Transfusion Reaction - Nursing Case Study
Pathophysiology
• Primary mechanism: Immune-mediated hemolysis occurs when the recipient's antibodies recognize donor red blood cells (RBCs) as foreign, leading to the destruction of these cells. This is often due to ABO or Rh incompatibility, causing acute hemolytic transfusion reactions.
• Secondary mechanism: Cytokine release can occur due to leukocyte antibodies or pre-stored blood products, resulting in febrile non-hemolytic transfusion reactions. The cytokines trigger an inflammatory response, manifesting as fever and chills.
• Key complication: Disseminated intravascular coagulation (DIC) may develop from massive hemolysis, leading to widespread clotting and subsequent bleeding due to consumption of clotting factors, posing a life-threatening risk.
Patient Profile
Demographics:
52-year-old female, registered nurse
History:
• Key past medical history: Hypertension, Type 2 Diabetes
• Current medications: Lisinopril, Metformin, Insulin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Fever and chills after blood transfusion
• Key symptoms: Shortness of breath, back pain, dark urine
• Vital signs: Temperature 101.3°F, Heart rate 110 bpm, Blood pressure 140/90 mmHg, Respiratory rate 24 breaths per minute, Oxygen saturation 92% on room air
Section 1
As the clinical team continues to monitor the patient, further diagnostic results come in, providing crucial insights into her status. Laboratory tests reveal a marked elevation in lactate dehydrogenase (LDH) and bilirubin levels, indicative of ongoing hemolysis. The patient's hemoglobin level has dropped significantly to 8.5 g/dL from a pre-transfusion level of 12 g/dL, confirming the suspicion of acute hemolytic transfusion reaction. Additionally, the direct antiglobulin test (DAT) returns positive, further supporting the diagnosis of immune-mediated hemolytic anemia. These findings suggest that the destruction of red blood cells is contributing to her symptoms of dark urine and back pain.
Compounding the situation, the patient's coagulation profile shows a prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), along with a decrease in platelet count to 90,000/mm³. Fibrinogen levels are also low, raising concerns about the development of disseminated intravascular coagulation (DIC). The presence of schistocytes on the peripheral blood smear corroborates this complication. As her clinical picture evolves, the patient's oxygen saturation drops further to 88% despite supplemental oxygen, necessitating a rapid response to address both her respiratory distress and the potential for further hematological instability.
In response to these developments, the care team initiates a series of targeted interventions aimed at stabilizing the patient. Intravenous fluids are administered to maintain renal perfusion and support hemodynamic stability, while supplemental oxygen is increased to improve her saturations. The administration of fresh frozen plasma and platelets is considered to address the coagulopathy associated with DIC. Meanwhile, the cessation of further blood transfusions is crucial to prevent exacerbation of the hemolytic process. The interdisciplinary team, including hematology and critical care specialists, convenes to reassess and optimize her management plan, emphasizing the importance of ongoing monitoring and prompt adjustment of treatment strategies to mitigate the risk of further complications.
Section 2
As the clinical team continues to closely monitor the patient's response to interventions, new complications emerge, necessitating further adjustments to her treatment plan. Despite the administration of intravenous fluids and increased supplemental oxygen, the patient's oxygen saturation remains critically low at 85%, indicating worsening respiratory compromise. Auscultation reveals bilateral crackles, suggesting pulmonary edema, possibly secondary to fluid overload or acute lung injury from the transfusion reaction. Her respiratory rate has increased to 28 breaths per minute, and she is using accessory muscles to breathe, highlighting her respiratory distress.
Concurrently, the patient's renal function begins to decline, as evidenced by an increase in serum creatinine to 2.1 mg/dL from a baseline of 0.9 mg/dL, raising concerns about acute kidney injury (AKI) due to hemoglobinuria and decreased renal perfusion. Urinary output has decreased to less than 30 mL/hour, prompting the team to reassess her fluid management strategy. Given the risk of exacerbating her pulmonary status, the balance between ensuring adequate renal perfusion and avoiding fluid overload becomes a critical component of her care.
In light of these developments, the interdisciplinary team decides to initiate diuretic therapy to address the pulmonary edema while carefully monitoring her fluid status. Hematology specialists recommend initiating corticosteroids to mitigate the immune response driving the hemolytic process. The care team also considers renal replacement therapy options if the patient's renal function continues to deteriorate. These adjustments aim to stabilize her condition and prevent further complications, underscoring the importance of vigilant monitoring and dynamic clinical decision-making in managing complex transfusion reactions.
Section 3
As the interdisciplinary team implements the new treatment plan, they observe the patient's response to the interventions with close attention. Despite the initiation of diuretic therapy, the patient's pulmonary status shows only slight improvement. Her oxygen saturation has modestly increased to 88%, but she remains tachypneic with a respiratory rate of 26 breaths per minute, and continues to exhibit the use of accessory muscles. Bilateral crackles persist upon auscultation, suggesting that the pulmonary edema is being partially managed but has not resolved. The team decides to adjust the diuretic dosage to further alleviate fluid overload while maintaining a cautious approach to avoid compromising renal perfusion.
In parallel, the hematology team starts the corticosteroid regimen, aiming to attenuate the immune response implicated in the ongoing hemolytic process. Over the next 24 hours, there is a slight stabilization in her hemoglobin levels, indicating a potential decrease in hemolysis. However, renal function remains a concern as her serum creatinine levels have climbed further to 2.4 mg/dL, and urine output remains low at 25 mL/hour. The nephrology consultants are called in to assess the need for renal replacement therapy, considering the patient's risk factors and current fluid balance.
As these developments unfold, the patient begins to show new signs of metabolic imbalance. Arterial blood gas analysis reveals a pH of 7.32, a bicarbonate level of 18 mmol/L, and a base deficit, indicating a developing metabolic acidosis. This finding prompts the team to evaluate the potential causes, including the reduced renal clearance of acid and the ongoing hemolysis. The interdisciplinary team recognizes the urgent need for continuous monitoring and frequent reassessments to pivot the treatment strategy effectively, emphasizing the critical interplay between respiratory, renal, and hematologic systems in the context of a complex transfusion reaction.
Section 4
As the interdisciplinary team continues to monitor the patient's condition, they begin to observe new complications that further challenge their comprehensive treatment plan. Despite the adjusted diuretic regimen, the patient's renal function continues to deteriorate. Her serum creatinine has further increased to 3.0 mg/dL, and her urine output has dropped to 15 mL/hour, signaling worsening renal failure. Concurrently, her metabolic acidosis has deepened, with recent arterial blood gas analysis showing a pH of 7.28 and bicarbonate level of 15 mmol/L. These findings indicate an urgent need to address both the renal insufficiency and the acid-base imbalance to prevent further systemic compromise.
In light of the worsening renal function and metabolic acidosis, the nephrology team decides to initiate continuous renal replacement therapy (CRRT) to support renal function and correct the acid-base disturbance. The decision is made to start CRRT cautiously, taking into account the patient's hemodynamic stability and the need to effectively manage fluid overload without exacerbating her pulmonary status. Meanwhile, the hematology team continues the corticosteroid regimen, monitoring for any signs of improvement in hemolysis and overall hematologic stability.
As the patient undergoes CRRT, the healthcare team remains vigilant in monitoring her vital signs and biochemical parameters. Her blood pressure has stabilized at 110/70 mmHg, and her heart rate remains elevated at 110 beats per minute. Oxygen saturation has improved slightly to 90% with supplemental oxygen, and her respiratory rate is holding steady at 24 breaths per minute. The team acknowledges the interconnected nature of her conditions, understanding that improvements in renal function and acid-base balance could positively impact her respiratory status. This ongoing situation demands careful coordination and frequent reassessments to ensure that each organ system is supported, with the ultimate goal of achieving a holistic recovery.
Section 5
As the patient's CRRT progresses, the healthcare team observes a mixed response to the interventions. Initially, there is a modest improvement in her metabolic parameters: the latest arterial blood gas shows a pH of 7.32 and bicarbonate level has increased to 18 mmol/L, indicating a slight correction in her metabolic acidosis. This improvement in acid-base balance is promising, yet her renal function remains a concern. Despite the CRRT, her serum creatinine has only marginally decreased to 2.8 mg/dL, and urine output remains low at 20 mL/hour, suggesting persistent renal insufficiency. Her vital signs show a stable blood pressure of 108/68 mmHg, but the heart rate persists at 112 beats per minute, hinting at ongoing stress on her cardiovascular system.
As the team continues monitoring, a new complication surfaces: the patient's oxygen saturation begins to fluctuate, intermittently dropping to 85% despite supplemental oxygen. A repeat chest X-ray reveals new bilateral pulmonary infiltrates, raising concerns about possible transfusion-associated circulatory overload (TACO) or transfusion-related acute lung injury (TRALI). This development prompts the team to adjust her fluid management strategy further, balancing diuresis with cautious fluid replacement to prevent exacerbation of her pulmonary status.
Given these new findings, the interdisciplinary team convenes to reassess the treatment plan. The possibility of TRALI necessitates collaboration with the hematology team to review her transfusion history and evaluate any signs of ongoing hemolysis. Meanwhile, the pulmonology team is consulted to provide additional insights into managing her respiratory complications. The integrated approach aims to address the interconnected challenges of renal failure, metabolic acidosis, and respiratory distress, with the ultimate goal of stabilizing her condition and guiding her toward recovery.