544xcdfszdserA caustic substance is one that will damage or destroy other tissues with which it comes into contact by means of a chemical reaction.
Caustic refers to any chemical that will dissolve the structure of an object.
Caustics are present at home and in industry.
Almost 1000 children with caustic ingestion or hospitalized each year.
In 2018 the Poison Control center reported that household cleaners ranked second among all exposures to poisons and foreign bodies, accounting for 9% of the total.
Caustic exposure can be divided on basis of intention with exposures in children best characterized as exploratory and typically involve small amounts.
Rarely alkali ingestions occur as a manifestation of child abuse.
Adolescents and adults usually ingest larger volumes in deliberate attempts at self harm.
Caustic substances cause injury after dermal, ocular, or gastrointestinal contact.
Commonly ingested household caustics include lye and hair relaxers, bleach, or ammonia, and highly concentrated acid.
Caustics include cleaning products, toilet bowl or a swimming pool cleaners, laundry detergent capsules,
They can be acids, oxidizers, or bases.
Caustics include desiccant, vesicants, and protoplasmic poisons.
When such substances come in contact with a surface, the surface deteriorates.
Surface deterioration can occur in minutes, or slowly over days or years.
At low concentrations, a corrosive substance is called an irritant.
At high concentrations, a corrosive substance causes a chemical burn.
Corrosives are immediately dangerous to the tissues they contact.
Common corrosives include: strong acids, strong bases, or concentrated solutions of certain weak acids or weak bases.
In general, acid with a pH of less than two and alkalis with a pH of more than 12 cause the most extensive injury.
pH alone does not explain the difference in caustic nature of injuries alone.
Titratable acid or alkaline reserve quantifies the amount of acid or base ion that the body’s physiological response donates to injured tissues to return them to a physiological pH.
Most neutralizing reactions are exothermic, and the heat released adds to the injury.
Corrosive forms can exist as any state of matter: liquids, solids, gases, mists or vapors.
Corrosive action on living tissue such as skin, flesh and cornea and is mainly based on acid-base reactions of amide hydrolysis, ester hydrolysis and protein denaturation.
Proteins bonds are destroyed via amide hydrolysis while lipids, which have ester bonds, are decomposed by ester hydrolysis.
The above reactions lead to chemical burns, the mechanism of the destruction posed by corrosives.
Other corrosives possess other chemical properties which may extend their corrosive effects.
Sulfuric acid at a high concentration is also a strong dehydrating agent, resulting in secondary thermal burns in addition to the chemical burns and may speed up its decomposing reactions on the contact surface.
Some corrosives-nitric acid and concentrated sulfuric acid, are strong oxidizing agents as well, contributing to the extra damage caused.
Hydrofluoric acid produces tissue damage and toxicity after being painlessly absorbed.
Strong bases such as calcium oxide, which has a strong affinity for water also releases heat capable of contributing thermal burns as well as delivering the corrosive effects of a strong alkali to moist flesh.
Some corrosive chemicals, mostly acids such as hydrochloric acid and nitric acid, are volatile.
Volatile corrosive chemicals can emit corrosive mists upon contact with air.
Inhalation can damage the respiratory tract.
Ingestion of corrosives can induce severe consequences, including serious damage of the gastrointestinal tract, which can lead to vomiting, severe stomach pains and death.
Common corrosive chemicals:
Strong acids: sulfuric acid, nitric acid and hydrochloric acid.
Weak acids: formic acid, acetic acid, and phosphoric acid.
Strong Lewis acids such as anhydrous aluminum chloride, boron trifluoride
and zinc chloride
Caustics or alkalis, such as sodium hydroxide, potassium hydroxide, and calcium hydroxide
Alkali metals in the metallic form and hydrides of alkali and alkaline earth metals, such as sodium hydride, function as strong bases and hydrate to give caustics.
Extremely strong bases, superbases, such as alkoxides, metal amides and organometallic bases such as butyllithium.
Fully alkalized salts of weak acids such as trisodium phosphate.
Some concentrated weak bases, such as ammonia when anhydrous or in a concentrated solution
Dehydrating agents such as concentrated sulfuric acid, phosphorus pentoxide, calcium oxide, anhydrous zinc chloride, also elemental alkali metals.
Strong oxidizers such as concentrated hydrogen peroxide.
Electrophilic halogens: elemental fluorine, chlorine, bromine and iodine, and electrophilic salts such as sodium hypochlorite or N-chloro compounds such as chloramine-T.
Organic halides and organic acid halides such as acetyl chloride and benzyl chloroformate.
Alkylating agents such as dimethyl sulfate
Most toxic product injury can be assessed on the pH, concentration, volume ingested, and duration of tissue contact, as well as the body surface affective the skin is involved.
Alkalis damage tissue by saponifying fats, resulting in liquefaction necrosis and creating a gelatinous substance, allowing for the penetration for tissue damage.
Acids denature proteins through coagulation necrosis and the coagulant that develops is thought to prevent the acid from reaching deeper tissues, thereby limiting the damage.
Hydrofluoric acid causes injury by releasing hydrogen ions, but also by direct cellular injury from the highly electronegative fluoride ions.
Free fluoride binds rapidly to cations such as calcium and magnesium resulting in life-threatening Hypocalcemia and hypomagnesemia.
Caustic ingestions are divided into immediate, delayed, and remote clinical manifestations.
Organs commonly involved with caustic exposure include the eyes, skin, airway, and gastrointestinal tract.
Pain is the immediate clinical effect, followed by loss of function.
Common caustic exposure manifestations include swelling of the tongue and mouth, drooling, vomiting, bleeding if injury is severe, swelling of the airway with stridor, respiratory compromise, and changes in voice.
The esophagus can perforate with the development of mediastinitis, additionally perforation of the stomach or bowel can lead to peritonitis.
For survival rate of an acute episode both delayed and remote complications can occur.
Ocular and cosmetic dermal injuries with functional limitations can appear.
Esophageal strictures occur over a period of weeks to months, and lead to chronic pain and impaired nutrition.
Chronic structures of the esophagus can lead to esophageal cancer.
After caustic ingestion, the most immediate risk to life is loss of the airway.
A change of voice frequently indicates impending airway compromise and placement of a definitive airway should be considered.
Principles of gastrointestinal decontamination are not applied to patients with caustic ingestions, since attempts to empty the stomach can potentially increase injury.
Activated charcoal does not adsorb caustics and obscures endoscopic visualization.
The use of glucocorticoids not been shown to be beneficial.
However, in 2B alkaline esophageal injuries a short course of methyl prednisone has demonstrated efficacy.
Sulcrafate may be beneficial in caustic esophageal injuries.
Mitomycin C minimizes the clinical effects of strictures by making the more amenable to mechanical dilation.
Mitomycin. c induces fibroblast apoptosis and reduces scarring, and requires your dilatations.
Mitomycin C can be given endoscopically.