DKA PROTOCOL
This protocol is
intended as a guide – individual patient modifications may be necessary.
Physiology
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.
Treatment
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
Fluid Therapy
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.
Fluid Rate
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
4 L/m2/day
Insulin
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.
Dextrose
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.
A B
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
Ongoing Monitoring
· Never put the patient on autopilot
· Check dextrose stick every 1 hour
· Check VBG every 2 – 4 hours (frequency is
dependent on severity of acidosis)
· Check serum electrolytes every 4 hours
· Make sure that Intake > Output
· Consider foley catheter placement in patients in
shock or if the resuscitation is not straightforward.
· Check UA every 8 hours for glucose and ketones
Neurologic Complications
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.
Recovery
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.
Summary
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
Appendix A
Table: Two bag system
method: calculating delivered dextrose.
|
Desired Dextrose Delivery Concentration |
Total Rate (as %) of Bag A (D0) |
% Total Rate of Bag B (D10) |
|
D0 |
100 % |
Off |
|
D2.5 |
75% |
25% |
|
D5 |
50% |
50% |
|
D7.5 |
25% |
75% |
|
D10 |
Off |
100 % |