Abomasal ulcers affect mature cattle and calves and have several different manifestations.
Etiology and Pathogenesis
Except for lymphosarcoma of the abomasum and the erosions of the abomasal mucosa that develop in viral diseases such as bovine viral diarrhea and bovine malignant catarrhal fever, the causes of abomasal ulceration are not well understood. Many different causes have been suggested. Although abomasal ulcers can be seen any time during lactation, they are common in high-producing, mature dairy cows within the first 6 wk after parturition. The most likely cause is prolonged inappetence, which results in sustained periods of low abomasal pH; hence, the adage “no acid, no ulcer.”
Abomasal ulcers may also arise in association with lymphosarcoma, abomasal disorders (displacement or volvulus), or increased luminal pressure causing ischemia of abomasal mucosa; they may also appear to be unrelated to other disease.
Abomasal ulcers are very common in milk-fed calves after they have consumed milk or milk replacer for 4–12 wk. Most of these ulcers are subclinical and nonhemorrhagic. Occasionally, milk-fed calves <2 wk old are affected by acute, hemorrhagic abomasal ulcers that may perforate and cause rapid death. Well-nourished suckling beef calves, 2–4 mo 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 syndrome varies, depending on whether ulceration is complicated by hemorrhage or perforation and by the severity of such hemorrhage or peritonitis.
A system of classification is based on the depth of penetration or the degree of hemorrhage or peritonitis caused by the ulcer: Type I is an erosion or ulcer without hemorrhage, Type II is hemorrhagic, Type III is perforated with acute localized peritonitis, Type IV is perforated with acute diffuse peritonitis, and Type V is perforated with peritonitis within the omental bursa. 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. Signs of blood loss are seen 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 it takes at least 8 hr for abomasal blood to be detected in the feces. As the condition progresses, body temperature drops, and the animal becomes recumbent and dies within 6–8 hr.
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 are seen together occasionally, usually in cases that are chronic or 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.
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.
In cases with only slight bleeding and mild clinical signs, diagnosis of abomasal ulcer is difficult and may 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 tests, including abdominocentesis. In cases with melena, the diagnosis can be based on physical examination alone. The PCV can help to determine the degree of hemorrhage, although it takes at least 4 hr after an acute hemorrhage before the PCV decreases. An occult blood test of the feces can confirm melena. Other conditions that result in blood in the feces should be eliminated. Blood from portions of the GI tract distal to the abomasum reacts on fecal occult blood tests; 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 do not respond to therapy. 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; if the blood is swallowed, this can also result in melena. Fecal occult blood may also be due to AV or rarely to bloodsucking helminths.
Diagnosis of perforating abomasal ulcers is based on physical examination and excluding other causes of peritonitis. Abomasal ulceration with perforation and local peritonitis may be indistinguishable from chronic traumatic reticuloperitonitis (see Traumatic Reticuloperitonitis). A magnet in the reticulum (confirmed by use of a compass) or an accurate history of having given the cow a magnet before the onset of signs decreases the likelihood of traumatic reticuloperitonitis. Reticular radiographs may confirm or exclude the presence of radiopaque foreign bodies in the reticulum. In some cases, there is a neutrophilia, possibly with a left shift. Evaluation of peritoneal fluid will confirm peritonitis if total protein or d-dimer concentration and nucleated cell count are increased. Intracellular bacteria or degenerate neutrophils are rarely seen because, in most cases, the infection is rapidly walled off. The diagnosis of diffuse peritonitis due to perforation is based on physical examination and excluding other causes. Rupture of a distended viscus, such as can occur with AV or cecal rotation, produces similar signs. Regardless of the cause of diffuse peritonitis, the prognosis is grave because of overwhelming infection and cardiovascular deterioration. There is neutrophilia with a marked left shift and hemoconcentration. Abdominal fluid is usually readily obtainable in large quantities, and the protein level is increased; the nucleated cell count may be increased, or it may be normal due to dilution or utilization.
Most cases of abomasal ulcers are undiagnosed and therefore untreated. Occasionally, a presumptive diagnosis is made and medical treatment instituted. 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 hr) is indicated for perforating ulcers. Antacids effectively increase abomasal pH in milk-fed calves when administered at 4- to 6-hr 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, tid) and ranitidine (50 mg/kg, tid) are high, making treatment expensive. Proton pump inhibitors, such as omeprazole (2 mg/kg, IV) effectively increase luminal pH, but again treatment is expensive. The efficacy of oral omeprazole (4 mg/kg) in adult ruminants is unknown, but it has some efficacy in milk-fed calves. Because NSAIDs can contribute to ulceration, their use is contraindicated. The prognosis for localized peritonitis associated with perforating abomasal ulcers is good with medical therapy and dietary alteration. Recovery generally takes 1–2 wk, and animals fully recovered for 1–2 wk generally do not experience recurrence. Surgery is indicated for perforating abomasal ulcers only when the abomasum is displaced; however, significant 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 antibiotics. 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 hr. 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 wk. The prognosis is good if weakness and lethargy have not developed before treatment is started.
Animals should be encouraged to keep eating to avoid prolonged periods of inappetence and low abomasal pH.
Last full review/revision May 2014 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM