Saturday 14 April 2012

Presentation

Velvety stellated leaves
Leaves, Wisley, August 2011
My presentation on Re-feeding Syndrome (RFS) went very well, although if I were to do it again I would make a few changes. The audience was small, and all were doctors. Last week was when all the junior doctors changed to a different department on rotation, so there were five brand new doctors in attendance, with their consultant and clinical educator who is one of my favourites. To be honest, any doctor that knows who I am is one of my favourites, but this one has been particularly helpful and welcoming.

The consultant kicked off by giving the new doctors a bit of information about how their placement was going to work, and then I was introduced by the registrar as a Senior Dietitian. I had to explain that despite my appearance I am actually a very Junior Dietitian, only two months old in Dietitian Years.

I embarked on the presentation, which I had been given ready-made by one of the senior Dietitians in the department, saving me no end of time in putting something together. I'd tweaked it a little bit, but not much. It wasn't designed for such a medical audience, so I had to supplement it with some hard facts about treatment, and then we talked a bit about how to manage ward procedures to cope with any patients who actually were at high risk of RFS.

So what exactly is Re-feeding Syndrome? It's "a potentially lethal derangement of blood electrolytes (potassium, phosphate, magnesium and sometimes others) caused by a switch to carbohydrate metabolism from fat and protein metabolism."

What that means in ordinary language is that in normal circumstances we use mainly carbohydrate for energy, adding to or removing from fat reserves if carb intake doesn't match energy expenditure. We don't store a whole lot of carbohydrate - I believe that when marathon runners hit the 'wall' it's when their stored glycogen is used up. For normal people, it would take about two days. After that, our metabolism switches to using mostly fat for energy, which works pretty well as a substitute, as you might expect. When the fat is gone (and to some extent, before the fat is gone) we turn to protein for energy, turning muscles into fuel.

The problem in RFS happens when carbohydrate intake starts up again, and metabolism switches from burning fat/protein to carbs. If the interruption was only a few days, and the individual was not underweight or malnourished to start with, then there's no problem. If it's a particularly thin person who hasn't eaten for more than 5 days (and there are a few other more obscure risk factors) then the risk rises with the rate of feeding. What actually happens is that energy generation using glucose starts up inside cells, which sucks the materials it needs out of the blood to make ATP for energy. The concentration of these electrolytes and vitamins in the blood drops, leading to potentially fatal consequences.

There are not many acute life-threatening conditions that a Dietitian encounters, so there is a good deal of emphasis on RFS in the Dietetics degree. I assess every patient I am asked to see, and if RFS is a possibility I will indicate it in every way I can - in the medical notes, nursing notes, and to the medical and nursing staff on duty.

The main approach for prevention of the Syndrome is to take great care not to feed the patient too much too quickly, and provide them with vitamin supplements. Monitoring the success of the approach is generally by way of monitoring levels of potassium, phosphate and magnesium in the blood, and replacing these if they drop. It is highly unlikely that someone will succumb following ordinary eating and drinking, but much more likely if they have had a period of no oral intake followed by tube feeding, as in the case of a stroke that has disrupted the process of swallowing, for example.

The way we manage tube feeding is that I write down the rate of delivery of the feed and the number of hours it should be given. On each successive day my regimen shows a slightly increased rate of feeding, and in someone at high risk, it is important to check blood results before the rate is increased. The main issue we face is that while I produce the feeding regimen, the nurses actually control the delivery of feed, and the doctors order blood results and review them. At the point when the rate of feeding increases, I definitely won't be there, but the nurse setting up the feed should check that a doctor has reviewed the blood results and approves the increase in feed rate. I wonder if this has ever happened. Mostly, I imagine, we've been lucky and nobody has died.

At the meeting, after I'd done my lecture, I presented this problem and asked for suggestions. The best that we could come up with was the liberal use of a highlighter pen in notes and other records to ensure that the risk is not overlooked, and checkboxes to be ticked to try and ensure that blood results are reviewed appropriately. I have two potential re-feeders at the moment, so we'll see if it makes any difference.

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