# Diabetic ketoacidosis
**Diabetic ketoacidosis** (DKA) is a life-threatening hyperglycemic emergency in which a severe lack of insulin causes the body to break down fat for fuel, producing acids called ketones that accumulate to dangerous levels in the blood[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html). It is most common in people with type 1 diabetes but also occurs in type 2 diabetes, and it requires urgent hospital treatment with intravenous fluids, insulin, and electrolytes[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html) • [2](https://www.nhs.uk/conditions/diabetic-ketoacidosis/). Together with the hyperglycemic hyperosmolar state (HHS), DKA accounts for approximately 1% of all hospitalizations in people with diabetes[3](https://doi.org/10.2337/dc25-s006).
| Key fact | Detail |
|---|---|
| Diagnostic criteria | Glucose ≥200 mg/dL (11.1 mmol/L) or prior diabetes history; β-hydroxybutyrate ≥3.0 mmol/L or urine ketones 2+; pH <7.3 and/or bicarbonate <18 mmol/L; all criteria must be met[3](https://doi.org/10.2337/dc25-s006) |
| Leading precipitants | Inadequate diabetes medication (40.9% of episodes) and infection (31.1%) in a systematic review of adult DKA[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review) |
| In-hospital mortality | Pooled estimate 2.64% (95% CI 1.22–5.61%) across eight studies, with high heterogeneity; most recent country-level data range from 0.2% in type 1 to 1.0% in type 2 diabetes[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review) • [3](https://doi.org/10.2337/dc25-s006) |
| Euglycemic DKA | About 10% of people with DKA present with plasma glucose <200 mg/dL (11.1 mmol/L), often linked to reduced food intake, pregnancy, alcohol use, liver failure, or SGLT2 inhibitor therapy[3](https://doi.org/10.2337/dc25-s006) |
| Typical resolution | Mean DKA resolution time of 18.4 hours (95% CI 13.9–22.9 hours) across 13 studies[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review) |
| Core treatment | Intravenous fluids, insulin, and electrolytes with close monitoring, timely transition to subcutaneous insulin, and treatment of the precipitating cause[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC11635037/) |
## Mechanism and presentation
DKA develops when the body does not have enough insulin to allow blood sugar into cells for energy. The liver instead breaks down fat, a process that produces ketones; when too many ketones are produced too fast, they build up to dangerous levels[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html).
The condition usually develops over hours to days. Early symptoms include thirst and frequent urination; more severe features include nausea, vomiting, and abdominal pain, fast deep breathing (Kussmaul respiration), fruity-smelling breath, tiredness, and confusion[2](https://www.nhs.uk/conditions/diabetic-ketoacidosis/) • [3](https://doi.org/10.2337/dc25-s006) • [1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html). DKA can be the first noticeable sign of diabetes in someone not yet diagnosed, particularly children[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html) • [2](https://www.nhs.uk/conditions/diabetic-ketoacidosis/).
Diagnosis requires all three criteria: hyperglycemia or a prior history of diabetes, significant ketosis (β-hydroxybutyrate ≥3.0 mmol/L or urine ketone strip 2+ or greater), and metabolic acidosis (pH <7.3 and/or bicarbonate <18 mmol/L)[3](https://doi.org/10.2337/dc25-s006). Blood ketone measurement by β-hydroxybutyrate testing is preferred because the older nitroprusside urine reaction measures acetoacetic acid but not β-hydroxybutyrate, the main ketoacid produced in DKA[6](https://pmc.ncbi.nlm.nih.gov/articles/PMC11343900/).
## Precipitants and risk factors
The two most common causes are illness, which disrupts eating and drinking and glucose management, and missed insulin doses, clogged insulin pumps, or incorrect dosing[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html). In a systematic review of 18 studies covering 1,344 adult DKA episodes, inadequate diabetes medication accounted for 40.9% of episodes and infection for 31.1%[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review). Other causes include heart attack, stroke, physical injury, alcohol or drug use, and certain medicines such as diuretics and corticosteroids[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html).
**SGLT inhibitors** deserve particular attention. These drugs are not approved for use in people with type 1 diabetes, in whom SGLT inhibitor–associated DKA occurs in approximately 4% and the risk can be 5–17 times higher than in people with type 1 diabetes not treated with SGLT inhibitors. In type 2 diabetes, DKA with these drugs is uncommon, at an estimated 0.6–4.9 events per 1,000 person-years. Risk factors include very-low-carbohydrate diets, prolonged fasting, dehydration, and excessive alcohol intake[7](https://doi.org/10.2337/dc25-S009). Up to a third of people treated with SGLT2 inhibitors who develop DKA present with glucose below 200 mg/dL, which is why ketone testing rather than glucose alone guides recognition[7](https://doi.org/10.2337/dc25-S009).
## Treatment
Hospital management follows recommendation 16.14 of the American Diabetes Association Standards of Care: administer intravenous fluids, insulin, and electrolytes, monitor closely, ensure a timely and bridged transition to maintenance subcutaneous insulin, and identify and treat the precipitating cause[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC11635037/). Presentation varies widely, from euglycemic DKA to severe hyperglycemia, dehydration, and coma, so treatment is individualized based on clinical and laboratory assessment[5](https://pmc.ncbi.nlm.nih.gov/articles/PMC11635037/).
The transition from intravenous to subcutaneous insulin is a defined step: basal insulin is given 2–4 hours before the intravenous insulin is stopped to prevent recurrence of ketoacidosis and rebound hyperglycemia[8](https://doi.org/10.2337/dc24-S016). In a systematic review of adult DKA, the mean time to DKA resolution was 18.4 hours (95% CI 13.9–22.9 hours)[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review).
## Outcomes and epidemiology
DKA mortality decreased in the first decade of the 21st century, but these improvements have plateaued in the past decade[3](https://doi.org/10.2337/dc25-s006). The most recently available inpatient mortality data during hospital admission for DKA range from 0.2% in type 1 diabetes to 1.0% in type 2 diabetes[3](https://doi.org/10.2337/dc25-s006). A 2026 systematic review and meta-analysis of eight studies estimated pooled in-hospital mortality at 2.64% (95% CI 1.22–5.61%), with a prediction interval of 0.61–10.7% and high heterogeneity[4](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review). Death rates in low- and middle-income nations substantially exceed those seen in wealthier nations, possibly owing to late identification and therapy[3](https://doi.org/10.2337/dc25-s006).
Crisis rates have been rising. Newer figures indicate that hyperglycemic crises affect as many as 44.5–82.6 individuals per 1,000 person-years who have type 1 diabetes, compared with a maximum of 3.2 per 1,000 person-years in those who have type 2 diabetes[3](https://doi.org/10.2337/dc25-s006). DKA and HHS often present concurrently, and one-third of hyperglycemic emergencies have a hybrid DKA-HHS presentation; the only study to examine inpatient mortality for mixed DKA-HHS found it higher than for either condition alone[3](https://doi.org/10.2337/dc25-s006).
A substantial proportion of people hospitalized with DKA experience recurrent episodes. Structured diabetes self-management education and support that includes problem-solving reduces DKA admissions, as do psychological interventions, peer support, individual coaching, and behavioral family systems therapy; access to continuous glucose monitoring may also decrease recurrence risk[3](https://doi.org/10.2337/dc25-s006).
## Prevention
People at risk are counseled on early signs and symptoms, given tools for urine or blood ketone measurement, and taught sick day advice for timely self-management of hyperglycemia and ketonemia[3](https://doi.org/10.2337/dc25-s006). Practical measures include checking blood sugar often, especially during illness, testing ketones when glucose is high or symptoms are present, and not stopping or skipping insulin even when not eating[1](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html) • [2](https://www.nhs.uk/conditions/diabetic-ketoacidosis/). People on intensive insulin therapy should not hold basal insulin during illness or fasting, and clinicians should provide detailed instructions for insulin dose adjustment in these settings[3](https://doi.org/10.2337/dc25-s006). Individuals who have experienced DKA should not be treated with SGLT inhibition[7](https://doi.org/10.2337/dc25-S009), and people with type 1 diabetes or other DKA risk are advised not to use recreational cannabis in any form because of the risk of cannabis hyperemesis syndrome[9](https://diabetesjournals.org/care/article/48/Supplement_1/S6/157564).
## History
Before insulin, DKA was a frequent cause of death in children with diabetes, and pre-1921 treatments relied on severe calorie restriction intended to reduce glycosuria, dehydration, and ketoacidosis development[10](https://doi.org/10.1136/bmjdrc-2021-002373). Within a year of the discovery and purification of insulin by Banting, Best, Collip, and Macleod at the [University of Toronto](https://www.edgepedia.org/university-of-toronto), insulin was used in early 1922 to successfully treat young children dying from diabetic ketoacidosis at Toronto General Hospital[11](https://journals.physiology.org/doi/full/10.1152/physiol.00007.2021). Insulin therapy was the first treatment that reversed and prevented DKA, transforming type 1 diabetes from a fatal diagnosis into a manageable chronic condition[10](https://doi.org/10.1136/bmjdrc-2021-002373).
## References
1. [Diabetic Ketoacidosis, CDC](https://www.cdc.gov/diabetes/about/diabetic-ketoacidosis.html)
2. [Diabetic ketoacidosis, NHS](https://www.nhs.uk/conditions/diabetic-ketoacidosis/)
3. [6. Glycemic Goals and Hypoglycemia: Standards of Care in Diabetes—2025, Diabetes Care](https://doi.org/10.2337/dc25-s006)
4. [2280-P: Diabetic Ketoacidosis: A Systematic Review of Precipitants, Treatment, and Outcomes with a Mortality Meta-Analysis, Diabetes (2026)](https://diabetesjournals.org/diabetes/article/75/Supplement_1/2280-P/168180/2280-P-Diabetic-Ketoacidosis-A-Systematic-Review)
5. [16. Diabetes Care in the Hospital: Standards of Care in Diabetes—2025, Diabetes Care](https://pmc.ncbi.nlm.nih.gov/articles/PMC11635037/)
6. [Hyperglycaemic crises in adults with diabetes: a consensus report, Diabetes Care (2024)](https://pmc.ncbi.nlm.nih.gov/articles/PMC11343900/)
7. [9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2025, Diabetes Care](https://doi.org/10.2337/dc25-S009)
8. [16. Diabetes Care in the Hospital: Standards of Care in Diabetes—2024, Diabetes Care](https://doi.org/10.2337/dc24-S016)
9. [Summary of Revisions: Standards of Care in Diabetes—2025, Diabetes Care](https://diabetesjournals.org/care/article/48/Supplement_1/S6/157564)
10. [100 years on: the impact of the discovery of insulin on clinical outcomes, BMJ Open Diabetes Research & Care](https://doi.org/10.1136/bmjdrc-2021-002373)
11. [Physiology in Perspective: Insulin—100 Years of Physiological Discovery, Physiology](https://journals.physiology.org/doi/full/10.1152/physiol.00007.2021)
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*Topic: Encyclopedia › Life and health › Human health and medicine › Diseases and injuries › Digestive, metabolic, and endocrine conditions › Diabetes mellitus*
*Initially written Sep 17, 2026 · Reviewed: Sep 17, 2026; Sep 30, 2026; Oct 21, 2026 · Edited: Sep 30, 2026; Oct 21, 2026 · Last review: Oct 21, 2026*
*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*
License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license