Management of Ben's condition
Okay, so the most likely diagnosis here is DKA (or diabetic ketoacidosis). This is often how a new diagnosis of Type 1 (insulin dependant) Diabetes presents, as the dehydration develops due to a build up of ketones.
When we initially met Ben, his dad was mainly concerned about the abdominal pain, vomiting and the problems with breathing. The breathing problems should alert you to a diagnosis other than the obvious ones suggested by the abdominal pain and vomiting (gastroenteritis, possible appendicitis). Heavy breathing may of course be caused by things like chest infections and asthma, and a nasty chest infection (pneumonia) can cause abdominal pain and vomiting; but thinking more broadly about why he is breathless is important.
Later on, Cam managed to get the history of excessive drinking in the weeks leading up this illness and this is an important clue that should immediately make you think of diabetes as a cause. Abdominal pain is a common presentation of children with early DKA. If you add to this the history of thirst and the breathlessness due to the patient being acidotic you arrive at your diagnosis. A simple bedside blood sugar test will help confirm the diagnosis.
Now Ben doesn’t look too unwell, and I think he has been caught early before he deteriorates. In DKA, build-up of ketones leads to acidosis and, as the patient becomes more acidotic, their symptoms become more severe. If Ben had presented a day or two later he would likely be very unwell, tachycardic (high heart rate) and tachypnoeic (fast breathing rate) with grossly acidotic breathing (deep sighing respirations). Children in this state will often have an altered conscious level.
So let’s look at the fluid bolus that Ben was given. Patients who are acidotic will generally be tachycardic and in severe DKA, have evidence of poor perfusion. But these children have lost total body water (severe dehydration) rather than the situation of reduced circulating volume which leads to shock. Until the acidotic state is corrected, their physiological parameters will not change. We know that giving fluid boluses to children with DKA can increase the risk of one of the most serious complications, cerebral oedema (brain swelling). Children can be shocked with DKA (if the episode was triggered by an infection and they have associated sepsis for example) but in most cases they are not.
So the take-home message in children with DKA is that fluid boluses will not usually be indicated (and definitely not in Ben’s case, as his condition was not too serious), based just on tachycardia alone.
If the blood pressure is normal it makes sense to get them to the nearest appropriate ED for further management. Of course if they have a blood pressure in their boots, a careful fluid bolus makes sense but I would definitely not give more than 10 ml/kg without having a chat with someone on the phone first (ring ahead to the hospital for advice).
The biggest risk factors for developing cerebral oedema are the age of the child (younger children are at grater risk) and how acidotic they are (the more acidotic they are the greater risk there is). In a child with DKA who develops signs of possible cerebral oedema (headache, worsening conscious level), go for a head up tilt and transfer to hospital following a pre alert.