diabetic ketoacidosis Flashcards
DKA is a triad of
hyperglycaemia
metabolic acidosis
increased total body ketone concentration
DKA results from
absolute or relative deficiency of circulating insulin and the effects of increased levels of counter-regulatory hormones
biochemical criteria for the diagnosis of DKA
- hyperglycaemia >11mmol/L
- Ketoanaemia (blood bethydroxybutyrate >3mmol/L or moderate or large ketonuria)
- acidosis: venous pH <7.3 or bicarbonate <15mmol/L
euglycaemia ketaacidosis
rarely DKA may present with near normal glucose levels
if a child is hyperosmolar with very high BGL >30mmol/L, with little or no acidosis or ketones
this is a hyperosmolar hyperglycaemia state (HHS)
requires completely different treatment
discuss with senior doctor
causes and precipitants of DKA
insufficient insulin, newly diagnosed type 1 diabetes
missed insulin dose
infection/illness
assessment
- is the patient shocked/haemodynamically stable?
- assess ABCs and fluid resuscitate
- contact ED consultant, PCC and endocrinology
- confirm diagnosis and determine causes
symptoms of DKA
polyuria
polydipsia
weight loss
abdominal pain
weakness
nausea and vomiting
confusion
signs of DKA
dehydration
deep sighing respiration (Kussmaul)
smell of ketones
biochemistry prior to arrival
elevated BGL >11mmol/L
acidaemia pH <7.3
moderate or large ketones in urine and/or blood ketonaemia
goals of therapy are to
correct dehydration
correct acidosis and reverse ketosis
restore normal BGL
avoid complications of therapy
priorities are fluid resus then insulin
children who are alert, not clinically dehydrated and not nauseated or vomiting
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
general resuscitation for shocked or haemodynamically unstable patients
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
APLS definition of shock
tachycardia, prolonged central capillary refill, poor peripheral pulses and hypotension (though this is a late sign of shock)
how much fluid should non shocked patients get
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
how much fluid should shocked patients get
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
why should excessive fluid be avoided
risk of cerebral oedema
initial investigations
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
raised white blood cell count in DKA
common, does not necessarily indicate infection
clinical assessment when admitting a patient with DKA
conscious level - hourly neurological examinations
comprehensive examination - look for cerebral oedema, infection, ileus (common in DKA)
weigh patient
signs of cerebral oedema
headache, irritabillity, slowing pulse, lethargy, incontinence, thermal instability
papilloedema is a late sign
potassium replacement therapy is required because
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)
monitoring during potassium infusion
continuous ECG monioring
if serum potassium is >5mmol cease potassium infusion
bicarbonate administration
not routinely recommended
except for rare circumstances in extremely sick children
what happens to phosphate levels in DKA
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
potential complications of DKA
- hyper/hyponatraemia
- hypoglycaemia
- cerebral oedema
preventing hypoglycaemia
if the blood glucose levels fall too low and the patient is still ketotic, give IV glucose, do not discontinue insulin
when might cerebral oedema develop
may suddenly develop clinically, usually between 6-12 hours after starting therapy
prevention of cerebral oedema
slow correction of fluid and biochemical abnormalities
very late signs of cerebral oedema
rising blood pressure, bradycardia and respiratory impairment