Type 1 diabetes and diabetic ketoacidosis in children

• Type 1 diabetes in children is an autoimmune disease in which the insulin-producing beta cells of the pancreas are destroyed, leaving an absolute deficiency of insulin. It cannot be prevented by diet, exercise or any lifestyle change presently known. ^[1][4]
• The classic picture is weeks of polyuria, polydipsia (often nocturnal enuresis in the young), polyphagia, weight loss and lethargy; children under 5 may have no symptoms except enuresis, so a high index of suspicion is needed.
• Diabetic ketoacidosis (DKA) is the life-threatening presentation. It is diagnosed by glucose above 11 mmol/L with acidosis (blood pH below 7.3 or plasma bicarbonate below 15 mmol/L) and ketonaemia (blood beta-hydroxybutyrate above 3 mmol/L). ^[1]
• In DKA the first treatment is fluid, not insulin: restore the circulation, then give insulin at 0.05 to 0.1 units/kg/hour one to two hours later. Insulin boluses are not given. ^[1][4]
• Cerebral oedema can occur in the first 24 hours of treatment. An unexplained headache, agitation, a falling heart rate or a rising blood pressure during DKA should be treated immediately with mannitol or hypertonic saline.
• Long term, a basal-bolus insulin regimen, an HbA1c target of 48 mmol/mol or lower (6.5%), real-time continuous glucose monitoring for every child, and sick-day rules are the standard of care.

By the end of this page you should be able to:

1. Recognise the presentation of type 1 diabetes in children of different ages, including those who present in DKA.
2. Define DKA and HHS in children, grade the severity of DKA, and explain why shock must be distinguished from acidosis-induced vasoconstriction.
3. Plan the first hours of DKA management: fluids (bolus, total requirement, composition and rate), insulin, potassium, glucose and monitoring.
4. Recognise and treat cerebral oedema in DKA, and explain why it can occur even with optimal care.
5. Set up long-term care: insulin regimen and dose, blood glucose and HbA1c targets, monitoring, sick-day rules, hypoglycaemia management and screening for complications.
6. Describe how DKA prevention and low-resource practice differ from ideal practice.

Type 1 diabetes is different from type 2 diabetes. In type 2 diabetes the child usually has obesity and insulin resistance and may retain substantial pancreatic insulin secretion; type 1 diabetes is defined by the near-total loss of insulin secretion. In practice NICE recommends that diabetes in a child is assumed to be type 1 unless there are strong indications of type 2 disease, such as obesity, a strong family history, an origin from a high-risk ethnic group, or a need for little or no insulin after the remission phase.^[1] Other types exist, such as monogenic diabetes and neonatal diabetes, and are considered when diabetes presents in the first year of life or behaves atypically.^[1]

Diabetic ketoacidosis (DKA) is the acute metabolic emergency of diabetes. In DKA absolute insulin deficiency causes hyperglycaemia, unrestrained lipolysis and ketone production, metabolic acidosis, osmotic diuresis and dehydration.^[4] Without treatment it progresses to coma and death.

Hyperglycaemic hyperosmolar state (HHS) is a related but different emergency that is more typical of type 2 diabetes: extreme hyperglycaemia and hyperosmolality with little or no ketosis or acidosis. Children can have a mixed picture, and that overlap matters because it changes fluid and insulin therapy.^[2]

T1D is the most common endocrine or metabolic disorder of childhood and adolescence. Incidence varies greatly by geography and genetics: annual rates of roughly 15 cases per 100,000 in the United States and 13.5 per 100,000 in the United Kingdom have been reported, with the highest rates in Scandinavia (Sardinia about 34.4 per 100,000; Finland about 40 per 100,000) and the lowest in many Asian and African populations.^[4] Incidence rates appear to have at least doubled in many countries over the last two decades.^[4]

The onset has a bimodal pattern, with peaks at 6 to 8 years and again during puberty; onset in the first year of life is unusual and there is no consistent sex predominance.^[4] Onset is seasonal, with a peak in the colder months.^[4]

DKA remains common at diagnosis. In Europe and North America between about 15% and 70% of children present with DKA at the onset of type 1 diabetes, and several countries have reported recent increases.^[2] In the United Kingdom, DKA accounts for roughly 2,700 admissions per year, of which about a quarter are in children with newly diagnosed diabetes.^[3] In resource-limited settings late presentation in DKA is the rule rather than the exception and is the most important driver of mortality in childhood diabetes.^[4]

Type 1 diabetes is not inherited in a simple Mendelian fashion, nor is it caused by sugar. It arises when an environmental trigger acts on a genetically susceptible person. The HLA class II region on chromosome 6 carries the strongest genetic risk (about half of the genetic contribution), and monozygotic twin concordance is only 30 to 50%, which shows that genes are not the whole story.^[4] Environmental triggers postulated to initiate beta cell damage include certain viruses (enteroviruses, mumps, rubella, cytomegalovirus, coxsackie B) and possibly early dietary exposures; episodes of intercurrent illness often precede clinical presentation.^[4]

Autoimmune markers (islet cell antibody, glutamic acid decarboxylase antibody, insulin antibody, IA-2 antibody) are present in most if not all children at diagnosis, but about 90% of beta cells must be destroyed before clinical disease appears.^[4] Because insulin deficiency develops gradually, the illness can be present biochemically long before it is noticed clinically.

Identified risk factors for DKA are mainly related to delay:

• younger age (under 5 years), in whom symptoms are few and easy to miss; ^[4]
• missed or delayed diagnosis, particularly in children without a family history of diabetes; ^[2]
• intercurrent illness; and
• in children with known diabetes, failure to give insulin, most often because of incorrect sick-day management, adolescence-related non-adherence, or pump infusion set failure. ISPAD states that DKA in a child with established diabetes is almost always due to failure to administer insulin.^[2]

Understanding why each symptom appears makes the illness easy to reason about.

Pancreatic beta cells secrete insulin, which is the hormone that moves glucose into cells and suppresses fat breakdown and ketone formation. When beta cells are destroyed, insulin falls and the counter-regulatory hormones (glucagon, cortisol, adrenaline and growth hormone) rise. Three consequences follow, in this order.^[4]

1. Hyperglycaemia and osmotic diuresis. Without insulin, glucose cannot enter muscle and fat, so it accumulates in the blood. Once the renal threshold for glucose is exceeded, glucose spills into the urine and drags water with it. The result is polyuria, nocturia, dehydration and secondary polydipsia. The child "passes through" urine (the original meaning of diabetes) and drinks to compensate.^[4]
2. Weight loss and ketosis. Without insulin, cells are starved of glucose despite high blood levels, so fat and protein break down. Fat breakdown releases free fatty acids, which the liver converts to ketone bodies (beta-hydroxybutyrate and acetoacetate). Ketones appear in urine and blood; their accumulation produces metabolic acidosis. The child loses weight even though appetite is often increased (polyphagia), and may develop vomiting.^[4]
3. Kussmaul breathing and coma. The acidosis is partly compensated by deep, rapid breathing (Kussmaul respiration), and acetone gives the characteristic "pear drops" or fruity breath. Coma, when it occurs, is the result of the combined effect of ketosis, acidosis, dehydration and hyperosmolality.^[4]

This explains the classic symptom cluster and why a child who is mildly ill one day can be dangerously acidotic the next: each of the three processes accelerates once the counter-regulatory hormone response is established.^[4]

The classical presentation of type 1 diabetes is polyuria, polydipsia, polyphagia and weight loss with lethargy.^[4] Other clues include recurrent or prolonged infections (urinary, skin, respiratory), candidiasis of the groin and flexures, anorexia, constipation, blurred vision and poor concentration. In children under 5 the only symptom may be new or worse nocturnal enuresis, which is easy to mistake for a behavioural issue and is the reason that this age group is at particular risk of presenting late in DKA.^[4] Onset may be acute, precipitated by an intercurrent illness, or insidious over weeks or even months.^{[4] [1]}

Children who are already diabetic and present unwell may have euglycaemic DKA, particularly if they continue to take some insulin or have a prolonged illness; a normal glucose does not exclude DKA.^[1]

Look for the consequences of the pathophysiology rather than for the disease itself:

• dehydration: dry mouth and reduced tears, sunken eyes, poor skin turgor, tachycardia, hypotension, reduced urine output;
• Kussmaul breathing (deep and rapid) and the acetone smell;
• weight loss and failure to gain weight, which in younger children may present as growth faltering;
• signs of hyperosmolality or raised intracranial pressure in severe DKA: bradycardia, hypertension or anisocoria, which are red flags for cerebral oedema.^[4]

A 9-year-old girl has had two weeks of drinking large amounts and passing urine every hour, including at night. She has lost 4 kg. Her mother thought it was a urinary tract infection. She now has abdominal pain and is breathing deeply and quickly. A finger-prick glucose is markedly raised (well above 11 mmol/L). This is not gastroenteritis: the abdominal pain and vomiting in DKA are real but arise from acidosis and ketosis.^[1][4]

The most useful question in a child with new polyuria and polydipsia is whether the cause is diabetes mellitus or something else (diabetes insipidus, high intake, renal disease), and once diabetes is likely whether it is type 1 or type 2.

Other distinctions that matter:

• Type 2 diabetes in an overweight adolescent with acanthosis nigricans and a strong family history can present without DKA, but such patients may still be in DKA at presentation, so do not rely on body habitus to exclude DKA.^[1]
• Monogenic and mitochondrial diabetes are considered when diabetes appears before 1 year of age, when there is no autoimmunity suggested by other features, or when the course is atypical.^[1]
• Stress hyperglycaemia is short-lived (1 to 5 hours) after acute illness, returns to normal without insulin and is not accompanied by ketonaemia.^[4]
• If a child with known diabetes has vomiting, abdominal pain, fast breathing, dehydration or reduced consciousness, think of DKA even with a normal glucose, and check blood ketones.^[1]

DKA is diagnosed clinically and biochemically, not radiologically. At presentation measure:

• capillary or venous glucose (finger-prick is enough at first contact);
• blood ketones (beta-hydroxybutyrate) if a near-patient method is available, otherwise urine ketones;
• pH and bicarbonate (capillary or venous blood gas);
• electrolytes (sodium, potassium, urea, creatinine);
• a full clinical assessment of level of consciousness, heart rate, blood pressure, temperature, respiratory rate and hydration.^[1]

NICE recommends that after a child with suspected or known DKA arrives in hospital the full set above is measured and recorded, and an intravenous line is established.^[1] Consider a near-patient ketone method for rapid diagnosis and monitoring.^[1]

For a child who is not in DKA, diagnosis of diabetes should be confirmed using the WHO plasma glucose criteria: symptoms plus random plasma glucose above 11 mmol/L, or fasting plasma glucose above 7 mmol/L, or a 2-hour value above 11 mmol/L during a glucose tolerance test.^[1][4] A formal glucose tolerance test is rarely needed in a thin child with classic symptoms.^[4]

Do not delay treatment to measure C-peptide or diabetes autoantibodies at initial presentation in order to decide type 1 versus type 2: that distinction is made clinically and can be revisited later if the course is atypical.^[1] Do not wait for autoantibody results before starting insulin when DKA is present.

Further investigations (full blood count, blood cultures, chest radiograph) are driven by the search for a precipitant, not by the DKA itself.

DKA is diagnosed when all three elements are present (ISPAD and NICE agree):^[1][2]

• hyperglycaemia (plasma glucose above 11 mmol/L); and
• acidosis (blood pH below 7.3 or plasma bicarbonate below 15 mmol/L); and
• ketonaemia (blood beta-hydroxybutyrate above 3 mmol/L) or significant ketonuria (2+ or more).

Note the ISPAD biochemical criteria use serum bicarbonate below 18 mmol/L, whereas NICE uses plasma bicarbonate below 15 mmol/L. This is a genuine difference between guidelines: check which convention your laboratory and local protocol use, and be consistent.^[1][2]

Children with known diabetes can be in DKA with normal blood glucose; measure ketones in any diabetic child who is unwell, vomiting, breathing fast, dehydrated or drowsy, even if the glucose is normal.^[1][4]

Severity is set by pH and bicarbonate. It drives staffing, monitoring, fluid assumptions and the risk of cerebral oedema.^[1][3]

HHS is diagnosed when all of the following hold: plasma glucose above 33.3 mmol/L (600 mg/dL), venous pH above 7.25 (arterial above 7.30), bicarbonate above 15 mmol/L, absent or mild ketonaemia, effective osmolality above 320 mOsm/kg. ^[2] A child with HHS needs much faster and larger initial fluid replacement than for DKA, and insulin should be delayed until glucose is no longer falling at 3 mmol/L per hour with fluids alone, then given at 0.025 to 0.05 units/kg/hour.^[2] Insulin boluses are not recommended in either condition.^[2]

DKA is treated in a hospital with acute paediatric facilities. It requires a senior clinician to be informed at diagnosis, one-to-one nursing for children under 2 years or with severe DKA (pH below 7.1), and a team experienced in fluids, insulin, potassium and neurological monitoring.^[1] Where geographic constraints prevent this, treatment should begin with telephone or video conferencing support from a physician expert in DKA.^[2]

A child under 2 with new-onset diabetes should be admitted, as the risk of rapid deterioration is higher.^[1]

Resuscitation follows the airway-breathing-circulation pattern, with these specifics:^[1][4]

• Oxygen by face mask if there are signs of shock.
• A nasogastric tube if consciousness is reduced and the child is vomiting.
• Urgent anaesthetic review and discussion with paediatric critical care if the airway cannot be protected.
• Inotropes if there is hypotensive shock, discussed with paediatric critical care.
• Consider sepsis if there is fever or hypothermia, hypotension, refractory acidosis or lactic acidosis.

Record the level of consciousness, vital signs, nausea and vomiting, clinical dehydration and body weight at diagnosis, and measure the baseline blood gas, electrolytes, urea, creatinine, glucose and ketones.^[1]

Fluid replacement begins before insulin. The key principles are universal; the volumes are where guidelines differ slightly.

Bolus

• In a child who is clinically dehydrated but not in shock: 10 mL/kg of 0.9% sodium chloride over 30 minutes, and discuss with the senior paediatrician before giving a second 10 mL/kg bolus.^[1][3]
• In shock (weak thready pulse and hypotension): 10 mL/kg of 0.9% sodium chloride as soon as possible, with further 10 mL/kg boluses up to 40 mL/kg, then inotropes.^[1][3]
• ISPAD describes the initial step as one or more boluses of 0.9% saline over 20 to 30 minutes to restore peripheral circulation without fixing the volume, while NICE and BSPED specify 10 mL/kg.^[1][2][3]

Total fluid requirement

• Calculate the total for the first 48 hours as fluid deficit plus maintenance.
• In mild-to-moderate DKA (blood pH 7.1 or above) assume 5% dehydration; in severe DKA (pH below 7.1) assume 10% dehydration. ^[1]
• Replace the deficit evenly over 48 hours; in critically ill children discuss the regimen early with the senior paediatrician or paediatric intensivist, because the risk of cerebral oedema is higher. ^[1]
• Use the Holliday-Segar formula for maintenance: 100 mL/kg for the first 10 kg, 50 mL/kg for the second 10 kg, 20 mL/kg for every kilogram after that, with a maximum weight of 75 kg. ^[1]
• Subtract any initial bolus volumes from the deficit unless the child is in shock.^[1]

Composition

• 0.9% sodium chloride without glucose for both rehydration and maintenance until the plasma glucose is below 14 mmol/L, then switch to 0.9% sodium chloride with 5% glucose. ^[1]
• Include 40 mmol/L potassium chloride in all fluids (except the initial boluses), unless the child is anuric or hyperkalaemic above the normal range; withhold adding potassium in hyperkalaemia (above 5.5 mmol/L) unless potassium is below 5.5 mmol/L or the child has passed urine; address hypokalaemia before starting insulin if present. ^[1]
• No sodium bicarbonate routinely; use it only for life-threatening hyperkalaemia or severe acidosis with compromised cardiac contractility, after discussion with a paediatric intensivist.
• Do not replace urinary losses.
• Monitor sodium throughout. As DKA resolves, serum sodium should rise as glucose falls. A falling sodium, or a rapid sustained rise in sodium, can indicate cerebral oedema.^[1]

Start an intravenous insulin infusion 1 to 2 hours after fluid replacement has begun; if the child uses an insulin pump, disconnect it when intravenous insulin starts.^[1]

• Use soluble insulin at 0.05 to 0.1 units/kg/hour. Do not give intravenous boluses.
• If beta-hydroxybutyrate is not falling within 6 to 8 hours, increase the insulin to 0.1 units/kg/hour or more. ^[1]
• Do not stop insulin because of normoglycaemia: when glucose falls below 14 mmol/L, change to glucose-containing fluid and keep insulin at least 0.05 units/kg/hour while ketosis persists. If glucose falls below 6 mmol/L, increase the glucose concentration of the infusion and continue insulin. ^[1]
• Continue intravenous insulin until ketosis is resolving, the child is alert and taking fluids, and pH has reached 7.3.
• Give subcutaneous insulin (basal and meal doses) at least 30 minutes before stopping the infusion; if an insulin pump is used, restart it at least 60 minutes before, with a new cannula site and new cartridge and set. ^[1]
• Consider continuing the child's usual subcutaneous basal insulin during DKA, in discussion with the diabetes specialist.
• Consider continuing subcutaneous basal insulin during DKA in discussion with the diabetes specialist.^[1]

Insulin therapy after DKA: start or restart on a multiple daily injection basal-bolus regimen, which NICE recommends from diagnosis. ^[1] Reinstating pump therapy after recovery follows the same 60-minute rule.

Dose at the start of treatment is weight-based. After stabilisation in moderate DKA, total daily dose in the first days is usually between 0.5 and 1.0 units/kg/day, but guidelines do not agree: ISPAD recommends 0.7 to 1.0 units/kg/day for pre-pubertal children, the American Diabetes Association 0.5 to 1.0, and AACE/ACE 0.4 to 0.5. ^[5] During the remission ("honeymoon") phase that often begins within weeks of starting insulin, children may need only 0.5 units/kg/day to maintain an HbA1c below 48 mmol/mol (6.5%). ^[1] A classic split is 30 to 40% of the total as long-acting basal insulin at bedtime and the remainder as rapid-acting insulin with meals. ^[4] Adolescents can require up to 2 units/kg/day. ^[4]

Trustworthy care of DKA is mostly monitoring. ^[1][2]

• Hourly: capillary blood glucose, heart rate, blood pressure, temperature, respiratory rate (watching for Kussmaul breathing), fluid balance input/output, and level of consciousness using the modified Glasgow Coma Scale.
• Every 30 minutes: level of consciousness and heart rate in children under 2 years, and in all children and young people with severe DKA (pH below 7.1), because they are at increased risk of cerebral oedema. ^[1]
• Continuous ECG monitoring to detect hypokalaemia (ST depression, prominent U waves).
• Blood tests at 2 hours after starting treatment and then at least every 4 hours: laboratory glucose, pH, pCO2, sodium, potassium, urea and beta-hydroxybutyrate. ^[1]
• Face-to-face medical review at diagnosis and at least every 4 hours, more often if the child is under 2 or severely affected. ^[1]
• Healthcare professionals performing this monitoring must know what to look for and when to escalate.

The child, and the parents, should be updated regularly about progress. ^[1]

If glucose, pH or ketones are not improving within 4 to 6 hours, reassess: the likely causes are an insulin error, inadequate rehydration or sepsis. ^[4]

Cerebral oedema is the most feared complication of DKA and the leading cause of diabetes-related death in children. It usually occurs in the first 24 hours of treatment, is more common under 10 years (especially under 5), and carries about 25% mortality with neurological sequelae in survivors. ^[4] The pathophysiology is still poorly understood: it can occur despite optimal management, and traditional explanations (rapid osmotic shifts) have been replaced by a multifactorial model of vasogenic and cytotoxic oedema. ^[3]

ISPAD lists the main risk factors for cerebral injury: age under 5 years, severe acidosis (pH below 7.1), severe hypocapnia (pCO2 below 21 mmHg) and an elevated blood urea nitrogen above 20 mg/dL (7 mmol/L). ^[2] Other recognised risks include severe dehydration or shock, hyponatraemia or hypernatraemia, and a deteriorating conscious state during treatment. ^[4]

Recognition is staged:

• Early signs (treat immediately): headache, agitation or irritability, an unexpected fall in heart rate, or a rising blood pressure. ^[1]
• Later, more dangerous signs: deterioration in level of consciousness, abnormal breathing pattern (including respiratory pauses), oculomotor palsies, pupillary inequality or dilatation. ^[1]

Treatment must not wait for a scan. Give the most readily available of:

• mannitol 20%, 0.5 to 1 g/kg over 10 to 15 minutes, or
• hypertonic sodium chloride (2.7% or 3%), 2.5 to 5 mL/kg over 10 to 15 minutes. ^[1]

Some older sources cite mannitol 1 to 2 g/kg over 20 minutes. ^[4] ISPAD additionally recommends that in children with several risk factors, mannitol or hypertonic saline should be calculated and kept at the bedside before trouble develops. ^[2] Reduce the fluid infusion rate, seek specialist advice immediately, and arrange transfer to paediatric intensive care and neurological imaging. ^[1][4]

Prevention is mostly good DKA care: slow, controlled fluid replacement over 48 hours in severe cases, frequent (half-hourly) neurological observations in high-risk children, close monitoring of sodium trends, and early senior review. ^[1]

• Hypokalaemia below 3.0 mmol/L: temporarily suspend insulin and involve paediatric critical care, as giving high-concentration potassium requires central access. ^[1]
• Hyperchloraemic acidosis: common during DKA and resolves without specific treatment. ^[1]
• Venous thromboembolism, particularly around a central venous catheter (a real risk in DKA, not the base rate). ^[1]
• Acute kidney injury from dehydration and hypoperfusion.
• Cerebral injury (above).

After recovery, discuss frankly what led to the DKA: non-adherence in established type 1 diabetes is the leading cause of recurrent DKA, especially in adolescence. ^[1] Revisit sick-day rules, ensure reliable insulin access and pump consumables, and assess emotional and psychological wellbeing in any young person with frequent episodes. ^[1][4]

Type 1 diabetes cannot be cured, but it can be managed so well that complications are delayed or prevented. Care is delivered by a multidisciplinary paediatric diabetes team (paediatrician or paediatric endocrinologist, diabetes nurses, dietitian, psychologist, social worker) with 24-hour telephone access for families. ^[1]

• Offer a multiple daily injection basal-bolus regimen from diagnosis; if multiple daily injections are not appropriate, consider continuous subcutaneous insulin infusion (pump). ^[1]
• Encourage adjustment of dose after each glucose reading in multiple-injection users; tell them to inject rapid-acting insulin analogues before meals. ^[1]
• Rapid-acting insulin analogues are provided for intercurrent illness or hyperglycaemia. ^[1]
• Review injection sites at every visit and provide needles of appropriate length for body fat, together with sharps disposal. ^[1]
• Aim for optimal glycaemic control; if targets are not met, offer more contact and consider an alternative regimen. ^[1]

A dietitian supports the family. Healthy eating, low glycaemic index choices, at least 5 portions of fruit and vegetables daily, and tailoring to insulin and activity are recommended. ^[1] For children using basal-bolus or a pump, level 3 carbohydrate counting education should be offered from diagnosis and repeated regularly. ^[1] An older practical guide that still informs practice suggests carbohydrates 50 to 60% of energy (no more than 10% from sucrose or refined carbohydrates), fat below 30% and protein 10 to 20%, with the aim of keeping blood glucose close to 6 to 12 mmol/L (100 to 200 mg/dL) in younger children and tighter targets in older ones. ^[4] Dietary advice should not be generic and must be individualised.

• Education is continuous from diagnosis and covers insulin action, dosing, glucose and ketone monitoring, sick-day rules, hypoglycaemia recognition, diet, activity and intercurrent illness. ^[1][4]
• Sick-day rules should be given in individualised written form: what to monitor (glucose, blood ketones), how to adjust insulin, fluid and food intake, and when and where to seek help, reviewed at least annually. ^[1]
• Every child should be offered blood ketone testing strips and a meter, and tested for ketonaemia when ill or hyperglycaemic. ^[1]
• Children should wear or carry something identifying type 1 diabetes. ^[1][4]

• Target ranges for short-term plasma glucose: 4 to 7 mmol/L on waking; 4 to 7 mmol/L before other meals; 5 to 9 mmol/L after meals. ^[1]
• HbA1c target of 48 mmol/mol or lower (6.5%) minimises the risk of long-term complications; any reduction from a higher value reduces risk. ^[1]
• Measure HbA1c 4 times a year; think about more frequent testing if management is difficult. Services should document the proportion achieving 53 mmol/mol (7%) or lower. ^[1]
• Real-time continuous glucose monitoring (rtCGM) is offered to all children with type 1 diabetes from diagnosis, alongside education in its use. ^[1] Intermittently scanned CGM (flash) is offered to those aged 4 years and over who cannot or do not want to use rtCGM. Children using CGM should still take some capillary measurements to check accuracy and as a back-up, and should be encouraged to wear the sensor at least 70% of the time. ^[1]
• Children not using CGM are advised to perform at least 5 capillary tests a day. ^[1]

Mild to moderate hypoglycaemia is treated with 10 to 20 g of fast-acting glucose, rechecked within 15 minutes, followed by a long-acting carbohydrate. ^[1] Severe hypoglycaemia (outside hospital, or without rapid intravenous access) is treated with intramuscular glucagon: 1 mg if the child is over 8 years or weighs 25 kg or more; 500 micrograms if under 8 years or under 25 kg. In hospital, 10% intravenous glucose is used at 500 mg/kg (5 mL/kg) maximum. Glucagon may be less effective when alcohol is involved. ^[1] Families, carers and (where appropriate) school nurses must be trained in glucagon administration. ^[1]

From diagnosis and throughout childhood:

• Thyroid disease: screen at diagnosis and annually. ^[1][4]
• Coeliac disease: screen as guided by the NICE coeliac guideline; annually in many services. ^[1][4]
• Complications (NICE): diabetic retinopathy screening from 12 years; moderately increased albuminuria (ACR 3 to 30 mg/mmol, early morning urine) and hypertension from 12 years; review of foot care and dental health. ^[1]
• Rare associated conditions to remember: juvenile cataract, necrobiosis lipoidica, Addison disease. ^[1]
• Growth, puberty and blood pressure at every visit, with 3 to 4-monthly clinic follow-up. ^[4]
• HbA1c in a range that most clinicians accept as 7 to 9%, with intensive regimens aiming lower as the child grows and matures. ^[4]

Children and young people with type 1 diabetes have a higher risk of emotional and behavioural difficulties, anxiety, depression and eating disorders, especially in adolescent girls. ^[1] Psychological support should be offered after diagnosis and refreshed thereafter, with access to mental health professionals who understand diabetes; every young person with frequent DKA should have their emotional and psychological wellbeing assessed. ^[1]

• Exercise reduces long-term cardiovascular risk; children need insulin and carbohydrate adjustments rather than exclusion from sport. ^[1]
• Practical advice on long-distance travel, sick-day rules and alcohol (with the increased nocturnal hypoglycaemia risk) should be given. ^[1]
• Annual influenza and pneumococcal immunisation (if on insulin) per the Green Book. ^[1]
• Smoking and substance misuse counselling. ^[1]
• Surgery only in centres with dedicated paediatric diabetes facilities. ^[1]

Transition should be planned over time, based on physical development and emotional maturity, occur at a time of relative stability, and be agreed in a local protocol. Parents and young people should be prepared for the changes in service. ^[1]

Acute complications. The main acute complications are DKA (the most important cause of mortality and severe morbidity), hypoglycaemia (which, if recurrent and severe in under-5s, carries a risk of learning and neurological problems) and hyperglycaemia during illness. ^[4]

Chronic complications. In children these are largely future risks driven by duration and level of hyperglycaemia: diabetic nephropathy (microalbuminuria first), retinopathy, neuropathy, hypertension, dyslipidaemia and poor growth. Periodontal disease risk is increased. The goal of tight glycaemic and blood pressure control is to delay or prevent these. ^[1][4]

Associated autoimmune disease. Thyroid disease and coeliac disease are the ones to remember. ^[1][4]

With good management children with type 1 diabetes can expect full, normal, healthy lives, although DKA at or after diagnosis remains the main cause of death and severe morbidity, particularly in low-resource settings. ^[4] Improved insulins, pumps and continuous glucose monitoring have reduced the burden of severe hypoglycaemia and improved control. Prospects such as islet cell transplantation or stem cell therapy are experimental and not standard care for children. ^[4]

DKA is potentially preventable in most children: late presentation and insulin omission are the dominant causes. ^[2][4] Prevention is therefore an education and systems issue as much as a medical one:

• public and professional awareness so that the classic symptoms (and isolated nocturnal enuresis in toddlers) are recognised early;
• universal access to finger-prick glucose testing: fingerstick glucose should be considered in every child presenting with rapid breathing, or vomiting and abdominal pain without diarrhoea. ^[2]
• individualised sick-day rules and ketone testing at home; ^[1]
• 24-hour access to the diabetes team and psychological support for adolescents with repeated episodes; ^[1]
• research screening for high-risk children through genetics and autoantibody testing remains a future prospect, not routine care. ^[4]

Symptomatic children, children of parents with T1D, and those with Down or Turner syndrome are groups in whom a lower threshold for glucose testing is reasonable in practice.

• Under 5s: symptoms are easily missed (often only enuresis); admission is recommended for newly diagnosed children, and management must consider family ability to cope. ^[1][4] High starting insulin doses (above 0.5 units/kg/day) are generally safe in older children but the youngest group has a higher rate of early hypoglycaemia, so caution is advised. ^[5]
• Adolescents: insulin requirements rise (up to 2 units/kg/day), non-adherence is the main cause of recurrent DKA, and transition planning begins years before the move to adult services. ^[1][4]
• Low-resource settings: missed diagnosis and lack of insulin are the critical gaps; insulin and 0.9% sodium chloride, potassium and 5% dextrose, plus a working blood gas or dipstick ketones, save lives when used in the 48-hour protocol above. ^[4]

The same protocol applies, but with substitutions that keep the essential physiology intact:

• Suspect DKA early: many children present late. Use glucose and ketone testing (finger-prick if possible, urine ketones otherwise) in every child with rapid breathing, vomiting or abdominal pain without diarrhoea. ^[2][4]
• Assume 5% or 10% dehydration by pH and replace over 48 hours using the Holliday-Segar formula with 0.9% saline (or the most available balanced crystalloid at first), with 40 mmol/L potassium once urination is established. ^[4]
• If laboratory potassium or sodium is unavailable, prioritise at least glucose, pH or bicarbonate, and creatinine.
• When glucose falls below about 14 mmol/L (250 mg/dL), add dextrose 5 to 10% to the same saline.
• Give insulin at 0.05 to 0.1 units/kg/hour by infusion; if pumps are unavailable, use a drip set and count carefully.
• Mannitol or hypertonic saline for cerebral oedema should be drawn up in advance in high-risk children; treat on clinical signs without waiting for imaging.
• Transfer early to any facility with intensive care; phone support from an experienced physician is better than no support. ^[2]

• Type 1 diabetes is autoimmune beta-cell destruction with absolute insulin deficiency; it is not caused by lifestyle.
• Classic symptoms in older children: polyuria, polydipsia, polyphagia, weight loss and lethargy; in under-5s perhaps only nocturnal enuresis.
• DKA is defined (NICE) as glucose above 11 mmol/L, pH below 7.3 or bicarbonate below 15 mmol/L, and beta-hydroxybutyrate above 3 mmol/L. ISPAD uses bicarbonate below 18 mmol/L.
• Shock (weak thready pulse, hypotension) is rare in DKA and is not the same as tachycardia and poor capillary refill from acidosis or hypocapnia.
• Fluids come first: 10 mL/kg bolus; total over 48 hours is 5% (pH 7.1 or above) or 10% (pH below 7.1) plus Holliday-Segar maintenance; 0.9% saline until glucose is below 14 mmol/L, then glucose-containing fluid; 40 mmol/L potassium.
• Insulin starts 1 to 2 hours later at 0.05 to 0.1 units/kg/hour intravenously, with no bolus; never stop insulin because the glucose has normalised while ketosis remains.
• Cerebral oedema can occur in the first 24 hours; treat headache, bradycardia, hypertension or any altered consciousness immediately with mannitol or hypertonic saline.
• Long-term standard: basal-bolus insulin, HbA1c target 48 mmol/mol or lower, rtCGM offered to all, sick-day rules and ketone testing at home.
• Screen thyroid and, from age 12, albuminuria and hypertension; retinopathy screening from 12 years.
• Prevention of DKA is education, access, and early recognition.

• Acute kidney injury (when dehydration is complicated by renal hypoperfusion)
• Acid-base disorders (the metabolic acidosis of DKA)
• Neonatal hypoglycaemia and neonatal diabetes (a different diabetic presentation in infancy)
• Diabetes chronic complications in adults (the long-term view for the same child grown up)
• Hypoglycaemia (detailed treatment)
• Trauma and shock (fluid resuscitation principles)
• Thyroid disease and coeliac disease (autoimmune associations of type 1 diabetes)

Sources named in this page: NICE guideline NG18 (last updated 11 May 2023), ISPAD clinical practice consensus guidelines 2022 for diabetic ketoacidosis and hyperglycaemic hyperosmolar state, BSPED DKA guideline 2021, an open-access review of childhood diabetes (Ayoola 2008), and a review of initial insulin dosing in children (Muller et al. 2018). Plain text links only: no internal topic links were added.