Ascites - Hepatic Encephalopathy - Gastroesophageal Varices – Spontaneous Bacterial Peritonitis (SBP) - Hepato renal Syndrome - Alcoholic Liver Disease

1. Ascites
Hepatic
Encephalopathy
Gastroesophageal
Varices
Spontaneous Bacterial
Peritonitis (SBP)
Hepato renal
Syndrome
Alcoholic
Liver Disease

2. Dr / Sayed Zaki 2
Ascites - Hepatic Encephalopathy - Gastroesophageal Varices –
Spontaneous Bacterial Peritonitis (SBP) - Hepato renal Syndrome - Alcoholic Liver Disease

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Variable Score
1 Point 2 Points 3 Points
Encephalopathy Absent Mild-moderate Severe to coma
Ascites Absent Slight Moderate
Bilirubin (mg/dL) < 2 2–3 > 3
Albumin (g/L) > 3.5 2.8–3.5 < 2.8
Prothrombin time (seconds
above normal)
1–4 4–6 > 6
 Scoring Systems for Severity of Liver Disease:
 Child-Pugh Classification of the Severity of Cirrhosis
Class A = total score of 5 or 6
class B = total score of 7–9
class C= total score of 10 or more.

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5.  Free fluid in the abdominal cavity secondary
to resistance within the liver and osmotic
pressure within the bloodstream
(hypo albuminemia).
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TREATMENT

7.  Dietary sodium restriction (< than 2g/day)
fluid restriction to <1.5 L/day if serum sodium is < 120–125 mmol/L
 furosemide + spironolactone (a ratio of 40 mg of furosemide to every 100
mg of spironolactone is an appropriate starting regimen)
 Amiloride 10–40 mg/day may be substituted for spironolactone in patients
who develop tender gynecomastia
 If refractory ascites is present, may consider midodrine 7.5 mg three times
daily as add-on therapy to diuretics
 If tense ascites is present, may use large-volume paracentesis.
 Administer albumin at a dose of 6–8 g/L of ascitic fluid removed (if more
than 5 L is removed at one time)
 No upper limit of weight loss if massive edema is present, 0.5 kg/day in
patients without edema
 drugs as NSAIDs. ACE and ARBs should be avoided also to prevent renal
failure

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sodium restriction
(< than 2g/day)
fluid restriction
to <1.5 L/day
if serum sodium
is < 120–125 mmol/L
40mg furosemide +
100mg spironolactone
patients who develop
tender gynecomastia
from spironolactone
40mg furosemide+
10–40 mg Amiloride
refractory
ascites
40mg furosemide+
100mg spironolactone +
midodrine 7.5 mg tid
Tense ascites
paracentesis
if more than 5 L
is removed
at one time
Albumin
at a dose of 6–8 ml/L
of ascitic fluid removed

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precipitation factors
 Constipation& GI bleeding.
 infection.
 hypokalemia, dehydration & hypotension.
 CNS-active drugs (benzodiazepines and narcotics).
Hepatic encephalopathy is a brain dysfunction caused by liver insufficiency or
portosystemic shunting; it manifests as a wide spectrum of neurological or psychiatric
abnormalities ranging from subclinical alterations to coma.
causes
 Accumulation of nitrogenous substances (mainly NH3) arising from the gut (mainly).
 Activation of GABA by endogenous benzodiazepine-like substances.
 Zinc deficiency, or altered cerebral metabolism.

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14.  Lactulose is first-line treatment
I. Metabolized by colonic bacteria to acetic and lactic acid;
NH3 present in the GI lumen is reduced to ammonium ion (NH4 +) through the
reduction in pH (“ammonia trapping”)
and is therefore unable to diffuse back into the bloodstream
II. Dose: 15- to 45-mL dose two or three times daily or
an enema (300 mL plus 700 mL of water retained for 1 hour, May be continued
over the long term to prevent recurrent encephalopathy
III. adverse effects: Flatulence, diarrhea, and abdominal cramping
 Neomycin or metronidazole may be used;
I. neomycin is considered as effective as lactulose
II. neomycin caution with long-term use in patients with renal insufficiency;
III. long-term metronidazole use may result in peripheral neuropathy.
 Rifaximin is as effective as lactulose in patients 18 years and older is 550 mg
twice daily. Drug cost may be greater.
 A recent trial showed that polyethylene glycol 3350 4 L given orally or by
nasogastric tube over 4 hours resulted in faster improvement in encephalopathy
than lactulose
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Flumazenil is used if the cause is benzodiazepine overdose
Zinc is used if the cause is zinc deficiency

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Lactulose syp
15 to 45mL tid
or
enema
(300 mL lactulose+
700 mL water for 1hr)
Neomycin
or
metronidazole
+ +
550 mg Rifaximin
bid
‫أو‬ polyethylene glycol 3350
4 L given orally or by nasogastric tube over 4 hours

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Resistance to blood flow within the liver
secondary to cirrhosis results in the development of
portal hypertension.
Collateral blood vessels (e.g., esophageal varices) are
formed because of this increased resistance to blood
flow.
DEFINITION

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22.  Nonselective β-blockers primary prophylaxis for patients with cirrhosis and small, medium or large
varices and no history of bleeding
I. MOA : block β1 reduces cardiac output,blockβ2 splanchnic constriction leads to reductions in portal
pressure
II. Therapy should aim for a heart rate of 55–60 beats/minute or a 25% reduction from baseline
 Fluid resuscitation and hemodynamic stabilization.Maintain Hb conc 8 g/Dl
 Sclerotherapy: Effective in discontinuing bleeding in 80%–90% of patients
I. sclerosing agents include ethanolamine and sodium tetradecyl sulfate
 Endoscopic variceal band ligation: may be used as an alternative to sclerotherapy
 Vasopressin plus nitroglycerin for 3–5 days
I. Vasopressin cause splanchnic vasoconstriction and coronary vasoconstriction /hypertension
II. so nitroglycerin is used to ¯ coronary vasoconstriction /hypertension
More adverse effects , less preferable
 Octreotide (sandostatin amp) Works possibly by reducing portal pressure (by reduced splanchnic
blood flow)
I. adverse effects include hyperglycemia and abdominal cramping.
II. dose/ 50 mcg iv bolus then 50mcg/hr iv for 3-5days
 patients with cirrhosis and variceal bleeding use
a) (norfloxacin or ciprofloxacin) orally for 7 days.
b)Ceftriaxone 1 g/day i.v may be used if high rates of fluoroquinolone resistance
 Secondary prophylaxis: combination of endoscopic variceal band ligation + nonselective β-blockers
 TIPS ( transjugular intrahepatic portosystemic shunt) is very effective at preventing recurrent bleeding;
however, it is associated with a 30%–40% incidence of encephalopathy
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‫عنده‬ ‫مريض‬
liver cirrhosis + varices
No
bleeding
Nonselective β-blockers
( indral )
1ry prophylaxis
bleeding
Fluid resuscitation
Hb conc 8 g/Dl
Sclerotherapy
ethanolamine and sodium tetradecyl sulfate
or
Endoscopic variceal band ligation Vasopressin
+nitroglycerin
for 3–5 days
norfloxacin or
ciprofloxacin
orally for 7 days
Octreotide
50 mcg iv bolus
then 50mcg/ hr for 3-5days
+ ‫أو‬ +
Ceftriaxone i.v
1 g/day
‫أو‬
+
Nonselective β-blockers
Secondary prophylaxis

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Gram-negative Bacilli (50%) Gram-positive Bacilli (17%)
Escherichia coli, 37% Streptococcus pneumoniae, 10%
Klebsiella spp., 6% Other streptococci, 6%
Other, 7% Staphylococcus aureus, 1%
Pathophysiology:
 The bacteria present are usually enteric pathogens; thus,
they may enter the blood because of increases in gut
permeability secondary to portal hypertension.
 gram-negative pathogens are most commonly involved.
Definition:
Infection of previously sterile ascitic fluid without an
apparent intra-abdominal source.
Most Commonly Isolated Bacteria Responsible for SBP:

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33. o The presence of more than 250 polymorphonuclear
cells/mm3 (PMN) is diagnostic for SBP
3rd generation cephalosporins:
Cefotaxime (2 g every 8–12 hours) or
ceftriaxone (2 g/day IV)for 5–10 days.
Ofloxacin 400 mg orally twice daily
Albumin: 1.5 ml/kg on admission;
1 ml/kg on hospital day 3
o Guidelines suggest using this albumin regimen with
antibiotics
if SCr is >1 mg/dL, BUN > 30 mg/dL, or total bilirubin
more than 4 mg/dL
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Cefotaxime
2 g every 8–12 hours
for 5–10 days
+
Ceftriaxone
2 g/day IV
for 5–10 days
‫أو‬
Ofloxacin 400 mg
orally twice daily +
Albumin
1.5 ml/kg on admission;
1 ml/kg on hospital day 3
Indicator for SBP:
more than 250 polymorphonuclear cells/mm3 (PMN)
SCr > 1 mg/dL
BUN > 30 mg/dL
total bilirubin > 4 mg/dL
Spontaneous Bacterial Peritonitis (SBP)

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39.  Development of Renal failure secondary to liver cirrhosis.
 Primary mechanism responsible for deterioration of renal functions is
renal hypo perfusion.
 Criteria in patients with cirrhosis and ascites: SCr greater than 1.5mg/dL.
 Subtypes:
Type 1: Doubling of SCr to greater than 2.5 mg/dL or a 50% reduction in
crcl to less than 20 mL/minute/1.73 m2 in less than 2 weeks.
Type 2: Non rapid progression of worsening of renal function. Associated
with high mortality
 Treatment:
 Albumin + octreotide (200 mcg subcutaneously three times daily)
 or midodrine (12.5 mg three times daily maximum) may be considered for
type 1 hepatorenal syndrome.
 Albumin + norepinephrine in ICU = intensive care unit patient
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‫أو‬
Hepatorenal Syndrome

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42. Patients may develop cirrhosis.
 TREATMENT:
I. 4-week course of prednisolone 40 mg/day,
followed by a 2-week taper
I. pentoxifylline 400 mg three times daily, especially if
there are contraindications to corticosteroids
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