Sirs, I read the article, ‘Assessment of Fluid responsiveness in the Acute Medical Patient and the Role of Echocardiography’ by Dr Parulekar and Dr Harris with interest. It rightly highlights the challenges posed when assessing for fluid resuscitation in a pressured setting with limited information. This scenario is a routine one for our speciality, which is why it is a concern that the evidence-base outside of intensive care remains limited. Of particular relevance to the Acute Medical specialist, the article acknowledges that performing a focussed-echocardiogram on all acutely-unwell patients is “impractical”. Developing a quick and straightforward approach to fluid resuscitation assessment should be a high research priority for Acute Medicine. However, there are several statements described in the article which warrant correction, particularly as they reflect misconceptions that are rife in the Intensive Care literature: The assumption that fluid responsiveness is equivalent to hypovolaemia: As the article acknowledges, “No suitably powered RCT has assessed the role of stroke volume guided fluid administration as a resuscitation goal.” Furthermore, fluid responsiveness has been demonstrated in healthy volunteers suggesting it may be a normal physiological condition. Even if there was a unanimous agreement for its use, it is currently a poorly-defined concept with no consensus definition. Therefore, significant question marks remain about the diagnostic ability of fluid responsiveness and much work is needed before it can be reliably used as a test for hypovolaemia. 2. The contradiction between the stated utility of IVC measurements and that of CVP: The article states that “IVC [inferior vena cava] size decreases in hypovolaemia” and later notes “a very small collapsing IVC in a shocked patient suggests fluid tolerance”. It goes on to say that “IVC diameter predicts central venous pressure [CVP]”. Then the article contradicts this link by stating that “CVP has little or no role in volume assessment”. The final statement is based on a systematic review in 2008, as acknowledged in the article. The review was updated in 2013. Both compared the ability of CVP to predict fluid responsiveness, however, they did so based on the assumption that fluid responsiveness predicts hypovolaemia. This is far from proven, as discussed above. Therefore, the utility of CVP remains unclear and should be explored along with IVC measurements as a fluid assessment tool. 3. The meaning of the transient response to a fluid bolus: Finally, the article suggests that a “fast response device” should be used to measure cardiac response before and after a passive leg raise, because the subsequent “changes in cardiac output may be transient”. This transient change is not unique to a passive leg raise. The haemodynamic improvements that follow an intravenous fluid bolus are similarly temporary. One study found that cardiac output returned to baseline values 90 minutes after a bolus in fluid responsive patients. Instead of finding a “fast response device” to measure transient haemodynamic improvements, we should be asking if the benefit of fluid resuscitation is also transient, particularly in conditions such as sepsis. We should also question whether rapid fluid boluses cause harm from subsequent oedema, and explore whether this harm persists after the haemodynamic benefit has disappeared. Are we temporarily boosting physiological markers whilst at the bedside, only for the fluid to leak into the interstitium after we have moved on to our next patient? In conclusion, I applaud the authors for the highlighting the important topic of fluid assessment. Despite nearly two centuries of use, the benefits and harms of intravenous fluid are still poorly understood. This is a vital research topic for our speciality, so I hope they will join me and others in addressing the evidence gaps and research questions that are highlighted by this letter. Yours faithfully, Adam Seccombe BSc (Hons) MBChB MRCP (Acute Medicine)
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