Transcript Diabetic Emergencies - Creighton University

Diabetic Emergencies
Andjela Drincic M.D.
Diabetic Emergencies
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Case Presentation
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Pt is a 32yo female with a hx of type 1
DM who presents with a cc of N/V, and
diffuse abdominal pain for 24 hours
What other questions would you like to
ask
Diabetic Emergencies
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Case Presentation
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Pt denies F/C, URI symptoms, urinary
symptoms except for frequency
Pt also states that she has been using
her insulin correctly, but she had not
taken any insulin for the last 24 hours
because she wasn’t able to eat
anything
Diabetic Emergencies
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Case Presentation
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PMHx: Diagnosed with DM after
episode of DKA approx 7 years ago.
Meds: Insulin 70/30 28UqAM, 16UqPM
NKMA
SHx: Single, no children, (+) Tob 1ppd
for 12 years, occ EtOH use, no
recreational drugs
FHx: (+) HTN
What are pertinent findings on physical
exam?
Diabetic Emergencies
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Physical Exam
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Gen: Mild distress but A&O x 3
97.4, 120, 34, 132/88
HEENT: WNL
Heart: RR Lungs: CTA-B
Abd: (+) BS, diffuse tenderness, no
rebound
Ext: WNL
Neuro: WNL
What Lab Data would you like to
obtain?
Diabetic Emergencies
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Case Presentation
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Lab Data
WBC 15.7, H/H 15/45 Plt 229
 NA 132, K 5.2, CL 96, HCO 11, BUN 10,
Cr 1.0 Glucose 612, Ca 12.1, Phos 6.6,
Mg 2.1
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Diabetic Emergencies
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Case Presentation
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Lab Data Analysis
NA 132, K 5.2, CL 96, HCO 11, BUN 10,
Cr 1.0 Glucose 612, Ca 12.1, Phos 6.6,
Mg 2.1
 What is the anion gap?
 What is the actual serum sodium?
 What is the differential diagnosis for wide
anion gap metabolic acidosis?
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Formulas you may need
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sOsm = 2 (Na + K ) + Glu/18 +
BUN/2.8 + ETOH/4.6
AG = Na - ( Cl + HCO3)
Na = Na + 1.6 x (Glu - 100)/100
Diabetic Emergencies
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Case Presentation
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Lab Data (Continued)
UA: Protein 3+, Large ketones
 Serum ketones were 1:16
 Serum osmolarity was 323mOsm/kg
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Diabetic Ketoacidosis (DKA)
Life-threatening emergency
 Gross insulin deficiency is the
predominant problem of DKA
 Most common in patients with
type 1 diabetes
 Can occur in patients with type 2
diabetes due to progressive loss of
β-cell reserve
 Mortality is ~5%–10%
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Fishsbein H, Palumbo PJ. Acute metabolic complications in diabetes. In: National
Diabetes Data Group. Diabetes in America. Bethesda (MD): National Institutes of Health,
Signs, Symptoms, and Treatment of Diabetic
Ketoacidosis
Symptoms
 Blurred vision
 Increased thirst
 Increased urination
 Nausea/vomiting
 Confusion
 Loss of consciousness
Signs
 Deep respirations
 Fruity breath
 Dehydration
 Hyperglycemia
 Ketosis
 Acidosis
Treatment
 Give insulin in a sufficient
amount
 Attention to the potassium
level is also important
 Hydration
Type 1 DM
hormonal pathophysiology
- Insuln deficiency:
decreased glucose utilization
- Elevations in counterregulatory
hormones:
increased lipolysis in adipose tissue
increased proteolysis in muscle
increased glycogenolysis
increased gluconeogenesis
hepatic ketogenesis
Leading to DKA
Hyperosmolar Hyperglycemic State
(HHS)
Life-threatening emergency
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Occurs in patients with type 2 diabetes
Characterized by very high blood glucose levels
without ketones
insulin secretion is maintained to prevent
peripheral lipolysis , liver able to metabolize
FFA in a nonketogenic manner
relative insulin deficiency : decreased
peripheral uptake and increased hepatic
gluconeogenesis
hyperglycemia, hyperosmolality
osmotic diuresis and volume and electrolyte
depletion
DKA/HHS
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not mutually exclusive !
Criteria for DKA
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hyperglycemia ( glu>250 mg/dl)
ketosis
acidemia ( pH <7.3)
Pathophysiology of DKA/HHS
Insulin Deficiency
Increased Lipolysis
Hyperglycemia
Increased ketogenesis
Osmotic Diuresis
Ketoacidosis
Pure Diabetic Ketoacidosis
Hyperosmolality
Pure Hyperosmolar State
DKA
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Absolute insulin deficiency and counterregulatory hormones promote lipolysis
shift in hepatic lipid metabolism of
incoming fatty acids due to high ratio of
glucagon to insulin in portal flow - fall in
malonyl co A levels and disinhibition of
CPT
CPT catalizes beta oxidative pathwayfatty acids are oxidized to form ketone
bodies rather than re-esterified into TG
Physiology of DKA
Insulin
glucagon
Triglyceride
Hormone Sensitive Lipase
Adipocyte
Serum
Free Fatty Acids
Free Fatty Acids
Hepatocyte
Free Fatty Acids
Mitochondria
Fatty Acyl Co A
Glucagon
Malonyl Co A
Carnitine palmitoyl transferase 1
Acetyl Co A
HMA Co A
Acetoaceteate
Acetone
3 hydroxybutyrate
Evaluation of patient
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history of DM , medications and symptoms
history of complications
utilization of medications
social history ( including alcohol)
vomiting
precipitating factor - pregnancy, infection,
omission of insulin, MI, CVA
asses hemodynamic status
examine for infection
Laboratory Evaluation
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BMP
CBC
serum ketones
calculate serum osmolality and AG
measure serum osmolality if ingestion of osmotically
active substance other than glucose suspected
UA and culture
consider blood culture
CXR
consider HCG
ABG if indicated clinically
HbA1c
“Euglycemic ketoacidosis “
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Glu < 300 mg/dl
HCO3 < 10 mEq/l
Usually in pump pts ( no “back-up
insulin)
Other expected labs in DKA
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Hyponatermia unless pt is
dehydrated
Hyperkalemia due to cellular shift
Leukocytosis in the absonce of
infection
Elevation of amylase and lipase in
the absence of pancreatitis
“Serum Ketone Negative DKA”
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Alcoholic ketoacidosis
Hypoxia
Beta hydroxybutirate is the
dominant ketone
Not detected by nitroprusside
reaction
Gudelines ofr therpay of DKA/HHS
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addapted from Joslin’s Diabetes
Mellitus 14th edtion , 2005
Suggested Fluid Replacement in
DKA/HHS
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Administer NS as indicated to
maintain hemodynamic status than
follow general guidelines:
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NS for first 4 hours
consider 1/2 NS thereafter
Change to D5 1/2 NS when BG < 259
mg/dl
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may need to adjust type and rate of fluid
administration in the elderly and in
patients with CHF and CRF
Suggested fluid replacement in
DKA /HHS
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1st hour : 1 l
2nd hour : 1 l
3rd hour : 500 ml
4th hour:
500 ml
5th hour : 500 ml
Total 1st - 5th hour
6th - 12th hour :
ml/hr
-1l
-1l
-1l
3.5 - 5 l
250 - 500
Guidelines for Insulin Management
in DKA/ HHS
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regular insulin 10U I.v. stat ( for adults) or 0.15 U/kg
I.v. stat
start regular insulin infusion 0.1 u /kg per hour or 5 U
per hour
Increase insulin by 1 U per hour every 1-2 hours if less
than 10 % decrease in glucose or no improvement in
acid - base status
decrease insulin by 1-2 U/hr when BG < 250 mg/dl
and/or progressive improvement in clinical status with
decrease in glucose >75 mg/dl /hr
do not decrease insulin infusion to < 1 u /hr
maintain BG 140 - 180 mg/dl
if BG < 80 mg/dl , stop insulin infusion for no more
than 1 hour and restart the infusion
if BG drops consistently to <100 mg/dl , change I.V.
Insulin Infusion Algorithm
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1. Discontinue all subcutaneous insulin
use
2. Measure blood glucose every hour
measure urine ketones after each void
every 4 hours
3. Give D5%W iv via insulin infusion
pump
4. Make insulin solution using regular
insulin to a concentration of 0.5 U/ml
Insulin Infusion Algorithm
Newton et al:Arch Intern Med 164,sept 27, 2004
Blood glucose
mg/dl
Insulin infusion
U/h
D5%W
ml/h
<70
71-100
101-150
151-200
201-250
251-300
301-350
351-400
401-450
451-500
>500
0.5
1.0
2.0
3.0
4.0
6.0
8.0
10.0
12.0
15.0
20.0
250
225
200
175
150
100
50
0
0
0
0
Guidelines for K replacement in
DKA/HHS
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Do not administer K if serum K > 5.5
mEq/l or if patient is anuric
Use KCl but alternate with KPO4 if there
is severe phosphorus depletion and
patient is unable to take phosphorus by
mouth
Add I.V. KCl to each liter of fluid
administered unless contraindicated
Guidelines for K replacement in
DKA/HHS
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serum K ( mEq/L)
required
<3.5
3.5 - 4.5
4.5 - 5.5
> 5.5
infusion
Additional K
40 mEq/L
20 mEq/L
10 mEq/L
Stop K
Guidelines for Bicarbonate Therapy in
DKA
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PRO: severe acidosis is associated with
adverese effects:hypotension, decreased
cardiac output decreased peripheral
vascular resistance, increased pulmonary
arterterial resistance , bardycardia,
arrhytimas , renal and mesenteric
ischemia, cerebral vasodilatation
CONS: no studies have shown any benefit
of bicarbonate if pH is 6.9-7.1
SIDE EFF : overshoot alkalosis,
paradoxical CSF acidosis , hypokalemia,
volume overload, overproduction of
Guidelines for Bicarbonate Therapy in
DKA
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Use clinical judgement in deciding if
bicarbonate therapy is indicated
if pH is < 7.0 consider 100 ml HCO3 over
45 min
( mix 100 ml NaHCO3 with 400 ml sterile
water and administer at rate of 200
ml/hr)
check ABG 30 min later
Phosphate replacement
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Phos depletion is common: renal loss,
intracellular uptake during insulin Rx
problem: low cardiac output, respiratory
muscle weakness, rhabdomyolisis , CNS
deppression , seizures , coma, renal
failure
CAVE : iv Phos leads to hypocalcemia
no benefit in routine replacement
reserve replacement Rx if phos < 1.5
mg/dl AND in whom Ca is normal
use of small amount of Kphos and KCL iv
is safe and effective
Monitoring of RX
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BG hourly
electrolytes and acid base status every 24 hours
ok to check venous pH if you can’t get art
line ( 0.03 unit less than arterial )
frequent measurement of ketones may be
misleading (  hydroxybutirate is
converted to acetoacetate)
consider using bedside measurement of ß
hydroxybutirate
repeat CXR after 4 l fluids administered
Complications of RX
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hypoglycemia
hypokalemia
hypophosphatemia
hyperchloremia and hyperchloremic
acidosis - chloride losses are less severe
than sodium losses but replacement
solutions have equal par tof Na and Cl
hypoalcemia
cerebral edema - children
DVT/PE ( dehydration as a risk factor)
DKA - is it always type 1 DM?
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Arch Int Med 1999 159:2317 epidemiology of pts admitted for DKA :
type 1 DM in
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80 % of whites
53% of African Americans
34 % of Hispanics
no difference in electrolytes,glu, pH, AG,
pOsm or level of ketosis
majority of pts with type 2 , no
preciptating event !
A” Real Life “ case
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55 y/o AAF
no previous h/o DM
comes with polyuria,, polydipsia, fatigue
Vitals: 96.9, 130, 24, 122/63
Labs: WBC 19, BS 502, K 6.0, Na 128,
CO2 5
Orders
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Dx DKA
IVF NS 3l bolus than 200 cc/hour
2 amps HCO3
blood cultures, sputum
cultures,accucheck q 1hour
diabetic education in am
cbc , bmp in am
bmp q 2hours x 4, UA
Mg, PO4 levels
Insulin gtt: U/hour
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0-50
70 - 100
101- 129
130 - 170
171 - 200
201 -230
231 - 270
271 - 300
300 - 330
>330
off
0.3
0.4
0.5
0.6
0.8
1.0
2.0
4.0
4.0
Orders - cont
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4 hours later - K 3.0 , BS 347
order : 40 mEq KCl now
change IVF to D5 NS with 40 KCl at 200
cc/hour
6 hours later: phos 1.2
order : 40 mEq K phos IV
soft diet for pt
24 hours later , BS 350
Diabetic Emergencies
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Hypoglycemia
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Whipple Triad
Consistent signs and symptoms
 Low blood glucose
 Relief with supplemental glucose
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Two categories of hypoglycemia
Reactive
 Nonreactive
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Diabetic Emergencies
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Hypoglycemia
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Reactive Hypoglycemia
Develops in response to a nutrient
challenge
 Seen in pts with type 2 DM (???) and
post GI surgery pts
 Idiopathic form
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Nonreactive Hypoglycemia
Iatrogenic
 Fasting/Factious
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Diabetic Emergencies
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Hypoglycemia
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Fasting/Factious Hypoglycemia
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3 main causes
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Factitious taking of oral
hypoglycemics/insulin
Autoimmune etiology
Insulinoma from an islet cell tumor
Heavy EtOH can also cause hypoglycemia
 Three tests for workup of nonreactive
hypoglycemia
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Serum insulin
C-peptide
Urinary sulfonylurea test
Diabetic Emergencies
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Hypoglycemia
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C-peptide
Elevated indicates endogenous insulin
secretion and is low if there is factitious
insulin injection
 High levels seen in autoimmune
hypoglycemia, insulinoma, and
sulfonylurea ingestion
 Urinary sulfonylurea test will rule in or out
oral hypoglycemic use
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Insulin levels
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< 100 suggest insulinoma