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Correspondence |
Montréal, Québec
To the Editor:
Intoxication by bleach ingestion causes mainly gastrointestinal irritation and ear, nose and throat lesions. Usually bleach ingestions are benign, leading most toxicologists to advocate ambulatory conservative management. Rare case reports of fatal bleach ingestions with hypernatremia and hyperchloremia have been reported.1 Chemical adult respiratory distress syndrome (ARDS) has been reported following ingestion of numerous agents such as organic solvents, fluoride or chlorine containing solutions. We present a case of ARDS following bleach ingestion and discuss the unique mechanism of bleach induced lung injury.
A 33-yr-old woman was admitted to the emergency department following an assault with sodium hypochlorite; presumably, she aspirated bleach. She presented without respiratory symptoms, a respiratory rate of 18 breaths•min–1, a saturation of 97% under room air. The first chest x-ray performed two hours after intoxication (Figure 1A
) showed a bilateral bi-basal infiltrate suggestive of aspiration pneumonia. Initial biochemistry showed a sodium of 139 mmol•L–1, a potassium of 3.8 mmol•L–1 and a chloride of 107 mmol•L–1 and liver tests were normal. Complete blood count showed a white blood cell of 17.8 G•L–1 with 75% neutrophils, 10% stab forms, vacuolated neutrophils with toxic granules.
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) showed progression to an ARDS which worsened during the next 24 hr. Evolution was marked by slow recovery requiring 26 days of mechanical ventilation. There was no hypernatremia or hyperchloremia. Bleach is a potent oxidant and has been used as a trigger for experimental lung injury. Infusion of sodium hypochlorite in an isolated rabbit lung induces a depletion of reduced glutathione.2 This oxydative stress on pulmonary neutrophils triggers an endothelial response with increased pulmonary artery pressure, increased alveolar permeability and ARDS.3 Although rabbit models involved perfusion of the lungs with hypochlorite containing perfusate, aspiration of bleach could also induce an alveolar neutrophil oxydation and ARDS.
Bleach is also a strong reagent in acids: ingestion of sodium hypochlorite reacts with gastric hydrochloric acid to form chlorine gas. Very small amounts of inhaled chlorine may cause acute lung injury: in rats, exposure to 500 ppm of chlorine during ten minutes, is able to reverse the alveolar fluid shift from absorption to massive translocation.4 Microvascular permeability increased by 150% and extravascular lung water doubled.
Aside ENT and gastrointestinal irritation, clinicians should be aware of the unique direct and indirect pulmonary toxicity of this common household product.
References
1 Ross MP, Spiller HA. Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis.Vet Hum Toxicol 1999; 41: 82–6.[Medline]
2 Hammerschmidt S, Buchler N, Wahn H. Tissue lipid peroxidation and reduced glutathione depletion in hypochlorite-induced lung injury. Chest 2002; 121: 573–81.
3 Wahn H, Hammerschmidt S. Influence of cyclooxygenase and lipoxygenase inhibitors on oxidative stress-induced lung injury. Crit Care Med 2001; 29: 802–7.[Medline]
4 Menaouar A, Anglade D, Baussand P, et al. Chlorine gas induced acute lung injury in isolated rabbit lung. Eur Respir J 1997; 10: 1100–7.[Abstract]
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