The Transfusion Trigger: A Data-Driven Look at When to Use Blood Products

Challenging dogma and applying patient-specific transfusion medicine

A Review Article for Postgraduate Medical Students in Internal Medicine

Dr Neeraj Manikath , claude.ai

Abstract

Blood transfusion remains one of the most common therapeutic interventions in hospitalized patients, yet its appropriate use continues to evolve. This comprehensive review examines contemporary evidence-based approaches to transfusion medicine, with particular emphasis on restrictive versus liberal transfusion strategies for red blood cells, evidence-based thresholds for platelet transfusions, rational use of plasma products, and recognition of life-threatening transfusion reactions. We challenge long-standing dogmas and provide practical, patient-specific guidance based on high-quality evidence from recent randomized controlled trials and international guidelines published through 2024.

Keywords: Blood transfusion, hemoglobin threshold, platelet transfusion, fresh frozen plasma, cryoprecipitate, TACO, TRALI

Introduction

The art and science of transfusion medicine has undergone a paradigm shift over the past two decades. What was once a liberal practice governed by arbitrary thresholds has evolved into a nuanced, evidence-based discipline that recognizes both the potential benefits and substantial risks of blood product administration. The restrictive transfusion strategy, once viewed with skepticism, has now become standard practice for most hospitalized patients. However, recent data suggest that certain patient populations may not benefit from—and may even be harmed by—overly restrictive approaches.

This review synthesizes the most current evidence to provide practical guidance for internists managing patients requiring blood products. We will explore the data supporting restrictive transfusion thresholds, identify critical exceptions where higher hemoglobin targets may be beneficial, examine evidence-based approaches to platelet and plasma transfusion, and provide a framework for recognizing and managing the most serious transfusion reactions.

The Restrictive Strategy (Hb <7-8 g/dL) in 2024: A New Standard with Important Exceptions

The Evidence Base for Restrictive Transfusion

The restrictive red blood cell (RBC) transfusion strategy represents one of the most significant advances in transfusion medicine. This approach, which considers transfusion when hemoglobin falls below 7-8 g/dL in hemodynamically stable patients, emerged from landmark trials demonstrating non-inferiority—and often superiority—compared to more liberal strategies.

The 2024 AABB guidelines, based on systematic review of 45 randomized controlled trials involving over 20,000 participants, provide strong recommendations for restrictive transfusion in most hospitalized adult patients. For hemodynamically stable adults, transfusion should be considered when hemoglobin concentration falls below 7 g/dL, with the caveat that clinicians may choose thresholds of 8 g/dL for patients with pre-existing cardiovascular disease or those undergoing orthopedic surgery.

The biological rationale for restrictive transfusion extends beyond simply conserving blood products. Each unit of transfused blood carries risks: immunomodulation, increased infection rates, transfusion reactions, and iron overload. Moreover, stored RBCs undergo progressive biochemical changes—the "storage lesion"—that may impair oxygen delivery despite increasing hemoglobin concentration. The restrictive approach acknowledges that the body's compensatory mechanisms (increased cardiac output, enhanced oxygen extraction, rightward shift of the oxygen-hemoglobin dissociation curve) can maintain adequate tissue oxygenation at lower hemoglobin levels in most patients.

The Cardiac Exception: When Restrictive May Be Too Restrictive

Recent high-quality evidence has challenged the universal application of restrictive transfusion thresholds in patients with cardiac disease. The landmark MINT (Myocardial Ischemia and Transfusion) trial, published in 2023, fundamentally altered our approach to transfusion in acute coronary syndromes (ACS).

This multicenter, randomized trial enrolled 3,504 patients with acute myocardial infarction and anemia (hemoglobin <10 g/dL). Patients were randomized to either a restrictive strategy (transfusion threshold 7-8 g/dL) or a liberal strategy (transfusion threshold <10 g/dL). The results were striking: while there was no significant difference in the primary composite outcome of death or myocardial infarction at 30 days, cardiac death rates were substantially higher in the restrictive group (5.5% vs 3.2%, relative risk 1.74, 95% CI 1.26-2.40).

Multiple meta-analyses have now corroborated these findings. A 2024 systematic review examining patients with cardiovascular disease found significantly increased risks of both myocardial infarction and death with restrictive transfusion strategies. The mechanistic explanation is physiologically intuitive: in the setting of acute myocardial ischemia with compromised coronary perfusion, maintaining higher hemoglobin levels enhances myocardial oxygen delivery and may limit infarct expansion.

The 2024 CHEST guidelines reflect this evolving evidence. While recommending restrictive transfusion for most critically ill patients, they conditionally recommend against restrictive strategies for those with acute coronary syndrome. The optimal target in ACS remains uncertain, but current evidence supports maintaining hemoglobin levels at or above 10 g/dL during the acute phase.

Pearl: An isolated elevation in troponin without other evidence of acute cardiac ischemia does NOT warrant a permissive transfusion strategy. Reserve higher thresholds for confirmed ACS with ongoing ischemia.

Other Potential Exceptions to Restrictive Transfusion

Beyond ACS, several clinical scenarios warrant careful consideration of transfusion thresholds:

Severe, symptomatic coronary artery disease: Patients with significant CAD and angina may benefit from higher hemoglobin targets (8-9 g/dL), though definitive trial data are lacking.

Active acute hemorrhage: In the setting of ongoing bleeding, transfusion decisions should focus on maintaining hemodynamic stability and adequate oxygen delivery, not arbitrary hemoglobin thresholds.

Cardiac surgery: Higher thresholds (7.5-8 g/dL) are reasonable during the perioperative period given the cardiovascular stress.

Neurologic injury: While not definitively proven, some experts advocate for higher thresholds (8-9 g/dL) in acute stroke or traumatic brain injury to optimize cerebral oxygen delivery.

Hack: Create a mental "rule of 10s" for cardiac patients: 10 g/dL for ACS, 8 g/dL for stable CAD undergoing surgery, 7 g/dL for all others. This simplification aids bedside decision-making while acknowledging the nuanced evidence.

Platelet Transfusions: Prophylactic vs. Therapeutic Thresholds

The Evolution of Platelet Transfusion Practice

Platelet transfusion practice has undergone remarkable transformation, moving from empiric, liberal approaches to evidence-based, restrictive strategies. The 2025 AABB platelet transfusion guidelines, published in collaboration with the International Collaboration for Transfusion Medicine Guidelines (ICTMG), represent the most comprehensive synthesis of evidence to date, incorporating data from 21 randomized controlled trials and 13 observational studies.

Prophylactic Transfusion: The 10,000 Threshold

For patients with hypoproliferative thrombocytopenia (bone marrow failure due to chemotherapy or hematopoietic stem cell transplant), robust evidence supports prophylactic platelet transfusion when platelet counts fall below 10 × 10³/µL. Multiple trials have demonstrated that this threshold adequately prevents WHO grade 2 or higher bleeding without exposing patients to unnecessary transfusions.

The TOPPS trial, one of the largest studies in this population, found no significant difference in bleeding outcomes between prophylactic transfusion at 10 × 10³/µL versus a "therapeutic only" strategy, though the prophylactic approach was associated with fewer bleeding days. The key insight: spontaneous major bleeding is rare above 10 × 10³/µL in stable patients.

Important exceptions to the 10 × 10³/µL threshold:

Consumptive thrombocytopenia in neonates: Transfuse at <25 × 10³/µL
Acute promyelocytic leukemia: Maintain platelets >30 × 10³/µL due to enhanced bleeding risk
Autologous stem cell transplant: Growing evidence suggests prophylactic transfusions may be unnecessary; consider therapeutic-only approach

Procedure-Related Thresholds: Balancing Risk and Benefit

The optimal platelet count for invasive procedures remains one of the most clinically relevant—and debated—aspects of transfusion medicine. The 2025 guidelines provide nuanced, procedure-specific recommendations:

Low-risk procedures (<20 × 10³/µL):

Bone marrow aspiration and biopsy
Peripheral and central venous catheter insertion (compressible sites)
Tunneled catheter removal
Lumbar puncture (though some guidelines recommend 40-50 × 10³/µL)

Intermediate-risk procedures (20-50 × 10³/µL):

Interventional radiology procedures (varies by complexity)
Bronchoscopy without biopsy
Endoscopy without biopsy in stable patients

High-risk procedures (50 × 10³/µL or higher):

Major non-neuraxial surgery
Epidural or spinal anesthesia
Neurosurgery (often 100 × 10³/µL)
Ophthalmologic surgery (often 100 × 10³/µL)
Liver biopsy (transjugular approach preferred if platelets low)

Pearl: For lumbar puncture, the devastating potential consequence of spinal hematoma warrants a conservative approach: target platelets 40-50 × 10³/µL and INR <1.5-2.0.

When NOT to Transfuse Platelets

Several clinical scenarios represent contraindications or situations where platelet transfusion is inappropriate:

Immune thrombocytopenia (ITP): Do not use prophylactic transfusions; platelets are rapidly destroyed and may worsen the condition. Reserve for serious bleeding, often with concurrent IVIG.

Thrombotic thrombocytopenic purpura (TTP): Contraindicated; may precipitate thrombotic events.

Heparin-induced thrombocytopenia (HIT): Contraindicated in absence of bleeding.

Portal hypertension with variceal bleeding: Recent data suggest platelet transfusion may paradoxically increase mortality and rebleeding, possibly through enhanced portal pressure.

Oyster: In cirrhosis with thrombocytopenia, remember that traditional coagulation tests (PT/INR) don't reflect the rebalanced hemostasis in liver disease. Thromboelastography (TEG/ROTEM) provides superior assessment and often reveals normal or even hypercoagulable states despite thrombocytopenia and elevated INR.

FFP and Cryoprecipitate: Busting the Myth of the "Little Bit Abnormal" INR

The Overuse of Fresh Frozen Plasma: A Persistent Problem

Fresh frozen plasma (FFP) remains one of the most inappropriately used blood products in modern medicine. A recurring scenario plays out daily in hospitals worldwide: a patient has an INR of 1.5-1.8 and requires a procedure, prompting a reflexive FFP order. This practice, rooted more in tradition than evidence, exposes patients to unnecessary risks without meaningful benefit.

The Evidence Against Routine FFP for Mildly Elevated INR

Multiple studies have demonstrated that FFP transfusion for mildly elevated INR (1.5-2.0) provides minimal coagulation factor repletion and does not reduce bleeding risk. A landmark study examining over 136 ICU patients with INR ≥1.5 found that only 32% achieved INR correction after FFP transfusion, and there was no difference in bleeding complications between those who received FFP and those who did not.

The biological explanation is straightforward: FFP contains coagulation factors at physiologic concentrations (approximately 1 unit/mL). To meaningfully increase factor levels in a normovolemic adult requires substantial volumes—typically 15-20 mL/kg (4 units for a 70 kg patient). Even then, the effect on INR is modest when baseline INR is <2.0. One cohort study demonstrated median INR reductions of only 0.1 for pre-transfusion INR 1.0-1.5 and 0.4 for INR 1.6-2.5.

When IS FFP Indicated?

FFP has legitimate, evidence-based indications:

Active bleeding with multiple factor deficiency:

INR >1.4-1.5 with clinically significant hemorrhage
Massive transfusion protocols (typically 1:1 or 1:2 ratio with RBCs)
DIC with active bleeding

Urgent reversal of warfarin:

Though prothrombin complex concentrate (PCC) is superior for emergency reversal
FFP remains acceptable if PCC unavailable

Thrombotic thrombocytopenic purpura:

Therapeutic plasma exchange is treatment of choice

Specific coagulation factor deficiencies:

Only when factor-specific concentrates unavailable

Pre-procedure in major hemorrhage risk:

Consider for high-risk procedures (neurosurgery, cardiothoracic surgery) if INR >1.5-2.0
NOT for low-risk procedures regardless of INR

Special Consideration: Cirrhosis and Coagulopathy

The "coagulopathy" of cirrhosis represents a fundamental misunderstanding of hepatic hemostasis. Patients with cirrhosis demonstrate rebalanced hemostasis with proportional reductions in both pro-coagulant and anti-coagulant factors. Standard coagulation tests (PT/INR) only measure pro-coagulant factors, creating an illusion of bleeding risk.

The American Association for the Study of Liver Diseases (AASLD) and American Gastroenterological Association (AGA) explicitly recommend against routine FFP use before low-risk procedures (paracentesis, thoracentesis, endoscopy) in cirrhotic patients. Studies have shown that FFP in portal hypertension may increase mortality through volume overload, worsened portal hypertension, and a paradoxical prothrombotic effect.

Hack: Create a personal "FFP refusal checklist": INR <2.0 without bleeding? No FFP. Low-risk procedure in cirrhosis? No FFP. Minor bleeding with stable vital signs? No FFP. This mental framework prevents reflexive, inappropriate transfusion.

Cryoprecipitate: The Fibrinogen Fix

Cryoprecipitate represents a concentrated source of fibrinogen, factor VIII, von Willebrand factor, and factor XIII. In modern practice, its primary indication is acquired hypofibrinogenemia, most commonly in the setting of major hemorrhage, DIC, or massive transfusion.

Evidence-Based Fibrinogen Thresholds

The optimal fibrinogen threshold for transfusion remains somewhat controversial, with different guidelines proposing varying targets:

British Society of Haematology (2024):

Active bleeding: fibrinogen <1.5 g/L
Obstetric hemorrhage: fibrinogen <2.0 g/L
Cardiothoracic bleeding: fibrinogen <2.0 g/L

European Trauma Guidelines:

Recommend supplementation for fibrinogen <1.5-2.0 g/L in bleeding trauma patients

Massive transfusion protocols:

Many institutions use threshold of 1.0-1.5 g/L
Higher thresholds (1.5-2.0 g/L) may be more appropriate given emerging data

The FIBRES randomized clinical trial, published in 2019, evaluated early high-dose fibrinogen concentrate versus placebo in trauma patients with bleeding and found no difference in mortality, though it was underpowered for this outcome. Observational data suggest that maintaining fibrinogen >1.5-2.0 g/L during major hemorrhage may reduce blood product requirements.

Practical Dosing of Cryoprecipitate

Each unit of cryoprecipitate contains approximately 150-250 mg of fibrinogen in 15-20 mL volume. Standard adult dosing:

Initial dose: 10 units (1-2 pooled packs), expected to raise fibrinogen by 50-100 mg/dL
Maintenance: Repeat every 6-8 hours based on fibrinogen levels and clinical bleeding
Pediatric dosing: 1 unit per 5-10 kg body weight

Pearl: Unlike FFP, cryoprecipitate's small volume (10 units ≈ 150-200 mL) makes it ideal for patients at risk of volume overload. This is particularly valuable in cardiac and renal patients requiring fibrinogen replacement.

Fibrinogen Concentrate: An Emerging Alternative

Lyophilized fibrinogen concentrate (RiaSTAP) offers several theoretical advantages over cryoprecipitate: standardized dosing, immediate availability (no thawing required), viral inactivation, and smaller volume. Currently licensed in many countries for congenital afibrinogenemia, it is increasingly used off-label for acquired hypofibrinogenemia.

The main barrier to widespread adoption is cost—fibrinogen concentrate costs approximately twice as much as cryoprecipitate per gram of fibrinogen. However, in emergency situations where rapid fibrinogen repletion is critical (massive trauma, obstetric hemorrhage), the immediate availability may justify the expense.

Oyster: In massive transfusion, fibrinogen is typically the first coagulation factor to reach critically low levels. Check fibrinogen levels early and often, and don't wait for obvious hypofibrinogenemia to develop before initiating replacement in major hemorrhage.

Recognizing and Managing Transfusion Reactions: TACO vs. TRALI

Introduction to Pulmonary Transfusion Reactions

Transfusion-associated circulatory overload (TACO) and transfusion-related acute lung injury (TRALI) represent the leading causes of transfusion-related morbidity and mortality in contemporary practice. Since 2011, these pulmonary complications have accounted for the majority of transfusion-related deaths reported to the FDA, with TACO comprising approximately 34% and TRALI 24% of fatal reactions.

The clinical challenge lies in their similar presentation: both cause acute respiratory distress and pulmonary edema within 6 hours of transfusion. However, their underlying pathophysiology, management, and prognosis differ substantially. Accurate differentiation is critical for appropriate treatment and prevention of future reactions.

TACO: Hydrostatic Pulmonary Edema

Pathophysiology: TACO represents cardiogenic pulmonary edema resulting from inability to tolerate the volume or rate of transfused blood products. The primary mechanism is volume overload leading to elevated left atrial pressure, increased pulmonary capillary hydrostatic pressure, and transudation of fluid into alveoli.

Risk factors extend beyond simple volume considerations:

Cardiac disease: Heart failure (particularly HFpEF), severe coronary disease, valvular disease
Renal dysfunction: Acute or chronic kidney disease with impaired fluid handling
Extremes of age: Elderly patients and neonates with limited cardiovascular reserve
Positive fluid balance: Pre-existing volume overload from aggressive resuscitation
Rapid transfusion: Rate >1 mL/kg/hour associated with increased risk

Interestingly, TACO can occur with relatively small transfusion volumes in susceptible patients, highlighting that individual patient factors matter more than absolute volume transfused.

Clinical Presentation:

Acute dyspnea, orthopnea, or cough during or within 6-12 hours of transfusion
Hypertension (key distinguishing feature from TRALI)
Tachycardia
Elevated jugular venous pressure
Widened pulse pressure
Peripheral edema (may be present)
Inspiratory crackles on auscultation
Chest radiograph: bilateral pulmonary infiltrates, often with cardiomegaly, pleural effusions, or Kerley B lines

Diagnostic Criteria (National Healthcare Safety Network, 2016): Three or more of the following within 6 hours of transfusion cessation:

Acute respiratory distress (dyspnea, orthopnea, cough)
Elevated brain natriuretic peptide (BNP)
Elevated central venous pressure (CVP)
Evidence of left heart failure
Evidence of positive fluid balance
Radiographic evidence of pulmonary edema

Biochemical Markers: BNP or NT-proBNP levels provide valuable diagnostic support:

Post-transfusion BNP >300 pg/mL or NT-proBNP >2000 pg/mL suggests TACO
Pre/post-transfusion NT-proBNP ratio >1.5 has good diagnostic accuracy
Values drawn within 24 hours of reaction onset most useful

Management:

Immediate actions:
- Stop the transfusion
- Sit patient upright
- Administer supplemental oxygen
- Notify blood bank and attending physician
Pharmacologic therapy:
- Diuretics: Furosemide 20-40 mg IV (or higher dose based on home regimen and renal function)
- Response to diuretics strongly suggests TACO diagnosis
- Monitor urine output; goal negative fluid balance
Respiratory support:
- Supplemental oxygen to maintain SpO₂ >90%
- Non-invasive positive pressure ventilation (CPAP/BiPAP) if needed
- Mechanical ventilation for severe respiratory failure
Hemodynamic management:
- Blood pressure control if severely hypertensive
- Avoid excessive fluid administration

Prevention:

Careful assessment of transfusion need—avoid unnecessary transfusions
Slower transfusion rates in high-risk patients (<1 mL/kg/hour)
Consider split-unit transfusion (transfuse half unit, reassess, then complete if needed)
Prophylactic diuretics in high-risk patients (20 mg furosemide IV before or between units)
Pre-transfusion volume status assessment

Pearl: The triad of hypertension, elevated BNP, and response to diuretics essentially confirms TACO. If your patient improves with furosemide, you've made the right diagnosis and initiated the right treatment.

TRALI: Permeability Pulmonary Edema

Pathophysiology: TRALI represents non-cardiogenic pulmonary edema resulting from acute lung injury. The leading hypothesis invokes a "two-hit" model:

First hit: Patient factors that prime neutrophils and activate pulmonary endothelium

Systemic inflammation (sepsis, SIRS)
Recent surgery
Mechanical ventilation
Massive transfusion
Hematologic malignancy

Second hit: Transfusion of biologically active substances

Anti-HLA or anti-HNA antibodies (most common in plasma from multiparous female donors)
Bioactive lipids that accumulate during blood storage
Other biological response modifiers

This dual-hit mechanism explains why TRALI occurs in specific patients receiving specific units. The antibodies or biological response modifiers activate primed neutrophils, leading to endothelial damage, increased vascular permeability, and protein-rich fluid extravasation into alveoli.

Clinical Presentation:

Acute dyspnea during or within 6 hours of transfusion
Hypoxemia (SpO₂ <90% on room air)
Hypotension or normotension (NOT hypertension)
Fever (often present, may precede respiratory symptoms)
Tachycardia
Normal or low CVP/PCWP
Bilateral crackles on auscultation
Chest radiograph: bilateral infiltrates WITHOUT cardiomegaly, pleural effusions, or vascular congestion

Diagnostic Criteria (Canadian Consensus/NHLBI Working Group):

TRALI:

Acute lung injury (hypoxemia, bilateral infiltrates)
Onset during or within 6 hours of transfusion
No temporal relationship with alternative ARDS risk factor
No evidence of left atrial hypertension/circulatory overload

Possible TRALI: 1-2 as above, PLUS 3. Temporal relationship with alternative ARDS risk factor (sepsis, aspiration, pneumonia, trauma, pancreatitis)

Management:

Immediate actions:
- Stop transfusion immediately
- Notify blood bank for donor antibody screening
- Supportive care
Respiratory support (similar to ARDS management):
- Supplemental oxygen
- Non-invasive ventilation if adequate
- Mechanical ventilation with lung-protective strategy if intubated:
  - Low tidal volume (6 mL/kg ideal body weight)
  - Plateau pressure <30 cmH₂O
  - PEEP as needed for oxygenation
Hemodynamic management:
- Judicious fluid administration—avoid both hypovolemia and hypervolemia
- Vasopressors if hypotensive (norepinephrine first-line)
- DO NOT use diuretics (ineffective and may worsen hemodynamics)
Avoid:
- Corticosteroids (NOT indicated, no proven benefit)
- Aggressive diuresis

Natural History:

Most patients improve within 48-96 hours with supportive care
Chest radiograph typically clears within 2-5 days
Mortality historically 5-10%, though improving with recognition and supportive care
Slow recovery suggests alternative diagnosis

Prevention:

Preferential use of male donor plasma (strategy dramatically reduced TRALI incidence)
Screening female donors for HLA/HNA antibodies
Leukoreduction of blood products (may reduce but not eliminate risk)
Avoiding plasma-rich products when possible in high-risk patients

Hack: Create a mental checklist for TRALI: "No BP elevation + No response to diuretics + Bilateral infiltrates + Recent transfusion = TRALI until proven otherwise."

Key Distinguishing Features: TACO vs. TRALI

Feature	TACO	TRALI
Blood Pressure	Usually hypertensive	Hypotensive or normotensive
JVP/CVP	Elevated	Normal or low
BNP/NT-proBNP	Elevated, ratio >1.5	Normal or minimally elevated
Response to Diuretics	Improves	No improvement
CXR Pattern	Vascular congestion, possible cardiomegaly, pleural effusions	Bilateral infiltrates without cardiomegaly
Fluid Balance	Positive	May be neutral or negative
Mechanism	Hydrostatic (cardiogenic)	Permeability (non-cardiogenic)
Time to Resolution	Hours to 1-2 days	2-4 days
Treatment	Diuretics	Supportive only

Oyster: Both TACO and TRALI can coexist in the same patient, and both can occur in the setting of underlying ARDS. When in doubt, treat for TACO first (diuresis is unlikely to harm TRALI patients significantly, whereas withholding diuretics from TACO patients may be deleterious). If no response to diuretics, shift management strategy to ARDS/TRALI protocols.

Conclusion: A Patient-Specific Approach to Transfusion Medicine

Modern transfusion medicine represents a paradigm shift from reflexive, threshold-based practices to individualized, evidence-informed decision-making. The key principles that should guide contemporary practice include:

Restrictive transfusion is the standard for most patients, with hemoglobin thresholds of 7-8 g/dL safe and appropriate for hemodynamically stable hospitalized adults.
Acute coronary syndrome is the critical exception, where maintaining hemoglobin ≥10 g/dL may reduce cardiac mortality.
Platelet transfusion thresholds should be procedure-specific, with prophylactic transfusion at 10 × 10³/µL for stable patients with hypoproliferative thrombocytopenia.
FFP is dramatically overused, particularly for mildly elevated INR without active bleeding. Reserve FFP for genuine multiple factor deficiency with bleeding.
Fibrinogen matters more than we historically appreciated in major hemorrhage. Monitor levels and maintain >1.5-2.0 g/L with cryoprecipitate.
TACO and TRALI are distinguishable with careful clinical assessment. Blood pressure, BNP, and response to diuretics provide the most useful discriminating features.

As transfusion medicine continues to evolve, the internist must remain current with emerging evidence, question traditional practices, and always ask: "Does this patient truly need this blood product, and what are the risks versus benefits for THIS patient?" This individualized approach, grounded in high-quality evidence, represents the future of transfusion medicine.

Key References

Natanson C, Applefeld WN, Klein HG. Hemoglobin-based transfusion strategies for cardiovascular and other diseases: restrictive, liberal, or neither? Blood. 2024;144(20):2075-2082.
Carson JL, Brooks MM, Hébert PC, et al. Restrictive or Liberal Transfusion Strategy in Myocardial Infarction and Anemia. N Engl J Med. 2023;389(26):2446-2456.
Association for the Advancement of Blood & Biotherapies. Updates in Red Blood Cell Transfusion Thresholds. AABB Clinical Practice Guidelines. 2024.
Metcalf RA, Delaney M, Slichter SJ, et al. Platelet Transfusion International Clinical Practice Guidelines. JAMA. 2025;329(19):1892-1902.
American College of Chest Physicians. Transfusion of Fresh Frozen Plasma and Platelets in Critically Ill Adults: An American College of Chest Physicians Clinical Practice Guideline. Chest. 2025;157(3):488-499.
Wikkelsø AJ, Wetterslev J, Møller AM, Afshari A. Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) to monitor haemostatic treatment in bleeding patients: a systematic review with meta-analysis. Anaesthesia. 2017;72(4):519-531.
Vlaar APJ, Toy P, Fung M, et al. A consensus redefinition of transfusion-related acute lung injury. Transfusion. 2019;59(7):2465-2476.
Lieberman L, Petraszko T, Yi QL, et al. Transfusion-associated circulatory overload and transfusion-related acute lung injury. Blood. 2019;133(17):1840-1853.

Questions for Self-Assessment

A 68-year-old man with known severe coronary artery disease presents with NSTEMI. His hemoglobin on admission is 8.2 g/dL. What is the appropriate transfusion threshold for this patient?
A patient with AML undergoing chemotherapy has a platelet count of 8 × 10³/µL without bleeding. A lumbar puncture is planned for intrathecal chemotherapy. What is your management approach?
A cirrhotic patient with INR 2.1 requires diagnostic paracentesis. The team requests FFP before the procedure. How do you respond?
A patient develops acute dyspnea and hypoxemia 2 hours after receiving 2 units of RBCs. Blood pressure is 180/95 mmHg, JVP is elevated, and BNP is 450 pg/mL. What is the diagnosis and immediate management?

Answers provided in supplementary material

This review article is intended for educational purposes and should be adapted to local institutional protocols and individual patient circumstances. Always consult with hematology and transfusion medicine specialists for complex cases.

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