approach to patient with hepatic disorders

8/14/2019 Approach to Patient With Hepatic Disorders

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Approach to Patient withApproach to Patient with

Hepatic DisordersHepatic Disorders


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Liver Structure and FunctionLiver Structure and Function

largest organ in the body;largest organ in the body;

weighs about 1-1.5kgweighs about 1-1.5kg

Located in the RUQ of the abdomenLocated in the RUQ of the abdomenunder the right lower rib age againstunder the right lower rib age against

the diaphragmthe diaphragm


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Blood SupplyBlood Supply

a.a. 20% from Hepatic Artery (oxygen-20% from Hepatic Artery (oxygen-

rich)rich)

b.b.80% from Portal Vein (nutrient-rich)80% from Portal Vein (nutrient-rich)

A mixture of venous and arterial bloodA mixture of venous and arterial blood

bathes the liver cellsbathes the liver cells


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HepaticArtery

Portal Vein

Liver

Common capillary bed/

sinusoids of liver

Central Veins

of each Lobule

Hepatic Vein

Inferior Vena Cava


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Liver CellsLiver Cells

Hepatocytes 2/3 of liver mass andHepatocytes 2/3 of liver mass and

does most of the liver functionsdoes most of the liver functions

Kupffer cells engulf particulateKupffer cells engulf particulate

matter (bacteria) that enter the livermatter (bacteria) that enter the liver

through portal bloodthrough portal blood

Ito cells fat-storing cellsIto cells fat-storing cells


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Functions of LiverFunctions of Liver


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Glucose MetabolismGlucose Metabolism

Meal Glucose absorption in

intestines

Portal Circulation Liver

Glucose converted

to glycogen

Stored in

hepatocytes

I.

II.

Exercise Protein/Fat

breakdown

Liver creates glucose

(gluconeogenesis)


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Ammonia ConversionAmmonia Conversion

Ammonia from: use of amino acids

from protein forgluconeogenesis

Ammonia from: production

of intestinal flora/ from diet

Portal Circulation

Liver: converts ammonia to urea

Systemic circulation

Excreted in the kidneys

(urine)


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Protein MetabolismProtein Metabolism

Synthesizes plasma proteinSynthesizes plasma protein

(albumin, alpha and beta globulin)(albumin, alpha and beta globulin)

Clotting factors (prothrombin)Clotting factors (prothrombin) -- liver needs Vit. K to synthesize prothrombinliver needs Vit. K to synthesize prothrombin


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Fat MetabolismFat Metabolism

Fatty acids are degraded into ketoneFatty acids are degraded into ketone

bodies for energy duringbodies for energy during

hypoglycemic state, starvation andhypoglycemic state, starvation and

uncontrolled DM.uncontrolled DM.


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Vitamin and Iron StorageVitamin and Iron Storage

Large amounts of Vit. A, B, and D andLarge amounts of Vit. A, B, and D and

several B-complex vitamins areseveral B-complex vitamins are

stored in the liverstored in the liver

Iron and copper are also stored in theIron and copper are also stored in the

liverliver


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Drug MetabolismDrug Metabolism

First-pass Effect

Oral meds pass the

G.I.T.

Portal

circulation

Liver (metabolized)

Decreased

bioavailability

Bioavailability fraction of drug that reaches the systemic

circulation


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Bile FormationBile Formation

Formed by the hepatocytesFormed by the hepatocytes

Primary bile acids are cholic acid andPrimary bile acids are cholic acid and

chenodeoxycholic acid (CDCA)chenodeoxycholic acid (CDCA)

Major components: water(82%), bileMajor components: water(82%), bile

acids(12%), lecithin &otheracids(12%), lecithin &other

phospholipids (4%) and unesterifiedphospholipids (4%) and unesterified

cholesterol (0.7%)cholesterol (0.7%)


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Bilirubin ExcretionBilirubin Excretion

Degradation ofSenescent RBCs in

the spleen

Release ofHemoglobin

Heme

moleculeCO & biliverdin

bilirubin

Heme oxygenase Biliverdin reductase


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Enterohepatic Circulation

Bile

(conjugated bilirubin)

Bile ducts

duodenum

Ileum and colon

(converted into urobilinogen)

Excreted in feces

(stercobilin)

Reabsorbed into

portal circulation

Systemic circulation

kidney

Excreted in urine

Liver:

reexcreted into bile


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Clinical HistoryClinical History


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Symptoms of Liver DiseaseSymptoms of Liver Disease

Nature of DiseaseNature of Disease

Pattern of OnsetPattern of OnsetDisease ProgressionDisease Progression

Potential Risk FactorsPotential Risk Factors


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Symptoms of Liver DiseaseSymptoms of Liver Disease

A.A. Fatigue - most commonFatigue - most commoncharacteristic ofcharacteristic of liverliverdiseasedisease

e.g. lethargy, weakness,e.g. lethargy, weakness,restlessnessrestlessness

B. Nausea/Vomiting provoked byB. Nausea/Vomiting provoked by

odor ofodor of food or fatty foodfood or fatty foodintakeintake

C. RUQ pain/discomfort arises fromC. RUQ pain/discomfort arises fromstretching/irritation ofstretching/irritation of

GlissonsGlissons capsule w/ccapsule w/c


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D. Pruritus/Itching related toD. Pruritus/Itching related to

accumulationaccumulation of bileof bile

salts in the dermissalts in the dermis

E. Jaundice hallmark of liver diseaseE. Jaundice hallmark of liver disease

andand most reliable markermost reliable marker

of severityof severity

- accompanied by acholic- accompanied by acholic

tools/tools/ tea-colored urine?tea-colored urine?

e.g.e.g. jaundice without dark urine indicatesjaundice without dark urine indicatesunconjugated hyperbilirubinuriaunconjugated hyperbilirubinuria


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Nature of DiseaseNature of Disease

Hepatocellular injury vs.Hepatocellular injury vs.Cholestatic injuryCholestatic injury

Hepatocellular: ALT/AST elevated outHepatocellular: ALT/AST elevated outof proportion to alkaline phosphataseof proportion to alkaline phosphatase

Cholestatic: Alkaline phosphatase outCholestatic: Alkaline phosphatase outof proportion to ALT/ASTof proportion to ALT/AST

Viral vs BacterialViral vs Bacterial( Viral Hepatitis/ Liver( Viral Hepatitis/ Liver

abscess)abscess)


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Pattern of Disease (Staging)Pattern of Disease (Staging)

Course of disease (acute vs. chronic)Course of disease (acute vs. chronic)

Early vs. lateEarly vs. late

Pre-cirrhotic, cirrhotic, end stagePre-cirrhotic, cirrhotic, end stage


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Disease ProgressionDisease Progression

(Grading)(Grading)Severity and activity of diseaseSeverity and activity of disease

Active vs. inactive; mild moderate,Active vs. inactive; mild moderate,

severesevere


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Potential Risk FactorsPotential Risk Factors

A.A. Alcohol consumptionAlcohol consumption

for women: 2 drinks(22-30g/day)for women: 2 drinks(22-30g/day)

for men: 3 drinks (33-45g/day)for men: 3 drinks (33-45g/day)

Assess presence ofAssess presence ofabuse orabuse or

dependencedependence

Alcoholism defined on behavioralAlcoholism defined on behavioral

patterns andpatterns and consequences of alcoholconsequences of alcohol

intake not on the basis fointake not on the basis fo amount ofamount of

consumption.consumption.


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Abuse repetitive pattern of drinking alcoholAbuse repetitive pattern of drinking alcohol

that has adverse effects on social, family,that has adverse effects on social, family,

occupational and health statusoccupational and health status

Dependence alcohol-seeking behavior despiteDependence alcohol-seeking behavior despiteits adverse effectsits adverse effects

Have you ever had a drink firstthing in the morning to steady yournerves and get rid of hangover?

Eye-opener

E

Have you ever felt Guilty or bad

about your drinking?G

Have people Annoyed you bycriticizing your drinking?

A

Have you ever felt you ought to Cutdown on drinking?C


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B. MedicationsB. Medications Currently taking meds? on maintenanceCurrently taking meds? on maintenance

drugs? Herbal medicines? Birth controldrugs? Herbal medicines? Birth control

pills? Self-medication? Illicit drug use?pills? Self-medication? Illicit drug use?

C.C.LifestyleLifestyle Personal habits/hygienePersonal habits/hygiene Eating habits/food preferenceEating habits/food preference Sexual activity/preferenceSexual activity/preference Recent travelRecent travel

Environment/sanitation/occupationEnvironment/sanitation/occupationTattoe, piercing, needle-stick injuryTattoe, piercing, needle-stick injury Exposure/contact with patients with liverExposure/contact with patients with liver

diseasedisease


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D. Past Medical HistoryD. Past Medical History Previous hospitalizationsPrevious hospitalizations

Previously acquired diseasesPreviously acquired diseases

Recent surgeryRecent surgery

Blood transfusionsBlood transfusions

E. Family HistoryE. Family History Related familial diseases of the liverRelated familial diseases of the liver


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Physical ExaminationPhysical Examination


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A. IcterusA. Icterus

Assess for these areas:Assess for these areas:

sclerae (under natural light)sclerae (under natural light)

skin ( for fair-skinned individuals)skin ( for fair-skinned individuals)

oral-mucosa ( for dark-skinnedoral-mucosa ( for dark-skinned

individuals)individuals)

Clinically evident when serum bilirubinClinically evident when serum bilirubin

exceeds 2.5mg/dLexceeds 2.5mg/dL


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Types of JaundiceTypes of Jaundice

A. HemolyticA. Hemolytic - increased destruction of red- increased destruction of redblood cellsblood cells

e.g. transfusion reactions, Hemophiliae.g. transfusion reactions, Hemophilia

B. HepatocellularB. Hepatocellular inability of damaged liver inability of damaged livercells to clear normal amounts of bilirubin from thecells to clear normal amounts of bilirubin from thebloodblood

e.g. viral hepatitis, cirrhosise.g. viral hepatitis, cirrhosis

C. ObstructiveC. Obstructive occlusion of bile duct by occlusion of bile duct bygallstone, inflammatory process, tumor orgallstone, inflammatory process, tumor orenlarged organ (extrahepatic)enlarged organ (extrahepatic)

- obstruction of small bile ducts within- obstruction of small bile ducts withinthe liver (intrahepatic)the liver (intrahepatic)


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D. Hepatomegaly/SplenomegalyD. Hepatomegaly/Splenomegaly

liver size varies; not a reliable signliver size varies; not a reliable sign

of liver diseaseof liver disease

Palpation: assess liver edge forPalpation: assess liver edge for

unusual firmness, irregularity andunusual firmness, irregularity and

nodules.nodules.

E. Hepatic TendernessE. Hepatic Tenderness

Most reliable P.E. findingMost reliable P.E. finding

Discomfort/pain on touching/pressingDiscomfort/pain on touching/pressing


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F. AscitesF. Ascites

accumulation of excess fluid withinaccumulation of excess fluid within

the peritoneal cavitythe peritoneal cavity

Percussion: shifting dullnessPercussion: shifting dullness

(+) abdominal fluid wave(+) abdominal fluid wave


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G. Hepatic EncephalopathyG. Hepatic Encephalopathy Accumulation of ammonia due to damagedAccumulation of ammonia due to damaged

liver cells fot to brain dysfunctionliver cells fot to brain dysfunction P.E. : a. changes in personality, sleepP.E. : a. changes in personality, sleep

patterns,patterns, irritability, mentalirritability, mentaldullnessdullness

(not due to meds, F&E imbalance,(not due to meds, F&E imbalance,etc.)etc.)

b. asterixis/flapping tremors of bodyb. asterixis/flapping tremors of bodyand tongueand tongue

c. Fetor hepaticus sweet ammonialc. Fetor hepaticus sweet ammonialodor, fruity-odor, fruity- odor ofodor ofbreathbreath

* Trail-making test N=15-30secs* Trail-making test N=15-30secs


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H. OthersH. Others

Umbilical Hernia due to ascitesUmbilical Hernia due to ascites

Caput Medusa collateral veins seenCaput Medusa collateral veins seen

radiating from umbilicusradiating from umbilicus

Hyperpigmentation/Xanthelasma- tendonHyperpigmentation/Xanthelasma- tendonxanthomata due to increased lipids andxanthomata due to increased lipids and

cholesterolcholesterol

Kayser-Fleischer rings- golden brownKayser-Fleischer rings- golden browncopper pigment deposited at periphery ofcopper pigment deposited at periphery of

corneacornea.. Hepatic Bruit sound produced in lungHepatic Bruit sound produced in lung

CA.CA.


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Diagnostic ProcedureDiagnostic Procedure


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i. Lab Tests/Liver Functioni. Lab Tests/Liver Function

TestsTests

a.a. Pigment studiesPigment studies

b.b. Protein StudiesProtein Studies

c.c. PTPTd.d. Serum AminotransferasesSerum Aminotransferases

e.e. GGT,LDHGGT,LDH

f.f. Cholesterol StudiesCholesterol Studies


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a. Pigment Studiesa. Pigment Studies

Measures the ability of the liverMeasures the ability of the liverto conjugate and excreteto conjugate and excretebilirubinbilirubin

Serum bilirubin (direct) 0-0.3mg/dLSerum bilirubin (direct) 0-0.3mg/dL

(total) 0-0.9mg/dL(total) 0-0.9mg/dL

Urine bilirubin 0(0)Urine bilirubin 0(0)

Urine urobilinogen 0.05-2.5mg/24hrUrine urobilinogen 0.05-2.5mg/24hr

Fecal urobilinogen 40-200mg/24hrFecal urobilinogen 40-200mg/24hr


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b. Protein Studiesb. Protein Studies

Albumin: cirrrhosisAlbumin: cirrrhosis

chronic hepatitischronic hepatitis

edema, ascitesedema, ascites

Globulin: cirrhosisGlobulin: cirrhosis

liver diseaseliver disease

chronic obstructive jaundicechronic obstructive jaundice

viral hepatitisviral hepatitis

A/G ratio is reversed in chronic liverA/G ratio is reversed in chronic liverdiseasedisease


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c. Prothrombinc. Prothrombin

Normal 100% or 12-16secsNormal 100% or 12-16secs

Prolonged in liver diseaseProlonged in liver disease


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d. Serum Aminotransferasesd. Serum Aminotransferases

A. ALT (SGOT) 10-40unitsA. ALT (SGOT) 10-40units

- to monitor coure of- to monitor coure ofhepatitis/cirrhosis and effects ofhepatitis/cirrhosis and effects of

treatments that may be toxic to livertreatments that may be toxic to liver- Increased : liver disorder- Increased : liver disorder

b. AST (SGPT) 5-35 unitsb. AST (SGPT) 5-35 units

- present n tissues high in- present n tissues high inmetabolic activity (heart, liver,metabolic activity (heart, liver,skeletal muscle)skeletal muscle)

- increase with damaged tissues- increase with damaged tissues


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e. GGT/ LDHe. GGT/ LDH

Elevated in alcohol abuseElevated in alcohol abuse

Marker for biliary cholestasisMarker for biliary cholestasis


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f. Cholesterol Studiesf. Cholesterol Studies

Elevated in damaged liverElevated in damaged liver

Normal values:Normal values:

HDL M: 35-70mg/dLHDL M: 35-70mg/dLF: 35-85mg/dLF: 35-85mg/dL

LDL


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ii. Diagnostic Imagingii. Diagnostic Imaging


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a. US/CT scana. US/CT scan

First option for suspected obstructiveFirst option for suspected obstructive

jaundicejaundice

Can also detect fatty liverCan also detect fatty liver


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b. ERCPb. ERCP

Both diagnostic (biliary treeBoth diagnostic (biliary tree

visualization) and therapeutic ( stonevisualization) and therapeutic ( stone

extraction, stents)extraction, stents)

Extrahepatic cholestasis: dilatedExtrahepatic cholestasis: dilated

ductsducts

Intrahepatic cholestasis: ducts notIntrahepatic cholestasis: ducts not

dilateddilated


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c. Doppler US/MRIc. Doppler US/MRI

Asses hepatic vasculature andAsses hepatic vasculature and

dynamicsdynamics


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iii. Liver Biopsyiii. Liver Biopsy

Gold standard in evaluation of liverGold standard in evaluation of liver


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Gold standard in evaluation of liverGold standard in evaluation of liver

diseasedisease


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AlcoholicAlcoholicLiverLiver

DiseaseDisease

d h i i


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due to chronic, excessivedue to chronic, excessive

alcoholalcohol ingestioningestion

a.a. Fatty liverFatty liver

b.b. Alcoholic hepatitisAlcoholic hepatitis

c.c.

CirrhosisCirrhosis


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Alcoholic Cirrhosis (Laennecs)Alcoholic Cirrhosis (Laennecs)

An irreversible chronic injury of theAn irreversible chronic injury of the

hepatic parenchyma and extensivehepatic parenchyma and extensive

fibrosis in association of regenerativefibrosis in association of regenerative

nodulesnodules


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ii. Clinical Manifestationsii. Clinical Manifestations

Anorexia, malnutrition, wt. lossAnorexia, malnutrition, wt. loss

Sx of hepatocellular dysfunction: jaundice, portalSx of hepatocellular dysfunction: jaundice, portal

hypertension, bleeding varices, ascites,hypertension, bleeding varices, ascites,

encephalopathyencephalopathy

Hormonal disturbances:Hormonal disturbances:

Men: gynecomastia, testicular atrophyMen: gynecomastia, testicular atrophy

Women: virilization, menstrual problemWomen: virilization, menstrual problem


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iii. Lab Findingsiii. Lab Findings

Anemia due to G.I. blood lossAnemia due to G.I. blood loss

- coexistent nutritional deficiency (folic &- coexistent nutritional deficiency (folic &

B12)B12)

Elevated transaminasesElevated transaminases

Prolonged PTT reduced synthesis of clottingProlonged PTT reduced synthesis of clotting

proteins;proteins; Vit. KVit. K

Decreased serum albumin impaired proteinDecreased serum albumin impaired protein

synthesissynthesis

Increased ammonia levels may lead toIncreased ammonia levels may lead to

encephalopathyencephalopathy


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iv. Prognosisiv. Prognosis

Abstinence to alcohol consumption decreasesAbstinence to alcohol consumption decreases

morbidity/mortality and delays/preventsmorbidity/mortality and delays/prevents

complicationscomplications


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Major ComplicationsMajor Complications


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a. Portal Hypertensiona. Portal Hypertension

Normal pressure in portal veinNormal pressure in portal vein

( 5-10mmHg); PH is > 10mmHg( 5-10mmHg); PH is > 10mmHg

Damaged liver structures leads toDamaged liver structures leads to

increased resistance to portal bloodincreased resistance to portal blood

flow (presinusoidal, postsinusoidal &flow (presinusoidal, postsinusoidal &

sinusoidal venous compartments)sinusoidal venous compartments)

In Cirrhosis, resistance is usually atIn Cirrhosis, resistance is usually at

sinusoidal areasinusoidal area

portal venous system has no valvesportal venous system has no valves


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portal venous system has no valvesportal venous system has no valves

facilitates retrograde blood flow from highfacilitates retrograde blood flow from highpressure portal venous system to a lowerpressure portal venous system to a lower

pressure systemic circulationpressure systemic circulation

Cardioesophageal

junction

Rectum Retroperitoneal

space

Falciform

ligament of liver

Esophagogastric

varices

hemorrhoids ascites Periumbilical/abdominal

wall collaterals

(caput medusa)


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b.b. EsophagealEsophagealVaricesVarices

i.i. Factors to Bleeding:Factors to Bleeding: Muscular exertion from lifting heavyMuscular exertion from lifting heavy

objects; straining at stool, sneezing,objects; straining at stool, sneezing,coughing or vomiting.coughing or vomiting.

EsophagitisEsophagitis Irritation of vessels by poorly chewedIrritation of vessels by poorly chewed

foods or irritating fluids; reflux offoods or irritating fluids; reflux of

stomach contentsstomach contents salicylatessalicylates

ii Treatment:ii Treatment:


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ii. Treatment:ii. Treatment: Life- threatening EMERGENCY!!!Life- threatening EMERGENCY!!!

- replacement of blood loss to maintain- replacement of blood loss to maintain

intravascular volume BEFORE Dx studiesintravascular volume BEFORE Dx studies

and interventions to stop bleedingand interventions to stop bleeding

(hemostasis)(hemostasis)

*** excessive fluid administration would*** excessive fluid administration wouldincrease portal pressure leading to furtherincrease portal pressure leading to further

bleedingbleeding

Close monitoring of CVP, urine output,Close monitoring of CVP, urine output,

mental statusmental status

Only when hemodynamically stable shouldOnly when hemodynamically stable should

we proceed to Dx procedure andwe proceed to Dx procedure and

hemostasishemostasis

iii Medical Management:iii Medical Management:


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iii. Medical Management:iii. Medical Management:

c.c. Vasoconstrictors:Vasoconstrictors: Vasopressin generalizedVasopressin generalized

vasoconstriction leading to decreasedvasoconstriction leading to decreased

blood flow to portal venous systemblood flow to portal venous system

Somatostatin/Octreotide directSomatostatin/Octreotide direct

splanchnic vasoconstrictionsplanchnic vasoconstriction


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b. Balloon Tamponadeb. Balloon Tamponade

- tube introduced to the- tube introduced to thestomach, gastric balloon inflated andstomach, gastric balloon inflated and

pulled back into the stomach cardia.pulled back into the stomach cardia.- done if bleeding is too- done if bleeding is too

vigorous and endoscopy is notvigorous and endoscopy is notavailableavailable

e.g. triple lumen (Sengstaken-e.g. triple lumen (Sengstaken-Blakemore)Blakemore)

c Endoscopic Interventionc Endoscopic Intervention


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c. Endoscopic Interventionc. Endoscopic Intervention

first line of treatment to controlfirst line of treatment to control

bleeding acutely.bleeding acutely.c.i.c.i. Endoscopic SclerosisEndoscopic Sclerosis varices varices

injected with sclerosing agents via ainjected with sclerosing agents via a

needle- tip catheter passed throughneedle- tip catheter passed throughthe endoscopethe endoscope

c.ii. Endoscopic Band Ligation c.ii. Endoscopic Band Ligation

varices are ligated withvarices are ligated withendoscopically placed small elasticendoscopically placed small elastic

O-ringsO-rings


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d. non-selective beta adrenergicd. non-selective beta adrenergic

blocker causes hypotension andblocker causes hypotension and

eventually causes hypovolemia.eventually causes hypovolemia.


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Cirrhosis

with portal

hypertension

Splanchnic

arterial

vasodilation

Decreased in

circulating arterial

blood volume

Activation ofrenin-

angiotensin and

SNS and ADH

Kidney retains

sodium and water

hypervolemia

Persistent activation of systems for

retention of sodium and water;

ascites and edema formation

Continued arterial

underfilling

Management:Management:


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Management:Management:

b.b. Dietary ModificationDietary Modification

-- low sodium diet (2g/d NaCl)low sodium diet (2g/d NaCl)- to create a (-) Na balance leading to- to create a (-) Na balance leading todiuresisdiuresis

e.e. DiureticsDiuretics Spironolactone (Aldactone) first line ofSpironolactone (Aldactone) first line of

treatment for ascites from cirrhosistreatment for ascites from cirrhosis Furosemide may produce hyponatremiaFurosemide may produce hyponatremia

with prolonged usewith prolonged use Ammonium Chloride/Acetazolamide Ammonium Chloride/Acetazolamide

contraindicated (precipitates hepaticcontraindicated (precipitates hepaticcoma)coma)

*** daily wt loss should not exceed:*** daily wt loss should not exceed:


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daily wt. loss should not exceed: daily wt. loss should not exceed:

1-2kg in patients with1-2kg in patients with

ascites/edemaascites/edema0.5-0.75kg in patients without0.5-0.75kg in patients withoutedemaedema

*** fluid restriction is not attempted*** fluid restriction is not attemptedunless Na isunless Na is very lowvery low

Complications:Complications: Fluid and electrolyte imbalanceFluid and electrolyte imbalance

Encephalopathy due toEncephalopathy due tohypovolemia and dehydrationhypovolemia and dehydration

Decrease potassium = increasedDecrease potassium = increased

ammonia in systemic circulationammonia in systemic circulation

c Bed Restc Bed Rest


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c. Bed Restc. Bed Rest

- upright posture promotes activation- upright posture promotes activation

of RAAS system leading to decreasedof RAAS system leading to decreasedGFR, Na excretion and decreasedGFR, Na excretion and decreased

response to loop diureticsresponse to loop diuretics

d. Paracentesisd. Paracentesis


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d. Hepatic Encephalopathyd. Hepatic Encephalopathy

A complex neuropsychiatricA complex neuropsychiatric

syndrome characterized by these 4syndrome characterized by these 4

major factors:major factors:

Hepatocellular disease/portal systemicHepatocellular disease/portal systemiccollateral shuntscollateral shunts

Disturbances of awareness and mentationDisturbances of awareness and mentation

Shifting combinations of neurologic signs:Shifting combinations of neurologic signs:asterixis,rigidity,hyperreflexiaasterixis,rigidity,hyperreflexia

A characteristic symmetric high voltageA characteristic symmetric high voltage

triphasic slow wave pattern on ECGtriphasic slow wave pattern on ECG


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Hepatocellular

dysfunction

Shunting ofportal

venous bood

into systemic

circulation

Liver is

bypassed

Toxic substances

not detoxified by

liver

Accumulation

in systemic

circulation

Metabolic

abnormalities in the

CNS

***Ammonia not converted to urea


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Common PrecipitantsCommon Precipitants

Increased NitrogenIncreased NitrogenLoadLoad

- GastrointestinalGastrointestinal

bleedingbleeding

- Excess dietary proteinExcess dietary protein

- AzotemiaAzotemia

- ConstipationConstipation

Electrolyte andElectrolyte andMetabolicMetabolic

imbalanceimbalance

-

HypokalemiaHypokalemia- AlkalosisAlkalosis

- HypoxiaHypoxia

- HyponatremiaHyponatremia

- hypovolemiahypovolemia

DrugsD

rugs MiscellaneousMiscellaneous


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DrugsDrugs

- NarcoticsNarcotics

-TranquilizersTranquilizers

- SedativesSedatives

- diureticsdiuretics

MiscellaneousMiscellaneous

- InfectionInfection

-SurgerySurgery

- SuperimposedSuperimposed

acute liver diseaseacute liver disease

- Progressive liverProgressive liver

diseasedisease

- Portal-systemicPortal-systemic

shuntsshunts

EEGAsterixiM t l St tSt


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Deltawaves

-Coma; initiallyresponsive to noxiousstimuli, later

IV

Triphasicwaves

+Marked confusion,incoherent speech,

sleeping butarousable

III

Triphasic

waves

+Lethargy, moderate

confusion

II

Triphasic

waves

+/-Euphoria or depression,

mild confusion, slurredspeech, disordered sleep

I

EEGAsterixis

Mental StatusStage


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Treatment:Treatment:

Elimination or treatment ofElimination or treatment ofprecipitating factorsprecipitating factors

Lowering of blood ammonia levels byLowering of blood ammonia levels by

decreasing the absorption of proteindecreasing the absorption of proteinand nitrogenous products from theand nitrogenous products from the

intestineintestine

approach to patient with hepatic disorders

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