We report a case of neuroblastoma diagnosed after adrenal haemorrhage following a minor trauma in a thirteen-month-old boy. Minor trauma is not commonly described as a cause of AH in the literature. Therefore when no accepted cause for AH can be found in a young child below the age of 5 years, it is important to look for a neuroblastoma and discuss the necessity of surgical exploration.
A heavily immunosuppressed, 43-kg, 9-year-old patient was recovering from a bone marrow transplant. Primary prophylaxis against invasive fungal infections was liposomal amphotericin B (AmBisome®, 2.3 mg/kg [100 mg] two times per week). Once home, following a first amphotericin B infusion, he presented with strong diarrhoea and vomiting; this was repeated after the second infusion. The clinical situation worsened rapidly and the patient was rehospitalised. On admission, he presented with acute renal failure. During the 2-week hospitalisation, renal function recovered progressively. A few days after returning home, a new administration of amphotericin B was again followed by diarrhoea and vomiting, together with shivering and fever. The child was again rapidly rehospitalised. Investigation revealed that the community pharmacist, relying on drug software, had selected an inappropriate substitute drug: the patient had been administered amphotericin B deoxycholate (Fungizone®) and not liposomal amphotericin B. Depending on the indication, intravenous AmBisome® is usually administered at a dose between 3 and 5 mg/kg bodyweight; this dose can be increased to up to 10 mg/kg/day. Intravenous Fungizone®, however, should be administered using an initial dose of 0.25 mg/kg bodyweight, up to a recommended 1-mg/kg/day dose. The child had thus received 100 mg of Fungizone®, or ten times the recommended dose.
Rationnal: In children with de novo acute lymphoblastic leukemia (ALL) event-free survival (EFS) and overall survival (OS) could be decreased when the diagnostic lumbar puncture is traumatic, as showed by two previous studies. The cerebrospinal fluid (CSF) should be contaminated with circulating leukemic blasts. Purpose: The aim of this study is to further investigate the influence of traumatic diagnostic lumbar puncture (LP) on CNS relapse rate as first endpoint and then on OS in a single center (Lille Academic Hospital, France) from 1989 to 2004. Patients and Methods: A total of 352 patients were restrospectively evaluated. These patients were treated according to the EORTC pediatric cooperative protocols 58 881 and 58 951. In these protocols, the neuroprophylaxy consisted in high-dose methotrexate (5g/m2/course x 4 to 11 courses according to the risk-group therapy) and intrathecal therapy (methotrexate +/− aracytine and corticosteroids), without any cranial irradiation. Traumatic lumbar puncture was defined as the presence of 10 erythrocytes/mm3 or more in cerebro-spinal fluid. Results: The median follow-up was 5.9 years (0.05–14). The CNS relapse rate is increased in patients with traumatic diagnostic LP (p=0.023), and their OS is also significantly decreased (p=0.04). However, a “true” CNS involvement (i.e. CNS 3) at diagnostis is a risk factor for further CNS relapse, and in this study, the number of CNS3 child was more important in the traumatic LP group. In order to avoid this major biased error, the analysis was repeated with CNS1 and CNS2 child (n=339)only and without CNS3 patients. In this subgroup, when the diagnostic LP is traumatic, the CNS relapse rate and the OS are not statistically different than in non traumatic LP group (p=0.06 and p=0.087, respectively). However, there is a trend for worse results. Conclusion: This study does not confirm the pejorative character of the traumatic diagnostic LP. Further investigations in larger study should be conducted to achieve more definitive conclusion. Moreover, an adequate biologic criteria is necessary to discriminate CSF contaminated with circulating leukemic blasts and real CNS primitive involvement to improve prognostic analysis and to adjust the treatment.
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