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TRIMETHYLAMINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Trimethylamine is an insect attractant, fungicide, and substrate for organic synthesis reactions in plastics.
    B) Trimethylamine occurs naturally; sources of normal exposure include the diet and conversion from choline by gut flora.

Specific Substances

    1) TMA
    2) N,N-Diethylmethamine
    3) CAS 75-50-3
    4) TMA (TRIMETHYLAMINE, AQUEOUS SOLUTION)
    5) TRIMETHYLAMINE, AQUEOUS SOLUTION
    1.2.1) MOLECULAR FORMULA
    1) C3-H9-N
    2) (CH3)3-N

Available Forms Sources

    A) FORMS
    1) Trimethylamine is sold as an aqueous solution containing 25, 30 or 40% water, or as liquified gas (anhydrous, 99% minimum grade) (Budavari, 1996; Lewis, 1996; Lewis, 1997; Snyder et al, 1990).
    B) SOURCES
    1) INDUSTRIAL SOURCES:
    a) Trimethylamine can be manufactured through synthesis between paraformaldehyde and ammonium chloride, or through reaction of formaldehyde and formic acid on ammonia (Budavari, 1996; Snyder et al, 1990).
    b) It can also be manufactured through the reaction between methanol and ammonia (in the presence of a catalyst and at high temperatures) (Ashford, 1994; Lewis, 1996; Lewis, 1997; Snyder et al, 1990).
    1) During this reaction, mono-, di-, and trimethylamines are generated; subsequent separation may be done using azeotropic or extractive distillation (Lewis, 1996; Lewis, 1997).
    2) ENVIRONMENTAL AND OTHER SOURCES:
    a) Trimethylamine commonly occurs in the environment as a decomposition product of plants and animals (especially fish) (Howard, 1990).
    1) In animal tissue, especially fish, it exists in conjugated form (Budavari, 1996; Clayton & Clayton, 1994).
    b) It is also released during decay of nitrogenous plant and animal wastes (e.g. manure in cattle feed lots) (Clayton & Clayton, 1994) ACGIH, 1991; (Howard, 1990).
    c) It forms during bacterial breakdown of the common plant and animal tissue constituents choline and betaine, and as a result of bacterial reduction of trimethylamine N-oxide, a commonly found metabolite and excretory product of aquatic organisms (Howard, 1990).
    d) Trimethylamine may be formed during degradation or distillation of sugar-beet pulp, (due to sugar beets' high levels of betaine) (HSDB , 2000).
    e) Trimethylamine has also been identified in cheese, caviar, beer, whiskey, cocoa, coffee, soups (HSDB , 2000). It has also been identified as a volatile constituent in boiled beef (Howard, 1990).
    f) Trimethylamine is contained in tobacco smoke (Howard, 1990).
    g) It has been detected in uncultivated soil and as volatile constituent in marine algae (Howard, 1990).
    h) When urine is stored at room temperature, trimethylamine may be generated (Budavari, 1996).
    i) Persons with a genetically determined deficiency in the capability to N-oxidize trimethylamine excrete large quantities of this compound in their urine after eating fish or other choline rich food items (Clayton & Clayton, 1994).
    j) Facilities that manufacture or use trimethylamine may release this compound to the environment through effluents or other emissions (Howard, 1990).
    C) USES
    1) This compound mainly finds use as an intermediate in the production of chlorine salts, especially choline chloride (which is used as animal feed supplement) (Snyder et al, 1990; Clayton & Clayton, 1994; Howard, 1990; OHM/TADS , 2000).
    a) In 1984, approximately 15,322 tons of trimethylamine were produced in the US (Snyder et al, 1990).
    2) This compound is also used in the manufacture of quaternary ammonium compounds and as a warning agent for natural gas (Lewis, 1997; Clayton & Clayton, 1994) ACGIH, 1991; (Snyder et al, 1990; Sittig, 1991; OHM/TADS , 2000);
    3) in the manufacture of disinfectants (Lewis, Clayton & Clayton, 1994; (Snyder et al, 1990; OHM/TADS , 2000);
    4) in the manufacture of plastics (organic synthesis) and floating agents (Lewis, 1997) ACGIH, 1991; (Snyder et al, 1990; OHM/TADS , 2000);
    5) in the manufacture of cationic emulsion polymers (Snyder et al, 1990);
    6) in the manufacture of insect attractants or repellants (Lewis, 1997) ACGIH, 1991; (Snyder et al, 1990; Sittig, 1991; OHM/TADS , 2000);
    7) as a fungicide and as a catalyst in gas chromatography (HSDB , 2000);
    8) as a corrosion inhibitor (Clayton & Clayton, 1994);
    9) as synthetic flavor agent in fish and seafood, and as ingredient in synthetically fermented egg protein products (used to attract coyotes and repel deer) (Snyder et al, 1990).
    10) Trimethylamine also finds medical use as a chemical initiator for the neuroregulator acetylcholine bromide (Snyder et al, 1990).

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: Trimethylamine, considered to be corrosive, is used as a fungicide, in the manufacture of plastics, disinfectants, quaternary ammonium compounds, and insect attractants or repellants, and as a warning agent for natural gas.
    B) TOXICOLOGY: Trimethylamine may cause liquefaction necrosis. It can saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue, an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
    C) EPIDEMIOLOGY: Trimethylamine is generally available for industrial use only. Exposure is unusual.
    D) WITH POISONING/EXPOSURE
    1) Trimethylamine is considered to be an alkaline corrosive. Although there is limited information regarding specific human toxicity following exposure, the following effects may occur, based on documented human exposures with other alkaline corrosives.
    2) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) and are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.
    a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
    b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.
    3) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
    4) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
    6) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.
    0.2.4) HEENT
    A) This substance is an eye irritant and may cause severe irritation, hemorrhagic conjunctivitis and possible corneal edema and opacities.
    0.2.5) CARDIOVASCULAR
    A) Shock may develop following significant oral or dermal exposures.
    0.2.6) RESPIRATORY
    A) Irritation of the lungs is expected with coughing, dyspnea, and a chemical pneumonitis.
    0.2.8) GASTROINTESTINAL
    A) Oral or inhalation exposures may result in nausea and vomiting, abdominal cramps, diarrhea, and risk of gastric perforation.
    0.2.14) DERMATOLOGIC
    A) Dermal exposure causes skin irritation, itching and tingling sensation, painful burning, painful ulcerations, skin feels slippery or soapy, and state of shock.

Laboratory Monitoring

    A) Obtain a complete blood count in symptomatic patients following an alkaline corrosive ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, serum electrolytes, INR, PTT, type and crossmatch for blood, and monitor urine output. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings DOES NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no information available about treatment of trimethylamine-induced corrosive injury; the following data is derived from experience with other corrosive agents.
    B) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY
    1) Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. If burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.
    C) SEVERE ORAL TOXICITY
    1) Resuscitate with 0.9% normal saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.
    D) DILUTION
    1) Dilute with 4 to 8 ounces of water may be useful if it can be performed shortly after ingestion in patients who are able to swallow, with no vomiting or respiratory distress; then the patient should be NPO until assessed for the need for endoscopy. Neutralization, activated charcoal, and gastric lavage are all contraindicated.
    E) AIRWAY MANAGEMENT
    1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury.
    F) ENDOSCOPY
    1) Endoscopy 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) CORTICOSTEROIDS
    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 it is effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use.
    H) STRICTURE
    1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation.
    I) SURGICAL MANAGEMENT
    1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome.
    J) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home.
    2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    K) PITFALLS
    1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
    2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air.
    3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
    4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with corrosive eye injury should be evaluated by an ophthalmologist.
    L) DIFFERENTIAL DIAGNOSIS
    1) Acid ingestion, gastrointestinal hemorrhage, or perforated viscus.
    0.4.3) INHALATION EXPOSURE
    A) DECONTAMINATION
    1) Administer oxygen as necessary. Monitor for respiratory distress.
    B) AIRWAY MANAGEMENT
    1) Manage airway aggressively in patients with significant respiratory distress, stridor or any evidence of upper airway edema. Monitor for hypoxia or respiratory distress.
    C) BRONCHOSPASM
    1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION
    1) Exposed eyes should be irrigated with copious amounts of 0.9% normal saline for at least 30 minutes, until pH is neutral and the cul de sacs are free of particulate material.
    2) An eye examination should always be performed, including slit lamp examination. Ophthalmologic consultation should be obtained. Antibiotics and mydriatics may be indicated.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION
    a) Remove contaminated clothes and any particulate matter adherent to skin. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer, depending on concentration, amount and duration of exposure to the chemical. A physician may need to examine the area if irritation or pain persist.

Range Of Toxicity

    A) TOXICITY: Serious burns are less likely if the pH is less than 11.5. Injury is greater with large exposures and high concentrations. With highly concentrated liquids, esophageal burns may occur in up to 100% of patients, even after accidental ingestion.

Clinical Effects

Summary Of Exposure

    A) USES: Trimethylamine, considered to be corrosive, is used as a fungicide, in the manufacture of plastics, disinfectants, quaternary ammonium compounds, and insect attractants or repellants, and as a warning agent for natural gas.
    B) TOXICOLOGY: Trimethylamine may cause liquefaction necrosis. It can saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue, an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
    C) EPIDEMIOLOGY: Trimethylamine is generally available for industrial use only. Exposure is unusual.
    D) WITH POISONING/EXPOSURE
    1) Trimethylamine is considered to be an alkaline corrosive. Although there is limited information regarding specific human toxicity following exposure, the following effects may occur, based on documented human exposures with other alkaline corrosives.
    2) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) and are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.
    a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
    b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.
    3) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
    4) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
    6) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.

Heent

    3.4.1) SUMMARY
    A) This substance is an eye irritant and may cause severe irritation, hemorrhagic conjunctivitis and possible corneal edema and opacities.
    3.4.3) EYES
    A) OCULAR EXPOSURE causes immediate, highly painful irritation of eyes and eyelids; intense watering of eyes; victim keeps eyelids tightly closed; burns and irreparable damage to mucous membranes of eyes; and serious injury to eyes (Lefevre, 1989).
    B) CONJUNCTIVITIS - Trimethylamine is an irritant to eyes (ITI, 1975). Single drops of a 1% solution causes severe irritation, 5% may cause hemorrhagic conjunctivitis, and a 16.5% solution causes severe reactions with conjunctival hemorrhages, corneal edema and opacities. This damage may be followed with clearing, but with significant vascularization (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) IRRITATION - Vapors of trimethylamine are irritating to the mucous membranes of the nose and throat.
    3.4.6) THROAT
    A) IRRITATION - Ingestions may cause an immediate burning sensation in the mouth and throat, pain on swallowing, swelling of the throat, and profuse salivation (Lefevre, 1989).

Cardiovascular

    3.5.1) SUMMARY
    A) Shock may develop following significant oral or dermal exposures.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Symptoms of shock, including weak and rapid pulse, cold sweat, pale complexion, light-headedness, and cold hands and feet, may develop following significant oral or dermal exposures (Lefevre, 1989).

Respiratory

    3.6.1) SUMMARY
    A) Irritation of the lungs is expected with coughing, dyspnea, and a chemical pneumonitis.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Irritation of the lungs is expected with trimethylamine, much like dimethylamine (CHRIS , 1999). Severe pulmonary irritation or pulmonary edema have NOT been reported in humans to date.
    B) PNEUMONITIS
    1) Because trimethylamine is caustic, symptoms of acute poisoning via INHALATION might include: throat irritation; sneezing; tingling sensation in respiratory tract; coughing; risk of chemical bronchitis; and, after an apparent delay, acute pulmonary edema (Lefevre, 1989).

Gastrointestinal

    3.8.1) SUMMARY
    A) Oral or inhalation exposures may result in nausea and vomiting, abdominal cramps, diarrhea, and risk of gastric perforation.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Oral or inhalation exposures may result in nausea and vomiting, hematemesis, abdominal cramps, diarrhea, which may be bloody, and risk of gastric perforation (Lefevre, 1989).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal exposure causes skin irritation, itching and tingling sensation, painful burning, painful ulcerations, skin feels slippery or soapy, and state of shock.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Trimethylamine is an irritant to the skin. Direct contact should be avoided (ITI, 1975).
    B) HYPERESTHESIA
    1) Dermal exposure causes itching and tingling sensation, painful burning, painful ulcerations, skin feels slippery or soapy, and state of shock (weak and rapid pulse, cold sweat, pale complexion, light-headedness, cold hands and feet) (Lefevre, 1989).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-50-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a complete blood count in symptomatic patients following an alkaline corrosive ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, serum electrolytes, INR, PTT, type and crossmatch for blood, and monitor urine output. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings DOES NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Obtain a complete blood count in patients with symptomatic alkaline corrosive ingestion.
    B) COAGULATION STUDIES
    1) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding, obtain renal function tests, PT or INR, PTT, and type and crossmatch for blood.
    4.1.3) URINE
    A) OTHER
    1) Monitor urine output in patients with significant gastrointestinal burns, perforation, or bleeding.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway burns.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain an upright chest x-ray in patients with significant signs and symptoms after ingestion to evaluate for pneumomediastinum or free air under the diaphragm.
    a) The absence of these findings does not rule out the possibility of necrosis or perforation of the esophagus or stomach (Davis et al, 1972; Allen et al, 1970).
    2) Obtain a chest x-ray in patients with significant pulmonary signs or symptoms.
    B) RADIOGRAPHIC-OTHER
    1) 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, as water soluble contrast causes less injury than barium if it extravasates into tissue (Chen et al, 1988; Kirsh & Ritter, 1976).
    2) Barium esophagogram performed once perforation has been excluded may be useful to evaluate extent of injury or presence of strictures (Chen et al, 1988; Lowe et al, 1979; Leape et al, 1971).

Methods

    A) CHROMATOGRAPHY
    1) TMA and its metabolites can be separated by thin-layer chromatography on silica gel G or cellulose plates and visualized with bromocresol green (Al-Waiz et al, 1987).
    2) TMA and its metabolites can also be determined quantitatively by gas-liquid chromatography with flame-ionization detector (Al-Waiz et al, 1987).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home.

Monitoring

    A) Obtain a complete blood count in symptomatic patients following an alkaline corrosive ingestion.
    B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, serum electrolytes, INR, PTT, type and crossmatch for blood, and monitor urine output. Serum lactate and base deficit may also be useful in these patients.
    C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings DOES NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) DILUTION
    1) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION
    1) 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) ENDOSCOPIC PROCEDURE
    1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated trimethylamine ingestion. The following information is derived from experience with other corrosives.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
    3) 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).
    4) 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)
    5) 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).
    6) 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.
    7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    8) 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.
    9) 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).
    B) CORTICOSTEROID
    1) 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.
    2) 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).
    3) 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).
    4) 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).
    5) 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).
    6) 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).
    7) 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).
    8) 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).
    C) 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).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) TOXIC EFFECT OF GAS, FUMES AND/OR VAPORS
    1) Trimethylamine is a gas at room temperature and most exposures are to the gaseous state.
    B) 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) Exposed eyes should be irrigated with copious amounts of water for at least 30 minutes. An examination should always be performed. Ophthalmologic consultation should be considered.
    2) In a medical facility: Irrigate with sterile saline for at least an hour or until the superior and inferior cul-de-sacs have been examined for particulate matter and returned to neutrality (pH paper touched to lower cul-de-sac) (Pfister & Koski, 1982).
    a) Irrigation with a "T" tube and irrigating scleral lens (Morgan, 1971) have not proved superior to simply retracting the lids and manually using IV tubing connected to the irrigating solution.
    B) INJURY OF GLOBE OF EYE
    1) EVALUATION
    a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000).
    b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000; Singh et al, 2013):
    1) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
    2) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
    3) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
    4) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.
    c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):
    1) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
    2) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
    3) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
    4) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
    5) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
    6) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.
    2) MINOR INJURY
    a) SUMMARY
    1) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) TOPICAL CYCLOPLEGIC
    1) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    d) TOPICAL ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008).
    e) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    3) SEVERE INJURY
    a) SUMMARY
    1) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    d) CARBONIC ANHYDRASE INHIBITOR
    1) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    e) TOPICAL STEROIDS
    1) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993b).
    2) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
    3) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000b).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    f) ASCORBATE
    1) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
    3) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993b). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000b).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    g) CITRATE
    1) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
    3) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993b). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000b).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000b).
    h) COLLAGENASE INHIBITORS
    1) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
    2) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
    3) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).
    i) ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000a; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).
    j) TOPICAL CYCLOPLEGIC
    1) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    k) SOFT CONTACT LENSES
    1) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.
    4) SURGICAL THERAPY
    a) SURGICAL THERAPY CAUSTIC EYE INJURY
    1) Early insertion of methylmethacrylate ring or suturing saran wrap over palpebral and cul-de-sac conjunctiva may prevent fibrinosis adhesions and reduce fibrotic contracture of conjunctiva, but the advantage of such treatments is not clear.
    2) Limbal stem cell transplantation has been used successfully in both the acute stage of injury and the chronically scarred healing phase in patients with persistent epithelial defects after chemical burns (Azuara-Blanco et al, 1999; Morgan & Murray, 1996; Ronk et al, 1994).
    3) In some patients, amniotic membrane transplantation (AMT) has been successful in improving corneal healing and visual acuity in patients with persistent epithelial defects after chemical burns. It can restore the conjunctival surface and decrease limbal stromal inflammation (Fish & Davidson, 2010; Sridhar et al, 2000; Su & Lin, 2000; Meller et al, 2000; Azuara-Blanco et al, 1999).
    4) Control glaucoma. Remove any cataracts formed (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    5) In patients with severe injury, tenonplasty can be performed to promote epithelialization and prevent melting (Tuft & Shortt, 2009).
    6) A keratoprosthesis placement has also been indicated in severe cases (Fish & Davidson, 2010). Penetrating keratoplasty is usually delayed as long as possible as results appear to be better with a greater lag time between injury and keratoplasty (Grant & Schuman, 1993a).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) TOXICITY: Serious burns are less likely if the pH is less than 11.5. Injury is greater with large exposures and high concentrations. With highly concentrated liquids, esophageal burns may occur in up to 100% of patients, even after accidental ingestion.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Exposure levels, other than the TLV and STEL have not been established for human exposures. The TWA is 10 ppm {approximately 24 mg/m(3)} and the STEL is 15 ppm {approximately 36 mg/m(3)}. Case histories are rare.

Workplace Standards

    A) ACGIH TLV Values for CAS75-50-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Trimethylamine
    a) TLV:
    1) TLV-TWA: 5 ppm
    2) TLV-STEL: 15 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT irr
    d) Molecular Weight: 59.11
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS75-50-3 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Trimethylamine
    2) REL:
    a) TWA: 10 ppm (24 mg/m(3))
    b) STEL: 15 ppm (36 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS75-50-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Trimethylamine
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Trimethylamine
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-50-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000 ITI, 1995 Lewis, 1996 OHM/TADS, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 946 mg/kg
    2) LD50- (ORAL)RAT:
    a) 500 mg/kg

Physicochemical

Physical Characteristics

    A) Trimethylamine (anhydrous) is a colorless gas; it is shipped as liquefied compressed gas (Lewis, 1997) Lewis, 1996).
    1) At temperatures below 37 degree F, it exists as a liquid (HSDB , 2000; NIOSH , 2000).
    2) At 15 degrees C and 1 atm pressure, it exists as a gas (CHRIS , 2000).
    B) This compound exists as a volatile liquid, emitting a fishy odor (Lewis, 1996).
    1) Its odor has been describes as unpleasant, pungent, fishy, ammoniacal (Budavari, 1996; Grant & Schuman, 1993; ITI, 1995; Lewis, 1997). Only 7% of the human population are not able to smell this compound (HSDB , 2000).
    2) At low concentrations, this compound has a characteristic fishy odor. At concentrations between 100 to 500 ppm, the odor resembles that of ammonia (Clayton & Clayton, 1994).
    C) It has a saline taste (Budavari, 1996; ITI, 1995).
    D) During decay, it is converted to the free tertiary amine (Budavari, 1996).
    1) At pH 3.3 and 100 degrees C, trimethylamine can be converted to dimethylnitrosamine (ACGIH, 1991).
    E) Decomposition products include: carbon monoxide, carbon dioxide, hydrocarbons, oxides of nitrogen and amine vapors (NFPA, 1997).
    F) Under anaerobic conditions, bacterial decomposition products include: dimethylamine, formaldeyde, formate and carbon dioxide. Under aerobic conditions, microbial decomposition products include: dimethylamine, ammonia and methane (Snyder et al, 1990).

Ph

    A) Strong base (Budavari, 1996).
    B) Dissolving the anhydrous gas in water generates a very strong alkaline solution (NFPA, 1997)

Molecular Weight

    A) 59.11

Other

    A) ODOR THRESHOLD
    1) The following thresholds have been reported (HSDB , 2000):
    2) 1.70 ppm (detection in water, chemically pure)
    3) 3.67X10(-4) ppm (detection in water, chemically pure)
    4) 5.00X10(-4) mg/kg (detection in water)
    5) 2.10X10(-4) ppm (recognition in air, chemically pure)
    6) 2.20X10(11) molecules/cm(3) (in air, purity not specified)
    7) Low: 0.36 mg/m(3); High: 1.12 mg/m(3)
    8) 0.00011 to 0.87 ppm (Clayton & Clayton, 1994)
    9) 0.00044 ppm (Sittig, 1991)
    10) 0.00021 ppm (OHM/TADS , 2000)

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