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Postoperative ileus (POI) is defined as a severe impairment of gut motility which unavoidably follows any type of abdominal and, to a lesser extent, extra-abdominal surgery.1 2 Clinically, this condition is characterised by symptoms and signs of intestinal subocclusion including nausea, vomiting, lack of passage of flatus and stool, along with abdominal distension and absence of borborygmi. Although the clinical outcome is essentially not life-threatening, POI is a markedly morbid condition accompanied by increased hospitalisation (ie, up to 10 days or longer in the most severe cases)3 and related costs.4 The need to improve the patient’s postoperative course and reduce time spent in hospital has fuelled basic and clinical research aimed at a better understanding of the pathogenetic mechanisms involved in POI. Several potentially relevant factors, including extrinsic and intrinsic neural reflexes, a variety of inflammatory mediators and pharmacological agents used during postoperative analgesia, have been implicated in the pathogenesis of POI.2 5–7 The clinical evidence that patients undergoing minimally invasive (ie, laparoscopic) surgery have a shorter period of POI suggests that manipulation of bowel loops during surgery plays an important pathogenetic role in this condition.8 9
Data from animal models indicate that abdominal surgery and bowel manipulation promote cessation of gut motility by at least two major mechanisms: (1) activation of neural reflexes; and (2) a remarkable inflammatory response within the enteric neuromuscular layer.5–7 Concerning neurogenic mechanisms, the activation of inhibitory reflex circuits has been proposed to contribute to POI. These reflexes can occur at different levels of the innervation supplying the gut, namely within the intrinsic (enteric) nervous system or via extrinsic nerve pathways involving prevertebral ganglia, the spinal cord or supraspinal centres.5–7 Although the hierarchy and sequence of these reflexes remain a matter of …
Competing interests: None.
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