Left Displacement of the Abomasum in a Cow: Case Study
Molly Murphy, DVM, PhD; Kenneth S. Latimer, DVM, PhD
Class of 2007 (Murphy) and Department of Pathology (Latimer), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388

Signalment - Cow, Holstein-Friesian, 3-year-old.
History - Decreased milk production and anorexia of 3 weeks duration.
Abdominal distension has been observed for the past week. This cow had been bred three months previously by artificial insemination.
Physical examination - The cow’s abdomen was distended both ventrally and dorsally on the left side, and ventrally on the right side. A “ping” was present following percussion and auscultation over the left abdomen (from the 9th rib at the level of the elbow extending caudodorsally to the left paralumbar fossa), and over the right abdomen (caudal to the last rib and at the level of the stifle). An orogastric tube was passed and 75 liters of reflux were removing, after which the right-sided ping resolved.
Diagnostics - Laboratory diagnostics included a complete blood cell count (CBC), fibrinogen determination, and biochemical profile. Survey radiographs also were taken.
Laboratory data:
| CBC |
Patient values |
Units |
Reference Range |
| HCT |
40.8 |
% |
24.0-46.0 |
| RBC |
8.20 |
x 106 /µl |
5.0-10.0 |
| HGB |
13.7 |
g/dl |
8.0-15.0 |
| MCV |
49.7 |
fl |
40-60 |
| MCH |
16.7 |
pg |
11.0-17.0 |
| MCHC |
33.6 |
g/dl |
30-36 |
| Platelets |
497 |
x 103 /µl |
100-800 |
| MPV |
4.5 |
fl |
3.5-6.5 |
| Platelet Estimate |
Adequate |
|
Adequate |
| Nucleated RBC |
0 |
/100 WBC |
0 |
| WBC |
10.2 |
x 103 /µl |
4.0-12.0 |
| Seg |
5.508 |
x 103 /µl |
0.6-4.0 |
| Band |
0.0 |
x 103 /µl |
0.0-0.1 |
| Lymph |
4.182 |
x 103 /µl |
2.5-7.5 |
| Mono |
0.510 |
x 103 /µl |
0.0-0.9 |
| Eos |
0.0 |
x 103 /µl |
0.0-2.4 |
| Baso |
0.0 |
x 103 /µl |
0.0-0.2 |
| Other |
0.0 |
x 103 /µl |
0.0-0.0 |
| Fibrinogen |
700 |
mg/dl |
100-600 |
RBC Morphology: Many echinocytes, few Howell-Jolly bodies
| Serum Chemistry |
Patient Values |
Units |
Reference Range |
Creatinine |
4.1 |
mg/dl |
0.7-2.4 |
| Total Protein |
8.8 |
g/dl |
6.8-7.6 |
| Albumin |
3.9 |
g/dl |
2.3-3.9 |
| Glucose |
103 |
mg/dl |
44-102 |
| Sodium |
139 |
mmol/L |
139-146 |
| Potassium |
2.7 |
mmol/L |
3.6-4.7 |
| Chloride |
80 |
mmol/L |
98-109 |
| Bicarbonate |
40 |
mmol/L |
22-31 |
| Anion gap |
23 |
mmol/L |
16-23 |
| Calcium |
9.0 |
mg/dL |
7.7-11.1 |
| Creatine Kinase |
271 |
U/L |
17-332 |
| GGTP |
21 |
U/L |
NRR |
| SDH |
10.5 |
U/L |
NRR |
Problem list and interpretation (2):
1. Mature neutrophilia: The neutrophilia could be a response to pain, abomasal displacement, ketosis, grain overload, indigestion, or mild inflammation.
2. Hyperfibrinogenemia: Hyperfibrinogenemia is a hallmark of inflammation in ruminants and may be a more sensitive indicator of inflammation than is the leukocyte count.
3. Increased creatinine: Creatinine is the metabolite of phosphocreatine, an energy store within muscle tissue. A certain amount of phosphocreatine is converted to creatinine daily. After traveling through the bloodstream, creatinine is freely filtered by the glomerulus and is not reabsorbed by the renal tubuar system. An increase in serum creatinine concentration may be the result of increased creatinine production (i.e., muscle breakdown), ingestion of exogenous creatinine (i.e., muscle-based foods), or decreased glomerular filtration rate (GFR). In this patient, decreased GFR is suspected secondary to dehydration and subsequent blood volume reduction. Fluid loss in this patient could result from a combination of decreased water intake, insensible water loss, and compartmentalization or loss of body water. Compartmentalization and loss of a large quantity of body water likely followed the removal of 75 liters of reflux fluid.
4. Hyperproteinemia: The hyperproteinemia is characterized by normoabluminemia at the maximum value of the reference interval and a calculated globulin concentration of 4.9 g/dl, indicating hyperglobulinemia. The A:G ratio is 0.80:1 which is within the reference interval (0.6:1 to 0.9:1). Thus, the hyperproteinemia is most likely due to dehydration and hyperfibronogenemia.
5. Hyperglycemia: The hyperglycemia is minimal and most likely due to excitement or stress.
6. Hypokalemia: Hypokalemia is associated with the depletion of intracellular potassium as due to decreased intake (anorexia), loss of potassium-rich gastric fluids (diarrhea, vomiting, abomasal sequestration, and/or removal of reflux fluid), or increased urinary loss in polyuria, metabolic alkalosis, early metabolic acidosis, or diuresis.
7. Hypochloremia: In this patient, the plasma sodium is within the reference interval, indicating that chloride loss is not entirely related to NaCl concentrations. Other sources of chloride loss include loss of HCl or KCl from gastric secretions due to reflux fluid removal (vomiting does not occur in ruminants), malabsorption in the lower gastrointestinal tract, or chloride sequestration in the rumen or abomasum.
8. Metabolic alkalosis: Metabolic alkalosis occurs due to the loss or sequestration of gastric HCl, and the relative excess of HCO3-.
Disease diagnosis: Left abomasal displacement with hypochloremic metabolic alkalosis (Figure 1).
 |
Figure 1. Left displacement of the abomasum. The abomasum is characterized by marked distension and congestion. It is positioned between the spinal column and the dorsal rumen. Image courtesy of Dr. John King, Cornell University, College of Veterinary Medicine, Ithaca, New York. |
Mechanism of disease:
In health, the formation of a ruminal raft of large hay particles serves to retain fermentable feed substrates within the rumen. Therefore, the majority of gas production occurs within the rumen, which is highly expansible. Ingesta is slowly passaged into the glandular abomasum by ruminal contractions (3). In glandular digestion, the abomasum secretes a large amount of HCl, which is later neutralized by HCO3- . The secretion of HCO3- occurs in the duodenum, and is stimulated by the passage of a food bolus. HCl and KCl are reabsorbed in the lower GI tract, maintaining the acid-base equilibrium (1).
In abomasal displacement, abomasal outflow is functionally obstructed as the abomasum folds itself upon the rumen and floats dorsally to wedge between either the rumen and the left body wall (left displaced abomasum, or LDA), or the rumen and the right-sided abdominal viscera (right displaced abomasum, or RDA). This obstruction entraps hydrogen, potassium, and chloride-containing gastric fluids, which are functionally lost to reabsorption. The decrease in appetite also contributes greatly to hypokalemia in ruminants because of decreased ion intake (3).
Without stimulation by the passage of ingesta, the duodenum does not secrete pancreatic HCO3-, creating a relative increase in HCO3- and producing metabolic alkalosis (1). Within the kidney, HCO3- is freely filtered by the glomerulus and reabsorbed in the proximal tubule regardless of plasma HCO3- concentration. In response to alkalosis, a net secretion of HCO3- occurs in the renal collecting duct via a Cl-/ HCO3- antiporter, creating an alkalotic urine (1).
In many cases of hypochloremic metabolic alkalosis, a paradoxical aciduria may occur. In response to dehydration-induced hypovolemia, aldosterone stimulates the kidneys to retain Na+ and water. In health, Cl- is the anion that is absorbed along with Na. However, due to Cl- sequestration in the displaced abomasum as well as the aforementioned Cl- absorption in exchange for HCO3- secretion, Cl- is unavailable for absorption with Na+. Therefore, HCO3- is the anion which is reabsorbed with Na+, decreasing the urine pH. Sodium (and water) can also be reabsorbed via exchange with intracellular K+ or H+. In the presence of hypokalemia, K+ is unavailable for exchange. Therefore, H+ ions are exchanged with Na+, creating an acidic urine. Finally, in response to systemic alkalosis, the cellular secretion of H+ ions into the bloodstream in exchange for an uptake of K+ ions can serve as a minor source of K+ depletion (2).
Displaced abomasum occurs more frequently in dairy versus beef breeds, and a variety of etiologies have been proposed including breed (4), dietary concerns (neutral detergent fiber content), hypocalcemia (5), and insulin resistance (6). Treatment usually involves medical correction of dehydration and surgical correction of the abomasal displacement via omentopexy or abomasopexy. The outcome of surgery is generally good, and the metabolic disturbances characteristic of displaced abomasum usually resolve spontaneously following surgery (3).
References
1. Cunningham JG: Textbook of Veterinary Physiology, 3rd ed. W.B.Saunders Company, Philadelphia, 2002, pp. 255-279 and 459-466.
2. Latimer KS, Mahaffey EA, Prasse KW: Veterinary Laboratory Medicine: Clinical Pathology, 4th ed. Iowa State Press, Ames, 2003, pp. 136-161.
3. Smith BP: Large Animal Internal Medicine, 3rd ed. Mosby, St. Louis, 2002, pp. 756-759.
4. Roussel AJ, Cohen ND, Hooper RN. Abomasal displacement and volvulus in beef cattle: 19 cases (1988-1998). J Am Vet Med Assoc 2000; 216: 730-733.
5. Stengarde LU, Pehrson BG. Effects of management, feeding and treatment on clinical and biochemical variables in cattle with displaced abomasum. Am J Vet Res 2002; 63: 137-142.
6. Pracettoni D, Doll K, Hummel M, Cavallone E, Re M, Belloli AG. Insulin resistance and abomasal motility disorders in cows detected by use of abomasal electromyography after surgical correction of left displaced abomasum. Am J Vet Res 2004; 65: 1319-1324.
Acknowledgement
"Cosmic Cows" by Barbara Ziff is from her Gallery on The Orange County Artists Guild website and is used with permission. |