Abomasal Ulcers

Abomasal ulcers, also known as Gastritis of Ruminants, Long-standing abomasitis leads to abomasal ulcers.

Definition of Abomasal Ulcers

Inflammation of the abomasal mucosa is clinically manifested by progressive anorexia, loss of production, and if damage to the mucosa is severe, it results in ulcers that are clinically manifested by progressive anaemia and black tarry-coloured pasty faeces.

Haemoglobin in the stomach combines with HCl, forming acid haematin, which imparts a brownish colour to the faeces.

Etiology

It is a stress-related disease that results in increased production of ACTH that stimulates the release of glucocorticoids, which impair mucosal turnover and the regeneration of epithelium. High-yielding animals are more susceptible to stress and, hence, more susceptible to abomasal ulcers.

Low-quality feed leads to more irritation to the gastric mucosa, especially in feed pellets if coarse and rough particles are present.

Infection agents like thielariasis cause button-shaped abomasal ulcers. Enzootic bovine leukosis is also associated with abomasitis and ulceration of the abomasal mucosa. Worm infestations, like Haemonchus spp., also cause abomasal ulcers.

Pathogenesis

Stress leads to the production of ACTH, which stimulates the release of steroid hormones, which impair mucosal turnover. There is diffusion of H⁺ and pepsin through the damaged mucosa that accelerates the deepening of ulcers, which may cause damage to the underlying blood vessels, leading to gastric haemorrhage.

Abomasal ulcers are categorised into four types based on the amount of erosion and haemorrhage associated with the ulcers (Smith et al., 1983):

Type I (Non-Perforating)

There is an incomplete ulceration of the abomasal wall. Usually, such types of ulcers undergo abomasal thickening and mild serositis with minimal haemorrhage.

Type II (Non-Perforating causing severe blood loss)

These ulcers, while invading, cause damage to major abomasal vessels in the submucosa, causing severe blood loss.

Type III (Perforating type with local peritonitis)

Ulcer has perforated the abomasal wall but resulted in local peritonitis. Here is also spread is arrested, because of local adhesions to adjacent viscera.

Type IV (Perforating type with diffused peritonitis)

Diffused peritonitis is due to widespread draining of abomasal contents.

Clinical Signs

Progressive development of inappetence, excessive thirst, signs of abdominal pain, and the passing of soft, pasty faeces. When abomasitis develops into the ulcerative stage, the signs are much more pronounced. Like progressive anaemia, the passing of dark-coloured pasty faeces (melena), pronounced signs of abdominal pain, jugular pulsation, a high pulse rate, and tachycardia are seen as compensatory mechanisms for profound anaemia.

Ulcers associated with peritonitis are indicated by signs like fluctuating fever, atony of rumen, progressive anorexia, the passing of dark brown tarry-coloured faeces, and pain on palpation on the right costal arch nearing xiphoid.

Diagnosis

• Based on the history: common in high-yielding animals of urban origin; history of the passing of dark, tarry-coloured faeces.
• Based on the clinical signs: progressive anaemia, passage of dark tarry-coloured faeces, signs of abdominal pain, toxaemia.
• Abdominocentesis: Paracentesis of the abomasum.

Differential diagnosis

• Abomasal impaction
• Omasal impaction
• Caecal dilatation

Treatment

• Change in the diet. The plane of nutrition should be changed with restrictions on indigestible components of food stuff for more nutritious components.
• Antacids: Mg(OH)₂ is preferred for ruminants. 1 g/kg body weight, but when administered orally, some quantity gets retained in the rumen. Under partial closure of the oesophageal groove with a special tube, the contents can be delivered into the Omaso-Abomasum. It can also be administered through a canula inserted at the abomasocentesis site.
• Mineral oils like liquid paraffin and linseed oil can be administered at 8 ml/kg B. Wt by oral route can smoothen gastric mucosa and decrease HCl secretion.
• Supportive treatment: fluids and electrolytes like normal saline or DNS are administered based on the exact cause of dehydration. Depending on the extent of abomasal damage, H₂ blockers can be used, like Cimetidine and Ranitidine, at 1-2 mg/kg body weight by the IM route and Protop pump inhibitors like pantoprazole also used.
• Gastric motility modifiers in abomasitis are indicated as there is delayed gastric emptying. (Metaclopramide at 0.3 mg/kg body weight by parentral route. Cisapride is used in monogastrics but has not yet been tried in ruminants.)
• Blood transfusion to counteract anaemia.
• A course of parental antibiotics to check for ongoing peritonitis is advised.