Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
2. Characteristics
Uncontrolled hyperglycaemia (generally >13.9 mmol/L)
Metabolic acidosis (arterial blood ph <7.3) and plasma
bicarbonate <15 mmol/L
High anion gap acidosis of >12 ± 2
Increase in circulating total body ketone concentration (β-
hydroxybutyric and acetoacetic acid) and ketonuria.
3. Precipitating causes
Infection
New-onset diabetes
Cessation of insulin
Myocardial infarction
Pancreatitis
Shock and hypovolaemia
Stroke
Other medical diseases
No precipitating event
6. Initial laboratory investigations
Immediate urine test for glycosuria and ketonuria
Plasma sample for:
∘ Glucose
∘ Electrolytes
∘ Bicarbonates
∘ Chloride
∘ Urea
∘ Creatinine
Arterial blood samples for blood gas analysis
Blood count (leucocytosis is frequent)
Urine culture
Blood culture if indicated
X-ray chest
Electrocardiogram (ECG)
7.
8. How does the body dispose of ketones?
Extrahepatic tissues have the capacity to utilize ketone
bodies but this is impaired in uncontrolled diabetes.
Oxidation of ketone anions during treatment neutralizes
the acidosis by generating bicarbonate ions.
Increased excretion of ketone bodies through the kidneys
and lungs is important in ketone body elimination.
9. What are the effects of acidosis?
Negative inotropic effect on cardiac muscle.
Systemic hypotension.
Peripheral vasodilatation.
Risk of ventricular arrhythmia.
Respiratory depression.
10. What is the impact of acute illness on
glucose metabolism?
Increased production.
Decreased tissue utilization.
Decreased renal clearance.
13. Rules for fluid replacement
Which fluid should be used?
∘ Isotonic saline: 0.9% normal saline.
∘ In severe hypernatraemia: 0.45% saline.
∘ In case of shock: volume expander.
How to replace fluid?
∘ There are several protocols based on the fact that volume depletion is
significant.
∘ The initial fluid of choice is isotonic saline at the rate of 15-20 ml/kg body
weight per hour or 1-1.5 L in adults during the first hour.
∘ Further repletion depends on the hydration status, serum electrolyte
levels and urine output.
14. Insulin replacement
DKA is a state of marked insulin resistance. Only short-
acting (regular) insulin should be used initially. The
optimum route of administration is intravenous.
A low-dose insulin regimen is given: 5–7 units of short-
acting insulin hourly through continuous intravenous
infusion till plasma glucose falls to 13.9 mmol/L.
The expected rate of decrease in plasma glucose is 4–5
mmol/L per hour.
Plasma glucose concentration should not be allowed to
drop to ≤11 mmol/L in the first 6–8 hours.
15. Rationale for low-dose insulin therapy
Low-dose insulin raises the circulating insulin level to 10–
20 times the normal fasting level and provides near-
maximal stimulation of each action of insulin, as follows:
inhibition of hepatic glucose production
inhibition of lipolysis
stimulation of glucose uptake by the peripheral tissues.
16. Potassium replacement
In established DKA, total body K+ deficits amount to
200–400 mmol or 3–5 mmol/kg body weight. The initial
plasma K+ value may be low, normal or high.
During the treatment of DKA, plasma K+ concentration will
drop because of:
rehydration (dilution)
correction of acidaemia
continued renal excretion
insulin-mediated cellular uptake.
17. Bicarbonate administration
There is no evidence that administration of bicarbonate
(HCO3) is either necessary or safe in DKA. Bicarbonate
should not be used in the initial resuscitation procedure.
The potential hazards of HCO3 therapy include:
paradoxical exacerbation of central nervous system
acidosis
hypokalaemia and altered calcium ionization
excessive osmolar load and volume overload
tissue hypoxia.
21. Clinical observations and monitoring
Monitoring Interval
Clinical
Mental status 1 h
Vital signs (temperature; pulse; respiratory rate;
blood pressure)
1 h
ECG As indicated
Weight As indicated
Therapy
Fluid intake and output (mL/h) 1–4 h
Insulin (unit/h) 1–4 h
Potassium (mmol/L) 1–4 h
Bicarbonate (mmol/L) 1–4 h
Laboratory
Glucose (bedside) 1 h
Potassium, pH 1–2 h
Sodium, chloride bicarbonate 2–4 h
BUN or creatinine 4–6 h
Urine ketones 2–4 h
Calcium As indicated
Haematocrit As indicated
22. Other considerations
Type and cross-match if necessary.
Take blood (and other) cultures if necessary.
Aspirate stomach contents if comatose.
Catheterize if needed for accurate urine output
measurement.
Keep patient nil by mouth.
23. Complications Attributable to the
Treatment of DKA
Premature discontinuation of insulin may result in
persistence and worsening of ketoacidosis.
Cerebral oedema may occur, particularly in children:
∘ Rapid correction of hyperglycaemia
∘ Excessive amounts of hypotonic fluid.
Early feeding may lead to vomiting and aspiration
pneumonia.
Too aggressive fluid replacement may induce congestive
heart failure.
24. Mortality
Mortality from DKA when there is a delay in treatment still
remains high and may reach 5%.
Major causes of mortality are associated with medical co-
morbidities that precipitate DKA.
Prevention of DKA and sick day guidelines remain the most
important aspects of management.
25. Prevention
Patients should be given the following advice:
Measure blood glucose at least four times a day.
Depending on blood glucose results, take an extra-short-
acting insulin.
Replace food with plenty of sugar-free liquids.
If blood glucose persists at ≥17 mmol/L, contact your
doctor.