Diabetic Ketoacidosis Management

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?

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