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Created page with "==Introduction== Grain overload is still a relatively common disease, and refers to the '''over-consumption of concentrates'''. This may be by '''accident''', or deliberately i..."
==Introduction==
Grain overload is still a relatively common disease, 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''', tchypnoea, 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'''.
{{Learning
|flashcards = [[Equine Internal Medicine Q&A 20]]
}}
==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''
[[Category:To Do - Helen]]
[[Category:To Do - Review]]
Grain overload is still a relatively common disease, 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''', tchypnoea, 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'''.
{{Learning
|flashcards = [[Equine Internal Medicine Q&A 20]]
}}
==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''
[[Category:To Do - Helen]]
[[Category:To Do - Review]]