liver disorders part 1 charlene morris, rn, msn austin community college addenda spring 2010 john...

Liver DisordersLiver DisordersPart 1Part 1

Charlene Morris, RN, MSNCharlene Morris, RN, MSN

Austin Community CollegeAustin Community College

Addenda Spring 2010 John Nation RN, MSNAddenda Spring 2010 John Nation RN, MSN

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4.4. Can you repeat Can you repeat the question?the question?

Overview of Today’s Overview of Today’s LectureLecture A & P ReviewA & P Review Hepatitis AHepatitis A Hepatitis BHepatitis B Hepatitis CHepatitis C Cirrhosis Cirrhosis Portal HypertensionPortal Hypertension Esophageal VaricesEsophageal Varices Hepatic EncephalopathyHepatic Encephalopathy Hepatorenal SyndromeHepatorenal Syndrome Liver Transplant Liver Transplant

Which letter points to Which letter points to the liver?the liver?

A B C D E F

17% 17% 17%17%17%17%1.1. AA

2.2. BB

3.3. CC

4.4. DD

5.5. EE

6.6. FF

A and P ReviewA and P Review

Largest Largest internalinternal organ- organ-weighs around 3 lbs!weighs around 3 lbs!

A and P ReviewA and P Review

A LiverA Liver B Hepatic veinB Hepatic vein C Hepatic C Hepatic

arteryartery D Portal veinD Portal vein E Common bile E Common bile

ductduct F StomachF Stomach G Cystic ductG Cystic duct H GallbladderH Gallbladder

Blood Supply – 2 sourcesBlood Supply – 2 sources

Hepatic arteryHepatic artery – 500cc/min oxygenated – 500cc/min oxygenated blood. blood. – 30% of Cardiac output goes to the liver30% of Cardiac output goes to the liver

Portal veinPortal vein – 1000cc/min partly – 1000cc/min partly oxygenated blood supplies 50 - 60% O2 oxygenated blood supplies 50 - 60% O2 plus rich supply of nutrients, toxins, drugsplus rich supply of nutrients, toxins, drugs

stomach, small and large intestines, pancreas stomach, small and large intestines, pancreas and spleenand spleen

Both empty into capillaries/sinusoidsBoth empty into capillaries/sinusoids Liver filters the bloodLiver filters the blood Hepatic vein to inferior vena cavaHepatic vein to inferior vena cava

Hepatic Circulation VideoHepatic Circulation Video

Lobule –

Functional unit of the liver

Capillaries

Metabolic Functions of Metabolic Functions of the liverthe liver

““Body’s Refinery” Over 400 functionsBody’s Refinery” Over 400 functions

Primary role in anabolism and Primary role in anabolism and catabolismcatabolism

Metabolic Functions of the LiverMetabolic Functions of the Liver

1. 1. Metabolism of GlucoseMetabolism of Glucose - glucose buffer - glucose buffer – When glucose levels rise When glucose levels rise

liver stores it as glycogenliver stores it as glycogen– When glucose levels lowWhen glucose levels low

Liver breaks glycogen to usable glucoseLiver breaks glycogen to usable glucose Amino acids to glucoseAmino acids to glucose Fatty acids/triglycerides into glucoseFatty acids/triglycerides into glucose

2. Protein2. Protein – major storage center for protein – major storage center for protein – When protein storage at full capacity, liver breaks it When protein storage at full capacity, liver breaks it

into glucose then forms glycogen and fatty acids for into glucose then forms glycogen and fatty acids for storagestorage

– Breakdown of amino acids releases ammoniaBreakdown of amino acids releases ammonia– Liver converts ammonia to urea and excreted by the Liver converts ammonia to urea and excreted by the

kidneyskidneys

Metabolic Functions of the liver cont.Metabolic Functions of the liver cont.

3. Fatty acids3. Fatty acids – Conversion of triglycerides into fatty acids & – Conversion of triglycerides into fatty acids & glycerol by enzymes in capillary walls of liver and adipose glycerol by enzymes in capillary walls of liver and adipose tissue tissue - Digestion & Storage of fats- Digestion & Storage of fats- Energy - Energy

Glycerol and fatty acids can enter the Kreb’s cycle. Glycerol and fatty acids can enter the Kreb’s cycle. Some triglycerides break down/are converted to new Some triglycerides break down/are converted to new

glucose releasing ketonesglucose releasing ketones Released Ketones can fuel heart & skeletal muscles/ lower Released Ketones can fuel heart & skeletal muscles/ lower

pHpH

4. Cholesterol4. Cholesterol– – produced by the liver & used for fat digestionproduced by the liver & used for fat digestion

- processed into lipoproteins- processed into lipoproteinsLDL metabolized – releases oxygen freeLDL metabolized – releases oxygen free

radicals/electrons – vessel & cell radicals/electrons – vessel & cell damagedamage

HDL carries cholesterol from cells back to the HDL carries cholesterol from cells back to the liver liver

Other functionsOther functions ImmunologicImmunologic – phagocytic Kupffer’s cells in liver – phagocytic Kupffer’s cells in liver

remove bacteria, dead cells and other foreign remove bacteria, dead cells and other foreign substances from blood substances from blood

Blood storageBlood storage – Emergency reserveEmergency reserve

– – may be up to 400-500cc with Rt. Heart failuremay be up to 400-500cc with Rt. Heart failure Plasma protein synthesisPlasma protein synthesis

- including albumin for maintaining plasma osmotic- including albumin for maintaining plasma osmotic pressurepressure ClottingClotting

– – factor synthesis fibrinogen, prothrombin andfactor synthesis fibrinogen, prothrombin and factor VIIfactor VII - absorption of vitamin K- absorption of vitamin K Storage of vitamins and mineralsStorage of vitamins and minerals

– BB12, 12, D, and AD, and A– Iron as ferritinIron as ferritin

Other transformation processesOther transformation processes

Waste products of hemoglobin -Waste products of hemoglobin - transformed to a water-soluble form of transformed to a water-soluble form of Bilirubin that can be excretedBilirubin that can be excreted

Indirect/unconjugated bilirubin is attached to albumin, goes Indirect/unconjugated bilirubin is attached to albumin, goes

to the liver to be changed to direct/conjugated water solubleto the liver to be changed to direct/conjugated water soluble form. Conjugated bilirubin is soluble and excreted in bile. A form. Conjugated bilirubin is soluble and excreted in bile. A small amount is reabsorbed by the blood.small amount is reabsorbed by the blood.

Formation and secretion of bileFormation and secretion of bile Contains cholesterol and bile salts for digestion of fats. Contains cholesterol and bile salts for digestion of fats. Used in fat soluble vitamin absorption Used in fat soluble vitamin absorption Bile transports bilirubin to the intestines to be excreted Bile transports bilirubin to the intestines to be excreted In the intestines, bacteria convert conjugated bilirubin to In the intestines, bacteria convert conjugated bilirubin to

stercobilinogen and urobilinogenstercobilinogen and urobilinogen Stercobilinogen causes brown color of stoolStercobilinogen causes brown color of stool Some urobilinogen is reabsorbed into blood, returned to Some urobilinogen is reabsorbed into blood, returned to

liver, and excreted as bile.liver, and excreted as bile.

Other transformation Other transformation processesprocesses Steroids and hormones - Steroids and hormones - acts on acts on

these to make them water soluble for these to make them water soluble for excretion – otherwise would excretion – otherwise would concentrate in body tissuesconcentrate in body tissues

AmmoniaAmmonia – neurotoxic byproduct of – neurotoxic byproduct of protein breakdown transformed into protein breakdown transformed into urea for excretion in urine urea for excretion in urine

Drugs, alcohol and toxins Drugs, alcohol and toxins metabolismmetabolism– transforms to water – transforms to water soluble for excretionsoluble for excretion

To Summarize….To Summarize….

The liver:The liver:– changes food into energy changes food into energy – removes alcohol and poisons from removes alcohol and poisons from

the bloodthe blood– makes bile, a yellowish-green liquid makes bile, a yellowish-green liquid

that helps with digestionthat helps with digestion

HepatitisHepatitis

Simply means inflammation of Simply means inflammation of the liverthe liver– ““itis” means inflammation, “hepa” itis” means inflammation, “hepa”

means liver. means liver. Viral hepatitis Viral hepatitis

– Most common causeMost common cause– Viral types include A, B, C, D, E, and Viral types include A, B, C, D, E, and

GG

HepatitisHepatitis

Other possible causesOther possible causes– Drugs (alcohol)Drugs (alcohol)– ChemicalsChemicals– Autoimmune liver diseaseAutoimmune liver disease– Bacteria (rarely)Bacteria (rarely)

Hepatitis Hepatitis EtiologyEtiology CausesCauses

– A, B, C, D, E, and G virusA, B, C, D, E, and G virus– CytomegalovirusCytomegalovirus– Epstein-Barr virusEpstein-Barr virus– Herpes virus Herpes virus – CoxsackievirusCoxsackievirus– Rubella virusRubella virus

Hepatitis AHepatitis AEtiologyEtiology Hepatitis A virus (HAV)Hepatitis A virus (HAV)

– RNA virusRNA virus– Transmitted fecal–oral route, Transmitted fecal–oral route,

parenteral (rarely)parenteral (rarely)– Frequently occurs in small outbreaksFrequently occurs in small outbreaks

Hepatitis AHepatitis A

61,000 cases of hepatitis A occur 61,000 cases of hepatitis A occur annually in the United Statesannually in the United States

10 million cases of hepatitis A 10 million cases of hepatitis A occur worldwideoccur worldwide– Nearly universal during childhood in Nearly universal during childhood in

developing countriesdeveloping countries

Hepatitis Statistics- CDCHepatitis Statistics- CDC

Hepatitis A Hepatitis A EtiologyEtiology Hepatitis A virus (HAV)Hepatitis A virus (HAV)

– Found in feces 2 or more weeks Found in feces 2 or more weeks before the onset of symptoms and before the onset of symptoms and up to 1 week after the onset of up to 1 week after the onset of jaundice jaundice

– Present in blood brieflyPresent in blood briefly– No chronic carrier state No chronic carrier state

Incubation PeriodIncubation Period

2-6 weeks2-6 weeks Acute onsetAcute onset Mild flu-like manifestationsMild flu-like manifestations Symptoms last up to 2 monthsSymptoms last up to 2 months Liver usually repairs itself, so no Liver usually repairs itself, so no

permanent effectspermanent effects


– Anti-HAV immunoglobulin M (IgM)Anti-HAV immunoglobulin M (IgM) Appears in the serum as the stool Appears in the serum as the stool

becomes negative for the virusbecomes negative for the virus Detection of IgM anti-HAV indicates Detection of IgM anti-HAV indicates

acute hepatitis acute hepatitis


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

lifelong immunity lifelong immunity

Mode of Transmission Mode of Transmission HAVHAV Mainly by ingestion of food or Mainly by ingestion of food or

liquid infected with the virusliquid infected with the virus– Poor hygiene, improper Poor hygiene, improper

handling of food, crowding handling of food, crowding housing, poor sanitation housing, poor sanitation conditions are all factors conditions are all factors related to Hepatitis Arelated to Hepatitis A

Mode of Transmission Mode of Transmission HAVHAV Occurs more frequently in Occurs more frequently in

underdeveloped countriesunderdeveloped countries Contaminated watersContaminated waters

– Drinking water, contaminated Drinking water, contaminated seafoodseafood

Food-borne Hepatitis A outbreaks Food-borne Hepatitis A outbreaks usually due to infected food handlerusually due to infected food handler– Contamination of food during Contamination of food during

preparationpreparation

Hepatitis A VaccineHepatitis A Vaccine

2 doses IM2 doses IM–Initial doseInitial dose–Booster in 6 to 12 Booster in 6 to 12 monthsmonths

Post-exposure Post-exposure ProphylaxisProphylaxis Standard IG-immune globulinStandard IG-immune globulin

– Given IM within 2 weeks of exposureGiven IM within 2 weeks of exposure Hepatitis A VaccineHepatitis A Vaccine

IG is recommended for persons who do not IG is recommended for persons who do not have anti-HAV antibodies and have had food have anti-HAV antibodies and have had food borne exposure or close contact with HAV-borne exposure or close contact with HAV-infected person infected person

Remember 2/2/2/2 Remember 2/2/2/2 RuleRule 2 doses IM to prevent2 doses IM to prevent Signs & symptoms last 2 monthsSigns & symptoms last 2 months Contagious 2 weeks before signs & Contagious 2 weeks before signs &

symptomssymptoms Post-exposure dose given IM within 2 Post-exposure dose given IM within 2

weeks of exposureweeks of exposure Must report within one dayMust report within one day

Hepatitis BHepatitis B

Nearly 400 million people infected Nearly 400 million people infected with Hepatitis Bwith Hepatitis B– 50% to 75% active viral replication50% to 75% active viral replication

73,000 new cases of Hepatitis B 73,000 new cases of Hepatitis B annually in United Statesannually in United States– Incidence Incidence decreased due to HBV decreased due to HBV

vaccinevaccine

Hepatitis B Hepatitis B EtiologyEtiology

Hepatitis B virus (HBV)Hepatitis B virus (HBV)– DNA virusDNA virus– Transmission of HBVTransmission of HBV

Perinatally by mothers infectedPerinatally by mothers infected Percutaneously (IV drug use)Percutaneously (IV drug use) Horizontally by mucosal exposure to Horizontally by mucosal exposure to

infectious blood, blood products, or other infectious blood, blood products, or other body fluidsbody fluids

Hepatitis B Hepatitis B EtiologyEtiology

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

Hepatitis BHepatitis BEtiologyEtiology

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

Hepatitis B- Hepatitis B- Precautions Precautions PREVENT INFECTION OF FAMILYPREVENT INFECTION OF FAMILY — Acute and chronic hepatitis B — Acute and chronic hepatitis B

are contagious. Thus, people with hepatitis B should discuss are contagious. Thus, people with hepatitis B should discuss measures to reduce the risk of infecting close contacts. This includes measures to reduce the risk of infecting close contacts. This includes the following:the following:

Discuss the infection with any sexual partners and use a latex Discuss the infection with any sexual partners and use a latex condom with every sexual encounter. condom with every sexual encounter.

Do not share razors, toothbrushes, or anything that has blood on it. Do not share razors, toothbrushes, or anything that has blood on it. Cover open sores and cuts with a bandage. Cover open sores and cuts with a bandage. Do not donate blood, body organs, other tissues, or sperm. Do not donate blood, body organs, other tissues, or sperm. Immediate family and household members should have testing for Immediate family and household members should have testing for

hepatitis B. Anyone who is at risk of hepatitis B infection should be hepatitis B. Anyone who is at risk of hepatitis B infection should be vaccinated, if not done previously. (See vaccinated, if not done previously. (See "Patient information: Adult immunizations""Patient information: Adult immunizations".) .)

Do not share any injection drug equipment (needles, syringes). Do not share any injection drug equipment (needles, syringes). Clean blood spills with a mixture of 1 part household bleach to 9 Clean blood spills with a mixture of 1 part household bleach to 9

parts waterparts water..

Source: UptoDateSource: UptoDate

Hepatitis B- Hepatitis B- PreventionPrevention

Hepatitis B cannot be spread by:Hepatitis B cannot be spread by: Hugging or kissing* (some Hugging or kissing* (some

disagreement)disagreement) Sharing eating utensils or cups Sharing eating utensils or cups Sneezing or coughing Sneezing or coughing BreastfeedingBreastfeeding

Source: UptodateSource: Uptodate

Hep B Incubation Hep B Incubation PeriodPeriod

6-24 weeks6-24 weeks PreventionPrevention

–Vaccine-3 dosesVaccine-3 dosesInitial doseInitial doseDose at 4 weeksDose at 4 weeksDose 5 months laterDose 5 months later

Post-exposure Hep BPost-exposure Hep B

Hepatitis B Immune globulinHepatitis B Immune globulin IM in 2 dosesIM in 2 doses

– First dose within 24 hours to 7 days of First dose within 24 hours to 7 days of exposureexposure

– Second dose 20 to 30 days post-Second dose 20 to 30 days post-exposureexposure

Provides short-term immunityProvides short-term immunity Give HBV vaccine concurrently- vaccine Give HBV vaccine concurrently- vaccine

can be beneficial post- exposurecan be beneficial post- exposure

Hepatitis B Hepatitis B EtiologyEtiology Hepatitis B virus (HBV)Hepatitis B virus (HBV)

– Complex structure with three Complex structure with three antigensantigens Surface antigen (HBsAg)Surface antigen (HBsAg) Core antigen (HBcAg)Core antigen (HBcAg) E antigen (HBeAg)E antigen (HBeAg)

– Each antigen—a corresponding Each antigen—a corresponding antibody may develop in response to antibody may develop in response to acute viral Hepatitis Bacute viral Hepatitis B

Hepatitis B VirusHepatitis B VirusEtiologyEtiology Presence of Hepatitis B Surface Presence of Hepatitis B Surface

AntibodiesAntibodies– Indicates immunity from HBV Indicates immunity from HBV

vaccinevaccine– Past HBV infectionPast HBV infection– With chronic infection, liver enzyme With chronic infection, liver enzyme

values may be normal or ↑values may be normal or ↑– 15% to 25% of chronically infected 15% to 25% of chronically infected

persons die from chronic liver persons die from chronic liver diseasedisease

Hepatitis CHepatitis C

Approximately 170 million people Approximately 170 million people are infected with the hepatitis C are infected with the hepatitis C virus (HCV)virus (HCV)

Estimated 30,000 new cases Estimated 30,000 new cases diagnosed annuallydiagnosed annually

Hepatitis CHepatitis C

8000 to 10,000 people in the 8000 to 10,000 people in the United States die each year from United States die each year from complications of end-stage liver complications of end-stage liver disease secondary to HCVdisease secondary to HCV

Approximately 30% to 40% of Approximately 30% to 40% of HIV-infected patients also have HIV-infected patients also have HCVHCV

Hepatitis C Hepatitis C EtiologyEtiology Hepatitis C virus (HCV)Hepatitis C virus (HCV)

– Transmitted percutaneouslyTransmitted percutaneously– Risk factorsRisk factors

IV drug useIV drug use–Most common mode of Most common mode of transmission in United transmission in United States and CanadaStates and Canada

Blood transfusionsBlood transfusions

Hepatitis CHepatitis CEtiologyEtiology

Hepatitis C virus (HCV)Hepatitis C virus (HCV)– Risk factors (cont’d)Risk factors (cont’d)– High-risk sexual behaviorHigh-risk sexual behavior

HemodialysisHemodialysis Occupational exposureOccupational exposure Perinatal transmissionPerinatal transmission

Hepatitis CHepatitis CMOTMOT

Hepatitis C virus (HCV)Hepatitis C virus (HCV)– Up to 10% of patients with HCV Up to 10% of patients with HCV

cannot identify a sourcecannot identify a source– Risk of body piercings, tattooing, Risk of body piercings, tattooing,

and intranasal drug use in and intranasal drug use in transmission of HCVtransmission of HCV

Hepatitis CHepatitis CDiagnostic StudiesDiagnostic Studies

Anti-HCV antibodyAnti-HCV antibodyHCV RNAHCV RNA

You Tube Hepatitis CYou Tube Hepatitis C

Hepatitis C Hepatitis C InterventionsInterventions Needle ExchangeNeedle Exchange Harm Reduction - Austin Harm ReHarm Reduction - Austin Harm Re

duction Coalitionduction Coalition

Hepatitis DHepatitis DEtiologyEtiology

Hepatitis D virus (HDV)Hepatitis D virus (HDV)– Also called Also called delta virusdelta virus– Defective single-stranded RNA Defective single-stranded RNA

virusvirus– Cannot survive on its ownCannot survive on its own– Requires the helper function of Requires the helper function of

HBV to replicateHBV to replicate

Hepatitis DHepatitis DEtiologyEtiology Hepatitis D virus (HDV) Hepatitis D virus (HDV)

(cont’d)(cont’d)– HBV-HDV co-infectionHBV-HDV co-infection

↑ ↑ Risk of fulminant Risk of fulminant hepatitishepatitis

More severe acute diseaseMore severe acute disease

Hepatitis EHepatitis EEtiologyEtiology Hepatitis E virus (HEV)Hepatitis E virus (HEV)

– RNA virusRNA virus– Transmitted fecal–oral routeTransmitted fecal–oral route– Most common mode of Most common mode of

transmission is drinking transmission is drinking contaminated watercontaminated water

– Occurs primarily in developing Occurs primarily in developing countriescountries

Hepatitis GHepatitis GEtiologyEtiology Hepatitis G virus (HGV)Hepatitis G virus (HGV)

– RNA virusRNA virus– Poorly characterized parenterally Poorly characterized parenterally

and sexually transmitted virusand sexually transmitted virus– Found in some blood donorsFound in some blood donors– Can be transmitted by blood Can be transmitted by blood

transfusiontransfusion

Hepatitis GHepatitis GEtiologyEtiology

Hepatitis G virus (HGV) Hepatitis G virus (HGV) (cont’d)(cont’d)– Coexists with other hepatitis Coexists with other hepatitis

viruses and HIVviruses and HIV– Does not appear to cause Does not appear to cause

liver damageliver damage

Pathophysiology of Pathophysiology of HepatitisHepatitis Acute infection- widespread Acute infection- widespread

inflammation of liver tissueinflammation of liver tissue– Liver damage mediated byLiver damage mediated by

Cytotoxic cytokines Cytotoxic cytokines Natural killer cells Natural killer cells

– Liver cell damage results in Liver cell damage results in hepatic cell necrosishepatic cell necrosis

Common Common ManifestationsManifestationsof Acute Hepatitisof Acute Hepatitis Predictable course among Predictable course among

all the virusesall the viruses Incubation Phase: after Incubation Phase: after

exposure to virus, no exposure to virus, no symptomssymptoms

Preicteric Phase of Preicteric Phase of HepatitisHepatitis Flu-like symptomsFlu-like symptoms

– General malaiseGeneral malaise– FatigueFatigue– Body aches, headacheBody aches, headache– GI symptoms- nausea/vomiting, GI symptoms- nausea/vomiting,

diarrhea, abdominal discomfortdiarrhea, abdominal discomfort– Chills, low grade feverChills, low grade fever

Icteric or Jaundice Icteric or Jaundice Phase Phase Usually 5-10 days after pre-icteric Usually 5-10 days after pre-icteric

symptomssymptoms Jaundice results when bilirubin diffuses Jaundice results when bilirubin diffuses

into tissuesinto tissues Sclera jaundicedSclera jaundiced Urine darkens due to excess bilirubin Urine darkens due to excess bilirubin

being excretedbeing excreted If bilirubin cannot flow out of liver, If bilirubin cannot flow out of liver,

stool will be light or clay-coloredstool will be light or clay-colored

Severe JaundiceSevere Jaundice

Hepatitis Hepatitis Clinical ManifestationsClinical Manifestations Pruritus can accompany jaundicePruritus can accompany jaundice

– Accumulation of bile salts beneath Accumulation of bile salts beneath the skinthe skin

When jaundice occurs, fever subsidesWhen jaundice occurs, fever subsides Liver usually enlarged and tenderLiver usually enlarged and tender

Convalescent PhaseConvalescent Phase Healing generally within 3-16 Healing generally within 3-16

weeksweeks Begins as jaundice is Begins as jaundice is

disappearingdisappearing GI symptoms minimalGI symptoms minimal

HepatitisHepatitis

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

Hepatitis Hepatitis ComplicationsComplications

Fulminant Hepatic FailureFulminant Hepatic FailureChronic HepatitisChronic HepatitisCirrhosisCirrhosisHepatocellular CarcinomaHepatocellular Carcinoma

Fulminant HepatitisFulminant Hepatitis

Results in severe impairment or Results in severe impairment or necrosis of liver cells and potential necrosis of liver cells and potential liver failure liver failure

Develops in small percentage of Develops in small percentage of patientspatients

Occurs because of Occurs because of Complications of Hepatitis BComplications of Hepatitis B Toxic reactions to drugs and Toxic reactions to drugs and

congenital metabolic disorderscongenital metabolic disorders

Diagnostic testsDiagnostic tests Liver function studiesLiver function studies

– ALTALT (Alanine aminotransferase) – elevates: (Alanine aminotransferase) – elevates: enzyme in liver cellsenzyme in liver cells released into bloodstream released into bloodstream with injury or disease (0 – 50) normalwith injury or disease (0 – 50) normal

– ASTAST (Aspartate aminotransferase) – elevates: (Aspartate aminotransferase) – elevates: enzyme in liver & heart cellsenzyme in liver & heart cells released into released into bloodstream (0 -41)bloodstream (0 -41)

– GGTGGT – gamma glutamyltransferase: – gamma glutamyltransferase: present in present in all cell membranesall cell membranes, inj or disease = elevates in , inj or disease = elevates in cell lysis, (8 – 55). increases when bile ducts cell lysis, (8 – 55). increases when bile ducts are blocked & hepatitis. Elevated until function are blocked & hepatitis. Elevated until function returns.returns.

Diagnostic testsDiagnostic tests– Alkaline phosphataseAlkaline phosphatase – present in – present in liver & bone liver & bone

cellscells. Elevated in hepatitis.(44-147 IU/L). Elevated in hepatitis.(44-147 IU/L)

– CBC CBC – low RBC, Hct, Hgb related to – low RBC, Hct, Hgb related to anemia, RBC anemia, RBC destruction, bleeding, folic acid and vitamin destruction, bleeding, folic acid and vitamin deficiencies.deficiencies.

– Low WBC and PlateletsLow WBC and Platelets Increased blood flow to spleen – cells Increased blood flow to spleen – cells

destroyed faster than neededdestroyed faster than needed

– AFP- alpha fetoprotein– liver cancer markerAFP- alpha fetoprotein– liver cancer marker

– Lactic dehydrogenase LDH5 specific for liver Lactic dehydrogenase LDH5 specific for liver damagedamage

Diagnostic testsDiagnostic tests CoagulationCoagulation – prolonged prothrombin – prolonged prothrombin

time due to poor production of time due to poor production of prothombin by liver and decreased prothombin by liver and decreased Vitamin K absorption (Normal PT 12-15 Vitamin K absorption (Normal PT 12-15 seconds, INR 0.8 to 1.2)seconds, INR 0.8 to 1.2)

HyponatremiaHyponatremia –hemodilution –hemodilution Hypokalemia, hypophosphatemia, Hypokalemia, hypophosphatemia,

hypomagnesemiahypomagnesemia –malnutrition & –malnutrition & renal lossrenal loss

BilirubinBilirubin – Total (2-14 umol/L) – Total (2-14 umol/L) Bilurubin – direct/conjugated (0-4 Bilurubin – direct/conjugated (0-4

umol/L)umol/L)

Diagnostic testsDiagnostic tests Serum albuminSerum albumin – low due to impaired liver – low due to impaired liver

production (3.3 – 5)production (3.3 – 5) Serum ammoniaSerum ammonia – high (0 – 150)(10 to 80 – high (0 – 150)(10 to 80

ug/l)ug/l) Glucose and cholesterolGlucose and cholesterol –abnormal due to –abnormal due to

impaired liver functionimpaired liver function Abd. UltrasoundAbd. Ultrasound – liver size, ascites, or – liver size, ascites, or

nodulesnodules EsophagascopyEsophagascopy – look for varices – look for varices Liver biopsyLiver biopsy CT, MRICT, MRI

Rx impacting liverRx impacting liver

A host of medications can cause abnormal liver enzymes A host of medications can cause abnormal liver enzymes levels. Examples include:levels. Examples include:

Pain relief medications such as aspirin, acetaminophen Pain relief medications such as aspirin, acetaminophen (Tylenol), (Tylenol), ibuprofen ibuprofen (Advil, Motrin), neproxen (Narosyn), (Advil, Motrin), neproxen (Narosyn), diclofenacdiclofenac (Voltaren), and phenylbutazone (Butazolidine) (Voltaren), and phenylbutazone (Butazolidine)

Anti-seizure medications such as Anti-seizure medications such as phenytoinphenytoin (Dilantin), (Dilantin), valproicvalproic acid acid, , carbamazepinecarbamazepine (Tegretol), and phenobarbital (Tegretol), and phenobarbital

Antibiotics such as the tetracyclines, sulfonamides, isoniazid Antibiotics such as the tetracyclines, sulfonamides, isoniazid (INH), (INH), sulfamethoxazolesulfamethoxazole, , trimethoprimtrimethoprim, , nitrofurantoinnitrofurantoin, etc. , etc.

Cholesterol lowering drugs such as the "statins" (Mevacor, Cholesterol lowering drugs such as the "statins" (Mevacor, Pravachol, Lipitor, etc.) and niacin Pravachol, Lipitor, etc.) and niacin

Cardiovascular drugs such as Cardiovascular drugs such as amiodaroneamiodarone (Cordarone), (Cordarone), hydralazine, hydralazine, quinidinequinidine, etc. , etc.

Anti-depressant drugs of the tricyclic type (ie elavil)Anti-depressant drugs of the tricyclic type (ie elavil) With drug-induced liver enzyme abnormalities, the enzymes With drug-induced liver enzyme abnormalities, the enzymes

usually normalize weeks to months after stopping the usually normalize weeks to months after stopping the medications.medications.

Needle biopsyMost 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

3 Types of Liver Biopsy

Liver BiopsyLiver Biopsy

Adequacy of clotting- PT/ INR, Platelets (Vit. K?)Adequacy of clotting- PT/ INR, Platelets (Vit. K?) Type and cross match for bloodType and cross match for blood Usually hold aspirin, ibuprofen, and Usually hold aspirin, ibuprofen, and

anticoagulantsanticoagulants Chest x-rayChest x-ray Consent form & NPO 4 to 8 hr. Consent form & NPO 4 to 8 hr. Vital signs & Empty bladderVital signs & Empty bladder Supine position, R arm above headSupine position, R arm above head Hold breath after expiration when needle Hold breath after expiration when needle

insertedinserted Be very still during procedure – 20 minutesBe very still during procedure – 20 minutes

Liver Biopsy VideoLiver Biopsy Video

Complications are:

Puncture of lung or gallbladder, infection, bleeding, and pain.

After Needle Liver After Needle Liver BiopsyBiopsy Pressure to site, place pt on Rt side to maintain Pressure to site, place pt on Rt side to maintain

site pressure minimum of 2 hrs. & flat 12-14 hrs.site pressure minimum of 2 hrs. & flat 12-14 hrs. Vital signs & check for bleedingVital signs & check for bleeding NPO X 2H afterNPO X 2H after Assess for peritonitis, shock, & pneumothoraxAssess for peritonitis, shock, & pneumothorax Rt. shoulder pain commonRt. shoulder pain common

– caused by irritation of the diaphragm muscle caused by irritation of the diaphragm muscle – usually radiates to the shoulder a few hours or usually radiates to the shoulder a few hours or

days.days. Soreness at the incision siteSoreness at the incision site Avoid aspirin or ibuprofen for pain control for the Avoid aspirin or ibuprofen for pain control for the

first week because they decrease blood clotting, first week because they decrease blood clotting, which is crucial for healing. CONSULT which is crucial for healing. CONSULT HEALTHCARE PROVIDER!HEALTHCARE PROVIDER!

Avoid coughing, straining, lifting x 1-2 weeksAvoid coughing, straining, lifting x 1-2 weeks

Hepatitis CareHepatitis Care Rest is a priority!Rest is a priority! Diet –High calorie & protein, Diet –High calorie & protein,

Low fatLow fat–Vitamin supplement – B Vitamin supplement – B complex & Kcomplex & K

–Avoid alcohol & drugs Avoid alcohol & drugs detoxed in liverdetoxed in liver

Life style changesLife style changes

Meds for Chronic Meds for Chronic HepatitisHepatitis Chronic HBVChronic HBV

Pegylated a-interferon (Pegasys, PEG-Intron)Pegylated a-interferon (Pegasys, PEG-Intron) Lamivudine (Epivir)Lamivudine (Epivir) Adefovir (Hepsera)Adefovir (Hepsera) Entecavir (Baraclude)Entecavir (Baraclude) Telbivudine (Tyzeka)Telbivudine (Tyzeka)

Chronic HCVChronic HCV Pegylated a-interferon (Pegasys, PEG-Intron)Pegylated a-interferon (Pegasys, PEG-Intron) Ribavirin (Rebetol, Copegus)Ribavirin (Rebetol, Copegus)

Hepatitis Hepatitis Nursing ManagementNursing Management

Nursing assessmentNursing assessment Past health historyPast health history

– Hemophilia Hemophilia – Exposure to infected persons Exposure to infected persons – Ingestion of contaminated food or Ingestion of contaminated food or

water water – Past blood transfusion (before 1992)Past blood transfusion (before 1992)


Nursing assessmentNursing assessment Medications (use and misuse)Medications (use and misuse)

– Acetaminophen Acetaminophen – Phenytoin Phenytoin – Halothane Halothane – Methyldopa Methyldopa


Nursing assessmentNursing assessment IV drug and alcohol abuseIV drug and alcohol abuse Weight lossWeight loss Dark urineDark urine FatigueFatigue Right upper quadrant painRight upper quadrant pain Pruritus Pruritus


Nursing assessmentNursing assessment Low-grade feverLow-grade fever JaundiceJaundice Abnormal laboratory Abnormal laboratory

valuesvalues


Nursing diagnosesNursing diagnoses Imbalanced nutrition: Less Imbalanced nutrition: Less

than body requirementsthan body requirements Activity intoleranceActivity intolerance Ineffective therapeutic Ineffective therapeutic

regimen managementregimen management


Overall goals: PlanningOverall goals: Planning–Relief of discomfortRelief of discomfort–Resumption of normal Resumption of normal activities activities

–Return to normal liver function Return to normal liver function without complicationswithout complications


Nursing implementationNursing implementation Health promotionHealth promotion

–Hepatitis A Hepatitis A EducationEducationVaccinationVaccinationGood hygiene practicesGood hygiene practices

Nursing implementationNursing implementation

Health PromotionHealth Promotion– Hepatitis BHepatitis B

VaccinationVaccination EducationEducationWorkplace safetyWorkplace safety



Nursing implementationNursing implementation Health promotionHealth promotion

–Hepatitis CHepatitis C EducationEducation Infection control precautionsInfection control precautions Modification of high-risk behavior Modification of high-risk behavior


Nursing implementationNursing implementation Acute interventionAcute intervention

–RestRest– JaundiceJaundice

Assess degree of jaundiceAssess degree of jaundiceSmall, frequent mealsSmall, frequent meals


Nursing implementationNursing implementation Ambulatory and home careAmbulatory and home care

–Dietary teaching Dietary teaching –Assessment for complicationsAssessment for complications–Regular follow-up for at least Regular follow-up for at least 1 year after diagnosis1 year after diagnosis


Nursing implementationNursing implementation Ambulatory and home careAmbulatory and home care

– Avoid alcoholAvoid alcohol


Evaluation Evaluation Expected outcomesExpected outcomes

– Adequate nutritional intake Adequate nutritional intake – Increased tolerance for activityIncreased tolerance for activity– Verbalization of understanding Verbalization of understanding

of of follow-up care follow-up care


Evaluation Evaluation Expected outcomesExpected outcomes

–Able to explain methods Able to explain methods of transmission and of transmission and methods of preventing methods of preventing transmission to otherstransmission to others

Hepatitis ReportingHepatitis Reporting

Which type of hepatitis Which type of hepatitis has few long term has few long term consequences?consequences?

Hep

atiti

s A

Hep

atiti

s B

Hep

atiti

s C

Hep

atiti

s D

25% 25%25%25%

1.1. Hepatitis AHepatitis A

2.2. Hepatitis BHepatitis B

3.3. Hepatitis CHepatitis C

4.4. Hepatitis DHepatitis D

Which statement Which statement about hepatitis is about hepatitis is true?true?

Hep

atiti

s A o

ften

lead

...

Hep

atiti

s B is

tran

smi..

.

Hep

atiti

s C is

tran

sm...

Hep

atiti

s D is

a b

enig

...

25% 25%25%25%1.1. Hepatitis A often Hepatitis A often

leads to fulminant leads to fulminant hepatitishepatitis

2.2. Hepatitis B is Hepatitis B is transmitted via blood transmitted via blood and other body fluidsand other body fluids

3.3. Hepatitis C is Hepatitis C is transmitted via fecal-transmitted via fecal-oral routeoral route

4.4. Hepatitis D is a Hepatitis D is a benign infectionbenign infection

Which types of Which types of hepatitis have hepatitis have vaccines?vaccines?

Hep

atiti

s A, B

, & C

Hep

atiti

s A &

B

Hep

atiti

s B &

C

Hep

atiti

s B, C

, & E

25% 25%25%25%

1.1. Hepatitis A, B, & Hepatitis A, B, & CC

2.2. Hepatitis A & BHepatitis A & B

3.3. Hepatitis B & CHepatitis B & C

4.4. Hepatitis B, C, & Hepatitis B, C, & EE

Juandice occurs during Juandice occurs during which stage of which stage of hepatitis?hepatitis?

1.1. IncubationIncubation

2.2. Pre-ictericPre-icteric

3.3. IctericIcteric

4.4. Post-ictericPost-icteric

Cirrhosis Video ClipCirrhosis Video Clip

Break!!

CirrhosisCirrhosis

Cirrhosis Cirrhosis PathophysiologyPathophysiology Cirrhosis is the end stage of Cirrhosis is the end stage of

chronic liver diseasechronic liver disease Progressive, leads to liver failureProgressive, leads to liver failure Insidious, prolonged courseInsidious, prolonged course Ninth leading cause of death in Ninth leading cause of death in

United StatesUnited States Twice as common in menTwice as common in men

Cirrhosis Cirrhosis PathophysiologyPathophysiology Hepatocytes are destroyed and portalHepatocytes are destroyed and portal

hypertension developshypertension develops Liver cells attempt to regenerateLiver cells attempt to regenerate Regenerative process is disorganizedRegenerative process is disorganized Functional liver tissue is destroyed and Functional liver tissue is destroyed and

scarring of liver occursscarring of liver occurs New fibrous connective tissue distorts New fibrous connective tissue distorts

liver’s normal structure, with impeded liver’s normal structure, with impeded blood flowblood flow

Four Types of CirrhosisFour Types of Cirrhosis

Alcoholic Cirrhosis – formerly Alcoholic Cirrhosis – formerly called called Laennec’sLaennec’s

Post necrotic CirrhosisPost necrotic Cirrhosis Biliary/obstructive - bile flow Biliary/obstructive - bile flow

obstructed causing damage to obstructed causing damage to liverliver

Cardiac- from right side heart Cardiac- from right side heart failurefailure

Alcoholic or Nutritional Alcoholic or Nutritional CirrhosisCirrhosis

(formerly called (formerly called Laennec’s)Laennec’s) Usually associated with Usually associated with

alcohol abusealcohol abuse Most common cause of Most common cause of

cirrhosiscirrhosis Causes metabolic changes in Causes metabolic changes in

liver; fat accumulates in liver liver; fat accumulates in liver (fatty liver)(fatty liver)

Fatty liver potentially Fatty liver potentially reversible if alcohol reversible if alcohol consumption ceasesconsumption ceases

Post Necrotic Post Necrotic CirrhosisCirrhosis

Results from complication of Results from complication of viral infections, Hepatitis, or viral infections, Hepatitis, or exposure to toxinsexposure to toxins

Liver shrinks because lobules Liver shrinks because lobules destroyed, broad bands of destroyed, broad bands of scar tissue form within the scar tissue form within the liverliver

Biliary CirrhosisBiliary Cirrhosis

Associated with chronic Associated with chronic biliary obstruction and biliary obstruction and infectioninfection

Retained bile damages and Retained bile damages and destroys liver cells, causing destroys liver cells, causing fibrosis of liverfibrosis of liver

Cardiac Cardiac CirrhosisCirrhosis

Results from long-standing Results from long-standing severe right sided heart severe right sided heart failurefailure

Elevated central venous Elevated central venous pressures cause stasis of pressures cause stasis of blood in veins of liver, which blood in veins of liver, which leads to fibrosisleads to fibrosis

Early Signs of Cirrhosis Early Signs of Cirrhosis ComplicationsComplicationsand Common Manifestationsand Common Manifestations

1.1. Hepatomegaly and RUQ painHepatomegaly and RUQ pain

2.2. Weight lossWeight loss

3.3. WeaknessWeakness

4.4. AnorexiaAnorexia

5.5. Diarrhea and constipationDiarrhea and constipation

CirrhosisCirrhosis Interventions- Interventions- DrugsDrugs

Diuretics-Diuretics-– Aldactone Aldactone (spironolactone): decreases (spironolactone): decreases

aldosterone levels, K+ sparingaldosterone levels, K+ sparing– Lasix (furosemide) Lasix (furosemide)

Salt-poor albuminSalt-poor albumin NeomycinNeomycin – decrease ammonia forming – decrease ammonia forming

organisms. Only recommended when unable to organisms. Only recommended when unable to tolerate lactulosetolerate lactulose

Lactulose Lactulose – decreases ammonia forming – decreases ammonia forming organisms and inc. acidity of bowel. Goal is 2-3 organisms and inc. acidity of bowel. Goal is 2-3 loose stools per day.loose stools per day.

Ferrous sulfate and folic acidFerrous sulfate and folic acid – to treat anemia/ – to treat anemia/ vitamin deficiency vitamin deficiency

Beta blocker: propranolol (Inderal), nadolol-Beta blocker: propranolol (Inderal), nadolol- to prevent bleeding of E varices in to prevent bleeding of E varices in conjunction with conjunction with isosorbide mononitrate isosorbide mononitrate (Imdur)(Imdur) lowers hepatic venous pressure lowers hepatic venous pressure

Proton Pump Inhibitors, H2 Receptor Proton Pump Inhibitors, H2 Receptor Blockers– decrease irritation of varicesBlockers– decrease irritation of varices

Serax (oxazepam)Serax (oxazepam) – benzodiazepine for – benzodiazepine for alcohol withdrawal, sedation, sleep. Is alcohol withdrawal, sedation, sleep. Is metabolized in the liver – use cautiously.metabolized in the liver – use cautiously.

Nursing Diagnoses - Nursing Diagnoses - CirrhosisCirrhosis

Fluid Volume deficitFluid Volume deficit Ineffective protection: bleedingIneffective protection: bleeding Disturbed thought processDisturbed thought process Ineffective breathing patternIneffective breathing pattern Impaired skin integrityImpaired skin integrity Imbalanced nutrition: less than Imbalanced nutrition: less than

body requirementsbody requirements

CirrhosisCirrhosis Interventions- Interventions- Diet and fluidsDiet and fluids Low protein (sometimes), high carbohydrate, Low protein (sometimes), high carbohydrate,

high calorie-if signs of acute hepatic high calorie-if signs of acute hepatic encephalopathyencephalopathy

With cirrhosis and no hepatic encephalopathy, With cirrhosis and no hepatic encephalopathy, high carbohydrate, high protein, low salthigh carbohydrate, high protein, low salt

Low sodium-500 mg-2gmsLow sodium-500 mg-2gms At first sign of encephalopathy or ammonia At first sign of encephalopathy or ammonia

level increasing- decrease protein intake level increasing- decrease protein intake (sometimes)(sometimes)

Early stage for liver regeneration- need high Early stage for liver regeneration- need high protein-(75-100gms)protein-(75-100gms)

Later Manifestations of Later Manifestations of Cirrhosis JaundiceCirrhosis Jaundice

Jaundice occurs as a result of Jaundice occurs as a result of the decreased ability to the decreased ability to conjugate and excrete conjugate and excrete bilirubinbilirubin

In the late stages of In the late stages of cirrhosis, patient is usually cirrhosis, patient is usually jaundicedjaundiced

JAUNDICEJAUNDICE

HepatocellularHepatocellular

ObstructiveObstructive

HemolyticHemolytic

Cirrhosis Cirrhosis Hepatocellular or Hepatocellular or intrahepatic jaundiceintrahepatic jaundice

Diseased liver cells can’t Diseased liver cells can’t clear normal amounts of clear normal amounts of bilirubin from the blood.bilirubin from the blood.

Obstructive or Obstructive or Extrahepatic JaundiceExtrahepatic Jaundice

Due to the interference with Due to the interference with the flow of bile in the hepatic the flow of bile in the hepatic duct. duct.

Liver is conjugating bilirubin Liver is conjugating bilirubin but it cannot reach small but it cannot reach small intestines so is released into intestines so is released into blood streamblood stream

Hemolytic Hemolytic JaundiceJaundice

Due to excessive destruction of Due to excessive destruction of RBC’s.RBC’s.– transfusion reactiontransfusion reaction

– Faulty hemoglobin – sickle cellFaulty hemoglobin – sickle cell

– Autoimmune destruction of RBC’sAutoimmune 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 A client is admitted with increased ascites related to cirrhosis. What is ascites related to cirrhosis. What is the priority nursing diagnosis?the priority nursing diagnosis?

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.

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25% 25%25%25%1.1. Fatigue Fatigue

2.2. Excessive fluid Excessive fluid volumevolume

3.3. Ineffective Ineffective breathing patternbreathing pattern

4.4. Imbalanced Imbalanced nutrition: less nutrition: less than body than body requirementsrequirements

BreakBreak!!

• 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 Hypertension

Portal Hypertention Portal Hypertention (Cont’d)(Cont’d)

– Increases in portal pressure cause development of Increases in portal pressure cause development of a portosystemic collateral circulation with resultant a portosystemic collateral circulation with resultant compensatory portosystemic shunting and compensatory portosystemic shunting and disturbed intrahepatic circulation. disturbed intrahepatic circulation.

– These factors are partly responsible for the These factors are partly responsible for the important complications of chronic liver disease, important complications of chronic liver disease, including variceal bleeding, hepatic including variceal bleeding, hepatic encephalopathy, ascites, hepatorenal syndrome, encephalopathy, ascites, hepatorenal syndrome, recurrent infection, and abnormalities in recurrent infection, and abnormalities in coagulation.coagulation.

– Variceal bleeding is the most serious Variceal bleeding is the most serious complicationcomplication and is an important cause of death and is an important cause of death in patients with cirrhotic liver disease. in patients with cirrhotic liver disease.

PORTAL HYPERTENSIONPORTAL HYPERTENSIONnormal 3 mmHg normal 3 mmHg 12 mmHg = esophageal rupture12 mmHg = esophageal rupture

Resistance to blood flow = Increase in Resistance to blood flow = Increase in pressure in portal venous system.pressure in portal venous system.– Swelling, inflammation, fibrosis, scarring of liverSwelling, inflammation, fibrosis, scarring of liver– Thrombus Thrombus – Resistance in Inferior vena cava: Rt.CHF, myopathyResistance in Inferior vena cava: Rt.CHF, myopathy

Blood takes collateral channelsBlood takes collateral channels - esophagus, - esophagus, stomach, spleen etc, veins, hemorrhoids stomach, spleen etc, veins, hemorrhoids

May need shunts or TIPS May need shunts or TIPS Transjugular Intrahepatic Transjugular Intrahepatic

Portosystemic ShuntPortosystemic Shunt to decrease pressure, beta to decrease pressure, beta blockers also helpblockers also help

TIPS!- You tubeTIPS!- You tube

Portal Hypertension

Esophageal

Varices

Caput medusae

(dilated abd. veins)

Hemorrhoids

Arteriovenous shunting

Hypersplenism

Moderate anemia

Neutropenia

Thrombocytopenia

Marked ascites

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 Treatment of esophageal varicesvaricesActive bleedingActive bleeding Central line & pulmonary artery pressuresCentral line & pulmonary artery pressures Blood transfusions & fresh frozen plasma for clotting Blood transfusions & fresh frozen plasma for clotting

factorsfactors Somatostatin or Vasopressin – constrict gut vesselsSomatostatin or Vasopressin – constrict gut vessels Nitroglycerin- to counter negative affects of Nitroglycerin- to counter negative affects of

vasopressinvasopressin Airway/trachAirway/trach

Later prevention of re-bleeding Later prevention of re-bleeding Beta-blockersBeta-blockers Long-acting nitratesLong-acting nitrates Soft food, chew well, avoid intra-abdominal pressure Soft food, chew well, avoid intra-abdominal pressure Protonix (pantoprazole) 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:Question:

There is a risk of damage to the oesophageal mucosa from an There is a risk of damage to the oesophageal mucosa from an inflated oesophageal balloon. Many centres have policies for inflated oesophageal balloon. Many centres have policies for routinely deflating and then reinflating the oesophageal routinely deflating and then reinflating the oesophageal balloon. This varies from 5 minutes deflation every hour to 30-balloon. This varies from 5 minutes deflation every hour to 30-60 minutes every 8 hours. There appears to be little consensus 60 minutes every 8 hours. There appears to be little consensus at this time. If the oesophageal balloon needs to be inflated at this time. If the oesophageal balloon needs to be inflated what is the most accurate general principle? what is the most accurate general principle?

A)A) The balloon should be deflated and the reinflated every hour.The balloon should be deflated and the reinflated every hour.

B)B) The balloon should be deflated and then reinflated every 8 The balloon should be deflated and then reinflated every 8 hours.hours.

C)C) The balloon should never be routinely deflated as the risk of The balloon should never be routinely deflated as the risk of rebleeding is too great.rebleeding is too great.

D)D) The Balloon should be inflated for the absolutely minimum The Balloon should be inflated for the absolutely minimum time necessary.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 Transjugular Intrahepatic Portosystemic ShuntPortosystemic Shunt

Special proceduresSpecial procedures – fistula created – fistula created with portal vein and hepatic vein and with portal vein and hepatic vein and then stents placed to keep it open. then stents placed to keep it open.

Bypasses the liver by returning blood Bypasses the liver by returning blood to hepatic vein to inferior vena cavato hepatic vein to inferior vena cava

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

YouTube- TIPS

TIPSTIPS Transjugular intrahepatic Transjugular intrahepatic portosystemic shuntportosystemic shunt

TIPS POSTTIPS POST

*Shunted blood containshigh ammonia

Which can lead to:hepatic encephalopathy*

SplenomegalySplenomegaly due to due to Portal hypertensionPortal hypertension The spleen enlarges as blood is The spleen enlarges as blood is

shunted to splenic veinshunted to splenic vein This increases rate of destruction This increases rate of destruction

of RBCs, WBCs, and plateletsof RBCs, WBCs, and platelets Decreases storage capacity of Decreases storage capacity of

spleenspleen Causes anemia, leukopenia and Causes anemia, leukopenia and

thrombocytopeniathrombocytopenia

AscitesAscites – Complication – Complication of Cirrhosisof Cirrhosis Blood flow diverted to mesenteric vesselsBlood flow diverted to mesenteric vessels

– Increased capillary pressure leads to fluid Increased capillary pressure leads to fluid leaving vessels out into peritoneal cavityleaving vessels out into peritoneal cavity

High pressure in liver causes fluid to leave High pressure in liver causes fluid to leave liver into peritoneal cavityliver into peritoneal cavity

This fluid is plasma filtrate with high This fluid is plasma filtrate with high concentration of albuminconcentration of albumin

Minerals- Ca++ is attached to albumin Minerals- Ca++ is attached to albumin decreases so phosphorus increases. decreases so phosphorus increases.

K+ is low due to aldosteroneK+ is low due to aldosterone

Increased capillary

permeability

Increased Na+

&H2O retention

Portal Hypertension

HypoproteinemiaFour Factors Lead to Ascites

Responses to third Responses to third spacingspacing Loss of albuminLoss of albumin to ascites leads to to ascites leads to

hypoproteinemia, depletion of plasma proteinshypoproteinemia, depletion of plasma proteins

Loss of blood volumeLoss of blood volume = lowered BP = lowered BP

ReflexesReflexes aimed at returning blood pressure to aimed at returning blood pressure to normal include release of aldosteronenormal include release of aldosterone– Increases reabsorption of NA+ back into Increases reabsorption of NA+ back into

blood and H2O follows, thus increasing blood and H2O follows, thus increasing blood volumeblood volume

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

ASCITES

Nursing Management ASCITESNursing Management ASCITES

Assess for Assess for Respiratory Respiratory Distress- Fowler’s Distress- Fowler’s position helps position helps ease work of ease work of breathing in breathing in ascitesascites

Measure Measure Abdominal GirthAbdominal Girth

Accurate I&OAccurate I&O

MEDICAL TREATMENTMEDICAL TREATMENT

Na+ restriction-Na+ restriction- 500 mg –2 gms500 mg –2 gms

Fluids-1500 ml/day Fluids-1500 ml/day

Diuretics-AldactoneDiuretics-Aldactone

Albumin - NaCl poorAlbumin - NaCl poor

ParacentesisParacentesis

To treat respiratory distress To treat respiratory distress Pt will loose 10-30 grams of proteinPt will loose 10-30 grams of protein Pt in sitting positionPt in sitting position Empty bladder firstEmpty bladder first Post--watch for hypotension,Post--watch for hypotension,

bleeding, shock & infectionbleeding, shock & infection

Additional Additional ComplicationsComplicationsLiver FailureLiver Failure

Liver FailureLiver Failure

Complex syndrome Complex syndrome characterized by impairment characterized by impairment of many organs and body of many organs and body functionsfunctions

Two conditions:Two conditions: Hepatic EncephalopathyHepatic Encephalopathy Hepatorenal SyndromeHepatorenal Syndrome

Hepatic Hepatic encephalopathy:encephalopathy:

Alteration in neuro status Alteration in neuro status due to accumulation of due to accumulation of

ammoniaammonia

Build-up of other substances Build-up of other substances such as hormones, such as hormones,

GI toxins, drugs also GI toxins, drugs also contributecontribute

Where does ammonia Where does ammonia come from?come from? A by-product of protein A by-product of protein

metabolismmetabolism Protein and amino acids are Protein and amino acids are

broken down by bacteria in GI broken down by bacteria in GI tract, producing ammonia.tract, producing ammonia.

Liver converts this to urea which Liver converts this to urea which is eliminated in the urineis eliminated in the urine

Precipitating Factors – all Precipitating Factors – all place demands on liverplace demands on liver

Bleeding esophageal varicesBleeding esophageal varices Ingestion of narcotics or barbiturates, Ingestion of narcotics or barbiturates,

anesthetics anesthetics Excessive protein intakeExcessive protein intake Electrolyte imbalanceElectrolyte imbalance Hemodynamic alterationsHemodynamic alterations DiureticsDiuretics Severe infectionSevere infection Blood transfusionsBlood transfusions

Stages of Hepatic Stages of Hepatic EncephalopathyEncephalopathy

Hepatic Encephalopathy - Onset Hepatic Encephalopathy - Onset PhasePhase

Personality Personality changes, changes, disturbances of disturbances of awareness, awareness, forgetfulness, forgetfulness, irritability, & irritability, & confusionconfusion

Hepatic Encephalopathy - Second Hepatic Encephalopathy - Second PhasePhase

HyperreflexiaHyperreflexia Asterixis or Asterixis or

flappingflapping– Altered hand Altered hand

writingwriting Violent, abusive Violent, abusive

behaviorbehavior

Hepatic EncephalopathyHepatic Encephalopathy - Coma - Coma

+ Babinski+ Babinski hyperactive hyperactive

reflexes obtained reflexes obtained with reflex with reflex hammerhammer

BabinskiBabinski Video Video

With thefirst signof hepatic

encephalopathydecreaseprotein intake!

Medical ManagementMedical Management Hepatic EncephalopathyHepatic Encephalopathy

NeomycinNeomycin -- intestinal antiseptic- -- intestinal antiseptic-decrease bacteria that produce decrease bacteria that produce ammonia but may cause renal toxicity ammonia but may cause renal toxicity or hearing impairment or hearing impairment

LactuloseLactulose

Converts to Converts to lactic and acetic acidslactic and acetic acids

Acid environment Acid environment decreases decreases bacterial growthbacterial growth

Increased acidity in the gut Increased acidity in the gut converts converts ammonia to ammonium ion which ammonia to ammonium ion which is excreted in fecesis excreted in feces thus decreases thus decreases amount of ammonia available for re-amount of ammonia available for re-absorption into the blood.absorption into the blood.

Laxative effect removes ammonia Laxative effect removes ammonia from bowelfrom bowel. Goal-2-3 loose . Goal-2-3 loose stools/daystools/day

Give diluted with fruit juice or water- Give diluted with fruit juice or water- very sweet! Avoid giving with meals. very sweet! Avoid giving with meals.

Hepatic Encephalopathy - Protein Hepatic Encephalopathy - Protein IntakeIntake

Decrease proteinDecrease protein intake 0-40 grams/day- intake 0-40 grams/day- meat protein most meat protein most toxictoxic

Add 10-20 grams Add 10-20 grams every 3-5 days to max every 3-5 days to max 60gms60gms

If tube feeding use If tube feeding use Hepatic-aidHepatic-aid. (reduce . (reduce ammonia from protein) ammonia from protein)

Increase Increase carbohydrates carbohydrates

Decrease fatsDecrease fats

A client with cirrhosis is receiving lactulose to prevent hepatic encephalopathy. What should

the nurse monitor to evaluate the effectiveness of this medication?

Ser

um a

lbum

in le

vel

Ser

um a

mm

onia le

vel

ALT

Unco

njugat

ed b

iliru

bin

25% 25%25%25%1. Serum albumin level

2. Serum ammonia level

3. ALT4. Unconjugated

bilirubin

A trained nurse can insert a Sengstaken- Blakemore

tube.

Tru

e

Fal

se

50%50%1. True2. False

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:

Ele

vate

d live

r enzy

m..

Hyp

ogly

cem

ia a

nd i...

Thro

mbocy

tope

nia

Hyp

ergly

cem

ia a

nd i...

25% 25%25%25%

1. Elevated liver enzymes and low serum protein

2. Hypoglycemia and increased serum ammonia

3. Thrombocytopenia

4. Hyperglycemia and increased creatinine

Hepatorenal syndromeHepatorenal syndromeComplication of Hepatic Complication of Hepatic

FailureFailure

Hepatorenal syndromeHepatorenal syndromeComplication of Hepatic FailureComplication of Hepatic Failure

kidneys may appear normal kidneys may appear normal physically but functioning physically but functioning impaired.impaired.

Usually sudden decrease Usually sudden decrease Urine production, Urine production, increase BUN & increase BUN & Creatinine, jaundice and Creatinine, jaundice and signs of liver failuresigns of liver failure

Poor prognosis- Poor prognosis- most die most die within 3 wks without within 3 wks without transplanttransplant

Think due to decreased Think due to decreased perfusion &/or toxins perfusion &/or toxins from failure of liverfrom failure of liver

Liver DialysisLiver Dialysis

Bridge to transplantBridge to transplant Dialyze 6 hours at a timeDialyze 6 hours at a time

Donors:Donors:

Live donor liver transplants are an excellent Live donor liver transplants are an excellent option. option.

Liver regenerates to appropriate size for their Liver regenerates to appropriate size for their individual bodies.individual bodies.

Survival rates increase / shorter wait timeSurvival rates increase / shorter wait time

The donor - a blood relative, spouse, or friend, will The donor - a blood relative, spouse, or friend, will have extensive medical and psychological have extensive medical and psychological evaluations to ensure the lowest possible risk.evaluations to ensure the lowest possible risk.

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

Blood type and body size are critical factors Blood type and body size are critical factors in determining who is an appropriate donor. in determining who is an appropriate donor.

Potential donors evaluated for:Potential donors evaluated for:– liver disease, alcohol or drug abuse, cancer, or liver disease, alcohol or drug abuse, cancer, or

infection. infection. – hepatitis, AIDS, and other infections. hepatitis, AIDS, and other infections. – matched according to blood type and body size. matched according to blood type and body size. – Age, race, and sex are not considered. Age, race, and sex are not considered.

Cadaver donor have to wait for brain dead Cadaver donor have to wait for brain dead donordonor

Liver TransplantLiver Transplant VideoVideo

Liver transplant Liver transplant complicationscomplications Rejection. Rejection. About 70% of all liver-transplant About 70% of all liver-transplant

patients have some degree of organ rejection patients have some degree of organ rejection prior to discharge. prior to discharge.

Anti-rejection medications are given to ward Anti-rejection medications are given to ward off the immune attack.off the immune attack.

InfectionInfection Most infections can be treated successfully Most infections can be treated successfully

as they occur. as they occur. CancerCancer

Review 1. Pathophysiology

1. Cirrhosis

2. Portal hypertension

3. Liver failure

1. Encephalopathy

2. Hepato-renal syndrome

2. Signs & Symptoms

3. Treatment

4. Nsg. Care

5. Complications

The EndThe End

liver disorders part 1 charlene morris, rn, msn austin community college addenda spring 2010 john...

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