Diabetic Ketoacidosis
Management
Presentation
A Nimalasuriyatitle
MD
SUB TITLE HERE
Maria Ureña RN, MHA
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:
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Severe insulin deficiency
Absolute type 1
Relative type 2
Associated with cocaine use
Atypical anti-psychotics
DKA
Precipitating Factors
Failure to take insulin
 Psychological
 Secondary gain
 Weight concerns
Failure to increase
insulin
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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 lipolysis
Absence of insulin
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Glucose accumulates in the blood
Liver
Uses amino acids for gluconeogenesis
Converts fatty acids into ketone bodies
Acetone, Acetoacetate, β-hydroxybutyrate
Counterregulatory Hormones DKA
Epinephrine
Increases
insulin
resistance
Activates
glycogenolysis and
gluconeogenesis
Activates
lipolysis
Inhibits insulin
secretion
X
X
X
X
X
X
Glucagon
X
Cortisol
X
Growth
Hormone
X
X
Insulin Deficiency
Glucose uptake
Lipolysis
Proteolysis
Glycerol
Free Fatty Acids
Amino Acids
Hyperglycemia
Ketogenesis
Gluconeogenesis
Glycogenolysis
Osmotic diuresis
Dehydration
Acidosis
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)
Acute abdomen
DKA
Pancreatitis
Acute surgical
Emergency
Amylase
Lipase
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 DKA
Fluids 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 DKA
Fluids 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 DKA
Fluids 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 DKA
Insulin Therapy
IV bolus of 0.15 units/kg (~ 10 units) regular insulin
IV infusion 0.1 units/kg /hr
If blood glucose does not drop by 50 mg double the
infusion rate
Do not give if K is less than 3.3 mEq/L
Hydrate first
Follow with hourly regular insulin infusion
Glucose levels
 Decrease 75-100 mg/dl hour not more than this
 Minimize rapid fluid shifts
Treatment of DKA
Glucose 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 Resolved
Treatment
Blood sugar less than 200 mg
Bicarbonate greater than 18 mEq/L
Venous pH greater than 7.3
Once DKA Resolved
Treatment
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 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
Prevention of DKA
Sick 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
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 300500 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 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
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 falling
Recurrent ketoacidosis
 Premature discontinuation of insulin and fluids when
ketones still present
Hypoglycemia
 Insufficient glucose administration
Successful Management
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
Time For Questions?
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