Type 1 diabetes in children

Overview

Type 1 diabetes (DM1) is the commonest endocrine disorder of childhood. It results from autoimmune destruction of the insulin-producing beta cells of the pancreatic islets, leaving the child permanently insulin-dependent. Onset in children is more acute than in adults and often follows an infection; many children first present in diabetic ketoacidosis (DKA). Good care needs insulin, diet, monitoring and a trained family.

Definition and diagnostic criteria

Diabetes is a chronic disorder of carbohydrate, protein and fat metabolism due to insulin lack, marked by hyperglycaemia and glycosuria. Any one of the following (repeat if there are no symptoms):

Classification

Epidemiology and genetics

• Peaks at 5 to 7 years and at puberty (Akbar).
• Siblings or children of a diabetic: risk about 2 to 8% (Akbar: 5%); identical twin: about 30 to 50%.
• HLA region on chromosome 6 is the strongest genetic factor; over 90% of children with DM1 carry HLA DR3, DR4 or both. Carrying both raises risk most.
• Possible environmental triggers: viruses (Coxsackie B, mumps, rubella, cytomegalovirus), early cow's milk or cereal exposure, vitamin D deficiency. Breastfed infants have a lower rate.
• It is not caused by diet or the child's nutrition.

Pathophysiology

• Mainly a T cell-mediated autoimmune attack. Antibodies appear months to years before symptoms: islet cell antibodies, insulin autoantibodies, anti-GAD (glutamic acid decarboxylase), anti-IA-2. More antibodies = higher risk.
• Symptoms start when about 80 to 90% of beta-cell mass is gone.
• Postprandial hyperglycaemia appears first, then fasting hyperglycaemia.
• Glucose above the renal threshold (160 to 190 mg/dL) spills into urine, causing osmotic diuresis (polyuria, salt and potassium loss) and thirst.
• Cells starved of glucose: hunger (polyphagia), breakdown of fat and muscle, weight loss, growth slowing.
• With more complete insulin lack, fatty acids are turned into ketones (beta-hydroxybutyrate, acetoacetate, acetone), leading to ketoacidosis.

Clinical features

• Polyuria, polydipsia, polyphagia and weight loss (classic tetrad).
• Nocturia or new bedwetting in a child who was dry.
• Recurrent infections and candidiasis.
• Often DKA is the first presentation: dehydration, vomiting, abdominal pain, Kussmaul breathing, fruity breath, drowsiness or coma (see the DKA chapter).

Investigations

• Blood glucose (fasting or random) and HbA1c.
• Urine: glycosuria, ketonuria.
• If unwell: electrolytes, venous blood gas (low pH and bicarbonate in DKA); haemoglobin and haematocrit may be high from dehydration; leucocytosis.
• Islet autoantibodies (anti-GAD, insulin, islet cell) support type 1; C-peptide response helps in suspected type 2.
• Baseline screening for associated autoimmune disease: thyroid function, coeliac serology.

Management

The team: doctor, diabetes nurse educator, dietitian, and psychologist or social worker. Goals: normal growth and an active life, no acute crises, and control good enough to reduce long-term complications.

Insulin types

Daily insulin dose

Regimens

1. Basal-bolus (multiple daily injections), the commonest modern regimen

• 30 to 50% of the total dose as long-acting basal insulin (glargine or detemir) once daily, often at bedtime.
• The rest as rapid-acting insulin with each meal, matched to carbohydrate and correction needs.
• Most flexible, but needs many injections and carbohydrate counting.

2. Twice-daily split-mixed regimen (common in our setting)

• Total dose: two-thirds intermediate (NPH), one-third short-acting (regular).
• Two-thirds of the day's dose is given before breakfast; the remaining third goes before the evening meal.
• Needs fixed meal times: 3 meals and 3 snacks, constant carbohydrate.

3. Insulin pump

• Continuous subcutaneous rapid insulin with boluses at meals; for motivated families. With no depot insulin, pump failure can quickly lead to DKA.

Glucose-based adjustment and the sliding scale

• Extra regular or rapid insulin is added when a reading is above target, using a sliding scale that sets a dose for each glucose band; the scale is written by the treating team.
• Nelson describes two rules used with basal-bolus regimens:
  • Correction (sensitivity) factor = 1800 ÷ total daily dose: the fall in glucose (mg/dL) from 1 unit of rapid insulin.
  • Insulin-to-carbohydrate ratio = 450 ÷ total daily dose: grams of carbohydrate covered by 1 unit.

Diet

• Normal, balanced diet adapted from the household diet, with enough calories for growth.
• Akbar: about 55% carbohydrate, 15% protein, 30% fat; Nelson: carbohydrate 50 to 65%, protein 12 to 20%, fat under 30% with saturated fat under 10%.
• Mostly complex carbohydrates, high fibre, avoid refined sugar.
• Regular meals and snacks; a bedtime snack for those on evening NPH.

Exercise

• Encouraged daily; it lowers insulin needs and improves control.
• Take extra carbohydrate or reduce insulin around exercise to prevent hypoglycaemia.

Education for child and caregivers

• Simple explanation of diabetes; insulin types, storage, injection technique and timing.
• Home glucose monitoring; urine or blood ketone testing.
• Recognising and treating hypoglycaemia; glucagon use.
• Sick-day rules: never stop insulin; test ketones when glucose is over 250 to 300 mg/dL, with fever, vomiting or illness.
• Education is repeated and adapted as the child grows.

Monitoring

Glucose targets (Nelson)

• Test before each meal and at bedtime, and at 2 to 3 am if night lows or unstable morning readings are suspected.
• HbA1c every 3 months (4 times a year): it reflects mean glucose over the past 2 to 3 months. Falsely unreliable in haemoglobinopathies (use fructosamine).

Clinic follow-up checklist

Growth (height and weight on charts), puberty, blood pressure, injection sites (lipoatrophy), HbA1c, diet, school progress, joint mobility, and fundus examination.

Complications

Acute

1. Hypoglycaemia

• The commonest complication of insulin therapy; Akbar defines it as glucose under 60 mg/dL in a diabetic child.
• Causes: too much insulin, missed or late meal, extra exercise.
• Adrenergic signs: sweating, tremor, tachycardia, hunger, anxiety. Neuroglycopenic signs: headache, behaviour change, confusion, visual change, seizures, coma.
• Mild: quick-acting oral sugar (glucose tablets or gel, juice), then a snack.
• Severe (fits, unconscious): intramuscular glucagon at home; intravenous glucose in hospital (Nelson: 2 mL/kg of 10% dextrose for emergency treatment).
• Hypoglycaemia unawareness occurs in about a quarter; strict avoidance of lows for 2 to 3 weeks can restore warning symptoms.

2. Diabetic ketoacidosis: see the DKA chapter.

3. Hyperosmolar state: very high glucose (over 600 mg/dL), dehydration and drowsiness with little ketosis.

4. Brittle diabetes: wide swings between hypo- and hyperglycaemia despite dose changes.

Morning hyperglycaemia

Chronic (long term)

• Microvascular: retinopathy, nephropathy (microalbuminuria first), neuropathy.
• Macrovascular: later heart attack and stroke.
• Rarely clinical before 10 to 15 years of diabetes.
• Growth failure, delayed puberty, and emotional problems with poor control.
• Infections: boils, candidiasis, urinary infection.
• Lipoatrophy at injection sites.
• Associated autoimmune disease: thyroiditis, coeliac disease, Addison disease, IgA deficiency.

Honeymoon period

• After starting insulin, surviving beta cells recover partly, so insulin needs fall and glucose is easy to control.
• Usually starts in the first weeks, lasts 3 to 6 months, and can last up to 2 years.
• It is temporary; insulin must not be stopped.

Long-term outcomes

• Intensive control (frequent testing, multiple injections or a pump) reduces retinopathy, microalbuminuria and neuropathy (large reductions shown in the Diabetes Control and Complications study), at the cost of more hypoglycaemia.
• In young children, whose developing brain is more vulnerable to low glucose, less tight targets are accepted.

Quick revision

• Autoimmune beta-cell loss; HLA DR3/DR4; anti-GAD, insulin, islet antibodies.
• Peaks 5 to 7 years and puberty; twin risk 30 to 50%.
• Fasting 126 or more; random 200 or more with symptoms; OGTT 200; HbA1c 6.5%.
• Polyuria, polydipsia, polyphagia, weight loss, bedwetting; DKA often first.
• Start about 0.5 to 1 U/kg/day; puberty 1 to 2 U/kg/day; honeymoon less.
• Twice-daily: 2/3 morning, 1/3 evening; each 2/3 NPH, 1/3 regular.
• Basal-bolus: 30 to 50% basal; 1800 and 450 rules.
• HbA1c every 3 months; yearly thyroid, microalbumin, eyes.
• Somogyi = night low then rebound; dawn = GH surge.
• Hypoglycaemia: oral sugar; glucagon IM; IV 10% dextrose.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

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