Liver Disorders Part 1 Charlene Morris, RN, MSN

Liver Disorders Part 1 Charlene Morris, RN, MSN
Austin Community College Addenda Spring 2010 John Nation RN, MSN

Have you finished reading the Lewis text?
3 Weeks ago 2 Weeks ago 1 Week ago Can you repeat the question?

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

Which letter points to the liver?
A B C D E F

A and P Review

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

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

Blood Supply – 2 sources Hepatic artery – 500cc/min oxygenated blood.
30% of Cardiac output goes to the liver Portal vein – 1000cc/min partly oxygenated blood supplies % O2 plus rich supply of nutrients, toxins, drugs stomach, small and large intestines, pancreas and spleen Both empty into capillaries/sinusoids Liver filters the blood Hepatic vein to inferior vena cava

Hepatic Circulation Video

Lobule – Functional unit of the liver Capillaries

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)

Metabolic Functions of the Liver
1. Metabolism of Glucose - glucose buffer When glucose levels rise liver stores it as glycogen When glucose levels low Liver breaks glycogen to usable glucose Amino acids to glucose Fatty acids/triglycerides into glucose 2. Protein – major storage center for protein When protein storage at full capacity, liver breaks it into glucose then forms glycogen and fatty acids for storage Breakdown of amino acids releases ammonia Liver converts ammonia to urea and excreted by the kidneys 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

Metabolic Functions of the liver cont.
3. Fatty acids – Conversion of triglycerides into fatty acids & glycerol by enzymes in capillary walls of liver and adipose tissue - Digestion & Storage of fats - Energy Glycerol and fatty acids can enter the Kreb’s cycle. Some triglycerides break down/are converted to new glucose releasing ketones Released Ketones can fuel heart & skeletal muscles/ lower pH 4. Cholesterol – produced by the liver & used for fat digestion - processed into lipoproteins LDL metabolized – releases oxygen free radicals/electrons – vessel & cell damage HDL carries cholesterol from cells back to the liver What really common class of medications do you see in the hospital? statins

Other functions Emergency reserve B12, D, and A Iron as ferritin
Immunologic – phagocytic Kupffer’s cells in liver remove bacteria, dead cells and other foreign substances from blood Blood storage Emergency reserve – may be up to cc with Rt. Heart failure Plasma protein synthesis - including albumin for maintaining plasma osmotic pressure Clotting – factor synthesis fibrinogen, prothrombin and factor VII - absorption of vitamin K Storage of vitamins and minerals B12, D, and A Iron as ferritin

Other transformation processes
Waste products of hemoglobin - transformed to a water-soluble form of Bilirubin that can be excreted Indirect/unconjugated bilirubin is attached to albumin, goes to the liver to be changed to direct/conjugated water soluble form. Conjugated bilirubin is soluble and excreted in bile. A small amount is reabsorbed by the blood. Formation and secretion of bile Contains cholesterol and bile salts for digestion of fats. Used in fat soluble vitamin absorption Bile transports bilirubin to the intestines to be excreted In the intestines, bacteria convert conjugated bilirubin to stercobilinogen and urobilinogen Stercobilinogen causes brown color of stool Some urobilinogen is reabsorbed into blood, returned to liver, and excreted as bile.

Other transformation processes
Steroids and hormones - acts on these to make them water soluble for excretion – otherwise would concentrate in body tissues Ammonia – neurotoxic byproduct of protein breakdown transformed into urea for excretion in urine Drugs, alcohol and toxins metabolism– transforms to water soluble for excretion

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

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

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

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

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

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 Hepatitis Statistics- CDC

Hepatitis A Etiology 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

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

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

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

Mode of Transmission HAV
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

Mode of Transmission HAV
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

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

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

Remember 2/2/2/2 Rule 2 doses IM to prevent
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

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 34

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

Hepatitis B Etiology 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

Sexually transmitted disease Can live on a dry surface for 7 days More infectious than HIV

Hepatitis B- Precautions
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. 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. Source: UptoDate

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

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

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

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

Hepatitis B Virus Etiology
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

Hepatitis C Approximately 170 million people are infected with the hepatitis C virus (HCV) Estimated 30,000 new cases diagnosed annually 44

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 45

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

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

Hepatitis C MOT 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

Hepatitis C Diagnostic Studies
Anti-HCV antibody HCV RNA 49

You Tube Hepatitis C

Hepatitis C Interventions
Needle Exchange Harm Reduction - Austin Harm Reduction Coalition

Hepatitis D Etiology 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

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

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

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

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

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

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

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

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

Severe Jaundice

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

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

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

Hepatitis Complications
Fulminant Hepatic Failure Chronic Hepatitis Cirrhosis Hepatocellular Carcinoma

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

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.

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

Diagnostic tests 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)

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

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), neproxen (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. 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.

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

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. Vital signs & Empty bladder Supine position, R arm above head Hold breath after expiration when needle inserted Be very still during procedure – 20 minutes

Liver Biopsy Video

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

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 a few hours or days. 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

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

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)

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

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

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

Nursing assessment Low-grade fever Jaundice Abnormal laboratory values

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

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

Nursing implementation Health promotion Hepatitis A Education Vaccination Good hygiene practices

Nursing implementation Health Promotion Hepatitis B Vaccination Education Workplace safety

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

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

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

Nursing implementation Ambulatory and home care Avoid alcohol

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

Evaluation Expected outcomes Able to explain methods of transmission and methods of preventing transmission to others

Hepatitis Reporting

Which type of hepatitis has few long term consequences?
Hepatitis A Hepatitis B Hepatitis C Hepatitis D

Which statement about hepatitis is true?
Hepatitis A often leads to fulminant hepatitis Hepatitis B is transmitted via blood and other body fluids Hepatitis C is transmitted via fecal-oral route Hepatitis D is a benign infection

Which types of hepatitis have vaccines?
Hepatitis A, B, & C Hepatitis A & B Hepatitis B & C Hepatitis B, C, & E

Juandice occurs during which stage of hepatitis?
Incubation Pre-icteric Icteric Post-icteric

Cirrhosis Video Clip Break!!

Cirrhosis

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

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

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

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.

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

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

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

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

Cirrhosis Interventions- Drugs
Diuretics- Aldactone (spironolactone): decreases aldosterone levels, K+ sparing Lasix (furosemide) Salt-poor albumin Neomycin – decrease ammonia forming organisms. 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

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.

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

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)

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

JAUNDICE Hepatocellular Obstructive Hemolytic

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

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

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

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

A client is admitted with increased ascites related to cirrhosis
A client is admitted with increased ascites related to cirrhosis. What is the priority nursing diagnosis? Fatigue Excessive fluid volume Ineffective breathing pattern Imbalanced nutrition: less than body requirements

Break!

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. Although the differential diagnosis is extensive, alcoholic and viral cirrhosis are the leading causes of portal hypertension in Western countries. Portal vein thrombosis is the most common cause in children.

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.

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 TIPS!- You tube

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

Ascites Caput medusae

Spider angiomas

Varices In Western countries variceal bleeding accounts for about 7% of episodes of gastrointestinal bleeding, although this varies according to the prevalence of alcohol related liver disease (11% in the United States, 5% in the United Kingdom). Patients with varices have a 30% lifetime risk of bleeding, and a third of those who bleed will die. Patients who have bled once from esophageal varices have a 70% chance of bleeding again, and about a third of further bleeding episodes are fatal. Several important considerations influence choice of treatment and prognosis. These include the natural course of the disease causing portal hypertension, location of the bleeding varices, residual hepatic function, presence of associated systemic disease, continuing drug or alcohol misuse, and response to specific treatment.

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)

Emergency endoscopy Emergency diagnostic fibreoptic endoscopy is essential to confirm that esophageal varices are present and are the source of bleeding. Most patients will have stopped bleeding spontaneously before endoscopy (60% of bleeds) or after drug treatment. Endotracheal intubation may be necessary during endoscopy, especially in patients who are bleeding heavily, encephalopathic, or unstable despite vigorous resuscitation. In 80% of patients variceal bleeding originates from esophageal varices. These are treated by injection with sclerosant or by banding.

Sclerotherapy In sclerotherapy a sclerosant solution (ethanolamine oleate or sodium tetradecyl sulphate) is injected into the bleeding varix or the overlying submucosa. Injection into the varix obliterates the lumen by thrombosis whereas injection into the submucosa produces inflammation followed by fibrosis. The first injection controls bleeding in 80% of cases. If bleeding recurs, the injection is repeated. Complications are related to toxicity of the sclerosant and include transient fever, dysphagia and chest pain, ulceration, stricture, and (rarely) perforation.

Band ligation Band ligation is achieved by a banding device attached to the tip of the endoscope. The varix is aspirated into the banding chamber, and a trip wire dislodges a rubber band carried on the banding chamber, ligating the entrapped varix. One to three bands are applied to each varix, resulting in thrombosis. Band ligation eradicates esophageal varices with fewer treatment sessions and complications than sclerotherapy. You Tube Band Ligation

Balloon tube tamponade
The balloon tube tamponade may be life saving in patients with active variceal bleeding if emergency sclerotherapy or banding is unavailable or not technically possible because visibility is obscured. In patients with active bleeding, an endotracheal tube should be inserted to protect the airway before attempting to place the esophageal balloon tube. The Minnesota balloon tube has four lumens, one for gastric aspiration, two to inflate the gastric and esophageal balloons, and one above the esophageal balloon for suction of secretions to prevent aspiration. The tube is inserted through the mouth, and correct placement within the stomach is checked by auscultation while injecting air through the gastric lumen. The gastric balloon is then inflated with 200 ml of air. Once fully inflated, the gastric balloon is pulled up against the esophagogastric junction, compressing the submucosal varices. The tension is maintained by strapping a split tennis ball to the tube at the patient's mouth. The esophageal balloon is rarely required. The main complications are gastric and esophageal ulceration, aspiration pneumonia, and esophageal perforation. Continued bleeding during balloon tamponade indicates an incorrectly positioned tube or bleeding from another source. After resuscitation, and within 12 hours, the tube is removed and endoscopic treatment repeated. Minnesota balloon for tamponade of esophageal varices

Minnesota Tube Sengstaken-Blakemore tube – has only 3 lumens
**Respiratory assessment**

Sengstaken-Blakemore tube – has only 3 lumens

Question: There is a risk of damage to the oesophageal mucosa from an inflated oesophageal balloon. Many centres have policies for routinely deflating and then reinflating the oesophageal balloon. This varies from 5 minutes deflation every hour to minutes every 8 hours. There appears to be little consensus at this time. If the oesophageal balloon needs to be inflated what is the most accurate general principle? The balloon should be deflated and the reinflated every hour. The balloon should be deflated and then reinflated every 8 hours. The balloon should never be routinely deflated as the risk of rebleeding is too great. The Balloon should be inflated for the absolutely minimum time necessary.

Long term management of esophageal varices
After acute variceal hemorrhage – prevent rebleeding, which occurs in many patients. 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. All patients should take beta blockers unless they have contraindications. Best results are obtained when portal blood pressure is reduced by more than 20% of baseline or to below 12 mm Hg. 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.

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 reduces portal venous pressures and thus controls bleeding and increases urine output by inc. venous return YouTube- TIPS

TIPS Transjugular intrahepatic portosystemic shunt

TIPS POST

*Shunted blood contains
high ammonia Which can lead to: hepatic encephalopathy*

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

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

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

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

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

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

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

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

Additional Complications Liver Failure

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

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

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

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

Stages of Hepatic Encephalopathy

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

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

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

With the first sign of hepatic encephalopathy decrease protein intake!

Medical Management Hepatic Encephalopathy
Neomycin -- intestinal antiseptic-decrease bacteria that produce ammonia but may cause renal toxicity or hearing impairment

Lactulose Converts to lactic and acetic acids
Acid environment decreases bacterial growth Increased acidity in the gut converts ammonia to ammonium ion which is excreted in feces thus decreases amount of ammonia available for re-absorption into the blood. Laxative effect removes ammonia from bowel. Goal-2-3 loose stools/day Give diluted with fruit juice or water- very sweet! Avoid giving with meals.

Hepatic Encephalopathy - Protein Intake
Decrease protein intake 0-40 grams/day- meat protein most toxic Add grams every 3-5 days to max 60gms If tube feeding use Hepatic-aid. (reduce ammonia from protein) Increase carbohydrates Decrease fats

Unconjugated bilirubin
A client with cirrhosis is receiving lactulose to prevent hepatic encephalopathy. What should the nurse monitor to evaluate the effectiveness of this medication? Serum albumin level Serum ammonia level ALT Unconjugated bilirubin

A trained nurse can insert a Sengstaken- Blakemore tube.
True False

Elevated liver enzymes and low serum protein
A client with acute liver failure exhibits confusion, a declinning level of consciousness, and slowed respirations. The nurse finds him very difficult to arouse. The diagnostic information which best explains the clint's behavior is: Elevated liver enzymes and low serum protein Hypoglycemia and increased serum ammonia Thrombocytopenia Hyperglycemia and increased creatinine

Hepatorenal syndrome Complication of Hepatic Failure

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

Liver Dialysis Bridge to transplant Dialyze 6 hours at a time

Donors: Video- What being a donor doesn't mean...
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. Video- What being a donor doesn't mean...

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 for brain dead donor Liver Transplant Video

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

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

The End

Liver Disorders Part 1 Charlene Morris, RN, MSN

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Liver Disorders Part 1 Charlene Morris, RN, MSN

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