DKA is a life-threatening complication that can occur in patients with type 1 or type 2 diabetes. It results from a lack of insulin and high levels of glucose and ketones in the blood. Symptoms may include nausea, vomiting, thirst, frequent urination, and abdominal pain. Treatment involves rapid fluid replacement, administration of insulin, and monitoring of electrolytes. Goals are to rehydrate the patient and lower glucose and ketone levels. Complications can include hypoglycemia, hypokalemia, and cerebral edema. With treatment, mortality rates for DKA are now below 5%. Prevention relies on patient education about sick day management of diabetes.

1. Diabeticketoacidosi
s
By
Dr.Hafsa Asim

2. • DKA is a potentially life threatening
complication in pts with
-IDDM
-Type 2 DM
• DKA is a medical emergency,without
treatment it can lead to death.
• DKA was 1st described in 1886 untill
introduction of insulin therapy in 1920,it was
fatal.
• Now mortalitiy rate is <5%.

3. Definition:
• BSL > 250mg/dl(13.9mmol/L)
• Blood pH < 7.3 / serum bicarb < 15meq/l
• Ketonuria +++ / ketones in serum > 5meq/l

4. In 2006 ADA,categorised DKA into 3 stages of
severity:
Mild
pH 7.25-7.30
S/bicarb 15-18
Pt is alert
Severe
pH <7.00
s/bicarb <10
Pt is in coma
Moderate
pH 7.00-7.25
s/bicarb 10-15
Pt-mild drowsy

5. Causes:

6. DKA
No cause
5%
Medical
surgical
emotional
stress
New
onset of
DM 20%

7. Recurrent
episodes of
DKA
In young pts
Eating disorder
Skipping
doses
Cocaine or
Alcohol
abuse

8. • DKA also occurs in TYPE 2 DM,more common
in african-american. This condition is called
ketosis-prone type 2 diabetes

9. Mechanism:
DKA absolute lack of insulin
Inc
glucagon
Inc glucagon
Dec insulin
ratio
Gluconeogenesis
(dec conc, of F2-6-
bisphosphate)
Inc glucose levels
Osmotic diuresis
Inc liberation of FFA
due to loss of
inhibitory action of
insulin on lipase
In liver
converted
into ketone
bodies
Dec pH
Metabolic
acidosis

10. Ketosis-prone ketogenesis:
• Exact mechanism is unknown.
• Occurs in type-2 diabetics.
Dec insulin
release due
to end
organ
insulin
resistance
Increase
level of
glucose
ketogenesis

11. Dehydration occurs as a result of 2 parallel
processes:
Inc
glucose
Inc
ketones
acidosisHyperglycemia
glycosuria
Osmotic
diuresis vomiting
Fluid & electrolyte depletion
(Renal hypoperfusion)

12. Clinical features:
symptoms
predominant symptoms severe DKA
• Nausea -confusion
• Vomiting -stupor
• Intense thirst -5% coma
• Polyuria
• Abdominal pain
• hyperventilation

13. Signs
• Signs of dehydration(dry mouth,skin turgor
dec)
• Tachycardia
• Hypotension
• abd tenderness
• Kussmoul sign
• Acetone breath
• hypothermia

14. How to approach
a pt with DKA?

15. • History:
can develpe over several days,
symptoms mostly occur within 24hr.
Ask abt symptoms of hyperglycemia e.g.
-polyuria,polydipsia,nocturia,wt loss,muscle
pains & cramps
Symptoms of acidosis & dehydration:
-abd pain,SOB,confusion,coma
Other symptoms
-vomiting,signs of inf(UTI,RTI),
weakness,nonspecific malaise

16. Physical examination:
• Dehydration: reported in 3-5 % pts
Mild <3% Moderate
3-8%
Severe 8%
Shock >10%
appearance Thirsty,alert lethargic drowsy
Tissue turgor Normal absent absent
Mucous mem moist dry very dry
BP normal normal or low low
pulse normal rapid rapid& weak
eyes normal sunken grossly sunken

17. • BP is usually normal untill last stage
• Tachycardia
• Capillary refill is maintained
• Pt have a smell of acetone
• Impaired consciousness 20%
level of consciousness depends on serum osmolality &not on
acidosis
>320mosm/l
s/osmolality=2(Na)+K+glucose/18
• Coma 10% pts
• Abd tenderness

18. Investigations:
• BSL
• Electrolytes
• Urine complete
• CBC
• ABGs
• RFTs
• X-ray chest
• ECG

19. Treatment goals:
• Fluid replacement
• Dec serum glucose
• Electrolyte replacement
• Antibiotics if infection

20. Management:

21. Typical deficits:
Water: 6 L, or
100 mL /kg
body wt
Sodium: 7 to
10 mEq/kg
body wt
Potassium: 3
to 5 mEq/kg
body wt
Phosphate:
~1.0 mmol/kg
body wt

22. Fluid replacement:
• Average fluid deficit is abt 6L
-3L from ECC(0.9%NaCl)
-3L from ICC (0.5%DW)
However 6L is not required by every pt,it depends upon degree of
dehydration.
fluid deficit in L=(0.6*wt in kg)[(Na/140)-1]
• Scheme: isotonic saline
1L in 1/2hr
1L in 1hr then
1L in 2hr i.e 500ml/hr

23. • Plasma osmolality can be used to measure
severity of dehydration
• 2(Na)+glucose/18+BUN/2.8
Subsequent fluid replacement:
-hypotonic saline 0.45% at 200-1000ml/hr
(because in DKA H2O loss>NaCl,both compartments will gradually be
replaced)
-5%DW added if BSL <250mg/dl

24. • Advantage of early rehydration:
-restores circulatory volume
-dec conc. Of catecholamines,glucagon
• Monitoring:
-by CVP,JVP
-urine output
-basal crepts
• Complication:
-ARDS
-cerebral edema
-hyperchloremic acidosis

25. Insulin therapy:
• Bolus dose 0.1unit/kg IV then 0.1 unit/kg/hr
in a continuous infusion or bolus dose 10unit IV
then 5-10units/hr
• If infusion not possible then 10units IM stat then
4-6units/hr IM
• BSL should dec by 100mg/dl/hr
• If BSL does not dec by 10 %,repeat loading
dose,double the infusion rate every 2 hour untill
BSL dec by 10%
• When BSL<250mg/dl,dec insulin to 1-4units/hr

26. Electrolyte
replacement:

27. Potassium:• At presentation K level is normal or high (K is shifted to
ECC in exchange for hydrogen ions that accumulate in acidosis)
so K is not added in 1st drip.
• Dec K level occurs because
-osmotic diuresis
-insulin shifts K insie the cells
-sec hyperaldosteronism
Total K loss equals 3-5meq/kg body wt
k 4.0-5.0 20mmol KCl/L
k3.0-4.0 30mmol KCL/L
k <3.5 40mmol KCL/L
Do not exceed >40meq/l. the goal is to maintain the s/K
concentration in the range of 4 to 5 mEq per L

28. ECG changes in hypokalemia:
• Inverted T wave
• Prominent U wave
• Long PR
• ST segment depression

29. Sodium:
• Initial plasma Na conc are low or normal despite
of H2O loss due to osmotic shift of H2O
• Hyponatremia occurs due to osmolar
compensation for hyperglycemia
• Add 1.6 meq to plasma Na for every 100 mg of
glucose
• Corrected Na=
[(plasma glucose-100)1.6/100]+ measured Na
Or =Na+2.4[(glucose-5.5)/5.5]

30. Bicarbonate:
• Its use is controversial because there is no diff
in reduction of glucose or ketoanion
• May aggravate hypokalemia
• Can be used in pts with pH<7.0
-pH 6.9-7.0---- 44meq of bicarb in
0.45%Nacl over 30 min to 1hour
-pH <6.9------88meq of bicarb

31. Phosphate:
• At presentation,serum PO4 may be normal or
inc
• Total body PO4 is dec by 1mmol/kg
• Dec PO4 occurs because it re-enters the cell
after administration of insulin & Osmotic
diuresis leads to inc urinary PO4 losses.
so while correcting hypokalemia give 2/3 Kcl
& 1/3 KPO4.( reduces the chloride load that might
contribute to hyperchloremic acidosis)

32. Complications of hypophosphatemia:
• Respiratory depression
• Skeletal muscle weakness
• Hemolytic anemia
• Cardiac dysfunction
Studies unable to prove that replacement of PO4 is beneficial in DKA
But may be helpful in pts with
• Anemia
• CCF
• Pneumonia
• hypoxia

33. • Antibiotics:
broad-spectrum antibiotics are given for
infections,while waiting for C/S

34. Special measures:
• Bladder cathetrization
• NG tubes
• CVP line in shocked pts
• For DVT prophylaxis,S/C heparin in comatose,
elderly or obese pts.

35. Subsequent monitoring:
• Monitoring is done by making a flow sheet:
Pts name age/sex
BSL
2hrly
Ketones
2hrly
Na/K
4hrly
Intake/
output
vitals insulin ABGs
4hrly

36. Complications:
• Hypotension:
-can lead to renal failure
-plasma expanders or whole blood is
given if sys BP< 80 & not responding to
NaCl
• Cerebral edema:
-caused by rapid reduction of BSL or
hypotonic fluids
• ARDS:
-hypoxemia on ABGs or pulse oximetry

37. thromboembolism DIC hypothermia
Hypoglycemia
Hypokalemia
Pulmonary edema

38. Resolution:
• Resolution of DKA is defined as general
improvement in symptoms e.g ability to
tolerate oral nutrition &fluids,
blood(pH>7.3),ketones in blood (<1 mmol/l)
or none in urine.
• Once this has been achieved, insulin may be
switched to the usual S/C regimen, one hour
after which the IV administration can be
discontinued.

39. • In pts with suspected ketosis-prone type 2
diabetes, determination of antibodies against
glutamic acid decarboxylase and islet cells
may aid in the decision whether to continue
insulin administration long-term (if antibodies
are detected), or whether to attempt
treatment with oral medication.

40. Follow up:
• Once pt is able to drink & anion gap dec &
ketonuria cleared S/C insulin is started
• Pt is discharged on S/C insulin
• Dietry plan
• BSL charting
• Weekly follow up initially

41. Prevention:
• Attacks of DKA can be prevented in known
diabetics to an extent by adherence to "sick day
rules"; these are clear-cut instructions to patients
on how to treat themselves when unwell.
• Instructions include advice on how much extra
insulin to take when sugar levels appear
uncontrolled, an easily digestible diet rich in salt
and carbohydrates, means to suppress fever and
treat infection, and recommendations when to
call for medical help.

42. THANKYOU