Abomasal lesions can be classified as ulcers if the necrosis of the abomasal wall reaches into the submucosal layer (deeper than the lamina muscularis mucosae into 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 degree of hemorrhage or peritonitis caused by the ulcer:
Type I - an 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, however, is very difficult to assess by physical examination and may be more applicable during necropsy examination. Ulcers seem to occur less frequently in small ruminants but they are very commonly found in South American Camelids (SAC).
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 Viral Diarrhea and Mucosal Disease Complex Bovine viral diarrhea/mucosal disease is a pestivirus infection of cattle and other ruminants. Infection leads to immunosuppression and can cause signs in multiple body systems in addition to... read more bovine leukemia virus Overview of Bovine Leukosis Cutaneous lymphosarcoma Lymphosarcoma in cattle may be sporadic or result from infection with bovine leukemia virus (BLV); the latter is often referred to as an enzootic bovine leukosis. Sporadic... read more , and bovine malignant catarrhal fever Malignant Catarrhal Fever in Animals Malignant catarrhal fever is a severe, often fatal, lymphoproliferative disease of artiodactyls caused by ruminant gammaherpesviruses. Clinical signs include fever, oral and nasal erosions,... read more , 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 Left or Right Displaced Abomasum and Abomasal Volvulus in Cattle Abomasal displacement and volvulus are common disorders of high-producing dairy cattle. Clinical signs include anorexia and decreased milk production. With abomasal volvulus, clinical deterioration... read more ), 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.
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 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.
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.
Diagnosis of Abomasal Ulcers in Cattle
Clinical Diagnosis and Ultrasonography
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 test evaluation, including abdominocentesis when perforated abomasal ulcers are suspected.
Diagnosis of perforating abomasal or Type III ulcers is based on physical examination and excluding other causes of peritonitis. Rupture of a distended viscus can occur with abomasal volvulus Left or Right Displaced Abomasum and Abomasal Volvulus in Cattle Abomasal displacement and volvulus are common disorders of high-producing dairy cattle. Clinical signs include anorexia and decreased milk production. With abomasal volvulus, clinical deterioration... read more or cecal rotation and produces similar signs. Furthermore, abomasal ulceration with perforation and local peritonitis may be indistinguishable from traumatic reticuloperitonitis Traumatic Reticuloperitonitis in Cattle Traumatic reticuloperitonitis of cattle occurs when animals ingest nails, pieces of wire, and other nonmetallic materials that injure the reticular wall. Sharp objects can puncture the reticulum... read more . 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. Traumatic reticuloperitonitis does not occur in SACs; however, peritonitis due to other causes (eg, dicrocoeliosis) may be considered. Ultrasonographic examination is a valuable tool to diagnose peritonitis and can be combined with abdominocentesis evaluation. However, ultrasonography is not suitable to diagnose nonperforating ulcers in the gastric wall.
In cases with melena, the diagnosis of abomasal ulcer can be based on 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 blood from portions of the GI tract distal to the abomasum reacts during fecal occult blood tests. It is usually bright red if from the large intestine or is 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; swallowing blood can also result in melena. Fecal occult blood may also be due to abomasal volvulus or rarely to bloodsucking helminths.
In cases of abomasal ulcer with diffuse peritonitis, there is neutrophilia with a marked left shift and hemoconcentration. In bleeding ulcers, the PCV can help to determine the extent of hemorrhage, although PCV decreases only 4 hours after an acute hemorrhage.
In perforated ulcers, abdominal fluid is usually readily obtainable in large quantities. Evaluation of fluid obtained by abdominocentesis will confirm peritonitis if total protein or d-dimer concentration and nucleated cell count are increased. Nucleated cell count may also be normal because of dilution or utilization.
Intracellular bacteria or degenerate neutrophils are rarely seen because, in most cases, the infection is rapidly walled off. However, bacteria may be present, glucose concentration is close to zero, and LDH activity and D-dimer concentration are increased in septic peritoneal fluid. Sucrose absorption tests as reported in horses have not been found suitable in cattle yet, and no studies seem to be available in SACs.
Treatment of Abomasal Ulcers in Cattle
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.
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.
Abomasal ulcers are underdiagnosed.
Clinical signs are often nonspecific, making a reliable clinical diagnosis difficult.
Animals that appear healthy may die quickly of perforating ulcers.
Early treatment is essential.