This protocol is intended as a guide – individual patient modifications may be necessary.
DKA is the result of a lack of insulin production by the pancreas. This leads to a characteristic physiologic change in patients:
1. The decreased insulin leads to an inability to draw glucose into cells. This in turn leads to increased serum glucose.
A. A serum glucose level > 250 exceeds the kidney’s threshold, leading to spilling of glucose into the urine. The loss of glucose draws water with it and leads to polyuria.
B. Polyuria leads to dehydration, which, in turn leads to polydipsia (which, as the patient gets sicker cannot keep up with the polyuria).
i. As a result all patients with DKA are dehydrated
2. The lack of glucose entry into cells leads to cellular energy deprivation.
A. To overcome this, he body increases gluconeogenesis, a process to create more glucose in an attempt to provide energy to cells. The process of gluconeogenesis breaks down fats to create glucose.
i. The glucose created is released into the serum and, because of lack of insulin, cannot enter cells and therefore leads to a further increase in serum glucose.
ii. As a by-product of breaking down fats ketoacids are produced – this leads to the acidosis of DKA.
iii. To compensate for the acidosis the patients “blow off” CO2 by breathing deeply and rapidly (Kussmaul respirations).
B. The lack of available energy leads to increased food consumption by the patients – polyphagia.
3. Potassium physiology
A. The cells of the body are filled with potassium (positively charged ion).
B. With increasing acidosis (i.e. an increase in hydrogen – also positively charged) hydrogen ions accumulate in the plasma.
C. The hydrogen ions move down their concentration gradient into the cells in an attempt to buffer the acidosis.
D. To keep the cell’s charge neutral, for each hydrogen ion that moves into the cell, a potassium ion is moved out into the plasma.
E. To keep the plasma potassium concentration normal, the kidney will increase potassium losses into the urine.
F. As the acidosis is corrected the process is reversed.
i. The hydrogen ions move back out of the cells
ii. The potassium moves back into the cells, BUT much has been lost in the urine, so the potassium level drops
G. Thus, the patient becomes total body potassium depleted.
Goals of Treatment
1. Restore perfusion
2. Stop ketogenesis (inhibit lipolysis and gluconeogenesis).
3. Permit glucose transport into cells
4. Correct dehydration and electrolyte disturbances
5. Avoid complications of therapy – cerebral edema, hypoglycemia and hypokalemia
Assessment of the Patient
1. Assess the patient with careful neurologic assessment – all patients with an altered mental status and/or severe dehydration and shock require immediate attending notification.
2. Initial labs: VBG, electrolytes, BUN, creatinine, calcium, magnesium, phosphate, serum glucose, dextrostick, UA, CBC
Types of Fluids
1. Administer 20 cc/kg of normal saline (0.9%) over 20 – 30 minutes. If the patient is in shock the initial fluid bolus should be given over 10 – 20 minutes. The PICU attending needs to be notified if the patient is in shock, as additional fluid boluses may be necessary to alleviate shock
2. The patient should be reevaluated after the initial 20 cc/kg fluid bolus and if no further boluses are needed, then fluids should be changed to:
˝ normal saline + 20 mEq/L KCl + 20 mEq/L Kphos
If the serum K+ is > 5, decrease the total K+ in the fluids to 20 mEq/L
If the serum K+ is > 5.5, omit the K+ from the fluids
*A note on using buffer therapy with bicarbonate: sodium bicarbonate is almost never necessary in the treatment of DKA, and its use is associated with increased risk of cerebral edema. Therapy with sodium bicarbonate may be considered in cases of severe acidosis with shock. Any consideration of bicarbonate administration requires the input of the PICU attending.
1. Total fluid rate is 1˝ times maintenance for 24 hours or until the acidosis is resolved. Make sure to include the rate of the insulin drip in the total fluids.
2. Continue to monitor urine output carefully, as significant polyuria may necessitate additional fluids – consult with attending.
*For uncomplicated DKA, the total fluids (including boluses) should not exceed
After the initial fluid bolus is finished or after the patient is out of shock, begin an insulin drip
Dose: 0.1 Units/kg/hr
Concentration: 50 Units Regular insulin/500 cc normal saline
Nursing note: run 50 cc through tubing before connecting to patient to saturate binding sites in the tubing.
The goal of insulin is to halt ketogenesis and stop gluconeogenesis – continue until the urine ketones are clearing, pH is improving (> 7.30), and the patient is able to eat.
Note: in very young children, the insulin drip may need to be reduced to 0.05 Unit/kg/hr, especially if the glucose is dropping to quickly.
The goal of dextrose management is to keep a serum glucose level of 200. Remember the primary goal of treatment is to halt ketogenesis and gluconeogensis: not to treat hyperglycemia per se. The act of providing fluids alone will cause the glucose level to fall, as the patient continues to have glucosuria. Dextrosticks are monitored every 1 hour. When the glucose reaches 300, add dextrose at 5% (D5).
Based on the hourly dextrosticks, the amount of glucose should be titrated up or down to maintain the serum glucose 200 – 300. This requires changing the glucose concentration hourly based on whether the patient’s glucose is falling too rapidly or rising again. An ideal rate of fall is by 50 mg/dl/hr. Since the patient’s needs will change faster than the pharmacy can mix new fluid bags, the easiest way to alter the dextrose concentration that the patient receives is via the 2 bag system.
2 Bag Fluid System to Allow Rapid Titration of Dextrose
The fluids are ordered in 2 bags that are identical in electrolyte concentration: each bag will contain ˝ normal saline + 20 mEq KCl/L + 20 mEq Kphos/L.
The first bag (A) will contain no dextrose.
The second bag (B) will contain D10.
The bags will run at the calculated fluid rate
(1˝ times maintenance minus the insulin drip rate).
The relative rates of the 2 bags will be adjusted
to change the amount of dextrose delivered to the
patient from D0 all the way to D10. See appendix A.
Thus: in the beginning of management,
run Bag A at the full rate and keep Bag B off
– this gives fluids with no dextrose.
Increase dextrose by increasing the rate of Bag B
and decreasing the rate of Bag A
Decrease dextrose by decreasing the rate of Bag B
and increasing the rate of Bag A
All patient in DKA are at risk for cerebral edema and herniation. This is especially true for young patients, those that present with altered mental status and those with their first episode of DKA. All patients require frequent (at least q 1 hour) neuro checks. At this time we do not know what causes cerebral edema. Theories include a rapid change in osmolality (via drop in glucose), too much fluid and impaired cerebral compliance. An ominous warning sign is a serum sodium concentration that doses not increase as the patient is treated. A decreasing sodium level should trigger a decrease in the IV rate and a conversation with the attending. If there is a neurologic deterioration, mannitol is given (0.5 grams – 1 gram/kg) and the most experienced person available intubates the patient using strict increased ICP precautions.
Once the ketones have cleared from the urine and ketogenesis has been halted, the insulin drip can be discontinued. If this occurs in the middle of night, continue the drip to until the morning, maintaining a serum glucose 200 – 300. Before discontinuation of the insulin drip, the patient must first receive subcutaneous insulin. Once the patient is feeding, the IV fluids can be discontinued. Insulin doses are then titrated to the patient’s need,
Subcutaneous insulin dosage:
Daily insulin dose can be calculated at 0.5 – 1 Unit/kg/day and is divided as ? of the daily dose in the morning and ? of the daily dose at night. For this dose give ? of each dose as regular and the remaining ? as NPH.
Note: many endocrinologists have treatment protocols for their patients. They should be consulted upon PICU admission and again prior to transitioning the patient to subcutaneous insulin. It is wise to ask their preference about long term care, as they will be managing these patients for years to come.
1. Prepare for the patient prior to their arrival
A. This protocol requires a minimum of 3 and perhaps 4 IV pumps
i. Insulin pump
ii. 2 pumps for fluids (1 for dextrose and 1 for non dextrose containing fluids)
iii. 1 pump for additional fluid replacement if necessary
B. The following fluids are needed
i. Normal Saline
ii. ˝ NS + 20 mEq KCl/L + 20 mEq KPhos/L
iii. D10 ˝ NS + 20 mEq KCl/L + 20 mEq Kphos/L
iv. Insulin Drip mixed at 50 units of regular insulin in 500 cc NS
2. Treat dehydration and shock with NS
3. Begin ˝ NS with KCl and Kphos at 1 ˝ times maintenance
4. Begin Insulin drip at 0.1 units/kg/hr
5. Add dextrose when dextrose stick falls below 300
6. Titrate dextrose with 2 bag system to maintain dextrose stick 200 – 300
7. Monitor I/O carefully
8. Monitor neurologic status closely
9. Endocrine consult early in the patient’s course
Table: Two bag system method: calculating delivered dextrose.
Total Rate (as %) of Bag A (D0)
% Total Rate of Bag B (D10)