- Email: [email protected]
Toxic effects of caustics (corrosives)
CHAPTER
Toxic effects of caustics (corrosives)
23
CHAPTER OUTLINE 23.1 Introduction ...................................................................................................267 23.2 Classification.................................................................................................267 23.3 Acids.............................................................................................................268 23.3.1 Inorganic Acids/Mineral Acids .....................................................268 23.3.2 Organic Acids.............................................................................271 23.4 Alkalis...........................................................................................................275
23.1 INTRODUCTION Corrosive poisons are those substances that corrode (or eat away) and destroy tissues through direct chemical action. They almost always act locally and have few systemic effects. The term caustic is often mistakenly presumed to denote an alkali; actually, it has a much broader meaning and refers to any substance that is corrosive and burning in nature. Obviously, this would also include the more important groups comprising acids. Table 23.1 summarizes the list of commonly used caustics/corrosive poisons.
23.2 CLASSIFICATION 1. Acids: a. Inorganic acids (mineral acids): Sulfuric, nitric, hydrochloric, and hydrofluoric acids. b. Organic acids: Carbolic, oxalic, and salicylic acids. These acids are weaker in action compared to inorganic acids and are usually absorbed into circulation, promoting local and remote action. 2. AIkalis: these include Alkalis include anhydrous ammonia, potassium hydroxide, sodium hydroxide, ammonium carbonate, potassium carbonate, and sodium carbonate.
Fundamentals of Toxicology. DOI: http://dx.doi.org/10.1016/B978-0-12-805426-0.00023-8 © 2016 BSP Books Pvt. Ltd. Published by Elsevier Inc. All rights reserved.
267
268
CHAPTER 23 Toxic effects of caustics (corrosives)
Table 23.1 Selective List of Commonly Used Caustics Strong Acids
Strong Alkalis
Others
Inorganic acids (mineral acids): Sulfuric, nitric, hydrochloric, and hydrofluoric acids Organic acids: Carbolic, oxalic, and salicylic acids
Anhydrous ammonia, potassium hydroxide, sodium hydroxide, ammonium carbonate, potassium carbonate, sodium carbonate
Hydrogen peroxide, iodine, potassium permanganate, quaternary ammonium compounds
Table 23.2 Comparative Characteristics of Sulfuric, Nitric, and Hydrochloric Acids Sulfuric Acid Synonymous
Oil of vitriol
Physical properties
Heavy Colorless Viscid/oily Nonfuming Gives heat with water Charring positive
Fatal dose Fatal period Commercial use
Burning acid taste 5 10 mL 12 24 min Textile, arts, and industry
Nitric Acid Aqua fortis, spirit of niter Heavy Colorless Not viscid/oily Fumes (yellow) in air Not so Xanthroproteic reaction positive Choking odor 10 15 mL 24 30 min Industries
Hydrochloric Acid Spirit of salts, muriatic acid Heavy Colorless Not viscid/oily Fumes in air Not so Not so Not so 15 20 mL 15 24 min Cleansing agent
23.3 ACIDS 23.3.1 INORGANIC ACIDS/MINERAL ACIDS Sulfuric, nitric, and hydrochloric acid Acids are hydrogen-containing substances that, on dissociation in water, produce hydrogen ions. They are potent desiccants with the ability to produce coagulation necrosis of tissues on contact (except hydrofluoric acid, which produces liquefactive necrosis). When a strong acid is dissolved in a solvent, an exothermic reaction ensues, resulting in the emanation of heat, which is referred to as the heat of solution. Table 23.2 summarizes comparative characteristics of sulfuric, nitric, and hydrochloric acids.
23.3 Acids
Mode of action Strong acids act as corrosives, burning all tissues in the upper gastrointestinal (GI) tract when digested and sometimes resulting in esophageal or gastric perforation. They produce coagulation necrosis characterized by the formation of a coagulum (eschar) as a result of the desiccating action of the acid on proteins in superficial tissues. The coagulum formed limits the penetrating ability of acids. However, strong alkalis create injury to tissue by the mechanism of liquefaction necrosis. Alkalis, unlike acids, produce extensive penetrating damage. Squamous epithelium of the esophagus is more resistant to acids than is the columnar epithelium of the stomach. Therefore, esophageal strictures are more common in alkali poisoning, and pyloric and gastric strictures are more common in acid poisoning. Dilute acids and alkalis act as irritants, and corrosion is not really a prominent feature. The mode of action of acids is summarized in Fig. 23.1. Signs and symptoms After oral consumption, corrosion of the GI and respiratory tracts is common but varies in intensity depending on the type and concentration of the acid. Fig. 23.1 shows the respiratory signs and symptoms after ingestion of all inorganic acid poisons, except hydrofluoric acid. The oral cavity shows chalky white teeth, swollen blackish tongue, and swollen lips. Acid burn (eschar) is
Corrosion (any part of the body)
Extraction of water
Liberation of heat
Coagulation and precipitation of cellular proteins
Conversion of hemoglobin to hematin
Corrosion and destruction of tissues
FIGURE 23.1 Schematic representation of the mechanism of coagulation necrosis.
269
270
CHAPTER 23 Toxic effects of caustics (corrosives)
commonly seen because vomited acid trickles down the angle of the mouth toward the neck and chest. The abdomen may be distended and tender. Immediate death may be due to suffocation and asphyxia due to edema of the glottis; exhaustion and shock may be due to circulatory collapse or perforation of stomach; and delay in death may be due to starvation and dehydration because of stricture of the esophagus or pylorus. The victim may also die due to peritonitis or secondary infections. The mind remains sound until death. Postmortem findings External Corrosion of parts that come in contact with the acid, especially the lips, mouth, throat, chin, angle of mouth, and hands. Internal The findings are restricted to the upper GI and respiratory tract and lead to corrosion. Treatment The management of poisoning should be carefully undertaken. Certain general measures such as respiratory distress due to laryngeal edema should be treated with 100% oxygen. Demulcents: Milk (canned condensed milk), egg white (beaten), vegetable oils, starch solution, barley water, and thin oatmeal should be administered. Immediate dilution with milk or water within 30 min of ingestion is strongly recommended for oral ingestions. Do not attempt to neutralize the acid with weak bases/dilute alkalizers such as milk of magnesia or lime water (ie, calcium hydroxide in water), because an exothermic reaction may extend the corrosive injury. Do not give alkalis such as sodium bicarbonate because they can produce carbon dioxide gas, which increases the risk of perforation of the stomach. Airway maintenance and artificial respiration are necessary if there is any respiratory distress. Use morphine/pethidine for relief of pain and IV fluids and electrolytes for dehydration. No oral feeding should be administered until endoscopy confirms the extent of injury. The use of antibiotics for controlling infections is recommended. There is controversy regarding the use of corticosteroids (although proven to be good for delaying or preventing stricture formation in experimental animal studies) in the treatment of acid poisoning. Skin care for any skin lesions involves copious saline irrigation. Treat with nonadherent gauze and wrapping. Deep second-degree burns may benefit from topical application of silver sulfadiazine. Eye care for any acid injuries requires copious irrigation with retraction of the eyelids for 20 30 min. Antibiotic eye drops can help combat infections. However, it may be necessary to refer the patient to an ophthalmologist for further treatment. Emesis and gastric lavage are contraindicated (to prevent gastric perforation; however, there is an exception with organic acids).
23.3.1.1 Hydrofluoric acid Hydrofluoric acid is a colorless gas that becomes a fuming liquid when dissolved in water. It is used for etching glass and clouding electric bulbs.
23.3 Acids
The fatal dose is approximately 15 mL. The fatal period varies from a few minutes to 2 h. However, there have been reports of deaths occurring within 7 h of poisoning. Mode of action The mode of action of hydrofluoric acid exposure is quite different from that of other inorganic acids. The fluoride anion produces liquefaction necrosis by binding with calcium and magnesium in the tissues, thus resulting in hypocalcemia and rendering hydrofluoric acid poisoning more serious. Signs and symptoms Following ingestion, the patient shows hematemesis, hypovolemic tonic convulsions, upper airway obstruction, severe hypocalcemia, acidosis, shock, and coma. Myocardial irritability and subsequent life-threatening cardiac arrhythmias may be due to binding of potassium, magnesium, and calcium ions. Skin exposure can result in severe and deep burns, which are extremely painful and slow to heal. Postmortem findings The lips, tongue, and mouth may show white patches or may be charred. The esophagus may show shredded epithelium with ecchymosis, inflammation, ulceration, and blackening of the stomach. Liver and kidneys show fatty and parenchymatous degeneration. Treatment The following treatment is recommended: • • •
Acid burn lesions need copious irrigation with water and application of calcium and gluconate gel. Debridement may also be needed. Intra-arterial infusion of 20% calcium gluconate or calcium chloride is effective. Oxygen inhalation after removal from fumes and tracheotomy, if needed, should be performed.
23.3.2 ORGANIC ACIDS 23.3.2.1 Carbolic acid (phenol) Carbolic acid is a poison that can be identified by its smell, which is commonly referred to as a phenolic odor or hospital odor. Pure phenol has a colorless, short, prismatic, needle-shaped, crystalline form. On exposure to air, it turns pink and liquefies. It is fat-soluble; therefore, it can attack the nervous system. It is also soluble in glycerin, ether, and alcohol, and it is slightly soluble in water. It is known specifically for its antiseptic or disinfectant property. Other members of phenol group: Phenol has several derivates, namely, cresol, creosote, lysol, and dettol. These are absorbed orally, through intact skin, by the GI tract, through inhalation by the respiratory tract, per rectum, and per vaginum. The toxicological actions of these compounds are similar to phenol but less severe. • •
Cresol is a methyl phenol with meta, ortho, and para isomers. It is used as a disinfectant and antiseptic. Creosote is a mixture of phenols consisting mainly of cresol and guiacol. It is used as a household remedy for coughs and is found in many proprietary preparations.
271
272
CHAPTER 23 Toxic effects of caustics (corrosives)
•
Resorcinol is a colorless crystalline substance used for the treatment of various skin diseases, including ringworm, psoriasis, and eczema. • Lysol is a 50% solution of cresol (3-methyl phenol) in saponified vegetable oil. • Thymol is an alkyl derivative of phenol obtained from volatile oils of Thymus vulgaris, Monarda punctata, or Trachyspermum ammi. It occurs in colorless crystals with a characteristic pungent odor and taste. Previously, it was used as an antihelminthic (for ankylostomiasis), antifungal, and antiseptic. Mode of action Phenol is a protoplasmic poison. It enters into loose combination with proteins and penetrates deep into the tissue. When applied to the skin or mucosa, it causes necrosis and gangrene. The local nerve endings are first stimulated and then paralyzed, resulting in anesthesia. After absorption, it causes widespread capillary damage and clotting in superficial blood vessels. It also acts on the cells of the central nervous system, heart, and kidneys. Phenol is mainly metabolized by the kidneys, wherein it gets converted into hydroquinone and pyrocatechol and then is excreted in urine. These products turn urine olive green or brown on standing, which is a phenomenon called carboluria. Complete elimination occurs in 36 h. Phenol is nephrotoxic (other nephrotoxics are heavy metals, methanol, oxalic acid, salicylates, phenacetin, EDTA, and penicillamine). Signs and symptoms Poisoning by carbolic acid is known as carbolism. The usual signs and symptoms of carbolism include headache, giddiness, tinnitus, vomiting, diarrhea, abdominal pain, and a burning sensation. Inhalation of vapors leads to laryngeal edema and stertorous breathing with cyanosis. Pupils are dilated. If the patient survives for 48 h, then carboluria followed by anuria are seen. The victim will pass dark, smoky urine, which soon turns olive green on standing. Nervous symptoms are common. Methemoglobinemia is a characteristic feature in severe cases. Muscular spasms and convulsions, collapse/unconsciousness, and coma followed by death occur due to respiratory and circulatory failure. Diagnosis: Corrosions on the face, around and inside the mouth (greyish white with phenol or brownish with lysol), phenolic odor (breath/vomit), carboluria, dilated pupils, and stertorous breathing. The fatal dose is 5 15 g. The fatal period varies from 2 to 12 h (rapid death, if injected intrauterine). Postmortem findings External Greyish or brownish corrosions at the angle of the mouth and thin cracks in the body, arms, and hands (splashes), with characteristic phenolic odor. Internal Corrosion of gastrointestinal mucosa and laryngeal and pulmonary edema have been observed in all orally ingested poisoning cases. However, there are certain specific findings, such as the stomach emitting a phenolic odor. Gastric mucosa will show marked corrosion and swelling of mucosal folds with coagulated greyish or brownish silvery mucus. Intervening normal mucosal folds appear dark red.
23.3 Acids
The kidneys will show hemorrhagic nephritis when the victim survives for some time after poisoning. Vomit and gastric lavage collection may show partially detached gastric mucosa. Treatment Symptomatic treatment should include artificial respiration, tracheal aspiration of secretions, and glucose saline to induce diuresis. In case of poisoning through skin absorption, use the following: • • • • •
Remove the contaminated garments. Cleanse the site by mopping with a wet cloth and wash with soap and water. Apply olive oil/methylated spirit/10% ethyl alcohol, which can prevent further absorption. Move the victim to fresh air. Give normal saline plus sodium bicarbonate (intravenous (IV) drip). In case of poisoning through the oral route, perform the following:
•
•
Gastric lavage: Although phenol corrodes the stomach wall, it also hardens it, unlike other corrosive poisons. Hence, gastric lavage is performed whenever possible with plenty of lukewarm water containing animal charcoal, olive oil, magnesium or sodium sulfate, or saccharated lime soap solution with 10% glycerin. When the lavage is completed, 30 g of magnesium sulfate or medicinal liquid paraffin should be left in the stomach. Give egg whites and Epsom salts/demulcents orally.
23.3.2.2 Oxalic acid (acid of sugar) Oxalic acid is a colorless, prismatic, crystalline substance (similar to magnesium sulfate (MgSO4) and zinc sulfate (ZnSO4)). It acts locally as a corrosive on the skin and mucosa (more severe). After absorption, it affects blood electrolytes. It can remove tissue calcium, leading to hypocalcemia, followed by cardiovascular shock, tubular necrosis, uremia, and death. The fatal dose is 15 20 mg. The fatal period ranges from 1 to 2 h. Signs and symptom With large oral doses (15 g or more), it can lead to a sour and acidic taste, followed by a sensation of constriction around the throat and burning pain from the mouth to the epigastrium, which radiates all over the abdomen. There will be tenderness in the epigastrium, nausea followed by vomiting (coffee ground colored vomit), severe thirst, diarrhea, electrolyte imbalance, and hypocalcemia, leading to muscle irritability, tenderness, tetany, convulsions, tingling of extremities, coma, collapse, and death. In case of slow poisoning, there is uremia. Urine is scanty, with traces of albumin. Microscopically, blood and calcium oxalate crystals are observed. Postmortem findings External There are no specific findings; however, sometimes, burns of the face and skin may be seen.
273
274
CHAPTER 23 Toxic effects of caustics (corrosives)
Internal Specific findings are that the mucosa of the mouth, tongue, pharynx, and esophagus may be bleached (whitened/scale/red) if a strong solution is consumed. Stomach Changes The stomach mucosa is reddened and punctate due to erosions, giving a “velvety red” or blackish appearance. The wall of the stomach is softened, but there are no perforations. The stomach contents are gelatinous brown (due to acid hematin formation). All other viscera are congested. Kidneys are swollen and congested. On histopathology, tubules are filled with oxalate crystals. Treatment General management should include gastric lavage with calcium lactate (two teaspoons per lavage), 10 mL calcium gluconate IV frequently, parathyroid extracts of 100 units IM, demulcent drinks, enema, and purgatives (castor oil). Symptom-based treatment should also be followed. Antidotes such as lime water, calcium lactate, calcium gluconate, calcium chloride, and chalk suspension in water or milk may be administered orally. These form insoluble calcium oxalate and are excreted easily.
23.3.2.3 Formic acid (methanoic acid, formylic acid) Formic acid is a colorless liquid with a pungent penetrating odor. It is completely soluble in water and is used as bath cleaner. Generally, airplane glue makers, cellulose format workers, and tanning salon workers are exposed to a 60% solution of formic acid. Signs and symptoms Skin contact produces brownish discoloration, dermatitis, pustules, vesicles, and sometimes sloughing. Formic acid is unique for its ability, in many patients, to cause death after a prolonged (several weeks) course of classical acid-induced gastrointestinal damage. Certain other complications include severe metabolic acidosis, intravascular hemolysis, and disseminated intravascular coagulation. Accidental ingestion in children usually does not lead to fatalities because the pungent taste prevents ingestion of a lethal dose. Nevertheless, it is a problem when used deliberately for suicide. It causes acute trachea bronchitis, which is characterized by cough, sore throat, chest pain, and light-headedness. Formic acid skin burns may also result in systemic toxicity. When absorbed by the body, it causes systemic acidosis, hematuria, and renal damage. The metabolism of methanol can also produce toxic metabolites of formic acid. Treatment Treatment is by correction of acidosis by infusion of sodium bicarbonate intravenously and hemodialysis for renal failure.
23.3.2.4 Salicylic acids An important therapeutic preparation of this is acetyl salicylic acid (aspirin). Details are discussed in another chapter dealing with therapeutic agents.
23.4 Alkalis
23.4 ALKALIS Like acids, alkalis also act as corrosive poisons when administered in the concentrated form, but they act as an irritant poison when diluted. Alkalis are present in a number of household products (eg, drain cleaners, oven cleaners, dishwasher products, some paint strippers, etc.) and are also used in industry. Alkalis commonly encountered in poisoning include ammonia (usually in the form of ammonium hydroxide) and carbonates of sodium and potassium. Hydroxides of sodium and calcium and sodium hydrochloride are also increasingly used in household cleaning agents such as detergent. Mode of action Alkalis generally contain hydroxyl groups, which on dissociation in water produce hydroxide ions. Alkali agents injure the GI tract by saponification of fats and solubilization of proteins that allow deep penetration into tissue. Thus, unlike acids, they produce extensive penetrating damage. This pathogenesis of injury is rapidly progressive and may extend weeks after onset. Alkalis have more severe corrosive effects on the esophagus (acids produce corrosive effects on the stomach). Severe esophageal damage can occur if the pH is lower than 11. However, with deliberate ingestion of large quantities, corrosive effects can be seen anywhere from the mouth to the small intestine. Locally, alkalis produce liquefaction necrosis, which results in extensive penetrating damage because of saponification of fats and solubilization of proteins. Ulcers are common and may persist for several weeks. Signs and symptoms The esophagus is often severely affected, resulting in dysphasia, vomiting, and hematemesis. Stridor is an important indicator of severe esophageal injury. Eye involvement can produce serious complications of ophthalmologic emergency. The fatal dose is 10 15 g for most alkalis and 15 to 20 mL for ammonia. Treatment Treatment involves removal from exposure and rest, and also symptom-based treatment. Corneal irrigation with water and topical use of antibiotics are recommended.
275
Toxic effects of caustics (corrosives)
23
CHAPTER OUTLINE 23.1 Introduction ...................................................................................................267 23.2 Classification.................................................................................................267 23.3 Acids.............................................................................................................268 23.3.1 Inorganic Acids/Mineral Acids .....................................................268 23.3.2 Organic Acids.............................................................................271 23.4 Alkalis...........................................................................................................275
23.1 INTRODUCTION Corrosive poisons are those substances that corrode (or eat away) and destroy tissues through direct chemical action. They almost always act locally and have few systemic effects. The term caustic is often mistakenly presumed to denote an alkali; actually, it has a much broader meaning and refers to any substance that is corrosive and burning in nature. Obviously, this would also include the more important groups comprising acids. Table 23.1 summarizes the list of commonly used caustics/corrosive poisons.
23.2 CLASSIFICATION 1. Acids: a. Inorganic acids (mineral acids): Sulfuric, nitric, hydrochloric, and hydrofluoric acids. b. Organic acids: Carbolic, oxalic, and salicylic acids. These acids are weaker in action compared to inorganic acids and are usually absorbed into circulation, promoting local and remote action. 2. AIkalis: these include Alkalis include anhydrous ammonia, potassium hydroxide, sodium hydroxide, ammonium carbonate, potassium carbonate, and sodium carbonate.
Fundamentals of Toxicology. DOI: http://dx.doi.org/10.1016/B978-0-12-805426-0.00023-8 © 2016 BSP Books Pvt. Ltd. Published by Elsevier Inc. All rights reserved.
267
268
CHAPTER 23 Toxic effects of caustics (corrosives)
Table 23.1 Selective List of Commonly Used Caustics Strong Acids
Strong Alkalis
Others
Inorganic acids (mineral acids): Sulfuric, nitric, hydrochloric, and hydrofluoric acids Organic acids: Carbolic, oxalic, and salicylic acids
Anhydrous ammonia, potassium hydroxide, sodium hydroxide, ammonium carbonate, potassium carbonate, sodium carbonate
Hydrogen peroxide, iodine, potassium permanganate, quaternary ammonium compounds
Table 23.2 Comparative Characteristics of Sulfuric, Nitric, and Hydrochloric Acids Sulfuric Acid Synonymous
Oil of vitriol
Physical properties
Heavy Colorless Viscid/oily Nonfuming Gives heat with water Charring positive
Fatal dose Fatal period Commercial use
Burning acid taste 5 10 mL 12 24 min Textile, arts, and industry
Nitric Acid Aqua fortis, spirit of niter Heavy Colorless Not viscid/oily Fumes (yellow) in air Not so Xanthroproteic reaction positive Choking odor 10 15 mL 24 30 min Industries
Hydrochloric Acid Spirit of salts, muriatic acid Heavy Colorless Not viscid/oily Fumes in air Not so Not so Not so 15 20 mL 15 24 min Cleansing agent
23.3 ACIDS 23.3.1 INORGANIC ACIDS/MINERAL ACIDS Sulfuric, nitric, and hydrochloric acid Acids are hydrogen-containing substances that, on dissociation in water, produce hydrogen ions. They are potent desiccants with the ability to produce coagulation necrosis of tissues on contact (except hydrofluoric acid, which produces liquefactive necrosis). When a strong acid is dissolved in a solvent, an exothermic reaction ensues, resulting in the emanation of heat, which is referred to as the heat of solution. Table 23.2 summarizes comparative characteristics of sulfuric, nitric, and hydrochloric acids.
23.3 Acids
Mode of action Strong acids act as corrosives, burning all tissues in the upper gastrointestinal (GI) tract when digested and sometimes resulting in esophageal or gastric perforation. They produce coagulation necrosis characterized by the formation of a coagulum (eschar) as a result of the desiccating action of the acid on proteins in superficial tissues. The coagulum formed limits the penetrating ability of acids. However, strong alkalis create injury to tissue by the mechanism of liquefaction necrosis. Alkalis, unlike acids, produce extensive penetrating damage. Squamous epithelium of the esophagus is more resistant to acids than is the columnar epithelium of the stomach. Therefore, esophageal strictures are more common in alkali poisoning, and pyloric and gastric strictures are more common in acid poisoning. Dilute acids and alkalis act as irritants, and corrosion is not really a prominent feature. The mode of action of acids is summarized in Fig. 23.1. Signs and symptoms After oral consumption, corrosion of the GI and respiratory tracts is common but varies in intensity depending on the type and concentration of the acid. Fig. 23.1 shows the respiratory signs and symptoms after ingestion of all inorganic acid poisons, except hydrofluoric acid. The oral cavity shows chalky white teeth, swollen blackish tongue, and swollen lips. Acid burn (eschar) is
Corrosion (any part of the body)
Extraction of water
Liberation of heat
Coagulation and precipitation of cellular proteins
Conversion of hemoglobin to hematin
Corrosion and destruction of tissues
FIGURE 23.1 Schematic representation of the mechanism of coagulation necrosis.
269
270
CHAPTER 23 Toxic effects of caustics (corrosives)
commonly seen because vomited acid trickles down the angle of the mouth toward the neck and chest. The abdomen may be distended and tender. Immediate death may be due to suffocation and asphyxia due to edema of the glottis; exhaustion and shock may be due to circulatory collapse or perforation of stomach; and delay in death may be due to starvation and dehydration because of stricture of the esophagus or pylorus. The victim may also die due to peritonitis or secondary infections. The mind remains sound until death. Postmortem findings External Corrosion of parts that come in contact with the acid, especially the lips, mouth, throat, chin, angle of mouth, and hands. Internal The findings are restricted to the upper GI and respiratory tract and lead to corrosion. Treatment The management of poisoning should be carefully undertaken. Certain general measures such as respiratory distress due to laryngeal edema should be treated with 100% oxygen. Demulcents: Milk (canned condensed milk), egg white (beaten), vegetable oils, starch solution, barley water, and thin oatmeal should be administered. Immediate dilution with milk or water within 30 min of ingestion is strongly recommended for oral ingestions. Do not attempt to neutralize the acid with weak bases/dilute alkalizers such as milk of magnesia or lime water (ie, calcium hydroxide in water), because an exothermic reaction may extend the corrosive injury. Do not give alkalis such as sodium bicarbonate because they can produce carbon dioxide gas, which increases the risk of perforation of the stomach. Airway maintenance and artificial respiration are necessary if there is any respiratory distress. Use morphine/pethidine for relief of pain and IV fluids and electrolytes for dehydration. No oral feeding should be administered until endoscopy confirms the extent of injury. The use of antibiotics for controlling infections is recommended. There is controversy regarding the use of corticosteroids (although proven to be good for delaying or preventing stricture formation in experimental animal studies) in the treatment of acid poisoning. Skin care for any skin lesions involves copious saline irrigation. Treat with nonadherent gauze and wrapping. Deep second-degree burns may benefit from topical application of silver sulfadiazine. Eye care for any acid injuries requires copious irrigation with retraction of the eyelids for 20 30 min. Antibiotic eye drops can help combat infections. However, it may be necessary to refer the patient to an ophthalmologist for further treatment. Emesis and gastric lavage are contraindicated (to prevent gastric perforation; however, there is an exception with organic acids).
23.3.1.1 Hydrofluoric acid Hydrofluoric acid is a colorless gas that becomes a fuming liquid when dissolved in water. It is used for etching glass and clouding electric bulbs.
23.3 Acids
The fatal dose is approximately 15 mL. The fatal period varies from a few minutes to 2 h. However, there have been reports of deaths occurring within 7 h of poisoning. Mode of action The mode of action of hydrofluoric acid exposure is quite different from that of other inorganic acids. The fluoride anion produces liquefaction necrosis by binding with calcium and magnesium in the tissues, thus resulting in hypocalcemia and rendering hydrofluoric acid poisoning more serious. Signs and symptoms Following ingestion, the patient shows hematemesis, hypovolemic tonic convulsions, upper airway obstruction, severe hypocalcemia, acidosis, shock, and coma. Myocardial irritability and subsequent life-threatening cardiac arrhythmias may be due to binding of potassium, magnesium, and calcium ions. Skin exposure can result in severe and deep burns, which are extremely painful and slow to heal. Postmortem findings The lips, tongue, and mouth may show white patches or may be charred. The esophagus may show shredded epithelium with ecchymosis, inflammation, ulceration, and blackening of the stomach. Liver and kidneys show fatty and parenchymatous degeneration. Treatment The following treatment is recommended: • • •
Acid burn lesions need copious irrigation with water and application of calcium and gluconate gel. Debridement may also be needed. Intra-arterial infusion of 20% calcium gluconate or calcium chloride is effective. Oxygen inhalation after removal from fumes and tracheotomy, if needed, should be performed.
23.3.2 ORGANIC ACIDS 23.3.2.1 Carbolic acid (phenol) Carbolic acid is a poison that can be identified by its smell, which is commonly referred to as a phenolic odor or hospital odor. Pure phenol has a colorless, short, prismatic, needle-shaped, crystalline form. On exposure to air, it turns pink and liquefies. It is fat-soluble; therefore, it can attack the nervous system. It is also soluble in glycerin, ether, and alcohol, and it is slightly soluble in water. It is known specifically for its antiseptic or disinfectant property. Other members of phenol group: Phenol has several derivates, namely, cresol, creosote, lysol, and dettol. These are absorbed orally, through intact skin, by the GI tract, through inhalation by the respiratory tract, per rectum, and per vaginum. The toxicological actions of these compounds are similar to phenol but less severe. • •
Cresol is a methyl phenol with meta, ortho, and para isomers. It is used as a disinfectant and antiseptic. Creosote is a mixture of phenols consisting mainly of cresol and guiacol. It is used as a household remedy for coughs and is found in many proprietary preparations.
271
272
CHAPTER 23 Toxic effects of caustics (corrosives)
•
Resorcinol is a colorless crystalline substance used for the treatment of various skin diseases, including ringworm, psoriasis, and eczema. • Lysol is a 50% solution of cresol (3-methyl phenol) in saponified vegetable oil. • Thymol is an alkyl derivative of phenol obtained from volatile oils of Thymus vulgaris, Monarda punctata, or Trachyspermum ammi. It occurs in colorless crystals with a characteristic pungent odor and taste. Previously, it was used as an antihelminthic (for ankylostomiasis), antifungal, and antiseptic. Mode of action Phenol is a protoplasmic poison. It enters into loose combination with proteins and penetrates deep into the tissue. When applied to the skin or mucosa, it causes necrosis and gangrene. The local nerve endings are first stimulated and then paralyzed, resulting in anesthesia. After absorption, it causes widespread capillary damage and clotting in superficial blood vessels. It also acts on the cells of the central nervous system, heart, and kidneys. Phenol is mainly metabolized by the kidneys, wherein it gets converted into hydroquinone and pyrocatechol and then is excreted in urine. These products turn urine olive green or brown on standing, which is a phenomenon called carboluria. Complete elimination occurs in 36 h. Phenol is nephrotoxic (other nephrotoxics are heavy metals, methanol, oxalic acid, salicylates, phenacetin, EDTA, and penicillamine). Signs and symptoms Poisoning by carbolic acid is known as carbolism. The usual signs and symptoms of carbolism include headache, giddiness, tinnitus, vomiting, diarrhea, abdominal pain, and a burning sensation. Inhalation of vapors leads to laryngeal edema and stertorous breathing with cyanosis. Pupils are dilated. If the patient survives for 48 h, then carboluria followed by anuria are seen. The victim will pass dark, smoky urine, which soon turns olive green on standing. Nervous symptoms are common. Methemoglobinemia is a characteristic feature in severe cases. Muscular spasms and convulsions, collapse/unconsciousness, and coma followed by death occur due to respiratory and circulatory failure. Diagnosis: Corrosions on the face, around and inside the mouth (greyish white with phenol or brownish with lysol), phenolic odor (breath/vomit), carboluria, dilated pupils, and stertorous breathing. The fatal dose is 5 15 g. The fatal period varies from 2 to 12 h (rapid death, if injected intrauterine). Postmortem findings External Greyish or brownish corrosions at the angle of the mouth and thin cracks in the body, arms, and hands (splashes), with characteristic phenolic odor. Internal Corrosion of gastrointestinal mucosa and laryngeal and pulmonary edema have been observed in all orally ingested poisoning cases. However, there are certain specific findings, such as the stomach emitting a phenolic odor. Gastric mucosa will show marked corrosion and swelling of mucosal folds with coagulated greyish or brownish silvery mucus. Intervening normal mucosal folds appear dark red.
23.3 Acids
The kidneys will show hemorrhagic nephritis when the victim survives for some time after poisoning. Vomit and gastric lavage collection may show partially detached gastric mucosa. Treatment Symptomatic treatment should include artificial respiration, tracheal aspiration of secretions, and glucose saline to induce diuresis. In case of poisoning through skin absorption, use the following: • • • • •
Remove the contaminated garments. Cleanse the site by mopping with a wet cloth and wash with soap and water. Apply olive oil/methylated spirit/10% ethyl alcohol, which can prevent further absorption. Move the victim to fresh air. Give normal saline plus sodium bicarbonate (intravenous (IV) drip). In case of poisoning through the oral route, perform the following:
•
•
Gastric lavage: Although phenol corrodes the stomach wall, it also hardens it, unlike other corrosive poisons. Hence, gastric lavage is performed whenever possible with plenty of lukewarm water containing animal charcoal, olive oil, magnesium or sodium sulfate, or saccharated lime soap solution with 10% glycerin. When the lavage is completed, 30 g of magnesium sulfate or medicinal liquid paraffin should be left in the stomach. Give egg whites and Epsom salts/demulcents orally.
23.3.2.2 Oxalic acid (acid of sugar) Oxalic acid is a colorless, prismatic, crystalline substance (similar to magnesium sulfate (MgSO4) and zinc sulfate (ZnSO4)). It acts locally as a corrosive on the skin and mucosa (more severe). After absorption, it affects blood electrolytes. It can remove tissue calcium, leading to hypocalcemia, followed by cardiovascular shock, tubular necrosis, uremia, and death. The fatal dose is 15 20 mg. The fatal period ranges from 1 to 2 h. Signs and symptom With large oral doses (15 g or more), it can lead to a sour and acidic taste, followed by a sensation of constriction around the throat and burning pain from the mouth to the epigastrium, which radiates all over the abdomen. There will be tenderness in the epigastrium, nausea followed by vomiting (coffee ground colored vomit), severe thirst, diarrhea, electrolyte imbalance, and hypocalcemia, leading to muscle irritability, tenderness, tetany, convulsions, tingling of extremities, coma, collapse, and death. In case of slow poisoning, there is uremia. Urine is scanty, with traces of albumin. Microscopically, blood and calcium oxalate crystals are observed. Postmortem findings External There are no specific findings; however, sometimes, burns of the face and skin may be seen.
273
274
CHAPTER 23 Toxic effects of caustics (corrosives)
Internal Specific findings are that the mucosa of the mouth, tongue, pharynx, and esophagus may be bleached (whitened/scale/red) if a strong solution is consumed. Stomach Changes The stomach mucosa is reddened and punctate due to erosions, giving a “velvety red” or blackish appearance. The wall of the stomach is softened, but there are no perforations. The stomach contents are gelatinous brown (due to acid hematin formation). All other viscera are congested. Kidneys are swollen and congested. On histopathology, tubules are filled with oxalate crystals. Treatment General management should include gastric lavage with calcium lactate (two teaspoons per lavage), 10 mL calcium gluconate IV frequently, parathyroid extracts of 100 units IM, demulcent drinks, enema, and purgatives (castor oil). Symptom-based treatment should also be followed. Antidotes such as lime water, calcium lactate, calcium gluconate, calcium chloride, and chalk suspension in water or milk may be administered orally. These form insoluble calcium oxalate and are excreted easily.
23.3.2.3 Formic acid (methanoic acid, formylic acid) Formic acid is a colorless liquid with a pungent penetrating odor. It is completely soluble in water and is used as bath cleaner. Generally, airplane glue makers, cellulose format workers, and tanning salon workers are exposed to a 60% solution of formic acid. Signs and symptoms Skin contact produces brownish discoloration, dermatitis, pustules, vesicles, and sometimes sloughing. Formic acid is unique for its ability, in many patients, to cause death after a prolonged (several weeks) course of classical acid-induced gastrointestinal damage. Certain other complications include severe metabolic acidosis, intravascular hemolysis, and disseminated intravascular coagulation. Accidental ingestion in children usually does not lead to fatalities because the pungent taste prevents ingestion of a lethal dose. Nevertheless, it is a problem when used deliberately for suicide. It causes acute trachea bronchitis, which is characterized by cough, sore throat, chest pain, and light-headedness. Formic acid skin burns may also result in systemic toxicity. When absorbed by the body, it causes systemic acidosis, hematuria, and renal damage. The metabolism of methanol can also produce toxic metabolites of formic acid. Treatment Treatment is by correction of acidosis by infusion of sodium bicarbonate intravenously and hemodialysis for renal failure.
23.3.2.4 Salicylic acids An important therapeutic preparation of this is acetyl salicylic acid (aspirin). Details are discussed in another chapter dealing with therapeutic agents.
23.4 Alkalis
23.4 ALKALIS Like acids, alkalis also act as corrosive poisons when administered in the concentrated form, but they act as an irritant poison when diluted. Alkalis are present in a number of household products (eg, drain cleaners, oven cleaners, dishwasher products, some paint strippers, etc.) and are also used in industry. Alkalis commonly encountered in poisoning include ammonia (usually in the form of ammonium hydroxide) and carbonates of sodium and potassium. Hydroxides of sodium and calcium and sodium hydrochloride are also increasingly used in household cleaning agents such as detergent. Mode of action Alkalis generally contain hydroxyl groups, which on dissociation in water produce hydroxide ions. Alkali agents injure the GI tract by saponification of fats and solubilization of proteins that allow deep penetration into tissue. Thus, unlike acids, they produce extensive penetrating damage. This pathogenesis of injury is rapidly progressive and may extend weeks after onset. Alkalis have more severe corrosive effects on the esophagus (acids produce corrosive effects on the stomach). Severe esophageal damage can occur if the pH is lower than 11. However, with deliberate ingestion of large quantities, corrosive effects can be seen anywhere from the mouth to the small intestine. Locally, alkalis produce liquefaction necrosis, which results in extensive penetrating damage because of saponification of fats and solubilization of proteins. Ulcers are common and may persist for several weeks. Signs and symptoms The esophagus is often severely affected, resulting in dysphasia, vomiting, and hematemesis. Stridor is an important indicator of severe esophageal injury. Eye involvement can produce serious complications of ophthalmologic emergency. The fatal dose is 10 15 g for most alkalis and 15 to 20 mL for ammonia. Treatment Treatment involves removal from exposure and rest, and also symptom-based treatment. Corneal irrigation with water and topical use of antibiotics are recommended.
275