Transfusion Related Acute Lung Injury

Introduction:

Transfusion-related acute lung injury is a clinical syndrome, acute, noncardiogenic pulmonary edema related to hypoxia that happens either during or after a transfusion. Transfusion reactions are the side effects after the blood products are transfused, such as whole blood, fresh frozen plasma, platelets, cryoprecipitate, granulocytes, intravenous immune globulin, allogeneic and autologous stem cells, and packed red blood cells. It is a fatal condition.

Transfusion-related acute lung injury was notified first in the 1950s but identified as a clinical syndrome in 1983. These conditions are analyzed clinically and verified by findings in the radiographs. The main diagnostic criteria are if the symptoms evolve within six hours of transfusion without any risk factors for producing acute lung injuries such as sepsis from pneumonia, aspiration, and shock.

Still, there are physical symptoms like fever, hypotension, and tachycardia on chest radiograph, there are exudative bilateral infiltrates, and there is no evidence of pulmonary vascular overload and hypoxemia of SpO2 less than ninety percent on room air with a ratio of the partial pressure of oxygen to a fractional inspired oxygen concentration of less than 300 mmHg. There is a chance of transfusion-related acute lung injury if risk factors for acute lung injury.

Delayed transfusion-related acute lung injury means when transfusion is completed after six to seventy-two hours, and this is a condition with a more elevated mortality rate. Transfusion-related circulatory overload needs to be found due to the resemblance of pulmonary edema, but due to actual volume overload.

What Is the Etiology of Transfusion-Related Acute Lung Injury?

According to the diagnostic factors, transfusion-related acute lung injury does not have many risk factors for lung injury. The deterioration of pulmonary vasculature induces it from neutrophil-mediated in the form of human neutrophil antigen or human leukocyte antigen antibodies in the donor's blood that binds to a recipient's antigens. Storage of blood products causes the accumulation of proinflammatory mediators, which can also cause transfusion-related acute lung injury. Neutrophil sequestration occurs in the pulmonary vasculature, and neutrophils activate to damage the endothelial layer and thus cause leakage of protein and fluid into the alveolar space.

What Is the Epidemiology of Transfusion-Related Acute Lung Injury?

The risk factors of transfusion-related acute lung injury include,

• Mechanical ventilation.

• Sepsis.

• Massive transfusion.

• Coronary artery bypass graft.

• End-stage liver disease.

• More elevated risk was informed with plasma from female donors because it is found in parous female donors with multiple human leukocyte antigen antibodies.

• Some studies suggested that female donor plasma has more anti-human leukocyte antigen class II and human neutrophil antigen-positive antibodies.

• Blood products with a high amount of plasma contents are related to a high risk of transfusion-related acute lung injury.

• Patients with terminating ill diseases have a higher incidence of transfusion-related acute lung injury. It is because they receive more blood products and have clinical manifestations that activate neutrophil sequestration before the blood transfusion, which places them at a higher risk of transfusion-related acute lung injury.

What Is the Pathophysiology of Transfusion-Related Acute Lung Injury?

• One reason is due to the priming of neutrophils from those patients who are diseased from shock, sepsis, or organ damage, those who had surgery, or those who have experienced severe trauma. Raised levels of interleukin-8, interleukin-6, and elastase-alpha 1-antitrypsin complex cause neutrophil recruitment to the pulmonary vasculature. Modification in beta-2 integrins permits neutrophils to attach to pulmonary capillaries.

• The next reason is the transfusion. Antibodies and bioactive lipids reserved in blood products will activate neutrophils, thus causing capillary leakage of intracellular content-releasing proteases and elastase from the activation of NADPH, thus oxidases and inducing pulmonary edema.

• Another assumption given is called the threshold hypothesis. Transfusion-related acute lung injury can occur in healthy patients transfused with plasma that has elevated amounts of antibodies whose neutrophil has already been activated.

• Histopathology includes early acute lung distress syndrome, exposing interstitial and intra-alveolar edema, and the existence of neutrophils in the interstitial and airway. Section of the lung shows multiple neutrophils in pulmonary capillaries and small pulmonary vessels.

What Are the Types of Transfusion-Related Acute Lung Injury?

There are two types of transfusion-type one and type two.

• Type one transfusion-related acute lung injury is related to acute lung injury. The onset is acute, which is within six hours of transfusion. Hypoxemia, on imaging in the chest, computed tomography, and ultrasound, there is evidence of bilateral pulmonary edema. No evidence of left atrial hypertension. If present, it causes hypoxia.

• Type two transfusion-related acute lung injury is related to type one in clinical criteria. There is the presence of acute respiratory distress syndrome risk factor.

How Is Evaluation Done for Transfusion-Related Acute Lung Injury?

Chest radiographs are used to see bilateral pulmonary infiltrate. Clinical characteristics include acute dyspnea, hypoxemia, fever, hypotension, tachycardia, leukopenia, thrombocytopenia, and pulmonary occlusion in the artery due to non-cardiogenic pulmonary edema.

How to Treat Transfusion-Related Acute Lung Injury?

Emergency treatment is done to arrest the transfusion and inform the blood bank to filter the donor unit for anti-leukocyte antibodies, anti-human leukocyte antigens, or anti-neutrophil-specific antibodies. There are no specific treatment measures available for this condition. Supportive measures must be taken to enhance oxygenation.

Low tidal volume application is possible in the condition as its pathophysiology is similar to acute lung distress syndrome. Prevention is the best treatment option for this condition. The incidence of this condition can be decreased by utilizing plasma from male donors and screening female donors for human leukocyte antigen and human neutrophil antigen antibodies because they are strong risk factors. Once the transfusion is discontinued, recovery may take two to four days. The chest x-ray will improve within two to five days.

Conclusion:

The diagnosis and treatment of transfusion-related acute lung injury is not easy. They are made with an interprofessional team that comprises a hematologist, cardiologist, pulmonologist, internist, and a specially trained nurse experienced with the care of these patients. It can evolve within six to seventy-two hours of blood transfusions rich in plasma. It should be prevented with the strategy of blood transfusions in patients more vulnerable to acquiring this condition. Due to no definitive treatment, prevention is the best way to manage.