Podrobný sprievodca čoskoro
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Diabetic Ketoacidosis (DKA) is a life-threatening acute metabolic complication of diabetes mellitus characterised by hyperglycaemia, ketoacidosis, and metabolic acidosis resulting from severe insulin deficiency, often accompanied by counter-regulatory hormone excess. DKA occurs predominantly in type 1 diabetes but also in insulin-deficient type 2 diabetes, particularly under physiological stress (infection, surgery, myocardial infarction) and increasingly due to SGLT-2 inhibitor use (euglycaemic DKA). The diagnostic triad is: blood glucose >11 mmol/L (>200 mg/dL), blood ketones >3 mmol/L or urine ketones 2+ or more, and bicarbonate <15 mmol/L or pH <7.3 on venous blood gas. DKA results from absolute or relative insulin deficiency causing: unopposed glucagon stimulation of hepatic gluconeogenesis and glycogenolysis; breakdown of adipose tissue releasing free fatty acids; hepatic beta-oxidation producing ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone); and osmotic diuresis from hyperglycaemia causing profound dehydration and electrolyte losses, particularly potassium. Initial management follows a structured protocol: immediate IV fluid resuscitation with 0.9% normal saline (1L over 60 minutes, then 500 mL/h for 4 hours, then 250 mL/h), fixed-rate IV insulin infusion (FRIII) at 0.1 units/kg/h, aggressive potassium replacement, and continuous monitoring of glucose and ketone clearance. The primary treatment target is ketone clearance (fall of >0.5 mmol/L/hour) rather than glucose normalisation. DKA carries a mortality of 0.2–0.5% in specialist centres but substantially higher outside these settings.
DKA diagnosis: Glucose >11 mmol/L + Ketones >3 mmol/L (or urine 2+) + pH <7.3 or HCO3 <15 mmol/L; Fluid: 1L NS over 1h → 500 mL/h × 4h → 250 mL/h; Insulin: 0.1 units/kg/h
- 1Step 1 — Confirm DKA: Blood glucose >11 mmol/L, blood ketones >3 mmol/L (or urine ketones 2+), venous pH <7.3 or bicarbonate <15 mmol/L. Check all three criteria are met.
- 2Step 2 — IV access and bloods: Establish two large-bore IV cannulae. Bloods: glucose, ketones, U&E, creatinine, VBG (pH, HCO3, lactate), FBC, LFTs, bone profile, cultures if infection suspected. ECG for T-wave changes (hyperkalaemia/hypokalaemia).
- 3Step 3 — IV fluid resuscitation: 1L of 0.9% NaCl over 60 minutes. Then 500 mL/h for 4 hours. Then 250 mL/h for 4 hours. Add dextrose saline when glucose falls below 14 mmol/L. Continue assessing fluid balance hourly.
- 4Step 4 — Fixed-rate IV insulin infusion (FRIII): 50 units Actrapid in 50 mL 0.9% NaCl (1 unit/mL). Infuse at 0.1 units/kg/hour. Do NOT give IV bolus insulin. Do NOT stop long-acting insulin if patient already taking it.
- 5Step 5 — Potassium replacement: Check serum K+ immediately. If K+ >5.5 mmol/L — no K+ replacement initially. If 3.5–5.5 mmol/L — add 40 mmol/L KCl to each litre of IV fluid. If <3.5 mmol/L — urgent senior review, may need central K+ replacement before insulin.
- 6Step 6 — Monitoring: Hourly bedside glucose and ketones. VBG at 1, 2, 4, 6 hours. Target ketone fall ≥0.5 mmol/L/hour and glucose fall ≥3 mmol/L/hour. If not meeting targets, increase insulin infusion by 1 unit/hour.
- 7Step 7 — Transition to subcutaneous insulin: When ketones <0.6 mmol/L, pH >7.35, and patient eating and drinking — restart SC insulin regimen, overlap IV insulin by at least 30–60 minutes before stopping infusion.
Target ketone fall 0.5 mmol/L/h; reassess VBG at 2h; add dextrose when glucose <14 mmol/L
All three DKA criteria met. FRIII = 0.1 × 70 = 7 units/h. K+ 4.0 = within normal range — add 40 mmol/L KCl to each litre. Monitor ketones every hour.
Insulin drives K+ intracellularly — starting insulin with K+ <3.5 can cause fatal arrhythmia
Potassium <3.5 mmol/L requires urgent replacement via central line before insulin. Replace K+ to ≥3.5 mmol/L first, then start FRIII at 6 units/h. Continuous ECG monitoring.
SGLT-2 inhibitors promote renal glucose excretion, masking hyperglycaemia while DKA is present
SGLT-2 inhibitors (gliflozins) cause euglycaemic DKA — glucose may be <11 mmol/L but ketosis and acidosis are present. Insulin infusion and fluid resuscitation still required. Add dextrose to maintain glucose >6 mmol/L.
In paediatric DKA, over-rapid fluid resuscitation risks cerebral oedema — the most feared complication
Children require cautious fluid management. Initial 10 mL/kg bolus 0.9% NaCl over 60 min (not 1L). Subsequent fluid deficit replaced over 48h. Insulin 0.1 units/kg/h = 4 units/h. Beware cerebral oedema: headache, bradycardia, deteriorating consciousness.
Emergency department initial assessment and resuscitation of DKA patients before handover to endocrinology/medicine. This application is commonly used by professionals who need precise quantitative analysis to support decision-making, budgeting, and strategic planning in their respective fields
JBDS DKA protocol implementation across acute hospital trusts for standardised care and mortality reduction. Industry practitioners rely on this calculation to benchmark performance, compare alternatives, and ensure compliance with established standards and regulatory requirements
Paediatric emergency medicine management of DKA with cerebral oedema prevention through careful fluid titration. Academic researchers and students use this computation to validate theoretical models, complete coursework assignments, and develop deeper understanding of the underlying mathematical principles
Endocrinology outpatient clinics educating patients on sick day rules to prevent hospital admission. Financial analysts and planners incorporate this calculation into their workflow to produce accurate forecasts, evaluate risk scenarios, and present data-driven recommendations to stakeholders
Critical care unit management of severe DKA with multi-organ involvement requiring HDU/ICU level care. This application is commonly used by professionals who need precise quantitative analysis to support decision-making, budgeting, and strategic planning in their respective fields
DKA in Pregnancy
Pregnant women develop DKA more rapidly at lower glucose levels due to altered metabolism and buffering. Even mild hyperglycaemia (glucose >8–10 mmol/L) with any ketonaemia should prompt urgent assessment. Fetal monitoring is essential. Aggressive fluid resuscitation and insulin are the mainstay; maternal acidosis must be corrected urgently to prevent fetal compromise and stillbirth.
Euglycaemic DKA from SGLT-2 Inhibitors
SGLT-2 inhibitor-associated DKA may present with glucose as low as 5.5 mmol/L. Standard diagnostic criteria based solely on glucose will miss these patients. Any sick diabetic patient on a gliflozin (empagliflozin, dapagliflozin, canagliflozin, ertugliflozin) must have blood ketones measured. Dextrose-containing fluids are particularly important in euglycaemic DKA to maintain glucose while clearing ketones.
Cardiac Arrhythmia from Electrolyte Disturbance
Hypokalaemia from insulin administration is the most common life-threatening complication in DKA management. Initial hyperkalaemia from acidosis can also cause fatal arrhythmias before treatment. All DKA patients require continuous cardiac monitoring. ECG changes: peaked T-waves (hyperkalaemia), U-waves and flat T-waves (hypokalaemia). Check electrolytes at 0, 1, 2, 4, 6 hours.
DKA in Patients with Renal Failure
Renal failure impairs urinary excretion of ketones and protons, worsening acidosis. It also prevents the compensatory excretion of potassium, risking severe hyperkalaemia with insulin administration. IV fluid volumes must be carefully titrated. Haemofiltration (CVVHF) may be required in severe cases. Close liaison with renal and endocrinology teams is essential.
| Severity | pH | HCO3 (mmol/L) | Blood Ketones (mmol/L) | Clinical Features |
|---|---|---|---|---|
| Mild | 7.25–7.30 | 15–18 | 3–6 | Alert; GCS 15; tolerating oral fluids |
| Moderate | 7.00–7.24 | 10–14 | >6 | Drowsy; GCS 12–14; vomiting; may manage fluids |
| Severe | <7.00 | <10 | >6 or unmeasurable | Confused/comatose; GCS <12; HDU/ICU care |
What is the difference between DKA and Hyperosmolar Hyperglycaemic State (HHS)?
DKA is characterised by significant ketosis and acidosis (pH <7.3, HCO3 <15) with moderate hyperglycaemia (typically 11–33 mmol/L). HHS has severe hyperglycaemia (>30 mmol/L), hyperosmolality (>320 mOsm/kg), profound dehydration but minimal or absent ketosis and acidosis. HHS occurs in type 2 diabetes and carries higher mortality due to degree of dehydration and patient age/comorbidities.
Why is a fixed-rate insulin infusion (FRIII) used instead of glucose-based sliding scale?
The primary goal of insulin in DKA is to suppress ketogenesis and clear ketones, not simply to lower glucose. FRIII at 0.1 units/kg/h provides consistent ketone clearance. Sliding scales vary insulin by glucose level and would provide insufficient insulin when glucose is near-normal but ketones remain high. When glucose falls below 14 mmol/L, dextrose is added to the fluids rather than reducing insulin.
Why is potassium replacement so critical in DKA?
In DKA, total body potassium is severely depleted due to osmotic diuresis, despite the serum K+ appearing normal or even high (due to acidosis driving K+ out of cells). When insulin is administered, K+ moves back intracellularly, and serum K+ can fall precipitously. If serum K+ is below 3.5 mmol/L before insulin is started, dangerous hypokalaemia and cardiac arrhythmias can be fatal.
When should bicarbonate be given in DKA?
Sodium bicarbonate is NOT routinely recommended in DKA. It may worsen intracellular acidosis by promoting CO2 production, cause hypokalaemia, and is not shown to improve outcomes. The only exception is severe metabolic acidosis with life-threatening hyperkalaemia (K+ >6.5 mmol/L) or pH <6.9 with haemodynamic instability, in which senior endocrinology or intensivist guidance is required.
What triggers DKA in known diabetics?
The classic trigger is infection (30–40% of cases), particularly urinary tract infection, pneumonia, or skin infection. Other triggers include insulin omission or inadequate insulin therapy (20–25%), myocardial infarction, pancreatitis, stroke, surgery, pregnancy, certain medications (corticosteroids, antipsychotics, SGLT-2 inhibitors), and new diagnosis of type 1 diabetes in 25–30% of cases. This is an important consideration when working with dka management calculations in practical applications.
What is the target for DKA resolution?
JBDS DKA targets: blood ketones <0.6 mmol/L, venous pH >7.35, bicarbonate >18 mmol/L, blood glucose between 6–12 mmol/L. Resolution is primarily defined by ketone clearance rather than glucose normalisation. The patient must be tolerating oral intake before transitioning to subcutaneous insulin. In practice, this concept is central to dka management because it determines the core relationship between the input variables.
What is cerebral oedema and why is it a feared complication in paediatric DKA?
Cerebral oedema is a life-threatening complication of DKA occurring almost exclusively in children, with a mortality of up to 20–25% when it occurs. It is thought to result from too-rapid fluid resuscitation and/or rapid glucose/osmolality correction causing water shift into brain cells. Warning signs: headache, deteriorating consciousness, bradycardia, hypertension. Treatment: immediate 3% hypertonic saline or mannitol 0.5–1 g/kg IV.
Can DKA occur with normal blood glucose (euglycaemic DKA)?
Yes — euglycaemic DKA (glucose <11 mmol/L with significant ketosis and acidosis) occurs predominantly in patients taking SGLT-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin), in pregnancy, with prolonged fasting, and in patients who have taken partial insulin doses. SGLT-2 inhibitors promote urinary glucose excretion, masking the hyperglycaemia while DKA develops. Any diabetic patient on a gliflozin presenting unwell should have ketones checked regardless of glucose.
Pro Tip
The key monitoring parameter in DKA is ketone clearance, not glucose. Target a ketone fall of at least 0.5 mmol/L per hour. If ketones are not clearing at 1–2 hours despite adequate fluid and insulin, increase the insulin infusion by 1 unit/hour and reassess. When glucose drops below 14 mmol/L, add dextrose-saline rather than reducing insulin — you still need insulin to clear the ketones.
Did you know?
The first clinical description of diabetic ketoacidosis was made by Apollinaire Bouchardat in Paris in 1875, who noted the sweetish smell of acetone on the breath of dying diabetic patients. Before insulin was discovered in 1921, DKA was universally fatal. Today, mortality in specialised centres is below 0.5%, representing one of the most dramatic improvements in medical outcomes of the 20th century.
References
- ›JBDS — The Management of Diabetic Ketoacidosis in Adults (2023 update)
- ›ISPAD Clinical Practice Consensus Guidelines — Diabetic Ketoacidosis in Children (2022)
- ›Kitabchi AE et al. — Hyperglycemic Crises in Adult Patients (Diabetes Care 2009)
- ›NHS England — DKA Management Pathway
- ›LITFL DKA Management Reference
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