Diabetic Ketoacidosis

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Diabetic Ketoacidosis Hyperosmolar
Hyperglycemic State- Inpatient management

• Susan Schayes M.D
• Assistant Professor-CT
• Family Medicine, Emory University School of
  Medicine

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High Impact Diseases

• /

Jonas Brothers
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Learning objectives

• Define diagnostic criteria for diabetic
  ketoacidosis
• Define diagnostic criteria for hyperosmolar
  hyperglyemia
• Understand the five key components to the
  treatment algorithm

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In 1552 BCDiabetes 1st Described In Writing

• Earliest known record of diabetes mentioned on
  3rd Dynasty Eqyptian papyrus by physician
  Hesy-Ra mentions polyuria as a symptom.
• 250 BC, Apollonius of Memphis coined the name
  "diabetes meaning "to go through" or siphon. He
  understood that the disease drained more fluid
  than a person could consume.

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The Word Diabetes MellitusFirst Used

• Gradually the Latin word for honey, "mellitus,"
  was added to diabetes because it made the urine
  sweet.
• Up to 11th century diabetes was commonly
  diagnosed by water tasters who drank the urine
  of those suspected of having diabetes, as it was
  sweet-tasting.

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Early Diabetes Discoveries

• In the 1869, Paul Langerhans, a German medical
  student announced in a dissertation, that the
  pancreas contains two systems of cells.
• 1889 Oskar Minkowski and Joseph von Mering in
  France, removed the pancreas from a dog to
  determine the effect of an absent pancreas on
  digestion

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Fredrick Banting Charles Best

• Boss leaves on vacation May 1921
• Banting and his assistant Best isolate insulin
  from dogs, and give it to diabetic dogs.
• Boss returns and is skeptical that insulin works
• Try extract on themselves, then on

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Leonard Thompson

• The first patient to receive injections of
  pancreatic extract on January 11, 1922. He was
  14. The young Toronto resident had been diabetic
  since 1919. He weighed only 65 pounds and was
  about to slip into a coma and die. At first he
  received Dr, F. Bantings and Dr. Charles Bests
  extract. Two weeks later he used the purified
  extract of Dr. J.B. Collip and Thompson's
  symptoms began to disappear his blood sugar
  returned to normal and he was brighter and
  stronger. Thompson lived another 13 years with
  the insulin. He died at the age of 27 due to
  pneumonia, a complication of his diabetes

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Type 1 vs. type 2 diabetesLambert P, et al.
Medicine 2006 34(2) 47-51Nolan JJ. Medicine
2006 34(2) 52-56

• Features of type 2 diabetes
• Usually presents in over-30s (but also seen
  increasingly in younger people)
• Associated with overweight/obesity
• Onset is gradual and diagnosis often missed (up
  to 50 of cases)
• Not associated with ketoacidosis, though ketosis
  can occur
• Immune markers in only 10
• Family history is often positive with almost 100
  concordance in identical twins

• Features of type 1 diabetes
• Onset in childhood/adolescence
• Lean body habitus
• Acute onset of osmotic symptoms
• Ketosis-prone
• High levels of islet autoantibodies
• High prevalence of genetic susceptibility

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Goals of management

• Manage symptoms
• Prevent acute and late complications
• Improve quality of life
• Avoid premature diabetes-associated death
• An individualized approach

Glycemic control
BP
Lipids
Lifestyle (e.g. diet exercise)
Patient education
Management
Eye care
Microalbuminuria kidneys
Foot care
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Normal Physiologic Insulin Sensitivity and
?Cell Function Produce Euglycemia
Normal Insulin Sensitivity
Normal ?Cell Function
Decreased Lipolysis
Pancreas
Liver
Decreased Plasma FFA
? Glucose Uptake
? Glucose Production
Islet ?Cell DegranulationInsulin Released in
Response to Elevated Plasma Glucose
Muscle
Adipose Tissue
Decreased Glucose Output
Normal Physiologic Plasma Insulin
Increased Glucose Transport
Euglycemia
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?Cell Dysfunction and Insulin Resistance Produce
Hyperglycemia in Type 2 Diabetes
Insulin Resistance
?Cell Dysfunction
Increased Lipolysis
Pancreas
Liver
Elevated Plasma FFA
?Glucose Uptake
?Glucose Production
Islet ?Cell DegranulationReduced Insulin
Content
Muscle
Adipose Tissue
Increased Glucose Output
Reduced Plasma Insulin
Decreased Glucose Transport Activity
(expression) of GLUT4
Hyperglycemia
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Diabetic Ketoacidosis

• Key features hyperglycemia, ketosis, acidosis
• Clinical presentation polyuria, polydipsia,
  polyphagia, weakness, Kussmaulsrespirations,
  nausea and vomiting
• Can be mistaken for AGE

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Diabetic Ketoacidosis
Cause reduced insulin levels, decreased glucose
use, increased gluconeogenesis Primarily affects
TIDM, but can be T2DM Precipitating factor
Infection, Noncompliance, Other acute event ie
MI

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Diabetic Ketoacidosis

• Treatment involves 5 key components
• Monitoring
• Fluid resuscitation
• Insulin and dextrose infusion
• Electrolyte repletion
• Treating underlying cause

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PATHOGENESIS
Ketoacidosis is a state of uncontrolled
catabolism associated with insulin deficiency.
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• Polyuria leading to Oliguria
• Dehydration, Thirst
• Hypotension, Tachycardia,
• Peripheral circulatory failure
• Ketosis
• Hyperventilation
• Vomiting
• Abdominal pain (acute abdomen)
• Drowsiness, Coma

CLINICAL FEATURES
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METABOLIC FEATURES

• Hyperglycemia
• Glycosuria
• Non-respiratory Acidosis
• Ketonemia
• Uremia
• Hyperkalemia
• Hypertriglyceridemia
• Hemoconcentration

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Dx Criteria for Mild DKA

• Glucose gt 250
• Arterial pH 7.25-7.30
• Serum bicarb 15-18 mEq
• Urine and Serum ketones
• B-hydroxybutyrate- high
• Anion gap gt10
• Patient is alert

Trachtenbarg David, Diabetic Ketoacidosis,
American Family Physician, 2005711705-1714
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Dx Criteria for Moderate DKA

• Glucose gt 250
• Arterial pH 7.00-7.24
• Serum bicarb 10 to lt15 mEq
• Urine and Serum ketones
• B-hydroxybutyrate- high
• Anion gap gt12
• Patient is alert/drowsy

Trachtenbarg David, Diabetic Ketoacidosis,
American Family Physician, 2005711705-1714
21
Dx Criteria for Severe DKA

• Glucose gt 250
• Arterial pH lt7.00
• Serum bicarb lt10 mEq
• Urine and Serum ketones
• B-hydroxybutyrate- high
• Anion gap gt12
• Patient is stupor/coma

Trachtenbarg David, Diabetic Ketoacidosis,
American Family Physician, 2005711705-1714
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Dx Criteria for HHS

• Glucose gt 600
• Arterial pH lt7.30
• Serum bicarb lt15 mEq
• Urine and Serum ketones- small
• B-hydroxybutyrate- n or elevated
• Anion gap-variable
• Patient is stupor/coma

Trachtenbarg David, Diabetic Ketoacidosis,
American Family Physician, 2005711705-1714
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DKA- Monitoring

• ICU
• 2 IVs, Oxygen, cardiac monitor,
• continuous vitals, pulse ox
• Foley to monitor I O
• Initially blood work every 1-2 hours
• If pH is less that 6.9 be frightened

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DKA- MonitoringStandard blood work

• Glucose, lytes with calculated anion gap, Mag
• Bun creatinine, calculate GFR
• Beta-hydroxybutyrate or serum ketones
• UA
• CBC
• EKG
• Infection-cultures,chest xray
• Cardiac status-cardiac enzymes

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DKA- Fluids

• Deficits are typically 100 ml per kg
• Fluid replacement will lower glucose
• Initial Tx usually fluid, fluid, fluid
• Initial resuscitation 15-20 ml/kg stat for severe
  dehydration with normal saline
• 1l,1l,1l,then 500ml X4 hours, reassess/reassess
• Once glucose below 250, switch to
• D5W/.45 N saline

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Insulin

• Initially 10 units R Insulin IV,
• .15 units/kg
• Insulin drip, most protocols 5-7 units per hour,
  .1 units/kg/hr
• Patient to ICU
• Stop insulin drip when sugar is less than 250

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Electrolytes- K

• Whole body potassium deficits exist. (3-5
  mmol/kg)
• Acidosis increases K
• Glucose Insulin lowers K
• Start K with K less than 5 mmol and adequate
  urine output
• If initial K less than 3.3 mmol
• replete, and then start insulin when K above
  3.3 mmol/L

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Electrolytes- K

• Commonly under repleted
• Resident mistakenly uses the replacement of
  potassium protocol, which vastly under repletes
  potassium
• Watch like a hawk!!!!
• Replace/repete/replace/repete

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Electrolytes- Mg

• A serum deficit usually exists
• of .5-1 mmol per L
• Consider repleting if less than 1.8 mg/dL

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DKA HONK

• Protocols- but use
• Common sense which
• is not common