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. Although abomasal ulcers can occur any time during lactation, they are common in high-producing, mature dairy cows within the first 6 weeks after parturition. Although in contrast to monogastric animals, and not scientifically proven, one cause may be a prolonged inappetence, which results in sustained periods of low abomasal pH—hence the adage “no acid, no ulcer.” Conversely, because in ruminating animals the abomasal volume does not vary substantially, the situation is very different from that in monogastric animals.

Abomasal ulcers may also arise in association with lymphosarcoma, abomasal disorders (displacement or volvulus), or increased luminal pressure causing ischemia of the abomasal mucosa; they may also appear to be unrelated to other disease. The role of stress (eg, transport, new groups, heat, dehorning of calves) in the pathogenesis is not completely understood and seems to vary substantially between animals; however, it is likely that stress is 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. Occasionally, milk-fed calves < 2 weeks old are affected by acute, hemorrhagic abomasal ulcers that may perforate and cause rapid death. Well-nourished suckling beef calves 2–4 months old may be affected by acute abomasal ulcers. Abomasal trichobezoars are common in these calves but do not appear to increase risk of ulcer formation.

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 may be only a single ulcer or many acute and chronic ulcers. Cattle with bleeding abomasal ulcers may be asymptomatic except for intermittent occult blood in the feces, or they can 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 may be intermittent. Because SACs have dark and dry feces, it is difficult to identify melena unless the bleeding is extensive. Signs of blood loss occur with major hemorrhage and may include tachycardia (100–140 bpm), pale mucous membranes, weak pulse, cool extremities, shallow breaths, tachypnea, and melena. More severe signs include acute rumen stasis, generalized abdominal pain with a reluctance to move and an audible grunt or groan with each breath, weakness, and dehydration. Melena may not be present in peracute cases, 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.

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 those associated with abomasal displacement.

Calves with abomasal ulceration and hairballs may have a distended gas- and fluid-filled abomasum that is palpable behind the right costal arch. Deep palpation may reveal abdominal pain associated with local peritonitis due to a perforated ulcer. In calves, perforating ulcers are more common than bleeding ulcers.

Lesions

Abomasal ulcer, cow

Image

Courtesy of Dr. Sameeh M. Abutarbush.

Ulceration 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. Most cases of 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 may infiltrate widely through the omental fat. Adhesions may form between the ulcer and surrounding organs or the abdominal wall.

• Transabdominal ultrasonography

• Laboratory testing

• Improve dietary intake

• Decreasing acid secretion in the abomasum

• Blood transfusion in severe cases

Most occurrences of abomasal ulcers are undiagnosed and therefore untreated. Occasionally, a presumptive diagnosis is made and medical treatment begun. The most important treatment is to get 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 increase abomasal pH. Broad-spectrum antimicrobial therapy (given 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 at 4- to 6-hour intervals 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, 3 times a day) and ranitidine (50 mg/kg, 3 times a day) are high, making treatment expensive.

Proton pump inhibitors, such as omeprazole (2 mg/kg, IV, or 4 mg/kg, PO in calves) effectively increase luminal pH, but, again, treatment is expensive. The efficacy of administration of oral omeprazole (4 mg/kg) in adult ruminants and SACs is difficult to assess because absorption rates vary substantially. Because it has been shown in monogastric animals that NSAIDs can contribute to ulceration (although there are no studies for cattle and SACs), their administration should be avoided if possible when abomasal ulcers are suspected.

The prognosis for localized peritonitis associated with perforating abomasal ulcers is good with medical therapy 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 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.

Animals with diffuse peritonitis after perforation of an abomasal ulcer rarely respond to therapy, and the prognosis is grave. Treatment consists of rapid and continued IV fluid therapy (based on the current metabolic status) and IV broad-spectrum antimicrobials. In valuable animals (SACs), 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 massive abdominal adhesions.

For bleeding ulcers, blood transfusions and fluid therapy may be necessary in addition to dietary management, stall confinement, and oral antacids. If hemorrhage is acute, the PCV may 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 are present; a decision regarding transfusion should be based on clinical signs rather than PCV. Cross-matching is not usually necessary; a single transfusion of 4–6 L of blood is required. Some cattle require more than one transfusion over the course of several days. Complete recovery usually takes 1–2 weeks. The prognosis is good if weakness and lethargy have not developed before treatment is started.

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.