In a 67-year-old male with O‑negative blood type who was transfused B‑positive packed red blood cells and within 20 minutes developed fever, hypotension, tachycardia, chills, flank pain, dark‑colored urine, and a positive direct Coombs test, what is the most likely diagnosis?

Acute Hemolytic Transfusion Reaction (AHTR)

Diagnosis

This patient is experiencing an acute hemolytic transfusion reaction (AHTR) due to ABO-incompatible blood transfusion—a life-threatening medical emergency caused by transfusing B-positive blood to an O-negative recipient. 1, 2

---

CJMM Phase 1: Recognize Cues

Four Abnormal Assessment Findings

• Hypotension (86/50 mm Hg) with tachycardia (118 bpm) indicating hemodynamic instability from complement activation and vasomotor disturbances 2
• Fever (101.2°F/38.4°C) with chills representing the systemic inflammatory response to intravascular hemolysis 2
• Dark-colored urine (hemoglobinuria) indicating massive intravascular red cell destruction with free hemoglobin release 3, 2
• Back/flank pain with chest tightness mediated by complement cleavage products (C3a, C5a) causing pain, restlessness, and dyspnea 2

Critical Transfusion-Related Cue

• ABO major incompatibility: B-positive blood transfused to O-negative patient represents the most dangerous transfusion error, as group O patients have naturally occurring anti-A and anti-B antibodies that immediately attack incompatible red cells 4, 5

---

CJMM Phase 2: Analyze Cues

How Incompatible Blood Caused Symptoms

• Anti-B antibodies in the O-negative recipient immediately bind to B-antigen on transfused red cells, activating the complement cascade leading to intravascular hemolysis 2, 6
• Complement activation releases C3a and C5a (anaphylatoxins) which mediate fever, hypotension, pain, dyspnea, nausea, and shock through histamine and kinin release 2
• Massive intravascular hemolysis releases free hemoglobin causing hemoglobinuria (dark urine) and potential acute kidney injury 3, 2
• Activation of intravascular clotting pathways can progress to disseminated intravascular coagulation (DIC) with bleeding complications 3, 2

Significance of Positive Direct Coombs Test

• The positive direct antiglobulin test (DAT/Coombs) confirms antibody coating on transfused red cells, proving immune-mediated hemolysis rather than non-immune causes 1
• This finding definitively establishes AHTR as the diagnosis by demonstrating IgG and/or complement (C3d) bound to the surface of red blood cells 1

---

CJMM Phase 3: Prioritize Hypotheses

Most Likely Problem

• Acute hemolytic transfusion reaction (AHTR) from ABO major incompatibility with ongoing intravascular hemolysis, hemodynamic instability, and risk of progression to DIC and acute kidney injury 1, 3, 2

Greatest Immediate Risk

• Cardiovascular collapse and acute kidney injury from continued hemolysis, hypotension, and free hemoglobin deposition in renal tubules 3, 2
• Disseminated intravascular coagulation (DIC) from activation of the clotting cascade by hemolyzed red cell membranes and tissue factor release 3, 2

Priority Concern

• Hypotension (86/50 mm Hg) with hemoglobinuria represents the most critical finding requiring immediate intervention to prevent irreversible organ damage, particularly acute renal failure 1, 3

---

CJMM Phase 4: Generate Solutions

Two Priority Nursing Interventions

• Maintain adequate blood pressure for organ perfusion (MAP >65-70 mmHg) with aggressive IV fluid resuscitation using normal saline bolus 1000-2000 mL to preserve renal perfusion and prevent acute kidney injury 1, 3
• Administer high-flow oxygen (high FiO2) and monitor respiratory status closely to address potential hypoxemia and prepare for potential intubation if respiratory distress worsens 7, 1

Additional Actions Related to Transfusion

• Contact the transfusion laboratory immediately to report the reaction and initiate investigation—this is a statutory requirement with 100% traceability mandated for 30 years 4, 1
• Send post-reaction blood samples immediately for: complete blood count, PT, aPTT, fibrinogen, direct antiglobulin test (DAT), repeat cross-match, and visual inspection of plasma for hemolysis to guide further management and document the reaction 7, 1
• Double-check all documentation for administration errors, particularly patient identification and blood component compatibility, as this represents a preventable sentinel event 1

---

CJMM Phase 5: Take Action

First Nursing Action When Transfusion Reaction Suspected

Stop the transfusion immediately and maintain IV access with normal saline—this is the single most critical intervention that can prevent progression to severe morbidity or mortality. 7, 1, 8

• Do not wait to confirm the reaction type before stopping the transfusion, as every minute of continued incompatible blood administration increases the severity of hemolysis 1
• Keep the IV line open with normal saline for medication administration and aggressive fluid resuscitation 7, 8

Anticipated Medications and Treatments

• Aggressive IV fluid resuscitation with normal saline or lactated Ringer's solution to maintain MAP >65-70 mmHg and preserve renal perfusion 7, 8, 3
• Vasopressors (norepinephrine or dopamine) if hypotension persists despite fluid resuscitation to maintain adequate organ perfusion 1
• Diuretics (furosemide) may be considered ONLY after adequate fluid resuscitation to maintain urine output >100 mL/hour and prevent hemoglobin precipitation in renal tubules 3
• Plasma exchange therapy should be considered for severe cases to remove anti-B antibodies and free hemoglobin, as it has been shown to decrease free hemoglobin from 13 to 2 mg/dL within 2 hours 3
• Eculizumab (complement C5 inhibitor) may be considered in severe cases to block complement-mediated hemolysis, though this is typically reserved for refractory cases 6
• Continuous renal replacement therapy (CRRT) or hemodialysis if acute kidney injury develops despite aggressive fluid management 3

---

CJMM Phase 6: Evaluate Outcomes

Findings Indicating Patient Stabilization

• Blood pressure normalizing (systolic >100 mmHg, MAP >65 mmHg) with heart rate decreasing toward baseline (<100 bpm) 1
• Urine output maintained >0.5-1 mL/kg/hour with clearing of hemoglobinuria (urine color lightening from dark red/brown to yellow) 3
• Temperature trending down toward normal with resolution of chills and subjective improvement in pain 1
• Hemoglobin stabilizing without further decline on serial measurements 3
• Laboratory improvement: decreasing LDH, decreasing indirect bilirubin, improving renal function (stable or decreasing creatinine) 3

Findings Indicating Worsening Condition

• Persistent or worsening hypotension despite aggressive fluid resuscitation requiring escalation to vasopressors 1, 3
• Oliguria or anuria (urine output <0.5 mL/kg/hour) indicating acute kidney injury progression 3
• Development of bleeding from multiple sites (IV sites, mucous membranes) suggesting disseminated intravascular coagulation 3, 2
• Worsening respiratory distress with hypoxemia requiring intubation and mechanical ventilation 7, 8
• Laboratory deterioration: rising creatinine, falling fibrinogen, prolonging PT/aPTT, falling platelet count, rising lactate indicating DIC and multi-organ dysfunction 3
• Continued hemoglobinuria despite aggressive fluid resuscitation suggesting ongoing hemolysis 3

---

Critical Pitfalls to Avoid

• Never administer diuretics before adequate fluid resuscitation, as this can worsen renal perfusion and precipitate acute tubular necrosis 8
• Do not transfuse additional blood products without consulting transfusion medicine, as further incompatible transfusions will worsen hemolysis 1
• Avoid assuming the reaction is mild based on initial presentation—AHTR can rapidly progress to cardiovascular collapse, DIC, and multi-organ failure within hours 3, 2
• Do not delay reporting to the blood bank, as this is both a legal requirement and critical for preventing future errors by removing implicated units from circulation 4, 1