10.Cirrhosis and treatment
Transcript of 10.Cirrhosis and treatment
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CIRRHOSISCIRRHOSIS
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Destruction of Regeneration of
liver cells liver cells
Fibrosis Noduleformation
Loss of normal architecture
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DiagnosisDiagnosis
Clinical featuresClinical features
Laboratory testsLaboratory tests
Imaging (US, CT, MRI)Imaging (US, CT, MRI) -- increasing roleincreasing role
OGD to detect evidence of portalOGD to detect evidence of portalhypertensionhypertension
Tests to detect aetiologyTests to detect aetiology
HistologyHistology ± ± not always requirednot always required
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CT scanningCT scanning ± ± cirrhosis of the liver cirrhosis of the liver
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OGD - oesophageal varices
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Aetiology Aetiology
Alcohol Alcohol
Chronic HBV and HCVChronic HBV and HCV
NonNon-- Alcoholic Steatohepatitis (N ASH) Alcoholic Steatohepatitis (N ASH)
Drugs and toxinsDrugs and toxins -- methotrexate, IN AH, antimethotrexate, IN AH, anti--psychotics methyldopa,psychotics methyldopa,
MetabolicMetabolic -- haemachromatosis, Wilson¶shaemachromatosis, Wilson¶s
disease,disease, EE1 anti1 anti--trypsin deficiencytrypsin deficiency
MiscellaneousMiscellaneous -- Biliary cirrhosis, ICCBiliary cirrhosis, ICC
CryptogenicCryptogenic
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Dynamic situation of hepatic necrosis,Dynamic situation of hepatic necrosis,fibrosis and regenerationfibrosis and regeneration
Regeneration > necrosis and fibrosis:Regeneration > necrosis and fibrosis:COMPENS ATED CIRRHOSISCOMPENS ATED CIRRHOSIS
Necrosis and fibrosis > regeneration:Necrosis and fibrosis > regeneration:
DECOMPENS ATED CIRRHOSISDECOMPENS ATED CIRRHOSIS[further reading: Child[further reading: Child--Pugh score]Pugh score]
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DecompensatedDecompensatedcirrhosiscirrhosis
Compensated cirrhosisCompensated cirrhosis
Features of chronic liverFeatures of chronic livercell failure and portalcell failure and portal
hypertensionhypertension
Abnormal LFT Abnormal LFT
-- Bilirubin elevatedBilirubin elevated
-- Albumin reduced Albumin reduced
-- PT elevatedPT elevated
Few clinical features (eg:Few clinical features (eg:hepatomegaly only)hepatomegaly only)
LFT minimally deranged andLFT minimally deranged andstablestable
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Decompensated cirrhosisDecompensated cirrhosis
Liver cellLiver cell
failurefailure
Portal hypertensionPortal hypertension
Ascites Ascites (SBP)(SBP)
Oesophageal & gastricOesophageal & gastric varicesvarices(haemorrhage)(haemorrhage)
SplenomegalySplenomegaly (hypersplenism)(hypersplenism)
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Liver cell failureLiver cell failure
Failure of the liver to perform its functionsFailure of the liver to perform its functions
usually leading to impairment of consciousnessusually leading to impairment of consciousness
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AetiologyAetiology
Acute diseases of the liver Acute diseases of the liver
Viral hepatitis / alcoholic hepatitis Viral hepatitis / alcoholic hepatitis
LeptospirosisLeptospirosis
Paracetamol overdoseParacetamol overdose Acute fatty liver of pregnancy Acute fatty liver of pregnancy
Fulminant Hepatic Failure (FHF) whereFulminant Hepatic Failure (FHF) whereonset of onset of encephalopathy is rapid andencephalopathy is rapid andspontaneous (v. poor prognosis)spontaneous (v. poor prognosis)
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AetiologyAetiology
Chronic diseases of the liver Chronic diseases of the liver
CirrhosisCirrhosis
Chronic active hepatitisChronic active hepatitis
Some factor precipitates hepaticSome factor precipitates hepaticencephalopathy / decompensationencephalopathy / decompensation
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1. Increased protein load (diet, GI bleed)
2. Electrolyte imbalance (dehydration,starvation, diuretics, paracentesis)
3. Drugs (sedatives, hepatotoxic drugs)
4. Alcohol binges
5. Infection (eg: SBP)
6. Constipation - ? more time for bacteria
to act on intestinal contents
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Clinical featuresClinical features
1 Jaundice1 Jaundice -- poor uptake, conjugation,poor uptake, conjugation,
excretion of bilirubinexcretion of bilirubin ± ± hepatocellular hepatocellular
jaundice jaundice
2 Ascites and hepato-renal syndromemainly due to portal hypertension +
hypoalbuminaemia
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3 Bleeding tendency3 Bleeding tendency
-- Reduced synthesis of clotting factorsReduced synthesis of clotting factorsii, vii, ix, x (vitamin K dependent)ii, vii, ix, x (vitamin K dependent)v, xi, xii, xiii, (vitamin K nonv, xi, xii, xiii, (vitamin K non--dep.)dep.)
- Production of abnormal clottingfactors - eg. Dysfibrinogenaemia
- Defective platelet function
- Reduced platelet count (lessproduction by bone marrow,sequestration in spleen)
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4 Endocrine and metabolic disturbances
- Hypoglycaemia, low serum cholesterol
- Osteomalacia / osteoporosis - #
- Hypogonadism- Reduced catabolism of oestrogen
- Reduced production of testosteroneimpotence, gynaecomastia, testicular atrophy, loss of
IIry
sexual characteristics, spider naevi, palmar erythema
- Altered drug metabolism ± drug toxicity
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5 Hepatic encephalopathy
Toxic substances from gut cause direct damage(eg. NH3) or act as false neurotransmitters
- EEG changes ± may be subclinical- Constructional apraxia
- Inverted sleep rhythm
- Flapping tremor - Confusion, drowsiness, convulsions, coma
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Treat / avoid cause if possible. eg.
Abstain from alcohol
Anti-viral drugs for HBV
Venesection for haemachromotosis Penicillamine for Wilson¶s disease
Treat decompensation Liver failure Portal hypertension
ManagementManagement of cirrhosisof cirrhosis
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Detect / prevent complications Clinical assessment
LFT, PT, FBC, creatinine, electrolytes - 3m
US abdomen and alpha-feto protein - 6m OGD - 12m
Liver transplantation
ManagementManagement of cirrhosisof cirrhosis
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Prognosis: ChildPrognosis: Child--Pugh scorePugh score
ScoreScore 11 22 33S. bilirubin (mg/dl)S. bilirubin (mg/dl) <2<2 22--33 >3>3
S. albumin (g/l)S. albumin (g/l) >35>35 2828--3535 <28<28
PT (sec. pr) / INRPT (sec. pr) / INR <4 / <1.7<4 / <1.7 44--6 / 1.76 / 1.7--2.32.3 >6 / >2.3>6 / >2.3
Ascites Ascites NoneNone MildMild MarkedMarked
EncephalopathyEncephalopathy NoneNone MildMild MarkedMarked
Score <7 = Child¶s grade 1, survival 15 - 20 yrs
7-9 = C grade 2, for liver transplantation evaluation
>9 = C Grade 3, survival < 1yr
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1 Mx of unconscious patient if appropriate
Nurse in semi-prone position, clear airway
NG tube
Bladder, bowel, skin care
2 Assessment V
ital functions Possible aetiology, ppt.ing factors avoid Basic investigations
ManagementManagement of liver failureof liver failure
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3 Reduce protein load and gut bacterial flora
Metronidazole 400mg tds or neomycin 1g 6H
Lactulose till BO and then ~20ml tds
Bowel washes or enemas if required Restrict oral protein intake
[If evidence of cerebral oedema: i.v. mannitol]
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4 Correct bleeding tendencyVitamin K, FFP, fresh blood, platelet
concentrates
5 Nutrition
~2000 cal/day (10% dextrose iv)
Vitamin and mineral supplements
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6 Correct / avoid risk factors
Avoid sedatives, diuretics, paracentesis
Try to reduce risk of GI bleeding: PPI
7 Management of ascites
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When a patient with portal hypertensionpresents with ascites
If there is evidence of encephalopathy
no active treatment as it will worsen HE
Exception: if there is acute distress
- Severe abdominal pain- Respiratory embarrassment
limited paracentesis (~500ml)
Management of ascites
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If there is no evidence of even early HE and
there is no acute distress
1. Restrict salt intake: 5g/day
2. Spironolactone: (aldosterone antagonist)25mg bd - double dose every 2-3 days.
Maximum dose 200mg bd
3. Add loop diuretic: Frusemide / AmilorideFrusemide 40mg/day to 80mg bd
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4. Monitor: weight, abdominal girth, UOP +
serum creatinine and electrolytes + look for early evidence of encephalopathy
If no response bad prognosis
5. Paracentesis: 5L/d
or more if intra-vascular
volume is maintained
eg: salt free albumin ±repeated paracentesis
often necessary
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If patient with ascites develops fever and/or abdominal pain probably SBP
Aspirate ascitic fluid (full report, culture)
Treatment with antibiotics: usually
cephalosporins or quinolones
[Further reading: Hepato-renal failure,
TIPPS, Liver transplantation]
6. Spontaneous Bacterial peritonitis