Saturday, March 21, 2015

The tremendous impact of sick sick days...

Like every parent, we've previously had our share of sick days: runny nose, flu like syndromes... The type of vague viral infection that doesn't warrant antibiotic therapy. While I always kept an eye on them, just in case, they didn't seem to have a significant impact on Max's BG levels. If they had one, it was lost in our daily variations.

This time was different. Max came back from a school trip in the UK with a runny nose and a slightly sore throat. For the first three days, nothing seemed different from the past innocuous events. Then, on the morning of the fourth day, the symptoms worsened. There was a bit of fever, the cough became rougher and wetter. Most tellingly, perhaps, Max lost interest in his smartphone and started dozing through the day. The time had come for a visit to the family MD and some amoxicillin.

Rough day -1

Here's his BG profile for that day. Slightly higher than our typical profile, but nothing alarming. There is a dawn phenomenon starting a bit earlier than usual, corrected at 3:45 (blood check and re-calibration visible), wake up at 7:00 (the correction was perfect) the breakfast spike, the lunch spike and the dinner spike. The total insulin dose for the day was around 34 units, including the correction, or about 0.64 U/kg.

Rough day

The next day was "interesting", to say the least. Max woke up, decided he was unable to eat and immediately headed for the couch where he basically slept through the day. The slope of the (very early) dawn phenomenon was steeper. The more aggressive correction at 3 AM only had a very short term effect. At 8:00 AM, BG confirmed value was at 250 mg/dL. This is why we decided to dose exactly as if he had eaten even though he had not (5U novo). As soon as that dose had run its course, his BG started to rise again at 11:00. At that point, having seen how resistant the 'high' was, I decided to take a strict control stance. We corrected at 11:15 and then again at 13:30 when it became clear that the BG was staying high despite, again, zero food intake at noon. Around 4:15, Max woke up a bit and moved around, immediately triggering a fall. A single 2 grams glucose tablet was sufficient to prevent what looked like an unavoidable low. And then, BG started its slow rise again, which we corrected again, and again and again.

Total food intake for the day: 2 grams of carbs and lots of water.
Total insulin for the day: 50 units (close to 1 U/kg), a 50% increase.

I thought I knew what to expect...

but to be honest, I was a bit surprised. I expected I would have to keep giving insulin even if food intake was low or non existent. Max is on MDI and I expected the Levemir to keep things relatively under control during what was, after all, a relatively benign infection.

If we had applied a stupid rule such as "no food, no fast acting insulin", my model predicts Max would have shot above 400 mg/dL before noon. I can't be sure it would actually have happened (and had no desire to test) but my model is very often quite accurate, as shown by the perfect correction the day before. Notes: no paracetamol was given at any point, around 1gr of aspirin was used per day for headaches, pre-correction and general levels were checked by BG meter to exclude any eventual sensor inaccuracy.

If I had applied a slightly less stupid rule, such as "keep giving the normal doses even if he does not eat", we would probably have spent the whole day in the 300 mg/dL range and that would have been a problem. Why?

The problem

Well, we have previously established that Max renal threshold is around a fairly 250 mg/dL. Any extended period above that range and glucose starts leaking in his urine. We have also established that somewhere between 250 mg/dL and 300 mg/dL his BG becomes much harder to control, especially if he starts to exercise a bit. Whereas aerobic exercise under 250 mg/dL always leads to a correction, it does not work well between 250 mg/dL and 300 mg/dL and not at all above 300 mg/dL. In that case, we have seen extremely steep increases rather than controlled decreases. This is again expected and fairly typical as acidosis and possibly ketosis show up.

We did test for ketones and had none (thanks to the strict control) but I can't help thinking that, had we taken another course of action or had the information a CGM provides, we would have experienced additional difficulties. The "no food, no bolus" rule, even if we are supposed to be somewhat covered by the morning Levemir, would have almost certainly brought us to the edge of DKA.

I won't dive into the DKA mechanisms in this post but, generally speaking, the vicious circles of acidosis and ionic disturbances are what makes the initial phase of DKA dangerous (correcting too quickly is what makes the correction phase dangerous). Those disturbances can lead to arrhythmias and, at the extreme, sudden death or death in bed.

And that is understandable. Here is a ECG I took from Max, as he was sleeping on the couch. He has a typical rest rate of 60 bpms. At the end of that no-food day, with a body temperature around 38C (fever, but not severe), he was pumping around 125 bpm. It seems to me that, had the fever and acido ketosis been severe, a very real cardiac risk exists even in relatively benign situations.  

It is one thing to read about such risk from a theoretical point of view. But seeing how hard it was to keep BGs in a relatively correct range, despite no food intake and the relative protection of MDI based therapy, real life was an eye opener.

Conclusion - rough day +1, rough day +2

Max has now recovered. Here are the profiles of the two following days. Amoxicillin was effective. Average BG normalized itself progressively Food intake resumed. And we were immediately able to lower the insulin doses back to our normal schedule.

And finally, Friday afternoon, after 72 hours of total or relative inactivity, Max started moving again and we started to see some hypos again. 

To be honest, the whole week that followed the sick week was a bit peculiar. Nothing dramatic, but a recurrent tendency to go in hypo faster than usual. A plausible reason for this would be that
  • the glucose that was mobilized during the sick period had to come from somewhere since it did not come from food.
  • those mobilized reserves had to be rebuild during the recovery period.

Plausible, but speculative at this point as I have no hard science references to explain the phenomenon. Lastly, it seems that Max needed more time to recover fully from that infection than he needed before he became T1D. It is highly subjective: I just noticed his tennis and endurance had taken a big hit when he resumed training.

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