Corrosive ingestion

Question 6 from the first paper of 2000 asks for the complications of corrosive ingestion, and Question 9 from the first paper of 2023 asked for the management options. The majority of these cases tend to be accidental, in children. The main things to look out for are airway injuries, hypovolemic shock and perforation of the oesophagus. The greatest harm is from alkaline liquids. The single most useful resource for this topic would have to be the LITFL page on this topic. Among the published literature, the 2014 article by Kyung Sik Park offers an excellent overview.  Unless otherwise stated, the information below is derived from this article.

Pathophysiological and aetiological considerations

Alkali ingestion

  • Alkaline substances are easier to swallow, as it hurts less than acid (they are a more common tool of suicide)
  • Alkaline material mainly damages the oesophagus, as the stomach contains neutralising acid.
  • Ingestion of alkaline substances leads to liquefactive necrosis, which does not stop until the alkaline substance is neutralized by the tissue fluids. It can eat its way into the mediastinum in this fashion.
  • This process includes protein dissolution, collagen destruction, fat saponification, cell membrane emulsification, and transmural thrombosis. Erythema and oedema occur within seconds.
  • Button type batteries contain alkaline substances and can also cause burns by creating a highly localised current (injury may occur within 4-6 hours)

Acid ingestion

  • Acidic materials usually do more harm to the stomach than the oesophagus
  • In contrast to alkali, ingestion of acid tends to result in coagulative necrosis, and the dessicated necrotic tissue forms an eschar which acts as a protective barrier preventing the propagation of acid.
  • The initial injury takes up to 2 weeks to run its course, at the end of which the oesophageal wall is thin and fragile; return to normality may take up to 3 months.
  • Stricture formation is a common complication

Complications of corrosive ingestion

As one might imagine, these scenarios are usually not consequence-free.

  • Airway:
    • Airway burns, leading to airway compromise
    • Potential acute tracheo-oesophageal fistula due to corrosive effect on oesophagus
    • Assessment and immediate airway control is a priority
    • Goldfranks Manual of Toxicologic Emergencies (2007, Chapter 100) recommends dexamethasone to reduce airway oedema (10mg), resorting to the use of authority ("most clinicians agree") but not offering any references.
    • Ideally, you will avoid tracheostomy. It interferes with future efforts to repair or resect the oesophagus.
  • Breathing:
    • Potential aspiration of caustic gastric/oesophageal contents, thus acute lung injury
    • Hypoxia may be present; supplemental oxygen may be required. NIV may be contraindicated in case of full-thickness oesophageal injury
  • Circulation:
    • Potential hypovolemic shock due to fluid loss into the corroded gut, or haemorrhage though ulcers
    • Need for rapid fluid replacement or surgical haemostasis
    • CVC access, as this patient is likely to require long-term TPN
  • Neurological state:
    • Potential for disorganised behaviour due to psychiatric condition, or obtundation due to shock
    • Analgesia issues need to be addressed
  • Electrolyte disturbance
    • Absorption of corrosive agent may result in electrolyte and acid-base disturbance.
  • Fluid balance
    • Likely, hypovolemia will exist and need correction
    • renal impairment may be present, with implications on drug dosing
  • Gastrointestinal problems:
    • Extent of corrosive damage will need to be assessed by CT and/or direct endoscopy (earlier is better, before significant tissue softenting makes endoscopy risky)
    • Perforation of hollow organs must be ruled out with CXR and/or CT
  • Specific issues
    • Decontamination by NG aspiration may be possible if it is safe to pass an NGT

Systemic consequences

The LITFL page on this topic contains an excellent list of corrosive substances which have systemic effects, which I will paraphrase here to simplify my own revision.

  • glyphosate  — metabolic acidosis, shock, multi-organ dysfunction
  • hydrofluoric acid — hypocalcemia
  • mercuric chloride  — renal failure, shock
  • oxalic acid — hypocalcemia, renal failure
  • paraquat — pulmonary fibrosis, multi-organ dysfunction and shock
  • phenol — coma, seizures, hepatotoxicity, renal failure
  • phosphorus — hepatotoxicity, renal failure
  • picric acid — renal failure
  • potassium permangante — methemoglobinemia, multi-organ failure
  • silver nitrate — methemoglobinemia
  • tannic acid — hepatotoxicity

Grading of severity of the oesophageal injury

  • Oesophageal injury can be graded (endoscopically) according to whether or not the burns are circumferential, ulcerated, or necrotic (Zargar et al, 1992). The grade of injury predicts the chances of stricture formation.
  • Grade I burns: oedema without ulcers. These carry no risk of stricture formation.
  • Grade II burns: ulceration, which may be circumferential. These burns lead to oesophageal stricture formation in approximately 75% of cases.
  • Grade III burns are deep ulcers and necrosis. These invariably progress to stricture formation.

Characteristic laboratory findings

  • Hydrochloric acid ingestion predictably produces a hyperchloraemic acidosis
  • Sulfuric acid ingestion may result in a high anion gap metabolic acidosis where the added unmeasured anion is the absorbed sulfate.
  • Lactic acidosis may result from any corrosive ingestion as a consequence of shock
  • DIC may develop

Management of corrosive ingestion

  • Intubation may be indicated for airway protection, in anticipation of swelling.
  • Fluid resuscitation to correct third space losses
  • Adequate analgesia (the pain is very severe)
  • Proton pump inhibitors
  • Antiemetics may be useful: emesis results in re-exposure to the agent.
  • Nasogastric tubes are either inserted early in the process, or are deferred until later (as is endoscopy)
  • Endoscopy is largely diagnostic (there is little you can do here endoscopically)
  • Perforated viscera are obviously in need of surgical repair
  • Oesophagectomy may become inevitable if the oesophagus is irreparably damaged or if severe strictures develop.
  • There is some controversy regarding the role of corticosteroids in the development of oesophageal strictures. It seems that stricture development is dependent mostly on the severity (depth) of the burn, and the steroids are useless in the setting of the most severe injuries.

Decontamination and neutralization

  • Generally speaking, this is either pointless or harmful.
  • Neutralisation reactions are exothermic, and may exacerbate the burns
  • Products of neutralisation may be either caustic (concentrated salt), toxic,  gaseous and rapidly expanding (increasing the risk of perforation), or all three.
  • One may think about diluting the swallowed substance by "chasing" it with something like water, but this is probably pointless unless it happens within moments of the actual toxic ingestion.
  • Charcoal is not indicated, as these substances do not tend to adsorb.

Exceptions to the rule

  • Substances with significant systemic toxicity may benefit from decontamination (to prevent that toxicity). These include zinc chloride (ZnCl2) and mercuric chloride (HgCl2). The corrosive damage is trivial compared to the systemic toxicity. Activated charcoal is the way to go.


Ramasamy, Kovil, and Vivek V. Gumaste. "Corrosive ingestion in adults." Journal of clinical gastroenterology 37.2 (2003): 119-124.

Kluger, Yoram, et al. "Caustic ingestion management: World Society of Emergency Surgery preliminary survey of expert opinion." World Journal of Emergency Surgery 10.1 (2015): 1-8.

Park, Kyung Sik. "Evaluation and management of caustic injuries from ingestion of acid or alkaline substances." Clinical endoscopy 47.4 (2014): 301-307.

Zargar, Showkat Ali, et al. "Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history." The American journal of gastroenterology 87.3 (1992): 337-341.