Category: Teaching

Teaching medical and technical staff transfusion medicine

Rh Discrepancy Workup

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This is an old lecture I gave to medical technologists at National Guard Health Affairs in Jeddah. This was prepared in the pre-molecular blood bank era, but there is good common sense in it to deal with many interferences.

Process: Donor Reactions

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5.6.1 PROCESS:  Donor Reactions

Process:

  1. Donor is continuously observed in the collection and post-donation areas by collection staff.
  2. Staff respond promptly to any adverse effect.
  3. Staff contact transfusion physician immediately if they cannot treat the reaction.
  4. Donor is referred promptly to emergency service if the transfusion physician cannot handle the situation or is not on premises.
  5. All reactions are documented in the adverse effects log and Hematos IIG.

References:

  1. HMC 1001 Setting Specification, Version 1.5, Hematos IIG, Medinfo
  2. Standards for Blood Banks and Transfusion Services, Current Edition, AABB, Bethesda, Maryland, USA

Policy: Donor Reactions

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Document Enumeration:  5.6

Policy:

  1. All donors must be continuously observed throughout and after the collection process.
  2. Donors showing any signs of an adverse reaction must be treated promptly.
  3. All collection staff should be trained and deemed competent to handle donor reactions.
  4. All adverse effects should be recorded in the appropriate log AND the Hematos IIG system.
  5. All policies, processes, and procedures must comply with Qatari, HMC, and applicable accreditation standards (i.e. AABB, CAP, and JCI).

References:

  1. HMC 1001 Setting Specification, Version 1.5, Hematos IIG, Medinfo
  2. Standards for Blood Banks and Transfusion Services, Current Edition, AABB, Bethesda, Maryland, USA

Opinion: Selecting a Pathogen Inactivation System

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Transfusion-transmitted infectious disease are a continuing threat.  Despite donor infectious marker testing and new donor questioning, there are many threats which are not addressed by these measures.  Also new pathogens are being identified for which there are no tests or specific donor questions available.  How can we handle these new threats?

Pathogen inactivation can significantly reduce infectious agents in blood components, although the degree varies depends on the agent.  Theoretically any agent with nucleic acid—RNA or DNA is affected.  The only class of agents not affected at all are prions, which have NO nucleic acid at all.

In general, a photoactive agent is added to the blood component which binds to the nucleic acid.  Photoactive agents include riboflavin, psoralen dyes, and methylene blue.  Then the component is irradiated, the time proportional to the volume of the unit.

The component is then exposed to ultraviolet light to photoactivate it, which disrupts the DNA and RNA present, including in the white cells.  Thus, NO irradiation or bacterial culture is required.

Here are my questions to consider when selecting a pathogen inactivation system:

Targets?  Platelets vs plasma vs whole blood?

Methylene may be used for plasma, but riboflavin or psoralens may be used for platelets or plasma.  Whole blood inactivation with riboflavin is CE-approved.

Photoactive dye:  Is it riboflavin vs psoralen vs methylene based?

Riboflavin is vitamin B2—the amount used is small and does not need to be removed whereas the psoralen must be removed for clinical use.

Does the photoactive material need to be removed before transfusion?

You can immediately use the riboflavin-treated component but the psoralen must be removed before transfusion—this may take 6 or 20 hours depending on the licensing of the product.

What is the loss of platelets or coagulation factors after treatment?

With treatment by all methods, there is some loss of platelets and coagulation factors.  The platelet loss may be greater in psoralen-based methods and require additional components be added to the pool to reach the desired dose.  Likewise, plateletpheresis components treated with psoralen may require a recalibration of the donor apheresis equipment to collect more platelets per dose to compensate.  There may be some RBC loss additionally in whole blood pathogen inactivation.

What is the efficacy of pathogen reduction for the infectious agents, particularly the ones in your region?

Example:  How well does the treatment handle local agents like Hepatitis E?  Psoralen agents may be less effective than riboflavin for this agent.

Does it work with platelet additive solution PAS?

There are minimum and maximum volumes for pathogen inactivation set by the manufacturer.  Can you get sufficient yields within these volumes?

How good is the data management system?  Can it be integrated with your blood bank computer system?

Can the equipment be integrated with your system?  This is important to set rules and enforce good manufacturing processes GMP.

Does it work well with an automated blood component production system?

Such automated systems like the Reveos can free up personnel for pathogen inactivation.  Can the volumes produced be handled effectively by the pathogen-inactivation method?  Do the timings for separation of components work synergistically with the pathogen inactivation method?

Vendor issues:  how well will the local agent provide support?  Is someone else in your country or region using the system?

You need an experienced vendor to provide optimal support.

Are These Garbage Antibodies?

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In my Middle Eastern experience, I have found antibody panels from a certain manufacturer show a lot of weak, nonspecific reactivity which disappears with another manufacturer’s panels, particularly when gamma-heavy-chain-specific reagents are used:

  • In the following example, 4/15 cells show weak or 1+ reactivity at AHG phase only using the manufacturer’s whole molecule IgG antiglobulin reagent—no reactions at enzyme phase.  This reagent detects both heavy and light chains.
  • When the panel from another manufacturer is used with a gamma-heavy-chain-specific reagent, there is no reactivity at either AHG or enzyme phases.

Normally, in my protocols, the first encounter in this situation, I would do extended RBC phenotyping beyond Rh and Kell systems as well.

In my experience, the nonspecific reactions detected are not clinically significant and they may be ignored if the conditions of the following algorithm is used:

  1. If nonspecific, enzyme-labile reactions found in the first manufacturer’s panels and AHG, then repeat with the second manufacturer’s panels using gamma-heavy-chain-specific reagents.
  2. If the second manufacturer’s panels are negative, use the latter for full AHG crossmatch and release crossmatch-compatible components if the panel is negative.

What do you do when you encounter this is in your laboratory?  Please share your thoughts.

Manufacturer 1’s Panel:

Manufacturer 2’s Panel: