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DIABETIC KETO ACIDOSIS/
DIABETIC COMA
ALIYA RAHMAN
DEFINITION
• It is a clinical syndrome arising as a
complication of diabetes and characterized by
hyperglycaemia and ketoacidosis
PRECIPITATING FACTORS
• New onset of type 1 DM: 25%
• Infections (the most common cause): 40%
• Drugs: e.g. Steroids, Thiazides, Dobutamine &
Turbutaline.
• Omission of Insulin: 20%. This is due to:
o Non-availability (poor countries)
o fear of hypoglycemia
o fear of weight gain
o stress of chronic disease
CLINICAL MANIFESTATIONS
• 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 low
• Temperature low
• Polyuria, polyphagia and polydipsia
DIAGNOSIS
To diagnose DKA, the following criteria must be
fulfilled The American Diabetes Association
diagnostic criteria for DKA are as follows:
• elevated serum glucose level (greater than
250 mg per dL [13.88 mmol per L])
• an elevated serum ketone level
• a pH less than 7.3
• a serum bicarbonate level less than 18 mEq
per L (18 mmol per L)
LAB EVALUATION
• The initial Lab evaluation includes:
• Plasma & urine levels of glucose & ketones.
• ABG, U&E (including Na, K, Ca, Mg, Cl, PO4, HCO3),
arterial pH and venous PH
• Complete Blood Count with differential.
• Further tests e.g., cultures, X-rays…etc , are done when
needed.
• BUN: may be elevated with perirenal azotemia secondary
to dehydration.
• Serum Amylase: is often raised, & when there is abdominal
pain, a diagnosis of pancreatitis may mistakenly be made.
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. Administer 0.9% Saline 4- 14 ml/kg/hour for
an initial hour, to restore blood volume and
renal perfusion.
2. If serum sodium is high or normal start with
0.45% saline.
FLUID REPLACEMENT
• When serum glucose reaches 250mg/dl
change fluid to 5% dextrose with 0.45 saline,
at a rate that allow complete restoration in 48
hours, & to maintain glucose at 150-
250mg/dl.
• Pediatric saline 0.18% Na Cl should not be
used even in young children.
INSULIN THERAPY
• start regular insulin 0.15 unit/kg as IV Bolus.
• start infusing regular insulin at a rate of
0.1U/kg/hour using a syringe pump.
Optimally, serum glucose should decrease in a
rate no faster than 100mg/dl/hour.
• 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 ACIDOSIS
• Insulin therapy stops lipolysis and promotes
the metabolism of ketone bodies. This
together with correction of dehydration
normalize the blood PH.
• Bicarbonate therapy should not be used
unless severe acidosis (pH<7.0) results in
hemodynamic instability. If it must be given, it
must infused slowly over several hours.
• If no adequate settings (i.e. no infusion or
syringe pumps & no ICU care which is the
usual situation in many developing countries)
Give regular Insulin 0.1 U/kg/hour IM till
acidosis disappears and blood glucose drops
to <250 mg/dl, then us SC insulin in a dose of
0.25 U/kg every 4 hours.
• When patient is out of DKA return to the
previous insulin dose.
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, & the
rest as potassium phosphate, this will provide
phosphate for replacement, & avoids excess
phosphate (may precipitate hypocalcaemia) &
excess Cl (may precipitate cerebral edema or
adds to acidosis).
• If K conc. < 3.3mEq/l, administer 40mEq/l of KCl
in IV saline over 1 hour. Withhold Insulin until K
conc. becomes>3.3mEq/l and monitor K conc.
hourly.
• If serum potassium is 5 or more, do not give
potassium recheck in every 2 hours.
• If intial potassium is ≥3.3 but <5mEq/l give 20- 30
mEq/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)
• IF PH < 6.9 Bicabonate (100 osmol) dilute in
400ml of H2O. Infused at 200 ml/h.
• IF PH < 6.9-7.0 Bicabonate (50 osmol) dilute in
200ml of H2O. Infused at 200 ml/h
• IF PH >7 No bicarbonate
PHOSPHATE REPLACEMENT
• Phosphate concentration decreases with insulin
therapy.
• To avoid cardiac and skeletal muscle weakness
and respiratory depression due to
hypophosphatemia, careful phosphate
replacement may sometimes be indicated in
patients with cardiac dysfunction, anemia, or
respiratory depression and in those with serum
phosphate concentration 1.0 mg/dl. When
needed, 20–30 mEq/l potassium phosphate is
administered.
ANTIBIOTICS
• Infections should be treated vigorously with
broad spectrum antibiotics.
• Carry out c&s study of blood and urine and
portable chest xray
CARE OF UNCONSCIOUS PATIENTS
• Monitor all vitals every hourly
• Sent daily blood samples for the estimation of
glucose, urea, ketone, PH, bicarbonate and
electrolytes
• Catheterization, change of posture , etc
according to patient’s need
MONITORING
• A flow chart must be used to monitor fluid
balance & Lab measures.
• serum glucose must be measured hourly.
• electrolytes also 2-3 hourly.
• Ca, Mg, & phosphate must be measured initially
& at least once during therapy.
• Neurological & mental state must examined
frequently, & any complaints of headache or
deterioration of mental status should prompt
rapid evaluation for possible cerebral edema.
COMPLICATIONS
• Cerebral Edema
• Intracranial thrombosis or infarction.
• Acute tubular necrosis.
• peripheral edema.
THANK YOU

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DIABETIC KETO ACIDOSIS

  • 2. DEFINITION • It is a clinical syndrome arising as a complication of diabetes and characterized by hyperglycaemia and ketoacidosis
  • 3.
  • 4. PRECIPITATING FACTORS • New onset of type 1 DM: 25% • Infections (the most common cause): 40% • Drugs: e.g. Steroids, Thiazides, Dobutamine & Turbutaline. • Omission of Insulin: 20%. This is due to: o Non-availability (poor countries) o fear of hypoglycemia o fear of weight gain o stress of chronic disease
  • 5. CLINICAL MANIFESTATIONS • 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 low • Temperature low • Polyuria, polyphagia and polydipsia
  • 6. DIAGNOSIS To diagnose DKA, the following criteria must be fulfilled The American Diabetes Association diagnostic criteria for DKA are as follows: • elevated serum glucose level (greater than 250 mg per dL [13.88 mmol per L]) • an elevated serum ketone level • a pH less than 7.3 • a serum bicarbonate level less than 18 mEq per L (18 mmol per L)
  • 7. LAB EVALUATION • The initial Lab evaluation includes: • Plasma & urine levels of glucose & ketones. • ABG, U&E (including Na, K, Ca, Mg, Cl, PO4, HCO3), arterial pH and venous PH • Complete Blood Count with differential. • Further tests e.g., cultures, X-rays…etc , are done when needed. • BUN: may be elevated with perirenal azotemia secondary to dehydration. • Serum Amylase: is often raised, & when there is abdominal pain, a diagnosis of pancreatitis may mistakenly be made.
  • 8.
  • 9.
  • 10. 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.
  • 11. DEHYDRATION WITHOUT SHOCK 1. Administer 0.9% Saline 4- 14 ml/kg/hour for an initial hour, to restore blood volume and renal perfusion. 2. If serum sodium is high or normal start with 0.45% saline.
  • 12. FLUID REPLACEMENT • When serum glucose reaches 250mg/dl change fluid to 5% dextrose with 0.45 saline, at a rate that allow complete restoration in 48 hours, & to maintain glucose at 150- 250mg/dl. • Pediatric saline 0.18% Na Cl should not be used even in young children.
  • 13.
  • 14. INSULIN THERAPY • start regular insulin 0.15 unit/kg as IV Bolus. • start infusing regular insulin at a rate of 0.1U/kg/hour using a syringe pump. Optimally, serum glucose should decrease in a rate no faster than 100mg/dl/hour. • 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.
  • 15. CORRECTION OF ACIDOSIS • Insulin therapy stops lipolysis and promotes the metabolism of ketone bodies. This together with correction of dehydration normalize the blood PH. • Bicarbonate therapy should not be used unless severe acidosis (pH<7.0) results in hemodynamic instability. If it must be given, it must infused slowly over several hours.
  • 16. • If no adequate settings (i.e. no infusion or syringe pumps & no ICU care which is the usual situation in many developing countries) Give regular Insulin 0.1 U/kg/hour IM till acidosis disappears and blood glucose drops to <250 mg/dl, then us SC insulin in a dose of 0.25 U/kg every 4 hours. • When patient is out of DKA return to the previous insulin dose.
  • 17. 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, & the rest as potassium phosphate, this will provide phosphate for replacement, & avoids excess phosphate (may precipitate hypocalcaemia) & excess Cl (may precipitate cerebral edema or adds to acidosis).
  • 18.
  • 19. • If K conc. < 3.3mEq/l, administer 40mEq/l of KCl in IV saline over 1 hour. Withhold Insulin until K conc. becomes>3.3mEq/l and monitor K conc. hourly. • If serum potassium is 5 or more, do not give potassium recheck in every 2 hours. • If intial potassium is ≥3.3 but <5mEq/l give 20- 30 mEq/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)
  • 20.
  • 21. • IF PH < 6.9 Bicabonate (100 osmol) dilute in 400ml of H2O. Infused at 200 ml/h. • IF PH < 6.9-7.0 Bicabonate (50 osmol) dilute in 200ml of H2O. Infused at 200 ml/h • IF PH >7 No bicarbonate
  • 22. PHOSPHATE REPLACEMENT • Phosphate concentration decreases with insulin therapy. • To avoid cardiac and skeletal muscle weakness and respiratory depression due to hypophosphatemia, careful phosphate replacement may sometimes be indicated in patients with cardiac dysfunction, anemia, or respiratory depression and in those with serum phosphate concentration 1.0 mg/dl. When needed, 20–30 mEq/l potassium phosphate is administered.
  • 23. ANTIBIOTICS • Infections should be treated vigorously with broad spectrum antibiotics. • Carry out c&s study of blood and urine and portable chest xray
  • 24. CARE OF UNCONSCIOUS PATIENTS • Monitor all vitals every hourly • Sent daily blood samples for the estimation of glucose, urea, ketone, PH, bicarbonate and electrolytes • Catheterization, change of posture , etc according to patient’s need
  • 25. MONITORING • A flow chart must be used to monitor fluid balance & Lab measures. • serum glucose must be measured hourly. • electrolytes also 2-3 hourly. • Ca, Mg, & phosphate must be measured initially & at least once during therapy. • Neurological & mental state must examined frequently, & any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema.
  • 26. COMPLICATIONS • Cerebral Edema • Intracranial thrombosis or infarction. • Acute tubular necrosis. • peripheral edema.