1) 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 esophageal. Some patients (particularly young children) may develop upper airway edema.
2) 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.
3) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
5) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.

1) Perform early endoscopy (within 12 hours) 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.

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.

1) 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.

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.

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 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 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, 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 corrosive eye injury should be evaluated by an ophthalmologist.

1) Acid ingestion, gastrointestinal hemorrhage, or perforated viscus.

1) Administer oxygen as necessary. Monitor for respiratory distress.

1) Manage airway aggressively in patients with significant respiratory distress, stridor or any evidence up upper airway edema. Monitor for hypoxia or respiratory distress.

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

1) Exposed eyes should be irrigated with copious amounts of 0.9% 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.

1) DECONTAMINATION

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.

1) Cardiovascular collapse can result from fluid loss and sequestration following ingestion, or from pulmonary congestion and noncardiogenic pulmonary edema following inhalation (EPA, 1985; Lewis, 1996; Kennedy & Chen, 1984).

1) Vapor inhalation causes irritation of the respiratory tract (Kennedy & Chen, 1984).

1) Pulmonary congestion and edema occur at higher exposure concentrations and can lead to death in circulatory collapse (Kennedy & Chen, 1984).

1) Drooling, gagging, vomiting, and chest or upper abdominal pain may occur following ingestion (EPA, 1985; Lewis, 1996).

1) This agent is highly corrosive and would be predicted to cause burns and edema of the mouth, throat, esophagus, and gastrointestinal tract (EPA, 1985; Lewis, 1996).

1) Early complications following ingestion could be perforation and bleeding (EPA, 1985; Lewis, 1996).

1) Late sequelae could be stricture formation in the esophagus or stomach (EPA, 1985; Lewis, 1996).

1) CBC CHANGES - Changes in hemoglobin, hematocrit, and leukocyte counts were seen in rats repeatedly exposed to DBHMD by inhalation (Kennedy & Chen, 1984). These effects have not been reported in exposed humans.

1) DBHMD is very corrosive to the skin (EPA, 1985; Lewis, 1996; Kennedy & Chen, 1984).

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

1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

1) Not Listed

1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

1) Obtain a complete blood count in symptomatic patients following ingestion.

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.

1) Monitor urine output in patients with 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, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.

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.

1) The use of diluents is controversial. Immediate dilution with small amounts of milk or water may help decontaminate the oral mucosa or dislodge particles of granular caustics from the esophageal mucosa. In a survey of the POISINDEX(R) editorial board (Consensus, 1988), 7 of 10 members routinely recommended dilution, provided that no airway compromise was present. Two other members expressed concern that dilution might precipitate vomiting, but this was not the experience of other members.
2) Swallowed milk may obscure esophagoscopy (Howell, 1987), but is not a problem with equipment containing water irrigation attachments. Maull (1987) found water to be an ineffective diluent in vitro. Other in vitro studies have demonstrated efficacy of milk or water (Rumack & Burrington, 1977).
3) The amount of diluent recommended by the POISINDEX(R) editorial board varied widely, ranging from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum amount of 8 ounces in adults and 4 ounces in children (Consensus, 1988).

1) Acidic agents (eg, vinegar, fruit juices) to neutralize the alkali are CONTRAINDICATED because of the high risk of exothermic burns (Rumack & Burrington, 1977). Once the alkaline agent has reached the stomach it will be effectively neutralized by the available gastric acid. Gastric tissue is resistant to burns from small amounts of these agents.

1) LAVAGE - should be AVOIDED to prevent reexposure of the esophagus to the corrosive agent.
2) Some clinicians may choose to insert a small nasogastric tube through the mouth, if the patient is alert and cooperative, in an attempt to dilute and remove the corrosive substance following a recent ingestion. The decision should be based on the amount of the ingestion, the concentration of the alkaline, the type of product ingested, and the risk and potential benefit to the patient. This is based on the fact that reports of perforations were from insertion of rigid endoscopes and on the benefit from removal of the corrosive substance, thereby preventing some tissue damage.

1) Activated charcoal may cause vomiting, which may be hazardous to a patient who has ingested a caustic substance. Furthermore, the administration of activated charcoal may obscure visualization of gastroesophageal lesions by endoscopy.

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) Do not exceed 15 milliliters/kilogram orally in a child (maximum 250 milliliters in a 16 kilogram or larger patient) as vomiting may occur with excessive fluid. The patient should be made NPO following initial dilution and kept NPO until after medical/surgical evaluation.

1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
2) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
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.
7) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
8) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).

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, 1973a). 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

1) Antibiotics should be used only for specific indications of infection. Intravenous antibiotics should be considered in patients with evidence of infection and esophageal or gastric perforation (Howell, 1987).

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).
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).

1) BETA AMINOPROPIONITRILE - Animal studies indicate that the use of beta aminopropionitrile (BAPN) may play a role in the future for preventing stricture formation after burns.
2) N-ACETYLCYSTEINE - Systemic N-acetylcysteine has been shown to decrease the incidence of esophageal stricture formation in rats (Liu & Richardson, 1985).
3) SUCRALFATE - The administration of 1 gram in 100 milliliters of water was reported to decrease odynophagia by 50 percent within 24 hours in a woman who ingested crystalline Drano(R); however, stricture formation was not prevented and cimetidine was given concurrently, making assessment of any therapeutic benefit from sucralfate difficult (Reddy & Budhraja, 1988). More studies will be needed before sucralfate can be recommended for treatment of caustic ingestions.
4) PANA - Oral administration (via gastric gavage) of sodium polyacrylate (PANA) to rats with sodium-hydroxide induced gastric burns resulted in a decreased burn area but not burn depth (Ehrenpreis et al, 1988).

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) Administer oxygen, determine blood gases, obtain chest x-ray and, if pulmonary edema is present, consider positive end expiratory pressure ventilation (PEEP). Steroids may provide benefit but antibiotics are useful only if there is evidence of infection.
2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
3) 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).
4) 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).
5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
7) 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).
8) 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) SUMMARY
2) DOPAMINE
3) NOREPINEPHRINE

1) 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).

1) Sticky lime paste may be removed from the conjunctiva or cul-de-sac by using a cotton tipped applicator soaked in 0.01 Molar sodium EDTA (Pfister & Koski, 1982).

1) EVALUATION
2) MINOR INJURY
3) SEVERE INJURY
4) SURGICAL THERAPY

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).

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

1) Chemical burns from alkalis should be frequently irrigated for 24 hours with normal saline. This should reduce the average time from burn to first skin graft. Hydrotherapy may not be effective for an alkaline corrosive burn if it is not begun within 1 hour of the burn (Saydjari et al, 1986).