Liver Disorders John Nation, RN, MSN Fall 2011 From the notes of Charlene Morris, RN, MSN Austin...
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Transcript of Liver Disorders John Nation, RN, MSN Fall 2011 From the notes of Charlene Morris, RN, MSN Austin...
Liver DisordersLiver Disorders
John Nation, RN, MSNJohn Nation, RN, MSNFall 2011Fall 2011
From the notes ofFrom the notes ofCharlene Morris, RN, MSNCharlene Morris, RN, MSNAustin Community CollegeAustin Community College
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
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::– 500ml/min of oxygenated blood. 500ml/min of oxygenated blood. – 30% of Cardiac output goes to the liver30% of Cardiac output goes to the liver
Portal veinPortal vein – 1000ml/min – 1000ml/min – partly oxygenated blood supplies 50 - 60% partly oxygenated blood supplies 50 - 60%
O2 O2 plus rich supply of nutrients, toxins, drugsplus rich supply of nutrients, toxins, drugs
– from stomach, small and large from stomach, small and large intestines, pancreas and spleenintestines, pancreas and spleen
Hepatic Blood Supply Hepatic Blood Supply (Cont’d)(Cont’d) Both empty into Both empty into
capillaries/sinusoidscapillaries/sinusoids
Liver filters the bloodLiver filters the blood
Hepatic vein to inferior vena Hepatic vein to inferior vena cavacava
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
2. Protein2. Protein StorageStorage
3. Fatty acids3. Fatty acids
4. Cholesterol4. Cholesterol
Other functionsOther functions
ImmunologicImmunologic
Blood storageBlood storage
Plasma protein synthesisPlasma protein synthesis
ClottingClotting
Waste products of hemoglobin Waste products of hemoglobin
Formation and secretion of bileFormation and secretion of bile
Steroids and hormonesSteroids and hormones
AmmoniaAmmonia
Drugs, alcohol and toxins metabolismDrugs, alcohol and toxins metabolism
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 – Coxsackie virusCoxsackie virus– Rubella virusRubella virus
Hepatitis AHepatitis A
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
3000 new cases of hepatitis A 3000 new cases of hepatitis A occur annually in the United occur annually in the United StatesStates
1.4 million cases of hepatitis A 1.4 million cases of hepatitis A occur annually worldwideoccur annually worldwide– Nearly universal during childhood in Nearly universal during childhood in
developing countriesdeveloping countries
Hepatitis A Hepatitis A
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 1-2 weeks after the onset of up to 1-2 weeks after the onset of jaundice jaundice
– Present in blood brieflyPresent in blood briefly– No chronic carrier state No chronic carrier state
Hepatitis A:Hepatitis A: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
Hepatitis AHepatitis A
Hepatitis A virus (HAV)Hepatitis A virus (HAV)– Anti-HAV immunoglobulin M (IgM)Anti-HAV immunoglobulin M (IgM)
Appears in the serum as the stool becomes Appears in the serum as the stool becomes negative for the virusnegative for the virus
Detection of IgM anti-HAV indicates acute Detection of IgM anti-HAV indicates acute hepatitis hepatitis
– Anti-HAV immunoglobulin G (IgG)Anti-HAV immunoglobulin G (IgG) IgG anti-HAV: Indicator of past infection or IgG anti-HAV: Indicator of past infection or
immunizationimmunization Presence of IgG antibody provides lifelong Presence of IgG antibody provides lifelong
immunity immunity
Hepatitis A:Hepatitis A:Mode of TransmissionMode of Transmission Mainly by ingestion of food or Mainly by ingestion of food or
liquid infected with the virusliquid infected with the virus– Poor hygiene, improper handling of Poor hygiene, improper handling of
food, crowding housing, poor food, crowding housing, poor sanitation conditions are all factors sanitation conditions are all factors related to Hepatitis Arelated to Hepatitis A
Hepatitis A:Hepatitis A:Mode of Transmission Mode of Transmission (Cont’d)(Cont’d) 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:Hepatitis A: Vaccine Vaccine
2 doses IM2 doses IM– Initial doseInitial dose– Booster in 6 to 12 monthsBooster in 6 to 12 months
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 for vaccination2 doses IM for vaccination 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
Worldwide, nearly 2 billion people Worldwide, nearly 2 billion people infected with Hepatitis B. 350 million infected with Hepatitis B. 350 million have chronic infectionhave chronic infection
43,000 new cases of Hepatitis B 43,000 new cases of Hepatitis B annually in United Statesannually in United States– Incidence Incidence decreased due to HBV vaccinedecreased due to HBV vaccine
1.25 million people chronically 1.25 million people chronically infected in the United Statesinfected in the United States
Hepatitis B Hepatitis B
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) Sexually transmittedSexually transmitted Mucosal exposure to infectious blood, blood Mucosal exposure to infectious blood, blood
products, or other body fluidsproducts, or other body fluids
Hepatitis BHepatitis B
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- PrecautionsPrecautionsSource: UptodateSource: Uptodate PREVENT INFECTION OF FAMILYPREVENT INFECTION OF FAMILY — Acute and — Acute and
chronic hepatitis B are contagious. Thus, people with chronic hepatitis B are contagious. Thus, people with hepatitis B should discuss measures to reduce the risk hepatitis B should discuss measures to reduce the risk of infecting close contacts. This includes the following:of infecting close contacts. This includes the following:
Discuss the infection with any sexual partners and use Discuss the infection with any sexual partners and use a latex condom with every sexual encounter. a latex condom with every sexual encounter.
Do not share razors, toothbrushes, or anything that Do not share razors, toothbrushes, or anything that has blood on it. 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 Do not donate blood, body organs, other tissues, or sperm. sperm.
Hepatitis B- Hepatitis B- PrecautionsPrecautionsSource: UptodateSource: Uptodate Immediate family and household members Immediate family and household members
should have testing for hepatitis B. Anyone should have testing for hepatitis B. Anyone who is at risk of hepatitis B infection should who is at risk of hepatitis B infection should be vaccinated, if not done previously. (See be vaccinated, if not done previously. (See "Patient information: Adult immunizations".) .)
Do not share any injection drug equipment Do not share any injection drug equipment (needles, syringes, etc). (needles, syringes, etc).
Clean blood spills with a mixture of 1 part Clean blood spills with a mixture of 1 part household bleach to 9 parts water.household bleach to 9 parts water.
Hepatitis B- Hepatitis B- PreventionPrevention
No Evidence Hepatitis B Spread by:No Evidence Hepatitis B Spread by: Sweating Sweating Urine (in free of blood)Urine (in free of blood) TearsTears BreastfeedingBreastfeeding
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
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 Virus
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
170 million people chronically infected 170 million people chronically infected worldwide worldwide
Approximately 4 million people in the USApproximately 4 million people in the US 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 disease complications of end-stage liver disease secondary to HCVsecondary 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
Hepatitis C virus (HCV)Hepatitis C virus (HCV)– Transmitted primarily Transmitted primarily
percutaneouslypercutaneously– Risk factorsRisk factors
IV drug useIV drug use–Most common mode of Most common mode of transmission in United States transmission in United States and Canadaand Canada
Blood transfusionsBlood transfusions
Hepatitis CHepatitis C
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 C:Hepatitis C:TransmissionTransmission
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 antibody- Anti-HCV antibody- marker marker for acute or chronic infection with HCVfor acute or chronic infection with HCV
HCV RNA- HCV RNA- indicates ongoing viral indicates ongoing viral replicationreplication
Enzyme Immunoassay (EIA)- Enzyme Immunoassay (EIA)- initial screening for HCVinitial screening for HCV
Hepatitis DHepatitis D
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 D
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 E
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 G
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 G
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 damage by itselfliver damage by itself
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
Acute HepatitisAcute Hepatitis
Hepatitis A: acute onset, flu-like Hepatitis A: acute onset, flu-like symptomssymptoms
Hepatitis B: Hepatitis B: – symptoms usually more severesymptoms usually more severe– 30% of patients asymptomatic30% of patients asymptomatic
Hepatitis C: Hepatitis C: – 80% asymptomatic80% asymptomatic– Often mildOften mild
Acute HepatitisAcute Hepatitis
Incubation Phase: after exposure to virus, no Incubation Phase: after exposure to virus, no symptomssymptoms
Preicteric Phase: Preicteric Phase: – General malaiseGeneral malaise– FatigueFatigue– Body aches, headacheBody aches, headache– GI symptoms- nausea/vomiting, diarrhea, GI symptoms- nausea/vomiting, diarrhea,
abdominal discomfortabdominal discomfort– Chills, low grade feverChills, low grade fever
Acute HepatitisAcute Hepatitis
Icteric or Jaundice Phase:Icteric or Jaundice Phase:– Usually 5-10 days after pre-icteric symptomsUsually 5-10 days after pre-icteric symptoms– Jaundice results when bilirubin diffuses into Jaundice results when bilirubin diffuses into
tissuestissues– Sclera jaundicedSclera jaundiced– Urine darkens due to excess bilirubin being Urine darkens due to excess bilirubin being
excretedexcreted– If bilirubin cannot flow out of liver, stool will be If bilirubin cannot flow out of liver, stool will be
light or clay-coloredlight or clay-colored– Pruritus can accompany jaundicePruritus can accompany jaundice
Accumulation of bile salts beneath the skinAccumulation of bile salts beneath the skin– When jaundice occurs, fever subsidesWhen jaundice occurs, fever subsides– Liver usually enlarged and tenderLiver usually enlarged and tender
Severe JaundiceSevere Jaundice
Acute HepatitisAcute Hepatitis Concalescent Phase:Concalescent Phase:
– Healing generally within 3-16 weeksHealing generally within 3-16 weeks– Begins as jaundice is disappearingBegins as jaundice is disappearing– 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 all present in all cell membranescell membranes, inj or disease = elevates in cell , inj or disease = elevates in cell lysis, (8 – 55). increases when bile ducts are lysis, (8 – 55). increases when bile ducts are blocked & hepatitis. Elevated until function returns.blocked & hepatitis. Elevated until function 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 destroyed Increased blood flow to spleen – cells destroyed
faster than neededfaster 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 time – prolonged prothrombin time due to poor production of prothombin by liver due to poor production of prothombin by liver and decreased Vitamin K absorption (Normal and decreased Vitamin K absorption (Normal PT 12-15 seconds, INR 0.8 to 1.2)PT 12-15 seconds, INR 0.8 to 1.2)
HyponatremiaHyponatremia –hemodilution –hemodilution Hypokalemia, hypophosphatemia, Hypokalemia, hypophosphatemia,
hypomagnesemiahypomagnesemia –malnutrition & renal –malnutrition & renal lossloss
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 production – low due to impaired liver production (3.3 – 5)(3.3 – 5)
Serum ammoniaSerum ammonia – high (0 – 150)(10 to 80 ug/l) – high (0 – 150)(10 to 80 ug/l) Glucose and cholesterolGlucose and cholesterol –abnormal due to impaired –abnormal due to impaired
liver functionliver 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 A host of medications can cause abnormal liver enzymes levels. Examples include:liver enzymes levels. Examples include:
Pain relief medications such as aspirin, Pain relief medications such as aspirin, acetaminophen (Tylenol), acetaminophen (Tylenol), ibuprofen (Advil, (Advil, Motrin), naproxen (Narosyn), Motrin), naproxen (Narosyn), diclofenac (Voltaren), and phenylbutazone (Butazolidine) (Voltaren), and phenylbutazone (Butazolidine)
Anti-seizure medications such as Anti-seizure medications such as phenytoin (Dilantin), (Dilantin), valproic acid, , carbamazepine (Tegretol), and phenobarbital (Tegretol), and phenobarbital
Antibiotics such as the tetracyclines, Antibiotics such as the tetracyclines, sulfonamides, isoniazid (INH), sulfonamides, isoniazid (INH), sulfamethoxazole, , trimethoprim, , nitrofurantoin, etc. , etc.
Rx Impacting LiverRx Impacting Liver
Cholesterol lowering drugs such as the Cholesterol lowering drugs such as the "statins" (Mevacor, Pravachol, Lipitor, "statins" (Mevacor, Pravachol, Lipitor, etc.) and niacin etc.) and niacin
Cardiovascular drugs such as Cardiovascular drugs such as amiodarone (Cordarone), hydralazine, (Cordarone), hydralazine, quinidine, etc. , etc.
Anti-depressant drugs of the tricyclic Anti-depressant drugs of the tricyclic type (ie elavil)type (ie elavil)
With drug-induced liver enzyme With drug-induced liver enzyme abnormalities, the enzymes usually abnormalities, the enzymes usually normalize weeks to months after normalize weeks to months after stopping the medications.stopping the medications.
Needle biopsyMost common in past
Laparoscopic biopsy:
Used to remove tissue from specific parts of the liver.
Liver Biopsy
Liver Biopsy (Cont’d)Liver Biopsy (Cont’d)
Transvenous biopsyTransvenous biopsy Catheter into a vein in the neck and Catheter into a vein in the neck and
guiding it to the liver. guiding it to the liver.
A biopsy needle is placed into the A biopsy needle is placed into the catheter and advanced into the catheter and advanced into the liver. liver.
Used for patients with blood-Used for patients with blood-clotting problems or excess fluid clotting problems or excess fluid
Liver BiopsyLiver Biopsy
Adequacy of clotting- PT/ INR, Adequacy of clotting- PT/ INR, Platelets (Vit. K?)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.
Liver Biopsy (Cont’d)Liver Biopsy (Cont’d)
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 Hold breath after expiration when
needle insertedneedle inserted Be very still during procedure – 20 Be very still during procedure – 20
minutesminutes
Liver 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 for a few hours or usually radiates to the shoulder for a few hours or
days.days.
After Needle Biopsy After Needle Biopsy (Cont’d)(Cont’d) Soreness at the incision siteSoreness at the incision site
Avoid aspirin or ibuprofen for pain control Avoid aspirin or ibuprofen for pain control for the first week because they decrease for the first week because they decrease blood clotting, which is crucial for blood clotting, which is crucial for healing. CONSULT HEALTHCARE healing. CONSULT HEALTHCARE PROVIDER!PROVIDER!
Avoid coughing, straining, lifting x 1-2 Avoid coughing, straining, lifting x 1-2 weeksweeks
Hepatitis CareHepatitis Care
Rest is a priority!Rest is a priority!
Diet –High calorie & protein, Low fatDiet –High calorie & protein, Low fat– Vitamin supplement – B complex & Vitamin supplement – B complex &
KK– Avoid alcohol & drugs detoxed in Avoid alcohol & drugs detoxed in
liverliver
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) Tenofovir (Viread)Tenofovir (Viread)
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)
Hepatitis Hepatitis Nursing ManagementNursing Management
Nursing assessmentNursing assessment Medications (use and misuse)Medications (use and misuse)
– Acetaminophen Acetaminophen – Phenytoin Phenytoin – Methyldopa Methyldopa
Hepatitis Hepatitis Nursing ManagementNursing Management
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
Hepatitis Hepatitis Nursing ManagementNursing Management
Nursing assessmentNursing assessment Low-grade feverLow-grade fever JaundiceJaundice Abnormal laboratory Abnormal laboratory
valuesvalues
Hepatitis Hepatitis Nursing ManagementNursing Management
Nursing diagnosesNursing diagnoses Imbalanced nutrition: Less Imbalanced nutrition: Less
than body requirementsthan body requirements Activity intoleranceActivity intolerance Ineffective therapeutic Ineffective therapeutic
regimen managementregimen management
Hepatitis Hepatitis Nursing ManagementNursing Management
Overall goals: PlanningOverall goals: Planning
– Relief of discomfortRelief of discomfort– Resumption of normal activities Resumption of normal activities – Return to normal liver function Return to normal liver function
without complicationswithout complications
Hepatitis Hepatitis Nursing ManagementNursing Management
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
Hepatitis Hepatitis Nursing ManagementNursing Management
Hepatitis Hepatitis Nursing ManagementNursing Management
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
Hepatitis Hepatitis Nursing ManagementNursing Management
Nursing implementationNursing implementation Acute interventionAcute intervention
–RestRest– JaundiceJaundice
Assess degree of jaundiceAssess degree of jaundiceSmall, frequent mealsSmall, frequent meals
Hepatitis Hepatitis Nursing ManagementNursing Management
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
Hepatitis Hepatitis Nursing ManagementNursing Management
Nursing implementationNursing implementation Ambulatory and home careAmbulatory and home care
– Avoid alcoholAvoid alcohol
Hepatitis Hepatitis Nursing ManagementNursing Management
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 follow-up care of follow-up care
Hepatitis Hepatitis Nursing ManagementNursing Management
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
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 called Alcoholic Cirrhosis – formerly called Laennec’sLaennec’s
Post necrotic CirrhosisPost necrotic Cirrhosis Biliary/obstructive - bile flow Biliary/obstructive - bile flow
obstructed causing damage to liverobstructed causing damage to liver Cardiac- from right side heart failureCardiac- from right side heart failure
Alcoholic or Nutritional Alcoholic or Nutritional CirrhosisCirrhosis(formerly called Laennec’s)(formerly called Laennec’s)
Usually associated with alcohol Usually associated with alcohol abuseabuse
Most common cause of cirrhosisMost common cause of cirrhosis 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 reversible Fatty liver potentially reversible if alcohol consumption ceasesif alcohol consumption 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 scar destroyed, broad bands of scar tissue form within the livertissue form within the liver
Biliary CirrhosisBiliary Cirrhosis
Associated with chronic biliary Associated with chronic biliary obstruction and infectionobstruction and infection
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 failuresevere right sided heart failure
Elevated central venous Elevated central venous pressures cause stasis of blood pressures cause stasis of blood in veins of liver, which leads to in veins of liver, which leads to fibrosisfibrosis
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 aldosterone (spironolactone): decreases aldosterone
levels, K+ sparinglevels, K+ sparing– Lasix (furosemide) Lasix (furosemide)
Salt-poor albuminSalt-poor albumin
NeomycinNeomycin – decrease ammonia forming organisms. – decrease ammonia forming organisms. Typically only Typically only
recommended when unable to tolerate lactuloserecommended when unable to tolerate lactulose
Lactulose Lactulose – decreases ammonia forming organisms and – decreases ammonia forming organisms and inc. acidity of bowel. Goal is 2-3 loose stools per day.inc. acidity of bowel. Goal is 2-3 loose stools per day.
Ferrous sulfate and folic acidFerrous sulfate and folic acid – to treat anemia/ vitamin – to treat anemia/ vitamin deficiency deficiency
Beta blocker: propranolol (Inderal), nadolol-Beta blocker: propranolol (Inderal), nadolol- to prevent to prevent bleeding of E varices in conjunction with bleeding of E varices in conjunction with isosorbide isosorbide mononitrate (Imdur)mononitrate (Imdur) lowers hepatic venous pressure lowers hepatic venous pressure
Proton Pump Inhibitors, H2 Receptor Blockers– Proton Pump Inhibitors, H2 Receptor Blockers– decrease irritation of varicesdecrease irritation of varices
Serax (oxazepam)Serax (oxazepam) – benzodiazepine for alcohol – benzodiazepine for alcohol withdrawal, sedation, sleep. Is metabolized in the liver withdrawal, sedation, sleep. Is metabolized in the liver – use cautiously.– use cautiously.
Cirrhosis Interventions- Drugs (Cont’d)
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 bilirubinconjugate and excrete bilirubin
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
• The portal vein carries about 1500 ml/min of blood from the small and large bowel, spleen, and stomach to the liver.
• Any obstruction or increased resistance to flow or, rarely, pathological increases in portal blood flow may lead to portal hypertension with portal pressures over 12 mm Hg.
• alcoholic and viral cirrhosis are the leading causes of portal hypertension in Western countries.
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, Resistance in Inferior vena cava: Rt.CHF,
myopathymyopathy Blood takes collateral channelsBlood takes collateral channels - -
esophagus, stomach, spleen etc, veins, esophagus, stomach, spleen etc, veins, hemorrhoids hemorrhoids
May need shunts or TIPS May need shunts or TIPS Transjugular Transjugular
Intrahepatic Portosystemic ShuntIntrahepatic Portosystemic Shunt to decrease to decrease pressure, beta blockers also helppressure, beta blockers also help
Portal Hypertension
Esophageal
Varices
Caput medusae
(dilated abd. veins)
Hemorrhoids
Arteriovenous shunting
Hypersplenism
Moderate anemia
Neutropenia
Thrombocytopenia
Marked ascites
Ascites &Caput medusae
Spider angiomas
Treatment of esophageal Treatment of esophageal varicesvarices
Active 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)
Rapid Endoscopy!
Sclerotherapy:
• A sclerosant solution (ethanolamine oleate or sodium tetradecyl sulphate) is injected into the bleeding varix or the overlying submucosa
• Complications can include fever, dysphagia and chest pain, ulceration, stricture, and (rarely) perforation.
Band ligation:
• Band ligation is achieved by a banding device attached to the tip of the endoscope
Band LigationBand Ligation
• The balloon tube tamponade may be life saving in patients with active variceal bleeding if emergency sclerotherapy or banding is unavailable
• The main complications are gastric and esophageal ulceration, aspiration pneumonia, and esophageal perforation.
Balloon Tube Tamponade:
Minnesota Tube-
Four lumens:• one for gastric aspiration
• two to inflate the gastric and esophageal balloons
• one above the esophageal balloon for suction of secretions to prevent
aspiration
Sengstaken-Blakemore Tube
Three Lumens:Three Lumens: Esophageal balloon Esophageal balloon
inflationinflation Gastric balloon Gastric balloon
inflationinflation Gastric aspirationGastric aspiration
Repeated endoscopic treatment Repeated endoscopic treatment eradicates esophageal varices in most
patients, recurrent variceal bleeding is uncommon. Because portal hypertension persists, patients at risk for recurrent
varices
Long term drug treatment The use of beta-blockers after variceal bleeding has been shown to
reduce portal blood pressures and lower the risk of further variceal bleeding.
Prophylactic management Most patients with portal hypertension never bleed, and it is difficult to
predict who will. Beta blockers have been shown to reduce the risk of bleeding.
Long term Management of Esophageal Varices
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
TIPSTIPS Transjugular intrahepatic Transjugular intrahepatic portosystemic shuntportosystemic shunt
TIPS POSTTIPS POST
• Shunted blood contains high ammonia • Can lead to: hepatic encephalopathy
TIPS:TIPS:
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 To treat respiratory distress distress
Pt will loose 10-30 grams Pt will loose 10-30 grams of proteinof protein
Pt in sitting positionPt in sitting position Empty bladder firstEmpty bladder first Post--watch for Post--watch for
hypotension, bleeding, hypotension, bleeding, shock & infectionshock & 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 Alteration in neuro status status due to accumulation of due to accumulation of ammoniaammonia
Build-up of other Build-up of other substances such as substances such as hormones, 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 Ingestion of narcotics or
barbiturates, anesthetics barbiturates, 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
Babinski VideoBabinski Video
Medical ManagementMedical Management Hepatic EncephalopathyHepatic Encephalopathy
NeomycinNeomycin
LactuloseLactulose
Protein reductionProtein reduction
- 44thth most common cancer in the most common cancer in the worldworld
- 22,600 new cases annually in US22,600 new cases annually in US- 80% of cases also have cirrhosis 80% of cases also have cirrhosis
of the liverof the liver- 50-60% causes by hepatitis C50-60% causes by hepatitis C- 20% caused by hepatitis B20% caused by hepatitis B- Often metastasizes to lungsOften metastasizes to lungs
Primary Liver Cancer Primary Liver Cancer
Liver Cancer Liver Cancer TreatmentTreatment Surgical resectionSurgical resection Radiofrequency ablationRadiofrequency ablation CryoablationCryoablation Percutaneous ethanol injectionPercutaneous ethanol injection ChemotherapyChemotherapy
Hepatorenal syndromeHepatorenal syndromeComplication of Hepatic Complication of Hepatic FailureFailure
Hepatorenal syndromeHepatorenal syndromeComplication of Hepatic FailureComplication of Hepatic Failure
kidneys may appear normal physically but kidneys may appear normal physically but functioning impaired.functioning impaired.
Usually sudden decrease Urine Usually sudden decrease Urine production, increase BUN & Creatinine, production, increase BUN & Creatinine, jaundice and signs of liver failurejaundice and signs of liver failure
Poor prognosis- Poor prognosis- most die within 3 wks most die within 3 wks without transplantwithout transplant
Think due to decreased perfusion &/or Think due to decreased perfusion &/or toxins from failure of livertoxins from 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 The donor - a blood relative, spouse, or friend, will have extensive medical and friend, will have extensive medical and psychological evaluations to ensure the psychological evaluations to ensure the lowest possible risk.lowest possible risk.
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 waitCadaver donor have to wait
Liver Transplant VideoLiver Transplant Video
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 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