Tasty Morsels of Critical Care 055 | Salicylate poisoning
Welcome back to the tasty morsels of critical care podcast. This time round we’ll look at an oldie but a goodie: salicylate poisoning. I have not seen one of these in quite some time but it is a classic tox question for exams in both EM and ICM. Oh Chapter 90 has the ambitious task of covering all poisonings so unsurprisingly it’s a little brief but this post is supplemented by a few other excellent resources linked to at the end. Salicylates are primarily found in our part of the world in aspirin. Locally the commonest use for aspirin these days is primary or secondary prevention of vascular disease, ie the baby aspirin tablets that come in 75mg. You would need to take a large number of these to get into trouble. The analgesic doses of nearer to 600mg are less commonly used, especially when compared to the ubiquitous paracetamol, but 15-20 of these big aspirins could get you into big trouble. It does exist in other forms, most notably in “oil of wintergreen” which, in kids can be a potentially fatal ingestion at low volume. Like most ingestions, the context or the patient will often be the give away to the diagnosis. But if they haven’t told you directly, you might start by asking questions about tinnitus, dizziness and vomiting. On exam you might find fever, tachypnoea and even impaired consciousness as things get more advanced. These clinical signs can be explained by looking at the pathophysiology. Aspirin, being salicylic acid is by nature an acid, one would think that this is the reason you get the metabolic acidosis. In overdose it does indeed form part of the anion gap of unmeasured anions along with lactate. But in reality the salicylate apparently contributes only a small amount of the gap here and other unmeasured anions like lactate and ketones form most of the gap. The metabolic acidosis induces an appropriate kussmaul like response observed in the tachypnoea. Minute ventilation is increased to lower CO2 as a “compensation” for the metabolic acidosis. More interestingly aspirin has a direct effect on the brainstem causing outflow to the respiratory centres to increase resulting an additional increase in minute volume beyond that appropriate to the metabolic acidosis. As a result you get the classic blood gas of someone with a mixed metabolic acidosis and respiratory alkalosis with a CO2 lower than that expected with something like Winter’s formula or perhaps a normal pH (remember respiratory compensation for acidosis should not correct so much as to normalise the pH). In general the pH in these patients will be normal or high and indeed if an acidaemia develops you’re really in trouble. The tinnitus and dizziness is thought to be a direct effect on vestibulocochlear centres inducing the symptoms. The fever is likely related to the uncoupling of oxidative phsophorylation and possibly on hypothalamic set points. Aspirin has multiple potential mechanisms of pathology that could potentially lead to death. * probably the biggest is uncoupling of oxidative phosphorylation, something so key to life that pretty much all aerobic life depends on it. High lactates are probably the best measure for this * penetration of the CNS with salicylates, leading to the usual tox spiral of seizures, coma, death * promotion of fatty acid metabolism creating severe ketosis and contributing to hypoglycaemia The non ionised form of aspirin causes all the nastiness and the dissociation between ionised and non ionised is highly pH dependant. An aspirin level of 400 at pH 7.4 might be tolerable but the same level at a pH of 7.2 is likely to be rapidly lethal. These 2 components, the aspirin and the blood pH form the subtleties of management at this stage. Levels are easily obtainable from every lab I’ve ever worked at.