Diabetic Ketoacidosis and Hyperosmolar Hyperglycaemic State Flashcards
Diagnostic criteria for DKA
- Random blood glucose > 15mmol/L (but <33.3mmol/L)
- Academia with arterial pH < 7.3, bicarbonate < 15mmol/L
- Ketonaemia (beta-hydroxybutyrate >/= 3mmol/L) or moderate ketonuria (>/= 3+)
Management of DKA (4 pillars)
- ABCs & supportive
+/- Supplemental O2
Pillar 1: Fluid replacement
- Corrected sodium = measured sodium + 0.3(current glucose - 5.5)
- Initial bolus 10ml/kg of normal saline over 1h, repeat until stable
- Replace fluid deficit (NS) over next 48h: Deficit + Maintenance (holiday-segar)
- Deficit: % dehydration x body weight (kg)
- Mild DKA ~5% dehydration
- Moderate DKA ~5-7% dehydration
- Severe DKA ~7-10% dehydration
Pillar 2: Treat underlying precipitate
Pillar 3: Correct potassium
- Insulin causes K+ to shift intracellularly, may worsen any pre-existing hypokalaemia
- K+ > 5.2: Give IV insulin
- 3.3 < K+ < 5.2: Replace K+ (IV KCL 40mmol/L/h) and give IV insulin
- K+ < 3.3: Replace K+ FIRST. Withhold insulin until K+ > 3.3
Pillar 4: Give IV insulin
- BOLUS 0.1unit/kg body weight of IV soluble insulin first (no need in paeds, infusion straight)
- Followed by continuous infusion of 0.1unit/kg body weight hourly (if <6yo then 0.05)
- Target 10% decrease in BSL in 1st hour then 3-4mmols decrease per hour
- Once BSL < 14, start IV D5% + Reduce IV insulin rate by 50%
- Aim for 8-12mmol/L (5-10 in paeds)
- Once DKA resolves, CBG < 11.1 and either 2 of the following:
BHOB < 0.3
pH > 7.3
HCO3- > 15
AG < 12
Change IV insulin to SC insulin
+ Monitoring: Vitals, ECG, SpO2
+ Check serum glucose hourly and ketones, potassium every 4 hourly (2 hourly if severe)
DKA: Clinical features
Abdominal pain
Nausea, vomiting
Kussmaul breathing (compensate metab acidosis)
Fruity breath (acetone)
+ Features shared with HHS:
Polyuria
Polydipsia
Polyphagia
LOW
Precipitants of DKA/HHS
DKA:
Insulin
- non-compliance
- missed dose
- undiagnosed
HHS:
Insulin
- increase insulin demand
Infection
- UTI, pneumonia, sepsis
Inflammation (‘itis’)
Infarction
- AMI
- Stroke
Intoxication
- Increase alcohol consumption
- Drugs
Iatrogenic
- Steroids (Corticosteroids increase blood glucose levels → increase insulin demand)
- Surgery (Wound healing requires glucose + general stress to the body)
Common cause of euglycaemic DKA
SGLT2 inhibitors
Where and what ketones can be found?
Blood: Beta hydroxybutyrate
Breath: Acetone
Urine: Acetoacetate
Pathophysio of DKA
Diabetic ketoacidosis (DKA) is caused by a combination of
- insulin deficiency (absolute or relative)
and an increase in counterregulatory hormones, leading to increased
- gluconeogenesis
- accelerated glycogenolysis
- impaired glucose utilisation by peripheral tissues
- lipolysis
- unrestrained hepatic fatty acid oxidation to ketone bodies
culminating in hyperglycaemia and ketonaemia
Investigation in DKA
POCTs
- CBG
- ABG
- Urine dipstick
- ECG tro preciptitating cardiac cause
Labs
- FBC
- Renal panel
- Serum beta hydroxybutyrate
- Serum glucose
- Urinanalysis
Imaging
- CXR tro precipitating cardiac cause
Potential complications while managing hyperglycaecmic crisis
Cerebral edema - rapid correction of hyperglycaemia
- patient drowsy, initial blood glucose levels >30mmol/L
Hypoglycaemia
Hypokalemia
Hyperchloremia
Fluid overload
ARDS
Thromboembolism
Rhabdomyolysis
Why does tachypnea occur in DKA?
Increased hydrogen ion concentration in the blood due to metabolic acidosis which stimulates the peripheral chemoreceptors (aortic and carotid bodies), leading to an increased respiratory rate (Kussmaul’s respiration) to exhale more CO2 as a form of compensatory mechanism
Why does fruity breath occur in DKA?
Acetoacetate can get further broken down, producing acetone → sent to the lungs and exhaled out → fruity breath odour
Pathophysiology of hyperosmolar hyperglycaemic state
1: Insulin resistance and/or deficiency
2: Inflammatory state with marked elevation in pro inflammatory cytokines and counter regulatory stress hormones that cause increased hepatic gluconeogenesis and glycogenolysis
· Increased stress to the body stimulates the sympathetic nervous system, releasing epinephrine and norepinephrine
· Epinephrine and norepinephrine will stimulate glucagon production by the pancreatic alpha cells
· Increase epinephrine, norepinephrine and glucagon will act on the liver → gluconeogenesis & glycogenolysis will occur
3: Osmotic diuresis followed by impaired renal excretion of glucose
· Excess glucose cannot be reabsorbed by the proximal convoluted tubules and excreted into urine
· Glucose in the urine (glucosuria) draws water out into the urine through osmotic diuresis
· Leads to dehydration
· Leads to decreased water concentration in the blood + a lot of glucose in the blood → hyperosmolar state
Diagnostic criteria for HHS
- Blood glucose > 33mmol/L
- Arterial pH > 7.3, HCO3 > 15mmol/L
- Serum osmolality > 320 mOsm/kg
How to calculate serum osmolality?
2 x Na + glucose
Management of HHS
Similar to DKA except insulin bolus is NOT required and more fluids are needed
Clinical features of HHS
A) Dehydration +++
-> Hypovolemia
– decreased skin turgor
– dry mucosa membrane
-> Hypotensive
– decrease urine output (due to decrease renal perfusion)
– reflex tachycardia and diaphoresis
B) Hyperosmolar (Glucose in blood will cause water inside the neurons of CNS and muscle cells to move out)
-> CNS neurons
– AMS, seizure, coma
-> Muscle cells
– muscle weakness
Difference between DKA & HHS
DKA
- Usually in T1 DM
- Rapid onset
- Kussmaul breathing, fruity breath, abdominal pain, N/V
- Anion gap: HAGMA > 12mEq/L
- Serum glucose > 15mmol/L (& less than 33)
- Arterial pH < 7.3
- Serum bicarbonate < 15mmol/L
- Urinanalysis: Ketonuria, glycosuria
- Presence of serum beta hydroxybutyrate
HHS
- Usually in T2 DM
- Insidious onset
- Dehydration +++
- Anion gap: NAGMA (within 8-12mEq/L)
- Serum glucose > 33mmol/L
- Arterial pH > 7.3
- Serum bicarbonate > 15mmol/L
- Urinanalysis: NO ketones, glycosuria +++
- Serum osmolality > 320mOsm/kg
How to calculate anion gap?
Anion gap = (Na+) + (K+) - (Cl-) - (HCO3-)
Or
Anion gap = unmeasured anions - unmeasured cations
Why is there HAGMA in DKA?
Anion gap = (Na+) + (K+) - (Cl-) - (HCO3-)
Or
Anion gap = unmeasured anions - unmeasured cations
Since acidic ketones will cause HCO3- (bicarbonate) buffer to decrease AND
ketone bodies are unmeasured anions, thus causing an increase in unmeasured anions
THEREFORE resulting in HAGMA
Severity of DKA can be determined by
pH
- Mild: pH 7.2-7.3, HCO3- 10-15
- Moderate: pH 7.1-7.19, HCO3- 5-10
- Severe: pH < 7.1, HCO3- <5
Blood glucose targets for paeds
5-10mmol/L
Why do we choose normal saline > Hartmann’s for DKA fluid management?
Hartmann’s solution contains lactate -> can worsen the metabolic acidosis
