Because the abomasum is suspended loosely by the greater omentum and lesser omentum, it can be moved from its normal position on the right ventral part of the abdomen to the left or right side (LDA, RDA), or it can rotate on its mesenteric axis while displaced to the right and lateral to the liver (AV). The abomasum can shift from its normal position to left displacement or to right displacement over a relatively short period. AV can develop rapidly or slowly from an uncorrected RDA.
Although LDA, RDA, and AV (previously incorrectly referred to as right torsion of the abomasum) are often considered separately, there is evidence of a common underlying etiology; they may be different manifestations of the same or a similar disease process.
The etiology is multifactorial, although abomasal hypomotility and dysfunction of the intrinsic nervous system are thought to play an important role in development of displacement or volvulus. Important contributing factors include abomasal hypomotility associated with hypocalcemia and possibly hypokalemia, as well as concurrent diseases (mastitis, metritis) associated with endotoxemia and decreased rumen fill, periparturient changes in the position of intra-abdominal organs, and genetic predisposition, particularly in deep-bodied cows. Genetic predisposition is correlated with milk yield, indicating that current selection practices for milk production are increasing the incidence of abomasal displacement. Hypomotility is also related to ingestion of high-concentrate, low-roughage diets, which reduce abomasal motility through a poorly defined mechanism that may involve hyperinsulinemia or increased concentrations of volatile fatty acids. One of the mechanisms of excessive gas accumulation in cattle with abomasal displacement is reticulum-mediated inflow of ruminal gas into the abomasum that is hypomotile. In addition, high-concentrate diets result in increased gas production in the abomasum (mostly carbon dioxide, methane, and nitrogen). Finally, subclinical and clinical ketosis increase the risk of abomasal displacement through an unknown mechanism that may be associated with decreased rumen fill.
Approximately 80% of displacements are seen within 1 mo of parturition; however, they can be seen at any time. LDA is much more common than RDA (30 LDA to 1 RDA); cases of AV are also more common than RDA (10 LDA to 1 AV). AV is preceded by RDA.
In LDA, as a result of abomasal hypomotility and gas production, the partially gas-distended abomasum becomes displaced upward along the left abdominal wall lateral to the rumen. The fundus and greater curvature of the abomasum are primarily displaced, which in turn causes displacement of the pylorus and duodenum. The omasum, reticulum, and liver are also rotated to varying degrees. The abomasal obstruction is partial, and although the segment contains some gas and fluid, a certain amount can still escape, and the distention rarely becomes severe. Because there is minimal interference with blood supply unless the gas distention is marked, the effects of displacement are entirely due to interference with digestion and passage of ingesta, which lead to decreased appetite and dehydration.
A mild metabolic alkalosis with hypochloremia and hypokalemia are common. The hypochloremic metabolic alkalosis is due to abomasal hypomotility, continued secretion of hydrochloric acid into the abomasum, and the partial abomasal outflow obstruction, with sequestration of chloride in the abomasum and reflux into the rumen. Hypokalemia is due to decreased intake of feeds high in potassium, sequestration of potassium in the abomasum, and dehydration. Secondary ketosis is common and may be complicated by development of hepatic lipidosis (fatty liver disease; see Fatty Liver Disease of Cattle).
In RDA, hypomotility, gas production, and displacement of the partially gas-filled abomasum occur as in LDA. Mild hypokalemic, hypochloremic, metabolic alkalosis develops as well. After this dilatation phase, rotation of the abomasum on its mesenteric axis leads to volvulus and local circulatory impairment and ischemia (hemorrhagic strangulating obstruction). The volvulus is usually in a counterclockwise direction when viewed from the rear and the right side of the animal. The omasum is displaced medially and can be involved in the volvulus with occlusion of its blood supply (called an omasal-abomasal volvulus) and displacement of the liver and reticulum. In rare cases, the reticulum can be involved (called a reticular-omasal-abomasal volvulus).
A large quantity of chloride-rich fluid (up to 50 L) accumulates in the abomasum, and hypochloremic, hypokalemic metabolic alkalosis develops. The blood supply to the abomasum, and often the omasum and proximal duodenum, is compromised, eventually resulting in ischemic necrosis of the abomasum and proximal duodenum as well as dehydration and circulatory failure. As circulatory failure progresses, a metabolic acidosis due to hyper-l-lactatemia and azotemia can become superimposed on the preexisting metabolic alkalosis.
The typical history of abomasal displacement includes anorexia (most commonly a lack of appetite for grain with a decreased or normal appetite for roughage) and decreased milk production (usually significant but not as dramatic as with traumatic reticuloperitonitis or other causes of peritonitis). In AV, anorexia is complete, milk production is more markedly and progressively reduced, and clinical deterioration is rapid. In abomasal displacement, temperature, heart rate, and respiratory rate are usually normal. The caudal part of the rib cage on the side of the displacement may appear “sprung.” Hydration appears subjectively normal with displacements except in some chronic cases. Rumen motility may be normal but often is reduced in frequency and strength of contraction. Feces are usually reduced in quantity and more fluid than normal.
The most important diagnostic physical finding is a ping on simultaneous auscultation and percussion of the abdomen, which should be performed in the area marked by a line from the tuber coxae to the point of the elbow, and from the elbow toward the stifle. The ping (detected during simultaneous percussion and auscultation) characteristic of an LDA is most commonly located in an area between ribs 9 and 13 in the middle to upper third of the left abdomen; however, the ping can be more ventral or more caudal, or both. Pings associated with a rumen gas cap are usually more dorsal, less resonant, and extend more caudally through the left paralumbar fossa. Rectal examination can confirm a gas-filled rumen or an extremely empty rumen that correlates with the rumen ping in these cases. Pings associated with pneumoperitoneum typically are less resonant, present on both sides of the abdomen, and are inconsistent in location on repeated evaluation. Frequently, secondary ketosis develops, and ketones are present in the urine or milk. Ketosis that develops in association with abomasal displacement responds only transiently to treatment and recurs (versus in primary ketosis, which develops early in lactation in high-producing cows and responds to therapy permanently if instituted early). (Also see Ketosis in Cattle.)
The ping associated with RDA also is most commonly located in the area between ribs 10 and 13 on the right abdomen. Differentiation between various causes of a right-side ping can be difficult in some cases, although a ping cranial to rib 10 usually indicates the presence of AV because the liver is displaced medially by the distended viscus. A small, right-side ping underlying ribs 12 or 13 and extending as far forward as rib 10 is common in cows with functional ileus from a number of causes. This ping is most often associated with gas in the ascending colon and resolves with correction of the underlying condition. Cecal dilatation and rotation are characterized by a right-side ping. The ping extends through the dorsal paralumbar fossa in cecal dilatation and usually is located more caudally (well into the paralumbar fossa) in cecal rotation than the ping of RDA. Palpation per rectum is helpful in differentiating an RDA from cecal dilatation or rotation. Other right-side pings are produced by pneumoperitoneum or gas in the rectum, descending colon, duodenum, or uterus.
Spontaneous fluid splashing or gas tinkling sounds may be heard on auscultation of the area of the ping or on simultaneous ballottement and auscultation of the abdomen (succussion). The characteristic rectal examination findings with LDA include a medially displaced rumen and left kidney. The abomasum is rarely palpable in LDA and only occasionally in RDA.
The clinical signs associated with abomasal volvulus are more severe than with simple displacements because of the vascular compromise. However, an early abomasal volvulus can be difficult to distinguish from an RDA except by the presence of a right-side ping cranial to rib 10 (indicating medial displacement of the liver by the abomasal volvulus) and the anatomic position identified at surgery. In contrast to cases of displacement, an animal with AV has tachycardia proportional to the severity of the condition. The area of the ping is usually larger (extending as far forward as rib 8), and the amount of succussible fluid is greater. The animal is more depressed, and signs of weakness, toxemia, and dehydration develop as the disease progresses. The caudal extent of the abomasum is usually palpable per rectum. Without therapy, the animal often becomes recumbent within 48–72 hr after developing volvulus. Death occurs from shock and dehydration and is sudden if the ischemic abomasum ruptures.
For displacement or volvulus, diagnosis is based on the presence of the characteristic ping on simultaneous auscultation and percussion and exclusion of other causes of left- or right-side pings. Ultrasonography may be helpful in confirming a diagnosis of LDA, RDA, or AV, but it cannot reliably differentiate RDA from AV. Recent parturition, partial anorexia, and decreased milk production suggest displacement. A ketosis that is only temporarily responsive to treatment is consistent with abomasal displacement, which may be intermittent. The typical signs on physical examination (in addition to the ping), rectal examination, and laboratory evaluation also support the diagnosis. Melena or signs of peritonitis (eg, fever, tachycardia, localized abdominal pain, pneumoperitoneum) with an LDA may indicate a bleeding or perforated abomasal ulcer, respectively. In cattle with AV, blood l-lactate concentrations ≤2 mmol/L indicate a positive outcome with surgical correction, whereas cattle with blood l-lactate concentrations ≥6 mmol/L have a high probability of a negative outcome.
Open (surgical) and closed (percutaneous) techniques can be used to correct abomasal displacements. Rolling a cow through a 180° arc after casting her on her right side corrects most LDAs; however, recurrence is very likely. LDA can be corrected surgically using right flank pyloric omentopexy, right paramedian abomasopexy, left paralumbar abomasopexy, combined left flank and right paramedian laparoscopy (two-step procedure), or left flank laparoscopy (one-step procedure). Blind suture techniques (toggle-pin fixation or the “big needle” [blind-stitch] method), performed in the right paramedian area, are percutaneous methods for correction of LDA; however, the exact location of the suture is not known. Potentially fatal complications can develop after blind suture techniques, and the reported success rate is less than that of surgical correction by right flank pyloric omentopexy. With toggle-pin fixation, the pH can be checked to confirm that the pin is in the abomasum, which reduces the likelihood of attaching rumen, small intestine, or omentum to the body wall rather than the abomasum. RDA and AV are corrected surgically (using right paralumbar fossa omentopexy) when economically feasible. The right paramedian abomasopexy should be used only to correct RDA and AV in cattle unable to stand.
Ancillary treatment of animals with abomasal displacement include treating any concurrent disease (eg, metritis, mastitis, ketosis). Calcium borogluconate or calcium gluconate SC or calcium gels PO help restore normal abomasal motility in many cases. Administration of erythromycin (10 mg/kg, IM) at the time of surgery increases abomasal emptying rate and milk production in the immediate postoperative period. Because surgical correction of abomasal displacement or volvulus is frequently done on the farm, the prokinetic effect of erythromycin suggests that it might be preferred if antimicrobials are administered to control intraoperative infection. However, administration of an antimicrobial for a nonantimicrobial effect should not be promoted.
In simple displacement, fluid and electrolyte abnormalities correct spontaneously with access to water and a salt block. Providing electrolyte water (60 g sodium chloride and 30 g potassium chloride in 19 L of water) via stomach tube is helpful in cases of longer duration. Animals with significant dehydration and metabolic derangement require IV therapy, typically administered as hypertonic saline (7.2% NaCl, 5 mL/kg, IV over 5 min).
Occasionally, animals with abomasal displacement or volvulus have atrial fibrillation, thought to be of metabolic origin and primarily due to concurrent hypokalemia and metabolic alkalosis. Correction of the displacement or volvulus almost always results in correction of the atrial fibrillation within 5 days.
Aggressive treatment of ketosis plays an important role in successful treatment of abomasal displacement, because most of the cattle that die after surgical correction of LDA and RDA do so from the metabolic consequences of prolonged anorexia.
The prognosis after correction of simple LDA or RDA is good, with survival rates of 95%. AV has a variable and less favorable prognosis (average survival rate of 70%); a high heart rate, moderate to severe dehydration, a longer period of illness, a large quantity of fluid in the abomasum, increased blood or plasma l-lactate concentration, and the presence of omasal-abomasal or reticulo-omasal-abomasal volvulus are associated with a poorer prognosis.
The incidence of abomasal displacements can be decreased by ensuring a rapid increase in rumen volume after calving, feeding a total mixed ration rather than feeding grain twice daily (“slug feeding”), avoiding rapid dietary changes, maintaining adequate roughage in the diet, avoiding postparturient hypocalcemia, and minimizing and promptly treating concurrent disease and ketosis.
Last full review/revision May 2014 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM