BACKGROUND: The known etiology of acute lung injury (ALI) is immensely varied and includes severe burns and trauma. Electrical and multiple defibrillation shocks can cause cutaneous burns and blunt chest trauma. The literature contains no reference to the association between ALI and cutaneous burns or blunt chest trauma secondary to defibrillation. OBJECTIVE: To report a patient with Acute Myocardial Infarction (AMI) who developed ALI possibly due to multiple defibrillation shocks. CASE REPORT: A 51 year-old man with AMI presenting with multiple episodes of ventricular fibrillation (VF) treated with defibrillation and subsequently cutaneous burns. He developed soon afterward respiratory failure due to ALI. Cardiac failure or any known etiology of ALI was ruled out. Medical treatment included oxygen therapy, cardiac frequency control with betablockers, in addition to antiplatelet therapy. Clinical and oxymetric evolution was favourable, with resolution of the radiological infiltrates. The patient was discharged alive and in good condition at the 19th day after admission. The authors discuss possible mechanisms of ALI development by multiple defibrillation shocks. CONCLUSIONS: In the absence of any other known etiology, multiple defibrillation shocks may have played a role in the genesis of ALI in our patient, but this remains speculative.
BACKGROUND: The known etiology of acute lung injury (ALI) is immensely varied and includes severe burns and trauma. Electrical and multiple defibrillation shocks can cause cutaneous burns and blunt chest trauma. The literature contains no reference to the association between ALI and cutaneous burns or blunt chest trauma secondary to defibrillation. OBJECTIVE: To report a patient with Acute Myocardial Infarction (AMI) who developed ALI possibly due to multiple defibrillation shocks. CASE REPORT: A 51 year-old man with AMI presenting with multiple episodes of ventricular fibrillation (VF) treated with defibrillation and subsequently cutaneous burns. He developed soon afterward respiratory failure due to ALI. Cardiac failure or any known etiology of ALI was ruled out. Medical treatment included oxygen therapy, cardiac frequency control with betablockers, in addition to antiplatelet therapy. Clinical and oxymetric evolution was favourable, with resolution of the radiological infiltrates. The patient was discharged alive and in good condition at the 19th day after admission. The authors discuss possible mechanisms of ALI development by multiple defibrillation shocks. CONCLUSIONS: In the absence of any other known etiology, multiple defibrillation shocks may have played a role in the genesis of ALI in our patient, but this remains speculative.