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7/31/2019 Ddf0Diabetic Ketoacidosis
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Medical emergency
DIABETIC KETOACIDOSIS
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contd medical emergency commonly in people with type 1 diabetes Mortality 10-15% in developed countriesPrecipitating factors
1. Infection2. Trauma3. Stress4. Missed or reduced insulin5. Myocardial infarction
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Pathogenesis Insulin helps in Triglyceride and Fatty acid
synthesis and inhibits fatty acid oxidation andketone production.
In absence of insulin, ketone production
increases Ketones- acetoacetate, 3-hydroxybutyrate or
acetone
Normally produced in small amount andutilized.
In DKA, production exceeds utilization andpass into urine.
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Cardinal features hyperglycaemia hyperketonaemia
metabolic acidosis
Osmotic diuresis leading to dehydration,hypotension & electrolyte loss, particularly ofsodium and potassium
metabolic acidosis forces hydrogen ions into cells,displacing potassium ions
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AVERAGE LOSS OF FLUID AND
ELECTROLYTES
Water: 6 litres
Sodium: 500 mmol
Chloride: 400 mmol
Potassium: 350 mmol
3 litres extracellular -replace with saline
3 litres intracellular -replace with dextrose
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CLINICAL FEATURES
(Symptoms)
Nausea, vomiting
Polyuria, thirst
Abdominal pain Weight loss
Weakness
Leg cramps Blurred vision
Note :- Abdominal pain is due to progression to
pancreatitis.
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Signs
Tachycardia
Dehydration (dry mucous membrane, reduced skin turgor)
Hypotension (postural or supine)
Cold extremities/peripheral cyanosis
Tachypnea, Air hunger (Kussmaul breathing)
Smell of acetone
Hypothermia Confusion, drowsiness, coma (10%)
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Precipitating Factors are
1. Inadequate insulin administration
2. Infection (Pneumonia/UTI/Sepsis/Gastroenteritis)
3. Infarction (Cerebral/coronory/mesentric/peripheral)
4. Drugs (cocaine)5. Pregnancy
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Investigations
1. Blood glucose ( 13.9 33.3 mmol/l or 250- 600 mg/dl)
2. Arterial blood gases (PH 6.8 7.3)
3. Plasma Bicarbonate < 12 mmol/l = severe acidosis
4. Urine and plasma ketone = ++++5. RFT :- urea , creatinine & electrolytes,
6. Osmolality 300 320 mosm/l
7. Anion Gap = Increase
8. ECG9. Infection screen: FBC, blood and urine culture,
CRP, CXR
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Monitoring In ketoacidosis
Serum Osmolality = [2 x (serum sodium + serumpotassium) + plasma glucose (mg/dL)/18 + BUN/2.8]
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The principal components of
treatment
The administration of short-acting (soluble) insulin
Fluid replacement
Potassium replacementAntibiotics if infection is present
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Fluid replacement 0.9% saline (NaCl) i.v.
1 litre over 30 minutes 1 litre over 1 hr 1 litre over 2 hrs 1 litre over next 4 hrs
When blood glucose < 15 mmol/l, Switch to 5% dextrose, 1 litre 8-hourly If still dehydrated, continue 0.9% saline and add 5%
dextrose 1 litre per 12 hrs
Typical requirement is 6 litres in first 24 hrsbut avoid fluid overload in elderly patients
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Insulin
50 units soluble insulin in 50 ml 0.9% saline i.v. viainfusion pump
6 units/hr initially
3 units/hr when blood glucose < 15 mmol/l (270 mg/dl)
2 units/hr if blood glucose declines < 10 mmol/l (180mg/dl)
Check blood glucose hourly initially-if no reduction in firsthour, rate of insulin infusion should be increased
Aim for fall in blood glucose of 3-6 mmol/l (55-110 mg/dl)per hour
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Potassium
If plasma potassium < 3.5 mmol/l, give 40 mmol addedpotassium
Avoid infusion rate of > 20 mmol/hr
If plasma potassium is 3.5-5.5 mmol/l, give 20 mmol addedpotassium
If plasma potassium is > 5.5 mmol/l, or patient is anuric,give no added potassium
Later, according to lab report. Note= If initial serum K+ < 3.3 mmol/l then stop insulin infusion
until K+ is corrected > 3.3mmol/l.
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Others treatment
Continue Above until pt is stable and glucose goal is 150 250mg/dl & Acidosis is resolved then
Insulin infusion is /may decreased to 0.05 0.1 U/kg/hr.
Catheterisation if no urine passed after 3 hrs
Nasogastric tube to keep stomach empty in unconscious orsemiconscious patients.
Central venous line if cardiovascular system compromised.
Plasma expander if systolic BP is < 90 mmHg or does notrise with i.v. saline.
Antibiotic if infection demonstrated or suspected
ECG monitoring in severe cases
Monitoring Vitals (BP, pulse, RR, Temp)
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Complication of DKA
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