Corrosives are agents which causes corrosion and destruction of tissues with which it comes in to contact.
Corrosive ingestion poisoning is the accidental or intentional intake (swallowing, breathing-in, or skin contact) of any product containing a corrosive agent, often acids or alkalis (hydroxides of sodium and potassium), most commonly used as household agents.
Rapidly obtaining reliable information on the particular agent involved is vital. This is particularly critical because some agents have important toxic concerns beyond those of a simple caustic ingestion.
Commonly available corrosive agents include:
Sodium hydroxide — detergents, drain and oven cleaners, button batteries. Alkaline agents are more dangerous as they cause deep and progressive mucosal burns injuries (liquefactive necrosis)
Sodium hypochlorite — bleaches and household cleaners
Ammonia — metal and jewellery cleaners, anti-rust products
Hydrochloric acid — metal cleaners
Sulfuric acid — drain cleaners, car batteries.
Glyphosate (toxicity may be due to the herbicide’s solvent, POEA surfactant) — metabolic acidosis, shock, multi-organ dysfunction
Paraquat — pulmonary fibrosis, multi-organ dysfunction and shock
Intoxications with these agents produce numerous and severe injuries of the upper gastrointestinal tract comprising oropharynx, larynx, esophagus, and stomach. Occasionally, corrosive agents may also cause injuries of the respiratory system.
Corrosive ingestion may be life-threatening due to airway compromise or GI perforation, or due to agent-specific systemic toxicity such circulatory collapse, metabolic acidosis and / or multi-organ failure.
If the patient survives the acute effects of caustic ingestion (characterized by necrosis, small vessel clotting, and sloughing of the mucosa), the reparative response leads to the development of esophageal strictures, gastric strictures of the antrum and pyloris, and rarely oesophageal and gastric cancer.
For a long time, it was believed that the acids cause more damage to the gastric mucosa, whereas alkalis have a tendency for greater damage to the esophageal mucosa. However, it is now known that these agents cause mucosal injuries in both the organs with no selective preference.
• Ingestion of concentrated sulfuric acid and sodium hydroxide solutions are associated with 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 multiple organ dysfunction syndrome
• Ingestion of <150 mL (< half a glass) 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
• Remove clothing soiled by corrosive agent.
• If household bleach such as Jik, has been ingested, swish fresh water in the mouth and spit out. After rinsing, drink water to help dilute out any bleach in the stomach, this will make it less irritating to the stomach lining.
• If household bleach has gotten on your skin or eye, flush the exposed area for several minutes (minimum 10-15 minutes) under tap water of a comfortable temperature.
• do not induce vomiting
• do not administer oral fluids
• do not administer activated charcoal
• do not attempt pH neutralisiation
Treatment of poisoning
Symptom-directed supportive care is the mainstay of management. No specific medical therapy can attenuate the extent of damage acutely nor alter the progression of chronic changes.
The gold standard for determination of the grade and extent of the lesion is upper gastrointestinal endoscopy performed in the first 24–48 hours in hemodynamically stable patients with no signs of perforation. CT thorax/abdomen is complimentary in assessing the severity of injury, risk of mortality and risk of subsequent stricture formation
if asymptomatic at 4 hours post-ingestion, perform a trial of oral fluids and discharge if well tolerated.
If symptomatic (e.g. throat pain, drooling, pain on attempting to swallow his own saliva, or has vomiting or abdominal pain); keep nil by mouth and admit for observation and an endoscopy.
If the eye is exposed, remove contact lenses if present. Use topical anaesthetic (if available), and immediately irrigate with 1L normal saline (via a giving set) for minimum 10-15 minutes regardless of pH.
If airway compromised; secure the airway and admit in ICU
If GI perforation, sepsis or hemodynamic instability, urgently begin surgical assessment and admit in ICU.
The long-term management is based on the presence, number, location, and tightness of the stricture as obtained from barium contrast studies.
Do not do gastric lavage, induce emesis, perform chemical neutralization or give any food orally (if symptomatic, pending endoscopic assessment). Blind placement of nasogastric tubes and attempts at dilution or neutralization of the ingested chemical are potentially hazardous and should be avoided.
Administer demulcents like susp antacids
Tracheostomy+Assisted ventilation in the presence of respiratory distress from upper airway edema
Administer IV fluids
Antibiotics if evidence of perforation exists or after severe dermal burns
Relieve severe pain with strong analgesics (e.g.Morphine)
Laparotomy for perforation
Commence intravenous PPI
Treat systemic toxicity if present, for example:
— hypocalemia: Administer calcium as calcium gluconate 0%,10ml i.v
— methemoglobinemia: Give methylene blue
— paraquat: Administer immunosuppressants and antiinflammatories