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A K M A S U D A I
DIABETIC KETOACIDOSIS
 Diabetic ketoacidosis (DKA) is an acute, major,
lifethreatening complication of diabetes that mainly
occurs in patients with type 1 diabetes, but it can
occur in some patients with type 2 diabetes.
 DKA is a complex disordered metabolic state
characterized by hyperglycemia, ketoacidosis, and
ketonuria.
 DKA has high morbidity and mortality in paediatric
patients.
PATHOPHYSIOLOGY
 Insulin normally elevates cellular uptake of glucose
from the blood
 Insulin deficiency with raised counter regulatory
hormones (glucagon, cortisol, catecholamines, GH)
 Can occur with lack of insulin (non-adherence,
inadequate dosage,1 st presentation) or increased
stress (surgery, infection, exercise)
 Unopposed hepatic glucose production
hyperglycemia cause osmotic diuresis then
dehydration and electrolyte disturbance Na+ (water
shift to ECF causing pseudohyponatremia)
 Fat mobilization increases FFA then ketoacids then
metabolic acidosis
 As a result of hyperglycemic hyperosmolality,
potassium shifts along with water from inside cells
to the extracellular space and is lost in the urine.
 Insulin normally promotes cellular potassium
uptake but is absent in DKA, compounding the
problem.
 A total body potassium deficit therefore develops in
the body, although serum potassium may be
normal or even paradoxically elevated.
SIGNS AND SYMPTOMS
 Polyuria ,Polydipsia
 Recent weight loss
 Nausea and vomiting
 Signs of volume depletion (i.e., dry mucous
membranes, decreased skin turgor), hypotension,
circulatory collapse
Neurological abnormalities
 Altered mental status
 Lethargy
 coma
 Other neurological exam abnormalities such as
blurred vision and weakness
 Rapid onset (< 24 h)
 Abdominal pain
 Fruity odor on the breath (from exhaled acetone)
 Hyperventilation: Kussmaul respirations: deep
breaths at a normal respiratory rate
DIAGNOSTICS
Initial approach
 ABCs: airway, breathing, and circulation
 Mental status check
 Fingerstick glucose
 History (taken from family members or friends if
need be), including possible precipitating factors
Diagnostic tests
 ◦ ↑ Serum glucose(< 600 mg/dL > 250 mg/dL
,Urine ketones Serum electrolytes, including
bicarbonate (with anion gap calculation)
 ◦ Hypertonic hyponatremia
 ◦ But if fluid loss due to osmotic diuresis is not
replaced, hypernatremia
 ◦ serum bicarbonate is reduced
 ◦ Urine dipstick with increased glucose and ketones
 ◦ Osmolarity (increased to >290 mOsm/L)
Additional tests
 Indications: may be ordered to rule out serious
precipitating factors, such as myocardial infarction,
pneumonia, or pancreatitis
 ↑ Blood urea nitrogen (BUN) and creatinine
 Full blood count, ABG
 Blood or urine cultures
 ECG
 Chest x-ray
MANAGEMENT
Principles
 Admission in high dependency area of Medical Ward
or ICU.
 Correction of fluid loss with intravenous fluids
 Correction of hyperglycemia with insulin
 Correction of electrolyte disturbances, particularly
hypokalemia
 Correction of acid-base balance but most of time
corrected with above mentioned measures
 Treatment of concurrent infection, if present
Correction of fluid loss
 Normal Saline or Ringer’s Lactate
 Administer 1-3 L during the first hour
 Administer 1 L during the second hour
 Administer 1 L during the following 2 hours
 Administer 1 L every 4 hours, depending on the
degree of dehydration
Correction of hyperglycemia
 critical to resolve acidosis, not only hyperglycemia
 Do not use with hypokalemia , until serum K+ is
corrected to >3.3 mmol/L
 – short-acting insulin(R)
 – maintain on 0.1 U/kg/h insulin R infusion
 – check serum glucose hourly
 If blood glucose stable and urine ketones negative,
then stop insulin infusion and start standard insulin
regimen
K+ replacement
 with insulin administration, hypokalemia may
develop
 If serum k+ <3.3mmol/L, hold insulin and give 40
mEq/L K+ replacement
 if serum K+3.3-4.5 mmol/L, give 20 mEq/L K+
replacement
 when K+ 4.5-6.0 mmol/L add KCL 10 mEq/L IV
fluid to keep K+ in the range of 3.5-5 mEq/L
Treatment of intercurrent infection
 Start empiric antibiotics on suspicion of infection
until culture results are available
REFERENCES
• Davidson’s Principles & Practice of Medicine- 21st
edition.
• Harrison’s Principles of internal Medicine-10th &
17th edition.
• Current Medical Diagnosis & Treatment – 2014
edition.
 THANK YOU

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Diabetic ketoacidosis [DK]

  • 1. A K M A S U D A I DIABETIC KETOACIDOSIS
  • 2.  Diabetic ketoacidosis (DKA) is an acute, major, lifethreatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it can occur in some patients with type 2 diabetes.  DKA is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.  DKA has high morbidity and mortality in paediatric patients.
  • 3. PATHOPHYSIOLOGY  Insulin normally elevates cellular uptake of glucose from the blood  Insulin deficiency with raised counter regulatory hormones (glucagon, cortisol, catecholamines, GH)  Can occur with lack of insulin (non-adherence, inadequate dosage,1 st presentation) or increased stress (surgery, infection, exercise)
  • 4.  Unopposed hepatic glucose production hyperglycemia cause osmotic diuresis then dehydration and electrolyte disturbance Na+ (water shift to ECF causing pseudohyponatremia)  Fat mobilization increases FFA then ketoacids then metabolic acidosis
  • 5.  As a result of hyperglycemic hyperosmolality, potassium shifts along with water from inside cells to the extracellular space and is lost in the urine.  Insulin normally promotes cellular potassium uptake but is absent in DKA, compounding the problem.  A total body potassium deficit therefore develops in the body, although serum potassium may be normal or even paradoxically elevated.
  • 6. SIGNS AND SYMPTOMS  Polyuria ,Polydipsia  Recent weight loss  Nausea and vomiting  Signs of volume depletion (i.e., dry mucous membranes, decreased skin turgor), hypotension, circulatory collapse
  • 7. Neurological abnormalities  Altered mental status  Lethargy  coma  Other neurological exam abnormalities such as blurred vision and weakness
  • 8.  Rapid onset (< 24 h)  Abdominal pain  Fruity odor on the breath (from exhaled acetone)  Hyperventilation: Kussmaul respirations: deep breaths at a normal respiratory rate
  • 9. DIAGNOSTICS Initial approach  ABCs: airway, breathing, and circulation  Mental status check  Fingerstick glucose  History (taken from family members or friends if need be), including possible precipitating factors
  • 10. Diagnostic tests  ◦ ↑ Serum glucose(< 600 mg/dL > 250 mg/dL ,Urine ketones Serum electrolytes, including bicarbonate (with anion gap calculation)  ◦ Hypertonic hyponatremia  ◦ But if fluid loss due to osmotic diuresis is not replaced, hypernatremia  ◦ serum bicarbonate is reduced  ◦ Urine dipstick with increased glucose and ketones  ◦ Osmolarity (increased to >290 mOsm/L)
  • 11. Additional tests  Indications: may be ordered to rule out serious precipitating factors, such as myocardial infarction, pneumonia, or pancreatitis  ↑ Blood urea nitrogen (BUN) and creatinine  Full blood count, ABG  Blood or urine cultures  ECG  Chest x-ray
  • 12. MANAGEMENT Principles  Admission in high dependency area of Medical Ward or ICU.  Correction of fluid loss with intravenous fluids  Correction of hyperglycemia with insulin  Correction of electrolyte disturbances, particularly hypokalemia  Correction of acid-base balance but most of time corrected with above mentioned measures  Treatment of concurrent infection, if present
  • 13. Correction of fluid loss  Normal Saline or Ringer’s Lactate  Administer 1-3 L during the first hour  Administer 1 L during the second hour  Administer 1 L during the following 2 hours  Administer 1 L every 4 hours, depending on the degree of dehydration
  • 14. Correction of hyperglycemia  critical to resolve acidosis, not only hyperglycemia  Do not use with hypokalemia , until serum K+ is corrected to >3.3 mmol/L  – short-acting insulin(R)  – maintain on 0.1 U/kg/h insulin R infusion  – check serum glucose hourly  If blood glucose stable and urine ketones negative, then stop insulin infusion and start standard insulin regimen
  • 15. K+ replacement  with insulin administration, hypokalemia may develop  If serum k+ <3.3mmol/L, hold insulin and give 40 mEq/L K+ replacement  if serum K+3.3-4.5 mmol/L, give 20 mEq/L K+ replacement  when K+ 4.5-6.0 mmol/L add KCL 10 mEq/L IV fluid to keep K+ in the range of 3.5-5 mEq/L
  • 16. Treatment of intercurrent infection  Start empiric antibiotics on suspicion of infection until culture results are available
  • 17. REFERENCES • Davidson’s Principles & Practice of Medicine- 21st edition. • Harrison’s Principles of internal Medicine-10th & 17th edition. • Current Medical Diagnosis & Treatment – 2014 edition.