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Diabetic Ketoacidosis Management. Heidi Chamberlain Shea, MD Endocrine Associates of Dallas. Goals of Discussion. Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome. Epidemiology. Annual incidence in U.S.

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diabetic ketoacidosis management

Diabetic Ketoacidosis Management

Heidi Chamberlain Shea, MD

Endocrine Associates of Dallas

goals of discussion
Goals of Discussion
  • Pathophysiology of DKA
  • Biochemical criteria for DKA
  • Treatment of DKA
  • Prevention of DKA
  • Hyperosmolar Nonketoic Syndrome
  • Annual incidence in U.S.
    • 5-8 per 1000 diabetic subjects
  • 2.8% of all diabetic admissions are due to DKA
  • Overall mortality rate ranges from 2-10%
    • Higher is older patients
dka precipitating factors
Failure to take insulin

Failure to increase insulin





Acute stress



Medical Stress

Counterregulatory hormones

Oppose insulin

Stimulate glucagon release


Increases glucagon and catecholamines

Decreased renal blood flow

Decreases glucagon degradation by the kidney

DKAPrecipitating Factors
diabetic ketoacidosis
Diabetic Ketoacidosis

Due to:

Severe insulin deficiency

Excess counterregulatory hormones




Growth hormone

role of insulin
Role of Insulin
  • Required for transport of glucose into
    • Muscle
    • Adipose
    • Liver
  • Inhibits lipolysis
  • Absence of insulin
    • Glucose accumulates in the blood
    • Liver
      • Uses amino acids for gluconeogenesis
      • Converts fatty acids into ketone bodies
        • Acetone, Acetoacetate, β-hydroxybutyrate
    • Increased counterregulatory hormones

Insulin Deficiency

Glucose uptake



Free Fatty Acids


Amino Acids






Osmotic diuresis


signs and symptoms of dka
Polyuria, polydipsia





Abdominal pain



Fruity breath


Kussmaul breathing

Mental status changes




Signs and Symptoms of DKA
lab findings
Lab Findings
  • Hyperglycemia
  • Anion gap acidosis
    • (Na + K) – (Cl + Bicarb) >12
    • Bicarbonate <15 mEq/L
    • pH <7.3
  • Urine ketones and serum ketones
  • Hyperosmolarity
differential diagnosis anion gap acidosis
Differential Diagnosis Anion Gap Acidosis
  • Alcoholic ketoacidosis
  • Lactic acidosis
  • Renal failure
  • Ethylene glycol or methyl alcohol poisoning
  • Starvation in late pregnancy or lactation (rare)
atypical presentations
Atypical Presentations
  • DKA can be present with BS <300
    • Impaired gluconeogenesis
      • Liver disease
      • Acute alcohol ingestion
      • Prolonged fasting
      • Insulin-independent glucose is high (pregnancy)
    • Chronic poor control but taking insulin
  • Bedside urine ketones false negatives
    • Measure acetoacetate not β-hydroxybutyrate
    • Send blood to lab
treatment of dka
Treatment of DKA
  • Initial hospital management
    • Replace fluid and electrolytes
    • IV Insulin therapy
    • Glucose administration
    • Watch for complications
    • Disconnect insulin pump
  • Once resolved
    • Convert to home insulin regimen
    • Prevent recurrence
treatment of dka fluids and electrolytes
Treatment of DKAFluids and Electrolytes
  • Fluid replacement
    • Restores perfusion of the tissues
      • Lowers counterregulatory hormones
    • Average fluid deficit 3-5 liters
  • Initial resuscitation
    • 1-2 liters of normal saline over the first 2 hours
    • Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours
      • When fluid overload is a concern
  • If hypernatremia develops ½ NS can be used
treatment of dka fluids and electrolytes1
Treatment of DKAFluids and Electrolytes
  • Hyperkalemia initially present
    • Resolves quickly with insulin drip
    • Once urine output is present and K<5.0, add 20-40 meq KCL per liter.
  • Phosphate deficit
    • May want to use Kphos
  • Bicarbonate not given unless pH <7 or bicarbonate <5 mmol/L
treatment of dka insulin therapy
Treatment of DKAInsulin Therapy
  • IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin
  • Follow with hourly regular insulin infusion
  • Glucose levels
    • Decrease 75-100 mg/dl hour
    • Minimize rapid fluid shifts
  • Continue IV insulin until urine is free of ketones
treatment of dka glucose administration
Treatment of DKAGlucose Administration
  • Supplemental glucose
    • Hypoglycemia occurs
      • Insulin has restored glucose uptake
      • Suppressed glucagon
    • Prevents rapid decline in plasma osmolality
      • Rapid decrease in insulin could lead to cerebral edema
  • Glucose decreases before ketone levels decrease
  • Start glucose when plasma glucose <300 mg/dl
complications of dka

Precipitates DKA


Leukocytosis can be secondary to acidosis


If not improving with fluids r/o MI

Vascular thrombosis

Severe dehydration

Cerebral vessels

Occurs hours to days after DKA

Pulmonary Edema

Result of aggressive fluid resuscitation

Cerebral Edema

First 24 hours

Mental status changes

Tx: Mannitol

May require intubation with hyperventilation

Complications of DKA
once dka resolved treatment
Once DKA ResolvedTreatment
  • Most patients require 0.5-0.6 units/kg/day
  • Pubertal or highly insulin resistant patients
    • 0.8-1.0 units/kg/day
  • Long acting insulin
    • 1/2-2/3 daily requirement
    • NPH, Lente, Ultralente or Lantus
  • Short acting insulin
    • 1/3-1/2 given at meals
    • Regular, Humalog, Novolog
  • Give insulin at least 2 hours prior to weaning insulin infusion.
prevention of dka sick day rules
Prevention of DKASick Day Rules
  • Never omit insulin
    • Cut long acting in half
  • Prevent dehydration and hypoglycemia
  • Monitor blood sugars frequently
  • Monitor for ketosis
  • Provide supplemental fast acting insulin
  • Treat underlying triggers
  • Maintain contact with medical team
goals of discussion1
Goals of Discussion
  • Pathophysiology of DKA
  • Biochemical criteria for DKA
  • Treatment of DKA
  • Prevention of DKA
  • Hyperosmolar Nonketoic Syndrome
hyperosmolar nonketotic syndrome
Hyperosmolar Nonketotic Syndrome
  • Extreme hyperglycemia and dehydration
    • Unable to excrete glucose as quickly as it enters the extracellular space
    • Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl
    • When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space.
hyperosmolar nonketotic syndrome1
Hyperosmolar Nonketotic Syndrome
  • Extreme hyperglycemia and hyperosmolarity
  • High mortality (12-46%)
  • At risk
    • Older patients with intercurrent illness
    • Impaired ability to ingest fluids
  • Urine volume falls
    • Decreased glucose excretion
  • Elevated glucose causes CNS dysfunction and fluid intake impaired
  • No ketones
    • Some insulin may be present
    • Extreme hyperglycemia inhibits lipolysis
hyperosmolar nonketotic syndrome presentation
Hyperosmolar Nonketotic SyndromePresentation
  • Extreme dehydration
  • Supine or orthostatic hypotension
  • Confusion coma
  • Neurological findings
    • Seizures
    • Transient hemiparesis
    • Hyperreflexia
    • Generalized areflexia
hyperosmolar nonketotic syndrome presentation1
Hyperosmolar Nonketotic SyndromePresentation
  • Glucose >600 mg/dl
  • Sodium
    • Normal, elevated or low
  • Potassium
    • Normal or elevated
  • Bicarbonate >15 mEq/L
  • Osmolality >320 mOsm/L
hyperosmolar nonketotic syndrome treatment
Hyperosmolar Nonketotic SyndromeTreatment
  • Fluid repletion
    • NS 2-3 liters rapidly
    • Total deficit = 10 liters
      • Replete ½ in first 6 hours
  • Insulin
    • Make sure perfusion is adequate
    • Insulin drip 0.1U/kg/hr
  • Treat underlying precipitating illness
clinical errors
Clinical Errors
  • Fluid shift and shock
    • Giving insulin without sufficient fluids
    • Using hypertonic glucose solutions
  • Hyperkalemia
    • Premature potassium administration before insulin has begun to act
  • Hypokalemia
    • Failure to administer potassium once levels falling
  • Recurrent ketoacidosis
    • Premature discontinuation of insulin and fluids when ketones still present
  • Hypoglycemia
    • Insufficient glucose administration
  • Successful management requires
    • Judicious use of fluids
      • Establish good perfusion
    • Insulin drip
      • Steady decline
      • Complete resolution of ketosis
    • Electrolyte replacement
    • Frequent neurological evaluations
    • High suspicion for complications
  • Determine etiology to avoid recurrent episodes