download the DKA Guideline Packet PDF

Diabetic Ketoacidosis
Clinical Practice Guidelines
Order BMP, VBG, UA
Check neuro status
Consider
New onset labs*
Patient arrives
with DKA
Rehydration
with normal
saline 20ml/kg
Signs of
uncompensated
shock after first
bolus?
No
Check neuro status
TIVF at 1.5-2.0x MIVF via 2 bag method*(below)
Glucose infusion rate determined by the
patient’s blood sugar (see chart on pg2)
Insulin infusion at 0.1 units/kg/hr
BMP q4h and start Insulin infusion at 0.1
units/kg/hr (for most patients).
pH > 7.0 with
trend of patient
improvement?
Obtain VBG q1h until
upward trend is
established AND pH > 7.0
Yes
Yes
No
Repeat fluid bolus
Continue rehydration with 1.5-2.0x MIVF by
2 bag method* without additional potassium
Recheck potassium in no more than 4 hours
Continue IVF at 1.5-2.0 x MIVF with NS as
the base solution for the 2 bag method*
with potassium as indicated until sodium is
corrected and neuro status is baseline.
No
K< 5.0?
Yes
Continue rehydration with 2 bag method*; add a total
of 40 mEq/L of K+ to IV fluids (as KCL 20mEq/L and KPO
20 mEq/L)
Continue q1h glucose checks & rehydration for 8-12hrs
of total fluids
No
Normal sodium
& baseline
neuro status?
Yes
Transition base IVF to ½ NS
solution with standard 2 bag
method
BMP every 8 hrs until
corrected
PO sugar free
Bicarb 18 or
greater?
Bicarb ≥ 16 x 2 with
gap <10?
Yes
No
Diabetic Ketoacidosis or DKA is a
condition that occurs when there are
critically low levels of insulin in the
body. The body responds by burning
fatty acids (ketogenesis) which
produce acetone and
betahydroxybutyric acid in very large
amounts (acidosis) resulting in
extreme dehydration, kidney failure,
cardio-respiratory collapse and death
if not treated.
General Information
This pathway is intended to treat mild to moderate uncomplicated DKA (pH > 7.0).
Symptomatic Cerebral Edema from DKA is a clinical emergency.
Warnings and emergency therapies
Pediatric DKA is associated with a higher incidence of cerebral edema and stroke
For concern of cerebral edema, consider hypertonic saline administration: 3-5ml/kg
over 10 minutes (max of 500ml).
Bicarbonate administration is associated with increased morbidity/mortality from
cerebral edema.
Infection can adversely affect the
recovery time from DKA and threaten the
clinical stability of the patient. When
fever of > 100 F is present , the work up
should include a fever/ infection
evaluation while treating DKA
*2 Bag Method
The first bag is non-dextrose fluid and the second bag is D10; Both will be infused
simultaneously via IV.
Each bag will infuse at different rates dependent on serum glucose levels .
Bicarbonate administration should be reserved for dire situations after
consultation with a Pediatric Endocrinologist
(information for glucose infusion w/ table on pg 2)
Transition as follows:
Allow patient to eat
regular diet
Give scheduled SQ
insulin
Stop insulin and
dextrose fluids 10 min
after SQ insulin
Inclusion Criteria
Patient must meet all of the following:
Blood glucose > 250
Ketosis by blood or urine testing
Acidosis by blood gas analysis
AND any of the three listed below:
History of previously diagnosed IDDM
History of significant NIDDM
History consistent with new onset IDDM
(polyuria, polydipsia, polyphagia)
Exclusion Criteria
Significant dehydration/ketosis without insulin
deficiency from any other cause, such as:
Appendicitis or other abdominal crisis
Steroid induced hyperglycemia
Ketosis from other metabolic/genetic causes
This guideline does not take into account individual patient situations, and does not substitute for clinical judgment
Diabetic Ketoacidosis
Clinical Practice Guidelines
Insulin Infusion
After initiation of insulin infusion:
Bedside glucose testing hourly.
Obtain BMP 4 hours for the first 8-12 hours of rehydration therapy.
Consult Endocrinology for long acting insulin (Lantus)
recommendations during rehydration.
If the patient returns to baseline neurologic status and does not have
documented hyponatremia (corrected for serum glucose), sugar-free clears
up to 1 ml/kg/hr are allowed keeping total intake less than 2.5x MIVF.
After 8-12 hours of rehydration therapy:
Obtain new BMP.
Provider team will assess patient for return to baseline neuro status,
signs of cerebral edema, and correction of hyponatremia (>135 mEq/L)
Continue rehydration per algorithm.
Obtain BMP every 8 hours until acidosis is corrected.
Transition from Insulin Infusion
Obtain pre-meal glucose level by finger stick.
Give patient the scheduled subcutaneous insulin injection including.
sliding scale and/ or meal correction dose.
Allow patient to eat 10 minutes after injection of meal insulin.
Stop insulin infusion 20 minutes after meal insulin injection.
If dehydration is still problematic, the pediatric endocrinology team
will decide on IV fluids type, infusion rate and glucose infusion rate.
Glucose Infusion
Glucose infusion rate is determined by the patient’s blood sugar while
on an insulin infusion as listed in the table below.
The purpose of glucose in intravenous fluids is to provide enough
dextrose to maintain the insulin infusion at all times in order to stop
the catabolic process (ketogenesis).
1st Bag
Patient’s Glucose
(D0 solution)
2nd Bag
(D10 solution)
BG <200
0% TIVF (0x MIVF)
100% TIVF (1.5-2.0x MIVF)
BG 201-300
50% TIVF (0.75-1.5x MIVF)
50% TIVF (0.75-1.5x MIVF)
BG >301
100% TIVF (1.5-2.0x MIVF)
0% TIVF (0x MIVF)
Patient Education
Patient education is performed by both the bedside staff and the
diabetes education nurse/endocrinology team. The provider places an
order to page the diabetic educator (during regular week day work
hours) for the standardized education pathway and approved
education materials.
REFERENCES
Dunger, D. B., Sperling, M. A., Acerini, C. L., Bohn, D. J., Daneman, D., Danne, T. P. A., … Lawson Wilkins Pediatric
Endocrine Society. (2004). European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society
consensus statement on diabetic ketoacidosis in children and adolescents. Pediatrics, 113(2), e133–140.
Felner, E. I., & White, P. C. (2001). Improving management of diabetic ketoacidosis in children. Pediatrics, 108(3), 735–
740.
Fiordalisi, I., Novotny, W. E., Holbert, D., Finberg, L., Harris, G. D., & Critical Care Management Group. (2007). An 18-yr
prospective study of pediatric diabetic ketoacidosis: an approach to minimizing the risk of brain herniation during
treatment. Pediatric Diabetes, 8(3), 142–149. doi:10.1111/j.1399-5448.2007.00253.x
Poirier, M. P., Greer, D., & Satin-Smith, M. (2004). A prospective study of the "two-bag system’’ in diabetic ketoacidosis
management. Clinical Pediatrics, 43(9), 809–813.
Rosenbloom, A. L. (2010). The management of diabetic ketoacidosis in children. Diabetes Therapy, 1(2), 103–120.
doi:10.1007/s13300-010-0008-2
Savage, M. W., Dhatariya, K. K., Kilvert, A., Rayman, G., Rees, J. A. E., Courtney, C. H., … Joint British Diabetes Societies.
(2011). Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine: A Journal
of the British Diabetic Association, 28(5), 508–515. doi:10.1111/j.1464-5491.2011.03246.x
Silverstein, J., Klingensmith, G., Copeland, K., Plotnick, L., Kaufman, F., Laffel, L., … American Diabetes Association. (2005).
Care of children and adolescents with type 1 diabetes: a statement of the American Diabetes Association. Diabetes Care,
28(1), 186–212.
So, T.-Y., & Grunewalder, E. (2009). Evaluation of the Two-Bag System for Fluid Management in Pediatric Patients with
Diabetic Ketoacidosis. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 14(2), 100–105. doi:10.5863/15516776-14.2.100
Wolfsdorf, J., Glaser, N., Sperling, M. A., & American Diabetes Association. (2006). Diabetic ketoacidosis in infants, children,
and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care, 29(5), 1150–1159.
doi:10.2337/diacare.2951150
This guideline does not take into account individual patient situations, and does not substitute for clinical judgment