Diabetic Ketoacidosis and Hyperosmolar Hyperglycaemic State Flashcards

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1
Q

Diagnostic criteria for DKA

A
  1. Random blood glucose > 15mmol/L
  2. Academia with arterial pH < 7.3, bicarbonate < 15mmol/L
  3. Ketonaemia (beta-hydroxybutyrate >/= 3mmol/L) or moderate ketonuria (>/= 3+)
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2
Q

Management of DKA (4 pillars)

A
  • ABCs & supportive
    +/- Supplemental O2

Pillar 1: Fluid replacement
- Corrected sodium = measured sodium + 0.3(current glucose - 5.5)

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+ 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
- Followed by continuous infusion of 0.1unit/kg body weight hourly
- 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
- 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)

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3
Q

DKA: Clinical features

A

Abdominal pain
Nausea, vomiting
Kussmaul breathing (compensate metab acidosis)
Fruity breath (acetone)

+ Features shared with HHS:
Polyuria
Polydipsia
Polyphagia
LOW

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4
Q

Precipitants of DKA/HHS

A

Insulin
- non-compliance
- missed dose
Infection
- UTI, pneumonia, sepsis
Inflammation
Infarction
Iatrogenic
- Steroids
- Surgery

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5
Q

Common cause of euglycaemic DKA

A

SGLT2 inhibitors

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6
Q

Where and what ketones can be found?

A

Blood: Beta hydroxybutyrate
Breath: Acetone
Urine: Acetoacetate

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7
Q

Pathophysio of DKA

A

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

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8
Q

Investigation in DKA

A

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

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9
Q

Potential complications while managing hyperglycaecmic crisis

A

Hypoglycaemia
Hypokalemia
Hyperchloremia
Fluid overload
ARDS
Thromboembolism
Rhabdomyolysis

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10
Q

Why does tachypnea occur in DKA?

A

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

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11
Q

Why does fruity breath occur in DKA?

A

Acetoacetate can get further broken down, producing acetone → sent to the lungs and exhaled out → fruity breath odour

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12
Q

Pathophysiology of hyperosmolar hyperglycaemic state

A

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

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13
Q

Diagnostic criteria for HHS

A
  • Blood glucose > 33mmol/L
  • Arterial pH > 7.3, HCO3 > 15mmol/L
  • Serum osmolality > 320 mOsm/kg
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14
Q

How to calculate serum osmolality?

A

2 x Na + glucose

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15
Q

Management of HHS

A

Similar to DKA except insulin bolus is NOT required and more fluids are needed

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16
Q

Clinical features of HHS

A

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

17
Q

Difference between DKA & HHS

A

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

18
Q

How to calculate anion gap?

A

Anion gap = (Na+) + (K+) - (Cl-) - (HCO3-)
Or
Anion gap = unmeasured anions - unmeasured cations

19
Q

Why is there HAGMA in DKA?

A

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