Pediatric DKA and cerebral edemaMANAGEMENT

PEDIATRIC-SPECIFIC PRESENTATIONS · 12 SECTIONS

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604 items

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

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Pediatric-Specific Presentations19▾

Bronchiolitis Croup Ductal-dependent congenital heart disease Emergency delivery Febrile seizure Hypercyanotic (tet) spell Inborn error of metabolism Intussusception Kawasaki disease Necrotizing enterocolitis Neonatal jaundice Neonatal resuscitation Nursemaid's elbow Pediatric DKA and cerebral edema Pediatric fever 0 to 28 days Pediatric fever 29 to 60 days Pediatric fever 61 to 90 days Pediatric septic shock Pyloric stenosis

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp41

Immediate priorities and the first hour

›Confirm the diagnosis at the bedside before committing to a pathway

›Capillary or venous glucose above 11 mmol/l

›Venous pH below 7.3 or bicarbonate below 15 mmol/l

›Blood beta-hydroxybutyrate 3 mmol/l or higher, or moderate to large ketonuria

›Documented weight in kilograms, because every fluid and drug dose is weight-based

›Assign biochemical severity, which drives fluid assumptions and level of care

›Mild: venous pH below 7.3 or bicarbonate below 15 mmol/l

›Moderate: venous pH below 7.2 or bicarbonate below 10 mmol/l

›Severe: venous pH below 7.1 or bicarbonate below 5 mmol/l

›Sequence the first hour deliberately

›Airway, breathing, circulation, and a documented Glasgow Coma Scale before any therapy

›Start 0.9% sodium chloride first and begin the insulin infusion 1 hour after fluids

›Two intravenous cannulas: one for fluids and insulin, one for repeated blood sampling

›Continuous cardiac monitoring and pulse oximetry attached before insulin starts

›Strict fluid balance and an hourly neurologic observation chart from time zero

›Identify the child at high risk of cerebral edema at first contact

›Age under 5 years

›New-onset diabetes

›Long symptom duration with severe acidosis

›Marked hypocapnia and an elevated serum urea

›Give the receiving team an explicit cerebral-edema risk statement at handover

›Establish disposition intent early

›Involve pediatric critical care and pediatric endocrinology at the first assessment

›Arrange transfer now if the treating unit cannot deliver hourly neurologic checks and 1 to 2 hourly biochemistry

›Place mannitol and 3% sodium chloride physically at the bedside for any high-risk child

Life-threatening features that mandate the resuscitation bay

›Depressed or fluctuating consciousness

02History/hx50

Presenting symptoms

›Osmotic symptoms

›Polyuria, including new nocturnal enuresis in a previously dry child

›Polydipsia and unquenchable thirst

›Nocturia

›Catabolic symptoms

›Unintentional weight loss over days to weeks

›Fatigue, weakness, and reduced activity tolerance

›Acidosis and ketosis symptoms

›Nausea, vomiting, and diffuse abdominal pain

›Rapid or deep breathing noticed by carers

›Fruity breath odor reported by the family

›Progression markers

›Reduced oral intake and falling urine output as dehydration advances

›Blurred vision

›Drowsiness, irritability, or confusion

›Symptom duration, which is prognostic

›Days from first polyuria to presentation

›Hours from onset of vomiting or reduced intake to presentation

›A longer prodrome raises the risk of cerebral edema

Diabetes history and precipitants

›Diabetes type and duration

›Known type 1, type 2, monogenic (neonatal), or cystic-fibrosis-related diabetes

›Age at diagnosis and baseline glycemic control

›Insulin delivery

›Regimen, last dose, and any missed or reduced doses

›Insulin pump use and time since the last successful bolus or a suspected set failure

›Deliberate omission, needle phobia, or diabetes-related distress

03Physical Exam/exam51

Vital signs and age-specific thresholds

›Heart rate, interpreted against age

›Sustained above 160 per minute in infants

›Above 140 per minute in preschool children

›Above 120 per minute in school-age children and adolescents

›Bradycardia for age, or a sustained fall of more than 20 per minute, suggests raised intracranial pressure rather than recovery

›Respiratory rate and pattern, interpreted against age

›Above 60 per minute in infants, above 40 in preschool children, above 30 in older children

›Deep sighing Kussmaul breathing reflects compensation, not primary lung disease

›A falling respiratory rate with persistent acidosis signals exhaustion

›Blood pressure

›Hypotension is a late sign: systolic below 70 mmHg in infants, below 70 mmHg plus twice the age in years from 1 to 10 years, below 90 mmHg over 10 years

›A rising blood pressure with a widening pulse pressure suggests raised intracranial pressure

›Diastolic blood pressure above 90 mmHg is a minor cerebral-edema criterion

›Oxygen saturation, target 94 to 98%

›Cyanotic congenital heart disease: the child's known baseline, often 75 to 85%

›Chronic lung disease or bronchopulmonary dysplasia: 90 to 92%

›Pulmonary hypertension: the child's baseline, avoiding both hypoxia and hyperoxia

›Temperature

›Fever indicates a likely precipitating infection; DKA alone does not cause fever

›Hypothermia is a poor prognostic sign and can mask infection

›Measured weight in kilograms

›Use a length-based estimate only if the child truly cannot be weighed

›Recheck the dosing weight against the estimate before drawing up resuscitation drugs

Hydration, perfusion, and general examination

›Estimate the fluid deficit, expecting clinical signs to underestimate it

›Assume 5 to 7% dehydration in moderate DKA

›Assume 7 to 10% dehydration in severe DKA

04Differential Diagnosis/ddx26

High anion gap metabolic acidosis and metabolic mimics

›Diabetic ketoacidosis

›Anion gap above 12 mmol/l with ketonemia and hyperglycemia

›Euglycemic DKA with glucose below 11 mmol/l in SGLT2 inhibitor use, pregnancy, or starvation

›Other ketoacidoses

›Starvation ketosis and alcoholic ketoacidosis in an adolescent, with glucose normal or low

›Inborn error of metabolism in an infant: organic acidemia or fatty-acid oxidation defect

›Non-ketotic high anion gap acidosis

›Lactic acidosis from sepsis, hypoperfusion, or a prolonged seizure

›Salicylate poisoning with a mixed respiratory alkalosis, tinnitus, and hyperthermia

›Toxic alcohol ingestion (ethylene glycol, methanol) with an osmolar gap

›Uremic acidosis in advanced kidney disease

›Hyperglycemic states without acidosis

›Hyperglycemic hyperosmolar state: glucose above 33 mmol/l, effective osmolality above 320 mmol/kg, pH above 7.25, minimal ketosis

›Ketosis-prone type 2 diabetes in an adolescent with obesity

Altered mental status and clinical mimics

›Neurologic causes of decline

›Cerebral edema complicating DKA, the default explanation for deterioration during treatment

›Meningitis or encephalitis, especially when fever is present

›Intracranial hemorrhage or cerebral venous thrombosis, to which DKA predisposes

›Non-accidental or accidental head injury

›Non-convulsive seizure

›Metabolic and toxic causes

›Hypoglycemia from an insulin error before or during treatment

›Toxic ingestion, including a carer's medication

›Misattributed presentations that delay the glucose check

›Kussmaul breathing mistaken for pneumonia, bronchiolitis, or an asthma exacerbation

›Abdominal pain mistaken for appendicitis or gastroenteritis

05Laboratory Tests/lt45

Diagnostic and severity laboratory tests

›Glucose

›Point-of-care and laboratory glucose for the diagnostic threshold above 11 mmol/l

›Serial glucose to confirm a controlled fall of 2 to 5 mmol/l per hour

›Acid-base

›Venous blood gas for pH and pCO2; arterial sampling is not required

›Bicarbonate for severity grading and for tracking resolution

›Ketones

›Blood beta-hydroxybutyrate for diagnosis at 3 mmol/l or higher and for resolution below 1 mmol/l

›Urine ketone strips detect acetoacetate, not beta-hydroxybutyrate

›Point-of-care ketone meters plateau near 8 mmol/l and understate severe ketonemia

Electrolytes, derived values, and precipitant workup

›Sodium

›Measured and corrected sodium: add 1.6 to 2.4 mmol/l to measured sodium for every 5.5 mmol/l that glucose exceeds 5.5 mmol/l

›Corrected sodium should rise as glucose falls

›A falling or static corrected sodium during treatment predicts cerebral edema

›Potassium and chloride

›Potassium at baseline and every 1 to 2 hours; expect a rapid fall once insulin and fluids run

›Chloride, to detect the hyperchloremic acidosis that large-volume saline produces

›Derived values

›Anion gap = sodium minus (chloride plus bicarbonate); normal 8 to 12 mmol/l

›Follow the anion gap, not bicarbonate, to judge resolution

›Effective osmolality = 2 times sodium (mmol/l) plus glucose (mmol/l); normal 275 to 295 mmol/kg

›Renal and mineral panel

›Urea and creatinine for degree of dehydration and kidney function

›Phosphate, magnesium, and calcium at baseline and during replacement

›Venous or capillary lactate if perfusion is poor or sepsis is possible

›Precipitant and diagnostic workup

06Diagnostic Tests/dt49

Scoring Systems

›Glasgow Coma Scale

›Use the age-modified verbal scale under 5 years

›Chart hourly and act on a fall of 2 or more points

›Muir bedside clinical criteria for cerebral edema

›Apply prospectively during treatment, not only at deterioration

›Treat on one diagnostic criterion, two major criteria, or one major plus two minor criteria

›The criteria were derived to give roughly 92% sensitivity and 96% specificity with a low false-positive rate

›Biochemical severity grading

›ISPAD mild, moderate, and severe categories by pH and bicarbonate

›Severity sets the assumed deficit and the level of care

›Escalation aids

›A pediatric early warning score standardizes ward escalation

›Do not wait for a score to cross a threshold when the bedside picture is deteriorating

›Indications

›Non-contrast head CT when the cause of neurologic decline is uncertain

›To exclude hemorrhage or thrombosis before anticoagulation or a lumbar puncture

›Sequencing

›Start cerebral-edema treatment first; imaging must not delay hyperosmolar therapy

›A normal CT does not exclude cerebral edema, which is a clinical diagnosis treated on clinical grounds

›Additional studies

›CT venography if cerebral sinovenous thrombosis is suspected from focal signs or seizures

›Repeat imaging for a new focal deficit, a sustained GCS fall, or no improvement after hyperosmolar therapy

MRI

›Role

›Not part of acute management; reserve for a diagnostic question CT cannot answer

›Transfer to the scanner is rarely justified while the child is unstable

07Disposition/dispo34

Level of care

›Pediatric intensive care

›Severe DKA with pH below 7.1

›Age under 2 years

›Depressed consciousness, hemodynamic instability, or any sign of cerebral edema

›Monitored pediatric ward or high-dependency unit

›Mild to moderate DKA only when hourly neurologic checks, hourly vital signs, and 1 to 2 hourly biochemistry are guaranteed

›One-to-one nursing for any child with a reduced or fluctuating GCS

›Specialist involvement

›Pediatric endocrinology for every child, including established diabetes

›Do not manage a child with DKA in an adult ICU without pediatric-competent staff and pediatric protocols

Transfer from non-tertiary centers

›Timing and communication

›Contact the regional pediatric critical care service at the first assessment, not after deterioration

›Do not withhold fluids, insulin, potassium, and monitoring pending transport

›Holding measures

›Keep the child in the resuscitation area with 1:1 nursing and cardiac monitoring until the retrieval team arrives

›Have mannitol and 3% sodium chloride physically at the bedside before and during transfer

›Transfer criteria

›Age under 2 years, severe acidosis, reduced consciousness, a sodium abnormality, or any center that cannot deliver hourly neuro-observations

›En route

›Continue an insulin infusion with dextrose-containing fluid and avoid abrupt glucose swings

›Avoid hyperventilation if intubated and keep pCO2 at the child's compensated value

›Treat a deteriorating GCS in transit as cerebral edema and give hyperosmolar therapy

Resolution criteria, step-down, and transition to subcutaneous insulin

›Biochemical resolution

›Venous pH above 7.3, bicarbonate 15 mmol/l or higher, and a closed anion gap

›Beta-hydroxybutyrate below 1 mmol/l

08Treatment/t176

Airway and breathing decisions

›Oxygen

›Give oxygen only for hypoxia, targeting SpO2 94 to 98%

›Target the child's baseline in cyanotic heart disease, 90 to 92% in chronic lung disease, and the baseline in pulmonary hypertension

›Avoid intubation whenever possible

›Loss of spontaneous hyperventilation removes the compensation for a severe metabolic acidosis and can precipitate cardiac arrest at induction

›If intubation is unavoidable, match minute ventilation to the child's pre-intubation effort and keep pCO2 at the compensated value, often 15 to 25 mmHg

›Do not acutely normalize pCO2; a sudden rise worsens CNS acidosis and a sudden fall lowers cerebral perfusion

›Never allow pCO2 below 22 mmHg

›Rapid-sequence induction agents if intubation is required

›Ketamine 1 to 2 mg/kg IV, which preserves respiratory drive and blood pressure

›Verify against current pediatric guideline before use

›Rocuronium 1 to 1.2 mg/kg IV for paralysis

›Verify against current pediatric guideline before use

›Avoid succinylcholine when potassium is high or unknown; if used, 1.5 to 2 mg/kg IV

›Verify against current pediatric guideline before use

›Supportive measures

›Nasogastric tube on free drainage if consciousness is reduced and the child is vomiting, to prevent aspiration

›A child who tires, whose respiratory rate falls while still acidotic, or whose pCO2 climbs needs senior airway and critical-care presence at the bedside

Fluid therapy

›Initial resuscitation

›0.9% sodium chloride 10 ml/kg IV over 30 to 60 minutes for poor perfusion

›Verify against current pediatric guideline before use

›Repeat to a usual maximum of 20 to 30 ml/kg in the first hour, then reassess with senior input

›Cap an individual adolescent bolus at 500 to 1000 ml and reassess perfusion before repeating

›In frank shock give further boluses with critical-care involvement and look actively for sepsis

›Deficit and maintenance

›Assume a 5 to 7% deficit in moderate DKA and 7 to 10% in severe DKA

›Replace the deficit evenly over 24 to 48 hours and add maintenance

›Total delivered fluid should not exceed 1.5 to 2 times routine maintenance, roughly 3.5 to 4 litres per square metre per day

›Subtract resuscitation boluses above 20 ml/kg from the calculated deficit

›Fluid composition

›Use 0.9% sodium chloride or a balanced isotonic crystalloid for the first several hours

›A balanced crystalloid reduces hyperchloremic acidosis and may shorten the time the anion gap stays open

›Do not use hypotonic fluid for resuscitation; move toward 0.45% sodium chloride only once corrected sodium is stable or rising

›Add potassium once potassium is below 5.5 mmol/l and urine is passed

›Add dextrose once glucose falls to 14 to 17 mmol/l

›Evidence and cautions

›The PECARN FLUID trial found neither infusion rate nor sodium content changed neurologic or cognitive outcomes, so extreme fluid restriction is not required

›Still avoid large repeated boluses beyond what perfusion needs and avoid an abrupt drop in effective osmolality

›Reassess for fluid overload with serial lung and inferior vena cava ultrasound and a running fluid balance

Insulin therapy and glucose targets

›Regular (soluble) insulin infusion

›0.05 to 0.1 unit/kg/hour IV, started 1 hour after fluids begin, with no bolus

›Verify against current pediatric guideline before use

›Use 0.05 unit/kg/hour for children under 5 years, early presentations, or high cerebral-edema risk

›Titrate by adding dextrose, not by cutting insulin, until the acidosis clears

›Do not reduce below 0.05 unit/kg/hour; maximum 0.1 unit/kg/hour

›Do not give an intravenous insulin bolus, which raises the risk of cerebral edema and a rapid potassium shift

›Do not start insulin until potassium is known and is 3.3 mmol/l or above

›Continue the infusion until the ketoacidosis clears

›Endpoint is pH above 7.3, bicarbonate 15 mmol/l or higher, a closed anion gap, and beta-hydroxybutyrate below 1 mmol/l

›Keep the infusion running even after glucose is normal, using added dextrose

›Glucose target and rate of fall

›Aim for a controlled fall of 2 to 5 mmol/l per hour and avoid a fall faster than 5 mmol/l per hour

›Once glucose reaches 14 to 17 mmol/l, add intravenous dextrose rather than cutting insulin

›Keep glucose at roughly 8 to 12 mmol/l while the infusion runs

›Neonates and small infants tolerate a narrower margin; keep them at the higher end and check glucose more often

›Dextrose delivery

›Use a two-bag system with identical electrolytes, one bag containing 10% dextrose and one without, to titrate dextrose without changing fluid or electrolyte rate

›Verify against current pediatric guideline before use

›If glucose keeps falling on 10% dextrose at an adequate rate, only then reduce insulin, and not below 0.05 unit/kg/hour

›Treat intercurrent hypoglycemia below 3.5 mmol/l with dextrose 10% 2 to 5 ml/kg IV and increase the infused dextrose; do not stop insulin

›Verify against current pediatric guideline before use

Potassium and phosphate replacement

›Potassium status at presentation dictates the next step

›Potassium below 3.3 mmol/l: withhold insulin, give potassium 0.5 mmol/kg IV over 1 hour, and recheck before starting insulin

›Verify against current pediatric guideline before use

›Potassium 3.3 to 5.5 mmol/l with urine output: add potassium 40 mmol/l to the infusion

›Potassium above 5.5 mmol/l or no urine passed: withhold potassium and recheck in 1 to 2 hours

›Replacement practicalities

›Give potassium as half chloride and half phosphate, or as chloride with acetate, to limit the chloride load

›Do not exceed 0.5 mmol/kg/hour of intravenous potassium without continuous ECG monitoring and central access

›Recheck potassium every 1 to 2 hours while insulin runs; the nadir is usually 2 to 6 hours in

›Phosphate

›Routine phosphate replacement does not improve outcomes and risks hypocalcemia

›Replace only for phosphate below 0.32 mmol/l or symptomatic depletion with respiratory muscle weakness, rhabdomyolysis, or cardiac dysfunction, using potassium phosphate within the potassium allowance

›Monitor ionized calcium during phosphate replacement

›Magnesium

›Replace symptomatic hypomagnesemia, which perpetuates hypokalemia and prolongs the QT interval

Bicarbonate (recommended against)

›Do not give sodium bicarbonate routinely in pediatric DKA

›It is associated with cerebral edema, paradoxical CNS acidosis, worsening hypokalemia, and a slower fall in ketones

›The acidosis corrects with fluid and insulin as ketogenesis stops

›Consider it only for life-threatening hyperkalemia, or profound acidemia with pH below 6.9 and cardiovascular collapse unresponsive to resuscitation, after critical-care discussion

›If used, sodium bicarbonate 1 to 2 mmol/kg IV over at least 60 minutes with continuous ECG monitoring and added potassium

›Verify against current pediatric guideline before use

Cerebral edema: recognition and treatment

›Recognize it with the Muir bedside criteria, applied prospectively

›Diagnostic criteria: abnormal motor or verbal response to pain, decorticate or decerebrate posturing, cranial nerve palsy, abnormal neurogenic respiratory pattern

›Major criteria: altered or fluctuating consciousness, sustained heart-rate deceleration of more than 20 per minute not explained by sleep or improved volume state, age-inappropriate incontinence

›Minor criteria: vomiting, headache, lethargy or difficulty rousing, diastolic blood pressure above 90 mmHg, age under 5 years

›Treat on one diagnostic criterion, two major criteria, or one major plus two minor criteria, without waiting for imaging

›Timing

›Usually 4 to 12 hours after treatment starts

›Can be present at diagnosis or appear up to 24 to 48 hours in

›Immediate actions

›Reduce the intravenous fluid rate by about one third

›Raise the head of the bed to 30 degrees and keep the head midline

›Give hyperosmolar therapy without delay, choosing one agent first and drawing up the second

›Hypertonic saline 3%: 2.5 to 5 ml/kg IV over 10 to 15 minutes, a typical adolescent dose being 150 to 250 ml

›Verify against current pediatric guideline before use

›Preferred when the child is hyponatremic or hypotensive

›Repeat once after 15 to 30 minutes if there is no neurologic improvement

›Mannitol 0.5 to 1 g/kg IV over 10 to 20 minutes

›Verify against current pediatric guideline before use

›May repeat after 30 minutes to 2 hours if there is no response

›Give through a filter and keep a repeat dose and 3% saline ready; avoid while the child is hypotensive or volume-depleted until perfusion is restored

›Airway support for a GCS at or below 8 or loss of protective reflexes

›Intubate with the pCO2 cautions above and never let pCO2 fall below 22 mmHg

›Prophylactic hyperventilation to a low pCO2 is associated with worse outcome and must be avoided

›Imaging and specialists

›Obtain a non-contrast head CT once the child is stabilized to exclude hemorrhage or thrombosis; do not delay drug treatment for the scan

›Involve pediatric neurology and neurosurgery and continue hourly, then more frequent, neurologic observation

Monitoring protocol during treatment

›Bedside observations

›Hourly heart rate, respiratory rate, blood pressure, SpO2, GCS or age-appropriate score, capillary glucose, and fluid balance

›More frequent neurologic checks in children under 5 years, in severe acidosis, and for the first 12 hours

›Laboratory cadence

›Venous gas, sodium, potassium, chloride, and glucose every 1 to 2 hours initially, then every 2 to 4 hours once trends are safe

›Beta-hydroxybutyrate every 2 to 4 hours where available, otherwise track the anion gap and bicarbonate

›Continuous monitoring

›Cardiac monitoring and pulse oximetry throughout the insulin infusion and potassium replacement

›Strict hourly input and output; catheterize if consciousness is reduced or output is unclear

›Derived trends and escalation

›Calculate corrected sodium and effective osmolality with each blood draw and chart the trend

›Escalate immediately for a GCS fall of 2 or more, any Muir criterion, a corrected sodium that fails to rise, or a glucose fall faster than 5 mmol/l per hour

Managing the precipitating illness

›Sepsis

›Treat on its own pathway if suspected; DKA and sepsis frequently coexist and fever points to infection

›Antibiotics outside the neonatal period: ceftriaxone 50 to 75 mg/kg IV once daily, maximum 2 g, for a suspected serious bacterial infection, adjusted to source and local guidance

›Infants under 12 weeks, including infant-onset and monogenic diabetes

›Ampicillin 50 mg/kg per dose IV every 6 to 8 hours, with a neonatal band of every 8 to 12 hours in the first week of life, plus cefotaxime 50 mg/kg per dose IV every 8 hours or gentamicin

›Ampicillin monotherapy is inadequate at this age; a second agent for Gram-negative and Listeria cover is mandatory

›Avoid ceftriaxone in the neonate because of bilirubin displacement and calcium-ceftriaxone precipitation

›Non-infective precipitants

›Review insulin pump function, place the child on an infusion, and remove a failed pump set

›Address the psychosocial precipitant of a missed-insulin presentation before discharge

›Symptom control

›Antiemetic for persistent vomiting: ondansetron 0.15 mg/kg IV per dose, maximum 4 mg per dose, with a baseline ECG given the electrolyte shifts and QT risk

Iatrogenic harms: routine interventions to modify or avoid

›Intubation and mechanical ventilation

›Removes respiratory compensation for the acidosis; induction or a low set minute ventilation can cause abrupt lethal acidemia

›If unavoidable, match minute ventilation to pre-intubation effort and keep pCO2 at the compensated value, never below 22 mmHg

›Sedation

›Masks the declining consciousness that is the earliest sign of cerebral edema

›Avoid routine sedation; if essential use ketamine 1 to 2 mg/kg IV and record a pre-sedation neuro score

›Verify against current pediatric guideline before use

›Fluid loading

›Boluses beyond what perfusion requires cause an abrupt osmolar drop; give only for shock and cap as in the fluid section

›The PECARN FLUID trial permits liberal-within-limits rehydration but not repeated unindicated boluses

›Oxygen

›Routine high-flow oxygen has no benefit and hyperoxia is undesirable; treat to the SpO2 target and its comorbidity exceptions

›Vasopressors

›Shock in DKA is almost always hypovolemic and responds to fluid; a reflex pressor treats a number, not the physiology

›If distributive shock from sepsis is genuinely present, norepinephrine 0.05 to 0.5 mcg/kg/min IV titrated to perfusion

›Verify against current pediatric guideline before use

›Mechanical circulatory support and the intra-aortic balloon pump

›Not indicated; the myocardial dysfunction of severe DKA reverses with correction of acidosis, potassium, and phosphate

›Anticoagulation

›DKA is prothrombotic and femoral central lines in young children carry a high thrombosis rate; prefer non-femoral access and remove lines early

›Reserve prophylactic enoxaparin 0.5 mg/kg SC every 12 hours for an adolescent with a central catheter and severe DKA, and only after intracranial hemorrhage is excluded

›Do not give therapeutic anticoagulation for a suspected stroke until imaging excludes hemorrhage

›Fibrinolysis

›Not used for DKA; systemic thrombolysis for arterial ischemic stroke in children is generally contraindicated and needs stroke-team direction

›Analgesia

›Abdominal pain usually resolves with rehydration and insulin

›Opioids blunt the sensorium, depress the respiratory drive compensating for the acidosis, and worsen ileus; NSAIDs risk acute kidney injury in a dehydrated child

›If analgesia is essential, fentanyl 0.5 to 1 mcg/kg IV with continuous monitoring

›Verify against current pediatric guideline before use

Therapy not working: troubleshooting

›Acidosis not improving after 4 to 6 hours

›Check the insulin: pump programming, line disconnection, tissue infiltration, an expired bag, or a rate below 0.05 unit/kg/hour

›Check for under-resuscitation and ongoing hypoperfusion

›Check for unrecognized sepsis or another acidosis such as lactate, salicylate, or toxic alcohol

›Distinguish a persistent open anion gap, meaning ongoing ketoacidosis, from a normal-gap hyperchloremic acidosis, which is expected; switch to a balanced crystalloid for the latter

›Glucose not falling despite insulin

›Almost always an insulin delivery failure; inspect the whole circuit and replace it

›Persistent tachycardia and poor perfusion despite adequate fluid

›Reconsider sepsis, evolving cerebral edema, myocardial dysfunction from hypokalemia or hypophosphatemia, or a pericardial effusion

›Rising lactate or a widening anion gap after initial improvement

›Look for a new infection, bowel ischemia from severe dehydration, or an insulin interruption

›Neurologic deterioration at any point

›Treat as cerebral edema immediately; do not attribute drowsiness to tiredness or to sedation

›Refractory hypokalemia

›Replace magnesium, reduce the insulin rate toward 0.05 unit/kg/hour, and confirm potassium is actually in the running fluid

09Special Populations/sp35

Pregnancy

›Applies to pregnant adolescents; confirm with a pregnancy test in any patient of childbearing potential

›Recognition

›Ketoacidosis develops at lower glucose in pregnancy and can occur with glucose below 11 mmol/l

›A lower threshold to check ketones for any unwell pregnant patient with diabetes

›Priorities

›Maternal stabilization is the priority and is the best fetal resuscitation

›Continuous fetal heart-rate monitoring if the fetus is potentially viable, with obstetric and neonatology involvement

›Nurse in the left lateral position to protect venous return

›Do not deliver for fetal heart-rate abnormalities until the mother is corrected unless there is an independent obstetric emergency

›Treatment adjustments

›Insulin infusion and fluid principles are unchanged; potassium requirements are often higher

›Maintain higher-normal maternal oxygenation because fetal reserve is small

›Ondansetron 0.15 mg/kg IV, maximum 4 mg per dose, is used for refractory vomiting after a shared discussion of first-trimester data

Geriatric

›Not applicable within the pediatric age range; the relevant edge is the older adolescent or young adult transitioning to adult services

›Physiologic contrasts in older patients

›A hyperglycemic hyperosmolar state predominates, carries higher mortality, and requires slower osmolar correction

›Coexisting kidney or cardiac disease limits the fluid rate and mandates closer potassium and volume monitoring

›Neurologic contrasts

›Classic pediatric cerebral edema is rare after adolescence

›Osmotic demyelination from rapid sodium shifts becomes the greater CNS concern

›Handover

›Transfer transition-age patients with an explicit statement of any cerebral-edema history and the usual insulin regimen

Pediatrics

›The entire topic is pediatric; every dose is weight-based and every neurologic assessment must be age-appropriate

›Highest-risk groups

›Children under 5 years and those with new-onset diabetes carry the highest cerebral-edema risk and warrant the lowest insulin rate of 0.05 unit/kg/hour and the closest neuro-observation

10Background/b37

Epidemiology

›Presentation at diagnosis

›DKA is present at the diagnosis of type 1 diabetes in about 30% of children, ranging roughly from 15% to 70% between countries and by access to care

›Type 1 diabetes incidence in children is rising by roughly 3% per year in many registries

›Recurrent DKA

›Among children with established type 1 diabetes, DKA recurs at roughly 1 to 10 episodes per 100 patient-years, concentrated in a minority with insulin omission

›Mortality and cerebral edema

›Overall mortality from pediatric DKA is about 0.15% to 0.3% in resource-rich settings and substantially higher where care is delayed

›Clinically overt cerebral edema complicates about 0.5% to 1% of pediatric DKA episodes

›Cerebral edema carries about 20% to 25% mortality and accounts for 60% to 90% of DKA-related deaths in children

›Roughly 10% to 25% of cerebral-edema survivors have persistent neurologic deficits

›Related states

›Subclinical cerebral edema on imaging or with subtle mental-status change is considerably more common than the overt syndrome

›The hyperglycemic hyperosmolar state is uncommon in children and is seen mainly in adolescents with type 2 diabetes

Pathophysiology

›Hormonal drivers

›Absolute or relative insulin deficiency with excess glucagon, catecholamines, cortisol, and growth hormone

›Unrestrained gluconeogenesis, glycogenolysis, and impaired peripheral glucose uptake produce hyperglycemia

›Ketogenesis and acidosis

›Lipolysis delivers free fatty acids that the liver converts to beta-hydroxybutyrate and acetoacetate, causing a high anion gap metabolic acidosis

›Kussmaul respiration is respiratory compensation; its loss unmasks the full acidosis

›Fluid and electrolyte losses

›Hyperglycemia drives an osmotic diuresis with large losses of water, sodium, potassium, and phosphate

›Total body potassium and phosphate are depleted even when serum values are normal or high, because acidosis and insulin lack shift them extracellularly

›Cerebral edema mechanism

›Not simply osmotic and not purely iatrogenic; cerebral hypoperfusion during untreated DKA followed by reperfusion, ion-transporter activation, and both cytotoxic and vasogenic mechanisms contribute

›The association with higher urea, greater hypocapnia, and a blunted rise in corrected sodium supports a perfusion-driven rather than a purely fluid-driven model

11Patient Discharge Instructions/pdi34

Discharge planning and safety-netting for clinicians

›Admission rules

›Never discharge a newly diagnosed child; admit for stabilization and structured education

›For established diabetes, discharge only after full biochemical resolution and when the child is eating

›Equipment and follow-up

›Confirm the family leaves with a working glucometer, a blood-ketone meter and strips, adequate insulin, and an in-date glucagon rescue kit

›Arrange endocrinology and diabetes-nurse review within 1 to 2 weeks and give a 24-hour contact number

›Teaching and precipitant

›Check that the family can state the sick-day rules and demonstrate a correction-dose calculation before discharge

›Provide a written sick-day plan and the specific fix for the identified precipitant, such as pump training, a prescription refill, or a psychosocial referral

›Document any cerebral-edema course and communicate it to the diabetes team and primary physician

copy discharge instructions

›About this visit

›Your child was treated for diabetic ketoacidosis, a serious problem that happens when there is not enough insulin

›Diabetic ketoacidosis can come back quickly if insulin is missed or an illness is not managed

›Insulin and blood sugar checks

›Give insulin every day and never skip a dose, even when your child is unwell or not eating

›On any sick day, check blood sugar every 2 to 3 hours, day and night

›Check blood ketones whenever the blood sugar is above 15 mmol/l or your child is unwell or vomiting

›If blood ketones are 0.6 to 1.5 mmol/l, give extra rapid-acting insulin as your team has instructed and recheck in 2 hours

›Food and fluids

›Give sugar-free fluids if the blood sugar is high, and sugar-containing fluids if the blood sugar is low or normal

›Keep offering fluids and carbohydrate in small frequent sips if your child will not eat

›Fever and pain relief

›You may give acetaminophen 15 mg/kg per dose by mouth or rectum every 4 to 6 hours, up to 75 mg/kg in 24 hours and never more than 4 g in a day

›You may give ibuprofen 10 mg/kg per dose by mouth every 6 to 8 hours, up to 40 mg/kg in 24 hours, but not if your child is vomiting, not drinking, or passing little urine

›Severe low blood sugar

›Use the glucagon rescue kit if your child cannot be woken or cannot safely swallow: 0.5 mg by injection if under 25 kg, 1 mg by injection if 25 kg or more, or nasal glucagon 3 mg if age 4 years or older, then call emergency services

12References/r26

Guidelines and consensus statements

›ISPAD Clinical Practice Consensus Guidelines: diabetic ketoacidosis and hyperglycemic hyperosmolar state

›International Society for Pediatric and Adolescent Diabetes, 2022 update

›Integrated care pathway for children and young people under 18 years with diabetic ketoacidosis

›British Society for Paediatric Endocrinology and Diabetes, 2021

›Standards of Care in Diabetes: children and adolescents

›American Diabetes Association, current annual edition

›Pediatric Advanced Life Support

›American Heart Association, current guidelines, for shock, airway, and resuscitation drug dosing

›BNF for Children

›Joint Formulary Committee, current edition, for insulin infusion, potassium, mannitol, and hypertonic saline dosing

Landmark trials and cohort studies

›PECARN FLUID trial of rehydration rate and tonicity in pediatric DKA

›Kuppermann N and colleagues, New England Journal of Medicine, 2018 — neither rehydration rate nor fluid sodium content altered neurologic or cognitive outcomes

›PECARN observational study of cerebral edema risk factors

›Glaser N and colleagues, New England Journal of Medicine, 2001 — higher serum urea, greater hypocapnia, and bicarbonate therapy were associated with cerebral edema

›Bedside diagnostic criteria for cerebral edema in pediatric DKA

›Muir AB and colleagues, Diabetes Care, 2004 — diagnostic, major, and minor bedside criteria

›UK case-control study of cerebral edema in childhood DKA

›Edge JA and colleagues — association with younger age, new-onset diabetes, and severity of acidosis

›Neuroimaging studies of DKA-related brain injury

›Glaser and colleagues, serial MRI showing vasogenic and cytotoxic contributions and pretreatment cerebral hypoperfusion

Pediatric dosing and airway references

›APLS: The Practical Approach

›Advanced Life Support Group, current edition, for weight estimation and rapid-sequence intubation

›Institutional pediatric DKA order set and two-bag intravenous fluid protocol

›Local pediatric endocrinology and critical care, reviewed against ISPAD 2022

›Lexicomp Pediatric and Neonatal Dosage Handbook

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed September 13, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.