Diabetic Ketoacidosis
Patient (condition)
 
Aliases:
DKA

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Absolute or relative deficiency of insulin resulting in a hyperglycemic ketoacidosis. Two standout processes are in action here. 1. An unopposed glycogenolysis and gluconeogenesis resulting in hyperglycemic glycosuria and significant total body water and potassium loss. 2. Increased fatty acid oxidation with ketoacid production for ongoing brain/muscle energy requirements resulting in a high anion gap metabolic acidosis. Management principles: initial volume resuscitation; commencement of an insulin bolus/infusion; replacement of total body potassium; monitoring in a high dependency environment.

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Insulin deficiency results in hyperkalemia which drives renal potassium excretion. This results in a total body potassium deficit of up to 5-10 mEq per kg body weight (eg 350-700mmol in 70kg adult) in severe cases despite an initially high measured serum potassium. The serum potassium will decrease first with volume resuscitation (dilutional), and then with insulin therapy (intracellularisation). Once the serum potassium falls below 4.5mmol replace at a rate of 20 mmol/hr. At 3-4.5mmol/L replace at a rate of 40mmol/hr. At <3 mmol/L replace at a rate of 40-60mmol/hr.

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If K+ <3.3mmol, delay insulin administration as insulin will exacerbate hypokalemia. Give 40mmol KCl over 1hr then recheck prior to commencing insulin #ohea

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Jun 22, 2011
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If K+ >3.3mmol, administer IV loading dose of 0.1u/kg insulin, then infusion of 0.1mg/kg/hr refl.in/40 #improve

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May 27, 2011
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Insulin infusion can be reduced when pH >7.3, HCO3 >18mmol.

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May 18, 2011
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NaHCO3 may be considered for severe acidemia (pH <7.1) refl.in/40. Concerns with its use include excessive CO2 production and additional Na load.

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Emergency surgery may be indicated to correct the precipitating pathology. Where required, correct potentially dangerous volume states & serum potassium concentrations that may place the patient at unacceptable risk at induction, prior to commencing the case.

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If intubation is required, maintain their pCO2 at the compensatory pre-op level to avoid an additional respiratory acidosis. Perform regular VBG or ABG gases to maintain this.

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Ensure normalisation of Na at the same time as glucose to prevent cerebral oedema refl.in/40 Keep in mind that serum Na may be low due to the osmotic effect of glucose #improve

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Adults may have up to 100ml/kg fluid deficit. (eg deficit in 70kg adult could be up to 7L)

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If the BSL falls by >5mmol/?hr, then reduce insulin infusion to 0.05 units/?kg/?hr

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May 18, 2011
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NHS GOSH DKA guidelines refl.in/41

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Resuscitate with large volumes of normal saline where appropriate. Rehydration alone will reduce blood sugar level by 30%-50% refl.in/40

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May 27, 2011
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These patient's can present critically unwell. Consider HDU/ICU if <2yo, pH <7.1 >10% dehyd, Na >160, K+>6.5, impaired conciousness, unstable CVS intra-operatively, or
sepsis requiring inotropes.

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Oct 04, 2011
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Replace PO4 with K2PO4

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May 18, 2011
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Resuscitate initially with 0.9% NaCl titrated to improvement of cardiovascular parameters. Take note that both serum glucose and K+ will initially fall due to dilution. Administer an insulin bolus of 0.1u/kg immediately (providing serum K+ is above 3.5mmol/L) and commence an insulin infusion at 0.1U/kg/hr aiming for a reduction in BGL to 14mmol/L at a rate of no greater than 3mmol/L/hr (to minimise the risk of cerebral oedema). At a serum glucose of 14mmol/L commence a D5W or D10W infusion whilst continuing the insulin infusion. When the serum K+ falls below 4.5mmol, replace at a rate of 20 mmol/hr. At 3-4.5mmol/L replace at a rate of 40mmol/hr. At <3 mmol/L replace at a rate of 40-60mmol/hr. (at these rates a central line will likely be required). Ensure precipitating condition is treated

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