Liver Cirrhosis

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Liver Cirrhosis

• Lamya Alnaim, PharmD

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Background

• Cirrhosis ?the end stage of any chronic liver
  disease.
• Hepatitis C and alcohol are the main causes
• Two major syndromes result
• Portal hypertension
• Hepatic insufficiency.
• peripheral and splanchnic vasodilatation with the
  resulting hyperdynamic circulatory state

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Background

• Cirrhosis can remain compensated for many years
  before the development of a decompensating event.
• Decompensated cirrhosis is marked by the
  development of any of the following
  complications
• Jaundice,
• Hemorrhage
• Ascites
• Encephalopathy.
• Other than liver transplantation, there is no
  specific therapy for this complication.

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Background

• Other complications occur as a consequence of
  PHTN and the hyperdynamic circulation.
• Gastroesophageal varices result from PHTN,
  although hyperdynamic circulation contributes
• Ascites results from sinusoidal HTN and sodium
  retention, which is 2ndry to vasodilatation and
  activation of neurohumoral systems.

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Background

• The hepatorenal syndrome results from severe
  peripheral vasodilatation that leads to renal
  vasoconstriction.
• Hepatic encephalopathy is a consequence of
  shunting of blood through portosystemic
  collaterals (due to PHTN), brain edema (cerebral
  vasodilatation), and hepatic insufficiency.

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Definition

• A chronic disease of the liver with wide spread
  hepatic parenchymal injury and hepatocyte
  destruction.
• It may lead to anatomic and functional
  abnormalities of blood vessels and bile ducts

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Causes

• Alcohol
• Viral illness
• Biliary dysfunction
• Metabolic disorders
• Inherited disorders
• Drugs
• The most common causes are alcoholism and viral
  hepatitis

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Clinical Features

• Insidious development
• Often produces no clinical manifestations
• Common symptoms
• Anorexia, nausea, abdominal discomfort, weakness,
  weight loss, and malaise

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Clinical Features

• Physical examination
• Enlargement of the liver and spleen due to PHTN
• ascities,
• peripheral edema,
• Jaundice
• Spider angiomas
• GI bleeding
• Palmer erythema
• Right upper quadrant pain

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Portal Hypertension

• Portal vein collects blood from GI tract,
  pancreas and spleen to the liver
• Contains oxygen, nutrients and bacterial waste
• A pathway for detoxification and metabolism of
  absorbed substance.
• Fibrosis and nodular regeneration of liver with
  distortion of hepatic veins is the main cause of
  ? intrahepatic resistance

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Portal Hypertension

• Persistent PHTN lead to
• Changes in blood and lymphatic flow ?
  hyperfiltration and ascites
• ? collateral circulation ? the risk for
  esophageal and gastric varices
• Hepatic encephalopathy and hepatorenal syndrome

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Lab Findings

• Bilirubingt 2mg/dl to 40 mg/dl
• AST, ALT, alkaline phosphatase
• Aid in early diagnosis, prognosis, and response
  to treatment
• ? ALkPo gt 3 times normal indicate billiray disease

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Lab Findings

• Albumin
• (non-specific protein) Factor V and VII
  (specific proteins) can provide information on
  the functional capacity of the liver
• Low albumin lt 3 that does not respond to therapy
  is bad prognosis

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Lab Findings

• PT
• Prolongation due to impaired synthesis of vitamin
  K dependant clotting factors
• No response to VIT K is poor prognosis
• BUN
• lt 5 due to inadequate protein intake and
  depressed hepatic capacity for urea synthesis
• Biopsy
• Confirm the presence of cirrhosis

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General Management

• Largely symptomatic
• Maintain fluid and electrolyte balance

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General Management

• Analgesics
• NSAIDs may worsen gastritis and GI bleeding
• Acetaminophen may lead to hepatoxicity
• Narcotics may lead to CNS and respiratory
  depression
• Sedatives and hypnotics should be avoided if the
  patient is in danger of hepatic coma

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General Management

• Diet
• 2000-3000 calorie diet with 1g protein/kg
• In encepalopathy, dietary supplentation of BCAAs
• Thiamine replacement 50-100mg/da
• Iron and folate if patient is anemic
• Vitamin K 10 mg sc if PT is elevated, if PT is
  not improved in 3-5 days D/C

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I-Ascities

• Definition
• Accumulation of protein rich fluid in the
  peritoneal cavity.
• The most common clinical feature
• Clinical features
• Inability to fit into one's clothes
• Abdominal and back pain
• Gateroesophageal reflux
• SOB secondary to impaired diaphragm movement Or
  pleural effusions

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Ascities

• Pathophysiology Underfill theory
• 1-? hydrostatic pressure in portal vein and ?
  oncotic pressure.
• Exudation of fluid from the splanic capillary bed
  and liver surface when drainage capacity of the
  lymphatic system is exceeded.

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Ascities

• Pathophysiology Underfill theory
• 2-Portal hypertension ? oncotic pressure ??
  arterial blood flow to vital organs ?
  vasoconstriction.
• Reduced circulation to kidney activate rennin
  angiotension sys ? ? aldosterone Na/ water
  retention.
• Renal K excretion gt Na excretion urinary Na K
  ratio abnormal.

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Ascities

• Goals of therapy
• Mobilize fluid
• Diminish abdominal discomfort, back pain, and
  difficulty in ambulation
• Prevent complications such as bacterial
  peritonitis, hernias, pleural effusion,
  hepatorenal syndrome, respiratory distress.
• Prevent complications of treatment such as
  acid-base imbalance, hypokalemia, and volume
  depletion

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Ascities -Treatment

• A- Sodium Restriction (500mg-2g/day)
• 10-20 mEq/day plus bed rest (to ?rennin)
• Degree of success depends on
• Duration of restriction
• Extent of hepatic injury
• Patient with urine Na gt10 mEq/l likely respond

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Ascities -Treatment

• B-Water Restriction
• Effective in dilutional hyponatremia (Nalt130)
• Patients with low urine sodium lt10 mEq/l
• Normal renal function
• Not effective in
• reduced 24-hour Na urinary excretion
• Reduced GFR free water clearance
• May lead ? renal blood flow and azotemia

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Ascities -Treatment

• C. Diuresis
• The cornerstone of treatment
• Must be slow
• If urinary losses gt reabsorption from ascites?
  volume depletion , hypotension and renal
  insufficiency
• Should be limited to 0.2-0.3 kg /day in patients
  without edema
• 0.5-1kg /day for patients with edema

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Ascities -Treatment

• I- Spironolactone
• An aldosterone-inhibiting agent
• Patients have high levels of aldosterone
• Increased production
• Portal hypertension, ascities, ? intravascular
  volume, ? renal blood flow activate rennin-ang
  system
• Decreased excretion
• Hepatic impairment prolongs half-life due to ?
  metabolism
• ? albumin ? unbound hormone in the blood
• Dose 100-200 mg/day, may be ? slowly every 2-4
  days

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Ascities -Treatment

• I- Spironolactone
• Monitoring Parameters
• weight
• urine output
• changes in abdominal girth
• BUN
• Increase in K/Na ratio from pretreatment baseline
• Table

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Complication of Spironolactone

• 1-Hypokalemic hyperchloremic metabolic alkalosis
  and hyponatermia
• May occur in untreated cirrhosis
• Initial deficiency of K due to diarrhea,
  vomiting, hyperaldosterone
• May be corrected with KCl supplement
• Hyponatermia corrected by temporary withdrawal of
  diuretic and free water restriction
• 2- Prerenal azotemia
• ARF due to overdiuresis with compromise in
  intravascular volume and decreased renal
  perfusion
• gradual rise in Scr and Bun
• If large fluid volume must be removed quickly,
  paracentesis should be preformed
• 3- Gynecomastia
• can be related to cirrhosis independent of drug
  use

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Ascities -Treatment

• II-Other Diuretics
• If spironolactone fails to produce diuresis or
  hyperkalmeia occurs additional diuretic are
  needed
• The dose should be started low 50 mg/day HCTZ or
  20-40 mg furosemide and gradually increased
• Loop and thiazide diuretics may affect the value
  of monitoring urinary electrolyte
• The may cause excessive sodium loss in the
  presence of continued hyperaldosteronism

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Ascities -Treatment D- Paracentesis

• Removal of large amount of ascetic fluid with a
  needle or catheter
• Uses
• Ascites unresponsive to diuretic therapy
• If respiratory and cardiac functions are
  compromised
• Not definitive because fluid quickly
  reaccumliated due to transudation of fluid from
  the interstitial and plasma

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D- Paracentesis

• Major complications
• 15-100 of the fluid reaccumlates with 24-48 hrs
  ? transient hypovolemia and possibility of shock,
  encaphalopathy and ARF
• Hypotension
• Hemconcentration

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D- Paracentesis

• Major complications
• Shock
• Oliguria
• Hepatorenal syndrome
• Hemorrhage
• Perforation of abdominal vicra
• Infection, bacterial peritonitis
• Protein depletion

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E- Albumin

• Combined with paracentesis
• Effective as the initial management in tense
  ascites
• Typical regimen
• Removal of 4-6 l/day with replacement of 40-50g
  of albumin

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E- Albumin

• Benefits of combination
• More ascetic fluid can be removed
• Shorter hospital stay
• Superior to diuretic therapy
• No worsening of hepatic, renal or CV function
• Albumin alone can promote diuresis in ascites
  edema by increasing intravascualr volume
• The effects are not long lasting
• Variceal hemorrhage may be precipitated

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F- Dextran 70

• Can be combined with paracentesis
• Equally effective to albumin in mobilizing
  ascities
• More cost-effective
• Does not correct the underlying hemodynamic
  abnormalities, so albumin is preferred

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G-Surgical therapy

• 1- Peritoneovenous shunt
• An implanted valve in the abdominal wall, with
  cannula that empties into the vena cava
• Urine output as high as 15 L in 24 hrs
• Supplemental fruosamide may be needed to prevent
  vascular overload

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G-Surgical therapy

• 1- Peritoneovenous shunt
• Contraindications
• Peritonitis,
• Recurrent coma
• Sever coagulopathy
• Significant cardiac failure
• Acute alcoholic hepatitis

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G-Surgical therapy

• 1- Peritoneovenous shunt
• Complication
• Pulmonary edema
• Coagualopahty
• Fever, Wound infection, Septicemia, GI bleeding
• Reserved for patients with good renal and hepatic
  function who fail standard therapies

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G-Surgical therapy

• 2-transjugular intrahepatic portosystemic shunt
  (TIPS)
• a radiologic procedure in which a stent is placed
  in the middle of the liver to reroute the blood
  flow.
• it makes a tunnel through the liver connecting
  the portal vein to one of the hepatic veins.
• A metal stent is placed in this tunnel to keep
  the track open.

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SBP

• SBP is an infection of ascites that occurs in the
  absence of a contiguous source of infection.
• SBP occurs in 10 to 20 of hospitalized
  cirrhotic patients.
• Early diagnosis is a key issue in the management
  of SBP.
• SBP pathogenesis in patients with cirrhosis is
  considered
• to be the main consequence of bacterial
  translocation.

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SBP-Predisposing factors

• Severity of liver disease
• Total ascites protein lt1 g/dL
• GI bleeding
• Bacteriuria
• Previous SBPRecurrence rates 43 by 6 mts, 69
  by 1 yr and 74 by 2 yrs

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SBP-Clinical features

• signs may be absent in up to 1/3
• fever/hypothermia
• abdominal pain and tenderness
• hepatic encephalopathy
• diarrhoea
• ileus
• shock
• Unexplained deterioration in a patient with
  cirrhosis and ascites should lead to diagnostic
  paracentesis

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SBP-diagnosis

• A diagnostic paracentesis should be performed in
• Any patient admitted to the hospital with
  cirrhosis and ascites,
• Any cirrhotic patient who develops compatible
  symptoms or signs
• Any cirrhotic patient with worsening renal or
  liver function.
• Diagnosis is established with an ascites PMN of gt
  250/mm3

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SBP- Treatment

• Once an ascites PMN count of gt250/mm3 is
  detected, and before obtaining the results of
  ascites or blood cultures, antibiotic therapy
  needs to be started.
• The antibiotic that has been most widely used in
  the treatment of SBP is IV cefotaxime (2g 8 hrly)
  with which SBP resolves in around 90 90 of
  treated patients

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SBP- Treatment

• The combination of amoxicillin and clavulanic
  acid was shown to be as effective and safe as
  cefotaxime
• Antibiotic treatment can be safely discontinued
  after the ascites PMN count decreases to below
  250/mm3
• duration of antibiotic therapy should be for a
  minimum of 8 days

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Prevention of recurrent SBP

• In patients who survive an episode of SBP, the
  1-year cumulative recurrence rate is high, at
  about 70 .
• It is essential that patients be started on
  antibiotic prophylaxis to prevent recurrence
  before they are discharged from the hospital.

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Prevention of recurrent SBP

• Long-term prophylaxis with oral norfloxacin at a
  dose of 400 mg QD
• treatment should be initiated as soon as the
  course of antibiotics for the acute event is
  completed.
• oral ciprofloxacin at a dose of 250 mg QD could
  be used, although levofloxacin may be a better
  alternative given its added gram-positive
  coverage.

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Prevention of recurrent SBP

• Weekly administration of quinolones is not
  recommended given a lower efficacy and an
  increase in the development of fecal
  quinolone-resistant organisms.
• Prophylaxis should be continuous until
  disappearance of ascites (i.e., patients with
  alcoholic hepatitis who stop drinking) or
  transplant

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Esophageal varices

• Definition
• Compensatory hemodynamic mechanism due to PHTN
• Shunting of blood supply through low-pressure
  collateral veins in the esophageaus, rectum.
• ? pressure in the gastric fundus and esophagus
  cause swelling and burst resulting in life
  threatening upper GI bleeding
• Bleeding may be ? by impaired clotting system
  caused by deficincies of vitamin K dependant
  clotting factors
• It is the leading cause of death in cirrhosis
• Considered a medical emergency

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Esophageal varices

• Goals of therapy
• Volume resuscitation
• Acute treatment of bleeding
• Prevention of recurrence

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EV-General Management

• Resuscitation
• Gastric lavage with suction of gastric fluid to
  prevent complication as aspiration pneumonia
• Pharmacological treatment to stop bleeding
• If PT gt 15 sec, INR. 1.7 give 10mg IV vitamin K
• Monitor electrolytes, blood gases, and urine
  output
• Hypovolemia
• Signs Pallor, cold clammy skin, rapid pulse, SBp
  lt 80 mmHg
• Blood and blood products transfusion
• Keep HCT gt 30
• Whole blood is preferred due to homeostatic
  properties

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Therapy of Bleeding Varices

• 1-Vassopressin
• Powerful non-specific vasoconstrictor that
  reduces blood flow in the splanchnic bed
• Effective in 60 of patients
• short half-life and must be given as CIV
• May be used before sclerotherpay to slow bleeding
  and visualize varices

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Therapy of Bleeding Varices

• 1-Vassopressin
• Dosing
• Use lowest effective dose because ADRs dose
  related
• IV bolus 20U ? IVI of 0.2-0.4 u/min Max 0.9 u/min
• Taper dose over 24-48 hrs when bleeding controlled

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1-Vassopressin

• SE
• Intense vasoconstrictor action decreases C.O. and
  may cause coronary ischemia
• Bradycardia due to stimulation of the vagus nerve
• Abdominal cramping and Skin blanching due to
  stimulation of smooth muscle contraction
• Phlebitis
• Hematoma at the site of infusion
• Excess water retention and dilutioanl hyponatremia

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Therapy of Bleeding Varices

• 2-Terlipressin
• A synthetic analogue
• 80 effective
• Longer half-life and can be give as bolus every 6
  hrs
• Dose 2 mg
• Less cardiac side effects have been reported

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Therapy of Bleeding Varices

• 3-Somatosatin
• Natural peptide with shorter half life
• Dose bolus 50-250 mcg, infusion 250- 500 mcg/hr
• Similar efficacy to vasopressin but les side
  effects and higher cost
• 4- Octreotide
• Synthetic analogue of somatostatin
• Selective, potent vasoconstrictor that reduces
  portal and collateral blood flow
• Comparable efficacy to vasopressin
• Dose bolus 50-100 mcg followed by infusion 25-50
  mcg/hr

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Sclerotherapy

• Insertion of a flexible fiberoptic esophagoscope
  to directly visualize and inject a sclerosing
  agent in varices to induce immediate homeostasis
  ?intense inflammation ? thrombus formation and
  cessation of bleeding in 2-5 minutes
• Permanent destruction of the vessel over several
  days
• Procedure may need to be repeated several times

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Sclerotherapy

• Treatment of choice
• 95 effective
• More effective that vasopressin and balloon
  tamponade
• Following scleotherapy, prophylaxis with
  antacids, histamine blockers, omeprazole or
  suclafate

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Sclerotherapy

• Complications
• Esophageal ulceration
• Stricture formation
• Esophageal perforation
• Retrosternal chest pain
• Temporary dysphasia
• Sclerosing agents
• Sodium tetradecyl sulfate
• Ethanolamine oleate
• 0.5-2 ml of the solution is injected

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Therapy of Bleeding Varices

• Alternative treatments Balloon tamponade
• After initial sclerotherapy fails before trying a
  second sclerotherapy
• Used for acute treatment
• 90 effective
• Direct compression of the varices
• Temporary procedure limited to time balloon is
  inflated
• An additional procedure required within 24 hrs

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Therapy of Bleeding Varices

• Alternative treatments Balloon tamponade
• Complication
• Aspiration
• Pneumonitis
• Esophageal ulceration
• And rupture
• Chest pain
• Asphyxia

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EV-Long-Term Management

• 1- Propranolol
• Used for secondary prophylaxis
• To reduce hepatic flow and portal pressure
• Beneficial in alcoholic cirrhosis and less
  advanced disease
• Does not decrease mortality
• Abrupt discontinuation may lead to rebreeding

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EV-Long-Term Management

• 2- Endoscopic Band Legation
• An elastic band is placed around the mucus a and
  submucosa of the esophageal area containing the
  varix
• Leading to strangulation and fibrosis of the
  varix as effective as sclerotherpay with less
  complications
• Effective in preventing rebreeding
• 3-Surgery

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EV-Long-Term Management

• Primary prophylaxis
• Primary prevention of bleeding episode
• 1-Beta-Blockers
• Studies shown beta blockers to prevent bleeding
• Using 25 reduction in heart rate or hepatic
  venous gradient
• Propranolol and nadolol have been used
• They do not increase survival

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EV-Long-Term Management

• Primary prophylaxis
• 2-Isosorbide mononitrate
• Can reduce portal pressure
• Combination with propranolol has greater
  reduction in pressure
• Similar efficacy to propranolol, with regard to
  bleeding and survival
• 3-Sclerotherpay
• As a primary preventive measure has a higher
  mortality rate and is not recommended

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3-Hepatic Encephalopathy

• a metabolic disorder of the CNS and occurs in
  patients with advanced cirrhosis or fulminate
  hepatitis.
• Clinical Features
• Altered mental status
• Fetor heapticus sweetish musty pungent odor of
  the breath
• Asterixis flapping tremor, nonspecific
• Personality changes
• Drowsiness and confusion
• Deep coma, reversible

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Pathogenesis-HE

• 1- Ammonia
• The byproduct of protein metabolism
• Large portion is derived from diet or blood in
  the GIT
• Ammonia is metabolized to urea, which is renally
  eliminated

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Pathogenesis-HE

• 1- Ammonia
• In cirrhosis serum and CNS ammonia are increased
• In the CNS it combines with alpha-ketogluarate to
  form glutamine an aromatic amino acid.
• High glutamine in CSF is characteristic of
  encephalopathy , but it may not be the only cause

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Pathogenesis

• 2-Amino acid balance
• normal ratio of branched to aromatic AA is 4-61
• Catabolic state ? -ve nitrogen balance and
  preferential use of BCAAs as a source of energy

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Pathogenesis

• 2-Amino acid balance
• Ammonia ? ? glucagons secretion stimulated ?
  stimulated hepatic gluconeogenesis ? glucose from
  AA ? insulin is secreted ? ? uptake and
  metabolism in skeletal muscles
• In liver failure , aromatic AA ? and branched
  either ? or stays the same ? ratio is altered

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Pathogenesis

• As liver failure progress ? liver no longer
  produce glucose for energy ? BCAA used by
  skeletal muscle ? ? their level in the blood.
• Plasma clearance of AAAs is ?
• The blood brain barrier become more permeable to
  AAA via exchange for glutamine in the CSF

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Pathogenesis

• In the CSF the aromatic compounds are metabolized
  into chemicals that disrupt normal
  neurotransmitter balance
• E.g. tryptophan is converted to serotonin, which
  can compete with norephineprine for normal CNS
  function

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Pathogenesis

• 3-Gamma-aminobuyteric acid (GABA)
• GABA is the primary inhibitory neurotransmitter
  in the CNS
• Activation of GABA receptors results in increased
  Chloride permeability, hyper polarization of the
  neuronal membrane, and inhibition of
  neurotransmission.
• GABA binds to postsynaptic receptors sites in the
  brain, and causes the neurological abnormalities
  associated with hepatic encephalopathy.

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Precipitating factors

• Increase the serum ammonia or produce excessive
  somnolence in patients with impending hepatic
  coma
• Excess nitrogen load and metabolic or electrolyte
  abnormalities may increase ammonia levels

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Treatment

• 1-removal of precipitating factor
• 2-reducing the amount of ammonia or nitrogenous
  products in the blood
• 3- Stop or limit protein intake at the onset of
  encephalopathy
• May be increased at 10-20 g/day every 2-5 days
  depending on the clinical condition.
• Vegetable protein may be better tolerated
  because they contain fewer methionine and
  aromatic amino acids are less ammoniagenic

82
Drug Therapy

• 1-Lactulose
• A disaccharide broken down by GI bacteria to
  lactic, acetic, and formic acid
• MOA
• acidification of the colon to convert NH3 ? less
  absorbed NH 4 ? lower plasma NH3
• Induce osmotic diarrhea decreases intestinal
  transient time available for NH3 production and
  absorption.
• Dose
• Syrup 10g/15 ml
• Acute 30-45 ml TID titrated to resolution of
  symptoms 3 soft stools /day.
• In coma rectal retention enema 13 lactulose in
  tap water
• Effects appear in 24-48 hrs

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Drug Therapy-Lactulose

• Precautions
• Avoid excessive diarrhea because it could lead to
  dehydration and hypokalemia which could
  exacerbate encephalopathy
• 20 may have gaseous distention, flatulence,
  belching

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Drug Therapy

• 2-Neomycin
• MOA
• reduces plasma ammonia levels by decreasing
  protein metabolizing bacteria in the GI tract
• Dose
• 1-2 g orally QID
• 1 retention solution as retention enema foe
  20-60 min QID

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Drug Therapy -Neomycin

• Precautions
• 1-3 of the dose can be absorbed and may cause
  ototoxicity or nephrotoxicity especially with
  chronic use in patients with renal failure.
• Monitor serum creatinine, protein in the urine,
  CrCl when using high doses are used for long
  periods
• May lead to reversible malabsorption syndrome
  that may decrease absorption of fat, iron, vit B
  digoxin, penicillin, and vit K
• Comparison
• Similar effectiveness
• Neomycin produces a faster response in acute case
• A patient who does not respond to one may respond
  to the other

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Drug Therapy

• Combination
• May be more effective than either drug alone
• Sterilization of gut bacteria by neomycin may
  impair bacterial degradation of lactulsoe and
  prevent colonic acidification
• A stool PH lt 6.0 reflects synergistic effects
• Lactulose alone is preferred for long term use
• Always try lactulose first if no response try
  neomycin, then try combination

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Drug Therapy

• 3-Branched chain amino acids
• Diets high in BCAA and low in AAAs may help
  restore normal AA balance and reduce
  encepalopathy
• Heptamine is marketed as an 8 AA solution and
  contains more BCAAs than standard parental
  solutions
• Indications
• Due to high cost and limited efficacy information
  Patients with life threatening encepalopathy
  refractory to conventional therapy and with
  documented elevated serum ammonia levels
• Hepatic-aid- Dietary supplement

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Drug Therapy

• 4-Flumazenil
• A benzodiazepine antagonist
• Bases on GABAergic neurotransmission in hepatic
  encephalopathy
• Demonstrated clinical improvement
• Dose chronic 25 mg BID

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Management of Compensated Cirrhosis

• Patients with compensated cirrhosis are not
  jaundiced and have not yet developed ascites,
  encephalopathy, or variceal hemorrhage.
• Median survival is around 10 years
• Management is preventive and consists of routine
  monitoring for the development of liver
  insufficiency and/or the development of
  complications of portal hypertension/cirrhosis.

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Assessments in compensated cirrhosis

• Liver synthetic function tests every 3 to 6
  months
• Screening for hepatocellular carcinoma
• Screening for EGD
• If no varices, repeat endoscopy in 2 years 
• If small varices, repeat endoscopy in 1 year 
• If large varices, therapy to prevent first
  variceal hemorrhage
• Alphafetoprotein serum levels and liver
  ultrasound every 6 months
• Vaccination against hepatitis A and B in
  susceptible individuals