title: Feed intolerance in critical illness is associated with increased basal and nutrient-stimulated plasma cholecystokinin concentrations.
abstract: OBJECTIVE
  Delayed gastric emptying and intolerance to gastric feeding occur frequently in the critically ill. In these patients, gastric motor responses to nutrients are disturbed. Cholecystokinin (CCK) slows gastric emptying. The aim of this study was to determine plasma CCK concentrations during fasting and in response to small-intestine nutrient infusion in critically ill patients.
  
  
  METHODS
  Randomized, controlled trial.
  
  
  METHODS
  Level 3, mixed medical and surgical intensive care unit.
  
  
  METHODS
  A total of 31 mechanically ventilated, critically ill patients (23 men, 51 +/- 3 yrs) and 28 healthy subjects (21 men, 43 +/- 2 yrs).
  
  
  METHODS
  Subjects received two 60-min duodenal infusions of Ensure (complete balanced nutrition), at 1 and 2 kcal/min, in a randomized, single-blind fashion. The nutrient infusions were separated by a 2-hr "washout" period. Blood samples for measurement of plasma CCK concentrations were obtained immediately before and every 20 mins during nutrient infusion.
  
  
  RESULTS
  Baseline and nutrient-stimulated plasma CCK concentrations were higher in critically ill patients compared with healthy subjects (p < .001). The magnitude of the rise in plasma CCK in response to nutrients was also greater in the critically ill (p < .01). Of the 23 patients who received enteral nutrition before the study, nine were intolerant of gastric feeding. In these patients, both the baseline plasma CCK concentration and the magnitude of CCK increase during nutrient infusions were greater than in patients with feed tolerance (p < .002). Impaired renal function was associated with an increased baseline CCK concentration but had no effect on the CCK response to nutrients.
  
  
  CONCLUSIONS
  Both fasting and nutrient-stimulated plasma CCK concentrations are increased in critically ill patients, particularly in those with feed intolerance. This may provide a humoral mechanism for delayed gastric emptying seen in critical illness.
authors.affiliation: Department of Gastroenterology, Hepatology, and General Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
authors.forename: Nam Q
authors.initials: NQ
authors.lastname: Nguyen
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Fraser
authors.forename: Marianne J
authors.initials: MJ
authors.lastname: Chapman
authors.forename: Laura K
authors.initials: LK
authors.lastname: Bryant
authors.forename: Richard H
authors.initials: RH
authors.lastname: Holloway
authors.forename: Rosalie
authors.initials: R
authors.lastname: Vozzo
authors.forename: Judith
authors.initials: J
authors.lastname: Wishart
authors.forename: Christine
authors.initials: C
authors.lastname: Feinle-Bisset
authors.forename: Michael
authors.initials: M
authors.lastname: Horowitz
mesh_terms: D018806:APACHE; D000328:Adult; D000704:Analysis of Variance; D002766:Cholecystokinin / Q000097:blood*; D016638:Critical Illness / Q000628:therapy; D019422:Dietary Sucrose / Q000008:administration & dosage*; D004386:Duodenum / Q000503:physiopathology; D004750:Enteral Nutrition / Q000009:adverse effects / Q000379:methods; D005215:Fasting / Q000502:physiology*; D025461:Feedback, Physiological; D005260:Female; D005526:Food, Formulated; D005746:Gastric Emptying / Q000502:physiology*; D005767:Gastrointestinal Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D005769:Gastrointestinal Motility; D006801:Humans; D007441:Intubation, Gastrointestinal; D007674:Kidney Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D007902:Length of Stay / Q000706:statistics & numerical data; D008297:Male; D008657:Metabolic Clearance Rate; D012121:Respiration, Artificial; D016037:Single-Blind Method; D013997:Time Factors
chemical_list: D019422:Dietary Sucrose; C082131:Ensure formulated food; D002766:Cholecystokinin