1) Acrylyl chloride exposure is unusual; limited data regarding specific toxicity following acrylyl chloride 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.
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.

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.

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.

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.

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.

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.

1) Treat with oxygen, inhaled beta agonists and consider systemic 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.

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.

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.

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.

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.

1) Alkaline corrosive ingestion, gastrointestinal hemorrhage, or perforated viscus.

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

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.

1) IRRITATION - Eye irritation or corneal burns may be predicted to occur with either vapor exposure or direct eye contact based on this agent's similarity to acrylic acid. Acrylyl chloride is a corrosive (HSDB , 1996).

1) IRRITATION - Irritation of the mucosa of the nose and throat may be predicted to occur following vapor exposure based on this agent's similarity to acrylic acid. Acrylyl chloride is a corrosive (HSDB , 1996).

1) IRRITATION - Irritation of the mucosa of the nose and throat may be predicted to occur following vapor exposure based on this agent's similarity to acrylic acid. Acrylyl chloride is a corrosive (HSDB , 1996).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) At the time of this review, no human data were available to assess the teratogenic potential of acrylyl chloride.

1) RELATED COMPOUNDS

1) LACK OF INFORMATION

1) Not Listed

1) LACK OF INFORMATION

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.

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.

1) Monitor urine output and urinalysis in patients will significant gastrointestinal burns, perforation, or bleeding.

1) MONITORING

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.

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.

1) Activated charcoal should NOT be used. It may cause vomiting which can worsen caustic gastrointestinal injury, and may obscure endoscopy findings.

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).

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).

1) It has been suggested that following a large ingestion of strong acids, a nasogastric tube should be passed and suction performed in an attempt to remove as much acid as possible prior to cold water dilution which may result in an exothermic reaction and worsen the burn (Penner, 1980).
2) Many authorities oppose this procedure fearing esophageal or gastric perforation. A soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.

1) Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. Early (within 24 hours) endoscopy should be performed to assess the severity of injury and guide future management.

1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
2) 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.
3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
5) GRADING
6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.

1) A small study suggests that esophageal ultrasonography may be useful in predicting the likelihood of strictures after corrosive ingestion (Kamijo et al, 2004).

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, 1989a; 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

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, 1984a).
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).

1) Depends on degree of damage as assessed by early endoscopy (Dilawari et al, 1984).
2) Observe for symptoms of gastric outlet obstruction, at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestions.

1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
2) A 3-year-old child developed esophageal stricture 2 years after the acid ingestion in a prospective study of 41 patients. This child had a normal barium study at one year after ingestion (Zargar et al, 1989).

1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.

1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

1) APPLICATION
2) DEBRIDEMENT
3) TREATMENT
4) TETANUS PROPHYLAXIS