Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Diabetic ketoacidosis and cerebral-oedema risk
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Neurological deterioration during DKA
New headache, irritability, unexpected bradycardia, rising blood pressure, altered breathing, falling consciousness, cranial-nerve signs or posturing may indicate cerebral injury.
Action: Give whichever is immediately available: hypertonic saline 2.7% or 3% 2.5 to 5 ml/kg over 10 to 15 minutes, or mannitol 20% 0.5 to 1 g/kg over 10 to 15 minutes. Summon senior paediatric intensive-care help, modify fluids under BSPED and do not delay treatment for CT.
Overview
Diagnose and grade childhood diabetic ketoacidosis, restore circulation and correct dehydration and ketosis using the current BSPED protocol, while detecting and treating cerebral injury immediately without waiting for neuroimaging.
DKA is caused by severe effective insulin deficiency with excess counter-regulatory hormones. It can reveal new diabetes or follow missed insulin, pump interruption, infection, vomiting, psychosocial crisis or inadequate sick-day correction. Ask about polyuria, thirst, weight loss, insulin delivery, last basal dose, pump alarms, ketone actions and preceding illness. Abdominal pain and vomiting can resemble a surgical abdomen, while deep Kussmaul breathing may be mistaken for primary respiratory disease.
Confirm glucose above 11 mmol/L, blood ketones above 3 mmol/L or urine ketones at least 2+, and venous pH below 7.3 or bicarbonate below 15 mmol/L using the current BSPED definition. Grade acidosis because severity influences location and monitoring. Venous samples are normally sufficient; repeated arterial puncture adds pain without improving routine decisions. Differential diagnoses include starvation ketosis, lactic acidosis, toxic ingestion and hyperosmolar states.
Practice
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Paediatrics and child healthOriginal SBA
Insulin timing and rate
A 30 kg child has confirmed DKA, is not shocked and has started the calculated intravenous fluid pathway. Which insulin plan best follows current BSPED principles?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Initial priorities are airway, breathing, circulation, disability, glucose and accurate weight. Shock is uncommon and must be distinguished from peripheral vasoconstriction caused by acidosis. Give 10 ml/kg isotonic crystalloid over 15 minutes for shock, reassessing after each bolus; up to 40 ml/kg may be required before inotropes are considered with critical-care input. Shock boluses are not subtracted from the calculated DKA deficit. Non-shocked children needing IV therapy receive 10 ml/kg 0.9% saline over 30 minutes under BSPED.
Calculate maintenance by the current paediatric formula and add estimated deficit according to pH, normally replacing over 48 hours with a maximum calculation weight of 75 kg in the BSPED pathway. Subtract the non-shock initial bolus from the deficit calculation. Account for fluid received elsewhere. Oral intake, urine and infusions must be charted. Do not improvise a simple adult DKA regimen because children's fluid physiology and cerebral-injury risk differ.
Start soluble insulin infusion after one to two hours of fluids, normally 0.05 units/kg/hour and up to 0.1 units/kg/hour for selected severe cases or adolescents. Do not bolus insulin. Insulin suppresses ketogenesis; glucose may fall before acidosis clears. At glucose 14 mmol/L, change to glucose-containing saline and titrate glucose strength to allow insulin to continue. A fall in ketones and improvement in pH are better evidence of metabolic recovery than glucose alone.
Total-body potassium is depleted through osmotic diuresis and vomiting even when acidosis raises the measured serum concentration. Add potassium chloride to ongoing fluid according to BSPED unless potassium is high or renal output is absent, and monitor closely. If potassium falls below 3.0 mmol/L, urgent critical-care advice and temporary insulin interruption may be necessary while potassium is replaced. Hyperchloraemic acidosis can persist after ketones resolve and should not be mistaken automatically for failed insulin therapy.
Cerebral injury is the feared acute complication. Establish and record neurological status from arrival, including headache and behaviour. Early signs include headache, irritability, unexpected slowing of heart rate and increasing blood pressure; later signs include deteriorating consciousness, abnormal breathing, cranial-nerve palsy, pupillary change or posturing. Treat at clinical suspicion with the immediately available hypertonic saline or mannitol regimen, reduce fluid as the protocol specifies, summon intensive care and image only after treatment and stabilisation.
Transition when the child is alert, drinking, no longer vomiting, ketones have cleared and acidosis has resolved sufficiently under the pathway. Give subcutaneous rapid-acting insulin before stopping the infusion and preserve basal insulin continuity. Revisit the precipitant: a cannula problem is treated differently from food insecurity, depression or family exhaustion. Before discharge, repeat injection or pump, ketone and sick-day education and verify supplies, contacts and follow-up.
Key points
Paediatric DKA requires hyperglycaemia, significant ketonaemia or ketonuria and metabolic acidosis; blood beta-hydroxybutyrate and venous pH are more useful for serial treatment than urine ketones alone.
Use ABCDE, weigh the child, establish neurological baseline and obtain senior paediatric and critical-care support early; record every fluid already received.
True shock means impaired central circulation, weak pulses and hypotension, not cool hands alone. Give isotonic crystalloid in 10 ml/kg boluses over 15 minutes with reassessment, up to 40 ml/kg before considering inotropes.
A non-shocked child needing intravenous treatment receives 0.9% sodium chloride 10 ml/kg over 30 minutes, then calculated maintenance plus deficit replacement generally over 48 hours under BSPED.
Start soluble insulin infusion 0.05 to 0.1 units/kg/hour one to two hours after fluids begin; 0.05 units/kg/hour is usually sufficient, especially under 5 years, and no insulin bolus is given.
Add potassium to ongoing fluids as directed unless hyperkalaemia or absent urine makes it unsafe; serum potassium can be high despite severe total-body depletion.
When glucose reaches 14 mmol/L, add 5% glucose to 0.9% sodium chloride and continue insulin to clear ketones; increase glucose concentration if needed rather than stopping insulin prematurely.
Aetiology
01
New autoimmune diabetes
Progressive beta-cell loss first becomes clinically apparent when insulin is insufficient to suppress lipolysis and ketone production.
02
Insulin delivery failure
Missed injections, empty reservoirs, displaced cannulas, spoiled insulin or device malfunction can remove effective insulin within hours.
03
Intercurrent physiological stress
Infection, trauma, surgery and vomiting increase catecholamines, cortisol and glucagon, raising insulin requirement and accelerating ketogenesis.
04
Psychosocial interruption
Diabetes distress, depression, eating disorder, safeguarding problems, poverty or family-system failure can lead to intentional or unintentional omission.
Pathophysiology
1
Unchecked ketogenesis
Low insulin and high counter-regulatory hormones release fatty acids that the liver converts to beta-hydroxybutyrate and acetoacetate.
2
Osmotic volume loss
Hyperglycaemia drives urinary water and electrolyte loss, while vomiting and reduced intake worsen extracellular and intracellular dehydration.
3
Acid-base compensation
Accumulating organic acids lower bicarbonate and pH, provoking deep respiratory compensation and contributing to abdominal pain and reduced myocardial performance.
4
Potassium redistribution
Acidosis and insulin deficiency move potassium extracellularly despite large urinary losses, so treatment can expose dangerous hypokalaemia.
5
Cerebral injury mechanisms
Hypoperfusion, inflammation, altered cerebral water handling and treatment-related osmotic change may combine; no single bedside fluid event explains every case.
Clinical features and red flags
Mild DKA
Hyperglycaemia and ketonaemia occur with venous pH below 7.3 but at or above 7.2 and bicarbonate below 15 mmol/L.
Moderate DKA
Venous pH from 7.1 to below 7.2 marks greater acidosis and usually requires closer inpatient monitoring.
Severe DKA
Venous pH below 7.1, major dehydration or impaired consciousness signals high complication and critical-care risk.
Shock pattern
Weak central pulses, prolonged central refill, tachycardia and hypotension indicate circulatory failure beyond acidotic peripheral vasoconstriction.
Early cerebral warning
New headache, irritability, unexpected bradycardia or rising blood pressure during treatment warrants immediate senior review.
A neurological trend or discordant cardiovascular change can reveal cerebral injury before profound coma develops.
04Serial ketones and acid-base status
Why
Measure metabolic response at least every two hours initially as specified by the pathway.
Interpretation and limitations
Falling beta-hydroxybutyrate and improving pH show insulin effect; isolated chloride-related acidosis can lag after ketosis clears.
05
Differential diagnosis
01
Starvation ketosis
Reduced intake causes ketones with normal or low glucose and usually milder acidosis, although young children can become significantly unwell.
02
Sepsis with lactic acidosis
Fever, shock, organ dysfunction and raised lactate may coexist with stress hyperglycaemia, requiring antimicrobial and perfusion management.
03
Toxic or metabolic acidosis
Salicylate, toxic alcohol, renal failure and inborn metabolic disease produce acidosis through mechanisms not corrected by standard DKA insulin.
04
Hyperosmolar hyperglycaemic state
Extreme glucose and osmolality with relatively little ketosis needs specialist fluid and insulin modification and can overlap with DKA.
Management
01Initial resuscitationRestore circulation and quantify DKAFirst stepA child has hyperglycaemia, ketones and suspected acidosis or impaired perfusion.+
1Use ABCDE, weigh, record neurological status and fluids, obtain IV access and send glucose, ketones, venous gas, electrolytes and renal tests.
2For shock give isotonic crystalloid 10 ml/kg over 15 minutes, reassess and repeat when needed up to 40 ml/kg with critical-care input.
3For a non-shocked child requiring IV therapy give 0.9% sodium chloride 10 ml/kg over 30 minutes and calculate the BSPED 48-hour plan.
02Ketone clearanceContinue insulin with controlled substrateCirculation is addressed and one to two hours of intravenous fluid have begun.+
1Start soluble insulin 0.05 to 0.1 units/kg/hour without a bolus, usually using 0.05 units/kg/hour.
Complications
01
Cerebral injury
Brain swelling or vascular injury can cause headache, neurological decline, herniation, permanent disability or death during treatment.
02
Potassium-related arrhythmia
Rapid intracellular potassium movement during insulin therapy can cause weakness, electrocardiographic change and malignant cardiac arrhythmia.
03
Hypoglycaemia
Continuing insulin without adequate glucose replacement can lower plasma glucose before ketones and acidosis have resolved.
04
Acute kidney injury
Severe dehydration, shock and rhabdomyolysis can impair renal filtration and complicate potassium, fluid and medicine management.
05
Venous thrombosis and aspiration
Dehydration, central access, immobility and reduced consciousness increase serious thrombotic and airway risks in severe illness.
Monitoring and follow-up
Record hourly neurological status, headache, pupils, Glasgow Coma Scale, heart rate, blood pressure, respiratory pattern and oxygen saturation.
Measure bedside glucose hourly and ketones, venous pH, bicarbonate and electrolytes at least every two hours initially or more often when unstable.
Maintain a cumulative chart of every oral and intravenous input, urine, emesis and fluid given before transfer.
Follow measured and glucose-corrected sodium trends and escalate an unexpected fall or other sign of adverse osmotic change.
Track potassium and ECG through insulin and replacement, particularly when the starting concentration is low or renal function changes.
Judge recovery from ketone clearance, acid-base improvement, alertness and oral tolerance rather than glucose alone.
After the crisis, review insulin delivery, illness, education, mood, eating behaviour, family capacity and access to equipment.
Special situations
Shock is a central diagnosis
Acidosis constricts peripheral vessels, so cool extremities alone do not justify repeated resuscitation boluses.
Insulin treats ketones
Glucose-containing fluid allows continued insulin after glucose falls, preventing biochemical recovery from being stopped halfway.
Serum potassium can deceive
An initially high concentration reflects extracellular shift while the child's whole-body potassium store is markedly depleted.
Cerebral treatment precedes scanning
Neurological delay can be fatal; imaging looks for alternatives only after immediate osmotherapy and stabilisation.
Chloride can prolong acidosis
A low bicarbonate after ketone clearance may reflect saline-related hyperchloraemia rather than ongoing diabetic ketogenesis.
Common pitfalls
01
Using an adult DKA protocol for a child.
02
Calling cool hands shock without assessing central perfusion and blood pressure.
03
Failing to include fluid already given during transfer in the calculation.
04
Giving an insulin bolus or starting insulin before initial fluid replacement.
05
Stopping insulin when glucose normalises despite persistent ketones.
06
Forgetting potassium because the admission serum value is high.
07
Waiting for CT confirmation before treating neurological deterioration.
08
Discharging after biochemical recovery without exploring the precipitant and rebuilding the sick-day plan.
Monitor hourly observations, neurological state, glucose and fluid balance, with at least two-hourly ketones, electrolytes and venous acid-base testing initially according to severity and protocol.
Headache, irritability, falling consciousness, unexpected bradycardia, rising blood pressure, abnormal breathing, cranial-nerve signs or posturing means suspected cerebral injury.
Treat suspected cerebral oedema immediately with available hypertonic saline 2.7% or 3% 2.5 to 5 ml/kg over 10 to 15 minutes, or mannitol 20% 0.5 to 1 g/kg over 10 to 15 minutes; do not wait for CT.
A glucose fall without ketone clearance is not recovery and must not prompt premature insulin cessation.
Falling measured sodium as glucose declines can indicate an adverse water shift and requires senior review of fluid calculations.
Persistent vomiting, worsening abdominal signs or lactate despite metabolic improvement suggests an additional diagnosis.
Recurrent DKA or an unexplained delay in presentation requires psychosocial, access and safeguarding assessment.
ECG when potassium is abnormal
Why
Detect conduction and repolarisation effects of important hypo- or hyperkalaemia during rapid biochemical change.
Interpretation and limitations
ECG change strengthens urgency but a normal trace does not make a dangerous potassium concentration safe.
06Brain imaging after stabilisation
Why
Look for haemorrhage, thrombosis, infarction or another cause when neurological deterioration has been treated.
Interpretation and limitations
CT is not a diagnostic prerequisite for cerebral-oedema therapy and waiting can worsen irreversible injury.
2
Add potassium to ongoing fluid when safe and repeat glucose, ketones, gas, sodium and potassium at protocol intervals.
3At glucose 14 mmol/L add 5% glucose and increase glucose concentration if necessary so insulin continues until ketosis resolves.
03Cerebral injuryTreat clinically before imagingHeadache, behaviour change, bradycardia, hypertension, abnormal breathing or neurological deterioration appears.+
1Give hypertonic saline 2.7% or 3% 2.5 to 5 ml/kg, or mannitol 20% 0.5 to 1 g/kg, over 10 to 15 minutes immediately.
2Call senior paediatrics and intensive care, follow the BSPED fluid modification and avoid inexperienced elective intubation.
3AlternativeStabilise first, then image for alternative intracranial pathology and repeat osmotherapy only with expert protocol-based review.
04Recovery transitionReturn safely to subcutaneous insulinConsciousness, oral tolerance, ketones and acidosis have improved sufficiently for transition.+
1Confirm the child can drink and the precipitant is treated, and distinguish resolved ketosis from residual hyperchloraemic acidosis.
2Give planned subcutaneous insulin with appropriate overlap before stopping intravenous insulin and preserve long-acting basal coverage.
3Re-educate on ketones, devices and sick days, assess psychosocial triggers and arrange prompt diabetes-team follow-up.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Restores effective circulation and begins controlled dehydration correction before insulin is introduced.
Isotonic crystalloid
For shock, give 10 ml/kg intravenously over 15 minutes, reassess and repeat as required up to a total 40 ml/kg before inotrope consideration; a non-shocked child needing IV therapy receives 0.9% sodium chloride 10 ml/kg over 30 minutes.
Document pre-hospital fluid, distinguish shock from cool acidotic peripheries, recalculate maintenance and deficit carefully and involve critical care for repeated boluses.
Suppresses lipolysis and ketone generation while gradually lowering glucose and permitting metabolic recovery.
Soluble insulin infusion
Start intravenously at 0.05 to 0.1 units/kg/hour one to two hours after fluid begins, usually 0.05 units/kg/hour and without an insulin bolus; continue until ketones and acidosis resolve.
Monitor glucose and potassium closely, add glucose-containing saline at 14 mmol/L, and never stop solely because glucose normalises before ketones clear.
Replaces severe total-body potassium loss unmasked as insulin and correction of acidosis move potassium into cells.
Potassium chloride in intravenous fluid
Use the BSPED fluid concentration, commonly 40 mmol/L, once potassium and renal output make replacement safe; temporarily stop insulin and obtain critical-care advice if potassium falls below 3.0 mmol/L.
Do not add during hyperkalaemia or absent urine without senior review; concentrated replacement may require central access and continuous cardiac monitoring.
Provides immediate osmotherapy for clinically suspected cerebral injury before imaging or definitive intensive-care management.
Hypertonic saline or mannitol
For suspected cerebral oedema, give hypertonic saline 2.7% or 3% at 2.5 to 5 ml/kg over 10 to 15 minutes, or mannitol 20% at 0.5 to 1 g/kg over 10 to 15 minutes.
Use whichever is available fastest, seek intensive-care support immediately, adjust fluids under BSPED and monitor haemodynamics, sodium, diuresis and neurological response.