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Acute complications in children with type 1 diabetes

In this topic:
Diabetic ketoacidosis
Algorithm for the immediate assessment and management of diabetic ketoacidosis (DKA) in children
(Figure 5.6)
Hypoglycaemia

Diabetic ketoacidosis
Diabetic ketoacidosis is a medical emergency requiring urgent hospital admission.
Diabetic ketoacidosis (DKA) is a medical emergency that requires hospital admission and intravenous fluid,
electrolyte, and insulin therapy. There are many different approaches to managing DKA in children. This section
provides one approachdifferent institutions may have varying local protocols.
An algorithm summarising the immediate assessment and management of DKA is shown in Figure 5.6.
In a child with DKA, fluid replacement should start immediately, before insulin therapy. Rapid rehydration increases
the risk of precipitating acute cerebral oedema, which has a high mortality rate. Urgent consultation with an expert in
paediatric diabetes is essential. Volume expansion (resuscitation) is required only if needed to restore peripheral
circulation.
Fluid and electrolyte replacement has to take into account:

child's body size

calculated losses of water, sodium, potassium and chloride

need for maintenance fluids

addition of glucose when the blood glucose concentration approaches 14 to 17 mmol/L, or sooner if the fall
in blood glucose concentration is precipitous.

There is always a total body deficit of potassium, even if serum potassium concentrations are normal or high at
presentation. Bicarbonate therapy is required only in extreme circumstances and may increase the risk of cerebral
oedema.
Short-acting insulin should be given by intravenous infusion, titrated against the response of hourly finger-prick blood
glucose concentrations. Use:

short-acting insulin 0.1 units/kg/hour by continuous IV infusion (see Table


5.4 for insulin formulations).
When oral intake of food and fluid is well tolerated and acidosis has resolved, convert insulin to a
subcutaneous multiple daily injection (basalbolus) insulin regimen.

Cerebral oedema is an uncommon (less than 1%) but serious life-threatening complication of managing DKA in
children. Risk factors include:

younger age

newly diagnosed diabetes and longer duration of symptoms

greater hypocapnia at presentation

increased serum urea concentration

more severe acidosis

attenuated rise in measured sodium during therapy

greater volumes of fluid given in the first 4 hours.

Early signs that cerebral oedema is developing are a falling serum osmolality, headache, and irritability or an altered
conscious state. While serum osmolality is the main risk factor, in practice often the corrected sodium concentration
[Note 1] is used as a surrogate marker of serum osmolality. Therefore the goal is to keep the corrected sodium
concentration stable during treatment.
Late signs of cerebral oedema are bradycardia, increased blood pressure and depressed respiration.
Patients should be nursed in an intensive care setting with neurological assessment that includes neuroradiological
imaging. Intubation and ventilation may be required.
Treat cerebral oedema when suspecteddo not delay treatment while waiting for confirmatory neuroimaging if
cerebral oedema is diagnosed on clinical grounds. Treatment involves lowering the rate of fluids being administered,
along with:

mannitol 20% 1.25 to 5 mL/kg (= 0.25 to 1 g/kg) IV as a bolus dose over 20


minutes. This can be repeated in 2 hours if there is no initial response
OR

sodium chloride 3% 5 to 10 mL/kg IV over 30 minutes.

Algorithm for the immediate assessment and management of diabetic ketoacidosis


(DKA) in children (Figure 5.6)
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Initial assessment of diabetic ketoacidosis

Management of diabetic ketoacidosis after initial


assessment

ECG = electrocardiogram; ICU = intensive care unit; IV = intravenous; NG


= nasogastric; SC = subcutaneous
Adapted with permission from Wolfsdorf J, Craig ME, Daneman D, Dunger
D, Edge J, Lee W, et al. Diabetic ketoacidosis in children and adolescents
with diabetes. Pediatr Diabetes 2009;10 Suppl 12:118-33. John Wiley &
Sons A/S.

Hypoglycaemia
Hypoglycaemia is of particular concern in children with diabetes who are younger than 5 years. This is because of its
potential to cause seizures, and children's greater susceptibility to brain injury, including seizure disorder and
intellectual damage. This is especially so when the child is unable to adequately recognise and communicate the
symptoms of hypoglycaemia to carers. Young people with diabetes should always have immediate access to glucose
tablets or sweets.
When treating hypoglycaemia, if the child is conscious and cooperative, use:

glucose 10 to 20 g, orally (see below for examples).


The following products in specified quantities contain 10 to 20 grams of glucose and are appropriate for use in
conscious and cooperative children with hypoglycaemia:

1 glass of oral glucose solution (eg Lucozade)

180 mL of juice (a small glass or small popper or box)

180 mL of soft drink (not 'diet')

1 tablespoon of honey

1 tablespoon of glucose gel

10 to 20 grams of easily absorbed carbohydrate (eg jelly beans).

If the child is unconscious, use:

glucagon (less than 25 kg) 0.5 mg SC or IM


or glucagon (25 kg or more) 1 mg SC or IM.
Once the child is conscious, oral feeding may start.
If the child is unconscious and in hospital, use:

glucose 10% 2 mL/kg IV as a bolus over a few minutes, until blood glucose
concentration normalises (more than 4 mmol/L)
FOLLOWED BY
sodium chloride 0.45% with glucose 5% IV (maintenance fluids), at

maintenance rate to prevent further hypoglycaemia. Increase concentration


of glucose in fluid if necessary to maintain a blood glucose concentration
above 4 mmol/L.
Using glucose 50% has caused deaths in children due to hyperosmolality. For this reason, glucose 10% is
recommended in children.

Note 1: Corrected sodium concentration = measured sodium concentration + (0.3 [blood glucose concentration
5.5]) (all concentration units in mmol/L)

Related topics:
Management of type 1 diabetes in children
Chronic complications
Key references for this topic:
Topic
Key references for this chapter

Revised October 2013. Thera

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