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GIFTASUP: A Missed Opportunity?

Volume 10, Number 2, April 2009 JICS 90 The great comparative anatomist and advocate of evolution, Thomas Henry Huxley stated that ‘every great advance in natural knowledge has involved the absolute rejection of authority.’ One wonders how such an individual would view the current world of evidence-based medicine, where guidelines and protocols are the norm in an attempt to standardise practice. The question that one must always ask, however, is ‘are we standardising good practice?’ And so to the recent development of the ‘British consensus guidelines on intravenous fluid therapy for adult surgical patients’ (GIFTASUP), which have been adopted as a clinical practice guideline by the Intensive Care Society and the Association of Surgeons of Great Britain and Ireland. The authors must be commended for taking on such a monumental endeavour; however one must question whether or not the production of generic recommendations on fluid management for the myriad of surgical procedures and pathologies encountered in patients from a multitude of demographic backgrounds is actually achievable. To tackle such an issue requires a comprehensive and balanced review of all aspects of assessment and management so that the treating clinician can make a rational, individualised regimen for each patient. While this document reviews many of the issues, it is not always comprehensive or balanced in its approach, producing often predictable recommendations given the authorship. For example, the emphasis and approach to assessing patient ‘volume status’ is logical and well established in much clinical practice. However, the management aspect is very much based on the approach of fluid loading according to increases in cardiac output or stroke volume. It is worth considering that in healthy euvolaemic individuals given an intravenous fluid bolus, stroke volume and cardiac output increase. However they weren’t in need of the fluid bolus; they were euvolaemic! Just because we can increase flow by fluid loading doesn’t mean we should. There are relatively recent studies (with the usual limitations) that throw this conventional fluid philosophy on its head.1 Yet these are not quoted in the review. This philosophy of ‘just because we can, doesn’t mean we should’ can also be applied to the practice of ‘goal-directed therapy’ using fluids and inotropes. Indeed, there is a paradox in the clinical evidence between patients who need to be ‘driven’ versus those who need to be beta-blocked in order to achieve improved clinical outcome. It is a shame that this paradox is neither mentioned nor implied in the recommendations. Indeed, it is hard to believe from the text that the area is controversial at all. It is a missed opportunity that the document fails to provide a comprehensive insight into the current problems and future progress of intravenous fluids with respect to their ‘ingredients’. The headline to recommendation 1 expounds the risks of hyperchloraemic acidosis. However, while evidence points increasingly clearly towards the harmful effects of hyperchloraemia, the same cannot be said of acidosis.2 When we look at the evolution of cellular energetics, we see that acidosis was present in our progeny cells about two billion years ago. Indeed, multicellular organisms have evolved around acidosis rather than the other way round, which makes the concept of acidosis causing direct harm seem a little tenuous. Transient mild-to-moderate acidosis is part of our normal daily life! Consideration of the ideal buffer takes us into far more interesting territory. While lactate also plays a part in our normal physiology, we are developing an increasing recognition of its complexity as an energy shuttle, buffer of intracellular acidosis and intermediate in numerous metabolic and biochemical pathways.3 Less is known about acetate, but given the many common metabolic pathways it shares with lactate, it is likely that there is still much to be elucidated. Given that these substances are metabolically active, there is a surprising paucity of studies examining the metabolic consequences of exogenous administration. There are isomeric issues. Lactate exists predominantly as an L-isomer in its natural physiological form, with the accumulation of D-lactate known to be associated with metabolic and clinical problems.4,5 We still continue to administer racemic lactate in our current intravenous fluids. We also remain ignorant of the metabolic effects of administering lactate in the absence of its ‘redox partner’ pyruvate.6 Exogenous acetate has been associated with increased oxygen utilisation,7 detrimental cardiovascular effects,8 uncoupling of oxidative phosphorylation,9 increased IL-1 production (more than chloride),10 and detrimental effects on cellular energetics.9 It is interesting that these compounds (in their racemic forms) appear to be becoming the mainstay buffers of our current intravenous fluids. These studies highlight the need for considerable focus on these potentially highly active ingredients in future clinical studies. On a more positive note, the nutrition review is concise and guides the way to modernising local starvation and perioperative nutrition policies, although to effect such change requires considerable systemic alterations (such as precise scheduling of operations), which may counter the current process trends for the surgical ‘conveyor belt.’ It will be interesting to see whether it is the clinical or system-related outcomes that are the greater drive for patient care in our ‘modern’ NHS. This document comprehensively states a position of where we are currently. In many respects, it highlights how little we know given the extensive period over which we have been using intravenous fluids. Many of the quoted studies, although GIFTASUP: a missed opportunity?