10.Cirrhosis and treatment

8/7/2019 10.Cirrhosis and treatment

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CIRRHOSISCIRRHOSIS



Destruction of Regeneration of

liver cells liver cells

Fibrosis Noduleformation

Loss of normal architecture





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



CT scanningCT scanning ± ± cirrhosis of the liver cirrhosis of the liver



OGD - oesophageal varices



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



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]



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



Decompensated cirrhosisDecompensated cirrhosis

Liver cellLiver cell

failurefailure

Portal hypertensionPortal hypertension

Ascites Ascites (SBP)(SBP)

Oesophageal & gastricOesophageal & gastric varicesvarices(haemorrhage)(haemorrhage)

SplenomegalySplenomegaly (hypersplenism)(hypersplenism)



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



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)



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



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



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



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)



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



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



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



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



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



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



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]



4 Correct bleeding tendencyVitamin K, FFP, fresh blood, platelet

concentrates

5 Nutrition

~2000 cal/day (10% dextrose iv)

Vitamin and mineral supplements



6 Correct / avoid risk factors

Avoid sedatives, diuretics, paracentesis

Try to reduce risk of GI bleeding: PPI

7 Management of ascites



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



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



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



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

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10.Cirrhosis and treatment