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Gastroparesis & Gastric Rupture in Friesian Horses



Research has indicated Friesians appear to be disproportionately affected by primary gastric rupture. One theory researchers have contemplated is that the increased presentation of primary gastric rupture in Friesians may be caused by gastric dysmotility as a result of a breed-specific collagen-related connective tissue disorder.


THE PHYSIOLOGY OF GASTRIC EMPTYING Gastric motor function and gastric emptying in horses is a complex process. Many horse owners don’t consider that liquids and solids are handled differently within the equine stomach. Solid food undergoes a process called trituration once it enters the stomach, which crushes and grinds food into

very small particles and mixes it with water and digestive juices to form “chyme”- a thick semifluid mass of partially digested food and digestive secretions. The process of trituration requires coordinated gastric motility consisting of peristaltic contractions, which generate pressure and move chyme down towards the exit of the stomach.


Compared to humans, the equine stomach has very limited potential as a reservoir for large meals. A horse’s stomach is relatively small, with an average capacity of approximately 2.5 gallons (20 lbs.) for a 1,000 lb. horse. A horse’s stomach is also unable to relax and accommodate food in response to gastric distention. Therefore, a horse’s stomach contents should not exceed more than 2/3 of its capacity (including forage) at any time. This equates to a maximum of 1.6 gallons (13. lbs) of total ingesta for a 1,000 lb. horse. This explains why, among many other reasons, horses should not receive large concentrate or grain meals and should ingest forage throughout the day at a slow pace. Additionally, soaking food items such as concentrates, grains, and hay pellets/cubes in water prior to feeding them assists in trituration.


The exit of the stomach is a thick circular muscle that remains partially contracted at all times called the pylorus. In order for chyme to exit through the pylorus, larger food particles must be triturated down to an acceptable size, ideally 1-2 mm. This process is referred to as gastric emptying, and the rate of emptying is influenced by the nature and volume of the meal ingested. Large-volume meals, large food particles, long-stemmed forage, and high carbohydrate meals all empty the stomach at a slower rate than their alternatives. The average rate of gastric emptying in healthy adult horses is 1.5 hours for solids and 10 – 70 minutes for liquids.

In order for food particles to exit the stomach they must be ground down to a very small size, ideally 1-2 mm.

GASTRIC ULCERS AND DELAYED GASTRIC EMPTYING There are two distinct types of gastric ulcers that affect horses. The first and most common type, accounting for up to 80% of ulcers in horses, is called Equine Squamous Gastric Disease (ESGD). ESGD describes ulcers that occur in the upper third portion of the stomach called the squamous region. Squamous ulcers are usually caused by human-induced environmental and management practices such as limited turnout, high-intensity training, high grain or concentrate intake, intermittent feeding practices, social stress, travel, and competition.


In contrast, Equine Glandular Gastric Disease (EGGD) accounts for only 20% of equine ulcer cases and affects the bottom two-thirds of the stomach, called the glandular region. The risk factors for EGGD include issues that weaken or lessen the integrity of the stomach’s protective functions in the glandular region. Examples of risk factors include limited turnout, low hay intake, long-term NSAID drug use, short and intense exercise, breed predisposition, unbalanced diet, and pathogenic bacteria.


The most common cause of delayed gastric emptying in horses is pyloric outflow obstruction secondary to Equine Glandular Gastric Disease (EGGD). The pylorus, the area where food exits the stomach, becomes ulcerated. This results in fibrosis (scar tissue), granulation of the pylorus tissue, and lesions that physically obstruct the outflow of the stomach contents, resulting in delayed gastric emptying. It should be noted that anytime delayed gastric emptying occurs, it can cause secondary ulcers in the upper squamous region of the stomach as well as gastroesophageal reflux due to exposure to gastric acid. Thankfully, both ESGD and EGGD are typically very responsive to treatment with the appropriate drugs and diet, and management changes if they are addressed early enough.



GASTROPARESIS AND DELAYED GASTRIC EMPTYING

Gastric Dysmotility, also known as Gastroparesis, can also cause delayed gastric emptying. In humans, a plethora of other conditions have also been associated with delayed gastric emptying, and it would be naïve to assume that similar conditions do not exist in horses. Of particular interest is gastroparesis, a motility disorder described in humans characterized by delayed gastric emptying in the absence of mechanical obstruction. This condition bears similarities with a poorly defined syndrome of gastric dysmotility in adult horses characterized by delayed gastric emptying of solid food and primary gastric impaction. Affected horses do not appear to have difficulty emptying liquids from their stomach and, therefore, rarely present with fluid distention of the stomach and do not develop secondary squamous gastric disease or gastroesophageal reflux. Clinical signs are vague and include many symptoms, which can be confused with ulcer symptoms such as inappetence, mild recurrent colic, reluctance to work, signs of pain, and sensitive skin or “girthiness”. Some affected horses are asymptomatic, and in such cases, the condition is identified incidentally at the time of gastroscopy.


Friesians appear to be disproportionately affected by primary gastric impaction and gastric rupture, and it has been postulated that this may be due to a breed-specific increase in collagen degradation of connective tissue. Interestingly, in Friesians with both megaesophagus and aortic rupture, researchers observed significantly more collagen deposited between large muscle fibers and collagen fibers in the esophagus and aorta of affected horses. Additionally, the collagen was disorganized, less condensed, and presented as small, clumped structures. Additional studies indicated a difference in the rate of collagen catabolism in Friesian horses. This could explain the predisposition of Friesians to connective tissue disorders.

Primary Gastric Impaction in a Friesian Mare

Humans with systemic sclerosis have a similar increase in collagen catabolism, and it is interesting to note that they are also disproportionately affected by gastric dysmotility. The pathogenesis is complex in humans but involves vascular changes, alterations of innate immunity, and the development of patchy fibrosis that may cause stiffness and loss of gastric contractility. Similar mechanisms may be at play in the Friesian breed and warrant further investigation.


DIAGNOSING GASTROPARESIS OR DELAYED GASTRIC EMPTYING Unfortunately, the diagnosis of gastroparesis or delayed gastric emptying in adult horses can be challenging. In most cases, the diagnosis is presumptively made based on characteristic clinical signs, such as a consistently enlarged stomach on ultrasonography or viewing the presence of food in the stomach via gastroscopy after an appropriate period of fasting.


One promising diagnostic technique is nuclear scintigraphy, a process that uses radiolabeled solids. Scintigraphy is accurate, sensitive, quantitative, easy to perform, and widely available. Scintigraphy is considered the gold standard for the investigation of gastric motility disorders in human medicine. Researchers encourage equine practitioners to consider nuclear scintigraphy for adult horses that present with signs suggestive of delayed gastric emptying. Having a reliable method of determining the rate of gastric emptying in adult horses will improve the understanding of the role delayed gastric emptying plays in disorders such as EGGD, gastric dysmotility, and primary gastric impactions. Furthermore, it will facilitate investigation into the effects of dietary modification and pharmacological modulation of gastric motility in these challenging cases.


GASTRIC RUPTURE Gastric rupture is rare in horses and is almost always fatal. There are two types of gastric rupture: primary gastric rupture and secondary gastric rupture.

  • Primary gastric rupture is caused by the abnormal expansion of the stomach with feed material due to delayed gastric emptying, often as a result of glandular gastric ulcers or gastric dysmotility (gastroparesis). Other less common causes of primary gastric rupture include severe gastric ulceration leading to perforation, death of stomach wall tissue due to localized loss of blood supply, or extreme overeating. Horses with primary gastric complications will often initially present with a slow onset of symptoms typically associated with gastric ulcers and delayed gastric emptying that may be missed by the owner. This, among several other reasons, is why it is particularly important to perform a gastroscopy prior to treating any horse for ulcers. If the horse is misdiagnosed with a simple case of ulcers and no gastroscopy is performed, gastroparesis or delayed gastric emptying could result in a subsequent gastric impaction and, ultimately, primary gastric rupture.

  • Secondary Gastric Rupture is caused by the abnormal expansion of the stomach as a result of an intestinal obstruction (colic) which then causes gas or the contents of the small intestines to backflow into the stomach.

Resolving gastric impaction can be difficult, particularly if it is left to progress for a significant amount of time. However, if gastric impaction is caught early enough, horses can be fasted for a period of time and then placed on a diet of soaked hay pellets and soaked concentrates to prevent future impactions. Additionally, there are medications that can be given, with varying degrees of success, in an attempt to improve gastric motility.


The best approach to preventing secondary gastric rupture is to treat all colic pain as an emergency. Acute cases will develop rapidly, and once the stomach ruptures, there is little that can be done. Fortunately, impending secondary gastric rupture as a result of intestinal obstruction can often be confirmed and relieved by passing a nasogastric tube into the stomach through the nostrils and draining gas and fluid from the stomach.


Regardless of whether related to primary or secondary causes, the hallmark sign of impending gastric rupture is intense and unbearable abdominal pain, which often causes an extremely violent reaction from the horse as the stomach nears rupture. This pain is nearly always unrelieved by the typical pain medications given for colic. If the horse is particularly stoic, as Friesians are reported to be, it may not show signs of intense pain until it is too late for intervention. Surgical repair of primary or secondary gastric rupture is very rarely possible, as the horse must already be at an equine hospital and prepared for surgery when the moment of gastric rupture occurs.

Treat colic as an emergency until proven otherwise.

THE PREDISPOSITION FOR PRIMARY GASTRIC RUPTURE IN FRIESIANS A study of primary gastric rupture in 47 horses from 1995-2011 that was published in the Canadian Veterinary Journal found an apparent breed predisposition of Friesians and Draft breeds to primary gastric rupture. Researchers hypothesize the predisposition may be related to breed-associated differences in pain tolerance or the presence of underlying connective tissue defects or gastric dysmotility (gastroparesis).


Subjectively, Draft horses and Friesians are more stoic breeds and may not manifest gastric pain until severe, possibly delaying treatment and predisposing them to gastric rupture. It is also possible that both Draft horses and Friesians have an underlying structural or functional defect in their stomach, making them more likely to rupture compared with other breeds. The Friesian breed suffers from several connective tissue-related diseases, including megaesophagus and aortic rupture, and it is conceivable that a connective tissue-related disorder could also affect the stomach of Friesian horses. The findings of this study underscore previous studies, which indicate that events leading to gastric rupture, even gastric impaction, may not be long-standing or may not be associated with easily recognizable clinical signs prior to rupture.



GASTRIC ISSUES SHOULD BE TAKEN SERIOUSLY BY FRIESIAN OWNERS It is critical that all horse owners understand the difference between Equine Squamous Gastric Disease and Equine Glandular disease. Horses that show symptoms of gastric ulcers should undergo gastroscopy to confirm the presence of ulcers, determine the type (squamous or glandular), and receive the specific medication appropriate for treating ulcers in that region of the stomach.


It’s also of great importance that owners understand the symptoms of delayed gastric emptying are often confused for symptoms of ulcers. If horses with delayed gastric emptying do not undergo a gastroscopy, the disease may be misdiagnosed for ulcers, go untreated and subsequently lead to gastric rupture.


Finally, due to the apparent breed disposition of Friesians to primary gastric rupture and their stoic nature, it is essential that owners take any signs of colic pain seriously and consult with their veterinarian without delay. If owners are able to recognize the signs of gastric issues and take action early enough, gastric rupture can hopefully be prevented.


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References: Hewetson, M. & McGuire, C.. (2021). Equine squamous gastric disease and delayed gastric emptying – the chicken or the egg?. Equine Veterinary Education. 10.1111/eve.13597.

Winfield, L. S., & Dechant, J. E. (2015). Primary gastric rupture in 47 horses (1995-2011). The Canadian veterinary journal = La revue veterinaire canadienne, 56(9), 953–958.



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