Pediatric Influenza-associated Acute Necrotizing Encephalopathy: Two Cases from Kazakhstan with a Comparative Review of the Literature

2026

Full text Open access: Hybrid Metadata (CSL-JSON)
DOI 10.4103/wkmj.wkmj_61_26
Data confidence 70 medium
How this score is calculated

It is built from checkable properties of the record itself: whether the article has a DOI, how many independent sources confirmed its data, whether the required fields are filled in, and how recent the latest confirmation is. Disagreement between sources and a missing identifier lower it. A value of 80 or above means the record was published without further checking; 60 to 79 means it is published at reduced confidence, with a manual check advisable. A record verified by an editor by hand is never pushed below 90 by a recalculation. This scores our data about the article, not the article itself.

Abstract

A BSTRACT Influenza-associated acute necrotizing encephalopathy (IANE) is a rare but devastating neurological complication predominantly affecting previously healthy young children. Characterized by rapid neurological deterioration, symmetric thalamic lesions on neuroimaging, and cytokine-mediated pathophysiology, IANE carries mortality rates of 30%–41%, with the majority of survivors experiencing permanent neurological sequelae. Clinical data from Central Asian populations remain limited. The objective of the study was to report the first cases of IANE from the Republic of Kazakhstan and compare clinical, laboratory, neuroimaging, and outcome data with published systematic reviews. We present two previously healthy 3-year-old children (one male and one female) with laboratory-confirmed influenza A (H1N1) infection who developed ANE. Both patients presented with high-grade fever and rapid neurological deterioration within 48 h of symptom onset. Case 1 exhibited diffuse cerebral edema with subarachnoid hemorrhage, fulminant multiorgan dysfunction, and disseminated intravascular coagulation, progressing to brain death despite receiving intravenous immunoglobulin (IVIG) and corticosteroid therapy. Case 2 demonstrated characteristic bilateral symmetric thalamic lesions with cerebellar involvement, received IVIG and corticosteroids, and was transferred to palliative care due to irreversible neurological injury with no prospect of central nervous system recovery. Cerebrospinal fluid (CSF) analysis in Case 2 revealed the pathognomonic albuminocytologic dissociation (elevated protein without pleocytosis). Both patients developed secondary nosocomial infections with multidrug-resistant Acinetobacter baumannii . Comparative analysis with five published reviews and case series (2020–2025) revealed strong concordance between our cases and global data regarding age distribution (peak incidence 2–5 years), clinical presentation (fever–seizures–coma triad), neuroimaging findings (bilateral thalamic involvement), laboratory abnormalities (elevated inflammatory markers, hepatic dysfunction, coagulopathy), and the critical importance of early immunotherapy. The divergent outcomes of our patients, fatal in Case 1 versus survival with severe neurological sequelae in Case 2, highlight the critical importance of early immunomodulatory intervention. These cases, representing the first reported IANE cases from Central Asia, demonstrate that the disease follows a consistent clinical pattern regardless of geographic location. Early clinical recognition, prompt neuroimaging for characteristic thalamic lesions, and early initiation of immunomodulatory therapy (corticosteroids and IVIG) are critical determinants of outcome. Clinicians should maintain a high index of suspicion for IANE in children presenting with acute encephalopathy during influenza season, even in the absence of pleocytosis on CSF analysis.