There are moments in transfusion medicine when the most uncomfortable part of a case isn’t the serology — it’s the realization that the literature can’t quite tell you what to do. Recently, on service, I encountered a patient with a rare A subgroup and a cold-reacting anti-A1. Genotyping suggested either an Aw allele or an Ael allele. The immediate question was practical and deceptively simple: Is it safe to transfuse group A red cells, or should we restrict the patient to gr

How the BEST Criteria Updated a Decade-Old AABB Approach to Septic Transfusion Reactions One of the most uncomfortable questions in transfusion medicine is deceptively simple: When should we culture the patient and the blood product after a transfusion reaction? Culture too often, and you trigger false positives, unnecessary lookbacks, and wasted resources.Culture too conservatively, and you risk missing a true septic transfusion reaction — one of the most dangerous complicat

It was a routine service morning — until it wasn’t. The patient wasn’t crashing in a cinematic way. No massive bleeding. No dramatic hypotension. But the labs were drifting in a direction that felt wrong: platelets falling, creatinine creeping, LDH elevated, hemoglobin sliding just enough to notice. Organ dysfunction without a single unifying explanation. Somewhere between the pattern and the unease it produced, the diagnosis surfaced quietly: TAMOF. What TAMOF Is — and Why I

I learned something new this week: you can buy an at-home ABO blood typing kit on Amazon. I didn’t know that. And I suspect many transfusion medicine physicians don’t either. I found out when a pediatrician called with a worried question. A newborn’s blood type had been determined appropriately in the hospital: A negative . The mother’s type was known: O negative . The father reported he was O negative , based on an at-home blood typing kit. The parents were now concerned abo

Donor infectious disease eligibility is one of those topics that feels straightforward until you’re asked to explain why  a donor with negative testing still isn’t eligible — or why some pathogens get NAT, others don’t, and some only get tested once. This post walks through donor eligibility the way the boards expect you to understand it: as a risk-assessment framework , not just a checklist of tests. What Is Donor Infectious Disease Eligibility? Donor eligibility  is the ass

Stem cell collection sits at the intersection of hematology, immunology, and procedural medicine. It’s conceptually simple — collect enough hematopoietic stem cells to reconstitute marrow — but operationally complex, with decisions at every step that affect engraftment, toxicity, and long-term outcomes. This post walks through stem cell collection from a practical, systems-level perspective: what we collect, where it comes from, how we mobilize it, and what determines whether

Most of us were taught to think of a low haptoglobin as a red flag for hemolysis. The logic seems airtight: free hemoglobin spills into the plasma, haptoglobin binds it, and the levels drop. End of story… right? Except it’s not. Clinically, low haptoglobin is one of the least  specific markers we use — and in some patients, it tells you absolutely nothing about hemolysis at all. This post is about those patients. I’m talking about the ones with clear plasma, normal LDH, norma

AI tools are showing up everywhere in medicine right now — in our inboxes, in meetings, and quietly in the background as we prepare talks or look up unfamiliar territory. Many of us are experimenting with them in real time, often between consults or after a busy clinic day, trying to figure out what they’re actually good at and how to use them without creating extra work. One place where AI can be genuinely helpful is in orienting yourself to a clinical question — especially

There are days in Transfusion Medicine when the most interesting teaching moments arrive quietly — between phone calls, in the apheresis unit hallway, or as someone leans back in a rolling chair and says, “Okay, but why can’t we just do a depletion exchange here?” Today it came up while troubleshooting an inpatient red cell exchange on a Sickle Cell patient who was a lot sicker than he’d been two weeks earlier. One person suggested adding a depletion phase to improve the effi

Introduction: The Problem With the "Second Brain" Metaphor Artificial intelligence in pathology and laboratory medicine is often marketed with an irresistible promise: a second brain that will spot what humans miss, automate the tedious parts of practice, and bring order to the overwhelming volume of data moving through modern health systems. It’s a compelling metaphor—but also a deeply misleading one. The truth is simpler and far more useful: most AI tools in lab medicine to

I’ve been thinking a lot about attribution bias lately — the reflex to explain someone’s behavior by pointing to their character instead of their circumstances. In medicine, this isn’t just a cognitive shortcut. It’s one of our favorite misdiagnoses, and it often shows up in the form of a single, damning label: the difficult patient. Two encounters from my own practice keep coming back to me. 1. “The Meanest Person I’ve Ever Met.” That was the handoff. The wife was “the meane

Two different patients. Two plasma exchange treatments. Two nurses asking me, gently and matter-of-factly, the same question: “Do you want to chase with some plasma?” Before becoming an attending, I had never heard the phrase. It wasn’t part of residency, fellowship, ASFA courses, or any protocol I’d ever followed. It certainly isn’t in textbooks. The first time someone asked me, I wondered whether this was a regional term or a long-standing tradition I’d somehow missed. What

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

1 | Finding the rhythm of replacement When people talk about plasma exchange, they usually focus on what  to replace. Less often...