Ascites

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DEFINITION
Diagnosis and management
Practically, surgeons deal with ascites usually in the context of cirrhosis.
Refractory Ascites = either diuretic resistant or diuretic intractable.
D E A B M I M

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AETIOLOGY

Sieve

Portal hypertension and causes

Lymphatic Obstruction
Congenital lymph disorders
- eg primary lymph hypoplasia.
Lymphoma
Lymph-node mets eg testicular, melanoma
GI carcinoids
- obstruct lymph at base of mesentry - dense fibrosis.
Chylous ascites - disruption to channels

Abdo / Peritoneal exudative
TB
Primary mesothelioma
Serous / mucinous carcinomas
Carcinomatosis
Pancreatitis / pseudocyst

Non-abdominal Starling Forces transudative
Myxoedema
Nephrotic syndrome
CHF
Chronic pericardial tamponade
Constrictive peritonitis.

D E A B M I M  

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BIOLOGICAL BEHAVIOUR

Pathophysiology

Cirrhosis
Ascites marks transition from compensated to decompensated cirrhosis
- attended by increase in predicted mortality from low (1-3%/year) to high (20-60%/year)

1. First, increase in vascular resistance at hepatic microcirculation
- due to mechanical alterations to hepatic architecture, and as a result of underlying liver disease
- and dynamic imbalance between vasodilator and vasoconstrictor stimuli
- i.e. relative deficiency of local NO leads to contraction of  myofibroblasts, stellate cells and vascular SM
(NO is a therapeutic target)

2. Results in portosystemic pressure gradient; sinusoidal portal hypertension

3. Portal backflow leads to pooling of blood in portal circulation
- and thus overproduction of NO in splanchnic circulation
- causes increased blood inflow, further exacerbating portal hypertension.
- bacterial translocation and ensuing cytokins probably also play a key role in splanchnic vasodilation

4. Pooling leads to decrease in effective circulating volume
- and activation of sympathetic nervous system and RAAS
- triggers vasopressing from posterior pituitary
--> avid retention of sodium, fluid and water in the kidneys

5. Coupled with decreased oncotic pressure from liver failure
--> increased inflow of lymph into liver, overwhelming congested liver
--> plasma ultrfiltrate containing retained sodium and water accumulates as ascites.

Malignancies
- multiple hepatic mets with stenosis / occlusion of portal vein branches
- multiple foci of malignant cells scattered through cavity
- obstruction of lymphatics.

Chylous ascites
- obstruction to major lymph channels
- direct leak of chyle through a lymphoperitoneal fistula due to abnormal / injured lymph
- exudation without fistula or obstruction

D E A B M I M  

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MANIFESTATIONS

Risk factors present
Underlying disease factors

Full bulging abdo with flank dullness on percussion.
- 1.5L must be present for this to be detectable

Ascites can dramatically impact on quality of life
- distension, discomfort, immobility
- umbilical hernia
- progressive renal insufficiency, sepsis and respiratory distress.

Chylous Ascites
Painless distention usual
Malnutrition and dyspnea occur in 50%.
Milky fluid on tapping (with high fat content)

D E A B M I M

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INVESTIGATIONS

Biochemistry

Abdominal Paracentesis
- all new patients should have this done.
- and those with possibility of infection
- only contraindicated where DIC and clinically evident fibrinolysis.
- otherwise perform in cirrhotics / coag abnormalities (See Sabiston for study)
Left lower quadrant tap is preferred.
- USS in the obese, where laparotomy scars / adhesions.
- aboid the inferior epigastrics.

Examining the Fluid
Examine the gross appearance
- normally yellow and transparent.
- cloudy if >5000 neutrophils / mm3.
- nearly clear if <1000.
- if blood clots = traumatic, else non-traumatic (clotting factors depleted in peritoneal cavity)

Lab Tests
Cell count
- leukocyte count usually <500cells/mm3, half being neutrophils
- more than 250cells/mm3 suggests bacterial peritonitis (both total WCC and absolute neuts elevated)
Serum-ascites-albumin gradient most reliable method for categorising various causes of ascites
- measure albumin of serum vs ascitic.
- if SAAG >= 1.1g/dL = portal hypertension
- if SAAG <= 1.1g/dL = not portal hypertension.
- accurate to about 97% (Sabiston).

>= 1.1g/dL	<=1.1g/dL
Cirrhosis	Peritoneal carcinomatosis
Alcoholic hepatitis	TB peritonitis
Cardiac ascites	Pancreatic ascites
Massive liver mets	Biliary ascites
Fulminant hepatic failure	Nephrotic syndrome
Budd-Chiari	Post-op lymph leak
Portal vein thrombosis	Serositis in CT disorders
Myxoedema

Complicance
Urinary Na/K
- if ratio >1, equivalent to sodium intake >2g; then probably non compliant with therapy
Or test dose of frusemide:
- if after 80mg, urine sodium over next 8h shows <50mEq Na+ then pts have diuretic-resistant ascites

Complications
Severely limits lifestyle
Risk of SBP
Renal failure
Increased mortality



D E A B M I M

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MANAGEMENT

Principles

1. Aside from transplantation there is no therapy proven to improve mortality.

2. These pts decompensated cirrhosis; are at risk of acute hepatic failure
- encephalopathy and variceal bleeding may be triggered by infection, e.g. SBP
--> prompt antibiotic therapy.

3. Avoid hepatotoxins (alcohol) and nephrotoxins (contrast, aminoglycosides, antibiotics)

4. Determine:
- is cirrhosis cause of ascites, or another problem, e.g. metastatic disease.
- does the pt truly have refractory ascites; has medical therapy been maximised?
- are they compliant? (see above)

5. Consider adjunctive medication with gastro advice, e.g.
- vasoconstrictors (ocreotide)
- Alpha2 agonist (clonidine; decreass sympathetic outflow, decreasing sodium reabsorption and inhibiting RAAS, increase spironolactone effect)
- colloid (albumin; prohibitory cost but in short term situations)

6. Interventional Therapy
- liver transplant = most effective, but never sole indication

Cirrhotic Ascites
Stop drinking.
- may resolve or become responsive.
Dietary sodium restriction and diuretics
- limit to 2g/day
- measure compliance by 24hr urinary sodium levels.
--> if excreting >78mmol/day, should lose weight.
--> if weight increasing, despite losses, pt is consuming salt.
Spironolactone and frusemide given in a 100mg & 40mg / day dosing  will promote natriuresis
- while maintaining normokalaemia
- if ineffective in increasing urinary sodium and decreasing body weight, increase in same 100:40 ratio.

'Intensive therapy'
Combination of both spironolactone 400 mg/day and furosemide 160 mg/day
With 1-2g sodium restricted diet of at least 1 wk duration.

Refractory ascites in cirrhosis
Occurs in <10% of patients.
Options:
- liver transplant
- repeated paracentesis
- see portal hypertension

Diuretic complications
Development of encephalopathy
Renal impairment (doubling of serum creatinine)
Hyponatraemia (<125 mEq/L)
Hyperkalaemia (serum K+ >6 mEq/L)
Gynecomastia and decreased libido from andosterone agonism.

Interventional Treatment Algorithm for Refractory Ascites


Large Volume Paracentesis (LVP)
draining >5L+
- can cause systemic hypovolaemia
- avoided by concurrent administration of albumin.
- also can accentuate hyponatraemia; delayed. must be undertaken with optimized diuretics.
Effective, fast, safe but transient.
Limited by
- need for repeat punctures and risk of gut puncture
- diuretic complications
- bacterial peritonitis
Technique:
- target LLQ, 2 finger breadths cephalad to ASIS; can get USS guidance to be safe (black = fluid).
- prep and drape
- use paracentesis kit containing hollow bore needle and sterile tubing.
- insert needle at an angle.

Peritoneovenous (PV) shunt
Palliate refractory ascites but moving fluid from peritoneal cavity back into circulating volume.
Thus improve renal fx.  But do not improve survival.
But shrinking role due to risks:
- DIC, infection, CHF, limited duration efficacy and risk of placement.
Prefer:

Portosystemic Shunting (TIPS)
Decompression of underlying sinusoidal hypertension.
Esp. when variceal bleeding.
Can result in dramatic improvements to BP, hepatorenal syndrome, hospitalizations


Chylous Ascites
Improve nutrition
- enteral / parenteral.
- low-fat medium-chain trig diet with duretics helped in one trial.
Reduce rate of chyle formation
Correct underlying process.
Paracentesis for symptomatic relief.
Surgical exploration for those not improving on above (50-66% of patients)
- ideally a discrete leaking channel is found for ligation.

Malignant Ascites
Due to direct invasion (carcinomatosis) or generated by cancer cells.
Harbinger of extremely poor prognosis.
Intraperitoneal chemotherapy, cytokine therapy and immunotherapy being evaluated.

Post-operative Abdominal Leaks of Ascites
High mortality
Contribute to wound failure, sepsis, systemic collapse and death.
1. Optimize medical therapy pre op! and post op.
2. Judicious fluid administration
3. Nylon skin sutures with a running / locking fashion.
4. If leak occurs and dehiscence suspected,  early re-exploration
--> survival experience vs leaving with wound care, binders and observation alone.

D E A B M I M

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REFERENCES
Sabiston

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