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
Critical Care
Compendium
Leave a Reply