Diabetic Ketoacidosis (DKA) - Zeineddin Etkaidek
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Etiology
o The most common precipitants of DKA
1. Noncompliance – 44%
2. Infection
3. Medications: beta blockers, diuretics, steroids, anti-convulsant
o Pathophysiology
1. ↓ Insulin deficiency, ↑ insulin counter-regulatory hormones (glucagon,
cortisol, catecholamines)
2. Hyperglycemia: ↓ glucose utilization, ↑ gluconeogenesis and
glycogenolysis
3. Ketone bodies (b-OHB, acetoacetate, acetone): ↑ lipolysis and conversion
of FA to ketone bodies
4. Dehydration: hyperglycemia-induced osmotic diuresis, polyuria
o Electrolyte
1. Insulin shifts K+ into the cells
 Insulin deficiency shifts K+ out of the cells
 (Serum K+) may be normal
 (Total body K+) is decreased because of urinary losses due to
osmotic diuresis
2. Mg+2
 Serum Mg+2: Hypermagnesemia
 Total body Mg+2: decreased because of urinary losses due to
osmotic diuresis
 After Rx: hypomagnesemia
3. PO4
 Total body PO4: decreased because of urinary losses due to
osmotic diuresis
 After Rx: hypophosphatemia
Epidemiology
o 20-40% of cases of T1DM presents as DKA
Clinical features
o 20-40% of cases of T1DM presents as DKA
o Hx
1. Nausea
2. Vomiting
3. Abdominal pain
4. Dehydration
5. Lethargy
6. Polyuria
7. Polydipsia
8. Weight loss s
o O/E
1.
2.
3.
4.
Vital signs
Mental status (alert, drowsy, stupor/coma)
Kussmaul respiration: hyperventilation with deep, sighing respiration
Fruity odor of the breath: due to acetone
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Investigations
o Dextro test (glucometer)
o UA
1. Glycosuria
2. Ketonuria
o ABGs
1. Metabolic acidosis
o CBC
o HbA1c
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Criteria and classification
Plasma glucose
(mg/dL)
Urine ketone
pH
Serum HCO3
Clinically
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Mild
>250
+
7.25-7.30
15-18
Alert
Moderate
Severe
7.00-7.25
10-15
Drowsy
<7
<10
Stupor
Management
o ICU
o Insulin
1. MOA
 ↑ movement of glucose into cells
 ↓ hepatic glucose production
 ↓ movement of FA to the liver
2. Don’t give insulin bolus
 Does not speed the recovery
 Increases the risk of hypokalemia and hypoglycemia
3. Start regular/plain insulin infusion at a rate of 0.1unit/kg/hr
o Rehydration
1. MOA
 Improves renal perfusion and enhances renal excretion of glu
2. Initial IV bolus
 10-20mL/kg 0.9NS over 1-2hrs
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0.9 NS (isotonic) because the pt is hypertonic to keep Fluid in the
intravascular space
3. IVF rate = (85cc/kg + maintenance – bolus) / 23hr
 85cc/kg comes from 8.5 % dehydration
 Bolus: 0.9 NS (isotonic)
 Maintenance: ½ NS (hypotonic)
4. D5: RBS <300mg/dL
5. D10: RBS <200mg/dL
Corrected Na = Na + 1.6 mEq/L for every 100mg/dL glucose above 100
E osm = 2 x Na(uncorrected) x Glu
1. Na and Glu in mmol/L
The use of base therapy (sodium bicarbonate)
1. Indications
 pH<7
 HCO3 <10
2. Complications:
 Hypernatremia and volume overload
 Generates CO2 which can accumulate in case of respiratory
 Rapid change from acidemia to alkalemia which causes
hypokalemia and hypophosphatemia
Complications
1. Cerebral edema
 If the decline in serum glu >100 mg/dL/hr
 Decline in Na