Corrosive Ingestion


Corrosive ingestion may be life-threatening due to airway compromise or GI perforation, or due to agent-specific systemic toxicity.

Commonly available corrosive agents include:

  • Sodium hydroxide — detergents, drain and oven cleaners, button batteries
  • Sodium hypochlorite — bleaches and household cleaners (unintentional ingestion in children is generally benign, dilute solutions less than 150 mL do not cause significant
  • corrosive injury)
  • Ammonia — metal and jewellery cleaners, anti-rust products
  • Hydrochloric acid — metal cleaners
  • Sulfuric acid — drain cleaners, car batteries
  • Button batteries — injury results from leakage of alkali, local electrical current discharge and direct pressure necrosis


  • ingestion of concentrated H2SO4 and NaOH solutions and solid preparations are associated with the severe corrosive injury
  • Ingestion of >60 mL of concentrated HCl leads to severe injury to the GI tract with necrosis and perforation, rapid onset of MODS and is usually fatal
  • Ingestion of <150 mL household bleaches containing dilute sodium hypochlorite does not cause significant corrosive injury
  • The absence of lip or oral burns does not exclude significant gastro-oesophageal injury
  • Assess if risk of systemic toxicity (see below)


  • Unintentional ingestion of household drain and oven cleaners or automatic dish-washing powders can cause severe corrosive injury.
  • Unintentional ingestion of household bleaches is usually benign.
  • Ingested button batteries may cause local corrosive injury if they lodge in the oesophagus


Direct chemical injury

  •  Extent depends on:
    — pH
    — concentration
    — volume ingested
  • Acidic agents cause protein denaturation resulting in coagulative necrosis.
  • Alkaline agents are more dangerous as they cause liquefactive necrosis resulting in deep and progressive mucosal burns.
  • Other corrosive agents may have reducing, oxidising, denaturing or defatting actions.

Some corrosive agents also have systemic effects, such as:

  • glyphosate (toxicity may be due to the herbicide’s polyoxyethyleneamine surfactant) — metabolic acidosis, shock, multi-organ dysfunction
  • hydrofluoric acid — hypocalcemia
  • mercuric chloride (inorganic mercury salts) — 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


Corrosive ingestion may result in immediate symptoms of injury to the gastrointestinal tract:

  • mouth and throat pain
  • drooling
  • odynophagia
  • vomiting
  • abdominal pain

Upper airway injury is the most important immediate life-threat. Laryngeal injury and edema presents with:

  • progressive stridor
  • hoarseness
  • respiratory distress

Look for evidence of complications — severe ingestions of concentrated acids may present with severe metabolic acidosis and shock.


Acute complications:

  • oral, oesophageal, gastric burns (varying thickness) – most effected = areas of anatomical narrowing (cricopharyngeal, diaphragmatic oesophagus, antrum, pylorus).
  • oesophageal, gastric perforation
  • shock
  • haemorrhage
  • mediastinitis
  • psychiatric behaviour management
  • organ failure
  • acidosis
  • external injury from corrosive exposure

Chronic complications

  • laryngopharyngo fibrosis with airway incompetence -> chronic aspiration
  • oesophageal fibrosis, stricture (30% with grade IIB or III injury), stenosis and pseudodiverticulum
  • gastric outlet obstruction
  • GORD
  • psychosocial problems
  • oesophageal carcinoma (risk increased 1000 times, may occur up to 40 years later)


  • Perform a chest x-ray and abdominal x-ray for evidence of perforation if suggestive symptoms or signs
  • endoscopy within 24 hours (unless asymptomatic at 4 hours)

The  endoscopic findings of corrosive injuries are graded as follows:

  • Grade 0 — normal
  • Grade I — mucosal edema and hyperemia
  • Grade IIA — superficial ulcers, bleeding and exudates
  • Grade IIB — deep focal or circumferential ulcers
  • Grade IIIA — focal necrosis
  • Grade IIIB — extensive necrosis


Life threats

  • airway compromise
  • GI perforation and sepsis
  • Systemic toxicity in special cases


  • Treat systemic toxicity if present:
    — hypocalemia -> calcium
    — methemoglobinemia -> methylene blue
    — paraquat -> avoid excess O2

Supportive care and Monitoring

  • keep the patient NBM if symptomatic, pending endoscopic assessment.
  • Do not insert a nasogastric tube until cleared of gastrointestinal injury (e.g. endoscopy)
  • Antibiotics is evidence of perforation
  • no role for coricosteroids (do not reduce strictures, may increase risk of perforation and sepsis)


  • Rinse the mouth with water as an immediate first aid measure.
  • do not induce vomiting
  • do not administer oral fluids
  • do not administer activated charcoal
  • do not attempt pH neutralisiation
  • do not perform gastric lavage or insert an nasogastric tube (until endoscopy is performed)

Enhanced Elimination and Antidotes

  • nil


  • if asymptomatic at 4 hours post-ingestion -> perform a trial of oral fluids and discharge if well tolerated  (avoid discharging a child at night)
  • Some experts advocate endoscopy following corrosive ingestion even in the asymptomatic patient
  • If symptomatic (e.g. throat pain, drooling, pain on attempting to swallow his own saliva, or has vomiting or abdominal pain) -> keep NBM and admit for observation and an endoscopy within 24 hours
  • If airway compromise -> secure the airway and admit ICU
  • If GI perforation, sepsis or hemodynamic instability -> urgent surgical assessment and ICU admission

References and Links

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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