01OverviewDefinition, clinical context and the essential points that orientate the chapter.
DKA results from absolute or marked relative insulin deficiency with excess counter-regulatory hormones. Lipolysis generates ketone bodies, causing high-anion-gap metabolic acidosis; osmotic diuresis produces water and electrolyte loss. Total-body potassium is depleted even when extracellular shift makes the first serum potassium normal or high. Vomiting and compensatory respiratory alkalosis can complicate the initial acid–base picture.
The clinical pattern includes polyuria, polydipsia, weight loss, dehydration, nausea, vomiting, abdominal pain, acetone breath and deep sighing respiration. Cerebral dysfunction, shock and hypothermia indicate severe illness. DKA may be the first presentation of diabetes, but recurrent episodes often reveal barriers such as insulin access, injection distress, eating disorder, substance use, mental illness, safeguarding concerns or inadequate sick-day support.
This is an adult learning framework. Children, young people and pregnancy require their dedicated urgent protocols because fluid, physiological and fetal risks differ. Concentrations, infusion devices and potassium charts vary between organisations; the live prescription bundle, local critical-care thresholds and current JBDS publication govern bedside delivery.
Key points
- JBDS adult diagnostic criteria combine diabetes or glucose above 11 mmol/L with blood ketones above 3.0 mmol/L or significant ketonuria and venous pH below 7.3 or bicarbonate below 15 mmol/L.
- A near-normal glucose does not exclude ketoacidosis, particularly with an SGLT2 inhibitor, pregnancy, starvation or partial insulin treatment; assess ketones and acid–base status when the syndrome fits.
- Give 0.9% sodium chloride through the weight-, circulation- and comorbidity-adjusted local schedule, documenting reassessment because both under-resuscitation and fluid overload are dangerous.
- Use a fixed-rate intravenous insulin infusion at 0.1 units/kg/hour in the standard adult pathway, while continuing the patient’s usual long-acting basal insulin unless the specialist protocol directs otherwise.
- Add glucose-containing fluid once blood glucose falls below 14 mmol/L so insulin can continue suppressing ketogenesis without driving hypoglycaemia.
- Aim for blood ketones to fall by at least 0.5 mmol/L/hour, bicarbonate to rise by at least 3 mmol/L/hour and glucose to fall by at least 3 mmol/L/hour.
- Manage potassium from measured values and repeat testing using the dedicated prescription chart; serum potassium can be high initially despite severe whole-body depletion.
- Do not finish at biochemical resolution: identify infection, missed insulin, pump failure, myocardial infarction, pancreatitis, medicines or psychosocial barriers and create a safe subcutaneous transition.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Absolute insulin deficiency
New type 1 diabetes, omitted insulin, pump interruption or inadequate basal replacement removes the restraint on hepatic glucose output and lipolysis.
Physiological stress
Infection, infarction, surgery, trauma or another acute illness raises counter-regulatory hormones and can overwhelm an existing insulin regimen.
Treatment and psychosocial barriers
Insulin access, injection distress, eating disorder, substance use, mental illness or limited sick-day support can contribute to recurrent episodes.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Effective insulin action falls
Insufficient insulin with excess counter-regulatory signalling increases hepatic glucose production and prevents normal glucose use by insulin-dependent tissues.
- 2Ketone production accelerates
Unrestrained lipolysis releases fatty acids that the liver converts to ketone bodies, consuming bicarbonate and producing a high-anion-gap metabolic acidosis.
- 3Osmotic diuresis depletes volume
Hyperglycaemia drives urinary glucose, water and electrolyte loss, causing dehydration, reduced kidney clearance and worsening hormone and acid accumulation.
- 4Potassium shifts conceal depletion
Acidosis and insulin deficiency move potassium out of cells, so serum potassium may appear normal or high despite substantial total-body loss.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Polyuria, thirst, nocturia, weight loss, dry mucosa, tachycardia and reduced skin perfusion reflect hyperglycaemia and substantial volume depletion.
Nausea, repeated vomiting, diffuse abdominal pain, acetone odour and deep laboured breathing should prompt immediate ketone and venous acid–base testing.
Hypotension, hypoxia, hypothermia, oliguria, altered consciousness, very low pH or a major potassium disturbance increases mortality and requires senior critical-care assessment.
An adult without a previous diagnosis may present in DKA; obtain appropriate classification later without delaying emergency insulin and fluid treatment.
Because pump therapy uses rapid-acting insulin without a long subcutaneous depot, cannula displacement or device interruption can produce ketosis quickly despite recent apparently normal glucose readings.
Symptoms and acidosis with glucose below the classic range occur with SGLT2 inhibitors and other settings; blood ketones prevent false reassurance from the glucose value.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Capillary blood ketonesFirst step - Why
- Confirm ketonaemia and provide a direct hourly marker of insulin-driven biochemical recovery.
- Interpretation and limitations
- A concentration above 3.0 mmol/L supports the JBDS diagnosis in the appropriate acidotic context; a fall under 0.5 mmol/L/hour should trigger a systematic delivery and diagnosis review.
- 02
Venous blood gas - Why
- Measure pH and bicarbonate rapidly without routine arterial puncture.
- Interpretation and limitations
- Venous pH below 7.3 or bicarbonate below 15 mmol/L fulfils the acidosis component; trend pH and bicarbonate while considering lactate and mixed disorders.
- 03
Glucose, electrolytes, urea and creatinine - Why
- Quantify hyperglycaemia, potassium risk, renal injury and dehydration while guiding fluid and replacement safety.
- Interpretation and limitations
- Interpret sodium in the context of changing glucose, recognise total-body potassium depletion, and increase senior oversight when renal impairment limits predictable potassium and fluid handling.
- 04
ECG and continuous cardiac assessment when indicated - Why
- Detect potassium-related conduction changes and an ischaemic precipitant or complication.
- Interpretation and limitations
- Peaked T waves, widening complexes, arrhythmia or ischaemic change requires immediate clinical action; a normal trace does not remove the need for serial serum potassium.
- 05
Precipitant screen - Why
- Identify infection, acute vascular disease, pancreatitis, pregnancy, medicine exposure or insulin-delivery failure.
- Interpretation and limitations
- Use symptoms and examination to direct cultures, chest imaging, troponin, lipase, pregnancy testing and other studies; do not prescribe antibiotics merely for stress leucocytosis.
- 06
Fluid balance and bedside observations - Why
- Track perfusion response and detect shock, overload or inadequate renal output during resuscitation.
- Interpretation and limitations
- Heart rate, pressure, respiratory status, oxygenation, consciousness and urine output must improve coherently; discordance warrants repeat examination and senior review rather than automatic fluid escalation.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Starvation ketosis
Restricted intake can raise ketones, but acidosis and the broader diabetic metabolic disturbance are generally less pronounced than in clinically significant DKA.
Lactic acidosis
Shock, sepsis, seizure or medicine accumulation may explain a raised anion gap; measured lactate and ketones show whether one or both processes are present.
Hyperosmolar hyperglycaemic state
More prolonged profound hypertonicity with little ketonaemia suggests HHS, although mixed DKA and HHS can occur and needs protocol-aware care.
Toxic ingestion
Salicylate or toxic alcohol exposure can cause high-gap acidosis; history, respiratory pattern and targeted toxicology provide discriminating evidence.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ConfirmEstablish DKA and severityFirst stepA patient with diabetes or hyperglycaemic symptoms is acutely unwell with vomiting, dehydration, abdominal pain or abnormal breathing.+
- 1Perform ABCDE, obtain capillary glucose and blood ketones, send a venous gas with renal profile, establish monitored venous access and record weight for the insulin calculation.
- 2Apply the full diagnostic triad rather than glucose alone, then assess consciousness, haemodynamics, oxygenation, pH, potassium, renal function and comorbidity for the appropriate care environment.
- 3Call senior acute and diabetes clinicians early, involving critical care immediately for shock, severe physiological derangement, pregnancy or inability to deliver safe ward monitoring.
02ResuscitateReplace circulation and stop ketogenesisAdult DKA has been diagnosed and a dedicated current protocol is available.+
- 1Start 0.9% sodium chloride at the protocol rate, modifying delivery for shock, age, pregnancy, heart failure or renal disease and examining repeatedly for perfusion and overload.
- 2Commence fixed-rate intravenous insulin at 0.1 units/kg/hour using a checked pump and continue established basal long-acting insulin, while prescribing potassium only from the live laboratory-based chart.
- 3When glucose drops below 14 mmol/L, add the protocol glucose substrate so fixed-rate insulin can continue until ketonaemia and acidosis resolve.
03TroubleshootAct on missed biochemical targetsKetones, bicarbonate or glucose are not changing at the expected hourly rate, or the patient deteriorates.+
- 1Return to the patient and ABCDE, repeat bedside ketones and gas, verify perfusion, renal output, diagnosis and whether another emergency such as sepsis or ischaemia is evolving.
- 2Trace the insulin from prescription through pump, line and cannula, confirm weight-based rate and check that fluid, glucose and potassium bags match the chart without interruption.
- 3EscalationEscalate to senior diabetes and critical-care teams before protocol deviation; follow the current JBDS troubleshooting step rather than repeatedly adding unstructured insulin boluses.
04TransitionResolve and hand over safelyBlood ketones are below 0.6 mmol/L, venous pH exceeds 7.3 and the patient is clinically recovered and able to eat.+
- 1Confirm resolution with the biochemical and clinical criteria, correct remaining electrolyte or precipitant issues and obtain a subcutaneous regimen agreed by an experienced diabetes clinician.
- 2Administer appropriate subcutaneous insulin with the protocol overlap before stopping intravenous insulin; never create an insulin-free gap in type 1 diabetes.
- 3Before discharge, review injection or pump technique, sick-day ketone rules, insulin supply, psychosocial drivers and early diabetes follow-up, documenting any safeguarding plan.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Fixed-rate intravenous human soluble insulin
Use 0.1 units/kg/hour by checked intravenous infusion for standard adult DKA under the current JBDS-aligned prescription chart; use actual protocol weight rules and obtain specialist direction for exceptional circumstances.Confirm pump, line, cannula and rate hourly; monitor ketones, glucose and potassium. Do not substitute a general variable-rate chart, omit continuing basal insulin, stop solely because glucose normalises, or use this adult rate for children or pregnancy without their protocol.
Glucose-containing intravenous fluid
Add the concentration and rate specified by the local adult DKA chart once blood glucose is below 14 mmol/L, alongside 0.9% sodium chloride and fixed-rate insulin as fluid status permits.Check bag strength, access, glucose trend and total fluid burden. Glucose substrate complements rather than replaces volume fluid, and its start does not justify reducing insulin when ketone clearance remains inadequate without senior protocol review.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Circulatory and kidney injury
Severe volume depletion causes hypotension, acute kidney injury and impaired clearance, amplifying both acidosis and electrolyte disturbance.
Potassium-related arrhythmia
Total-body depletion and rapid treatment-related shifts can produce dangerous hypokalaemia or hyperkalaemia, requiring repeated biochemical and cardiac assessment.
Cerebral or pulmonary injury
Severe illness or poorly controlled fluid and osmotic change can contribute to neurological deterioration or pulmonary complications, prompting critical-care review.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Measure bedside glucose and blood ketones hourly during active treatment, recording whether ketones fall at least 0.5 mmol/L/hour and responding explicitly when they do not.
- Repeat venous bicarbonate or pH and serum potassium at the schedule defined by the DKA chart, with more frequent review for severe derangement, renal impairment or replacement changes.
- Track respiratory rate, oxygen saturation, pulse, blood pressure, temperature, consciousness and an accurate fluid balance; worsening physiology overrides an apparently improving glucose.
- Inspect infusion pumps, labels, tubing and cannula at every handover and after any transfer because accidental insulin or substrate interruption is a preventable cause of non-resolution.
- Review for cerebral symptoms, pulmonary oedema, hypoglycaemia, potassium disturbance, thrombosis and treatment-associated hyperchloraemic acidosis without assuming all post-treatment abnormality is persistent ketoacidosis.
- Continue monitoring through the subcutaneous transition, confirming oral intake and post-overlap glucose before leaving the high-frequency observation pathway.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Ketones guide insulin effectiveness
Glucose may fall with fluid before ketogenesis stops, so an improving meter value cannot substitute for serial blood ketones and acid–base assessment.
Potassium is depleted overall
Acidosis and insulin deficiency shift potassium out of cells, masking urinary losses; insulin treatment can reveal dangerous hypokalaemia rapidly.
Basal overlap prevents rebound
Continuing established long-acting insulin and using timed subcutaneous overlap reduces the insulin-free interval that can restart ketone production.
Bicarbonate is not routine
The adult JBDS pathway does not use bicarbonate routinely; profound exceptional acidosis requires senior critical-care judgement, not reflex ampoule prescribing.
Abdominal pain should improve
DKA itself can cause striking abdominal pain, but persistent focal pain after metabolic improvement warrants investigation for a precipitant such as pancreatitis or surgical disease.
Recurrence has a story
Repeated DKA should prompt respectful assessment of access, technique, mental health, disordered eating, housing, substance use and safeguarding instead of a label of non-compliance.
11Common pitfallsFrequent interpretation and management errors.
- 01
Diagnosing and tracking DKA from glucose alone, thereby missing euglycaemic disease or stopping insulin while clinically important ketonaemia persists.
- 02
Using a variable-rate intravenous insulin regimen designed for general hyperglycaemia instead of the dedicated fixed-rate DKA protocol.
- 03
Replacing potassium from memory without checking the current measured value, renal function, urine output and organisation-specific prescription chart.
- 04
Giving identical rapid fluid volumes to a young dehydrated adult and an older patient with advanced heart or kidney failure without reassessment.
- 05
Stopping the infusion when the patient feels better but before ketone, pH and safe subcutaneous overlap criteria are met.
- 06
Treating the metabolic numbers yet failing to resolve infection, pump failure, insulin access or psychosocial factors responsible for the episode.