APACHE = Acute Physiology and Chronic Health Evaluation; ICU = intensive care unit; MI = myocardial infarction; SMART = Systemic MediatorAssociated Response Test.

Available online http://ccforum.com/content/6/4/295

The glutton digs his grave with his teeth

Anonymous English proverb

Over the past few months yet more information bombards us.Several papers have concentrated on nutrition and markersthereof, in an attempt to make sense of much data.

Current interest in blood glucose levels focuses on examiningpatients’ glucose tolerance to predict outcomes. This isparticularly pertinent to high-dependency and coronary carepractice, as well as intensive care unit (ICU) work. TheDIGAMI study highlighted the long-term post-myocardialinfarction (MI) risk in patients with a deranged glycometabolicstate [1]. Similarly, the intensive care population has beenscrutinized with regard to glycometabolic control in septiccritically ill patients. Strict glycaemic control in suchindividuals is now hopefully commonplace, with the aim ofimproving survival. This has prompted much work todelineate those individuals with impaired glycometaboliccontrol, and the same group presented further evidence thatabnormal glucose metabolism is associated with a highprevalence of acute MI [2]. A total of 181 consecutivenondiabetic patients admitted with acute MI were givenstandard glucose tolerance testing at discharge and3 months later. Fewer than 35% of patients had normalglucose tolerance at 3 months of follow up. It would appearlikely, then, that early detection of impaired glycometaboliccontrol might improve outcome by allowing introduction ofsecondary preventative measures. This probably has littleimmediate relevance to the ICU, but for those of us who areinvolved in coronary care it is worthwhile bearing in mind thatan HbA1c on admission may well indicate long-term risk andis a relatively quick and inexpensive test.

Nutritional support is often regarded as the Cinderella of theintensivist’s armamentarium, probably because it does notgenerate the same excitement as the latest test forinflammatory mediators or suchlike. However, rather liketoothache, it is best not ignored. Intense debate continues asto the preferred route of administration. The recent report byMontejo and colleagues [3] does little to help. A prospectiverandomized study comparing the efficacy and complicationsof early jejunal versus gastric feeding was undertaken in asample group of some 101 ICU patients who were deemedto need enteral nutrition for more than 5 days. Interestingly,the sample group comprised fewer than 6% of patientsadmitted to the 14 centres involved, with more than 12%being given mandatory total parenteral nutrition. Little overalldifference between the two groups was identified, which inpart may be explained by the small numbers involved. Asexpected, the jejunal route resulted in significantly lowerresidual volume, but this did not translate into higher volumesof diet or indeed increased caloric intake, principally becauseof increased frequency of tube-related complications (i.e.occlusion, withdrawal [accidental] and displacement). Forthose of us who have struggled with nasogastrojejunal tubes,some solace is found within this paper. Furthermore, therewas no difference in the incidence of nosocomial pneumoniain the two groups, again possibly reflecting the numbersstudied. The authors point out that the study shows that thetranspyloric tube is as useful as a nasogastric tube for earlynutrition in the critically ill. One may argue that this implies alot more effort for little or no benefit. No doubt further studieswill address this. The alternative is of course to befriend anamenable surgeon.

An alternative approach to accelerate recovery ofgastrointestinal motility may be effective salt and waterbalance. In a study by Lobo and colleagues [4], prompted by

CommentaryRecently published papers: We are what we eat?LG Forni

Consultant, Worthing General Hospital, Lyndhurst Road, Worthing, West Sussex, UK

Correspondence: Lui G Forni, Lui.Forni@wash.nhs.uk

Published online: 9 July 2002 Critical Care 2002, 6:295-297This article is online at http://ccforum.com/content/6/4/295© 2002 BioMed Central Ltd (Print ISSN 1364-8535; Online ISSN 1466-609X)

Critical Care August 2002 Vol 6 No 4 Forni

animal models, 20 patients were randomized to standardpostoperative intravenous fluids (at least 1 litre 0.9% NaClplus 2 litres 5% dextrose per day) or restricted sodium andwater intake (2 litres of water plus 77 mmol sodium per day).Those in the restricted group showed significantly improvedsolid-phase and liquid-phase gastric emptying times onpostoperative day 4, as well as a reduction in loosely definedcomplications and in hospital stay. Although intriguing, thatstudy is open to several criticisms. Those in the restrictedgroup were managed remotely from those offered standardtreatment, and fluid input was managed solely by one of theinvestigators. The standard treatment implied little thought asto volume balance, which I am sure was not the case. Also,the elegant studies on gastric emptying were incomplete inthe standard group. It may well be that other units approachthe problem of postoperative ileus in a different manner,utilizing epidural analgesia, laparoscopic surgery and earlymobilization to improve results. The authors also suggestedthat moderate restriction of salt and water may benefit somecritically ill patients. Although this may be the case in a fewinstances, there is considerable evidence that earlyaggressive volume resuscitation in septic patients can havedramatic effects on mortality. As such I would take their lastcomments with a pinch of brine! For those interested, abalanced view to this work is provided by Heyland andPaterson [5].

An interesting alternative with respect to volume resuscitationwas recently described. Horstick and colleagues [6]subjected rats to volume-controlled haemorrhagic shock andexamined the mesenteric microcirculation as well as otherparameters following resuscitation with similar volumes ofeither 20% albumin infusion or 0.9% NaCl. A significantimprovement in global haemodynamics was found, togetherwith an improvement in the microcirculation, when albuminwas used as the resuscitation fluid. Clearly, the albumin storycontinues to run but, as Horstick and colleagues pointed out,this experimental scenario is vastly different from that which isoften encountered clinically, and not surprisingly they suggesta need for further experimentation and clinical studies.

Albumin is also the subject of a recent study reported by Yapand coworkers [7]. They retrospectively studied more than1000 patients over an 18-month period, their hypothesisbeing that serum hypoalbuminaemia may be predictive ofmortality risk in the critically ill. This was no doubt triggeredby the Acute Physiology and Chronic Health Evaluation(APACHE) III as well as the study reported by McCluskeyand colleagues [8]. Unlike the latter study, Yap andcoworkers failed to show that serial measurement of albuminwas as accurate as APACHE II in predicting outcome,although they agreed that serum albumin is associated withacute physiological illness and mortality. They pointed outthat their data suggest that serum albumin is a poor predictorof hospital mortality, and the referees should becongratulated on publishing relatively negative results.

Another surrogate of nutritional and overall health status ishaemoglobin concentration. An observational studyconducted in over 2000 patients who underwent coronaryartery bypass surgery [9] examined in-hospital mortality withrespect to haemoglobin concentration. The crude mortalityrate was five times higher among patients with ahaemoglobin of 100 g/l or less. The authors concluded thatcomorbidity probably had the greatest effect on outcome, asindicated by the reduced haemoglobin levels. There was noevidence to support perioperative correction of anaemia. Nodoubt studies will soon be focused on the use oferythropoietin preoperatively.

Acute sepsis and markers thereof continue to provide muchexcitement, although the prognostic value of certain markerssuch as procalcitonin remain in doubt. Claeys and colleagues[10] studied procalcitonin in septic patients and tried todetermine its relationship with more conventional markers,including C-reactive protein and white cell count. Individualswith septic shock (n = 53), as defined by the AmericanCollege of Chest Physicians Consensus, were studied. Allpatients had elevated procalcitonin and C-reactive proteinlevels within 24 hours of diagnosis. However, baseline valueswere of no predictive value. Indeed, single measures ofprocalcitonin did not discriminate between survivors andnonsurvivors when examined within the first 5 days ofadmission. There was some evidence that time-dependantchanges in procalcitonin may provide an earlier indicator ofsurvival, but equally other nonquoted variables such asinotrope usage, fractional inspired oxygen, or indeed bloodpressure may be just as good pragmatically.

Continuing the procalcitonin story, yet another article onproinflammatory cytokine clearance using continuousvenovenous haemofiltration was reported [11]. Curiously, thispaper infers that procalcitonin is an important clinicalprognostic marker in septic patients, which is rather at oddswith the findings described above. Using an AN69membrane, concentrations of the inflammatory mediatorsmeasured were significantly reduced, but in keeping withother studies this effect was decreased after 12 hours,probably reflecting progressive membrane saturation. Onepoint that this paper does highlight is that clearance of suchmediators is entirely membrane dependent. Whatimplications do those findings have for the use of continuousvenovenous haemofiltration in sepsis? My personal view isthat the jury is still out. If one views the circulation as thedumping ground for cytokines, one wonders whether suchremoval has any effect at the cellular level.

Finally, what predictions can be made in critically ill patients?In intensive care we are blessed with a variety of scoringsystems of varying complexity, most of which predict mortalitywith similar efficacy. To date, scoring systems have not beenparticularly good at predicting the events that determine ICUmortality, such as the development of organ failure. Slotman

[12] described a multivariate predictive model imaginativelydescribed as the SMART (Systemic Mediator AssociatedResponse Test) system. In an impressively thrifty manner, heused the data obtained from the placebo arm of a phase IIIclinical trial. An impressive array of data had been collected,including interleukin-6, interleukin-8 and granulocyte colony-stimulating factor levels, which were used randomly todevelop a training cohort (200), the further 103 data setsbeing used to provide prospective validation. Through usingthe training cohort, multivariate models were developed topredict acute respiratory distress syndrome, renalinsufficiency, hepatobiliary dysfunction and disseminatedintravascular coagulation, as defined according toestablished criteria. The aim of such a SMART model couldbe to predict the development of organ dysfunction, and inthe future it may enable tailored therapies to be introducedearly. The author points out valid criticisms of the model andhighlights some of its limitations. However, he should becommended. With the growth of fully automated clinicalinformation systems, it may not be too long before SMART-like models, allied with clinical judgement (hopefully!),become commonplace in ICUs. ‘He that would know whatshall be, must consider what hath been’ (quotation: Fuller T[1654–1734]). Slotman has taken that advice, and we waitto see what the future brings.

Competing interestsNone declared.

References1. Malmberg K, Norhammer A, Wedel H, Ryden L: Glycometabolic

state at admission: important risk marker of mortality in con-ventially treated patients with diabetes mellitus and acutemyocardial infarction: long-term results from the diabetes andinsulin-glucose infusion in acute myocardial infarction(DIGAMI) study. Circulation 1999, 99:2626-2632.

2. Norhammar A, Tenerz A, Nilsson G, Hamsten A, Efendic S, RydenL, Malmberg K: Glucose metabolism in patients with acutemyocardial infarction and no previous diagnosis of diabetesmellitus: a pospective study. Lancet 2002, 359:2140-2144.

3. Montejo JC, Grau T, Acosta J, Ruiz-Santana S, Planas M, Garcia-De-Lorenzo A, Mesejo A, Cervera M, Sanchez-Alvarez C, Nunez-Ruiz R, Lopez-Martinez J; Nutritional and Metabolic WorkingGroup of the Spanish Society of Intensive Care Medicine andCoronary Units: Multicenter, prospective, randomized, single-blind study comparing the efficacy and gastrointestinal com-plications of early jejunal feeding with early gastric feeding incritically ill patients. Crit Care Med 2002, 30:796-800.

4. Lobo DN, Bostock KA, Neal KR, Perkins AC, Rowlands BJ, AllisonSP: Effect of salt and water balance on recovery of gastroin-testinal function after elective colonic resection: a randomisedcontrolled trial. Lancet 2002, 359:1812-1818.

5. Heyland DK, Paterson WG: Fluid restriction for postoperativepatients? [Comment]. Lancet 2002, 359:1792-1793.

6. Horstick G, Lauterbach M, Kempf T, Bhakdi S, Heimann A, Hor-stick M, Meyer J, Kempski O: Early albumin infusion improvesglobal and local haemodynamics and reduces inflammatoryresponse in hemorrhagic shock. Crit Care Med 2002, 30:851-855.

7. Yap FHY, Joyn GM, Buckley TA, Wong ELY: Association ofserum albumin concentration and mortality in critically illpatients. Anaesth Intensive Care 2002, 30:202-207.

8. McCluskey A, Thomas AN, Bowles BJM, Kishen R: The prognos-tic value of serial measurements of serum albumin concen-tration in patients admitted to an intensive care unit.Anaesthesia 1996, 51:724-727.

9. Zindrou D, Taylor KM, Peder Bagger J: Preoperative haemoglo-bin concentration and mortality rate after coronary arterybypass surgery. Lancet 2002, 359:1747-1748.

10. Claeys R, Vinken S, Spapen H, ver Elst K, Decochez K, HuyghensL, Gorus FK: Plasma procalcitonin and C-reactive protein inacute septic shock: clinical and biological correlates. Crit CareMed 2002, 30:757-762.

11. Dahaba AA, Elawady GA, Rehak PH, List WF: Procalcitonin andproinflammatory cytokine clearance during continuous ven-ovenous haemofiltration in septic patients. Anaesth IntensiveCare 2002, 30:269-274.

12. Slotman GJ: Prospectively validated prediction of physiologicvariables and organ failure in septic patients: The SystemicMediator Associated Response Test (SMART). Crit Care Med2002, 30:1035-1045.

Available online http://ccforum.com/content/6/4/295