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Diabetic Ketoacidosis 
Done by: 
Mohammed Qazzaz
Diabetic Ketoacidosis 
It is a life threatening but reversible 
complication of type 1 diabetes due to 
absolute insulin deficiency. 
Ketoacidosis: 
High anion gap metabolic acidosis due to 
excessive blood concentration of ketone 
bodies (Ketoanion).
Diabetic Ketoacidosis 
153,000 Hospital admission. 
2.4 billion US $
Diabetic Ketoacidosis
Diabetic Ketoacidosis
Diabetic Ketoacidosis 
A-The basic underlying mechanisms are: 
-Absolute deficiency of circulating insulin. 
-secretion of insulin counterregulatory 
hormones; glucagon, adrenaline, cortisol and 
growth hormone.
Diabetic Ketoacidosis 
B-This leads to disturbances in the following 
physiological processes: 
-glucose utilization (hyperglycemia). 
- proteolysis ( amino acids, glutamine and 
alanine). 
- lipolysis ( glycerol and FFAs). 
- glycogenolysis (breakdown of muscle glycogen 
 lactate). 
- gluconeogensis (glutamine & alanine & glycerol 
& lactate are the precursors).
Diabetic Ketoacidosis 
acetone, 
acetoacetic acid, 
beta-hydroxybutyric acid
Diabetic Ketoacidosis 
C-This results in the following metabolic abnormalities: 
1-Hyperglycemia. 
2-Hyperketonemia: 2 main mechanisms: 
a- Production of ketone bodies (ketogenesis): 
-Increase FFAs  hepatic uptake  FFAs enter the 
mitochondria  oxidation to form acetoacetic acid. 
-Large part of acetoacetic acid  reduced to  - 
hydroxy butyric acid ( -HBA). 
-Small part of acetoacetic acid is decarboxylated to 
acetone. 
The 3 ketone bodies are released to the blood in a ratio 
between acetoacetic acid to -HBA of 8 : 1 . 
b- Utilization of ketone bodies.
Diabetic Ketoacidosis 
D-The consequences of these metabolic abnormalities are: 
a-Hyperglycemia: 
-Osmotic diuresis. 
-Excessive urinary losses of H2O & Na, K. 
-Dehydration and hypotension. 
b-Hyperketonemia: 
-Ketonuria. 
-  Blood acidity (acetoacetic acid and -HBA are strong 
acids). 
-Acetone is a CNS anaesthetic.
Diabetic Ketoacidosis 
E-Electrolytes and acid base disturbances during DKA: 
a-Serum K: Usually high (hyperkalemia) secondary 
to: 
1-Shift of K from intracellular to extracellular 
compartment due to: 
-Insulin deficiency and hyperglycemia. 
-Extracellular hyperosmolarity. 
-Acidosis. 
- Catabolism and breakdown of cellular 
protein. 
2-Impaired cellular uptake of K.
Diabetic Ketoacidosis 
b-Serum sodium: Usually low secondary to: 
-Hyperglycemia leads to  osmotic flux of H2O from 
intracellular to extracellular space. 
-Obligate sodium loss with ketonuria. 
c-Metabolic acidosis: Secondary to: 
- Production and  utilization of strong acids; 
acetoacetic acid and -HBA. 
- Alkaline reserve (sodium and K losses).
Diabetic Ketoacidosis 
Clinical features of DKA 
A-Symptoms of DKA: 
1-Classic symptoms of hyperglycemia: short period of time: 
Polyuria, polydipsia, wt loss and thirst. 
2-Other symptoms: 
- General weakness, malaise and lethargy. 
-Nausea, vomiting and abdominal pain. 
- Perspiration. 
- Disturbed consciousness and confusion. 
3-Symptoms of underlying infections or other conditions; 
fever, abdominal pain, dysuria, chest pain…etc.
Diabetic Ketoacidosis 
Precipitating Factors: 
Stress 
Infections: UTI, Chest, Fungal 
Stroke, MI, PE 
Pregnancy 
Steroids 
Trauma 
Pancreatitis 
Surgery 
Hyperthyroidisim
Diabetic Ketoacidosis 
B- Physical signs of DKA: 
a-General signs: Ill appearance and disturbed consciousness. 
b-Signs of dehydration: 
-Skin: Dry, hot, flushed, and loss of skin turgor. 
-Tongue: Dry (sometimes woody tongue). 
-Eyes: Sunken eyes and dark circles under the eyes. 
c-Vital signs: 
-Tachycardia, hypotension and tachypnea. 
d-Specific signs: 
-Ketotic breath: A strong, fruity breath odour (similar to nail 
polish remover or acetone). 
-Acidotic breath (Kussmaul's respiration): deep and rapid. 
-Abdominal tenderness.
Diabetic Ketoacidosis 
Diagnostic criteria of DKA: 
• Blood glucose > 250 mg/dl. 
• Mild to moderate dehydration. 
• Ketonuria: (++). 
• Serum bicarbonate < 15 m Eq/L. 
• pH is acidic (Metabolic acidosis): 
Arterial < 7.3. Or 
Venous < 7.25.
Diabetic Ketoacidosis 
Complications of DKA 
1-Complications of associated illnesses e.g. 
sepsis or MI. 
2-Adult respiratory distress syndrome. 
3-Thromboembolism (elderly). 
4-Complications of treatment: 
a-Hypokalemia: Which may lead to: 
-Cardiac arrhythmias. 
-Cardiac arrest. 
-Respiratory muscle weakness.
Diabetic Ketoacidosis 
b-Hypoglycemia. 
c-Overhydration and acute pulmonary edema: 
particularly in: 
-Treating children with DKA. 
-Adults with compromised renal or cardiac 
function. 
-Elderly with incipient CHF.
Diabetic Ketoacidosis 
d-Neurological complications: Cerebral Edema. 
-It occurs only in children with DKA. 
-Very dangerous and increases mortality. 
-The risk is related to the severity, duration and rapid 
correction of DKA. 
Mechanism: The brain adapts by producing intracellular osmoles 
(idiogenic osmoles) which stabilize the brain cells from 
shrinking while the DKA was developing. When the 
hyperosmolarity is rapidly corrected, the brain becomes 
hypertonic towards the extracellular fluids  water flows into 
the cells  cerebral edema
Diabetic Ketoacidosis 
ER Evaluation 
ABC 
V/S 
Cardiac monitoring 
Physical examination 
IV access : 2 large bore lines (16-18gauge ) 
CVP may be needed 
Blood sugar 
Foley catheter
Diabetic Ketoacidosis 
Lab!!?? 
Baseline 1 hr 2 hr 3 hr 6 hr 12 hr 24 hr 
Glucose2 √ √ √ √ √ √ √ 
Urea, electrolytes √ √ √ √ √ √ 
Creatinine √ √ √ √ 
Bicarbonate √ √ √ √ √ √ √ 
Blood gases )√( 3√ 3√ 
• Urinalysis for ketones 
• ECG 
• Infection screen: full blood count, blood and urine culture, C-reactive 
protein, chest X-ray. Although leucocytosis invariably occurs, this 
represents a stress response and does not necessarily indicate 
infection
Diabetic Ketoacidosis 
Management of DKA 
• The main lines of management include: 
1. Fluid replacement 
2. Insulin 
3. Potassium
Diabetic Ketoacidosis 
Fluid replacement 
•0.9% saline (NaCl) i.v. 
• 1 L over 30 mins 
• 1 L over 1 hr 
• 1 L over 2 hrs 
• 1 L over next 2-4 hrs 
•When blood glucose < 15 mmol/L (270 mg/dL) 
• Switch to 5% dextrose, 1 L 8-hourly 
• If still dehydrated, continue 0.9% saline and add 5% dextrose, 
1 L per 12 hrs 
•Typical requirement is 6 L in first 24 hrs but avoid fluid overload in 
elderly patients 
•Subsequent fluid requirement should be based on clinical response 
including urine output
Diabetic Ketoacidosis 
Insulin 
IV bolus of 0.10 units/kg (~ 6 units) regular 
insulin 
 6 U/hr 
 3 U/hr when blood glucose < 15 mmol/L (270 
mg/dL) 
 2 U/hr if blood glucose < 10 mmol/L (180 mg/dL) 
•Check blood glucose hourly initially; if no reduction in 
first hour, rate of insulin infusion should be increased 
•Aim for fall in blood glucose of 3-6 mmol/L 
(approximately 55-110 mg/dL) per hour
Diabetic Ketoacidosis 
Potassium 
•None in first L of i.v fluid unless plasma potassium < 3.0 
mmol/L 
•When < 3.5 mmol/L, give 20 mmol/hr 
•When plasma potassium is 3.5-5.0 mmol/L, give 10 mmol/hr
Diabetic Ketoacidosis 
Additional procedures: 
•Catheterisation if no urine passed after 3 hrs((do it from the 
start)) 
•Nasogastric tube to keep stomach empty in unconscious or 
semiconscious patients, or if vomiting is protracted 
•Central venous line if cardiovascular system compromised, to 
allow fluid replacement to be adjusted accurately 
•Plasma expander if systolic BP is < 90 mmHg or does not rise 
with i.v. saline 
•Antibiotic if infection demonstrated or suspected 
•ECG monitoring in severe cases
Diabetic Ketoacidosis 
Aim of treatment 
a-Fluids: 
1- Correct volume deficit and hypotension. 
2- Improve tissue perfusion. 
3-Improve insulin sensitivity (insulin counterregulatory 
hormones). 
4-Improve glomerular filtration rate: 
i-↑ excretion of large amount of glucose in urine. 
ii-Clears hyperketonemia. 
5- Correct metabolic acidosis.
Diabetic Ketoacidosis 
b-Insulin: Reversal of metabolic abnormalities : 
i-Corrects hyperglycemia. 
ii-Inhibits ketogenesis. 
c-Potassium: Prevents complications associated 
with hypokalemia.
Diabetic Ketoacidosis

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Diabetic Ketoacidosis

  • 1. Diabetic Ketoacidosis Done by: Mohammed Qazzaz
  • 2. Diabetic Ketoacidosis It is a life threatening but reversible complication of type 1 diabetes due to absolute insulin deficiency. Ketoacidosis: High anion gap metabolic acidosis due to excessive blood concentration of ketone bodies (Ketoanion).
  • 3. Diabetic Ketoacidosis 153,000 Hospital admission. 2.4 billion US $
  • 6. Diabetic Ketoacidosis A-The basic underlying mechanisms are: -Absolute deficiency of circulating insulin. -secretion of insulin counterregulatory hormones; glucagon, adrenaline, cortisol and growth hormone.
  • 7. Diabetic Ketoacidosis B-This leads to disturbances in the following physiological processes: -glucose utilization (hyperglycemia). - proteolysis ( amino acids, glutamine and alanine). - lipolysis ( glycerol and FFAs). - glycogenolysis (breakdown of muscle glycogen  lactate). - gluconeogensis (glutamine & alanine & glycerol & lactate are the precursors).
  • 8. Diabetic Ketoacidosis acetone, acetoacetic acid, beta-hydroxybutyric acid
  • 9. Diabetic Ketoacidosis C-This results in the following metabolic abnormalities: 1-Hyperglycemia. 2-Hyperketonemia: 2 main mechanisms: a- Production of ketone bodies (ketogenesis): -Increase FFAs  hepatic uptake  FFAs enter the mitochondria  oxidation to form acetoacetic acid. -Large part of acetoacetic acid  reduced to  - hydroxy butyric acid ( -HBA). -Small part of acetoacetic acid is decarboxylated to acetone. The 3 ketone bodies are released to the blood in a ratio between acetoacetic acid to -HBA of 8 : 1 . b- Utilization of ketone bodies.
  • 10. Diabetic Ketoacidosis D-The consequences of these metabolic abnormalities are: a-Hyperglycemia: -Osmotic diuresis. -Excessive urinary losses of H2O & Na, K. -Dehydration and hypotension. b-Hyperketonemia: -Ketonuria. -  Blood acidity (acetoacetic acid and -HBA are strong acids). -Acetone is a CNS anaesthetic.
  • 11. Diabetic Ketoacidosis E-Electrolytes and acid base disturbances during DKA: a-Serum K: Usually high (hyperkalemia) secondary to: 1-Shift of K from intracellular to extracellular compartment due to: -Insulin deficiency and hyperglycemia. -Extracellular hyperosmolarity. -Acidosis. - Catabolism and breakdown of cellular protein. 2-Impaired cellular uptake of K.
  • 12. Diabetic Ketoacidosis b-Serum sodium: Usually low secondary to: -Hyperglycemia leads to  osmotic flux of H2O from intracellular to extracellular space. -Obligate sodium loss with ketonuria. c-Metabolic acidosis: Secondary to: - Production and  utilization of strong acids; acetoacetic acid and -HBA. - Alkaline reserve (sodium and K losses).
  • 13. Diabetic Ketoacidosis Clinical features of DKA A-Symptoms of DKA: 1-Classic symptoms of hyperglycemia: short period of time: Polyuria, polydipsia, wt loss and thirst. 2-Other symptoms: - General weakness, malaise and lethargy. -Nausea, vomiting and abdominal pain. - Perspiration. - Disturbed consciousness and confusion. 3-Symptoms of underlying infections or other conditions; fever, abdominal pain, dysuria, chest pain…etc.
  • 14. Diabetic Ketoacidosis Precipitating Factors: Stress Infections: UTI, Chest, Fungal Stroke, MI, PE Pregnancy Steroids Trauma Pancreatitis Surgery Hyperthyroidisim
  • 15. Diabetic Ketoacidosis B- Physical signs of DKA: a-General signs: Ill appearance and disturbed consciousness. b-Signs of dehydration: -Skin: Dry, hot, flushed, and loss of skin turgor. -Tongue: Dry (sometimes woody tongue). -Eyes: Sunken eyes and dark circles under the eyes. c-Vital signs: -Tachycardia, hypotension and tachypnea. d-Specific signs: -Ketotic breath: A strong, fruity breath odour (similar to nail polish remover or acetone). -Acidotic breath (Kussmaul's respiration): deep and rapid. -Abdominal tenderness.
  • 16. Diabetic Ketoacidosis Diagnostic criteria of DKA: • Blood glucose > 250 mg/dl. • Mild to moderate dehydration. • Ketonuria: (++). • Serum bicarbonate < 15 m Eq/L. • pH is acidic (Metabolic acidosis): Arterial < 7.3. Or Venous < 7.25.
  • 17. Diabetic Ketoacidosis Complications of DKA 1-Complications of associated illnesses e.g. sepsis or MI. 2-Adult respiratory distress syndrome. 3-Thromboembolism (elderly). 4-Complications of treatment: a-Hypokalemia: Which may lead to: -Cardiac arrhythmias. -Cardiac arrest. -Respiratory muscle weakness.
  • 18. Diabetic Ketoacidosis b-Hypoglycemia. c-Overhydration and acute pulmonary edema: particularly in: -Treating children with DKA. -Adults with compromised renal or cardiac function. -Elderly with incipient CHF.
  • 19. Diabetic Ketoacidosis d-Neurological complications: Cerebral Edema. -It occurs only in children with DKA. -Very dangerous and increases mortality. -The risk is related to the severity, duration and rapid correction of DKA. Mechanism: The brain adapts by producing intracellular osmoles (idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing. When the hyperosmolarity is rapidly corrected, the brain becomes hypertonic towards the extracellular fluids  water flows into the cells  cerebral edema
  • 20. Diabetic Ketoacidosis ER Evaluation ABC V/S Cardiac monitoring Physical examination IV access : 2 large bore lines (16-18gauge ) CVP may be needed Blood sugar Foley catheter
  • 21. Diabetic Ketoacidosis Lab!!?? Baseline 1 hr 2 hr 3 hr 6 hr 12 hr 24 hr Glucose2 √ √ √ √ √ √ √ Urea, electrolytes √ √ √ √ √ √ Creatinine √ √ √ √ Bicarbonate √ √ √ √ √ √ √ Blood gases )√( 3√ 3√ • Urinalysis for ketones • ECG • Infection screen: full blood count, blood and urine culture, C-reactive protein, chest X-ray. Although leucocytosis invariably occurs, this represents a stress response and does not necessarily indicate infection
  • 22. Diabetic Ketoacidosis Management of DKA • The main lines of management include: 1. Fluid replacement 2. Insulin 3. Potassium
  • 23. Diabetic Ketoacidosis Fluid replacement •0.9% saline (NaCl) i.v. • 1 L over 30 mins • 1 L over 1 hr • 1 L over 2 hrs • 1 L over next 2-4 hrs •When blood glucose < 15 mmol/L (270 mg/dL) • Switch to 5% dextrose, 1 L 8-hourly • If still dehydrated, continue 0.9% saline and add 5% dextrose, 1 L per 12 hrs •Typical requirement is 6 L in first 24 hrs but avoid fluid overload in elderly patients •Subsequent fluid requirement should be based on clinical response including urine output
  • 24. Diabetic Ketoacidosis Insulin IV bolus of 0.10 units/kg (~ 6 units) regular insulin  6 U/hr  3 U/hr when blood glucose < 15 mmol/L (270 mg/dL)  2 U/hr if blood glucose < 10 mmol/L (180 mg/dL) •Check blood glucose hourly initially; if no reduction in first hour, rate of insulin infusion should be increased •Aim for fall in blood glucose of 3-6 mmol/L (approximately 55-110 mg/dL) per hour
  • 25. Diabetic Ketoacidosis Potassium •None in first L of i.v fluid unless plasma potassium < 3.0 mmol/L •When < 3.5 mmol/L, give 20 mmol/hr •When plasma potassium is 3.5-5.0 mmol/L, give 10 mmol/hr
  • 26. Diabetic Ketoacidosis Additional procedures: •Catheterisation if no urine passed after 3 hrs((do it from the start)) •Nasogastric tube to keep stomach empty in unconscious or semiconscious patients, or if vomiting is protracted •Central venous line if cardiovascular system compromised, to allow fluid replacement to be adjusted accurately •Plasma expander if systolic BP is < 90 mmHg or does not rise with i.v. saline •Antibiotic if infection demonstrated or suspected •ECG monitoring in severe cases
  • 27. Diabetic Ketoacidosis Aim of treatment a-Fluids: 1- Correct volume deficit and hypotension. 2- Improve tissue perfusion. 3-Improve insulin sensitivity (insulin counterregulatory hormones). 4-Improve glomerular filtration rate: i-↑ excretion of large amount of glucose in urine. ii-Clears hyperketonemia. 5- Correct metabolic acidosis.
  • 28. Diabetic Ketoacidosis b-Insulin: Reversal of metabolic abnormalities : i-Corrects hyperglycemia. ii-Inhibits ketogenesis. c-Potassium: Prevents complications associated with hypokalemia.
  • 29.