Management of Diabetic ketoacidosis from A-Z.

Posted on: Saturday, September 22nd, 2018 @ 9:26 PM - By: Mohemet - Seen 235 Times

Diabetic ketoacidosis (DKA) is a medical emergency. The patient may have already been diagnosed of having diabetes mellitus or may be first time presentation without being  diagnosed. When it’s not known that the patient is diabetic, the clinical triad of kussmaul respiration (deep & rapid breathing), dehydration and coma in a child should always raise the possibility of DKA. Also there may be repeated vomiting,  abdominal pain, signs of intercurrent infection. Diagnosis is then confirmed by the following:

  • Blood glucose level > 300mg/dl.
  • Metabolic acidosis by ABG analysis >> pH < 7.3 and  bicarbonate  HCO3−   < 15meq/L.
  • Glucosuria and ketonuria.

*Causes of developing DKA: 

  • First time presentation without knowing of having DM (the patient is not on treatment).
  • Missing an insulin dose or due to poor compliance (over eating of sweet food).
  • Intercurrent infection might precipitate development of DKA.

Having diagnosed the case as DKA, continuous observation of the level of consciousness, state of hydration and vital signs is essential.

**Immediately put the patient on Oxygen therapy, in comatose patients if there is vomiting suctioning is needed, and might also need nasogastric tube insertion to evacuate the stomach and prevent aspiration of vomited material. Establish 2 intravenous accesses and infuse shock therapy 10-20ml/kg NS 0.9% over 1hr. Withdraw blood and send for the following investigations:

  • Blood glucose level
  • Arterial blood gas
  • Serum electrolytes and RFT.
  • CBC, CRP, Blood culture if infection suspected as triggering factor.
  • Send Urine for Sugar and Ketone

**Lines of management according to Milwaukee protocol:

1-ABC: Oxygen, suctioning of secretions if any, establish 2 IV lines, withdraw blood for investigations and send urine for analysis, nil by mouth, hourly chart for vital signs, blood glucose level and input-output, frequent neurologic checks.

2- Correction of shock, acidosis and dehydration by IV fluids as follow:

  • a- Shock therapy:  A bolus of 10-20ml/kg NS 0.9% or RL over 1hr will be given. It may be repeated if still dehydrated but should not exceed 30ml/kg.
  • b- Deficit therapy: The deficit amount in DKA is constant, it’s almost always 85ml/kg NS 0.45% (not 0.9%) when blood glucose is > 300mg/dl or GS 1/2 when blood glucose is < 300mg/dl. For duration of infusing deficit therapy see below.
  • c- Maintenance therapy: Calculate maintenance therapy according to Holliday-Segar method ( click here to learn more ), the type of fluid is NS 0.45% (not 0.9%) when blood glucose is > 300mg/dl or GS 1/2 when blood glucose is < 300mg/dl. The deficit and maintenance amount with the initial bolus subtracted will be given over 23 hour period whereas those with severe DKA and a greater volume deficit require 30-36 hours with this protocol for rehydration to avoid cerebral edema. See below for more information.
  • d- Correction of metabolic acidosis with sodium bicarbonate will be considered only if there is sever acidosis (pH < 7.15 and HCO3−  < 10meq/L). A single dose of sodium bicarbonate 5% 2ml/kg slow IV over 10 minutes is sufficient as complete correction will occur with with IV fluid therapy and insulin therapy.
  • e- K replacement: If available (20 mEq/L KPhosphate and 20 mEq/L KAcetate), if not available 40mEq/L KCl will be added to deficit and maintenance therapy (not to the initial IV bolus) after serum K is <6 mEq/L or urine flow is established. If K <3 mEq/L increase IV K to 80 mEq/L.

3- Intravenous insulin therapy: Regular insulin must be given at the beginning of therapy (i.e. with initial IV bolus in the first hr via second IV line) at a rate of 0.1 units/kg/hr.

Insulin will be infused with the infusion pump. For e.g. if the patient is 20kg, 20*0.1IU= 2IU/hr should be provided. To calculate the insulin requirement, divide wt by 2 (20/2 =10), put 10IU of regular insulin in 50ml NS and infuse 1oml/hr. Another e.g. if the patient’s wt is 28, 28*0.1IU= 2.8IU/hr is required, divide 28 by 2 (28/2=14), so put 14IU of regular insulin in 50ml NS and infuse 10ml/hr. Notice that 50ml of NS and infusion rate 10ml/hr are constant, only amount of putting insulin is changing according to wt.

An infusion pump set to deliver 10ml/hr.

  • Insulin infusion can be lowered to 0.05IU/kg/hr but not stopped once hyperglycemia resolved. To continue the insulin infusion without causing hypoglycemia, glucose must be added to the infusion. It’s recommend that glucose be added as a 5% solution when the serum glucose has decreased <300 mg/dL and as a 10% solution when the serum glucose has decreased <200 mg/dL.
  • If the condition managed accurately hypoglycemia should not develop. When it occurs, it means mismanagement: either rapid insulin infusion, improper dosage calculation, delay follow up of the patient’s glucose level and delay in changing NS 0.45% to GS1/2,…etc.

4-Cerebral edema: Radiographic imaging is frequently unhelpful in making the diagnosis of cerebral edema. Hence frequent neurologic checks for any signs of increasing intracranial pressure, such as a change of consciousness, depressed respiration, worsening headache, bradycardia, apnea, pupillary changes, papilledema, posturing, and seizures is necessary. Mannitol must be readily available for use at the earliest sign of cerebral edema.

  • Mannitol administered  intravenously in a dosage of 1 g/kg over 20 minutes with repeat as necessary in 1–2 hours.
  • Reduction in the rate of fluid administration and elevation of the head of the bed.
  • Intubation should be reserved for those with respiratory compromise.

5- Control of precipitating infection: when an infection seems to be the precipitating factor, a broad spectrum antibiotic is given for instance Ceftriaxone vial or an antibiotic according to the result of cultures.

Miwaukee protocol for DKA management

6- Subcutaneous insulin: After fully rehydrating the patient and resolving of acidotic state, it’s time to start oral intake and shift to subcutaneous insulin.

  • Criteria for transition to oral intake and subcutaneous insulin:
  • plasma glucose is <200–250 mg/dL
  • pH >7.30 & total HCO3− >15 mEq/L
  • sodium stable between 135 and 145 mEq/L
  • anion gap is ≤12
  • no emesis

When the above criteria met, the patient can be easily transitioned to oral intake and subcutaneous insulin.

  • IV fluids can be stopped 1–2 hours after substantial consumption of oral fluids without vomiting.
  • Subcutaneous insulin injection can be started when IV fluids are no longer needed, the first dose of short-acting subcutaneous insulin is given with a meal, and the insulin drip is discontinued approximately 30 min later.
  • Regular insulin is given in a dose of 0.2-0.4IU/kg every 6-8 hrs before meal.
  • Blood glucose level should be monitored before and 2 hrs after each meal and insulin dosage can be adjusted to keep blood glucose level between 100-180mg/dl.

**Having the patient fully controlled, then refer the case to a diabetic center for putting the patient on lifelong management.

***Case scenario: An 8 year-old (30 kg) male child who is previously healthy, presented with severe dehydration, vomiting and labored breathing. He is conscious. His RBS is 700mg/dl, pH is 7.2,  HCO3− is 15mEq/L, temp is 37.1°. How to manage this case?

Management will be:

1-Initial management: Hospitalization and ABC: give oxygen, nil by mouth, establish 2 IV lines, withdraw blood for investigations, put NG tube for gastric emptying, make a follow up chart hourly.

2-IV fluid therapy:

  • Shock bolus: 30*10= 300ml NS 0.9% (100 drops/min) over 1 hr.
  • Deficit therapy: Is 85ml/kg >> 85*30= 2550 ml.
  • Maintenance therapy: For 30 kg child according to Holliday-Segar method is 1750ml.

According to Milwaukee protocol >>

So 175 ml/hr of NS 0.45% should be given, when RBS < 300mg/dl change to GS 1/2 and when RBS further drops to below < 200mg/dl add another 5% of glucose to the fluid to avoid hypoglycemia. The rate of infusion can be easily controlled with infusion pump or flow regulator.

3- IV insulin therapy: 0.1IU/kg of regular insulin is given via 2nd IV line. Patient’s wt is 30 kg, (30/2=15) so put 15IU of regular insulin inside 50ml NS and infuse 10ml/hr via infusion pump.

4-Add KCL to fluid: add 40mEq/L (1ml=2mEq), so add 10ml/pint when urine output is positive or serum K level is < 6 mEq/L. Increase KCL to 20ml/pint if serum K level is < 3mEq/L.

NOTE: there is no need for sodium bicarbonate, antibiotics or mannitol because pH is > 7.15, no signs of infection with no fever (temp is 37.1°) and patient is conscious with no signs of cerebral edema.

5-Subcutaneous insulin therapy: when above criteria met and DKA resolved, oral feeding will be started, if tolerated with no emesis, IV fluid will be stopped and a dose of SC regular insulin 0.2IU*30=6IU will be given, 30 minutes later IV insulin therapy will be discontinued. 0.2-0.4IU/kg (30*0.2-0.4=6-12IU) of regular insulin will be given SC every 8 hrs 30min before meal with blood glucose level checking 3omin before and 2 hours after meal. Adjust insulin dose according to blood glucose level. When patient fully recovered refer him to a diabetic center for long term management.


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