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MANAGEMENT OF DIABETIC
KETOACIDOSIS
KEERTHIKA.V
1 ST YEAR
PERIODONTICS AND IMPLANTOLOGY
CONTENTS
 Introduction
 Causes
 Pathophysiology
 Symptoms
 Diagnosis
 Management
DIABETIC KETOACIDOSIS
 Diabetic ketoacidosis is an acute, major, life-threatening complication of
diabetes.DKA mainly occurs in patient with type I diabetes, but it is also not
uncommon in some patients with type 2diabetes.
 Also it can be the very initial presentation of the previously undiagnosed pt with
type 1 diabetic mellitus.
 This condition is a complex disordered metabolic state characterized by
hyperglycemia, ketoacidosis, and ketouria.
CAUSES OF DKA
TYPE I DIABETIC MELLITUS
 In 25% of patients, DKA is present at
diagnosis of type 1 diabetes due to
acute insulin deficiency.
 Poor compliance with insulin.
 Bacterial infection and recurrent
illness[eg,urinary tract infection[UTI],
vomiting]
 Medical,surgical, or emotional stress.
 Idiopathic
TYPE II DIABETIC
MELLITUS
 Intercurrent illness [eg.myocardial
infarction,pneumonia,prostatitis,UTI].
 Medication[eg,corticosteroids,pentami
dine,clozapine.]
 Diabetic ketoacidosis[DKA] usually evolves rapidly, over 24-hr period.
 The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and
weight loss
 Dehydration
 Acidotic [Kussmaul’s]breathing, with a fruity smell[acetone].
 Abdominal pain or distension.
 Vomiting.
 An altered mental status ranging from disorientation to coma.
 Blood pressure and pulse.
 Temperature.
TO DIAGNOSE DKA ,THE FOLLOWING CRITERIA MUST BE FULFILLED.
The American Diabetes association diagnostic criteria for DKA are as follow:
 Elevated serum glucose level
 An elevated serum ketone level.
 A PH less than 7.3 and
 A serum bicarbonate level less than 18 mEq per L
MANAGEMENT
PRINCIPLES OF MANAGEMENT OF DIABETIC
KETOACIDOSIS
 Rapid correction of dehydration.
 Rapidly acting regular insulin,early and enough.
 Correction of acidosis.
 Treatment of precipitating cause, if found.
 Correction of hypokalemia and hypophosphatemia.
 Nursing management.
 Measure capillary glucose every 1-2 h and electrolytes every 4h for 24h.
DKA
INSULIN
BICARBONATES
INFUSION
ELECTROLYTES FLUIDS
FLUID
REPLACEMENT
FLUID REPLACEMENT
 Determine hydration status:
Hypovolemic shock
Administer 0.9% saline, Ringer’s lactate or a plasma expander as a bolus dose of
15-20 ml/kg. This can be repeated if the state of shock persists.
 Dehydration without shock ;
1. Adminster 0.9% Saline4-14 ml/kg/hr for an initial hr, to restore blood volume and
renal perfusion.
2. If serum sodium is high or normal start with 0.45% saline.
When serum glucose reaches 250mg/dl change fluid to 5% dextrose with 0.45% saline,at a
rate that allow complete restoration in 48 hrs, and to maintain glucose at 150-250
mg/dl.
INSULIN THERAPY
 Start regular insulin 0.5 unit/kg as IV Bolus.
 Start infusing regular insulin at a rate of 0.1%/kg/hr using a syringe pump.Optimally,
serum glucose should decrease in a rate no faster than 100mg/dl/hr.
 If serum glucose falls <200 prior to correction of acidosis, change IV fluid from D5 to
D10, but don’t decrease the rate of insulin infusion.
CORRECTION OF ELECTROLYTE IMBALANCE
 Regardless of K conc.at presentation,total body K is low.So, as soon as the
urine output is restored potassium supplementation must be added to Iv fluid at
a conc. Of 20-40 mmol/l, where 50% of it given as KCL, and the rest as
potassium phosphate, this will provide phosphate for repalcement, and avoids
excess phosphate[may precipitate hypocalcaemia].
POTASSIUM AND PHOSPHATE
 If k conc.<3.3mEq/l,administer 40mEq/l of KCL in IV saline over 1
hr.Withhold insulin until K conc.becomes >3.3mEq/l and moniter K
conc.hourly.
 If serum potassium is 5 or more,do not give potassium recheck in every2 hrs.
 If initial potassium is > 3.3 but < 5mEq/l give 20-30mEq/l of K in each liter in
each liter of Iv fluids[2/3 as KCL and 1/3 as KPO4 to keep K to 4-5mEq/l].
BICARBONATE
 If ph<6.9
Bicarbonate [100 osmol] dilute in 400 ml of H2O.infused at 200 ml/h.
 If ph <6.9-7.0
Bicarbonate [50 osmol] dilute in 200ml of H2O.
Infused at 200ml/h
 If ph >7
No bicarbonate.
MONITORING
 A flow chart must be used to moniter fluid balance and lab measures.
 Serum glucose must be measured hourly.
 Electrolyte also 2-3 hourly.
 Ca,Mg,and phosphate must be measured initially and atleast once during
therapy.
 Neurological and mental state must examined frequently and any complaints of
headache or deterioration of mental status should prompt rapid evaluation for
possible cerebral edema.
…

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DIABETIC MELLITUS -MANAGEMENT OF DIABETIC KETOACIDOSIS 'PHARM'.pptx

  • 1. MANAGEMENT OF DIABETIC KETOACIDOSIS KEERTHIKA.V 1 ST YEAR PERIODONTICS AND IMPLANTOLOGY
  • 2. CONTENTS  Introduction  Causes  Pathophysiology  Symptoms  Diagnosis  Management
  • 3. DIABETIC KETOACIDOSIS  Diabetic ketoacidosis is an acute, major, life-threatening complication of diabetes.DKA mainly occurs in patient with type I diabetes, but it is also not uncommon in some patients with type 2diabetes.  Also it can be the very initial presentation of the previously undiagnosed pt with type 1 diabetic mellitus.  This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketouria.
  • 4. CAUSES OF DKA TYPE I DIABETIC MELLITUS  In 25% of patients, DKA is present at diagnosis of type 1 diabetes due to acute insulin deficiency.  Poor compliance with insulin.  Bacterial infection and recurrent illness[eg,urinary tract infection[UTI], vomiting]  Medical,surgical, or emotional stress.  Idiopathic TYPE II DIABETIC MELLITUS  Intercurrent illness [eg.myocardial infarction,pneumonia,prostatitis,UTI].  Medication[eg,corticosteroids,pentami dine,clozapine.]
  • 5.
  • 6.
  • 7.
  • 8.  Diabetic ketoacidosis[DKA] usually evolves rapidly, over 24-hr period.  The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss
  • 9.  Dehydration  Acidotic [Kussmaul’s]breathing, with a fruity smell[acetone].  Abdominal pain or distension.  Vomiting.  An altered mental status ranging from disorientation to coma.  Blood pressure and pulse.  Temperature.
  • 10. TO DIAGNOSE DKA ,THE FOLLOWING CRITERIA MUST BE FULFILLED. The American Diabetes association diagnostic criteria for DKA are as follow:  Elevated serum glucose level  An elevated serum ketone level.  A PH less than 7.3 and  A serum bicarbonate level less than 18 mEq per L
  • 11.
  • 12. MANAGEMENT PRINCIPLES OF MANAGEMENT OF DIABETIC KETOACIDOSIS  Rapid correction of dehydration.  Rapidly acting regular insulin,early and enough.  Correction of acidosis.  Treatment of precipitating cause, if found.  Correction of hypokalemia and hypophosphatemia.  Nursing management.  Measure capillary glucose every 1-2 h and electrolytes every 4h for 24h.
  • 15. FLUID REPLACEMENT  Determine hydration status: Hypovolemic shock Administer 0.9% saline, Ringer’s lactate or a plasma expander as a bolus dose of 15-20 ml/kg. This can be repeated if the state of shock persists.
  • 16.  Dehydration without shock ; 1. Adminster 0.9% Saline4-14 ml/kg/hr for an initial hr, to restore blood volume and renal perfusion. 2. If serum sodium is high or normal start with 0.45% saline. When serum glucose reaches 250mg/dl change fluid to 5% dextrose with 0.45% saline,at a rate that allow complete restoration in 48 hrs, and to maintain glucose at 150-250 mg/dl.
  • 18.  Start regular insulin 0.5 unit/kg as IV Bolus.  Start infusing regular insulin at a rate of 0.1%/kg/hr using a syringe pump.Optimally, serum glucose should decrease in a rate no faster than 100mg/dl/hr.  If serum glucose falls <200 prior to correction of acidosis, change IV fluid from D5 to D10, but don’t decrease the rate of insulin infusion.
  • 19. CORRECTION OF ELECTROLYTE IMBALANCE  Regardless of K conc.at presentation,total body K is low.So, as soon as the urine output is restored potassium supplementation must be added to Iv fluid at a conc. Of 20-40 mmol/l, where 50% of it given as KCL, and the rest as potassium phosphate, this will provide phosphate for repalcement, and avoids excess phosphate[may precipitate hypocalcaemia].
  • 20. POTASSIUM AND PHOSPHATE  If k conc.<3.3mEq/l,administer 40mEq/l of KCL in IV saline over 1 hr.Withhold insulin until K conc.becomes >3.3mEq/l and moniter K conc.hourly.  If serum potassium is 5 or more,do not give potassium recheck in every2 hrs.  If initial potassium is > 3.3 but < 5mEq/l give 20-30mEq/l of K in each liter in each liter of Iv fluids[2/3 as KCL and 1/3 as KPO4 to keep K to 4-5mEq/l].
  • 21. BICARBONATE  If ph<6.9 Bicarbonate [100 osmol] dilute in 400 ml of H2O.infused at 200 ml/h.  If ph <6.9-7.0 Bicarbonate [50 osmol] dilute in 200ml of H2O. Infused at 200ml/h  If ph >7 No bicarbonate.
  • 22. MONITORING  A flow chart must be used to moniter fluid balance and lab measures.  Serum glucose must be measured hourly.  Electrolyte also 2-3 hourly.  Ca,Mg,and phosphate must be measured initially and atleast once during therapy.  Neurological and mental state must examined frequently and any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema.
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