Pathophysiology

The inciting factors involved in AE remain unknown. The isolation of C difficile and C perfringens strains from reflux fluid in limited numbers of affected horses, compared with those with small intestinal strangulating obstruction, suggests that either of these organisms may initiate the inflammatory response seen in the small intestine. Feeding practices, such as giving rations with a high grain content, have also been proposed as a contributing cause. However, to date, only a weak association between ration and AE has been reported. Regardless of the cause, an inflammatory response mediated by endotoxin and inflammatory mediators, such as eicosanoids, ensues and leads to small intestinal stasis. These mediators also account for hypersecretory mechanisms, which account for the accumulation of fluid in the affected portions of intestine.

The serosa of affected segments may have petechial to ecchymotic hemorrhages, and the mucosal surfaces are usually diffusely hyperemic with varying degrees of petechiation or ulceration. The fluid contents of the affected small intestine may be red-brown.

Clinical Pathology

The clinicopathologic changes seen in horses with AE stem from a combination of inflammation and endotoxemia as well as accumulation of fluids within the proximal gastrointestinal tract (a third space). As a result, affected horses are characteristically azotemic, hemoconcentrated (high PCV), hyperlactatemic, and hyperproteinemic. Of these, the severity of hemoconcentration and azotemia are negatively associated with survival. White blood cell counts vary from leukopenia to leukocytosis.

Metabolic acidosis with a large anion gap character­ized by enteric bicarbonate loss, hypochloremia, and hyperlactatemia is often observed. An anion gap greater than or equal to 15 mEq/L has been associated with a high mortality rate in affected cases.

Horses with AE are at greater risk for sustaining hepatic injury relative to horses with other forms of small intestinal obstruction. High values for γ-glutamyl transferase (GGT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST) are commonly seen. These increases may be incited by ascending infection through the common bile duct and concomitant endotoxemia. Horses with AE were 12 times as likely to have high values for GGT activity as horses with a small intestinal strangulating obstruction. Use of serum GGT activity greater than 22 U/L as a cutoff point was only moderately sensitive at differentiating horses with AE from those with obstruction in one study, but this cutoff was highly specific and had a high positive-predictive value.

Peritoneal fluid accumulates secondary to serosal inflammation and distension of affected small intestine segments. High peritoneal fluid protein concentration (>3.5 g/dL) and mild to moderate increases in peritoneal white cell count may be observed. Analysis of peritoneal fluid may aid in determination of the prognosis. High fluid total protein concentration is significantly associated with death in horses with AE.

Clinical Manifestation of Disease

The primary challenge faced in evaluating horses with AE is differentiating the condition from forms of small intestinal obstruction, which may require surgical intervention. Signs of abdominal discomfort in horses with AE typically abate upon gastric decompression, in contrast to the unrelenting pain often observed in those with strangulating or obstructive lesions. In the southeastern United States, differentiating the disease from ileal impactions can also be challenging.

Horses with AE typically are presented with mild to severe abdominal discomfort; the heart rate is typically high, ranging from 60 to 100 beats/minute in accordance with severity of the condition, and horses are often also tachypneic. Many are febrile at the time of presentation (temperature >101.5° F [38.6° C]); mucous membranes may appear congested, and a toxic rim can be observed in horses with endotoxemia. Capillary refill time is often prolonged. Gastrointestinal borborygmus is generally decreased, and in severe cases, the horse may have spontaneous reflux at the nares. Patients may also present with concurrent laminitis or may develop laminitis over the course of treatment. The incidence of laminitis in horses with AE ranges from 7.5% to 28.4%. Other secondary complications include pneumonia and thrombophlebitis.

Diagnosis

A definitive diagnosis of AE can only be made at the time of surgery or necropsy. A tentative diagnosis may be reached on the basis of clinical progression and response to gastric decompression, along with the clinicopathologic changes previously described. Rectal palpation before nasogastric intubation may reveal turgid, distended loops of small intestine. Palpation of an impacted ileum may rule out a diagnosis of AE.

Nasogastric intubation typically yields large volumes of reflux, usually reddish brown to bloody in appearance. Signs of abdominal pain subside until fluid reaccumulates in the stomach.

Abdominal ultrasound may provide useful information to support a diagnosis of AE. Evidence of gastric distension is provided by the presence of anechoic fluid along with a gas–fluid interface within the stomach, which may extend beyond the 12th intercostal space, in the cranial and lateral aspect of the left side of the abdomen. A distended duodenum with poor or absent motility may be seen coursing caudodorsally around the caudal pole of the right kidney. The distended duodenum and more distal portions of small intestine may exceed 5 cm in diameter. Wall thickness of the small intestine can also be assessed and may become increasingly thick as the disease persists. Patients with small intestinal strangulating obstructions characteristically have more significant wall thickening and edema in affected portions of bowel than horses with AE. The lungs in the cranioventral aspects of both hemithoraces should be evaluated for pneumonia secondary to aspiration.

Ultrasonography should also be used to assess the presence, volume, and character of peritoneal fluid. In general, horses with strangulating obstructions have more substantial increases in fluid total protein than those with AE. Patients with an abdominal total protein of 3.5 g/dL or greater were four times as likely to succumb to AE as horses having an abdominal PF total protein of less than 3.5 g/dL in one study.