When curiosity turns toxic: accidental hydrocarbon aspiration in a pediatric patient - a case report with literature review

When curiosity turns toxic: accidental hydrocarbon aspiration in a pediatric patient - a case report with literature review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report When curiosity turns toxic: accidental hydrocarbon aspiration in a pediatric patient - a case report with literature review Alice Bianchi, Michele Ghezzi, Mirko Gambino, Elisabetta Bungaro, and 8 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9226833/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 8 You are reading this latest preprint version Abstract Background Accidental hydrocarbon ingestion is a common cause of pediatric toxic exposure, particularly among those under 6 years of age, and primarily causes injury through aspiration leading to chemical pneumonitis. Clinical presentation is variable, ranging from mild symptoms to severe respiratory failure, with potential early deterioration and rare delayed complications such as pneumatoceles. Case report: We report the case of a 17-month-old previously healthy boy admitted after accidental ingestion of printer fluid containing low-viscosity hydrocarbons. He initially presented with mild respiratory symptoms and stable vital signs but developed progressive chemical pneumonitis within hours, requiring Pediatric Intensive Care Unit admission and ventilatory support. The clinical course was complicated by bilateral pulmonary consolidations and subsequent development of large pneumatoceles, with gradual radiological resolution and complete clinical recovery at 6- and 12-month follow-up, without residual sequelae. Conclusions Our case illustrates that accidental hydrocarbon ingestion may lead to severe and progressive respiratory injury even after an apparently mild initial presentation, thus warranting close in-hospital observation for at least 48 hours. Although radiological complications such as pneumatoceles may develop several days after exposure, long-term outcomes are generally favorable, highlighting the remarkable capacity for pulmonary recovery in children and the importance of structured follow-up. children hydrocarbon inhalation chemical pneumonitis pneumatoceles pediatric pulmonology pediatric intensive care Figures Figure 1 Figure 2 Figure 3 Introduction Accidental hydrocarbon poisoning remains a significant cause of toxic exposure in the pediatric population worldwide, particularly among children under 6 years of age 1 . The reported incidence varies by geographic region and socioeconomic context. In high-income countries such as the United States, data from the American Association of Poison Control Centers indicate that hydrocarbons account for approximately 1–3% of all pediatric poisoning exposures reported annually 2,3 . Poisoning events are more frequent in males, with a peak incidence between 1 and 4 years of age, due to exploratory behaviour, hand-to-mouth activity, and the storage of fuels in easily accessible containers, often beverage bottles 1 . Hydrocarbons commonly implicated include kerosene, gasoline, lamp oil, lighter fluids, mineral spirits, and other petroleum distillates frequently stored in households. The primary mechanism of toxicity is related to aspiration during the ingestion of hydrocarbon-containing products, which can lead to chemical pneumonitis. Consequently, respiratory complications represent the most common clinically significant outcomes, whereas systemic complications resulting from absorption of the substance are rare 1,4 . The clinical presentation is highly variable, ranging from initially asymptomatic patients to children presenting with established respiratory distress requiring ventilatory support. In cases of chemical pneumonitis, clinical deterioration may occur within the first 6–8 hours after exposure, with a peak in severity typically observed around 48 hours. However, severe complications, such as the development of pneumatoceles, may arise several days after the initial event. The present case describes an episode of accidental hydrocarbon aspiration leading to severe chemical pneumonitis, further complicated by the development of pneumatoceles, ultimately necessitating respiratory support and admission to the Pediatric Intensive Care Unit (PICU). Despite the severity of the clinical and radiological findings during the hospitalization, the patient experienced a completely favourable outcome, with no detectable sequelae at follow-up in the subsequent months. Case Report We report the case of a 17-month-old boy with no relevant medical history, who was admitted at our Pediatric Emergency Department following accidental ingestion of an unknown quantity of printer fluid (petroleum oil at low viscosity, containing hydrocarbons - HC) at his parents' workplace. Immediately after ingestion, the child developed facial flushing, coughing and respiratory distress. At the initial evaluation, vital signs were stable (HR 132 bpm, SO₂ 96%, BP 107/64 mmHg). On clinical examination, the child appeared alert and responsive, with normal skin perfusion and hydration. The oral cavity was unremarkable, and cardiovascular and pulmonary examination was normal, except for the presence of transmitted upper airway sounds. Venous blood gas analysis showed: pH 7.44, pCO₂ 30 mmHg, HCO₃⁻ 20.4 mmol/L, BE -3.8 mmol/L. Blood tests revealed: WBC 18,150/mm³, CRP negative, blood glucose 185 mg/dL, ALT 323 U/L, AST 148 U/L, renal and hepatic function tests and electrolytes within normal limits. A rapid antigen nasal swab for SARS-CoV-2 was negative. Electrocardiogram findings were normal. Chest X-ray demonstrated mild bilateral pulmonary hyperinflation and a slightly accentuated peribronchovascular pattern, with a small area of consolidation in the left paracardiac region. The Local Poison Control Center of Pavia was contacted and recommended clinical monitoring for at least 24 hours due to the risk of chemical pneumonitis from hydrocarbon aspiration. The patient was admitted for continuous vital sign monitoring, intravenous hydration with electrolyte solution, empiric broad-spectrum antibiotic therapy with ampicillin/sulbactam and intravenous N-acetylcysteine due to elevated transaminase levels. Several hours after admission, the child developed fever. Approximately eight hours post-ingestion, pulmonary auscultation worsened with audible crackles, although vital signs remained stable. On the following day, blood gas analysis was good. Laboratory results showed an increasing CRP and decreased transaminase levels. A follow-up chest X-ray revealed new pulmonary consolidations in the left basal, right basal, and right upper paramedian zones. Due to worsening respiratory mechanics, the patient was admitted to the Pediatric Intensive Care Unit (PICU). Here, ventilatory support was started using helmet CPAP, along with intravenous corticosteroid therapy, gastroprotective agents and antibiotic therapy for 8 days. On day 3, a chest CT scan revealed extensive bilateral heterogeneous pulmonary consolidations with partial air bronchograms and numerous obliterated bronchi, large hypodense areas compatible with reduced vascularization and pleural effusion in the scissural region and at the left lung base (Fig. 1 ). The child remained febrile but gradually improved in terms of respiratory mechanics. On day 5, he was transferred to the Pediatric ward, after CPAP support was progressively reduced and replaced with high-flow nasal cannula (HFNC) therapy. On day 8, the patient experienced a new episode of respiratory worsening, with tachypnea (60 breaths/min) and bilateral diffuse crackles on auscultation. He was subsequently transferred back to the PICU, where respiratory support with CPAP was re-initiated, resulting in clinical improvement. A bronchoscopy with bronchoalveolar lavage (BAL) was performed: the trachea showed edematous and erythematous mucosa, with poorly defined tracheal rings. The main bronchi showed erythematous mucosa that bled easily, abundant, tenacious whitish secretions and the bronchial carinae appeared markedly swollen. On day 15, a new chest CT scan revealed large, bilateral round cavitary lesions with wall enhancement, containing heterogeneous material with both fluid and air components forming air-fluid levels (Fig. 2 ). Since day 17, respiratory support was discontinued and a progressive improvement in respiratory mechanics was observed, with vital signs remaining consistently good. Subsequently serial chest X-rays were performed, showing a gradual reduction of pulmonary lesions. He was ultimately discharged on day 37 in good clinical conditions and with daily inhaled corticosteroid therapy. During follow-up evaluations, 2 months after the ingestion, lung ultrasound showed a reduction in the left posterior basal air-filled lesion (2.5 cm diameter) with minimal pleural effusion. On chest X-ray a reduction of the known pulmonary cavitations was described and the fluid component appeared diminished. At 3 months general well-being was reported, with no respiratory symptoms and no signs at pulmonary clinical evaluation. 4 months after the ingestion, the clinical condition continued to be good, with no longer recognizable bilateral cavitated lesions on chest X ray, as well as on a chest X-ray at 6 months (Fig. 3 ). The last pulmonological assessment, performed 12 months after ingestion, reported no respiratory infections or respiratory symptoms, with normal pulmonological findings. Discussion Mechanisms of Hydrocarbon-Associated Lung Toxicity Pulmonary injury results from aspiration during or after hydrocarbon ingestion. Increased volatility, low viscosity, and decreased surface tension are related to increased risk of aspiration and lung injury because these characteristics facilitate penetration of the HC into the bronchial tree. Vomiting, choking, or coughing during or after the ingestion increases the risk of aspiration, so induced emesis and gastric lavage should be avoided as they increase the risk of aspiration 1,3,5,6 . Pulmonary penetration of HC results in both direct chemical injury to the surfactant system 7 and the alveolar epithelium, as well as indirect damage mediated by a secondary inflammatory response. At the alveolar level, HC become incorporated into the surfactant film, leading to surfactant inactivation and increased surface tension, thereby predisposing to alveolar collapse, atelectasis, and reduced pulmonary compliance. Owing to their lipophilic properties, HC also penetrate the cell membranes of type I and type II pneumocytes, causing epithelial injury with subsequent alveolar edema and protein-rich exudation, which represents the initial substrate for sterile inflammation. Collectively, these mechanisms result in chemical pneumonitis, which triggers a secondary inflammatory cascade characterized by the recruitment of inflammatory cells (including neutrophils and macrophages) and the release of pro-inflammatory cytokines that further exacerbate lung injury 6 . Even minimal exposure to these substances appears to be sufficient to cause severe toxicity, including chemical pneumonitis; however, in most cases reported in the literature, as well as in the case just described, the actual amount of inhaled HC is unknown. Clinical Manifestations of Hydrocarbon Inhalation Immediately after HC ingestion, approximately 46–65% of children remain asymptomatic 8–10 . The absence of initial symptoms suggests a lower risk of developing chemical pneumonitis and subsequent complications. When present, the most common symptoms are tachypnea (74% of cases), fever (63.5%), and cough (38%). Vomiting occurs in approximately 51% of cases and represents a clinical warning sign, as it is associated with an increased risk of inhalation and subsequent pulmonary injury 11 . Less frequently, central nervous system manifestations are observed, and include signs of either agitation or depression, such as drowsiness and restlessness (31%) 12 . In approximately 15% of pediatric patients with a history of HC exposure, symptoms of chemical pneumonitis appear within 6–8 hours and progressively worsen over the first 48 hours 5,13,14 . This phase is characterized by increasing cough, tachypnea, and dyspnea, and in some cases, hemoptysis. In approximately 5% of cases complicated by pneumonitis, the clinical course is rapidly progressive and characterized by severe manifestations, including acute respiratory distress syndrome (ARDS), hypoxemia, and respiratory failure 15 . Between days 3–10, approximately 90% of patients show clinical improvement, with gradual resolution of cough and dyspnea. However, in more severe cases, complications such as air-leak syndromes may occur. Persistence or recurrence of fever during this phase may indicate secondary bacterial superinfection. Beyond the first 10 days, most patients experience gradual clinical recovery. In cases of severe pneumonitis, however, persistent lung disease may develop, with the appearance of pneumatoceles detectable on radiographic imaging 6,16 . Laboratory and instrumental findings On laboratory evaluation, leucocytosis appears to be suggestive of pneumonia, as it was observed in 75% of patients with pneumonia, compared with 32% of patients without pneumonia following hydrocarbon ingestion 13 . On instrumental evaluation, a poor correlation was observed between clinical manifestations and chest radiographic findings, which may appear several hours after hydrocarbon ingestion 10,17,18 . Notably, most of symptomatic patients who had normal chest radiographs at presentation developed radiographic abnormalities later in the clinical course (60%), most commonly within 4–8 hours after hydrocarbon ingestion. Bilateral interstitial pneumonitis is the most common radiographic pattern (53%), followed by unilateral interstitial pneumonitis (23%) and lobar pneumonia (9.5%) 13 . Pneumatoceles is the most frequent complication of chemical pneumonitis (2–4% of cases) 13,19 . Pneumatocele formation is thought to result from parenchymal necrosis combined with a check-valve mechanism in the small airways, leading to focal air trapping and the development of air-filled cystic spaces 19,20 . As in the case described, pneumatoceles may develop days after the toxic insult (typically 6–10 days 6,21 , up to 15 days in the present case); therefore, close clinical monitoring and serial imaging during hospitalization are justified, particularly in the presence of clinical deterioration or the onset of new respiratory symptoms. Fortunately, these lesions are often transient in children, although complications (e.g., secondary infection or pneumothorax) may occur. Management of Hydrocarbon Inhalation There are no well-defined guidelines for the management of patients with hydrocarbon inhalation pneumonia, and the limited available recommendations are largely based on outdated retrospective studies 10,13,16–19,22 . In the review by Makrygianni et al. 6 , it is suggested that all children who remain asymptomatic after hydrocarbon inhalation should be observed for 6–8 hours in the he emergency department and undergo chest radiography. If they remain asymptomatic and the chest X-ray is normal, discharge home may be considered. Conversely, patients with radiographic abnormalities should be hospitalized for prolonged monitoring, even though approximately 95% of patients remain asymptomatic and have a benign clinical course 10 . Similarly, children who are symptomatic at presentation or who develop symptoms during the observation period warrant hospital admission, as the presence of symptoms is associated with an increased risk of chemical pneumonitis. Patients presenting with respiratory distress, altered mental status, and/or seizures should be evaluated for admission to the intensive care unit 13,16 . Management is primarily supportive and includes close monitoring of cardiorespiratory status, serial arterial blood gas analysis, and oxygen supplementation to correct hypoxemia when necessary 6 . In the presence of wheezing, inhaled bronchodilators may be considered. The use of antibiotics and the optimal timing for their initiation remain uncertain. In the retrospective descriptive study by Tenembaum et al. 1 , most children (52.3%) received prophylactic antibiotics, whereas 37.2% were hospitalized for observation without any specific therapy. When bacterial superinfection is suspected, empiric broad-spectrum antibiotic therapy (e.g., amoxicillin–clavulanate, cefuroxime, or cloxacillin combined with gentamicin) should be initiated and subsequently adjusted according to microbiological findings 23 . In our case, empiric antibiotic therapy with amoxicillin–clavulanate was started early after hospital admission because of progressive radiological abnormalities and a concomitant rise in inflammatory markers, which increased the suspicion of a possible bacterial superinfection. The use of systemic corticosteroids remains controversial 22,24,25 . Some studies suggest that corticosteroids may attenuate inflammation and potentially reduce the subsequent development of fibrosis; however, their use has also been associated with an increased risk of secondary infections. In a retrospective study by Sen et al. including 54 pediatric patients with HC inhalation pneumonia 22 , 18 children (33%) required admission to the intensive care unit for respiratory failure and were treated with systemic corticosteroids. Among these, 17 patients (94%) showed normalization of oxygen saturation within 24 hours, with no reported cases of secondary infection. However, the only randomized controlled trial available demonstrated no clinical benefit of systemic corticosteroids over placebo in children with mild-to-moderate hydrocarbon-induced lung disease, with no significant differences in fever duration, respiratory or heart rate, or length of hospital stay 25 . With regard to the management of severe disease, mechanical ventilation should be considered in cases of hypoxemia refractory to supplemental oxygen 16 . Given that pulmonary surfactant depletion represents one of the key pathogenetic mechanisms of hydrocarbon-induced pneumonitis, intratracheal administration of exogenous surfactant may also be considered 26,27 . Beyond the initial chest radiograph obtained in the emergency department, we emphasize the importance of repeat chest imaging during follow-up in patients with HC inhalation pneumonia, particularly at 10–14 days, in order to rule out the development of pneumatoceles 19 . Prognosis of Hydrocarbon Inhalation Fortunately, literature data from systematic reviews and poison center registries indicate a generally favourable prognosis for pediatric patients following HC inhalation 9,10,13,16 . Uncomplicated pneumatoceles typically resolve spontaneously over a period of weeks to months, whereas complicated pneumatoceles—such as infected pneumatoceles, tension pneumatoceles, or those rupturing with resultant pneumothorax—require prompt intervention 5,21 . Management primarily involves image-guided percutaneous drainage, with surgical resection considered in cases of multiple complicated lesions 28,29 . In pediatric patients with HC inhalation pneumonia, follow-up with a pulmonologist is consistently recommended to monitor for the potential development of small airway obstructive disease and loss of elastic recoil, both of which have been reported in the literature, albeit with variable prevalence 30,31 . In this context, patients may benefit from a course of inhaled corticosteroid therapy to reduce airway inflammation and the risk of small airway obstruction, as observed in our case. The mortality rate associated with HC inhalation is generally low (< 1%; 0.2–0.5%) and is closely linked to the progression of severe pneumonia 6,9,10 . Conclusions Accidental hydrocarbon ingestion in children represents a significant cause of toxic exposure in the pediatric population and a potentially life-threatening event; however, evidence-based management guidelines remain limited 10,13,16–19,22 . The available literature indicates that even minimal quantities of ingested hydrocarbons may result in severe toxicity, including chemical pneumonitis and progressive respiratory failure. Our case highlights a particularly severe presentation of hydrocarbon aspiration pneumonia, requiring admission to the pediatric intensive care unit and advanced respiratory support, thereby underscoring the potential for rapid and clinically significant deterioration and the need for close observation 5,13,14 . Therefore, we recommend in-hospital monitoring for at least 48 hours, even in initially asymptomatic patients. Pulmonary injury is primarily related to aspiration occurring during or shortly after ingestion. Radiological complications such as pneumatoceles may become apparent 6–10 days following the acute event and can persist for up to six months 6,21 . In uncomplicated cases, pneumatoceles generally resolve spontaneously over weeks to months, regardless of the specific therapeutic interventions administered during the acute phase. Careful post-discharge follow-up is warranted, as long-term outcomes are often favourable and demonstrate a substantial capacity for pulmonary recovery in the pediatric population. Consistent with the available literature, our patient also showed a completely favourable clinical evolution despite the severity of the initial presentation, with progressive respiratory recovery and no long-term sequelae observed during follow-up. Further reports of comparable cases may help to better define the clinical evolution and optimal management of these rare complications. In this context, collaboration and data sharing between different centers could facilitate the comparison of clinical experiences and contribute to improving therapeutic strategies. Abbreviations HR Heart Rate SO2 Saturation of Oxygen BP Blood Pressure pCO2 Partial pressure of Carbon dioxide HCO3- Bicarbonate ion BE Base Excess WBC White Blood Count CRP C-reactive Protein ALT Alanine Transaminase CPAP Continuous Positive Airway Pressure FiO2 Fraction of Inspired Oxygen PEEP Positive End-Expiratory Pressure Chest CT Chest Computed Tomography Declarations Clinical trial number: not applicable Funding Statement: This research received no external funding. Conflict of interest: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Ethical Statement: According to the italian directive (AIFA directorial decision of August 2024 ), single case report is not considered clinical research and therefore does not require formal approval by an Ethics Committee. Consent for publication An informed consent was obtained from the parents of the patients to either describe the case report and use the pictures. All the authors approved the final manuscript for submission and agreed to the publication of this study Acknowledgments: The authors would like to thank the staff of the Pediatric Emergency Department, the Pediatric Intensive Care Unit, and the Pediatric Ward for their dedicated care of the patient. References Tenenbaum A, Rephaeli R, Cohen-Cymberknoh M, Aberbuch D, Rekhtman D. Hydrocarbon Intoxication in Children: Clinical and Sociodemographic Characteristics. 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Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 13 May, 2026 Reviewers agreed at journal 07 May, 2026 Reviewers agreed at journal 04 May, 2026 Reviewers invited by journal 16 Apr, 2026 Editor invited by journal 02 Apr, 2026 Editor assigned by journal 31 Mar, 2026 Submission checks completed at journal 31 Mar, 2026 First submitted to journal 25 Mar, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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Buzzi","correspondingAuthor":false,"prefix":"","firstName":"Elena","middleName":"","lastName":"Zoia","suffix":""},{"id":627180620,"identity":"b7a10702-2f87-4ab3-8a22-1285da334643","order_by":9,"name":"Gianvincenzo Zuccotti","email":"","orcid":"","institution":"Ospedale dei Bambini Vittore Buzzi","correspondingAuthor":false,"prefix":"","firstName":"Gianvincenzo","middleName":"","lastName":"Zuccotti","suffix":""},{"id":627180621,"identity":"7fc11fd9-7578-40fc-9679-43a7b26e1c4b","order_by":10,"name":"Enza D'Auria","email":"","orcid":"","institution":"Ospedale dei Bambini Vittore Buzzi","correspondingAuthor":false,"prefix":"","firstName":"Enza","middleName":"","lastName":"D'Auria","suffix":""},{"id":627180622,"identity":"39e172cc-fde3-411e-98db-ed4c54c604c7","order_by":11,"name":"Stefania Ferrario","email":"","orcid":"","institution":"Ospedale dei Bambini Vittore Buzzi","correspondingAuthor":false,"prefix":"","firstName":"Stefania","middleName":"","lastName":"Ferrario","suffix":""}],"badges":[],"createdAt":"2026-03-25 20:08:43","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9226833/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9226833/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":107652006,"identity":"97bfe7c4-c6fd-4805-810f-a48745f386b4","added_by":"auto","created_at":"2026-04-23 15:11:12","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":928159,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eChest TC scan on day 3 - \u003c/strong\u003eextensive bilateral heterogeneous pulmonary consolidations with partial air bronchograms and numerous obliterated bronchi.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-9226833/v1/4f0036629db5532c3d0c380c.png"},{"id":107652022,"identity":"6bf1f039-ccf6-49e7-8f26-fe7a03700c3a","added_by":"auto","created_at":"2026-04-23 15:11:17","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":383561,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eChest TC scan on day 15\u003c/strong\u003e -large, round cavitary lesions with wall enhancement, containing heterogeneous material with both fluid and air components forming air-fluid levels.\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-9226833/v1/8959c28979e7fa0ac4976d35.png"},{"id":107652033,"identity":"2bba93af-7368-45db-94f0-0f63cc870819","added_by":"auto","created_at":"2026-04-23 15:11:19","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":207781,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eClinical and radiological temporal course from time 0 (T0) to time 4 (T4). \u003c/strong\u003eLegend: C = clinical status; R = chest X-ray.\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-9226833/v1/a36fc14d49dc0ff96e9b0d01.png"},{"id":108803619,"identity":"ac7d25f5-4105-48de-b24d-3596045f990d","added_by":"auto","created_at":"2026-05-08 15:01:30","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1746744,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9226833/v1/bc1387ae-9c33-40cd-b248-7da91c5ca8c7.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"When curiosity turns toxic: accidental hydrocarbon aspiration in a pediatric patient - a case report with literature review","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAccidental hydrocarbon poisoning remains a significant cause of toxic exposure in the pediatric population worldwide, particularly among children under 6 years of age\u003csup\u003e1\u003c/sup\u003e. The reported incidence varies by geographic region and socioeconomic context. In high-income countries such as the United States, data from the American Association of Poison Control Centers indicate that hydrocarbons account for approximately 1\u0026ndash;3% of all pediatric poisoning exposures reported annually\u003csup\u003e2,3\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003ePoisoning events are more frequent in males, with a peak incidence between 1 and 4 years of age, due to exploratory behaviour, hand-to-mouth activity, and the storage of fuels in easily accessible containers, often beverage bottles\u003csup\u003e1\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eHydrocarbons commonly implicated include kerosene, gasoline, lamp oil, lighter fluids, mineral spirits, and other petroleum distillates frequently stored in households. The primary mechanism of toxicity is related to aspiration during the ingestion of hydrocarbon-containing products, which can lead to chemical pneumonitis. Consequently, respiratory complications represent the most common clinically significant outcomes, whereas systemic complications resulting from absorption of the substance are rare\u003csup\u003e1,4\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eThe clinical presentation is highly variable, ranging from initially asymptomatic patients to children presenting with established respiratory distress requiring ventilatory support. In cases of chemical pneumonitis, clinical deterioration may occur within the first 6\u0026ndash;8 hours after exposure, with a peak in severity typically observed around 48 hours. However, severe complications, such as the development of pneumatoceles, may arise several days after the initial event.\u003c/p\u003e \u003cp\u003eThe present case describes an episode of accidental hydrocarbon aspiration leading to severe chemical pneumonitis, further complicated by the development of pneumatoceles, ultimately necessitating respiratory support and admission to the Pediatric Intensive Care Unit (PICU). Despite the severity of the clinical and radiological findings during the hospitalization, the patient experienced a completely favourable outcome, with no detectable sequelae at follow-up in the subsequent months.\u003c/p\u003e"},{"header":"Case Report","content":"\u003cp\u003eWe report the case of a 17-month-old boy with no relevant medical history, who was admitted at our Pediatric Emergency Department following accidental ingestion of an unknown quantity of printer fluid (petroleum oil at low viscosity, containing hydrocarbons - HC) at his parents' workplace. Immediately after ingestion, the child developed facial flushing, coughing and respiratory distress. At the initial evaluation, vital signs were stable (HR 132 bpm, SO₂ 96%, BP 107/64 mmHg). On clinical examination, the child appeared alert and responsive, with normal skin perfusion and hydration. The oral cavity was unremarkable, and cardiovascular and pulmonary examination was normal, except for the presence of transmitted upper airway sounds. Venous blood gas analysis showed: pH 7.44, pCO₂ 30 mmHg, HCO₃⁻ 20.4 mmol/L, BE -3.8 mmol/L. Blood tests revealed: WBC 18,150/mm\u0026sup3;, CRP negative, blood glucose 185 mg/dL, ALT 323 U/L, AST 148 U/L, renal and hepatic function tests and electrolytes within normal limits. A rapid antigen nasal swab for SARS-CoV-2 was negative. Electrocardiogram findings were normal. Chest X-ray demonstrated mild bilateral pulmonary hyperinflation and a slightly accentuated peribronchovascular pattern, with a small area of consolidation in the left paracardiac region. The Local Poison Control Center of Pavia was contacted and recommended clinical monitoring for at least 24 hours due to the risk of chemical pneumonitis from hydrocarbon aspiration. The patient was admitted for continuous vital sign monitoring, intravenous hydration with electrolyte solution, empiric broad-spectrum antibiotic therapy with ampicillin/sulbactam and intravenous N-acetylcysteine due to elevated transaminase levels.\u003c/p\u003e \u003cp\u003eSeveral hours after admission, the child developed fever. Approximately eight hours post-ingestion, pulmonary auscultation worsened with audible crackles, although vital signs remained stable. On the following day, blood gas analysis was good. Laboratory results showed an increasing CRP and decreased transaminase levels. A follow-up chest X-ray revealed new pulmonary consolidations in the left basal, right basal, and right upper paramedian zones. Due to worsening respiratory mechanics, the patient was admitted to the Pediatric Intensive Care Unit (PICU). Here, ventilatory support was started using helmet CPAP, along with intravenous corticosteroid therapy, gastroprotective agents and antibiotic therapy for 8 days.\u003c/p\u003e \u003cp\u003eOn day 3, a chest CT scan revealed extensive bilateral heterogeneous pulmonary consolidations with partial air bronchograms and numerous obliterated bronchi, large hypodense areas compatible with reduced vascularization and pleural effusion in the scissural region and at the left lung base (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The child remained febrile but gradually improved in terms of respiratory mechanics. On day 5, he was transferred to the Pediatric ward, after CPAP support was progressively reduced and replaced with high-flow nasal cannula (HFNC) therapy. On day 8, the patient experienced a new episode of respiratory worsening, with tachypnea (60 breaths/min) and bilateral diffuse crackles on auscultation. He was subsequently transferred back to the PICU, where respiratory support with CPAP was re-initiated, resulting in clinical improvement. A bronchoscopy with bronchoalveolar lavage (BAL) was performed: the trachea showed edematous and erythematous mucosa, with poorly defined tracheal rings. The main bronchi showed erythematous mucosa that bled easily, abundant, tenacious whitish secretions and the bronchial carinae appeared markedly swollen.\u003c/p\u003e \u003cp\u003eOn day 15, a new chest CT scan revealed large, bilateral round cavitary lesions with wall enhancement, containing heterogeneous material with both fluid and air components forming air-fluid levels (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eSince day 17, respiratory support was discontinued and a progressive improvement in respiratory mechanics was observed, with vital signs remaining consistently good.\u003c/p\u003e \u003cp\u003eSubsequently serial chest X-rays were performed, showing a gradual reduction of pulmonary lesions. He was ultimately discharged on day 37 in good clinical conditions and with daily inhaled corticosteroid therapy.\u003c/p\u003e \u003cp\u003eDuring follow-up evaluations, 2 months after the ingestion, lung ultrasound showed a reduction in the left posterior basal air-filled lesion (2.5 cm diameter) with minimal pleural effusion. On chest X-ray a reduction of the known pulmonary cavitations was described and the fluid component appeared diminished.\u003c/p\u003e \u003cp\u003eAt 3 months general well-being was reported, with no respiratory symptoms and no signs at pulmonary clinical evaluation.\u003c/p\u003e \u003cp\u003e4 months after the ingestion, the clinical condition continued to be good, with no longer recognizable bilateral cavitated lesions on chest X ray, as well as on a chest X-ray at 6 months (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e3\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThe last pulmonological assessment, performed 12 months after ingestion, reported no respiratory infections or respiratory symptoms, with normal pulmonological findings.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eMechanisms of Hydrocarbon-Associated Lung Toxicity\u003c/h2\u003e \u003cp\u003ePulmonary injury results from aspiration during or after hydrocarbon ingestion. Increased volatility, low viscosity, and decreased surface tension are related to increased risk of aspiration and lung injury because these characteristics facilitate penetration of the HC into the bronchial tree. Vomiting, choking, or coughing during or after the ingestion increases the risk of aspiration, so induced emesis and gastric lavage should be avoided as they increase the risk of aspiration\u003csup\u003e1,3,5,6\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003ePulmonary penetration of HC results in both direct chemical injury to the surfactant system\u003csup\u003e7\u003c/sup\u003e and the alveolar epithelium, as well as indirect damage mediated by a secondary inflammatory response. At the alveolar level, HC become incorporated into the surfactant film, leading to surfactant inactivation and increased surface tension, thereby predisposing to alveolar collapse, atelectasis, and reduced pulmonary compliance. Owing to their lipophilic properties, HC also penetrate the cell membranes of type I and type II pneumocytes, causing epithelial injury with subsequent alveolar edema and protein-rich exudation, which represents the initial substrate for sterile inflammation. Collectively, these mechanisms result in chemical pneumonitis, which triggers a secondary inflammatory cascade characterized by the recruitment of inflammatory cells (including neutrophils and macrophages) and the release of pro-inflammatory cytokines that further exacerbate lung injury \u003csup\u003e6\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eEven minimal exposure to these substances appears to be sufficient to cause severe toxicity, including chemical pneumonitis; however, in most cases reported in the literature, as well as in the case just described, the actual amount of inhaled HC is unknown.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eClinical Manifestations of Hydrocarbon Inhalation\u003c/h3\u003e\n\u003cp\u003eImmediately after HC ingestion, approximately 46\u0026ndash;65% of children remain asymptomatic\u003csup\u003e8\u0026ndash;10\u003c/sup\u003e. The absence of initial symptoms suggests a lower risk of developing chemical pneumonitis and subsequent complications. When present, the most common symptoms are tachypnea (74% of cases), fever (63.5%), and cough (38%). Vomiting occurs in approximately 51% of cases and represents a clinical warning sign, as it is associated with an increased risk of inhalation and subsequent pulmonary injury\u003csup\u003e11\u003c/sup\u003e. Less frequently, central nervous system manifestations are observed, and include signs of either agitation or depression, such as drowsiness and restlessness (31%)\u003csup\u003e12\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eIn approximately 15% of pediatric patients with a history of HC exposure, symptoms of chemical pneumonitis appear within 6\u0026ndash;8 hours and progressively worsen over the first 48 hours\u003csup\u003e5,13,14\u003c/sup\u003e. This phase is characterized by increasing cough, tachypnea, and dyspnea, and in some cases, hemoptysis. In approximately 5% of cases complicated by pneumonitis, the clinical course is rapidly progressive and characterized by severe manifestations, including acute respiratory distress syndrome (ARDS), hypoxemia, and respiratory failure\u003csup\u003e15\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eBetween days 3\u0026ndash;10, approximately 90% of patients show clinical improvement, with gradual resolution of cough and dyspnea. However, in more severe cases, complications such as air-leak syndromes may occur. Persistence or recurrence of fever during this phase may indicate secondary bacterial superinfection.\u003c/p\u003e \u003cp\u003eBeyond the first 10 days, most patients experience gradual clinical recovery. In cases of severe pneumonitis, however, persistent lung disease may develop, with the appearance of pneumatoceles detectable on radiographic imaging\u003csup\u003e6,16\u003c/sup\u003e.\u003c/p\u003e\n\u003ch3\u003eLaboratory and instrumental findings\u003c/h3\u003e\n\u003cp\u003eOn laboratory evaluation, leucocytosis appears to be suggestive of pneumonia, as it was observed in 75% of patients with pneumonia, compared with 32% of patients without pneumonia following hydrocarbon ingestion\u003csup\u003e13\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eOn instrumental evaluation, a poor correlation was observed between clinical manifestations and chest radiographic findings, which may appear several hours after hydrocarbon ingestion\u003csup\u003e10,17,18\u003c/sup\u003e. Notably, most of symptomatic patients who had normal chest radiographs at presentation developed radiographic abnormalities later in the clinical course (60%), most commonly within 4\u0026ndash;8 hours after hydrocarbon ingestion. Bilateral interstitial pneumonitis is the most common radiographic pattern (53%), followed by unilateral interstitial pneumonitis (23%) and lobar pneumonia (9.5%)\u003csup\u003e13\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003ePneumatoceles is the most frequent complication of chemical pneumonitis (2\u0026ndash;4% of cases)\u003csup\u003e13,19\u003c/sup\u003e. Pneumatocele formation is thought to result from parenchymal necrosis combined with a check-valve mechanism in the small airways, leading to focal air trapping and the development of air-filled cystic spaces\u003csup\u003e19,20\u003c/sup\u003e. As in the case described, pneumatoceles may develop days after the toxic insult (typically 6\u0026ndash;10 days\u003csup\u003e6,21\u003c/sup\u003e, up to 15 days in the present case); therefore, close clinical monitoring and serial imaging during hospitalization are justified, particularly in the presence of clinical deterioration or the onset of new respiratory symptoms. Fortunately, these lesions are often transient in children, although complications (e.g., secondary infection or pneumothorax) may occur.\u003c/p\u003e\n\u003ch3\u003eManagement of Hydrocarbon Inhalation\u003c/h3\u003e\n\u003cp\u003eThere are no well-defined guidelines for the management of patients with hydrocarbon inhalation pneumonia, and the limited available recommendations are largely based on outdated retrospective studies \u003csup\u003e10,13,16\u0026ndash;19,22\u003c/sup\u003e. In the review by Makrygianni et al.\u003csup\u003e6\u003c/sup\u003e, it is suggested that all children who remain asymptomatic after hydrocarbon inhalation should be observed for 6\u0026ndash;8 hours in the he emergency department and undergo chest radiography. If they remain asymptomatic and the chest X-ray is normal, discharge home may be considered. Conversely, patients with radiographic abnormalities should be hospitalized for prolonged monitoring, even though approximately 95% of patients remain asymptomatic and have a benign clinical course\u003csup\u003e10\u003c/sup\u003e. Similarly, children who are symptomatic at presentation or who develop symptoms during the observation period warrant hospital admission, as the presence of symptoms is associated with an increased risk of chemical pneumonitis. Patients presenting with respiratory distress, altered mental status, and/or seizures should be evaluated for admission to the intensive care unit \u003csup\u003e13,16\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eManagement is primarily supportive and includes close monitoring of cardiorespiratory status, serial arterial blood gas analysis, and oxygen supplementation to correct hypoxemia when necessary\u003csup\u003e6\u003c/sup\u003e. In the presence of wheezing, inhaled bronchodilators may be considered.\u003c/p\u003e \u003cp\u003eThe use of antibiotics and the optimal timing for their initiation remain uncertain. In the retrospective descriptive study by Tenembaum et al.\u003csup\u003e1\u003c/sup\u003e, most children (52.3%) received prophylactic antibiotics, whereas 37.2% were hospitalized for observation without any specific therapy. When bacterial superinfection is suspected, empiric broad-spectrum antibiotic therapy (e.g., amoxicillin\u0026ndash;clavulanate, cefuroxime, or cloxacillin combined with gentamicin) should be initiated and subsequently adjusted according to microbiological findings\u003csup\u003e23\u003c/sup\u003e. In our case, empiric antibiotic therapy with amoxicillin\u0026ndash;clavulanate was started early after hospital admission because of progressive radiological abnormalities and a concomitant rise in inflammatory markers, which increased the suspicion of a possible bacterial superinfection.\u003c/p\u003e \u003cp\u003eThe use of systemic corticosteroids remains controversial\u003csup\u003e22,24,25\u003c/sup\u003e. Some studies suggest that corticosteroids may attenuate inflammation and potentially reduce the subsequent development of fibrosis; however, their use has also been associated with an increased risk of secondary infections. In a retrospective study by Sen et al. including 54 pediatric patients with HC inhalation pneumonia\u003csup\u003e22\u003c/sup\u003e, 18 children (33%) required admission to the intensive care unit for respiratory failure and were treated with systemic corticosteroids. Among these, 17 patients (94%) showed normalization of oxygen saturation within 24 hours, with no reported cases of secondary infection. However, the only randomized controlled trial available demonstrated no clinical benefit of systemic corticosteroids over placebo in children with mild-to-moderate hydrocarbon-induced lung disease, with no significant differences in fever duration, respiratory or heart rate, or length of hospital stay\u003csup\u003e25\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eWith regard to the management of severe disease, mechanical ventilation should be considered in cases of hypoxemia refractory to supplemental oxygen\u003csup\u003e16\u003c/sup\u003e. Given that pulmonary surfactant depletion represents one of the key pathogenetic mechanisms of hydrocarbon-induced pneumonitis, intratracheal administration of exogenous surfactant may also be considered\u003csup\u003e26,27\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eBeyond the initial chest radiograph obtained in the emergency department, we emphasize the importance of repeat chest imaging during follow-up in patients with HC inhalation pneumonia, particularly at 10\u0026ndash;14 days, in order to rule out the development of pneumatoceles\u003csup\u003e19\u003c/sup\u003e.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003ePrognosis of Hydrocarbon Inhalation\u003c/h2\u003e \u003cp\u003eFortunately, literature data from systematic reviews and poison center registries indicate a generally favourable prognosis for pediatric patients following HC inhalation\u003csup\u003e9,10,13,16\u003c/sup\u003e. Uncomplicated pneumatoceles typically resolve spontaneously over a period of weeks to months, whereas complicated pneumatoceles\u0026mdash;such as infected pneumatoceles, tension pneumatoceles, or those rupturing with resultant pneumothorax\u0026mdash;require prompt intervention\u003csup\u003e5,21\u003c/sup\u003e. Management primarily involves image-guided percutaneous drainage, with surgical resection considered in cases of multiple complicated lesions\u003csup\u003e28,29\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eIn pediatric patients with HC inhalation pneumonia, follow-up with a pulmonologist is consistently recommended to monitor for the potential development of small airway obstructive disease and loss of elastic recoil, both of which have been reported in the literature, albeit with variable prevalence\u003csup\u003e30,31\u003c/sup\u003e. In this context, patients may benefit from a course of inhaled corticosteroid therapy to reduce airway inflammation and the risk of small airway obstruction, as observed in our case. The mortality rate associated with HC inhalation is generally low (\u0026lt;\u0026thinsp;1%; 0.2\u0026ndash;0.5%) and is closely linked to the progression of severe pneumonia\u003csup\u003e6,9,10\u003c/sup\u003e.\u003c/p\u003e \u003c/div\u003e"},{"header":"Conclusions","content":"\u003cp\u003eAccidental hydrocarbon ingestion in children represents a significant cause of toxic exposure in the pediatric population and a potentially life-threatening event; however, evidence-based management guidelines remain limited\u003csup\u003e10,13,16\u0026ndash;19,22\u003c/sup\u003e. The available literature indicates that even minimal quantities of ingested hydrocarbons may result in severe toxicity, including chemical pneumonitis and progressive respiratory failure. Our case highlights a particularly severe presentation of hydrocarbon aspiration pneumonia, requiring admission to the pediatric intensive care unit and advanced respiratory support, thereby underscoring the potential for rapid and clinically significant deterioration and the need for close observation\u003csup\u003e5,13,14\u003c/sup\u003e. Therefore, we recommend in-hospital monitoring for at least 48 hours, even in initially asymptomatic patients.\u003c/p\u003e \u003cp\u003ePulmonary injury is primarily related to aspiration occurring during or shortly after ingestion. Radiological complications such as pneumatoceles may become apparent 6\u0026ndash;10 days following the acute event and can persist for up to six months\u003csup\u003e6,21\u003c/sup\u003e. In uncomplicated cases, pneumatoceles generally resolve spontaneously over weeks to months, regardless of the specific therapeutic interventions administered during the acute phase.\u003c/p\u003e \u003cp\u003eCareful post-discharge follow-up is warranted, as long-term outcomes are often favourable and demonstrate a substantial capacity for pulmonary recovery in the pediatric population. Consistent with the available literature, our patient also showed a completely favourable clinical evolution despite the severity of the initial presentation, with progressive respiratory recovery and no long-term sequelae observed during follow-up.\u003c/p\u003e \u003cp\u003eFurther reports of comparable cases may help to better define the clinical evolution and optimal management of these rare complications. In this context, collaboration and data sharing between different centers could facilitate the comparison of clinical experiences and contribute to improving therapeutic strategies.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHeart Rate\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSO2\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eSaturation of Oxygen\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eBP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBlood Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003epCO2\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePartial pressure of Carbon dioxide\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHCO3-\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBicarbonate ion\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eBE\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBase Excess\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eWBC\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eWhite Blood Count\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCRP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eC-reactive Protein\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eALT\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAlanine Transaminase\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCPAP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eContinuous Positive Airway Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eFiO2\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eFraction of Inspired Oxygen\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePEEP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePositive End-Expiratory Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eChest CT\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eChest Computed Tomography\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eClinical trial number: \u003c/strong\u003enot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding Statement:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received no external funding.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of interest:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eEthical Statement:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAccording to the italian directive (AIFA directorial decision of August 2024 ), single case report is not considered clinical research and therefore does not require formal approval by an Ethics Committee.\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAn informed consent was obtained from the parents of the patients to either describe the case report and use the pictures.\u003c/p\u003e\n\u003cp\u003eAll the authors approved the final manuscript for submission and agreed to the publication of this study\u003c/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eAcknowledgments:\u003c/strong\u003e\u003cbr\u003e The authors would like to thank the staff of the Pediatric Emergency Department, the Pediatric Intensive Care Unit, and the Pediatric Ward for their dedicated care of the patient.\u003c/p\u003e\n"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eTenenbaum A, Rephaeli R, Cohen-Cymberknoh M, Aberbuch D, Rekhtman D. Hydrocarbon Intoxication in Children: Clinical and Sociodemographic Characteristics. \u003cem\u003ePediatr Emerg Care\u003c/em\u003e. 2021;37(10):502-506. doi:10.1097/PEC.0000000000002111\u003c/li\u003e\n\u003cli\u003eGummin DD, Mowry JB, Beuhler MC, et al. 2023 Annual Report of the National Poison Data System\u0026reg; (NPDS) from America\u0026rsquo;s Poison Centers\u0026reg;: 41st Annual Report. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2024;62(12):793-1027. doi:10.1080/15563650.2024.2412423\u003c/li\u003e\n\u003cli\u003ePalmer SB, Spiller HA, Kistamgari S, et al. Hydrocarbon ingestions among individuals younger than 20 years old reported to United States Poison Centers, 2000\u0026ndash;2021. \u003cem\u003eInj Epidemiol\u003c/em\u003e. 2023;10(1):48. doi:10.1186/s40621-023-00461-6\u003c/li\u003e\n\u003cli\u003eGhezzi M, Odoni M, Testagrossa O, et al. Pneumonia in a Teenager Hiding a Fire-Eating Stunt. \u003cem\u003ePediatr Emerg Care\u003c/em\u003e. 2019;35(8):e147-e149. doi:10.1097/PEC.0000000000001316\u003c/li\u003e\n\u003cli\u003eThalhammer GH, Eber E, Zach MS. Pneumonitis and pneumatoceles following accidental hydrocarbon aspiration in children. \u003cem\u003eWien Klin Wochenschr\u003c/em\u003e. 2005;117(4):150-153. doi:10.1007/s00508-004-0304-9\u003c/li\u003e\n\u003cli\u003eMakrygianni EA, Palamidou F, Kaditis AG. Respiratory complications following hydrocarbon aspiration in children. \u003cem\u003ePediatr Pulmonol\u003c/em\u003e. 2016;51(6):560-569. doi:10.1002/ppul.23392\u003c/li\u003e\n\u003cli\u003eSchneider S, Sch\u0026uuml;rch D, Geiser M. Aspiration toxicology of hydrocarbons and lamp oils studied by in vitro technology. \u003cem\u003eToxicol Vitro Int J Publ Assoc BIBRA\u003c/em\u003e. 2013;27(3):1089-1101. doi:10.1016/j.tiv.2013.01.015\u003c/li\u003e\n\u003cli\u003eSheikh S, Chang A, Kieszak S, et al. Characterizing risk factors for pediatric lamp oil product exposures. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2013;51(9):871-878. doi:10.3109/15563650.2013.839028\u003c/li\u003e\n\u003cli\u003eMachado B, Cross K, Snodgrass WR. Accidental hydrocarbon ingestion cases telephoned to a regional poison center. \u003cem\u003eAnn Emerg Med\u003c/em\u003e. 1988;17(8):804-807. doi:10.1016/s0196-0644(88)80558-4\u003c/li\u003e\n\u003cli\u003eAnas N. Criteria for Hospitalizing Children Who Have Ingested Products Containing Hydrocarbons. \u003cem\u003eJAMA J Am Med Assoc\u003c/em\u003e. 1981;246(8):840. doi:10.1001/jama.1981.03320080026021\u003c/li\u003e\n\u003cli\u003eVictoria MS, Nangia BS. Hydrocarbon poisoning: a review. \u003cem\u003ePediatr Emerg Care\u003c/em\u003e. 1987;3(3):184-186. doi:10.1097/00006565-198709000-00014\u003c/li\u003e\n\u003cli\u003eTormoehlen LM, Tekulve KJ, Na\u0026ntilde;agas KA. Hydrocarbon toxicity: A review. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2014;52(5):479-489. doi:10.3109/15563650.2014.923904\u003c/li\u003e\n\u003cli\u003eLifshitz M, Sofer S, Gorodischer R. Hydrocarbon poisoning in children: a 5-year retrospective study. \u003cem\u003eWilderness Environ Med\u003c/em\u003e. 2003;14(2):78-82. doi:10.1580/1080-6032(2003)014[0078:hpicay]2.0.co;2\u003c/li\u003e\n\u003cli\u003eGupta P, Singh RP, Murali MV, Bhargava SK, Sharma P. Kerosene oil poisoning--a childhood menace. \u003cem\u003eIndian Pediatr\u003c/em\u003e. 1992;29(8):979-984.\u003c/li\u003e\n\u003cli\u003eYu MC, Lin JL, Wu CT, Hsia SH, Lee F. Multiple organ failure following lamp oil aspiration. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2007;45(3):304-306. doi:10.1080/15563650601072241\u003c/li\u003e\n\u003cli\u003eJayashree M, Singhi S, Gupta A. Predictors of outcome in children with hydrocarbon poisoning receiving intensive care. \u003cem\u003eIndian Pediatr\u003c/em\u003e. 2006;43(8):715-719.\u003c/li\u003e\n\u003cli\u003eThe WHO EMRO Pediatric Hydrocarbon Study Group, Cairo, Egypt, Bond GR, Pi\u0026egrave;che S, et al. A clinical decision rule for triage of children under 5 years of age with hydrocarbon (kerosene) aspiration in developing countries. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2008;46(3):222-229. doi:10.1080/15563650701801218\u003c/li\u003e\n\u003cli\u003eBeamon RF, Siegel CJ, Landers G, Green V. Hydrocarbon ingestion in children: a six-year retrospective study. \u003cem\u003eJACEP\u003c/em\u003e. 1976;5(10):771-775. doi:10.1016/s0361-1124(76)80307-3\u003c/li\u003e\n\u003cli\u003eHarris VJ, Brown R. Pneumatoceles as a complication of chemical pneumonia after hydrocarbon ingestion. \u003cem\u003eAm J Roentgenol Radium Ther Nucl Med\u003c/em\u003e. 1975;125(3):531-537. doi:10.2214/ajr.125.3.531\u003c/li\u003e\n\u003cli\u003eLeuchter D, St\u0026uuml;becke W, Oberschulte-Beckmann D. Pneumatozele nach Kohlenwasserstoffaspiration. \u003cem\u003eKlin P\u0026auml;diatr\u003c/em\u003e. 1998;210(06):422-424. doi:10.1055/s-2008-1043916\u003c/li\u003e\n\u003cli\u003eBergeson PS. Pneumatoceles Following Hydrocarbon Ingestion: Report of Three Cases and Review of the Literature. \u003cem\u003eAm J Dis Child\u003c/em\u003e. 1975;129(1):49. doi:10.1001/archpedi.1975.02120380031008\u003c/li\u003e\n\u003cli\u003eSen V, Kelekci S, Selimo H, et al. An evaluation of cases of pneumonia that occurred secondary to hydrocarbon exposure in children.\u003c/li\u003e\n\u003cli\u003eBalme KH, Zar H, Swift DK, Mann MD. The efficacy of prophylactic antibiotics in the management of children with kerosene-associated pneumonitis: a double-blind randomised controlled trial. \u003cem\u003eClin Toxicol\u003c/em\u003e. 2015;53(8):789-796. doi:10.3109/15563650.2015.1059943\u003c/li\u003e\n\u003cli\u003eGurkan F, Bosnak M. Use of nebulized budesonide in two critical patients with hydrocarbon intoxication. \u003cem\u003eAm J Ther\u003c/em\u003e. 2005;12(4):366-367.\u003c/li\u003e\n\u003cli\u003eMarks MI, Chicoine L, Legere G, Hillman E. Adrenocorticosteroid treatment of hydrocarbon pneumonia in children--a cooperative study. \u003cem\u003eJ Pediatr\u003c/em\u003e. 1972;81(2):366-369. doi:10.1016/s0022-3476(72)80315-9\u003c/li\u003e\n\u003cli\u003eMastropietro CW, Valentine K. Early administration of intratracheal surfactant (calfactant) after hydrocarbon aspiration. \u003cem\u003ePediatrics\u003c/em\u003e. 2011;127(6):e1600-1604. doi:10.1542/peds.2010-3229\u003c/li\u003e\n\u003cli\u003eHoroz OO, Yildizdas D, Yilmaz HL. Surfactant therapy in acute respiratory distress syndrome due to hydrocarbon aspiration. \u003cem\u003eSingapore Med J\u003c/em\u003e. 2009;50(4):e130-132.\u003c/li\u003e\n\u003cli\u003eDiBardino DJ, Espada R, Seu P, Goss JA. Management of complicated pneumatocele. \u003cem\u003eJ Thorac Cardiovasc Surg\u003c/em\u003e. 2003;126(3):859-861. doi:10.1016/S0022-5223(03)00367-2\u003c/li\u003e\n\u003cli\u003eZuhdi MK, Spear RM, Worthen HM, Peterson BM. Percutaneous catheter drainage of tension pneumatocele, secondarily infected pneumatocele, and lung abscess in children. \u003cem\u003eCrit Care Med\u003c/em\u003e. 1996;24(2):330-333. doi:10.1097/00003246-199602000-00024\u003c/li\u003e\n\u003cli\u003eGurwitz D, Kattan M, Levison H, Culham JA. Pulmonary function abnormalities in asymptomatic children after hydrocarbon pneumonitis. \u003cem\u003ePediatrics\u003c/em\u003e. 1978;62(5):789-794.\u003c/li\u003e\n\u003cli\u003eTaussig LM, Castro O, Landau LI, Beaudry PH. Pulmonary function 8 to 10 years after hydrocarbon pneumonitis. Normal findings in three children carefully studied. \u003cem\u003eClin Pediatr (Phila)\u003c/em\u003e. 1977;16(1):57-59. doi:10.1177/000992287701600109\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"children, hydrocarbon inhalation, chemical pneumonitis, pneumatoceles, pediatric pulmonology, pediatric intensive care","lastPublishedDoi":"10.21203/rs.3.rs-9226833/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9226833/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cb\u003eBackground\u003c/b\u003e\u003c/p\u003e \u003cp\u003eAccidental hydrocarbon ingestion is a common cause of pediatric toxic exposure, particularly among those under 6 years of age, and primarily causes injury through aspiration leading to chemical pneumonitis. Clinical presentation is variable, ranging from mild symptoms to severe respiratory failure, with potential early deterioration and rare delayed complications such as pneumatoceles.\u003c/p\u003e\u003cp\u003e\u003cb\u003eCase report:\u003c/b\u003e\u003c/p\u003e \u003cp\u003eWe report the case of a 17-month-old previously healthy boy admitted after accidental ingestion of printer fluid containing low-viscosity hydrocarbons. He initially presented with mild respiratory symptoms and stable vital signs but developed progressive chemical pneumonitis within hours, requiring Pediatric Intensive Care Unit admission and ventilatory support. The clinical course was complicated by bilateral pulmonary consolidations and subsequent development of large pneumatoceles, with gradual radiological resolution and complete clinical recovery at 6- and 12-month follow-up, without residual sequelae.\u003c/p\u003e\u003cp\u003e\u003cb\u003eConclusions\u003c/b\u003e\u003c/p\u003e \u003cp\u003eOur case illustrates that accidental hydrocarbon ingestion may lead to severe and progressive respiratory injury even after an apparently mild initial presentation, thus warranting close in-hospital observation for at least 48 hours. Although radiological complications such as pneumatoceles may develop several days after exposure, long-term outcomes are generally favorable, highlighting the remarkable capacity for pulmonary recovery in children and the importance of structured follow-up.\u003c/p\u003e","manuscriptTitle":"When curiosity turns toxic: accidental hydrocarbon aspiration in a pediatric patient - a case report with literature review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-23 15:10:17","doi":"10.21203/rs.3.rs-9226833/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-05-13T07:52:06+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"25946643337841693941475155432239275066","date":"2026-05-07T11:18:57+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"312713101811232289945165460593989023709","date":"2026-05-04T08:16:01+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-04-16T05:16:35+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-04-02T08:57:10+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-04-01T02:59:18+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-04-01T02:58:32+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Pediatrics","date":"2026-03-25T20:05:18+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"579335d6-8847-4179-bc12-a654d84d6b5b","owner":[],"postedDate":"April 23rd, 2026","published":true,"recentEditorialEvents":[{"type":"editorInvitedReview","content":"","date":"2026-05-13T07:52:06+00:00","index":54,"fulltext":""},{"type":"reviewerAgreed","content":"25946643337841693941475155432239275066","date":"2026-05-07T11:18:57+00:00","index":53,"fulltext":""},{"type":"reviewerAgreed","content":"312713101811232289945165460593989023709","date":"2026-05-04T08:16:01+00:00","index":43,"fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-04-23T15:10:17+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-23 15:10:17","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9226833","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9226833","identity":"rs-9226833","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}