6.13 DKA Flashcards
You are asked to review an 18-year-old male in the emergency department who has been found obtunded at home. He is an insulin-dependent diabetic with a history of poor control. Capillary blood glucose is 23.4mmol/L.
a) List the biochemical findings that confirm the diagnosis of
diabetic ketoacidosis (DKA).
The diagnostic triad of DKA is:
● Ketonaemia >3.0mmol/L
or significant ketonuria
(more than 2+ on urine sticks).
● Blood glucose >11.0mmol/L
or known diabetes mellitus.
● Bicarbonate <15.0mmol/L,
venous pH <7.3,
or both.
b) What are the clinical features of DKA? List at least two signs and two symptoms.
Symptoms:
● Thirst, polyuria, polydipsia.
● Nausea, vomiting.
● Abdominal pain.
● Lethargy.
● Could even be the first presentation of DM.
Signs:
● Dehydration.
● Tachycardia, hypotension.
● Kussmaul respiration.
● Ketotic breathing.
● Altered consciousness, confusion.
c) What other clinical and biochemical findings are seen in severe DKA?
The presence of one or more of the following:
● GCS less than 12 or abnormal AVPU scale.
● Oxygen saturation below 92% on air assuming normal baseline respiratory function.
● Systolic BP below 90mmHg.
● Pulse over 100 or below 60 bpm.
● Blood ketones over 6mmol/L.
● Bicarbonate level below 5mmol/L.
● Venous/arterial pH below 7.0.
● Hypokalaemia on admission
(under 3.5mmol/L).
● Anion gap above 16
(anion gap = [Na+ + K+] – [Cl- + HCO3 -]).
d) What is the pathophysiology of DKA?
●Relative or absolute insulin deficiency.
● Increase in counter-regulatory hormones.
● Hyperglycaemia due to gluconeogenesis,
glycogenolysis, and impaired glucose utilisation
by peripheral tissues.
● Free fatty acid release and their oxidation
in the liver to ketones.
● Hydrogen ions produced by the
dissociation of the ketone bodies
cause metabolic acidosis.
● Hyperglycaemia causes an osmotic fluid
shift from intracellular to
extracellular compartments.
● Hyperglycaemia causes osmotic diuresis
and loss of sodium, potassium, phosphate,
water and glucose.
e) What are the three most common causes of DKA?
● An underlying infection.
● Missed insulin treatment.
● First presentation of diabetes mellitus.
f) What investigations would you request in such a presentation
of DKA?
Mandatory investigations:
● Capillary ketone levels/urinalysis for ketones.
● Blood sugar.
● Blood gas for pH, bicarbonate, or both.
Routine investigations:
● Full blood count.
● Urea.
● Creatinine.
● Potassium.
● Sodium.
● Chloride.
● CRP.
● Liver function tests.
Investigations to detect the cause:
● ECG.
● Cultures.
● Amylase.
● Pregnancy test.
Ongoing investigations:
● Hourly CBG/arterial blood glucose and capillary blood ketones.
● 2-hourly pH, bicarbonate and potassium
g) Outline the management plan for severe DKA within the first hour.
Resuscitation — ABCDE approach.
● Intravenous fluid — normal saline.
● Fixed rate IV insulin infusion at 0.1 units/kg/hour.
● Establish appropriate monitoring and investigations.
● If systolic BP <90mmHg, then administer a 500ml normal saline infusion over 15 minutes.
Repeat if the patient remains hypotensive.
Refer to intensive care if haemodynamic instability continues.
● Treatment of hyperkalaemia or hypokalaemia.
● If the patient takes a long-acting insulin,
continue this at the normal dose and normal time.
h) What are the serious complications that can follow the
management of DKA?
● Cerebral oedema.
● Hypoglycaemia.
● Hypokalaemia, hyperkalaemia.
● Pulmonary oedema.
i) What is the mechanism of hypokalaemia in DKA and how is it
managed?
Potassium loss is caused by:
● A shift of potassium from the intracellular to extracellular space in exchange for hydrogen ions which accumulate in acidosis.
● A loss of extracellular potassium through osmotic diuresis.
Management:
● No potassium should be added to the initial litre of fluid.
● Subsequent fluids should have 40mmol/L of potassium chloride, provided the serum potassium is <5.5mmol/L, and the patient is not oliguric.
