EM Flashcards
Methanol poisoning
Methanol is pure distilled alcohol, more likely to be consumed by those with a history of alcohol abuse.
Visual impairment typically occurs with methanol and in severe cases result in permanent blindness. Initial presentation of methanol or ethylene glycol mimics those of ethanol ingestion and when co-ingested, protects the patient from the toxic effects of methanol and ethylene glycol (possibly delaying the diagnosis).
This is because alcohol dehydrogenase has a higher affinity for ethanol, hence methanol and ethylene glycol are excreted unchanged in the kidneys, preventing the formation of toxic metabolites formate (methanol) and oxalic acid (ethylene glycol).
Raised anion garp (normail is 10-18)
salicylate posioning
The patient should then be rehydrated and the urine alkalinised to promote urinary excretion. This is achieved by giving an infusion of 1.25% or 8.4% sodium bicarbonate. The ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. The administration of an intravenous infusion of sodium bicarbonate aiming for a urinary pH of 7.5-8 will increase the excretion of the acid 10-fold.
Severe cases of salicylate poisoning where plasma levels of salicylate are high >800 mg/L, severe metabolic acidosis, acute kidney injury, or have neurological impairment (coma, hallucinations or seizures) may require early haemodialysis. tinnitus
salicylate posioning
The patient should then be rehydrated and the urine alkalinised to promote urinary excretion. This is achieved by giving an infusion of 1.25% or 8.4% sodium bicarbonate. The ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. The administration of an intravenous infusion of sodium bicarbonate aiming for a urinary pH of 7.5-8 will increase the excretion of the acid 10-fold.
Severe cases of salicylate poisoning where plasma levels of salicylate are high >800 mg/L, severe metabolic acidosis, acute kidney injury, or have neurological impairment (coma, hallucinations or seizures) may require early haemodialysis. tinnitus
methanol poisoning
metabolic acidosis with a raised anion gap.
CNS and cardiovascular depression.
optic nerve toxicity
Methanol is often found in contraband alcohol so a raised blood alcohol level is not surprising.
Toxicity is a result of an accumulation of products produced by the action of alcohol dehydrogenase on methanol. Management is aimed at inhibiting production of toxic metabolites. Fomepizole is an alcohol dehydrogenase inhibitor and the treatment of choice in this situation.
Ethanol may be administered in the event that fomepizole cannot be immediately obtained as it competes with methanol for metabolism by alcohol dehydrogenase. Fomepizole is preferable as the effect of ethanol is less predictable, titration more difficult, and the consequent CNS depression makes it significantly less safe.
Gastric decontamination, either by aspiration or activated charcoal, is rarely indicated in the management of toxic alcohol poisoning, except where presentation is very soon after ingestion.
Haemodialysis may be necessary when there is profound acidosis which is refractory to treatment with bicarbonate or a significant deterioration in renal function. It takes time to arrange and is not an appropriate initial treatment.
pre-clampsia and seizures treatment
severe pre-eclampsia with a likely either and intracerebral bleed or cerebral oedema. The most important initial therapy is to control any further seizures and control her blood pressure - intravenous magnesium is the therapy of choice.
TCA OD
Overdose of tricyclic antidepressants can readily be fatal and is often associated with seizures and arrhythmias. Treatment is broadly supportive. If signs of a severe overdose are present, administration of sodium bicarbonate can treat arrhythmias and prevent their development if the QTc interval is prolonged.
Paracetamol OD
Paracetamol overdose is a common question.
The essentials of management are:
Check paracetamol level four hours after ingestion, check levels against the Rumack-Matthew nomogram.
Gastric lavage if large dose ingested (more than 7.5 g) and/or presenting within eight hours of ingestion; consider oral charcoal.
Give N-acetylcysteine or methionine.
Hourly BMs monitored.
Check INR 12 hourly.
Signs associated with poor prognosis (and indicating need for transfer to a liver unit) include:
INR greater than 2.0 within 48 hours or greater than 3.5 within 72 hours of ingestion
Creatinine greater than 200 µmol/L
Blood pH less than 7.3
Signs of encephalopathy
Hypotension (SBP less than 80 mmHg).
Liver enzymes are a poor marker of the degree of hepatocellular damage; synthetic function (as determined by INR or PT) is the best indicator.
lead poisoninbg
Mild cases of lead poisoning are associated with:
Lethargy Anorexia Abdominal discomfort, and Arthralgia. Moderate cases exhibit:
Anaemia Headache Abdominal cramps A gingival blue lead line, and Peripheral motor neuropathy. In severe cases there are:
Convulsions Coma Encephalopathy, and Renal failure. Blood tests reveal a hypochromic, microcytic anaemia and basophilic stippling of red cells.
Chelating agents, for example, dimercaprol, edetate, penicillamine and/or succimer may be used as treatment.
brain stem death asessment
Assessment involves the observation that all brain stem reflexes are absent (for example, corneal reflex) and this assessment must be carried out by two medical practitioners either together or separately. These practitioners must be registered for more than five years and at least one (but not both) must be a consultant.
iron poisoning
Acute iron poisoning typically presents with gastrointestinal symptoms - vomiting, diarrhoea, abdominal pain and gastrointestinal haemorrhage are typical of a toxic iron overdose.
Following this initial presentation symptoms typically abate until the development of severe metabolic acidosis, cardiovascular complications and CNS depression. Patients who survive this stage of iron toxicity go on to develop hepatic dysfunction.
Resolution is characterised by scarring of the gastrointestinal tract with stricture formation and possible gastrointestinal obstruction. Iron tablets are radiopaque and thus may be visualised on plain films or CT.
normal anion gap
Post-extubation stridor (PES)
Post-extubation stridor (PES) is a frequent complication of intubation, occurring in 2-16% of cases. It is caused by laryngeal oedema that results from damage to the mucosa of the larynx. Mucosal damage is caused by pressure and ischaemia resulting in an inflammatory response. Laryngeal oedema, in severe cases, can lead to acute respiratory compromise necessitating emergency reintubation.
Female gender is a risk factor for both laryngeal oedema and PES. This predisposition has been hypothesised to be due to the female mucous membrane being less resistant to trauma and thinner than that in men.
Other risk factors include:
Female gender Intubation >36 hours Excessive cuff pressure Large tube size, and Tracheal infection.
