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Basics

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BASICS

Definition!!navigator!!

DPJ is an inflammation of the proximal SI. However, this descriptive name is inaccurate because other segments of the GI tract can be affected. Ileus with SI and gastric distention occurs as a result of excessive fluid and electrolyte secretion and accumulation.

Pathophysiology!!navigator!!

  • Idiopathic condition
  • Lesions are more consistently found in the duodenum and proximal jejunum, but the pylorus, distal esophagus, and stomach can be affected
  • Fluid and electrolyte accumulation occurs in the SI and stomach
  • Signs of abdominal pain are common, likely as a result of inflammation and intestinal distention from increased secretion, decreased absorption, and poor perfusion
  • The cause of the ileus is unknown, but could result from direct damage, distention, pain, toxemia, hypokalemia, and/or other electrolyte disturbances
  • Net fluid movement into the SI combined with lack of aboral movement eventually results in gastric distention

Systems Affected!!navigator!!

GI

  • Increased fluid secretion, decreased fluid absorption, and lack of aboral movement cause SI distention, mainly in the duodenum and proximal jejunum
  • Fluid accumulation in the SI, reflux into the stomach causing gastric distention
  • Signs of abdominal pain (colic)
  • Some horses may develop diarrhea
  • Liver enzymes can be increased, but the mechanism involved is unknown

Cardiovascular

Dehydration and hypovolemia. Cardiac arrhythmias can occur.

Musculoskeletal

  • Laminitis
  • Muscle mass loss can result from the severe catabolic state and restricted food intake

Genetics!!navigator!!

No known genetic basis.

Incidence/Prevalence!!navigator!!

  • Anecdotally, a greater incidence in the southern USA; however, cases can occur in any region
  • Can occur throughout the year; however, it is reported more often during the summer months in some areas

Signalment!!navigator!!

  • Horses >1 year are primarily affected, with a high proportion in those >9 years
  • No sex predilection

Signs!!navigator!!

Historical Findings

  • Acute onset of colic signs
  • Occasionally there is recent introduction of a high-energy diet or access to too-lush pasture

Physical Examination Findings

  • Tachycardia, with 40–80 bpm
  • Moderate to severe dehydration
  • Animals appear more depressed than painful, especially after gastric decompression; however, some horses may be severely painful
  • Fever is common
  • Gastric reflux with variable volumes
  • Appearance of gastric reflux varies from green to brownish-red, with or without a fetid odor
  • Distended SI is usually palpable per rectum
  • Clinical signs resemble those of an obstructive SI lesion. Differentiation of horses with obstructive lesions requiring surgery is critical. Horses with DPJ tend to be more depressed and to have a greater resolution of pain and lower heart rate after gastric decompression, significantly more reflux, less palpably distended SI, more GI sounds, and lower peritoneal WBC counts than horses with surgical SI lesions. None of these signs alone is diagnostic and a definitive diagnosis can be confirmed only during surgical exploration or necropsy

Causes!!navigator!!

  • Unknown, but infectious cause is suspected
  • Clostridium difficile was consistently recovered from the reflux in some horses and also occasionally from the feces of affected horses. Some horses inoculated with C. difficile toxins developed clinical signs and lesions consistent with those found in naturally occurring disease cases
  • Clostridium perfringens has been inconsistently recovered from reflux or feces of clinical cases
  • Salmonella spp. and mycotoxins have been suggested as possible causes but not proven
  • Intestinal dysbacteriosis is likely to occur as well and could play a role in the pathogenesis

Risk Factors!!navigator!!

A recent dietary change.

Diagnosis

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DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Any condition causing colic and gastric reflux
  • Strangulating or nonstrangulating obstructive SI lesions
  • Ileus
  • Large colon impaction, causing SI compression

CBC/Biochemistry/Urinalysis!!navigator!!

A leukocytosis may be present but is not diagnostic.

Other Laboratory Tests!!navigator!!

  • Metabolic acidosis can occur due to hypovolemia, decreased tissue perfusion, and electrolyte imbalance. Metabolic alkalosis also possible due to gastric reflux
  • Abdominocentesis—increased peritoneal fluid protein level (>30 g/L, and possibly >45 g/L) with normal WBC numbers (<5–10 × 109 cells/L) is suggestive but is not diagnostic

Imaging!!navigator!!

Abdominal ultrasonography—SI distention.

Pathologic Findings!!navigator!!

Gross

  • Lesions are present invariably in the duodenum, often in the jejunum, and occasionally in the pyloric region of the stomach
  • Petechial and ecchymotic hemorrhages on serosal surface
  • Thickened intestinal wall due to edema and inflammation
  • Hyperemic mucosa

Histopathologic

  • Lesions include fibrinopurulent exudation on the serosal surface, intramural hemorrhage, and hyperemia and edema of the mucosa and submucosa
  • Depending on severity, there may be villous epithelial degeneration, epithelial cell sloughing, and neutrophilic infiltration
  • In some cases, no gross or histologic lesions are present

Treatment

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TREATMENT

Appropriate Health Care!!navigator!!

Intensive treatment and monitoring required; affected horses should be managed on an inpatient basis.

Nursing Care!!navigator!!

  • Frequent monitoring is essential, especially when the presence of a surgical lesion remains unclear
  • Signs of colic and tachycardia could indicate the need for gastric decompression
  • Deep bedding and prophylactic feet icing could be beneficial to laminitis

IV Fluid Therapy

  • Balanced electrolyte solution
  • Administer daily maintenance (30–50 mL/kg/day) plus correction of fluid deficits from dehydration and replacement of the fluid volume lost with reflux
  • Monitor plasma electrolyte levels
  • IV potassium supplementation—20–40 mEq/L of KCl can be added to lactated Ringer's solution or saline. Infusion rate should not exceed 0.5 mEq/kg/h
  • Hypocalcemia—slow 500 mL IV infusion of 23% calcium borogluconate

Gastric Decompression

  • A siphon must be established each time, because passage of a nasogastric tube does not always result in reflux. Initially, nasogastric intubation may be needed every 1–2 h
  • If <5 L of fluid is obtained, the interval between refluxing can be increased
  • If colic or tachycardia are observed, the stomach should be refluxed
  • The tube is commonly left in place until refluxing has either ceased or decreased to 1–2 L in 4 h

Activity!!navigator!!

If no signs of laminitis are present, it may be beneficial to walk the horse frequently for short periods of time to stimulate GI motility.

Diet!!navigator!!

  • Nothing should be given orally until the nasogastric tube is removed, after which a slow reintroduction of feed can begin
  • Partial or total parenteral nutrition may be indicated

Client Education!!navigator!!

  • This condition can be frustrating and expensive to treat
  • Owners should be made aware that the affected horses could reflux for >1 week, and that expensive therapy (e.g. total or partial parenteral nutrition) may be indicated
  • Laminitis can occur, especially in larger horses
  • Reported survival rate is generally good
  • Death occurs from complications (e.g. laminitis, adhesions), or horses are euthanized because of economic concerns

Surgical Considerations!!navigator!!

  • Surgical intervention is common during the early stages of this condition to differentiate from a surgical SI lesion
  • Surgery may be beneficial by confirming the diagnosis and decompressing the SI, but secondary complications such as risks associated with anesthesia and adhesion formation should be considered

Medications

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MEDICATIONS

Drug(s) of Choice!!navigator!!

  • The use of antimicrobials has been suggested but their efficacy has not been proven:
    • For intestinal clostridiosis, penicillin may be administered—sodium penicillin (20 000–40 000 IU/kg IV every 6 h) or metronidazole (15–25 mg/kg per rectum every 8 h)
    • Broad-spectrum antibiotics may be indicated with signs of toxemia or bacteremia. Options include a penicillin–aminoglycoside combination (sodium penicillin 20 000–40 000 IU/kg IV every 6 h/gentamicin 6.6 mg/kg IV every 24 h), trimethoprim–sulfamethoxazole (24 mg/kg IV every 12 h), or ceftiofur sodium (2 mg/kg IV every 12 h)
  • Low-dose flunixin meglumine 0.25–0.5 mg/kg IV every 8 h can be administered for its purported antiendotoxin as well as anti-inflammatory effects
  • Once the stomach is decompressed, there usually is little need for analgesics
  • Analgesics should be administered judiciously because they may mask the progression of clinical signs that might indicate a surgical lesion. If analgesia is required, flunixin meglumine 1.1 mg/kg IV every 12 h can be administered
  • H2-receptor antagonists (e.g. ranitidine 6.6 mg/kg PO every 8 h) or proton pump inhibitors (e.g. omeprazole 4 mg/kg PO every 24 h) may be indicated after refluxing has ceased because of gastric irritation from distention, the primary disease process, and prolonged nasogastric intubation
  • Efficacy of prokinetic agents has not been proven

Contraindications!!navigator!!

Prokinetic agents are contraindicated in obstructive SI lesions. Consider their use once an obstructive lesion has been ruled out or when DPJ has been confirmed via exploratory laparotomy/laparoscopy.

Precautions!!navigator!!

  • Aminoglycosides and NSAIDs are potentially nephrotoxic and should not be administered until hydration status is normal
  • Antibiotics have been implicated in the development of colitis

Follow-up

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FOLLOW-UP

Patient Monitoring!!navigator!!

During the recovery period, monitor for signs of recrudescence of disease.

Prevention/Avoidance!!navigator!!

Because an intestinal dysbacteriosis may be involved in pathogenesis, institute feeding changes gradually.

Possible Complications!!navigator!!

  • Laminitis
  • Intestinal adhesions after surgical exploration
  • Other less common complications—peritonitis, aspiration pneumonia, and myocardial or renal infarcts

Expected Course and Prognosis!!navigator!!

  • Duration of reflux may be short (24 h) but typically lasts for 3–7 days or longer
  • Survival rates range from 25% to 98%
  • Prognosis is good for horses that stop refluxing within 72 h
  • Death most often results from economic concerns or complications such as laminitis or adhesions

Miscellaneous

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MISCELLANEOUS

Associated Conditions!!navigator!!

  • Aspiration pneumonia
  • Intestinal adhesions
  • Laminitis
  • Peritonitis

Pregnancy/Fertility/Breeding!!navigator!!

Pregnant mares may be at greater risk for abortion.

Synonyms!!navigator!!

  • Anterior enteritis
  • Gastroduodenojejunitis
  • Proximal enteritis

Abbreviations!!navigator!!

  • DPJ = duodenitis–proximal jejunitis
  • GI = gastrointestinal
  • NSAID = nonsteroidal anti-inflammatory drug
  • SI = small intestine
  • WBC = white blood cell

Suggested Reading

Arroyo LG, Stämpfli HR, Weese JS. Potential role of Clostridium difficile as a cause of duodenitis-proximal jejunitis in horses. J Med Microbiol 2006;55:605608.

Cohen ND, Toby E, Roussel AJ, et al. Are feeding practices associated with duodenitis-proximal jejunitis? Equine Vet J 2006;38:526531.

Freeman DE. Duodenitis-proximal jejunitis. Equine Vet Educ 2000;12:322332.

Author(s)

Authors: Luis G. Arroyo and J. Scott Weese

Consulting Editors: Henry Stämpfli and Olimpo Oliver-Espinosa