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CHLOROSILANES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chlorosilanes are organic or inorganic derivatives of silicon and chlorine with the general formula RCl Si.

Specific Substances

    A) Tetrachlorosilane
    1) Molecular Formula: Cl4-Si
    2) Chlorosilane
    3) CAS 10026-04-7
    Methyltrichlorosilane
    1) Molecular Formula: C-H3-Cl3-Si
    2) CAS 75-79-6
    Dimethyldichlorosilane
    1) Molecular Formula: C2-H6-Cl2-Si
    2) CAS 75-78-5
    Ethyltrichlorosilane
    1) Molecular Formula: C2-H5-Cl3-Si
    2) CAS 115-21-9
    Diethyldichlorosilane
    1) Molecular Formula: C4-H10-Cl2-Si
    2) CAS 1719-53-5

Available Forms Sources

    A) USES
    1) Tetrachlorosilane (SiCl4) is an irritant gas used as a warfare agent and to prepare smoke screens.

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: Chlorosilanes are organic or inorganic derivatives of silicon and chlorine. Tetrachlorosilane (SiCl4) is an irritant gas used as a warfare agent and to prepare smoke screens.
    B) TOXICOLOGY: Chlorinated silanes are very corrosive to skin and mucous membranes and liberate hydrochloric acid in the presence of water. Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars.
    C) EPIDEMIOLOGY: Exposure is rare; limited data regarding specific human toxicity following chlorosilanes exposure.
    D) WITH POISONING/EXPOSURE
    1) Chlorosilanes exposure is unusual; limited data regarding specific human toxicity following acrylic acid exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    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) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema.
    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. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication.
    a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
    4) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis and systemic toxicity.
    0.2.4) HEENT
    A) Severe ocular irritation may occur.
    B) Rats exposed to vapors developed nasal discharge, lacrimation, salivation, and pulmonary irritation.
    0.2.6) RESPIRATORY
    A) Three cases of permanently disabling reactive airway syndrome have been reported in adults exposed for several hours to fumes of sodium hydroxide, trichlorosilane, and silicon tetrachloride.
    B) Rats exposed to vapors developed shallow and difficult respiration.
    0.2.8) GASTROINTESTINAL
    A) Gastrointestinal tissue corrosion was observed in animals given single oral doses and may occur in humans following ingestion.
    0.2.10) GENITOURINARY
    A) Renal toxicity following chronic vapor exposure in animals has been observed.
    0.2.13) HEMATOLOGIC
    A) Tetrachlorosilane vapor exposure may produce red blood cell destruction.
    0.2.14) DERMATOLOGIC
    A) The application of chlorosilanes to shaved rabbit skin produced various degrees of irritation. Complete denaturation and tissue sloughing occurred within one minute after exposure to dichlorodimethylsilane, within 2 to 3 minutes after exposure to methyltrichlorosilane, ethyltrichlorosilane, and dichlorodiethylsilane, and within 10 minutes after exposure to tetrachlorosilane.

Laboratory Monitoring

    A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid 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, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. 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 2 or 3 burns, to evaluate for strictures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is very little information available regarding the treatment of chlorosilane-induced injury; the following data is derived from experience with other acids.
    B) MILD TO MODERATE ORAL TOXICITY
    1) Within the first 12 hours of exposure, 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% 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. Severe edema may make intubation difficult; be prepared for surgical airway management (cricothyroidotomy) in patients with severe upper airway edema.
    F) ENDOSCOPY
    1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with acid ingestion. 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) BRONCHOSPASM
    1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids.
    H) 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, so routine use is not recommended.
    I) 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.
    J) 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.
    K) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to 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, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    L) 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 acidic eye injury should be evaluated by an ophthalmologist.
    M) DIFFERENTIAL DIAGNOSIS
    1) Alkaline corrosive ingestion, gastrointestinal hemorrhage, or perforated viscus.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: 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, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

    A) TOXICITY: Serious burns are less likely if the pH >3. Injury is usually greater with either a large ingestion (usually deliberate), or a high concentration acid (usually not a household product).
    B) In a case series of unintentional caustic ingestions (mixed liquid and solid, acids and bases) among children, the incidence of significant esophageal or gastric burns was 5% to 35%. However, adults with deliberate acid ingestions are more likely to develop significant esophageal and/or gastric burns (40% to 95%).

Clinical Effects

Summary Of Exposure

    A) USES: Chlorosilanes are organic or inorganic derivatives of silicon and chlorine. Tetrachlorosilane (SiCl4) is an irritant gas used as a warfare agent and to prepare smoke screens.
    B) TOXICOLOGY: Chlorinated silanes are very corrosive to skin and mucous membranes and liberate hydrochloric acid in the presence of water. Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars.
    C) EPIDEMIOLOGY: Exposure is rare; limited data regarding specific human toxicity following chlorosilanes exposure.
    D) WITH POISONING/EXPOSURE
    1) Chlorosilanes exposure is unusual; limited data regarding specific human toxicity following acrylic acid exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    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) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema.
    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. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication.
    a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
    4) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis and systemic toxicity.

Heent

    3.4.1) SUMMARY
    A) Severe ocular irritation may occur.
    B) Rats exposed to vapors developed nasal discharge, lacrimation, salivation, and pulmonary irritation.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION - Severe ocular irritation may occur following exposure to vapors or liquids. The instillation of a small drop of any of the chlorosilanes produced severe damage to rabbit eyes, including corneal and eyelid burns (HSDB , 2001; Rowe et al, 1948).
    2) LACRIMATION was reported in rats exposed to vapors (HSDB , 2001; Rowe et al, 1948).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) NASAL DISCHARGE was reported in rats exposed to vapors (HSDB , 2001; Rowe et al, 1948).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) SALIVATION was reported in rats exposed to vapors (HSDB , 2001; Rowe et al, 1948).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Circulatory collapse with clammy skin, weak and rapid pulse, shallow respiration, and anuria may occur following ingestion or dermal exposure of chlorosilanes. Death may occur due to circulatory shock (HSDB , 2001).

Respiratory

    3.6.1) SUMMARY
    A) Three cases of permanently disabling reactive airway syndrome have been reported in adults exposed for several hours to fumes of sodium hydroxide, trichlorosilane, and silicon tetrachloride.
    B) Rats exposed to vapors developed shallow and difficult respiration.
    3.6.2) CLINICAL EFFECTS
    A) REACTIVE AIRWAYS DYSFUNCTION SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Promisloff et al (1990) report 3 cases of reactive airway dysfunction syndrome (RADS) associated with a chemical spill which included sodium hydroxide, silicon tetrachloride, and trichlorosilane. The patients developed permanently disabling exertional dyspnea and wheezing following several hours' exposure to the fumes (Promisloff et al, 1990).
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Caustic burning and irritation of the respiratory tract may be noted (HSDB , 2001).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSPNEA
    a) RATS - Shallow and difficult breathing was noted in rats exposed to vapors (HSDB , 2001; Rowe et al, 1948).

Gastrointestinal

    3.8.1) SUMMARY
    A) Gastrointestinal tissue corrosion was observed in animals given single oral doses and may occur in humans following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Chlorosilanes liberate hydrochloric acid in the presence of water and may cause corrosion of mucous membranes of mouth, esophagus, and stomach accompanied by pain, dysphagia, nausea, and vomiting of "coffee-ground" material following ingestion. Necrotic areas may first appear grayish-white but will change to a blackish discoloration with a wrinkled texture (HSDB , 2001).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CHEMICAL BURN
    a) The chlorosilanes were markedly corrosive to the gastrointestinal tissues when given orally to animals (Rowe et al, 1948).

Genitourinary

    3.10.1) SUMMARY
    A) Renal toxicity following chronic vapor exposure in animals has been observed.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) Renal toxicity has been observed with chronic exposure to vapors in animals.

Hematologic

    3.13.1) SUMMARY
    A) Tetrachlorosilane vapor exposure may produce red blood cell destruction.
    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) Red blood cell destruction may occur after exposure to tetrachlorosilane vapors.

Dermatologic

    3.14.1) SUMMARY
    A) The application of chlorosilanes to shaved rabbit skin produced various degrees of irritation. Complete denaturation and tissue sloughing occurred within one minute after exposure to dichlorodimethylsilane, within 2 to 3 minutes after exposure to methyltrichlorosilane, ethyltrichlorosilane, and dichlorodiethylsilane, and within 10 minutes after exposure to tetrachlorosilane.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DERMATITIS EXFOLIATIVE
    a) RABBITS - The application of chlorosilanes to shaved rabbit skin produced various degrees of irritation.
    1) Complete denaturation and tissue sloughing occurred within one minute after exposure to dichlorodimethylsilane, within 2 to 3 minutes after exposure to methyltrichlorosilane, ethyltrichlorosilane, and dichlorodiethylsilane, and within 10 minutes after exposure to tetrachlorosilane (Rowe et al, 1948).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS10026-04-7 (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
    B) IARC Carcinogenicity Ratings for CAS75-79-6 (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
    C) IARC Carcinogenicity Ratings for CAS75-78-5 (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 and electrolytes in all patients with significant burns after acid 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, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. 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 2 or 3 burns, to evaluate for strictures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion. 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 and liver enzymes.
    B) COAGULATION STUDIES
    1) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain INR, PT, PTT, fibrinogen, fibrin degradation products, and type and crossmatch for blood.
    4.1.3) URINE
    A) OTHER
    1) Monitor urine output and urinalysis in patients will 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 signs and symptoms to evaluate for pneumomediastinum or free air under the diaphragm.
    2) The absence of these findings does NOT rule out the possibility of necrosis or perforation of the esophagus or stomach.
    3) Obtain a chest radiograph in patients with pulmonary signs or symptoms.
    B) RADIOGRAPHIC-OTHER
    1) Esophagrams in the acute and subacute phase demonstrate edema, hemorrhage, ulcerations, atony, and dilation. Strictures of the esophagus may be present in the chronic phase. These radiographic findings are not different from those found in alkaline corrosive esophagitis (Muhletaler et al, 1980).
    2) Krypton esophageal transit studies and manometric measurements correlated better with residual clinical symptoms and functional outcomes than did morphological findings of stenosis late (3 months to 7 years) after caustic ingestions (Cadranel et al, 1990).
    C) CT SCAN
    1) Abdominal CT scans were performed on 5 patients who ingested glacial acetic acid. Diffuse edematous thickening of the walls of the esophagus and stomach were found in all patients. Wedge-shaped low density areas in the liver were found in 3 patients; clinically these 3 developed hepatic failure, hemolysis, metabolic acidosis and coagulopathy, and 2 of these patients died. The authors postulated that wedge-shaped low densities in the liver after acid ingestion may represent areas of hepatic necrosis secondary to toxin absorption into the portal circulation (Kim et al, 2007).

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, or extensive grade II 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 an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to home.

Monitoring

    A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid 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, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. 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 2 or 3 burns, to evaluate for strictures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL/NOT RECOMMENDED
    1) Activated charcoal is NOT recommended as it has not been shown to reduce corrosive gastrointestinal injury and may obscure endoscopy findings.
    B) IRRIGATION
    1) Irrigate the mouth with copious amounts of water.
    C) 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).
    2) Follow dilution with appropriate demulcents - milk, cornstarch, and water.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Activated charcoal should NOT be used. It may cause vomiting which can worsen caustic gastrointestinal injury, and may obscure endoscopy findings.
    B) IRRIGATION
    1) Irrigate the mouth with copious amounts of water.
    C) 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).
    2) Follow dilution with appropriate demulcents - milk, cornstarch, and water.
    6.5.3) TREATMENT
    A) CONTRAINDICATED TREATMENT
    1) Do not induce vomiting or give bicarbonate to neutralize. Addition of buffer to strong acid causes an exothermic reaction and an immediate rise in solution temperature (Maull et al, 1985; Penner, 1980).
    2) A report concerning emergency surgical resection of the alimentary tract following caustic ingestions has indicated that 5 out of 6 patients sustained injuries beyond the pylorus as a result of gastric lavage (Wu & Lai, 1993).
    B) DIETARY FINDING
    1) Put patient on clear liquid or full liquid diet as tolerated.
    C) BURN
    1) If severe burns occur in the mouth then esophageal burns may exist. Most burns occur in the pyloric region of the stomach. Esophagoscopy in severe cases will determine presence or absence of burns.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    3) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (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; Nuutinen et al, 1994)
    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.
    D) OBSTRUCTION
    1) Observe for symptoms of acute obstruction (pyloric spasm), at which time parenteral fluids and/or hyperalimentation should be considered.
    E) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993a). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, 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).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.
    F) 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).

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.

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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) 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).

Range Of Toxicity

Summary

    A) TOXICITY: Serious burns are less likely if the pH >3. Injury is usually greater with either a large ingestion (usually deliberate), or a high concentration acid (usually not a household product).
    B) In a case series of unintentional caustic ingestions (mixed liquid and solid, acids and bases) among children, the incidence of significant esophageal or gastric burns was 5% to 35%. However, adults with deliberate acid ingestions are more likely to develop significant esophageal and/or gastric burns (40% to 95%).

Maximum Tolerated Exposure

    A) ANIMAL DATA
    1) Single oral doses of 100 or 300 mg/kg in rats did not result in mortality, whereas doses of 1000 mg/kg were lethal in most of the animals (Rowe et al, 1948).

Workplace Standards

    A) ACGIH TLV Values for CAS10026-04-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) ACGIH TLV Values for CAS75-79-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) ACGIH TLV Values for CAS75-78-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    D) NIOSH REL and IDLH Values for CAS10026-04-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    E) NIOSH REL and IDLH Values for CAS75-79-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    F) NIOSH REL and IDLH Values for CAS75-78-5 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    G) Carcinogenicity Ratings for CAS10026-04-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    H) Carcinogenicity Ratings for CAS75-79-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    I) Carcinogenicity Ratings for CAS75-78-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    J) OSHA PEL Values for CAS10026-04-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    K) OSHA PEL Values for CAS75-79-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    L) OSHA PEL Values for CAS75-78-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ETHYL TRICHLOROSILANE
    1) LD50- (ORAL)RAT:
    a) 1330 mg/kg (RTECS , 2001)
    B) TETRACHLOROSILANE
    C) TRICHLOROSILANE
    1) LD50- (ORAL)RAT:
    a) 1.03 g/kg (HSDB, 2001)

Physicochemical

Physical Characteristics

    A) All of the chlorosilanes are water-white liquids which fume on exposure to moist air.
    B) Vapors have a sharp acrid odor.

Molecular Weight

    A) DICHLORODIETHYLSILANE: 157.05
    B) DICHLORODIMETHYLSILANE: 129.02
    C) ETHYLTRICHLOROSILANE: 163.47
    D) METHYLTRICHLOROSILANE: 149.46
    E) TETRACHLOROSILANE: 169.89

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