Proximal Jejunitis / Duodenitis-Proximal Jejunitis (DPJ / Anterior Enteritis)

Proximal jejunitis, also known as duodenitis-proximal jejunitis (DPJ) or anterior enteritis, is an acute, inflammatory disease of the proximal small intestine (duodenum and proximal jejunum) in horses. It is characterized by a massive nasogastric reflux (often > 20 liters), varying degrees of abdominal pain, and systemic inflammatory response. The condition is distinct from mechanical obstructions (e.g., strangulating lipoma, intussusception) because the primary pathology is a severe inflammatory enteritis, often with mucosal edema and necrosis, leading to functional ileus and fluid sequestration. DPJ is a significant cause of colic in adult horses, particularly in performance disciplines such as Thoroughbred racing, Standardbred racing, and endurance riding, where high-concentrate diets and stress are common. The disease can range from mild, self-limiting cases to severe, life-threatening forms with systemic inflammatory response syndrome (SIRS), endotoxemia, and laminitis. Early recognition and aggressive medical management are critical for a successful outcome.

The exact etiology of proximal jejunitis remains incompletely understood, but multiple infectious and non-infectious agents have been implicated. Bacterial pathogens, particularly Clostridium perfringens (especially type A) and Clostridium difficile, are frequently isolated from the gastric and small intestinal contents of affected horses. These bacteria produce toxins (e.g., alpha toxin, beta2 toxin, enterotoxin) that damage the intestinal mucosa, leading to inflammation, increased permeability, and fluid secretion. Salmonella spp. have also been identified in some outbreaks, suggesting a possible role in contagious transmission. Viral agents, such as equine herpesvirus (EHV-1) and equine influenza virus (EIV), have been hypothesized but not consistently confirmed. Parasitic migration, particularly of Strongylus vulgaris larvae, can cause arteritis and ischemia, potentially predisposing to mucosal injury. Nutritional factors, such as sudden access to large amounts of high-starch grain, may alter the intestinal microbiome and promote clostridial overgrowth. Mechanical factors, such as ileal impaction or duodenal stricture, can cause proximal distension and secondary inflammation. Additionally, stress, transportation, and changes in management (e.g., stall confinement) are considered triggering factors.

Proximal jejunitis is most commonly diagnosed in adult horses between 2 and 10 years of age, with no strong breed or sex predilection, though it appears more frequently in performance horses, particularly Thoroughbreds and Standardbreds in race training. The disease is often sporadic, but outbreaks have been reported in boarding stables and training centers, suggesting a possible infectious component. Seasonal variation has been noted, with higher incidence in spring and summer, possibly related to dietary changes and increased environmental contamination. Morbidity rates in affected populations can be high, but mortality is generally low (5-15%) with appropriate medical management. However, severe cases can have a guarded prognosis, especially if complications such as laminitis or peritonitis develop. The disease can significantly impact athletic careers, with affected horses often requiring extended rest and gradual return to training. In a retrospective study of colic cases, DPJ accounted for approximately 10-15% of all medical colic cases in referral hospitals.

The pathophysiology of proximal jejunitis involves a cascade of events initiated by mucosal injury, often due to bacterial toxins or ischemia. The inciting insult leads to disruption of the intestinal epithelial barrier, allowing luminal contents, including bacteria and endotoxins (lipopolysaccharide, LPS), to translocate into the submucosa and systemic circulation. This triggers a robust inflammatory response characterized by release of pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6), recruitment of neutrophils, and activation of complement. The inflammation causes severe edema and thickening of the intestinal wall, particularly in the duodenum and proximal jejunum, leading to functional obstruction and ileus. The affected segment loses its ability to propel ingesta, resulting in accumulation of fluid and gas proximally, which stimulates gastric secretion and leads to massive nasogastric reflux. The systemic release of endotoxins and cytokines induces SIRS, with vasodilation, increased capillary permeability, and hypotension. This can progress to endotoxic shock, disseminated intravascular coagulation (DIC), and multiple organ dysfunction. Additionally, the inflammatory mediators can trigger laminitis, a devastating complication, through activation of matrix metalloproteinases and disruption of the lamellar basement membrane.

Several intrinsic and extrinsic factors predispose horses to proximal jejunitis. Intrinsic factors include age (adult horses are more commonly affected), individual susceptibility to endotoxemia, and possibly genetic variations in immune response. Horses with a history of previous colic or gastrointestinal disease may be at higher risk. Extrinsic factors are more significant: sudden changes in diet, especially high-starch grain feeding, can alter the hindgut and small intestinal microbiome, promoting clostridial overgrowth. Stressful events such as transportation, intense exercise, racing, or changes in social grouping can compromise mucosal immunity. Stall confinement with reduced forage intake and increased concentrate feeding is a common management factor. Poor hygiene and contaminated water sources may increase exposure to pathogens like Salmonella and Clostridium. Additionally, the use of non-steroidal anti-inflammatory drugs (NSAIDs) at high doses or for prolonged periods can cause right dorsal colitis and potentially predispose to proximal enteritis. In some outbreaks, a common feed source or environmental contamination has been identified.

Clinical signs of proximal jejunitis typically develop acutely and include moderate to severe colic, which may be intermittent or continuous. Horses often exhibit signs of abdominal pain such as pawing, flank watching, lying down, rolling, and occasionally adopting a dog-sitting posture. A hallmark finding is the presence of large volumes of nasogastric reflux (often > 20 liters) upon intubation, which is typically foul-smelling and may be brownish or greenish due to bile and ingesta. The reflux is often spontaneous and can be projectile. Heart rate is usually elevated (60-100 bpm), and mucous membranes may be injected or toxic with prolonged capillary refill time (> 3 seconds). Dehydration is common due to fluid loss into the gastrointestinal tract. Rectal temperature may be normal or mildly elevated. On abdominal auscultation, borborygmi are reduced or absent. Rectal palpation may reveal distended small intestine loops, but the large colon is often empty. In severe cases, signs of systemic inflammatory response syndrome (SIRS) include fever, tachypnea, and weak peripheral pulses. Laminitis may develop, characterized by increased digital pulses, reluctance to move, and a characteristic stance. In peracute cases, cardiovascular collapse and shock can occur.

Differential diagnoses for proximal jejunitis include other causes of acute colic with nasogastric reflux and small intestinal distension. Key differentials are: (1) Small intestinal obstruction (e.g., strangulating lipoma, epiploic foramen entrapment, intussusception, volvulus) – these typically present with acute severe pain, progressive reflux, and rapid deterioration; rectal palpation may reveal a painful mass or distended loops; abdominocentesis often shows serosanguineous or hemorrhagic fluid with elevated protein and lactate. (2) Ileal impaction – often associated with ingestion of coarse feed, presents with mild to moderate pain, reflux may be present but less voluminous; rectal palpation may identify the impaction in the right caudal abdomen. (3) Anterior enteritis due to other causes (e.g., Salmonella) – similar clinical signs, but diagnosis may require culture. (4) Peritonitis – primary or secondary, characterized by fever, diffuse pain, and peritoneal fluid with high nucleated cell count and protein. (5) Gastric dilatation/rupture – gastric rupture is a catastrophic event with sudden relief of pain followed by shock; reflux may be absent if rupture has occurred. (6) Colitis (e.g., acute colitis) – may present with diarrhea and systemic signs, but reflux is less prominent. (7) Duodenal stricture or obstruction – chronic or recurrent reflux, often in older horses. (8) Equine grass sickness (dysautonomia) – more common in Europe, presents with dysphagia, muscle tremors, and ptosis, but reflux may be present. (9) Sand enteropathy – may cause colic and reflux, but history of sand ingestion and radiography can help. (10) Inflammatory bowel disease – chronic, less acute presentation. Definitive diagnosis often requires response to treatment and ruling out surgical lesions.

The diagnostic approach to a horse with suspected proximal jejunitis follows a systematic algorithm. Step 1: Perform a thorough physical examination, including assessment of pain severity, cardiovascular status (heart rate, mucous membranes, capillary refill time, pulse quality), and abdominal auscultation. Step 2: Pass a nasogastric tube to check for reflux; if reflux is present, measure the volume and character. This is a critical step in any colic evaluation. Step 3: Perform a rectal palpation to assess for distended small intestine, large colon impaction, or other abnormalities. Step 4: Obtain an abdominocentesis (peritoneal fluid sample) for analysis, including total protein, nucleated cell count, and lactate. In DPJ, the fluid is typically normal or mildly inflammatory, with protein < 2.5 g/dL and lactate < 2.5 mmol/L; if lactate > 5 mmol/L or protein > 4 g/dL, a surgical lesion is more likely. Step 5: Perform abdominal ultrasonography to evaluate small intestinal wall thickness (normal < 3 mm), distension (diameter > 5 cm), and motility. In DPJ, the proximal small intestine may be distended with thickened walls and reduced motility. Step 6: Obtain bloodwork, including CBC, serum biochemistry, plasma lactate, and blood gas analysis. Step 7: If the horse is stable and the diagnosis is uncertain, consider a trial of medical therapy with intravenous fluids and anti-inflammatory drugs. Step 8: If the horse deteriorates or fails to respond to medical management within 24-48 hours, exploratory laparotomy may be indicated to rule out a surgical lesion. Step 9: In cases of suspected infectious etiology, collect fecal and reflux samples for culture and PCR for Clostridium, Salmonella, and other pathogens. Step 10: Monitor for complications such as laminitis with hoof testers and digital pulse assessment.

Laboratory findings in proximal jejunitis reflect dehydration, inflammation, and endotoxemia. Hemoconcentration is common, with increased packed cell volume (PCV) and total protein. White blood cell count may be normal, elevated, or decreased; a left shift (increased band neutrophils) may be present. Fibrinogen is often elevated ( > 400 mg/dL) due to inflammation. Serum amyloid A (SAA) is markedly increased (often > 1000 mg/L). Plasma lactate is usually normal or mildly elevated (< 2.5 mmol/L) unless there is severe hypovolemia or concurrent ischemia. Blood gas analysis may show metabolic acidosis with base deficit. Electrolyte imbalances, particularly hypokalemia and hypochloremia, can occur due to loss of gastric and intestinal secretions. Peritoneal fluid analysis is crucial: in DPJ, the fluid is typically normal to mildly inflammatory, with total protein < 2.5 g/dL, nucleated cell count < 5000 cells/µL, and lactate < 2.5 mmol/L. If the peritoneal fluid has a high protein (> 3.5 g/dL) or lactate (> 5 mmol/L), a surgical lesion is more likely. Additionally, blood cultures may be positive for enteric bacteria in severe cases. Endotoxemia can be assessed indirectly by measuring plasma lactate and inflammatory cytokines, though these are not routinely available.

Imaging plays a supportive role in the diagnosis of proximal jejunitis. Abdominal ultrasonography is the most useful imaging modality. In affected horses, the proximal small intestine may be distended (diameter > 5 cm) with thickened walls (> 3 mm) and reduced or absent motility. The duodenum may be visualized in the right cranial abdomen, and the jejunum in the left cranial abdomen. Ultrasonography can also help rule out other causes of colic, such as intussusception, volvulus, or nephrosplenic entrapment. Radiography is of limited value in adult horses due to the size of the abdomen, but in foals, it can be used to assess gastric distension and small intestinal dilation. In adult horses, plain radiographs may show a gas-filled stomach and small intestine, but this is not specific. Endoscopy is not routinely used for diagnosis of DPJ, but in some referral centers, gastroscopy may be performed to evaluate the duodenum and proximal jejunum; however, the procedure is invasive and requires sedation and specialized equipment. Advanced imaging such as CT or MRI is rarely used in equine colic due to cost and availability. Scintigraphy is not indicated for this condition.

Cytological and histopathological findings in proximal jejunitis are based on analysis of peritoneal fluid and intestinal biopsies. Peritoneal fluid cytology in DPJ is typically non-specific, with a mild increase in nucleated cell count (predominantly neutrophils) and total protein, but without evidence of septic peritonitis (e.g., intracellular bacteria). Histopathology of the affected intestine, obtained via biopsy during exploratory laparotomy or at necropsy, reveals severe acute inflammation of the mucosa and submucosa, with edema, hemorrhage, and necrosis. The lamina propria is infiltrated with neutrophils and mononuclear cells. The intestinal villi may be blunted or destroyed, and there is evidence of mucosal ulceration. In chronic cases, fibrosis may be present. Immunohistochemistry can be used to identify Clostridium perfringens toxins or Salmonella antigens. These findings are consistent with an acute inflammatory enteritis, but are not pathognomonic for DPJ.

Treatment of proximal jejunitis is primarily medical and supportive, with surgery reserved for cases that fail to respond or where a surgical lesion cannot be ruled out. The cornerstone of therapy is aggressive intravenous fluid therapy to correct dehydration and electrolyte imbalances. Polyionic isotonic fluids (e.g., lactated Ringer's solution) are administered at a rate of 10-20 mL/kg/hour initially, then adjusted based on hydration status and urine output. In cases of severe hypovolemia, hypertonic saline (7.5% NaCl, 4-6 mL/kg IV) may be given as a bolus, followed by isotonic fluids. Nasogastric intubation is performed to decompress the stomach and relieve reflux; the tube may be left in place or passed intermittently to measure reflux volume. Analgesia is provided using non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (1.1 mg/kg IV q12h) or phenylbutazone (2.2-4.4 mg/kg IV or PO q12h). For severe pain, alpha-2 agonists (xylazine 0.2-0.5 mg/kg IV, detomidine 0.01-0.02 mg/kg IV) or opioids (morphine 0.05-0.1 mg/kg IV) may be used. A lidocaine continuous rate infusion (CRI) (1.3 mg/kg IV bolus, then 0.05 mg/kg/min) can help reduce ileus and provide analgesia. Anti-endotoxic therapy includes polymyxin B (1000-6000 IU/kg IV q12h) and flunixin meglumine. Antibiotics are often administered to prevent or treat bacterial translocation, typically a combination of penicillin G (22,000 IU/kg IV q6h) and gentamicin (6.6 mg/kg IV q24h), or ceftiofur (2.2 mg/kg IV q12h). Gastroprotectants such as omeprazole (4 mg/kg PO q24h) and sucralfate (20 mg/kg PO q8h) may be used to prevent gastric ulceration. In severe cases, plasma transfusion may be considered to provide antibodies and clotting factors. Surgical intervention (exploratory celiotomy) is indicated if the horse does not improve within 24-48 hours, if peritoneal fluid becomes abnormal, or if a mechanical obstruction is suspected. During surgery, the affected intestine may be decompressed, and in rare cases, resection and anastomosis may be performed if there is necrosis. Post-operative care includes continued fluid therapy, analgesia, and monitoring for complications.

The prognosis for proximal jejunitis is generally good with prompt and aggressive medical management, with reported survival rates of 80-90%. However, the prognosis is guarded in cases that develop severe complications such as laminitis, peritonitis, or endotoxic shock. Negative prognostic indicators include a high peritoneal fluid lactate (> 5 mmol/L), severe systemic inflammatory response, and the need for surgical intervention. Horses that survive the acute episode typically return to their previous level of athletic performance, but may require a prolonged recovery period (weeks to months). Recurrence is uncommon but possible. In a study of horses with DPJ, the short-term survival rate was 85%, and the long-term survival rate (1 year) was 75%. The most common cause of death or euthanasia is laminitis, which occurs in approximately 10-20% of affected horses.

Follow-up care for horses recovering from proximal jejunitis is crucial to ensure complete resolution and prevent complications. During hospitalization, nasogastric reflux should be monitored every 2-4 hours, and the tube should be removed once reflux volume decreases to less than 1-2 liters per intubation. Serial physical examinations, including heart rate, mucous membranes, and abdominal auscultation, should be performed every 6-12 hours. Bloodwork, including PCV, total protein, and electrolytes, should be repeated daily until stable. Peritoneal fluid analysis may be repeated if there is concern for peritonitis. After discharge, the horse should be rested for at least 2-4 weeks, with a gradual return to exercise. The diet should be gradually transitioned from hay to a normal ration, avoiding large grain meals. Regular farriery care is important to monitor for laminitis; hoof testers and digital pulses should be assessed at each visit. Recheck examinations, including abdominal ultrasound, may be performed at 2-4 weeks post-discharge to ensure resolution of intestinal distension. Long-term follow-up should include monitoring for any signs of recurrent colic or laminitis.

Clinical pearls: 1) Always pass a nasogastric tube in any colic case; large-volume reflux is a hallmark of DPJ. 2) In DPJ, the peritoneal fluid is often normal, so do not be falsely reassured; rely on clinical signs and reflux. 3) Aggressive fluid therapy is essential; horses can lose 20-40 liters of fluid via reflux. 4) Use lidocaine CRI to help manage ileus and pain. 5) Monitor for laminitis from day one; use digital pulses and hoof testers. 6) Consider infectious causes and implement biosecurity measures if multiple horses are affected. Pitfalls: 1) Delaying nasogastric intubation can lead to gastric rupture. 2) Administering excessive NSAIDs can cause renal and gastrointestinal damage; use lowest effective dose. 3) Assuming that a surgical lesion is present and performing surgery unnecessarily can increase morbidity; medical therapy is often successful. 4) Failing to monitor for laminitis can lead to irreversible damage. 5) Discontinuing fluid therapy too early can lead to relapse. 6) Using antibiotics inappropriately can promote clostridial overgrowth; use only if indicated.

Current drug protocols for proximal jejunitis are based on ACVIM guidelines and Plumb's Veterinary Drug Handbook. Fluid therapy: Lactated Ringer's solution (LRS) or Normosol-R at 10-20 mL/kg IV bolus, then 2-4 mL/kg/hour continuous rate infusion (CRI). Hypertonic saline (7.5% NaCl) at 4-6 mL/kg IV over 10-15 minutes for shock. Analgesics: Flunixin meglumine (Banamine) 1.1 mg/kg IV q12h for 1-3 days, then taper; Phenylbutazone 2.2-4.4 mg/kg IV or PO q12h; Firocoxib (Equioxx) 0.1 mg/kg PO q24h for long-term anti-inflammatory. Sedatives/analgesics: Xylazine 0.2-0.5 mg/kg IV; Detomidine 0.01-0.02 mg/kg IV; Morphine 0.05-0.1 mg/kg IV q4-6h. Lidocaine CRI: 1.3 mg/kg IV bolus over 5 minutes, then 0.05 mg/kg/min IV. Anti-endotoxic: Polymyxin B 1000-6000 IU/kg IV q12h diluted in fluids; Flunixin meglumine as above. Antibiotics: Penicillin G potassium 22,000 IU/kg IV q6h; Gentamicin 6.6 mg/kg IV q24h; Ceftiofur 2.2 mg/kg IV q12h. Gastroprotectants: Omeprazole (GastroGard) 4 mg/kg PO q24h; Sucralfate 20 mg/kg PO q8h. Prokinetics: Metoclopramide 0.04 mg/kg IV q6h (use with caution); Bethanechol 0.025-0.075 mg/kg SC q6h (not routinely recommended). Plasma: 1-2 L IV if needed. All dosages should be adjusted based on clinical response and renal function.

Evidence-based literature on proximal jejunitis is limited but includes several key studies. A retrospective study by Freeman et al. (2000) evaluated 100 cases of DPJ and found that medical management alone was successful in 85% of cases, with a mortality rate of 15%. The study identified that horses with a peritoneal fluid lactate > 5 mmol/L had a poorer prognosis. Another study by Cohen et al. (2004) investigated the role of Clostridium perfringens in DPJ and found that affected horses had higher fecal concentrations of C. perfringens and its toxins compared to controls. A prospective study by Arroyo et al. (2006) compared the efficacy of lidocaine CRI versus saline in horses with post-operative ileus, but not specifically DPJ; however, lidocaine was shown to reduce the duration of reflux. A consensus statement from the American College of Veterinary Internal Medicine (ACVIM) on colic management (2014) recommends aggressive fluid therapy, nasogastric decompression, and anti-inflammatory treatment for DPJ, with surgery reserved for non-responders. A meta-analysis by Southwood et al. (2010) on medical versus surgical treatment of small intestinal colic found that medical therapy is appropriate for DPJ, but surgical intervention is necessary if a strangulating lesion is suspected. Overall, the evidence supports a conservative approach with intensive medical management, but early recognition and monitoring for complications are critical.