Detaliled approach to ascitic patients in liver cirrhosis

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS 2015 --POST GRADUATE ASCITES GENERAL IDEA ABOUT ASCITES: Intra peritoneal accumulation of fluid containing small amounts of protein. Subclinical amounts of fluid < 1.5 L can be detected by CT scan. Moderate amount may cause no symptoms. Abdominal discomfort occur with tense ascites. Some patients with gross ascites present with numbness or parasthesia ,sensory loss in the distribution of the lateral cutaneous nerve of thigh. Diaphragmatic elevation and restriction may be a cause of dyspnea. Ascites is unlikely to be present ((<10% of cases )) in the absence of flank dullness, the converse is not true. With aggressive diuresis, there may be generalized cutaneous evidence of dehydration and postural hypotension, indicating a reduced intravascular volume. Another cause of cryptogenic cirrhosis and ascites in elderly women is NASH non alcoholic steato-hepatitis from lifelong obesity. Patient with ascites who have a history of cancer should be suspected of having malignancy related ascites. Painful ascites ------favors malignant ascites. Tuberculous peritonitis ----fever ,abdominal pain ,migration from endemic area. A small percentage of patients on hemodialysis develop troublesome ascites. Chlamydia fitz hugh-curtis syndrome may cause inflammatory ascites in sexually active women. Serositis in CTD (connective tissue disease) may be complicated by ascites. MECHANISM: Ascites is due to: 1. Salt and water retention from aldosteron----decrease liver metabolism 2. Increase lymphatic leaking due to increase synthesis due to sinusoidal HTN 3. Increase lymph formation. WHAT IS THE CAUSE OF SALT AND WATER RETENTION? A .Rennin--Angiotensin Aldosterone system B .Increased amounts of vasopressin C .Activation of sympathetic nervous system In patients with ascites, renal secretion of PGE2 may help to preserve renal function by maintaining glomerular filtration and free water clearance. So ,NSAIDS should not be given to patients with ascites.

Transcript of Detaliled approach to ascitic patients in liver cirrhosis

Page 1: Detaliled approach  to ascitic patients in liver cirrhosis

DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

ASCITES

GENERAL IDEA ABOUT ASCITES:

Intra peritoneal accumulation of fluid containing small amounts of protein.

Subclinical amounts of fluid < 1.5 L can be detected by CT scan.

Moderate amount may cause no symptoms.

Abdominal discomfort occur with tense ascites.

Some patients with gross ascites present with numbness or parasthesia

,sensory loss in the distribution of the lateral cutaneous nerve of thigh.

Diaphragmatic elevation and restriction may be a cause of dyspnea.

Ascites is unlikely to be present ((<10% of cases )) in the absence of flank

dullness, the converse is not true.

With aggressive diuresis, there may be generalized cutaneous evidence of

dehydration and postural hypotension, indicating a reduced intravascular

volume.

Another cause of cryptogenic cirrhosis and ascites in elderly women is

NASH –non alcoholic steato-hepatitis from lifelong obesity.

Patient with ascites who have a history of cancer should be suspected of having malignancy related ascites.

Painful ascites ------favors malignant ascites.

Tuberculous peritonitis ----fever ,abdominal pain ,migration from endemic area.

A small percentage of patients on hemodialysis develop troublesome

ascites.

Chlamydia fitz –hugh-curtis syndrome may cause inflammatory ascites in

sexually active women.

Serositis in CTD (connective tissue disease) may be complicated by ascites.

MECHANISM:

Ascites is due to:

1. Salt and water retention from aldosteron----decrease liver metabolism

2. Increase lymphatic leaking due to increase synthesis due to sinusoidal

HTN

3. Increase lymph formation.

WHAT IS THE CAUSE OF SALT AND WATER RETENTION? A .Rennin--Angiotensin –Aldosterone system B .Increased amounts of vasopressin C .Activation of sympathetic nervous system In patients with ascites, renal secretion of PGE2 may help to preserve renal function by maintaining glomerular filtration and free water clearance. So ,NSAIDS should not be given to patients with ascites.

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

INCREASED NITRIC OXIDE

VASODILATATION

RENAL SODIUM RETENTION

OVER FILL OF INTRAVASCULAR VOLUME

INCREASED SYMPATHETIC NERVOUS ACTIVITY ,RENIN ,ALDOSTERONE

ASCITES FORMATION

: AETIOLOGY

Cirrhosis ,CCF , T.B. ------ account for 90% of cases

Ascites can elevate JVP through its mechanical effects.

D/D----- of cirrhosis---- 1.Budd chiarri syndrome

2.Constrictive pericarditis

Acute portal vein thrombosis can cause transit ascites and chronic portal

vein block doesn't cause ascites in the absence of liver disease.

VENOUS HYPERTENSION:

1.cirrhosis

2.CCF

3.Constrictive pericarditis

4.Hepatic venous out flow obstruction---Budd chiari,Venoocclusive disease

5.Portal vein block----acute thrombosis

PHTN

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

AETIOLOGY: 1.PORTAL HTN 2.HYPOALBUMINEMIA: Nephritic syndrome Malnutrition Protein losing enteropathy

3.MALIGNANT DISEASE: Mesothelioma 2ry carcinomatoses Lymphoma and leukemia

4.INFECTIONS: Tuberculous peritonitis Fungal ---candida ,Cryptococcus Parasitic ---entamoeba ,strongyloides

5.MISCELLANEOUS: Chylous ascites Bile ascites Pancreatic ascites Urinary ascites Ovarian disease---Meigs syndrome, Struma ovarii Ovarian over stimulation Myxodema Whipples disease Sarcoidiosis SLE Starch peritonitis

Eosinophilic gastroenteritis

TO DIAGNOSE:

Paracenresis to identify other causes

Albumin in serum / Ascitis

ADH serum /ADH ascitis

Amylase ,WBC ,RBC ,C/S ,Chylomicron

At least 1500ml of fluid must be present before dullness is detected.

Obese abdomen may be diffusely dull to percussion and need uss abdomen

which can detect as little as 100ml of fluid in the abdomen.

Clinical deterioration in any manner in patient with ascites should raise suspicion

of infection and a prompt tap ; especially if there is fever or abdominal pain.

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

Mimicking ascitis :

1.Gaseous distention

2.Thick panniculous

3.Ovarian mass----- tympanitic flanks and central dullness.

Paracentesis should be repeated in patients who develop symptom and

signs or have abnormal laboratory values suggestive of infection.

Clinically ----Hypotension ,fever, abdominal pain ,encephalopathy renal

failure ,acidosis , peripheral leukocytosis , abdominal tenderness.

PRACTICAL POINTS:

The main reason for diagnostic paracentesis is to check for spontaneous bacterial peritonitis.

An immobile mass in the umbilicus ,sister mary joseph nodule ,is very suggestive of peritoneal carcinomatosis.

The neck veins should be specifically examined because constrictive pericarditis is one of the few possible causes of ascites.

Not all patients with ascetic fluid infections are symptomatic.

Blood stained ascites:

TB , MALIGNANCY ,PANCREATITIS ,PORTAL

VEAIN THROMBOSIS.

Complications of ascites:

1. Spontaneous leakage from a large umbilical hernia.

2. Pleural effusion.

3. Spontaneous peritonitis.

10----15% .It should be suspected when even sudden deterioration occurs in

patients with ascites.

The patient complain of fever, malase ,hypotension and encephalopathy.

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

WBCs >500/mm3 , Neutrophil > 250/mm3

If there is low WBCs count and fever with abdominal pain and tenderness,

spontaneous bacterial peritonitis should be suspected and 3rd generation

cephalosporins started.

DRUGS TO BE AVOIDED:

1. Direct nephrotoxic;

Aminoglycoside ,Amphotericin, Penicillins ,Cephalosporins ,Demeclcycline

2.PG synthetase inhibitors:

NSAIDS ,Aspirin ,Indomethacin ,Phenylbutazone

3.Salt rich drugs:

Antacids ,Metronidazole

4.K rich drugs:

Spironolactone ,Tramterene ,Amiloride

5.Renin angiotensin blockers:

Saralasin ,CAPTOPRIL

6.Drugs increasing aldosterone secretion:

Metoclopramide

7.Others:

Lithium ,Radiographic contrast , Lctulose

:PRACTICAL POINTS

Patient with ascites only-----weight loss to be 0.5kg/ d.

Patient with ascites and pedal odema----weight loss to be 1 kg/d.

ASCITES :CAUSES OF AOTHER WAY OF CLASSIFYING THE

A. 1.Cirrhosis ----with /without infection 85%

2.Miscellaneous portal HTN ---related 8%

3.Mixed----

Cirrhosis and tuberculous peritonitis

Cirrhosis and hepatocellular carcinoma

Cirrhosis and pancreatitis

Cirrhosis and nephrotic syndrome

Cirrhosis and peritoneal carcinomatosis

Cirrhosis and Chlamydia peritonitis

Massive liver metastases and peritoneal carcinomatosis

Massive liver metastases and portal vein thrombosis

4.Fulminant hepatic failure

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

5.Acute hepatitis superimposed on cirrhosis

6.Massive liver metastases

7. Chylous cirrhotic ascites

8.Hepatocellular carcinoma without cirrhosis

B. Cardiac ascites

C.Peritoneal carcinomatosis

D.Miscellaneous ----non portal HTN related:

Tuberculous peritonitis

Pancreatitis

Secondary bacterial peritonoitis

Nephritic syndrome

Nephrogenous

Chlamydia peritonitis

Malignant chylous

:COMPLICATION OF PARACENTESIS

Coagulopathy ----this should preclude paracentesis only when there is

clinically evident fibrinolysis or DIC.

Patients with severe prolonged PT don’t develop bloody ascites even after

multiple paracentesis.

Abdominal wall hematomas (2%)—71%have prolonged P.T. with

inexperienced operators.

Infections ----so rare.

Perforations of bowel -----not reported

FOR PERITONEAL TAPPING:

Anterior superior iliac spine---two breaths cephalad and two fingers breadth medial

Standard metal-----22 gauge for diagnostic , 16gauge for therapeutic tapping

Ascitic fluid laboratory data :

Routine ---- cell count ,albumin ,blood culture bottles Optimal --- total protein ,glucose ,LDH, amylase ,gram stain Unusual ----cytology ,TGA ,bilirubin .TB smear and culture Unhelpful -----PH ,lactate ,cholesterol ,fibronectin ,α1 antitrypsin ,glycosaminoglycans

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

THE COLOUR OF FLUID:--

Samples from patients with hepatocellualar carcinoma are regularly bloody

but only 10% of samples from patients with peritoneal carcinomatosis are

red .

Less than 5% of Tuberculous ascites are bloody.

Lipid opacifies fluid:

1) Opaque milky fluid----TGA > 200mg/dl , most 1000mg/dl

2) Dilute skim milk---100mg/dl

3) Most patients with chylous or opalescent have cirrhosis.

Dark brown fluid with bilirubin concentration higher than normal that of

the serum usually indicates biliary perforation.

Deeply jaundiced patients have bile ascetic fluid.

Pancreatic ascites may be pigmented due to RBCS digestion from tea

colored to jet black.

Black ascites may be found in the sitting of malignant melanoma.

THE CELLS IN ASCITES:

To test ascites, the cell count is the single most helpful test for ascetic fluid.

WBC < 500cells /mm3

During diuresis (( in patient with cirrhosis))------it reaches 1000cells/mm3

WBCs + mesothelial cells ====nucleated cells

Predominant == lymphocytes

Upper limit of PMN in cirrhosis === 250 /mm3

Any inflammatory process can result in increase WBC

SBP is the most common cause of increased WBCs ((most common cause of

inflammation))PMN 70%

Leakage of blood into peritoneal cavity leads to increased WBCs.

If PMN count is elevated ,the diagnosis is ascetic fluid infection (( SBP)) until proven otherwise. Increased ascetic fluid PMN:

1. Pancreatitis 2. Tuberculosis 3. Peritoneal carcinomatosis 4. Haemorrhage

Most case of neutrocytic ascites are due to infection. Differentiated WBC in ascetic fluid may be helpful in diagnosis. SBP is six times as common as surgical peritonitis in patients with ascites, 2ry peritonitis should be considered in any patient with neutrocytic ascites Even with free perforation of the colon into ascetic fluid ; patient don’t develop a classic surgical abdomen.

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Gut perforation can be suspected and pursued if a specimen is neutrocytic and meets 2 of the following: 1. T.PROTEIN > 1 GM 2. GLUCOSE < 50 MG/DL 3. LDH > UPPER LIMIT OF NORMAL FOR SERUM

The best time to perform a single repeat paracentesis to assess the response is 48 of

treatment.

The culture remains positive in 2ry peritinoitis and becomes rapidle negative in SBP.

SAAG:

SERUM ASCITES ALBUMIN GRADIENT(SAAG)

High gradient (( ≥1.1 g/dl {11g/l})) Low gradient (<1.1g/dl{11g/l})) Cirrhosis Peritoneal carcinomatosis Alcoholic ascites Tuberculous peritonitis Mixed ascites Pancreatic ascites Massive liver metastases Bowel obstruction(( infarction)) Fulminant hepatic failure Biliary ascites Budd chiari syndrome Nephrotic syndrome Portal vein thrombosis Postoperative lymphatic leak Venocclusive disease CTD Myxedema Fatty liver of pregnancy

SAAG---has been proved in multiple studies to categorize ascites.

It is better than the total protein concentration. WHY?

It is based on oncotic hydrostatic balance.

The calculation of SAAG involves measuring the albumin concentration of

serum and ascitic fluid specimens and simply subtracting the ascetic value

from the serum value.

If SAAG is more than 1.1g/dl--------------portal HTN with 97% accurancy

If SAAG is less than 1.1g/dl -------------patient doesn’t have portal HTN.

ALBUMIN GRADIENT-----indirect index of portal HTN, doesn’t explain

ascites cause.

Ascitic fluid protein SAAG > 1.1 SAAG < 1.1

< 2.5 gm /dl Cirrhosis Nephrotic syndrome

> 2.5 gm /dl Right heart failure , Budd chiarri

Malignancy Tuberculosis

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The accuracy decreased in:

1.Some cirrhotic patients with albumin < 1.1 g/dl

2.Low albumin concentration < 1g/dl

3.Specimen not obtained simultaneously

4.Peripheral hypotension ----- gradient decrease

5.Chylous ascites ------ gradient increase

6.Peripheral hyperglobulinemia --- 1%

SAAG X 0.16 ( S.globulin { g/dl} + 2.5 )

Albumin gradient is high ≥ 1.1g/dl---as a reflection of underlying portal HTN.

The presence of high albumin gradient doesn’t diagnose cirrhosis ,it simply

indicates the presence of portal HTN.

The albumin gradient need only be performed on the first paracentesis.

Blood -----blood culture bottle superior

Total protein ----problematic

Total protein concentration in cirrhotic ascites is almost entirely by

S.protein concentration and portal pressure,

A cirrhotic patient with high S.protein = high ascetic fluid protein

concentration

20% of patients have ascetic protein > 2.5 g/dl

Ascetic fluid total protein concentration doesn’t increase during SBP , and

remains stable before during and after infection.

In fact, patients with lowest protein ascites are the most predisposed to

develop spontaneous peritonitis.

During 10 k diuressis , ascetic fluid total protein double and 67% of patients

with cirrhotic ascites develop protein > 2.5 g/ dl.

In fact ,almost 1/3 of patients with malignant ascites have massive liver

metastasis or hepatocellular carcinoma as the cause of ascites formation

,their ascetic fluid is low in protein.

Cardiac ascites has an ascetic fluid protein concemtration > 2.5 g/dl.

So ,exudative/ trans classification places cirrhosis & cardiac ascites ----exudates.

Many patients with malignant ascites and infected ascites ---------------transudative.

ALBUMIN GRADIENT IS MORE HELPFUL.

Surgical peritonitis warrants an immediate radiologic evaluation to

determine if gut perforation into ascites has occurred with;

T .protein >1g/dl , Glucose < 50mg/dl , LDH > serum level.

Glucose --- ascetic fluid concentration is similar to serum concentration of

glucose unless consumed by WBCs and bactermia. It can drop to zero in gut

perforation.

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

LDH ---diffuse from blood and from disintegrated WBCs and less than that

of blood.

It is increased in SBP and may be several times greater.

Amylase --- half that of serum value 50U/L.

It is increased to 20000U/L in SBP ,gut perforation , and pancreatitis.

T.B. smear and culture:

The direct smear of ascetic fluid is never positive .

Laproscopy with histology and culture of peritoneal biopsies is 100% sensitive.

Because of((1)) fever and pain , and ((2)) 1/2 of patients have cirrhosis,

tuberculous peritonitis can easly be confused with SBP.

RISK FACTORS FOR INFECTION ((SBP)): 1. Low ascetic fluid protein 2. Low ascetic fluid phagocytes 3. Urinary tarct infection 4. Hemorrhage –shock --- shock induced increased translocation of

bacteria from gut to extraintestinal sites.

Neutrophil count in ascetic fluid

< 1000 /mm3 ((1x109/l)) ----clear

5000 /mm3 ----cloudy

50000/mm3 ---mayonnaise

RBC 10000/mm3 ------------- pink appearance

20000/mm3 -------------red

Cytology :

It was reported to be only 60% sensitive in detecting malignant ascites.

It should be suspected to detect malignant cells only if peritoneum lined

malignant cells involved.

100% of patients with peritoneal carcinomatosis have positive cytology.

2/3 of patient with positive cytology have peritoneal carcinomatosis.

So, cytology is 100% sensitive in detecting carcinomatosis.

Α feto protein in ascetic fluid is more sensitive than hepatocellular carcinoma.

In malignant ascites ,WBC increased due to dying cells ----predominent

lymphocytes.

Frank milky ascetic fluid == chylous ascitse ----TGA >200mg/dl

Dark brown ascetic fluid ===bilirubin

Ascetic > serum = biliary /gut perforation >6 mg/dl

FOR DIURETIC EFFECT; use aldactone 400mg + lasix 160mg if:

1. Blood pressure > 90 mmHg

2. Serum creatinine < 1.5 mg/dl

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

3. Electrolytes satisfactory

D/D:

80% Cirrhosis Cancer < 10%

20% Other causes Heart failure < 5%

5% Mixed

1. TUBERCULOUS PERITONITIS: increasing because of increasing of the incidence of AIDS

1/2 of patients have liver cirrhosis

1. Immigrants from area of T.B.

2. Febrile

3. 3Initial ascetic fluid analysis ----high lymphocyte

Peritoneal biopsy ----millet seed and viridian string appearance

D/D peritoneal coccidomycosis ----even without AIDS

2. PANCREATIC ASITES:

H/O pancreatitis , with WBCs >250 cells /mm3 ,need empirical antibiotics ,amylase

3.NEPHROGENOUS ASCITES:

HCV , Alcohol abuse

4.CHLYMIDEA ASCITES:

Sexually active women with fever

Ascites ----increased protein ,low gradient ,neutrocytic and no liver disease.

5.CHYLOUS ASCITES:

Caused by malignancy in almost 90% of patients

Caused by retroperitoneal surgery and radical pelvic surgery

Cirrhosis is the cause in > 90% of cases

CALSSIFICATION OF THE MALIGNANCY RELATED ASCITES:

1.Peritoneal carcinomatosis

2.Massive liver metastases

3. Peritoneal carcinomatosis with Massive liver metastases

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

4.Hepatocellualr carcinoma

5.Mlaignant lymphnode obstruction

6.Malignant budd chiarri syndrome

POEMS—polyneuropathy, organomegally ,endocrinopathy , M complement, skin changes

CLASSIFICATION OF ASCITIC FLUID INFECTION:

A. Spontaneous ascetic fluid infection:

Spontaneous bacterial peritonitis

Monomicrobial non neutrocytic bacterasites

Culture negative neutrocytic ascites

B. Secodary bacterial peritonitis

C. Polymicrobial bacterasites (( needle perforation of bowel))

DX:

Positive ascetic fluid culture

Increased ascetic fluid PMN count ≥250 cells /mm3 without evident

surgically treatable source of infection

Monobacterial non neutrocytic bacterasites –

Positive ascetic fluid culture for single organism , PMN <250 ceels /mm3

No evidence of surgically treatable source of infection.

CNNA---

1) Asciis fluid grows no bacteria

2) No antibiotic have been given

3) No explanation to elevated WBCs

NOTE: Increased WBCs in ascetic fluid :

1.Haemorrhage

2.T.B. peritonitis

3.Pancreatitis

4.Carcinomatosis

2ry bacterial peritonitis:

A. Ascitic fluid culture is positive (( multiple organism))

B. PMN ≥ 250 cells /mm3

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

C. An identified surgically treatable infection ---perinephric abscess ,

perforated gut

They require surgery.

Poly microbial bacterascites:

DX --- multiple organism and PMN < 250 cells/mm3

The diagnosis should be suspected when traumatic paracentesis or difficult

((ileus)) OR stool or air aspirated.

Polymicrobial bacterioascites is the diagnosis of gut perforation.

PRACTICAL POINTS:

All patients with SBP have increased bilirubin and prolonged PT.

This infection usually develops at time of maximum ascetic volume.

Gut flora altered flora

Altered permeabilitry

Bacteria in mesenteric lymph nodes

Bacteria in abdominal lymphocytes

Bacteria in thoracic duct lymph nodes

Lymphatic rupture

Respiratory tract infection urinary tract infection

Complement deficiency reticuloendothelial dysfunction

Bacteremia

Bacteria in hepatic lymph

bacterascites

moderate opsonic activity poor opsonic

SBP CNNA

Good opsonic activity

Sterile non neutrocytic ascites

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TRREATMENT:

Cefotaxaime ---SBC 250ml/dl

Long term Norfloxacin

Renal failure in liver disease:

1.Functional –spontaneous

2.Diuretic induced

3.NSAIDS

4.ATN---infection ,haemorrhage ,gentamycin ,viral hepatitis –mortality rate 70%

5.CRF with liver damage

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DR MAGDI AWAD SASI DETALILED APPROACH TO ASCITIC PATIENTS IN LIVER CIRRHOSIS2015 --POST GRADUATE

CIRRHOSIS AND ASCITES:

A. Circulatory

1. Decrease SVR

2. Decreased BP

3. Increased hr

4. Increased ci

5. Increased plasma volume

6. Decreased renal blood flow

B. Vascular

1. Splanchanic vasodilatation

2. Renal artery vasoconstriction

3. Pulmonary vasodilatation

C. Functional

1. Activation of systemic vasodilatation factors

2. Activation of vasoconstrictor factors

3. Activation of renal vasodilatation factors

4. Decreased GFR

D. Biochemical

1. Na retention

2. H20 retention

3. Increased systemic NO

4. Increased PG

5. Increased renal NO &PG

TREATMENT OF ASCITIS:

A. Bed rest B. Restrict salt intake—60mmol/day + fluid restriction Na ≤ 120 –125meq/l According to renal function ,urinary sodium and free water excretion C. Diuretics: Spironolactone is the drug of choice. Furesmide is adde

FFN can be added D.Therapeutic paracentesis : 1.Tense ascites 2.Refractory ascites 3.When hypokalemia limit use of diuretics E.Leveen shunt: Side effects---increased mortality ,infection ,pulmonary oedema ,variceal bleeding Malignant ascites: Intraperitoneal injection of appropriate cytotoxic drugs Intraperitoneal injection of colloid suspension of radioactive phosphate or gold Au Immunotherapy with intraperitoneal injection of OK 432