Acute Hemolytic Transfusion Reactions

An acute hemolytic transfusion reaction (HTR) occurs when the recipient of a blood transfusion is incompatible with the donor (most commonly an ABO incompatibility). The specific red blood cell (RBC) antigens and the recipients’ antibody titer determine the reaction severity.

The recipients’ antibodies bind to transfused RBC antigens. IgM is released, and the complement system is activated, causing immediate intravascular hemolysis. The membrane attack complex causes complement proteins to create pores in the RBC membrane, leading to cell lysis. Histamine is released through the binding of complement proteins to mast cell surfaces, causing degranulation. This results in increased vessel permeability, vessel dilation, bronchoconstriction, and release of proinflammatory cytokines. The rupture of RBCs releases free hemoglobin, which causes renal tubule occlusion and renal vasoconstriction, resulting in acute tubular necrosis and renal failure. Antibodies from the recipient opsonize the transfused RBCs, leading to phagocytosis by macrophages and phagocytes (extravascular hemolysis). Over time, RBCs circulating through the liver and spleen (where macrophages are highly concentrated) break down slowly, quickly becoming fragile (osmotically fragile spherocytes).

To diagnose an acute HTR, ABO and Rh typing, antibody screening and crossmatching should be repeated. Antibodies not originally detected may now be present post-reaction. Elevated hemoglobinemia (due to free hemoglobin released by RBC moving into plasma), hemoglobinuria, (free hemoglobin excreted into urine), as well as hyperbilirubinemia (buildup of hemoglobin breakdown) would be seen. Haptoglobin (which binds to free hemoglobin) would be low. Lactate dehydrogenase (an enzyme found in RBCs, released through cell lysis) would be elevated. PT, APTT, fibrinogen, NR and platelet count are coagulation tests that would reveal if disseminated intravascular coagulation has occurred. Next, a renal panel would likely indicate renal impairment (free hemoglobin buildup leading to kidney damage). Finally, an ECG should be done to monitor heart function (arrhythmias, myocardial stress, or electrolyte imbalances can occur).

Common side effects include hypotension, tachycardia, fever, tachypnea, hypoxia, chest or back pain, hematuria, low urine output, restlessness, nausea, vomiting, anxiety, rash or headache.

If an acute HTR is suspected, the transfusion should be stopped, normal saline should be run, ABCs, vitals, and urine output should be assessed, and treatment of symptoms should begin (ex. fluid resuscitation). Furosemide can be used to prevent an AKI (increasing renal blood flow and urine output), and corticosteroids, antihistamines or epinephrine may be used if the airway is compromised. In severe cases, an exchange transfusion may be required.

This video was well-researched and I felt that it was well done, however, there were a few pieces of content that I wish were added that would have enhanced my understanding of the topic. First, I would have liked if the type of hypersensitivity reaction that HTRs are was discussed, as I felt it would have helped to relate the content to our class learning a bit more. I would have also found it beneficial to mention other types of hemolytic issues discussed in class, such as newborn hemolytic disease, and how this differs as it may have been interesting and helpful to my overall understanding.

Next, I would have liked to hear you discuss the activation of the complement system in a more clear or organized manner. I felt that the content jumped back and forth between the complement system and other pathologic processes, such as what was occurring in the kidneys, making it hard to follow at times. Chemotaxis was also the only piece of the complement system activation that was not discussed. This is also just my opinion and others may have not found it confusing, and it all did come together well in the end.

Finally, I would have liked it if you had spoken a bit more about why the coagulation labs are important and what disseminated intravascular coagulation is. I have heard of this before, but I was a bit confused about its relation to HTRs and the pathophysiology behind why this is happening. These are all very minor gaps, and I still learned a lot from this video and enjoyed watching it.

One teaching-learning strategy that was well implemented and supported my learning was the visuals that were included throughout the video presentation. I am a very visual learner and find it much easier to understand topics (especially related to pathophysiology) when I can look at an image or diagram.

The photos you chose were simple enough to quickly glance at and understand while still being able to listen and comprehend what was being discussed. I felt that you had the perfect number of photos and that I had enough time to look at each one without feeling rushed or losing interest.

Each photo also helped to trigger my memory and think back to past pathophysiology or anatomy classes, for example, the photo of the glomerulus and renal tubule. As you were speaking, I thought back to our previous pathophysiology class and was able to recall the normal functions of the kidneys and how acute tubular necrosis can occur. This helped me to better understand the pathophysiology of HTRs.

Another image I found helpful was of Interior Health’s protocol for responding to a transfusion reaction. This is very beneficial as a reference and reminder of how to respond when a transfusion reaction occurs. There was also an image that labelled a diagram of a human and organized the main symptoms of an HTR based on the system. This was very beneficial for memorizing and categorizing the common symptoms. Overall, the integration of visuals was appropriate throughout and aided in learning. It was a very well-done video project.

Although I thought the presentation was very well done, I would have loved for the case study and acting scene to be presented at the start of the video or integrated throughout, instead of at the end. This is because I feel it would have eased viewers into the video and set up the presentation well, engaging the audience. Instead, it felt as though we jumped right into the pathophysiology without setting up the topic. This was also a bit confusing as the patient’s name from the case study was mentioned before the case was introduced.

Furthermore, I had a hard time following some of the content at the beginning, and having a case study to draw from and refer to could have been helpful. The acting in your video was well done, it made sense, and I loved how you progressed through the decision-making process for giving blood. The patient’s symptoms were clearly portrayed, and treatment options were well demonstrated. I felt as though it may have been helpful to either discuss common symptoms before showing the video, or discuss them immediately following that scene, and the same with the treatment options, breaking the video up into sections.

I also would have liked it if you read out the character’s names or showed photos of them rather than just displaying them on the screen, making them more memorable so if you referred to the patient’s name or the family member, viewers would be more likely to know who you were talking about. Overall, very well done and I enjoyed watching it.

This presentation was incredibly beneficial to my nursing practice not only in terms of the pathophysiology but also the connection and rationale of diagnostics and treatments. It has made it much easier to understand why patients respond to blood transfusions in the way they do and will help me to better integrate this knowledge into my nursing practice.

Currently, I work at Royal Inland Hospital as an employed student nurse in obstetrics. When women in delivery experience postpartum hemorrhages, they are sometimes so severe that we need to give blood either immediately following delivery, or in the first days postpartum. We often draw CBC labs and a group and screen before delivery and assess hemoglobin levels. If after delivery their hemoglobin is below 80 g/L, we will likely provide a blood transfusion to the patient postpartum. These patients are often stable, and there is no rush to give the transfusion immediately, therefore allowing ample time for double-checking blood products.

In contrast, when we are giving blood in emergency situations, it is often needing to be transfused very quickly because of the patient’s condition. This can make it difficult to complete double checks thoroughly and calmly, increasing the risk of human error. Furthermore, it can also be hard to assess for symptoms of an HTR because signs such as hypotension or tachycardia can also be a result of blood loss. Because of this, knowing the pathophysiology and specific HTR symptoms, as well know what lab work and testing we do to confirm HTRs will help me stay vigilant and observe my patient closely for changes in their clinical presentation and respond appropriately. I also now feel more competent in the rationale for treatment and why specific medications, like furosemide, are given when an HTR is suspected or confirmed.

Additionally, knowing that the most common type of HTR is caused by ABO incompatibility due to errors in testing or administration has made me even more aware of the importance of safety checks when administering blood or blood products, especially in an emergent situation where we may be trying to move quickly. Overall, this has been very beneficial to my practice, and I will absolutely use the knowledge I have gained.