Iron poisoning - anion-gap or non-anion gap acidosis?

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Phloston

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Uworld QID# 6559 (on UWSA1) says that iron poisoning can cause a non-anion-gap metabolic acidosis.

P. 514 of FA, via MUDPILES, lists iron poisoning as anion-gap.

Any thoughts on that?

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Iron acidosis is one of the easier ones, because you simply have a bunch of extra cations in the serum compared to normal. Iron isn't considered for the anion gap calculation, therefore there's a greater gap than usual.
 
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Gap. There's a greater gap than usual (therefore anion gap acidosis). It's most helpful to consider the formula for the anion gap: Na - (Cl + HCO3). To protect the gap, any loss in HCO3 has to be made up by Cl or vice versa.

In non-anion gap acidosis, there is a drop in bicarb (acidosis) but a concomitant rise in Cl, making the net anion gap the same as normal serum. This is also called hyperchloremic acidosis. The best way to remember these is that they involve direct HCO3 loss or direct Cl gain.

In anion gap (aka high anion gap) acidosis, there is a change in unmeasured ions in the serum. Sometimes this is because there are extra anions (e.g. lactic acid) that acidify the blood, sometimes it's the direct addition of cations (e.g. iron) that also acidify the blood. Both of these drive the extra H+ to combine with HCO3, consuming HCO3 without a rise in Cl. There isn't a rise in Cl because the extra unaccounted for ions take care of the balance (which is another way of saying the HCO3 buffering system has done its job). A loss of HCO3 without a rise of Cl necessarily implies an increase anion gap.

It's kind of a confusing topic, but the central takeaway is that a direct gain or loss of Cl or HCO3 (respectively) has a non-gap anion acidosis.
 
Iron has Four Separate, but slightly overlapping actions that cause acidosis. Three of those mechanisms lead to lactic acidosis, while the fourth mechanism can lead to normal anion gap acidosis:

1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production
2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis
3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis

4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O
--> FeOH3 + 3H+
This will then deplete Bicarb buffering system resulting in non-gap acidosis.

Source: http://www.derangedphysiology.com/php/Acid-Base-Disturbance/iron-overdose.php
 
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