Academe Learn
CBME Curriculum Preview

Page 27 of 27

PA21.1-6 | Blood Groups & Transfusion Medicine — PBL Case

CLINICAL SETTING

Kavitha, a 32-year-old homemaker from Chennai, is admitted to a busy government hospital for an elective laparoscopic cholecystectomy. She has no known comorbidities. The ward is short-staffed on the morning of her surgery, and in the pre-operative chaos, the blood bank technician draws a sample from the patient in the adjacent bed — also a woman in her early thirties — without confirming the wristband. The label 'Kavitha / 32F / ward 4B' is written from memory on the tube. The blood is grouped, crossmatched, and a unit of packed red blood cells (PRBC) is kept ready as a precaution. During surgery, mild haemorrhage occurs and the anaesthetist transfuses the crossmatched unit. Within 15 minutes, Kavitha develops rigors, her temperature climbs to 39.6°C, her BP drops from 118/74 to 78/46 mmHg, and she passes dark reddish-brown urine through the urinary catheter. The scrub nurse calls a code.

Trigger 1: Initial Presentation — Something Is Terribly Wrong

The operating surgeon stops the procedure. The anaesthetist stops the blood transfusion immediately and infuses normal saline wide open. Emergency investigations from the theatre: • The transfused unit bag label: 'Group A Rh-negative, crossmatched for Kavitha' • Point-of-care blood group of Kavitha (from a fresh finger-prick sample taken in theatre): Group O Rh-negative • Urine: grossly haemoglobinuric (dark port-wine colour) • BP 78/46 mmHg despite 500 mL saline • Temperature 39.8°C, HR 128/min • The blood bank is called and confirms that the group A unit was crossmatched against the mislabelled sample — not against Kavitha's actual blood

DISCUSSION POINTS

  • Explain the immunological mechanism of the acute haemolytic reaction occurring in Kavitha. What specific antibodies does she carry in her plasma as a group O individual, and how do they trigger intravascular haemolysis when exposed to group A red cells?
  • Why does ABO incompatibility cause INTRAVASCULAR haemolysis (rather than extravascular)? Which component of the immune system is activated, and what is the direct cause of the haemoglobinuria?
  • What is the single most common ROOT CAUSE of acute haemolytic transfusion reactions in clinical practice worldwide? Identify the specific error that occurred in this case and at which step in the transfusion safety chain it happened.
  • The crossmatch was performed and was 'compatible' — how is it possible for a crossmatch to appear compatible if the blood was grouped incorrectly? What is the limitation of the crossmatch when the input sample itself is wrong?
Click to reveal Trigger 2: Investigations — Diagnosing the Reaction and Containing the Damage (discuss previous trigger first!)

Trigger 2: Investigations — Diagnosing the Reaction and Containing the Damage

The anaesthetist sends a comprehensive 'transfusion reaction workup' panel to the laboratory. The blood bank technician retrieves the original sample tube and the transfused unit. Laboratory results: • Direct antiglobulin test (DAT) on Kavitha's post-transfusion blood: POSITIVE (4+) • Haemoglobin in plasma (free haemoglobin): markedly elevated • Serum bilirubin: rising (indirect fraction predominant) • Serum haptoglobin: undetectable • Urine haemoglobin: positive; urine haemosiderin: positive • Serum creatinine 2 hours later: 1.9 mg/dL (was 0.7 mg/dL pre-op) • Repeat grouping of the original sample confirms blood group A; repeat grouping from Kavitha confirms group O • Platelet count: 85 × 10⁹/L (was 210 × 10⁹/L preoperatively); PT prolonged; fibrinogen falling — DIC pattern emerging

DISCUSSION POINTS

  • Interpret the complete post-transfusion laboratory panel: what is the significance of undetectable haptoglobin, elevated plasma haemoglobin, and haemoglobinuria together? Trace the fate of haemoglobin once it is released from haemolysed red cells.
  • The DIC pattern is emerging (falling platelets, falling fibrinogen, prolonged PT). What is the mechanistic link between intravascular haemolysis and the onset of DIC in an acute haemolytic transfusion reaction?
  • The investigation protocol for a suspected transfusion reaction requires a strict, ordered sequence of steps. Enumerate the steps in the correct order — starting from 'stop the transfusion' and ending with 'inform the blood bank'.
  • Compare this acute haemolytic reaction with a febrile non-haemolytic transfusion reaction (FNHTR): how would you distinguish them clinically and laboratory-wise in the first 15 minutes, before the full workup returns?
Click to reveal Trigger 3: Diagnosis & Management — Prevention and Safe Transfusion (discuss previous trigger first!)

Trigger 3: Diagnosis & Management — Prevention and Safe Transfusion

Kavitha survives after aggressive ICU management. The hospital's transfusion medicine committee conducts a root-cause analysis. The investigation identifies: (1) blood sample collected from wrong patient; (2) no wristband identity check performed; (3) no bedside identity verification at the time of transfusion. Six weeks later, Kavitha (who has now fully recovered, blood group O Rh-negative, normal renal function) requires elective surgery again. She is anxious and asks the surgeon: 'Can you guarantee I won't receive the wrong blood again?' The blood bank team is also asked to counsel her on autologous transfusion options — and to counsel a pregnant patient in the antenatal clinic (Kavitha's roommate, who is also Rh-negative and 28 weeks pregnant with her second child, whose first child was born jaundiced). Additionally, the blood bank is investigating a bag of platelets that a nurse flagged as 'cloudy and smelling odd' — the bag is 4 days old. The transfusion officer has to decide whether to issue it.

DISCUSSION POINTS

  • Describe preoperative autologous blood donation (PAD) as an option for Kavitha's elective second surgery. What are its advantages, contraindications, and the specific clinical scenarios where autologous transfusion is most valuable? Why is it particularly relevant for her blood group?
  • Kavitha's roommate is Rh-negative, second pregnancy, first child was jaundiced. Explain the mechanism of haemolytic disease of the newborn (HDN) in Rh incompatibility — why was the first child unaffected but the second child at risk? What is the rationale for anti-D immunoglobulin prophylaxis and at what points should it be given?
  • The platelet bag is cloudy and malodorous at day 4. Explain why platelets are specifically at high risk of bacterial contamination compared to PRBC, what organisms are most commonly responsible, and what the correct action is when contamination is suspected.
  • Design a systematic pre-transfusion safety checklist (at the bedside) that would have PREVENTED Kavitha's reaction. Which of the five mandatory NACO screening tests on donated blood also contributes to safety from a different angle — and what does each test specifically screen for?

Group Task Assignments

Group 1: ABO and Rh blood group systems — genetics, serology, clinical consequences

  • Construct the ABO blood group table: for each of the four groups (A, B, AB, O), list the red cell antigen, the serum antibody, the antibody class (IgM/IgG), and whether it fixes complement. Explain Landsteiner's law.
  • Describe the Bombay phenotype (hh): why do these individuals fail to express A, B, or H antigens, and why is their blood uniquely dangerous to transfuse — even to group O recipients? How common is it in South India?

Competencies: PA21.1

Group 2: Blood components and clinical uses

  • Create a reference table for all major blood components (PRBC, FFP, platelets, cryoprecipitate, granulocytes, albumin): preparation method, volume, storage conditions and duration, key contents, and one specific clinical indication for each.
  • Explain why massive transfusion (>10 units PRBC in 24 hours) causes hypothermia, hypocalcaemia, and dilutional coagulopathy — describe the metabolic complications collectively known as the 'lethal triad' and the '1:1:1' resuscitation ratio rationale.

Competencies: PA21.2

Group 3: Transfusion-transmitted infections and NACO screening

  • List the five NACO-mandated screening tests for donated blood in India, state the pathogen each detects, and identify the window period for each — highlighting why HIV NAT testing has reduced (but not eliminated) the window period risk.
  • Explain why bacterial contamination of platelets is the most common infectious cause of transfusion-related death (more common than HIV/HBV/HCV combined), and describe the specific storage conditions that make platelets uniquely vulnerable to bacterial proliferation.

Competencies: PA21.3

Group 4: Transfusion reactions — classification, mechanisms, investigation

  • Classify transfusion reactions using the 2×2 matrix (acute vs delayed × immune vs non-immune). Give one example and the key mechanism for each of the four quadrants. Include TRALI (leading cause of mortality in high-income settings) and TACO (leading cause in elderly patients).
  • Write the complete, step-by-step investigation algorithm for a suspected acute transfusion reaction, beginning with 'stop the transfusion' and ending with 'complete transfusion reaction report to the blood bank'.

Competencies: PA21.4

Group 5: Blood grouping technique, crossmatch, and autologous transfusion

  • Describe the forward and reverse ABO grouping procedure: what reagents are used, what reactions are expected, and what constitutes a discrepancy requiring investigation? Explain the weak-D problem in Rh typing and its clinical significance.
  • Compare the three types of autologous transfusion (preoperative autologous donation, intraoperative cell salvage, acute normovolaemic haemodilution): indications, contraindications, and the specific advantage each offers over allogeneic transfusion.

Competencies: PA21.5, PA21.6

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [PA21.1] What are the ABO and Rh blood group systems — their antigens, antibodies, inheritance, and clinical consequences of incompatibility including haemolytic disease of the newborn?
  2. [PA21.2] What are the major blood components (PRBC, FFP, platelets, cryoprecipitate), their preparation, storage, and specific clinical indications including massive transfusion?
  3. [PA21.3] What infections can be transmitted by blood transfusion, what are the five NACO-mandated screening tests, what is the concept of the window period, and why is bacterial contamination of platelets the leading infectious cause of transfusion death?
  4. [PA21.4] How are transfusion reactions classified (acute vs delayed, immune vs non-immune), what are the mechanisms of the major reactions (AHTR, FNHTR, TRALI, TACO, DHTR), and what is the step-by-step investigation algorithm for a suspected reaction?
  5. [PA21.5] What are the indications, types, advantages, and contraindications of autologous transfusion (preoperative autologous donation, intraoperative cell salvage, acute normovolaemic haemodilution)?
  6. [PA21.6] What is the technique of ABO and Rh blood grouping (forward and reverse), what constitutes a discrepancy, how is crossmatching performed (immediate-spin and AHG phases), and what are the common sources of error in blood grouping and crossmatching?