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Gastrointestinal motility and prokinetics in the critically ill Current Opinion in Critical Care 2007, 13:187 – 194. Ri 趙基安 Supervisor VS 葉育彰. Introduction. Early enteral administration of nutrition is currently considered to be best practice

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Gastrointestinal motility and prokinetics in the critically illCurrent Opinion in Critical Care 2007, 13:187–194


Supervisor VS葉育彰

  • Early enteral administration of nutrition is currently considered to be best practice
  • 50~60% of critically ill patients have delayed gastric emptying
  • The aetiologies of abnormal UGI motor activity remain unclear; related: pre-existing comorbidities, admission diagnoses, drugs, electrolyte abnormalities including hyperglycaemia, recent surgery, shock, and circulating cytokines
Sequelae of abnormal UGI motility:

☆ poor nutrition

☆ bacterial colonization of the gastrointestinal


☆ gastro-esophageal reflux

☆ esophagitis

☆ gastrointestinal bleeding

☆ pulmonary aspiration

☆ ventilator-associated pneumonia

Current treatment for abnormal UGI motility has major limitations
  • Better understanding  target therapy new agents
upper gastrointestinal motility in health
Upper gastrointestinal motility in health
  • Lower esophageal sphincter tone prevents reflux of food, acid and bile
  • Proximal stomach functions as a reservoir and an important determinant of liquid gastric emptying; nutrient redistribution
  • Antro-pyloro-duodenal motility: Contractions can be localized or propagated (antegrade or retrograde)
Chyme into the duodenum  nutrient receptor feedback  fundal relaxation, decrease in fundic and antral contractions, increased pyloric activity  slow gastric emptying
  • Fasting motility consists of migratory motor complexes, which are divided into 3 phases:

☆Phase I: quiescence

☆Phase II: variable period of irregular contractile


☆Phase III: short period (5~10 min) of intense, frequent, regular contractions (motilin receptor) clear bowel

Gastrointestinal motility control: mixture of neural and humoral mechanisms
  • Interstitial cell of Cajal  fluctuated RMP  rhythm of smooth muscle activity
  • Neural and humoral mechanisms  to or not to initiate a mechanical contraction
  • Intrinsic: myenteric plexus
  • Extrinsic: parasympathetic↑; sympathetic↓
  • CCK, released in response to nutrients  slow gastric emptying
gastric emptying in the critically ill
Gastric emptying in the critically ill
  • Delayed gastric emptying occurs frequently in critical illness
  • Gastric residual volumes  surrogate marker to determine the success or failure of nasogastric nutrition, and the risk of regurgitation and aspiration
  • The incidence of delayed gastric emptying in the critically ill appears to be affected by age, illness severity, and admission diagnosis
Delayed gastric emptying is more frequent in:


☆multiple trauma (with and without head injury)

☆severe sepsis

►80% head injuries (IICP associated)

►Hyperglycemia delays gastric emptying (pre-

existing DM doesn’t affect)

Drugs administered in ICU, particularly inotropes and those used for sedation, may impact on gastrointestinal motility
  • Opiates μreceptors  may contribute to

abnormal upper gastrointestinal motor


  • Neuromuscular blockers  no effect
High levels of circulating catecholamines commonly seen  negative effect
  • Adrenaline reduces gastric emptying by a β-adrenergic effect
  • Dopamine reduces antral contractions and slows orocaecal transit
  • High-dose catecholamines may reduce the prokinetic effect of erythromycin
  • Anticholinergics and calcium channel blockers
esophageal dysmotility
Esophageal dysmotility
  • Reflux oesophagitis occurs in approximately 50% of patients  hemorrhage, microaspiration  ventilator-associated pneumonia.
  • Lower esophageal sphincter tone is reduced or absent in mechanically ventilated patients  free oral flow of gastric contents
gastric dysmotility
Gastric dysmotility
  • Motor disturbances have been described in all regions of the stomach.

★Proximal stomach

  • Fundic wave frequency is reduced
  • Subsequent recovery of nutrient-induced relaxation to baseline is markedly delayed
★Whole stomach
  • Intragastric meal distribution is abnormal
  • Proximal gastric meal retention  GE reflux

★Distal stomach

  • Antral motor activity is greatly reduced
  • Pyloric activity is increased
  • Exaggeration in response to the presence of nutrients in the duodenum
duodenal dysmotility
Duodenal dysmotility
  • Frequency of duodenal contractions is relatively well
  • Organization of duodenal activity is abnormal
  • 50% of these contractions are retrograde in critically ill
control mechanisms
Control mechanisms
  • During fasting, ghrelin and peptide YY (PYY) concentrations are abnormal
  • Nutrient-stimulated concentrations of cholecystokinin and PYY are markedly elevated  delayed gastric emptying
intestinal absorption
Intestinal absorption
  • Glucose absorption is substantially reduced in the critically ill
  • Fat absorption may also be reduced
  • The reasons for impaired absorption are unclear
  • 5-HT4 agonist  Acetylcholine increase in enteric nervous system (parasympathomimetic)  increase esophageal sphincter tone and gastric emptying
  • Limited use due to enteral formulation and the risk of cardiac arrhythmias
  • Widely used in ICU
  • Antagonizes the inhibitory effect of dopamine on motility; weak 5-HT3 antagonist
  • Less effective than erythromycin
  • With repeated administration tachyphylaxis develops
  • Ineffective and contraindicated in patients with head injuries
  • Low doses (1~3 mg/kg IV) of erythromycin act as a motilin agonist, triggering phase 3-like activity in the stomach and small intestine
  • In critically ill, itincreases antral motility, accelerates gastric emptying and improves the success of feeding
  • Efficacy reduced after 7-day use
  • Cardiac toxicity (use low dose:70 vs 200mg) and bacterial resistance
combination therapy
Combination therapy
  • Combination of erythromycin and metoclopramide for failure of nasogastric feeding, both as first-line treatment and after the failure of monotherapy, is superior to either drug alone and with less tachyphylaxis
5 ht 4 receptor agonists
5-HT4 receptor agonists
  • Activation of the 5-HT4 receptor is important in the initiation of peristalsis


  • A selective, 5-HT4 receptor partial agonist
  • Improve gastric hypomotility in a small number of critically ill patients
  • Ischemic colitis?
receptor antagonists
μreceptor antagonists
  • Opiates slow gastric emptying  opiate antagonist


  • administered directly into the gut  avoid antagonism of the central effects of parenteral opiates
  • improves the success of feeding and reduces ventilator-associated pneumonia
  • High affinity for μreceptors
  • Does not cross the blood–brain barrier
  • No effect on gastric emptying
  • hastened gut recovery and shortened time to hospital discharge in patients after bowel resection or hysterectomy
cholecystokinin receptor antagonists
Cholecystokinin receptor antagonists
  • Elevated cholecystokinin levels slow gastric emptying and motility and are associated with feed intolerance in critically ill patients


  • Selective and highly potent CCK-1 receptor antagonist
  • Inhibits gallbladder contraction,
  • Improves lower oesophageal sphincter function,
  • Hastens colonic transit.
  • Potential treatment
postpyloric feeding
Postpyloric feeding
  • As small intestinal motor function appears to be relatively preserved, successful feeding may be achieved with postpyloric feeding tubes
  • Blind placement  often failure
  • Radiological or endoscopic support are required
  • Postpyloric tubes v.s. intravenous erythromycin  failed nasogastric feeding and unresponsive to prokinetics
  • New insights into the pathophysiology underlying failed enteral feeding
  • Commonly used prokinetics have limited efficacy
  • New agents are yet to undergo systematic clinical evaluation in the critically ill
  • Real time localization of the path of the tube
  • Use of frictional nasal jejunal feeding tubes