We report a previously healthy 15-year-old male (weight 62 kg, height 172 cm) who was discovered unconscious with a Glasgow Coma Scale score of 3 following exposure to a malfunctioning gas heater in a poorly ventilated bathroom. The estimated exposure duration was approximately 6 h overnight. Upon arrival at our Pediatric Trauma Center emergency department, the patient was comatose and unresponsive to painful stimuli. His respiratory status was critically compromised, with severe hypoxemia manifesting as SpO₂ of 70% despite high-flow oxygen at FiO₂ = 1.0. Abundant vomiting had resulted in upper airway obstruction. Cardiovascular assessment revealed hemodynamic instability with tachycardia (heart rate 150 bpm) and hypotension (blood pressure 73/50 mmHg). Laboratory investigations demonstrated a carboxyhemoglobin level of 45%, severe mixed acidosis on arterial blood gas analysis (pH 7.12, PaCO₂ 53 mmHg, PaO₂ 62 mmHg, base excess −12.5 mmol/L), and marked hyperlactatemia at 8.5 mmol/L. Additionally, troponin I was significantly elevated at 2.8 μg/L (normal 25% 5, 6, creating a challenging clinical dilemma. Our management strategy diverged from conventional protocols by prioritizing respiratory stabilization before HBOT. This sequential approach was informed by the evidence from Kao et al., 3 who documented improved survival when HBOT was delayed until respiratory stabilization was achieved in CO patients with acute respiratory failure. The ventilatory management strategy followed lung-protective ventilation principles established for ARDS 1. We employed a tidal volume of 6 mL/kg predicted body weight (407 mL) and optimized positive end-expiratory pressure (PEEP), starting at 12 cmH₂O and titrating based on P/F ratio response. Prone positioning was implemented for 18 h per day for 48 h, a strategy with proven mortality benefit in severe ARDS 1. We accepted permissive hypercapnia with PaCO₂ up to 55 mmHg while maintaining plateau pressure below 30 cmH₂O to minimize ventilator-induced lung injury. Recognizing the dual insult of CO toxicity and aspiration injury, we implemented an aggressive anti-inflammatory regimen (detailed in Table 1). High-dose intravenous vitamin C was administered at 200 mg/kg/day divided every 6 h, based on its role as a potent antioxidant in mitigating oxidative stress from both CO toxicity and aspiration injury. Pentoxifylline, a phosphodiesterase inhibitor with anti-inflammatory and rheological properties, was infused continuously at 30 mg/kg/day. Additionally, methylprednisolone was administered at 2 mg/kg/day divided every 12 h. Early initiation of low-dose corticosteroids within 72 h has been associated with reduced duration of mechanical ventilation in ARDS 1. Supportive care included targeted temperature management at 36°C using surface cooling, a neuroprotective strategy that reduces cerebral metabolic demand and may limit secondary brain injury. We implemented a conservative fluid strategy after initial resuscitation, targeting a central venous pressure of 8–10 mmHg. Prophylactic antibiotics (ampicillin-sulbactam 50 mg/kg every 6 h) were administered for aspiration pneumonia prevention. Continuous renal replacement therapy was not required. Table 2 summarizes the temporal evolution of ventilator parameters and clinical milestones, demonstrating the rapid improvement in respiratory mechanics achieved through this approach. By hour 24, the P/F ratio had improved from 62 to 233 mmHg, representing a 275% increase. Lung compliance improved to 28 mL/cmH₂O, and the patient was successfully weaned from vasoactive support. Following this dramatic improvement in oxygenation (P/F ratio > 300) and lung compliance, HBOT was safely initiated at hour 30 post-admission. The protocol consisted of three sessions of 90 min each at 2.5 atmospheres absolute (ATA), administered at 30, 48, and 66 h post-admission. This approach aligned with current evidence suggesting that neuroprotective benefits of HBOT persist even when delayed up to 72 h in CO poisoning 3-8. The patient tolerated all HBOT sessions excellently, with no barotrauma or hemodynamic instability. Figure 2 illustrates the temporal evolution of P/F ratio, FiO₂, and mean airway pressure during the first 48 h, clearly demonstrating the stepwise improvement that enabled safe HBOT initiation. The patient demonstrated remarkable recovery following the sequential management approach. By day 2, the P/F ratio had improved to 325 mmHg with FiO₂ weaned to 0.40. Successful extubation to high-flow nasal cannula was achieved on day 4, and the patient transitioned to room air on day 6. He was discharged from the pediatric intensive care unit to the pediatric ward on day 8 and ultimately discharged home on day 12 with a normal neurological examination. Neurological follow-up was comprehensive and encouraging. Complete neurological recovery was confirmed at 3-month follow-up using the standardized Montreal Cognitive Assessment, with a MoCA score of 28/30 (normal for age). Brain MRI at 3 months demonstrated complete resolution of the initial subtle hyperintensities in the bilateral globus pallidus that had been noted on diffusion-weighted imaging. No delayed neuropsychological sequelae (DNS) were detected, and the patient returned to school with normal academic performance. At 6-month follow-up, the patient remained asymptomatic with normal exercise tolerance, no cognitive deficits, and normal quality of life assessment. Carbon monoxide poisoning represents a significant toxicological emergency, with intensive care unit mortality rates as high as 14%, substantially exceeding the general mortality of 1–3%.⁴ While carboxyhemoglobin levels traditionally guide management decisions, the optimal approach for severe respiratory failure complicating CO poisoning remains poorly defined in current emergency resuscitation guidelines 8, 9. Recent evidence indicates that initial lactate levels > 6 mmol/L are associated with increased mortality and neurological sequelae, proving more reliable outcome predictors than COHb levels alone⁵—a finding consistent with our patient's initial lactate of 8.5 mmol/L. The development of true ARDS in CO poisoning is uncommon but carries a particularly poor prognosis. Our literature review (Table 3) identified only 3 previously reported pediatric or mixed-age cases, with mortality exceeding 50%. 6, 7 Previous fatal cases, such as that reported by Penning et al., 7 highlight the lethal potential of this combination. The challenge lies in balancing two competing priorities: early HBOT, which is strongly recommended within 6 h for neurological protection 8, 9, and respiratory stability, which is critical for safe HBOT chamber transport and treatment. Most guidelines recommend early HBOT for patients with COHb > 25%, neurological symptoms, or cardiovascular involvement 8, 9. However, these recommendations do not adequately address the subset of patients with life-threatening ARDS, where immediate HBOT may be technically impossible or medically inadvisable. Unstable oxygenation requiring high PEEP and FiO₂, risk of barotrauma in non-compliant lungs, difficulty managing critically ill patients in hyperbaric chambers, and limited monitoring and intervention capabilities during HBOT all present formidable obstacles in this patient population. Our management strategy was guided by the evidence from Kao et al., 3 who documented improved survival when HBOT was delayed until respiratory stabilization in CO patients with acute respiratory failure. The pathophysiological rationale centers on immediate priorities during the first 24 h: preventing refractory hypoxemia (more immediately life-threatening than delayed DNS), optimizing lung mechanics before exposure to pressure changes, establishing hemodynamic stability, and initiating neuroprotective strategies such as temperature management and avoidance of hypotension. The aggressive anti-inflammatory regimen, while not standard in all pediatric ARDS protocols, was justified by the dual pathology of CO toxicity and aspiration injury. High-dose vitamin C acts as a potent antioxidant, potentially mitigating oxidative stress from both insults. Pentoxifylline, a phosphodiesterase inhibitor with anti-inflammatory and rheological properties, has shown benefit in adult ARDS. Low-dose methylprednisolone for early ARDS, when started within 72 h, is supported by updated evidence showing reduced duration of mechanical ventilation 1. We acknowledge that the Murray Lung Injury Score is an adult-derived tool, not specifically validated in pediatric populations. However, for this 62 kg, 172 cm adolescent patient approaching adult size, we felt its use was appropriate alongside contemporary pediatric metrics. The patient clearly met PALICC-2015 criteria² for severe pediatric ARDS with an OI of 30.6 (severe ARDS defined as OI ≥ 16), OSI of 27.1, bilateral infiltrates, acute onset ( 25), clinicians should prioritize respiratory stabilization through lung-protective ventilation, prone positioning, and adjunctive therapies. Early anti-inflammatory approaches should be considered based on institutional protocols and emerging evidence. Respiratory mechanics should be monitored every 6–12 h, with HBOT initiated once the P/F ratio exceeds 200 mmHg and FiO₂ is below 0.60. Importantly, the HBOT course should be completed despite delay, as neuroprotective benefit persists up to 72 h post-exposure 3-8. For CO poisoning without severe ARDS, standard early HBOT protocols should be followed as recommended in current guidelines 8, 9. This is a single case report and cannot establish causation. We cannot definitively attribute the excellent outcome to our specific approach versus the patient's young age, previously healthy status, or other factors. Additionally, the optimal anti-inflammatory regimen remains to be defined through controlled trials. The economic and resource implications of prolonged pediatric intensive care unit management versus immediate HBOT attempts were not analyzed. Further research through multicenter studies or randomized controlled trials would be necessary to validate this sequential approach. DNS occurs in 10–30% of CO poisoning survivors 10, with substantially increased risk in patients with initial unconsciousness, cardiac involvement, and elevated lactate—all risk factors present in our patient. The complete neurological recovery at 6 months is particularly encouraging and may support the neuroprotective value of delayed HBOT combined with temperature management and hemodynamic optimization during the acute phase. This case demonstrates that a sequential approach—prioritizing severe ARDS stabilization before delayed HBOT—can achieve excellent outcomes in CO poisoning complicated by life-threatening respiratory failure. The dramatic respiratory improvement achieved through lung-protective ventilation, prone positioning, and adjunctive anti-inflammatory therapy enabled successful delayed HBOT with complete neurological recovery. While immediate HBOT remains the standard for most CO poisoning cases, 8, 9, our experience suggests that when true ARDS with severe hypoxemia complicates the clinical picture, respiratory stabilization should take precedence, with HBOT delayed until safe administration becomes feasible. This strategy may reduce mortality in this challenging subset of patients and should be incorporated into future management algorithms pending validation in larger case series or multicenter studies. Conceptualization: Marco Piastra, Giorgio Conti. Methodology: Marco Piastra, Paolo Maurizio Soave. Investigation: Marco Piastra, Ivonne Portaccio, Riccardo Maviglia, Silvia Maria Pulitanò. Formal Analysis: Silvia Maria Pulitanò, Marco Piastra. Resources: Riccardo Maviglia, Giorgio Conti. Data Curation: Ivonne Portaccio, Riccardo Maviglia. Writing – Original Draft: Marco Piastra, Ivonne Portaccio. Writing – Review and Editing: All authors. Visualization: Silvia Maria Pulitanò, Marco Piastra. Supervision: Marco Piastra, Giorgio Conti, Paolo Maurizio Soave. Project Administration: Marco Piastra. Validation: Giorgio Conti, Paolo Maurizio Soave. The authors received no specific funding for this work. This case report was conducted in accordance with the Declaration of Helsinki and followed recognized ethical standards for clinical research involving human participants. Institutional Review Board: Comitato Etico della Fondazione Policlinico Universitario “A. Gemelli” IRCCS – Università Cattolica del Sacro Cuore. Ethics Approval Number: Prot. N. 0015288/22 - Del 03/05/2022. Study Protocol ID: 4788. The study protocol was reviewed and approved by the Ethics Committee of Fondazione Policlinico Universitario “A. Gemelli” IRCCS on May 3, 2022. Informed Consent: Written informed consent was obtained from the patient's legal guardians for medical treatment, publication of this case report and associated clinical data, and use of clinical images and radiological findings for educational and research purposes. Data Protection: Patient anonymity has been maintained throughout. All identifying information has been removed from the case presentation while preserving clinical and educational value. The authors declare no conflicts of interest related to this case report. No funding was received for this work, and no commercial or financial relationships exist that could be construed as potential conflicts of interest. The data supporting the findings of this case report are available from the corresponding author upon reasonable request, subject to ethical and privacy considerations and institutional data protection policies in accordance with Italian national regulations and European Union General Data Protection Regulation (GDPR).
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