2019
Introduction
It is estimated that adhesions may develop in up to 90% of patients
undergoing major abdominal surgery and 55–100% of
women undergoing pelvic surgery.
Although most patients are asymptomatic, adhesions can be associated with significant
morbidity including small bowel obstruction, chronic pelvic
pain, deep dyspareunia and female subfertility.
Pathophysiology
Adhesion formation is multifactorial and depends on patient healing (peritoneal repair), surgical technique and equipment factors.
The inciting event for adhesion formation is injury to the peritoneal mesothelium, which initiates a peritoneal repair response.
Subsequently, the development of adhesions depends on the balance between fibrin deposition and degradation (fibrinolysis) that begins within hours of surgery.
the organisation of fibrin into adhesions is potentiated by two risk factors associated with surgical injury: inflammation and tissue ischaemia.
At a biomolecular level, this injury causes damaged tissues to release cytokines, growth factors, cell adhesion molecules and histamine, which mediate a local inflammatory response
that promotes fibrin deposition.
This inflammatory reaction involves processes such as coagulation and the recruitment of
leucocytes (macrophages and neutrophils) and fibroblasts.
In particular, macrophages are involved in the recruitment of adjacent mesothelial cells and fibroblasts, which migrate to the site of peritoneal injury and re epithelialize the injured peritoneal surface over 3–5 days.
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