Diabetic Emergencies

Andjela Drincic M.D.

Diabetic Emergencies

Case Presentation
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

Case Presentation
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 wasnt able to eat
anything

Diabetic Emergencies

Case Presentation
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

Physical Exam
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

Case Presentation
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

Diabetic Emergencies

Case Presentation
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?

Formulas you may need

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

Case Presentation
Lab

Data (Continued)

UA: Protein 3+, Large ketones

Serum ketones were 1:16
Serum osmolarity was 323mOsm/kg

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
-cell reserve
Mortality is ~5%10%

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

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

not mutually exclusive !

Criteria for DKA

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

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
Triglyceride
Adipocyte
Serum

Insulin

glucagon

Hormone Sensitive Lipase

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

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

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

Glu < 300 mg/dl

HCO3 < 10 mEq/l
Usually in pump pts ( no back-up
insulin)

Other expected labs in DKA

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

Alcoholic ketoacidosis
Hypoxia
Beta hydroxybutirate is the
dominant ketone
Not detected by nitroprusside
reaction

Gudelines ofr therpay of DKA/HHS

addapted from Joslins Diabetes

Mellitus 14th edtion , 2005

Suggested Fluid Replacement in

DKA/HHS

Administer NS as indicated to
maintain hemodynamic status than
follow general guidelines:
NS

for first 4 hours

consider 1/2 NS thereafter
Change to D5 1/2 NS when BG < 259
mg/dl

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

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

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. fluids to D 10
to maintain BG 140 - 180 mg/dl

Insulin Infusion Algorithm

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

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

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

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 ketoacids

Guidelines for Bicarbonate Therapy in

DKA

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

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
but oral replacement preferred to I.V.

Monitoring of RX

BG hourly
electrolytes and acid base status every 2-4
hours
ok to check venous pH if you cant 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
hydroxybutirate
repeat CXR after 4 l fluids administered

Complications of RX

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?

Arch Int Med 1999 159:2317 epidemiology of pts admitted for DKA :
type 1 DM in

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

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

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

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

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

Hypoglycemia
Whipple

Triad

Consistent signs and symptoms

Low blood glucose
Relief with supplemental glucose

Two

categories of hypoglycemia

Reactive
Nonreactive

Diabetic Emergencies

Hypoglycemia
Reactive

Hypoglycemia

Develops in response to a nutrient

challenge
Seen in pts with type 2 DM (???) and post
GI surgery pts
Idiopathic form

Nonreactive

Hypoglycemia

Iatrogenic
Fasting/Factious

Diabetic Emergencies

Hypoglycemia
Fasting/Factious

Hypoglycemia

3 main causes
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

Serum insulin
C-peptide
Urinary sulfonylurea test

Diabetic Emergencies

Hypoglycemia
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

Insulin

levels

< 100 suggest insulinoma

> 100 suggest autoimmune