Diabetic emergencies in children

Published on 23/06/2015 by admin

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10.2 Diabetic emergencies in children

Kam Sinn

Essentials

1 Diabetes mellitus is one of the most common chronic diseases in childhood.
2 The incidence of childhood diabetes has been increasing over the last decade.
3 Diabetic ketoacidosis is defined as BGL >11 mmol L−1, pH < 7.3 and bicarbonate <15 mmol L−1.
4 As obesity becomes more prevalent in childhood, type II diabetes has started to present in younger and younger adolescents.
5 Type I diabetes remains the major (>90%) cause of childhood diabetes.

Diagnosis

The classic symptoms of polyuria, polydipsia and weight loss may be present for a few weeks before parental concern is raised.

The diagnosis should be confirmed by a random blood glucose level (BGL >11 mmol L–1) in addition to urine analysis for glucose and ketone.

Once the diagnosis is confirmed, initial management is dictated by the severity of dehydration, presence of shock, degree of acidosis, hyperglycaemia and osmolality.

In a child with no past history of diabetes the initial diagnosis may be misled by non-specific symptoms such as abdominal pain, weight loss, drowsiness, fever, secondary enuresis and dyspnoea. Beware of tachypnoea due to metabolic acidosis, intercurrent infection in a new diabetic, abdominal pain related to diabetic ketoacidosis (DKA) and drowsiness in a child. In such children, diabetes should be excluded as a possible cause with a random blood glucose.

Diabetic ketoacidosis

Diabetic ketoacidosis is the major cause of mortality in diabetic children. It often presents in newly diagnosed type I diabetic children. In established diabetics, it occasionally presents in the midst of intercurrent febrile illness or poor adherence to management.

Diabetic ketoacidosis is caused by insulin deficiency, leading to hyperglycaemia, osmotic diuresis, hyperosmolar dehydration, lipolysis, ketosis and acidosis. It may be defined by the combination of:

• hyperglycaemia;
• ketosis and ketonuria;
• acidosis (pH < 7.3, bicarbonate <15);
• dehydration and/or shock.

Management starts with rapid assessment, resuscitation and meticulous replacement of fluid, electrolyte and insulin infusion.

Like all medical emergencies, assessment of airway, breathing and circulation (ABC) is vital. Ketotic breath, degree of tachypnoea and respiratory distress should be noted. Degree of shock or dehydration should be assessed. Initial level of consciousness should be noted, and hourly neurological observation commenced. It is also important to look for a focus of infection and sepsis.

Initial investigations should include venous blood glucose, electrolytes, urea, creatinine, full blood count, venous or arterial blood gases. In addition, if sepsis is suspected, blood culture, urine culture and chest X-ray may be considered.

Resuscitation

Intravenous access should be established; ideally with two intravenous (IV) cannulae so that further venous sampling of BGL and electrolyte may be undertaken easily.

In children with shock, noted to be hypotensive and poorly perfused, resuscitation should start immediately with facial mask oxygen and intravenous fluid bolus. Normal saline (0.9% Na Cl) 10 mL kg–1 should be given as a bolus. The normal saline bolus (10 mL kg–1) should be repeated if the child remains shocked upon reassessment in 10 minutes.

Careful and frequent monitoring should continue for the next 24–48 hours. Monitoring should include all vital signs, including neurological assessment, urine output and ECG monitoring.

Fluid

After the initial resuscitation, IV fluid consisting of maintenance fluid and deficit replacement should be calculated and replaced over 48 hours. The child’s degree of dehydration should be assessed clinically, including an accurate weight.

The calculation of maintenance fluid is based on the child’s weight or surface area.

Dehydration in the form of deficit in percentage of body weight would allow calculation of an estimated volume to be replaced over the next 48 hours. Maintenance and deficit replacement should be given as normal saline (0.9% Na Cl) until the BGL falls to 12–15 mmol L–1. Once the BGL falls to 12–15 mmol L–1, the IV fluid should be changed to half normal saline with glucose 5% (0.45% Na Cl with 5% glucose).

Beware of giving deficit replacement too rapidly, which decreases intravascular osmolality and may contribute towards cerebral oedema.

Insulin

Insulin infusion should only be started after shock has been resuscitated with normal saline intravenously as above. The BGL would fall rapidly during the resuscitation phase with fluid replacement alone.

Insulin infusion with short-acting insulin (soluble or regular) should be started with maintenance IV fluid. An initial bolus of insulin is not recommended, as it may reduce the BGL and osmolality too rapidly. The infusion is made up by diluting soluble or regular insulin in normal saline to a concentration of 1 U mL–1, to be given in an electronic IV syringe pump. The infusion is started at a rate of 0.05–0.1 U insulin kg–1 hr–1. The insulin infusion rate can be titrated to achieve a fall in BGL of 4–5 mmol hr–1.

Once the BGL falls to the normal range (5–10 mmol L−1), the insulin infusion should continue until the child is ready to change over to subcutaneous insulin. As DKA is caused by Type I diabetes, the insulin infusion should not be stopped or decreased in rate of infusion below 0.05 U kg–1 hr–1 until subcutaneous insulin can be started, despite a normal BGL. Insulin is required to suppress lipolysis and clear ketosis. If there is a concern about hypoglycaemia, the glucose concentration in the maintenance IV fluid can be increased from 5% up to 10%.

The change over from IV insulin to subcutaneous insulin is often most conveniently performed at mealtime, when the child is no longer acidotic, is alert and able to tolerate an oral meal. At such time, rapid- or short-acting insulin can be given subcutaneously before a meal; the insulin infusion should continue during the meal and then cease 30 minutes after the meal.

Potassium

The initial serum potassium may be high, normal or low, despite a low total body potassium. Potassium replacement should be given intravenously once resuscitation is completed and there are no ECG changes of hyperkalaemia, anuria or severe renal impairment.

The measured serum potassium goes up by 0.6 mmol L–1 for every 0.1 drop in pH. As the acidosis gets corrected with fluid resuscitation and insulin, serum potassium will drop rapidly in exchange for H+ ions.

The potassium requirement may be as high as 4–5 mmol kg–1 day–1 in the first 24 hours. Initially, potassium chloride 40 mmol is usually added to each litre of normal saline for replacement. It is important that serum electrolyte is checked frequently every 2 to 4 hours in the first 12 to 24 hours of DKA management.

Sodium

Serum sodium is a major determinant of osmolality. Rapid change and fall in serum sodium should be avoided to minimise the risk of cerebral oedema. The measured sodium is initially affected by hyperglycaemia.

The corrected sodium can be calculated by:

image

If there is hypernatraemia with a corrected serum sodium >150 mmol L−1, rate of rehydration should be slowed down further to 72 hours, to minimise rapid changes in osmolality and fluid shift.

Bicarbonate

Bicarbonate is not indicated despite metabolic acidosis. Bicarbonate may increase central nervous system acidosis and worsen hypokalaemia and hypernatraemia. Blood gas should be repeated at frequent intervals if the initial pH is below 7.1.

Phosphate

Serum phosphate is often low initially. It is controversial whether replacement of phosphate makes any difference to outcome.

Complications

Approximately 0.5% children develop cerebral oedema as a complication of DKA. The warning signs are changes in level of consciousness, irritability, headache, cranial nerve palsies and seizures. Treatment includes slowing the rehydration infusion, IV mannitol, intubation and assisted ventilation.

Careful and close observation of vital signs, frequent review of clinical status and laboratory values of BGL, electrolytes, and acid–base status are vital in the first 24–48 hours of DKA to minimise complications.

Hypoglycaemia and hypokalaemia can be minimised by frequent monitoring of BGL and electrolytes, followed by the adjustment of rehydration fluid and insulin infusions.

Hypoglycaemia

Hypoglycaemia is a common complication in all diabetics. Education and ongoing support for the diabetic child and his/her family is the key to preventing and managing hypoglycaemia when it does occur.

Hypoglycaemia can be caused by insulin excess (e.g. ‘honeymoon period’), overdose of oral hypoglycaemic (in type II diabetes), intercurrent illness (e.g. gastroenteritis), vigorous exercise and other metabolic/endocrine disorders (e.g. Addison’s disease).

Hypoglycaemia is often defined as a BGL <2.5 mmol L–1. However, symptoms of hypoglycaemia may appear with a BGL <4.0 mmol L–1 in a diabetic. Therefore, the level of BGL in a child with diabetes should be maintained above 4 mmol L–1.

Hypoglycaemia may cause symptoms related to neuroglycopenia and autonomic activation.

In mild to moderate cases, where the patient remains conscious, treatments include ingestion of rapidly absorbed simple carbohydrate such as sugar or fruit juice, followed by more complex carbohydrate and medical review of the cause of the hypoglycaemia.

In severe hypoglycaemia, the patient may present with seizure or coma. Treatment includes stabilisation of airway, breathing and circulation.

• If IV access is available, 2–5 mL kg–1 of glucose 10% can be given as an IV bolus.
• If IV access is not available; intramuscular or deep subcutaneous infusion glucagon should be given.

The dose of glucagons is 0.5 U (0.5 mg) for children up to 8 years of age and 1 U (1 mg) for older children and adolescents.

In the recovery phase of severe hypoglycaemia, close monitoring of BGL, medical review of insulin dosage, diabetic control, IV infusion of glucose-containing crystalloid solution and/or additional oral complex carbohydrate would be required.

In all children with diabetes, education for the parents, patient, teachers and other carers on symptoms and management of hypoglycaemia, sick-day management, and the availability and use of glucagons are vital.

Some form of wearable identification (e.g. Medic-Alert bracelet) for the child would also help in the management of hypoglycaemic coma.

Long-term management

The key to good long-term management of children with diabetes is a team and holistic approach to education for the affected child and his/her parents.

Regular medical review of insulin dosage, diet, exercise, medium-term control and complications should be undertaken with a paediatrician, diabetic educator and dietician. It is beyond the scope of this chapter to deal with the details of long-term management of childhood diabetes.

Further reading

Australasian Paediatric Endocrine Group for the Department of Health and Ageing. Clinical practice guidelines: Type 1 diabetes in children and adolescents. 2005. Available from http://www.chw.edu.au/prof/services/endocrinology/apeg/apeg_handbook_final.pdf [accessed 19.10.10]

National Collaborating Centre for Women’s and Children’s Health. Type 1 diabetes diagnosis and management of type 1 diabetes in children and young people. 2004. Available from http://www.nice.org.uk/nicemedia/live/10944/29394/29394.pdf [accessed 19.10.10]

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