Detaliled approach to ascitic patients in liver cirrhosis

DR MAGDI AWAD SASIDETALILED 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.

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

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.

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.

 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 OFAOTHER 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

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

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.

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

 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.

 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

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

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

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 activitypoor opsonic
SBP CNNA
Good opsonic activity
Sterile non neutrocytic ascites

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

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

Detaliled approach to ascitic patients in liver cirrhosis

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Detaliled approach to ascitic patients in liver cirrhosis