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Cetoacidose diabética: insights

Estes são compilados recentes de publicações que reorientam a conduta na cetoacidose diabética. Para preservar a intenção e a informação trazida nos artigos, mantive os textos originais.

Seven myths about diabetic ketoacidosis [1]

Myth 1: DKA is a state of extreme hypovolemia with a need for large volume resuscitation (e.g. 100 mL/Kg)

Although substantial renal losses can occur due to hyperglycemia, especially over a longer duration, true hypovolemia usually ensues when patients are unable to drink due to nausea and vomiting. The body usually compensates for osmotic diuresis through increased oral intake through activation of physiologically effective circulating volume operators such as increased thirst and other neuro-hormone pathways. Some patients may not be hypovolemic, e.g. patients undergoing chronic dialysis or those with euglycemic DKA, where fluid losses are smaller.

Myth 2: NaCl 0.9% should be the standard of care for volume repletion in DKA

NaCl 0.9% causes iatrogenic hyperchloremic acidosis and does not prevent cerebral oedema. Buffered crystalloids such as Plasmalyte-148® or Hartmann’s solution will hasten pH correction but with no difference in anion-gap closure. Potassium replacement may however need to be given separately.

Myth 3: Weight-fixed fluid infusion rates are necessary for the treatment of DKA

A lower rate of fluid infusion leads to less hyperchloremic acidosis, reduces the risk of fluid overload, and does not affect overall DKA correction rates. Treatment should be personalized to patient needs.

Myth 4: Glucose-corrected serum sodium follows a linear relationship

A non-linear relationship for glucose-corrected serum sodium is most likely. The clinical significance of glucose-corrected serum sodium is usually low since fluid tonicity does not influence the rate of clinically significant cerebral oedema.

Myth 5: Hyperchloremic acidosis in DKA is the sole consequence of iatrogenesis

Hyperchloremic acidosis is not only a function of large volumes of salt-containing solutions, but also of the severity and duration of DKA before treatment is started. In DKA, renal reabsorption of chloride is increased to allow renal excretion of ketoacids, especially β-hydroxybutyrate.

Myth 6: DKA should be treated only with intravenous insulin

In patients who are not very sick, an ultra-rapid subcutaneous insulin regimen (hourly dose of 0.1 U/Kg) may shorten time to DKA treatment and avoid the need for intravenous insulin. With current very long-acting insulins, it is advisable to use only small doses (usually 0.2 U/Kg) in patients with severe DKA at the onset of treatment. This allows a smoother transition from an IV to a SC insulin regimen.

Myth 7: DKA correction criteria include glucose levels and ketonemia

pH > 7.30 and bicarbonate > 15 mEq/L are the usual minimum criteria for DKA correction. Full correction of hyperglycemia does not ensure DKA reversal, neither is it necessary. Although point-of-care ketonemia may hasten the diagnosis of DKA, its use as a routine treatment target has not been compared to standard approaches. Optimal monitoring and rate of reduction have not been identified.

Keypoint of care in ketoacidosis[2]


  1. BESEN, Bruno AMP; RANZANI, Otavio T.; SINGER, Mervyn. Management of diabetic ketoacidosis. Intensive Care Medicine, v. 49, n. 1, p. 95-98, 2023.
  2. EVANS, Kate. Diabetic ketoacidosis: update on management. Clinical Medicine, v. 19, n. 5, p. 396, 2019.