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Diabetic Ketoacidosis Management Heidi Chamberlain Shea, MD Endocrine Associates of Dallas

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. - PowerPoint PPT Presentation

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Page 1: Diabetic Ketoacidosis Management

Diabetic Ketoacidosis Management

Heidi Chamberlain Shea, MDEndocrine Associates of Dallas

Page 2: Diabetic Ketoacidosis Management

Goals of Discussion

• Pathophysiology of DKA

• Biochemical criteria for DKA

• Treatment of DKA

• Prevention of DKA

• Hyperosmolar Nonketoic Syndrome

Page 3: Diabetic Ketoacidosis Management

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

Page 4: Diabetic Ketoacidosis Management

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

Page 5: Diabetic Ketoacidosis Management

Diabetic Ketoacidosis

Due to:

Severe insulin deficiency

Excess counterregulatory hormones

Glucagon

Epinephrine

Cortisol

Growth hormone

Page 6: Diabetic Ketoacidosis Management

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

Page 7: Diabetic Ketoacidosis Management

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

Page 8: Diabetic Ketoacidosis Management

Insulin Deficiency

Glucose uptakeProteolysis

Lipolysis

Amino Acids

Glycerol Free Fatty Acids

GluconeogenesisGlycogenolysisHyperglycemiaHyperglycemia Ketogenesis

AcidosisAcidosisOsmotic diuresis DehydrationDehydration

Page 9: Diabetic Ketoacidosis Management

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

Page 10: Diabetic Ketoacidosis Management

Lab Findings• Hyperglycemia• Anion gap acidosis

– (Na + K) – (Cl + Bicarb) >12

– Bicarbonate <15 mEq/L– pH <7.3

• Urine ketones and serum ketones

• Hyperosmolarity

Page 11: Diabetic Ketoacidosis Management

Differential Diagnosis Anion Gap Acidosis

• Alcoholic ketoacidosis

• Lactic acidosis

• Renal failure

• Ethylene glycol or methyl alcohol poisoning

• Starvation in late pregnancy or lactation (rare)

Page 12: Diabetic Ketoacidosis Management

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

Page 13: Diabetic Ketoacidosis Management

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

Page 14: Diabetic Ketoacidosis Management

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

Page 15: Diabetic Ketoacidosis Management

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

Page 16: Diabetic Ketoacidosis Management

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

Page 17: Diabetic Ketoacidosis Management

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

Page 18: Diabetic Ketoacidosis Management

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

Page 19: Diabetic Ketoacidosis Management

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

Page 20: Diabetic Ketoacidosis Management

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

Page 21: Diabetic Ketoacidosis Management

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

Page 22: Diabetic Ketoacidosis Management

I

Page 23: Diabetic Ketoacidosis Management

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

Page 24: Diabetic Ketoacidosis Management

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

Page 25: Diabetic Ketoacidosis Management

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

Page 26: Diabetic Ketoacidosis Management

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

Page 27: Diabetic Ketoacidosis Management

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

Page 28: Diabetic Ketoacidosis Management

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

Page 29: Diabetic Ketoacidosis Management

Goals of Discussion

• Pathophysiology of DKA

• Biochemical criteria for DKA

• Treatment of DKA

• Prevention of DKA

• Hyperosmolar Nonketoic Syndrome

Page 30: Diabetic Ketoacidosis Management

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.

Page 31: Diabetic Ketoacidosis Management

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

Page 32: Diabetic Ketoacidosis Management

Hyperosmolar Nonketotic Syndrome Presentation

• Extreme dehydration

• Supine or orthostatic hypotension

• Confusion coma

• Neurological findings– Seizures– Transient hemiparesis– Hyperreflexia– Generalized areflexia

Page 33: Diabetic Ketoacidosis Management

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

Page 34: Diabetic Ketoacidosis Management

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

Page 35: Diabetic Ketoacidosis Management

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

Page 36: Diabetic Ketoacidosis Management

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