19th July – Does Bedside US Measurement of the IVC Diameter Correlate with CVP in the Assessment of Intravascular Volume in Children?

190713 Paper

Where can I find this paper?

http://www.ncbi.nlm.nih.gov/pubmed/23426248

What is this paper about (what is the research question)?

Can we use bedside ultrasound measurement of IVC diameter as a proxy for fluid status (as determined by CVP measurement) in children?

Summary of the Paper

Design: prospective observational study

Objective: to compare bedside US assessment of volume status with CVP measurement in critically ill paediatric patients

Outcomes: correlation of US assessment of volume depletion with CVP assessment

Test of interest: beside US measurement of IVC diameter and calculation of IVC/aorta ratio, defining dehydration as “collapsability index of 50% or greater and an IVC/Ao ratio of 0.8 or less.” Diameter measured in subxiphoid sagittal and subxiphoid transverse views.

Reference Standard: invasive CVP measurement by digital transduction at distal port of previously sited CVC

Participants: convenience sample of patients aged <21y admitted to the Paediatric Critical Care Unit (Intensive Care) at a single centre between July 2010 and June 2011

  • Inclusions: patients requiring invasive haemodynamic monitoring
  • Exclusions: patients in whom US measurement of IVC could not be performed due to technical limitations

Results: 

72 eligible patients of whom 51 enrolled to the study. Sagittal view was obtained in 100%, transverse view in 84% of subjects.

Correlation of collapsibility index and CVP: -0.23 (P=0.11)

Correlation of IVC/Ao ratio and CVP: -0.19 (P=0.22)

Authors’  conclusions

We did not find a correlation between the 1-point measurement of either the collapsibility index or the IVC/Ao ratio and CVP measurements in critically ill paediatric patients.

On the study design

This paper is an interesting one; the use of ultrasound to determine the need for and response to fluid resuscitation is controversial in adult patients, so it is not surprising to see that the uncertainty about clinical usefulness translates to paediatric practice. In addition, assessment of hydration/dehydration in children is notoriously difficult and the search for objective measures which reflect clinical endpoints is clearly relevant.

This paper is an observational study which means that there was no change made to the patient’s care in response to the measured data. The population may or may not reflect our ED patients; by definition, patients already admitted to PICU (at least in the UK) have usually a) been unwell for some time and b) had some level of resuscitation – so it is difficult to know how their volume status might be affected by preceding use of fluid boluses (particularly if hypertonic solutions were used). That said, the vast majority of critically ill paediatric patients in the ED do not have central access amenable to CVP monitoring and there are obvious issues with designing a study which necessitates insertion of CVCs which might not be necessary (unethical) or are going to be inserted in the ED (impractical – numbers likely to be very small). The fact that the recruitment was a convenience sample also reflects the otherwise small numbers and unpredictable nature of critical illness in children and while a more robust sampling method would be preferable, convenience sampling is often seen in studies where a single investigator has a particular skill set necessary for the collection of study data.

A bigger problem is the use of CVP as a marker of haemodynamic status; although it is frequently measured in the ICU and PICU, it is notoriously poor at reflecting volume status as a single measure and demonstrating clinically relevant response to fluid bolus when measured continuously, as raised in this review paper from 2008. So the study is comparing a questionable method of determining fluid status with one which is equally questionable – not exactly a great starting point. Perhaps a longer term outcome – such as fluid balance over the subsequent 24-48h, urine output, need for fluid boluses – might have given a clearer and more reliable picture.

There was also little consistency between the patients; CVC measurement occurred at a variety of anatomical sites and there was no correction or account taken for other variables which might affect CVC readings (such as abdominal surgery or positive pressure ventilation).

What were the results and what does this mean?

This is a great opportunity to revise correlation!

There’s a great wikipedia article on Spearman’s rank correlation coefficient here, but essentially correlation measures the level of interdependence between two non-parametric variables. It tells us whether as one variable increases, the other increases, and the strength of this relationship.

In the paper, both correlation co-efficients quoted in the results section were negative, suggesting that as CVP increases the IVC variable (IVC/Ao ratio or collapsibility index) decreases, and vice versa. The small numbers (-0.11 and -0.23) imply a near random relationship (remember, the nearer the correlation coefficient is to zero the less related the two variables appear to be; the nearer to 1 or -1, the stronger the relationship and the more predictive one variable is of the other). The performance characteristics (sensitivity, specificity, NPV and PPV) for both US-calculated variables were poor.

However, there are very small numbers here; of the 52 children included, only 21 actually had a CVP <8mmHg (the cutoff used by the authors to determine intravascular volume depletion). In any study where such a small number of patient have the target condition we have to wonder whether different patterns might be seen in a larger sample – the probability of a type II error is high.

What can we take from this paper into clinical practice?

So, assessment of paediatric intravascular volume status remains a mystery for now. Previously published studies have suggested that IVC/Ao ratio is lower in children who are otherwise clinically assessed as being dehydrated and that the value rises following fluid boluses, but we cannot be sure from this current paper that US measurement reflects CVP. Should we use ultrasound to assess intravascular status? This paper finds it a poor proxy for CVP – which again is a poor proxy for volume status. So on the basis of this study – no, but there is clearly more work to be done here.

More questions to ask

  • Do serial IVC measurements reflect response to fluid bolus in a clinically meaningful way?
  • Would we see better correlation using a single CVC line site, or excluding “less central” central lines such as femoral CVC?
  • Should we be aggressively fluid-resuscitating children anyway?! – see this interesting FOAM paper on new insights from the FEAST trial

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