Colic - effects of inflammation
By Dr Zofia Lisowski, Prof. Scott Pirie & Dr Neil Hudson
Overview of colic
Colic is a term used to describe the display of abdominal pain in the horse. It is the most common emergency in horses with four to ten out of every 100 horses likely to experience at least one episode of colic each year. It is also the single most common cause of equine mortality. In the US, one study showed that thoroughbreds were more likely to develop colic1 than other breeds. It is of great welfare concern to horse owners, and with the estimated costs associated with colic in the US exceeding $115 million dollars per year2 and the average cost of a horse undergoing colic surgery that requires a resection in the UK being £6437.803, it is also a significant economic issue for horse owners.
Horses with abdominal pain show a wide range of clinical signs, ranging from flank watching and pawing the ground in mild cases, to rolling and being unable to remain standing for any significant period of time in more severe cases. There are numerous (over 50) specific causes of colic. In general, colic occurs as a result of disruption to the normal function of the gastrointestinal tract. This may be attributable to mechanical causes such as an obstruction (constipation), distension (excess gas) or a volvulus (twisted gut). It may also have a functional cause, whereby the intestine doesn’t work as normal in the absence of an associated mechanical problem; for example, equine grass sickness is associated with a functional derangement of intestinal motility due to loss of nerves within the intestine.
Management of colic depends on the cause and can necessitate either a medical or surgical approach. Most horses with colic will either improve spontaneously or with simple medical treatment alone; however, a significant proportion may need more intensive medical treatment or surgery. Fortunately, due to improvements in surgical techniques and post-operative management, outcomes of colic surgery have improved over the past few decades with up to 85% of horses surviving to discharge. Crucially for the equine thoroughbred racehorse population, several studies focussed on racehorses that had undergone colic surgery and survived to discharge, reporting that 63-73% returned to racing. Furthermore, surgical treatment did not appear to negatively impact athletic performance. A similar finding was also seen in the general sport horse population.
Despite significant advancement in colic surgery per se, complications following surgery can have a significant impact on post-operative survival and return to athletic function. Common post-operative complications include:
Complications at the site of the incision (surgical wound)
Infection: Infections at the site of the surgical incision are relatively common. Antibiotics are usually administered before surgery and after surgery. Infections are not normally severe but can increase treatment costs. Horses that develop infections are at greater risk of developing an incisional hernia.
Hernia: Incisional hernias occur when the abdominal wall muscles fail to heal leaving a ‘gap’. Hernia size can vary from just a few centimetres, up to the full length of the incision. Most hernias will not require further treatment, but in more severe cases, further surgery may be required to repair the hernia.
Complications within the abdomen
Haemoperitoneum: A rare complication where there is blood within the abdomen from bleeding at the surgical site.
Anastomosis complications: The anastomosis site is where two opposing ends of intestine that have been opened are sutured back together again. It is important that at this site no leakage of intestinal contents occurs. Leakage or breakdown at this site can lead to peritonitis, which is inflammation or infection within the abdominal cavity and is a potentially life threatening complication.
Adhesions: Scar tissue can form within the abdomen following abdominal surgery. Occasionally this may cause further colic episodes
Further colic episodes
Further colic episodes can occur following surgery. These can occur days to months following discharge.
Endotoxaemia
In some rare cases, horses may develop sepsis in response to toxins released by damaged intestine
Diarrhoea
This is a rare complication. It can develop as a result of infections with C. difficile or Salmonella. As a consequence, some horses may need to be treated in isolation to ensure infection doesn’t spread to other horses or humans.
Post-operative ileus
Post-operative ileus is one of the potential post-operative complications which can lead to a significant increase in hospital stay duration, increased treatment costs and is also associated with reduced survival rates. Post-operative ileus is a condition that affects the muscle function in the intestinal wall. The intestine is a long tube-like structure that has a muscular wall throughout its entire length from the oesophagus to the anus. The function of this muscle is to contract in waves to mix and move food along the length of the intestinal tract, within which digestion occurs and nutrients are absorbed, terminating in the excretion of waste material as faeces. In post-operative ileus these contractions stop and thus intestinal contents are not moved throughout the intestinal tract. In most cases, it is transient and lasts for up to 48 hours following surgery; however, in some cases it can last longer. A build-up of fluid develops within the intestine as a result of the lack of propulsion. This stretches the intestines and stomach, resulting in pain and the horse’s inability to eat. Unlike humans, the horse is unable to vomit; consequently, this excess fluid must be removed from the stomach by other means, otherwise there is a risk of the stomach rupturing with fatal consequences. Post-operative ileus may occur in up to 60% of horses undergoing abdominal surgery and mortality rates as high as 86% have been reported. Horses in which the small intestine manipulated is extensively manipulated during surgery and those that require removal of segments of intestine are at higher risk. Despite the significant risk of post-operative ileus following colic surgery in horses, there is a lack of studies investigating the mechanisms underpinning this condition in horses; consequently, the precise cause of this condition in horses is not fully known.
What causes the intestine to stop functioning?
For many years it was thought that post-operative ileus occurred as a result of a dysfunction of the nerves that stimulate contraction of the muscles in the intestinal wall. This theory has now mostly been superseded by the concept that it primarily results from inflammation in the intestinal wall. Based on human and rodent studies, it has been shown that immune cells in the intestine (macrophages) play a key role in development of this condition. Macrophages are important cells found everywhere in the body, with the largest population being in the intestine. These cells become activated by the inevitable manipulation of the horses’ intestines during colic surgery, with subsequent initiation of a sequence of events which ultimately results in dysfunction of the muscle in the intestinal wall. We know macrophages are present within the wall of the horses’ intestine and that at the time of colic surgery there is an inflammatory response at this site. Although the significance of these findings in relation to post-operative ileus in the horse remains unknown, they provide sufficient justification for ongoing research focused on the inflammatory response in the intestine of horses during and immediately following colic surgery…
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Equine Gastric Ulcer Syndrome
Vets and other professionals recognise that gastrointestinal function and health in horses exists in a finely balanced state. Most conditions relating to the intestinal tract, for example colic and diarrhoea are well understood and are most commonly treated either medically or surgically.
Dr Mark Dunnett & Dr Catherine Dunnett (European Trainer - issue 15 - Autumn 2006)
Vets and other professionals recognise that gastrointestinal function and health in horses exists in a finely balanced state. Most conditions relating to the intestinal tract, for example colic and diarrhoea are well understood and are most commonly treated either medically or surgically. There has been, however, less appreciation of how frequently the health of a horse’s stomach can be compromised. The true prevalence of equine stomach lesions (gastric ulcers) was recognised only with the introduction of gastric endoscopy. How prevalent are ulcers? Numerous studies conducted in the 1980s and ‘90s in varied horse populations within differing sporting disciplines identified EGUS as a much more a widespread problem than commonly assumed. Many of these studies focussed on thoroughbred racehorses, and produced remarkably similar findings.
Between 80 and 90% of horses in training were found to have gastric ulcers. And, somewhat surprisingly, over 50% of racehorses temporarily out of training also had lesions. Moreover, this health and welfare issue was not confined to thoroughbred racing; horses competing in other equestrian sporting disciplines were also prone to this condition. In contrast, less than 5% of permanently grazed horses appear to suffer from gastric ulceration. Prevalence of EGUS in horses engaged in different equestrian sporting disciplines Population Prevalence (%) Racing (thoroughbreds) 80 - 90 Trotting/pacing (standardbreds) 72 - 88 Endurance racing 67 Show horses 58 Foals (thoroughbred) > 50 Symptoms to look for that may suggest gastric ulceration include chronic recurrent colic, episodic colic, acute colic, reduced appetite, poor body condition and chronic diarrhoea. Whilst these clinical signs are not always indicative of gastric ulcers, as can be seen from the table below there is a clear relationship.
The strongest indicator appears to be an inability to thrive as indicated by poor body condition and reduced appetite. Incidence of overt clinical signs in horses subsequently found to have EGUS Clinical signs Incidence (%) Chronic recurrent colic, for 7 days or more 25 Episodic colic (1+) for 7 or more days 13 Acute colic 10 Reduced appetite 53 Poor body condition 40 Diarrhoea 9 Unfortunately, however, in about 52% of horses where gastroscopy reveals ulceration there will have been no obvious prior clinical signs.
What causes gastric ulcers? Gastric lesions (ulcers) are now recognised as a common condition in stabled horses, whether involved in racing or other equine sports, and in foals, yet they appear to be absent in wild horses. You may be familiar with the fact that gastric ulcers in humans are frequently caused by infection with a bacterium called Helicobacter pylori, it was not surprising therefore that this was investigated but then dismissed as a possible cause in horses. So, what is the cause and why is the prevalence in racehorses so high? To answer this question we need to examine the manner in which we train, house and feed our racehorses. All the clinical evidence to date indicates that the high incidence of gastric ulcers in racehorses is a ‘man-made’ phenomenon that is related to the feeding and management practices that we employ during training.
There are four key contributory factors involved in the development and progression of ulcers:
1) Dietary makeup and feeding practices
2) Intensity of exercise (level of work)
3) Stress factors
4) Prolonged use of non-steroidal antiinflammatory drugs, such as phenylbutazone, and corticosteroids. When considering these factors we need to appreciate that the horse has evolved over millennia as an exclusively grazing animal with a digestive system that is reliant on the continual ingestion of fresh forage to meet its dietary requirements. In EGUS the damage caused to the lining of the stomach arises from prolonged exposure of the gastric mucosa to gastric acid, without sufficient protection from the buffering effect of saliva.
Dietary makeup and feeding practices Racehorses are most often fed a diet that is high in starch rich cereal and low in forage. Horses produce gastric acid continuously, and high starch diets tend to further increase its production through stimulation of a hormone known as gastrin. In addition, where these starch-rich meals are large, inadequate mixing in the stomach can lead to some of the starch being fermented here, which further contributes to the overall acidity. During feeding, chewing normally stimulates the production of saliva, which contains a natural buffer ‘bicarbonate’, to offer some protection of the gastric mucosa against the corrosive effects of gastric acid. However, the amount of saliva produced for each kilogram of concentrate feed consumed is about 2.5 times less than that produced for the same weight of forage, as proportionally less chewing is involved. Minimal forage intake therefore takes its toll on gastric health, as during periods when the horse has no access to feed or forage, the protective effects of saliva are lost and these are key danger times for gastric ulceration.
A recent study published in the Equine Veterinary Journal also suggests that repeated electrolyte or salt administration may exacerbate or even induce gastric ulceration. But before we all cast aside our daily electrolyte or salt administration, which has great physiological benefit, we need to take these recent findings in context. This latest study used an endurance model of electrolyte administration using a concentrated electrolyte syringe 8 times within an 8-hour period. Whilst this may be common practice during endurance races, this type of administration in racing is in my experience not practised. It is, however, a difficult conundrum for endurance trainers as electrolyte depletion during races is a significant issue.
Certainly electrolyte or salt products that dissolve more slowly in the stomach may be an advantage. Exercise intensity The level of work that horses undertake has also been found to be a significant contributory factor in the development of EGUS. Although ulcers are present in about 40% of horses undertaking light exercise this increases to over 95% in horses with busy racing schedules. This effect probably arises through the physical movement of the organs and tissues within the horse’s body that occurs during exercise. Mechanical movement and compression of the stomach forces the most sensitive non glandular regions of its lining into further contact with gastric acid, and this effect is exacerbated when exercise intensity is increased.
Stress Although training and racing by necessity place horses under physiological stress, psychological stress is also implicated in ulcer development. Recent studies in the USA indicate that sudden stressful changes from the normal daily routine and environment, including transport and new stabling, promote rapid changes to the integrity of the stomach lining. Indeed, gastroscopy showed the appearance of ulcers within only 6 days. Medical treatment of gastric ulcers Gastric ulcers in horses rarely heal spontaneously, so veterinary intervention is necessary. Methods for the treatment and prevention of gastric ulcers in horses follow those employed in human medicine and generally involve the use of antacids alone, or in conjunction with anti-ulcer drugs.
Antacids neutralise gastric acid. Those based on sodium and calcium carbonates and bicarbonates have the potential drawback of releasing carbon dioxide (gas) in the gut. In addition, bicarbonate supplementation can increase blood bicarbonate levels that could potentially result in a breach of doping rules. Antacids containing aluminium or magnesium hydroxides and silicates may be preferential.
Drugs used to inhibit gastric ulcers include, the H2-receptor blockers cimetidine and ranitidine and the so-called ‘proton-pump inhibitor’ omeprazole. Omeprazole is the most widely used and effective treatment in horses and is marketed as an oral paste under the trade name Gastroguard. Dietary supplement products available for gastric health Product Company Active ingredients Function Product Form Dose (500kg horse) Neigh-Lox Saracen (KER) Dihydroxy-aluminium, sodium carbonate, calcium carbonate, aluminium phosphate Antacid Coats & protects Pellet 340g Settlelex Feedmark Calcium carbonate, aluminium hydroxide, magnesium carbonate, dicalcium phospahte Antacid Powder 30-100g Acti-Soothe Nelson Veterinary Ltd high fibre ingredients, calcium carbonate. Magnesium carbonate, probiotic, prebiotic Antacid Pellet 400g Gastro Ardmore Equine phytochemicals, mucosal agents,, natural antibiotics, natural stress reducers Other Paste 1 syringe Ulseraze NAF Powder, lactoferrin, ginger, marshmallow, Liquorice,psyllium seeds, phosphotidylcholine, Other Powder 60g U-Guard Equine America Calcium carbonate, kaolin, liquorice, aloe Vera, iron oxide, dried apple pectin pulp, magnesium silicate, vitamin B5 and magnesium oxide. Antacid Coats & protects Powder 40g Stomacare Twydil polyunsaturated fatty acids, phospholipds, chitosan glucosamine fibre Antacid Coats & protects Syringe 1-2 syringes (60-120g) Dietary prevention of ulceration Mark Tompkins chairman of the Newmarket Trainers Federations takes the view that “a common sense approach to gastric ulcers is what's needed, with care being taken over the feeding regime and any stress on horses being kept to a minimum”. In essence he is absolutely correct and as we largely know what the dietary trigger factors are, this should be a fairly straightforward process.
Firstly, whilst the need to minimise gut fill from forage is appreciated, we should try to maximise forage intake whenever possible. This serves two purposes by increasing the amount of protective saliva produced, but also reducing the amount of time that horses in training spend without access to feed. Racehorses could benefit from the best of both worlds, if they were fed more hay or haylage for the majority of the time, with the level being reduced to a minimum (1% of bodyweight for hay and 1.25% of bodyweight for haylage) in the 2-3 days before racing. Additionally, any horses that suffer from recurrent ulcers would certainly benefit from turnout onto pasture for some part of the day. Ensuring meal size is minimised can mollify the negative effects of a high cereal intake. Greater number of small meals, rather than a few large ones is the better option.
It is usually the second and third meals of the day that often need to be reduced and be redistributed to a fourth late feed. Addition of generous double handful of alfalfa chaff to concentrate feeds will also encourage chewing and improve saliva production. Supplements fed to help maintain gastric mucosal health are unlikely to be as effective as drug treatments such as Omeprazole. However, they can be used as an adjunct to veterinary therapy following an initial course of treatment, or during periods where drug treatment has to be withdrawn to avoid contravening doping regulations. In choosing a product however, selecting those from companies that have tested the efficacy of their product in a scientific environment is a wise strategy.