Gastrointestinal motility and prokinetics in the critically ill
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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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Ri supervisor vs

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


Supervisor VS葉育彰

Introduction ill

  • 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

Ri supervisor vs

  • Sequelae of abnormal UGI motility: ill

    ☆ poor nutrition

    ☆ bacterial colonization of the gastrointestinal


    ☆ gastro-esophageal reflux

    ☆ esophagitis

    ☆ gastrointestinal bleeding

    ☆ pulmonary aspiration

    ☆ ventilator-associated pneumonia

Ri supervisor vs

Upper gastrointestinal motility in health
Upper gastrointestinal motility in health limitations

  • 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)

Ri supervisor vs

  • Chyme into the duodenum limitations 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

Ri supervisor vs

  • 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 humoral mechanisms

  • 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

Ri supervisor vs

  • Delayed gastric emptying is more frequent in: humoral mechanisms


    ☆multiple trauma (with and without head injury)

    ☆severe sepsis

    ►80% head injuries (IICP associated)

    ►Hyperglycemia delays gastric emptying (pre-

    existing DM doesn’t affect)

Ri supervisor vs

Ri supervisor vs

  • High levels of circulating catecholamines commonly seen used for sedation, may impact on gastrointestinal motility 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 critically ill

  • 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 critically ill

  • 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

Ri supervisor vs

critically illWhole 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 critically ill

  • 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 critically ill

  • 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 critically ill

  • Glucose absorption is substantially reduced in the critically ill

  • Fat absorption may also be reduced

  • The reasons for impaired absorption are unclear

Therapeutic options
Therapeutic options critically ill

Cisapride critically ill

  • 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

Metoclopramide critically ill

  • 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

Erythromycin critically ill

  • 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 critically ill

  • 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

Novel drug therapies
Novel drug therapies critically ill

5 ht 4 receptor agonists
5-HT critically ill4 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
μ critically illreceptor 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

Ri supervisor vs

critically illAlvimopan

  • 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 critically ill

  • 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 critically ill

  • 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

Conclusion critically ill

  • 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