Transfusion-related acute lung injury

Transfusion-related acute lung injury (TRALI) is a serious, potentially life-threatening complication associated with the transfusion of blood products. It is characterized by the sudden onset of acute respiratory distress and non-cardiogenic pulmonary edema within 6 hours following a transfusion. TRALI is considered one of the leading causes of transfusion-related mortality. Despite its severity, the exact pathogenesis of TRALI remains incompletely understood, though it is believed to involve immune-mediated mechanisms.

Etiology and Pathogenesis

TRALI is thought to result from an immune response that leads to damage of the pulmonary endothelium. Two main theories have been proposed to explain its pathogenesis:

• The antibody-mediated hypothesis suggests that donor antibodies, directed against recipient leukocyte antigens, activate the recipient's neutrophils, which then damage the pulmonary capillary endothelium.
• The two-hit hypothesis posits that the first hit is a priming event of the recipient's neutrophils, caused by factors such as surgery, infection, or inflammation, making the lungs more susceptible to injury. The second hit is then delivered by the transfusion, which could be due to bioactive substances in the blood product or the infusion of antibodies, leading to an exaggerated immune response and capillary leak.

Risk Factors for TRALI include recent surgery, active infection, chronic alcohol abuse, higher volumes of transfused blood products, and the presence of specific donor antibodies.

Clinical Presentation

Patients with TRALI typically present with symptoms of acute respiratory distress, including dyspnea, hypoxemia, and bilateral pulmonary infiltrates on chest X-ray, without evidence of circulatory overload. Fever, hypotension, and tachycardia may also be present. The onset of symptoms usually occurs within 2 to 6 hours after the start of a transfusion.

Diagnosis

The diagnosis of TRALI is primarily clinical and based on the exclusion of other causes of acute lung injury. Key diagnostic criteria include:

• Acute onset within 6 hours of transfusion
• Hypoxemia, as indicated by a PaO2/FiO2 ratio ≤300 mmHg or the presence of bilateral infiltrates on chest imaging
• No evidence of left atrial hypertension
• Absence of an alternative risk factor for acute lung injury

Laboratory tests may show neutropenia and elevated inflammatory markers. However, these findings are not specific to TRALI.

Management and Treatment

The mainstay of treatment for TRALI is supportive care, focusing on oxygen therapy and mechanical ventilation if necessary. Fluid management should be cautious to avoid exacerbating pulmonary edema. There is no specific therapy for TRALI, but corticosteroids are sometimes used, although their efficacy is not well established.

Prevention strategies include the reduction of plasma from high-risk donors, particularly those with known leukocyte antibodies, and the use of male-only plasma donations to reduce the risk of antibody-mediated TRALI.

Prognosis

The prognosis of TRALI has improved with better recognition and supportive care. Most patients recover within 48 to 96 hours. However, mortality rates of 5-10% have been reported, emphasizing the need for prompt recognition and management.

Conclusion

TRALI is a significant complication of blood transfusion, requiring immediate recognition and supportive treatment. Ongoing research into its pathogenesis and prevention strategies is essential to reduce its incidence and improve patient outcomes.