PO-01. Neurological complications in children after hematopoietic stem cell transplantation: Single-center experience
Natalia V. Bronina, Evgeniy A. Burtsev, Inna O. Schederkina, Gleb O. Bronin
Morozov Children’s Hospital, Moscow, Russia
Dr. Natalia V. Bronina, phone: +7(919) 770 2278, e-mail: email@example.com
The neurological complications (NCs) incidence and severity in children receiving hematopoietic stem cell transplantation (HSCT) varies in different trials. Among some most common causes of NCs are infections, drug toxicity, metabolic, immune-related and cerebrovascular complication.
Materials and methods
We analyzed NCs incidence, structure and severity in Morozov Children’s hospital (Moscow, Russia) pediatric HSCT Department for a 3-year period. The clinical, laboratory, and magnetic resonance imaging (MRI) was collected and analyzed for all cases.
A total of 109 pediatric patients receiving HSCT in 2018-2020 were analyzed for a history of acute neurological symptoms after HSCT. Acute NCs were registered in 7.3 % (8/109) cases at a median of D+43(3-162) after transplant. The median age of patients with NCs was 8.8 (2-15) years. Pre-engraftment NCs were detected in 25% (2/8) of cases and were associated with drug toxicity. The early post-transplant NCs (before D+100) were observed in 62.5% (5/8) and included toxic and infections complications. The late post-transplantation NCs (after D+100) were registered in one patient (1/8; 12.5%). In accordance to the Common Terminology Criteria for Adverse Events (CTCAE), NCs were classified as Gr2 in 37.5% (3/8), Gr3 in 25% (2/8), Gr4 in 25% (2/8), and Gr5 in 12,5 % (1/8) cases. The causes of NCs were as follows: toxic leukoencephalopathy in 25% (2/8), human herpesvirus 6 (HHV-6) encephalitis in 25% (2/8), both of these causes, in 12.5% (1/8), сyclosporin A-associated posterior reversible encephalopathy syndrome (PRES) in 12.5%, metabolic Wernicke’s encephalopathy (WE – thiamine deficiency) in 12.5 % (1/8), and immune encephalitis (IE) in 12.5% (1/8) cases. The latter developed 6 months after HSCT. In 62.5% (5/8) patients complete recovery was observed. Two (25 %) children died later due to leukemia relapse (a girl with Gr 5 neurotoxicity) and systemic mould infection after second HSCT (the boy recovered from WE after the first HSCT). One child with IE remains alive in permanent coma 3 state (Glasgow Coma Scale).
Severe NCs are a very important post-HSCT morbidity and mortality cause in studied cohort. The NCs CTCAE grade correlates with chances for recovery. Two patients (with Gr 4-5 NCs) died. Mild NCs could be prevented, e.g. our experience with antiepileptic drugs given in proper dose regimen during high-dose busulfan administration suggests that it can prevent seizures. The adequate nutrition is necessary for WE prophylaxis. Regular viral load and serum drug concentration monitoring can help to control severe toxic and viral NCs. Repeat competent neurological examination must be an essential part of post-HSCT surveillance.
Success of HSCT depends on effective and early prevention and treatment of different complications including NCs. There are various causes of NCs in pediatric patients after HSCT: drug toxicity, infections, metabolic disorders, immune-related damage and stroke. It is important to know a complete spectrum of possible neurological complications for timely and early treatment initiation.
Neurological complications, leukoencephalopathy, encephalitis, hematopoietic stem cell transplantation.