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DIABETIC KETOACIDOSIS. Andrew J. Bauer Pediatric Endocrinology WRAMC. GOALS. REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA. CLINICAL DIAGNOSIS and MISLEADING LABS TREATMENT and CONTROVERSIES TREATMENT GUIDELINES. Type 1 DM.

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Diabetic ketoacidosis l.jpg

DIABETIC KETOACIDOSIS

Andrew J. Bauer

Pediatric Endocrinology

WRAMC


Goals l.jpg
GOALS

  • REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA

  • CLINICAL DIAGNOSIS and MISLEADING LABS

  • TREATMENT and CONTROVERSIES

  • TREATMENT GUIDELINES


Type 1 dm l.jpg
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

Honeymoon

100% Islet loss

“Diabetes threshold”


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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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PathophysiologyCounter-Regulatory Hormones

  • Insulin Deficiency is the Primary defect

  • Stress hormones accelerate and exaggerate the rate and magnitude of metabolic decompensation

  • 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

b-cell destruction

Insulin Deficiency

Decreased Glucose Utilization &

Increased Production

Epi,Cortisol

GH

Stress

Muscle

Glucagon

Amino

Acids

Adipo-

cytes

Increased

Protein

Catabolism

Liver

Increased

Ketogenesis

Gluconeogenesis,

Glycogenolysis

FattyAcids

IncreasedLipolysis

Threshold

180 mg/dl

Polyuria

Volume Depletion

Ketonuria

Hyperglycemia

Ketoacidosis

HyperTG


Pathophysiology l.jpg
Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin


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Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin

Dec Glucose Utilization

Lipolysis


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Decreased Utilization

 post-prandial

and

Stress-Induced

hyperglycemia

DKA - Early

  • Relative Insulin Deficiency

     Glycogenolysis &

    gluconeogenesis restrained

    Peripheral glucose

    uptake

    Elevates

    blood glucose


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Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin

Gluconeogenesis

Glycogenolysis

Lipolysis

Ketogenesis


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DKA - Late

Increased Production &

Decreased Utilization

 Fasting

hyperglycemia

  • Insulin Deficiency

    Glycogenolysis

    Gluconeogenesis

    Hepatic glucose output

    Peripheral glucose

    uptake

    Elevates blood glucose

    Lipolysis

    Release FFA -> liver

    VLDL & ketones

    Ketonemia

    and hyperTG

    Acidosis & Diuresis


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DKAInitial 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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700

24.4

518

16.8

47.5

9 yo lab Evaluation

  • 148| 109| 32

    5.6 | <5 | 1.4

  • Blood Gas - pH 7.0 5/1.020

    Glu >1000, (+) Ketones


9 yo lab evaluation20 l.jpg

700

24.4

518

16.8

47.5

9 yo lab Evaluation

  • 148| 109| 32

    5.6 | <5 | 1.4

  • Blood Gas - pH 7.0 5/1.020

    Glu >1000, (+) Ketones


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Misleading Labs

  • Sodium

  • Potassium

  • Ketones

  • WBC


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Misleading LabsSodium

  • 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 LabsSodium

  • Triglycerides also artificially lower Na

Lipid

Lipid

Serum

Na Na Na

Na Na Na

Na Na Na

Na Na

Gluc Na

Na Gluc


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Misleading LabsPotassium

  • 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


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DKA- Risks of TherapyHypokalemia/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


Misleading labs ketones l.jpg
Misleading LabsKetones

  • In the absence of insulin, FFA go to the liver, and into mitochondria via carnitine

  • ß-oxidation excess acetylCoA

Nitroprusside

reaction

  • Acetyl-CoA condenses to acetoacetate

  • Insulin prevents utilization of acetoacetate

  • so levels and shunt to ß-hydroxybutyrate and acetone


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Misleading LabsScreening for Ketonemia

  • Urine Dip stick vs. anion gap/serum bicarb

    SensitivitySpecificity

    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 LabsWBC 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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Controversies and Risks of Therapy

  • Fluids - composition, bolus

    amount and total fluids/day

  • Use of Bicarbonate

  • Phosphate replacement

Cerebral

Edema


Dka controversy cerebral edema truths l.jpg
DKA – ControversyCerebral Edema - Truths ?

Acute

  • 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

Late

Sequelae


Dka cerebral edema actualities l.jpg
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 EdemaTotal 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

J Peds 113:10-14, 1988

Attention to fluid rate and tonicity is essential, but may not be sufficient to predict subset that will develop neurologic complications

JCEM 85:509-513, 2000


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DKA – Cerebral EdemaTotal 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

J Peds 113:10-14, 1988

Attention to fluid rate and tonicity is essential, but may not be sufficient to predict subset that will develop neurologic complications

JCEM 85:509-513, 2000


Dka cerebral edema variable time of onset l.jpg

Prior to therapy; longer duration

symptoms before diagnosis

DKA – Cerebral EdemaVariable Time of Onset

# of Children with Neurologic Deterioration

NEJM 344:264-69, 2001

Hours after Initiation of Therapy


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DKA – Cerebral EdemaOther

  • 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

Neurosurg 21: 147-156, 1987

JCEM 85: 509-13, 2000


Dka cerebral edema signs and symptoms l.jpg
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

Cerebral Edema is a clinical diagnosis.

Need to treat BEFORE imaging.

JCEM 85:509-513, 2000


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DKA – Risks of TherapyBicarbonate 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 TherapyBicarbonate Administration

  • 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: PaCO2BUNGlucoseBicarb

    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

NEJM 344:264-269, 2001


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****

****

****

****

****

****

****

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DKA – Risks of TherapyBicarbonate 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


Dka controversy phosphate l.jpg
DKA- Controversy Phosphate

Theoretical

  • Essential phosphate deficit

  • W/treatment serum phosphate and 2,3-DPG fall

  • Shift oxyhemoglobin curve reducing O2 deliver

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 hypocalcemia

Endo Met Clin 29:Dec 2000



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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


Typical therapy fluids l.jpg
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


Typical therapy fluids47 l.jpg
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


Dka risks of therapy insulin l.jpg
DKA – Risks of TherapyInsulin

100%

Biological

effect

0.1 units/kg/hr

Current therapy uses

continuous insulin drip

 Drop glucose

50-100 mg/dl/hr

100 uU/ml

Insulin Level


Typical therapy insulin l.jpg
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


Typical therapy glucose 2 bag method l.jpg
Typical TherapyGlucose - 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


Typical therapy l.jpg
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


Monitor l.jpg
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


Monitor53 l.jpg
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


Monitor54 l.jpg
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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DKAGuidelines

  • 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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DKAFlowsheet

  • 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


9 yo lab evaluation57 l.jpg

700

24.4

518

16.8

47.5

9 yo lab Evaluation

  • 27 Kg - assume 10% dehydrated

  • 148| 109| 32

    5.6 | <5 | 1.4

  • Anion Gap =

  • Osm =

  • Corrected Na =

  • Fluid Def =

  • Maintenance =

  • IV rate (24hrs) =


Transport of patient with dka l.jpg
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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DKAPrevention

  • 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


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