OVERVIEW

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

RISK ASSESSMENT

• 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)

Children

• 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

MECHANISM

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

CLINICAL FEATURES

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.

COMPLICATIONS

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)

INVESTIGATIONS

• 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

MANAGEMENT

Life threats

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

Resuscitation

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

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)

Decontamination

• 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

Disposition

• 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

• LITFL Toxicology Conundrum 032 — Corrosive Ingestion