A 3-year-old male was admitted to the ED after his mother had witnessed him drinking caustic soda. Whilst cleaning the house she had accidentally left open a cupboard where he was able to access drain cleaner containing the substance.
The patient had been triaged by the nursing team (who had consulted TOXBASE) and an initial 2ml/kg oral bolus of milk had been given.
Examination revealed an ulcerated tongue, mild soft palate swelling, a blister to his left posterior tonsillar pillar and excessive oral secretions that required regular oropharyngeal suction. Respiratory, cardiovascular and abdominal examinations were unremarkable.
After assessment and management by ED and anaesthetic teams, there was no worsening of the symptoms and the patient was subsequently transferred to a tertiary centre for further management under the joint care of burns and ENT.
Caustic soda (or sodium hydroxide) ingestion continues to be a major health hazard in developed and developing countries despite continuing educational programs and legislation limiting the strength and availability of corrosive substances (Riffat and Cheng 2009).
It is a manufactured chemical which odourless, white in colour and mainly used in a solid or 50% solution (HPA 2014). Main uses include the production of other industrial chemicals such as in the pulp, paper, metal, food and textile industries, in water treatment processes and various household products including drain and oven cleaners (HPA 2014).
Cases presenting to healthcare providers mainly occur as a result of accidental indigestion from unmarked containers within reach of children at home (Riffat and Cheng 2009). Due to the appearance and the odourless nature, it can make this corrosive chemical appear benign and potentially appealing to a young child.
Caustic ingestions commonly occur in children less than six years and the incidence peaks at around two years when children develop skills of localisation but cannot discriminate between harmless and harmful substances (Riffat and Cheng 2009). Due to the accidental nature of ingestions, the case fatality rate for these patients is significantly less than that of adolescents and adults (Riffat and Cheng 2009).
Substances with a pH <2 or >12 are extremely corrosive (caustic soda has a pH of 13.5-15) and the clinical spectrum of paediatric caustic ingestion can vary from mild damage to potentially fatal sequela (Riffat and Cheng 2009).
During an exposure the mast cells play a key role in the inflammatory process and when activated, histamine is rapidly released into the local microenvironment, dilating post-capillary venules and activating the endothelium which increases blood vessel permeability leading to localised oedema (Tortora and Grabowski 2002). This is maximal at 24 hours post injury (Ahrns 2004), although pulmonary oedema may take up to 36 hours to develop (PHE 2015).
In light of this oedema, early intubation is often required in both adults and children when there is evidence of airway or breathing abnormalities. Whilst this case appeared to involve isolated upper airway exposure (and subsequent injury), it is important to thoroughly assess for evidence of chemical inhalation and lung injury and be aware that they may be progressive over time, making reassessment.
Subtle signs of chemical inhalation may include:
– shortness of breath
– sore thoat
– chest tightness
Additional points of interest:
An ECG should be performed on all patients with alkali ingestion as it can cause serious cardiac dysrhythmias (Ward 2013), in particular QT prolongation occurring due to electrolyte disturbance (TOXBASE 2013).
Early endoscopy (within 24 hours) is recommended to grade the severity of the injury (Riffat and Cheng 2009), as the long-term effects of ingestion include oesophageal strictures and an increased risk (3,000 times higher) of developing squamous cell carcinoma in patients with oesophageal lesions (Andreoni et al 1995).
Caustic soda to the aero-digestive tract remains a significant medical and social concern despite efforts to minimise the hazards of caustic household products.
Initial pre-hospital and ED management of ingestion requires careful and meticulous examination combined with specific guidance from specialist resources (e.g. Toxbase), once the substance has been identified.
Clinicians should consider the immediate life threatening nature and how this is managed, but also the wider issues of health and safety in the home, safeguarding and education.
Ahrns, K (2004) Trends in burn resuscitation: Shifting the focus from fluids to adequate endpoint monitoring, edema control, and adjuvant therapies. Critical Care Nursing Clinics of North America: Vol 16 pp 75–98. Cited in: Latenser, B (2009) Critical Care of the Burn Patient: The First 48 hours. Critical Care Medicine: Vol 37 Issue 10 p 2819-2826.
Andreoni, B., Farina, M & Biffi, R (1995) Esophageal perforation and caustic injury: Emergency management of caustic ingestion. Surgery Today: Vol 25 Issue 7 p 119–124.
Tortora and Grabowski (2002) Principles of Anatomy and Physiology 10th Ed. John Wiley and Sons: USA.