Modified Transudate

Introduction

Modified transudates are a type of effusion whose cell count and protein content are intermediate between a transudate and an exudate. In some cases, modified transudates may represent a transitional stage before the development of an exudate (as with uroabdomen, which begins as a modified transudate but develops into a chemical exudative peritonitis over time). Modified transudates arise as a result of disruptions to the endothelium or imbalances in the Starling forces. Common causes include:

• Increased vascular hydrostatic pressure resulting from inappropriate activation of the renin-angiotensin-aldosterone system (RAAS) in portal hypertension or congestive heart failure.
• Vasculitis, caused by feline infectious peritonitis virus (FIPV) or neoplasia. (Further discussion of the effusion encountered with FIP.)
• Strangulation of abdominal or thoracic organs may lead to the production of a modified transudate (which will develop into an exudate if untreated). This may occur with lung lobe torsion, torsion of the spleen or of a liver lobe or if part of the liver becomes strangulated within a diaphragmatic rupture.
• Chylous effusions are sometimes considered to be a type of modified transudate.

Diagnosis

Clinical Signs

Effusions may occur in any of the major body cavities, causing ascites, hydrothorax or pericardial effusion. Ascites is often of a high volume. An abdominal fluid thrill will often be palpable and the abdomen may appear to be grossly swollen.

Hydrothorax will cause coughing, tachypnoea and dyspnoea if severe. Dullness will be evident on thoracic percussion if a pleural effusion has developed and the heart sounds will be muffled on auscultation.

Pericardial effusion may be sufficiently severe to cause cardiac tamponade and right-sided heart failure. The heart sounds will be muffled on auscultation and there may be hepatojugular reflux, a jugular pulse or signs of left-sided forward failure. In horses and cattle, ventral oedema is much more likely to be encountered than ascites in animals with congestive heart failure.

Diagnostic Imaging

Effusions are easily diagnosed by ultrasonography and this modality may also be used to guide fine needle aspiration to obtain a sample of the fluid. Effusions also produce a distinctive pattern on plain radiographs:

• With pericardial effusion, the heart may appear to be generally enlarged with a globular shape. There may be a crisp cardiac silhouette (as the heart is moving within a stationary bag of fluid) and a hypovascular lung pattern due to pulmonary underperfusion.
• With ascites, there is a loss of serosal detail due to the presence of fluid in the abdominal cavity. This appearance may also occur with large abdominal masses and in emaciated animals.
• With pleural effusions, the lung lobes are contracted and lobulation is evident. Areas of peripheral radio-opacity should be evident, especially peripherally in the chest.

Cytology

Definitive diagnosis of any effusion relies on collection of a sample and cytological analysis. A refractometer can be used to measure the specific gravity of the fluid. The following features are typical of a modified transudate:

Appearance	Yellow to serosanguinous, turbid fluid
Specific gravity	1.018 - 1.030
Total protein	25 - 50g/l
Nucleated cells	0.3 - 5.5 x10e9/L (up to 7 x 10e9/L), of which the majority are mesothelial cells, macrophages, non-degenerate neutrophils and small lymphocytes

If the effusion has been caused by a neoplasm, exfoliated cells may be observed in the fluid but this is unlikely to be useful in identifying the origin of the tumour.

Treatment

Unless the effusion is causing clinical signs, it is generally not advisable to drain it as it will quickly recur. Drainage will also deplete body protein reserves even further. However, pleural or pericardial effusions should certainly be drained in animals with dyspnoea or signs of heart failure.

Diuretics are often used as first-line therapeutic agents for congestive heart failure and these will help to prevent fluid accumulation in body cavities. Consideration should be given to the use of spironolactone because, as well as sparing body potassium, it acts to prevent further activation of the RAAS. Bodyweight and abdominal girth can be measured regularly (including by owners) to give a crude estimate of the effectiveness of diuretic therapy.

The presence of neoplastic cells in an effusion should prompt further investigation through diagnostic imaging or exploratory surgery.

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