Grain Overload - Horse
Introduction
Grain overload is still a relatively common problem, and refers to the over-consumption of concentrates. This may be by accident, or deliberately induced.
It is the amount of soluble carbohydrate in the concentrate that is the problem, and maize/corn-containing products are a greater danger than a grain product such as oats. Barley is also very high in soluble carbohydrates.
Some owners feed extra corn over the winter hoping to increase heat production and help the horse keep warm. This does not occur and the caecum and colon produce a lot more heat through the fermentation of fibre.
As the carbohydrates enter the stomach and intestines, the pH decreases and there is a change in the microbial flora. This results in acidosis and an increased risk of endotoxaemia.
Grain overload is also a major contributor to the development of laminitis.
Clinical Signs
Signs can vary from mild colic and diarrhoea to death due to gastric rupture.
Other signs include: abdominal distension, lameness caused by laminitis, trembling, sweating.
If endotoxaemia and hypovolaemic shock, gastritis and ileus develop, signs may include: purple mucous membranes, tachycardia, tachypnoea, gastric reflux, colonic distension, decreased intestinal motility.
Diagnosis
This is usually based on the history, which may include an episode of eating large amounts of grain.
Clinical signs are also usually suggestive.
- Rectal examination may reveal: colonic distention with tight bands
- Haematology may reveal: polycythemia, neutropenia with a left shift and toxic changes in the neutrophils.
Treatment
The most immediate concern is gastritis and stomach distension. In such cases the passage of a nasogastric tube is essential to prevent gastric rupture. The tube can then be left in place, or continuous monitoring for repeat distension should be performed.
If no reflux is obtained, activated charcoal or mineral oil can be given to reduce toxin absorption from the gastrointestinal system.
If clinical signs have not developed yet, magnesium sulphate and water can be administered per os to speed evacuation of the grain from the gastrointestinal system.
Systemic therapy includes: flunixin for its anti-inflammatory and anti-endotoxic effects, aspirin may be of benefit in maintaining digital perfusion, an antihistamine may also be beneficial.
Dehydration and acidosis can be addressed by administering lactated Ringers fluid, possibly with added bicarbonate.
If the horse is showing signs of hypovolaemic shock, hypertonic saline can help expand the intravascular volume, but must be followed by isotonic fluids. Calcium and potassium may need to be supplemented.
Plasma may be helpful if signs of endotoxaemia are present.
Frog supports can be placed on the feet and the stall bedding should be deep and soft, to maintain laminar perfusion and prevent laminitis.
Nitroglycerine ointment at the coronary band has been shown to increase blood flow to the feet.
Prognosis
It is good if treatment is instituted before clinical signs develop. The prognosis is poor if there are moderate or severe clinical signs. Significant colic and abdominal distension often leads to death within 48 hours, even with the most aggressive therapy.
If laminitis occurs along with intestinal signs, the prognosis is grave.
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References
Orsini, J. (2008) Equine Emergencies Elsevier Health Sciences
Mair, T. (2002) Manual of equine gastroenterology Elsevier Health Sciences
Snyder, J. (2006) The equine manual Elsevier Health Sciences
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