Diabetic Ketoacidosis &

Hyperosmolar Hyperglycemic
State- Inpatient management
Susan Schayes M.D
Assistant Professor-CT
Family Medicine, Emory University
School of Medicine

2
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

.


In 1552 BC
Diabetes 1st Described In Writing
Earliest known record of diabetes
mentioned on 3
rd
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.



.


The Word Diabetes Mellitus
First Used
Gradually the Latin word for honey,
"mellitus," was added to diabetes because
it made the urine sweet.


Up to 11
th
century diabetes was commonly
diagnosed by water tasters who drank the
urine of those suspected of having
diabetes, as it was sweet-tasting.




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

7

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:


8
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

Type 1 vs. type 2 diabetes
Lambert P, et al. Medicine 2006; 34(2): 47-51
Nolan 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
Goals of management
Manage symptoms
Prevent acute and late complications
Improve quality of life
Avoid premature diabetes-associated death
An individualized approach


Management
Glycemic
control
BP
Lipids
Patient
education
Lifestyle
(e.g. diet & exercise)
Foot care
Eye care Microalbuminuria
& kidneys
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Normal Physiologic Insulin
Sensitivity and Cell Function
Produce Euglycemia
Pancreas
Normal Insulin Sensitivity
Liver
Euglycemia
Islet Cell Degranulation;
Insulin Released in Response to
Elevated Plasma Glucose
Muscle
Adipose Tissue
Increased Glucose
Transport

Decreased
Lipolysis
Glucose
Production
Glucose
Uptake
Normal Physiologic
Plasma Insulin
Decreased Glucose Output
Normal Cell Function
Decreased
Plasma FFA
12
Cell Dysfunction and Insulin
Resistance Produce Hyperglycemia in
Type 2 Diabetes
Pancreas
Insulin Resistance
Liver
Hyperglycemia
Islet Cell Degranulation;
Reduced Insulin Content
Muscle
Adipose Tissue
Decreased Glucose
Transport & Activity
(expression)
of GLUT4
Increased
Lipolysis
Glucose
Production
Glucose
Uptake
Reduced
Plasma Insulin
Increased Glucose Output
Cell Dysfunction
Elevated
Plasma FFA
13
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

PATHOGENESIS
Osmotic
Diuresis
Renal Hypoperfusion
Impaired Excretion of
Ketones & Hydrogen ions
Fluid & Electrolyte
Depletion
Vomiting
Acidosis Hyperglycemia
Glycosuria
Glucose
Ketones
Ketoacidosis
is a state of
uncontrolled catabolism
associated with
insulin deficiency.
CLINICAL FEATURES
Polyuria leading to Oliguria
Dehydration, Thirst
Hypotension, Tachycardia,
Peripheral circulatory failure
Ketosis
Hyperventilation
Vomiting
Abdominal pain (acute abdomen)
Drowsiness, Coma
METABOLIC FEATURES
Hyperglycemia
Glycosuria
Non-respiratory Acidosis
Ketonemia
Uremia
Hyperkalemia
Hypertriglyceridemia
Hemoconcentration
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Dx Criteria for Mild DKA
Glucose > 250

Arterial pH 7.25-7.30
Serum bicarb 15-18 mEq
Urine and Serum ketones
B-hydroxybutyrate- high
Anion gap >10
Patient is alert

Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician,
2005;71:1705-1714
20
Dx Criteria for Moderate DKA
Glucose > 250

Arterial pH 7.00-7.24
Serum bicarb 10 to <15 mEq
Urine and Serum ketones
B-hydroxybutyrate- high
Anion gap >12
Patient is alert/drowsy

Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician,
2005;71:1705-1714
21
Dx Criteria for Severe DKA
Glucose > 250

Arterial pH <7.00
Serum bicarb <10 mEq
Urine and Serum ketones
B-hydroxybutyrate- high
Anion gap >12
Patient is stupor/coma

Trachtenbarg David, Diabetic Ketoacidosis, American Family Physician,
2005;71:1705-1714
22
Dx Criteria for HHS
Glucose > 600

Arterial pH <7.30
Serum bicarb <15 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,
2005;71:1705-1714
23
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- Monitoring
Standard 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