It’s rare, devastating and usually totally unexpected: that dreaded call from a parent of one of your patients with type 1 diabetes telling you that their son or daughter has been discovered dead in bed. These are rarely the wild ones who have had multiple admissions with diabetic ketoacidosis because of insulin omission; instead, they are usually below the radar, with neither high nor dangerously low HbA1c.
We’ve known about dead in bed syndrome for at least three decades but the cause has remained a mystery. The Sheffield University research group, led by Professor Simon Heller, has long suspected hypoglycaemia as the cause, but since hypoglycaemia is so common and dead in bed syndrome so rare, this has remained difficult to explain.
The study by Novodvorsky and colleagues (summarised alongside) adds further evidence that hypoglycaemia can be proarrhythmogenic and that the effects on the heart have a diurnal difference, with nocturnal hypoglycaemia causing bradycardia and electrocardiogram changes not seen during daytime episodes.
The case is not proven, but these findings do suggest arrhythmia during hypoglycaemia as a possible cause of dead in bed syndrome. This does not mean that dead in bed syndrome is caused by hypoglycaemia, but it does lead to speculation that some individuals may be more at risk than others. What is clear is that insulin treatment must aim to improve glycaemic control and reduce the risk of microvascular complications, but achieve this without risking daytime and especially nocturnal hypoglycaemia.
We are fortunate that a new generation of basal insulins that reduce this risk is available. We must not limit their use on the basis of cost if there are obvious benefits for the individual with T1D.
To read the article summaries, please download the PDF