Influenza A (H5N1) is a highly pathogenic zoonotic virus with a human fatality rate of approximately 60%. Pediatric cases and associated neurological manifestations remain poorly documented in Latin America. This report describes the first confirmed Ecuadorian pediatric case of H5N1-associated encephalitis and multisystem organ failure in a previously healthy 9-year-old female following direct contact with infected poultry. The clinical course was characterized by an atypical initial presentation of bilateral periorbital edema and headache, progressing to acute encephalitis, cerebral ischemia, flaccid tetraplegia, central diabetes insipidus, and refractory septic shock. Diagnostic confirmation was achieved via nasopharyngeal RT-PCR, with additional RT-PCR and sequencing performed on cerebrospinal fluid, which identified conserved influenza A M1/M2 gene fragments, while laboratory markers—including marked elevations in IL-6, ferritin, and CRP—indicated a severe hyperinflammatory state. Management involved an intensive multidisciplinary approach utilizing oseltamivir, intravenous immunoglobulin, modulated-dose corticosteroids, desmopressin, and mechanical ventilation. Despite a severe clinical course, the patient achieved a favorable recovery, with a Glasgow Coma Scale score of 15/15 at discharge and only partial residual paresis and left hypoacusia as sequelae. This landmark case provides rare evidence of H5N1 neuroinvasion in a pediatric patient and demonstrates that timely detection combined with aggressive immunotherapy and antiviral treatment can improve survival. Furthermore, it underscores the critical necessity for strengthened regional molecular surveillance and clinical training to recognize atypical presentations of emerging zoonoses in Latin America, especially in cases involving contact with sick poultry.

Hemophagocytic lymphohistiocytosis (HLH) remains one of the greatest diagnostic challenges in pediatric critical care because of its high mortality and the complexity of its clinical presentations. We report the case of an 18-month-old boy who presented with persistent fever, a respiratory tract infection, pancytopenia, hepatosplenomegaly, and progressive neurological deterioration, fulfilling the diagnostic criteria of the HLH-2004 protocol [2]. His clinical course was complicated by concurrent viral infections (adenovirus and parainfluenza virus type III) and antibody-mediated neurological autoimmunity (anti-NMDA receptor encephalitis), an association rarely reported in the current literature [4,5]. A broad differential diagnosis was evaluated with immunologic, genetic, and neuroimaging studies. The combination of autoimmunity, recurrent infections, and positive family history suggested secondary HLH on the background of an underlying primary immunodeficiency [9]. The patient's outcome and the death of a sibling with a similar clinical picture indicate that this episode was not merely secondary HLH, but the first manifestation of a severe primary immune dysregulation, possibly related to mutations in genes such as CTLA4, LRBA, or STAT3—genes recognized within the spectrum of autoimmune lymphoproliferative immunodeficiency disorders (ALPID) [9,10]. This case illustrates the most aggressive facet of pediatric HLH and underscores the need to suspect hidden primary immunodeficiencies in patients with recurrent infections and early autoimmunity. Early recognition of this phenotype can make the difference between a fatal outcome and the possibility of offering targeted immunomodulatory or potentially curative therapies [12,13]. In critical pediatrics, HLH should no longer be considered a final diagnosis but rather a warning sign of an underlying genetic immune dysregulation.

Pediatric trauma is one of the leading causes of childhood morbidity and mortality worldwide. Optimizing early management in specialized units may substantially improve survival and functional outcomes. We therefore evaluated the impact of implementing a specialized Pediatric Trauma Unit on in-hospital mortality among children with moderate and severe trauma at Baca Ortiz Children's Hospital (HPBO) in Quito, Ecuador. Methods: We conducted a retrospective cohort study with historical controls including pediatric patients with moderate or severe trauma admitted before ( n = 104) and after ( n = 183) implementation of the Pediatric Trauma Unit. Descriptive statistics were used to summarize demographic and clinical characteristics. Chi-square and Fisher's exact tests were applied to compare categorical variables. Logistic regression was performed to assess the association between unit implementation and in-hospital mortality, adjusting for clinical severity scores and other potential confounders. Results: In-hospital mortality decreased from 16.3% in the pre-implementation period to 3.3% after implementation of the Pediatric Trauma Unit. Unit implementation was associated with an 88% reduction in the odds of death (adjusted OR 0.12; 95% CI 0.04–0.36; p < 0.001). Deceased patients had significantly higher pre-implementation BIG scores than survivors ( p = 0.02). Survival among patients with abdominal trauma also improved after protocol implementation ( p = 0.01). Conclusions: Implementation of a specialized Pediatric Trauma Unit at Baca Ortiz Children's Hospital was associated with a marked reduction in in-hospital mortality among children with moderate and severe trauma. These findings support the development and strengthening of pediatric trauma care systems in similar settings.

Hemophagocytic lymphohistiocytosis (HLH) continues to pose a diagnostic challenge in pediatric critical care, not only because of its severity but also due to the wide range of conditions that can underlie its presentation. Among these, metabolic disorders are often overlooked. We describe an 18-month-old boy who initially presented with persistent fever and respiratory symptoms, later evolving to pancytopenia, hepatosplenomegaly, and neurological deterioration, the patient fulfilled seven of the eight HLH-2004 criteria. Along the way, adenovirus and parainfluenza virus type III were identified, and anti-NMDA receptor encephalitis was confirmed, adding further complexity to the clinical picture. What proved decisive was the identification of a homozygous pathogenic variant in the IVD gene (c.1174C > T; p.Arg392Cys), establishing the diagnosis of isovaleric acidemia. This finding reframed the case. Rather than an isolated hyperinflammatory syndrome, the clinical course can be better understood as the result of a metabolic disorder capable of amplifying immune dysregulation, particularly in the setting of intercurrent infection. In this context, the features of HLH appear not as a separate entity but as part of a broader process, where metabolic decompensation, accumulation of toxic intermediates, and systemic inflammation converge. This overlap is likely underrecognized in clinical practice. Recognizing this possibility has practical implications. It shifts the diagnostic focus, but also opens the door to more tailored management strategies. In similar cases, HLH may be less an endpoint diagnosis and more a signal pointing toward an underlying metabolic or genetic condition that requires specific attention.