Equis ISSN 2398-2977

Gastrointestinal: enterolith

Contributor(s): Roberta Baxter, Peter Rakestraw

Introduction

  • Enteroliths are masses that build up in the intestinal system, particularly the right dorsal colon.
  • Cause: usually form as concretions around foreign bodies or food material.
  • Signs: include colic, although they may be non-pathogenic, they can cause partial obstructions, particularly at the entrance to the transverse colon, and within the small colon if they move.
  • Diagnosis: rectal palpation, radiography or at laparotomy.
  • Treatment: surgical removal.
  • Prognosis: good, provided prompt treatment is carried out when necessary.

Pathogenesis

Etiology

  • Enteroliths are mineral concretions within the guts.
  • They usually have a foreign body nidus such as a nail/piece of wire.
  • They are slow growing, but can reach large sizes.

Predisposing factors

General
  • Intestinal foreign bodies.
  • Diets high in magnesium, nitrogen and phosphorus.

Pathophysiology

  • Masses develop in the intestines, particularly the right dorsal colon.
  • They rarely cause problems there, though they may cause intermittant, low-grade chronic colic due to progressive partial obstruction of the gut lumen.
  • They may move into the entrance to the transverse colon and cause colic due to partial obstruction in this situation.
  • They may move into the narrower small colon and cause complete obstruction.
  • Complete obstruction results in the development of signs of severe colic that requires surgery.
  • Partial intermittent obstruction of the colonic lumen results in blockage of the intestinal transit. Mild pain can result due to stretching of the bowel.
  • In cases involving complete obstruction of the colonic lumen, the pathologic mechanisms are as follows:
    • Stasis of intestinal fluid proximal to the obstruction results in the multiplication of intestinal bacteria and the release of gas.
    • Increased pressure within the bowel due to fluid and gas build up causes distension, which results in an increase in pain, as well as a decrease in peristalsis.
    • The result is progressive filling and swelling of the gut, and atonia of the gut wall.
    • The enterolith can get tightly wedged in the small colon. The bowel spasms around the foreign body and pressure necrosis occurs. This can lead to rupture (ie the necrotic small colon is the site and cause of gut rupture with enteroliths, not degeneration of the proximal distended bowel).
    • Endotoxins and bacteria leak into the bloodstream and peritoneal cavity, causing damage to epithelial cells and platelets.
    • Platelets release thromboxane and serotonin causing vasoconstriction.
    • Endothelial cell damage causes the stimulation of neutrophils.
    • Endotoxemia   Endotoxemia: overview  may result, and this can cause further sensitization of the pain receptors.
    • Electrolyte and fluid sequestration contribute to the development of circulatory collapse.
    • Hypovolemia, endotoxic shock, electrolyte and acid/base abnormalities develop.
    • Pain due to the stretching of proximal bowel wall, as well as to gut and vascular compromise at the site of the lesion is generally continuous, and shows no, or only temporary response to analgesics.
    • Cardiovascular compromise is reflected by tachycardia, a decrease in pulse quality, mucous membrane congestion or cyanosis, and an increase in capillary refill time. Secondary increases in packed cell volume (PCV) and plasma proteins (TPP)are seen, and metabolic acidosis causes tachypnoea.
  • In cases that involve colonic, rather than small intestinal, obstruction, the development of clinical signs is gradual, and the resulting pain is usually mild, until severe bowel wall compromise is present.

Timecourse

  • Even when complete bowel obstruction occurs, it may take several hours for severe signs to develop.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references fromPubMedandVetMedResource.
  • Barrett E J & Munsterman A S (2013)Parainguinal laparotomy as an alternative surgical approach for removal of an enterolith in the small colon of a horse.Equine Vet Educ25(9), 442-446VetMedResource.
  • Hassel D Met al(1999)Evaluation of enterolithiasis in equids - 900 cases (1973-1996).JAVMA214(2), 233-237PubMed.
  • Cummings C A, Copedge K E & Confer A W (1997)Equine gastric impaction, ulceration and perforation due to persimmon (Diopyros virginiana) ingestion.J Vet Disgn Invest9(3), 311-313PubMed.
  • Peloso J Get al(1992)Obstructive enterolith in an 11-month-old miniature horse.JAVMA201(11), 1745-1746PubMed.
  • Lloyd Ket al(1987)Enteroliths in horses.Cornell Vet77(2), 172-186PubMed.
  • Blue M Get al(1981)Clinical and structural features of equine enteroliths.JAVMA179(1), 79-82PubMed.
  • Blue M Get al(1979)Enteroliths in horses - a retrospective study of 30 cases.Equine Vet J11(2), 76-84PubMed.
  • Blue M G (1979)Colonic obstructions due to enteroliths in four horses.Vet Rec104(10), 209-211PubMed.


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