Diabetic Emergencies Flashcards
when does DKA occur
in absolute/ relative insulin deficiency accompanied by an increase in the counter regulatory hormones (glucagon, adrenaline, cortisol, growth hormone)
what is the biochemical triad of DKA
hyperglycaemia, ketonaemia, acidaemia
does DKA occur in T1 or T2 DM
can occur in both
why does stress hormone activation cause DKA
increased lipolysis
decreased glucose utilisation
increased proteolysis
increased glycogenolysis
how does hyperglycaemia cause decreased renal function
glycosuria
electrolyte loss
dehydration
decreased renal function
what increases lactate in DKA
dehydration
what causes increases ketogenesis in DKA
increases liplysis, increased free fatty acids= ketogenesis
what causes osmotic diuresis
glycosuria
what causes hyperosmolarity in DKA
dehydration (osmotic diuresis)
what are the biochemical diagnostic markers for ketacidosis
ketonaemia > 3mmol/L (or significant ketonuria)
blood glucose > 11.0mmol/L
bicarb<15 mmol/L or venous pH < 7.3
(ketones and acids rise, bicarb falls)
what causes death is DKA
adults: hypokalaemia, aspiration pneumonia, ERDS, co morbidities
children: cerebral oedema
what can precipitate DKA
newly diagnosed
infection
illicit drug and alcohol use
poorly managed diabetes (most common cause)
what are the typical symptoms and signs of DKA
osmotic related- thirst and polyuria, dehydration
ketone body related- flushed, vomiting, abdo pain and tenderness, breathlessness (kussmauls respiration), ketone smell of breath
associated conditions- underlying sepsis, gastroenteritis
what happens to potassium in DKA
is often raised > 5.5 mmol/K
BEWARE OF A LOW READING- treatment for DKA will further lower potassium
what happens to creatinine in DKA
often raised
what happens to sodium in DKA
often low or
what happens to lactate in DKA
common to be raised
why might amylase be raised in DKA
rarely pancreatitis
origin can be salivary
what happens to white cell count in DKA
often raised- not always due to infection
what do you lose in DKA
fluid
sodium
potassium
phosphate
what are the 4 main complications of DKA
cardiac arrest secondary to kypokalaemia
ARDS
cerebral oedema
gastric dilatation- risk of aspiration (aspiration pneumonia)
what are the principles of management for DKA
manage in HDU
replace losses- fluid, insulin, potassium, (rare- phosphate and bicarbonate)
address risks- NG tube required?, monitor K+, prescribe LMWH (thrombo embolic risk), source sepsis (CXR, blood culture, MSSU)
describe the process by which insulin deficiency causes DKA
insulin deficiency switches metabolic balance in a catabolic direction
liver produces gluconeogenesis (from proteins and glycogen)
fat in adipose is reduce to triglycerides and fatty acids
increasing levels of ketone bodies
rising level of glucose increases urine production- loss of electrolytes and ions
metabolic acidosis
what is kussmaul respiration
involuntary attempt to remove carbon dioxide from the blood (would form carbonic acid and worsen the ketoacidosis)
what is a normal level of ketones
<0.6 mmol/L
what does urine ketone testing measure
acetoacetate - indivated levels of ketones 2-4 hours previously
why does ketonuria persist after clinical improvement
mobilisation of ketones from fat tissue
what is hyperglycaemic hyperosmolar syndrome
when hyperglycaemia results in osmolarity without significant ketoacidosis
what are the biochemical markers of HHS
marked hypovolaemia, marked hyperglycaemia, no/mild ketonaemia, bicarbonate >15 mmol/L, venous pH >7.3
osmolarity > 320 mosmol/kg
what are the features of HHS presentation
often older, or younger afro-caribbean
high refined COH intake beforehand
what are the risk associations of HHS
CVD (MI and stroke), sepsis, medication (steriods/ thiazide diuretics)
what has higher glucose DKA or HHS
HHS
happens to renal function in HHS
significant renal impairment
what is sodium like in HHS
normal or raised
compare DKA to HHS:
age of presentation
DKA- younger
HHS- older
compare DKA to HHS: type of diabetes
DKA- Type 1
HHS- type 2
compare DKA to HHS:
causes
DKA- insulin deficiency
HHS- diuretics and/or steroids, Fizzy drinks
compare DKA to HHS:
precipitant
DKA- insulin omission
HHS- new diagnosis, infection
compare DKA to HHS:
mortality
DKA- <2%
HHS- 10-50%
compare DKA to HHS:
treatment
DKA- insulin
HHS- diet/ oral hypoglycaemic agents/ (insulin)
what are the differences in treating HHS rather than DKA
- fluids- more increased risk of fluid overload (caution)
- insulin- more sensitive, slower- may not require insulin
- sodium- avoid rapid flucuations
- co morbidities more likely- screen for vascular event (silent MI), sepsis, LMWH for all unless contraindicated
what are the biochemical diagnostics of alcoholic/ starvation ketoacidosis
ketonaemia raised
biocarbonate low
venous pH <7.3
glucose normal, may be low
do patients with diabetes stay in hospital longer
yes
when should you admit someone with T1DM to hospital
unable to tolerate oral fluids persisting vomiting persisting hyperglycaemia persisting positive/ increasing levels of ketones abdominal pain/ breathlessness
what is the CPR in patient foot care
check, protect, refer
what does clearance of lactate require
hepatic uptake, aerobic conversion to pyruvate then glucose
what can lactic acidosis be caused by
type A- tissue hypoxaemia- sepsis, haemorrhage
type b- liver disease, leukaemic states, diabetes
what are the clinical features of lactic acidosis
hyperventilation, mental confusion, stupor or coma if severe
what are the biochemical features of lactic acidosis
raisaed bicarbonate, raised anion gap, abscence of ketonaemia, raised phosphate
after diagnosing DKA what other blood tests should be done
U&Es as dehydration can cause renal failure and potassium disorders common
if you suspect infection FBC (for WBC) and CRP and possibly cultures
