The clinical presentation of TRALI is variable. Symptoms and signs may include dyspnea, hypoxia, tachycardia, hypotension, fever, and pulmonary edema [8]. Chest radiography may show bilateral infiltrates. TRALI may occur during transfusion or within 6 h of transfusion [9]. TRALI can be classified as mild, moderate, or severe, depending on the immediacy of onset, the duration, and the degree of patient disability.

Large multinational collaborations, such as the National Heart Lung and Blood Institute Working Group on TRALI and the Canadian Consensus Conference on TRALI, have developed the following diagnostic criteria [8, 9]:

TRALI has been reported to occur later than 6 h after transfusion [10]. This has led other agencies and authors to extend the window for diagnosis to up to 24–72 h after transfusion [11]. Despite the presence of these diagnostic criteria, TRALI is frequently classified as possible, probable, or definite, depending on the temporal relationship to blood transfusion or coexisting alternative risk factors for ALI [8]. Additionally, it is sometimes difficult make a distinction between TRALI and transfusion-associated circulatory overload (TACO). TACO is a second type of lung injury related to blood transfusion. It is characterized by the rapid accumulation of fluid within the interstitial tissue of the lung, resulting from increased intravascular volume and increased hydrostatic pressure after blood transfusion [12]. The clinical presentation of TACO is similar to that of TRALI. However, patients with TACO show symptoms of venous overload, such as an elevated jugular venous pulse, hypertension, and elevated levels of B-type natriuretic peptide, which are not seen with TRALI [12].

TRALI is a self-limited condition that generally lasts for 48–96 h and has a good prognosis [13]. Its treatment is usually supportive, including oxygen supplementation, but it frequently requires intensive care unit (ICU) admission [11]. The reported rates of requirement for mechanical ventilation are variable. In a study from Canada, Silliman et al. [1] found that only 3 % of TRALI patients required mechanical ventilation, whereas a surveillance program in the United Kingdom reported that 45 % of TRALI patients required mechanical ventilation [11]. In a series of 37 patients with TRALI, all patients required oxygen supplementation and 72 % required mechanical ventilation [14]. In a study of ICU patients who developed TRALI, 78 % of patients were treated with mechanical ventilation, the median duration of support being 3.6 days (interquartile range, 1.6–7.1 days) [1, 2].

TRALI frequently results in acute hypoxemic respiratory failure. Noninvasive ventilation (NIV) has been established as a treatment modality for respiratory failure, with variable rates of success depending on the cause, severity, and patient characteristics. The beneficial physiological effects of NIV include reduced work of breathing, decreased inspiratory effort, increased dynamic lung compliance, increased tidal volume, improved pulmonary gas exchange, and improved arterial blood gas content [2–6].

The use of NIV in ARDS is controversial, as large and specific randomized controlled trials on this topic are lacking. Ferrer et al. randomized 105 patients with severe hypoxemic respiratory failure, 15 of whom had ARDS, to NIV or high O₂ [7, 8, 15]. NIV prevented intubation and was associated with better survival. However, in another study of 123 patients with acute hypoxemic respiratory failure, 102 had ARDS, NIV did not reduce intubation or mortality [7, 9]. A meta-analysis of six randomized controlled trials involving 227 patients concluded that early use of NIV can decrease the endotracheal intubation rate in patients with ALI, but does not change the mortality of these patients [2, 10, 12]. A more recent systematic review and meta-analysis evaluating the efficacy of NIV in non-chronic obstructive pulmonary disease and non-trauma patients with acute hypoxemic respiratory failure concluded that using NIV as adjunctive therapy in patients with heterogeneous causes of acute hypoxemic respiratory failure decreases the need for intubation, ICU length of stay, and mortality rate [10, 13]. However, the use of NIV in ARDS is associated with a failure rate as high as 83 %. In fact, ALI and ARDS have been found to be independent risk factors for NIV failure in patients with acute hypoxemic respiratory failure, together with age >40 years, a Simplified Acute Physiology Score II of > 35, and PaO₂/FiO₂ < 146 after 1 h of NIV [2, 11, 14, 16, 17].