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Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
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).
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.
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
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.