Metoclopramide improves gastric motility

Sir: Dr. Jooste and colleagues have shown that metoclopramide improves gastric emptying in a miscellaneous group of critically ill patients [1]. In common clinical practice, however, prokinetic drugs are considered a therapeutic option only in patients who demonstrate gastric intolerance, as demonstrated by phenomena such as large nasogastric aspirates, reflux, or vomiting. While we acknowledge that the relationship between large gastric aspirates and decreased gastric motility is still speculative [2], it would be much more relevant to assess the efficacy of metoclopramide in critically ill patients who have been demonstrated
clinically to have impaired gastric emptying. The likelihood of these patients having markedly impaired gastric emptying of a magnitude sufficient to cause clinically detectable gastric intolerance is uncertain, although we acknowledge they may have impaired gastric emptying relative to normals. Factors previously shown to be associated with impaired gastric emptying include being critically ill (Simplified Acute Physiology Score 9.5 ± 3), older age and female sex, opiate use [3], dopamine [4], and other drugs such as anticholinergics. Apart from opiate and inotrope use, the authors give little information regarding these factors. The paper by Dr. Jooste et al. therefore does not address the relevant clinical question: Does metoclopramide improve gastric emptying in patients with gastric stasis or gastric feed intolerance?

Assuming that blood paracetamol levels accurately reflect gastric emptying, the magnitude of the difference between the two groups is not substantial when compared with the control group's standard deviation [metoclopramide group 1387.2 ± 560.4 (mean ± SD); saline group 994 ± 623.6]. While the authors have shown a statistically significant increase in the AUC 120 (area under the curve over 120 min) in patients given metoclopramide, we would question the clinical significance of this result.

Lastly, in patients with documented gastric intolerance, we have noticed that the use of 1.5 g paracetamol is frequently associated (25% of cases studied) with detectable serum levels of paracetamol 24 h after the first dose. We would be interested to know whether the authors experienced this problem, and, if so, how did they compensate for this phenomenon (which we believe is merely a consequence of prolonged gastric emptying).

In conclusion, we believe that "the administration of intravenous metoclopramide improved gastric emptying in a heterogeneous group of critically ill patients" may have been shown in this study, that 'metoclopramide is a useful prokinetic drug in this patient population" has yet to be demonstrated.