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DIABETICS
KETOACIDOSIS
Intern Anup
13TH Batch KUSMS
• DKA is an acute, life threatening medical emergency
• Occurs in both type1 (more common) and type 2 diabetic
patients
PRECIPITATING FACTORS:
-Infection (pneumonia, UTI, sepsis, gastroenteritis)
-inadequate insulin treatment or noncompliance
-infraction (cerebral, coronary, mesenteric, peripheral)
-severe stress (physical, emotional)
-hyperthyroidism, pheochromocytoma
-drugs( thiazides, steroids, cocaine)
-pregnancy
CARDINAL BIOCHEMICAL FEATURES
(triad of hyperglycemia, high anion gap metabolic acidosis
and ketonemia)
PATHOPHYSIOLOGY
- Occurs as a consequences of absolute or relative insuline
deficiency that is accompanied by an increase in counter-
regulatory hormones ( glucagon, cortisol, growth
hormone, epinephrine).
- This imbalance enhances hepatic gluconeogenesis,
glycogenolysis, lipolysis and ketogenesis.
- Two ketone bodies namely acetoacetic acid and B-
hydroxybutyric acid are strong acid and are responsible
for acidotic state.
INVESTIGATIONS
Investigations shouldnot delay the institution of IVF and
insulin replacement.
URINE TESTS:
-Urine R/E (shows glucose in urine)
-Urine Ketone
BLOOD TESTS:
-Blood glucose, RFT( Ur, Cr, Na, K)
-Arterial Blood Gas Analysis
INFECTION SCREEN:
-Full blood count, blood and urine culture, CRP, C-XR
TREATMENT OF DKA
The goals of therapy:
1. Improvement of circulatory volume and tissue perfusion
2. Gradual reduction of serum glucose and osmolality
3. Correction of electrolyte imbalance
4. Identification and prompt treatment of co-morbid
precipitating causes
5. Frequent monitoring of patients by clinical and
laboratory parameters
Fluid Therapy
• DKA is volume-depleted states with total body water
deficit of approximately 6 L
• Use of isotonic saline at the rate of 15–20 ml /kg body
weight per hour or 1–1.5 L during the first hour
• hypernatremic or eunatremic condition 0.45% NaCl is
infused
• Recommended schedule:
- administer 1-3 litre over 1st hour
- 1 litre during second hour
- 1 litre during following 2 hour
- 1 litre every 4 hours depending on the degree of
dehydration state and CVP
Insulin Therapy
-Insulin should only be started after serum potassium value is >
3.3 mmol/L
-IV bolus of regular insulin (0.1 u/kg body weight) followed by a
continuous infusion of regular insulin at the dose of 0.1u/kg/hr.
-The optimal rate of glucose reduction is between 50-70 mg/hr. If
desirable glucose reduction is not achieved in the first hour, an
additional insulin bolus at 0.1 u/kg can be given
-when plasma glucose reaches 200-250 mg/dL , insulin rate
should be decreased to 0.05 U/kg/hr and IVF is changed to D5
½ NS.
-Revert to S/C insulin after patient begins to eat (iv insulin
infusion is continued for 1-2 hrs)
Potassium Therapy
-If the initial serum potassium is below 3.3 mEq/L, IV
potassium chloride is started with saline (20-40 mEq/hour)
-if the initial serum potassium is between 3.3 and 5.3
mEq/L, IV KCL (20-30 mEq) is added to each litre of Iv
replacement fluid and continued until serum potassium
concentration has increased to 4.0-5.0 mEq/L range
-If the serum potassium is initially >5.3 mEq/L, then
potassium replacement should be delayed
CORRECTION OF ACIDOSIS
-The use of bicarbonate in treatment of DKA remains
controversial (A/E- hypokalemia, decreased tissue oxygen
uptake and cerebral edema)
-If arterial pH < 6.9 bicarbonate should be given :100 mmol
sodium bicarbonate in 400 ml isotonic solution over 2
hours and repeat dose until pH>7.0
MONITORING
• capillary blood glucose and ketone: hourly
• Venous bicarbonate and potassium: after 1 and 2 hrs then
every 2 hrly
• Plasma electrolytes: every 4 hrly
• Clinical monitoring of O2 saturation, pulse, BP, RR and
urine output every hourly
ADDITIONAL
• Treatment of any precipitating factors
• Catheterisation if no urine passed after 3 hrs
• Measure ABG and repeat C-XR if O2 saturation < 92%
• ECG monitoring in severe case
HYPERGLYCEMIC HYPEROSMOLAR STATE
-severe hyperglycaemia (>600 mg/dl or 30 mmol/l)
-Hyperosmolality (serum osmolality >320 mOsm/kg)
-Dehydration
Absence of significant hyperketonaemia (<3 mmol/l) or
acidosis (PH>7.3, bicarbonate >15 mmol/l)
Onset is insidious, presents with a several week history of
polyuria, weight loss and diminished oral intake (dka <24
hrs)
Management
FLUID REPLACEMENT:
1-3 litres of NS over first 2-3 hours
After the patient is hemodynamically stable free
water defecit (9-10 litre) is reverse over next 1-2
days with 0.45% saline
When blood glucose reaches 250 mg/dl IVF is
changed to D5 ½ NS.
INSULIN:
IV bolus of regular insulin (0.1 u/kg body weight) followed
by a continuous infusion of regular insulin at the dose of
0.1u/kg/hr
when plasma glucose reaches 200-250 mg/dL , insulin rate
should be decreased to 0.05 U/kg/hr
Infusion is continued until patient has resumed eating and
can be transferred to a S/C regimen
PPT agents should be treated
Potassium correction
DKA

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DKA

  • 2. • DKA is an acute, life threatening medical emergency • Occurs in both type1 (more common) and type 2 diabetic patients PRECIPITATING FACTORS: -Infection (pneumonia, UTI, sepsis, gastroenteritis) -inadequate insulin treatment or noncompliance -infraction (cerebral, coronary, mesenteric, peripheral) -severe stress (physical, emotional) -hyperthyroidism, pheochromocytoma -drugs( thiazides, steroids, cocaine) -pregnancy
  • 3. CARDINAL BIOCHEMICAL FEATURES (triad of hyperglycemia, high anion gap metabolic acidosis and ketonemia)
  • 4. PATHOPHYSIOLOGY - Occurs as a consequences of absolute or relative insuline deficiency that is accompanied by an increase in counter- regulatory hormones ( glucagon, cortisol, growth hormone, epinephrine). - This imbalance enhances hepatic gluconeogenesis, glycogenolysis, lipolysis and ketogenesis. - Two ketone bodies namely acetoacetic acid and B- hydroxybutyric acid are strong acid and are responsible for acidotic state.
  • 5.
  • 6.
  • 7.
  • 8. INVESTIGATIONS Investigations shouldnot delay the institution of IVF and insulin replacement. URINE TESTS: -Urine R/E (shows glucose in urine) -Urine Ketone BLOOD TESTS: -Blood glucose, RFT( Ur, Cr, Na, K) -Arterial Blood Gas Analysis INFECTION SCREEN: -Full blood count, blood and urine culture, CRP, C-XR
  • 9. TREATMENT OF DKA The goals of therapy: 1. Improvement of circulatory volume and tissue perfusion 2. Gradual reduction of serum glucose and osmolality 3. Correction of electrolyte imbalance 4. Identification and prompt treatment of co-morbid precipitating causes 5. Frequent monitoring of patients by clinical and laboratory parameters
  • 10.
  • 11. Fluid Therapy • DKA is volume-depleted states with total body water deficit of approximately 6 L • Use of isotonic saline at the rate of 15–20 ml /kg body weight per hour or 1–1.5 L during the first hour • hypernatremic or eunatremic condition 0.45% NaCl is infused • Recommended schedule: - administer 1-3 litre over 1st hour - 1 litre during second hour - 1 litre during following 2 hour - 1 litre every 4 hours depending on the degree of dehydration state and CVP
  • 12. Insulin Therapy -Insulin should only be started after serum potassium value is > 3.3 mmol/L -IV bolus of regular insulin (0.1 u/kg body weight) followed by a continuous infusion of regular insulin at the dose of 0.1u/kg/hr. -The optimal rate of glucose reduction is between 50-70 mg/hr. If desirable glucose reduction is not achieved in the first hour, an additional insulin bolus at 0.1 u/kg can be given -when plasma glucose reaches 200-250 mg/dL , insulin rate should be decreased to 0.05 U/kg/hr and IVF is changed to D5 ½ NS. -Revert to S/C insulin after patient begins to eat (iv insulin infusion is continued for 1-2 hrs)
  • 13. Potassium Therapy -If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride is started with saline (20-40 mEq/hour) -if the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCL (20-30 mEq) is added to each litre of Iv replacement fluid and continued until serum potassium concentration has increased to 4.0-5.0 mEq/L range -If the serum potassium is initially >5.3 mEq/L, then potassium replacement should be delayed
  • 14. CORRECTION OF ACIDOSIS -The use of bicarbonate in treatment of DKA remains controversial (A/E- hypokalemia, decreased tissue oxygen uptake and cerebral edema) -If arterial pH < 6.9 bicarbonate should be given :100 mmol sodium bicarbonate in 400 ml isotonic solution over 2 hours and repeat dose until pH>7.0
  • 15. MONITORING • capillary blood glucose and ketone: hourly • Venous bicarbonate and potassium: after 1 and 2 hrs then every 2 hrly • Plasma electrolytes: every 4 hrly • Clinical monitoring of O2 saturation, pulse, BP, RR and urine output every hourly
  • 16. ADDITIONAL • Treatment of any precipitating factors • Catheterisation if no urine passed after 3 hrs • Measure ABG and repeat C-XR if O2 saturation < 92% • ECG monitoring in severe case
  • 17. HYPERGLYCEMIC HYPEROSMOLAR STATE -severe hyperglycaemia (>600 mg/dl or 30 mmol/l) -Hyperosmolality (serum osmolality >320 mOsm/kg) -Dehydration Absence of significant hyperketonaemia (<3 mmol/l) or acidosis (PH>7.3, bicarbonate >15 mmol/l) Onset is insidious, presents with a several week history of polyuria, weight loss and diminished oral intake (dka <24 hrs)
  • 18.
  • 19. Management FLUID REPLACEMENT: 1-3 litres of NS over first 2-3 hours After the patient is hemodynamically stable free water defecit (9-10 litre) is reverse over next 1-2 days with 0.45% saline When blood glucose reaches 250 mg/dl IVF is changed to D5 ½ NS.
  • 20. INSULIN: IV bolus of regular insulin (0.1 u/kg body weight) followed by a continuous infusion of regular insulin at the dose of 0.1u/kg/hr when plasma glucose reaches 200-250 mg/dL , insulin rate should be decreased to 0.05 U/kg/hr Infusion is continued until patient has resumed eating and can be transferred to a S/C regimen PPT agents should be treated Potassium correction