diabetic ketoacidosis andrew j. bauer pediatric endocrinology wramc
TRANSCRIPT
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DIABETIC KETOACIDOSIS
Andrew J. Bauer
Pediatric Endocrinology
WRAMC
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GOALS
• REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA
• CLINICAL DIAGNOSIS and MISLEADING LABS• TREATMENT and CONTROVERSIES• TREATMENT GUIDELINES
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Type 1 DM
• Autoimmune destruction of the pancreatic islet cell
• Hallmark = lymphocytic infiltration of islets
• Progresses over years• Leads to insulin
deficiency• Later may be associated
with glucagon deficiency as well
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Progression to Type 1 DM
Autoimmune destruction
“Diabetes threshold”
Honeymoon
100% Islet loss
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Typical Presentation
• Polyuria, polydypsia, weight loss
• Vomiting
• Rapid-deep respiration
• CNS depression – coma
• Precipitating event
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“Typical” Setting…..
• 9 yo boy presents to clinic with CC “ 6 day history of stomach pain and diarrhea.” “Vomiting started 2 days ago and has persisted.” – (+) weight loss– PE: HR 140, RR 28, T97.8 Weight: 27 Kg
• Tachy mucous membranes• Abd - soft, (+)BS, mild left CVA tenderness
– DX: viral gastroenteritis with mild dehydration
• Returned to ER 24 hours later– PE: cachectic, quiet, tired, cooperative, (+) ketotic breath
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Background
• 15-30% of new diabetics present in DKA– < 4 yrs of age = 40% with DKA @ diagnosis
• Most common cause of death in diabetics less than 20 years of age– 70% of related deaths in diabetics less than 10
yrs of age
• Mortality: 5-15% (1-2% at MEDCEN)
• Preventable
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Diagnostic Criteria
• Blood glucose > 250 mg/dl
• pH < 7.35
• HCO3 < 20 mEq/L
• Anion Gap > 12
• ketonemia
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Etiology
• Results from inadequate insulin– Accidental or intentional omission– Inappropriate intervention when stressed
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Etiology
DKA violates rules of common sense• Increased insulin requirement despite decreased
food intake• Marked urine output in setting of dehydration• Catabolic state in setting of hyperglycemia and
hyperlipidemia
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• Insulin Deficiency is the Primary defect
• Stress hormones accelerate and exaggerate the rate and magnitude of metabolic decompensation
Pathophysiology Counter-Regulatory Hormones
Pathophysiology Hormone• Impaired insulin secretion Epi• Anti-insulin action Epi, cortisol, GH• Promoting catabolism All• Dec glucose utilization Epi, cortisol, GH
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Islets of Langerhans
-cell destruction Insulin Deficiency
Adipo-cytes
Muscle
Liver
Decreased Glucose Utilization &Increased Production
GlucagonIncreasedProtein Catabolism Increased
KetogenesisGluconeogenesis,GlycogenolysisIncreasedLipolysis
HyperglycemiaKetoacidosis
HyperTG
PolyuriaVolume Depletion
Ketonuria
AminoAcids
FattyAcids
StressEpi,Corti
sol
GH
Threshold180 mg/dl
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Pathophysiology
Insulin
GlucagonEpinephrine
CortisolGrowth Hormone
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Pathophysiology
Dec Glucose UtilizationLipolysis
Insulin
GlucagonEpinephrine
CortisolGrowth Hormone
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DKA - Early• Relative Insulin Deficiency Glycogenolysis &
gluconeogenesis restrained
Peripheral glucose
uptake
Elevates
blood glucose
Decreased Utilization
post-prandial and Stress-Induced
hyperglycemia
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Pathophysiology
GluconeogenesisGlycogenolysis
LipolysisKetogenesis
Insulin
GlucagonEpinephrine
CortisolGrowth Hormone
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• Insulin Deficiency GlycogenolysisGluconeogenesisHepatic glucose outputPeripheral glucose uptakeElevates blood glucoseLipolysisRelease FFA -> liverVLDL & ketones Ketonemia and hyperTG Acidosis & Diuresis
DKA - Late Increased Production &Decreased Utilization
Fasting hyperglycemia
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DKA
Initial Evaluation
• Hx and PE - – Duration of onset – Level of dehydration– Evidence of infection
• Labs - STAT – Electrolytes – Venous blood gas– Serum Osmolality– U/a
Osmolality= 2 x (Na + K) + Glucose/18
+ BUN/3
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9 yo lab Evaluation
• 148| 109| 32
5.6 | <5 | 1.4
• Blood Gas - pH 7.0 5/1.020
Glu >1000, (+) Ketones
700 16.847.5
51824.4
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9 yo lab Evaluation
• 148| 109| 32
5.6 | <5 | 1.4
• Blood Gas - pH 7.0 5/1.020
Glu >1000, (+) Ketones
700 16.847.5
51824.4
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Misleading Labs
• Sodium
• Potassium
• Ketones
• WBC
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Misleading Labs
Sodium
• Na+ depressed 1.6 mEq/L per 100 mg% glucose
• Corrected Na+ = measured Na +
1.6 meq/L x (glucose-100)/100))
• Example:– Na+ = 123 meq/L and Glucose = 1,250 mg/dl– 1,250 – 100 = 1,150 / 100 = 11.5 x 1.6 = 18 meq/L – Corrected Na+ = 123 + 18 = 141 meq/L
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Misleading Labs
Sodium
• Triglycerides also artificially lower Na
Lipid LipidNa Na Na Na Na NaNa Na Na
Na Na Gluc NaNa Gluc
Serum
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• Acidosis leads to flux of K+ out of cells as H+ enters cells to buffer
• Dehydration and volume depletion– Aldosterone Na reabsorption and K+
wasting Serum K+ usually normal or high, but total
body K+ is low
Misleading Labs
Potassium
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DKA- Risks of Therapy
Hypokalemia/Hyperkalemia
• With insulin therapy– K+ moves into cells (1 meq/L / 0.1 unit pH )
• Even with K+ you must– Give large doses (40 meq/L) K+
– Monitor K+ levels and EKG • High K - tall peaked T, long PR, wide QRS
• Low K - depressed ST, diphasic T, Prom U-wave
– Cardiac dysrythmia
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• Acetyl-CoA condenses to acetoacetate• Insulin prevents utilization of acetoacetate • so levels and shunt to ß-hydroxybutyrate and acetone
Misleading Labs
Ketones
• In the absence of insulin, FFA go to the liver, and into mitochondria via carnitine
• ß-oxidation excess acetylCoA
Nitroprusside reaction
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Misleading Labs
Screening for Ketonemia
• Urine Dip stick vs. anion gap/serum bicarb
Sensitivity Specificity
DKA 99 % 69 %
Diabetic with minor signs and symptoms and negative urine ketone dip stick is unlikely to have acidosis
= high negative predictive value for excluding DKA
Am J Emer Med 34: 1999
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Misleading Labs
WBC count
• N = 247 DKA admissions over 6 years– Mean WBC = 17,519/mm3 (+/- 9,582)– 69% without infection– 17.8% presumed viral infection– 12.9% bacterial infection - more common in
children < 3 years of age
All need to be evaluated and re-evaluated if persistent acidosis
Am J Emer Med 19: 270-3, 2001
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Let’s start treatment…..
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Controversies and Risks of Therapy
• Fluids - composition, bolus
amount and total fluids/day
• Use of Bicarbonate
• Phosphate replacement
CerebralEdema
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DKA – Controversy
Cerebral Edema - Truths ?
• Idiogenic osmoles in CNS accumulate fluid
• Cerebral edema – present in 100% of patients prior to therapy
• Treatment exacerbates cerebral edema– Vigorous fluid
administration– Hypotonic fluids– Bicarbonate
Acute
LateSequelae
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DKA – Cerebral Edema
Actualities
• Etiology is not known• Occurs exclusively in pediatric patients• Mortality Rate = 21%• Morbidity Rate = 27% (permanent neurologic
sequelae)
Difficulty is relatively rare occurrence (1-3 %) with subsequent small numbers of patients in retrospective or prospective studies
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DKA – Cerebral Edema
Actualities
• NEJM - Jan 2001– N = 6977 DKA patients from 10 centers over 15
years– 61 developed cerebral edema (0.9%)
• Pediatrics - Sep 2001– N = 520 DKA patients over 5 1/2 years– 2 developed cerebral edema
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DKA – Cerebral Edema
Total Fluids
• > 4 L/m2/day, or > 50 ml/kg in first 4 hrs α hyponatremia α herniation– May occur in patients that receive less
– Of 52 patients with neurologic complications 21 had either a rise of serum Na or fall less than 4 mmol/L
JCE
M 8
5:50
9-51
3, 2
000
Attention to fluid rate and tonicity is essential, but may not be sufficient to predict subset that will
develop neurologic complications
J P
eds
113:
10-1
4, 1
988
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DKA – Cerebral Edema
Total Fluids
• > 4 L/m2/day, or > 50 ml/kg in first 4 hrs α hyponatremia α herniation– May occur in patients that receive less
– Of 52 patients with neurologic complications 21 had either a rise of serum Na or fall less than 4 mmol/L
JCE
M 8
5:50
9-51
3, 2
000
Attention to fluid rate and tonicity is essential, but may not be sufficient to predict subset that will
develop neurologic complications
J P
eds
113:
10-1
4, 1
988
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DKA – Cerebral Edema Variable Time of Onset
0
1
2
3
4
5
6
7
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 21 25
Hours after Initiation of Therapy
# of
Ch
ild
ren
wit
h N
euro
logi
c D
eter
iora
tion
NE
JM 3
44:2
64-6
9, 2
001
Prior to therapy; longer durationsymptoms before diagnosis
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DKA – Cerebral Edema
Other
• Hypoxemia– Children’s brains have higher oxygen
requirement, 5.1 mL/100g vs. 3.3 mL/100g
– Hypophosphatemia with resultant decreased 2,3-DPG decreases O2 delivery to brain cells
– Mannitol - earliest effects are related to decreased viscosity, not to shift of fluid from extravascular space
JCEM 85: 509-13, 2000Neurosurg 21: 147-156, 1987
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DKA – Cerebral Edema
Signs and Symptoms
1. Sudden and persistent drop in heart rate
- not bradychardia - not assoc with HTN
- not related to hydration status
2. Change in sensorium 7. Fall in serum
3. Headache Na, or failure
4. Emesis to rise
5. Incontinence
6. Unexplained tachypnea
JCEM 85:509-513, 2000
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DKA – Cerebral Edema
Evaluation
• CT may be non-diagnostic at time of symptoms– 9 of 30 - no edema, 6 read as normal– 5 of 9 - 2.5 to 8 hours after onset of coma, read as
normal
JCEM 85:509-513, 2000
Cerebral Edema is a clinical diagnosis.Need to treat BEFORE imaging.
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DKA – Risks of Therapy
Bicarbonate Administration
• Administration to acidotic patient generates rapid rise in CO2
• CO2 enters CNS rapidly• HCO3
- is delayed by blood-brain barrier• Increased CNS CO2 exacerbates cerebral acidosis CO2 + H2O H2CO3 H+ + HCO3
-
• May also reduce partial pressure of O2 in CSF vasoconstriction brain hypoxia/ischemia
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DKA – Risks of Therapy
Bicarbonate Administration
NEJM 344:264-269, 2001
• Multi-center study from 10 pediatric centers, USA and Melbourne, Australia over 15 yr period– 6977 DKA hospitalizations: 61 cases cerebral edema (0.9%)
• Presentation: PaCO2 BUN Glucose Bicarb Cerebral Edema 11.3 27 758 23/61 (32%) Controls 15.1 21 700 43/174 (23%) fluid, insulin, or sodium administration, nor rate of
fall in glucose was associated
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DKA – Risks of Therapy
Bicarbonate Administration
• Variations in treatment exacerbate an on-going pathologic process• Brain ischemia is major underline etiology
– Hyperglycemia increases extent of neurologic damage– Extreme dehydration, hypocapnia – Concept of idiogenic osmotically active substances not supported (no relationship to change in glucose, rate of fluid
or Na administration)
Risk related to duration and severity of DKA
NEJM 344:264-269, 2001
**** ******** ****
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DKA- Controversy
Phosphate
• Essential phosphate deficit
• W/treatment serum phosphate and 2,3-DPG fall
• Shift oxyhemoglobin curve reducing O2 deliver
Theoretical
Practical
• No evidence of direct benefit, but less Cl-
• Give ½ K+ replacement as K-phos x 8 hours
• Limit to 2 mEq/kg/day to avoid hypocalcemiaEndo Met Clin 29:Dec 2000
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Elements of Therapy
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Elements of Therapy
• Fluids – treat shock, then sufficient to reverse dehydration and replace ongoing losses (will correct hyperglycemia)
• Insulin – sufficient to suppress ketosis, reverse acidosis, promote glucose uptake and utilization (will stop ketosis)
• Electrolytes – replace profound Na+ and K+ losses
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Typical Therapy - Fluids
• 10% dehydration is standard estimate (use weight if known)– Bolus: treat shock, usual 20-30cc/kg
given 10cc/kg at a time– Replace deficit over 48-72 hours– ie. 10 % in 20 Kg pt = 2000ml over 48hrs
= maintenance + 42cc/hr x 48 hours
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Typical Therapy - Fluids
• Use ½ NS to NS • Average = 2 x maintenance
– 4:2:1 cc/kg/hr or 100:50:20 cc/kg/day – ie. 25 kg patient
• (4 x 10) + (2 x 10) + (1 x 5) = 65 cc/hr• (100 x 10) + (50 x 10) + (20 x 5)/24 hours
= 66.7 cc/hr
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DKA – Risks of Therapy
Insulin
Insulin Level
Biological effect
100%
100 uU/ml
Current therapy usescontinuous insulin drip Drop glucose 50-100 mg/dl/hr
0.1 units/kg/hr
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Typical Therapy - Insulin
• 0.1 unit/kg/hr continuous drip (regular)– Flush tubing with 50 ml– 250 units regular in 250 cc NS (1.0
units/ml)= 0.1 u/kg/hr = 0.1 ml/kg/hr
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Typical Therapy Glucose - 2 Bag Method
• Goal - decrease blood glucose by 50-100 mg/dl/hr
• Must continue insulin therapy to correct acidosis
• Order D10 NS to bedside– when serum glucose < 300: add D5NS ( = 1/2
D10NS + maintenance bag)– when serum glucose < 200: Change to D10NS
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Typical Therapy
• K+ 40 meq/L (split between KCl and Kphos)
• Reverse insulin resistance– Treat infection– Treat underlying illness - stress
• Bicarb - only if severe circulatory failure and high risk of cardiac decompensation from profound acidosis
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Monitor
• ICU - pH < 7.3 and/or HCO3 < 15
• Available staff
• Strict I/O (NPO)– Fluid calculations must account for ongoing
losses – vomiting, diarrhea, excessive urine– ? If > 4 L/m2/day
• CNS activity - headache, change in sensorium
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Monitor
• Vitals - sudden drop in HR, tachypnea• Neurologic checks - q30-60 minutes• Weight - bid• Labs
– dstick q1 hour– Urine dip q void - resolution of ketonuria may lag behind clinical improvement
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Monitor
• Labs – Lytes, VBG q 2-4 hours
Drop in Na - increase risk of cerebral edema, ? SIADH vs. cerebral salt wasting
HCO3- / pH in first 2-3 hours may drop further due
to re-perfusion of tissue, lactic acidosis
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DKA
Guidelines
• Common ground to start from
• Does not eliminate need to individualize therapy
• Large deviations should be an opportunity to critically review clinical and therapeutic course
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DKA
Flowsheet
• CIS is not a flow sheet, but rather a database
• Inability to review all data at one time decreases ability to make sound decisions
• Maintenance of flowsheet is the first step in critical analysis of response to therapy
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9 yo lab Evaluation
• 27 Kg - assume 10% dehydrated• 148| 109| 32
5.6 | <5 | 1.4 70016.847.5
51824.4
• Anion Gap = • Osm = • Corrected Na =
• Fluid Def = • Maintenance = • IV rate (24hrs) =
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Transport of Patient with DKA
• 2 large bore PIV• Must have documentation of previous treatments
– PE with vitals and notes on mental status – Fluids - bolus and current– ? SQ Insulin given - time and amount– Contact phone number for labs/cultures
• Must have glucagon, mannitol and IV glucose with patient at ALL times
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DKA
Prevention
• 50% DKA admissions are in known diabetics
• Failure of Physician-Patient relationship– non-compliance– Inappropriate intervention– Sick day rules need to be understood and
followed– Availability is essential