The Approach to Ascites

36 The Approach to Ascites



Anthony P. Carr



1. What clinical signs are associated with ascites?

The clinical signs associated with ascites can be either masked or exacerbated by the signs resulting from the cause of the ascites. As an example, a dog with heart failure and ascites will have exercise intolerance and dyspnea both from the ascites and from the heart disease. In general, significant fluid accumulation in the abdomen will result in cardiovascular (decreased venous return) and respiratory (pressure on the diaphragm limits breathing ability) compromise. Ascites, if significant enough, can result in a fluid wave that can be noted either spontaneously or after ballottement.


2. What are the general pathophysiologic ways in which fluids can accumulate?

Fluid can accumulate because of decreased colloidal pull (generally, hypoalbuminemia), increased resistance to flow (e.g., heart failure or tumor obstruction), increased permeability of the blood vessels, or increased lymphatic leakage.


3. What kinds of fluids can accumulate in the abdomen?

The fluids that can accumulate are blood, chyle, exudates, modified transudates, and pure transudates. Some authors classify hemorrhage as an exudate.


4. What could cause hemorrhage into the abdomen?

Hemorrhage into the abdomen can result either because of a hemostatic disorder or because of a bleeding lesion in the abdomen. Generally only a coagulopathy would result in cavity bleeding; this would not be expected with disorders of primary hemostasis (e.g., thrombocytopenia, von Willebrand’s disease). The most common coagulopathy to cause hemoabdomen is vitamin K antagonist rodenticide toxicity. Bleeding into the abdomen with normal hemostasis can occur because of trauma, ruptured blood vessels (e.g., splenic torsion or gastric dilatation-volvulus [GDV]), or bleeding tumors (mainly involving the spleen or liver).


5. What are the characteristics of exudates and what can cause them?

Exudates are rich in protein (>2.5 g/dl) and nucleated cells (>7,000/μl) and have a specific gravity of more than 1.025. They almost always are a result of increased permeability either through inflammation or infection. Nonseptic exudates can result from severe inflammatory conditions such as pancreatitis, bile peritonitis, or uroabdomen (although initially the inflammation would be absent and the fluid would not contain cells or protein). Tumors can also cause nonseptic exudates.


Visible bacteria confirm that a fluid is septic, although neutrophils with signs of degeneration or toxic changes raise the suspicion of an infection even if bacteria are not visible. Septic exudates can result from bile peritonitis (if the bile was infected), gastrointestinal (GI) tract rupture, a penetrating wound, or ruptured pyometra.


6. What is the difference between a transudate and a modified transudate? Name some potential differentials for each.

A transudate is low in specific gravity (<1.015), protein (<2.5 g/dl), and cells (<1500/μl). Modified transudates have specific gravities between 1.015 and 1.025, protein between 2.5 and 6.0 mg/dl, and cell concentrations of less than 7,000 cells/μl. Over time the presence of a pure transudate in the abdomen will lead to peritoneal irritation with resultant increases in protein and cell count. This will change the transudate to a modified transudate.


Pure transudates can be caused by decreased oncotic pressure, such as occurs in dogs with severe hypoalbuminemia (e.g., protein-losing enteropathy, protein-losing nephropathy). In these dogs it is not uncommon to find peripheral edema as well. Low levels of albumin can also be observed with liver disease, although the development of ascites in these dogs is usually exacerbated by the presence of portal hypertension. Portal hypertension can also lead to the formation of a transudate. Portal hypertension can be classified as prehepatic, hepatic, or posthepatic depending on the location of the obstruction to flow. In many dogs with liver disease the lesion can be at multiple sites. Pure prehepatic portal hypertension is associated with restriction of blood flow at the level of the portal vein and results initially in the formation of a transudate.


Modified transudates have higher protein levels and higher cell counts. Hepatic or posthepatic portal hypertension can cause the accumulation of a modified transudate. Posthepatic portal hypertension results when the level of the obstruction to flow is in either the hepatic vein or the caudal vena cava such as by kinking of the vein, right-sided heart failure, or cardiac tamponade. This results in increased hepatic lymph formation in the sinusoids, with subsequent leakage into the abdomen through the capsule of the liver.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on The Approach to Ascites

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