[Airbag-related death in a toddler. A poorly known danger?]. / Conséquences fatales de l'ouverture d'un « airbag ¼ chez un nourrisson. Un danger méconnu ?

We report the case of an 8-month-old baby killed by the deployment of an airbag. He was correctly positioned, in a safety seat designed for his age class, on the passenger side, and rear-facing. The accident occurred at low speed, on the left front of the car, without provoking any harm to the mother who was driving the vehicle, but the impact led to airbag deployment. A CT scan showed an occipital fracture, hemorrhagic parenchymal contusions, subarachnoid hemorrhage and edema, which quickly led to fatal intracranial hypertension. Severe retinal hemorrhages were also noted. Brain death was declared 24h later. Both direct impact and violent projection of the head are involved in the severity of brain lesions. Retinal hemorrhages are similar to what is observed in shaken-baby syndrome. To our knowledge, this is the first French publication on this topic in childhood. In France, children are allowed to be positioned on the passenger side seat, but the airbag, if present, is supposed to be deactivated, which is not always possible. In recent cars, depowering the airbag is easy, with on/off switches, but these systems are not uniform between models. Moreover, it is very likely that this possibility is ignored by numerous parents. A widespread communication on this topic should be initiated in France to prevent such events. Banning infants from front passenger seats completely does not seem possible. Nevertheless, greater attention on the part of police departments and better information to drivers appear necessary.

Natural history of platelet antibody formation against αIIbß3 in a French cohort of Glanzmann thrombasthenia patients.

Treatment of the bleeding syndrome in Glanzmann thrombasthenia (GT) is often complicated by naturally occurring isoantibodies directed against the αIIbß3 integrin that cause the removal of or render ineffective transfused donor platelets. Such antibodies are produced after transfusion or pregnancy when the patient's immune system comes into contact with normal platelets. Despite many reports of anti-αIIbß3 antibodies in GT patients, there is no consensus pertaining to their frequency, their long-term evolution in the circulation, or their formation in relation to either (i) the extent of the αIIbß3 deficiency in the patient's platelets or (ii) the nature of the genetic defect (ITGA2B or ITGB3 genes). Antibody screening was performed on a large series of 24 GT patients in South-West France dividing the patients into two cohorts: (i) 16 patients with the French gypsy mutation (c.1544 + 1G>A) within ITGA2B that gives platelets totally lacking αIIbß3 and (ii) 8 patients carrying other defects of ITGA2B or ITGB3 with different expression levels of αIIbß3. Our results confirm that patients with premature termination mutations resulting in platelets lacking αIIbß3 are the most susceptible to form isoantibodies, a finding that may be useful in deciding the choice of therapy between platelet transfusion and the use of recombinant factor VIIa (FVIIa).