Corrosive Poisoning

Corrosive Poisoning



Edited By :

Dr.Salim Al Mamun







Any chemical when ingested causing tissue injury to the gastrointestinal mucosa may termed as caustics- which are also known as corrosive poisons-i-e. strong acids locally produce corrosion and tissue necrosis, when they come in contact. They coagulate tissue proteins; fix the tissue, extract tissue fluid, and if the person survives for a reasonable period, then there is ulcer formation, sloughing of the necrosed tissue and scar formation with contracture.

Mineral acids and alkalies (corrosive agents) have direct local action, but may have indirect action, when ingested and absorbed in the system viz, circulatory and respiratory systems. Organic corrosive agents cause direct local and remote action as they are absorbed and reache to the different systems.


According to chemical action, corrosive agents may classify as:

Corrosive Poison



Mode of Action:

When ingested, moderately strong acids produce coagulation necrosis of the gut mucosa, and formation of Escher limits the damage up to the superficial layers, while alkalies cause liquifactive nercosis of the mucosa with saponification and continued deeper penetration into the underlying tissues causing extensive damage.

In both strong acids and alkalies, tissues immediately become corroded, soft and some times dissolved, disintegrated and perforated and thus the whole or part of it, or part of the intestine turns into a small soft pulpy mass.


Domestic Use: Many of acids are used in various household products like toilet. Bowl cleaner. Metal cleaner, antirust compound, battery fluid and pool sanitizer. Industrial use of acids includes electroplating, photography, calico printing, rayon manufacturing and in different chemical laboratory.

A)   Sulphuric acid: It is a colourless, heavy, oily, odourless hygroscopic liquid. It causes brittle chalky white teeth, ulceration of the mouth, oesophagus and stomach, where there may be perforation followed by generalized peritonitis.

Vitriolage: Throwing of the corrosive substance specially sulphuric acid ( Oil of vitriole) on any person usually on the face for disfiguration due to enemity or rivality is called vitriolage, which is a grievous hurt and a punishable offence.

B)   Nitric acid: Pure nitric acid is a clear, colourless, pungent choking odour liquid and emits white fumes when exposed in open air. Locally it is corrosive agent causing yellow colouration of the teeth and produce respiratory distress.

C)   Hydrochloric acid: Pure hydrochloric acid is a volatile colourless, odourless (Liquid) having burning sour taste. Shock usually occur due to severe pain. There may be no significant change in the teeth.

D)   Oxalic acid: It is a colourless transparent prismatic crystals and sour in taste. It is used in calico printings, manufacturing of straw hats, removing ink from the paper and cloths, removing rust stains from the metallic and wooden articles and preparation of various pickles and chanachurs. Its common clinical features are feeble pulse, cold and clammy skin, low blood pressure and shallow respiration. Coma and death due to asphyxia followed by respiratory failure.

E)   Acetic acid: It is a colourless liquid with sour taste and pungent smell. In concentrated form it is corrosive, but in diluted form it is irritant. Vinegar contains 4-5% acetic acid.

F)   Picric acid: Locally it produces corrosion with tissue necrosis. When ingested, it causes muscular cramping, drowsiness, stupor, decomposes red blood cells, meth-haemoglobinaemia and irritate CNS following convulsion coma and death. In low dose it causes cramping pain in the stomach, yellow vomiting, diarrhea of yellow liquid stool, yellow colouration of the skin and conjunctiva, dilatation of pupil with marked dehydration. Urine first becomes dark yellow, then turns into ruby red colouration with dysuria, even anuria.

G)   Formic acid: When ingested it produces cramping pain in the stomach, petechieal haemorrhage, intravascular haemolysis, disseminated intravascular coagulalation, severe acidosis, renal failure etc.

H)   Carbolic acid: It is a dark magenta coloured liquid with a typical phenol odour. Carbolic acid poisoning (Carbolism) includes- hot burning pain extending from the mouth to the stomach. Skin- becomes cold and clammy with subnormal temperature. Pupil constricted, feeble thready pulse, hypotension, slow laboured stertorous respiration with convulsion and lock jaw.  Oliguria or anuria may be present. Urine contains albumin, blood casts and metabolic products i.e. hydroquinone and pyrocatechol- colouring the urine Olivo green-known as carboluria.

Summary feature of acid poisoning:

Skin contact with acid causes pain, blistering, ulceration and lacerating necrosis, with severe scarring after weeks.

Ingestion by mouth causes immediate pain with pharyngeal edema and burns. Pain and mucosal edema causes difficulty in swallowing. Features of pharyngeal involvement includes hoarseness, stridor, respiratory distress and laryngeal and/or epiglottic edema. Perforation of the esophagus and/or stomach may occur, which can lead to chemical peritonitis. Abdominal pain, vomiting, diarrhea and haematmesis occur in more severe cases. Systemic effect includes circulatory collapse, metabolic acidosis, hypoxia, respiratory failure, intravascular coagulation and hemolysis. Renal failure occurs as the end result of ATN. Later effect of acid ingestion includes pyloric stenosis, stricture formation and achlorohydria.


Grading system for corrosive burns of the alimentary tract with endoscopy:

Grade             Features

v  1                Erythema and oedema only

v  2a              Localized,superficial friability,blistes or ulceration

v  2b              Features as for grade 2a,but with circumferential ulceration

v  3                Multiple deep ulcers,area of necrosis

Diagnosis is based on the history of exposure

Management and treatment:

1.            Emesis should not be induced.It is contraindicated.

2.            Attempt at gastric lavage is contraindicated due to danger of perforation.

3.            Dilution and /or neutralization is also contraindicated

4.            Steroids confer no benefit & may mask abdominal sign of perforation

5.            Early endoscopy as soon as possible.

6.            Inj Morphine / Diclofenac sodium for pain

7.            Soluable calcium tablet for hydrofluric acid ingestion if patient able to swallow followed by I.V. Inj. of 10% calcium gluconate 10ml with I.V. infusion of dextrose in normal saline.

8.            Oxygen inhalation and artificial respiration if necessary.

9.            For external burn and eye injury  wash immediately with water or saline for 10 to 30 minutes. Then use oint silver sulphadiazine for skin, and chloramphenicol eye point for eye.

10.         For oedema of the glottis- tracheostomy should be done.

11.         Surgery: For esopheseal stricture and gastric outlet obstruction. Usually done after 4-6 weeks of ingestion.

12.         Management of complications (e.g. peritonitis) if any.



Sodium Hydroxide (Caustic soda) is a constituent of oven and drain cleaners and dishwashers.

Sodium carbonate (washing soda) having strong alkaline taste is less toxic than potassium carbonate.

Potassium hydroxide (caustic Potash) is a soapy viscid in touch, used in hearing aid batteries.

Potassium carbonate is a white crystalline powder having a caustic and alkaline taste used as a cleaning and washing agent.

Bleach: Common house hold bleach has 3-6% of sodium hypochlorite. Its PH is about 11, more of which cause oesophagial ulceration.

Detergents: Most of the detergents contain sodium tripolyphosphate and sodium carbonate which are weakly alkaline and usually do not produce significant toxicity.

Ammonium hydroxide- contains 32.5% of ammonia and is used at home for removing paint, oil and dirt usually from the clothing.


Clinical Features:

  • Alkali damage to the oesophagus may produce diffused blurred oesophageal mucosul ulceration, sloughing, with petechial haemorrhagic spottings throughout the whole mucosa and its underlying tissues. Perforation of gastric or intestinal wall is less common. Oesophageal perforation can develop and as its sequel medistinitis pneumonitis, cardiac injury and tracheo oesophageal & aortico-enteric fistula may ensue.
  • Metabolic acidosis may develop in patients with severe gastrointestinal bleeding.
  • Renal failure is a rare complication, may be accompanied by Gl bleeding and shock.
  • Inhalation of alkaline vapour may cause hoarseness,stridor,upper airway oedema, wheezing, pneumonitis and respiratory failure.
  • Ocular exposure may produce severe conjunctival irritation, chemosis, corneal epithelial defects, limbal ischemia and permanent visual loss may occur in severe cases.
  • Dermal contact with alkaline corrosives may produce redness, irritation, pain and sometimes-full thickness burns of the skin.

Diagnosis: Is based on history of the exposure and PH of the collected gastric lavage.

Management/ Treatment:

  1. Dilution or neutralization, induce emesis, gastric aspiration and lavage are contraindicated.
  2. Irrigate exposed eyes with sterile cold water or saline at least for 20 minutes and continue until the PH returns to normal.
  3. Emulcents- egg white, olive oil, butter, cold milk should be avoided.
  4. Clear air way and support with O2 inhalation and artificial respiration, if necessary intensive care unit support including ventilator.
  5. I.V. fluid for maintaining nutrition and electrolyte balance.
  6. As there is no specific antidote for alkaline corrosives, symptomatic treatments are to be done. Neutralisation with alkali now-a-days is not done.
  7. Surgical treatment must be considered for any patient with grade II or III esophageal injury.
  8. Analgesia including Narcotics,or NSAID (Inj. Diclofenac)  may be given to relieve pain
  9. Diagnostic endoscopy should be performed within 12-24 hrs of alkali ingesion.
  10. Corticosteroids have no role in the management of a case and complication. It is rather harmful.

Medico legal importance:

  1. Usually accidental poisoning due to over dose
  2. Suicidal poisoning very rare
  3. Homicidal Poisoning not adopted

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