Yesterday I posted a poll showing CBC data from a patient with severe iron deficiency anemia and asked: assuming she receives 4 units pRBCs (which of course would be excessive here), does she need iron therapy on top of that?
70% answered YES.
2/6
Each unit of RBC contains about 250 mg Fe. So she will have received about 1000 mg of Fe, not far off from her total needs. However, such is iron is bound up in Hb inside the donor RBCs and is not readily accessible for erythropoiesis.
3/6
I ran through some rough numbers (see graphic):
1. Oral iron will deliver about 20 mg Fe to the bone marrow each day.
4/6
2. IV iron will deliver its full payload (Fe sequestered in a carbohydrate shell) to macrophages, where Fe will leach out and be slowly released to the bone marrow (I can't find data on how much is released daily, but presumably >20 mg since response to IV Is faster vs PO).
5/6
3. RBCs have a turnover of about 1%/day. So if 1 L pRBCs are transfused (4 units), 10 ml will be endocytosed and processed by macrophages each day, releasing 10 mg Fe/day for use by the bone marrow (these numbers gradually diminish over time as donor cells are destroyed).
6/6
Bottom line: while transfused RBCs provide a depot of iron, it is too little (unless >3-4 units are given) and its release is too slow to meet the demands of patients with severe iron deficiency in a timely manner - thus, such patients should also receive supplemental Fe.
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Yesterday, I posted a poll showing Hb 10.4 and Hct 41 and asked whether or not the patient had anemia.
About 62% of respondents answered YES.
That is the CORRECT answer.
2/4
Anemia is best defined by the Hb because patients with anemia have a deficit in oxygen carrying capacity. Hb binds and carries oxygen. The Hct, by contrast, is a function of cell size (MCV) and RBC count. It is impervious to the contents of the RBC.
3/4
RBCs could contain Swiss cheese for all the Hct cares. The Hb and Hct happen to correlate with each other only because RBCs package Hb.
This patient has severe iron deficiency (the only other explanation for the discordant Hb/Hct [i.e. low MCHC] would be thal major).
I posted a poll yesterday asking whether you would refer a patient with pernicous anemia (PA) to a gastroenterologist for consideration of upper endoscopy.
Most of you answered YES.
2/12
There is no evidence that initial or surveillance endoscopy affects the outcome of patients with PA.
That being said, most GI practice guidelines recommend endoscopy, whereas the sole hematology guideline (BSH) does not.
3/12
All recommendations are consensus based. The justification for endoscopy is that PA is a manifestation of chronic autoimmune gastritis and that the latter is associated with an increased risk of carcinoid tumors and gastric adenocarcinoma.
Yesterday, I posted a time series of CBCs and reticulocyte counts and asked a series of questions.
Let's address each question in turn.
2/7
Q1. Describe the CBC on 2/11.
A1. Leukocytosis (WBC > 11 x 10^9/L) with normocytic, normochromic anemia (Hb < 12-13 g/dL, MCV 80-100 fL, MCHC 32-36 g/dL), anisocytosis (RDW-SD > 46 fL) and thrombocytosis (PLT > 400 x 10^9/L).
3/7
Q2. Why does the MCV increase?
A2. There are only two ways to acutely increase the MCV above normal: reticulocytosis and in vitro artifact. In this case, the retic count is increasing, accounting for the new macrocytosis.
I posted a poll asking whether and how you would anticoagulate a patient with superficial vein thrombosis (SVT) of the leg. There was a pretty even split in votes between the 4 options.
2/5
Most respondents chose to anticoagulate, though there was no clear consensus on the type/duration of anticoagulation.
In fact, clinical practice guidelines would recommend anticoagulating this patient with either fondaparinux or rivaroxaban for 45 days.
3/5
Guideline recommendations for treating patients with SVT of the leg depend on:
1. The proximity of the clot is to the junction with the deep vein.
2. The length of the clot.
3. Whether there are severe symptoms and/or higher than normal risk factors for extension.