Chemical pneumonitis in a 9-year-old following chlorine gas exposure

Abstract

A previously fit and well 9-year-old boy developed shortness of breath and chest pain after playing with friends on a building site where bonfire materials were being collected. Firstline investigations failed to explain his symptoms, which worsened over the next 24 hours, necessitating endotracheal intubation and mechanical ventilation. When public health and the police retraced his steps, they found barrels of sodium hypochlorite and red diesel at the bonfire site, which when mixed had the potential to form chlorine gas leading to the diagnosis of a chemical pneumonitis secondary to chlorine gas inhalation. Supportive care was continued, and he was successfully extubated after 48 hours. At 6-week follow-up, he had no ongoing pulmonary symptoms.

Background

While chlorine gas has been used as a chemical weapon, most cases of poisoning now come from mixing of household cleaners, occupational exposure and transport or storage accidents. Sodium hypochlorite dissolved in water is more commonly known as bleach and can be household or industrial strength. Sodium hypochlorite is a strong oxidizer and, when mixed with organic materials such as diesel fuel oil, undergoes an exothermic reaction that generates heat and releases chlorine gas, sometimes violently.¹ As the child in this case presented with classical signs and symptoms of chlorine gas poisoning, this case should help raise awareness of this uncommon but potentially life-threatening diagnosis.

Case presentation

A 9-year-old boy presented to the emergency department of a tertiary paediatric hospital with a 12 hours history of non-productive cough, shortness of breath and central chest pain. His only past medical history was group B strep sepsis in the neonatal period, and more recently, he had been started on omeprazole for epigastric pain. His symptoms developed the night before when he was outside playing with friends on a building site where bonfire materials were being collected, and the symptoms increased in severity overnight. At presentation, he denied any inhalation or ingestion of any substances. His parents did not notice any unusual smell when he came home, and there were no complaints of eye irritation or stinging of mucosal membranes. No focal neurological symptoms, but the patient noted his limbs to feel ‘heavy’.

At presentation, he had a low-grade fever of 37.2°C, heart rate was 165 bpm, respiratory rate was 50 breaths/min and peripheral oxygen saturations were 93% in room air. On examination, heart sounds 1+2 were heard with no added sounds or murmurs. He had signs of respiratory distress with indrawing and recession. On auscultation of his chest, wide spread expiratory wheeze was noted. His abdominal and ENT exam were unremarkable.

Investigations

He had a chest radiograph performed (figure 1), which was unremarkable, apart from some bronchial wall thickening bilaterally. An ECG showed sinus tachycardia at 169 bpm, but no other abnormality. An echocardiogram was performed, which demonstrated a structurally normal heart with good function.

Figure 1.

Chest radiograph on admission.

Initial blood work showed haemoglobin 138 g/L, white cell count 15.2×10⁹/L, platelets 207×10⁹/L (neutrophils 12.8×10⁹/L, lymphocytes 0.8×10⁹/L), sodium 139 mmol/L, potassium 3.2 mmol/L, urea 3.1 mmol/L, creatinine 47 umol/L, C-reactive protein 27.2 mg/L and high-sensitivity troponin T <3 ng/L. A venous blood gas showed a lactic acidosis—pH 7.30, pCO₂5.3 kPa, PO₂6.4 kPa, bicarbonate (Bic) 19.6 mmol/L, base excess (BE) −6.3 and lactate 5.6 mmol/L. Urine screen for drugs of abuse was negative. Blood cultures and nasal swab for respiratory strip were sent.

Treatment

The initial working diagnosis was a lower respiratory tract infection with wheeze, and he was treated with intravenous ceftriaxone, oral prednisolone and nebulised bronchodilators, before escalating to intravenous magnesium and aminophylline when his symptoms failed to respond. Following the aminophylline loading dose, his chest pain worsened, and he was noted to have developed an erythematous blotchy rash. He was given intramuscular epinephrine, intravenous hydrocortisone and chlorpheniramine for possible anaphylaxis. Following this, he still had marked respiratory distress, and his blood gas had deteriorated further (lactate 9.9 mmol/L), so paediatric intensive care admission was organised.

He was transferred to the paediatric intensive care unit where high-flow nasal cannula oxygen therapy was started at 40 L/min. Antibiotic cover was broadened to cover atypical organisms with clarithromycin, and oseltamivir was added to cover influenza. Initially, the high-flow oxygen provided some benefit, and both his work of breathing and lactic acidosis improved. However, the following morning, his oxygen requirements had increased, he was requiring 90% oxygen to maintain oxygen saturations >92%, and endotracheal intubation was uneventfully performed with good effect.

At this stage, it became clear that some of the other children who had been at the bonfire site had developed similar but milder symptoms, which prompted public health involvement and a site inspection by the police and fire service. When the bonfire site was visited, chemical barrels were found, which had been illegally dumped. These barrels contained sodium hypochlorite and red diesel, which if mixed could result in the liberation of chlorine gas. There was no evidence on the scene to prove mixing had occurred. Site control and removal of substances were the responsibilities of the police service and landowner or city council.

Outcome and follow-up

Supportive management was continued, and he was successfully extubated to humified oxygen after 48 hours of mechanical ventilation. His blood and secretion cultures were negative, allowing antibiotics and oseltamivir to be discontinued. He completed a 5-day course of steroids and was discharged home 5 days after presentation. On further discussion with the patient and his parents, he admitted to mixing the chemicals found at the site by pouring them onto an abandoned mattress and leaning over to smell them.

He was reviewed at outpatient clinic 6 weeks later and was doing very well. Immediately postdischarge from hospital, he had regular headaches; however, these had reduced in frequency, and he had no ongoing respiratory symptoms. Mast cell tryptase sent during the first 24 hours was noted to be normal.

Discussion

Although chlorine gas was first synthesised by Jan Baptist van Helmont in 1630, it was Carl Wilhelm Scheele in 1774 who first studied it in detail, noting that it was a dense yellow-green gas with a strong odour.² He discovered that it had a bleaching effect and was poisonous. It has been used for both these properties in the past, with Claude Louis Berthollet using it to first bleach textiles in 1785, before converting it to a liquid sodium hypochlorite in 1789, which is still used as household bleach today.² Sodium hypochlorite can also be found in laundry detergents and surface cleaners. Although stable as a liquid at room temperature, when sodium hypochlorite is either heated or mixed with an acid, chlorine gas is released.³ Chlorine gas was first used as a chemical weapon by the Germans in 1915 during World War I.⁴ Although it has been used as a chemical weapon in a number of wars since World War I, today, the most common sources of chlorine gas poisoning come from mixing of household cleaners, occupational exposure and transport or storage accidents.⁵

As chlorine is in a gaseous state at room temperature, ingestion is uncommon, and most poisoning episodes involve injury to the eyes, skin or respiratory tract from direct contact with the irritant gas.⁶ Like with most poisons, the extent of the injury is determined by both the amount of the poison and the duration of exposure.⁷ At less than 15 ppm of chlorine gas, symptoms are generally limited to mucous membrane irritation, above 30 ppm tends to cause a chemical pneumonitis with immediate onset of cough, chest pain and shortness of breath, and exposure to concentrations greater than 400 ppm normally causes death within an hour.⁸ The exact mechanism of injury is unclear; however, it is believed that the formation of hypochlorous and hydrochloric acid and generation of free oxygen radicals lead to cellular injury.⁹

If a patient with chlorine gas exposure presents for emergency care, it is important that staff wear personal protective equipment.⁶ Decontamination should ideally be performed at the scene; however, if it has not been performed already, resuscitation should be performed prior to decontamination.⁶

Management of an inhalational injury is largely supportive with administration of oxygen and treatment of any bronchospasm with nebulised bronchodilators and steroids.⁶ Due to the smaller diameter of the airway in children, where even a small amount of oedema can cause significant symptoms, early endotracheal intubation should be considered if stridor is present. Chemical pneumonitis can cause pulmonary oedema, which is best treated with the use of positive pressure support such as continuous positive airway pressure or invasive ventilation as required.⁶ Due to the direct lung injury, patients are at risk of developing acute respiratory distress syndrome.¹⁰ Some references suggest nebulised sodium bicarbonate as a possible therapy for chlorine gas inhalation in an attempt to neutralise any acid produced on the surface of the pulmonary epithelium. While no adverse effects from this therapy were reported, the evidence is inconclusive regarding its efficacy.¹¹

On reviewing the literature, the majority of previously published cases involving chlorine gas poisoning have been caused by occupational exposure or transport accidents. An accidental release of chlorine fumes from the swimming pool chlorinating system in a recreation centre in Rome in 1998 led to a total of 134 children and 126 adults being affected.¹² The most common symptoms in children were respiratory and included shortness of breath, cough and wheeze. Children with chronic respiratory disease tended to a higher incidence of all symptoms compared with healthy children. Ongoing respiratory symptoms were reported in 21% of affected children at 15–30 days following exposure, and this was also higher in those with a history of chronic respiratory disease.

In 2005, a train in South Carolina was derailed leading to the release of 42–60 tons of chlorine gas.¹³ Eight people died at the scene, and 71 people required hospital admission for treatment. Of those admitted to hospital, 25 patients were admitted to intensive care, and one person died in hospital. On demographic characteristic analysis, no characteristics were significantly associated with the need for hospitalisation or intensive care support. This population of patients is currently being followed up to determine long-term effects.

In 2013, the accidental release of chlorine gas from a factory in South Korea affected 211 people, two of which required hospitalisation.¹⁴ Out of the 209 patients who did not require hospital admission, the most commonly reported symptoms were headache, eye irritation, nausea and sore throat. Of the two patients who required admission, the first developed dyspnoea after exposure, and the second developed cough, chest discomfort and palpitations. Both were diagnosed with chlorine-induced reactive airways dysfunction syndrome; however, there was no follow-up to determine if there were long-term effects.

There is evidence that acute exposure to chlorine gas can lead to long-term problems. A case series of three patients with occupational exposure to chlorine gas showed that all three patients developed long-term symptoms.¹⁵ Two cases of acute high-dose chlorine gas inhalation in previously well men resulted in chronic respiratory disease. In the first case, the patient developed steroid dependent asthma, requiring six hourly nebuliser therapy, and the other developed bilateral bronchiectasis with episodes of exacerbation. The third case in this series was of repeated inhalations of chlorine gas sustained while working in the chemical industry. The patient developed chronic cough and wheeze during his career, and spirometry at retirement demonstrated an obstructive pattern.

Learning points.

• Public education on the dangers of inappropriate disposal, storage or mixing of bleach is important for the primary prevention of chloride gas poisoning.

• If a patient fails to respond to treatment as you would expect, consider an alternative diagnosis.

• Inhalation of a toxic gas should be considered in a patient who presents with sudden onset of symptoms affecting the eyes, skin or respiratory tract.

• Children with inhalational airway injury will tolerate airway oedema poorly, and securing the airway by endotracheal intubation should be considered at an early stage.

• The role of other agencies such as public health or the police in assisting with making a diagnosis should not be forgotten about.