Small animal clinicians are frequently presented with animals showing abnormalities of the abdomen. In many cases these abnormalities result from primary intra-abdominal disease, although the clinical signs may merely be an abdominal manifestation of extra-abdominal disease. This presentation focuses on diseases causing abdominal distension or effusion in dogs and cats and is aimed at assisting the practitioner to develop an approach to diagnosis and treatment.
Fluid accumulations in the abdomen may take the form of air (pneumoperitoneum), blood (hemoperitoneum), septic or non-septic exudates, pure and modified transudates, bile, chyle or urine or a combination of the above. In some cases, diagnosis is obvious, in others further work-up is required to determine the exact nature of the effusion, the likely aetiology and the most appropriate plan of action.
Pneumoperitoneum: Air can enter the peritoneal cavity by a number of different routes. Most commonly, pneumoperitoneum is an indication of gastrointestinal tract rupture and is considered to be a surgical emergency. However it may also arise as a result of penetrating trauma, migration of air from other sites such as the pleural space, or rupture of an intraabdominal viscii (gall bladder or urinary bladder) that has been infected with gas-producing bacteria. Pneumo-peritoneum may be iatrogenic, resulting from laparoscopy, abdominocentesis or surgical exploration; air persists for up to a week after laparotomy. Pneumoperitoneum can occur in man as an idiopathic event; idiopathic pneumoperitoneum has also been reported in a dog.
Bile peritonitis: The most common cause of intra-abdominal bile accumulation is traumatic rupture of the gall bladder or biliary tract. Previous case series suggest that rupture is most likely to occur in the biliary tree near the openings of the lobar bile ducts. Surgical treatment requires good retraction, lighting, suction, knowledge of surgical anatomy and skills with delicate soft tissue surgery. Bile peritonitis may also occur after gall bladder rupture as a result of ascending cholangiohepatitis; in this case, resection of the necrotic gall bladder, treatment with appropriate antibiotics and possibly also open peritoneal drainage is required.
Uroperitoneum: As with the biliary tree, perforation of the urinary tract most commonly follows external trauma such as automobile accidents or falling from a height. However, ureteral rupture may result from occlusion with calculi descending from the renal pelvis. Iatrogenic rupture of the urinary bladder, or perforation of the urethra is unfortunately common in cases with obstructive urinary tract disease where repeated attempts to unblock the animal fail. Some small ruptures of the urinary tract are amenable to conservative treatment providing urinary diversion and decompression of the urinary tract can be accomplished. Others require prompt surgical intervention. Management of animals at the University Veterinary Centre, Sydney, that have undergone traumatic attempts to unblock them, includes a retrograde urinary contrast study. Urinary tract perforation or stricture is commonly noted.
Chyloperitoneum: While chylothorax may often be idiopathic, chyloperitoneum usually results from a severe pathological process such as lymphatic or other neoplasia. It has also been encountered as a sequel to thoracic duct ligation. In general, the prognosis for animals with chyloperitoneum is poor.
Septic Exudate: Septic exudate (septic peritonitis) usually results from perforation of the gastrointestinal or genitourinary tract. Identification of the underlying disease process (foreign body, neoplasia, ulcerative disease) is important, as it is critical to prognosis. Hepatic and splenic abscesses may occur; there is a strong association between hepatic abscessation and underlying hepatic neoplasia.
Ascites: In general, the term 'ascites' refers to serous abdominal fluid accumulation. Ascites may be a manifestation of either a transudate, or a modified transudate.
The term 'transudate' refers to low-protein fluid that has escaped from the intravascular space as a result of reduced oncotic, or increased hydrostatic, pressure. Typical examples include the ascites of hypoproteinaemia and ascites due to portal vein obstruction. Clinical evaluation should include measurement of plasma protein and, if low, evaluation for liver disease, protein-losing enteropathy or nephropathy. If the plasma albumin concentration is above 15 g/L, the portal circulation should be evaluated for evidence of an obstructive lesion.
A modified transudate has an elevated protein content, usually as a result of inflammation or a contribution of high-protein hepatic lymph. Note that right-sided congestive heart failure (including cardiac tamponade due to pericardial effusion) results in a modified transudate as venous obstruction occurs at a post-sinusoidal level and results in loss of hepatic lymph into the ascitic fluid. As the amount of intravascular protein available to be lost into ascitic fluid is dependent on plasma protein concentration, the plasma:ascites protein ratio is more important in determining whether ascites is 'high protein' or 'low protein' than any arbitrary guidelines. Other causes of modified transudate in the abdomen include neoplasia (may or may not be accompanied by abnormal cell types although reactive mesothelial cells can be difficult to differentiate from neoplastic cells), lymphocytic/plasmacytic cholangiohepatitis in cats (treatable with immunosuppressive agents) and sclerosing-encapsulating peritonitis (in which abdominal viscera are incarcerated within an inflammatory fibrous membrane.
Effusion of high-protein fluid may occur in response to peritoneal irritation by substances such as bile and urine, and may disguise the underlying aetiology. It is important to check the urea content of the fluid (and plasma:fluid urea concentration) if leakage from the urinary tract is considered a possibility.
ALGORITHM FOR DIAGNOSIS OF ASCITES IN DOGS AND CATS
Causes of fluid accumulation in small animal patients at the UVC, Sydney
Hepatic amyloidosis (cats)
Trauma (iatrogenic, automobile, other)
Secondary to thoracic duct ligation
Rupture of the gastrointestinal tract
Splenic torsion and necrosis
Pre-sinusoidal portal vascular occlusion (portal vein thrombosis, portosystemic shunt ligation)
Post-sinusoidal portal or hepatic vascular occlusion (e.g., right-sided congestive heart failure, Budd-Chiari syndrome)
Feline Infectious Peritonitis (FIP)
Lymphocytic/plasmacytic cholangiohepatitis (cats)
Bacterial or chemical peritonitis