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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

DIABETIC KETOACIDOSIS

Andrew J. Bauer

Pediatric Endocrinology

WRAMC

goals
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
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
progression to type 1 dm
Progression to Type 1 DM

Autoimmune destruction

Honeymoon

100% Islet loss

“Diabetes threshold”

typical presentation
Typical Presentation
  • Polyuria, polydypsia, weight loss
  • Vomiting
  • Rapid-deep respiration
  • CNS depression – coma
  • Precipitating event
typical setting
“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
background
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
diagnostic criteria
Diagnostic Criteria
  • Blood glucose > 250 mg/dl
  • pH < 7.35
  • HCO3 < 20 mEq/L
  • Anion Gap > 12
  • ketonemia
etiology
Etiology
  • Results from inadequate insulin
    • Accidental or intentional omission
    • Inappropriate intervention when stressed
etiology10
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
pathophysiology counter regulatory hormones
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
slide12

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
Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin

pathophysiology14
Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin

Dec Glucose Utilization

Lipolysis

dka early

Decreased Utilization

 post-prandial

and

Stress-Induced

hyperglycemia

DKA - Early
  • Relative Insulin Deficiency

 Glycogenolysis &

gluconeogenesis restrained

Peripheral glucose

uptake

Elevates

blood glucose

pathophysiology16
Pathophysiology

Glucagon

Epinephrine

Cortisol

Growth Hormone

Insulin

Gluconeogenesis

Glycogenolysis

Lipolysis

Ketogenesis

dka late
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

dka initial evaluation
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

9 yo lab evaluation

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

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

misleading labs
Misleading Labs
  • Sodium
  • Potassium
  • Ketones
  • WBC
misleading labs sodium
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
misleading labs sodium23
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

misleading labs potassium
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

dka risks of therapy hypokalemia hyperkalemia
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
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
misleading labs screening for ketonemia
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

misleading labs wbc count
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

controversies and risks of therapy
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
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
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

dka cerebral edema actualities33
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
dka cerebral edema total fluids
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 total fluids35
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

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

dka cerebral edema other
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
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

dka cerebral edema evaluation
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

dka risks of therapy bicarbonate administration
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
dka risks of therapy bicarbonate administration41
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

dka risks of therapy bicarbonate administration42

****

****

****

****

****

****

****

****

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
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

elements of therapy45
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
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
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
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
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
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
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
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
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
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

dka guidelines
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
dka flowsheet
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

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
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
dka prevention
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