Diabetes ketoacidosis(DKA)
Dr. Chalachew T.(Emergency and Critical Care
Medicine Physician
Course outline
• Objectives
• Introduction
• Precipitating factors
• Clinical presentation
• Investigation
• Treatment
• Disposition
• Summary
Learning objectives
• By the end of this session, participants will be
able to:
– Define diabetic ketoacidosis
– Describe the clinical features of DKA
– Diagnose DKA
– Manage DKA according to the standard protocol
Introduction
• Diabetic ketoacidosis(DKA)
– A metabolic disorder characterized by the triad of
• Hyperglycemia
• Anion gap metabolic acidosis (increased anion gap)
• Ketonemia.
– serious complication of diabetes mellitus
– occurs when uncontrolled blood sugar rises and
the body can’t produce enough insulin to use the
glucose.
Precipitating factors
• The most common precipitating factors
– Infection
– Discontinuation of insulin treatment
Other precipitating factors
– Acute major illnesses such as MI, CVA, or
pancreatitis.
– New onset type 1 diabetes
– Drugs (glucocorticoids, higher dose thiazide
diuretics, sympathomimetic agents (e.g.,
dobutamine and terbutaline).
– Cocaine use ..etc
Clinical presentation
• Directly related to the three primary
metabolic derangements
– hyperglycemia,
– volume depletion
– acidosis.
• Symptoms
– Nausea/vomiting ,Thirst/polyuria, Abdominal pain,
Shortness of breath etc
Clinical presentation
• Physical Findings
– Tachycardia
– Dehydration/hypotension
– Tachypnea / Kussmaul respirations/respiratory
distress
– Abdominal tenderness (may resemble acute
pancreatitis or surgical abdomen)
– Lethargy/obtundation/cerebral edema/possibly
coma
Investigation
• Serum Glucose:
– The serum glucose will be elevated(>200mg/dl)
• Serum bicarbonate
– is frequently <10 mmol/L
• Arterial PH
– ranges between 6.8 and 7.3- depending on the
severity of the acidosis
Investigation…
– sodium, chloride, phosphorus, and magnesium are
reduced in DKA.
• are not accurately reflected by their levels in the serum
because of dehydration and hyperglycemia.
– Renal function test-
• Elevated blood urea nitrogen (BUN) and serum
creatinine levels
– reflect intravascular volume depletion.
Treatment
• Stabilize ABC of life
• Fluid management
• Insulin
• K+ repletion
• Treatment of precipitating factors
• Monitoring
• Long term management
Treatment
General measures
Stabilize the ABC of life
 Obtain IV access
Monitor RBS every hour ,urine ketone every 2-4
hrs
Identify and treat Precipitating cause of DKA
Treatment…
Repletion of fluid deficit
 The usual fluid deficit is about 3-6 liters
 Give as much NS/RL rapidly for a patient in shock
In general
 The first 2 L over 0 - 2 hours
 The next 2 L over 2 - 6 hours
 Then 2 L more over 6 -12 hours.
 Change the fluid to DNS when blood sugar falls to
below 250
 Replace ongoing fluid loss
Treatment..
Repletion of K+ deficit
 If baseline K+ is <3.3meq/L
avoid insulin and administer 20 to 30 mEq/hour K+ IV
until [K+] is above 3.3 mEq/L.
 If base line K+ is 3.3-5.3meq/L or is unknown
administer 40meq/L to run over 4-8 hrs after confirming
adequate urine output (≥50ml/hr)
 If baseline k+ is above 5.3meq/L
don’t administer k+
 The target is to keep it between 4-5meq/L
Treatment..
Insulin administration
 If perfuser and trained staff for monitoring of
the rate of infusion is available:
 Administer short-acting insulin: IV (0.1 units/kg),
then 0.1 units/kg per hour by continuous IV
infusion
 serum potassium is <3.3 mmol/L (3.3 meq/L),
do not administer insulin until the potassium is
corrected.
Treatment…
Insulin administration
 Give initial bolus of 10IU IV and 10 IU IM of regular
insulin (if there is no Perfuser)
 Then give 5 IU IV every one hour until blood sugar falls
below 250 and urine ketone is twice negative
 If RBS doesn’t drop by at least 50mg/dl or is
persistently above 350-400,double the dose of insulin
i.e. give 10 IU IV
 Overlap the last dose of regular insulin with the
standing dose of long acting insulin
DKA follow up chart..
Disposition
• Most patients with DKA require hospital
admission, often to the intensive care unit.
• Patients who have mild DKA may be
discharged from ED
– The underlying causes do not require inpatient
therapy
– Close follow-up is pursued.
Summary
• DKA is a metabolic disorder characterized by the triad
– hyperglycemia
– anion gap metabolic acidosis (increased anion gap)
– Ketonemia.
• The most common precipitating factors are
– infection
– discontinuation of insulin treatment
• The main principles of DKA management
– fluid replacement
– correction of electrolyte abnormalities
– Insulin administration
– treating the precipitating factors
Questions?
Thanks

final DKA emergency for medicine student c2.pptx

  • 1.
    Diabetes ketoacidosis(DKA) Dr. ChalachewT.(Emergency and Critical Care Medicine Physician
  • 2.
    Course outline • Objectives •Introduction • Precipitating factors • Clinical presentation • Investigation • Treatment • Disposition • Summary
  • 3.
    Learning objectives • Bythe end of this session, participants will be able to: – Define diabetic ketoacidosis – Describe the clinical features of DKA – Diagnose DKA – Manage DKA according to the standard protocol
  • 4.
    Introduction • Diabetic ketoacidosis(DKA) –A metabolic disorder characterized by the triad of • Hyperglycemia • Anion gap metabolic acidosis (increased anion gap) • Ketonemia. – serious complication of diabetes mellitus – occurs when uncontrolled blood sugar rises and the body can’t produce enough insulin to use the glucose.
  • 5.
    Precipitating factors • Themost common precipitating factors – Infection – Discontinuation of insulin treatment
  • 6.
    Other precipitating factors –Acute major illnesses such as MI, CVA, or pancreatitis. – New onset type 1 diabetes – Drugs (glucocorticoids, higher dose thiazide diuretics, sympathomimetic agents (e.g., dobutamine and terbutaline). – Cocaine use ..etc
  • 7.
    Clinical presentation • Directlyrelated to the three primary metabolic derangements – hyperglycemia, – volume depletion – acidosis. • Symptoms – Nausea/vomiting ,Thirst/polyuria, Abdominal pain, Shortness of breath etc
  • 8.
    Clinical presentation • PhysicalFindings – Tachycardia – Dehydration/hypotension – Tachypnea / Kussmaul respirations/respiratory distress – Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen) – Lethargy/obtundation/cerebral edema/possibly coma
  • 9.
    Investigation • Serum Glucose: –The serum glucose will be elevated(>200mg/dl) • Serum bicarbonate – is frequently <10 mmol/L • Arterial PH – ranges between 6.8 and 7.3- depending on the severity of the acidosis
  • 10.
    Investigation… – sodium, chloride,phosphorus, and magnesium are reduced in DKA. • are not accurately reflected by their levels in the serum because of dehydration and hyperglycemia. – Renal function test- • Elevated blood urea nitrogen (BUN) and serum creatinine levels – reflect intravascular volume depletion.
  • 11.
    Treatment • Stabilize ABCof life • Fluid management • Insulin • K+ repletion • Treatment of precipitating factors • Monitoring • Long term management
  • 12.
    Treatment General measures Stabilize theABC of life  Obtain IV access Monitor RBS every hour ,urine ketone every 2-4 hrs Identify and treat Precipitating cause of DKA
  • 13.
    Treatment… Repletion of fluiddeficit  The usual fluid deficit is about 3-6 liters  Give as much NS/RL rapidly for a patient in shock In general  The first 2 L over 0 - 2 hours  The next 2 L over 2 - 6 hours  Then 2 L more over 6 -12 hours.  Change the fluid to DNS when blood sugar falls to below 250  Replace ongoing fluid loss
  • 14.
    Treatment.. Repletion of K+deficit  If baseline K+ is <3.3meq/L avoid insulin and administer 20 to 30 mEq/hour K+ IV until [K+] is above 3.3 mEq/L.  If base line K+ is 3.3-5.3meq/L or is unknown administer 40meq/L to run over 4-8 hrs after confirming adequate urine output (≥50ml/hr)  If baseline k+ is above 5.3meq/L don’t administer k+  The target is to keep it between 4-5meq/L
  • 15.
    Treatment.. Insulin administration  Ifperfuser and trained staff for monitoring of the rate of infusion is available:  Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg per hour by continuous IV infusion  serum potassium is <3.3 mmol/L (3.3 meq/L), do not administer insulin until the potassium is corrected.
  • 16.
    Treatment… Insulin administration  Giveinitial bolus of 10IU IV and 10 IU IM of regular insulin (if there is no Perfuser)  Then give 5 IU IV every one hour until blood sugar falls below 250 and urine ketone is twice negative  If RBS doesn’t drop by at least 50mg/dl or is persistently above 350-400,double the dose of insulin i.e. give 10 IU IV  Overlap the last dose of regular insulin with the standing dose of long acting insulin
  • 17.
  • 18.
    Disposition • Most patientswith DKA require hospital admission, often to the intensive care unit. • Patients who have mild DKA may be discharged from ED – The underlying causes do not require inpatient therapy – Close follow-up is pursued.
  • 19.
    Summary • DKA isa metabolic disorder characterized by the triad – hyperglycemia – anion gap metabolic acidosis (increased anion gap) – Ketonemia. • The most common precipitating factors are – infection – discontinuation of insulin treatment • The main principles of DKA management – fluid replacement – correction of electrolyte abnormalities – Insulin administration – treating the precipitating factors
  • 20.
  • 21.