Abstract

Background:

Chlorine is a potent irritant gas with asphyxiant toxicity. Depending on the concentration and duration of exposure, intentional or accidental inhalation can rapidly cause marked injury to the respiratory tract and, in some cases, leave patients with sustained ventilatory impairment. At present, there is no approved antidote that specifically targets chlorine intoxication. In this context, extracorporeal membrane oxygenation (ECMO) has been applied as a salvage therapy to provide temporary cardiopulmonary support for life-threatening respiratory failure that persists despite maximal conventional management. Among available configurations, veno-venous ECMO (VV-ECMO) delivered through a dual-lumen cannula (DLC) was designed to permit single-site cannulation and may lessen cannulation-related complications, reduce recirculation, and support earlier mobilization—including getting patients out of bed.

Case presentation:

To our knowledge, this is among the first reports in adolescents with longitudinal functional follow-up using chest computed tomography (CT) scans and pulmonary function tests in an adolescent with chlorine intoxication–induced severe acute respiratory distress syndrome (ARDS) who was successfully rescued with dual-lumen cannula veno-venous ECMO (DLC-VV-ECMO).

Conclusion:

In severe ARDS resulting from chlorine intoxication, VV-ECMO may function as a salvage strategy when conventional treatment is insufficient, providing temporary extracorporeal oxygenation and thereby preserving a window for pulmonary recovery and stabilization of other organ systems. During the acute phase of chlorine intoxication, prophylactic antibiotics are generally not recommended because the underlying lung injury is primarily caused by chemical insult and oxidative damage rather than established infection. Our findings also suggest that recovery of pulmonary function in adolescents after chlorine intoxication-induced severe ARDS may take longer than 6 months. Moreover, early suicide risk identification and timely mental health intervention are essential to prevent subsequent catastrophic outcomes.

Introduction

Chlorine is a highly irritating, asphyxiant gas. After intentional or accidental exposure, inhalation can rapidly trigger a wide range of respiratory injuries—from upper-airway irritation and bronchial obstruction to increased vascular permeability, pulmonary edema, and, in severe cases, acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Clinical severity and the likelihood of persistent ventilatory impairment vary with both the concentration and the duration of exposure, and individuals with underlying chronic respiratory disease (including asthma) appear particularly vulnerable (1–4). A major component of this toxicity is oxidative injury: chlorine hydrolyzes on contact with moist airway surfaces, generating hypochlorous and hydrochloric acids that damage the respiratory epithelium and may set the stage for longer-term ventilatory dysfunction (5). Injury may also be amplified by chlorination by-products (CBPs), which form when chlorine reacts with natural organic matter and have been implicated in related toxic pathways (6). In routine practice, β2-agonists and corticosteroids are often administered for chlorine-induced respiratory injury, yet the evidentiary base remains modest. No specific antidote for chlorine intoxication has been approved by the U.S. Food and Drug Administration (FDA) to date (7, 8). Over recent years, chlorine exposure has drawn increasing clinical attention, in part because reports of chlorine-related incidents have risen in a sustained manner (9, 10). Even so, the full spectrum of life-threatening presentations and longer-term sequelae after chlorine intoxication is still incompletely described, with the knowledge gap especially apparent in children and adolescents (11, 12).

Extracorporeal membrane oxygenation (ECMO) is widely regarded as a salvage therapy, offering temporary cardiopulmonary support for patients with life-threatening respiratory failure and/or cardiogenic shock that does not respond to conventional management. As devices, expertise, and clinical workflows have matured, ECMO deployment has expanded rapidly across the globe and is now commonly used as a bridge to recovery or transplantation (13–16). One refinement is veno-venous ECMO (VV-ECMO) delivered via a dual-lumen cannula (DLC), which was introduced to simplify cannulation. Performed in the intensive care unit (ICU) under bedside imaging guidance—such as ultrasonography and/or portable radiography—this approach can avoid multiple access sites, reduce cannulation-related complications, limit recirculation, and support earlier mobilization, including out-of-bed activity (17–21). At the same time, ECMO remains a double-edged intervention. Contact between blood and the extracorporeal circuit may provoke immune activation and a systemic inflammatory response syndrome (SIRS), which can amplify inflammation and potentially worsen outcomes, particularly when layered onto the patient's underlying disease process (22). Sivelestat sodium (SIV), a selective neutrophil elastase (NE) inhibitor, has been proposed as a means to attenuate organ injury by suppressing NE activity and dampening downstream inflammatory cascades (23–25).

To the best of our knowledge, we report the first adolescent case of severe ARDS following chlorine intoxication that was successfully supported with VV-ECMO using a dual-lumen cannula. We also provide a staged six-month follow-up, tracking longer-term evolution on chest imaging alongside pulmonary function testing. This report underscores not only the acute organ injury that chlorine exposure can precipitate, but also the persistent respiratory consequences that may extend well beyond the initial crisis, and it offers clinical pointers for tailoring supportive care to lessen early injury, curb downstream morbidity, reduce mortality risk, and improve post-recovery quality of life.

Case presentationChief complaints

On April 23, 2025, a 15-year-old boy was transferred to the Department of Critical Care Medicine at the Sixth Affiliated Hospital of Harbin Medical University, a tertiary women's and children's hospital, for further recovery and rehabilitation. He had been successfully rescued from chlorine-induced severe ARDS with dual-lumen cannula veno-venous ECMO (DLC-VV-ECMO) in the Department of Critical Care Medicine at the First Affiliated Hospital of Harbin Medical University.

History of present illness

Ten days before admission, the adolescent was exposed to a large amount of chlorine gas that he had generated himself and was subsequently admitted to the Department of Critical Care Medicine at the First Affiliated Hospital of Harbin Medical University. He was diagnosed with severe ARDS caused by chlorine intoxication. Continuous analgesia and sedation were administered with remifentanil and midazolam. Invasive mechanical ventilation (IMV) was initiated using a lung-protective approach, and intermittent prone positioning was continued for 8 days. Despite mechanical ventilation with an inspired oxygen fraction of 100%, peripheral oxygen saturation remained between 59% and 77% on that day. The PaO2/FiO2 ratio (P/F) was 38.7 mmHg and remained at that level for 4 h, leading to initiation of VV-ECMO, which was maintained for 7 days. The system included a single-use dual-lumen venous cannula for a cardiopulmonary bypass system (MAQUET Cardiopulmonary, model 70126), an extracorporeal circulation tubing pack (MAQUET Cardiopulmonary, model BE-PLS2050), and extracorporeal circulation cannulae and puncture accessories (MAQUET Cardiopulmonary, model PIK150). Four days before admission, the gas inlet and outlet of the ECMO oxygenator were completely closed. The patient remained hemodynamically stable, and arterial blood gas results were satisfactory, after which decannulation was performed. High-flow nasal cannula (HFNC) oxygen therapy was then continued for 2 days. Antimicrobials comprised empirical biapenem for 7 days, followed by cefoperazone/sulbactam plus tigecycline for 3 days to treat Acinetobacter baumannii (AB). Intravenous methylprednisolone sodium succinate was given in a tapering regimen of 400 mg/day, 80 mg/day, and 40 mg/day, each for 3 days. SIV was administered at 4.8 mg/kg/day for 5 days to reduce the inflammatory response. Additional supportive care included transfusion of blood products for coagulopathy and vasopressor therapy. After successful discontinuation of DLC-VV-ECMO and IMV, followed by transition to HFNC, he was transferred to the Sixth Affiliated Hospital of Harbin Medical University for further recovery and rehabilitation. Laboratory findings and chest imaging obtained during his stay at the First Affiliated Hospital are presented in Table 1 and Figures 1, 2, respectively.

The First Affiliated Hospital of Harbin Medical University/ICUHospitalization/ICURehabilitation wardAfter dischargeday of illnessDAY-10DAY-9DAY-8DAY-7DAY-6DAY-5DAY-4DAY-3DAY-2DAY-1DAY0DAY1DAY2DAY4DAY6DAY7DAY12DAY19DAY33DAY103DAY220Disease courseWBC (×109/L)43.2622.6927.1521.8310.0810.9410.8310.7416.269.5430.2123.095.9611.1215.977.35NEUT%79.687.5959188.382.282.683.677.469.690.378.24257.971.736.1NEUT (×109/L)34.4219.8725.7719.889.438.998.948.9812.586.6327.2818.042.56.4411.452.65LYMPH% (%)17.64.83.64.46.19.510.710.512.413.63.48.624.62.0910.932.8HGB (g/L)21815214612710811110399113111132113108113118108HCT (%)70.244.545.138.233.135.43230.734.333.239.634.831.934.135.733.8PLT (×109/L)25713912595526099129185300498464443507558348PT (s)25.715.81614.113.711.711.711.615.111.5PT (%)27.952.151.259.261.184.884.88954.990.7INR2.271.351.361.21.150.960.980.961.321APTT (s)57.6031.20000029.928.9FIB (g/L)0.54.624.883.090.451.171.781.986.484.58TT (s)36.118.215.617.628.321.318.918.614.514.9DD (mg/L)72.1226.7969.7340.9141.6834.8529.0312.162.09LDH(U/L)450.09299.32198.27254.12AST (U/L)54.352.7125.557.142.528.32120243419ALT (U/L)15.927.165.350.652.157.940.633.764.387.731.8ALB (g/L)26.933.231.233.939.641.841.0832.4733.5534.2532.93BUN (mmol/L)5.597.76.6213.917.635.12SCr (μmol/L)84.88560.641.145354041hs-cTnI (ng/L)262.7405.487.314.211CRP (mg/L)14.3113.59111.7840.9915.894.660.91PCT (ng/mL)4.7724.38169.145.613.0610.322.972.120.630.380.06Oxygen therapyInvasive mechanical ventilationHigh-flow nasal cannulaNasal catheter oxygen inhalationPEEP (cmH₂O)658888855FiO₂100404040403540353537403533333325pH7.0897.4167.4077.4277.4127.4197.517.4637.4257.5467.4597.4617.4937.5127.4727.421PCO₂(mmHg)55.242.246.545.249.147.838.137.842.931.937.438.241.244.138.640.6PO₂ (mmHg)38.794.311883.188.510115514614813180.892.276.677.471.575.6P/F (mmHg)38.7235.75295207.75221.25288.57387.5417.14422.86354.04202.2263.43232.12234.55216.67302.4LAC (mmol/L)7.12.41.41.72.1