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DKADiabetic ketoacidosis
DIAGNOSIS AND TEATEMENT
2/1/2019 DKA BY DR.BAKUNDA 1
Diabetic ketoacidosis (DKA) is an acute, major, life-
threatening 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 paediatic
patients.
2/1/2019 DKA BY DR.BAKUNDA 2
Pathophysiology
Insulin normally elevates cellular uptake of
glucose from the blood
Insulin defciency with rised counter regulatory
hormones (glucagon,cortisol, catecholamines,
GH)
Can occur with lack of insulin (non-adherence,
inadequate dosage, 1st presentation) or
increased stress (surgery, infection, exercise)
2/1/2019 DKA BY DR.BAKUNDA 3
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
2/1/2019 DKA BY DR.BAKUNDA 4
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.
2/1/2019 DKA BY DR.BAKUNDA 5
A total body potassium deficit therefore
develops in the body, although serum
potassium may be normal or even
paradoxically elevated.
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 7
Neurological abnormalities
Altered mental status
Lethargy
coma
Other neurological
exam abnormalities such
as blurred vision and weakness
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 9
Diagnostic
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
2/1/2019 DKA BY DR.BAKUNDA 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)
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 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
2/1/2019 DKA BY DR.BAKUNDA 15
K+ replacement
with insulin administration, hypokalemia may develop
if serum K+<3.3 mmol/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
2/1/2019 DKA BY DR.BAKUNDA 16
Treatment of intercurrent
infection
Start empiric antibiotics
on suspicion of infection
until culture results are
available
2/1/2019 DKA BY DR.BAKUNDA 17
REFERENCES
 www.uptodate.com
www.amboss.com
Toronto Notes 34th
Edition
http://www.moh.gov.r
w/fileadmin/templates
/Clinical/Internal-
Medicine-Clinical-
Treatment-Guidelines-
9-10-2012-1.pdf
Kumar and Clark's
Clinical Medicine, 9th
Edition
2/1/2019 DKA BY DR.BAKUNDA 18

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Dka

  • 1. DKADiabetic ketoacidosis DIAGNOSIS AND TEATEMENT 2/1/2019 DKA BY DR.BAKUNDA 1
  • 2. Diabetic ketoacidosis (DKA) is an acute, major, life- threatening 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 paediatic patients. 2/1/2019 DKA BY DR.BAKUNDA 2
  • 3. Pathophysiology Insulin normally elevates cellular uptake of glucose from the blood Insulin defciency with rised counter regulatory hormones (glucagon,cortisol, catecholamines, GH) Can occur with lack of insulin (non-adherence, inadequate dosage, 1st presentation) or increased stress (surgery, infection, exercise) 2/1/2019 DKA BY DR.BAKUNDA 3
  • 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 2/1/2019 DKA BY DR.BAKUNDA 4
  • 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. 2/1/2019 DKA BY DR.BAKUNDA 5
  • 6. A total body potassium deficit therefore develops in the body, although serum potassium may be normal or even paradoxically elevated. 2/1/2019 DKA BY DR.BAKUNDA 6
  • 7. 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 2/1/2019 DKA BY DR.BAKUNDA 7
  • 8. Neurological abnormalities Altered mental status Lethargy coma Other neurological exam abnormalities such as blurred vision and weakness 2/1/2019 DKA BY DR.BAKUNDA 8
  • 9. Rapid onset (< 24 h) Abdominal pain Fruity odor on the breath (from exhaled acetone) Hyperventilation: Kussmaul respirations: deep breaths at a normal respiratory rate 2/1/2019 DKA BY DR.BAKUNDA 9
  • 10. Diagnostic 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 2/1/2019 DKA BY DR.BAKUNDA 10
  • 11. 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) 2/1/2019 DKA BY DR.BAKUNDA 11
  • 12. 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 2/1/2019 DKA BY DR.BAKUNDA 12
  • 13. 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 2/1/2019 DKA BY DR.BAKUNDA 13
  • 14. 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 2/1/2019 DKA BY DR.BAKUNDA 14
  • 15. 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 2/1/2019 DKA BY DR.BAKUNDA 15
  • 16. K+ replacement with insulin administration, hypokalemia may develop if serum K+<3.3 mmol/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 2/1/2019 DKA BY DR.BAKUNDA 16
  • 17. Treatment of intercurrent infection Start empiric antibiotics on suspicion of infection until culture results are available 2/1/2019 DKA BY DR.BAKUNDA 17
  • 18. REFERENCES  www.uptodate.com www.amboss.com Toronto Notes 34th Edition http://www.moh.gov.r w/fileadmin/templates /Clinical/Internal- Medicine-Clinical- Treatment-Guidelines- 9-10-2012-1.pdf Kumar and Clark's Clinical Medicine, 9th Edition 2/1/2019 DKA BY DR.BAKUNDA 18

Editor's Notes

  1. acetoacetic acid and beta-hydroxybutyric acid
  2. Increase in BG by 10 mmol/L there is a decreases in Na+ by 3 mmol/L Osmolarity (increased to >290 mOsm/L) Calculation = 2 (Na + K) + urea/3 + glucose(mg/dl)/18 Anion gap (elevated) Calculation = ([Na + K] - [Cl + HCO3] >13 mEq/L)
  3. Te maximum decrease rate of glucose is 100 mg/dL/h Blood glucose should not fall below 200 mg/dl during the frst 6 hours Serum anion gap reduced to normal (12 ± 2 mEq/L), or serum BOHB ≤1 mmol/L (10.4 mg/dL) Venous pH >7.30, or serum bicarbonate (HCO3) >15 mEq/L ● Blood glucose <200 mg/dL (11.1 mmol/L) ● Patient is tolerating oral intake