Definition

Functional obstruction
Intestinal distension and the slowing, or absence, of passage of luminal contents
Without a demonstrable mechanical obstruction

Aetiology

Trauma
- Post-abdominal surgery
- Post-spinal or pelvic surgery
Metabolic and electrolyte derangements
- Hypokalaemia
- Hyponatraemia
- Hypomagnesaemia
- Diabetic coma
- Hypoparathyroidism
Medications
- Opiates
- Anticholinergics
- Antihistamines
- Psychotropic agents (Haloperidol, TCAs)
Intra-abdominal infection
- Retroperitoneal inflammation or haemorrhage
- Intestinal ischaemia
- Systemic sepsis from infection

Impaired Intestinal Motility
- Normal peristalsis is driven by the enteric nervous system and modulated by the autonomic nervous system.
In ileus, there is:
- Suppression of enteric nerve activity.
- Disruption of the balance between excitatory (acetylcholine) and inhibitory (nitric oxide) signals.
- Leads to paralysis of smooth muscle, preventing coordinated contractions.
Neurogenic Factors
- Surgical manipulation, trauma, or inflammation stimulates afferent sensory nerves.
- Activation of the sympathetic nervous system causes inhibitory effects on intestinal smooth muscle.
- Reflex arcs in the central nervous system further suppress peristalsis.
Inflammatory Response
- Inflammatory mediators such as cytokines (IL-6, TNF-α) and prostaglandins are released:
- Activate inhibitory pathways in the enteric nervous system.
- Cause edema and disrupt neuromuscular signaling.
Electrolyte Disturbances
- Electrolytes (e.g., hypokalemia, hypocalcemia, hypomagnesemia) are crucial for muscle contraction.
- Disruptions impair the depolarization and repolarization required for normal peristalsis.
Hormonal and Opioid Effects
- Stress hormones (e.g., cortisol and catecholamines) increase inhibitory signaling in the gut.
- Use of opioids inhibits gut motility by acting on μ-opioid receptors in the enteric nervous system, reducing acetylcholine release.