Ascites Flashcards

1
Q

What is ascites?

A

Excessive accumulation of fluid in the abdominal cavity

  • Variable amounts depending on the origin and severity of the pathology
  • To be detectable on examination, must have >500mls in someone of average build
  • Graded according to amount of distension

Some types are resistant to diuretics

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2
Q

What is the difference between an exudate an a transudate?

A

Transudate = increased hydrostatic pressure in veins leading to pressure gradient between vessels and abdominal cavity and the subsequent leakage of a transudative fluid

Exudate = actively secreted fluid secondary to inflammation (and resultant increased vascular permeability) or malignancy

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3
Q

What are the causes of transudative ascites?

A
  • Cirrhosis*
  • c. 75% of patients
  • Associated with poor prognosis

Right heart failure

Splenic or portal vein thrombosis

Budd-Chiari syndrome

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4
Q

What are the causes of exudative ascites?

A

Malignancy:

  • c. 15% of ascites
  • GI tract (carcinoma of stomach, colon, pancreas, HCC, mets)
  • Carcinoma of the ovary: Meigs’ syndrome = rare complication of ovarian cancer, leading to ascites out of proportion to the size of the tumour and (unilateral) pleural effusion
  • Hodgkin’s and NH-lymphoma

Pancreatitis

TB

Hypoalbuminaemia:

  • Nephrotic syndrome
  • Severe malnutrition
  • Protein losing enteropathy
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5
Q

How does ascites present?

A

Abdominal distension:

  • +ve shifting dullness
  • Weight gain

Abdominal discomfort/pain
- Esp if becomes infected

Shortness of breath
- As diaphragm gets splinted
and venous return reduces (from pressure on IVC)
- +/- concomitant pleural effusions

Peripheral oedema

Reduced appetite and nausea

Signs of underlying cause:

  • ALD e.g. jaundice, alcohol Hx etc
  • Malignancy e.g. masses, Virchow’s node, Ca Hx etc
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6
Q

How do you investigate ascites?

A

Clinical Ex

Look for cause:
- FBC, LFT, U+E, Clotting, TFT, Hep Abs etc

USS:

  • Can detect volumes <500ml
  • Also good to view other organs for origin of pathology e.g. pancreatitis, carcinomas etc

Ascitic tap:

  • Insertion of a needle in the flank to drain a small amount of fluid for analysis
  • Can also be done therapeutically for massive ascites (+ drains inserted to the same effect) causing respiratory distress or abdominal pain
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7
Q

What do you look for when assessing ascitic fluid from a tap?

A

ABC SAAG

Appearance:

  • Clear/straw coloured = liver cirrhosis
  • Cloudy = SBP, pancreatitis; perforated bowel
  • Bloody = malignancy, haemorrhagic pancreatitis (often seen with Grey-Turners flank sign)
  • Chylous/milk coloured = lymphoma, TB, malignancy

Biochemistry:

  • Total protein = 0.3-4g/dL normal; >4g SBP/TB
  • Glucose = similar to serum is normal; higher than serum level is pancreatitis

Cells (microscopy):
- RCC = none is normal; >100/microL is TB/malignancy; >100,000 microL is haemorrhage/trauma
WCC = <250microL is normal; >250 and mostly neutrophils is SBP; >250 and mostly lymphocytes is TB
- May also find Ca cells themselves

Serum ascitic albumin gradient - SAAG
- Indirect measure of portal pressure and can be used to tell if ascites is due to portal HTN i.e. if exudate vs transudate

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8
Q

How do you interpret the SAAG?

A

SAAG = (serum albumin) - (ascitic fluid albumin)

High SAAG:

  • > 1.1g/dL
  • ascitic fluid is a transudate i.e. caused by high portal HTN

Low SAAG:

  • <1.1g/dL
  • ascitic fluid is an exudate
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9
Q

How else can you differentiate between transudate and exudate on ascitic tap?

A

LDH:

  • <225U/L = transudate
  • > 225U/L = exudate

But SAAG is used more frequently

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10
Q

How do you manage ascites?

A

Manage underlying cause

Salt restriction:

  • <90mmol/day (5.2g salt/day)
  • Useful in cirrhosis, but not if other aetiologies i.e. Ca.

Diuretics:

  • Spironolactone = best initial choice; monitor serum K as hyperK often limits use
  • Loop diuretics = useful adjuncts, but only when max dose spiro used

Therapeutic paracentesis/drain

  • Infection risk can be reduced by limiting catheter time to <6-8hrs
  • Fluid replacement +/- albumin often given to combat the hypotension caused by reducing IVC pressure

TIPS - for chronic ascites
- Notable side effect is increased risk of hepatic encephalopathy

Beware:
- Long history of stable cirrhosis with acute development of ascites - must exclude HCC

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11
Q

What is spontaneous bacterial peritonitis and how do you prevent it?

A

A complication of ascites

  • Thought to be caused by translocation of gut bacteria across gut wall and/or haematogenous spread
  • E.coli is the most common bacteria implicated

Presents like classical peritonitis

Prevent by:

  • Proper treatment of ascites =
  • Empirical treatment of those with high neutrophil counts in their ascitic fluid (>250neutrophils/ml) with IV Abx and albumin
  • Lactulose - to expedite gut transit time/reduce faecal stasis and time for bacteria to translocate

Subsequent prophylaxis for individuals recovering from SBP:
- Long term oral Abx e.g. norfloxacin, levofloxacin, trimethoprim etc

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