Left side displacement of abomasum (LDA)
Etiology: It occurs commonly in large-sized, high producing adult dairy cows, immediately after parturition. High yielders are at a greater risk. The exact etiology is unknown. Occasional cases may also occur before parturition. Feeding of a low roughage and high concentrate diet is associated with LDA. Older cows suffer more than the younger ones. Following heavy grain feeding, flow of rumen ingesta to abomasum is increased. This causes distension of the abomasum with gases, predisposing its displacement. Increase in volatile fatty acids (VFA) contents of rumen reduces the motility of the smooth muscles and may cause abomasal distension. Concurrent diseases like hypocalcemia, metritis, mastitis, indigestion and traumatic reticuloperitonitis were also associated with LDA.
Right side displacement of abomasum (RDA)
Etiology: It is a subacute disease of mostly high yielding dairy cows few weeks after parturition. It occurs either due to obstruction of pylorus or primary atony of abomasal musculature. Atony of abomasum may occur to grain feeding, relative inactivity during winter housing and stress of parturition.
Pathogenesis: In LDA, abomasal atony is the primary dysfunction. The atonic organ is displaced upward along the left abdominal wall, lateral to the spleen and dorsal sac of the rumen. Hypomotality of abomasum is associated with high concentrate and low roughage diet. Due to abomasal atony there is a mild metabolic alkalosis, hypokalemia and hypochloremia.
In RDA, there is abomasal atony resulting in the accumulation of gases and fluid leading to gradual distension and displacement in caudal direction on the right side. During this period there is continuous secretion of hydrochloric acid, sodium chloride and potassium in the abomasum. This also leads to the metabolic alkalosis, hypokalemia and hypochloremia and the animal is dehydrated.
Clinical signs: The clinical signs of left displacement of abomasums and right displacement of abomasum are discussed here.
Left displacement of abomasum: Animal shows inappetance within few days following parturition. There is marked fall in milk production. Temperature, heart and respiratory rates are within the normal range. Faeces are pasty and scanty. Auscultation of left paralumber fossa reveals splashing sounds. Rumen contractions are decreased in frequency and amplitude. On rectal examination, emptiness in the right upper abdomen is observed and rumen size is small. Mild abdominal pain is evident by shifting weight from one leg to another (treading).
Right displacement of abomasum: History of calving within last few weeks can be known from the owner. Affected animal has low milk production and inappetance to anorexia. There is no interest in feed and the animal is dehydrated. Temperature, heart and respiration rates are normal. Mucus membranes are pale or muddy. Rumen is atonic. Distended abomasum may be palpated behind and below the right costal arch. Splashing sounds are heard on auscultation on right abdomen. Faeces are scanty, soft and dark in colour. Sudden death may follow after rupture of abomasum.
Laboratory diagnosis: Mild haemoconcentration is revealed by increase in PCV, Hb (hemoglobin) and plasma protein. There is increased level of BUN (blood urea nitrogen) and metabolic alkalosis. Paracentesis of the distended abdomen (10-11 intercostal space) may reveal pH of 2 to 3 with no protozoa. Mild hypocalcaemia is also present.
Treatment: Non-surgical correction attempt may be taken. Animal has to be casted on left side by tying the feet together and rolling the animal from side to side in 70° arc while the animal is in dorsal recumbency. Rolling and manipulation may be successful. Intravenous glucose therapy may be required once as ketotic signs appear. Animal should not be fed with grains for 3-5 days. Fluids and electrolytes may be given. To evacuate contents of abomasum mineral oil or magnesium hydroxide may be given.