Diabetic Ketoacidosis Management

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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.
        – 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       • Medical Stress
• Failure to increase insulin      – Counterregulatory
                                     hormones
   – Illness/Infection
                                      • Oppose insulin
       • Pneumonia
                                      • Stimulate glucagon
       • MI
                                        release
       • Stroke
   – Acute stress               • Hypovolmemia
       • Trauma                    – Increases glucagon and
       • Emotional                   catecholamines
                                      • Decreased renal blood
                                        flow
                                      • Decreases glucagon
                                        degradation by the kidney
      Diabetic Ketoacidosis
Due to:
 Severe insulin deficiency
 Excess counterregulatory hormones
         Glucagon
         Epinephrine
         Cortisol
         Growth hormone
                 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
     Counterregulatory Hormones - DKA
              Increases        Activates     Activates   Inhibits insulin
                insulin     glycogenolysis   lipolysis     secretion
              resistance         and
                           gluconeogenesis
Epinephrine
                 X               X             X               X
 Glucagon
                                 X
  Cortisol
                 X               X
  Growth
 Hormone         X                             X               X
                   Insulin Deficiency
 Glucose uptake                                    Lipolysis
                        Proteolysis


                                        Glycerol        Free Fatty Acids
                       Amino Acids


                      Gluconeogenesis
Hyperglycemia         Glycogenolysis                     Ketogenesis




Osmotic diuresis       Dehydration                      Acidosis
     Signs and Symptoms of DKA
• Polyuria, polydipsia   • Fruity breath
  – Enuresis               – Acetone
• Dehydration            • Kussmaul breathing
  – Tachycardia          • Mental status
  – Orthostasis            changes
• Abdominal pain           – Combative
  – Nausea                 – Drunk
  – Vomiting               – Coma
                    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
•   Alcoholic ketoacidosis
•   Lactic acidosis
•   Renal failure
•   Ethylene glycol or methyl alcohol poisoning
•   Starvation in late pregnancy or lactation
    (rare)
         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
        • 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
• 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 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.
• Normo/Hypokalemia
   – Malnourished individuals (alcoholics)
   – Start K replacement and have K > 3.0 prior to start of
     insulin
   – Remember to check Magnesium
• Phosphate deficit
   – May want to use Kphos
• Bicarbonate not given unless pH <7 or
  bicarbonate <5 mmol/L
           Treatment of DKA
              Insulin 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
• 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
   Insulin-Glucose Infusion for DKA
Blood glucose   Insulin Infusion   D5W Infusion
     <70          0.5 units/hr       150 cc/hr
   70-100             1.0              125
   101-150            2.0              100
   151-200            3.0              100
   201-250            4.0               75
   251-300            6.0               50
   301-350            8.0                0
   351-400           10.0                0
   401-450           12.0                0
   451-500           15.0                0
    >500             20.0                0
            Complications of DKA
• Infection                          • Cerebral Edema
   – Precipitates DKA                  –   First 24 hours
   – Fever                             –   Mental status changes
   – Leukocytosis can be secondary     –   Tx: Mannitol
     to acidosis                       –   May require intubation with
• Shock                                    hyperventilation
   – 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
         Once DKA Resolved
                 Treatment
• 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, Levemir or Lantus
• Short acting insulin
  – 1/3-1/2 given at meals
  – Regular, Humalog, Novolog or Apidra
           Once DKA Resolved
                     Treatment
• Give SQ insulin at least 2 hours prior to stopping
  insulin infusion.
• Lantus or Levemir
   – Steady state at 2-4 hrs
• Short acting analogs for meal times
• If transitioning to the pump
   – Restart the pump and after 30 minutes stop insulin
     infusion
• May still be more insulin resistant so will need
  more than usual dose
• Check blood sugars in 2 hrs
   – Offer supplemental
I
Insulin Types and Action
 INSULIN    ONSET OF    PEAK         DURATION
 TYPE       ACTION      EFFECT       OF ACTION

 Humalog    15 MIN      1 ½ HOURS    3 HOURS
 Novolog
 Apidra
 REGULAR    30 MIN      2-3 HOURS    4-6 HOURS


 NPH        2-3 HOURS   6-8 HOURS    12-16 HOURS


 LENTE      3-4 HOURS   8-12 HOURS   12-18 HOURS


 Glargine   1-2 hrs                  24 hrs
 Detemir
Prevention of DKA
  Sick 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
                     Preventing DKA
• Education
  – Sick days
      • Do not stop insulin but adjust
  – Hyperglycemia
      • If > 300 mg/dl, then check urine
        ketones
      • If ketones positive
          – Increase fluids
          – Take supplemental insulin Q2 hrs
  – Insulin temperature sensitive
      • < 77 degrees
      • Teenagers, homeless, pen and pump
        users
      • Do not store insulin in the car
      • Traveling and summer outdoor
        activities
      • May need to replace more frequently
         Goals of Discussion
•   Pathophysiology of DKA
•   Biochemical criteria for DKA
•   Treatment of DKA
•   Prevention of DKA
•   Hyperosmolar Nonketoic 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
             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
•   Extreme dehydration
•   Supine or orthostatic hypotension
•   Confusion     coma
•   Neurological findings
     – Seizures
     – Transient hemiparesis
     – Hyperreflexia
     – Generalized areflexia
Hyperosmolar Nonketotic Syndrome
                Presentation
• 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
• 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
• 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
                       Conclusion
• 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

				
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