Equine proximal enteritis

Last updated January 03, 2021

Proximal enteritis, also known as anterior enteritis or duodenitis-proximal jejunitis (DPJ), is inflammation of the duodenum and upper jejunum. It produces a functional stasis of the affected intestine (ileus) and hypersecretion of fluid into the lumen of that intestine. This leads to large volumes of gastric reflux, dehydration, low blood pressure, and potentially shock. Although the exact cause is not yet definitively known, proximal enteritis requires considerable supportive care.

Epidemiology

DPJ is most commonly seen in the Southeastern US, although cases have been reported throughout the United States and Canada, as well as sporadically in the United Kingdom and Europe.^[1] Horses in the Southeastern US tend to have a more severe form of the disease relative to other locations.^[1] Age, breed, and gender appear to have no effect on disease prevalence.^[1]

Pathophysiology

The cause of proximal enteritis is not definitively known.^[2] Both Salmonella and Clostridial species have been isolated from gastric reflux contents of affected horses. Salmonella has not been consistently found in all horses with DPJ, although one study cultured toxigenic Clostridial species in 100% of affected horses.^[2] Other potential causes include Fusarium infection and recent increase in dietary concentrate levels, which can alter the microbial population within the intestinal lumen.^[2]

Inflammation of the intestine leads to the secretion of a large amounts of electrolytes, primarily sodium and chloride, into its lumen, resulting in the osmotic movement of water.^[2] The production of fluid is thought to be due to active hypersecretion, passive secretion of proteins secondary to damage to epithelium of the mucosa and capillaries, and a functional ileus which prevents removal of this fluid.^[2] Massive fluid production results in extensive reflux, usually produced at a rate of 50–100 mL/min,^[3] in addition to distention of the proximal small intestine, dehydration, and possible shock secondary to hypovolemia.^[2] Proximal enteritis can also occur with inflammation of other organs in the gastrointestinal tract, including gastritis, ileitis, typhlitis, and colitis.^[2]

Clinical signs

Signs include acute onset of moderate to severe pain, large volumes of gastric reflux (4–20 L per decompression)^[2] which is usually orange-brown and fetid, distended small intestine (up to 5–7 cm in diameter)^[2] palpable on rectal examination, fever, depression, increased heart rate (>60 bpm),^[2] increased respiratory rate, prolonged CRT, and darkened mucous membranes.^[2] After gastric decompression, the horse may show signs of malaise and act lethargic, but pain level usually improves.^[2]

Abdominocentesis usually reveals a yellow, turbid fluid with an increased white blood cell count (usually 5,000–10,000 cells/microliter) and protein level (>3.5 g/dl),^[2] although the fluid may be serosanginous in severe cases.^[2]^[3] A chemistry panel will often show electrolyte abnormalities (hypokalemia, hyponatremia, hypochloremia) due to electrolyte loss into the lumen of the intestine. Leukocytes may be normal, increased, or decreased. PCV and total protein are usually both increased due to fluid loss, and the horse displays a prerenal azotemia.^[2] On the chemistry panel, liver enzymes such as GGT, ALP, AST are increased, likely due to ascending infection from the common bile duct, endotoxin absorption, and hypoperfusion.^[2] A metabolic acidosis with a high anion gap is often seen due to loss of bicarbonate in gastric reflux and an increase in lactic acid in the blood, secondary to hypovolemia and decreased tissue perfusion.^[2]

Differential diagnoses

It is important to differentiate DPI from small intestinal obstruction, since obstruction may require surgical intervention, but this can at times be difficult.^[3] Horses suffering from DPI usually have a higher protein concentration in their peritoneal fluid compared to horses with small intestinal obstruction, often without a concurrent increase in nucleated cell count.^[2] They usually have some relief and decrease in pain after gastric decompression, while horses with an obstruction often still act colicky after nasogastric intubation.^[2] Distention of the small intestine may be less than what is felt on rectal examination of horses with obstruction, especially after gastric decompression. Horses with DPJ usually produce larger volumes of reflux (usually greater than 48 liters in the first 24 hours)^[1]^:322–332 than those with obstruction, and are often pyretic (temperatures of 101.5–102.5) and have alterations in white blood cell levels, while those with obstructions usually have a normal or lower than normal temperature and normal leukocyte levels.^[2]

Ultrasound can also be helpful to distinguish DPJ from obstruction. Horses with small intestinal obstruction will usually have an intestinal diameter of −10 cm with a wall thickness of 3–5mm. Horses with proximal enteritis usually have an intestinal diameter that is narrower, but wall thickness is often greater than 6mm,^[3] containing a hyperechoic or anechoic fluid, with normal, increased, or decreased peristalsis.^[2] However, obstructions that have been present for some time may present with thickened walls and distention of the intestine.^[2]

DPJ can only be definitively diagnosed during surgery or at necropsy, when its gross appearance of the small intestine may be evaluated.^[2]

Treatment

Proximal enteritis usually is managed medically. This includes nasogastric intubation every 1–2 hours to relieve gastric pressure secondary to reflux,^[3]^[4] which often produces to 2–10 L,^[2] as well as aggressive fluid support to maintain hydration and correct electrolyte imbalances. Maintaining hydration in these patients can be very challenging. In some cases, fluid support may actually increase reflux production, due to the decreased intravascular oncotic pressure from low total protein and albumin levels, leading to loss of much of these IV fluids into the intestinal lumen. These horses will often display dependent edema (edema that collects in locations based on gravity).^[2] Colloids such as plasma or Hetastarch may be needed to improve intravascular oncotic pressure, although they can be cost prohibitive for many owners. Reflux levels are monitored closely to help evaluate fluid losses, and horses recovering from DPJ show improved hydration with decreased reflux production and improved attitude.^[2]

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain relief, reduction of inflammation, and for their anti-endotoxin effects, but care must be taken since they may produce gastrointestinal ulceration and damage the kidneys.^[2] Due to a suspected link to Clostridial infection, anti-microbials are often administered, usually penicillin or metronidazole. Aminoglycosides should be used with extreme caution due to the risk of nephrotoxicosis (damage to the kidney).^[2] The mucosa of the intestines is damaged with DPJ, often resulting in absorption of endotoxin and risking laminitis, so therapy to combat and treat endotoxemia is often employed. This includes treatment with drugs that counteract endotoxin such as Polymyxin B and Bio-Sponge, fluid support, and laminitis prevention such as icing of the feet.^[2] Prokinetic drugs such as lidocaine, erythromycin, metoclopramide, and bethanechol are often used to treat the ileus associated with the disease.

Horses are withheld food until reflux returns to less than 1–2 L of production every 4 hours, and gut sounds return, often requiring 3–7 days of therapy. Parenteral nutrition is often provided to horses that are withheld feed for greater than 3–4 days. It is suspected to improve healing and shorten the duration of the illness, since horses often become cachexic due to the protein losing enteropathy associated with this disease.^[2]

Surgery may need to be performed to rule out colic with similar presenting signs such as obstruction or strangulation,^[4] and in cases that are long-standing (> 7 days) to perform a resection and anastomosis of the diseased bowel.^[3] However, some horses have recovered with long-term medical support (up to 20 days).^[2]

Complications and survival

Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube.^[2] Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss.^[2] Horses are also at increased risk of hepatic injury.^[5]

Survival rates for DPJ are 25–94%.^[2] Horses that survive the incident rarely have reoccurrence.^[2]

Related Research Articles

Peritonitis is inflammation of the peritoneum, the lining of the inner wall of the abdomen and cover of the abdominal organs. Symptoms may include severe pain, swelling of the abdomen, fever, or weight loss. One part or the entire abdomen may be tender. Complications may include shock and acute respiratory distress syndrome.

Bowel obstruction, also known as intestinal obstruction, is a mechanical or functional obstruction of the intestines which prevents the normal movement of the products of digestion. Either the small bowel or large bowel may be affected. Signs and symptoms include abdominal pain, vomiting, bloating and not passing gas. Mechanical obstruction is the cause of about 5 to 15% of cases of severe abdominal pain of sudden onset requiring admission to hospital.

Enteritis is inflammation of the small intestine. It is most commonly caused by food or drink contaminated with pathogenic microbes, such as serratia, but may have other causes such as NSAIDs, cocaine, radiation therapy as well as autoimmune conditions like Crohn's disease and coeliac disease. Symptoms include abdominal pain, cramping, diarrhea, dehydration, and fever. Related diseases of the gastrointestinal system include inflammation of the stomach and large intestine.

Gastric acid, gastric juice, or stomach acid, is a digestive fluid formed within the stomach lining. Composed of hydrochloric acid, potassium chloride, and sodium chloride, gastric acid plays a key role in digestion of proteins by activating digestive enzymes, which together break down the long chains of amino acids of proteins. Gastric acid is regulated in feedback systems to increase production when needed, such as after a meal. Other cells in the stomach produce bicarbonate, a base, to buffer the fluid, ensuring a regulated pH. These cells also produce mucus – a viscous barrier to prevent gastric acid from damaging the stomach. The pancreas further produces large amounts of bicarbonate and secretes bicarbonate through the pancreatic duct to the duodenum to neutralize gastric acid passing into the digestive tract.

Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and a variety of anaemias.

Achlorhydria and hypochlorhydria refer to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively. It is associated with various other medical problems.

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the oesophagus, stomach, small intestine, large intestine and rectum, and the accessory organs of digestion, the liver, gallbladder, and pancreas.

Ileus is a disruption of the normal propulsive ability of the intestine. It can be caused by lack of peristalsis or by mechanical obstruction. The word 'ileus' is from Ancient Greek εἰλεός eileós, "intestinal obstruction". The term 'subileus' refers to a partial obstruction.

Colic in horses is defined as abdominal pain, but it is a clinical symptom rather than a diagnosis. The term colic can encompass all forms of gastrointestinal conditions which cause pain as well as other causes of abdominal pain not involving the gastrointestinal tract. The most common forms of colic are gastrointestinal in nature and are most often related to colonic disturbance. There are a variety of different causes of colic, some of which can prove fatal without surgical intervention. Colic surgery is usually an expensive procedure as it is major abdominal surgery, often with intensive aftercare. Among domesticated horses, colic is the leading cause of premature death. The incidence of colic in the general horse population has been estimated between 4 and 10 percent over the course of the average lifespan. Clinical signs of colic generally require treatment by a veterinarian. The conditions that cause colic can become life-threatening in a short period of time.

Volvulus Twisting of part of the intestine, causing a bowel obstruction

A volvulus is when a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction. Symptoms include abdominal pain, abdominal bloating, vomiting, constipation, and bloody stool. Onset of symptoms may be rapid or more gradual. The mesentery may become so tightly twisted that blood flow to part of the intestine is cut off, resulting in ischemic bowel. In this situation there may be fever or significant pain when the abdomen is touched.

Gallstone ileus is a rare form of small bowel obstruction caused by an impaction of a gallstone within the lumen of the small intestine. Such a gallstone enters the bowel via a cholecysto-enteric fistula. The presence of large stones, >2.5 cm in diameter, within the gallbladder are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus. Once a fistula has formed, a stone may travel from the gallbladder into the bowel and become lodged almost anywhere along the gastrointestinal tract. Obstruction occurs most commonly at the near the distal ileum, within 60 cm proximally to the ileocecal valve. Rarely, gallstone ileus may recur if the underlying fistula is not treated.

Ogilvie syndrome is the acute dilatation of the colon in the absence of any mechanical obstruction in severely ill patients.

Intestinal pseudo-obstruction is a clinical syndrome caused by severe impairment in the ability of the intestines to push food through. It is characterized by the signs and symptoms of intestinal obstruction without any lesion in the intestinal lumen. Clinical features can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved. The condition can begin at any age and it can be a primary condition or caused by another disease (secondary).

Whole bowel irrigation (WBI) is a medical process involving the rapid administration of large volumes of an osmotically balanced macrogol solution, either orally or via a nasogastric tube, to flush out the entire gastrointestinal tract.

Gastric outlet obstruction (GOO) is a medical condition where there is an obstruction at the level of the pylorus, which is the outlet of the stomach. Individuals with gastric outlet obstruction will often have recurrent vomiting of food that has accumulated in the stomach, but which cannot pass into the small intestine due to the obstruction. The stomach often dilates to accommodate food intake and secretions. Causes of gastric outlet obstruction include both benign causes, as well as malignant causes, such as gastric cancer.

Clostridial necrotizing enteritis (CNE), is a potentially fatal type of food poisoning caused by a β-toxin of Clostridium perfringens, Type C. It occurs in some developing countries, but was also documented in Germany following World War II, where it was called "Darmbrand". The toxin is normally inactivated by certain proteolytic enzymes and by normal cooking, but when these protections are impeded, and high protein is consumed, the disease emerges.

Jejunoileal bypass (JIB) was a surgical weight-loss procedure performed for the relief of morbid obesity from the 1950s through the 1970s in which all but 30 cm (12 in) to 45 cm (18 in) of the small bowel were detached and set to the side.

Nausea is a diffuse sensation of unease and discomfort, often perceived as an urge to vomit. While not painful, it can be a debilitating symptom if prolonged, and has been described as placing discomfort on the chest, upper abdomen, or back of the throat.

Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be Clostridium difficile, but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, an association with prior antibiotic use also exists. Immediate and aggressive treatment can sometimes save the horse, but even in such cases, 75% mortality is considered a best-case scenario.

Intestinal bypass is a bariatric surgery performed on patients with morbid obesity to create an irreversible weight loss, when implementing harsh restrictions on the diets have failed. Jejunocolic anastomosis was firstly employed. Nonetheless, it led to some unexpected complications such as severe electrolyte imbalance and liver failure. It was then modified to jejunoileal techniques. Viewed as a novel form of treatment for obesity, many intestinal bypass operations were carried out in the 1960s and 1980s. Significant weight loss was observed in patients, but this surgery also resulted in several complications, for instance, nutritional deficiencies and metabolic problems. Due to the presence of surgical alternatives and anti-obesity medications, intestinal bypass is now rarely used.

References

1 2 3 4 Edwards, G. B. (2000). "Duodenitis-proximal jejunitis (anterior enteritis) as a surgical problem". Equine Veterinary Education. 12 (6): 318–321. doi:10.1111/j.2042-3292.2000.tb00068.x.
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 Reed, Stephen M.; Waewick M. Bayly; Debra C. Sellon (2010). Equine Internal Medicine (Third ed.). St Louis, MO: Saunders. pp. 846–850. ISBN 978-1-4160-5670-6.
1 2 3 4 5 6 Smith, Bradford (2002). Large Animal Internal Medicine (3rd ed.). St. Louis, Missouri: Mosby, Inc. ISBN 978-0-323-00946-1.
1 2 Larson, Erica. "Colic in the Horse: When is Surgery Necessary". www.thehorse.com. The Horse. Retrieved 11 July 2014.
↑ Davis, J. L.; Blikslager, A. T.; Catto, K.; Jones, S. L. (2003). "A Retrospective Analysis of Hepatic Injury in Horses with Proximal Enteritis (1984–2002)". Journal of Veterinary Internal Medicine. 17 (6): 896–901. doi: 10.1111/j.1939-1676.2003.tb02530.x . PMID 14658728.

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[Freeman-1] 1 2 3 4 Edwards, G. B. (2000). "Duodenitis-proximal jejunitis (anterior enteritis) as a surgical problem". Equine Veterinary Education. 12 (6): 318–321. doi:10.1111/j.2042-3292.2000.tb00068.x.

[EIM-2] 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 Reed, Stephen M.; Waewick M. Bayly; Debra C. Sellon (2010). Equine Internal Medicine (Third ed.). St Louis, MO: Saunders. pp. 846–850. ISBN 978-1-4160-5670-6.

[LAIM-3] 1 2 3 4 5 6 Smith, Bradford (2002). Large Animal Internal Medicine (3rd ed.). St. Louis, Missouri: Mosby, Inc. ISBN 978-0-323-00946-1.

[NeedsSx-4] 1 2 Larson, Erica. "Colic in the Horse: When is Surgery Necessary". www.thehorse.com. The Horse. Retrieved 11 July 2014.

[5] Davis, J. L.; Blikslager, A. T.; Catto, K.; Jones, S. L. (2003). "A Retrospective Analysis of Hepatic Injury in Horses with Proximal Enteritis (1984–2002)". Journal of Veterinary Internal Medicine. 17 (6): 896–901. doi: 10.1111/j.1939-1676.2003.tb02530.x . PMID 14658728.

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