diabetic ketoacidosis management heidi chamberlain shea, md endocrine associates of dallas
TRANSCRIPT
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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.
• 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
• Give insulin at least 2 hours prior to weaning insulin infusion.
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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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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