Welcome back to the tasty morsels of critical care podcast.
Sometimes the tasty morsels are exam sized snippets of my knowledge on a given topic. More frequently they are literally all I know on the subject. Today’s topic of parenteral nutrition is a good example of this. I have no doubt there is a lot more I should know about what goes into those plastic shrouded bags at the end of the bed but I am afraid I do not.
Firstly, indications. From our point the overall message should be that we use PN when we fail to establish enteral nutrition. The definition of when we have failed to establish EN is a little less well defined, but comes in somewhere around the 5-7 day mark. In real life clinical practice we often start much earlier , particularly when the surgeons feel that the gut, or perhaps more accurately, the anastamosis mightn’t handle it.
In terms of complications, the maintouted one has been infection, with a long standing belief that PN increases the risk of sepsis. This is probably not true. However the need for central access on an ongoing basis does certainly increase the risk of line related infections but it does seem unfair to blame the PN for that.
The bogey man of refeeding syndrome rears its head in particular in relation to PN as the insulin that has lain dormant for so long in the starved patient finally comes out to play and cause havoc as the body moves from catabloism to anabolism. Again, this may not be due to PN specifically and maybe more reflects the fact that the calories are actually delivered in PN as opposed to calories being aspirated up the NG every 4-6 hrs in enteral nutrition.
There is a NAGMA or hyperchloraemic metabolic acidosis described that is associated with PN and may be caused by the amino acid solutions it contains. One to add to the list of NAGMA causes for me.
Hypercapnoea, causing a resp acidosis and hyperventilation is described as “overfeeding” in PN and I think I have seen this once but more commonly this tends to crop up on the data interpretaton section of any fellowship exam. If too many calories (eg >4mg/kg/min of glucose in the septic patient) are delivered then the body will covert these to lipids. This is a CO2 generating process and may contribute to difficulty weaning or tachypnoea driven by a high CO2.
LFTs are frequently monitored and are frequently abnormal and are frequently ignored. That being said there are a variety of potential issues with PN and LFTs, in particular, hepatic steatosis, intrahepatic cholestasis, and biliary sludge are all an issue. Unfortunately most of these are already common in the critically ill and would be hard to tease out which is which.
In terms of what is actually in the bag, while you can get pre made bags, in reality the composition is determined by the super clever dieticians in the units I’ve worked in.
Calories can come from any of the components (eg carbs or lipids) but the energy split is typically 70:30 carb:lipid with the carbs being generally 50% dextrose. Lipids are a more concentrated way of providing energy and can avoid some of the hyperglycaemia, though there is apparently concern for an immunosuppression effect. As I’m sure you already know the lipids are typically provided from intralipid – the magic white stuff we use when we give too much local anaesthetic. The required nitrogen comes from l-amino acids solutions. It will also include some tasty vitamins (though thiamine, folate and vit k are particuarly prone to depletion)
There are a number of important nutrition trials that occurred early in my career before I was really paying attention. LITFL has a good summary but my TLDR is that there is insufficient evidence to say PN is better than EN for now we go enterally when we can and parenterally when we can’t.
Oh’s Manual Chapter 96
From Twitter, after publishing, Lisa, one of my excellent dietician colleagues, added a grerat summary of the guidelines that you can access here.