Chronic liver disease (CLD) can result from a wide range of causes like viral hepatitis, alcohol use, autoimmune conditions, and genetic disorders. Common complications of CLD include portal hypertension, which can lead to gastroesophageal varices and ascites. Ascites, the accumulation of fluid in the abdominal cavity, is diagnosed through physical examination, ultrasound, and abdominal paracentesis. Spontaneous bacterial peritonitis is a frequent complication of ascites and occurs when ascitic fluid becomes infected without an evident source. Treatment involves antibiotics and monitoring for circulatory dysfunction following paracentesis.

1. Chronic liver Disease (CLD)
Andualem F. (MD)

2. CLD
• Chronic liver disease encompasses a wide
spectrum of disorders, including infectious,
metabolic, genetic ,drug-induced , idiopathic,
structural, and autoimmune diseases.
• It includes: A. Chronic Hepatitis
B .Cirrhosis
C.Hepatocellular Carcinoma
3/5/2018 2Andualem Firdie (MD)

3. CAUSES OF CLD
1.Viral(most common)
A. Hep. B-likelihood of chronicity after acute hepatitis
B.Hep.B + delta virus
C.Hepatitis C- >85% to chronic hepatis
-20-30% to cirrhosis
- 15% to HCC
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4. 2.Alcoholic Liver Diseas
(1) fatty liver,
(2) alcoholic hepatitis, and
(3) cirrhosis
• Quantity and duration of alcohol intake are the most
important risk factors involved in the development of
alcoholic liver disease
• The threshold for developing alcoholic liver disease
• Management;
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5. 3.Autoimmune Hepatitis
Diagnostic Criteria
• Exclusion other causes of liver disease .
• predominantly young to middle-aged women
• predominant aminotransferase elevation
• concurrent other autoimmune diseases
• with marked hyperglobulinemia and high-titer
circulating ANA
• and other autoantibodies;
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6. 4.Toxic and Drug-Induced Hepatitis
Dose dependant
• direct toxic hepatitis occurs
• More frequent
• predictable
• dose-dependent.
• The latent period is usually
short
Acetaminophen ,Carbon
Tetrachloride ,Oral
Contraceptive Agents,
idiosyncratic drug reactions
• idiosyncratic drug reactions
• Infrequent occurrence
• unpredictable;
• not clearly dose-dependent
• liver injury may occur at
any time during or shortly
after exposure to the drug
• isoniazid, valproate,
phenytoin,.halothene
methyldopa amiodarine
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7. 5.inherited metabolic liver diseases
hemochromatosis,
Wilson's disease,
1 antitrypsin (1AT) deficiency
cystic fibrosis (CF).
6.,biliary cirrhosis
primary biliary cirrhosis (PBC),
autoimmune cholangitis (AIC),
primary sclerosing cholangitis (PSC),
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8. Clinical History
• Fatigue is the most common and most characteristic
symptom of liver disease
• Arthralgia ,myalgia
• Loss of appetite,aversion to food ,nausea,vomiting.wt loss
• Low grade fever
• Dark urine and clay colored stool
• Jaundice
• Right upper quadrant discomfort or ache ("liver pain")
• Splenomegally and cervical LAP
• Itching
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9. Major risk factors for liver disease
• alcohol use,
• medications including herbal compounds, birth control pills,
and over-the-counter medications),
• sexual activity,
• travel,
• exposure to jaundiced or other high-risk persons,
• injection drug use
• transfusion with blood and blood products,
• occupation,
• accidental exposure to blood or needlestick, and
• familial history of liver disease
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10. Complications
• Abdominal distention,leg swelling
• GI bleeding
• Altered mentation,hepatic encepalophaty
• Respiratory symptoms hepato pulmonary
syndrome
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11. Physical Examination
• HEENT; sclera ,conjuctiva,fetor hepaticus,
• LGS; LAP,parotid enlargment,testicular
atophy,gynecomastia
• RS; signs for HPS,pleural effusion
• ABDOMINAL; ascites ;hepetosplenomagally,distended
viens
• MSS; muscle wasting,pedal edema
• INTEGUM; axillary hair loss,pamar erythema,spider
angiomata,pallor,excoration
• CNS; mental status,astrexis
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12. INVESTIGATIONS
• ALT,AST
• Bilirubin
• Serum albumin
• ALP
• PT,PTT,INR
• RFT
• HBSag
• Anti HBSag
• CBC
• UA
• Abdominal US
• Paracentesis
• Upper GI endoscopy
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13. Complications of CLD
1.Portal hypertension
 Gastroesophageal varices
 Ascites
 Spontaneous bacterial
peritonitis
 Splenomegaly,
hypersplenism
2.Hepatic encephalopathy
3.Hepatorenal syndrome
4.Hepatopulmonary
syndrome
Others
• Malnutrition
• Coagulopathy
• Hematologic
abnormalities
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14. Ascites
Def.Ascites is the accumulation of f luid with in the
peritoneal cavity
Pathogenesis
 increased portal pressure increased
hydrostatic pressure
 hypoalbuminemia decreased oncotic pressure
 RAAS activation hyperaldosteronism
 hepatic lymph oozing
DIAGNOSIS —a physical examination
,ultrasonography and Abdominal paracentesis
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15. ABDOMINAL PARACENTESIS
Indications:
– New onset ascites
– Hospitalization of a patient with ascites
– Clinical deterioration of an inpatient or outpatient
with ascites
Ascitic Fluid Analysis……… we see the f/f;
A.Appearance; straw (Clear), chylous( Milky), hgic,
Turbid or cloudy,green
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16. B. Serum-to-ascites albumin gradient
C. Total protein
D. Cell count and differential
E. Cultures
F.Gram stain,AFB
G. Glucose
H. LDH
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17. Ascites Grading
• Grade 1 – mild ascites detectable only by
ultrasound examination
• Grade 2 – moderate ascites manifested by
moderate symmetrical distension of the
abdomen
• Grade 3 – large or gross ascites with marked
abdominal distension.
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18. Management
Goal of the treatment;
To lose no more than 0.5kg/day for a
patient with ascites alone.
 No upper limit for those with periphera
edema
A. Grade 1
 Salt restriction to 1g/day
 bed rest
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19. Diuretics
A. Spironolactone
Start with initial dose 100mg/day escalate the dose a
maximum dose of 400mg/day
B. Fruesmide added
start with initial dose of 40mg/day and escalate up
to a maximum dose of 160mg/day.
If not responsive consider
 Repeated large-volume paracentesis( 4-6 l over 1-
2hr) +Albumin 6gl of removed fluid
 Trans jugular Intrahepatic Porto systemic Shunt
(TIPS)
 Liver Transplantation
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20. Complication-postparacentesis circulatory dysfunction
Monitor;
Vital signsS
The body weight,
 Urine outPut
 Electrolyte.
Watch out for azotemia, volume deplation
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21. Spontaneous bacterial peritonitis SBP
Is Spontaneous infection of ascitic fluid without
an intra-abdominal source.
pathogenesis–
Bacterial translocation and hematogenous
route
Etiology :Escherichia coli and other gut
bacteria;
gram-positive bacteria, including
Streptococcus viridans, Staphylococcus
aureus, and Enterococcus sp., can also be3/5/2018 21Andualem Firdie (MD)

22. Clinical manifestation
fever, abdominal pain and tenderness ,diarrhea ,
worsening of jaundice , encephalopathy or
they may present without any of these features.
Therefore, it is necessary to have a high degree of
clinical suspicion
Diagnosis
Positive ascitic fluid bacterial culture and
Elevated ascitic fluid absolute PMN count ≥ 250
cells/mm3
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23. Spontaneous bacterial
peritonitis
 without an intra-
abdominal source.
 protein concentration
less than 1 gm/dL has
the highest risk for SBP
 The glucose
concentration generally
remains above 50
mg/dL
 LDH less elevated
secondary bacterial
peritonitis
 with an evident
intraabdominal source
of infection .
 Total protein
concentration >1 g/dL
 Glucose concentration
<50 mg/dL
 LDH greater than the
upper limit of normal
for serum
3/5/2018 23Andualem Firdie (MD)

24. Variants of SBP
Variant Ascitic fluid culture Absolute PMN per mm3
Spontaneous bacterial
peritonitis
Positive ≥250
Culture-negative neutrocytic
ascites
No growth ≥250
Monomicrobial non-
neutrocytic bacterascites
(single organism)
Positive <250
Polymicrobial bacterascites Positive <250
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25. Antibiotic
Cefotaxime or
similar3-rd generation cephalosporin
Ceftriazone 1g IV BID for 5-7 days
ciprofloxacin
Ampicillin plus gentamicin
We also generally repeat a paracentesis after 48 hours of
treatment if there is clinical suspicion of secondary
peritonitis.
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26. Prophylaxis :
Indications
 history of SBP
an ascitic protein concentration <1.5 g/dL
gastrointestinal bleeding
Drugs
 norfloxacin 400 mg/day
ciprofloxacin 750 mg once q wk
trimethoprim-sulfamethoxazole 960mgday
3/5/2018 26Andualem Firdie (MD)