Soaps

Soaps are generally low in oral toxicity. However, some soaps, such as homemade soaps and laundry soaps, have an appreciable content of free alkali, thus presenting a possible corrosive hazard.^2,3 Commercial bar soaps generally have a low order of toxicity, but may cause emesis and diarrhea because of gastrointestinal irritation. This irritation may result in part from the essential oils used as fragrances in bar soaps.² Treatment involves the use of demulcents and diluents, such as milk or water. Induction of emesis may be considered if the ingested quantity exceeds 20 g of soap/kg BW, and the soap is nonalkaline (noncorrosive), or if spontaneous emesis has not occurred within 30 minutes of ingestion. If diarrhea or excessive vomiting occurs, symptomatic treatment and efforts should be started to maintain fluid and electrolyte balance.

Nonionic detergents

Many products contain nonionic synthetic detergents formulated into hand dishwashing detergents, shampoos, and some laundry detergents. Nonionic surfactants are uncharged in aqueous solutions at neutral pH. Nonionic detergents are alkyl ethoxylate, alkyl phenoxy polyethoxy ethanols, and polyethylene glycol stearate.⁴

The majority of nonionic detergents have a low order of irritation and thus low toxicity. Ingestions of nonionic detergents usually result in only vomiting and diarrhea, and ocular exposures to nonionic detergents generally do not produce extensive liquefaction of the corneal epithelium.² Depending on the exposure route, treatments for nonionic detergent exposures should include diluting ingestions with milk or water, rinsing exposed eyes with copious amounts of water, or thorough rinsing of detergents from skin and hair coats. If protracted vomiting occurs, treatments to reverse the effects and measures should be performed to maintain fluid and electrolyte balance.

Anionic detergents

Anionic surfactants are primarily sulfonated or phosphorylated straight-chain hydrocarbons. These compounds are used commonly in laundry detergents, electric dishwashing detergents, and in some shampoos. Among the more common anionic detergents are alkyl sodium sulfates, alkyl sodium sulfonates, dioctyl sodium sulfosuccinate, sodium lauryl sulfate, tetrapropylene benzene sulfonate, and linear alkyl benzene sulfonates.⁴ Many of these materials contain alkali builders, such as sodium phosphate, sodium carbonate, sodium metasilicate, or sodium silicate, to increase their effectiveness in hard water.

Most anionic detergents are slightly to moderately toxic. Electric or automatic dishwashing detergent products are considered most toxic because of their high alkalinity. The caustic potential of automatic dishwashing detergents has recently been evaluated and remains the topic of great controversy. The pH of 1% solutions of automatic dishwashing detergents is less than the supposedly critical pH of 12.5 traditionally associated with corrosive injury to the esophagus⁵; however, large ingestions of automatic dishwasher detergents are still practical risks to cause corrosive damage, depending on the composition, concentration, physical form, duration of exposure, and viscosity of the product. In general nonphosphate-containing electric dishwashing detergents induce greater tissue irritation and injury than phosphate-containing automatic dish detergents.⁶

Ingested anionic detergents are well absorbed from the intestinal tract. Healthy skin appears to be a good barrier to anionic surfactants, but such surfactants can be absorbed through irritated or broken skin. Anionic detergents are metabolized by the liver, and the metabolites are excreted in the urine.² Intravascular hemolysis may occur with anionic detergent exposure in patients with impaired liver function; the liver dysfunction is thought to be related to the detergent concentrations in the blood.² Prolonged or repeated cutaneous exposure to anionic detergents may result in irritation. Ocular exposure to automatic dish detergents has been reported to cause corneal erosion and opacity.⁵ Ingestions of anionic detergents often result in vomiting, nausea, diarrhea, and gastrointestinal discomfort. Most exposures cause illness but are not fatal.

Oral administration of milk or water to dilute the detergent is advised. Activated charcoal should be given if large quantities of detergent have been ingested and if corrosive injury has not occurred to the gastrointestinal tract. With ocular exposure, the eyes should be rinsed with copious amounts of water. Thorough bathing and rinsing is recommended for dermal exposures. If protracted vomiting occurs, symptomatic treatment and measures should be instituted to maintain systemic fluid and electrolyte balance. The patient should be monitored for the development of hemolysis. If hemolysis does occur, intravascular fluids and alkalinization of the urine are recommended to prevent renal tubular damage from the precipitation of hemoglobin in renal tubules or the resultant hypoxia, and renal function should be monitored. In patients that have ingested automatic dishwashing detergent, evaluation may be warranted of the mouth, oropharynx, and esophagus for corrosive injury. Treatment for corrosive injuries should be started as described later in the Corrosives section.

Cationic detergents

Cationic detergents are used as fabric softeners, germicides, and sanitizers and are considered highly or extremely toxic. The cationic surfactants are quaternary ammonium compounds with aryl or alkyl substituent groups, one of which is often a long hydrophobic carbon chain. Generally a halogen, such as bromide, iodide, or chloride, is also attached. These agents include benzethonium chloride, benzalkonium chloride, alkyl dimethyl 3,4-dichlorobenzene, and cetyl pyridinium chloride.⁴

Toxicoses in animals and humans have been reported from quaternary ammonium compounds.^7–9 The observed toxicity of cationic detergents can be divided into local effects, dependent on concentration and systemic effects, which are dose related.⁹ Cationic detergent concentrations as low as 1% are damaging to mucous membranes, and solutions containing more than 7.5% of cationic detergents may cause corrosive burns of the mouth, pharynx, and esophagus.

Quaternary ammonium compounds are absorbed from the gastrointestinal tract, but several factors modify this systemic absorption. Ethanol and isopropanol, which are often found in cationic detergent preparations, significantly enhance gastrointestinal absorption. In contrast, food and chyme in the stomach reduce absorption by forming unabsorbable complexes.^2–10 Percutaneous absorption through intact skin is not a major route of absorption for these compounds, although quaternary ammonium compounds may be absorbed through damaged skin.² Ingestion of these detergents from licking or grooming irritated skin surfaces and paws is also a significant exposure pathway for dogs and cats.

A mechanism explaining the systemic effects of cationic detergent toxicity has not been established. There are conflicting reports of cholinesterase inhibition caused by quaternary ammonium compounds.³ These compounds also possess ganglionic blocking potential and a curare-like action that causes paralysis of the neuromuscular junctions of striated muscles.^2,3,9 This hypothesis is supported by the structural similarities between quaternary ammonium compounds and decamethonium, a neuromuscular blocking agent, and hexamethonium, a ganglionic blocking agent.³

The principal clinical signs of these poisonings are profuse salivation, vomiting with possible hematemesis, muscle weakness, fasciculations, central nervous system (CNS) and respiratory depression, fever, seizures, collapse, and coma. These effects are very similar to, and must be differentiated from, those of pesticide poisonings. Cationic detergent ingestions usually result in corrosive damage to the mucous membranes of the mouth, tongue, pharynx, and esophagus. Shock may develop early or as the toxicosis progresses. Hair loss and skin ulcerations are frequently seen in cats,⁸ and inflammatory lesions of the paws are reported in dogs after exposure to quaternary ammonium compounds.⁷ Ocular exposure may result in clinical effects of mild discomfort to very serious corneal damage, depending on the concentration of the detergent.

Treatment of ingestions requires the giving of milk, water, or egg whites. Vomiting should not be induced when the concentration of cationic detergent in the product consumed is greater than 7.5%. Oral dilution may be followed by the administration of activated charcoal and a saline cathartic. Esophagoscopy for evaluation of the degree of corrosive damage is appropriate if stridor, dysphagia, or prolonged hypersalivation is present. General supportive care should include maintenance of respiration, adequate caloric intake (e.g., placement of a percutaneous esophageal gastric [PEG] tube), antibiotics, analgesics, IV fluid therapy (monitor blood gas and acid-base status, and serum electrolytes), and treatment of any seizures that may occur. Patients should be monitored closely for shock. The exposed skin should be gently but thoroughly washed with soap and water. The eyes should be thoroughly evaluated, and if ocular exposure has occurred, the eyes should be lavaged with isothermic isotonic saline for 20 to 30 minutes. Corneal ulcers should be promptly and persistently treated if present.²

Corrosives

A number of household products are capable of causing corrosive injury to contacting membranes. Most corrosives are classified as acids or alkalis, depending on their pH in solutions. Strongly alkaline or basic compounds tend to produce more severe injury than acidic materials.^11,12

Acidic household products typically contain hydrochloric (muriatic), sulfuric, nitric or phosphoric acid, or sodium bisulfite, which forms sulfuric acid in water. In addition, aqueous solutions of free halogens (e.g., chlorine, bromine, or iodine) can also be corrosive. Common acidic products include antirust compounds, toilet bowl cleaners, gun barrel cleaning fluid, automobile batteries, and swimming pool cleaning agents. Acids typically produce a localized coagulative necrotic lesion. Because of the rapid surface protein coagulation, acidic burns rarely penetrate the entire thickness of the mucosal membrane. Contact with strong acids induces immediate intense pain, so most animals become alerted to the danger and do not ingest significant quantities.³

Alkaline agents are also found in a variety of household products, such as drain cleaners, washing products, liquid cleansers, and toilet bowl products. Common ingredients are lye formulations (e.g., sodium and potassium hydroxide or potash, sodium and potassium carbonate), ammonium hydroxide, and potassium permanganate.² These alkaline products cause immediate liquefactive necrosis on contact. The lesions tend to be deeper and more penetrating than those caused by acidic materials. Full-thickness esophageal burns may occur. The strength of pH has an important effect on the degree of injury.^2,11,13 Most cases of severe esophageal injury and resulting secondary stricture have occurred from contact with substances with a pH greater than 10.

Concentrated ammonia solution ingested by a cat was shown to cause obliteration of the esophageal wall, seizures, and death within 5 minutes. The increased viscosity of alkalis may contribute to faster and deeper penetration of the esophageal mucosa.¹³

In general corrosive burns of mucosal membranes first appear milky white or gray. Soon, however, the area turns black and may look wrinkled because of eschar formation. The animal may vocalize or become depressed; some animals manifest pain by panting. Inability to swallow may be noted. Other effects are hematemesis, abdominal pain, polydipsia, epiglottic edema with secondary respiratory distress, and possible shock. Secondary pneumonitis may result from aspiration or exposure to acid vapors.^2,11

Esophageal involvement is less common with acid exposures than with alkali ingestions. The character of the commercial formulation also affects the resulting toxicity—solid or granular substances tend to be more painful initially, and burns are more common in the perioral area.¹² Liquids may be less painful initially and thus tend to be swallowed, leading to esophageal and/or gastric injuries. One cannot assume that the absence of oral lesions indicates that the esophagus and/or gastric mucosa will not be damaged—0% to 30% of patients with esophageal burns have no oral lesions; the reverse can also be true.^11,13

Once a corrosive substance comes into contact with mucosal membranes, blood vessel thrombosis, cellular necrosis, bacterial infiltration, and lipid saponification occur and are followed by mucosal sloughing. There is an increase in fibroblastic activity. Strictures may form several weeks after the initial injury. It is believed that strictures are most likely to occur after circumferential burns.¹¹

Food and fluid tend to buffer alkaline substances in the stomach; however, corrosive substances tend to induce pylorospasm. The most severe gastric injuries thus occur around the pylorus, and pyloric stenosis or perforations with secondary peritonitis are possible sequelae.^3,11 In addition to strictures and perforation, other clinical complications are gastrointestinal bleeding, edema, aspiration, fistulae, and gastric outlet obstruction.

If ocular or dermal exposure occurs, serious burns can result. Ocular exposures to either alkaline or acidic solutions are extremely painful and can lead to corneal and/or conjunctival necrosis. The extent of corneal damage may not be immediately evident. When the stroma of the cornea is injured, perforation or opaque scarring may result. Acids tend to penetrate the eye more slowly than do bases.^2,3,11

Treatment consists of immediate dilution of the exposure with milk or water. Dilution with milk in vitro causes the lowest peak temperature, whereas water produces the quickest return to physiological normalcy. Attempts to neutralize the burn chemically (e.g., acids added to basic exposures and basic solutions added to acid exposures) are contraindicated because exothermic reactions will result, producing elevated local heat and causing thermal burns. Unfortunately the action of corrosives is so rapid that dilution is sometimes of little apparent benefit. Controversially, excessive dilution may lead to vomiting, thus increasing esophageal contact time and the opportunity for secondary aspiration. In general, however, dilution is recommended and should be appropriately performed.¹¹

Gastric lavage is contraindicated in caustic ingestions, and charcoal is ineffective in binding caustics. After administration of a diluent, the animal should be given supportive care. Intravenous (IV) fluids are often indicated. If severe pharyngeal edema is present, an endotracheal or tracheostomy tube may be placed to ensure unobstructed respirations. Careful endoscopy with a flexible scope is valuable the first 12 to 24 hours after ingestion, since outward clinical signs do not always correlate with the severity of injury. The procedure should be halted at the first sign of esophageal mucosal injury. Radiographic evaluation is another alternative. Surgical resection of damaged tissue is sometimes advised; however, it is not always possible to easily identify the damaged area, and after-resection leaking of esophageal contents may occur at sites of anastomoses. Steroids, because they decrease fibroblastic activity and inflammation, have been recommended to reduce stricture from circumferential alkali burns. Steroid treatment should be started within the first 48 hours and be accompanied by prophylactic antibiotic therapy. Analgesics are often indicated for pain control. Antibiotics are specifically indicated in animals with perforations. Severely affected patients may require placement of a PEG tube for alimentary nutritional support. It is useful to monitor blood gas and acid-base status and concentrations of serum electrolytes. Therapy for shock may also be required; uncorrected circulatory collapse can lead to renal failure, ischemic lesions of vital organs, and acute death. Affected skin should be aggressively flushed with copious amounts of water, and exposed eyes must be flushed with sterile saline for at least 30 minutes. Topical anesthetics are helpful in patient manipulations and comfort.^2,3,11–13