DKA Current Practices in Africa 02 - 02 - 2022-1
DKA Current Practices in Africa 02 - 02 - 2022-1
◼ Definitions
◼ Conclusions
Definition of Diabetes Keto Acidosis
◼ A life threatening complication of diabetes characterized by
hyperglycaemia, acidosis and ketosis
◼ Biochemical criteria
❑ Hyperglycemia(blood glucose>11 mmol/l or 200mg/dl)
❑ Venous pH < 7.3
❑ Bicarbonate(HCO3=)<15mmol/l
❑ Ketonaemia or ketonuria
◼ Severity of DKA
❑ Mild-Venous pH<7.3 or HCO3=<15 mmol/l
❑ Moderate-Venous pH<7.2 or HCO3=<10 mmol/l
❑ Severe-Venous pH<7.1 or HCO3=<5 mmol/l
Clinical Manifestation of Diabetes Keto Acidosis
◼ Dehydration
evidence of infection.
◼ Beta hydroxybutyrate
◼ ECG monitoring
Supportive measures
◼ Secure the airways
❑ Labs(U&E, Ca++, Mg++, PO4=, glucose, haematocrit every 4 hours for the first 12 hours in
severe cases.
❖ If the laboratory cannot provide timely results, a portable biochemical analyzer that measures plasma glucose,
serum electrolytes and blood ketones on fingerstick blood samples at the bedside is a useful adjunct to laboratory-
based determinations.
Additional Calculations
❑ Anion gap = Na − (Cl + HCO3): normal is 12 ± 2 (mmol/L)
◼ Goals of Therapy
❑ Correct dehydration
Diagnosis confirmed
Diabetic Ketoacidosis
Contact senior staff
Dehydration >5%,
Shock (reduced peripheral pulses) Minimal dehydration
Not in shock
Reduced conscious level/coma Tolerating oral fluids
Acidotic(hyperventilation)
Vomiting
Critical Observations
Hourly blood glucose
Hourly fluid input & output
Neurological status at least hourly
Electrolytes 2 hourly after starting IV fluid therapy
Monitor ECG for T-wave changes Neurological deterioration
WARNING SIGNS:
Severe or progressive
Acidosis not improving headache, slowing heart
Blood glucose ≤17mmol/L (300 mg/dL) rate, irritability, confusion,
or decreased consciousness,
Blood glucose falls 5mmol/L/hour (90 mg/dL) incontinence, specific
Re-evaluate neurologic signs
IV fluid calculations
Insulin delivery system and dose
Need for additional resuscitation IV Therapy
Consider sepsis Change to 0.45% or 0.9% saline; add glucose to Exclude hypoglycemia
fluids (5%-12.5%) to prevent hypoglycemia Is it cerebral edema (CE)?
Adjust sodium infusion to promote an increase
in measured serum sodium
CE management
Give mannitol 0.5-1 g/kg or
3% hypertonic saline
Improved, clinically well, ketoacidosis resolved Adjust IV fluids to maintain
tolerating oral fluids normal BP but avoid over-
hydration
Call senior staff
Move to ICU
Consider cranial imaging
Transition to SC Insulin
only after patient stabilizing
Start SC insulin then stop IV insulin after an appropriate interval
◼ Among the existing challenges are inadequate nursing staff to provide the
ICU level of care and lack infusion pumps, therefore making it difficult to
give insulin infusion and do close monitoring
◼ There is limited choices of the types of insulin you can use, with insulin
◼ Therefore, the current guidelines have been modified to fit into the resource
limited setting without compromising patient care
KEY POINTS ON OUR CURRENT PRACTICES
◼ The starting insulin dose is 0.3 Units/kg of regular short acting human
insulin (Actrapid) stat intramuscularly, followed by a dose of 0.1
Units/kg/hour intramuscularly until acidosis improves HCO3 > 12-
15mmol/L.
◼ Where, the insulin pumps are available, the starting insulin dose is 0.1
Units/kg/hour and this dose should continue to be used until acidosis
improves. Sometimes a higher dose may be required or in special
circumstances this dose may be lower e.g. very young patients or
known sensitivity to insulin.
◼ The rate of fluid (IV and oral) should be calculated to rehydrate evenly
over 48 hours
◼ Requirements=maintenance+deficit
◼ Hourly rate=([maintence for 48 hours+deficit]-all fluid already given)/48
◼ Eg 20 kg 6 years old boy who is 10% dehydrated, has already received 20L/kg saline.
Maintenance; 60 mL X 20 kg=1200 mL in 24 hrs=2400mL in 48 hr
◼ Deficit(mL); 10% X 20kg(≈20000mL)= 2000mL.
◼ Minus 20mL X 20kg=400 mL
◼ Therefore the hourly rate is ([2400+2000]-400mL)/48 =83mL/hr
◼ ALTERNATIVELY, the fluid requirement after initially resuscitation is calculated as Hourly
rate= 1.5 x maintenence rate
Principles of Water and Salt Replacement
❑ Initial dose SC: 0.3 unit/kg, followed 1 hour later by SC insulin lispro or
aspart at 0.1 unit/kg every hour, or 0.15–0.20 units/kg every two hours
❑ If blood glucose falls to <15 mmol/L (250 mg/dL) before DKA has
resolved, (pH still <7.30), add 5% glucose (e.g., 5% glucose in 0.45%
saline) and continue with insulin as above.
❑ An IV bolus is unnecessary , may increase the risk of cerebral edema , and should not be used at the start of
therapy
❑ The dose of insulin should usually remain at 0.1 unit/kg/hour at least until resolution of DKA (pH >7.30,
bicarbonate >15 mmol/L and/or closure of the anion gap), which invariably takes longer than normalization of
blood glucose concentrations
❑ If the patient demonstrates marked sensitivity to insulin (e.g., some young children with DKA, patients with
HHS, and some older children with established diabetes), the dose may be decreased to 0.05 unit/kg/hour, or
less, provided that metabolic acidosis continues to resolve.
❑ During initial volume expansion the plasma glucose concentration falls steeply . Thereafter, and after
commencing insulin therapy, the plasma glucose concentration typically decreases at a rate of 2–5
mmol/L/hour, depending on the timing and amount of glucose administration
❑ To prevent an unduly rapid decrease in plasma glucose concentration and hypoglycemia, 5% glucose should
be added to the IV fluid (e.g., 5% glucose in 0.45% saline) when the plasma glucose falls to approximately
14–17 mmol/L (250–300 mg/dL), or sooner if the rate of fall is precipitous
◼ If the patient is hypokalemic, start potassium replacement at the time of initial volume
expansion and before starting insulin therapy
• If the patient is hyperkalemic, defer potassium replacement therapy until urine output
is documented
◼ Inadequate rehydration
◼ Hypoglycaemia
◼ Hypokalaemia
◼ Hypochloremic acidosis
◼ Cerebral edema
Introduction of oral fluids and transition to SC
insulin injections