1. Thrombocytopenia occurs in about 50% of patients in the ICU.
2. Sepsis accounts for approximately 50% of all thrombocytopenia in the severely ill.
3. Platelet count is included in the SOFA score.
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4. Platelet count is inversely associated with sepsis severity and mortality.
5. Mechanisms of thrombocytopenia in sepsis include:
-- a) Increased activation/consumption
-- b) Increased apoptosis
-- c) Decreased platelet production (uncommon)
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One of my favorite studies exploring mechanisms of sepsis-associated TP showed that injection of endotoxin in wild-type and TRL4 null. mice resulted in massive sequestration of platelets in the pulmonary microcirculation in WT, but not TRL4-deficient animals (graphic).
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NORMOCYTIC, NORMOCHROMIC IRON DEFICIENCY ANEMIA (IDA)
We tend to think of IDA as being microcytic (more consistently than hypochromic). However, there are certain situations in which the MCV is normal in IDA.
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Examples include:
1. A patient with high-normal baseline MCV whose MCV falls within the normal range in IDA (see first graphic for an example).
2. A patient with baseline macrocytosis, for example from concomitant liver disease, B12 deficiency, MDS or hydroxyurea use.
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3. Rare cases where the MCV simply doesn't budge from baseline despite clear cut evidence of IDA (i.e. anemia +/- low MCHC with low ferritin that responds to iron treatment).
We are used to considering variation in RBC size (increased variation = anisocytosis) by examining a blood smear or evaluating the RDW.
What about variation in RBC Hb concentration ([Hb]) (anisochromia)?
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We can often identify cell-to-cell differences in central pallor on a blood smear.
While we may make mental note of such differences, we rarely incorporate the finding in a summary of the smear. And there is no lab equivalent to the RDW for Hb concentration or "chromia".
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Or is there? If we plot single cell [Hb], we would likely find a normal distribution with a bell shaped curve (I have not seen any such data published). The mean would provide us with the MCHC and the standard deviation with the RDW for [Hb].
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.
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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.
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I ran through some rough numbers (see graphic):
1. Oral iron will deliver about 20 mg Fe to the bone marrow each day.
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.
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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.
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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).