DKA: Critical
Care Lecture
Series
PICU Fellows Lecture
Objectives
 Review
of the pathophysiology of DKA
 Review of Fluid Management
 Current DKA Management Guidelines
 Review of Common complications
 Current Protocols
Biochemical criteria
 Hyperglycemia
~200mg/dL
 Venous pH<7.3 or bicarbonate <15
 Ketonemia and ketonuria
Pathophysiology
Steel, S.
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1
3
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2
HHS vs DKA
Kitabchi, A., Et Al.
Comparing DKA And HHS
DKA
 Hyperglycemia
~200mg/dL
 Venous pH<7.3 or
bicarbonate <15
 Ketonemia and
ketonuria
HHS
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Glucose >600
pH>7.3
Bicarbonate>15
Small ketonuria
Effective serum
osmolarity
>330mOsom
Stupor or coma
Clinical Manifestations
 Dehydration
 Rapid,
deep sighing (Kussmaul
respirations)
 Nausea, vomiting and abdominal pain
 Progressive obtundation and loss of
consciousness
 Increased leukocyte count with Left shift
 Non-specific elevation of serum amylase
 Fever only when infection is present
Severity of DKA
 Mild:
Venous pH <7.3 or bicarbonate
<15mmol/L
 Moderate: Venous pH <7.2, bicarbonate
<10
 Severe: Venous pH <7.1, bicarbonate
<5mmol/L
Stamatis P, Et al.
Frequency of DKA
More common at diagnosis in younger children
 Families who do not have access to medical
care
 Risk is increased in patients with:
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Poor metabolic control, and previous DKA
Peripubertal and adolescent girls
Children with psychiatric disorders
Children with difficult family situations
Children who omit insulin
Insulin pump therapy
Clinical Assessment
 Assess
the Fluid Status
 Assess the degree of consciousness
Challenges in the ER
 Accurate
fluid assessment of these
children is difficult
 Urine OP is obscured
 Inevitably tachycardic
 Kussmal respirations
 History of the type of fluid to rehydrate is
extremely important as well
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Prospective consecutive case series
Percentage loss of weight
Parents weight at presentation, inpatient
discharge, and first follow-up clinic visit were
used to calculate percent loss of body weight
33 episodes of DKA
Patients had moderate DKA 4-8%
67% of patients in their study were assessed to
be severely dehydrated when only 12% , using
percent loss of body weight
Biochemical Assessment
 Obtain
plasma glucose, electrolytes,
osmolarity, venous pH, pCO2, calcium,
phosphorus and Magnesium, HbA1C,
CBC
 UA
 B-hydroxybutyrate
 Potassium
 Cultures
Goals of Therapy
 Correct
Dehydration
 Correct acidosis and reverse ketosis
 Restore blood glucose to near normal
 Avoid complications of therapy
 Identify and treat precipitating event
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Retrospective cohort study
Use of rehydration fluids with higher sodium
content would positively influence natremia
possibly reducing the incidence and severity
of cerebral edema
Found that increases in sodium were an
independent predicting factor against brain
edema
Issues: Hypernatremia, change to hypotonic
fluids hours after admission
Initial Fluid Management
Wolfsdorf et al.
Fluids
 Replace
deficit for next 4-6 hours with NS
or LR
 Can change fluids to ½ NS or a fluid of
greater tonicity if the physician deems this
necessary
 The goal is then to rehydrate evenly over
48 hours
 Extremely
common during treatment
 Two PICUs, Liverpool and London
 Retrospective Chart review
 Incidence of hyperchloremia increased
from 6% to 94% over 20 hours of treatment
 Base deficit decreased over treatment
time however proportion due to
hyperchloremia increased from 2-98%
An Example Calculation..
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Body weight in kilograms
Establish extent of dehydration
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Infants
Children
Mild: 5% = 50 ml/kg
3% = 30 ml/kg
 Moderate:10% = 100 ml/kg 6% = 60 ml/kg
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Severe: 15% = 150 ml/kg
9% = 90 ml/kg
An Example Calculation
 Calculate
maintenance fluid
requirements for the next 48 hours:
 200 ml/kg for the first 10 kg body weight
 + 100 ml/kg for the next 10 kg
 + 40 ml/kg for the remaining kg
 Calculate the total amount of fluid to be
given for our patient over the next 48
hours
More Fluid Calculations…
 Maintenance
plus your deficit will equal
what you need to give over 48 hours
 Divide that number by 48 hours
Two Bag Method
Metzger DL.
Two Bag Method
 Glucose
> 350 mg/dl: Run NS + additives
at 100% of calculated rate
 Glucose 250 – 350 mg/dl: Run NS at 50%
rate, run D10 NS at 50% rate
 Glucose < 250 mg/dl: Run D10 NS +
additives at 100% rate
Insulin therapy
 To
be started after our initial fluids after
the first 1-2 hours in DKA
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If given before this it has been shown in a
case control study in the UK to have a 12
fold increased risk of cerebral edema
 Dose:
0.1 unit/kg/hour
Woldfsdorf, J. Et Al.
 20
episodes of DKA in 19 children
 Bolus group and no bolus group
 Significantly lowers glucose in first hour
 “osmotic disequilibrium”
 Precipitous drop in blood glucose
Fort, P. Et al.
 38
children with 56 episodes of DKA
 No statistically significant different change
in serum glucose, osmolarity
Potassium
 Total
body potassium deficits
 Major losses from the Intracellular space
 May be normal on presentation
 Potassium
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Hypokalemic
Normal potassium
Hyperkalemic
Woldfsdorf, J. Et Al.
Acidosis
 Severe
acidosis reversible by fluid and
insulin replacement
 Stops further ketoacid production
 Allows ketoacids to be metabolized
 Bicarbonate administration may cause
paradoxical CNS acidosis(Hale, Pj., Et Al.)
 Retrospective
consecutive case series
 Initial pH < 7.15, Glucose >300
 106 children in 16 yr time period, at tertiary
university medical centers
 57 treated with bicarb
 No improved clinical outcome with
adjunctive bicarbonate therapy
 Possible longer hospitalization for the
patients who received the bicarb
Green, SM. Et al.
Mortality and Morbidity
 Cerebral
edema accounts for 75-87% of
all DKA deaths(Nichols, D. Et Al.)
 10-25% have significant residual morbidity
 Other complications
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Electrolyte abnormalities
DIC, Dural Sinus Thrombosis
Sepsis
Carlotti A P C P et al. Arch Dis Child 2003;88:170-173
Late risk factors for the development of cerebral oedema.
Carlotti A P C P et al. Arch Dis Child 2003;88:170-173
 2001,
multicenter study
 Children <18 yr
 61 children with CE
 181 randomly selected with DKA
 174 match to the CE group
 Using logistic regression, they found that
lower CO2 and higher BUN, and children
treated with bicarbonate
Glaser, Nicole, Et al.
Cerebral Edema
Diagnostic criteria
Abnormal motor or verbal response to
pain
 Decorticate or decerebrate posture
 Cranial nerve palsy
 Abnormal neurogenic respiratory pattern
o
Cerebral edema
Major
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Altered
mentation/fluctuatin
g level of
consciousness
Sustained heart rate
deceleration-not
from improved
volume or sleep
Age inappropriate
incontinence
Minor
 Vomiting
 Headache
 Lethargy or difficult
to rouse
 Diastolic blood
pressure >90mmHg
 Age <5yrs
One diagnostic, Two major, or one major
and one minor have a sensitivity of 92%
Treatment of cerebral edema
 Reduce
fluid volume by 1/3
 Mannitol 0.5-1gm/kg
 Hypertonic saline 5-10ml/kg (alternative or
second line therapy)
 Intubation if impending respiratory failure,
aggressive hyperventilation
 Elevate the head of the bed
 Then---CT to rule out thrombosis or other
intracerebral causes
 Retrospective
Observational study, in
Royal Children’s Hospital In Melbourne
 67 children with DKA
 Were in two groups equally distributed
 Plasma osmolarity had a more gradual
reduction in the 0.05u/kg/hr group
 Younger children
 Further research as whether this may
reduce the risk of cerebral edema
Hanshi, S, Et Al.l
Protocolized approach
 Minimizes
risks for young children with DKA
especially for Cerebral Edema
 ISPAD guidelines are currently the gold
standards internationally
Woldfsdorf, J. Et Al.
Protocols, protocols,
protocols….
Additional Protocols
Nursing Flowsheets
Consensus Statements
In Summary
 Caution
use of Hypotonic fluids in the first
12-24 hours of DKA management
 Assess the ECF contraction
 Increased attention to serum sodium
levels and Chloride levels
 Delay in the introduction of insulin infusions
 Protocols
Thank you!
Any Questions?
References
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British Columbia DKA Toolkit. January 8, 2010.
Cefalu W. Diabetic Ketoacidosis. Critical Care Clinics 7(1): 89-108, 1991.
Carlotti A P C P et al. Arch Dis Child 2003;88:170-173
Jeha, G, Et al. Treatment and Complication of Diabetic Ketoacidosis in
children. Uptodate. September 2010.
Kawamata,,T, Et At. Tissue Hyperosmolality and Brain Edema in Cerebral
Contusion. Neurosurg Focus. 2007;22(5):E5 © 2007 American Association of
Neurological Surgeons.
Kitabchi, A. Et Al. Hyperglycemic Crices In Patients with diabetes: DIiabetic
Ketoacidosis (DKA), and Hyperglycemic Hyperosmolar State. 2007.
Fort, P., Et Al. Low Dose insulin infusion in the the treatment of diabetic
ketoacidosis: bolus versus no bolus. The journal of Pediatrics. January 1980.
Glaser, Nicole, Et al. Risk Factors for Cerebral Edema in Children with Diabetic
Ketoacidosis. NEJM. Volume 344, No. 4, Jan. 25, 2001.
Green SM., Et Al. Failure of Adjunctive Bicarbonate to improve outcome in
severe Diabetic Ketoacidosis Ann Emerg Med. 1998 Jan: 31(1): 41-8. .
Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the
treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed) 1984 Oct 20:
289(6451): 1035 – 8.
Hanshi, S, Et Al. Insulin infusion at 0.05 versus 0.1 unit/kg/hr in children admitted
to intensive care with diabetic ketoacidosis. Pediatric Critical Care Medicine
2011 Vol 12, no 2. 137-140.
References
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Metzger, D. Diabetic Ketoacidosis in children and adolescents: an update
and revised treatment protocol. BC Medical Journal. Vol. 52. no 1, Jan/Feb
2010.
Nicols, D. Disorders of glucose homeostasis. Rogers’ Textbook of Pediatric
Intensive Care. 2008 : 1599-1614.
Orlowski, james., Et al. Diabetic Ketoacidosis in the Pediatric ICU. Pediatric
Clin N Am 55 (2008) 577-587.
Steel, S., Et al. Contin Educ Anaesth Crit Care Pain (2009) 9 (6): 194-199. doi:
10.1093/bjaceaccp/mkp034
Taylor, D., Et Al. The influence of hyperchloraemia on acid base interpretation
in diabetic ketoacidosis. Intensive Care medicine. (2006) 32:295-301.
Toledo, J., Et al. Sodium Concentration in rehydration Fluids for children with
ketoacidotic Diabetes: Effect on serum Sodium Concentration. J Pediatr
2009;154:895-900.
Woldfsdorf, J. Et Al. Diabetic Ketoacidosis in children and Adolescents with
Diabetes. Pediatric Diabetes. 2009:10(suppl. 12): 118-113.
Zeitler, P. Et al. Hyperglycemic Hyperosmolar Syndrome in Children:
Pathophysiological Considerations and suggested guidelines for treatment.
The Journal of Pediatrics. Vol 158, P9- 14. January 2011.