Ileus pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

Ileus is defined as temporary cessation of intestinal peristalsis in the absence of mechanical obstruction. The pathogenesis of ileus is multifactorial. Intestinal peristalsis is primarily regulated by enteric nervous system, autonomic nervous system and interactions with central nervous system. However, certain medications and metabolism products may also alter the normal intestinal equilibrium leading to temporary dysfunction in intestinal movements. With increasing time, intestinal aperistalsis results in accumulation of air and fluid in the bowel lumen.

Normal physiology

  • The gastrointestinal tract is are regulated by the enteric nervous system, autonomic nervous system and interactions with central nervous system.
  • The enteric nervous system (ENS) is also known as intrinsic neural network consists of neurons are located in the walls of GI tract.
    • ENS includes myenteric plexus (Auerbach's) and submucosal (Meissner's) plexuses.
    • The myenteric plexus is located in the muscular layer and is also known as Auerbach's plexus.
    • The submucosal plexus is located in the submucosal layer and is also known as Meissner's plexus.
  • The autonomic nervous system (ANS) is also known as extrinsic nervous system.
    • The ANS consists of sympathetic and parasympathetic nervous system which control GI function.
    • The sympathetic nervous system is inhibitory to visceral smooth muscle activity and increases peristalsis and GI motility.
    • The parasympathetic nervous system is stimulatory to visceral smooth muscle activity and increases peristalsis and GI motility.
    • The GI tract visceral sensory afferents located in the parasympathetic ANS while the visceral motor efferents are located in both sympathetic and parasympathetic ANS.
    • In addition, the extrinsic nervous system synapse with enteric nervous system and relay information to central nervous system.
Neural control of gut.(By Boumphreyfr (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons)

Pathophysiology

  • The most common cause of ileus is abdominal surgery.[1][2][3]
    • The risk of postoperative ileus depends upon the type of surgery; with the highest risk associated with colorectal surgery. In fact, post-operative ileus is so common that it is sometimes regarded as a normal sequelae of surgery. Post-operative ileus lasting longer than 3 days is termed as paralytic ileus.
        • The site of the surgery is the most commonly affected part of the GI tract. However, recent research has shown that inflammation of the intestinal muscle may extend from site of surgery to other parts of the intestinal tract.[4]
    • Abdominal incision leads to activation of inhibitory spinal reflexes which results in decreased movements of intestine, as a regulatory mechanism.
      • The painful stimuli stimulates the spinal afferents that synapse in the spinal cord. In the spinal cord, the pre-vertebral adrenergic neurons are activated which leads to inhibition of intestinal motility via efferent nerves.
      • Additionally, manipulation of intestine leads to activation of afferent pathways that travel to the brainstem. In turn, the brainstem sends increased autonomic output to the sympathetic neurons located in the inter-medio-lateral column of the thoracic cord. An increased activity of sympathetic neurons results in increased secretion of adrenergic output and decreased intestinal motility.
    • When a patient is undergoing a surgical procedure, it often puts the body under significant stress. This stress may lead to release of inflammatory and neuroendocrine mediators (such as nitric oxide, VIP and substance P) that may result in the development of ileus.
    • Stress inducing conditions may lead to increased recruitment of dendritic cells, natural killer cells, monocytes, T cells, macrophages, and mast cells. The macrophages and mast cells are considered the key cells in initiating the inflammatory process and release of chemical mediators.
    • Recent research has shown that inhibition of inflammatory mediators (such as nitric oxide & VIP) may lead to improved gastrointestinal peristalsis and function.
  • Another chronic and a more severe form of ileus is known as chronic intestinal pseudo-obstruction (CIPO).[5][6][7]
    • CIPO is a more severe form of ileus resulting from disturbances in autonomic nervous system and smooth muscle cell function.
    • The cause of CIPO can be idiopathic, sporadic, or secondary to metabolic, connective tissue, endocrinological, neurological, and paraneoplastic disorders.
    • CIPO is often due to dysfunction in the innervation of smooth muscle by the interstitial cells of Cajal resulting in partial or complete ineffective intestinal propulsion. However, any condition affecting the autonomic nervous system (both intrinsic or extrinsic), smooth muscle cells and neuromuscular junction may lead to development of CIPO.
    • The lack of intestinal propulsive movements may lead to increased intra-bowel pressure. The enhanced intra-bowel pressure may lead to malabsorption and bacterial translocation. Over time, it can progress to present with malnutrition and blood stream infection (sepsis).



  • The other common cause of ileus are the drugs that affect intestinal motility and alteration in electrolyte levels.
    • Drugs affecting intestinal motility primarily includes antimotility agents and other drugs such as opiates, vincristine.
    • Abdominal conditions such as gastroenteritis and peritonitis may also affect the intestinal motility leading to ileus.
    • Electrolyte abnormalities such as hypokalemia, hypercalcemia, hypermagnesemia, acidosis


    • Anesthetic drugs: Anesthetic agents have a direct inhibitory effect on the intestinal motility. Long acting anesthetic agents such as bupivacaine are more frequently associated with postopertaive ileus as compared to short acting agents such as propofol.
    • Opiates: The use of opiates for pain alleviation is not without side effects. Infact opiod use has been asssociated with significant increase in the occurence of postoperative ileus. Opiod medications that activate the µ receptors have been associated with decreased release of acetylcholine from cholinergic neurons, resulting in delayed intestinal motility. The most common opiod pain medication, morphine initially activates the migrating myoelectric complex and later on results in atony resulting in inhibition of propulsion and delay in intestinal transit.
  • Inhibitory neural reflexes
  • Inflammation: Ileus may increase adhesion formation, because intestinal segments have more prolonged contact, allowing fibrous adhesions to form, and intestinal distention causes serosal injury and ischemia. Intestinal distention has been shown to cause adhesions in foals. [8] In a recent survey of ACVS diplomates on drugs to prevent ileus and therefore prevent adhesions. The drug used in this survey was lidocaine, erythromycin, and cisapride. [9] Some respondents also mentioned the importance of walking horses postoperatively to stimulate motility. Repeat celiotomy to decompress chronically distended small intestine and remove fibrinous adhesions is also a useful method of treating ileus and reducing adhesions, and it has been associated with a good outcome. [10][11]
  • Neurohumoral peptides

References

  1. Kalff JC, Schraut WH, Simmons RL, Bauer AJ (1998). "Surgical manipulation of the gut elicits an intestinal muscularis inflammatory response resulting in postsurgical ileus". Ann. Surg. 228 (5): 652–63. PMC 1191570. PMID 9833803.
  2. Espat NJ, Cheng G, Kelley MC, Vogel SB, Sninsky CA, Hocking MP (1995). "Vasoactive intestinal peptide and substance P receptor antagonists improve postoperative ileus". J. Surg. Res. 58 (6): 719–23. doi:10.1006/jsre.1995.1113. PMID 7540700.
  3. Kalff JC, Schraut WH, Billiar TR, Simmons RL, Bauer AJ (2000). "Role of inducible nitric oxide synthase in postoperative intestinal smooth muscle dysfunction in rodents". Gastroenterology. 118 (2): 316–27. PMID 10648460.
  4. Bederman SS, Betsy M, Winiarsky R, Seldes RM, Sharrock NE, Sculco TP (2001). "Postoperative ileus in the lower extremity arthroplasty patient". J Arthroplasty. 16 (8): 1066–70. doi:10.1054/arth.2001.27675. PMID 11740765.
  5. Di Nardo, G.; Di Lorenzo, C.; Lauro, A.; Stanghellini, V.; Thapar, N.; Karunaratne, T. B.; Volta, U.; De Giorgio, R. (2017). "Chronic intestinal pseudo-obstruction in children and adults: diagnosis and therapeutic options". Neurogastroenterology & Motility. 29 (1): e12945. doi:10.1111/nmo.12945. ISSN 1350-1925.
  6. Iida H, Ohkubo H, Inamori M, Nakajima A, Sato H (2013). "Epidemiology and clinical experience of chronic intestinal pseudo-obstruction in Japan: a nationwide epidemiologic survey". J Epidemiol. 23 (4): 288–94. PMC 3709546. PMID 23831693.
  7. Yeung AK, Di Lorenzo C (2012). "Primary gastrointestinal motility disorders in childhood". Minerva Pediatr. 64 (6): 567–84. PMID 23108319.
  8. Lundin C, Sullins KE, White NA and al. Induction of peritoneal adhesions with small intestinal ischaemia and distention in the foal. Equine Vet J 21: 451, 1989
  9. Van Hoogmoed and Snyder
  10. Vachon AM, Fisher AT. Small intestinal herniation through the epiploic foramen: 53 cases (1987-1993). Equine Vet J 27: 373, 1995
  11. Southwood LL, Baxter GM. Current concepts in management of abdominal adhesions. Vet Clin North Am Eq Prac 13:2 415 1997