Diabetic Ketoacidosis (DKA): Emergency Recognition, Assessment and Management

Learning objectives

• Explain the pathophysiology and diagnostic triad of hyperglycaemia or known diabetes, ketonaemia and metabolic acidosis.
• Recognise early symptoms, severe DKA, euglycaemic DKA and dangerous complications.
• Perform a rapid ABCDE assessment, bedside glucose/ketone testing, focused history and severity triage.
• Describe safe pre-hospital stabilisation and the hospital sequence of fluids, insulin, potassium, dextrose and monitoring.
• Identify common precipitants, special populations, treatment complications and prevention strategies.

Definition and pathophysiology

DKA occurs when there is too little effective insulin for the body’s needs, together with excess glucagon, adrenaline, cortisol and growth hormone. Glucose cannot be used adequately by cells, so the liver increases glycogenolysis and gluconeogenesis. At the same time, fat is broken down into free fatty acids; the liver converts them into beta-hydroxybutyrate and acetoacetate. These ketones consume bicarbonate and produce a high-anion-gap metabolic acidosis.

High glucose exceeds the renal reabsorption threshold and causes osmotic diuresis. Water and electrolytes (sodium, chloride, potassium, phosphate and magnesium) are lost through urine. Vomiting and reduced intake intensify the deficit. Serum potassium may initially be normal or high because acidosis and insulin deficiency shift potassium out of cells, even though total-body potassium is depleted. When insulin and fluids are started, potassium moves back into cells and the serum level can fall rapidly.

Diagnostic concept

Common precipitants

• Insulin omission or interruption: missed doses, wrong dose, vomiting, insulin pump blockage, empty/expired insulin, poor injection technique or inability to obtain medicines.
• Infection: pneumonia, urinary infection, skin/soft-tissue infection, malaria, gastroenteritis, tuberculosis or sepsis.
• Acute physiological stress: myocardial infarction, stroke, pancreatitis, trauma, burns, surgery or severe asthma.
• Medicines: corticosteroids, sympathomimetics, atypical antipsychotics and SGLT2 inhibitors.
• New diabetes: first presentation of type 1 diabetes, especially in a child or young adult, or ketosis-prone type 2 diabetes.
• Pregnancy and fasting: accelerated starvation and altered metabolism can produce DKA with lower glucose.
• Psychosocial factors: fear of hypoglycaemia, eating disorder, depression, cognitive impairment, substance use, homelessness or lack of family support.

Clinical features and progression

First contact and scene management

1. Use standard precautions and assess for vomit, sharps, insulin needles, pump equipment, alcohol, medicines and other hazards.
2. Identify the patient, introduce yourself and ask relatives to bring the insulin, diabetes card, glucose/ketone meter, medication list and sick-day plan.
3. Activate emergency transport and senior clinical support early. DKA is not safely managed at home or in an unmonitored clinic.
4. Keep the patient resting; prevent exertion. If vomiting, use a safe lateral position while protecting the airway and considering spinal/trauma precautions.
5. Do not give oral food or fluids to a drowsy, actively vomiting or aspiration-risk patient. A fully alert patient may take small sips while transfer is arranged unless fluid restriction applies.

ABCDE assessment

A — Airway

• Assess speech, secretions, vomit, airway reflexes and ability to protect the airway. Reduced consciousness in DKA is a serious finding.
• Suction, position and use basic airway adjuncts as trained. Prepare advanced airway support if airway protection fails.

B — Breathing

• Count respiratory rate and assess depth, effort and Kussmaul pattern. A falling respiratory rate in an exhausted patient may signal impending respiratory failure, not improvement.
• Measure SpO₂ and give oxygen for hypoxaemia or respiratory distress according to local protocol. Do not suppress compensatory hyperventilation without expert help.

C — Circulation

• Measure pulse, blood pressure, capillary refill, temperature, peripheral perfusion and urine output. Check for shock and fluid overload risk.
• Insert a large-bore IV cannula if trained; collect venous blood for glucose, ketones, electrolytes, urea/creatinine, full blood count, blood gas and cultures when indicated.
• Begin isotonic crystalloid only under the local DKA protocol. Use smaller aliquots and close reassessment in heart failure, kidney failure, elderly patients and pregnancy.

D — Disability

• Record AVPU/GCS, pupils, behaviour and focal neurological signs. Check capillary glucose and blood ketones immediately.
• Confusion or coma may be due to acidosis, hyperosmolality, hypoglycaemia from treatment, stroke, sepsis, intoxication or cerebral oedema; never assume one cause.

E — Exposure

• Check temperature, skin, injection sites, pump tubing, feet, wounds, pressure areas and signs of infection or trauma.
• Look for pregnancy, dehydration, abdominal tenderness, chest pain, focal neurological deficit and medication interruption while preserving warmth and dignity.

Focused history: SAMPLER plus sick-day questions

Investigations and interpretation

• Glucose: repeat bedside value and send venous plasma glucose. Do not exclude DKA because the glucose is only modestly elevated.
• Ketones: use blood beta-hydroxybutyrate when available. NHS guidance treats blood ketones over 3 mmol/L or urine ketones over 2+ as a medical emergency; local pathways may differ.
• Venous blood gas: pH, bicarbonate, pCO₂ and lactate; calculate the anion gap when appropriate. Arterial sampling is reserved for specific respiratory/critical-care indications.
• Electrolytes/renal function: sodium, potassium, chloride, bicarbonate, urea, creatinine, magnesium and phosphate; calculate corrected sodium and osmolality with senior input.
• Precipitant tests: full blood count, cultures, urinalysis, malaria test where relevant, ECG/troponin, chest imaging, pregnancy test, lipase or other targeted tests.
• Monitoring baseline: weight if safe, fluid balance, urine output, temperature, neurological status and medication reconciliation.

Immediate pre-hospital and emergency-department priorities

1. Recognise DKA early, call the receiving facility and communicate the glucose, ketones, mental state, vital signs, suspected cause and treatment already given.
2. Protect airway and breathing; position safely, suction vomit and give oxygen only when indicated by hypoxaemia or respiratory compromise.
3. Obtain IV access and collect blood without delaying circulation support. Treat shock with isotonic crystalloid under protocol and reassess after each bolus.
4. Do not give an insulin bolus or start an unsupervised infusion in the field unless a written local protocol, monitoring, pump and trained prescriber support it.
5. Transfer urgently to a facility able to measure electrolytes/ketones, provide IV insulin and manage dysrhythmias, renal failure, pregnancy or critical deterioration.

Hospital treatment sequence

1. Fluids

• Isotonic crystalloid is usually started first to restore intravascular volume and renal perfusion. JBDS notes that fluid replacement precedes insulin and aims to restore circulation, clear ketones and correct electrolyte imbalance.
• Use the local adult protocol for rate and volume. Reassess blood pressure, pulse, urine output, lung sounds, sodium and osmolality frequently.
• Modify fluid volume/rate in heart failure, renal failure, older adults, pregnancy and adolescents; excessive fluid can cause pulmonary oedema or neurological harm.

2. Insulin

• Once initial fluids are running and potassium is known/managed, start a fixed-rate IV soluble insulin infusion in a monitored setting. JBDS commonly uses 0.1 units/kg/hour; the actual order must follow local policy.
• Insulin suppresses ketogenesis; it is continued until ketones/acidosis resolve, not merely until glucose becomes normal.
• When glucose falls below approximately 14 mmol/L in the JBDS pathway, add 10% dextrose and consider reducing insulin to 0.05 units/kg/hour to prevent hypoglycaemia and hypokalaemia while ketones clear.

3. Potassium and other electrolytes

• Measure potassium before insulin and repeat frequently. Total-body potassium is depleted even when the admission serum value is high.
• Do not add potassium when serum potassium is high or the patient is anuric; replace according to the result and local protocol. Severe hypokalaemia requires urgent senior/critical-care review before insulin.
• Magnesium and phosphate may fall. Routine phosphate replacement is not recommended by JBDS, but specialist replacement may be considered for severe deficiency, respiratory weakness, cardiac dysfunction or rhabdomyolysis.

4. Dextrose and transition

• Add IV dextrose when glucose falls while ketones remain, so insulin can continue to clear ketones safely.
• Continue IV insulin and dextrose until the patient is clinically improved, ketones have cleared, acidosis has resolved and oral intake is reliable.
• Start subcutaneous basal/bolus insulin before stopping IV insulin, with an overlap period specified by the hospital protocol, to avoid rebound ketosis.

Targets and monitoring in a monitored unit

DKA resolution and escalation

• Use local biochemical criteria. JBDS defines resolution as blood ketones below 0.6 mmol/L and venous pH above 7.3; bicarbonate alone may be misleading after large volumes of saline.
• Escalate to HDU/ICU for severe acidosis, shock, altered consciousness, severe potassium abnormality, respiratory failure, anuria, pregnancy, renal/heart failure, sepsis or inability to provide required monitoring.
• If ketones are not falling at the expected rate, check the infusion pump, line, insulin preparation, fluid delivery, sampling accuracy, ongoing infection and missed diagnosis.
• If consciousness deteriorates, reassess airway, glucose, sodium/osmolality, cerebral oedema, stroke, seizure, sepsis and other causes; urgent senior review and imaging may be required.

Complications of DKA and its treatment

• Hypokalaemia: insulin and correction of acidosis drive potassium intracellularly; weakness, ECG changes, ventricular dysrhythmia and arrest can occur.
• Hyperkalaemia: acidosis, renal failure and tissue breakdown can cause life-threatening conduction abnormalities before treatment.
• Hypoglycaemia: occurs when insulin continues without timely dextrose or monitoring.
• Cerebral oedema/neurological injury: more common in children and young people but neurological deterioration in any patient is an emergency.
• Pulmonary oedema: excessive fluid in renal or cardiac failure; monitor crackles, oxygenation, work of breathing and weight.
• Thrombosis, aspiration, acute kidney injury, rhabdomyolysis and myocardial injury: result from dehydration, inflammation, immobility or electrolyte shifts.
• Hyperchloraemic acidosis: may persist after ketones resolve following large volumes of 0.9% saline; interpret the whole clinical and biochemical picture.

Special populations

• Pregnancy: DKA can develop faster and at lower glucose. Treat as an obstetric emergency with medical, diabetes and obstetric teams; monitor mother and fetus.
• Children/adolescents: use a paediatric pathway, weight-based fluid calculation and specialist support; do not apply adult boluses or infusion rates.
• Renal failure/dialysis: volume, potassium and insulin clearance differ; avoid routine large fluid loads and involve nephrology/critical care.
• Heart failure/older adults: give smaller aliquots with frequent lung, perfusion and urine reassessment.
• SGLT2 inhibitors: consider euglycaemic DKA during illness, fasting, surgery or reduced insulin; check ketones even when glucose is not very high.

Nursing and EMT responsibilities

• Use a DKA observation chart; document every glucose, ketone, electrolyte, infusion rate, fluid volume, urine output, neurological score and clinical response.
• Check IV lines, insulin pump settings, infusion-pump programming and dextrose/potassium compatibility with an independent second checker where policy requires.
• Maintain aspiration, seizure, falls and pressure-injury precautions; provide oral care and reposition safely.
• Monitor for infection, chest pain, ECG changes, abdominal deterioration, worsening work of breathing, fluid overload and reduced urine output.
• Explain procedures calmly, involve family with consent, provide culturally appropriate education and use teach-back to confirm understanding.
• Escalate any unexpected trend rather than waiting for the next scheduled sample. A falling glucose with persistent ketones is not treatment failure if insulin and dextrose are being used correctly; a rising ketone level is concerning.

Discharge planning and prevention

1. Identify and address the precipitant: infection treatment, insulin access, pump education, medicine reconciliation, mental-health support or diabetes-team review.
2. Confirm the patient can eat and drink, administer insulin correctly, recognise hypo/DKA symptoms and access glucose/ketone testing.
3. Provide a written sick-day plan: continue prescribed basal insulin, check glucose frequently, test ketones during illness/high readings, maintain fluids if safe and seek help early.
4. Explain never to stop insulin simply because food intake is reduced; obtain professional advice for dose adjustment.
5. Arrange diabetes specialist and primary-care follow-up, review injection sites and technique, and assess social barriers, literacy and family support.

Clinical scenarios

Common errors to avoid

• Ruling out DKA because glucose is below 14 mmol/L or because the patient has type 2 diabetes.
• Starting insulin before checking potassium, perfusion and the local monitored protocol.
• Stopping insulin as soon as glucose normalises while ketones/acidosis persist.
• Using bicarbonate routinely, replacing phosphate routinely or giving potassium without a result and urine assessment.
• Giving large fluid volumes without reassessing lungs, urine output, sodium/osmolality, heart failure or kidney failure.
• Missing infection, myocardial infarction, pregnancy, SGLT2 medicine use, pump failure or social barriers as the trigger.

Revision questions

1. Describe how insulin deficiency produces ketones, acidosis, osmotic diuresis and total-body potassium loss.
2. What three biochemical components support a diagnosis of DKA?
3. Why can a patient with euglycaemic DKA be missed?
4. List six precipitants and explain how the history may identify each one.
5. Why is potassium checked before insulin, and why can it fall rapidly during treatment?
6. What are the indications for adding IV dextrose while continuing insulin?
7. Write a structured handover for Scenario 2, including the urgency and key treatment already given.

Key takeaways

References for further study

• Umpierrez et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report. Diabetes Care, 2024.
• Joint British Diabetes Societies. The Management of Diabetic Ketoacidosis in Adults, current 2023 guideline.
• NHS. Diabetic ketoacidosis — symptoms, ketone thresholds, urgent referral and sick-day prevention.
• NICE Clinical Knowledge Summaries. When to suspect hyperglycaemic emergencies.
• Follow current Uganda Ministry of Health, hospital and specialist protocols for adult, paediatric, pregnancy and renal-failure DKA.