DKA

DEPARTMENT OF INTERNAL MEDICINE

FMUI RSCM
FMUIRSCM
DKA: life threatening
 DKA
Unique
U i phenomenon
h iin diabetic
di b i due
d to
absolute or relative insulin deficiency that
accelerate lipolysis with all of consequences
 What is DKA?
High blood glucose, ketones, acidosis,
and dehydration

Absolute
b l or relative
l insulin
l deficiency
d f
Increase in counterregulatory hormones
Breakdown of fat and muscle
Biochemical triad:
hyperglycaemia
ketoacids
metabolic acidosis
 Incidence of DKA
V i 48
Varies: 8 episodes
i d per 1,000 patients
ti t
Death: 118
8 %, depend on facilities
Death in type 1: mainly from cerebral oedema
Death in type 2: due to comorbidities

Kitabchi et al 2009, Joint Brotish Diabetes Societies 2010

DKA cause or ttrigger
i
I id
Incidence
New-onset type 1 5-40%
Acute illness 10-20%

Insulin omission/non
omission/non-adherence
adherence 33%

Infection 20-38%

Heart attack, stroke, <10%

pancreatitis

Booth 2001, Joslin 2005

 Pathogenesis DKA
Counterregulatory Hormones RelativeInsulin
Relative Insulin
Deficiency
Deficiency
Absolut Insulin Deficiency

Absent or Minimal
Lipolysis Protein synthesis Proteolysis Absent or Minimal
Ketogenesis

++
FFA to Liver Gluconeogenic substrates

Ketogenesis Glucose utilization Gluceneogenesis Glycogenolysis

Alkali reserve Hyperglycemia

Ketoacidosis Glycosuria osmotic diuresis

Loss of water and electrolytes

Triacylglycerol
Decreased fluid intake
Dehydration Hyperosmolarity

Hyperlipidemia Impaired renal function

HHS
DKA
DKA
 Ketones
U d as fuel
Used f l when
h calories
l i are restricted
i d
Physiological ketosis when fasting or with
prolonged
l d exercise
i
Insulin deficiency lypolysis and ketone
production
d i acidosis
id i
betahydroxybutyrate
acetoacetate
acetone
Fasted State: Catabolic
 Ketones
Betahydroxybutyrate
y y y p
predominant
Ketoacidosis may be present without
detectable urinary ketones
Blood ketone testing may enable early
id tifi ti off DKA
identification
Earlier symptoms and signs of DKA

Polyuria
Polyuria
Polydipsia
Tiredness
Muscle
M l cramps
Flushed facial appearance
Later symptoms and signs of DKA
Weight loss
Nausea and vomiting
Abdominal pain
p
Dehydration
Acidotic breath
Hypotension
Shock
Altered consciousness
Coma
DKA investigations
g
Immediate for diagnosis
Capillary
p y blood g
glucose and ketones
Urgent for assessment and treatment
Blood glucose
Blood gases
Electrolytes, urea, creatinine
WBC
Consider
Cardiac monitor
Blood culture, urine culture
Chest Xray
Diagnostic criteria for DKA and HHS

DKA HHS

Mild Moderate Severe Plasma glucose

>250 mg/dl >600 mg/dl

Arterial pH 7.257.30 7.00 to < 7.24 < 7.00 > 7.30

Serum bicarbonate ( mEq/l) 1518 10 to < 15 < 10 > 18

Urine ketone* Positive Positive Positive Small

Serum ketone* Positive Positive Positive Small

Effective serum osmolality Variable Variable Variable > 320 mosm/kg

Anion gap+ > 10 > 12 > 12 Variable

Mental Status Alert Alert/drowsy Stupor/coma Stupor/coma

*Nitroprusside reaction method .Effective serum osmolality: 2[measured Na * (mEq/l)] + glucose (mg/dl)/18. Anion gap : (Na )
[(CI + HCO, (mEq/I)] (Data adapted from ref 13. )
Kitabchi 2009
 DKA laboratory
y findings
g
Blood glucose >250 mg/dL
Ketones Urine: moderate to large
Blood: >0.6 mmol/L
y
Osmolality Increased high
g blood glucose
g and
urea/creatinine, dehydration
Electrolytes Low/normal Na+ and Cl-
Low/normal/high K+(often misleading)
Low HCO3 (normal 23-31)

Anion gap >10

10 mild
>12 moderate to severe
Blood gases pH <7.30, HCO3 <15 (mild)

pH <7.00, HCO3 <10 (severe)

Admission biochemical data in patient with HHS or DKA

HHS DKA
Glucose (mg/dl) 930 83 616 36
Na + (mEq/l) 149 3.2
32 134 1
1.0
0
K + (mEq/i) 3.9 0.2 4.5 0.13
BUN (mg/dl) 61 11 32 3
Creatinine (mg/dl) 1.4 0.1 1.1 0.1
pH 7.3 0.03 7.12 0.04
Bicarbonate (mEq/l) 18 1.1 9.4 1.4
3hydroxybutyrate (mmol/l) 1.0 0.2 9.1 0.85
Total osmolality* 380 5.7 323 2.5
IRI (nmol/l) 0.08 0.01 0.07 0.01
Cpeptide
C peptide (nmol/l) 1 14 0.1
1.14 01 0.21 0
0 0.03
03
Free fatty acids (nmol/l) 1.5 0.19 1.6 0.16
Human growth hormone (ng/ml) 1.9 0.2 6.1 1.2
Cortisol (ng/ml) 570 49 500 61
IRI (nmol/l) 0.27 0.05 0.09 0.01
CPeptide l/l)
d ((nmol/l) 1.75 0.23 0 25 0.05
0.25 0 05
Glucagon (ng/ml) 689 215 580 147
Catacholamines (ng/ml) 0.28 0.09 1.78 0.4
Growth hormone (ng/ml) 1.1 7.9
Gap p : anion ggap
p 12(mEq/l)
( q/ ) 11 17

*According to the formula 2( Na + K) + urea (mmol/l) + glucose (nmol/i). Values following

interavenous administration of tolbutamide. IRI. Immunoreactive insulin (Adapted from ref 4)
Kitabchi 2009
 DKA treatment
Rehydration 1. Correct shock with bolus saline
2. Rehydration rate depends on clinical
status, age and kidney function
Normall saline
N li (0.9%)
(0 9%) ffor resuscitation
i i
and rehydration initially
Glucose/saline
/ solution when g
glucose
around 250 mg/dL
Rehydrate steadily over 48 hours
3. Consider NG tube

Potassium Essential after resuscitation and when

urine output confirmed
Kitabchi et al 2009
 DKA treatment
Insulin Infusion: 0.1 units/kg/hour after
resuscitation, saline established and BG
falling
Rate should be increased by 10-20%
10 20% if
glucose not fallen by 50-75 mg/dL over
first hour

Monitoring BG, BP, urine output and hourly

neurological status
Blood gases and electrolytes 2-hourly
initially
Kitabchi,2009
 DKA complications
Hypoglycaemia +/ hypokalaemia
Acidosis not improving consider continuing
dehydration
y or infection
Pulmonary oedema
Headache
H d h +/ / falling
f lli llevell off awareness consider
id
cerebral oedema and urgent treatment with
Mannitol

Joslin 2005
 DKA recovery
Rapid improvement
Continue IV insulin while ketosis present
Oral intake when possible
p
Rapidacting insulin 60120 minutes before
discontinuing IV insulin
Usual insulin regimen
Consider drinks and food containing
p
potassium
 DKA
DKA resolution
Clinical finding
Blood glucose < 200 mg/dl
Bicarbonat> 15 mEq/l
Anion gap 12 mEq/l
Decrease ketone bodies
 New Recommendations

1. Venous
V rather
th than
th arterial
t i l HCO
HCO3 and
d pH
H
2. Ketonometer used bedside testing
g
3. Long acting analogue should be continued
4. Do not use a priming bolus insulin
5. Bicarbonate
Bi b not used
d routinely
i l
Prevention is Key
y
Can be prevented by:
Better public awareness

Improved
I d access to medical
di l care

Improved education in treating

hyperglycaemia during illness

Emergency communication with

healthcare provider