Miscellaneous Flashcards
Dose of ibuprofen indicating admission
> 200mg/kg
a. <200 mg/kg = asymptomatic
b. 200-400 mg/kg = mild GI and CNS effects
c. >400 mg/kg = risk of multi-organ dysfunction
Activated charcoal uses
1-2g/kg, ideally within 1hr of ingestion
Salicyclates
Amphetamines, cocaine, ectstasy
Barbiturates
Theophyllines
Dose of salicylate indicating admission
> 150mg/kg - consider use of charcoal
<150mg/kg Minimal symptoms
150-300mg/kg Mild-moderate symptoms: Tinnitus, vomiting, hyperventilation
>300mg/kg Severe symptoms: Acidosis, seizures, hyperthermia
Contraindications to activated charcoal/when is it unhelpful
Iron
Hydrocarbons (e.g. petrol)
Caustic/corrosive substances
Alcohol
Ibuprofen
Paracetamol
Benzodiazepines
Essential oils (risk of aspiration)
Is salicylate blood level accurate/helpful?
Yes to a degree, peaks around 2-4hrs post ingestion, however can be misleading as there is a poor correlation between salicylate concentration and toxicity and deterioration may still occur with falling serum concentrations due to rising CNS concentration
Endoscopic grading in caustic/corrosive substances
- Grade 0 — normal
- Grade I — mucosal edema and hyperemia
- Grade IIA — superficial ulcers, bleeding and exudates
- Grade IIB — deep focal or circumferential ulcers
- Grade IIIA — focal necrosis
- Grade IIIB — extensive necrosis
What volume of essential oil can cause toxicity?
5-15ml in adults, 2-3ml in children
Mimic fat soluble drugs, absorbed through mucous membranes/skin
Admit any dose >5ml
How many times greater is the affinity of CO to haemoglobin c/w O2
240x
Binds to iron moiety of haem, causing allosteric changes in the haem protein = reduced ability of the other 3 O2 binding sites to offload haem into the peripheral tissues i.e. causes a LEFT SHIFT of O2 dissociation curve
Also binds to myoglobin, cytochromes and NAPH –> impaired oxidative phosphorylation in mitochondria
Indications for hyperbaric O2
patients with COHb >25%, end-organ ischaemia, LOC, pregnancy
Children have a higher risk of hypothermia, and do a CXR first to exclude congenital anomalies
Mechanism of cyanide poisoning
Normal aerobic metabolism = ATP generated from ETC following TCA cycle
Cyanide binds to Ferric ion (Fe3+) of cytochrome oxidase a3 –> inhibits final enzymes in ETC –> can’t make ATP so cell does anaerobic metabolism –> lactic acidosis, increased anion gap, metabolic acidosis
What is the antidote for cyanide and is it really needed?
YES. Hydroxycobalamin (B12)