Clinical profile: Admitted for hemorrhagic shock, right upper extremity destruction injury and right lower extremity skin decortication injury. There was a previous history of sulfonamide allergy. No history of blood transfusion. He was admitted to the hospital for emergency surgery and transferred to the intensive care unit. 3 days later, he was transferred to our department. On the same day, the coagulation test was normal. Hemoglobin: 65g/L, red blood cells. After cross-matching, 2 units of homogeneous concentrated red blood cells were transfused. During 30 minutes of transfusion of about 40 ml, the patient suddenly had panic attacks, dyspnea, cyanosis of lips, faint consciousness, fecal incontinence, and vomiting of white mucous sputum, and cardiac monitoring showed a progressive decrease in oxygen saturation to a minimum of 60%. Blood gas analysis showed that: physical examination: restlessness, cyanosis of the lips and mouth, a few rales in both lungs, more moderate and fine wet rales, heart rate increased to 128 beats per minute. The patient was immediately stopped from blood transfusion, administered oxygen by facemask, injected finasteride, intravenous dexamethasone, doxorubicin, tachyphylaxis, methylprednisolone, etc. The patient’s breathing stabilized after 40 minutes, and the croup disappeared after 2 hours, and the signs and symptoms completely disappeared after 3 hours. The patient’s blood and the remaining blood from the blood bag were then taken for bacterial culture and the results were negative. Discussion: Blood transfusion is a clinically important therapeutic tool, but it can also produce serious complications. Transfusion-associated acute lung injury (TRALI) is a dangerous and little-known complication of transfusion. It is characterized by non-cardiogenic pulmonary edema following transfusion. As reported in this paper, this 1 case was not a case of pulmonary edema due to an acute increase in blood volume caused by too much blood transfusion too quickly. Foreign scholars have shown that during the blood storage phase, lipids are produced and released into the plasma. In murine lung animal models stock blood plasma and stock blood erythrocyte lipids can induce transfusion-associated acute lung injury, manifested by dramatic changes in pulmonary artery pressure and significant pulmonary edema. Lindgre-L reported a case of transfusion-associated acute lung injury in a cholecystectomized patient who developed transfusion-associated acute lung injury after transfusion of frozen plasma, and tested the transfused plasma with granulocyte and HLA antibodies. It is believed that transfusion-associated acute lung injury occurs due to a specific antigen-antibody reaction between donor leukocytes or granulocyte antibodies and recipient antigens, which accumulates on small pulmonary vessels and leads to osmotic destruction. Autopsy of patients who died from transfusion-related acute lung injury due to respiratory distress showed extensive pulmonary edema with granulocytes aggregating in the pulmonary vascular system and infiltrating into the alveoli. Electron microscopy showed capillary endothelial damage with activated granulocytes aggregating on the alveolar basement membrane. In conclusion, the understanding of its pathophysiology is based on animal models of antibody-induced production of lung injury and a limited number of autopsies. Currently, there is no good means of detecting these antibodies in order to predict them, and it is important to have an adequate understanding of the disease. During the transfusion process, the patient’s condition should be closely observed and patients with transfusion-related acute lung injury should be treated promptly with a combination of adequate oxygen administration, early application of adrenocorticotropic hormones to inhibit the antigenic antibody response, improvement of pulmonary circulation, and protection of cardiac function.