Enteritis, Proximal
Basic Information 
Clinical Presentation
History, Chief Complaint
Depression, inappetence, fever, and variable signs of colic (mild to severe)
Physical Exam Findings
• Pyrexia is commonly observed.
• Variable tachycardia and tachypnea
• Variable signs of colic, which are almost always relieved by passage of a nasogastric tube and gastric decompression
A significant volume of gastric reflux (5–25 L) is usually obtained initially. Reflux volume may increase with therapy when the patient is rehydrated.
The reflux may be orange to dark brown in color and often has a fetid odor. Hemorrhagic gastric reflux is occasionally encountered.• Injected, hyperemic mucous membranes with a “toxic line” are usually encountered.
• Moderate to severe dehydration, with prolonged capillary refill time, prolonged skin tent, and poor jugular refill.
• Decreased to absent gastrointestinal borborygmi.
• Mild abdominal distension may be present.
Etiology and Pathophysiology
• The specific cause of proximal enteritis is unknown, although several infectious or toxic agents have been proposed. It is likely that a variety of causes result in a similar clinical syndrome.
Toxigenic Clostridium difficile is the pathogen most often isolated from horses with proximal enteritis, although C. difficile infection is not documented in all cases.
Clostridium perfringens and Salmonella spp. infection also occasionally manifest with signs consistent with proximal enteritis.
Cantharidin toxicity may result in small intestinal as well as colonic damage, and affected horses may present with clinical signs of proximal enteritis.
Lesions consistent with proximal enteritis have been produced experimentally in horses exposed to toxins produced by Fusarium moniliforme. However, neurologic signs and central nervous system lesions typical of leukoencephalomalacia were also observed in those horses and are not described in most cases of proximal enteritis.• Regardless of the specific inciting cause, the gross pathologic findings in horses with proximal enteritis include duodenal and proximal jejunal serositis with mucosal and submucosal hyperemia and edema. Histopathologic findings include loss of intestinal villi and necrosis of epithelial cells with neutrophilic infiltration and submucosal and serosal hemorrhages and fibrinopurulent exudates.
• Several factors may contribute to the large-volume enterogastric reflux in proximal enteritis.
With severe intestinal mural inflammation and epithelial cell necrosis, fluid, electrolytes, and plasma protein are lost passively through the damaged mucosa.
In addition, an active secretory component may be induced by bacterial toxins and likely plays a role in most cases, resulting in further enteric fluid and electrolyte loss.
Intestinal mural edema and inflammation and villus loss also decrease the small intestinal absorptive capacity and inhibit normal peristalsis, resulting in enterogastric reflux.
Finally, in some cases of proximal enteritis, pancreatic secretions are increased because of concurrent pancreatitis.• Bacterial toxins enter the systemic circulation through the compromised enteric mucosal barrier or via the portal circulation, resulting in the clinical signs of endotoxemia and the systemic inflammatory response syndrome.
Diagnosis 
Differential Diagnosis
• Strangulating or nonstrangulating small intestinal obstruction
• Ulcerative duodenitis or gastric outflow obstruction (see “Ulcerative Duodenitis” and “Pyloric Stenosis” in this section)
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