Diabetic Ketoacidosis

Question 1

List some DDx for a presentation of:

• weakness, lethargy
• polydipsia
• vague abdo pain
• dry mucosal membranes
• sweat smelling breath
• urinalysis ketone +++

Answer 1

PDx. DKA
DDx.
- Ketoacidosis- diabetic, starvation, alcoholic
- Hyperglycaemic hyperosmolic state (HHS) (80% T2DM)
- anion gap metabolic acidosis causes (MUDPILES mnemonic): methanol, uremia, DKA, propylene glycol, iron, lactic acidosis, ethylene glycol, salicylates)

Question 2

Account for the signs and symptoms of DKA?

Answer 2

• Polyuria: hypergycaemia -> glycosuria -> osmotic diuresis
• Polydipsia: osmotic diuresis (RAAS) -> dehydration -> hypothalamus osmoreceptors -> angiotensin II -> thirst
• weakness: hyperglycaemia -> decrease substate available for muscle energy
• decreases LOC: dehydration and acidosis
• ketotic fetor: acetoacetate carboxylation to acetone
• hypotension: glycosuria -> osmotic diuresis
• weight loss: insulin deficiency -> accelerated breakdown of muscle/fat
• tachycardia: volume depletion
• tachypnoea (Kussmal breathing): metabolic acidosis -> attempt to release CO2 and increase pH

Question 3

What investigations would you do?

Answer 3

Ensure haemodynamically stable
Bedside
- vitals, weight
- glucose
- osmolality 
- ABG (high anion gap metabolic acidosis)
- EUC (esp K+)
- urinalysis (glucose, ketones)
- ECG (arrhythmia/ hyperkalaemia)
Bloods
- HbA1c (acute)
- infection screen: urine MCS, CXR, blood culture, FBC
- auto-antibodies to islet cells: anti-glutamic acid decarboxylase Ab and insulin auto Abs
- C-peptide (degree of endogenous insulin production)
- screen coeliac disease
- TFT

Question 4

Explain how this pt develops hyperkalaemia?

Answer 4

High anion gap metabolic acidosis w resp compensation

• renal tubule K+/H+ exchanger: H+ enters and K+ exits tubule -> attempt to prevent increased acidosis
• insulin normally acts to transport K+ into cell -> remains extracellular

Question 5

How do you calculate an anion gap?

Answer 5

Anion gap = Na (+ K) – (Cl + HCO3)

Question 6

List some causes of an increased anion gap metabolic acidosis?

Answer 6

Increased anion gap (KUSMAL mnemonic):
K- ketoacidosis
U- uraemia
S- starvation
M- methanol
A- alcohol and other drugs (salicylates)
L- lactic acidosis

Question 7

Differentiate between polyuria and polydipsia?

Answer 7

Polyuria: increased urine vol >3L/day
- causes: DM, overhydration, DI, renal failure (polyuric phase)
Polydipsia: increased thirst
- controlled by hypothalamus osmoreceptors swelling/shrinking based on osmolality -> angiotensin 2 stimulates thirst
- causes: DM, DI, dehydration, hypercalcaemia, psychogenic, anticholinergics, hyperaldosteronism

Question 8

List some effects of low pH?

Answer 8

Respiratory
- increased resp stimulus, increased WOB
CVS
- decreased cardiac output (electrolyte disturbance and impaired muscle contraction)
- arrhythmia
- decreased vascular tone
- pulm vasoconstriction
Neuro
- cerebrovasodilation -> raised ICP
Electrolyte
- hyperkalaemia (H+/K+ exchange)
- hypercalcaemia (renal failure)
Renal
- increased ammonia production -> increased O2 demand
- diuresis
GIT
- decreased stomach emptying (impaired msucle activity) -> N/V
Haem
- coagulopathy (clotting factors impaired)
- impaired platelet aggregation (acidosis -> hyperchloraemia)

Question 9

Describe the pathophysiology of DKA?

Answer 9

T1DM: type 4 hypersensitivity reaction -> autoimmune destruction of B cells in pancreatic islets of Langerhans -> insulin deficiency
- due to genetics (HLA alleles) and eviro
DKA: due to absolute insulin deficiency
-> impairs glucose uptake into cells -> “starving”
-> increased counter-regulatory hormones
-> TG broken down to FFAs
(FFA normally broken down to acetyl-CoA then combines to oxaloacetate to form citrate and enter TCA cycle)
-> oxaloacetate used in gluconeogenesis -> FFA diverted to ketone body production (acetoacetate and B-hydroxybutyric acid)
-> ketones are acidic -> consume HCO3-> metabolic acidosis
-> compensatory Kussmal breathing -> respiratory acidosis

Question 10

What can trigger DKA?

Answer 10

• insulin non-compliance or inappropriate Rx (most common)
• 1st T1DM presentation
• acute illness (w T1DM hx)
• infection (pneumonia, UTI, gastro, sepsis)
• CVA
• MI
• acute pancreatitis
• exercise
• starvation, dehydration
• ETOH
• surgery
• iatrogenic (adrenaline, glucocorticoids, clozapine, olanzapine, lithium)

Question 11

List some complications of DKA?

Answer 11

Acute:
- hypoglycaemia
- hypovolemic shock -> end organ damage
Long-term:
- endothelial damage (advanced glycosylation end products)
- sorbitol accumulation -> osmotic injury, neuropathy, diabetic cataracts

Question 12

List some complications of T2DM?

Answer 12

Macro:
- stroke
- peripheral arterial disease
- coronary artery disease
Micro:
- diabetic retinopathy
- diabetic nephropathy- glomerulosclerosis, interstitial fibrosis, ESKD (35%)
- diabetic neuropathy (sorbitol accumulation in myelin sheath -> osmotic swelling -> impaired neural transmission)
- immunosuppression (neutrophils) -> pyelonephritis, foot ulcers

Question 13

How would you manage DKA?

Answer 13

• primary survey
• bolus 0.9% normal saline (NO dextrose)
• wait for fluid to wash out glucose for 1hr -> remeasure
• give rapid acting insulin (once K >3.3)