| (Waterbelly, Right ventricular failure, Pulmonary hypertension syndrome) Ascites is an accumulation of noninflammatory transudate in one or more of the peritoneal cavities or potential spaces.  The fluid, which accumulates most frequently in the two ventral hepatic, peritoneal, or pericardial spaces, may contain yellow protein clots. Ascites may result from increased vascular hydraulic pressure, vascular damage, increased tissue oncotic pressure, decreased vascular oncotic (usually colloidal) pressure, or blockage of lymph drainage. The most common cause of ascites is increased vascular hydraulic pressure in the venous system, which is most commonly caused by right ventricular failure (RVF) or hepatic fibrosis. In poultry, RVF is usually secondary to valvular insufficiency and may result from inflammatory (myocarditis, valvular endocarditis) or degenerative disease of the myocardium or valves or from congenital heart disease. In turkeys, spontaneous cardiomyopathy (Round Heart Disease Of Turkeys) is a common cause of ascites. However, the most common cause of ascites in meat-type chickens is RVF in response to increased pulmonary arterial resistance. Pulmonary hypertension occurs frequently in chickens secondary to the hypoxia of altitude with the resultant polycythemia and increased blood viscosity. It also occurs frequently secondary to the red blood cell rigidity of sodium toxicity and less frequently from lung pathology. When ascites occurs at low altitudes in meat-type chickens, which have a high metabolic oxygen requirement, it is usually caused by primary or spontaneous pulmonary hypertension because of insufficient capacity of the pulmonary capillaries. In poultry, liver damage may be caused by aflatoxin or by toxins from plants such as Crotalaria. In broiler chickens, obstructive cholangiohepatitis (caused by Clostridium perfringens infection) is the most common cause of the liver damage, which results in ascites. In both meat-type ducks and breeders, amyloidosis of the liver frequently causes ascites. Pathogenesis and Epidemiology: Pulmonary hypertension syndrome (PHS) is caused by increased pressure in the pulmonary arteries when the heart tries to pump more blood through the lungs to meet the body's oxygen requirement. The resultant volume and pressure overload on the right ventricle cause dilatation and hypertrophy of the right ventricular wall, valvular insufficiency, RVF, and ascites. Bird lungs are rigid and fixed in the thoracic cavity. The small capillaries can expand very little to accommodate increased blood flow. Lung size in proportion to body weight, and particularly to muscle mass, decreases as meat-type chickens grow. Increased blood flow results in primary pulmonary hypertension and cor pulmonale with sporadic cases of RVF and ascites in fast-growing broilers. Predisposing factors that increase oxygen demand (eg, cold), reduce oxygen-carrying capacity of the blood (eg, acidosis, carbon monoxide), increase blood volume (eg, sodium), or interfere with blood flow through the lung (eg, by lung pathology that narrows or occludes capillaries, by increased RBC rigidity, or by polycythemia with increased blood viscosity) may result in flock outbreaks of PHS with or without ascites. The incidence of PHS is >2% in some broiler and many roaster flocks and is occasionally 15-20% in other roaster flocks. Right ventricular hypertrophy is the response to an increased workload and eventually leads to RVF if the volume or pressure load persists. Hypertrophy of the right ventricular wall is directly related to pulmonary hypertension, and the ratio of the right ventricle to the total ventricular mass can be used as a measure of the increased pressure load on the right ventricle. Clinical Findings: Occasionally, young broilers develop PHS, particularly if increased sodium or lung pathology (eg, aspergillosis) is involved, but in primary pulmonary hypertension, mortality is greatest after 5 wk of age. Clinical signs are not seen until RVF occurs and ascites develops. Clinically affected broilers are cyanotic, the abdominal skin may be red, and peripheral vessels congested. Because growth stops as RVF develops, affected broilers are smaller than their pen mates. The ascites increases the respiratory rate and reduces exercise tolerance. Affected broilers frequently die on their back, and differential diagnosis includes flip-over disease (Flip-over Disease). Not all broilers that die from PHS have ascites. Death may occur suddenly before clinical signs are seen. Lesions: Most lesions are the result of increased venous hydraulic pressure secondary to RVF. There is a variable amount of clear yellow fluid and clots of fibrin in the hepatoperitoneal spaces. The liver may be swollen and congested, or firm and irregular with edema, and have clotted protein adherent to the surface. It may be nodular or shrunken; it may be white with subcapsular edema and a thickened capsule, or have large or small blebs of fluid between the capsule and the visceral peritoneum. Hydropericardium is mild to marked, and occasionally there is pericarditis with adhesions. There is right ventricular dilatation and mild to marked hypertrophy of the right ventricular wall. The right atrium and vena cava are very dilated. Occasionally, there is thinning of the left ventricle. The lungs are extremely congested and edematous. The intestine may or may not be empty. Diagnosis: Broilers that die from ascites or suddenly as the result of RVF or pulmonary hypertension can be identified by the enlarged heart; enlarged, thickened right ventricle; or fluid in the body cavities and heart sac. If the wall of the right ventricle is enlarged or thickened, the broiler has probably died from PHS, even if there is no fluid in the body or heart sac. Control: Ascites caused by PHS can be prevented by reducing the birds' oxygen requirement; slowing growth or reducing feed lowers the metabolic oxygen requirement. Environmental temperature, humidity, and air movement should be controlled to prevent excessive loss of body heat. Ascites caused by other factors (eg, sodium, lung damage, liver damage, etc) can be prevented by avoiding the etiologic agents involved. Altitudes >3000 ft (900 m) are unsatisfactory for meat-type chickens, and growth must be slowed to prevent mortality. More care to prevent chilling is also necessary at higher altitudes. See Also:
Breast Blisters
Cannibalism
Fluke Infections
Gout
Pendulous Crop
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