Diabetic Emergencies Flashcards

1
Q

What are the 2 HYPERglycaemic emergencies?

A

DKA (diabetic ketoacidosis)

HHS (hyperosmolar hyperglycaemic state)

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2
Q

What is the triad of DKA?

A

Hyperglycaemia
Hyperketonaemia
Metabolic Acidosis

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3
Q

What is the DKA diagnostic criteria?

A

BM >11mmol/L (diabetic level) or KNOWN diabetic
Blood ketones >3mmol/L or ketonuria >2+
Bicarb <15mmol/L or venous pH <7.3

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4
Q

Other than low insulin, what else can cause increased ketone production and therefore DKA?

A

Increase stress hormones (cortisol, catecholamines) which also promote the ketone pathway

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5
Q

What is the role of insulin with respect to potassium?

How does this affect DKA?

A

Insulin causes potassium to move INTO cells

In DKA in T1DM patients, the lack of insulin causes K leak from cells causing a high extracellular K (hyperkalaemia)

This causes K loss via urine = whole body K depletion

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6
Q

Why in DKA treatment is it important to think about K?

A

When DKA is treated K moves into the cells quickly from the plasma, and with total body K depletion this means K levels in plasma fall quickly

Arrhythmias can therefore occur

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7
Q

Why can cerebral oedema, PE and ARDS occur in DKA?

A

Fluid shifts

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8
Q

What are breathing signs of DKA?

Why does this occur?

A

Kussmaul breathing = deep, sighing breaths

To respiratory compensate for acidosis by removing CO2 from the body

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9
Q

What are the principles and steps of treatment of DKA?

A

Fluid replacement (helps acid/base balance)
Insulin replacement
Potassium replacement as fluids + insulin will cause K shift into cells
Indemnify and treat cause (?infection)
VTE prophylaxis

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10
Q

What is the insulin treatment dose for DKA?

A

0.1unit/kg/hr

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11
Q

Which fluid do you use as replacement in DKA?

A

0.9% sodium chloride

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12
Q

In which patient groups is DKA most likely seen?

What about HHS?

A

DKA = T1DM patients

HHS = T2DM patients, as enough insulin production to suppress ketogenesis

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13
Q

What is the clinical definition/diagnosis of HHS?

A

No precise definition

  • hypovolaemia (due to osmotic diuresis)
  • hyperglycaemia >30mmol/L!!!!!
  • hyperosmolarity of serum >320mosm/kg

KEY FACTOR:
- ketones <3mmol/L, no acidosis (pH>7.3) and bicarb >15mmol/L

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14
Q

Which condition has greater mortality risks and why, DKA or HHS?

A

HHS as metabolic disturbance is greater

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15
Q

Compare the DKA and HHS onset times?

A

HHS happens over days, DKA is quicker

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16
Q

How would you calculate the osmolarity from a blood gas?

A

(2 X Na) + glucose + urea

17
Q

How does HHS treatment differ from DKA?

A

Slow replacement of fluids

Lower insulin infusion (0.05units/kg/hr)

18
Q

What are the main differences in measurements (values) seem between DKA and HHS?

A

DKA = ketones high = low pH and low bicarb, GLUCOSE >11mmol/L

HHS = ketones normal (or just raised), pH normal, bicarb normal, GLUCOSE&raquo_space;30mmol/L!!!!

19
Q

What does ‘sick day rules’ mean?

What are some of these?

A

Rules of what to do or stop if “sick”

  • never stop background insulin
  • check BM and for ketones frequently
  • extra short acting insulin needed if BM or ketones rising
  • drink fluid = 100ml/hr
  • seek medical help if not handling well
20
Q

What is the diagnostic criteria/definition of hypoglycaemia?

A

BM <3.5mmol/L (4.0mmol/L if in hospital)

21
Q

Why do hypos occur?

A

Over treatment with:

  • insulin
  • sulphonylureas (gliclazide)

Or normal doses without eating properly

E.g. insulin requirement:level mismatch