Equis ISSN 2398-2977

Umbilicus: hernia (strangulating)

Contributor(s): David Moll, Prof Jonathon Naylor

Introduction

  • Umbilical hernias occur in approximately 1% of foals; most cases are easily reducible, asymptomatic and heal spontaneously. Strangulating umbilical hernia is a relatively rare cause of severe abdominal pain in the horse.
  • As the gut becomes strangulated, obstruction of both lumen and blood supply occurs.
  • Cause: common congenital defect.
  • Signs: development of severe abdominal pain with circulatory compromise.
  • Diagnosis: clinical signs, rectal and laparotomy findings.
  • Treatment: resection of affected bowel and anastomosis.
  • Prognosis: guarded to good.

Pathogenesis

Etiology

  • Umbilical hernias are the most common congenital defect of horses.
  • Most hernias are small and cause no disease.
  • Hernias that are large enough to accomocdate a section of bowel, or even just a section of intestinal wall (Richter's hernia), can result in disease such as strangulation and the development of enterocutaneous fistulae.

Predisposing factors

General

  • Failure of normal development and closure of the umbilicus.
  • Damage to the root of the umbilical cord at birth.
  • Infection of the umbilicus.
  • Excessive straining.
  • Genetic factors.

Pathophysiology

  • Incarceration of intestine into an umbilical hernia occurs in 2-10% of cases. In most cases of umbilical hernia reduction of the hernia daily is all that is necessary. However hernias that have not resolved by 12 months of age should be closed (herniorraphy Umbilicus: herniorrhaphy).
  • Strangulating umbilical hernia consists of passage of a section of bowel through the body wall defect to lie within hernial sac.
  • Pain results due to stretching of the obstructed bowel, to mesenteric traction, and to bowel compromise and toxin leakage.
  • Enterocutaneous fistulae can develop.
  • The circulatory effects of bowel compromise may be minimized by the fact that the devitalized bowel is trapped outside the peritoneal cavity.
  • However, bacteria and toxins can enter the blood stream and collapse and death due to endotoxemia Endotoxemia: overview can occur.
  • Passage of a length of small intestine into an umbilical hernial sac may initially cause no problems.
  • However passage of food into the incarcerated section of gut can cause a build up of pressure, and this, together with increased tightness of the defect around the gut loop contributes to pathology of the bowel loops at the points where they enter and leave the hernia.
  • This can cause inflammation, and commonly adhesions between the bowel wall and the edges of the body wall defect.
  • Reduced blood supply to the incarcerated section of bowel results in some devitalization of the bowel wall. This can be very mild, resulting merely in some release of toxins and inflammatory mediators into the hernial sac, or may be more serious leading to bowel and body wall necrosis and the development of enterocutaneous fistulae.
  • Effects on the blood supply of the bowel rarely cause systemic signs, but can do so via the following process:
    • Venous drainage of the area is impaired resulting in swelling, edema, and congestion.
    • There may be 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 leaks into the gut lumen, as well as the hernial, and occasionally peritoneal cavities.
    • Endotoxins and bacteria may leak into the bloodstream and peritoneal cavity, causing damage to endothelial cells and platelets. Platelets release thromboxane and serotonin causing vasoconstriction. Endothelial cell damage causes the stimulation of neutrophils.
    • Hypovolemia, endotoxic shock, electrolyte and acid/base abnormalities may develop.
  • Partial obstruction of the gut lumen as it enters and leaves the hernial sac also results in pathology due to stretching and hypertrophy of the bowel proximal to the lesion - see Pathophysiology of ileal impaction Ileum: impaction.
  • Pathology due to vascular compromise (where it exists) is, however, more serious; the severity depends on the extent of vascular compromise.
  • 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) may be seen, and metabolic acidosis can occur causing tachypnoea.
  • Where gut compromise is severe, peritoneal fluid may become sero-sanguinous, to turbid in appearance.

Timecourse

  • This depends on the degree of vascular obstruction; some cases may take a chronic course over several weeks, but in rare cases where severe circulatory compromise is present, bowel wall damage can lead to endotoxic shock, and death can follow within hours.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Smith M (2006) Management of umbilical disorders in the foal. In Pract 28 (5), 280-287 VetMedResource.
  • Orsini J A (1997) Management of umbilical hernias in the horse: treatment options and potential complications. Equine Vet Educ 9 (1), 7-10 VetMedResource.
  • Rijkenhuizen A B M, van der Velden M A & Back W (1997) Incarcerated umbilical hernia with enterocutaneous fistulae in two foals. Equine Vet Educ 9 (1), 3-6 VetMedResource.
  • Tinker M K et al (1997) Prospective study of equine colic incidence and mortality. Equine Vet J 29 (6) 448-453 PubMed.
  • Riley C B et al (1996) Comparison of herniorraphy versus clamping of umbilical hernias in horses: a retrospective study of 93 cases (1982-1994). Can Vet J 37 (5), 295-298 PubMed.
  • Bristol D G (1994) Enterocutaneous fistulae in horses: 18 cases (1964-1992). Vet Surg 23 (3), 167-171 PubMed.
  • McGladdery A J (1992) Ultrasonography as an aid to the diagnosis of equine colic. Equine Vet Educ 4 (5), 248-251 WileyOnline.
  • Edwards G B (1991) Equine colic - the decision for surgery. Equine Vet Educ 3 (1), 19-23 WileyOnline.
  • Freeman D E et al (1991) Evaluation of age, breed, and gender as risk factors for umbilical hernia in horses of an hospital population. Am J Vet Res 52 (4), 637-639 PubMed.
  • Freeman D E et al (1988) Complications of umbilical hernias in horses: 13 cases (1972-1986). JAVMA 192 (6), 804-807 PubMed.
  • Markel M D et al (1987) Strangulated umbilical hernias in horses: 13 cases (1974-1985). JAVMA 190 (6), 692-694 PubMed.
  • Fretz P B et al (1983) Management of umbilical hernias in cattle and horses. JAVMA 183 (5), 550-552 PubMed.
  • Peyton L C (1981) Surgical correction of equine umbilical hernias. Vet Med Small Anim Clin 76 (8), 1212-1215 PubMed.

Other sources of information

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


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