Proximal Enteritis, also called Anterior Enteritis or Duodenitis-Proximal Jejunitis, is an inflammatory condition of the small intestine of horses that causes a syndrome of depression, colic, ileus, and endotoxemia, with the accumulation of large volumes of gastric reflux. The cause of proximal enteritis is not completely understood, however recent research has shown that toxigenic Clostridium difficile strains may play an important role. The symptoms of proximal enteritis are similar to those of strangulating small intestinal lesions, which means that proximal enteritis is occasionally diagnosed during exploratory laparotomy. Surgical intervention was once considered to be superior to medical management when treating proximal enteritis, however recent research has shown that medical treatment is preferable.
Epidemiology and Pathophysiology of Proximal Enteritis in Horses
Proximal Enteritis (PE) is an acute-onset inflammatory condition of the proximal small intestine that affects the duodenum, and variable portions of the jejunum. PE usually affects adult horses, and the majority of affected horses are between 5-10 years of age (Freeman 2003).
PE is considered to be an idiopathic disease, however a bacterial etiology is suspected. Clostridia and Salmonella are the two bacterial species that have long been considered the most likely causative agents of PE, however, until recently, conclusive evidence was scarce. Evidence is now available that Clostridium difficile (and possibly Clostridium perfringens) may play an important role.
Arroyo (2006) performed bacterial cultures on the refluxed stomach contents of 10 horses with PE, trying to isolate species of Clostridia and Salmonella. Toxigenic strains of Clostridium difficile were cultured from all 10 horses. Only one (out of 16) of the control horses was positive for toxigenic C. difficile. Salmonella was not isolated from any reflux sample. C. perfringens was isolated from 4 of 10 reflux samples, and from 12 of 16 control horses. C. perfringens was not considered to be a pathologic agent in this study. Research is ongoing to discover if C. difficile is the primary cause of PE, or if C. difficile is only a component of a disease complex that results in PE.
C. difficile produces two virulent toxins, Toxin A and Toxin B. Toxin B has been shown to cause electromechanical disturbances to small intestinal smooth muscle (Arroyo 2006). The toxins can also act synergistically by binding to epithelial cell-surface receptors, and gaining access to the inside of the cell where they can disrupt a variety of important intracellular enzymatic processes. The consequences can include disintegration of epithelial tight junctions, breakdown of cell cytoskeletons and formation of pores that leak electrolytes and fluid. The toxins can also cause intestinal inflammation and increase the permeability of blood vessels. Diarrhea, epithelial necrosis, endotoxemia, septicemia and the formation of a pseudomembranous lining of the intestinal tract are potential outcomes. The concentration and potency of the toxins plays a significant role in the progression and outcome of the disease.
Freeman (2003) summarized the pathologic findings in horses with PE, which included:
- Serosal edema, with hemorrhagic patches, sometimes arranged in a circumferential striping pattern.
- Mucosal lesions, which range from a normal appearance, to dark red, hemorrhagic, necrotic, and ulcerated.
- Peritonitis can occur with necrosis
- Liver pathology that includes moderate to marked congestion, bile duct hyperplasia and inflammatory changes.
Davis (2003) found that horses with PE had much higher liver enzyme concentrations (GGT, AST, ALP) than horses with a strangulating small intestinal obstruction. The proposed reasons for this include ascending infections from the common bile duct (secondary to small intestinal stasis), endotoxemic effects, extension of inflammation, and hepatic hypoxia from dehydration and hypovolemia (Davis 2003; Freeman 2003).
A geographic predisposition for the occurrence of PE has been reported, however the attributes of these regions have not been defined.
Research by Cohen (2006) suggested that horses that eat more concentrates, or that are grazing pasture, might be more at risk of developing PE.
Clinical Signs of Proximal Enteritis in Horses
The common clinical signs of PE include:
- Depression, lethargy, anorexia.
- Colic – colic symptoms can vary from mild to severe.
- Tachycardia – usually above 60 beats per minute (bpm), in severe cases as high as 80-100 bpm.
- Gastric reflux – the appearance can vary, but is typically reddish-brown to bloody in color.
- +/- Fever.
- +/- Signs of endotoxemia – in particular, the presence of a “toxic line”; a bright pink to bluish-purple line of discoloration at the periphery of the gingiva, around the incisors (Barton 2001).
- +/- Cardiac arrhythmias that usually resolve with treatment.
- Laminitis has been reported to occur in 28.4% of cases (Freeman 2003).
Diagnosis of Proximal Enteritis in Horses
Diagnosis is based on the above clinical findings, particularly the finding of large volumes of gastric reflux.
It is important to rule out clinically similar diseases that require urgent surgical intervention such as strangulating small intestinal lesions and impactions of the small intestine. These lesions tend to produce smaller volumes of gastric reflux than PE. A horse with PE will usually become more comfortable after decompression of the stomach, whereas strangulating lesions tend to be persistently painful.
The blood work of horses with PE often shows the following:
- Azotemia – usually prerenal, due to dehydration +/- hypotension.
- Elevated lactate and increased hematocrit, also due to dehydration and/or hypotension.
- Electrolyte derangements.
- Metabolic acidosis is common, however metabolic alkalosis can also occur.
- White cell count may be increased or decreased.
- Elevated liver enzyme concentrations (GST, ALP, ALT).
Abdominocentesis results for PE generally show less severe changes compared to strangulating obstructions, however intestinal necrosis can occurred in both diseases, and the findings can then reflect peritonitis.
Abdominal Ultrasound. The duodenum can be imaged ventral to the right kidney, in the 6th-7th intercostal space. The duodenum is usually fluid-filled, with varying degrees of motility. The thickness of the duodenal wall and the echogenicity also varies. The jejunum can be located in the left ventral flank. The finding of fully distended, amotile loops of small intestine should lead to serious consideration of surgical intervention, as this appearance is more commonly seen with strangulating lesions.
Treatment for Proximal Enteritis in Horses
- Gastric decompression with a wide-bore nasogastric tube (preferably indwelling), every 2 hours. Complications may include pharyngitis, esophagitis, nasal trauma and gastric ulceration. Keeping a record of the volumes collected is advised.
- IV fluid administration to correct electrolyte imbalances.
- Parenteral nutrition may be required, particularly for weak or debilitated horses.
- Restore intestinal function by instigating treatments that control inflammation and endotoxemia, maintain hydration and perfusion of the intestine, and minimize fluid overload and distension of the small intestine. The benefits of promotility agents, such as Metoclopramide, are not clear.
- Control inflammation and pain
- Judicious use of non-steroidal anti-inflammatory medications.
- Lidocaine infusions have been shown to be beneficial for controlling gastric reflux (Malone 2006). Systemic lidocaine has analgesic, and anti-inflammatory effects, which assist in returning motility to the intestine.
- Opioids (i.e. Butorphanol or Fentanyl) for analgesia.
- Polymixin B to minimize the effects of endotoxemia – the horse should be adequately hydrated prior to use.
- Plasma – plasma contains a variety of components that assist in minimizing the effects of endotoxemia, fighting infection, and it has nutritional value (particularly proteins)
Antibiotic administration is controversial, because, if C. difficile is the causative agent; it has been associated with the development of antibiotic-induced colitis. Metronidazole administration should be considered, either intravenously or per rectum. Little research is available on antibiotic use and if there are any deleterious effects to horses with PE. Many horses with PE are treated with broad-spectrum antibiotics.
Gastric ulcer medication. Once gastric reflux has been controlled, gastric ulcer medication (omeprazole, +/- sucralfate) should be commenced, as horses with PE are prone to developing gastric ulcers.
Surgical intervention was once considered a valid treatment for PE, however, Underwood (2008) found that surgery did not lead to faster resolution of PE than medical therapy, and that horses that had surgery were more likely to develop diarrhea.
Clinical signs of PE usually resolve in 3 days, but recovery can be prolonged.
Arroyo, L.G. et al. (2006) Potential role of Clostridium difficile as a cause of duodenitis-proximal jejunitis in horses. J Medical Microbiology, 55:605-608.
Arton, M. (2001) Endotoxemia: The Movie. Dorothy R. Havemeyer Foundation Neonatal Septicemia Workshop.
Cohen, N.D. et al. (2006) Are feeding practices associated with duodenitis-proximal jejunitis? Equine Vet. J., 38:526-531.
Davis, J.L. et al. (2003) A Retrospective Analysis of Hepatic Injury in Horses with Proximal Enteritis (1984–2002). JVIM, 17:896-901.
Freeman, D.E. (2003) Duodenitis-Proximal Jejunitis. In: Current Therapy in Equine Medicine 6, ed. N.E. Robinson. Saunders, St Louis, Missouri p. 120-123.
Malone, E. et al. (2006) Intravenous continuous infusion of lidocaine for treatment of equine ileus. Veterinary Surgery 35(1): 60-66.
Underwood, C. et al. (2008) Complications and survival associated with surgical compared with medical management of horses with duodenitis-proximal jejunitis. Equine Vet J., 40(4): 373-8.