For years, transfusion-associated circulatory overload (TACO) has been framed as a purely hemodynamic problem — a case of too much blood, too fast.  But hemovigilance data are challenging that simplicity. A growing body of work suggests that in a significant subset of patients, TACO runs hot. Yes, fever. Not chills from contamination, not cytokine-release fever from a leukocyte-rich product, but true fever within hours of transfusion — sometimes the only obvious clue that som

A patient was admitted with a congestive heart failure exacerbation. Their hemoglobin was drifting downward — nothing dramatic, but enough to warrant a type and screen. The result wasn’t surprising: a known warm autoantibody. What was  surprising was the note that popped up beside it — “Requires washed RBCs.” We looked into it. The patient’s IgA level was reported as < 5 mg/dL on two separate occasions — a true, complete selective IgA deficiency. No history of anaphylactic re

Two weeks after a massive transfusion protocol for hemorrhagic shock, one of our patients developed profound thrombocytopenia — counts dropping to single digits despite transfusions. Each additional platelet unit seemed to make things worse, not better. Within days, she developed intra-abdominal bleeding that required surgical exploration and an open abdomen. When the post-transfusion purpura (PTP) panel came back, it revealed an alloantibody against HPA-1b — an uncommon find

When the phone rings mid-transfusion and the words “the patient is hypotensive”  hit your ears, there’s a short list of life-threatening reactions you can’t afford to miss. Four share a similar opening act — fever, hypotension, and sometimes respiratory distress. The fifth looks different but can end the same way if unrecognized. Here’s how to triage the call, fast. 1️⃣ Anaphylaxis Clue:  Sudden hypotension, respiratory distress, flushing, or urticaria — often within minutes

Every so often a case comes along that refuses to fit into our tidy categories. An adult male presented to the emergency department with profound weakness and striking jaundice. His hemoglobin was 3.7 g/dL, yet he was mentating normally and his lactate was within range — clear evidence of physiologic compensation. The chemistry panel featured a total bilirubin >70 mg/dL, direct fraction ≈ 40 mg/dL, with biliary dilation on CT abdomen/pelvis. On the hematology side, LDH was el

The patient was a premature infant, six weeks old and just 2.5 kilograms, already on ECMO for primary cardiopulmonary failure. Sepsis developed secondarily, and the critical-care team requested plasmapheresis for a presumed cytokine storm — a Category III indication  under the current ASFA guidelines. On paper, the rationale made sense. But when I calculated the total blood volume — only 250 mL  (≈ 100 mL/kg for a premature infant) — it was immediately clear this baby was too

The antibody screen looked straightforward at first glance — an O positive patient with apparent anti-D reactivity in plasma. But the autocontrol was positive, and the eluate was a panagglutinin. Those two results change the entire story. Working the Differential When a D-positive patient’s plasma reacts like anti-D, the immediate differentials are familiar: Partial D variant (missing epitope exposure) Passive anti-D (recent RhIg or IVIG) Autoantibody with apparent Rh specifi

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1 | A brief historical arc In the early years of therapeutic plasma exchange (TPE), replacement was simple: plasma when coagulation...

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Most of the time, our red cells are polite. They keep their surface antigens tucked away, only showing the parts of themselves that...

Most days in the blood bank, we’re juggling the usual suspects — ABO, Rh, Kell, Duffy, Kidd, MNS. But every now and then, an antibody...

One of the challenges in transfusion medicine is that the most important areas of knowledge are not always the most glamorous. Beyond the...

When I first wrote my Fresh Frozen Facts  series, I focused on the workhorses. But plasma isn’t a single product: it’s a whole family,...