Ascites

• Ascites - clinical signs

  Dependant on the underlying cause, ascites itself is not a diagnosis.

  • Abdominal distension and discomfort.
  • Dyspnoea - either from pressure on diaphragm, or if also have pleural effusion.
  • Lethargy
  • Owners may report weight gain, difficulty getting up/down.
  • Other signs depending on underlying cause - vomiting and diarrhoea, liver disease, coughing/syncope - CHF).
• Ascites - differential diagnosis

  Organomegaly (e.g. splenomegaly, hepatomegaly).

  Abdominal mass

  Pregnancy

  Bladder distension

  Obesity

  Gastric distension.
• Ascites - identifying it

  History - both past and present

  • When did this start, the order of the signs, want a clue to the underlying disease.

  Clinical examination - look at the whole animals.

  Ballottement - tapping of the abdomen, fluid thrill.

  Ultrasound.
• Ascites - sampling the fluid


  Abdominocentesis or ‘peritoneal tap’

  Blind vs ultrasound guided:

  • Blind does not need an ultrasound so is quicker but you can’t see where you’re going. This is fine when there is a lot of fluid, but if there is less fluid or there is possibly an abdominal mass then you should do ultraosund. Usually you will have conformed the ascites with an ultrasound scan anyway so the ultrasound will already be out.
• Ascites - identifying the fluid


  Gross appearance (and smell) - e.g. septic - opaque and foul smelling.

  Cellularity - number and type - good quality smears.

  Protein content

  Easy to do - refractometer, microscope

  If less urgent, can send to lab.
• Ascites types of fluid - protein poor transudate

  Clear, colourless or pale straw colour. Total protein <20 often <15. Total nucleated cell count <1.5. Neutrophils and macrophages with some mesothelial cells.
• Ascites types of fluid - protein rich transudate 


  Often yellow, blood tinged, turbid. Total protein usually >20. Total nucleated cell count <5. Macrophages and mesothelial cells, increasing number of neutrophils and small lymphocytes.
• Ascites types of fluid - exudate

  Typically turbid, various colour. Total protein >20, Total nucleated cell count >5. Neutrophils or nuetrophils and macrophages. May see neoplastic cells in the fluid if there is a mass but not always due to the high inflammatory cell count.
• Pathophysiology of protein poor transudate in ascites

  Watery-clear appearance.

  If you get a low plasma level (marked decreased in albumin - hypoalbuminaemia), then get decrease in plasma colloid oncotic pressure so fluid leaks out as there is not oncotic pressure to retain the fluid.

  Quite late on in the disease process:

  • Due to loss (protein losing nephropathy (kidney)), protein losing enteropathy (through the gut).
  • Can get it from liver disease.

  Ultrasound is of limited use to determine the cause of exudate
• Differentials of protein poor transudate in ascites

  Protein-losing nephropahty.

  Hepatic failure (due to either hypoalbuminaemia or pre-hepatic portal hypertension, or a combination).

  Protein losing enteropathy.
• Pathophysiology of protein rich transudate

  Increased hydraulic pressure within blood and/or lymphatic circulation - usually lungs or liver.

  Protein leaks from permeable capillaries, ascites develops when resoprtive capacity of regional lymphatics is overwhelmed.

  Total protein is the important characteristic - over time, transudate will irritate the mesothelium, leading to inflammation, and increased total nucleated cell count.
• Differentials of protein rich transudate

  Cardiovascular disease.

  Chronic liver disease - post-hepatic portal hypertension.

  Neoplasia

  Thrombosis - rare, due to fluid backlog.
• Pathophysiology of exudate in ascites

  Inflammatory process - chemotactants and vasoactive substances attract inflammatory cells, and cause increased vascular permeability.

  Hight TNCC - neutrophils and other phagocytic/inflammatory cells.

  Can be septic or non-septic.

  If septic - can be bacteria, fungi or mycoplasma.
• differential for septic exudate in ascites

  Penetrating wound

  Surgical complication - i.e enterectomy causing septic peritonitis.

  Rupture of surgical lesion

  Bacteraemia (rare).
• Investigations for septic exudate in ascites

  Abdominocentesis

  Appearance/ smell of fluid.

  Cytology - numerous degenerate neutrophils +/- intracellular bacteria.

  Culture and sensitivity

  Lactate, glucose.
• Differentials for non-septic exudate in ascites

  Neoplasia

  Uroperitoneum

  Bile peritonitis

  FIP
• Investigations for non-septic exudate in ascites

  Abdominocentesis

  Appearance of fluid

  Cytology - non-degenerate neutrophils, absence of bacteria.

  Fluid analysis - high urea, creatinine and potassium in fluid if uroperitoneum, green-gold material of bile peritonitis.

  Biochemistry (especially for uroperitoneum).

  Ultrasound
• Ascites - lymphatic compromise pathophysiology

  Rare (more commonly chylothorax)

  Chylous or non-chylous

  Obstruction or destruction of lymphatics.

  Leakage of lymph and lipids.
• Ascites - lymphatic compromise investigations

  Appearance - may look milky.

  Cytology - numerous small lymphocytes, over time, irritation leads to increase in nuetrophils and macrophages.

  Fluid analysis - triglyceride higher than serum, cholesterol lower due to size of the molecules.

  Ultrasound

  Biochemistry.
• Ascites - lymphatic compromise differentials

  Cardiac disease

  Hepatic disease

  Neoplasia

  Steatitis - inflamed fat (not common).
• Ascites - haemorrhagic effusion diagnosis and investigations

  Differentials:

  • Surgical and non-surgical trauma.
  • Haemostatic defects.
  • Neoplasia

  Investifactions:

  • PCV & TP of fluid
  • Presence of platelets
  • Cytology
  • Ultrasound.