This is a lecture by Dr. Andrew Wong from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.

1. Project: Ghana Emergency Medicine Collaborative
Document Title: Diabetic Emergencies
Author(s): Andrew Wong (University of Michigan/St. Joseph Mercy
Hospital), MD 2012
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3. 3

4. Objectives
— Pathophysiology
of
diabetes
— Signs,
symptoms,
diagnosis
and
management
of
acute
complications
of
diabetes:
— Hypoglycemia
— Diabetic
ketoacidosis
— Hyperglycemic
hyperosmolar
nonketotic
coma
4

5. Case
1
— 23yo
F
with
history
of
DM
Type
I
presents
to
the
ED
for
difficulty
breathing.
— 7
days
ago,
she
began
having
vaginal
spotting,
and
dysuria
— She
lost
her
glucometer
earlier
this
week
and
was
unable
to
measure
blood
sugars
— Today,
she
began
to
have
nausea
and
vomiting
and
complained
of
abdominal
pain.
— Mother
also
noticed
that
she
was
having
a
hard
time
breathing
— Found
glucometer
today
and
it
read
“high”
5

6. Case
1
— PMH:
Type
I
DM
— PSH:
None
— Medications:
Cannot
recall—uses
both
short
acting
and
long-­‐acting
insulin
— Allergies:
None
— SH:
Sexually
active;
denies
any
illicit
drug,
alcohol
or
tobacco
use.
Senior
in
high
school
6

7. Case
1
— Physical
Exam:
— VS:
T37
BP100/70
HR120
RR38
O2sat100%ra
— General:
ill-­‐looking
thin
female
who
appears
to
have
labored
respirations
— HEENT:
PERRL,
EOMI,
MM
dry,
OP
clear
— Neck:
soft,
supple
with
no
lymphadenopathy
— Lungs:
CTAB,
no
w/r/r
— CV:
tachycardic
but
regular
rhythm,
no
m/r/r
— Abdomen:
+BS.
Diffusely
tender
with
area
of
maximal
tenderness
in
the
LLQ.
No
lesions
found.
No
adnexal
masses
palpated
— Pelvic:
White
creamy
exhudate
with
+CMT
and
left
adnexal
tenderness
— Extremities:
cool
to
touch.
2+
radial,
DP
and
posterior
tibial
pulses
cap
refill
3
seconds.
— Skin:
No
rash,
+skin
tenting
7

8. Normal
Physiology
— Glucose
rise
triggers
pancreatic
beta
cells
to
release
insulin
— Insulin
lowers
serum
glucose
levels
— Stimulate
glucose
uptake
and
storage,
facilitate
use
by
fat
and
muscle
— Inhibit
glycogen
breakdown
in
liver
— Degraded
in
3-­‐10
min
in
liver
and
kidney
— Inhibits
hepatic
gluconeogenesis
and
glycogenolysis
— Stimulate
glycogen
(stored
form
of
glucose)
storage
— Fasting
state
stimulates
pancreatic
alpha
cells
to
release
glucagon
— Glucagon
increases
levels
of
glucose
in
blood
— Stimulate
liver
to
break
down
glycogen
and
release
glucose
— Kidney
release
glucose
in
prolonged
starvation
— Increases
ketone
production
to
enhance
gluconeogenesis
8

9. Background
— Diabetes
— Most
common
endocrine
disease
— Spectrum
of
disorders
characterized
by
hyperglycemia
and
disturbances
in
carbohydrate
and
lipid
metabolism
— Four
types
of
Diabetes
—
—
—
—
Type
I:
Immune-­‐mediated
or
idiopathic
failure
to
produce
insulin
Type
II:
Hyperinsulinemic
state
due
to
resistance
to
insulin
Gestational
Diabetes
Mellitis:
during
pregnancy;
similar
to
DMII
Impaired
Glucose
Tolerance:
increased
risk
of
developing
DMII
9

10. Epidemiology
— Prevalence
of
DM
in
US
is
6.6%
— 5-­‐10%
have
Type
I
— 90-­‐95%
have
Type
II
— Groups
at
risk
for
DM
— More
in
whites
than
nonwhites
— Native
Americans
— Age
of
onset
— Peak
age
of
onset
of
Type
I
DM
is
10-­‐14years
— Onset
of
Type
II
DM
tend
to
be
older;
younger
people
getting
disease
due
to
obesity
10

11. Clinical
Features
Clinical
Features
Type
I
Diabetes
Type
II
Diabetes
Body
habitus
Lean
Obese
Age
Younger
than
40yo
Middle-­‐aged
or
older
Insulin
levels
Absent
or
low
Normal
to
high
Onset
Abrupt
Gradual
—
Initial
presentation
of
Type
I
DM
usually
DKA
—
Type
II
DM
is
being
Dx
in
younger
people
—
Diagnosis:
—
Any
random
plasma
glucose
>200mg/dL
(11.1
mmol/dL)
with
symptoms
of
diabetes
—
Fasting
plasma
glucose
>126mg/dL
(7mmol/dL)
—
Plasma
glucose
>200mg/dL
(11.1
mmol/dL)
on
2
hour
oral
glucose
tolerance
test.
11

12. Hypoglycemia
— Background
—
—
Below
70
mg/dL
(3.8mmol/
dL),
most
symptomatic
Precipitants:
—
—
—
—
—
—
—
—
—
—
—
—
—
—
Addison’s
disease
Akee
fruit
Anorexia
nervosa
Antimalarials
Decrease
in
usual
food
intake
Ethanol
Factitious
hypoglycemia
Hepatic
impairment
Hyperthyroidism
Hypothyroidism
Increase
in
usual
exercise
Insulin
Islet
cell
tumors
Malfunctioning,
improperly
—
—
—
—
—
—
—
—
—
—
—
—
adjusted,
or
incorrectly
used
insulin
pump
Malnutrution
Old
age
Oral
hypoglycemics
Overaggressive
treatment
of
DKA
or
HHNC
Pentamidine
Phenylbutazone
Propranolol
Recent
change
of
dose
or
type
of
unsulin
or
oral
hypoglycemic
Salicylates
Sepsis
Some
antibacterial
sulfonylureas
Worsening
Renal
Insufficiency
12

13. Hypoglycemia
— Background
(cont’d)
— Hypoglycemia
unawareness
— Somogyi
phenomenon
— Signs
and
Symptoms
— Secondary
to
secretion
of
epinephrine
and
CNS
dysfunction
— Sweating,
nervousness,
tremor,
tachycardia,
hunger,
bizarre
behavior,
confusion,
seizures,
and
coma.
— Diagnostic
Strategies
— Obtain
blood
glucose
and
other
tests
to
find
cause
— Factitious
hypoglycemia:
testing
for
insulin
antibodies
and
C
peptide
level
13

14. Oral
hypoglycemic
agents
— Non
hypoglycemic
(taken
individually)
—
Biguanides
(metformin)
— decreases
hepatic
glucose
production
—
Alpha-­‐Glucosidase
inhibitors
(acarbose,
pioglitazone)
— Decrease
GI
tract
absorption
of
glucose
—
Thiazolidinediones
(rosiglitazone,
pioglitazone)
— Increase
peripheral
tissue
glucose
use
— Hypoglycemic
—
—
Insulin
Sulfonylurea
(i.e.
glipizide)
— Increases
pancreatic
insulin
secretion
—
Nonsulfonylurea
secretagogues
(repaglinide,
nateglinide)
— Increased
pancreatic
insulin
secretion
—
Glucagon-­‐like
peptide
(Exanatide)
OsamaK,
Wikimedia
Commons
— Stimulates
release
of
insulin
from
pancreatic
cells
—
Dipeptidyl
peptidase-­‐4
inhibitors
— Inhibits
DPP-­‐4
to
prevent
degredation
of
endogenous
GLP
14

15. Hypoglycemia
— Management
— If
patient
is
awake
and
cooperative,
give
sugar
containing
food
or
beverage
PO
— If
unable
to
take
PO
— 25-­‐75
gm
glucose
as
D50W
(1-­‐3
amps)
IV
— Children:
0.5-­‐1
g/kg
glucose
as
D25W
(2-­‐4mL/kg)
— Neonates:
0.5-­‐1
g/kg
glucose
(5-­‐10mL/kg)
as
D10W
— If
unable
to
obtain
IV
access:
— 1-­‐2
mg
glucagon
IM
or
SQ;
may
repeat
20
min
Intropin,
Wikimedia
Commons
15

16. Diabetic
Ketoacidosis
— Pathophysiology
— Caused
by
cessation
of
insulin
intake
or
by
physical
emotional
stress
Source
undetermined
16

17. Diabetic
Ketoacidosis
— Clinical
Features
— History
— c/o
polydipsia,
polyuria,
polyphagia,
visual
blurring,
weakness,
weight
loss,
nausea,
vomiting,
and
abdominal
pain.
— Seek
reason
for
DKA
— Physical
—
—
—
—
Altered
mental
status
Tachypnea
with
Kussmaul
respirations
Hypotension
and
other
signs
of
dehydration
Acetone
breath
17

18. Diabetic
Ketoacidosis
— Diagnostic
Strategies
— Laboratory
Tests
— Glucose:
>350
mg/dL
(19.4
mmol/dL)
— Euglycemic
DKA:
18%
pts
may
have
glucose
less
than
300
(16.6
mmol/
dL)
— Sodium:
Low
to
normal
— Correct
for
hyperglycemia:
0.016
x
(Glucose
-­‐100)
— High
lipid
content
may
cause
falsely
low
levels.
— Potassium:
Normal
to
high
— Technically,
potassium
deficit
due
to
K+
and
H+
shifts
— Correct
potassium
for
pH
— (Serum
potassium)-­‐[0.6
(7.4-­‐pH)
x
10]
— Acetoacetate
and
beta-­‐hydroxybutyrate:
elevated
— BUN
and
Cr:
elevated
18

19. Diabetic
Ketoacidosis
— Management
— ABCs,
IV,
O2,
Monitor
— Blood
glucose,
labs
— Dehydration
— Fluids
mainstay
of
therapy;
pts
usually
down
3-­‐5L
— Adult:
1-­‐2L
over
1-­‐3
hrs;
Child:
20
mL/kg
over
1
hour
— Follow
with
fluid
resuscitation
to
maintain
UOP
of
1-­‐2mL/kg/hr
— Insulin
— Infusion
of
0.1
units/kg/hr
up
to
5-­‐10
units/kg/hr
— Bolus
of
insulin
prior
to
drip
optional
in
adults;
contraindicated
in
children
— Check
glucose
every
1
hour
— Switch
IV
fluids
to
contain
dextrose
to
prevent
hypoglycemia
when
BS
250-­‐300
mg/dL
(13.8-­‐16.7
mmol/dL)
19

20. Diabetic
Ketoacidosis
— Correct
electrolyte
abnormalities
(check
basic,
pH,
ketones
every
2
hours)
— Potassium
— <4:
20mEq/hr
— 4-­‐6:
10mEq/hr
— >6:
none
— Magnesium
— Supplement
0.30
to
0.35
mEq/kg/day
of
magnesium
if
deficient
(1-­‐3
grams
in
70kg
pt)
20

21. Diabetic
Ketoacidosis
— Acidosis
— Bicarbonate
may
be
indicated
in
pts
pH
≤
7.0
— Usually
not
warranted
— Worsen
O2
release
by
shifting
oxygen
dissociation
curve
to
left
— Acidosis
correction
terminates
Kussmaul
respirations
needed
to
get
rid
of
CO2
— Increases
K+
requirement
— May
produce
alkalosis
which
induces
dysrhythmias
because
of
electrolyte
shifts
— Inhibit
feedback
mechanism
in
which
low
pH
inhibits
ketogenesis
— Studies
show
bicarbonate
worsens
prognosis
in
pts
even
with
pH
as
low
as
6.9-­‐7.1
21

22. Diabetic
Ketoacidosis
— Complications
—
—
—
—
—
Hypokalemia
Hypoglycemia
Alkalosis
(from
bicarb
therapy)
CHF
Cerebral
edema
— Occurs
6-­‐10
hrs
after
initiation
of
therapy
and
unless
if
glucose
is
below
250mg/dL
(13.8
mmol/dL)
— Consider
if
pt
remains
comatose
or
lapses
into
coma
— Mortality
90%
— Use
Mannitol
0.25-­‐2
mg/kg
22

23. Diabetic
Ketoacidosis
— Disposition
— Admit
to
hospital/ICU
— Consider
outpatient
if
—
—
—
—
—
Initial
pH>7.35
Initial
HCO3
≥
20
mEq/L
Can
tolerate
PO
fluids
Symptoms
resolve
in
ED
No
underlying
precipitant
requiring
hospitalization
23

24. Hyperglycemic
Hyperosmolar
Nonketotic
Coma
(HHNC)
— Background
— Characterized
by
hyperglycemia
(38.8),
hyperosmolarity,
dehydration,
and
altered
mental
status
— Ketosis
and
acidosis
are
minimal
or
absent
Source
undetermined
24

25. HHNC
— Pathophysiology
— Similar
to
DKA
— Absence
of
ketoacidosis
is
unknown
— Theory:
patients
continue
to
secrete
insulin
to
block
ketogenesis.
— Etiology
— More
common
in
type
II
DM
— May
occur
in
non
diabetic
pts
(20%
of
cases)
especially
after
burns,
hyperalimentation,
peritoneal
dialysis,
or
hemodialysis
Виталий
Поспелов,
Wikimedia
Commons
25

26. HHNC
— Clinical
Features
— History
— Fever,
thirst,
polyuria,
or
oliguria
— Associated
with
chronic
renal
insufficiency,
gram-­‐negative
PNA,
GI
bleeding,
gram-­‐negative
sepsis.
— Physical
Exam
—
—
—
—
—
—
—
hypotension
and
other
signs
of
dehydration
Tachycardia
Fever
Altered
mental
status
Seizures
Signs
of
stroke
Less
commonly:
choreoathetosis,
ballismus,
dysphagia,
segmental
myoclonus,
hemiparesis,
hemianopsia,
central
hyperpyrexia,
nystagmus,
visual
hallucinations,
and
acute
quadriplegia
26

27. HHNC
— Diagnostic
strategies
— Laboratory
Testing
— Blood
glucose
>600
mg/dL
(33.3
mmol/dL)
— Serum
osmolarity
>
350
mOsm/L
— May
have
metabolic
acidosis
2/2
lactic
acidosis,
starvation
ketosis
— Electrolytes:
decreased
sodium,
elevated
potassium
27

28. HHNC
— Management
— Dehydration
— Usually
9L
fluid
deficit
in
a
70
kg
pt
— 2-­‐3L
of
NS
initially;
may
change
to
0.45%NS
afterwards
— Sterile
water
to
be
considered
concommitently
for
pts
with
CHF
— Insulin
— Electrolytes
28

29. Case
1
— Work-­‐up
29

30. Case
1
— Laboratory
results:
Phos
7.3
Na
134
WBC
6.2
K
7.0
Hbg
3.6
Cl
106
Hct
9.9
HCO3
3
Plt
310
BuN
16
VBG
pH
7.2
Cr
1.4
Wet
Smear:
+
for
clue
cells
Glucose
770
(42.7)
Urine
Dip:
+LE,
Nitrite
Ca
9.4
Urine
Micro
15-­‐30wbc/hpf
Mg
2.6
30

31. Case
1
— EKG:
Sinus
tachycardia
with
normal
axis,
intervals.
+Peaked
T
waves
in
leads
V1-­‐6
— CXR:
no
infiltrates
— Pelvic
Ultrasound:
no
acute
abnormalities.
31

32. Case
1
— Hospital
course
— Started
on
IV
fluids,
Insulin
drip
— Started
on
Flagyl,
Cefotetan,
Doxycycline
— Blood
and
urine
cultures
were
positive
for
E.
coli
32

33. Sources
Marx
J.
Rosen’s
Emergency
Medicine,
7th
Ed,
2009.
Rucker
D.
“Diabetic
Ketoacidosis.”
eMedicine
Emergency
Medicine,
4
Jun
2010.
33