diabetic ketoacidosis management
DESCRIPTION
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. - PowerPoint PPT PresentationTRANSCRIPT
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Diabetic Ketoacidosis Management
Heidi Chamberlain Shea, MDEndocrine Associates of Dallas
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Goals of Discussion
• Pathophysiology of DKA
• Biochemical criteria for DKA
• Treatment of DKA
• Prevention of DKA
• Hyperosmolar Nonketoic Syndrome
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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
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DKAPrecipitating Factors
• Failure to take insulin• Failure to increase insulin
– Illness/Infection• Pneumonia
• MI
• Stroke
– Acute stress• Trauma
• Emotional
• Medical Stress– Counterregulatory
hormones• Oppose insulin
• Stimulate glucagon release
• Hypovolmemia– Increases glucagon and
catecholamines• Decreased renal blood
flow
• Decreases glucagon degradation by the kidney
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Diabetic Ketoacidosis
Due to:
Severe insulin deficiency
Excess counterregulatory hormones
Glucagon
Epinephrine
Cortisol
Growth hormone
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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
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Counterregulatory Hormones - DKAIncreases
insulin resistance
Activates glycogenolysis
and gluconeogenesis
Activates lipolysis
Inhibits insulin secretion
Epinephrine X X X XGlucagon XCortisol X XGrowth
Hormone X X X
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Insulin Deficiency
Glucose uptakeProteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
GluconeogenesisGlycogenolysisHyperglycemiaHyperglycemia Ketogenesis
AcidosisAcidosisOsmotic diuresis DehydrationDehydration
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Signs and Symptoms of DKA
• Polyuria, polydipsia– Enuresis
• Dehydration– Tachycardia– Orthostasis
• Abdominal pain– Nausea– Vomiting
• Fruity breath– Acetone
• Kussmaul breathing• Mental status
changes– Combative– Drunk– Coma
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Lab Findings• Hyperglycemia• Anion gap acidosis
– (Na + K) – (Cl + Bicarb) >12
– Bicarbonate <15 mEq/L– pH <7.3
• Urine ketones and serum ketones
• Hyperosmolarity
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Differential Diagnosis Anion Gap Acidosis
• Alcoholic ketoacidosis
• Lactic acidosis
• Renal failure
• Ethylene glycol or methyl alcohol poisoning
• Starvation in late pregnancy or lactation (rare)
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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
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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
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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
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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.• 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
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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
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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
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Insulin-Glucose Infusion for DKABlood 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
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Complications of DKA• Infection
– Precipitates DKA– Fever– Leukocytosis can be secondary
to acidosis
• Shock– 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
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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, Levemir or Lantus
• Short acting insulin– 1/3-1/2 given at meals– Regular, Humalog, Novolog or Apidra
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Once DKA ResolvedTreatment
• 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
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I
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Insulin Types and ActionINSULIN TYPE
ONSET OF ACTION
PEAK EFFECT
DURATION OF ACTION
Humalog Novolog Apidra
15 MIN 1 ½ HOURS 3 HOURS
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 Detemir
1-2 hrs 24 hrs
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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
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Preventing DKA• Education
– Sick days or NPO• Do not stop insulin but adjust• Continue basal insulin• NPH insulin- decrease by 30-50%• Use short acting
– Q2-3 hrs with Novolog, Humalog and Apidra– Q4 hrs with regular insulin
– 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
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Pump patients
• If blood sugars are increasing (>200 mg/dl)– Bolus– Check 2 hrs later, if
climbing– Give SQ correction– Change site– Make sure pump is working– Change insulin
• Pump patients need long acting back up at home and when traveling
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Pump patients
• If in DKA– Disconnect the pump
• Transitioning back to pump– Start pump with basal
x 2 hrs, then stop insulin drip
– Check blood sugars every 2 hrs to make sure they are in range
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Clinical Trials
• Immune modulating studies– www.jdrf.org– www.ClinicalTrials.gov
• Anti CD3- monoclonal AB– Phase 3 trials– Newly diagnosed Type 1 Diabetes
• Call Research Institute of Dallas 214-363-5535
• Immune modulating vaccines
• Stem cell and pancreas transplants
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Goals of Discussion
• Pathophysiology of DKA
• Biochemical criteria for DKA
• Treatment of DKA
• Prevention of DKA
• Hyperosmolar Nonketoic Syndrome
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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.
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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
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Hyperosmolar Nonketotic Syndrome Presentation
• Extreme dehydration
• Supine or orthostatic hypotension
• Confusion coma
• Neurological findings– Seizures– Transient hemiparesis– Hyperreflexia– Generalized areflexia
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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
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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
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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
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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