Clinical nutrition (Edinburgh, Scotland) · 2015
Gastric feeding intolerance is not caused by mucosal ischemia measured by intragastric air tonometry in the critically ill.
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Streefkerk Jörn O, Beishuizen Albertus, Groeneveld A B Johan
Аннотация
BACKGROUND: Gastric mucosal ischemia may be a risk factor for gastrointestinal intolerance to early feeding in the critically ill.
AIMS: To study intragastric PCO2 air tonometry and gastric residual volumes (GRV) before and after the start of gastric feeding.
METHODS: This is a two-center study in intensive care units of a university and teaching hospital. Twenty-nine critically ill, consecutive and consenting patients scheduled to start gastric feeding were studied after insertion of a gastric tonometry catheter and prior to and after start of gastric feeding (500 ml over 1 h), when clinically indicated.
RESULTS: Blood gasometry and intragastric tonometry were performed prior to and 2 h after gastric feeding. The intragastric to arterial PCO2 gap (normal <8 mm Hg) was elevated in 41% of patients prior to feeding and measured (mean ± standard deviation) 13 ± 20 and 16 ± 23 mm Hg in patients with normal (<100 ml, 42 ± 34 ml, n = 19) and elevated GRV (250 ± 141 ml, n = 10, P = 0.75), respectively. After feeding, the gradient did not increase and measured 27 ± 25 and 23 ± 34 mm Hg, respectively (P = 0.80).
CONCLUSION: Gastric mucosal ischemia is not a major risk factor for intolerance to early gastric feeding in the critically ill.
AIMS: To study intragastric PCO2 air tonometry and gastric residual volumes (GRV) before and after the start of gastric feeding.
METHODS: This is a two-center study in intensive care units of a university and teaching hospital. Twenty-nine critically ill, consecutive and consenting patients scheduled to start gastric feeding were studied after insertion of a gastric tonometry catheter and prior to and after start of gastric feeding (500 ml over 1 h), when clinically indicated.
RESULTS: Blood gasometry and intragastric tonometry were performed prior to and 2 h after gastric feeding. The intragastric to arterial PCO2 gap (normal <8 mm Hg) was elevated in 41% of patients prior to feeding and measured (mean ± standard deviation) 13 ± 20 and 16 ± 23 mm Hg in patients with normal (<100 ml, 42 ± 34 ml, n = 19) and elevated GRV (250 ± 141 ml, n = 10, P = 0.75), respectively. After feeding, the gradient did not increase and measured 27 ± 25 and 23 ± 34 mm Hg, respectively (P = 0.80).
CONCLUSION: Gastric mucosal ischemia is not a major risk factor for intolerance to early gastric feeding in the critically ill.