Abomasal ulcers affect calves and mature cattle and have several different manifestations. Common clinical signs include anorexia, bruxism, abdominal pain, occult blood in feces, and tachycardia. Ultrasonography and laboratory tests can aid diagnosis. Treatment is based on decreasing acid secretion in the abomasum. Blood transfusion might be required in severe cases.
Abomasal ulcers occur in dairy and beef cattle of all ages.
Abomasal lesions can be classified as ulcers if necrosis of the abomasal wall penetrates the submucosal layer. In contrast, more superficial lesions are defined as erosions.
A system of abomasal ulcer classification is based on the depth of penetration or the extent of hemorrhage or peritonitis caused by the ulcer:
Type I: erosion or ulcer without hemorrhage
Type II: hemorrhagic
Type III: perforated, with acute localized peritonitis
Type IV: perforated, with acute diffuse peritonitis
Type V: perforated, with peritonitis within the omental bursa
This classification is very difficult to assess by physical examination and might be more applicable during necropsy examination.
Etiology and Pathogenesis of Abomasal Ulcers in Cattle
Except for lymphosarcoma of the abomasum and the erosions of the abomasal mucosa that develop in viral diseases such as bovine viral diarrhea, bovine leukemia virus, and bovine malignant catarrhal fever, the causes of abomasal ulceration are not well understood. Many causes have been suggested.
Abomasal ulcers can occur anytime during lactation, but they are most common in high-producing, mature dairy cows within the first 6 weeks after parturition. Although not scientifically proven, one cause might be prolonged inappetence, which results in sustained periods of low abomasal pH.
Abomasal ulcers can arise in association with lymphosarcoma, abomasal disorders (displacement or volvulus), or increased luminal pressure causing ischemia of the abomasal mucosa. They can also appear to be unrelated to other disease.
The role of stress (eg, transport, new groups, heat, dehorning of calves) in the pathogenesis of abomasal ulcers is not completely understood and seems to vary substantially between animals; however, stress is likely a major contributing factor.
Abomasal ulcers are very common in milk-fed calves after they have consumed milk or milk replacer for 4–12 weeks. Most of these ulcers are subclinical and nonhemorrhagic. Perforating ulcers in young calves, particularly veal calves, are typically located in the pyloric region of the abomasum (1).
Occasionally, milk-fed calves < 2 weeks old are affected by acute, hemorrhagic abomasal ulcers that can perforate and cause rapid death. Well-nourished suckling beef calves 2–4 months old can be affected by acute abomasal ulcers. Abomasal trichobezoars are common in these calves but do not appear to increase the risk of ulcer formation (2).
Clinical Findings of Abomasal Ulcers in Cattle
The abomasal ulcer syndrome varies, depending on whether ulceration is complicated by hemorrhage or perforation and by the severity of such hemorrhage or peritonitis.
There can be only a single ulcer or many acute and chronic ulcers. Cattle with bleeding abomasal ulcers might be subclinically affected, except for intermittent occult blood in the feces, or they might die acutely from massive hemorrhage. Common clinical signs include mild abdominal pain, bruxism, sudden onset of anorexia, tachycardia (90–100 bpm), and fecal occult blood or melena that might be intermittent.
Major hemorrhage is accompanied by signs of blood loss, which can include tachycardia (100–140 bpm), pale mucous membranes, weak pulse, cool extremities, shallow breathing, tachypnea, and melena. More severe signs include acute rumen stasis, generalized abdominal pain with reluctance to move and an audible grunt or groan with each breath, weakness, and dehydration.
Melena might not be present in peracute cases of abomasal ulcers, because only after 8 hours can abomasal blood be detected in the feces. As the condition progresses, body temperature drops, and the animal becomes recumbent and dies within 6–8 hours.
Clinical signs of perforating abomasal ulcers are consistent with the extent of peritonitis; they include tachycardia, fever, grunting, bruxism, and diarrhea (3).
In general, bleeding ulcers do not perforate, and perforating ulcers do not bleed into the GI tract sufficiently to produce melena. However, hemorrhage and perforation occur together occasionally, usually in chronic cases or in cases associated with abomasal displacement.
Calves with abomasal ulceration and hairballs might have a distended gas- and fluid-filled abomasum that is palpable behind the right costal arch. Deep palpation might reveal abdominal pain associated with local peritonitis due to a perforated ulcer. In calves, perforating ulcers are more common than bleeding ulcers.
Lesions of Abomasal Ulcers in Cattle
Ulceration of the abomasum is most common in the fundic region in adult cattle and in the pyloric antrum in milk-fed calves. The single or multiple ulcers measure from a few millimeters to 5 cm in diameter. The affected artery is usually visible after ingesta and necrotic tissue are removed from a bleeding ulcerated area (see ).
Numerous nonbleeding abomasal ulcers in a cow.
Courtesy of Dr. Sameeh M. Abutarbush.
Most cases of abomasal ulcer perforation are walled off by the omentum, which forms a cavity 12–15 cm in diameter that contains degenerated blood and necrotic debris. Material from this cavity can infiltrate widely through the omental fat. Adhesions can form between the ulcer and surrounding organs or the abdominal wall.
Diagnosis of Abomasal Ulcers in Cattle
Transabdominal ultrasonography
Presence of melena or occult blood in feces
Presence of anemia in some cases
Abdominocentesis
Clinical Diagnosis and Ultrasonography of Abomasal Ulcers in Cattle
In abomasal ulcer cases with only slight bleeding and mild clinical signs, diagnosis is difficult and can require repeated fecal evaluations for occult blood. Other conditions that can cause partial anorexia and decreased milk production should be excluded by physical examination and laboratory test evaluation, including abdominocentesis when perforated abomasal ulcers are suspected.
Diagnosis of perforating abomasal ulcers is based on physical examination and exclusion of other causes of peritonitis. Rupture of a distended viscus can occur with abomasal volvulus or cecal rotation and produces similar signs. Furthermore, abomasal ulceration with perforation and local peritonitis can be indistinguishable from traumatic reticuloperitonitis (3).
Ultrasonography is a valuable tool for diagnosing peritonitis and can be combined with abdominocentesis. However, ultrasonography is not suitable to diagnose nonperforating ulcers in the gastric wall.
Occult Blood Testing for Diagnosis of Abomasal Ulcers in Cattle
When abomasal ulcers are accompanied by melena, they can be diagnosed by physical examination alone. An occult blood test of the feces can confirm melena.
Other conditions that result in blood in the feces should be eliminated, because the blood can originate in portions of the GI tract distal to the abomasum. It is usually bright red if from the large intestine or raspberry-colored if from the small intestine.
Animals with abomasal lymphosarcoma can have a bleeding syndrome similar to that associated with abomasal ulcers, but they do not respond to treatment.
Occasionally, oral, pharyngeal, and laryngeal lesions bleed, and the swallowed blood appears in the feces. Similarly, pulmonary abscesses that form as a sequela of rumenitis by embolization to the lungs and liver can erode blood vessels and result in hemoptysis; swallowing blood can also result in melena.
Fecal occult blood can also be due to abomasal volvulus or, rarely, to bloodsucking helminths.
Hematologic Testing for Diagnosis of Abomasal Ulcers in Cattle
When abomasal ulcers are accompanied by diffuse peritonitis, there is neutrophilia with a marked left shift and hemoconcentration. With bleeding ulcers, the PCV can help to determine the extent of hemorrhage; however, the PCV decreases only 4 hours after acute hemorrhage.
Pearls & Pitfalls
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Abdominocentesis for Diagnosis of Abomasal Ulcers in Cattle
With perforated ulcers, ascites is usually readily obtainable in large quantities. Evaluation of ascites obtained by abdominocentesis will confirm peritonitis if the appearance is abnormal (yellow, opaque fluid with visible fibrin), or if total protein concentration and nucleated cell count are increased during laboratory analysis. Nucleated cell count can also be normal because of dilution or utilization.
Intracellular bacteria or degenerate neutrophils are rarely observed in cases of peritonitis, because usually the infection is rapidly walled off. However, bacteria can be present, glucose concentration is close to zero, and LDH activity and D-dimer concentration are increased in septic peritoneal fluid.
Treatment of Abomasal Ulcers in Cattle
Improving dietary intake
Decreasing acid secretion in the abomasum
Blood transfusion in severe cases
Most abomasal ulcers in cattle are undiagnosed and therefore untreated. Occasionally, a presumptive diagnosis is made and medical treatment begun.
The most important treatment for abomasal ulcers is getting the animal to eat, because food is an excellent buffer, and continual flow of forestomach contents (pH 6.0–7.0) into the abomasum helps to increase abomasal pH.
Broad-spectrum antimicrobials (administered for ≥ 5 days or until the rectal temperature is normal for 48 hours) is indicated for perforating ulcers.
Antacids effectively increase abomasal pH in milk-fed calves when administered every 4–6 hours in a manner that induces esophageal groove closure. However, their efficacy is extremely questionable in adult ruminants because of dilution by the large rumen volume.
H2 receptor antagonists effectively increase abomasal pH in milk-fed calves; however, the oral dosages required for cimetidine (100 mg/kg, every 8 hours) and ranitidine (50 mg/kg, every 8 hours) are high, making treatment expensive (4).
The use of proton pump inhibitors has been investigated in calves, and omeprazole (4 mg/kg, PO, every 24 hours [5]) or pantoprazole (1 mg/kg, IV, or 2 mg/kg, SC, every 24 hours [6]) effectively increases luminal pH. However, this treatment is also expensive, and its efficacy has not been conclusively demonstrated in affected populations.
Because it has been shown that NSAIDs can contribute to ulceration in monogastric animals (even though there are no studies for cattle), their administration should be avoided when abomasal ulcers are suspected.
Pearls & Pitfalls
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The prognosis for cows that have localized peritonitis associated with perforating abomasal ulcers is good with medical treatment and dietary alteration. Recovery generally takes 1–2 weeks, and patients fully recovered for 1–2 weeks generally do not experience recurrence.
Surgery is indicated for perforating abomasal ulcers in cattle only when the abomasum is displaced. However, extensive abdominal contamination can occur in the process of breaking down adhesions and resecting or oversewing the ulcer.
Cows with diffuse peritonitis after perforation of an abomasal ulcer rarely respond to treatment, and the prognosis is grave. Treatment consists of rapid and continued IV fluid therapy (depending on the current metabolic status), pain control, and IV broad-spectrum antimicrobials. In valuable animals, surgery to close the perforation and intensive lavage of the peritoneal cavity can be performed. The few animals that recover from diffuse peritonitis usually have extensive abdominal adhesions.
For bleeding ulcers, blood transfusions and fluid therapy might be necessary in addition to dietary management, stall confinement, and oral antacids. If hemorrhage is acute, the PCV might not reflect the severity, because equilibration between intravascular and extravascular fluid after blood loss takes at least 4 hours.
Generally, a blood transfusion is required whenever weakness and lethargy accompany an abomasal ulcer. The decision regarding transfusion should be based on additional clinical signs of anemia (tachycardia, tachypnea, respiratory distress, prolonged capillary refill time) rather than PCV alone; however, a PCV of < 12% has been recommended as an indication for transfusion (7).
In cases of chronic blood loss, the following formula has been suggested to estimate the necessary volume for transfusion (7):
Up to 20% of a healthy donor's blood volume (10–15 mL/kg body weight) can typically be collected safely (7).
Blood typing in cattle is impractical, and crossmatching is not usually necessary for a single whole blood transfusion. Some cattle require more than one transfusion over the course of several days, and repeated transfusions increase the risk for transfusion reactions (7).
Complete recovery after blood transfusion for an abomasal ulcer usually takes 1–2 weeks. The prognosis depends on the severity of anemia and response to treatment.
Prevention of Abomasal Ulcers in Cattle
To prevent abomasal ulcers, stressors such as transportation, regrouping, and overcrowding should be avoided. Feeding coarse roughage to veal calves with an underdeveloped rumen should be avoided. Animals should be encouraged to keep eating to avoid prolonged periods of inappetence and low abomasal pH.
Key Points
Abomasal ulcers are underdiagnosed.
Clinical signs are often nonspecific, making a reliable clinical diagnosis difficult.
Animals that appear healthy can die quickly of perforating ulcers.
Blood transfusion is warranted in animals with hemorrhagic ulcers, clinical signs of anemia, and critical PCV.
References
Bus JD, Stockhofe N, Webb LE. Invited review: abomasal damage in veal calves. J Dairy Sci. 2019;102(2):943-960. doi:10.3168/jds.2018-15292
Marshall TS. Abomasal ulceration and tympany of calves. Vet Clin North Am Food Anim Pract. 2009;25(1):209-220. doi:10.1016/j.cvfa.2008.10.010
Braun U, Nuss K, Warislohner S, Reif C, Oschlies C, Gerspach C. Diagnostic reliability of clinical signs in cows with traumatic reticuloperitonitis and abomasal ulcers. BMC Vet Res. 2020;16(1):359. doi:10.1186/s12917-020-02515-z
Ahmed AF, Constable PD, Misk NA. Effect of orally administered cimetidine and ranitidine on abomasal luminal pH in clinically normal milk-fed calves. Am J Vet Res. 2001;62(10):1531-1538. doi:10.2460/ajvr.2001.62.1531
Ahmed AF, Constable PD, Misk NA. Effect of orally administered omeprazole on abomasal luminal pH in dairy calves fed milk replacer. J Vet Med A Physiol Pathol Clin Med. 2005;52(5):238-243. doi:10.1111/j.1439-0442.2005.00715.x
Olivarez JD, Mulon P-Y, Ebner LS, et al. Pharmacokinetic and pharmacodynamic properties of pantoprazole in calves. Front Vet Sci. 2023;9:1101461. doi:10.3389/fvets.2022.1101461
Balcomb C, Foster D. Update on the use of blood and blood products in ruminants. Vet Clin North Am Food Anim Pract. 2014;30(2):455-474. doi:10.1016/j.cvfa.2014.04.001
