I tweeted a pair of CBCs earlier today and asked for a diagnosis in two words.
Lots of great responses!!
Kudos to @AaronBoothby2 for getting the right answer:
CLOSTRIDIAL SEPSIS
In this thread we will systematically work through the case.
2/7
1. The first thing to note is that the two CBCs were taken a mere 7 h apart. Many notable changes occurred during this short time span, including a sudden drop in Hb and MCV and an increase in MCHC and RDW.
... it is the CHANGES in values that are meaningful.
3/7
2. How can we explain such a rapid drop in Hb? Certainly not by a production problem. If I completely shut off my bone marrow production of RBCs, my Hb will only drop by 0.1 g/dL/day because of the long survival time of RBCs.
So, this must be hemolysis or hemodilution.
4/7
3. Let's consider hemodilution first (which would most likely occur in the context of a bleed). If we work through the numbers we find that the patient would have had to receive a ridiculous quantity of fluid to explain this degree of drop in Hb.
5/7
4. That leaves hemolysis as the most likely cause of the reduction in Hb. The ddx of hemolysis includes immune and non-immune causes (extracorpuscular and intracorpuscular).
6/7
5. Considering causes of HA that are associated with elevated MCHC, the ddx narrows to AIHA (real), CAD (artifact) and infection with clostridial perfringens (real).
6/7
6. The MCV in CAD is artificially elevated, whereas this patient's MCV actually decreased (albeit within the normal range). The latter result is c/w AIHA or clostridium sepsis (especially the latter owing to microspherocytes).
7/7
7. It would very unusual for a warm antibody to result in such rapid hemolysis. Moreover, the leukocytosis is a hint that there may be an underlying infection.
In fact this patient had fulminant clostridial sepsis (including classical microspherocytes on his blood smear).
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A woman with ferritin 10 and Hb 12.2 (baseline 14). How should this be described?
Here’s how you answered:
• non-anemic Fe deficiency: 35%
• Fe deficiency anemia: 32%
• Fe deficiency with relative anemia: 27%
• none: 6%
Really interesting spread!
2/11
This tells us something important: clinicians sense a mismatch between definition-based language and physiology-based thinking, even if we disagree on terminology.
3/11
By strict WHO criteria, she is not anemic.
Hb ≥12 in women = normal.
So formally the correct label is: iron deficiency without anemia.
In acute GI bleed anemia, would you give 1 g IV iron regardless of ferritin?
Results:
• 27% yes — anticipate iron debt
• 12% sometimes
• 21% only if ferritin is low
• 41% no
2/13
First, an important acknowledgment:
There is no right answer here.
There are no firm guidelines that tell us what to do in this situation. Reasonable clinicians land in different places.
This is a gray zone where physiology, timing, and judgment matter.
3/13
So rather than argue what we should do, I want to walk through the numbers and biology and explain why some clinicians anticipate iron debt even when ferritin is normal.
Yesterday I posted a CBC + reticulocyte count and asked for your diagnostic thoughts. Many of you offered great reasoning. The correct diagnosis was hemoglobin C disease.
Let’s unpack why this case is such a good learning example. 👇
2/9
Microcytosis often triggers a reflex binary:
iron deficiency vs thalassemia trait.
That’s a useful starting point. But it’s incomplete. Structural hemoglobin variants (like HbC and HbE) also belong on that list.
3/9
Several people calculated the Mentzer index (MCV/RBC):
75 / 4.0 ≈ 18 → “suggests iron deficiency (ID).”
Important teaching point:
The Mentzer index was designed to distinguish thal trait vs ID. It is not validated for structural hemoglobinopathies like HbC or HbE.