Equis ISSN 2398-2977

Cecum: intussusception - cecocecal / cecocolic

Contributor(s): Peter Rakestraw


  • Cecocecal and cecocolic intussusception can occur due to changes in cecal motility which together account for approximately 0.3% of surgical colic cases. Cecocecal intussusception is approximately twice as common as cecocolic intussusception.
  • Cause: often unknown, but abnormal motility that may be secondary to tapeworm infestation, or the use of organophosphate anti-parasiticides, have been implicated.
  • Signs: sudden onset severe pain, often eases off after a few hours and then becomes intermittent.
  • Diagnosis: rectal examination or laparotomy may be necessary.
  • Treatment: surgery, in the case of cecocecal intussusception treatment involves surgical reduction of the intussusception and partial amputation of the cecum; cecocolic intussusceptions are much harder to treat.
  • Prognosis: guarded to good.



  • Etiology is usually unknown. However, a variety of factors can predispose to the development of intussusceptions.
  • The disease appears to follow changes in gastrointestinal activity, involving a reduction in the production of co-ordinated smooth muscle activity.
  • Tapeworm presence or recent tapeworm treatment is a possible predisposer, as is the use of organophosphate anti-parasiticides.

Predisposing factors

  • Abnormal gut motility, the cause of this is usually unknown, but hypermotility is usually involved. Drinking large amounts of cold water straight after exercise may cause abnormal motility and act as a predisposing factor.
  • Motility modifying drugs.
  • Cecal abscess.
  • Parasites, egEimeria lucarti,Anoplocephala perfoliata.


  • Tapeworm infestation   Tapeworm infection  .
  • Use of organophosphate anti-parasiticides.


  • Telescoping of a section of the cecum into itself results in partial obstruction of the bowel lumen, and partial occlusion of it's blood supply.
  • Pain results due to mesenteric traction, stretching of the more proximal gut, and potentially, to bowel compromise and toxin leakage.
  • Bowel compromise due to ischemia can occur, particularly in cases of cecocolic intussusception. It results in circulatory compromise via release of bacteria and toxins into the bloodstream. Circulatory compromise is rarer in cases of cecal intussusception than it is in cases of small intestinal intussusception.
  • Bacteria and toxins can also be released into the peritoneum causing fluid and white blood cell sequestration to this area. Hypovolemic and endotoxic shock result. Collapse and death due to endotoxemia or gut rupture can follow.
  • More commonly, in cases of cecocecal intussusception, the disease takes a chronic course, and pathology is largely related to the presence of a partial bowel obstruction.
  • Abnormal intestinal motility   →   invagination of the apex of the cecum. Intussusception of the body of the cecum into the base -> a cecocecal intussusception most commonly. Alternatively, telescoping of the invaginated cecal apex through the cecocolic opening into the right ventral colon causes a more serious cecocolic intussusception.
  • This results in acute abdominal pain, due to stretching and mesenteric traction, and devitalization of the intussuscepiens. The associated circulatory and peritoneal pathology that one would expect to occur is rarely a problem, because the blood supply to the cecum is often only partially affected, and any vascular compromise that takes place is largely contained within the intussuscepiens.
  • Devitalization of the telescoped section of cecum can cause reduction in pain sensation.
  • Chronic intermittent pain usually follows the initial acute stage, and this is mostly due to partial obstruction of the intestinal lumen which can cause pathology due to stretching of the bowel proximal to the lesion.
  • More serious pathology due to vascular compromise can, however occur, particularly in cases of cecocolic intussusception, and is characterised by the following process:
    • Venous drainage of the area is impaired resulting in swelling, edema and congestion.
    • There is progressive arterial obstruction, which causes cyanosis and ischemia of the affected bowel, which causes gut spasm, and contributes to proximal distension of bowel with accumulation of gas and fluid.
    • Intraluminal distension results in progressive ischemia and disruption of the mucosal layers, which leads to necrosis and cell sloughing.
    • Protein rich fluid, endotoxins and bacteria leak into the cecal lumen, and can also leak into the peritoneal cavity.
    • Hypovolemia, endotoxic shock, electrolyte and acid/base abnormalities may develop in such cases.
  • Pain due to gut and vascular compromise at the site of the lesion may become continuous and show little or only temporary response to analgesics.


  • This depends on the degree of vascular obstruction. In some cases of cecocecal intussusception, symptoms may continue for days with little worsening of clinical signs. In cases of cecocolic intussusception symptoms tend to be more acute and to necessitate emergency treatment.


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Hubert J D et al (2000) Cecal amputation within the right ventral colon for surgical treatment of nonreducible cecocolic intussusception in 8 horses. Vet Surg 29, 317-325 PubMed.
  • Dart A J, Dowling B & Hodgson D R (1999) Caecal disease. Equine Vet Educ 11 (4), 182-188 VetMedResource.
  • Wiemer P & Van der Veen H (1999) Nonreducible caecocolic intussusception. Equine Vet Educ 11 (4), 179-181 VetMedResource.
  • Edwards G B (1992) The clinical presentation and diagnosis of cecal obstruction in the horse. Equine Vet Educ (5), 237-240 Wiley Online Library.
  • Proudman C J (1992) A two year, prospective study of equine colic in general practice. Equine Vet J 24 (2), 90-93 PubMed.
  • Edwards G B (1991) Equine colic - the decision for surgery. Equine Vet Educ (1), 19-23 VetMedResource.

Other sources of information

  • Rose R J & Hodgson D R (1993) Manual of Equine Practice. W B Saunders. ISBN 0 7216 3739 6.