Brainstem Hemorrhage and Obstructive Hydrocephalus as an Early Complication of Acute Promyelocytic Leukemia in a Filipino Adolescent: A Case Report

Abstract

Background: Acute promyelocytic leukaemia (APL) is a distinct subtype of acute myeloid leukaemia characterised by a severe bleeding diathesis that may lead to life-threatening haemorrhagic complications. Intracranial haemorrhage remains an important cause of early morbidity and mortality, while brainstem haemorrhage with obstructive hydrocephalus is an uncommon and particularly severe presentation. Early recognition and prompt initiation of APL-directed therapy are therefore essential. Aims: To report a rare and severe early complication of paediatric acute promyelocytic leukaemia (APL) – brainstem haemorrhage and obstructive hydrocephalus – and to highlight the diagnostic and management lessons for clinicians. Case Presentation: A 16-year-old Filipino male with glucose-6-phosphate dehydrogenase deficiency presented with a six-week history of gingival bleeding initially treated as gingivitis, followed by fatigability and a petechial rash. Work-up showed anaemia, thrombocytopenia, 22% circulating blasts, and a prolonged prothrombin time. Peripheral smear showed promyelocytes with Auer rods, and bone marrow flow cytometry demonstrated a blast immunophenotype characteristic of APL, with confirmatory FISH for PML::RARA sent to a reference laboratory. On hospital day 4, before molecular confirmation returned, the patient developed acute neurological decline. Cranial computed tomography revealed a 5.4-mL left hemipontine haemorrhage with obstructive hydrocephalus. He was intubated, managed in intensive care with intracranial pressure-directed therapy and blood product support, and started on empirical all-trans retinoic acid (ATRA); idarubicin was added once counts allowed. Serial imaging confirmed gradual resolution, and he was extubated on day 11 and discharged on day 27 in stable condition. Discussion: This case illustrates that gingival bleeding, APL’s most common presenting complaint, is easily mistaken for a dental cause, and that its coagulopathy can produce catastrophic haemorrhage even after treatment has begun. Empirical initiation of ATRA before molecular confirmation, aggressive correction of coagulopathy, and close multidisciplinary intensive care were central to a favourable outcome. Conclusion: Catastrophic intracranial haemorrhage can complicate APL very early in its course. Survival with good neurological recovery is achievable with prompt recognition and aggressive, protocol-based management.