Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are acute, life-threatening metabolic emergencies of diabetes mellitus characterized by severe hyperglycaemia, dehydration, and electrolyte disturbances. DKA is distinguished by the presence of ketosis and metabolic acidosis, whereas HHS is characterized by profound hyperglycaemia and hyperosmolality with minimal or absent ketosis. Both conditions require prompt recognition, hospital admission, aggressive fluid replacement, electrolyte correction, insulin therapy, and treatment of the underlying precipitating cause.

Pathophysiology

Diabetic ketoacidosis (DKA)

Absolute or relative insulin deficiency results in:

• Increased hepatic glucose production

• Reduced peripheral glucose utilization

• Lipolysis with production of ketone bodies

• Metabolic acidosis

• Osmotic diuresis causing severe dehydration

• Electrolyte depletion, particularly potassium

Hyperosmolar hyperglycaemic state (HHS)

Relative insulin deficiency is sufficient to prevent significant ketosis but inadequate to control hyperglycaemia, resulting in:

• Severe hyperglycaemia

• Marked hyperosmolality

• Profound dehydration

• Altered consciousness

• Minimal or absent ketoacidosis

Common precipitating factors

• Newly diagnosed diabetes mellitus

• Poor adherence to insulin therapy

• Infection (pneumonia, urinary tract infection, sepsis)

• Myocardial infarction

• Stroke

• Pancreatitis

• Trauma or surgery

• Pregnancy

• Corticosteroid therapy

• Thiazide diuretics

• Antipsychotic medications

• Substance abuse

Clinical presentation

Symptoms

• Thirst

• Polyuria

• Nausea

• Vomiting

• Abdominal pain

• Shortness of breath

• Fruity-smelling breath

• Fever

• Weakness

• Lethargy

• Confusion

• Drowsiness

• Altered mental status

• Coma

Signs

• Severe dehydration

• Tachycardia

• Hypotension

• Kussmaul breathing (DKA)

• Reduced level of consciousness

• Signs of precipitating infection

Diagnostic criteria

Diagnostic criteria for DKA and HHS

Important notes

• Suspected DKA should be confirmed immediately.

• All patients require hospital admission for intensive management.

Investigations

Initial investigations

• Capillary blood glucose

• Urine ketones

• Blood ketones (if available)

• Arterial or venous blood gas

• Serum electrolytes

• Serum bicarbonate

• Serum osmolality

• Urea

• Serum creatinine

• Full blood count

Search for precipitating causes

• Urinalysis

• Blood cultures (if indicated)

• Chest X-ray

• ECG

• Cardiac biomarkers when indicated

Management

Treatment of DKA and HHS follows the same general principles:

• Frequent clinical monitoring

• Rapid restoration of circulating volume

• Correction of electrolyte abnormalities

• Insulin therapy

• Identification and treatment of precipitating factors

Average time to resolution:

• DKA: 10–18 hours

• HHS: 9–11 hours

Management algorithm

The following algorithm summarizes the management of paediatric diabetic ketoacidosis in a low-resource centre, including assessment of dehydration, fluid therapy, insulin initiation, monitoring, recognition of cerebral oedema, and recovery.

Fluid management

Fluid replacement is the first priority.

Benefits include:

• Restores circulating volume

• Improves tissue perfusion

• Lowers plasma glucose

• Reduces plasma osmolality

• Restores renal perfusion

• Improves insulin sensitivity

Adults

Initial fluid:

• 0.9% sodium chloride (normal saline)

Recommended infusion rate:

• 15–20 mL/kg/hour

• Approximately 1 L/hour

• Maximum 50 mL/kg during the first four hours

Estimated water deficit:

• Approximately 100 mL/kg body weight

Children

Use:

• Normal saline (NS)

• OR Ringer's lactate (RL)

Continue fluids over 48 hours

Fluid requirement =

Deficit + 48-hour maintenance

Maintenance fluid requirements

Electrolyte management

Almost every patient has a significant total body potassium deficit.

Potassium loss results from:

• Osmotic diuresis

• Secondary hyperaldosteronism

• Gastrointestinal losses

• Acidosis

Despite depletion, serum potassium may initially appear normal or elevated because:

• Insulin deficiency

• Hyperosmolality

• Movement of potassium from intracellular to extracellular space

ECG should be reviewed for evidence of hyperkalaemia or hypokalaemia.

Potassium replacement protocol

Important notes

• Delay insulin if potassium is <3.3 mEq/L.

• Insulin worsens hypokalaemia by driving potassium into cells.

• Correcting potassium first reduces the risk of cardiac arrhythmias, respiratory muscle weakness, and cardiac arrest.

Insulin therapy

Continuous intravenous regular insulin is the treatment of choice.

Before starting insulin:

• Correct hypovolaemic shock.

• Correct severe hypokalaemia.

Contraindication

Do not start insulin if serum potassium is <3.3 mEq/L.

Standard insulin regimen

Option 1

Regular insulin:

• IV bolus 0.1 units/kg

Follow within 5 minutes by:

• Continuous infusion 0.1 units/kg/hour

Option 2

Omit bolus and start:

• Continuous infusion 0.14 units/kg/hour

Practical preparation

Examples:

• 100 IU insulin in 100 mL normal saline

• Infuse approximately 5–7 mL/hour

OR

• 60 IU insulin in 60 mL normal saline

• Infuse approximately 6–7 mL/hour

Monitoring insulin response

If plasma glucose does not decrease by 2.8–4.2 mmol/L during the first hour:

• Increase insulin infusion by 50–100%

Target glucose decline:

• Approximately 5.5 mmol/L/hour

Avoid reducing glucose below:

• 14 mmol/L during the first 4–5 hours

Ketones may require 12–24 hours to clear after glucose normalizes.

Monitoring

Continuous monitoring is essential.

Monitor:

• Blood glucose (hourly)

• Vital signs

• Fluid balance

• Neurological status

• Serum electrolytes

• Serum potassium

• Renal function

• Ketones

• Acid-base status

Watch carefully for:

• Cerebral oedema

• Hypoglycaemia

• Hypokalaemia

• Pulmonary oedema

• Acute kidney injury

Cerebral oedema

Suspect if there is:

• Reduced consciousness

• Irritability

• Severe headache

• Bradycardia

• Hypertension

• Cranial nerve palsies

• Neurological deterioration

Management

• Exclude hypoglycaemia

• Mannitol 0.5–1 g/kg IV

• Urgent ICU transfer

• CT brain once clinically stable

Transition to subcutaneous insulin

Transition once:

• Patient is clinically stable

• Able to tolerate oral feeding

• Acidosis has resolved

• Ketones have cleared or are improving

Continue IV insulin for approximately 1–2 hours after the first subcutaneous insulin dose to prevent rebound hyperglycaemia.

Management Algorithm for Paediatric Diabetic Ketoacidosis (DKA) in Low-Resource Settings

Step 1: Assess the Child

A. Shock, reduced conscious level, or coma

• Follow the ABC (Airway, Breathing, Circulation) approach.

• Start intravenous (IV) fluid resuscitation immediately.

• Proceed to IV therapy.

If there is no improvement:

• Reassess the patient.

• Review fluid balance and continue IV therapy.

• Correct acidosis if present.

• Check insulin dose and adjust if necessary.

• Consider sepsis or another underlying cause.

B. Moderate dehydration (5–10%)

Features include:

• Clinical dehydration (5–10%)

• Clinical acidosis

• Vomiting

Management:

• Correct dehydration over 48 hours using 0.9% normal saline (NS).

• Add 20 mmol potassium chloride (KCl) to every 500 mL of IV fluid when indicated.

• Start regular insulin infusion at 0.1 IU/kg/hour.

Proceed to close observation.

C. Mild dehydration (<5%)

Features include:

• Clinically well

• Mild dehydration (<5%)

• Able to tolerate oral fluids

Management:

• Start subcutaneous insulin.

• Encourage oral fluids, such as oral rehydration solution (ORS).

If there is no improvement, switch to intravenous therapy.

Step 2: Observation and Monitoring

Monitor the patient closely:

• Blood glucose every 1–2 hours

• Neurological status every hour

• Fluid intake and output

• Serum electrolytes:

  • 2 hours after starting IV therapy

  • Then every 4–6 hours

Step 3: Blood Glucose Falls Below 14 mmol/L

When blood glucose is <14 mmol/L:

• Change IV fluid from normal saline to 5% dextrose.

• Continue insulin therapy.

• Continue frequent monitoring.

Step 4: Clinical Improvement

The child is improving when:

• Clinically well

• Drinking normally

• Tolerating food

Note: Urine ketones may remain positive despite clinical improvement.

Step 5: Insulin After Recovery

Continue maintenance insulin therapy.

• Children previously receiving insulin should resume their usual insulin regimen before developing DKA.

• Newly diagnosed patients should commence long-term insulin therapy according to the recommended insulin regimen.

Management of Neurological Deterioration

Suspect cerebral oedema if the child develops:

• Reduced level of consciousness

• Irritability

• Signs of raised intracranial pressure

• Headache

• Slowing heart rate (bradycardia)

First:

• Exclude hypoglycaemia.

If cerebral oedema is suspected:

• Administer mannitol 0.5–1 g/kg IV immediately.

• Transfer the patient to the intensive care unit (ICU) if available.

• Perform a CT scan only after the patient is clinically stable.

Management of Failure to Improve

If there is no clinical improvement despite treatment:

• Reassess hydration status.

• Review fluid balance.

• Continue IV therapy.

• Correct acidosis if required.

• Review insulin dosage and administration.

• Investigate and treat precipitating causes, particularly sepsis.

Prevention

• Never stop insulin during illness (sick-day rules)

• Early treatment of infections

• Regular blood glucose monitoring

• Home ketone monitoring where available

• Adequate hydration during illness

• Patient education on early symptoms of DKA

• Regular diabetes follow-up

• Proper insulin storage and adherence

Outcome

With prompt recognition and appropriate treatment, most patients with diabetic ketoacidosis (DKA) show progressive improvement over 10–18 hours, while hyperosmolar hyperglycaemic state (HHS) usually resolves within 9–11 hours. Clinical improvement is indicated by restoration of adequate circulation and hydration, normalization of blood glucose and electrolyte levels, resolution of metabolic acidosis and ketosis (in DKA), improvement in mental status, stable vital signs, and the ability to tolerate oral fluids and food. Patients can be transitioned from intravenous to subcutaneous insulin once ketoacidosis has resolved, they are clinically stable, and oral intake has resumed. Ongoing monitoring and treatment of the underlying precipitating cause are essential to prevent recurrence. In children with DKA, urine ketones may remain positive despite clinical recovery and should not be used alone to determine treatment success or hospital discharge.