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Oil of vitriol; Oleum; Battery acid.
Sulfuric acid is a heavy, oily, colourless, odourless, non-fuming liquid (Fig 5.1). It is hygroscopic, i.e. it has great affinity for water with which it reacts violently, giving off intense heat Sulfuric acid is mainly used in two forms:
· Commercial concentrated sulfuric acid is usually a 93–98% solution in water.
· Fuming sulfuric acid is a solution of sulfur trioxide in sulfuric acid.
Sulfuric acid is probably the most widely used industrial chem-ical in most parts of the world including India.
· It is used as a feedstock in the manufacture of a number of chemicals, e.g. acetic acid, hydrochloric acid, phosphoric acid, ammonium sulfate, barium sulfate, copper sulfate, phenol, synthetic fertilisers, dyes, pharmaceuticals, detergents, paint, etc
· Storage batteries utilise sulfuric acid as an electrolyte.
· Sulfuric acid is also used in the leather, fur, food processing, wool, and uranium industries, for gas drying, and as a laboratory reagent.
· Sulfuric acid can be formed in smog from the photo- chemical oxidation of sulfur dioxide to sulfur trioxide and subsequent reaction with water. It is a major component of acid rain.
About 20 to 30 ml of concentrate sulfuric acid. Deaths have been reported with ingestion of as little as 3.5 ml.
Systemic absorption of sulfuric acid is negligible.
Produces coagulation necrosis of tissues on contact.
· Burning pain from the mouth to the stomach. Abdominal pain is often severe.
· Intense thirst. However, attempts at drinking water usually provoke retching.
· The vomitus is brownish or blackish in colour due to altered blood (coffee grounds vomit), and may contain shreds of the charred wall of the stomach.
· If there is coincidental damage to the larynx during swal-lowing or due to regurgitation, there may be dysphonia, dysphagia, and dyspnoea.
· Tongue is usually swollen, and blackish or brownish in colour. Teeth become chalky white. There may be constant drooling of saliva which is indicative of oesophageal injury.
· There is often acid spillage while swallowing with conse-quent corrosion of the skin of the face (especially around the mouth), neck, and chest (Fig 5.2). Burnt skin appears dark brown or black.
· Features of generalised shock are usually apparent.
· Renal failure and decreased urine output can occur after several hours of uncorrected circulatory collapse.
· Because it is a strong acid, exposure to sulfuric acid may produce metabolic acidosis, particularly following ingestion. Acidosis may be due to severe tissue burns and shock, as well as absorption of acid.
· Leukocytosis is common after exposure to strong mineral acids.
· If perforation of stomach occurs, a severe form of chemical peritonitis can result. Rarely, perforation of duodenum (or even further down the small intestine) may occur.
· If the patient recovers, there are usually long-term sequelae such as stricture formation which may lead to pyloric obstruction, antral stenosis, or an hour glass deformity of the stomach. The oesophagus may also be involved resulting in stenosis. There are indications of increased propensity for carcinomas.
· Contact with the eyes can cause severe injury including conjunctivitis, periorbital oedema, corneal oedema and ulceration, necrotising keratitis, and iridocyclitis.
· Chronic Exposure –
a.Occupational exposure to sulfuric acid mist can cause erosion of teeth over a period of time, as also increased incidence of upper respiratory infections.
b. Sulfuric acid can react with other substances to form mutagenic and possibly carcinogenic products such as alkyl sulfates. Case reports suggest that chronic exposure to sulfuric acid fumes may be linked to carcinoma of the vocal cords and nasopharyngeal carcinoma. Occupational exposure to sulfuric acid may contribute to cases of laryngeal cancer.
· Litmus test: The pH of the saliva can be tested with a litmuspaper to determine whether the chemical ingested is an acid or an alkali (turns red in acid, and blue in alkaline solution).*
· Fresh stains in clothing may be tested by adding a few drops of sodium carbonate. Production of effervescence (bubbles) is indicative of an acid stain.
· If vomitus or stomach contents are available, add 10% barium chloride. A heavy white precipitate forms which is insoluble on adding 1 ml nitric acid.
· Respiratory distress due to laryngeal oedema should be treated with 100% oxygen and cricothyroidotomy.**
· Some authorities recommend administration of water or milk if the patient is seen within 30 minutes of ingestion (120–240 ml in an adult, 60–120 ml in a child). But no attempt must be made at neutralisation with alkalis, since the resulting exothermic reaction can cause more harm than benefit. Studies indicate that even administration of buffering agents such as antacids can produce significant exothermic reaction.
· Remove all contaminated clothes and irrigate exposed skin copiously with saline. Non-adherent gauze and wrapping may be used. Deep second degree burns may benefit from topical silver sulfadiazine.
· Eye injury should be dealt with by retraction of eyelids and prolonged irrigation for at least 15 to 30 minutes with normal saline or lactated Ringer’s solution, or tap water if nothing else is available. Anaesthetic agents and lid retractors may be necessary. It is desirable to continue with the irigation until normal pH of ocular secretions is restored (7.4), which can be tested with litmus paper or urine dipstick. Slit lamp examination is mandatory after decontamination, to assess the extent of corneal damage.
· The following measures are contraindicated: oral feeds, induction of vomiting, stomach wash, and use of acti-vated charcoal.
· Oral feeds: Depends on degree of damage as assessedby early endoscopy. The following is a rough guide—
a. Mild (grade I): may have oral feedings on first day.
b. Moderate (grade II): may have liquids after 48 to 72 hours.
c. Severe (grade III): jejunostomy tube feedings after 48 to 72 hours.
· Administration of steroids has been shown to delay stricture formation (in animals) when given within 48 hours of acid ingestion, but the practice is generally not recommended because of increased risk of perforation.
a. In case it is embarked upon, the dosage recommended is 60 to 100 mg/day of prednisolone for the first 4 days, followed by 40 mg/day for the next 4 days, and finally 20 mg/day for the subsequent 7 to 10 days. In children, the appropriate dose is 2 mg/kg/day.
b.Alternatively 0.1 mg/kg of dexamethasone or 1 to 2 mg/kg of prednisone can be given for 3 weeks and then tapered off.
· Administer antibiotics only if infection occurs. Prophy-lactic use is not advisable unless corticosteroid therapy is being undertaken.
· Since there is often severe pain, powerful analgesics such as morphine may have to be given.
· The use of flexible fibreoptic endoscopy is now stan-dard practice in the first 24 to 48 hours of ingestion to assess the extent of oesophageal and gastric damage. If there are circumferential 2nd or 3rd degree burns, an exploratory laparotomy should be performed. If gastric necrosis is present, an oesophagogastrectomy may have to be done.
· Emergency laparotomy is mandatory if there is perfora-tion or peritonitis.
· If the patient recovers, there may be long-term sequelae such as stenosis and stricture formation.* Follow-up is therefore essential to look for signs of obstruction—nausea, anorexia, weight loss. Surgical procedures such as dilatation, colonic bypass, and oesophagogastrostomy may have to be undertaken.
The most important first-aid measure for all patients with ocular caustic exposures should be immediate decontamination by irrigation, using copious amounts of water or any readily available safe aqueous solution such as normal saline, lactated Ringer’s solution, or balanced salt solution. An ocular topical anaesthetic is usually required for effective irrigation. A complete irrigation must be done including the conjunctival recesses, internal and external palpebral surfaces, and corneal and bulbar conjunctiva. Lid retraction is invariably necessary. While concern has been expressed over the use of aqueous solutions for ocular irrigation in the case of exposure to substances which react with water leading to heat or mechanical injury (e.g. white phosphorus), there are hardly any documented case reports where this has actually happened.
The duration of ocular irrigation varies with the nature of exposure. After exposure to acids or alkalies, normalisation of the conjunctival pH is often suggested as a useful endpoint. A minimum of 2 litres of irrigant per affected eye should be used before any assessment of pH is done. After waiting for 5 to 10 minutes, the pH of the lower conjunctival fornix is checked. Thereafter, rechecks are done in cycles until the pH reaches 7.5 to 8.
Adjunctival treatment of ocular burns include application of topical antibiotic providing antistaphylococcal and antipseudomonal coverage, cycloplegics which not only reduce pain from ciliary spasm, but also decrease the likelihood of posterior synechiae forma-tion, and the use of eye patches and systemic analgesics. Topical anaesthetic agents are not desirable. Topical steroids may help lessen the inflammation, but can interfere with healing and so must not be used for more than the first 7 days.
In every case of caustic ocular exposure, consultation with an ophthalmologist is essential after administration of first-aid and decontamination, to assess visual acuity, and to undertake slit lamp examination for detecting corneal damage. It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage. The basis of such an evaluation is the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischaemia.
• Grade 1: Corneal epithelial damage; no ischaemia.
• Grade 2: Cornea hazy; iris details visible, ischaemia less than one-third of limbus.
• Grade 3: Total loss of corneal epithelium; stromal haze obscures iris details; ischaemia of one-third to one-half of limbus.
Grade 4: Cornea opaque; iris and pupil
obscured, ischaemia affects more than one-half of limbus.
· Corroded areas of skin and mucous membranes appear brownish or blackish. Teeth appear chalky white.
· Stomach mucosa shows the consistency of wet blotting paper.
· There may be inflammation, necrosis, or perforation of the GI tract (Fig 5.3).
· Accidental poisoning may arise from mistaken identity since sulfuric acid resembles glycerine and castor oil. It is therefore imperative that it is stored in a distinctive bottle, clearly labelled, and kept in a safe place.
· Sulfuric acid is a rare choice for either suicide or homicide.
· In addition to routine viscera and body fluids, a portion of corroded skin should be cut out, placed in rectified spirit or absolute alcohol and sent for chemical analysis. Stained clothing must also be sent (preservative not necessary).
o This term refers to the throwing of an acid on to the face or body of a person in order to disfigure or blind him (Fig 5.4). The motive is usually revenge or jealousy.
o Though sulfuric acid is commonly used (hence the term vitriolage which is derived from “oil of vitriol”), other acids are also employed. In fact any corrosive which is easy to hand may be used, including organic acids, alkalis, and irritant plant juices.
o Going by newspaper reports, vitriolage is a fairly common crime in India, though it is regarded as a serious offence (grievous hurt), and carries stiff punishment.*
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