Chloramine gas can be generated by mixing bleach, which contains sodium hypochlorite, with ammonia. Similar to chlorine gas, inhaling chloramine can cause a range of respiratory symptoms, from mild mucosal irritation to acute respiratory failure. In severe cases, exposure can be fatal. Both chlorine and chloramine have historically been used as chemical warfare agents. Most incidents involving chlorine-containing substances occur due to the improper use of household cleaning products or the accidental mixing of incompatible agents [1] [2] . While chlorine gas typically forms when bleach is combined with an acidic cleaner (e.g., drain cleaner), chloramine gas arises from mixing bleach with ammonia, producing mono-, di-, and trichloramine compounds (NH₂Cl, NHCl₂, and NCl₃). These compounds are highly irritating and react with moisture in the airways to form hydrochloric acid and reactive oxygen species, leading to epithelial injury and inflammation [3] . Despite the widespread domestic use of these products, case reports of chloramine intoxication remain rare, and data on its effects during pregnancy are lacking. A comprehensive review of the extant literature in the PubMed database revealed that this is the first reported case of chloramine poisoning in a pregnant patient resulting from the accidental mixing of bleach and ammonia.

A 27-year-old biologic female (G3P2A0) who was five months pregnant presented to our emergency department with dyspnea and chest pain. Approximately 15 minutes after accidentally using a mixture of bleach (sodium hypochlorite) and ammonia to clean her bathroom with the window and door closed, she developed symptoms. Thirty minutes after the onset of symptoms, she arrived at the emergency department in respiratory distress. Her past medical history was unremarkable aside from active tobacco use. She reported no allergies, was not taking any chronic medications and had no significant comorbidities.

On initial assessment, her airway was patent. However, she exhibited overt respiratory distress, with a respiratory rate of 40 breaths per minute, an oxygen saturation of 86% on ambient air and bilateral wheezing and crackles on auscultation. Her heart rate was 104 beats per minute (sinus tachycardia), her blood pressure was 142/81 mmHg and her capillary refill time was two seconds. No cardiac murmurs were audible. She was alert and neurologically intact. Her temperature was 36.6˚C. Physical examination confirmed a gravid uterus consistent with approximately five months of gestation. There was no rash, conjunctivitis or peripheral edema.

The patient was immediately transferred to a resuscitation room. Oxygen was initially administered via a non-rebreather mask at a flow rate of 15 liters per minute. Bronchodilator therapy (aerosolized salbutamol and ipratropium bromide) was initiated. Two peripheral intravenous lines were established. Initial arterial blood gas analysis revealed the following: pH: 7.4; pCO₂: 29 mmHg; pO₂: 67 mmHg; ${\text{HCO}}_3^{-}$: 18 mmol/L, lactate: 1.1 mmol/L. An electrocardiogram (ECG) showed sinus tachycardia at 110 beats per minute without arrhythmia or signs of acute ischaemia. Point-of-care ultrasound (POCUS) performed by a clinician with expertise in point-of-care ultrasound revealed bilateral lung sliding, diffuse B-lines without pleural effusion, a hyperdynamic left ventricle without evidence of pericardial effusion, right ventricular dilation, or D-shaping. Given the pregnancy and a clear clinical picture confirmed by POCUS, no chest X-ray was performed.

The fetal heart rate was 135 beats per minute. Laboratory results were unremarkable, showing no signs of infection and indicating normal cardiac enzyme levels and preserved renal function.

A differential diagnosis of acute pulmonary edema was considered due to the presence of acute respiratory distress in combination with a bilateral B-line pattern on POCUS. Given the temporal correlation between the onset of symptoms and exposure to chloramine gas, we proposed a diagnosis of acute non-cardiogenic pulmonary edema secondary to chloramine inhalation. Other differential diagnoses, such as primary cardiogenic pulmonary edema, were considered less probable due to the absence of a known medical history of cardiac disease in an otherwise healthy female patient, the absence of acute ECG abnormalities, and a POCUS examination demonstrating normal left ventricular function on visual estimation. The likelihood of bilateral pneumonia was considered low due to the absence of symptoms such as productive cough or fever. The patient’s history indicated that alternative etiologies for acute non-cardiogenic pulmonary edema, including neurological conditions, drowning, drug-induced causes, aspiration, or transfusion-related events, were considered unlikely.

Non-invasive ventilation was initiated using continuous positive airway pressure (CPAP) with positive end expiratory pressure (PEEP) at 8 cm H₂O and FiO₂ at 100 %. Additionally, intravenous methylprednisolone (40 mg) and furosemide (20 mg) were administered. Over time, the FiO₂ requirement was gradually reduced to 40 %. After two hours of CPAP use in our emergency department, non-invasive ventilation was discontinued and oxygen was administered via a nasal cannula at a flow rate of 2.5 L/min. The patient reported significant improvement in her symptoms and expressed a wish to be discharged. Our reassuring fetal findings were confirmed by a bedside obstetric transabdominal ultrasound examination.

Following a multidisciplinary consultation, she was admitted to the pulmonology ward for further monitoring. Over the subsequent 24 hours, pulmonary function testing and ongoing fetal surveillance revealed no abnormalities. She was discharged in a stable condition with no recurrence of symptoms. The patient gave birth to a healthy child. At the nine-month follow-up, the patient reported complete resolution of symptoms. Pulmonary function testing was not repeated.

Our patient exhibited features consistent with severe, chlorine-related inhalation injury. These features included the rapid onset of dyspnea and hypoxemia, as well as the presence of bilateral B-lines on ultrasound, despite the absence of underlying cardiac pathology. These features are suggestive of acute, non-cardiogenic pulmonary edema. The following discussion addresses the epidemiology, clinical spectrum, management strategies (including current controversies), and potential fetal implications in the context of the available literature.

Acute chloramine inhalation from mixing household cleaning products (e.g., bleach and ammonia) can manifest as acute non-cardiogenic pulmonary edema in a patient who is five months pregnant. The appropriate initial management includes early removal from the source of exposure, supplemental oxygen, and non-invasive ventilation (e.g., CPAP). For pregnant patients, the priority should be maternal stabilization and fetal monitoring. There is limited high-quality evidence supporting the use of bronchodilators, corticosteroids, or nebulized sodium bicarbonate. Observation for at least 24 hours is recommended in cases of moderate exposure. Long-term follow-up may reveal chronic pulmonary diseases.

Niels Oversteyns: Conceptualization and writing. Hans De Puydt: Writing. Stefanie Vandervelden: Writing.

Written informed consent was obtained from the patient to publish this report in accordance with the journal’s patient consent policy.