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Diabetic ketoacidosis
Background
Overview
Definition
DKA is an acute metabolic complication occurring mostly in patients with T1DM, characterized by a triad of hyperglycemia, ketosis, and acidemia.
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Pathophysiology
DKA is caused by absolute or relative insulin deficiency and increased levels of counterregulatory hormones, typically ocurring at the time of new diagnosis of untreated T1DM or due to inadequate insulin therapy, infection (such as pneumonia, UTI, sepsis), concomitant medications (corticosteroids, SGLT-2 inhibitors, thiazide diuretics, sympathomimetics, certain antipsychotics), illicit drug use, surgery, trauma, physiologic stress, or pregnancy.
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Epidemiology
The age-adjusted hospitalization rate for DKA in the US was estimated at 6.3% annually in 2014, with an in-hospital case fatality of 0.4%. The rate of hopsitalization for DKA per 10,000 admissions was reported as 53.4 in 2014 and 61.6 in 2017.
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Risk factors
Risk factors include inconsistent caloric intake, poor medication adherence, poor glucose control, alcohol use, and dehydration.
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Disease course
Clinical manifestations include nausea, vomiting, abdominal pain, weakness, polydipsia, polyuria, dehydration, weight loss, polyphagia, fruity odor of breath, dyspnea, tachypnea, Kussmaul breathing, hypotension, tachycardia, and altered mental status. Laboratory findings in DKA include hyperglycemia, anion gap metabolic acidosis, and ketonemia/ketonuria.
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Guidelines
Key sources
The following summarized guidelines for the evaluation and management of diabetic ketoacidosis are prepared by our editorial team based on guidelines from the American Diabetes Association (ADA 2025,2024,2006), the American Academy of Family Physicians (AAFP 2024), the Kidney Disease: Improving Global Outcomes Foundation (KDIGO 2024), the United Kingdom Kidney Association (UKKA 2021), the French Society of Emergency Medicine (SFMU/SRLF 2019), ...
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Screening and diagnosis
Indications for screening: as per ADA 2025 guidelines, review history of hyperglycemic crises (DKA and hyperglycemic hyperosmolar state) at every clinical encounter in all patients with diabetes at risk for these events.
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Diagnostic criteria
Diagnostic investigations
Beta-hydroxybutyrate: as per AAFP 2024 guidelines, obtain serum testing of β-hydroxybutyrate, when available, instead of urine ketones to diagnose and monitor treatment of DKA.
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Urine ketones
Blood gas analysis
Evaluation of patients on SGLT-2 inhibitors
Medical management
General principles: as per ADA 2025 guidelines, administer IV fluids, insulin, and electrolytes for the management of DKA and hyperglycemic hyperosmolar state. Identify and treat the precipitating cause. Obtain close monitoring during treatment, ensuring timely and bridged transition to maintenance subcutaneous insulin administration.
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Insulin infusion (FICS)
Insulin infusion
Fluid resuscitation
Potassium replacement
Sodium bicarbonate
Inpatient care
Inpatient monitoring: as per ADA 2025 guidelines, monitor serum electrolytes, renal function, venous pH, osmolality, and glucose every 2-4 hours until stable. Initiate subcutaneous multi-dose insulin plan after resolution of DKA or hyperglycemic hyperosmolar state and when patient is able to eat and drink. Continue intravenous insulin infusion for 1-2 hours after subcutaneous insulin when transferring from intravenous to maintenance subcutaneous insulin.
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Glucose monitoring
Patient education
Preventative measures
Managing sick days: as per AAFP 2024 guidelines, manage sick days to minimize the risk of DKA by obtaining frequent glucose and ketone monitoring, administering supplemental insulin as indicated, and encouraging patients to contact their healthcare team with any questions.
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Withholding SGLT-2 inhibitors