Abomasal ulcers in cattle (Proceedings)

Description

An ulcer is defined as a loss of epithelium from the mucosal surface of the abomasum. The pathologic description, in fact, is an excavation in the mucosa that penetrates through to the muscularis mucosae. This excavation originates from coagulative necrosis. Excavation only partway through the depth of the mucosa is called an erosion. The cause of the excavation is generally due to a breakdown of the gastric mucosal barrier, permitting back diffusion of hydrogen ions. Bile reflux may alter the mucosal barrier as well as non-steroidal anti-inflammatory drugs.1

Categories

1. non-perforating

2. non-perforating, bleeding

3. perforating, local peritonitis

4. perforating, diffuse peritonitis

Epidemiology

According to the literature, while many calves have been shown to have clinically insignificant ulcers on necropsy, clinically affected calves tend to have type IV ulcers more frequently than any other category. Extensive research has been performed on abomasal ulcers in milk-fed calves. Lesions in calves tend to be located around the pylorus and pyloric antrum. In adults, one study from a referral population examining 69 clinically significant abomasal ulcers on postmortem, found that approximately one-third of these ulcers were type II, while the other two-thirds had types III or IV. Of the cattle with type II, one-half were associated with tumors, wile the other half were not. These tumor associated cases were generally older than 6 years, while the non-tumor associated cases were younger. Of the cattle with perforating ulcers, one-half had local peritonitis and the other half had diffuse peritonitis.2,3 The ventral most portion of the fundic region of the abomasum is a common location of lesions in the adult.4,5,6

Etiology

There has been extensive research into the etiology of abomasal ulcers in cattle. It is well established that nonsteroidal anti-inflammatory drugs alter the mucosal barrier by interfering with local prostaglandin synthesis. In my experience, as long as an animal is well hydrated and dosed correctly, I have not recognized an induction of an ulcer from therapy with flunixin meglumine. However, that's not to say we should not exercise some caution and discretion in the use of NSAID's. I do believe I've seen cases of abomasal ulcers that were the result, or partially the result of phenylbutazone even at the proper dose. In adults, stress, diets high in starch, concurrent postpartum disease (displaced abomasum, metritis, mastitis, ketosis) and lymphosarcoma have all been incriminated as contributors to the formation of abomasal ulcers. In calves, suckling frequency, route of milk administration (tube vs. suckling), composition of the milk replacer, nature of roughage diet and the presence of enteric bacteria, most notably Clostridium perfringens type A, Campylobacter spp. and Helicobacter pylori have been investigated as possible contributors to disease. 7,8,9 The role of Clostridium perfringens type A, in particular, in the development of abomasal ulcers in calves still remains elusive due to mixed findings. In one study, Clostridium perfringens type A was isolated in 7 of 8 calves diagnosed with abomasitis, and abomasal ulceration, while the remaining calf's abomasum contained Clostridium perfringens type E.7 The same investigators in another study, were able to successfully induce abomasal tympany, abomasitis and abomasal ulceration in 8 calves following intraruminal inoculation.9 However, despite this evidence, one Canadian study found no significant association between isolation of these bacteria and the presence of abomasal ulcer.8

Hairballs in calves have been implicated as well, however, a Canadian study concluded that it was unlikely that the presence of hairballs played a role in the development of fatal perforating ulcers.10 Therefore, the conclusion that can be drawn is that the etiology of abomasal ulcer formation is multi-factoral and intervention/prevention should be aimed at controlling all the factors, which for the most part, should be part of any good herd health program.

Clinical signs

1. Mild abdominal pain – partial anorexia

a. Decreased rumen motility, Ruminal tympany

2. Signs of anemia – pale mucous membranes, tachycardia, tachypnea

a. Tarry black feces (melena) – hematochezia, Complete rumen stasis and anorexia, Rumen may have a fluid consistency, May have some pain

3. Moderately febrile

a. Partially or totally anorexic

b. Acute drop in milk production

c. Abdominal pain – localized to right ventral abdomen

d. Mild bloat – absent rumen motility

e. Signs may subside as infection is contained

4. Rapid course – septic shock

a. Total anorexia, rumen stasis

b. Tachycardia, tachypnea, weak pulse

c. Bruxism, groaning – pain

d. Recumbency

e. Cool extremities

f. Dehydration, abdominal enlargement

Diagnostics

1. Clinical pathology

a. CBC/fibrinogen – not generally affected

b. Serum chemistry – not generally specific (metabolic alkalosis)

c. Urinalysis – non-specific

d. Fecal occult blood – one study found that about two-thirds were positive12

e. Ancillary diagnostics

f. Ultrasound – used to rule out other causes of abdominal pain

2. Clinical pathology

a. CBC/fibrinogen – decreased packed cell volume

b. Serum chemistry – non-specific (metabolic alkalosis)

c. Urinalysis – non-specific

d. Ancillary diagnostics

e. BLV gp51 – need to see if lymphosarcoma is a possibility, especially in cattle older than 3

f. Plasma Gastrin – study found that plasma gastrin levels were significantly higher13 Study used 29 adult cows with bleeding abomasal ulcers and six healthy cows. The mean plasma gastrin level was 103.2 in healthy cows and 213.6 in the cows with bleeding ulcers.

g. Rumen chloride levels – not found to be specific in one study14 In this study, they performed various diagnostic tests (hematology, serum chemical and rumen chemical) on cows prior to euthanasia and necropsy. Cattle that had ulcers were not significantly different than those without ulcers in regards to the antemortem test results.

3. Clinical pathology

a. CBC/fibrinogen – leukocytosis, neutrophilia, elevated fibrinogen

b. Serum chemistry – non-specific (metabolic alkalosis)

c. Urinalysis – non-specific

d. Ancillary diagnostics

e. Ultrasound – used to rule out traumatic reticuloperitonitis/pericarditis

4. Clinical pathology

a. CBC/fibrinogen – packed cell volume may be increased with decreased levels of protein, leukocytosis/neutrophilia or leukopenia/neutropenia

b. Serum chemistry – non-specific (metabolic alkalosis)

c. Urinalysis – may see "paradoxic aciduria" due to severe stasis of forestomachs and sequestration of chloride – leading to systemic alkalosis and hydrogen ion excretion in urine

d. Ancillary diagnostics

e. Ultrasound – looking for free fluid

f. Abdominocentsis – elevated protein, highly cellular, primarily consisting of neutrophils, may have free or phagocytosed bacteria

Treatment:

In general, addressing some of the suspected factors associated with the etiology of abomasal ulcers such as dietary problems, stressors and concurrent diseases applies for all of the categories. Symptomatic therapy is indicated as well.

Diet

Adults

Remove high starch feedstuffs, Good quality hay, Balanced minerals

Calves

Good quality milk replacer – milk proteins

Whole milk vs. milk replacer – study showing pH was lower in those calves on cow's milk15 In this study, six calves suckled cow's milk, all milk-protein milk replacer and combined milk and soy-protein milk replacer every 12 hours. Mean 24 hour abomasal luminal pH was 2.77 for cow's milk, 3.22 for all milk-protein milk replacer and 3.27 for the combined milk and soy-protein milk replacer. There was no significant difference between the two types of milk replacer, but they were both significantly higher than that of cow's milk. They suggested that due to the clotting of the cow's milk, this extruded the very low pH whey creating a lower pH.

Stressors/concurrent disease

Isolate from others

Identify and correct any other underlying disease such as metritis, mastitis, rumenitis, indigestion, ketosis, displaced abomasum, etc.

Histamine H2 antagonists

Cimetidine/Ranitidine – administered orally to normal milk-fed calves Three groups of calves; group one suckled milk replacer, group two suckled milk replacer and cimetidine (50 or 100 mg/kg), group three suckled milk replacer and ranitidine (10 or 50 mg/kg.). Found a significant dose-dependent increase in pH.16

Parenteral administration – found no significant effect on abomasal pH with cimetidine dosed in the range of 4 – 16 mg/kg17

Proton – pump inhibitors

Oral omeprazole – study looked at intraluminal pH of calves fed non-enteric coated omeprazole (4mg/kg) in paste form Fed this once daily (fed milk replacer without omeprazole 3 times a day) for five days. Found that intraluminal pH increased significantly the first day from 2.89 to 4.17. On days 2, 3, 4, and 5, the mean pH was 3.85, 4.02, 3.97 and 3.39, respectively. Therefore, while the conclusion was that pH did increase, the effects were diminished over time.18

Antacids/protecting agents

Aluminum hydroxide – absorbs pepsin, thereby decreasing proteolytic activity, binds bile acids to protect from bile reflux

Magnesium hydroxide – binds bile acids

In one study, they concluded that administration in this manner caused a transient, dose-dependent increase in intraluminal pH (< 3hours).19

Oral medication in adults

Oral medication, as described in calves, allows a significant portion of the medication to pass into the abomasum even if the calf is tube fed. However, administration of these products in an adult is largely ineffective due to dilution in the rumen. Closing the esophageal groove in adults would assist in delivery of more drug to the abomasum. To do this, various means have been studied including solutions of copper sulfate, hypertonic saline and sodium bicarbonate as a drench. Most recently, vasopressin (ADH) has been found to be a reliable stimulus to close the esophageal groove in ruminants that lack a suckle reflex (older calves, adults).20 According to this study, 0.25 IU/kg intravenously is an effective dose.

Antibiotics

Due to the potential role of bacteria in the etiology and the possibility of perforation of developing abomasal ulcers, antibiotics are probably indicated regardless of the type of ulcer present. That being said, they are particularly indicated for types III and IV (local and diffuse peritonitis, respectively).

Blood transfusions

Prevention:

Dietary management that reduces abomasal disease (LDA, RDA, abomasal volvulus)

Minimizing stress

Eliminating BLV positive animals

References

Van Kruiningen HJ, Gastrointestinal system, In: Thompson RG, Special Veterinary Pathology, BC Decker Inc, Philadelphia, 1988; pp 151-152.

Palmer JE, Whitlock RH, Bleeding abomasal ulcers in adult cairy cattle, J Am Vet Med Assoc 183:448-451, 1983.

Palmer JE, Whitlock RH, Perforated abomasal ulcers in adult dairy cattle, J AM Vet Med Assoc 184:171-174, 1984.

Aukema JJ, Breukink HJ, Abomasal ulcer in adult cattle with fatal hemorrhage, Cornell Vet, 64:303-317, 1974.

Hemmingsen I, Erosiones et ulcera abomasi bovis, Nord Vet Med 18:354-365, 1976.

Hemmingsen I, Ulcus perforans abomasi bovis, Nord vet Med 19:17-30, 1967.

Roeder BL, Chengappa MM, Nagaraja TG, et. al., Isolation of Clostridium perfringens from neonatal calves with ruminal and abomasal tympany, abomasitis, and abomasal ulceration. J Am Vet Med Assoc, 190(12):1550-5, 1987.

Jelinski MD, Ribble CS, Chirino-Trejo M, The relationship between the presence of Helicobacter pylori, Clostridium perfringens type A, Campylobacter spp, or fungi and fatal abomasal ulcers in unweaned beef calves.

Roeder BL, Chengappa MM, Nagaraja TG, et. al., Experimental induction of abdominal tympany, abomasitis, and abomasal ulceration by intraluminal inoculation of Clostridium perfringens type A in neonatal calves. Am J Vet Res 49(2):201-7, 1988.

Jelinski MD, Ribble CS, Campbell JR, et. al., Investigating the relationship between abomasal hairballs and perforating abomasal ulcers in unweaned beef calves. Can Vet J, 37(1):23-6, 1996.

Guard C, Abomasal ulcers. In: Smith BP, Large animal internal medicine. Reinhardt RW, (ed), CV Mosby Company, St. Louis, pp. 797-800, 1990.

Smith DF, Munson L, Erb HN, Predictive values for clinical signs of abomasal ulcer diseased in adult dairy cattle. Prev Vet Med 3:573-580, 1986.

Ok M, Sen I, Turgut K, et. al., Plasma gastrin activity and the diagnosis of bleeding abomasal ulcers in cattle. J Vet Med, 48:563-568, 2001.

Braun U, Eicher R, Ehrensperger F, Type 1 abomasal ulcers in dairy cattle. Zentralbl Veterinarmed A, 38(5):357-366, 1991.

Constable PD, Ahmed AF, Misk NA, Effect of suckling cow's milk or milk replacer on abomasal luminal pH in dairy calves. J Vet Int Med, 19:97-102, 2005.

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, 62:1531-38, 2001.

Whitlock RH, Becht JL, Probantheline bromide and cimetidine in the control of abomasal acid secretion. Bovine Proc (abstract) 15:140, 1983.

Ahmed AF, Constable PD, Misk NA, Effect of orally administered omeprazole on abomasal luminal ph in dairy calves. J Vet Med, 52:238-243, 2005.

Ahmed AF, Constable PD, Misk NA, Effect of orally administered antacid agent containing aluminum hydroxide and magnesium hydroxide on abomasal luminal pH in clinically normal milk-fed calves. J Am Vet Med Assoc, 220:74-79, 2002.

Mikhail M, Brugere H, Le Bars H, et. al., Stimulated esophageal groove closure in adult goats. Am J Vet Res, 49(10):1713-, 1988.

Mills KW, Johnson JL, Jensen RL, et. al., Laboratory findings associated with abomasal ulcers/tympany in range calves. J Vet Diagn Invest, 2(3):208-, 1990.

Ahmed AF, Constable PD, Misk NA, Effect of feeding frequency and route of administration on abomasal luminal pH in dairy calves fed milk replacer. J Dairy Sci 85:1502-08, 2002.