History and exam

Other diagnostic factors

Symptom of hyperglycemia.

Symptom of hyperglycemia.

Symptom of hyperglycemia.

Symptom of hyperglycemia.

Symptom of hyperglycemia.

Abdominal pain, nausea, and vomiting in DKA correlate with the degree of acidosis and may be confused with acute abdominal crisis.[1]

Abdominal pain, nausea, and vomiting in DKA correlate with the degree of acidosis and may be confused with acute abdominal crisis.[1]

Sign of volume depletion.

Sign of volume depletion.

Sign of volume depletion.

Sign of volume depletion.

Sign of volume depletion.

Rapid and deep respiration due to acidosis. Common in DKA.

Sign of ketosis. Common in DKA.

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]

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

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]

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]

Underlying cardiovascular events, particularly myocardial infarction, provoke the release of counter-regulatory hormones that are likely to result in DKA in patients with diabetes.[1][21]

Medical conditions such as pancreatitis, characterized by increased levels of counter-regulatory hormones and compromised access to water and insulin, may contribute in the development of hyperglycemic crises.[1][22]

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]

Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones and development of DKA in patients with concomitant diabetes.[23]

Hormonal derangements in some endocrine glands lead to increased counter-regulatory hormones and development of DKA in patients with concomitant diabetes.[24]

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]

Hypercortisolism leads to insulin resistance and may occasionally precipitate DKA in patients with concomitant diabetes; it more commonly precipitates hyperosmolar hyperglycemic state.

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]

DKA has been reported in patients with type 1 diabetes who have had bariatric surgery.[32]

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