Corrosive Poisoning

Robert P. Dowsett

Christopher H. Linden

Initially referring to acids, the term corrosives is now used synonymously with caustics, a term originally applied to alkalis. In solution, acids and bases donate or accept a proton altering the hydrogen ion concentration. This is measured as pH, the negative logarithm of the H⁺ ion concentration (M/L) Water, at 25°C, has a pH of 7 and is considered neutral. Solutions with a pH of less than 2 or greater than 12 are considered strongly acidic or basic. The pH levels of some common solutions are listed in Table 130.1.

Corrosives cause injury by reacting with organic molecules and disrupting cell membranes. They also cause thermal burns if heat is generated by dissolution and neutralization reactions. Reactions between strong acids and strong bases are usually highly exothermic. Metallic lithium, sodium, potassium, some aluminum and lithium salts, and titanium tetrachloride react violently when placed in water, producing large amounts of heat. Chlorine reacts with water in an exothermic reaction to form hydrochloric and hypochlorous acids, elemental chlorine, and free oxygen radicals. Similar reactions occur with bromine. Ammonia combines with water to form ammonium hydroxide in a reaction that liberates heat; the hydroxide formed is then responsible for corrosive effects. Nitrogen dioxide reacts with water to release heat and produce nitric and nitrous acid. Hydrogen peroxide liberates oxygen on contact with water.

The mixing of chemicals can result in reactions that liberate caustic gases. Mixing ammonia with hypochlorite (household bleach) generates chloramine gases (NH₂Cl and NHCl₂), which are highly irritating to mucosal epithelia. Combining bleach with acid (acid toilet bowl or drain cleaners) produces chlorine gas. A number of metallic compounds react with acids, resulting in the liberation of potentially explosive hydrogen gas. Hydrogen sulfide and sulfur oxide gas result from the action of acids on sulfur-containing compounds such as orthopedic plaster casting material in sink drains [1]. Zinc hydroxide, present in soldering flux, is corrosive in an acidic environment such as the stomach [2].

Table 130.1 Approximate pH of Common Solutions

Solution	pH
1.0 M hydrochloric acid	0
1 M hydrochloric acid solution	0
1 M nitric acid solution	0
0.1 M sulfuric acid	0.96
Battery acid (1% solution)	1.4
Gastric juice	1.2–3.0
Lemon juice	2
Domestic toilet cleaner (1%)	2.0
1 M acetic acid solution	2.37
1 M carbonic acid	5.7
Rain water	6.5
Water (pure, at 25°C)	7.0
Bleach (1% solution)	9.5–10.2
Automatic dishwasher detergents	10.4–13.0
Laundry detergents	11.6–12.6
Domestic ammonium cleaners	11.9–12.4
Ammonia 10%	12.5
Oven cleaner	13
Drain cleaner	13.3–14.0
1.0 M potassium hydroxide	14
1.0 M NaOH	14
Saturated ammonia solution	15

During 2007, 147,703 exposures to corrosive chemicals were reported by U.S. poison centers; actual exposures are estimated to be several times greater [3]. Lethal exposures constituted 1.9% of all reported deaths due to poisoning [3]. Exposures to chemicals accounted for 7.6% of poisonings in children younger than 6 years of age. Only a few of these cases resulted in serious injury, with only three deaths. Adults, usually by deliberate intent, ingest a larger amount of corrosive [4]. Deaths most commonly result from intentional exposure to drain cleaners and acidic cleaners [3].

Concentrated lye (sodium or potassium hydroxide) solutions used for laundering and plumbing purposes caused most of the serious injuries due to corrosive ingestions before 1970 [5]. Currently available liquid lye drain cleaners are less concentrated (less than 10%) but are still responsible for the largest number of severe gastrointestinal injuries; however, acid bowl cleaners now account for almost as many deaths [3]. Severe alkali injuries can result from the ingestion of powdered automatic dishwasher detergents and oven cleaners [6,7]. Household ammonia and bleaches, and hydrogen peroxide solutions are in general much less potent than industrial ones but can cause significant injury if ingested in large amounts [4,6].

Table 130.2 Grading of Severity of Ocular Chemical Burns

Grade	Cornea	Limbal ischemia	Prognosis
I	Epithelial loss	None	Good
II	Stromal haze, iris details visible	< 1/3 of vessels affected	Good
III	Total epithelial loss, iris details obscured	1/3–½ of vessels affected	Doubtful, vision reduced
IV	Opaque, no view of iris or pupil	> ½ of vessels affected	Poor

Pathophysiology

Alkalis cause liquefaction necrosis, a process resulting from the saponification of fats, dissolution of proteins, and emulsification of lipid membranes. The resultant tissue softening and sloughing may allow the alkali to penetrate to deeper levels. Tissue injury progresses rapidly over the first few minutes but can continue for several hours [8]. Over the ensuing 4 days, bacterial infection and inflammation cause additional injury. Granulation tissue then develops, but collagen deposition may not begin until the second week. The tensile strength of healing tissue is lowest during the first 2 weeks. Epithelial repair may take weeks to months. Scar retraction begins in the third week and continues for months.

Acid burns are characterized by coagulation necrosis. Protein is denatured, resulting in the formation of a firm eschar [9]. The release of heat is typically higher than for alkali reactions [10]. Subsequent responses are similar to those seen with alkalis.

Hydrocarbons can produce injury by dissolving lipids in cell membranes and coagulating proteins. Significant damage may occur with ingestion or after prolonged dermal contact [11]. Ingestion of a toluene containing glue can cause caused corrosive esophagitis [12]

Alkaline solutions with a pH of greater than 12.5 are likely to cause mucosal ulceration, with deeper tissue necrosis resulting if the pH approaches 14 [13]. However, solutions with a pH of less than 12.5 can still cause significant injury, and solutions of different chemicals but the same pH produce different degrees of tissue damage [13].

The physical state of a chemical also influences its toxicity. Corrosives that are gases at room temperature primarily affect the skin, eyes, and airways. Saturated acid solutions may liberate significant amounts of acid fumes, particularly if heated. Solid compounds tend to produce highly concentrated solutions on contact with body fluids and cause more severe injuries [14]. Solutions with a high viscosity tend to cause deeper burns [13].

Most systemic effects that occur after exposure to corrosives are secondary to inflammation, acidosis, infection, and necrosis [15]. Fluid and electrolyte shifts occur, resulting in hypovolemia, acidosis, and organ failure. Some chemicals, such as phenol, hydrazine, and chromic acid, can be absorbed after dermal exposure or ingestion and cause systemic toxicity [16,17].

Clinical Manifestations

Chemical burns to the eye range from irritation to severe and permanent damage [18]. Eye pain, blepharospasm, conjunctival hemorrhages, and chemosis are seen in all grades of injury. Decreased visual acuity may result from excessive tearing, corneal edema and ulceration, anterior chamber clouding, or lens opacities. Roper-Hall’s classification of injury predicts severity of subsequent vision loss [19] (Table 130.2).
Severe burns can result in increased intraocular pressure, anterior chamber clouding, lens opacities, and perforation of the globe [18]. Severity can be assessed by the extent of ischemia of conjunctival vessels at the limbus of the eye. If more than half of these vessels are obliterated, the prognosis is poor [19].

Significant differences exist between thermal and chemical burns of the skin. Although pain usually occurs immediately, it may be delayed several hours after corrosive exposure [20]. Assessing the depth of dermal injury can be difficult. Chemical burns rarely blister, and the affected skin is usually dark, insensate, and firmly attached regardless of the burn depth [21]. Healing usually takes longer than for thermal burns.

Some chemical warfare agents cause severe dermal injury. Sulfur mustard, the most common antipersonnel agent used, and lewisite (chlorovinylarsine dichloride) are potent alkylating agents, resulting in severe vesiculation of the skin 4 to 12 hours after exposure. Phosgene oxide has a similar action, but its effects are almost immediate. Respiratory burns are nearly always associated with sulfur mustard exposure [22]. White phosphorus is used in incendiary devices and in the manufacture of fertilizers and insecticides. It ignites spontaneously when exposed to air.

Ingested corrosives typically injure the oropharynx, esophagus, and stomach but may cause damage as distal as the proximal jejunum [23,24]. Areas most commonly affected are those of anatomic narrowing: the cricopharyngeal area, diaphragmatic esophagus, and antrum and pylorus of the stomach [23]. Multiple sites are affected in up to 80% of patients [24]. Esophageal lesions are seen predominantly in the lower half, and gastric burns are usually most severe in the antrum [24]. In the presence of food, gastric injuries tend to be less severe and involve the lesser curve and pylorus [10]. Vomiting is associated with a higher incidence of severe esophageal injuries [25].

Ingestion of alkali is associated with a higher incidence and severity of esophageal lesions than ingestion of acid, which typically causes stomach injury although this is not a consistent finding [4,25]. Alkaline agents have little taste, but acids are extremely bitter and more likely to be expelled if accidentally ingested.

Alkaline solids may adhere to mucosa of the oropharynx and cause oral pain that limits the quantity swallowed, thus sparing the esophagus [26]. If alkaline solids are swallowed, severe upper esophageal burns are seen [27]. Shallow ulcers may result when tablets become lodged in the esophagus (pill esophagitis). Hemorrhage and stricture formation may occur after esophageal impaction of potassium chloride, iron, quinidine, etidronate, antibiotics, and anti-inflammatory agents [28].

Common symptoms from corrosive ingestion are oropharyngeal pain, dysphagia, abdominal pain, vomiting, and drooling [29]. Less commonly, stridor, hoarseness, hematemesis, and melena are seen. Patients who are asymptomatic are unlikely to have significant injuries, although this may be difficult to assess in children who may appear to have no or minimal symptoms [29]. Vomiting, drooling, and stridor appear to be predictive of more severe injuries [29].

The absence of burns in the oropharynx does not exclude burns further along the gastrointestinal tract, and it is not predictive of less severe distal injuries [29]. Patients with laryngeal burns have a greater incidence and severity of esophageal lesions [25].

Hemorrhage, perforation, and fistula formation may occur in patients with full-thickness esophageal necrosis [24]. Untreated, perforations rapidly progress to septic shock, organ failure, and death. Some gastric perforations may become walled to form an abscess around the liver or in the lesser sac.

Severe gastric burns may extend to adjacent organs [30]. Perforation of the anterior esophageal wall may lead to formation of a tracheoesophageal fistula and tracheobronchial necrosis [31,32]. Tracheoesophageal–aortic and aortoesophageal fistulas, rare and uniformly fatal complications, are suggested by hemoptysis or hematemesis, which develops into torrential bleeding [33,34].

Burns to the larynx occur in up to 50% of patients and are the most common cause of respiratory distress [25]. Typically, the epiglottis and aryepiglottic folds are edematous, ulcerated, or necrotic. The absence of respiratory symptoms on presentation does not exclude the presence of laryngeal burns that may eventually require intubation [25]. Respiratory distress may also be due to the aspiration of corrosives [35].

Esophageal strictures develop in up to 70% of burns that result in deep ulceration, whether discrete or circumferential, and nearly all burns resulting in deep necrosis [24]. Strictures do not develop after superficial mucosal ulceration [35]. Strictures may become symptomatic as early as the end of the second week; half develop during initial hospitalization, and 80% are evident within 2 months [36]. Those that develop early often progress rapidly and require urgent intervention. Gastric outlet strictures may also occur, but only 40% become symptomatic [24]. Strictures can develop in the mouth and pharynx [25].

Esophageal pseudodiverticulum may occur in patients with esophageal stricture as early as 1 week after corrosive ingestions. It appears to result from incomplete destruction of the esophageal wall and usually resolves with dilation of associated strictures [37].

Deaths that occur are in patients who have extensive necrosis in the upper gastrointestinal tract. Sepsis secondary to perforation is the most common cause of death; severe hemorrhage or aspiration may also contribute [24].

Esophageal carcinoma, usually squamous cell, is a well-documented complication of alkali burns [38]. It occurs most commonly at the level of the tracheal bifurcation and is estimated to occur 1,000 times more frequently in patients who have had corrosive injuries than in the general population. Symptoms can develop 22 to 81 years after the initial insult.

Systemic toxicity has occurred with burns caused by arsenic and other heavy metals, cyanide, acetic acid, formic acid, fluoride, hydrazine, hydrochloric acid, nitrates, sulfuric acid, and phosphoric acid [39,40,41,42,43]. Severe acid burns may be accompanied by a metabolic acidosis and hypotension. The anion gap is usually elevated, although a hyperchloremic acidosis may be seen in hydrochloric acid and ammonium chloride ingestion. After hydrochloric acid ingestion, cardiovascular collapse is the most common cause of early death; myocardial infarction has occurred after large ingestions. Other findings associated with severe acid injuries include hemolysis, hemoglobinuria, nephrotoxicity, and pulmonary edema [40,41,43].

Only gold members can continue reading. Log In or Register to continue