Ascites

Hepatic Encephalopathy

Gastroesophageal Varices

Spontaneous Bacterial Peritonitis (SBP)

Hepato renal Syndrome

Alcoholic Liver Disease

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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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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

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 restrictionto <1.5 L/day

if serum sodium is < 120–125 mmol/L

40mg furosemide + 100mg spironolactone

patients who developtender gynecomastia

from spironolactone

40mg furosemide+10–40 mg Amiloride

refractory ascites

40mg furosemide+100mg spironolactone +

midodrine 7.5 mg tid

Tense ascites

paracentesisif more than 5 L

is removedat one time

Albuminat 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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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 overdoseZinc is used if the cause is zinc deficiency

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Lactulose syp15 to 45mL tid

orenema

(300 mL lactulose+ 700 mL water for 1hr)

Neomycinor

metronidazole+ +

550 mg Rifaximin bid

أو polyethylene glycol 33504 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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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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مريض عنده

liver cirrhosis + varicesNo

bleedingNonselective β-blockers

( indral )

1ry prophylaxis

bleeding

Fluid resuscitationHb conc 8 g/Dl

Sclerotherapy ethanolamine and sodium tetradecyl sulfate

orEndoscopic variceal band ligation Vasopressin

+nitroglycerinfor 3–5 days

norfloxacin or ciprofloxacin

orally for 7 days

Octreotide50 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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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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Cefotaxime2 g every 8–12 hours

for 5–10 days

+Ceftriaxone2 g/day IV

for 5–10 days

أوOfloxacin 400 mg orally twice daily +

Albumin1.5 ml/kg on admission;

1 ml/kg on hospital day 3

Indicator for SBP:more than 250 polymorphonuclear cells/mm3 (PMN)

SCr > 1 mg/dLBUN > 30 mg/dL

total bilirubin > 4 mg/dL

Spontaneous Bacterial Peritonitis (SBP)

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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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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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