Chronic liver disease pdf - سمنارات كروب C

Chronic liver Diseases

Supervised By

Dr. Ismael dawood saeed

What is Cirrhosis???

• Cell necrosis

• Fibrosis

• Nodules formation

• Loss of normal architecture

CAUSES OF CIRRHOSIS

???

1. Alcohol

2. Chronic viral hepatitis Bor C

3. Non-alcoholic fatty liver disease

4. Immune

Primary sclerosing cholangitis

Autoimmune liver disease

5. Biliary

Primary biliary cirrhosis

Cystic fibrosis

Genetic

Haemochromatosis

-antitrypsin deficiency

Wilson's disease

7. Cryptogenic (unknown)

8. Drugs

amiodarone, methyldopa, methotrexate

The Approach to a patient with cirrhosis

• History

• Physical examination

• Investigations

• Management & follow-up

History of the present illness and review of other systems

• asymptomatic !!! Or non-specific symptoms : weakness,

fatigue, muscle cramps, weight loss, anorexia, nausea,

vomiting and upper abdominal discomfort “

Compensated

”

• Symptoms of

“decompensation”

: abdominal distension,

coffee-ground vomiting and/or black tarry stool

“melaena”,bleeding from the nose, menorrhagia, altered

mental status, lower extremity swelling, jaundice, and

pruritus.

• Other less common symptoms : SOB

Past medical history

•

Jaundice (very important!!!)

•

chronic liver disease.

•

metabolic syndrome (diabetes, dyslipidaemia, obesity, HTN)

•

autoimmune disorders.

•

blood transfusion

Past surgical history

•

Previous operations and dental procedures

Drug history

• Medications with hepatotoxic effects.

• Over-the-counter medications, vitamins, and herbal and dietary

supplementation

Social history

• alcohol history

• intravenous drug use

• unprotected intercourse

• tattoos.

• Sharing of toothbrushes

Family history

• Haemochromatosis.

• Wilson's disease.

• Alpha-1 antitrypsin deficiency.

General examination

Head and neck

• Spider naevi

• Yellowish discoloration of sclerae

• Skin pigmentation

• Parotid gland swelling

• Bruising

• Epistaxis

• Bluish discoloration of lips

and mucous membrane

General examination

Upper limbs

• Palmar erythema

• Leukonychia (white nails)

• Finger clubbing

• Flapping tremor

• Spider naevi

• Bruising

• Dupuytren contracture

General examination

Limbs

Lower

• Bilateral pitting edema

• Loss of hair

Chest examination

• Gynaecomastia and loss of secondary sexual hair in

men

• Breast atrophy in women.

• Spider naevi

Abdominal examination

• Generalized Abdominal distension (especially in the flanks) ,shifting

dullness , transmitted thrill

• Caput Medusae

• Hepatomegaly

???

• Splenomegaly

• Bruising

• Loss of secondary sexual hair and testicular atrophy in men.

•Blood tests :

Full blood count , B suger ,B.uria, S.creatinin ,S. Electrolytes.

•Liver Function Test :ALT, AST, ALP, S.Bilirubine ,S.Albumin , PT
• U\S of liver ,Biliary Passage ,abdomen
•Liver Biopsy Gold stander
•Investigation of the Cause :viral study ,Haemochromayosis ,
•Investigation of complication : Ascites ,portal hypertension,hepatic
encephalopathy , renal failure, liver cancer

Lifestlyle and diet modifications (avoid alcohol,

avoid hepatotoxic drugs, limit salt ….etc).

treat underlying cause

3Treat complications ( ascites, esophageal varices ,
hepatic encephalopathy ….etc).

4regular screening for esophageal varices and

hepatocellular carcinoma

5Liver transplantation

???

Liver transplantation

Indicted in :

 Sign of liver failure
 First episode of bacterial pertonitis
 Diuretic resistant Ascites
 Recurrent variceal bleeding
 Liver cancer less than 5 cm
  persistent hepatic encephalopathy

Liver transplantation

contraindication

 sepsis
 Extrahepatic malignancy
 Active Alcoholic or substance misuse
 Cardiopulmonary dysfunction

• Portal hypertension develops when there is

elevation of portal pressure greater than 12
mmHg, while normal portal pressure is 5 –
10mmHg.

Portal hypertension

Features

In abdominal examination you may see

this

• Clinical

• CBC : pancytopenia

• endoscopy.

• Abdominal imaging, either by CT or MRI can

be helpful in demonstrating a nodular liver
and in finding changes of portal hypertension
with intraabdominal collateral circulation.

Diagnosis

• Treat the cause !

• Gastroesophageal variceal hemorrhage is the

most dramatic and lethal complication of
portal hypertension; therefore, Medical care
includes emergent treatment, primary and
secondary prophylaxis, and surgical

intervention

• Pharmacologic therapy Includes the use of

beta-blockers, most commonly propranolol
and nadolol

Treatment

• Endoscopic procedures such as sclerotherapy

and variceal ligation can be used to prevent
the recurrence of variceal hemorrhage.

Complications of this procedure ?

Now what if the patent presented with

Ascites

Ascites is usually diagnosed clinically or by ultrasound

New development of ascites in a cirrhotic patient does not

routinely require paracentesis only if :

1 General condition deteriorates.

2 In presence of unexplained fever, abdominal pain,

encephalopathy.

3 Admission to hospital for any cause (SBP.)

4 Laboratory investigations indicating infection:

- Leucocytosis

- Acidosis

- Worsening of renal functions

Paracentesis

• Serum-ascites albumin gradient

(SAAG) = serum albumin - ascitic fluid albumin.

If > 1.1 g/dL, the patient has PH-related ascites.

If < 1.1 g/dL (about 97% accurate), the patient does

not have PH-related ascites.

The SAAG does not need to be repeated after the initial

measurement.

•

Bed Rest

Not recommended

• Bed rest promote muscle atrophy and other

complications and extends hospital stay

Treatment

• Restriction of dietary Na to 80 mmol/day (no

adding table salt.)

• If there is severe ascites we should restrict Na

to (40 mmol/day) and should avoid drugs
cause salt retention like

NSAIDs

• Restriction of water to about 0.5-1 L/day

which is important especially when Na fall
below 125 mmol/L (because dilutional
hyponatremia may occur.)

• Diuretic treatment: the best one is

spironolacton in (100-400mg/day). Side
effects are painful gynecomastia &
hyperkalemia

• Paracenthesis (aspiration of fluid LVP): 3-4 L

can be taken over 1-2 hours specially in
emergency to relieve the patient distress

• common and severe complication of ascites

• occurs in the absence of a visceral perforation and in

the absence of an intraabdominal inflammatory focus

• Its usually monomicrobial infection the presence of

more microorganisms in the culture (>1), must raise
the suspicion of secondary peritonitis

• The most common organisms are

Escherichia coli

and

other gut bacteria; however, grampositive bacteria,
including

Streptococcus viridans, Staphylococcus

aureus

, and

Enterococcus

sp., can also be found.

Spontaneous Bacterial Perotonitis

• Approximately 10% of the patients with SBP

are asymptomatic

• usually non specific symptoms

• The most frequently encountered symptoms

and signs are fever (69%), abdominal pain
(59%), signs of hepatic encephalopathy,
abdominal tenderness (very rare), diarrhoea,
ileus, shock and hypothermia.

Features

• The SBP diagnosis is established by analysis of

the ascitic fluid obtained at paracentesis.

• Paracentesis should be avoided only in case of

a suspicion of fibrinolysis or DIC

Diagnosis

• From the ascitic fluid a series of tests can be

performed, mandatory even in the case of a
therapeutic paracentesis

leucocyte count , serum and ascitic fluid

albumin levels

• SBP is suspected when the PMN number in

the ascitic fluid is over 250/mm 3

• .After paracentesis, the ascitic fluid should be

inoculated immediately (at the patient‘s
bedside) into blood-culture bottles (10ml in
each bottle). Using these recipients instead of
the usual ones increases the diagnosis rate of
ascites with neutrophils from 50 to  80%

• Immediate use of broad spectrum antibiotic

such as Cefotaxim

Treatment

There are three categories of cirrhotic patients
which are more at risk of developing SBP:
patients with digestive hemorrhage;

patients with ascitic fluid protein level less than

patients who survived a prior SBP episode.

Prevention

• For those who have low protein level >>> give

Norfloxacin is administrated during
hospitalization

• Patients with digestive hemorrage 20% of

them have SBP at admission and 30-40% will
develop an infection during hospitalization.
These patients will receive 800 mg/ day
Norfloxacin through the nasogastric tube for 7
days

• In patients who survive an episode of SBP, a

long term prophylactic treatment (for
preventing recurrence) with Norfloxacin 400
mg/day will be administered.

Hepatorenal Syndrome

There are two
types

• Type 1 hepatorenal syndrome is characterized by

progressive oliguria, a rapid rise of the serum
creatinine and a very poor prognosis (without
treatment, median survival is less than 1
month.)

• There is usually no proteinuria, a urine sodium

excretion of less than 10 mmol/day

• Type 2 hepatorenal

yndrome usually occurs

in patients with refractory ascites, is
characterised by a moderate and stable
increase in serum creatinine, and has a better
prognosis.

• Tarlipressin

• Live transplantation is the treatment of choice

even after improvement in renal fuction since
prognosis is soo poor

Treatment

• alteration in mental status and cognitive

function

• occurring in the presence of liver failure

Hepatic encephalopathy

HEPATICUS

• H

aemorrhage

• E

lectrolye imbalance

• P

rotein

• A

lcohol/ Analgesics

• T

rauma

• I

nfxn

• C

onstipation

• U

raemia

• S

urgery (post systemic shunt)

Triggers

• Features of alterned mental state , personality

• Emotions and consciousness

• Convusion sometimes occur

In Examination

Fetor hepaticus , sweet musty breath odor
Asterixis

Hyperreflexia and bilateral planter response

Features

• Lactuloses: The goal of lactulose therapy is to

promote 2–3 soft stools per day.

• Antibiotics

Drugs like neomycin

• Change diet habit

• Skip

alcohol

: Even a little bit can be risky

• Stop some medications

Treatment