E RNA virus Is possibly a variant of the HBV – not much is Hepatitis F known about the virus Non-A, non-E hepatitis RNA flavivirus-like agent Hepatitis Copyright G © 2007 by Thomson Delmar Learning. ALL RIGHTS RESERVED. HGV or GB virus-C (GBV-C)  Types Spread / Route Fecal – oral route (eating food or drinking water Hepatitis A contaminated with HAV) – eating raw shellfish Blood and body fluids (semen, saliva, or vaginal secretions) via skin and mucous membranes Unprotected sex Hepatitis B Sharing needles & other drug paraphernalia Mother infected can inoculate the baby during birthing process Accidental needlesticks Blood & plasma to skin & mucous membranes Rarely spreads by sexual contact Hepatitis C Rarely spread from HCV-infected mother to baby during birthing process  Types Spread / Route Similar to HBV Coinfection is when HDV is acquired at the Hepatitis D same time as HBV Superinfection is when patients with chronic HBV acquire a subsequent HDV infection Fecal – oral route Waterborne epidemics, especially in Asia, Middle East, Africa, and Central and South Hepatitis E America Eating foods contaminated with HEV – often eating raw shellfish Hepatitis G Blood and plasma to skin and mucous membranes  Types Prevention / Vaccination HAV (Havrix, Vaqta) Handwashing with soap and water after using the bathroom, after changing diaper, before Hepatitis A preparing a food, and before eating. Once infected with HAV, the person will be immune HB vaccine is available Hepatitis B Testing of mothers with HBsAg Vaccination of all newborns No vaccine exists Prevention concentrates on standard Hepatitis C precautions and infection control Donor screening  Types Prevention / Vaccination Preventing HBV also prevents HDV Avoid contact with infected blood, contaminated Hepatitis D needles and an infected person’s personal items HE vaccine is available(effectiveness is uncertain) Always wash hands with soap and water after Hepatitis E using the bathroom, after changing diaper, before preparing a food, and before eating Hand sanitizers No vaccine exists Hepatitis G Prevention concentrates on standard precautions and infection control  Types Who is at risk? People living with infected people Hepatitis A Sex partners of infected people Traveling to countries where HAV is common Health care workers Inmates of long-term correctional facilities Sexually active men who have sex with men Men and women more than one sexual partner in the last six months. Hepatitis B Those who have history of STDs Hemodialysis patients Babies born to HBsAg (+) mothers Baby comes in contact with maternal secretions in the birth canal. Exposure to maternal blood, saliva, stool, urine.  Types Who is at risk? IV drug users are at higher risk Tattoos and body piercings Hepatitis C People who receive blood products Recipients of clotting factors Hepatitis D See HBV list People traveling to countries where HEV is Hepatitis E endemic IV drug users Hepatitis G Health care professionals  Types Incubation period Hepatitis A 2 – 6 weeks; average of 28 days 30 – 180 days; average is 120 days Hepatitis B HBV is 100 times more infectious than HIV and 10 times more infectious than HCV 15 – 160 days Chronic infection occurs in about 85% of HCV (+) Hepatitis C Can lead to cirrhosis, liver failure, liver failure, and liver cancer 30 – 150 days Hepatitis D Chronic hepatitis usually develops Hepatitis E 15 – 65 days Hepatitis G Chronic infection can occur  Types Signs and Symptoms / Diagnostic Tests Many are anicteric, asymptomatic Mild, viral flu-like symptoms Jaundice is not usually evident Hepatitis A Anorexia, dark urine, indigestion, epigastric distress, nausea, heartburn Anti-HAV is detected in serum to confirm diagnosis Anorexia, nausea, vomiting, jaundice, fatigue, low-grade fever, arthralgias, rashes, light-colored stools, and dark urine Infants will have low birth weight, jaundice, lethargy, failure to Hepatitis B thrive, abdominal distension and clay-colored stools Liver biopsy may be done Elevated AST, ALT, bilirubin, PT and LFTs. HBsAg, IG anti-HBc, IG anti-HBs Anti-HCV antibodies in serum Hepatitis C Influenza-type symptoms may be more severe than with HAV  Types Signs and Symptoms / Diagnostic Tests Coinfection symptoms are more severe than with solitary HBV infection Hepatitis D Some are asymptomatic Anti-HDV antibodies in serum and the presence of HBsAg confirms the diagnosis Mild, viral flu-like symptoms, jaundice, fatigue, abdominal pain, decreased appetite, nausea, Hepatitis E vomiting, and dark urine Anti-HEV is detected in serum to confirm diagnosis Anti-HGV antibodies in serum Hepatitis G Influenza-type symptoms  Types Treatment Hepatitis A IG = immediately after exposure After diagnosis: care is supportive, treating fever and flu-like symptoms Hepatitis A The disease usually resolves on its own Avoiding alcohol Has no known chronic carrier state HBIG administered within 7 days of percutaneous exposure and two weeks after sexual exposure. HBIG can be given within 12 hours of birth = for Hepatitis B infants born to HBV (+) mothers HBV vaccine = 12 – 24 hours postexposure HBV vaccine = can be given before the child leaves the hospital, and at one and six months after delivery.  Types Treatment After diagnosis: Interferon-alpha (injection 3x a week) Lamivudine (taken orally daily for one year) Hepatitis B Adefovir (taken orally daily for one year) Corticosteroids are contraindicated since viral replication is enhanced. IG is not proven effective after exposure After diagnosis: interferon, pegylated interferon, Hepatitis C and Ribavirin in combination are most effective Accounts for 50% of all liver transplants. HBIG = preexposure or postexposure Hepatitis D Alpha interferon for chronic HDV  Types Treatment After exposure = IG After diagnosis: supportive care, treating fever and flu-like symptoms Hepatitis E Avoiding alcohol Has no known carrier state More severe in pregnant women, especially in third trimester Supportive care after diagnosis Hepatitis G Avoiding alcohol  Nursing Care Standard precautions must be practiced at all times. Hand sanitizers help decrease infection. Needleless system for administering IVF. Patient education about handwashing after using the bathroom, before meal preparation, and before eating. Avoid raw shellfish. Avoid using anyone else’s personal items such as toothbrushes, razors, dental floss, nail clippers. Use condoms during sexual intercourse. Ensure sterility before obtaining tattoos or piercings. If traveling, drink only water that is purified. Peel fruits and vegetables before eating.  Choose cooked food over raw vegetables. Be sure milk products are pasteurized. During illness: – Promote adequate physical and psychological rest. – Limit fat and protein in the diet. – Small frequent meals should be offered. – Increasing antioxidants in the diet. – Vitamins and dietary supplements can improve nutrition. Avoid Prochlorperazine (Compazine), an antiemetic, because of potential hepatotoxic effects. Avoidance of alcohol in all types of hepatitis.  Alcoholic Hepatitis Inflammation of the liver caused by alcohol other than viruses. Nursing Management: Teach the use of corticosteroids and its side effects. Antioxidants to lessen the negative effects of free radicals. Antibiotics to combat increased permeability to intestinal bacteria. Vitamins and minerals supplementation. Observe for alcohol withdrawal symptoms Place the patient in seizure precautions.  Toxic & Drug-Induced Hepatitis Inflammation of the liver caused by toxic substances and prescribed medications. – Toxic substances: Carbon tetrachloride (e.g., Freon), hydrocarbons, and phosphorus – Medications: Isoniazid Indomethacin Halothane Methyldopa Propylthiouracil Acetaminophen Amiodarone Phenytoin Tetracycline MAOI Diclofenac  Fulminant Hepatic Failure Clinical syndrome of sudden and severely impaired liver function in a previously healthy person. This develops after the first symptom of jaundice. Jaundice progressing to encephalopathy is the characteristic. Categories: ❏ Hyperacute = the duration of jaundice before the onset of encephalopathy is 0 – 7 days ❏ Acute = 8 – 28 days ❏ Subacute = 28 – 72 days Causes: – Viral hepatitis – Toxic medications (acetaminophen) – Chemicals (carbon tetrachloride) – Metabolic disturbances (Wilson’s disease) – Structural abnormalities (Budd-Chiari syndrome - an obstruction to outflow in major hepatic veins) Treatment: – Plasmapheresis – Bioartificial liver = exposes separated plasma to a cartridge containing porcine liver cells after the plasma has flowed through a charcoal column that removes substances toxic to hepatocytes – Liver transplantation Complication: Cerebral edema due to encephalopathy Cause: not fully understood; but thought to be due to the disruption of the blood-brain barrier and plasma leakage into the CSF. Hereditary Diseases of the Liver  Wilson’s Disease This is an autosomal recessive disorder related to copper metabolism Copper is secreted in the bile, but becomes accumulated in the body. Manifestations: – Tremors – Deterioration of work – Rigidity – Personality changes – Kayser-Fleischer rings – Inappropriate behavior – Difficulty with speech Complications & Dx Tests: Complications: – Bone fractures – Infection – Impaired kidney function Diagnostics: – ↓ ceruloplasmin in blood and urine. – Liver biopsy = reveals liver tissue accumulation of copper. Treatment: – Avoid foods high in copper – Copper-binding drugs (chelating agents) Penicillamine (Cuprimine or Depen) Trientine (Syprine) Zinc acetate (Gatzin) = helps interfere with copper absorption in the stomach and intestine.  Hemochromatosis Excessive accumulation of iron in the liver, heart, joints, testicles, and thyroid Manifestations: – Fatigue – Bronze or grayish skin – Decreased libido (iron stimulates skin cells – Amenorrhea to produce more melanin) – Abdominal pain – Joint pain Complications: – Cirrhosis – Liver failure – Liver cancer – CHF – Cardiac arrhythmias – Impotence – Hypothyroidism – Diabetes Mellitus Diagnostic Tests: – Abnormal liver function tests Increased serum ferritin = measures the amount of iron stored in the body Increased serum transferrin saturation = measures the amount of iron that binds to protein in the blood – Liver biopsy = reveals excessive accumulation of iron Treatment: – Phlebotomy = letting of blood to decrease the iron load in the body. – Avoid foods like red meat, dried peas and lentils, and iron-enriched breads and pasta – Avoid Vitamin C supplements – Avoid alcohol = causes hepatotoxicity  Liver Cirrhosis A chronic, progressive condition characterized by destruction of the liver cells and subsequent formation of fibrotic tissue that reconfigures normal, healthy liver tissue. Major Types: 1. Alcoholic cirrhosis (Laennec’s cirrhosis) 2. Postnecrotic cirrhosis 3. Biliary cirrhosis 4. Cardiac cirrhosis  Alcoholic Cirrhosis (Laennec’s Cirrhosis) Alcohol interferes with lipid metabolism, creating hyperlipidemia, in turn would result to hypoxia, congestion, and inflammation. Persons with alcoholism and hepatitis C virus develop alcoholic cirrhosis  Postnecrotic Cirrhosis Occurs most frequently in the wake of hepatitis infections. Hepatitis C is the predominant cause of viral-related cirrhosis.  Biliary Cirrhosis Blocked bile ducts cause congestion, inflammation, and damage to liver tissue. Biliary atresia = bile ducts are absent or improperly formed, depriving the bile of avenues of exit from the liver and ultimately causing tissue damage.  Cardiac Cirrhosis (Vascular Cirrhosis) Occurs when blood flow out of the liver is restricted by severe right sided-heart failure. – Tricuspid regurgitation When the blood is not able to exit , liver engorgement occurs, and the pressure in the liver vasculature increases, causing venous congestion, anoxia, or hypoxia, and hepatic cell necrosis and subsequent fibrosis. Complications: Ascites = accumulation of fluid in the peritoneal cavity and the most common complication of cirrhosis. Pathophysiology: With congestion of blood and lymph in the fibrotic liver, plasma can seep from the liver vasculature into the peritoneum. Liver sweats = refer to movement of plasma from the lymphatic system into this potential space in the abdomen.  Ascites When volume is decreased in the intravascular space because of plasma moving out, the body perceives this as low blood volume, conserves water and sodium, and makes the problem worse. Refractory Ascites = means unresponsive to 400 mg of spironolactone (or 30mg of amiloride) plus 120 mg of furosemide daily for two weeks. Causes: – Noncompliance with fluid or sodium restrictions – Bacterial peritonitis  Spontaneous Bacterial Peritonitis (SBP) – Ascitic fluid becomes infected with bacteria in the absence of an obvious precipitating events. Manifestations: Increased fever or abdominal pain PMN (polymorphonuclear) count is greater than 250 cells/ µL Cefotaxime (Cefizox) = antibiotic of choice Complications: Impaired storage of fat soluble vitamin. Impaired synthesis of clotting factors Impaired metabolism and transport of bilirubin Type of diabetes mellitus High levels of ammonia Impaired lipid metabolism Inadequate albumin production Treatment: Fluid restriction = 1000 – 1500 ml/day Sodium restriction = limited to 200 – 500 mg/day Diuretic therapy – Spironolactone (Aldactone) = is the diuretic of choice, because of its potassium-sparing properties – Amiloride (Moduretic) – Triamterene (Dyazide or Maxzide)  Paracentesis Limited removal of fluid from the peritoneal cavity for diagnostic or therapeutic purposes. – This can be performed at the bedside. – Used palliatively to reduce abdominal pressure, which can cause respiratory distress and abdominal pain. – 750 – 1000 ml are removed at a time. Preparation: Have the patient empty his/her bladder to decrease the possibility of injury to the bladder. Elevate the head of the at 15° – 60° to allow fluid to accumulate in the lower abdomen. Monitor vital signs, ECG, weight, LOC, and abdominal girth. Check the consent. Monitor for cardiac arrhythmias. Result from depletion of potassium or hypovolemia. Monitor temperature to assess for infection. Keep the head of the bed at 30 degrees to allow for maximal respiratory expansion and minimize shortness of breath.  LeVeen Peritoneovenous Shunt (LPVS) Diverts ascitic fluid via a pressure sensitive one-way valve from the peritoneum to the internal jugular vein and ultimately into the superior vena cava. On inspiration, pressure in the abdomen increase, allowing fluid to move toward the heart and re-enter the vascular system.  Portal Hypertension The constant pressure of the blood, bile, and lymphatics within the liver. – When the blood meets with resistance, it tries to find another routes around the obstruction (collateral circulation). Complications: – Esophageal Varices = when the blood backs up, the vessels become distended, and walls become thinner and more friable. Complications: – Splenomegaly – Hemorrhoids – Caput Medusae Surgical Treatments: Distal Splenorenal Shunt (DSRS) → splenic vein is joined to the left kidney vein, thereby selectively decompressing the esophageal and gastric varices. – Used to reroute blood only from the veins coming from the esophagus and stomach, while preserving the blood flow through the portal vein. – Less encephalopathy but higher surgical mortality  Transjugular Intrahepatic Portosystemic Shunt (TIPS) A catheter is introduced into the jugular vein and advanced into the hepatic vein. The catheter is threaded into a large branch of the portal vein and a stent is placed connecting the portal vein with hepatic vein. Advantages: Local anesthetic and mild sedation only are used. Major surgery is avoided. Reduces ascites and relieving portal hypertension, but DSRS does not. Disadvantage: 25 % of patients suffer encephalopathy.  Sclerotherapy A technique of injecting sclerosing drugs into the varices, causing a narrowing of the swollen veins, thus preventing bleeding and reducing swelling. – This procedure is done endoscopically.  Hepatic Encephalopathy Known as Portal-Systemic Encephalopathy (PSE) or hepatic coma. This is a neurological condition leading to changes in LOC, slurred speech, behavioral changes and emotional lability, drowsiness, muscle twitching progressing to rigidity, asterixis, and seizures. – Asterixis = liver flaps, or flapping tremor  Asterixis When asked to hold the arms and hands stretched out, the patient is unable to do this position, and there will be series of rapid flexion and extension movements of the hands  Other Signs: – Rhythmic movements of the legs with dorsiflexion of the foot – Rhythmic movements in the face with strong closure of the eyelids. – Fetor hepaticus = musty, sweet odor of the patient’s breath. Cause: Impaired metabolism of ammonia (NH3) – Ammonia levels are toxic to nerve tissue and can cause negative effects to the brain. – Ammonia is catabolized from protein and is then converted into urea to be excreted by the kidneys. – Bacteria in the gut also produce ammonia.  Treatment: Lactulose = is a synthetic sugar that is used as laxative. – It works by pulling water into the gut to soften stool and increase peristalsis. – It also helps to pull ammonia from the blood into the colon for expulsion. – 2 – 4 stools/ day is recommended to treat high levels of ammonia Neomycin (Bleomycin) = is used to decrease amounts of ammonia-producing bacteria in the intestines. – Given orally because IV antibiotics do not have positive effect.  Fatty Liver (Hepatic Steatosis) A condition of excessive lipids in the liver that account more than 5% of liver weight. Three major types of fats (lipids): – Cholesterol – Triglycerides – Phospholipids (principal serum is phosphatidylcholine, commonly known as lecithin)  Lipids are hydrophobic (insoluble in water). – Lipids are modified by the liver to become lipoproteins (making it more water-soluble). – Lipoproteins are necessary for energy, membrane integrity, and synthesis of variety of molecules needed in metabolic processes. Causes: – Chronic alcohol ingestion = the most common cause of fatty liver – Conditions that increase fatty acids: Obesity Pregnancy DM Malnutrition or kwashiorkor Corticosteroids Prolonged TPN Pathophysiology: – Alcohol interferes with fat metabolism by causing lipidemia, and increasing VLDL. – Alcohol can damage membrane integrity of organelles within the hepatocytes by the release of free radicals. Clinical Manifestations: – Macrovesicular fatty liver = exhibits large fat droplets that balloon the liver cell and pushes the nucleus to the periphery of the cell. – Microvesicular fatty liver = small fat droplets fill the cell, the nuclei are not displaced, and the cells have a foamy appearance. Microvesicular fatty liver is most often seen with: – Pregnancy – Reye’s syndrome – Valproic acid – Tetracycline – Salicylate Microvesicular fatty liver can be much more concerning clinically. – Fatigue – Nausea – Vomiting – Jaundice – Hypoglycemia – Coma – DIC Macrovesicular fatty liver can be a reversible condition. – Hepatomegaly = most common finding of fatty liver – Many are asymptomatic – RUQ pain – Tenderness – Jaundice – Fatigue Dx & Interventions: Diagnostic test: – Liver biopsy = confirmatory diagnostic Planning & Implementation: – Avoid alcohol – Follow low fat diet  Hepatic Abscesses An area of infection in the liver caused by bacteria, amoeba, or protozoa. Etiology: – Cholangitis – Choledocholithiasis – Biliary-enteric anastomosis “ANCHOVY” PASTE Predisposing Factors: Bacteria – E. coli – Klebsiella pneumoniae – Streptococcal species Primary Conditions: – Appendicitis – Diverticulitis – IBD – Proctitis  Mycobacterium Tuberculosis = hepatic abscess occurs probably when a tuberculosis patient swallows infected sputum into the GI tract Amoebic Dysentery = caused by Entamoeba histolytica that can also lead to hepatic abscess. Clinical Manifestations: – Fever and RUQ pain – Chills – Malaise – Pleuritic chest pain – Right shoulder pain – Anorexia – Weight loss – Hepatomegaly – Jaundice Diagnostic Tests: – Stool cultures identify amoebic dysentery. – Percutaneous drainage removes the fluid from the abscess. The fluid can be used to analyze the offending agent. Planning & Implementation: – Anti-infective therapy: Metronidazole Clindamycin / Ciprofloxacin – Drainage of the abscess by percutaneous catheter guide by ultrasound or CT scan. Complications: – Pneumothorax – Hemorrhage – Leakage into the abdominal cavity Post-procedure, the nurse should be alert of: – Changes in vital signs, DOB, and increasing abdominal or chest pain.  Liver Transplantation The first human liver transplant was performed in 1963, but the first successful liver transplant was done in 1967. Reasons for liver transplantation: – Alcoholic cirrhosis – Cancer of the liver – Ulcerative colitis – Crohn’s disease – Biliary atresia  Types of Liver Transplantation Orthotopic – patient’s own liver is removed entirely – the most common type of transplant Auxiliary – involves leaving part or all of patient’s liver in place & grafting in a healthy whole or partial liver. – this type of surgery is used for patient with Crigler- Najjar syndrome  Liver Donors Cadaveric Organs = comes from people who have been declared brain dead, but other vital organs are healthy & have been adequately perfused – Smaller left lobe is implanted into a smaller person or child. – Larger right lobe is implanted to the larger recipient.  Liver Donors Live Donors (Living Donor Liver Transplants [LDLT]) = organs usually donated to related family members (parents, siblings, other relatives)  Liver Recipients Conditions to Prioritize: – Candidates who have life expectancy of less than 7 days. – A person who has nonfunctioning transplanted liver after 7 days Defined as aspartate aminotransferase (AST) greater than or equal to 5000 and an international normalized ratio (INR) greater than 2.5 or acidosis with pH less than 7.3 – Hepatic artery thrombosis in first 7 days of liver implant – Decompensated Wilson’s disease  Liver Recipients Disqualification of Transplant Recipient: – Continuing use of alcohol prior to & after surgery – Noncompliance with previous medical care – Lack of support people to care for the patient after the operation – Advanced cancer of the liver – Advanced diseases of the kidney, heart, vasculature, or lungs – HIV or AIDS  Post-Operative Care Monitoring for hemorrhage, acute renal failure, bile leakage, HAT, fluid and electrolyte imbalance, infection, and acute graft rejection Signs of Acute Graft Rejection: Fever Abdominal pain Abdominal tenderness Nausea, Pain Jaundice  Liver biopsy is necessary to determine if the liver is actively being rejected. Monitoring strict I&O. Abdominal UTz is performed to assess for HAT, where a clot forms in the hepatic artery. V/s monitoring to determine early signs of infection and rejection.  Infection is high in liver recipient because of anti-rejection medications. Prevention of infection: – Avoiding swimming in lakes and pools – Avoiding closed conditions, such as being in a movie theater – Avoiding sick children and adults or who have been immunized with live vaccine  Patient Education Advice patient to abstain from alcohol. Do not self-medicate with OTC because some drugs are hepatotoxic. Normal activity can resume after 6 – 12 months of transplant. Mothers who become pregnant after transplantation should be discouraged to breastfeed because the immunosuppressant medications can be transmitted to the baby.  Pharmacology – Corticosteroids (Prednisone) Side effects: osteoporosis, hyperglycemia, edema, fluid and electrolyte problems – Cyclosporine (Neoral, Sandimmune or, Gengraf) – blocks interleukins and TNF (tumor necrosis factor) Side effects: hypertension, growth of body hair, and kidney damage  FK-506 – Tacrolimus (Prograf) – inhibits T cell activation Side effects: seizure, GI bleeding, anaphylaxis, ascites, hypertension, UTI, pruritus, rash, anemia, and generalized pain. – Sirolimus (Rapamune) – inhibits T cell activation Side effects: leukopenia, thrombocytopenia, hyperlipidemia, arthralgia, and tremors  Mycophenolate mofetil (CeelCept) – inhibits T and B lymphocyte proliferation – Side effects: GI bleeding and diarrhea, vomiting, leukemia, and sepsis Basiliximab (Simulect) – Side effects: heart failure, anaphylaxis, and wound complication  Daclizumab (Zenapax) – Side effect: pulmonary edema Azathioprine (Imuran) - immunosuppressant – Side effects: serum sickness, fever and chills, nausea, vomiting, anorexia, and pancreatitis