Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.

1. DIABETIC
KETOACIDOSIS
IN ER
Presented By:
Dr. Ismat Alborhan

2. Learning Objective
 Recognize symptoms and signs of DKA
 Accurately assess degree of dehydration
 Prescribe appropriate fluid and electrolyte
replacement
 Appropriately manage insulin infusion
 Understand principles to minimize risk of
cerebral edema
 Appropriately manage cerebral edema if
occurs

3. What is Diabetic Ketoacidosis
• Diabetic ketoacidosis (DKA) is a state of absolute or
relative insulin deficiency aggravated by ensuing
hyperglycaemia, dehydration, and acidosis
producing derangements in intermediary
metabolism.
• DKA is a far more characteristic feature of type 1
than of type 2 diabetes but may be seen in persons
with type 2 diabetes under conditions of stress.

4. Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis*
4

5. Diagnostic Criteria
• Blood glucose > 250 mg/dl
• pH < 7.35
• HCO3 < 15 mEq/L
• Anion Gap > 12
• Ketonemia

6. Causes of DKA :
The most common scenarios for diabetic ketoacidosis are-
1. Underlying or concomitant infection (40%) – UTI is the
most common.
2. Missed insulin treatments (25%)
3. Newly diagnosed, previously unknown diabetes (15%).
4. Other associated causes (20%)
 Myocardial Infarction, Cerebrovascular accident,
Acromegaly, Complicated pregnancy, Trauma, Stress,
Surgery
 Heavy use of concentrated carbohydrate beverages such
as sodas Dental abscess and sports drinks.

7. Pathophysiology Counter-
Regulatory Hormones :
 Insulin Deficiency is the Primary defect.
 There is excess secretion of primarily glucagon as well as catecholamine,
glucocorticoids, and growth hormone
 Stress hormones accelerate and exaggerate the rate and magnitude of
metabolic decompensation
Pathophysiology Counter-Regulatory Hormones
• Impaired insulin secretion Epi
• Anti-insulin action Epi, cortisol, GH
• Promoting catabolism All
• Dec glucose utilization Epi, cortisol, GH

8. Pathogenesis of DKA
Insulin
Deficiency
Beta-cell
failure
D/C
Insulin
Glucotoxicity

9. Insulin
deficiency
Increased
glucagon
GH
cortisol
catecholamines
Pathogenesis of DKA

10. Carbohydrate Metabolism in DKA
Relative or absolute insulin deficiency
glucose output
glycogenolysis
liver
glucose uptake
muscle

11. Increased Glucose Production in DKA
Gluconeogenesis Glucose
Protein breakdownLipolysis
Glycerol Amino acids
Lactate
TG
Activity of gluconeogenic
enzymes
(PEPCK, PC, PFK)

12. Increased Production of Ketones in DKA
Lipolysis
FFA Glycerol
Ketogenesis
B-OH-B
Acetoacetate
TG

13. Pathogenesis of DKA
Liver
Increased
glucose
production
Decreased
glucose
uptake
Peripheral
tissue
HYPERGLYCEMIA
Increased
release
FFA
Increased
ketogenesis
Adipose
tissue
Liver
KETOACIDOSIS
Osmotic diuresis
Volume depletion Metabolic acidosis
Decreased alkali reserve

14. Diagnostic Criteria for DKA
DKA
Mild Moderate Severe
Plasma glucose (mg/dl)
pH
Anion gap
Bicarbonate (mEq/l)
Urine ketones*
Serum ketones*
Effective serum Osmol
(mOsm/kg)†
Alteration in sensoria
or mental obtundation
>250
7.25-7.3
>10
15-18
positive
positive
variable
alert
>250
7.0-<7.24
>12
10- <15
positive
positive
variable
alert/
drowsy
>250
<7.0
>12
<10
positive
positive
variable
stupor/
coma

15. Clinical Presentation of DKA
Sign
Hypothermia
Tachycardia
Tachypnea
Kussmaul breathing
Ileus
Acetone breath
Altered sensorium
Symptoms
Polydipsia
Polyuria
Weakness
Weight loss
Nausea
Vomiting
Abdominal pain
The onset of DKA is usually relative short, ranging from hours
to a day or two.

16. Initial Clinical Evaluation
• History and physical examination
Secure patient’s ABC
Mental status
Cardiovascular-renal status
Source of infection
• Evaluation of volume and hydration status
• Laboratory studies

17. • Immediate determination of blood glucose by finger
stick, and serum ketones (3-BH) by finger stick or
urinary ketones.
• Laboratory studies:
ABG’s
CBC with differential
CMP (glucose, electrolytes, bicarbonate, BUN, creatinine)
Serum ketones
Urinalysis
Bacterial cultures*
Cardiac enzymes*
Initial Laboratory Studies
* If clinically indicated

18. “Typical” Case….. :
Location : Emergency Room
Vital Signs : BP : 90/ 60 mm Hg, HR : 128/ min
regular, Temp : 100F, RR: 30/min rapid and shallow
C/C : Vomiting and Abdominal Pain
HPI : A 20 yr old woman presents to ER with 5
episodes of vomiting, abdominal pain, weakness and
increasing drowsiness of 1 day duration. During the
last 2 months she has noticed increased thirst and
increased urination. The abdominal pain is diffuse, 4-
5/10 in severity, constant, non radiating and there are
no aggravating or relieving factors. Vomiting is non
bloody. She has a family history positive for type 1
diabetes.

19. Typical” Case…..continue :
Lab Results –
Urine Pregnancy test is negative
WBC – 10,000 and normal differential
Na – 129, K – 5, Cl – 90, Ca – 8
RBS – 600
Serum Amylase – mildly elevated
Serum Lipase – WNL
UA showed 4+ sugar, 2+ketones but no evidence of
infection ABG showed metabolic acidosis compensated
by respiratory alkalosis ( Ph 7.3)

20. Clinical Features - History :
 Classic symptoms of hyperglycaemia
Thirst
Polyuria
polydipsia
Nocturia
 Other symptoms
Generalized weakness
Malaise/lethargy, fatigue
Nausea/vomiting
Decreased perspiration
Anorexia or increased appetite
Confusion
 Symptoms of associated infections and conditions
Fever/ Dysuria/ Chills /Chest pain/ Abdominal pain /Shortness of breath

21. Clinical Features – Physical
Examination :
General signs
Ill appearance
Dry skin
Labored respirations
 Dry mucous membranes
Decreased skin turgor
Decreased reflexes

22. Clinical Features – Physical
Examination :
• Vital signs
Tachycardia
Hypotension
Tachypnea
Hypothermia
Fever, if infection
• Specific signs
Ketotic breath (fruity, with acetone smell)
Confusion
Coma
Abdominal tenderness

23. Differential Diagnosis :
Hyperosmolar Hyperglycaemic Nonketotic Coma
Alcoholic Ketoacidosis
Abdominal Pathology like Appendicitis,
Gastroenteritis, Pancreatitis, Acute Intestinal
Obstruction
Pregnancy
Drug Intoxication

24. Work Up – Laboratory Studies :
 Glucose:
 Sodium: The osmotic effect of hyperglycaemia
moves extravascular water to the intravascular
space. For each 100 mg/dL of glucose over 100
mg/dL, the serum sodium level is lowered by
approximately 1.6 mEq/L. When glucose levels fall,
the serum sodium level rises by a corresponding
amount.
 Potassium: This needs to be checked frequently, as
values drop very rapidly with treatment. An ECG
may be used to assess the cardiac effects of
extremes in potassium levels.

25. Work Up – Laboratory Studies :
 Bicarbonate: It is used in conjunction with the anion gap to
assess degree of acidosis.
 Complete blood cell (CBC) count: High white blood cell
(WBC) counts (>15 X 109/L) or marked left shift may
suggest underlying infection.
 Arterial blood gas (ABG) levels: pH is often <7.3. Venous pH
may be used for repeat pH measurement. It has been
studied that pH on a venous blood gas level in patients with
DKA was 0.03 lower than pH on an ABG. Because this
difference is relatively reliable and not of clinical significance,
there is almost no reason to perform the more painful ABG.
End tidal CO2 has been reported as a way to assess acidosis
as well.

26. Work Up – Laboratory Studies :
 Ketones: The Acetest and Ketostix products
measure blood and urine acetone and acetoacetic
acid. They do not measure the more common
ketone body, beta-hydroxybutyrate.
 Beta hydroxybutyrate: Serum or capillary beta
hydroxybutyrate can be used to follow response to
treatment. Levels greater than 0.5 mmol /L are
considered abnormal, and levels of 3 mmol /L
correlate with need for diabetic ketoacidosis (DKA)
treatment.

27. Work Up – Laboratory Studies :
 Urinalysis (UA): Look for glycosuria and urine
ketosis. Use this to detect underlying urinary
infection.
 Osmolality: Measured as 2(Na+) (mEq/L) + glucose
(mg/dL)/18 + BUN(mg/dL)/2.8. Patients with
diabetic ketoacidosis who are in a coma typically
have osmolalities >330 mOsm/kg H2 O. If the
osmolality is less than this in a patient who is
comatose, search for another cause of obtundation.
 Phosphorous: If the patient is at risk
for hypophosphatemia (e.g., poor nutritional status,
chronic alcoholism), then the serum phosphorous
level should be determined.

28. Work Up – Laboratory Studies :
Hyperamylasaemia may be seen, even in the
absence of pancreatitis.
BUN level is increased.
Anion gap is higher than normal.

29. Work Up – Imaging Studies :
 Chest radiography:
To rule out pulmonary infection.
 CT scanning:
The changes of cerebral edema may be seen late on
head imaging and should not delay administration of
hypertonic saline or mannitol in those pediatric cases
where cerebral edema is suspected

30. Work Up – Other Tests :
 Electrocardiography (ECG):
Diabetic ketoacidosis may be precipitated by a cardiac
event, and the physiological disturbances of diabetic
ketoacidosis may cause cardiac complications. An
ECG is also a rapid way to assess
significant hypokalemia or hyperkalemia
 Telemetry:
Consider telemetry in those with comorbidities
(especially cardiac), known significant electrolyte
abnormalities, severe dehydration, or profound
acidosis

31. Cardinal Principles of
management- :
Replace fluids Replace insulin
Correct electrolytes
Treat the cause
Supportive treatment
Prevent complications

32. Typical Therapy - Fluids :
The Fluid of choice to correct dehydration is 0.9% NS
IV
 Administer 1 liter over the first 30 minutes.
 Administer 1 liter over the following 1 hour.
 Administer 1 liter over the following 2 hours.
 Administer 1 liter every 4 hours, depending on the
degree of dehydration and central venous pressure
(CVP) readings.

33. Typical Therapy - Fluids :
 When the glucose levels begin to approach 270 mg/
dl
 Switch to 5 % dextrose, 1 litre 8 hourly.
 If the patient is still dehydrated, continue 0.9 % saline and add 5
% dextrose 1 litre per 12 hours.
 Typical requirement is 6 litres in first 24 hrs but
avoid fluid overload in elderly patients.
 Subsequent fluid replacement should be based on
clinical response including urine output.

34. Typical Therapy - Insulin :
 Insulin Initially an iv bolus of 10- 15 U insulin is
administered.
 This is followed by 50 units soluble insulin in 50 ml
0.9 % saline i.v. via infusion pump.
 6 units / hr initially
 3 units / hr when the blood glucose is < 270 mg / dl
 2 units / hr when the blood glucose is < 180 mg / dl
 Check Blood glucose hourly initially – if no reduction
in first hour, rate of insulin infusion should be
increased.
 The goal should be to decrease blood glucose by
50- 100 mg/dl/hr.

35. Typical Therapy - Potassium :
 Potassium None in first litre of i.v. fluid unless < 3
mmol / L
 If potassium < 3.5 mmol / L, give 40 mmol added
potassium.
 Give in 1 litre of Fluid
 Avoid infusion rate of > 20 mmol / hr
 If potassium is 3.5 – 5 mmol / L, give 20 mmol
added potassium.
 If potassium is > 5 mmol / L, or patient is anuric,
give no potassium.
 Potassium can be given as follows: two thirds as
KCl, one third as KPO4.

36. EKG Changes During DKA

37. Role of - Bicarbonate :
 Administration to acidotic patient generates rapid
rise in CO2
 CO2 enters CNS rapidly
 HCO3- is delayed by blood-brain barrier
 Increased CNS CO2 exacerbates cerebral acidosis
CO2 + H2O H2CO3 H+ + HCO3-
 May also reduce partial pressure of O2 in CSF
>vasoconstriction > brain hypoxia/ischemia

38. Role of - Bicarbonate :
 Not routinely necessary.
 Indicated only in the following cases –
1. Shock or Coma
2. Severe Acidosis ( 6.9- 7.1)
3. Severe depletion of buffer reserve ( HCO3 <5 mEq/l)
4. Acidosis induced cardiac or respiratory dysfunction
5. Severe Hyperkalaemia

39. Procedures :
 Catheterisation if no urine passed after 3 hrs.
 Nasogastric tube to keep stomach empty in
unconscious or semiconscious patients, or if
vomiting is protracted.
 Central Venous line if CVS is compromised to allow
fluid replacement to be adjusted accurately.
 Airway management and Intubation in any patient
with a significantly depressed mental status or with
respiratory distress.

40. Complications :
 Cerebral Edema - The leading cause of diabetic
ketoacidosis (DKA) mortality in children.
The child presents with abnormal response to pain, decorticate
and decerebrate posturing, cranial nerve palsies, abnormal CNS
respiratory patterns, fluctuating level of consciousness,
sustained heart rate deceleration, incontinence, as well as more
nonspecific criteria such as vomiting, headache, lethargy, and
elevated diastolic blood pressure.
Mannitol or hypertonic saline should be available if cerebral
edema is suspected.

41. Complications :
 Hypokalaemia is a complication that is precipitated by failing
to rapidly address the total body potassium deficit brought
out by rehydration and insulin treatment, which not only
reduces acidosis but directly facilitates potassium reentry
into the cell.
 Hypoglycaemia may result from inadequate monitoring of
glucose levels during insulin therapy.
 Acute pulmonary oedema is potentially related to aggressive
or excessive fluid therapy. Although initial aggressive fluid
replacement is necessary in all patients, particular care must
be taken in those with comorbidities such as renal
failure or congestive heart failure.

42. During Discharge :
Discontinue IV Insulin
IVF Regular Insulin
NPH Insulin
Diabetic Diet
Patient Education, Diabetes
Home Glucose Monitoring

43. Thank You for your attention :
Thank you for saving me from DKA

44. Serum Sodium
Hyponatremia is common in patients with DKA
H2O
H2O
H2O
Serum glucose
Na+
H2O
Correction of Serum sodium:
Corrected Na+ = [Na+] 1.6 x glucose (mg/dl) – 100
100

45. Serum Potassium
Admission serum potassium is frequently elevated (due to a
shift of K- from the intracellular to the extracellular space)
K+
Osmolality
Acidosis
K+
Insulin
regulates
Activity of
Na+/K+
pump
Na+
K-
K+ K+
K+

46. Anion Gap Formula
• Anion gap can be measured as
• AG=[(Na)-(Hco3+CL)]

47. Fluid Therapy in DKA
Normal saline, 1-2 L over 1-2 h
NS or ½ NS at 250-500 mL/h
Glucose < 250 mg/dl
D5%1/2NS saline

48. Caution during fluid management
• Fluid should be replace over 12-24hr
• patients are generally depleted 3-6lit in DKA.
• Monitor urine output,heart rate,blood
pressure and respiratory status.
• CARE must b taken in patient with CCF and
kidney disease.

49. Blood Glucose monitoring in DKA
• Check initial blood glucose q1h.Goal decrease
in blood glucose is 50-75mg/dl/hr
• Once stable(3consecutie values decrease in
target range)change blood glucose
monitoringq2h.Resume q1h blood glucose
monitoring for each change in the insulin
infusion rate.
• Add dextrose5% to IV fluid when blood
glucose <250mg/dl.
• For DKA goal blood glucose 150-200mg/dl
until anion gap close.

50. Intravenous Insulin Therapy in DKA
I.V. Bolus: 0.1 U/kg
I.V. drip: 0.1 U/kg/h
Glucose < 250 mg/dl and
HCO3 > 15 mmol/l, then,
I.V. drip: 0.05 – 0.1 U/kg/h
Until c0rrection of anion gap

51. CHANGING THE INSULIN INFUSION
RATE
• Decrease IV insulin by 50%if blood glucose
decrease by >100mg/dl/hr in any 1hr period
• Increase insulin drip by 50%/hr if change in
blood glucose is <50mg/dl/hr
• When blood glucose decrease to 250mg/dl
insulin infusion may need to be decrease
50% to maintain glucose at target levels(150-
200mg/dl).

52. Transition to Subcutaneous Insulin
Patients with DKA should be treated with IV insulin until
ketoacidosis is resolved.
 Criteria for resolution of DKA:
 BG ≤ 200 mg/dL
 Serum bicarbonate level ≥ 18 mEq/L
 Venous pH ≥ 7.3 and anion gap closed

53. WHEN TO STOP IV INSULIN
• Give short acting insulin SC at twice the
hourly IV rate(if iv rate 5u/hr give 10u)
• Failure to give SC insulin may result in
rebound hyperglycemia and ketosis due to its
short acting effect.
• ENSURE pt has a meal and is eating and
awake.

54. Potassium replacement
K+ = > 5.5 mEq/l; no supplemental is required
K+ = 4 - 5 mEq/l; 20 mEq/L of replacement fluid
K+ = 3 - 4 mEq/l; 40 mEq/L of replacement fluid
If admission K+ = <3 mEq/l give 10-20 mEq/h until
K+ >3 mEq/l, then add 40 mEq/L to replacement fluid

55. pH > 7.0  no bicarbonate
pH < 7.0 and bicarbonate < 5 mEq/l  44.6 mEq
in 500 ml 0.45% saline over 1 h until pH > 7.0
Bicarbonate administration

56. Complications of DKA
1-Complications of associated illnesses e.g. sepsis
or MI.
2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly).
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Cardiac arrhythmias.
-Cardiac arrest.
-Respiratory muscle weakness.

57. b-Hypoglycemia.
c-Overhydration and acute pulmonary edema: particularly
in:
-Treating children with DKA.
-Adults with compromised renal or cardiac function.
-Elderly with incipient CHF.

58. d-Neurological complications: Cerebral Edema.
-It occurs mostly in children with DKA.
-Very dangerous and increases mortality.
-The risk is related to the severity, duration and rapid
correction of DKA.
Mechanism: The brain adapts by producing intracellular
osmoles (idiogenic osmoles) which stabilize the brain
cells from shrinking while the DKA was developing.
When the hyperosmolarity is rapidly corrected, the brain
becomes hypertonic towards the extracellular fluids 
water flows into the cells  cerebral edema

59.  Diabetic Ketoacidosis is a common, serious
and expensive complication in patients with
type 1 and type 2 diabetes
 Prevention of metabolic decompensation
through patient education, strict surveillance of
glucose homeostasis and aggressive diabetes
management might reduce the high morbidity
and mortality associated with diabetic
ketoacidosis
Summary

60. HbA1c every 3-6 months
Yearly dilated eye examinations
Annual microalbumin checks
Foot examinations at each visits
Blood pressure < 130/80 mm Hg, lower in
diabetic nephropathy
Statin therapy to reduce low-density
lipoprotein cholesterol
Message to take it home

61. Reference:
ADA guidelines for management of DM 2016
ABEDLRHMAN ALBORHAN MOHAMMED, Ismat. Describe the Various Types of Neuropathy
Observed in Patients with Diabetes. Global Journal of Medical Research, [S.l.], nov. 2016.
Available at: <https://medicalresearchjournal.org/index.php/GJMR/article/view/1217>. Date
accessed: 11 aug. 2018.

62. THANK YOU