MOBILE VIEW  | 

AUTOMATIC DISHWASHER DETERGENTS

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) ADDs can be classified as both corrosives and nonionic/anionic surfactants.
    B) Alkaline salts which may include any combinations of sodium tripolyphosphate, pentasodium tripolyphosphate, chlorinated trisodium phosphate, sodium silicate, sodium metasilicate, sodium carbonate, and sodium sulfate. A variety of surfactants are also used in ADDs.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) Sodium silicate
    2) Sodium metasilicate
    3) Sodium carbonate
    4) Sodium phosphate
    5) Trisodium polyphosphate
    6) Chlorinated phosphates
    7) Sodium tripolyphosphates
    8) Sodium dichloroisocyanurate
    9) Sodium borate
    10) Sodium perborate
    11) Sodium sulfate
    12) Anionic surfactants
    13) Nonionic surfactants
    14) Sodium chloride
    15) DISHWASHER DETERGENTS
    16) ELECTRIC DISHWASHER DETERGENTS

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Automatic dishwasher detergents (ADD) consist of a variety of products used for dishwashers to clean dishes and silverware. They come in various forms such as powders, liquids, and tablets.
    B) TOXICOLOGY: Most automatic dishwasher detergents are alkaline with pH values above 10. There alkalinity is responsible for their corrosive and caustic properties, which can lead to injuries ranging from mild tissue irritation to necrosis. Toxicity depends on pH, concentration, composition, physical form, amount and duration of exposure. Liquid products tend to have a higher pH. However, powder and tablet forms can affix to mucosal surfaces resulting in prolonged exposures.
    C) EPIDEMIOLOGY: These are common household products, and a common inadvertent pediatric exposure. Severe toxicity is uncommon/rare and can occur with an industrial strength products or ingestion during a self-harm attempt.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: With small exposures, local mucosal or skin irritation can occur.
    2) SEVERE TOXICITY: Skin burns may occur following exposure to solubilized granular or liquid ADD. Following large ingestions or ingestion of industrial strength products, there can be significant gastrointestinal caustic injury, necrosis and perforation, or mediastinitis. Spontaneous vomiting, diarrhea, dysphagia, and drooling may occur. Esophageal burns may occur without the presence of oral burns especially when a liquid containing the ADD is ingested. Respiratory distress can develop due to aspiration or oropharynx edema and inflammation. Extensive corneal erosion may result with prolonged exposure.

Laboratory Monitoring

    A) In significant ingestions, monitor CBC, serum electrolytes, and blood gases.
    B) In significant ingestions, radiographs should be considered to evaluate for perforation or aspiration.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Initial management includes irrigation if patient has had symptomatic dermal or ocular exposure. If product is ingested, rinse the mouth with water with the immediate removal of obvious granules or gels, and dilution of exposed area.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Respiratory support may be needed for respiratory distress, or airway edema. Initial circulatory support with adequate fluid resuscitation may be needed for dehydration, gastrointestinal bleed, and/or acid-base abnormalities due to large intentional ingestions. Endoscopy will be needed to evaluate the extent of injury.
    C) DECONTAMINATION
    1) PREHOSPITAL: Removal of obvious granules or gels, and dilution/irrigation of exposed areas can be initiated.
    2) HOSPITAL: After an ingestion, rinse mouth and administer small amounts of water. Lavage and activated charcoal are not indicated as toxicity is secondary to local tissue injury.
    D) AIRWAY MANAGEMENT
    1) Respiratory support may be needed for respiratory distress or airway edema.
    E) ANTIDOTE
    1) None.
    F) ENDOSCOPY
    1) INDUSTRIAL PRODUCTS/SIGNIFICANT INGESTIONS: Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after inadvertent ingestion. Endoscopy should also be considered in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion. Children and adults who are asymptomatic after inadvertent ingestion do not require endoscopy. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns.
    G) ENHANCED ELIMINATION PROCEDURE
    1) There is no routine role for hemodialysis.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Most small unintentional ingestions can remain at home. If an industrial product is involved, symptoms persist, self-harm ingestion, healthcare facility referral should be recommended.
    2) OBSERVATION CRITERIA: Patients who are symptomatic should be observed in the emergency department until patient is asymptomatic and tolerating oral intake. Patients with eye exposures should generally be referred to a healthcare facility for evaluation and treatment.
    3) ADMISSION CRITERIA: Patients who have persistent symptoms, respiratory difficulties, intolerance of oral intake, or intentional ingestions, may need to be admitted for further evaluation and endoscopy.
    4) CONSULT CRITERIA: If patients are symptomatic and/or after large ingestions, call your regional poison center. For significant or symptomatic ingestions, gastroenterology may need to be consulted for endoscopic evaluation. In pediatric patients, any stridor, persistent vomiting, or drooling may be indication for endoscopy. For ocular injuries, ophthalmology consultation may be needed.
    I) PITFALLS
    1) Failure to recognize symptoms of gastrointestinal injury, significant ingestion, or attempts to neutralize the product. Absence of oropharyngeal burns do not rule out the possibility of esophageal or gastric burns. Activated charcoal is not indicated, and will interfere with visualization of mucosa if endoscopy is indicated.
    J) TOXICOKINETICS
    1) With alkaline caustics, hydroxide is dissociated and penetrate tissue surfaces and produce a liquefactive necrosis. This process, among other things includes, fat saponification, protein dissolution, and cell death. This is in contrast to acidic caustics, which cause a coagulation necrosis. Common ingredients in detergents include benzalkonium chloride, sodium hydroxide, sodium borates, sodium carbonates, sodium phosphates, sodium silicates, and sodium hypochlorite.
    K) DIFFERENTIAL DIAGNOSIS
    1) Other alkaline and acidic caustic agents such as cleaning agents.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) Irrigate with water or normal saline until pH is neutral. Perform a slit lamp exam to evaluate for corneal.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Small oral or dermal exposures are not likely to cause significant caustic injury.
    B) Sodium metasilicate and sodium carbonate produce more titratable alkali than a comparable amount of a phosphate-containing product.
    C) In general, ADDs which are primarily composed of nonphosphate alkaline chemicals are associated with greater tissue irritation and injury than those containing a majority of phosphate alkaline chemicals.

Summary Of Exposure

    A) USES: Automatic dishwasher detergents (ADD) consist of a variety of products used for dishwashers to clean dishes and silverware. They come in various forms such as powders, liquids, and tablets.
    B) TOXICOLOGY: Most automatic dishwasher detergents are alkaline with pH values above 10. There alkalinity is responsible for their corrosive and caustic properties, which can lead to injuries ranging from mild tissue irritation to necrosis. Toxicity depends on pH, concentration, composition, physical form, amount and duration of exposure. Liquid products tend to have a higher pH. However, powder and tablet forms can affix to mucosal surfaces resulting in prolonged exposures.
    C) EPIDEMIOLOGY: These are common household products, and a common inadvertent pediatric exposure. Severe toxicity is uncommon/rare and can occur with an industrial strength products or ingestion during a self-harm attempt.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: With small exposures, local mucosal or skin irritation can occur.
    2) SEVERE TOXICITY: Skin burns may occur following exposure to solubilized granular or liquid ADD. Following large ingestions or ingestion of industrial strength products, there can be significant gastrointestinal caustic injury, necrosis and perforation, or mediastinitis. Spontaneous vomiting, diarrhea, dysphagia, and drooling may occur. Esophageal burns may occur without the presence of oral burns especially when a liquid containing the ADD is ingested. Respiratory distress can develop due to aspiration or oropharynx edema and inflammation. Extensive corneal erosion may result with prolonged exposure.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CORNEAL DAMAGE
    a) SUMMARY: The eyes are exquisitely sensitive to both the irritant/corrosive effects and mechanical irritation from particulate matter which constitute both liquid and granular ADD's. However, the majority of patients will sustain only minor effects (Krenzelok, 1989).
    b) The eyes, nose, mouth, and throat are all susceptible to the irritant/corrosive properties of ADD. The eyes are the most sensitive organ to the toxic effects of ADD (Seabrough et al, 1977; Krenzelok, 1989).
    c) LIMITED EXPOSURE: Mild reversible irritation manifest as conjunctivitis and iritis may result from limited exposures.
    d) EXTENSIVE EXPOSURE may result in the development of corneal ulceration and opacities and irreversible destruction of ocular tissue (Scharpf et al, 1972; Seabrough et al, 1977).
    e) INCIDENCE: In one study, ocular exposure to liquid ADD resulted in a 91.3% incidence of symptoms which included discomfort, minor corneal abrasions, or more severe corneal abrasions (Krenzelok, 1989).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) SUMMARY: The pH of some ADDs is in excess of pH 12.5 and the ingestion of those products can result in the development of oropharyngeal irritation or burns (Lee et al, 1972; Muhlendahl et al, 1978; Krenzelok & Clinton, 1979; Temple & Veltri, 1979).
    a) The absence of oral burns does not rule out an ingestion since esophageal and gastric burns may occur without overt oral toxicity. This is more likely to occur following the ingestion of commercial grade ADDs rather than with small amounts of household granular or liquid products.
    2) GRANULAR PRODUCTS
    a) SUMMARY: The oropharynx, lips, and tongue may have signs of irritation, edema, or frank burns. Oral pain may be intense. The absence of oropharyngeal burns does not rule out the possibility of esophageal or gastric burns (Bertinelli et al, 2006; Cello et al, 1980; Kirsh & Ritter, 1976; Madarikan & Lari, 1990).
    b) INCIDENCE: One series showed a 29% incidence of esophageal and/or gastric burns without any evidence of oropharyngeal burns following ingestion of a commercial ADD containing sodium metasilicate (Krenzelok & Clinton, 1979).
    c) SEVERE EXPOSURES may result in drooling, epiglottitis, dyspnea, stridor and dysphagia (Bertinelli et al, 2006). One series of human exposures to ADD describes mucosal irritation in 11.6% of patients and actual oral mucosal erosion in 4.7% of patients (Temple & Veltri, 1979).
    d) ORAL BURNS
    1) The absence of oral lesions does not preclude the possibility of esophageal injury. In a series of 18 children who ingested automatic dishwasher detergents, 2 of 5 children with no evidence of oral burns had positive endoscopic findings (Kynaston et al, 1989).
    2) It is unlikely that the ingestion of a dry granular product will result in the development of esophageal or gastric injury without the presence of oropharyngeal irritation or burns.
    e) CHILDREN: In a series of 39 cases of accidental ingestion of dishwashing detergent, 18 had patchy erythema of the esophagus, and 1 had a mucosal ulceration and false membrane. These cases involved an institutional use product (Dabadie et al, 1989).
    f) Oral burns from the lips to the uvula occurred in 10 of 11 children (ages ranging from 11 to 30 months) who ingested automatic dishwasher powder detergents. Amounts of ingestion varied from dipping a hand into the dishwasher tray to taking a bite out of a dishwasher detergent tablet (Bertinelli et al, 2006).
    3) LIQUIDS
    a) SUMMARY: Although liquid ADD have a higher pH than their granular counterparts, they do not appear to be associated with significant toxicity when small quantities are ingested.
    b) INCIDENCE: In one study, oral exposure to no more than one teaspoonful of liquid ADD resulted in a 8.9% incidence of symptoms which included oral irritation, emesis, nausea, or small buccal lesions (Krenzelok, 1989).
    c) The volume of liquid ADD is often limited due to package design or the use of child resistant closures. One study revealed that less than 1/4 teaspoonful was the most frequently ingested amount (Sublet et al, 1988).
    d) The ingestion of large amounts of liquid ADD, however, may be associated with corrosive toxicity and should be evaluated as such.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FINDING
    1) WITH POISONING/EXPOSURE
    a) Respiratory compromise is unlikely following the ingestion of small amounts of ADDs. Aspiration of the substance may produce irritant effects and consequent complications. Ingestions which are capable of producing oropharyngeal burn have the potential to produce respiratory compromise.
    B) INJURY OF UPPER RESPIRATORY TRACT
    1) WITH POISONING/EXPOSURE
    a) Granular ADD do not generally contain respirable size particles, therefore, respiratory irritation is usually limited to the upper respiratory tract. Intense irritation to this region may occur.
    b) However, aspiration of granular ADD or the liquid form may produce respiratory difficulties consistent with exposure to an irritant or corrosive substance: stridor, dyspnea, pneumonitis, and pulmonary edema.
    c) CASE SERIES: In a series of 11 children (ages 11 to 30 months) who ingested powdered automatic dishwasher detergent, 5 required intubation within 4 hours of ingestion. Two children underwent tracheostomy because of upper airway injury (Bertinelli et al, 2006).
    d) CASE REPORT: Third-degree burns to the oropharynx, false vocal cords, and upper esophagus were reported in a 16-month-old girl who ingested an unknown amount of granular ADD. Supraglottal and pharyngeal stenosis subsequently developed, necessitating tracheostomy (Kynaston et al, 1989).
    C) REACTIVE AIRWAYS DYSFUNCTION SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 43-year-old cook developed intense coughing following inhalational exposure to automatic dishwashing detergent powder. Lung auscultation, performed at the hospital, was normal. Following treatment with a bronchodilator and inhaled corticosteroid, the patient's cough subsided, although spirometry indicated mild airflow obstruction (maximal expiratory flow of 50% of vital capacity (MEF50) was 3.12 (58% of the predicted value) and forced expiratory volume in 1 second (FEV1) was 3.12 (81% of the predicted value)). A repeat spirometry examination, performed approximately one month after discharge, indicated a more obvious mild obstruction (MEF50 of 2.33 (43% of the predicted value) and FEV1 of 2.74 (71% of the predicted value)). Over the course of several months, the patient experienced occasional dyspnea and slight bronchial hyperreactivity, necessitating the continued use of an inhaled corticosteroid (Hannu et al, 2012).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and diarrhea are associated with the ingestion of ADDs due to the presence surfactants. Esophageal and gastric irritation and ulceration can occur. The absence of oropharyngeal irritation or burns does not rule out the presence of esophageal or gastric burns.
    B) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and spontaneous emesis may occur (Krenzelok, 1989).
    b) A retrospective review, involving 11 children (ages ranging from 11 to 30 months) who ingested automatic dishwasher powder detergents, showed that all of the children experienced drooling and had vomited at least once. Amounts of ingestion varied from dipping a hand into the dishwasher tray to taking a bite out of a dishwasher detergent tablet (Bertinelli et al, 2006).
    C) BURN
    1) WITH POISONING/EXPOSURE
    a) Corrosive burns of the gastrointestinal tract can develop.
    b) CASE SERIES: In a series of 11 children (ages 11 to 30 months) who ingested powdered automatic dishwasher detergent, 6 (55%) developed esophageal injuries, 3 of whom had deep esophageal burns that required esophageal dilatation; 2 required gastrotomy (Bertinelli et al, 2006).
    D) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea may also develop.
    E) ESOPHAGITIS
    1) WITH POISONING/EXPOSURE
    a) Esophagitis and gastritis may develop. Esophageal and gastric erosion occur more frequently following ingestion of NONPHOSPHATE ADD (Krenzelok & Clinton, 1979; Seabrough et al, 1977; Lee et al, 1972).
    b) Esophageal ulceration with eschar formation may also occur. In a comprehensive animal study evaluating detergent toxicity, ADD produced significantly more esophageal corrosion than other types of detergents (Seabrough et al, 1977).
    F) COLITIS
    1) WITH POISONING/EXPOSURE
    a) Detergent enemas may produce a pseudomembranous colitis terminating in extensive necrosis (Kerchner, 1977).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN FINDING
    1) WITH POISONING/EXPOSURE
    a) Skin irritation, even blister formation may accompany dermal exposure to liquid ADDs or granular ADD which has been dissolved in water. Dry granular ADD which comes into contact with the skin is unlikely to produce irritation.
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Quantitatively, dermal irritation appears to be more dependent upon the concentration of the ADD and the duration of exposure rather than the actual substance itself. Skin appears to be more resistant to the irritant/corrosive effects of ADD.
    b) GRANULAR: Skin irritation may occur following exposure especially if the ADD has been solubilized. Burns may result in some cases. An animal study evaluated the dermal toxicity of 23 ADD and revealed that 74% of the ADD produced dermal irritation while 26% produced corrosive effects (Seabrough et al, 1977).
    c) LIQUID: Blisters of the hand were reported in one patient who used a liquid ADD for hand dishwashing (Krenzelok, 1989).
    C) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) LIQUID: Minor skin irritation or rash was described in 26.1% and no effects in 69.6% of patients with dermal exposures to liquid ADD in one study of 192 liquid ADD exposures (total number of exposures by all routes) (Krenzelok, 1989).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) In significant ingestions, monitor CBC, serum electrolytes, and blood gases.
    B) In significant ingestions, radiographs should be considered to evaluate for perforation or aspiration.

Radiographic Studies

    A) RADIOGRAPHIC-OTHER
    1) Although it is unlikely that esophageal perforation will occur following the ingestion of ADDs, a water-soluble contrast material can be used at 10 days to 3 weeks postingestion initially to exclude esophageal perforation in patients with GI burns associated with alkaline ingestions (Chen et al, 1988).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients who have persistent symptoms, respiratory difficulties, intolerance of oral intake, or intentional ingestions, may need to be admitted for further evaluation and endoscopy.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most small unintentional ingestions can remain at home. If an industrial product is involved, symptoms persist, self-harm ingestion, healthcare facility referral should be recommended.
    B) Most ingestions of ADD involve small amounts which do not produce oral, pharyngeal, or esophageal irritation. If the patient is asymptomatic and not refusing liquids due to the discomfort of swallowing and no drooling is present, home observation is sufficient. Products with a pH of less than 11.4 are rarely associated with significant sequelae (Howell, 1987).
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) If patients are symptomatic and/or after large ingestions, call your regional poison center. For significant or symptomatic ingestions, gastroenterology may need to be consulted for endoscopic evaluation. In pediatric patients, any stridor, persistent vomiting, or drooling may be indication for endoscopy. For ocular injuries, ophthalmology consultation may be needed.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients who are symptomatic should be observed in the emergency department until patient is asymptomatic and tolerating oral intake. Patients with eye exposures should generally be referred to a healthcare facility for evaluation and treatment.
    6.3.4) DISPOSITION/EYE EXPOSURE
    6.3.4.2) HOME CRITERIA/EYE
    A) Ocular exposure to ADD rarely results in the need to admit. However, since these products have the potential to produce both mechanical and chemical injury, any patient suffering ocular exposure to ADDs should undergo immediate ocular irrigation followed by referral to an emergency department or ophthalmologist since over 90% of these patients will develop at least minor irritation (Krenzelok, 1989).

Monitoring

    A) In significant ingestions, monitor CBC, serum electrolytes, and blood gases.
    B) In significant ingestions, radiographs should be considered to evaluate for perforation or aspiration.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL: Removal of obvious granules or gels, and dilution/irrigation of exposed areas can be initiated.
    B) DILUTION
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) After an ingestion, rinse mouth and administer small amounts of water. Lavage and activated charcoal are not indicated as toxicity is secondary to local tissue injury.
    B) DILUTION
    1) Immediately remove any obvious granules from the lips and oral mucosa and dilute with milk or water, whichever is most accessible. The goal of dilution is to rinse the product from the mouth and pharynx.
    2) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    3) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    4) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    5) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    6) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    7) Following immediate dilution the patient should remain NPO until a thorough ENT evaluation is completed. Excessive fluid intake may promote emesis and aggravation of existing injury.
    C) GASTRIC LAVAGE
    1) Spontaneous emesis may occur. Induced emesis and gastric lavage are not indicated. Emesis or lavage may aggravate an existing corrosive injury.
    D) ACTIVATED CHARCOAL
    1) Avoid activated charcoal since it may interfere with visualization of oral, esophageal, and gastric irritation/necrosis.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) In significant ingestions, monitor CBC, serum electrolytes, and blood gases.
    2) In significant ingestions, radiographs should be considered to evaluate for perforation or aspiration.
    B) DILUTION
    1) Immediately remove any obvious granules from the lips and oral mucosa and dilute with milk or water, whichever is most accessible.
    2) Following immediate dilution the patient should remain NPO until a thorough ENT evaluation is completed. Excessive fluid intake may promote emesis and aggravation of existing injury.
    3) NEUTRALIZATION
    a) Avoid this procedure. It may accentuate preexisting pathology and waste time that could be dedicated to proper therapy.
    C) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    7) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
    8) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).
    D) CORTICOSTEROID
    1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that they are effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use, so routine use is not recommended.
    2) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    3) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    4) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    5) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    6) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    7) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    8) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    9) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    E) SURGICAL PROCEDURE
    1) SUMMARY: Initially if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed. If dilation is unsuccessful colonic intraposition or gastric tube placement may be needed. Early laparotomy should be considered in patients with evidence of severe esophageal or gastric burns on endoscopy.
    2) STRING - If a second degree or circumferential burn of the esophagus is found a string may be placed in the stomach to avoid false channel and to provide a guide for later dilation procedures (Gandhi et al, 1989).
    3) STENT - The insertion of a specialized nasogastric tube or stent immediately after endoscopically proven deep circumferential burns is preferred by some surgeons to prevent stricture formation (Mills et al, 1978; (Wijburg et al, 1985; Coln & Chang, 1986).
    a) STUDY - In a study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).
    4) DILATION - Dilation should be performed at 1 to 4 week intervals when stricture is present(Gundogdu et al, 1992). Repeated dilation may be required over many months to years in some patients. Successful dilation of gastric antral strictures has also been reported (Hogan & Polter, 1986; Treem et al, 1987).
    5) COLONIC REPLACEMENT - Intraposition of colon may be necessary if dilation fails to provide an adequate sized esophagus (Chiene et al, 1974; Little et al, 1988; Huy & Celerier, 1988).
    6) LAPAROTOMY/LAPAROSCOPY - Several authors advocate laparotomy or laparoscopy in patients with endoscopic evidence of severe esophageal or gastric burns to evaluate for the presence of transmural gastric or esophageal necrosis (Cattan et al, 2000; Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993).
    a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    F) ANTIBIOTIC
    1) Should not be used prophylactically but should be used only for specific indications of infection. Intravenous antibiotics should be considered in patients with evidence of esophageal or gastric perforation (Howell, 1986).
    G) SUCRALFATE
    1) CASE REPORT: The administration of 1 gram in 100 milliliters of water was reported to decrease odynophagia by 50 percent within 24 hours in a woman who ingested crystalline Drano(R); however, stricture formation was not prevented and cimetidine was given concurrently, making assessment of any therapeutic benefit from sucralfate difficult (Reddy & Budhraja, 1988).
    2) CONCLUSION - More studies will be needed before sucralfate can be recommended for treatment of caustic ingestions.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move the patient to fresh air. Observe for respiratory distress. If respiratory compromise develops, evaluate for respiratory tract irritation, pneumonitis and pulmonary edema. Evaluate the patient for esophageal, oral, nasal and dermal irritation/burns.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) All patients suffering ocular exposure to ADDs should undergo immediate ocular irrigation followed by referral to an emergency department or ophthalmologist since over 90% of those patients will develop at least minor irritation (Krenzelok, 1989).
    B) Remove contact lenses. The exposed eyes and contiguous dermal surfaces should be immediately irrigated with large volumes of lukewarm water. This is most easily accomplished in the nonhealth care facility setting by pouring a continuous gentle stream of water into the exposed eye(s) for a minimum of 15 minutes.
    C) In the healthcare facility, irrigate the exposed eye(s) with sterile normal saline for a minimum of 1 to 2 hours. Eyelid retractors should be utilized to ensure that thorough irrigation occurs and that particulate matter is not trapped beneath the lids. Irrigation should continue until the cul de sac pH returns to normal. Severe cases may require prolonged irrigation.
    6.8.2) TREATMENT
    A) OCULAR SLIT LAMP EXAMINATION
    1) An ophthalmologic examination should follow irrigation to determine the extent of injury. This should include fluorescein staining and a slit lamp examination.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Remove any contaminated clothing and irrigate the exposed area with a large volume of water. Gentle soap and water washes should follow the general irrigation procedure. If irritation or pain persists, medical evaluation is necessary.

Summary

    A) TOXICITY: Small oral or dermal exposures are not likely to cause significant caustic injury.
    B) Sodium metasilicate and sodium carbonate produce more titratable alkali than a comparable amount of a phosphate-containing product.
    C) In general, ADDs which are primarily composed of nonphosphate alkaline chemicals are associated with greater tissue irritation and injury than those containing a majority of phosphate alkaline chemicals.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Automatic dishwasher detergents can be irritants as well as corrosives. The individual product composition, duration of exposure, pH, and concentration are the best prognostic indicators of potential toxicity.
    2) Contacting manufacturers concerning case reports may be helpful in evaluating irritancy or causticity of individual products. For example, Procter and Gamble Co, the makers of Cascade(R) state that this product is of a low order of toxicity, is an irritant, but not corrosive, an emetic, and GI irritant.
    3) Generally speaking, the NONPHOSPHATE alkaline builders which comprise the majority of the ADD composition are more irritating and corrosive than phosphate alkaline builders (Scharpf et al, 1972; Gosselin et al, 1984; Seabrough et al, 1977). Nonphosphate alkaline builders have more titratable alkalinity than a comparable amount of a phosphate builder.
    a) For example, sodium metasilicate 0.5% has a pH value of 12.5 (Gosselin et al, 1984), whereas sodium phosphate 1.4% has a pH value of 7.0 to 7.5 (Grant & Schuman, 1993) and sodium carbonate 10% has a pH of 10.7 (Grant & Schuman, 1993). The higher the percentage of nonphosphate salts relative to phosphate salts, the more potential for extensive damage (Lee et al, 1972; Muhlendahl et al, 1978).
    b) Ocular toxicity research using rabbit eyes demonstrates that phosphates have a relatively low toxicity index compared to nonphosphates (Scharpf et al, 1972). However, phosphates can be as damaging as nonphosphates if the concentration is high and the duration of exposure prolonged. Nonphosphates produce more irreversible conjunctival and corneal damage than the phosphates (Scharpf et al, 1972; Seabrough et al, 1977).
    c) Sodium metasilicate greatly enhances the corrosive action of phosphate-containing compounds.
    4) The duration of exposure and concentration may also dictate the degree of injury.
    a) Dilute solutions of sodium metasilicate can produce irreversible ocular injury within 60 seconds (Scharpf et al, 1972). A 10% sodium carbonate solution (pH 10.7) dripped into a rabbit eye for 30 seconds followed by irrigation with water produced no detectable injury (Grant & Schuman, 1993).
    b) Although the typical sodium carbonate solutions with pH values of up to 11.6 would be expected to produce injury to the corneal epithelium prompt irrigation makes permanent corneal damage unlikely (Grant & Schuman, 1993).
    c) In general, the higher the concentration and the longer the exposure, the more extensive the tissue damage (Seabrough et al, 1977; Vancura et al, 1980).
    B) CASE REPORTS
    1) One series of 232 patients who ingested ADD revealed visible oral burns in 131 patients (Muhlendahl et al, 1978).
    2) In 1970, the National Clearinghouse collected 317 cases involving ADD; 67 had undescribed symptoms and 27 were hospitalized. Mucosal irritation was observed in 11.6% of patients ingesting ADD in a Utah series and 4.7% of patients had actual oral mucosal erosion (Temple & Veltri, 1979).
    3) Four of 14 who ingested a dilute solution of an ADD in water developed esophageal and gastric erosions. None of the patients, including those who developed esophageal and gastric erosion, had any oropharyngeal irritation. (Krenzelok & Clinton, 1979).
    4) Two of 8 children who ingested undiluted granular ADDs developed serious esophageal and pharyngeal injury. In the total series of 18 children (including ingestions of "sludge" remaining in the dishwasher), 11 had evidence of esophageal injury, including mild erythema, non-circumferential burns, and one case of third-degree pharyngeal and esophageal burns (Kynaston et al, 1989).
    5) A French study of 24 cases of pediatric ingestion of ADD powder observed 3 cases of grade 3 esophageal lesions with an uncomplicated clinical course (Martinot et al, 1989). In another series of 47 cases of ADD ingestion, there were 3 cases of grade 2 esophagitis; one child had limited gastric cardia ulceration, which resolved over 3 days, and one child had extensive grade 2 esophageal ulceration, necessitating 25 days of parenteral nutrition. The product ingested in the first case was a liquid ADD, and in the second case "sludge" remaining the dishwasher from a powdered ADD (Dabadie, 1989).
    C) ROUTE OF EXPOSURE
    1) Small amounts of granular or liquid ADD orally or dermally are not likely to produce caustic injury (Krenzelok, 1989). Ocular exposure to liquid ADD was very likely to produce corneal injury and these patients should be evaluated in a health care facility after prompt irrigation at incident site (Krenzelok, 1989).
    2) The nonionic and anionic surfactants contained in these products add little to the corrosive nature of the products.

Toxicologic Mechanism

    A) ADD produce their toxic effects through a direct corrosive effect on tissues. Concentrated solutions or solids can produce irritation and corrosion. Corrosive effects can occur very rapidly. Emesis and diarrhea may be secondary to both the irritant characteristics as well as the surfactants contained in the products.

Physical Characteristics

    A) They have no characteristic odor.

Ph

    A) GRANULAR: In general, these products have a pH range of 10.5-12.5.
    B) LIQUID: Liquid ADD generally have a higher pH (11.8-12.7) than solid granular products (Krenzelok, 1989).

Molecular Weight

    A) Varies

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