Abstract
Gallbladder dysmotility has been implicated as a putative mechanism underlying acute acalculous cholecystitis and lipid malabsorption in the critically ill, despite nutrient-stimulated gallbladder emptying never having been quantified in this population. In health, endogenous cholecystokinin (CCK) stimulates gallbladder emptying.
Highlights
Gallbladder dysmotility has been implicated as a putative mechanism underlying acute acalculous cholecystitis and lipid malabsorption in the critically ill, despite nutrient-stimulated gallbladder emptying never having been quantified in this population
Nutrient-stimulated gallbladder emptying is incomplete during critical illness as assessed by 3D ultrasound
The ejection fraction was less in the critically ill [50[10-82] vs 77[72-82]%; P = 0.01], but there was no difference in the change in gallbladder volume [22[11-32] vs 16[12-20]ml; P = 0.18]
Summary
To determine fasting and nutrient-stimulated gallbladder volumes in critically ill patients
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