Ascietesby

dr naila masood

Cirrhosis is the late result of any disease that causes scarring of the liver.

Patients with cirrhosis are susceptible to a variety of complications that include ascites, hepatic encephalopathy, and portal hypertension. Quality of life and survival are often improved by the prevention and treatment of these complications.

Ascites is defined as the accumulation of free fluid in the peritoneal cavity. It is a common clinical finding with a variety of both extraperitoneal and peritoneal etiologies.

It is most often caused by liver cirrhosis which accounts for over 75% of patients while the remaining 25 % is due to malignancy (10%), heart failure (3%), pancreatitis (1%), TB (2%), or other rare causes.

Nonperitoneal Causes of Ascites Non-peritoneal causes Examples

Intrahepatic portal hypertension

CirrhosisFulminant hepatic failureVeno-occlusive disease

Extrahepatic portal hypertension

Hepatic vein obstruction

(ie, Budd-Chiari syndrome)Congestive heart failure

Hypoalbuminemia Nephrotic syndromeProtein-losing enteropathy Malnutrition

Miscellaneous disorders MyxedemaOvarian tumorsPancreatic & Biliary ascites

Chylous Secondary to malignancy, trauma

Peritoneal Causes of Ascites Peritoneal Causes Examples

Malignant ascites Primary peritoneal mesotheliomaSecondary peritoneal carcinomatosis

Granulomatous peritonitis Tuberculous peritonitisFungal and parasitic infections SarcoidosisForeign bodies (cotton ,starch, barium)

Vasculitis Systemic lupus erythematosusHenoch-Schönlein purpura

Miscellaneous disorders Eosinophilic gastroenteritisWhipple diseaseEndometriosis

Prognosis

The development of ascites is an indication of deterioration in clinical status and poor prognosis.

Prognosis is worse for those with refractory ascites and SBP.

Approximately 60% of patients with cirrhosis will develop ascites requiring therapy and/or liver transplantation in 10 years duration.

Mortality in cirrhotic patients hospitalized with ascites is 40% at 2 years.

PATHOPHYSIOLOGY

Ascites is derived from the vascular compartment subserving the hepatosplanchnic viscera.

Factors important in the formation of ascites: Increased total body sodium and water Increased sinusoidal portal pressure.

In cirrhosisHepatic dysfunction and sinusoidal portal pressure send a message to the kidney to retain excess sodium and fluid.

PH serves to localize excess fluid to the peritoneal cavity rather than the periphery.

The pathogenesis of ascites formation remains controversial.

“Underfill" theory Ascites occurs as a primary event.

Sequestration of fluid into the peritoneal cavity as a result of changes in Starling's forces leads to reduction of the circulatory volume and stimulation of the sympathetic nervous & RAAS that promote renal sodium & water retention.

“Overflow theory" Renal Na retention occurs as a primary event.

It may be due to increased production of a sodium retaining factor or reduced synthesis of a natriuretic factor by the diseased liver.

The circulatory volume is expanded & the retained fluid is preferentially localized to the peritoneal cavity as ascites.

The currently accepted theory of ascites formation which include features of both the underfill and overflow theories is the

“Peripheral Arterial Vasodilation Hypothesis"

According to this theory, Portal pressure >12 mm Hg is required for the development of PH which will lead to formation of ascites.

As PH develops, vasodilators are released affecting the splanchnic arteries resulting in decrease in effective arterial blood flow and arterial pressures .

The precise agent (or agents) responsible for vasodilation is a subject of wide debate; however, most recent literature has focused on the role of:

Nitric Oxide

Chronic endotoxemia associated with cirrhosis may stimulate the synthesis and release of a potent endothelin-derived relaxing factor, Nitric oxide.

NO is the likely mediator in cirrhosis:(1) Increased activity of NO synthase .(2) High serum nitrite and nitrate levels (an index of NO synthesis). (3) Inhibition of NO leads to increased arterial pressures and systemic vascular resistance.

Portal hypertension

Vasodilatation, Decrease Splanchnic Systemic vascular resistance

Reduction in arterial blood volume

Activation of neurohumoral pressor systems

Renal sodium & water retention

When Na reabsorption cannot compensate for vasodilation, arterial underfilling leads to further activation of vasoconstrictor & antinatriuretic mechanisms which leads to increased Na retention & ultimately ascites is formed.

In the late stages of cirrhosis, free water accumulation is more pronounced than the Na retention leading to dilutional hyponatremia.

DIAGNOSIS

I) History

Approximately 85% of patients with ascites have cirrhosis.

Patients who don’t have cirrhosis should be questioned about lifetime body weight as NASH may be the cause.

Past history of cancer, heart failure, or TB.

II) Physical Examination Approximately 1.5 L must be present before flank dullness is detected. If no flank dullness is present, the patient has less than 10% chance of having ascites.

Shifting dullness & fluid thrill mean that more fluid is present.

Abdominal ultrasound to determine with certainty if fluid is present and in obese.

Two grading systems for ascites have been used in the literature.

An old system which grades ascites from 1+ to 4+, depending on the detectability of fluid on physical examination.

More recently, the International Ascites Club has proposed a system of grading from 1 to 3.

The older system 1+ is minimal and barely detectable. 2+ is moderate. 3+ is massive but not tense. 4+ is massive and tense.

The International Ascites Club grading (2003) Grade 1: mild ascites detectable only by US. Grade 2: moderate ascites manifested by moderate symmetrical abdominal distension. Grade 3: large or gross ascites with marked abdominal distension.

III) Diagnostic ParacentesisIndications(1)Evaluation for a non-cirrhotic patient developing clinically apparent ascites of recent onset. (2)New development of ascites in a cirrhotic patient does not routinely require paracentesis only if :(a) General condition deteriorates.(b) In presence of unexplained fever, abdominal pain, encephalopathy.(c) Admission to hospital for any cause (SBP).(3)Laboratory investigations indicating infection: Leucocytosis Acidosis Worsening of renal functions

SiteMidline was usually chosen. Abdominal wall in the left lower quadrant, 2 finger breadths cephalic & 2 finger breadths medial to ASIS, has been shown to be thinner with larger pool of fluid than midline.

Complications (1% of patients) Abdominal wall hematomas. Hemoperitoneum or bowel entry.

ContraindicationsClinically evident fibrinolysis or DIC.

Color Appearance

Translucent or yellow Normal/sterile

Brown Hyperbilirubinemia

GB or biliary perforation

Cloudy or turbid Infection

Pink or blood tinged Mild Trauma

Grossly bloody Malignancy

Abdominal trauma

Milky ("chylous") Cirrhosis

Thoracic duct injury

Lymphoma

Gross Appearance of Ascitic Fluid

Ascitic Fluid Testing

Routine Sometimes useful Rarely helpful

Cell count & differential

Total protein pH

Albumin LDH Lactate

Culture Glucose Gram stain

Amylase

Triglycerides

Bilirubin

Cytology

TB smear and culture

Ascitic fluid analysis (Routine)I) Cell count with differential Abnormal results are an indication for further non routine tests.

If the PMN count is >250 cells/mm3, another specimen is injected into blood culture bottles at bedside.

Bacterial growth occurs in about 80% of specimens with count of >250 cells/mm3.

The PMN count is calculated by multiplying the white cells/mm3 by the percentage of neutrophils in the differential.

In a "bloody" sample that contains a high concentration of RBC, the PMN count must be corrected: one PMN is subtracted from the absolute PMN count for every 250 red cells/mm3 in the sample.

The results must be available within 1 hour, so that important diagnostic and therapeutic decisions can be made.

A Gram stain is of particular low yield unless free gut perforation, is suspected.

II)Total protein ,albumin & serum albumin . Serum-ascites albumin gradient (SAAG) = serum albumin - ascitic fluid albumin.

If > 1.1 g/dL, the patient has PH-related ascites. If < 1.1 g/dL (about 97% accurate), the patient does not have PH-related ascites.

The SAAG does not need to be repeated after the initial measurement.

III)Based on clinical judgment, additional testing can be performed :

a) Cytology ,smear & culture for mycobacteria.

b) Cytology : in peritoneal carcinomatosis (sensitivity increased by centrifuging large volume).

c) Elevated bilirubin level suggest biliary or gut perforation.

d) LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and multiple organisms on gram stain suggest secondary bacterial peritonitis.

e) High level of TG's confirms chylous ascites.

f) Elevated amylase level suggest pancreatitis or gut perforation.

AASLD Recommendations 1.Paracentesis should be performed ,ascitic fluid should be obtained from inpatients & outpatients with clinically apparent new-onset ascites 2. Since bleeding is uncommon ,prophylactic use of FFP or platelets is not recommended. 3. Initial evaluation of ascitic fluid should include cell count ,differential, total protein & SAAG.4. If infection is suspected, ascitic fluid should be cultured at the bedside in blood culture bottles.5. Other studies can be ordered based on pretest probability of disease.

• Treat the Underlying Cause

• Childs C – 75% 3-year survival Vs. 0%

• Non-Alcoholic less reversible therefore consider referral for transplant earlier

Management of Ascites -Guideline

• Bed rest• Diet• Diuretics• Fluid Restriction• Paracentesis• TIPSS• Shunts• Transplant

Treatment Options

• Bed rest : No clinical trials• Upright posture activates sodium retaining

mechanisms , impairs renal perfusion and sodium excretion.

Management of ascites -Bed Rest

Sodium restriction :Water will follow SodiumEducate the PatientAim for 2000mg (88 mmol) per dayStudies show severe restriction (22mmol/day)

compared with less restricted is associated with longer duration of evolution of ascites, but higher incidence of diuretic induced renal impairment and hyponatraemia

Management of ascites-Sodium Restriction

• One controlled study, showed slightly reduced salt diet (120mmol/day) was equally effective when compared to a low salt diet ( 50mmol/day).

• No significant survival difference, although low salt diet (50mmol/day ) improved survival in those with previous GI bleed

MANAGEMENT OF ASCITES- Salt restriction (cont)

• Central hypovolaemia - > stimulates ADH receptors• - > decreases free water clearance - > dilutional

hyponatraemia.• • Therefore, treat by water restriction – no trials to

assess effect of water restriction in patients with cirrhosis and dilutional hyponatraemia. Restriction may worsen central hypovolaemia.

• Water restriction not first option, sodium restriction appropriate first line, water restrict if Na <125mmol/L

MANAGEMENT OF ASCITES-

WATER RESTRICTION

• Antimineralocorticoids – • Secondary hyperaldosteronism promotes sodium

retention in distal tubules and collecting ducts• Controlled and uncontrolled trials - >

Spironolactone effective antimineralocorticoid • S.E gynaecomastia, renal impairment,

hyperkalaemia• Other K sparing diuretics: amiloride, triamterene• Loop Diuretics : Frusemide – S.E : hyponatraemia,

hypokalaemia, hypovolemia, renal impairment of prerenal origin

MANAGEMENT OF ASCITES-

DIURETICS

• Weight loss of 0.5kg/day in absence of oedema and 1kg/day when oedema present

• Use Spironolactone & Frusemide 100mg/40mg ratio

• Medical treatment based on sodium restricted diet, diuretics – response in 90 % without renal failure.

ASCITES-Assess response to diuretics :

• Weight loss of 0.5kg/day in absence of oedema and 1kg/day when oedema present

• Use Spironolactone & Frusemide 100mg/40mg ratio

• Medical treatment based on sodium restricted diet, diuretics – response in 90 % without renal failure.

ASCITES-Assess response to diuretics :

• Unresponsive to Salt restriction & high dose diuretics (400mg Spironolactone & 160mg Frusemide)

• Recurs rapidly after Paracentesis (< 4/52)

• Diuretic induced complication – encephalopathy, renal impairment, hyponatraemia (<125mmol/L), hypo (3mmol/L) or hyperkalaemia (6mmol/L)

Ascites-Refractory Ascites

• Repeated daily paracentesis ( 5L/day )

• Single total paracentesis- reduced hospital stay

Ascites-Paracentesis

• Serial Paracentesis• Liver Transplantation• TIPSS• Peritoneovenous Shunts

Refractory Ascites -Treatment Options

• Liver Transplantation

Refractory Ascites -Treatment Options

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