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A Nimalasuriya MD Maria Ureña RN, MHA. Diabetic Ketoacidosis Management. 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 - PowerPoint PPT Presentation
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Presentation titleSUB TITLE HERE
A Nimalasuriya MD
Maria Ureña RN, MHA
Diabetic Ketoacidosis Management
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
Diabetic Ketoacidosis
Due to:
Severe insulin deficiency Absolute type 1 Relative type 2 Associated with cocaine use Atypical anti-psychotics
DKAPrecipitating Factors
Failure to take insulin
Psychological Secondary gain Weight concerns
Failure to increase insulin
Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional
Diabetic Ketoacidosis
Also…• Excess counterregulatory hormones• Glucagon• Epinephrine• Cortisol• Growth hormone
Role of Insulin
Required for transport of glucose into: Muscle Adipose Liver
Inhibits lipolysisAbsence of insulin
Glucose accumulates in the blood Liver Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies Acetone, Acetoacetate, β-hydroxybutyrate
Counterregulatory Hormones - DKA
Increases insulin
resistance
Activates glycogenolysis and
gluconeogenesis
Activates lipolysis
Inhibits insulin secretion
Epinephrine X X X XGlucagon XCortisol X XGrowth
Hormone X X X
Insulin Deficiency
Glucose uptakeProteolysis
Lipolysis
Amino Acids
GlycerolFree Fatty Acids
GluconeogenesisGlycogenolysis
HyperglycemiaHyperglycemia Ketogenesis
AcidosisAcidosisOsmotic diuresis DehydrationDehydration
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
Signs and Symptoms of DKA (continued)
DKA
Pancreatitis
Acute surgical Emergency
Amylase
Lipase
Acute abdomen
Lab Findings
Hyperglycemia blood sugar greater than 250
Anion gap acidosis 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)
Treatment of DKA
Initial hospital management Replace fluid and electrolytes IV Insulin therapy Glucose administration Watch for complications Treat causes Disconnect insulin pump
Once resolved Convert to home insulin
regimen Prevent recurrence
Flow sheet
STAT•Arterial ABG•CBC with differential• urinalysis• blood glucose•blood urea nitrogen (BUN)•Electrolytes• chemistry profile• creatinine levels •electrocardiogram chest X-ray and cultures as needed.
Serum Na should be corrected for •hyperglycemia
Follow up labs•plasma glucose• Lytes• BUN/creatinine •venous pH every 2 -4 hr
Treatment of DKAFluids and Electrolytes
Fluid replacement Restores perfusion of the tissues 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
After the first Liter consider ½ NS
Treatment of DKAFluids and Electrolytes
Sodium replacement Calculate effective serum sodium Serum sodium + 1.6 ( blood glucose-100)/100 isotonic saline (0.9% NaCl) is infused at a rate of 15–20
ml · kg−1 body wt · h−1 or greater during the 1st hour ( 1–1.5 l in the average adult). Subsequent choice for ∼fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output.
In general, 0.45% NaCl infused at 4–14 ml · kg−1 · h−1 is appropriate if the corrected serum sodium is normal or elevated; 0.9% NaCl at a similar rate is appropriate if corrected serum sodium is low.
Treatment of DKAFluids and Electrolytes
Hyperkalemia initially present Resolves quickly with insulin drip Once urine output is present and K<5.5,
add 20-40 meq KCL per liter.
Phosphate deficit May want to use Kphos
Bicarbonate not given unless pH <7
Treatment of DKAInsulin Therapy
IV bolus of 0.15 units/kg (~ 10 units) regular insulinIV infusion 0.1 units/kg /hrIf blood glucose does not drop by 50 mg double the
infusion rateDo not give if K is less than 3.3 mEq/LHydrate firstFollow with hourly regular insulin infusionGlucose levels
Decrease 75-100 mg/dl hour not more than this Minimize rapid fluid shifts
Treatment of DKAGlucose Administration
plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS,
decrease the insulin infusion rate to 0.05–0.1 unit · kg−1 · h−1 (3–6 units/h),
Add dextrose (5–10%) to the intravenous fluids. maintain the above glucose values until acidosis in
DKA or mental obtundation and hyperosmolarity in HHS are resolved
DKA ResolvedTreatment
Blood sugar less than 200 mg
Bicarbonate greater than 18 mEq/L
Venous pH greater than 7.3
Once DKA ResolvedTreatment
Most patients require 0.5-0.6 units/kg/day
highly insulin resistant patients 0.8-1.0 units/kg/day
Long acting insulin 1/2-2/3 daily requirement NPH 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.
Complications of DKA
Infection Precipitates DKA Fever Leukocytosis can be secondary
to acidosisShock
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
Prevention of DKASick Day Rules
Never omit insulin
Cut long acting in halfPrevent dehydration and hypoglycemiaMonitor blood sugars frequentlyMonitor for ketosisProvide supplemental fast acting insulinTreat underlying triggersMaintain contact with medical team
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 hyperosmolarityHigh 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 fallingRecurrent 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
Successful Management
Time For Questions?
THANK YOU FOR ATTENDING!