European Journal of Cardiovascular Medicine

Hydrochloric acid (HCl) is a widely used industrial and household chemical known to release corrosive, irritant vapors upon exposure to air. These acidic fumes can cause significant respiratory tract injury when inhaled, leading to chemical pneumonitis and, in severe cases, acute respiratory distress syndrome (ARDS).2,3 Inhalational injury from chemicals such as chlorine and hydrochloric acid has been described predominantly in occupational settings; however, cases from household exposures are emerging, especially in industrial hubs, where concentrated HCl products pose public health risks due to accidental inhalation during routine cleaning.4,5

Diagnosis of HCl-induced chemical pneumonitis relies primarily on clinical history, symptomatology, and radiological evidence because no specific biomarkers exist for HCl inhalation.7 Treatment remains predominantly supportive, encompassing oxygen therapy, corticosteroids, bronchodilator nebulization, and prophylactic antibiotics to prevent secondary infections.9,10

Case Presentation

A 41-year-old woman from north-east Rajasthan, exposed to 31% concentrated hydrochloric acid fumes for approximately one minute while cleaning a bathroom floor in a poorly ventilated area, developed acute shortness of breath, cough, and blood tinged sputam production.

On admission: SpO₂ of 89% on room air, pulse rate 124 bpm, blood pressure 126/84 mmHg, on auscultation bilateral crepitations and rhonchi in middle and lower lung zones.

Treatment included humidified oxygen via nasal prongs at 6 L/min (FiO2 44%), nebulized bronchodilators, intravenous methylprednisolone 40 mg twice daily, and prophylactic intravenous antibiotic. Symptomatic treatment continued for 7 days.

Laboratory investigations showed leukocytosis with neutrophilia, mild anemia (Hb 9.3 g/dL), elevated CRP (9.7 mg/L), and slightly raised AST, ALT, ALP. Arterial blood gases revealed mild hypoxemia (PaO2 80 mmHg) with pH 7.43. Infectious workup including tuberculosis serology was negative.

Chest X-ray and high-resolution CT thorax demonstrated diffuse alveolar opacification and GGO noted in both lungs in perihilar region with sparing of sub pleural & lung apices s/o diffuse alveolar hemorrhage consistent with chemical pneumonitis.

By day 7, SpO2 improved to 97% on room air, pulse rate reduced to 84 bpm, blood pressure normalized at 124/82 mmHg. Mild crepitations remained bilaterally. The patient was stable and discharged with inhaled corticosteroids and pulmonary rehabilitation and follow-up.

HCl inhalation causes chemical pneumonitis through corrosive injury to airways and alveoli, causing inflammation, edema, hemorrhage, and impaired gas exchange. Severity relates to concentration, exposure duration, and ventilation.2,7 Supportive management is key. Oxygen supplementation corrected hypoxemia via nasal prongs (FiO2 44%).9 Nebulized bronchodilators relieve airway obstruction; corticosteroids reduce inflammation and lung injury progression.8,10 Prophylactic antibiotics prevent secondary infection.1 Inhaled corticosteroids combined with bronchodilators improve lung compliance and oxygenation after chlorine or HCl inhalation.10,11 Nebulized sodium bicarbonate may neutralize acid fumes, reducing lung injury, but lacks standardized dosing and clear evidence.12-14 Diffuse alveolar hemorrhage visible on HRCT indicates severe membrane injury. Timely supportive care enabled near-complete recovery by day 7. Long-term follow-up is important for detecting reactive airway dysfunction syndrome, which requires prolonged bronchodilator therapy.2,9 This case adds to sparse Indian data on household HCl inhalation injuries, highlighting need for public education about safe chemical use, ventilation, protective equipment, and clinician awareness for early recognition and multidisciplinary care.4,9

Brief household exposure to concentrated HCl fumes can cause serious chemical pneumonitis and diffuse alveolar hemorrhage. Early diagnosis through history and imaging combined with supportive oxygen, corticosteroids, bronchodilators, and antibiotics leads to good outcomes. Public health measures and clinician vigilance are key to reducing morbidity.

Acknowledgement

I would like to thank Dr. Ayush Senger, Dr. Jay Manchanda for their guidance in paper writing.

No conflict of interest or financial support declared.

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