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, or decreased vascular oncotic (usually colloidal) pressure, but is most commonly associated with venous hypertension resulting from right heart failure in response to increased pulmonary resistance.
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), also associated with hepatic fibrosis. It is well documented that most cases are caused by a genetic predisposition to pulmonary hypertension, which progresses to congestive heart failure and terminal ascites in many cases.
Pulmonary hypertension occurs frequently in chickens secondary to high altitude-associated hypoxia with resultant polycythemia and increased blood viscosity. It also occurs frequently secondary to the RBC rigidity of sodium toxicity and less frequently from lung pathology. When ascites occurs at high 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. Cold stress, even briefly, during the first 3 wk of life is known to markedly increase predisposition to ascites syndrome.
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 may also cause ascites.
Pulmonary hypertension syndrome 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 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, lung pathology that narrows or occludes capillaries, increased RBC rigidity, or polycythemia with increased blood viscosity) may result in flock outbreaks of pulmonary hypertension syndrome with or without ascites.
The incidence of pulmonary hypertension syndrome 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 and dilatation 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.
Occasionally, young broilers develop pulmonary hypertension syndrome, particularly if increased sodium or lung pathology (eg, aspergillosis) is involved, but mortality is greatest after 5 wk of age. There are no signs 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 may be smaller than their pen mates. However, rapid growth rate is a known predisposing factor, and sometimes the largest broilers are affected, with occurrence in males more frequent than in females. The ascites increases the respiratory rate and reduces exercise tolerance. Affected broilers frequently die on their backs. Not all broilers that die from pulmonary hypertension syndrome have ascites. Death may occur suddenly before signs are seen.
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, usually from secondary infections. Right ventricular dilatation and mild to marked hypertrophy of the right ventricular wall may be noted. The right atrium and vena cava are markedly dilated in most cases. Occasionally, there is thinning of the left ventricle. The lungs are extremely congested and edematous. The intestine may or may not be empty.
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 pulmonary hypertension syndrome, even if there is no fluid in the body or heart sac.
Reducing the birds’ metabolic oxygen requirement by slowing growth or reducing feed density or availability can prevent ascites caused by pulmonary hypertension syndrome. Environmental temperature, humidity, and air movement should be controlled to prevent excessive loss of body heat, particularly in the early neonatal period. Even brief exposure to cold stress during the first weeks of life is known to predispose flocks to this condition. Ascites caused by other factors (eg, sodium, lung damage, liver damage, etc) can be prevented by avoiding the etiologic agents involved. Altitudes >3,000 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. Research has demonstrated that broilers can be genetically selected for both resistance and susceptibility to pulmonary hypertension syndrome and associated ascites.