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IRRITANTS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Irritants are substances that cause inflammation and swelling, but not cellular death and tissue damage; a corrosive causes cellular damage and death. They are generally classified as weak, strong or corrosive.

Specific Substances

    1) Tear gas devices
    2) AETHYLENININ (GERMAN)
    3) CALCIUM CHLORIDE (CAS 10043-52-4)
    4) DIATHANOLAMIN (GERMAN)
    5) ETHYLAMINE, ANHYDROUS
    6) ETHYLENEIMINE, INHIBITED
    7) IRRITATING AGENT, N.O.S.
    8) METHYLETHYLIMINE
    9) NATURAL GRAPHITE
    10) PENTACHLOROETANO (ITALIAN)
    11) PHOSPHORUS CHLORIDE
    12) RAW COTTON DUST
    13) TEAR GAS SUBSTANCE, LIQUID, N.O.S.
    14) TSPP VICTOR
    15) XYLENE CHLORIDE

Available Forms Sources

    A) FORMS
    1) DECOMPOSITION: Some compounds which are not irritants in their intact state may decompose upon exposure to heat or other factors into irritant compounds. Examples include compounds such as phosphorus pentachloride, that disintegrate into chlorides.
    2) INERT MATERIALS: Compounds such as wood dust and polypropylene fibers may create mild irritant effects or act in synergy with other irritants to amplify adverse clinical effects in humans and animals (Hesterberg et al, 1992; Leclerc et al, 1994; Holt, 1994).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Irritants are a broad category of substances that cause inflammation and swelling but not cellular death or tissue damage, while corrosives cause cellular damage and death. Whether a substance is labeled a "corrosive" or "irritant" typically depends on several factors including concentration, viscosity, pH, molarity, oxidation-reduction potential, complexing affinity toward bivalent ions, etc. It can be difficult to determine whether a substance is a corrosive or irritant and the distinction may be concentration-dependent.
    B) TOXICOLOGY: Irritants cause inflammation and swelling with local tissue irritation; this can lead to rhinorrhea, cough, shortness of breath, bronchospasm, irritation of oral mucous membranes and esophagus, and rarely upper airway swelling or acute lung injury.
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Irritants may cause swelling, redness, and pain at any site, especially at mucous membranes. The mouth, nose, and eyes are commonly affected. After inhalation, cough, tachypnea, and wheezing are common. With ingestion, nausea, vomiting, and diarrhea are common. With dermal exposure, redness, swelling, and pain may occur.
    0.2.20) REPRODUCTIVE
    A) Pregnant female rats were exposed to N- methylpyrrolidone. Exposed offspring had normal motor function, activity levels, and low-level learning abilities. On higher-level learning tests, their performance was impaired compared to unexposed offspring.
    0.2.21) CARCINOGENICITY
    A) Development of sinonasal neoplasms has been associated with exposure to wood dust and other irritants.

Laboratory Monitoring

    A) No specific lab tests are indicated.
    B) Patients with severe hypoxia may require pule oximetry/ABG monitoring and a chest radiograph.
    C) Patients with large ingestions or more severe symptoms (stridor, inability to swallow, pain on swallowing, persistent vomiting) should have endoscopy to evaluate for upper GI corrosive burns.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment consists of predominantly symptomatic and supportive care. For patients with ingestion, dilution with 4- to 8 ounces of fluid may decrease symptoms. Neutralization is not recommended.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Although irritants by definition should not produce tissue damage, it is almost impossible to assure that a particular substance under a particular set of circumstances could not act as a corrosive instead of an irritant. Patients with severe symptoms after ingestion of an irritant should be evaluated with upper GI endoscopy for possible corrosive injury with mucous membrane damage.
    C) DECONTAMINATION
    1) PREHOSPITAL: The patient should be removed from the exposure; remove contaminated clothing and wash exposed skin; irrigate exposed eyes. Emesis is NOT indicated due to the irritant nature of these agents. Activated charcoal is NOT recommended.
    2) HOSPITAL: Dermal or eye exposures should be irrigated as above. For patients with ingestion, dilution with 4 to 8 ounces of fluid may decrease symptoms. Emesis is NOT indicated due to the irritant nature of these agents. Charcoal is NOT recommended.
    D) AIRWAY MANAGEMENT
    1) Rarely, patients with signs and symptoms of respiratory failure and severe hypoxia may required intubation for acute lung injury.
    E) ANTIDOTE
    1) None
    F) ENHANCED ELIMINATION PROCEDURE
    1) There is no role for hemodialysis in irritant exposure.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with inadvertent small exposures who have no more than mild symptoms can be observed home.
    2) OBSERVATION CRITERIA: Patients with deliberate exposures or moderate to severe symptoms should be referred to a healthcare facility for evaluation and treatment. They should be observed in the ED until asymptomatic.
    3) ADMISSION CRITERIA: Patients with persistent symptoms, upper GI burns, persistent bronchospasm or hypoxia should be admitted.
    4) CONSULT CRITERIA: Contact your local poison center or a medical toxicologist for any patient with severe toxicity or in whom the diagnosis is unclear.
    H) PITFALLS
    1) Failure to monitor patients who are at risk for delayed-onset pulmonary edema and acute lung injury. Failure to recognize corrosive rather than irritant exposure.
    I) DIFFERENTIAL DIAGNOSIS
    1) Occupational or environmental asthma, heart failure, allergic reactions, caustic exposure.
    0.4.3) INHALATION EXPOSURE
    A) Patients should be removed from exposure into fresh air and monitored for respiratory distress. Oxygen should be administered as needed for hypoxia. Treat bronchospasm with inhaled beta-2 agonist and steroids. Patients with acute lung injury may require intubation for hypoxia; these patients should be managed with lung-protective ventilation techniques.
    0.4.4) EYE EXPOSURE
    A) Irrigate eyes with copious amounts of water or saline; the pH of the ocular cul de sac can be evaluated and the eyes should be irrigated until symptoms improve and this pH is neutral.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Skin should be thoroughly irrigated. Contact dermatitis may arise after repeated exposure to irritants.

Range Of Toxicity

    A) TOXICITY: The range of toxicity varies among the many substances categorized as irritants. Toxicity depends on a number of factors including concentration, mechanism of action, pH, free acidity and alkalinity, molarity and oxidation-reduction potential.

Clinical Effects

Summary Of Exposure

    A) USES: Irritants are a broad category of substances that cause inflammation and swelling but not cellular death or tissue damage, while corrosives cause cellular damage and death. Whether a substance is labeled a "corrosive" or "irritant" typically depends on several factors including concentration, viscosity, pH, molarity, oxidation-reduction potential, complexing affinity toward bivalent ions, etc. It can be difficult to determine whether a substance is a corrosive or irritant and the distinction may be concentration-dependent.
    B) TOXICOLOGY: Irritants cause inflammation and swelling with local tissue irritation; this can lead to rhinorrhea, cough, shortness of breath, bronchospasm, irritation of oral mucous membranes and esophagus, and rarely upper airway swelling or acute lung injury.
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Irritants may cause swelling, redness, and pain at any site, especially at mucous membranes. The mouth, nose, and eyes are commonly affected. After inhalation, cough, tachypnea, and wheezing are common. With ingestion, nausea, vomiting, and diarrhea are common. With dermal exposure, redness, swelling, and pain may occur.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MODERATE IRRITANTS: Animal studies have shown the following to cause corneal irritation that resolves within seven days (Griffith et al, 1980):
    1) Granular sodium chloride
    2) Sulfuric acid 10%
    3) Sodium hypochlorite 5%
    4) Isopropyl alcohol
    5) Coconut soap powder and 10% solution
    6) Powdered laundry soap
    7) Phosphate laundry detergent
    8) Sodium carbonate - sodium sulfate mixture
    9) Acetic acid 3%

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Tachypnea, wheezing, and coughing occurred in 25% of patients with inhalational irritant exposures whose respiratory symptoms lasted 12 to 24 hours. Immediate irritation of the upper respiratory mucosa is caused by irritant gases that are highly water soluble, such as ammonia, sulfur dioxide, and hydrogen chloride. Injury to the lower airways and alveoli is often seen with inhalation of gases with lower water solubility, such as oxides of nitrogen, phosgene, and ozone. Gases with intermediate water solubility, such as chlorine and acrolein, cause damage throughout the respiratory tract (Weiss & Lakshminarayan, 1994).
    1) Irritants with greater particle size (10 microns or more) and high water solubility generally cause upper airway and oral/nasal mucosal injury (Tarlo, 2000).
    b) Signs and symptoms in 24 cases of irritant inhalation included tachypnea (25%), wheezing (25%), coughing (25%), chest infiltrate (8%) (Blanc et al, 1991).
    B) REACTIVE AIRWAYS DYSFUNCTION SYNDROME
    1) WITH POISONING/EXPOSURE
    a) The term RADS (reactive airways dysfunction syndrome) refers to a persistent asthma-like syndrome developing after irritant exposure. Characteristics of RADS are: 1) onset within 24 hours of high-level irritant exposure; 2) positive methacholine challenge test; 3) persistence of respiratory symptoms and airway hyperreactivity for at least 3 months; 4) symptoms simulating asthma, with cough, wheezing, and dyspnea; 5) airflow obstruction measured via pulmonary function tests; 6) response to methacholine challenge; 7) absence of preceding respiratory complaints; and 8) other types of pulmonary disease excluded (Tarlo, 2000; Brooks et al, 1998; Brooks et al, 1985).
    b) Persistent symptoms lasting more than 14 days occurred in 6% of 160 patients with moderate-severe irritant exposures; risk factors were preexisting lung conditions and cigarette smoking (Blanc et al, 1991).
    C) VOCAL CORD DYSFUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 45-year-old nurse presented with wheezing, cough, and dyspnea several months after starting a new job at a gastroenterology unit. She was required to clean endoscopy instruments with irritating chemicals (ie, isopropyl alcohol, formaldehyde, peracetic acid) for 8 hours a day 5 days a week. Despite antiasthmatic therapy with inhaled budesonide at that time, her symptoms persisted. A video-laryngoscopy, that visualized the paradoxical motion of the vocal cords during symptoms, revealed vocal cord dysfunction (Tonini et al, 2009).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Inhalation exposure may result in pulmonary edema (Hajela et al, 1990; Proctor et al, 1988; Clayton & Clayton, 1981).
    E) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Irritant induced asthma can also develop after longer term (more than 24 hours) lower concentration exposures. These patients may be more likely to have a history of atopy and have a previous history of asthma that has been in remission (Brooks et al, 1998; Quirce et al, 2000).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY INFILTRATION
    a) POLYPROPYLENE FIBERS - In rats exposed for 90 days to airborne fibers, Hesterberg et al (1992) found a dose-dependent increase in pulmonary macrophages but no fibrosis. Histologic changes were reversible in about 90 days.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting and diarrhea are possible if ingested.
    B) ULCERATION OF INTESTINE
    1) WITH POISONING/EXPOSURE
    a) Ulcers or perforations should NOT occur.
    C) VASCULAR INSUFFICIENCY OF INTESTINE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: RECTAL ADMINISTRATION of 50 mL of 9% acetic acid in a 5-year-old boy resulted in colonic necrosis complicated by shock, ARDS, hemolysis, coagulopathy, acute renal failure, hepatic dysfunction and sepsis (Kawamata et al, 1994).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dermal inflammation with epidermal cellular swelling is seen. Redness, swelling, pruritus, blister formation, and pain may occur(Began, 2002).
    B) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Allergic contact dermatitis may arise after repeated exposure to irritants. Prolonged exposure to terpenes (found in turpentine and essential oils) has been associated with allergic dermatitis (Brun, 1975; Dooms-Goosens et al, 1977).
    b) Allergic contact dermatitis requires prior sensitization usually involving repeated exposure to irritants producing a type IV hypersensitivity reaction. Initially, the irritant chemical binds to a T cell. Upon re-exposure, the sensitized T cell initiates the allergic skin reaction(Began, 2002).

Reproductive

    3.20.1) SUMMARY
    A) Pregnant female rats were exposed to N- methylpyrrolidone. Exposed offspring had normal motor function, activity levels, and low-level learning abilities. On higher-level learning tests, their performance was impaired compared to unexposed offspring.
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Hass et al (1994) exposed pregnant female rats daily to 150 ppm N- methylpyrrolidone, a widely-used organic solvent, on days 7 - 20 of gestation. After birth, offspring were subjected to a battery of neurological and behavioral tests. Exposed offspring had normal motor function, activity levels, and low-level learning abilities. On higher-level learning tests, their performance was impaired compared to unexposed offspring.

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) Development of sinonasal neoplasms has been associated with exposure to wood dust and other irritants.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) NASAL CANCER - Development of sinonasal neoplasms has been associated with exposure to wood dust and other irritants. See Holt (1994) for a selected literature survey of these studies.
    a) One case-control study (non-blind) found that both duration and average level of exposure to hardwood dust in male subjects independently contributed to risk of neoplasm (nasal adenocarcinoma). The authors did not associate smoking with neoplasm development (Leclerc et al, 1994).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific lab tests are indicated.
    B) Patients with severe hypoxia may require pule oximetry/ABG monitoring and a chest radiograph.
    C) Patients with large ingestions or more severe symptoms (stridor, inability to swallow, pain on swallowing, persistent vomiting) should have endoscopy to evaluate for upper GI corrosive burns.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) SUMMARY: Patients with persistent symptoms, upper GI burns, persistent bronchospasm or hypoxia should be admitted.
    B) Admission is suggested for patients with moderate symptoms, pulmonary signs, radiological abnormalities, or impaired oxygenation (Mitchell & Carroll, 1989).
    6.3.3.2) HOME CRITERIA/INHALATION
    A) Patients with inadvertent small exposures who have no more than mild symptoms can be observed home.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Contact your local poison center or a medical toxicologist for any patient with severe toxicity or in whom the diagnosis is unclear.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) SUMMARY: Patients with deliberate exposures or moderate to severe symptoms should be referred to a healthcare facility for evaluation and treatment. They should be observed in the ED until asymptomatic.

Monitoring

    A) No specific lab tests are indicated.
    B) Patients with severe hypoxia may require pule oximetry/ABG monitoring and a chest radiograph.
    C) Patients with large ingestions or more severe symptoms (stridor, inability to swallow, pain on swallowing, persistent vomiting) should have endoscopy to evaluate for upper GI corrosive burns.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL: The patient should be removed from the exposure; remove contaminated clothing and wash exposed skin; irrigate exposed eyes. Emesis is NOT indicated due to the irritant nature of these agents. Activated charcoal is NOT recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Dermal or eye exposures should be irrigated as above. For patients with ingestion, dilution with 4 to 8 ounces of fluid may decrease symptoms. Emesis is NOT indicated due to the irritant nature of these agents. Charcoal is NOT recommended.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The 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).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment consists of predominantly symptomatic and supportive care. For patients with ingestion, dilution with 4- to 8 ounces of fluid may decrease symptoms. Neutralization is not recommended.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Although irritants by definition should not produce tissue damage, it is almost impossible to assure that a particular substance under a particular set of circumstances could not act as a corrosive instead of an irritant. Patients with severe symptoms after ingestion of an irritant should be evaluated with upper GI endoscopy for possible corrosive injury with mucous membrane damage.
    B) MONITORING OF PATIENT
    1) No specific lab tests are indicated.
    2) Patients with severe hypoxia may required pulse oximetry/ABG monitoring and a chest radiograph.
    3) Patients with large ingestions or more severe symptoms (stridor, inability to swallow, pain on swallowing, persistent vomiting) should have endoscopy to evaluate for upper GI corrosive burns.
    C) BURN OF GASTROINTESTINAL TRACT
    1) Tissue damage rarely occurs. Except under unusual circumstances, esophagoscopy, steroids, and antibiotics are not indicated.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Patients should be removed from exposure into fresh air and monitored for respiratory distress. Oxygen should be administered as needed for hypoxia. Treat bronchospasm with inhaled beta-2 agonist and steroids. Patients with acute lung injury may require intubation for hypoxia; these patients should be managed with lung-protective ventilation techniques.
    6.7.2) TREATMENT
    A) OXYGEN
    1) If symptoms are not relieved by exposure to fresh air, oxygen should be administered until pulse oximetry or blood gases can be measured. Assisted ventilation may be required if symptoms are severe or prolonged.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    8) A chest x-ray may be needed. Some irritants may rarely cause delayed acute lung injury.
    C) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) IRRIGATION
    1) Irrigate eyes with copious amounts of water or saline; the pH of the ocular cul de sac can be evaluated and the eyes should be irrigated until symptoms improve and this pH is neutral.
    2) A slit lamp examination should be considered following thorough irrigation. Some alkali exposures may require prolonged irrigation. Application of an ophthalmic local anesthetic will increase patient comfort and facilitate irrigation of the eye.
    B) INJURY OF CORNEA
    1) Administration of topical antibiotics, cycloplegics, mydriatics, and patching may be necessary in rare instances of corneal burns.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) PEDIATRIC
    1) One study reported a case of unintentional rectal instillation of 50 mL of 9% acetic acid solution in a 5-year-old male, who consequently developed extensive necrosis of the colon down to smooth muscle. Complications resulting from the colonic necrosis included disseminated intravascular coagulation (DIC), acute renal failure, acute liver dysfunction, sepsis, shock and respiratory distress. Following resection of the colon, hemodialysis, administration of blood products and antibiotics, and symptomatic care, the child improved (Kawamata et al, 1994).

Range Of Toxicity

Summary

    A) TOXICITY: The range of toxicity varies among the many substances categorized as irritants. Toxicity depends on a number of factors including concentration, mechanism of action, pH, free acidity and alkalinity, molarity and oxidation-reduction potential.

Pharmacology Toxicology

Toxicologic Mechanism

    A) Chemical "burns" may occur by several different mechanisms.
    1) Oxidizing agent (chromic acid, potassium permanganate).
    2) Reducing agent (alkyl mercury agent, hydrochloric acid, HNO3).
    3) Corrosives (phenol, phosphorous, dichromate, various hydroxides).
    4) Protoplasmic poisons
    a) Salt formers (picric, tungstic, tannic, formic or acetic acid).
    b) Metabolic competitor/inhibitor (oxalic and HF acids).
    5) Desiccants (H2SO4 or concentrated hydrochloric acid).
    6) Vessicants (cantharides, DMSO, mustard gas).

References

General Bibliography

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