Globally, approximately 750,000 cases of infantile meningitis occur annually[1]. Clinical data show infantile postmeningitis subdural fluid collection (IPSFC) is the most common complication of infantile bacterial meningitis (IBM), with a progression rate of 30-60% (39% in standardized treatment cohorts)[2]. Pathogens, predominantly Escherichia coli and Streptococcus pneumoniae, account for 70% of IPSFC cases[3]. IPSFC progresses to subdural empyema (IPSE) in 3.7-17.6% of cases, with 87.1% of IPSE cases occurring in infants <1 year old[4]. Collectively termed infantile postmeningitis subdural space lesions (IPSSL), these conditions impose the highest burden in Sub-Saharan Africa's "Meningitis Belt" and Southeast Asia[5]. IPSE progresses rapidly in infants, with a mortality rate of 18% and 50% of survivors developing neurological sequelae (e.g., epilepsy, motor/intellectual disability, sensory impairment)[6]. While spontaneously resolved IPSFC shows no significant sequelae, prolonged IPSE disrupts brain development, requires extended treatment, and incurs substantial familial burdens.

Causes of IPSFC secondary to IBM include increased subdural capillary permeability (with plasma exudation), cerebrospinal fluid (CSF) circulation/absorption disturbance, immature infantile blood-brain barrier (BBB), and underdeveloped arachnoid granulations[7]. IPSFC typically develops on days 7-10 of IBM and is staged by fluid thickness: Stage I (<0.3 mm), Stage II (3-8 mm), Stage III (>8 mm)[8]. Uncontrolled IBM infection, due to inappropriate antibiotics, inadequate dosage, delayed treatment, or infantile immunocompromise, e.g., preterm infants, allows pathogens to invade and proliferate in the subdural space, inducing local secondary infection, inflammatory cell infiltration, and accumulation of pathogen metabolites/necrotic tissue-ultimately progressing to IPSE[9]. Fibrinogen exudation and fibroblast activation may further form subdural fibrous cords, septa, purulent plaques, inflammatory pseudomembranes, and other fibro-inflammatory proliferative lesions (FIPLs)[10]. IPSE causes more severe mass/toxic effects, requiring aggressive surgical intervention. Cranial MRI shows empyema cavity rim enhancement, heterogeneous internal signals due to fluid collection septa, and dural thickening.

The progression rate of IPSFC to IPSE ranges from 3.7% to 17.6%, influenced by IBM pathogen types, therapeutic intervention, and host immunity[11]. However, large-scale cohort studies on risk factors for this progression remain lacking. Early adequate antibiotic therapy reduces IPSFC incidence by nearly 50%, whereas delayed intervention may accelerate IPSFC onset (day 3-7) via unremitting meningeal permeability[12]. Inadequate antibiotic courses may promote persistent IPSFC progression with FIPLs formation. Some pediatric neurosurgeons advocate extending antibiotic therapy beyond 21 days for IPSFC to prevent progression to IPSE[13].

Despite early antibiotic therapy reducing IBM mortality, IPSSL management remains challenging. A clinical study showed 22.4% of IPSFC cases required surgery, but occult inflammation in infants can prolong IPSFC up to 2 months[14]. Infantile unclosed fontanelles and cranial elasticity increase neurosurgical complication risks. Current consensus suggests asymptomatic/small-volume fluid collections (thickness <5 mm) often resolve spontaneously, obviating intervention[15]. Ultrasound-guided subdural puncture (US-SP-AF) is the first-line invasive treatment, curing about 50% of infants acutely but with a 30-50% recurrence rate. Whether US-SP-AF reduces IPSFC-to-IPSE progression remains controversial. For US-SP-AF-resistant cases, minimally invasive burr hole irrigation (BHID) with silicone tube drainage (3-5 days) is used; BHID shows higher cure rates than US-SP-AF but still has a 20-33% recurrence rate in small cohorts[16].

Neuroendoscopic technique allows rigid endoscope entry into the subdural space for visualized resection of pathological tissues, management of multiloculated cavities, adhesion lysis, and FIPLs irrigation. This approach directly targets the pathological substrate under vision, reducing residual lesions and recurrence rates compared to traditional methods. In adult cohorts, 6-month postoperative fluid collection recurrence rates are only 8% with neuroendoscopy, versus 33% with BHID[17]. However, neuroendoscopic exploration is technically demanding and equipment-dependent. The Ommaya reservoir offers advantages in postoperative management of cerebrospinal fluid-related disorders, including precise drainage, dynamic monitoring of disease progression, and local drug administration. However, it may be prone to catheter obstruction by pathological components[18].

Severe IPSSL causes intracranial hypertension and neurodevelopmental impairment, requiring comprehensive pediatric neurosurgical and pharmacologic strategies. Treatment selection depends on IPSFC/IPSE pathological features. Current stu

Inclusion Criteria:

- All enrolled children had received ≥3 weeks of standardized anti-infection therapy, including empirical or susceptibility-guided antibiotics administered intrathecal (post-lumbar puncture) or intravenous and dexamethasone administered intrathecal or intravenous. During conservative management, vital/neurological signs were closely monitored, with regular imaging to assess fluid thickness and empyema progression. Cranial ultrasound (primary modality, ≤3-day intervals) was performed, while CT/MRI were conducted ≤weekly.

Exclusion Criteria:

• subdural fluid collections secondary to viral meningitis; secondary collections with confirmed craniocerebral trauma history; diagnosed tuberculous subdural fluid collection; intracranial space-occupying lesions.

Children undergoing surgical treatment should meet at least one imaging criterion (persistent short-term widening of the subdural space or compression of lateral ventricles; unilateral fluid collection thickness >1 cm for two consecutive weeks; formation of empyema abscess wall or mature empyema) and at least two clinical criteria (head circumference growth rate exceeding normal range or increased fontanelle tension; worsening IPSSL symptoms or persistent poor infection control; manifestations of intracranial hypertension such as repeated vomiting or lethargy; frequent neurological abnormalities like epileptic seizures; asymptomatic cases with fluid/empyema thickness >1 cm for >2 weeks).