History and exam
Other diagnostic factors
common
polyuria
Symptom of hyperglycemia.
polyphagia
Symptom of hyperglycemia.
polydipsia
Symptom of hyperglycemia.
weight loss
Symptom of hyperglycemia.
weakness
Symptom of hyperglycemia.
nausea or vomiting
Abdominal pain, nausea, and vomiting in DKA correlate with the degree of acidosis and may be confused with acute abdominal crisis.[1]
abdominal pain
Abdominal pain, nausea, and vomiting in DKA correlate with the degree of acidosis and may be confused with acute abdominal crisis.[1]
dry mucous membranes
Sign of volume depletion.
poor skin turgor
Sign of volume depletion.
sunken eyes
Sign of volume depletion.
tachycardia
Sign of volume depletion.
hypotension
Sign of volume depletion.
Kussmaul respiration
Rapid and deep respiration due to acidosis. Common in DKA.
acetone breath
Sign of ketosis. Common in DKA.
altered mental status
Mental status may be altered, and varies from alert in mild DKA to stupor/coma in severe DKA. Studies have shown that acidosis is independently associated with altered sensorium in DKA patients, but hyperosmolarity and serum ketone levels are not. Combination of hyperosmolarity and acidosis predicts altered sensorium with good sensitivity (61%) and specificity (87%) in DKA patients.[43]
uncommon
hypothermia
Although concomitant infection is common, patients usually are normothermic or hypothermic due to peripheral vasodilation. Severe hypothermia is a poor prognostic sign.[44]
Risk factors
strong
inadequate or inappropriate insulin therapy
Reduction in the net effective concentration of insulin leads to impaired carbohydrate, lipid, and ketone metabolism in DKA. Decreased insulin results in increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues.[1]
Non-compliance with insulin therapy has been found to be the leading precipitating factor in black people and is present in over 30% of patients with DKA.[18][9] Psychological and social factors may impact on glycemic control, and low socio-economic status is correlated with a higher risk for DKA.[19][20]
infection
The most common precipitating factor in DKA is infection. Increased counter-regulatory hormones, particularly epinephrine, as a systemic response to infection lead to insulin resistance, increased lipolysis, ketogenesis, and volume depletion, which may contribute to the development of hyperglycemic crises in patients with diabetes.[1]
weak
pancreatitis
stroke
Acute medical events such as stroke, with increased levels of counter-regulatory hormones and compromised access to water and insulin, may contribute to the development of hyperglycemic crises.[1]
acromegaly
Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones and development of DKA in patients with concomitant diabetes.[23]
hyperthyroidism
Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones and development of DKA in patients with concomitant diabetes.[24]
drugs (e.g., corticosteroids, thiazides, pentamidine, sympathomimetics, second-generation antipsychotics, cocaine, immune checkpoint inhibitors, or SGLT-2 inhibitors)
Drugs that affect carbohydrate metabolism may precipitate hyperglycemic crises.[25][11][26][27] Cocaine abuse may be an independent risk factor associated with recurrent DKA.[28][10]
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors (e.g., canagliflozin, dapagliflozin, empagliflozin), used for glycemic control of type 2 diabetes, have been the subject of an FDA warning about a risk for DKA.[29]
Immune checkpoint inhibitor therapy for cancer (PD-1 and PD-L1 blocking antibodies such as nivolumab, pembrolizumab, and avelumab) appears to be associated with a risk for DKA and type 1 diabetes mellitus.[30][31]
Cushing syndrome
Hypercortisolism leads to insulin resistance and may occasionally precipitate DKA in patients with concomitant diabetes; it more commonly precipitates hyperosmolar hyperglycemic state.
Hispanic or black ancestry
Ancestry plays a role in ketosis-prone diabetes, with DKA a presenting manifestation of undiagnosed type 2 diabetes in young adults. Approximately 80% of obese black patients with DKA have type 2 diabetes, characterized by higher insulin secretion, the absence of autoimmune markers, and a lack of human leukocyte antigen (HLA) genetic association compared with lean patients with type 1 diabetes.[3]
bariatric surgery
DKA has been reported in patients with type 1 diabetes who have had bariatric surgery.[32]
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