Introduction

• Cause: common complication of abdominal surgery, peritonitis or possibly strongyle migration.
• Signs: none or colic - varies from mild discomfort (following surgery) to severe (if volvulus or herniation involved).
• Diagnosis: history, signs, laparotomy.
• Treatment: mild cases → NSAIDs; severe cases → surgery.
• Prognosis: depends on extent of adhesion and damage to bowel. One of the limitations on survival rate post-abdominal surgery.

Pathogenesis

Etiology

• The true incidence of post-operative adhesions is not really known as the reported studies have differences in their protocols for inclusion, in the population studied, and the way the results are reported. Most studies report the incidence based on those cases taken back to a repeat laparotomy, whereas the true incidence, based on a PM study of all originally operated cases, is probably considerably higher.
• Reported incidences have varied as widely as 1.5-33% of all post-operative colic surgery cases. In general, an incidence of between 5-15% is commonly cited in many studies which look across a wide range of colic surgery.

Predisposing factors

General

• Abdominal surgery.
• Peritonitis Abdomen: peritonitis.

Specific

• Small intestine disease.
• Intestinal resection and anastomosis Intestine: resection and anastomosis.
• Abdominal surgery in foals or Miniature horses.
• Poor surgical technique.
• Failure to address pre- and post-operative problems such as endotoxemia Endotoxemia: overview and ileus Gastrointestinal: ileus.
• Migrating strongyles Strongyle infestation: large.

Pathophysiology

• Fibrous and omental adhesions are a normal response after peritoneal injury and inflammation. Many cause no clinical problems. They can become a problem if the fibrinous adhesion matures into a fibrous one that restricts, compresses or distorts the gut leading to obstruction of normal passage of ingesta. Some can lead to intestinal incarceration, strangulation and volvulus Gastrointestinal: small intestine - torsion. All these adverse effects on gut function will present with varying degrees of abdominal pain or colic Abdomen: pain - adult.
• Injury or inflammation of the peritoneal membrane stimulates procoagulant activity within it, which is characterized by serofibrinous exudate secretion and subsequent deposition of fibrin. This fibrin matrix provides access for healing tissues to repair and re-establish the damaged peritoneum. Once this occurs there are local peritoneal fibrinolytic enzymes that can lyse the fibrin or fibrinous adhesions within 48-72 h. If the damage or inflammation is more severe, then the fibrin matrix is not lysed before it matures into fibrinous adhesions between adjacent viscera or peritoneal surfaces. Peritoneal fibrinolytic activity may be depressed by intestinal ischemia and inflammation caused by distension and strangulation, surgical trauma and excessive handling.
• All sorts of biological processes such as coagulation, fibrinolysis, kinin/bradykinin, arachidonic acid metabolism, and complement activation are involved in adhesion formation. The fibrinolytic system is the main modulator through its control of fibrin lysis under the action of the enzyme plasmin. Plasmin is derived from plasminogen via tPA (tissue plasminogen activator), the latter also being controlled by plasminogen activator inhibitors. The precise role of this fibrinolytic control system in the lack of fibrinolysis and therefore formation of mature adhesions is not yet known.
• The most common sites for adhesions are between loops of small intestine, and between the cecum and ventral body wall.

Timecourse

• Horses with adhesions that cause partial obstruction of the intestine often begin to show colic clinical signs 5-7 days post-operatively. Strangulation and incarceration, related to adhesions, often occur later on in the horse's life.

Diagnosis

Treatment

Prevention

Outcomes