endocrinology Flashcards
define DKA
person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when they body does not have enough insulin to use and process glucose. The main problems are ketoacidosis, dehydration and potassium imbalance.
ketoacidosis
no fuel and think they are starving, they initiate the process of ketogenesis so they have a usable fuel
glucose and ketone levels increase
ketone acids start to build up
dehydration in DKA
Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration. The dehydration stimulates the thirst centre to tell the patient to drink lots of water. This excessive thirst is called polydipsia.
potassium imbalance
insulin normally drives potassium into cells.
no potassium stored in the cells therefore it will be really low
when insulin starts lead to hypokalaemia -> arrhythmias
children with DKA at a high risk of developing what
cerebral oedema
dehydration and high blood sugar concentration cause water to move from the intracellular space in the brain to the extracellular space. This causes the brain cells to shrink and become dehydrated. Rapid correction of dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells. This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death.
signs
Mx of cerebral oedema
headaches, altered behaviour, bradycardia or changes to consciousness.
slowing IV fluids, IV mannitol and IV hypertonic saline
presentation of DKA
Polyuria Polydipsia Nausea and vomiting Weight loss Acetone smell to their breath Dehydration and subsequent hypotension Altered consciousness Symptoms of an underlying trigger (i.e. sepsis)
diagnosis of DKA
- Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
- Ketosis (i.e. blood ketones > 3 mmol/l)
- Acidosis (i.e. pH < 7.3)
Mx of DKA
Correct dehydration evenly over 48 hours. This will correct the dehydration and dilute the hyperglycaemia and the ketones. Correcting it faster increases the risk of cerebral oedema.
Give a fixed rate insulin infusion. This allows cells to start using glucose again. This in turn switches off the production of ketones.
Avoid fluid boluses to minimise the risk of cerebral oedema, unless required for resuscitation.
Treat underlying triggers, for example with antibiotics for septic patients.
Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l.
Add potassium to IV fluids and monitor serum potassium closely.
Monitor for signs of cerebral oedema.
Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin.§
complications of DKA
Hypoglycaemia.
Hypokalaemia.
Systemic infections.
Aspiration pneumonia.
Venous thromboembolism.
Appendicitis - consider if there is ongoing abdominal pain.
Others - eg, pneumothorax, interstitial pulmonary oedema, hyperosmolar hyperglycaemic non-ketotic coma.
persistent/severe hypo may be caused by
preterm birth (< 37 weeks) maternal diabetes mellitus IUGR hypothermia neonatal sepsis inborn errors of metabolism nesidioblastosis Beckwith-Wiedemann syndrome
features of neonatal hypo
may be asymptomatic autonomic (hypoglycaemia → changes in neural sympathetic discharge) 'jitteriness' irritable tachypnoea pallor neuroglycopenic poor feeding/sucking weak cry drowsy hypotonia seizures other features may include apnoea hypothermia
Mx of hypo
asymptomatic encourage normal feeding (breast or bottle) monitor blood glucose symptomatic or very low blood glucose admit to the neonatal unit intravenous infusion of 10% dextrose
causes of failure to thrive
nutrition - poor diet abuse and neglect problems with feeding - cerebral palsy unable to retain food - coeliac disease metabolic disease downs syndrome/congenital ongoing illness
