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Risk of bloodstream infection can be strongly decreased by a very moderate caloric intake or strongly increased by a very low caloric intake in severely ill patients in intensive care?

T he publication of Dr. Rubinson and colleagues (1) in this issue of Critical Care Medicine opens an important element of discussion: In severely ill patients in intensive care, an increase in bloodstream infections (BSIs) was only observed with a very low-level caloric intake ( 25% of guidelines, about 6 kcal/day). In contrast, with a caloric intake 25% of guidelines, the rate of BSI was low and didn’t change with higher caloric intake (25–100% of guidelines). In fact, although prospective, this study analyzes the consequences to the risk of bacteremia of very different nutritional practices, according to patients and physicians, without clear explanation and justification of therapeutic choices. Clearly the methodology used cannot give an absolute reply to these results, and the authors admit it. Nevertheless, disturbing questions are asked. The authors tried, by a statistical approach, to eliminate a maximum of confounding factors and bias. Some points merit discussion and question. First, we are surprised than the authors could collect four groups of patients with apparently the same severity of illness but receiving such different caloric intakes in a same unit. The nutritional supply is known to be very variable in intensive care units, and recommendations rarely are correctly followed for several reasons (2–5). Vigilance frequently is inadequate concerning the nutritional component of care, which is often pushed to the background in light of hemodynamic, infectious, and respiratory disturbances (2, 4). Moreover, in the past year, the level of caloric intake has been discussed with contradictory conclusions. In the acute phase of multiple-organ failure, hypocaloric intake has been recommended to reduce the risk of metabolic complications, but nevertheless recommendations are rarely 14 kcal/day (6). The consequences of inadequate caloric intake are rarely obvious for a patient with multipleorgan failure. The high level of glycemia in this situation leads to a restriction in glucose infusion. The consequences of high levels of glycemia on mortality rate have recently intensified this approach (7), but some works are conflicting (8). The route of administration also has to be considered. The enteral route often involves a caloric intake that is lower and delayed due to digestive intolerance (3, 4, 9, 10). According to meta-analysis, it seems that early enteral nutrition is associated with a lower incidence of infectious complications (11) and contributes to less immunosuppression (12), but conversely early enteral nutrition with high level of calories was followed by an increase of infectious complications compared with a control group who received enteral nutrition with only 20% of calories (13). In a large study, no difference was observed between enteral and parenteral nutrition on septic morbidity (14). The debate is always present. The first finding of the study of Dr. Rubinson and colleagues (1) would be that severely ill intensive care patients care rarely receive an adequate caloric intake and even often receive a very small quantity. Two surprises are associated with this finding. It is only if the caloric intake was 25% of recommendations than a drastic increase of rate of BSI was observed. An intake just above 25% would be sufficient to obtain a “normal” rate of BSI and there would appear to be no benefit, at this point, to increase the level of caloric intake. Second, a change in the level of caloric intake would modify the rate of bacteremia as early as 2 days. We could conclude that a very low caloric intake (about 400–500 kcal/day) would be sufficient to avoid an increase of infectious risk but that a lower intake drastically increases risk after only 2 days. We must emphasize that during the 1,420 study days, the patients did not receive any nutritional supply during 23.6% of days and that the group with low caloric intake had a significantly greater number of days without nutrition. These conclusions must be prudent for several reasons. The use of BSI, like pertinent criteria of infectious risk, can be questionable. The criteria for this diagnosis actually are debatable, although this is less true for bacteremia with Staphylococcus epidermidis, the microorganism largely isolated in primary BSI in the study of Dr. Rubinson and colleagues (1) (half of cases). Bloodstream infection is a relatively rare nosocomial infection in intensive care and is not an absolute reflection of the rate of nosocomial infection in a unit. We do not know the rate of other nosocomial infections that are better indicators of the onset of immunodepression, and nosocomial pneumonia can be a source of bacteremia. The high rate of nosocomial BSI (22.5% of patients), primary in 61% of cases, in the population studied is surprising (15, 16), although it is a group of severely ill patients with multiple organ failure and multiple parenteral access for heavy treatment. Moreover, the parenteral nutrition was less used than enteral nutrition in the study of Dr. Rubinson and colleagues (1). Enteral nutrition was given alone during 55.8% of days, whereas parenteral nutrition alone was given during only 16.6% of days. In fact, the intravenous access was probably largely used to give other medications, and the role of nutrition in the risk of BSI was secondary. We cannot exclude that a small amount of nutrients given by the enteral route can reduce the rate of BSI by intestinal translocation. In the group with a low caloric intake and high rate of BSI, use of the enteral route was very low. *See also p. 350.