The following article describes a clinical diagnosis encountered by nurses in Critical Care. The author aims to present the condition using current patho-physiologic theories surrounding its cause and discusses the condition using a systematic approach to diagnosis and nursing care.
SpecialtiesCriticalCase Study
CJ is a 65-year old female who tripped and fell inside her home landing on her right side. She felt immediate excruciating pain in her R hip and couldn't manage to get herself off the floor. Fortunately, she had a mobile phone in her housecoat pocket and she was able to call her son who arrived in her home within ten minutes. She was taken by ambulance to the ED where an x-ray revealed that she had sustained a hip fracture. CJ is otherwise healthy aside from a medical history that is notable for HTN and hyperlipidemia that are adequately managed with oral medications.
Orthopedic Consultation / Evaluation
CJ was seen by an Orthopedic Surgeon who recommended surgical intervention to repair her fractured hip. She was cleared medically to undergo surgery.
Orthopedic Surgery / Post-Operative
CJ was taken to the OR for an ORIF and was intubated for general anesthesia. She had significant blood loss from the surgical procedure and required blood transfusions during the case. At the conclusion of her 3-hour surgical procedure, she had received 3 Units of PRBC's. Additional 2 Units of FFP's were ordered because her surgical drain had significant output. CJ was transferred to the ICU intubated because she was slow to wake up from anesthesia. The nurse received report from the Anesthesiologist that CJ already received the first unit of FFP and the second unit is half-way transfused.
After receiving the second unit of FFP, her nurse noted an acute onset of oxygen desaturation to 75% and tachycardia. She was triggering the high peak airway pressure alarm on her ventilator. The nurse and respiratory therapist noticed copious amounts of pink, frothy secretions coming out of her oral endotracheal tube. Her FiO2 and PEEP were increased to 100% and 10 cmH2O respectively in order to maintain oxygen saturations above 90%. Chest x-ray was immediately obtained and showed bilateral pulmonary infiltrates with a normal cardio-mediastinal silhouette.
The Intensivist is concerned that CJ suffered a Transfusion Related Acute Lung Injury or TRALI.
Background
As nurses working in critical care, transfusing blood products is a common role we perform. While blood product transfusion reactions come in many forms, a distinct type of blood product transfusion reaction known as TRALI is a rare but life-threatening condition that we must be aware of because it is the leading cause of transfusion-related mortality described in the range of 40-60%. The true incidence of TRALI is difficult to estimate not only because cases of TRALI are under-reported but also because of previous disagreements among clinicians as to which cases meet the criteria for this diagnosis.
Pathophysiology
The exact mechanism of TRALI is not well understood, however, experts accept the two-hit mechanism which involves:
Neutrophil sequestration and priming - patient has intrinsic condition that causes neutrophil sequestration and priming in the lung microvasculature. This happens before the blood transfusion.
Neutrophil activation - when patient receives blood product, factors present in the blood product causes the recipient's neutrophils to release cytokines that damage the lung microvasculature leading to pulmonary edema.
Neutrophil Activation Can Happen in Two Ways
Immune mediated - via anti-HLA antibodies and anti-HNA antibodies in the donor blood
Biological response - biologically active lipids present in WBC's, platelets, and red blood cell breakdown.
TRALI Diagnostic Criteria
In an effort to standardize this clinical diagnosis, a consensus by the National Heart Lung and Blood Institute of the National Institutes of Health defines TRALI as new acute lung injury (ALI) or ARDS occurring during or within six hours of blood product administration.
Conventional criteria for the diagnosis of ALI/ARDS as defined by the Berlin Criteria
Acute onset
Bilateral infiltrates on chest x-ray
PaO2 to FiO2 ratio (P/F ratio) less than 300 with a minimum PEEP of 5 cmH2O
Etiology must not be fully explained by cardiac failure of fluid volume overload
Possible TRALI
The above clinical diagnosis is made using strict criteria that only implicates the blood product transfusion as the culprit in the development of ALI/ARDS. In cases where the development of ALI/ARDS coincides with blood product transfusion but other confounding events exist such as aspiration, infection, or trauma, then a diagnosis of Possible TRALI is preferred.
TRALI vs TACO
A similar presentation of transfusion related respiratory insufficiency is Transfusion-Associated Circulatory Overload or TACO. In order to distinguish from TRALI, TACO is associated with rapid blood product administration in the setting of fluid volume overload and compromised cardiac function. The mechanism for pulmonary edema is of a hydrostatic process in nature, that is, elevated pressures in the pulmonary circulation causes fluid to shift to the extravascular space into the lung parenchyma.
Nursing Care Planning
Nursing diagnoses that may apply to TRALI include:
Impaired Gas Exchange related to alveolar fluid accumulation as evidenced by dependence on mechanical ventilation with increased oxygen and PEEP requirements.
Anxiety related to difficulty breathing and increased respiratory effort as evidenced by inability to maintain adequate oxygen saturation without mechanical ventilator assistance.
Treatment
Treatment for TRALI is supportive. Transfusion should be stopped immediately if TRALI is suspected. Follow your facility protocol in terms of triggering blood bank evaluation of a transfusion reaction. It is important that cases of TRALI are reported and confirmed to protect future recipients of the donor blood. In many cases, patients are profoundly hypoxemic enough to require intubation and mechanical ventilation.
Traditional ARDS ventilatory strategies are employed. Hemodynamic monitoring is indicated as some patients develop hypotension and must be supported with fluid resuscitation and/or vasopressors. Education and emotional support to patients and families are important. The clinical course of TRALI has been described as short with quick resolution in mild cases to as long as 40 hours in severe cases though longer periods have been reported.
Prevention
It should be noted that cases of TRALI have declined significantly in recent years due to efforts at prevention. Blood donors implicated in TRALI cases should be deferred from future blood donation. Also recall that the mechanism thought to trigger TRALI partly involves immune mediated antibodies present in the donor blood particularly anti-HLA and anti-HNA antibodies. Some specialty laboratories in the US have the capability for neutrophil antibody testing to detect the risk of reaction from donor to recipient although this testing is expensive and still not widespread.
More importantly, blood products donated from multiparous women and individuals who received multiple blood transfusions in the past have been found to contain the antibodies implicated in TRALI. As a consequence of this finding, most centers preferentially obtain blood products from male donors and screen female donors in order to eliminate the possibility of donation by multiparous women and individuals who has a history of receiving multiple blood transfusions. Lastly, blood transfusions must be utilized with reasonable indication and with thorough consideration of its risks.
