Aspirin toxicity

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yankees527

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FREE 150 SPOILER ALERT:

I will be forever grateful if someone clarifies a timeline of aspirin toxicity (i.e. going from respiratory alkalosis to metabolic acidosis).

Just did the free 150 where someone with 3 hours post aspirin overdose presents with metabolic acidosis.

On the other hand, Uworld clearly states that the 12 hours is the transition

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I will be forever grateful if someone clarifies a timeline of aspirin toxicity (i.e. going from respiratory alkalosis to metabolic acidosis).

Just did the free 150 where someone with 3 hours post aspirin overdose presents with metabolic acidosis.

On the other hand, Uworld clearly states that the 12 hours is the transition

Up to date says that the onset of the acid/base stuff depends on the amount and type of aspirin (such as is it enteric coated) and whether the ingestion was acute or chronic or anything else was coingested. It usually presents as mixed, pure primary metabolic acidosis is rare in adults but can be seen in children soon after the ingestion. Acute respiratory acidosis can occur in the later stages.

So it seems that it just depends and you should think about it based on the case scenario. Is there anything else in the question that could have made you choose this. Like was it as simple as there was an anion gap, and aspirin overdose was the only choice available which can cause that?
 
Up to date says that the onset of the acid/base stuff depends on the amount and type of aspirin (such as is it enteric coated) and whether the ingestion was acute or chronic or anything else was coingested. It usually presents as mixed, pure primary metabolic acidosis is rare in adults but can be seen in children soon after the ingestion. Acute respiratory acidosis can occur in the later stages.

So it seems that it just depends and you should think about it based on the case scenario. Is there anything else in the question that could have made you choose this. Like was it as simple as there was an anion gap, and aspirin overdose was the only choice available which can cause that?
It was an arrow question, where you need to say what happens to bicarb, ph and pco2
 
It was an arrow question, where you need to say what happens to bicarb, ph and pco2
Haha so did you say they stayed the same because not enough time elapsed? I think it might be one of those step things where you just have to interpret what they are trying to test you on.
 
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Haha so did you say they stayed the same because not enough time elapsed? I think it might be one of those step things where you just have to interpret what they are trying to test you on.
There actually wasnt any baseline to compare to. It just said what would his ABG look like.

Im surprised no one else had this conflict lol
 
The rule of thumb I went by for the purposes of step tests was that anything <1hr after the ingestion would be the respiratory alkalosis (as this is an immediate reaction), and anything after that is mixed or metabolic acidosis. A few hours is a good rule of thumb for when to assume they could be squarely in the metabolic acidosis category.
 
The rule of thumb I went by for the purposes of step tests was that anything <1hr after the ingestion would be the respiratory alkalosis (as this is an immediate reaction), and anything after that is mixed or metabolic acidosis. A few hours is a good rule of thumb for when to assume they could be squarely in the metabolic acidosis category.

Yup, you're spot on. Basic physiology 101. When someone overdoses on a drug, the toxicity is described as an "acute" phase, meaning the first few hours (1-3). In the acute phase the body responds "acutely". It reacts, in this case, to aspirin with the salicylates triggering the medullary respiratory center where the patient blows air rapidly. Blowing air results in loss of CO2, depressed PaCO2, elevated pH, ergo respiratory alkalosis.


As in all things with human physiology, the body goes into "compensatory" mode but delayed ~ 12 hours. The body compensates by shifting the pH in the opposite direction, lowering the pH but in an ABG it will appear WNL. Such is the purpose of compensatory mechanisms. Thus the delayed compensatory phase has mixed respiratory alkalosis / metabolic acidosis. The pH has dropped away from its former elevated acute phase, PaCO2 remains depressed with the bicarbonate lowering as expected to compensate...


pH shifts downward yet WNL, PaCO2 remains low, serum HCO3 is low, delayed compensatory response.


Basic respiratory physiology concept explained in any decent medical physiology textbook.
 
Ugh, please put spoilers in the title (i.e. from free 150, from nbme X, etc).
haha sorry about that.
Yup, you're spot on. Basic physiology 101. When someone overdoses on a drug, the toxicity is described as an "acute" phase, meaning the first few hours (1-3). In the acute phase the body responds "acutely". It reacts, in this case, to aspirin with the salicylates triggering the medullary respiratory center where the patient blows air rapidly. Blowing air results in loss of CO2, depressed PaCO2, elevated pH, ergo respiratory alkalosis.


As in all things with human physiology, the body goes into "compensatory" mode but delayed ~ 12 hours. The body compensates by shifting the pH in the opposite direction, lowering the pH but in an ABG it will appear WNL. Such is the purpose of compensatory mechanisms. Thus the delayed compensatory phase has mixed respiratory alkalosis / metabolic acidosis. The pH has dropped away from its former elevated acute phase, PaCO2 remains depressed with the bicarbonate lowering as expected to compensate...


pH shifts downward yet WNL, PaCO2 remains low, serum HCO3 is low, delayed compensatory response.


Basic respiratory physiology concept explained in any decent medical physiology textbook.
Thanks, wasnt really asking about the basic physiology, but instead the actual time frame.
You say 12 hours (which i originally thought), however the question (#38 in block 1) states it is 3 hours post ingestion, and ABG has a DOWN arrow for HCO3, pH, and PCO2 indicating it is at a metabolic alkalosis at this point with respiratory compensation.

Guess ill just go with the hour cutoff then
 
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Yup, you're spot on. Basic physiology 101. When someone overdoses on a drug, the toxicity is described as an "acute" phase, meaning the first few hours (1-3). In the acute phase the body responds "acutely". It reacts, in this case, to aspirin with the salicylates triggering the medullary respiratory center where the patient blows air rapidly. Blowing air results in loss of CO2, depressed PaCO2, elevated pH, ergo respiratory alkalosis.


As in all things with human physiology, the body goes into "compensatory" mode but delayed ~ 12 hours. The body compensates by shifting the pH in the opposite direction, lowering the pH but in an ABG it will appear WNL. Such is the purpose of compensatory mechanisms. Thus the delayed compensatory phase has mixed respiratory alkalosis / metabolic acidosis. The pH has dropped away from its former elevated acute phase, PaCO2 remains depressed with the bicarbonate lowering as expected to compensate...


pH shifts downward yet WNL, PaCO2 remains low, serum HCO3 is low, delayed compensatory response.


Basic respiratory physiology concept explained in any decent medical physiology textbook.

You're so busy raving about medical textbooks have made you so smart that you didn't even take time to see what OP was asking.
 
I got this wrong on the free 150 too, lol. I changed my answer at the last minute because I thought maybe 3 hours might still be in the "acute" phase. Also UWorld said something about how the overall pH in the mixed part isn't usually acidotic enough that your pH actually decreases, its usually around normal (and the mixed answer had a decreased pH down arrow). I guess I will try to base my test answer off of the free 150 now, but if anyone has a better timeline rule to go by, I'd appreciate it!
 
Guess ill just go with the hour cutoff then

sounds reasonable. I think you'll agree that it takes the body time to "compensate" on a physiological basis so that it can rectify the assault. However, 12 hours is a reasonable time frame to believe the body is in compensatory mode assuming all physiological processes are intact and otherwise normal.

The problem with a lot of the basic medical sciences is that to understand the exact minutiae of what, when, where and why (and arrows and timing), is that this type of understanding is achieved through bench top science. This requires money to fund research. Sadly alot of research is done b/c there is a financial goal: bring a new drug to market, a new medical device, find a cure which translates into profits, discover the toxic agent to earn recognition in published journals, followed by drug discovery, etc. Rarely are questions answered just because we seek understanding.

e.g. "Let's do a clinical study to learn what the cutoff period is between acute and compensatory! How do we get someone to pay for it?" results: Trial is dead.

1 hour, 3 hours, 4.5 hours, 5.25 hours....who knows.
 
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