Liver Cirrhosis
Defined anatomically as a diffuse process with fibrosis and nodule formation.
Child –Turcotte-Pugh classification
Clinical parameter
1
--to access severity.
2
3
Bilirubin(mg/dl)
<2
2-3
>3
Albumin (g/dl)
> 3.5
Ascites
None
Encephalopathy(grade)
None
1-2
3-4
PT (sec prolonged)
<4
4-6
>6
OR INR
< 1.7
1.7 - 2.3
> 2.3
Prognosis
Good
2.8 - 3.5
Easily controlled
< 2.8
Poorly controlled
Fair
poor
Class A => 5 - 6, B = >7 - 9, C = >10-15
Symptoms:fatigue, weight loss, anorexia, leg swelling, hemorrhage (nose, gum, GI
tract), any Hx of jaundice, hepatitis, drug ingested, blood transfusion in the past and
alcohol consumption.
Signs
1. Skinvascular spider, purpura,
2. Eyejaundice, K-F ring, anemia
3. Bodygynaecomastia, testicular atrophy, distribution of body hair.
4. ExtremitiesDupuytren’s contracture, palmar erythema, nail changes (clubbing,
white nails), peripheral edema.
5. Abdomenascites, dilated veins, liver, spleen enlargement.
6. Neurohepatic encephalopathy, fetor hepaticus, flapping tremor.
Diagnosis
1. Anemia (microcystic due to blood loss, macrocystic due to folate deficiency),
pancytopenic ( hypersplenism), prolong PT (INR)
2. Biochemistry- elevated Bilirubin, GOT/GPT, ALK-P, reversed AG ratio, low
immunoglobulin, hyponatremia, hypokalemic alkalosis.
3. Etiology ; HBV, HCV marker, AFP, smooth muscle, mitochordrial and nuclear
antibodies, ceruloplasmin, α1 antitrypsin
4. Endoscopy.(for EV)
5. Hepatic echo , CT
6. Definitive diagnosisliver biopsy.
Prognosis factors
1. Aetiology ( alcohol is best)
2. Decompensation due to hemorrhage, infection and alcohol, better.
3. The response to therapy.
4. Jaundice ( esp; persistent)
5. Neurological complication
6. Liver size (large liver better- more functioning cells)
7. Portal venous pressure
8. EV bleeding
9. Biochemical test ( albumin< 2.5, Na+ < 120, )
10. Persistent hypotension ( SBP < 100)
11. Hepatic histological change
 Major Complication of Cirrhosis
• Portal hypertension ( < 60% of patients, > 10 mmHg) presenting as variceal
bleeding, hypersplenism
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Ascites
Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatopulmonary syndrome
Hepatocellular carcinoma
Ascites
Accumulation of fluid within the peritoneal cavity.
Symptoms:distended abdomen, fullness sensation, and other symptoms of cirrhosis
(above).
Signs:protruded abdomen, fluid thrill, associated with scrotal edema, umbilical or
inguinal herniation, pleural effusion esp; at RT side ( hepatic hydrothorax) and other
signs of cirrhosis (above).
Laboratory: check serum Na+, K+, HCO3─, CL─, urea, creatine, 24 hr urine volume
and Na+ excretion.
Diagnostic paracentesis: protein, albumin, glucose, cell count and differential,
culture, cytology. In selected case may need to check amylase, LDH, triglycerides, TB
culture.
Treatment
1. General Measurement of Ascites
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Education for dietary salt ( 2Gm/d = 88mmol/d )
Fluid restriction of 1- 1.5L if hyponatremia.
Bed rest
Check serum - urinary electrolyte and renal function.
Weigh daily,
Measure urinary volume.
• Sample ascites
• Spironolactone 100-200 mg/day
• After 4 days consider to add furosemide 40 g/d (100mg: 40 mg ratio) to Mx400mg: 160 mg, ** check electrolyte.
• Stop diuretic if pre-coma (flap) akalosis, azotemia or decrease K+
• Continue monitor weight, increase diuretics as necessary.
• Albumin supply
2. Tense ascites
Large volume paracentesis and supply I.V salt poor albumin- 6-8 gm/L removed
ascites.
Patient selection:
Child’s B, PT – normal, Platelets > 40x103/mm3,
Serum creatinine < 3 mg/dl, urinary Na + > 10 mmol/d
3. Refractory ascites
Serial therapeutic paracentesis, TIPS, peritoneovenous shunt and liver transplant.
Goal of Treatment
• To increase urinary excretion of Na + > 80mmol/d
• Random spot urine Na + concentration is > K + concentration can correlates
with a 24 hr Na + excretion > 78 mmol/d with approximately 90% accuracy.
Spontaneous Bacterial Peritonitis
-Suspect Grade B and C cirrhosis with ascites.
-Clinical feature may be absent and WBC may be normal.
-Ascites protein usually < 1 g/dl.
-Others ; sudden rise of fever, chill, generalizes abdominal pain with rebound
tenderness and progress of hepatic encephalopathy.
Diagnosis
Ascites fluid neutrophil count > 250 /mm3
Positive blood culture(E-coli, pneumococcus, streptococcus, Klebsiella)
Treatment
-Cefotaxime 2 G q 8H 5 days followed by more narrow spectrum therapy after
susceptibility results are available.
-Prophylaxis with Norfloxacin 400 mg PO qd 5 days a week or Cipro 50 mg PO once
a week.
Hepatic Encephalopathy
 A state of disordered CNS function associated with severe acute or chronic liver
disease; may be acute and reversible or chronic and progressive.
Clinical features
Stage 1: euphoria or depression, slurred speech, disordered sleep, asterixis (flapping
tremor), mild confusion.
Stage 2: lethargy, moderate confusion.
Stage 3: marked confusion, sleeping but arousable, inarticulate speech.
Stage 4: coma.
Differential diagnosis :
1. Alcohol related (intoxication, withdrawl)
2. Drug toxicity (sedatives or psychoactive drugs)
3. Infections ( sepsis, meningitis, encephalitis)
4. Intracranial lesions ( CVA, abscess, tumor)
5. Metabolic ( DKA, electrolyte imbalance, hypoglycemia, uremia)
6. Neuropsychiatric disorders
 Factors That May precipitate Hepatic Encephalopathy in Cirrhosis
Nitrogenous Encephalopathy
Non-nitrogenou Encephalopathy
1.
2.
3.
4.
5.
6.
7.
8.
Uremia/azotemia
GI bleeding
Dehydration
Metabolic alkalosis
Hypokalemia
Constipation
Excessive dietary protein
Infection
1.
2.
3.
4.
5.
Sedatives, benzodiazepines
Barbituates
Hypoxia, hypoglycemia
Hypothyroidism
Anemia
 Treatment of Hepatic Encephalopathy
1. Identify and correct the precipitating causes
a. Access volume statue and vital sign
b. Evaluate GI bleeding
c. Eliminate sedatives. tranquilizers or similar drugs
d. Perform screening test for hypoxia., hypoglycemia, anemia, hypokalemia, and
other possible metabolic or endocrine factors and correct as indicated.
2. Initiate ammonia –lowering therapy
a. NG lavage,
b. lactulose enema—100 ml in water or N/S 100 – 200 ml (retension enema)
oral—20 – 40 ml qid (at least 2 - 4 bowel movement/day)
c. Minimize or eliminate dietary protein
d. Oral non –absorbable antibiotic to reduce intestinal bacterial counts.
- Neomycin (1 – 3 g /day) or Metronidazole (250 mg qid/day)
e. Consider flumazenil or other benzodiazepine receptor antagonist
3. Minimize the potential complications of cirrhosis and depressed consciousness
a. Provide supportive care with protect airway, hemodynamic and metabolic status.
Hepatorenal syndrome
A progressive functional renal failure that occurs in patients with severe liver disease.
Clinical features
worsening azotemia, hyponatremia, progressive oliguria with urinary Na +
concentration < 10 mmol/L, hypotension which lack of response to volume challenge.
Precipitating factors
GI bleeding, excessive diuresis, paracentesis, or drugs (NSAID, ACEI,
aminoglycosides).
Treatment
1. Effective  liver transplantation.
2. Symptomatic  correct underlying or precipitating factors as much as possible.
(Volume challenge, stop NSAID).
Hepatocellular carcinoma
An epithelial tumor arising from malignant transformation of the hepatocyte. It is the
most common primary malignancy of the liver.
Symptoms: abdominal pain, weight loss, abdominal swelling, weakness, jaundice.
Signs: hepatomegaly, splenomegaly, hepatic bruit, ascites, jaundice.
Laboratory: usually reflect with underlying chronic liver disease, raised Alk-P and
AFP.
Imaging:
Abdominal US, CT, MRI, angiography, laparoscopy, biopsy.
Risk factors
1. Major chronic HBV and HCV infection, cirrhosis, aflatoxin B.
2. Minor OC pills, smoking, Wilson’s disease, hemochromatosis, α1
antitrypsin deficiency.
Treatment:
Choice of a particular therapy must be individualized because no single therapy has
emerged as a treatment of choice.
1.
2.
3.
4.
Surgery (offers best chance of cure)
Liver transplantation
TAE ( trans arterial embolization)
US-guided PEI (percutaneous ethanol injection), PAI (percutaneous acetic acid
injection) and RFA (radiofrequency ablation).
5. Chemotherapy.
6. Radiation