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Complications of chronic liver disease
Ibrahim Masoodi
Objectives
Understand the basic mechanisms of portal hypertension
Recognize the classic presentations of portal hypertension complications
Brief management of these complications
What is CLD?
❖ Diffuse fibrosis of the liver with nodule formation
❖ Abnormal response of the liver to any chronic injury
Causes of Chronic liver disease
❖ Chronic viral hepatitis
❖ Metabolic: hemochromatosis, Wilson disease, alfa-1-antitrypsin, NASH
❖ Prolonged cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis)
❖ Autoimmune diseases (autoimmune hepatitis)
❖ Drugs and toxins
❖ Alcohol
Diagnosis of CLD
❖ Clinical : Stigmata of CLD
❖ CBC/ LFT : Hb/Platelets ,Bil/ low albumin , PT elevation, AST /ALT levels
❖ USG : Portal vein dia, Shrunken liver, splenomegaly ,ascites
❖ Fibroscan : Normal is between 2 to 7 kPa.
❖ A score of over 7.2 kPa indicates higher likelihood of significant fibrosis.
❖ A score over 14.5 kPa in someone with HCV/HIV coinfection indicates cirrhosis.
USG features
❖ Shrunken liver, Nodular surface, Elevated caudate to right lobe ratio (> 0.73 has 99%
specificity for cirrhosis)
❖ Portal hypertension : Distorted liver architecture, Regenerating nodules.-
❖ Distorted vascular channels Dilated MPV, Collaterals, Splenomegaly.
❖ Various doppler findings. Collateral veins , Gastroesophageal varices
CLD Imaging
Anatomy of the portal venous system
❖ Portal pressure >15mm
❖ Hepatic venous portal gradient
❖ HVPG ,Invasive technique
❖ Routinely not advocated
❖ Anastomotic sites ….varices
The Effect of The Liver Nodule
Mechanism of Portal HTN
❖ Cirrhosis
❖ Resistance portal flow
❖ Mechanical : Nodules
❖ Dynamic : Nitric oxide
1.Varices
❖ Esophageal varices
❖ Fundal varices
❖ GOV1 F1, F2,F3
❖ Rectal varices
❖ Ectopic varices
Classification
❖ Grade I
❖ Grade II
❖ Grade III-IV
❖ Fundal varices
❖ F1,F2 ,F3
Portal hypertensive Gastropathy
❖ Mild PHG : A mosaic-like
pattern without other findings.
❖ Severe PHG : mosaic-like pattern with flat
or bulging red or black-brown spots
and/or active bleeding
Fundal varices
Glue injection in Fundal varices
Management of variceal bleed
❖ Presents : Hematemesis/Melena /Occult blood positive /Iron def anemia
❖ O/E :Stigmata of CLD on clinical exam should clinch the diagnosis/Labs
❖ ABC, 2 IV Lines ,Type and crossmatch
❖ Blood @ 7gm/dl. Do not over transfuse -Target Hb 9gm/dl
❖ Platelet transfusion (platelet <50,000) Fresh frozen plasma (Correct Pt) ,
❖ Antibiotics : Ceftriaxone 1gm OD X 7 Days ,Meta analysis 12 trials (N=1200)
Management
❖ IV vasoconstrictors (Octreotide) 50 mcg bolus - continuous infusion of 50 mcg per
hour and is also continued for 3-5 days
❖ Endoscopic therapy
❖ Banding
❖ Sclerotherapy but EVL preferred.
❖ Shunting , Surgical, T . I . P . S
EVL
Varices prevention
❖ Treat underlying disease
❖ Endoscopic banding protocol
❖ B-blockers : No contraindication . Dose : Upto 160 mg daily in patients without
ascites or 80 mg daily in patients with ascites
❖ Shunt surgery (only if no cirrhosis)
❖ Liver transplantation
2. Ascites
Mechanism
Ascites
❖ Liver disease: cirrhosis
❖ Right sided heart failure
❖ Kidney disease (nephrotic syndrome)
❖ Low albumin (malnutrition, bowel loss)
❖ Peritoneal infection (TB…)
❖ Peritoneal cancer
Clinical presentation
❖ History: Increased abdominal girth, Increased wt
❖ Physical exam: stigmata of CLD
❖ Bulging flanks,Shifting dullness
❖ Fluid wave
Diagnosis
❖ Physical examination Ultrasound
❖ Ascitic tap :WBC (>250 PMN: SBP) ,RBC
❖ SAAG (serum albumin to ascitic fluid albumin gradient)
❖ >11 mg/dl : portal hypertension
❖ <11 mg/dl : Other
Management
❖ Treat the underlying disease
❖ Salt restriction (<2gm/d)
❖ Diuretics Loop diuretic (Lasix) , Daily weight Target wt loss of 1 kgm daily
❖ Aldosterone inhibitor (Spironolactone)
❖ Up to 400 mg spironolactone and 160 mg furosemide per day
Treatment resistant Ascites
❖ Recurrent tapping
❖ Peritoneal-venous shunt
❖ TIPS
❖ Liver transplantation
Spontaneous Bacterial Peritonitis
❖ Infection of ascitic fluid
❖ Usually gram negative (E.Coli) , Secondary Peritonitis when to suspect
❖ Presentation variable : Pain abdomen , fever, deranged RFT, HE,
❖ Mortality is high
❖ Dx: ascitic tap = PMN>250
❖ Treatment : Third generation cephalosporin IV, SBP prophylaxis for 5-10 days
SBP
❖ IV albumin (1.5 g per kg body weight within six hours of diagnosis and 1.0 g/kg body
weight on day three) - 30-40% Develop Renal failure
❖ Albumin infusion should be given if the creatinine is >1 mg/dL ,Total bilirubin is >4
mg/dL
❖ Once renal failure :Octreotide and midodrine may be helpful, in addition to infusion
of 25 grams of 25 percent albumin daily, unless there is massive fluid overload.
3. Hepatic Encephalopathy
❖ Reversible decrease in neurological function secondary to liver disease
❖ Acute: seen with acute liver failure
❖ Acute on chronic: established cirrhosis
Clinical features of hepatic encephalopathy
❖ Reversal of sleep pattern
❖ Disturbed consciousness
❖ Personality changes
❖ Intellectual deterioration
❖ Fetor hepaticus
❖ Asterixis , Fluctuating
Clinical test
Diagnosis
❖ Clinical (most important)
❖ The drawing tests
❖ EEG
❖ CT/MRI may show cerebral atrophy
Management
❖ Identify and treat precipitation factor
❖ Treat underlying liver disease
❖ Stop Beta blockers
❖ Antibiotics (Rifaxamin, metronidazole) Inj.Cefotaxime 2gm IV 8 hrly
❖ Lactulose till diarrhea sets in via NG tube
❖ Transplantation.
SBP Prophylaxis
❖ GI bleeding.
❖ Patients who have had one or more episodes of SBP. Recurrence > 70 percent
❖ Ascitic fluid protein is <1.5 g/dL +impaired renal function or liver failure.(C ≥1.2
BUN ≥25 mg/dL ,Na = ≤130 mEq/L .Liver failure CTP ≥9 and a bilirubin ≥3 mg/dL.
❖ CLD hospitalized for other reasons As protein < 1 g/dL (10 g/L).
❖ Cipro 500mg /OD , Norflox 400 mg OD/ Septran DS OD
Hepatorenal Syndrome
❖ Progressive renal failure
❖ Type 1 : rapidly progressive, high mortality
❖ Type 2: slower progression
❖ R/O volume depletion secondary to diuretics
❖ IV vasoconstrictors
❖ Liver transplantation
Complications of CLD
❖ Hepatic hydrothorax
❖ Hepatopulmonary syndrome
❖ Portopulmonary hypertension
❖ Cirrhotic cardiomyopathy
❖ Portal cholangiopathy
HCC
❖ Treatment of chronic HBV , HCV underlying cause of CLD
❖ 6 monthly USG & AFP levels AFP> 500 µ/L diagnostic
❖ AFP elev: Pregnancy ,Tumors of gonadal origin
❖ Sensitivities of US, CT, and MRI 46%, 65%, and 72%, respectively.
❖ Resection of lesions < 5cms without vascular invasion
❖ TACE, RFA , OLT ,Tyrosine kinase inhibitor (TKI) sorafenib Advanced HCC
Take home message
❖ Mechanical compression of blood flow plus hemodynamic changes leads to portal
hypertension
❖ Common complications of portal hypertension are:
❖ Collateral formation (Varices)
❖ Ascites
❖ Hepatic encephalopathy
Take home message
❖ The most important step in variceal bleed management is resuscitation
❖ The most important step in management of hepatic encephalopathy is the
identification of the precipitating factor
Chronic liver disease and it s complications

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Chronic liver disease and it s complications

  • 1. Complications of chronic liver disease Ibrahim Masoodi
  • 2. Objectives Understand the basic mechanisms of portal hypertension Recognize the classic presentations of portal hypertension complications Brief management of these complications
  • 3. What is CLD? ❖ Diffuse fibrosis of the liver with nodule formation ❖ Abnormal response of the liver to any chronic injury
  • 4. Causes of Chronic liver disease ❖ Chronic viral hepatitis ❖ Metabolic: hemochromatosis, Wilson disease, alfa-1-antitrypsin, NASH ❖ Prolonged cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis) ❖ Autoimmune diseases (autoimmune hepatitis) ❖ Drugs and toxins ❖ Alcohol
  • 5. Diagnosis of CLD ❖ Clinical : Stigmata of CLD ❖ CBC/ LFT : Hb/Platelets ,Bil/ low albumin , PT elevation, AST /ALT levels ❖ USG : Portal vein dia, Shrunken liver, splenomegaly ,ascites ❖ Fibroscan : Normal is between 2 to 7 kPa. ❖ A score of over 7.2 kPa indicates higher likelihood of significant fibrosis. ❖ A score over 14.5 kPa in someone with HCV/HIV coinfection indicates cirrhosis.
  • 6. USG features ❖ Shrunken liver, Nodular surface, Elevated caudate to right lobe ratio (> 0.73 has 99% specificity for cirrhosis) ❖ Portal hypertension : Distorted liver architecture, Regenerating nodules.- ❖ Distorted vascular channels Dilated MPV, Collaterals, Splenomegaly. ❖ Various doppler findings. Collateral veins , Gastroesophageal varices
  • 8. Anatomy of the portal venous system ❖ Portal pressure >15mm ❖ Hepatic venous portal gradient ❖ HVPG ,Invasive technique ❖ Routinely not advocated ❖ Anastomotic sites ….varices
  • 9. The Effect of The Liver Nodule
  • 10. Mechanism of Portal HTN ❖ Cirrhosis ❖ Resistance portal flow ❖ Mechanical : Nodules ❖ Dynamic : Nitric oxide
  • 11. 1.Varices ❖ Esophageal varices ❖ Fundal varices ❖ GOV1 F1, F2,F3 ❖ Rectal varices ❖ Ectopic varices
  • 12. Classification ❖ Grade I ❖ Grade II ❖ Grade III-IV ❖ Fundal varices ❖ F1,F2 ,F3
  • 13. Portal hypertensive Gastropathy ❖ Mild PHG : A mosaic-like pattern without other findings. ❖ Severe PHG : mosaic-like pattern with flat or bulging red or black-brown spots and/or active bleeding
  • 15. Glue injection in Fundal varices
  • 16. Management of variceal bleed ❖ Presents : Hematemesis/Melena /Occult blood positive /Iron def anemia ❖ O/E :Stigmata of CLD on clinical exam should clinch the diagnosis/Labs ❖ ABC, 2 IV Lines ,Type and crossmatch ❖ Blood @ 7gm/dl. Do not over transfuse -Target Hb 9gm/dl ❖ Platelet transfusion (platelet <50,000) Fresh frozen plasma (Correct Pt) , ❖ Antibiotics : Ceftriaxone 1gm OD X 7 Days ,Meta analysis 12 trials (N=1200)
  • 17. Management ❖ IV vasoconstrictors (Octreotide) 50 mcg bolus - continuous infusion of 50 mcg per hour and is also continued for 3-5 days ❖ Endoscopic therapy ❖ Banding ❖ Sclerotherapy but EVL preferred. ❖ Shunting , Surgical, T . I . P . S
  • 18. EVL
  • 19.
  • 20. Varices prevention ❖ Treat underlying disease ❖ Endoscopic banding protocol ❖ B-blockers : No contraindication . Dose : Upto 160 mg daily in patients without ascites or 80 mg daily in patients with ascites ❖ Shunt surgery (only if no cirrhosis) ❖ Liver transplantation
  • 22. Ascites ❖ Liver disease: cirrhosis ❖ Right sided heart failure ❖ Kidney disease (nephrotic syndrome) ❖ Low albumin (malnutrition, bowel loss) ❖ Peritoneal infection (TB…) ❖ Peritoneal cancer
  • 23. Clinical presentation ❖ History: Increased abdominal girth, Increased wt ❖ Physical exam: stigmata of CLD ❖ Bulging flanks,Shifting dullness ❖ Fluid wave
  • 24. Diagnosis ❖ Physical examination Ultrasound ❖ Ascitic tap :WBC (>250 PMN: SBP) ,RBC ❖ SAAG (serum albumin to ascitic fluid albumin gradient) ❖ >11 mg/dl : portal hypertension ❖ <11 mg/dl : Other
  • 25.
  • 26.
  • 27. Management ❖ Treat the underlying disease ❖ Salt restriction (<2gm/d) ❖ Diuretics Loop diuretic (Lasix) , Daily weight Target wt loss of 1 kgm daily ❖ Aldosterone inhibitor (Spironolactone) ❖ Up to 400 mg spironolactone and 160 mg furosemide per day
  • 28. Treatment resistant Ascites ❖ Recurrent tapping ❖ Peritoneal-venous shunt ❖ TIPS ❖ Liver transplantation
  • 29. Spontaneous Bacterial Peritonitis ❖ Infection of ascitic fluid ❖ Usually gram negative (E.Coli) , Secondary Peritonitis when to suspect ❖ Presentation variable : Pain abdomen , fever, deranged RFT, HE, ❖ Mortality is high ❖ Dx: ascitic tap = PMN>250 ❖ Treatment : Third generation cephalosporin IV, SBP prophylaxis for 5-10 days
  • 30. SBP ❖ IV albumin (1.5 g per kg body weight within six hours of diagnosis and 1.0 g/kg body weight on day three) - 30-40% Develop Renal failure ❖ Albumin infusion should be given if the creatinine is >1 mg/dL ,Total bilirubin is >4 mg/dL ❖ Once renal failure :Octreotide and midodrine may be helpful, in addition to infusion of 25 grams of 25 percent albumin daily, unless there is massive fluid overload.
  • 31. 3. Hepatic Encephalopathy ❖ Reversible decrease in neurological function secondary to liver disease ❖ Acute: seen with acute liver failure ❖ Acute on chronic: established cirrhosis
  • 32.
  • 33. Clinical features of hepatic encephalopathy ❖ Reversal of sleep pattern ❖ Disturbed consciousness ❖ Personality changes ❖ Intellectual deterioration ❖ Fetor hepaticus ❖ Asterixis , Fluctuating
  • 35. Diagnosis ❖ Clinical (most important) ❖ The drawing tests ❖ EEG ❖ CT/MRI may show cerebral atrophy
  • 36.
  • 37. Management ❖ Identify and treat precipitation factor ❖ Treat underlying liver disease ❖ Stop Beta blockers ❖ Antibiotics (Rifaxamin, metronidazole) Inj.Cefotaxime 2gm IV 8 hrly ❖ Lactulose till diarrhea sets in via NG tube ❖ Transplantation.
  • 38. SBP Prophylaxis ❖ GI bleeding. ❖ Patients who have had one or more episodes of SBP. Recurrence > 70 percent ❖ Ascitic fluid protein is <1.5 g/dL +impaired renal function or liver failure.(C ≥1.2 BUN ≥25 mg/dL ,Na = ≤130 mEq/L .Liver failure CTP ≥9 and a bilirubin ≥3 mg/dL. ❖ CLD hospitalized for other reasons As protein < 1 g/dL (10 g/L). ❖ Cipro 500mg /OD , Norflox 400 mg OD/ Septran DS OD
  • 39. Hepatorenal Syndrome ❖ Progressive renal failure ❖ Type 1 : rapidly progressive, high mortality ❖ Type 2: slower progression ❖ R/O volume depletion secondary to diuretics ❖ IV vasoconstrictors ❖ Liver transplantation
  • 40. Complications of CLD ❖ Hepatic hydrothorax ❖ Hepatopulmonary syndrome ❖ Portopulmonary hypertension ❖ Cirrhotic cardiomyopathy ❖ Portal cholangiopathy
  • 41. HCC ❖ Treatment of chronic HBV , HCV underlying cause of CLD ❖ 6 monthly USG & AFP levels AFP> 500 µ/L diagnostic ❖ AFP elev: Pregnancy ,Tumors of gonadal origin ❖ Sensitivities of US, CT, and MRI 46%, 65%, and 72%, respectively. ❖ Resection of lesions < 5cms without vascular invasion ❖ TACE, RFA , OLT ,Tyrosine kinase inhibitor (TKI) sorafenib Advanced HCC
  • 42. Take home message ❖ Mechanical compression of blood flow plus hemodynamic changes leads to portal hypertension ❖ Common complications of portal hypertension are: ❖ Collateral formation (Varices) ❖ Ascites ❖ Hepatic encephalopathy
  • 43. Take home message ❖ The most important step in variceal bleed management is resuscitation ❖ The most important step in management of hepatic encephalopathy is the identification of the precipitating factor

Editor's Notes

  1. The use of a beta blockers alone reduces the risk of rebleeding and of death due to rebleeding. In a meta-analysis of 19 trials including 1050 patients with variceal bleeding, use of a beta blocker resulted in lower rates of rebleeding (37 versus 58 percent) and of death from rebleeding (9 versus 15 percent) compared with placebo or control group
  2. Child A 5-6 B 7-9 C 10-15 one-year survival rates for patients with Child-Pugh class A, B, and C cirrhosis are approximately 100, 80, and 45 percent, respectively
  3. The risk may be decreased with an infusion of intravenous albumin (1.5 g per kg body weight within six hours of diagnosis and 1.0 g/kg body weight on day three) [30]. Albumin infusion should be given if the creatinine is >1 mg/dL (88 micromol/L), the blood urea nitrogen is >30 mg/dL (10.7 mmol/L), or the total bilirubin is >4 mg/dL (68 micromol/L) [31]. Once renal failure has developed, treatment with a combination of octreotide and midodrine may be helpful, in addition to infusion of 25 grams of 25 percent albumin daily, unless there is massive fluid overload.