Liver Function tests
Enzyme tests? 3
Synthetic Function? 2
1. Aminotransferases—ALT & AST
2. Alkaline phosphatase—AP
3. Gamma glutamyl transpeptidase—GGT
1. Serum albumin
2. PT—prothrombin time
History, History, History
for Liver problems?
1. Exposure to chemicals, meds, herbs
2. Accompanying symptoms
3. Parenteral exposure
4. IV and intranasal drug use
5. Tattoos and piercings
6. Sexual activity
7. Travel and exposure history
8. Alcohol history
for liver problems?
1. Cachexia suggests malnutrishment - drinking or drug use
2. Stigmata of longstanding liver disease
3. Signs of alcoholic liver disease
4. Enlarged left supraclavicular node- Cancer
5. JVP suggests RHF secondary to portal HTN
6. Right pleural effusion in the absence of advanced ascites can be seen in cirrhosis
1. Two types?
2. Characterized by what? 2
-Type 1 (Classic): occurs in women of all age groups
-Type 2 (ALKM-1): occurs in girls and young women
2. Characterized by
-circulating autoantibodies (not thought to be part of the pathophysiology)
-High levels of serum globulin concentrations
Histopathology Autoimmune Hepatitis
Clinical Manifestations of Autoimmune Hepititis? 3
2. Subclinical and those presenting w/ advanced cirrhosis
3. Fulminant hepatitis
1. Presence of serological markers
2. Generally aminotransferases more elevated than bilirubin and AP
Extrahepatic Manifestations of autoimmune anemia?
1. Hemolytic anemia
3. Celiac sprue
5. Type I DM
6. Ulcerative colitis
ALL of these tend to be AUTOIMMUNE
1. Treatment of Autoimmune Hepatitis?
2. Acute risks and complications with steriods? 5
3. Long term risks? 6
4. 2nd line?
1. Corticosteriods for sympatomatic disease
-high blood sugar,
-Clouding of the lens in one or both eyes (cataracts)
-High blood sugar, which can trigger or worsen diabetes
-Increased risk of infections
-Thinning bones (osteoporosis) and fractures
-Suppressed adrenal gland hormone production
-Thin skin, bruising and slower wound healing
3. Azathioprine a 2nd line agent
1. Hemachromatosis is what?
2. What gene?
1. Genetic disease due to autosomal recessive
2. Identified gene HFE
Most common single gene disorder:
10% Caucasians heterotozygous
0.5% Caucasians homozygous
Very rare in other populations
1. Gene defect results in what?
2. What does this cause?
3. Eventual fibrosis & organ failure leads to what? 4
1. Gene defect results in increased iron absorption in the intestinal tract from the diet
2. Iron overload in the body
1. Normal iron content in the body?
2. Normally iron storage is controlled so there is no what?
3. Accumulation of _______ mg/yr. of iron occurs in hemochromatosis
4. Symptoms usually occur when? 2
5. Females have delayed symptoms because of what? 2
1. 3-4 mg /day
2. no excess accumulation
3. 500-1000 mg/yr.
-around age 40
-when iron stores reach 15-40 g!
Hemochromatosis Clinicical Manifestations are influenced by?
3. Alcohol use
4. Dietary iron
5. Menstruation & breast feeding
6. Unknown factors
1. Hemochromatosis is accelerated by what? 2
2. Classic presentation?
-Alcohol abuse &
-hepatitis C accelerate the process
2. Classic presentation:
-cutaneous hyperpigmentation w/ diabetes & cirrhosis
Reversible Manifestations of hemachromatosis?
1. CV? 2
2. Liver? 3
3. Skin? 2
4. Infections? 3
-bronzing (melanin deposition)
- grayness (iron deposition)
Irreversible Manifestations of Hemacromatosis
1. Liver? 2
2. Anterior pituitary gland?
1. Liver: : cirrhosis, hepatocellular CA **
2. Anterior pituitary gland: gonadotropin insufficiency leading?
3. Pancreas: diabetes mellitus (30-60%)
4. Thyroid: hypothyroidism
5. Genitalia: primary hypogonadism
6. Joints: pseudogout
Diagnosis of Hemochromatosis
Diagnosis of Hemochromatosis
1. Laboratory? 2
2. Gold Standard?
-Elevated serum transferrin saturation > 45%**
-Elevated serum ferritin
2. -Confirmation = ‘Gold Standard’ = liver biopsy (also defines extent of disease)
Treatment of Hemacromatosis
1. Education for evidence of iron overload/complications? 4
2. Mainstay of treatment?
1. Education for evidence of iron overload/complications:
-Avoid red meat, iron supplements
-Avoid handling or eating raw seafood (increased risk of infections)
-Receive vaccinations for hepatitis A & B
2. Mainstay of treatment--Phlebotomy
1. Removal of 500 ml of blood removes ______mg Iron
2. Do weekly until iron depletion:
Hgb = ?
Transferritin saturation ?
3. Maintenance: ?
2. Do weekly until iron depletion:
Hgb = 10 – 12 gm/dL
Ferritan < 50
Transferritin saturation < 50%
3. Maintenance: phlebotomy every 2-4 months
Hemacromatosis Genetic Testing
1. Screen who?
2. Likely to uncover who?
3. Screening test cost: ?
1. Screen 1st degree relatives unless under 18 YO
2. Likely to uncover homozygotes who are asymptomatic
3. Screening test cost: $200; done on whole blood sample
2. Inheritated how?
3. Affects what kind of metabolism?
4. Organ damage due to what?
5. Easily treated if what?
1. a.k.a. “hepatolenticular degeneration”
2. Autosomal recessive
3. Affects copper metabolism
4. Organ damage due to copper build up in the liver and brain
5. Easily treated if diagnosed early
-Difficult to diagnose!!!
1. The abnormal gene ATP7B affects the carrier protein of copper which is primarily in hepatocytes
2. It also impairs the excretion of copper via bile
Wilson's Disease Clinical manifesations?
1. Presents when?
2. What kind of symptoms? 3
Presentation varies widely and is often non-specific
1. Generally presents between the 1st and 3rd decade:
-Liver disease (usually presenting sx in young children)
1. Ceruoplasmin level
2. 24-hour urine for copper excretion
3. Look for Kayser-Fleischer rings in eyes
1. Once diagnosed chelation therapy w/ D-penicillamine is the treatment of choice (lifelong)
Universally fatal if untreated
Alcoholic liver dz: three stages?
1. Fatty liver (steatosis)
2. Alcoholic hepatitis
3. Alcoholic fibrosis and cirrhosis
1. Most patients present how?
2. Can occur how soon after a large alcohol binge & if continues to drink can progress?
3. May have tender what?
4. What is mildly elevated?
5. Can also occur in what other populations? 2
1. Most patients asymptomatic
2. Can occur within hours of a large alcohol binge & if continues to drink can progress
3. May have tender hepatomegaly
4. Transaminases mildly elevated
5. Can also occur in obese individuals and pregnancy
1. Range of presentation?
2. Symptoms? 8
1. Asymptomatic to extremely ill
-poor nutritional status
-Fever is common
Physical Exam for alcoholic hepatitis?
1. Spider angiomas
2. Palmar erythema
4. Parotid enlargement
5. Testicular atrophy
Lab findings for alcoholic hepatitis?
1. Leukocytosis w/ left shift (in severe disease)
2. Anemia (Macrocytic- B12*** or GI blood loss/microcytic)
3. Transaminases elevated: AST: ALT ratio usually greater than 2:0 (ratio rarely seen in other forms of liver disease)
4 Increased AP (> 3x normal)
5. Hyperbilirubinemia (60-90%)
6. Hypoalbunemia (severe disease)
7. Coagulopathy (severe disease)
8. Elevated ammonia level (severe disease)
Complications of Alcoholic LD
1. Alcoholic fatty liver is reversible
2. Alcoholic hepatitis—usually is reversible, but may run a fulminant course progressing to fibrosis and death
3. Long standing alcoholic liver disease can lead to cirrhosis
4. GI bleeds
5. esophageal varices
What are these?
1. Treatment of Alcoholic LD? 2
2. Supportive therapy? 5
-CESSATION of ALCOHOL!
-Liver transplant in appropriate patients
2. Supportive treatment:
- Folic Acid
& Vitamin B12
-R/O other causes for fever, liver disease such as Hep C, Hemochromatosis, neoplasm
-Glucocorticosteroids for severe hepatitis
Toxic Hepatitis: Factors influencing toxicity?
1. Excessive intake
2. Excessive cytochrome P450 activity
3. Decrease metabolism pathways in liver
4. Depletion of glutathione stores
5. Concomitant us of alcohol or other drugs
6. Comorbid illness
7. Advancing age
8. Nutritional status
What is the most common cause of liver failure in the US?
Drug-induced liver injury (DILI):
DILI: What kind of liver injury could it cause?
Least likely to cause?
2. cytotoxic or
less likely steatosis
Toxic Hepatitis: Most common drugs implicated in DILI in U.S.? 2
Treatment for acetaminophen overdose: 3
1. Acetaminophen level
2. Activated charcoal if ingested within 2-3 hours
3. N-acetylcysteine for severe overdose
Chronic Acetaminophen Intoxication
1. Signs and symptoms are nonspecific and often confused with what?
2. Patients who are at greater risk for developing hepatotoxicity:? 4
1. Signs and Sx are nonspecific: confused w/ viral diagnosis
-Ingestion of > 7.5 to 10 g over 24 hours
-Ingestion of less than 4g w/ increased susceptibility
-Liver tenderness, jaundice or ill-appearing
-Supratherapeutic acetaminophen concentrations (> 20 mcg/mL)
Treatment Chronic Acetaminophen Toxicity: Treatment w/ NAC recommended for?
1. All patients w/ liver tenderness &
2. Elevated aminotransferases &
3. Serum acetaminophen concentrations >10 mcg/mL
4. If serum acetaminophen concentrations are potentially toxic by the nomogram
What are the types?6
A, B, C, D, E, & G
Hepatitis A (HAV)
Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)
Hepatitis G (HGV)
GB virus type C (GBV-C)
Primarily seen w/ HAV, HBV, HCV, HEV: Many cases can be asymptomatic especially in children
1. Usually prodrome after exposure: this consists of what? 5
1. Malaise and fatigue
2. Anorexia, N/V
4. Pale stools, dark urine (urobiligen- direct being excreted in the urine and not in the stool like usual)
General Signs on Exam of viral hep?
2. RUQ pain
3. +/- Hepatomegaly
Labs for viral hep?6
1. Transaminases elevated, usually in thousands w/ ALT > AST
4. Alkaline phosphatase mildly elevated
5. WBC normal to low
6. May have prolonged PT
Acute Viral Hepatitis Management
1. Supportive care***
2. Manage symptoms
No other liver toxins:
5. Avoid exposure to other hepatitis viruses
How is HAV different from the other Hep viruses?
NO Chronic infection
HAV Routes of Transmission
1. Which one predominates?
2. Close personal contact such as? 3
3. Contaminated what?
4. Exposure to?
Maternal-fetal transmission has NOT been reported
1. Fecal-oral route predominates
2. Close personal contact
-day care centers)
3. Contaminated food/water
4. Blood exposure
Hepatitis A Vaccinatioin
1. What kind of vaccine?
2. SE? 4
1. Inactivated vaccine (Part of childhood vaccinations since 2006)
-injection site reactions,
3. Regimen: two doses 6-12 months apart
Hepatitis A Vaccinatioin: CDC recommendations
1. Persons w/ clotting factor disorders or chronic liver dz
2. Men who have sex with men
3. Users of illegal drugs
4. Those traveling to countries w/ high or intermediate levels
5. Any person wishing to obtain immunity
1. Postexposure Prophylaxis HAV treatment?
2. Situations? 6
1. Hep A vaccine or IG
-Close personal contact
-Sharing IV drug apparatus
-Child care centers—depends on number of cases
-Food handler case
Schools, hospitals, other work settings
HBV Modes of Transmission
1. Sexual contact
1. What is the major mode of transmission in developed countries?
2. Major mode in underdeveloped countries?
1. Sexual contact
2. Perinatal. Most infections occur at or near birth
1. How is HBV transmitted horizontally?
2. How long can HBV last outside the body?
3. How can HBV be spread percutaneously? 3
Post exposure prophylaxis? 2
1. Hepatitis vaccine
2. Post-exposure prophylaxis:
-Give first dose of vaccine
-Administer HBIG at same time—different site than vaccine
Hep B clinical outcomes of accute infection
Chronic HBV Infection
1. Most patients present how?
2. Other presentations? 4
1. Many patients asymptomatic
-Exacerbations similar to the acute infection
-Hepatic cell carcinoma (HCC)
1. 10-20% of these are due to what?
2. What are they? 5
1. 10-20% due to circulating immune complexes:
1. Hepatitis B surface antigen (HbsAg)
2. Hepatitis B core antigen (HbcAg)
4. Hepatitis B e antigen (HbeAg)
5. HBV DNA assays
Hepatitis B surface antigen (HbsAg)
1. Appears when?
2. Resolved infection becomes undetectable in how many months?
3. What makes it a chronic infection?
Hepatitis B surface antigen (HbsAg):
1. Appears prior to onset of symptoms
2. 4-6 months
3. Persistence past 6 m = chronic infection
Hepatitis B core antigen (HbcAg)
1. Intracellular antigen in what?
2. Presence of Anti-HBc of IgM class indicates what?
1. affected hepatocytes
2. acute infection
1. Follows the disappearance of what?
2. Usually persists for how long?
3. When coexists with HBsAg these persons are regarded as what?
4. Presence of anti-HBs only, indicates what?
1. Follows the disappearance of HBsAg
2. Usually persists for life
3. When coexists with HBsAg these persons are regarded as carriers of HBV**
4. Presence of anti-HBs only, indicates immunity by vaccination
Hepatitis B e antigen (HbeAg):
1. What is it?
2. Marker of what?
3. HBeAg to anti-HBe occurs early in patients w/ what?
4. Seroconversion is delayed for years in patients w/ what?
5. when they do seroconvert usually means what?
1. Secretory protein
2. replication and infectivity
3. acute infection
4. chronic HBV,
5. remission of their disease
HBV DNA assays:
1. USed for what?
2. Recovery from HBV associated w/ what?
3. Major role is in patients with HBV to monitor for what?
Treatment for Chronic HBV Infection
1. What is the agent of choice?
2. Patients who show evidence of virus replication are candidates for therapy. Who are these patients? 3
3. Patients who have decompensated cirrhosis or are carriers should be managed how?
1. Interferon or peginterferon is the agent of choice
2. Patients who show evidence of virus replication are candidates for therapy:
-HBeAg positive patients
-High serum HBV DNA levels
-Active liver disease (chronic hepatitis on liver biopsy) or elevated LFTs
3. SHOULD NOT receive treatments
Side Effects of Peginterferon
1. Flu-like symptoms
3. Abdominal pain, N/V, dry mouth
4. Hair loss
5. Blurred vision
Other Meds for Treating Hep B
1. Hep B easily becomes resistant so often what has to be used?
2. Treatment is for how long?
3. What are the meds? 4
The meds are complicated and have multiple side effects so I would defer to a specialist
1. a combo
2. Treatment is for months
A patient presents with these lab serology's:
IgM anti-HBc +
What does this patient have?
Acute Hep B infection
A patient presents with the following lab results:
HBsAg + (> 6 months)
HBV DNA +
ALT and AST moderately elevated ALT > AST
What does this patient have?
Chronic Hep B
Transmission of HCV
1. **IVDU/having sex with IVDU
2. Having been in jail more than 3 days
3. Religious scarification
4. Blood transfusion—since routine testing risk very low****
5. Having been struck or cut w/ bloody object
6. Pierced ears or body parts
7. Immunoglobulin injection
8. Perinatal transmission can occur
9. Solid organ transplant
Who Should be Screened for HCV?
1. Ever injected illegal drugs
2. Received clotting factors made before 1987
3. Received blood/organs before July 1992
4. Were ever on chronic hemodialysis
5. Have evidence of liver disease (increased ALT)
6. Are infected w/ HIV
7. Healthcare workers after needle stick/mucosal exposure to HCV + blood
Children born to HCV + mothers
Chronic HCV Infection
1. What percent of patients remain HCV RNA positive?
2. What percent of patietns have persistently elevated liver enzymes
3. Most common presentation/symptom?
4. HCV accounts for what percent of HCC cases in the US?
3. Symptoms: most common complaint is fatigue;
symptoms are rarely incapacitating, but may lead to a decrease in quality of life
4. HCV accounts for 1/3 of HCC cases in the U.S.!!!
Diagnosis of HCV
1. HCV RNA rises within what time frame following exposure?
2. Anti-HCV is positive within what tie frame after exposure?
3. Why is it difficult to distinguish acute from chronic HCV?
1. 8 days to 8 weeks
2. 12 weeks
3. both HCV RNA and anti-HCV are present in both
Management of Chronic HCV
1. Assess for severity of disease
2. Treat as indicated
3. Counsel to reduce further harm to liver- No tylenol
4. If not already done vaccinate against ?? Vaccinate Hep B or A
Patient Selection for Therapy for Chronic HCV
Patient evaluation for therapy? 4
1. Liver biopsy—almost all patients undergo this
2. Test for HIV
3. Evaluation for other types of liver disease
4. Continued IVDU or alcohol abuse
Treatment for Chronic HCV Infection
1. Combination of antivirals? 3
2. How do we assess treatment response? 2
Combination of antivirals:
3. Protease inhibitors
Assessing treatment response:
1. HCV RNA negativity
2. Sustained response HCV RNA negativity 6 months after treatment is stopped
Side Effects of Peginterferon/Ribavirin
1. Bone marrow suppression
2. Myalgia's, HAs, low grade fevers—common 1st 48 hours after infusion
3. Neuropsychiatric symptoms (irritability)—must screen for?
4. Non-productive cough and dyspsnea
5. Ocular: ischemic retinopathy, retinal hemmorrhage—evaluate by ophthalmologist
6. Thyroid dysfunction—monitor
7. Rash, hair loss, hearing loss, insomnia
Protease Inhibitors: Can be used to treat Hep C
1. What med is this?
2. Side effects?
-Harvoni is a tablet of 2 protease inhibitors that is showing promise—VERY expensive
-Many side effects including death!
Liver Transplant for HCV Patients
1. Describe what would happen in a liver transplant with an HCV patient?
2. What meds may prolong survival?
3. What other strategies may prolong survival? 2
1. A non-infected liver transplanted into an HCV infected patient becomes infected and decreases survival
2. Treatment w/ peginterferon + ribavirin may prolong survival
3. Using a younger liver or a liver that is already HCV infected also seems to help
1. Requires what for replcation?
3. Describe its structure?
1. Requires HBV for replication
2. HBsAg coat
3. Single stranded RNA rod-like structure
1. What activates replication of the HDV RNA in hepatocyte?
2. What directs packaging HD virion into HBsAg?
3. What envelope provided by HBV?
1. Small HDAg
2. Large HDAg
1. What type is most common in the western world?
2. Compare its prognosis with acute HBV?
3. Describe its progression?
1. Western world**
2. Increased risk of fulminant course when compared to acute HBV
3. Progression toward cirrhosis rapid
Genotype II for HDV is found where?
Genotype II: far East
Genotype III: Venezuela, Columbia, Brazil, Peruvian and Amazon bases
Transmission of HDV? 4
10% of HBV patients have HDV
HDV may be cytotoxic
2. Close personal contact
3. Multiple transfusions
4. Contaminated dialysis equipment
Clinical Features of HDV
1. Coinfection with HBV? 2
2. Superinfection on top of chronic HBV? 2
Coinfection w/ HBV:
1. Severe acute disease B + D; usually self-limited (direct cytopathic damage)
2. Low risk of chronic infection
Superinfection on top of chronic HBV:
1. Usually develop chronic HDV infection, HBV suppressed
2. High risk of severe, progressive chronic liver disease (immune damage)
1. HDV Prevention & Treatment?
2. HBV-HDV Coinfection?
3. Chronic HDV?
1. Hep B vaccine
2. HBV-HDV Coinfection:
Pre- or post-exposure prophylaxis to prevent HBV infection
3. Chronic HDV treated w/ peginterferon
1. What kind of virus?
2. Transmitted how?
3. Usually have a hx of what?
4. Infects in what forms?
1. RNA virus
2. Enterically transmitted, waterborne virus
3. U.S. cases usually have travel history to HEV-endemic area
4. NO chronic form
1. Spread by what most commonly?
2. What transmission is uncommon?
3. Can also be transmitted by what other things? 2
1. Spread by fecally contaminated water
2. Person-person transmission uncommon
-Can be transmitted by blood transfusion in endemic areas
-CAN BE transmitted from mother to newborn
HGV = GB virus type C (GBV-C)
3 different agents isolated: A, B, C—C is identical to HGV
1. How is it spread?
2. Evidence suggests it doesnt cause what?
3. How does it affect HIV pts?
1. Flavivirus, can be spread through contaminated blood and sexual contact
2. Evidence suggests doesn't cause hepatitis in humans
3. Protective effect on patients coinfected w/ HIV
Acute Hepatitis Complications
1. Cholestatic hepatitis
2. Raging fulminant hepatitis
3. Chronic hepatitis
Chronic Hepatitis: Liver Biopsy
What do we do before treatment?
Typical presentation? 4
1. Disease staging before treatment
1. Chronic inflammation in portal areas
2. Necrosis/inflammation (moderate activity)
3. Fibrosis (Marked activity)
4. Cirrhosis (non-reversible)
Definition: development of fibrosis of liver with formation of regenerative nodules; results in impairment of synthetic, metabolic and hemodynamic functions of the liver.
1. Imaging studies such as what can suggest dx? 3
2. What is the gold standard?
3. Determine underlying etiology using Hx & labs? 3
1. US, CT, MRI
2.Biopsy is gold standard**
3. Determine underlying etiology using Hx & labs:
1. What causes account for 1/2 of transplant pts? 2
2. Other etiologies? 6
1. Alcohol and Chronic HCV in U.S. account for ½ of transplant patients
-10-15% cryptogenic—diagnosis of exclusion
-Primary biliary cirrhosis (PBC)
1. Cirrhosis is a process of what of the liver?
2. Normally the extracellular matrix has different types of what that are in balance? 2
3. As chronic insult to the liver persists over years the collagen production in the liver does what?
4. The ECM becomes what and the normal functions of the liver are compromised?
5. The change in the ECM affects hepatic what cells?
6. Early fibrotic changes are ________, as progression occurs the changes become_________?
2. ollagen and glycoproteins
3. increases 4-10 fold
5. stellate cells
6. reversible, irreversible
Laboratory Abnormalities in Cirrhosis
2. Alkaline phosphatase
5. Prothrombin time
6. Serum sodium
Lab Abnormalities in Cirrhosis
How will the following be affected?
2. Alkaline phosphatase?
5. Prothrombin time?
6. Serum sodium? 2
1. Aminotransferases: AST/ALT--moderately elevated
2. Alkaline phosphatase: Elevated, but < 2-3 x normal
3. Bilirubin: levels rise as cirrhosis progresses
4. Albumin: levels fall as cirrhosis worsens
5. Prothrombin time: increases as ability of cirrhotic liver to synthesize clotting factors diminishes
6. Serum sodium: Hyponatremia seen w/ ascites and High levels of ADH (Why?)
Higher levels of Alkaline phosphatase would lead us to suspect what?
primary sclerosing cholangitis or PBS
Cirrhosis Hematologic lab abnormalities 3
What is the first hematologic change to occur in cirrhosis and why?
Thrombocytopenia: usually the first; secondary to portal hypertension and attendant congestive splenomegaly
1. Leukopenia occurs in cirrhosis why?
2. What is anemia from in cirrhosis? 5
1. Leukopenia: hypersplenism w/ margination
-Acute/chronic GI blood loss
-Folate deficiency (Occurs early in malnutrition, B12 deficiency occurs quite late)
-Bone marrow suppression
-Anemia of chronic disease (inflammation)
What is portal HTN?
What does it result in? 5
Increased blood pressure in the portal vein due to increased resistance to the blood passing through the vessels in the liver
1. Esophageal varices
2. Enlarged abdominal wall vessels(caput medusa)
5. Ascites (protein rich fluid)
Managing Portal Hypertension
1. Temporary measures: remove ascitic fluid
2. Portal shunts
3. Treat liver disease
4. Liver transplant
Hepatic Encephalopathy (HE)
1. Spectrum of potentially reversible neuropsychiatric abnormalities: 3
2. Syndrome observed in patients with cirrhosis
-Whats a prerequisite for this?
-Can occur in what kind of patients that dont have cirrhosis?
Spectrum of potentially reversible neuropsychiatric abnormalities:
-Motor impairment, including focal neurologic findings
2. Syndrome observed in patients with cirrhosis:
-Prerequisite is a diversion of portal blood to the systemic circulation
-Can occur in patient’s without cirrhosis who have surgically created portosystemic shunts
Hepatic Encephalopathy (HE): What other causes need to be ruled out before diagnosis?
Other precipitating causes need to be ruled out:
2. GI bleed
3. Hypokalemia/metabolic alkalosis
5. Sedatives or tranquilizers
7. Infection (including SBP)
Rarely hepatoma or vascular occlusion
Diagnosing Hepatic encephalopathy: What two staging techniques are used for this?
1. West-Haven Classification system grades HE stages 0-4
2. Glasgow Coma Scale may be used in severe HE
Describe Stages 0-4 for the West-Haven Criteria for HE?
Tests for diagnosing HE?
1. Ammonia and manganese are neurotoxins that precipitates HE
2. Serial ammonia levels are inferior to clinical assessment in gauging improvement or deterioration in patient who is being treated for HE
3. EEG findings are not specific to HE, but if seizure activity needs to ruled out an EEG may be helpful
4. CT and MRI are helpful in ruling intracranial lesions
1. What is the first thing we need to do in treatment?
2. How much should we give?
3. SE? 3
4. Another option?
5. What other correction do we need to make if present?
1. Need to lower ammonia levels: Lactulose:
2. Give enough so that the patient has 3-4 soft stools a day
3. SE: abdominal cramping, bloating, flatulence
Differential Diagnosis for HE?
1. Intracranial Lesions (?)
2. Infections (?)
3. Metabolic encephalopathy
4. Toxic encephalopathy
5. Organic brain syndrome
6. Postseizure encephaolpathy
Treatment of HE
1. Determine the stage of HE
2. Exclude nonhepatic causes of altered mental function
3. For overt HE lactulose may suffice
4. Low protein diet may be helpful
5. Rifampin orally effects the metabolic function of the gut microbiota and is as effective as lactulose with less SE’s
6. For more severe HE the patient may be at risk of aspiration and may need to intubated
Severe SE? 2
1. severe diarrhea,
2. eletrolyte abnormalities
to the point of worsening HE