diabetic ketoacidosis Flashcards

1
Q

DKA is a triad of

A

hyperglycaemia
metabolic acidosis
increased total body ketone concentration

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2
Q

DKA results from

A

absolute or relative deficiency of circulating insulin and the effects of increased levels of counter-regulatory hormones

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3
Q

biochemical criteria for the diagnosis of DKA

A
  1. hyperglycaemia >11mmol/L
  2. Ketoanaemia (blood bethydroxybutyrate >3mmol/L or moderate or large ketonuria)
  3. acidosis: venous pH <7.3 or bicarbonate <15mmol/L
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4
Q

euglycaemia ketaacidosis

A

rarely DKA may present with near normal glucose levels

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5
Q

if a child is hyperosmolar with very high BGL >30mmol/L, with little or no acidosis or ketones

A

this is a hyperosmolar hyperglycaemia state (HHS)
requires completely different treatment
discuss with senior doctor

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6
Q

causes and precipitants of DKA

A

insufficient insulin, newly diagnosed type 1 diabetes
missed insulin dose
infection/illness

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7
Q

assessment

A
  1. is the patient shocked/haemodynamically stable?
  2. assess ABCs and fluid resuscitate
  3. contact ED consultant, PCC and endocrinology
  4. confirm diagnosis and determine causes
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8
Q

symptoms of DKA

A

polyuria
polydipsia
weight loss
abdominal pain
weakness
nausea and vomiting
confusion

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9
Q

signs of DKA

A

dehydration
deep sighing respiration (Kussmaul)
smell of ketones

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10
Q

biochemistry prior to arrival

A

elevated BGL >11mmol/L
acidaemia pH <7.3
moderate or large ketones in urine and/or blood ketonaemia

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11
Q

goals of therapy are to

A

correct dehydration
correct acidosis and reverse ketosis
restore normal BGL
avoid complications of therapy

priorities are fluid resus then insulin

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12
Q

children who are alert, not clinically dehydrated and not nauseated or vomiting

A

do not always require IV fluids even if their ketone levels are high
usually tolerate oral rehydration and subcut insulin
they do require monitoring regularly to ensure they are improving and their ketone levels are falling

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13
Q

general resuscitation for shocked or haemodynamically unstable patients

A

airway
ensure airway is patent or provide airway support eg. airway manouvres, gueddel airway or endotracheal tube
Breathing
give oxygen by facemask
Circulation
measure blood pressure and heart rate and capillary refill time
cardiac monitor for T waves (peaked in hyperkalaemia)
insert two IV cannulas for resuscitation and blood sampling

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14
Q

APLS definition of shock

A

tachycardia, prolonged central capillary refill, poor peripheral pulses and hypotension (though this is a late sign of shock)

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15
Q

how much fluid should non shocked patients get

A

all children and young adults with mild, moderate or severe DKA who are not shocked and are felt to require Iv fluids should recieve a 10ml/kg sodium chloride 0.9% bolus over 60 minutes

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16
Q

how much fluid should shocked patients get

A

20ml/kg bolus of sodium chloride 0.9% over 15 minutes
following this, reassess and administer further boluses of 10ml/kg if required
to a limit of 40ml/kg, at which point ionotropes should be considered

17
Q

why should excessive fluid be avoided

A

risk of cerebral oedema

18
Q

initial investigations

A

blood glucose
blood gasses (venous or capillary)
FBC
urea and electrolytes, electrolytes on blood gas machine are acceptable and the same measuring system should be used throughout management of DKA
ketones (beta-hydroxybutyrate)
new diagnosis bloods including HbA1c when possible during first admission

19
Q

raised white blood cell count in DKA

A

common, does not necessarily indicate infection

20
Q

clinical assessment when admitting a patient with DKA

A

conscious level - hourly neurological examinations
comprehensive examination - look for cerebral oedema, infection, ileus (common in DKA)
weigh patient

21
Q

signs of cerebral oedema

A

headache, irritabillity, slowing pulse, lethargy, incontinence, thermal instability
papilloedema is a late sign

22
Q

potassium replacement therapy is required because

A

there will be a total body deficit of potassium and correction of the acidosis in the absence of potassium therapy will usually rapidly result in hypokalaemia (levels in the blood will fall once insulin is commenced)

23
Q

monitoring during potassium infusion

A

continuous ECG monioring
if serum potassium is >5mmol cease potassium infusion

24
Q

bicarbonate administration

A

not routinely recommended
except for rare circumstances in extremely sick children

25
Q

what happens to phosphate levels in DKA

A

depletion of intracellular phoshate occurs in DKA and phosphate is also lost form osmotic diuresis
plasma phosphate levels fall after starting treatment and this is execerbated by insulin promoting phosphate netry into cells
consider phosphate replacement

26
Q

potential complications of DKA

A
  1. hyper/hyponatraemia
  2. hypoglycaemia
  3. cerebral oedema
27
Q

preventing hypoglycaemia

A

if the blood glucose levels fall too low and the patient is still ketotic, give IV glucose, do not discontinue insulin

28
Q

when might cerebral oedema develop

A

may suddenly develop clinically, usually between 6-12 hours after starting therapy

29
Q

prevention of cerebral oedema

A

slow correction of fluid and biochemical abnormalities

30
Q

very late signs of cerebral oedema

A

rising blood pressure, bradycardia and respiratory impairment

31
Q
A