William Aird Profile picture
Nov 15, 2023 8 tweets 3 min read Read on X
1/7

NAME THAT CBC

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. Image
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. Image
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. Image
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. Image
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). Image
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). Image

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More from @WilliamAird4

Mar 19
1/10

Yesterday’s oral exam case (MCV 140) generated a lot of discussion.

Before I share my approach, I want to slow things down and think through two questions.
2/10

1. How do you structure the physical exam?

Do you:

– move disease by disease (B12, liver disease, hypothyroidism…), or

– move head to toe, mapping findings onto the body?

Both are acceptable.

But they are not the same.
3/10

A disease-by-disease approach follows the differential.

A head-to-toe approach reorganizes the differential into anatomy.

It forces you to translate ideas into space.
Read 10 tweets
Feb 13
1/9

I’ve long taught a simple framework for hypoproliferative normocytic anemia that I still love:

• nutritional deficiency
• inflammation
• organ dysfunction (kidney, liver, endocrine, marrow)

Clinically useful. Memorable. Teachable.

And it still holds up. Image
2/9

But conceptually, something interesting is happening.

These categories aren’t actually the same kind of explanation.

Nutritional deficiency and inflammation are mechanisms.
Organ dysfunction is different.

And even within organs, not all behave the same way.
3/9

Take kidney disease.

We often say “anemia from CKD” as if that explains it.

And in a way, it almost does.

Because kidney disease sits very close to mechanism:
↓ EPO → ↓ erythropoiesis

It’s only one step away.
Read 9 tweets
Feb 13
1/11

I posted a poll:

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! Image
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.
Read 11 tweets
Feb 10
RETICS IN PV

I recently ran a poll asking whether polycythemia vera (PV) is associated with:

• ↑ absolute reticulocyte count
• ↑ % reticulocytes
• both
• neither

The most popular answer was also the best answer: ↑ absolute reticulocyte count. Image
2/10

At first glance, that can feel counterintuitive.

PV is a disease of excessive red cell production, so why wouldn’t the reticulocyte percentage also be increased?

The answer depends on what reticulocytes actually measure.
3/10

Two metrics that are often conflated:

• Absolute reticulocyte count = how many reticulocytes are circulating

• Reticulocyte percentage = reticulocytes ÷ total red cell mass

They answer different physiologic questions.
Read 11 tweets
Feb 2
1/13

I posted a poll asking:

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.

Let’s take a concrete example.
Read 13 tweets
Jan 23
1/9

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. 👇 Image
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.
Read 9 tweets

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