ABCDE disability Flashcards
Assessment disability ABCDE
Vitals:
GCS
Look:
Pupils
Move:
Move all limbs
Invetsigations disability ABCDE
Blood glucose
Ketones
If GCS <8 what do you do
anaesthetics!
Management of hypoglycameia
If the patient is alert, a quick-acting carbohydrate may be given (as above).
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein
Management of DKA
- Fluid resucitation until SBP >90
- Once SBP is >90mmHg, give 1L of normal 0.9% sodium chloride over 1 hour. Monitor K+ with ABG/VBG and add it to the fluids accordingly.
- Commence a fixed rate intravenous insulin infusion. 0.1 units/kg/hr (prescribed as Actrapid)
+ Make sure to continue the patient’s long acting insulins subcutaneously
diagnosing DKA?
Blood glucose > 11mmol/L or known diabetes mellitus*
Ketonaemia ≥ 3.0 mmol/L or significant ketonuria (more than 2+ on standard urine stick).
Bicarbonate <15mmol/L and/or venous pH < 7.3. (Use venous readings to assess acidosis rather than arterial unless gas exchange must be assessed)
what elements of DKA pathogenesis will kill the pt
dehydration, potassium imbalance and acidosis.
why does GCS need to be monitored closely DKA
CEREBRAL OEDEMA
Neurological observations (i.e. GCS) should be monitored very closely (e.g. hourly) to look for signs of cerebral oedema. Be concerned when patients being treated for diabetic ketoacidosis develop headaches, altered behaviour, bradycardia or changes to consciousness.
Management options for cerebral oedema are slowing IV fluids, IV mannitol and IV hypertonic saline. These should be guided by an experienced paediatrician.
what trigger should you look for DKA
sepsis
presentation 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)
why is it important that fluid and hyperglycaemia correction is done slowly DKA
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.
causes of seizures?
Vascular: haemorrhagic stroke
Infectious: meningitis, encephalitis, systemic infection lowering seizure threshold, febrile seizures paeds
Trauma: head injury
Metabolic: Electrolyte disturbances: hyponatraemia, hypernatraemia, hypoglycaemia, hypocalcaemia, hypokalaemia, ammonia (hepatic encephalopathy)
Iatrogenic: tricyclic overdose, alcohol and benzodiazepine withdrawal
Neoplastic: space occupying lesion,
Environment: alcohol, stress, sleep deprivation
Functional: non-epileptic seizure
Pregnancy: eclampsia
what are breakthrough seizures
seizures that occur in known epileptics. These can be caused by poor medication compliance or precipitating factors such as sleep deprivation, alcohol and stress.
complications of prolonged seizures?
Airway:
Hypoxic brain injury due to airway occlusion and aspiration
Develop epilepsy after a prolonged seizure w hypoxic brain injury
Aspiration pneumonia
Injury:
Anterior dislocation of shoulder
Trauma and injury eg falling down stairs
Muscles contracting:
Electrolyte complications- lactic acidosis -
Creatinine kinase as a result of muscle breakdown - raised - rhabdomyolysis - kidney failure
Potassium intracellular so as muscles breakdown it is released - hyperkalaemia
Heart:
Arrhythmias
