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Intestinal insufflation of small volume of oxygen increases systemic oxygenation in acute respiratory distress sуndrome patients

Mazurok, Vadim; Belikov, Vladimir L.; Slivin, Oleg A.

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European Journal of Anaesthesiology: July 2015 - Volume 32 - Issue 7 - p 507-508
doi: 10.1097/EJA.0000000000000146
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Enteral oxygen administration is an old and intriguing technique previously used to treat local gastrointestinal tract disorders or to alleviate toxic effects of halothane anaesthesia.1,2 In this report we present preliminary results of enteral oxygen insufflation on systemic oxygenation.

Ethical approval for this study (ethical committee protocol no. 12) was provided by the local ethical committee of North-Western State Medical University named after I.I. Mechnikov, Saint-Petersburg, Russian Federation (Chairperson Prof Shevyakov), on 2 October 2013.

Twenty-one patients [18 men and three women, average age 48 ±19 years] with severe (five patients) or moderate (16 patients) acute respiratory distress syndrome according to the Berlin definition of different cause (polytrauma, pneumonia, mandibular phlegmon; 16 patients had sepsis criteria) were mechanically ventilated (pressure control ventilation or bilevel modes, FiO2: 0.6 ± 0.1; Pmax: 33 ± 5 cmH2O; positive end-expiratory pressure: 10 ± 3 cmH2O) during 5 ± 1 days before inclusion.

A nasointestinal tube (Ø 2.2 mm, 240-cm tube; Meditec, Saint-Petersburg, Russia, was placed after the ligament of Treitz using endoscopy. Patients with recent surgical anastomoses and gastric ulcers detected during endoscopy were not included. Intra-abdominal pressure was monitored using bladder pressure.3

By means of a 3-way cock, 100% oxygen was insufflated using a 60-ml syringe through a nasointestinal tube. Several boluses were slowly insufflated until intra-abdominal pressure increased by 2 to 3 mmHg. Average initial bladder pressure was 9 ± 2 mmHg, upon completion of oxygen administration 10 ± 3 mmHg. The total insufflated volumes were from 0.8 to 2.4 l, and the total duration of insufflation was 60 to 90 min.

Arterial blood gases were monitored at baseline and at 1, 3, 6, 9, 19 and 32 h after the insufflation. None of the ventilation variables was changed during the insufflation and the evaluation period. Taking into account the pressure regimens used the only flexible ventilation variable was tidal volume. Mean arterial blood pressure did not change significantly before (90 ± 11 mmHg) and after (88 ± 15 mmHg) oxygen administration (P > 0.05). The results are presented as the mean value ± SD. Analysis of variance was used with Holm–Sidak post-hoc test for pairwise comparison between each time point. P < 0.05 was accepted as statistically significant.

The earliest and most notable effect of enteral oxygenation was intestinal peristalsis activation, first described about 40 years ago,4 lasting several hours. Two to three hours after oxygen administration, the ‘inflated’ abdomen returned to its previous shape and the bladder pressure went back to the initial level. Defecation was quite common in the same time period.

PaO2/FiO2 ratio was significantly increased (P < 0.001 on analysis of variance) reaching its maximum 9 h after the oxygen insufflation, and lasting for more than 32 h (Fig. 1).

Fig. 1
Fig. 1:
PaO2/FiO2 dynamics after intestinal oxygenotherapy.

No significant changes in pH, BE, PaCO2, HCO3 dynamics were observed.

We speculate that the increase in systemic oxygenation was not due to direct intestinal absorption of oxygen because the total quantity of insufflated oxygen was definitely not enough for such prolonged improvement of oxygenation. Moreover, we did not observe a dose-dependence effect. So we speculate the existence of some other indirect mechanism(s), such as metabolic effect.

A serious limitation of our study was the absence of a control group.

In conclusion, we observed an increase of systemic oxygenation after enteral insufflation of small volume of oxygen in acute respiratory distress syndrome patients. Nevertheless, further investigations are needed to clarify the mechanisms.

Acknowledgements relating to this article

Assistance with the study: none.

Financial support and sponsorship: none.

Conflicts of interest: none.


1. Gelman SI. The effect of enteral oxygen administration on the hepatic circulation during halothane anaesthesia: experimental investigation. BJA 1975; 47:1253–1259.
2. Gelman SI. The effect of enteral oxygen administration on the hepatic circulation during halothane anaesthesia: clinical observation. BJA 1975; 47:1261–1264.
3. WSACS consensus definitions for IAP measurement
4. Gelman SI, Paz M, Levy E. Influence of enteral oxygen administration on the slow electrical activity of the intestine and stomach. Arch Surg 1976; 111:566–574.
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