Diabetic ketoacidosis Flashcards
Definition
Complication of DMT1
Triad of:
- Hyperglycaemia
- Ketosis (raised plasma ketones)
- Metabolic acidosis
Aetiology
- interruption of insulin therapy in type 1 diabetics (patients often omit insulin therapy if they feel nauseous or unable to eat, but this should NOT be done)
- previously undiagnosed diabetes
- In type 1 diabetics on insulin therapy: stress due to intercurrent illness (e.g. surgery, infection) leads to adrenaline release ⇒ glucagon release & ketogenesis.
- myocardial infarction (diabetics experience silent MI due to peripheral neuropathy)
Pathophysiology
-
Ketoacidosis is a state ofuncontrolled catabolism
(break down) associated withinsulin deficiency - Low insulin results in HIGH circulating glucagon (no paracrine feedback b/w alpha & beta cells in pancreatic Islets of Langerhans) ⇒ unrestrained lipolysis releasing FFA ⇒ increased FFA oxidation to acetyl coA ⇒ acidic ketone bodies (acetoacetic acid, beta hydroxybutyrate) produced during ketogenesis in the mitochondria ⇒ acidosis (blood pH < 7.35)
- Ketones are acidic and lower blood pH causing Kussmaul’s respiration (deep laboured breathing) & K+ imbalance (high serum K+ but low ttotal body K+ as less K+ inside cells).
- Absolute insulin deficiency means there is high glucagon resulting in: increased lipolysis releasing glycerol as a gluconeogenic substrate for hepatic gluconeogenesis, increasing glycogenolysis & decreased peripheral uptake of glucose by muscle & adipose tissue. This all leads to hyperglycaemia.
- High circulating glucose leads to osmotic diuresis causing dehydration & loss of electrolytes in urine.
- Vomiting leads to further loss of fluid and electrolytes
Explain why there is K+ imbalance in diabetic ketoacidosis
Serum K+ may be high (hyperkalemia) or normal but total body K+ is low because:
Increased acidity of blood = more protons in blood. H+ ions are transported into cells in exchange for K+ out of cells via a H+/K+ antiporter so total body K+ is low because no more K+ is stored inside cells, but serum K+ is high.
Also, complete insulin deficiency means insulin is not available to transport K+ into cells via Na+/K+ exchanger ⇒ more K+ outside of cells results in high serum K+ but low body K+ (as less K+ inside cells).
Explain why deep laboured breathing is a sign of DKA
Kussmaul’s respiration occurs as body tries to compensate for metabolic acidosis by blowing off more CO2 to increase blood pH to normal & reduce acidity of blood.
H+ + HCO3- → H2CO3 (carbonic acid) → CO2 + H20
Signs and symptoms
T1DM symptoms (polyuria, polydipsia, sudden unexplained weight loss, glycosuria) +
- Reduced tissue turgor (skin on dorsum of hand is pulled back & takes long time to return to original shape) = sign of dehydration)
- Dehydration (due to glycosuria & osmotic diuresis)- can cause hypotension
- Nausea & vomiting
- Kussmaul’s respiration (hyperventilation- deep, laboured breathing - lungs try to compensate for metabolic acidosis by blowing off more CO2 to reduce acidity of blood)
- Pear drop breath- due to acetone (fruity ketone) being expired
- Acute abdominal pain (confused with appendicitis)
- Ketonuria (ketones in urine)
- Drowsiness/confusion
Investigations & diagnosis
DKA should be recognised from clinical features and confirmed with a blood glucose measurement (hyperglycaemia) and an arterial blood gas sample (metabolic acidosis with respiratory compensation).
Diagnose if:
- hyperglycaemia (RPG >11.1 mmol/L)
- Ketosis ( blood ketones > 3mmol/L)
- AND acidosis (HCO3- < 15 mmol/L and/or pH < 7.3)- ABG
Other 1st line investigations:
- Urine dipstick- glycosuria & ketonuria
- U & E- shows raised serum K+ due to absence of insulin, raised urea & creatinine due to dehydration
Treatment
- Immediate ABC (airway, breathing, circulation) if Px is unconscious
- 1st line = Rehydrate with IV fluids 0.9% NaCl - to treat dehydration (most patients die from dehydration first)
- then Insulin (to replace deficient insulin & suppress hepatic ketogenesis) + glucose (to prevent hypoglycaemia)
- then potassium replacement with KCL infusion added to IV fluid infusion (because in DKA even if serum K+ is normal, total body K+ is low as K+ has been kicked out of cells via H+/K+ antiporter)
Complications
- If fluid is replaced too quickly, brain can swell leading to cerebral oedema (children more at risk).
- Acute respiratory distress syndrome-ARDS (extension of hyperventilation- Kussmaul’s respiration)
- Hyperkalemia (high serum K+) leading to arrythmias. Insulin therapy can lead to hypokalemia as insulin shoves K+ into cells via Na+/K+ ATPase pump
Why can cerebral oedema occur?
Rapid fluid replacement leads to hyponatremia. This causes an osmotic shift of water from the blood into the tissues, which in the brain causes cerebral oedema. Cerebral oedema can lead to rapid deterioration, coma therefore fluid boluses are not advised & fluid resuscitation is advised to be undertaken slowly over 48 hours.
