1) MILD TO MODERATE TOXICITY: Milder exposures (generally to concentrations less than 10%) may only cause irritation of the skin, upper airway and GI mucosa.
2) SEVERE TOXICITY: SUMMARY: Sulfuric acid is corrosive to the skin, eyes, nose, mucous membranes, respiratory tract and gastrointestinal tract, or any tissue with which it comes in contact.

1) INGESTION: Perform endoscopy within the first 12 hours of exposure; if burns are absent or grade l severity, the patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for IV 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) INGESTION: 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 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. INHALATION: Oxygen, inhaled beta agonists, early endotracheal intubation if upper airway burns are a concern or significant respiratory distress. Early bronchoscopy in patients with respiratory distress or upper airway edema. DERMAL: Copious irrigation, antibiotic ointment and referral to a burn specialist. OCULAR: Copious irrigation until pH neutral and emergent ophthalmology consultation. 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) PREHOSPITAL: INGESTION: Rinse mouth, administer small amounts of water or milk if the patient is not in respiratory distress and can swallow (child: up to 4 oz in or adult: 8 oz). DERMAL: Remove contaminated clothing and irrigate skin with copious amounts of water. INHALATION: Remove from exposure. OCULAR: Irrigate with copious amounts of water.
2) HOSPITAL: INGESTION: Irrigate mouth, administer small amounts of water or milk if the patient is not in respiratory distress and can swallow (child: up to 4 oz or adult: 8 oz). Consider insertion of a small, flexible nasogastric tube to aspirate stomach contents in large, recent ingestions. The risk of further mucosal injury must be weighed against potential benefit. DERMAL: Remove contaminated clothing and irrigate skin with copious amounts of water. INHALATION: Administer oxygen. OCULAR: Irrigate with copious amounts of water.

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) ENDOSCOPY: Should be performed as soon as possible (preferably within 12 hours not more than 24 hours) in any patient with an 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.
2) CORTICOSTEROIDS: 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 they are 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.
3) STRICTURE: 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.
4) SURGICAL MANAGEMENT: Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns or endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of a large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, and early resection and repair in these patients is associated with improved outcome.
5) HYPOTENSION: Patients with severe burns may develop hypotension secondary to third spacing of fluid and/or GI bleeding. Resuscitate with IV fluids and blood products as appropriate.

1) INHALATION: Administer oxygen. If respiratory symptoms develop obtain a chest x-ray, monitor pulse oximetry and/or blood gases. Treat bronchospasm with inhaled beta agonists. Perform endotracheal intubation early if upper airway burns are a concern or if significant respiratory distress develops. Early bronchoscopy may be useful to clear debris and assess extent of injury.

1) Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. After irrigation, apply antibiotic ointment and sterile dressing to dermal burns.

1) IRRIGATION: Irrigate with sterile 0.9% saline for at least an hour or until the cul-de-sacs are free of particulate matter and returned to neutrality (confirm with pH paper). Perform a slit lamp exam. Emergent ophthalmology consultation and close follow-up is recommended. Antibiotics and mydriatics may be indicated. The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after a burn.

1) HOME CRITERIA: Asymptomatic patients with inadvertent exposures to low concentration household products (ie, lick or sip, small dermal exposure to a product with less than 10% sulfuric acid) can be decontaminated and followed at home.
2) OBSERVATION CRITERIA: The following patients should be referred to a healthcare facility for evaluation: any patients with an eye exposure, any symptomatic patient, any deliberate exposure, any ingestion exposure to a high concentration product (10% or more sulfuric acid). 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.
3) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher GI burns should be admitted. Patients with respiratory distress, grade III GI burns, or extensive grade II GI burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting. Patients with deep or extensive dermal burns should be admitted to a burn center.
4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity. Consult a gastroenterologist for endoscopic evaluation of patients with ingestion exposures. Consult an ophthalmologist for any patient with ocular splash exposure. Consult a burn surgeon for any patient with severe or large body surface area burns, or any burns involving the face, hands, feet or genitals. Consult a pulmonologist or critical care physician for bronchoscopy in patients with significant respiratory distress.

1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal or gastric 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 sulfuric acid eye injury should be evaluated by an ophthalmologist.

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

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.
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) INHALATION: Respiratory effects of acute exposure include irritation of the nose and throat, coughing, sneezing, reflex bronchospasm, dyspnea and pulmonary edema. Death may occur from sudden circulatory collapse, glottic edema and airway compromise, or from acute lung injury.
b) INGESTION: Ingestion of sulfuric acid may cause immediate epigastric pain, nausea, hypersalivation and vomiting of mucoid or "coffee ground" hemorrhagic material. Occasionally vomiting of fresh blood has been seen. Ingestion of concentrated sulfuric acid may produce esophageal corrosion, necrosis and perforation of the esophagus or stomach especially at the pylorus. Occasionally injury to the small bowel has been reported. Delayed complications may include strictures and fistula formation. Metabolic acidosis may develop following ingestion.
c) DERMAL: Severe dermal burns can occur with necrosis and scarring. These may be fatal if a large enough area of the body surface is affected.
d) OCULAR: The eye is especially sensitive to corrosive injury. Irritation, lacrimation and conjunctivitis can develop even with low concentrations of sulfuric acid. Splash contact with high concentrations causes corneal burns, visual loss and occasionally perforation of the globe.

1) One study reported these findings with chronic exposures in the range of 12.6 to 35 mg/m(3): central and lateral incisors are mainly affected with etching of the dental enamel and erosion of the enamel and dentine with loss of tooth substance, progressive destruction of the crown occurs on the labial surface, painless erosion ceases at the lip level (Finkel, 1983; Proctor & Hughes, 1978; Sittig, 1985; El-Sadik et al, 1972).

1) CONCENTRATED SULFURIC ACID can cause severe pain, necrosis of the conjunctiva or corneal epithelium, corneal ulcers, or severe burns of the corneal epithelium if splashed in the eye (Gosselin et al, 1984; Finkel, 1983). The anterior segment of the globe can be dissolved; glaucoma and cataract can ensue as complications following exposure (Grant & Schumann, 1993).
2) Even DILUTE SULFURIC ACID can cause permanent corneal damage, blindness and scarring of the eyelids (Sittig, 1985). However, there are also many cases of transient injury with complete recovery following exposure to dilute sulfuric acid (Grant & Schumann, 1993).
3) With strong acid exposures, the cornea may become vascularized and opaque or may soften with sloughing of the whole stroma. Perforation of the globe and loss of ocular contents may occur (Grant & Schumann, 1993). Short of such drastic sequelae, permanent damage and visual impairment can occur from sulfuric acid (Proctor & Hughes, 1978).
4) A common cause of eye injuries from sulfuric acid is splashing of battery acid while working on car batteries. Of 93 cases most involved the conjunctiva, followed by injuries to the cornea; however, damage to the lids, anterior chamber, and retina were also seen (Holekamp & Becker, 1977).

1) CASE REPORT: A 36-year-old jeweler presented to the emergency department with severe burns to his face, neck, thorax, and abdomen 30 minutes after he inadvertently ingested an unknown quantity of highly concentrated sulfuric acid. Tracheal necrosis and severe trismus with insensitive spongy yellow tongue, gums, buccal mucosa, and palate were also observed. Despite an emergency tracheotomy and aggressive resuscitation efforts, the patient died of progressive hemodynamic decompensation and multiorgan failure (Aouad et al, 2011).

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) PULMONARY FUNCTION: Inhalation of sulfuric acid mist causes a reflex increase in respiratory rate and diminution of the depth of respiration with a compensatory increase in respiratory rate. It may also cause laryngospasm and bronchoconstriction resulting in increased pulmonary air flow resistance (Finkel, 1983; Sittig, 1985).
2) In 15 subjects exposed to concentrations ranging from 0.35 to 0.5 mg/m(3) (mean diameter 1 micron) for 15 minutes, respiratory rate increased by 30% over controls, maximum inspiratory and expiratory flow rates decreased by approximately 20%, and tidal volume increased by about 28%. At 5 mg/m(3) there was a decrease in minute volume and prolongation of the expiratory phase of the respiratory cycle (Amdur et al, 1952).

1) WITH POISONING/EXPOSURE

1) Chronic exposure to sulfuric acid mists may be associated with chronic bronchitis (ACGIH, 1987; Finkel, 1983).

1) Emphysema has resulted from long-term exposures to sulfuric acid mist (Sittig, 1985).

1) Chronic exposure to sulfuric acid mist has been associated with frequent respiratory infections (Sittig, 1985).

1) WITH POISONING/EXPOSURE

1) PULMONARY FUNCTION: Inhalation of sulfuric acid mist causes a reflexive diminution of the depth of respiration with a compensatory increase in the respiratory rate. Laryngospasm and bronchoconstriction may result in increased pulmonary air flow resistance (Sittig, 1985).
2) Patients with asthma are likely to develop transient bronchospasm at low exposure levels (51 to 176 mcg/m(3)) that may not affect other populations (Hanley et al, 1992; Koenig et al, 1993).

1) Studies in normal subjects performing moderate exercise in chamber atmospheres at 100 mcg/m(3) and 450 mcg/m(3) of sulfuric acid revealed no changes in pulmonary function immediately or 24 hours after inhalation. All subjects inhaled carbachol following each 4-hour exposure and 24 hours after exposure. Twenty-four hours after exposure to 450 mcg/m(3), 8 of 14 subjects reported mild throat irritation. Significant enhancement of the carbachol bronchoconstrictor response was also observed 24 hours after the 450 mcg/m(3) exposure (Utell, 1985).

1) In one study, carbachol-sensitive asthmatics inhaled sulfuric acid concentrations of 100 mcg/m(3), 450 mcg/m(3) and 1000 mcg/m(3) for 16 minutes via a mouthpiece. At 450 mcg/(3) and 1000 mcg/m(3), significant reductions in specific airway conductance and FEV(1) were observed. No significant change in airway function occurred at 100 mcg/m(3) (Utell, 1985).

1) RESPIRATORY DISORDER

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) WITH POISONING/EXPOSURE

1) Exposure to dilute concentrations may produce dermatitis; generally the epithelium becomes indurated without being destroyed (Proctor & Hughes, 1978).

1) Immunological alterations were reported from occupational exposure to sulfuric acid (Scheller, 1977).
2) SENSITIZATION: In all studies examining respiratory sensitization to sulfuric acid it would be important to distinguish between the reflex bronchoconstriction, which is possibly a pharmacologic effect, and true immunologic mechanisms of sensitization.
3) Although most studies of the effect of aerosolized sulfuric acid on bronchial hypersensitivity in asthmatics have found no effect of inhaled H2SO4, most have examined the effects of very low concentrations of 100 mcg/m(3). One study that compared the change in forced expiratory volume in one second (FEV1) in response to inhaled grass pollen after asthmatic subjects breathed air, 100 mcg/m(3) of aerosolized sulfuric acid, or 1000 mcg/m(3) of sulfuric acid found that the change in FEV1 with the lower concentration of sulfuric acid compared to air only approached significance, while the higher concentration of acid produced significantly more bronchial hyperreactivity (Tunnicliffe et al, 2001).

1) SKELETAL MALFORMATION
2) LACK OF EFFECT

1) ABORTION

1) Not Listed

1) Several epidemiological studies of workers chronically exposed to sulfuric acid have suggested increased risk for respiratory and nasopharyngeal cancers.

1) Monitor CBC, serum electrolytes and renal function tests after significant ingestions, dermal exposures or symptomatic inhalation injury.
2) An elevated anion gap acidosis or signs of renal insufficiency may be important signs of inadequate volume resuscitation and early shock. Although it is nonspecific, one study found that leukocytosis was an independent predictor of high-grade esophageal injury after corrosive ingestion (Havanond & Havanond, 2007).

1) Monitor urine output in patients with significant gastrointestinal or dermal burns. A drop in urine output may be an early indicator of volume depletion or inadequate resuscitation.

1) MONITORING
2) PULMONARY FUNCTION TESTS

A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher GI burns should be admitted. Patients with respiratory distress, grade III GI burns, or extensive grade II GI burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting. Patients with deep or extensive dermal burns should be admitted to a burn center.

A) Asymptomatic patients with inadvertent exposures to low concentration household products (ie, lick or sip, small dermal exposure to a product with less than 10% sulfuric acid) can be decontaminated and followed at home.

A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity. Consult a gastroenterologist for endoscopic evaluation of patients with ingestion exposures. Consult an ophthalmologist for any patient with ocular splash exposure. Consult a burn surgeon for any patient with severe or large body surface area burns, or any burns involving the face, hands, feet or genitals. Consult a pulmonologist or critical care physician for bronchoscopy in patients with significant respiratory distress.

A) The following patients should be referred to a healthcare facility for evaluation; any patients with an eye exposure, any symptomatic patient, any deliberate exposure, any ingestion exposure to a high concentration product (10% or more sulfuric acid). 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) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact 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) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).

1) Activated charcoal is of no value, may induce vomiting and may obscure endoscopy findings. It is NOT recommended.

1) Monitor vital signs, CBC and electrolytes after significant ingestion.
2) Monitor renal function tests, liver enzymes, serial CBC, INR, PTT, type and crossmatch for blood, serum lactate and base deficit, monitor urine output and urinalysis in patients with severe burns or deliberate ingestion.
3) Monitor for occult GI hemorrhage, respiratory distress and increasing pain.
4) Obtain chest radiograph and pulse oximetry in any patient with respiratory signs or symptoms.

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, 1980a).
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) The mouth should be irrigated with copious amounts of water.
2) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact 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).
3) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
4) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
5) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
6) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).

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, 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
9) A systematic pooled analysis was conducted over a 50-year-period and involving only those studies with patients diagnosed with endoscopically documented caustic-induced grade II burns that were either treated with a minimum 10-day course of steroid therapy or with no steroid therapy. A total of 328 patients with grade II esophageal burns were included in the analysis: 244 patients (from 3 prospective and 8 retrospective studies) given a minimum 10-day course of steroid therapy and 84 patients (from 4 prospective and 1 retrospective study) with no steroid therapy. Thirty patients (12.3%) in the steroid group developed strictures and 16 patients (19%) in the non-steroid group developed strictures, which was not statistically significant, indicating that there appears to be no proven benefit for the use of steroid therapy in patients with grade II esophageal burns (Fulton & Hoffman, 2007).

1) Seven patients who developed esophageal strictures 3 weeks to 3 months after intentional acid ingestions were treated by endoscopic balloon dilatation upon diagnosis. The diameter of the initial balloon was 8 to 12 millimeters. Following the first successful dilatation, the interval between successive dilatations was 1 to 4 weeks. The progressive widening of the esophageal lumen to 15 millimeters was achieved after 3 to 7 dilatations. Endoscopic balloon dilatation was successful in 5 of the 7 patients with annular or short tubular strictures, and they currently are able to eat regular diets (Jovic-Stosic et al, 2001).
2) A retrospective study, involving 11 children (ages ranging from 1 to 14 years) who developed esophageal strictures following ingestion of a corrosive substance and subsequently underwent balloon dilatation, showed that the dilatation procedure was technically successful in 10 patients (91%) and in 35 dilatation sessions (97%), with improvement of the luminal diameter as seen with an esophagram performed immediately after dilatation. However, clinical success, defined as improved food intake and reduced dysphagia within one month of the first dilatation procedure, only occurred in 7 patients (64%). During the 35-month follow-up period, 10 of the 11 patients experienced recurrence of the esophageal strictures following the initial balloon dilatation. Seven patients underwent additional dilatations and 3 patients underwent either stent placement or surgery or both (Doo et al, 2009).
3) Early intraluminal esophageal stenting with a special nasogastric tube was recommended after caustic ingestion to prevent later esophageal stricture formation (Wijburg et al, 1989).
4) Esophageal reconstruction, involving colon interposition, has been performed in patients with esophageal strictures due to ingested caustic substances. According to a retrospective review, conducted in Belgrade, Serbia, over a 40-year-period, 336 patients with caustic-induced esophageal strictures underwent colon interposition, with 12.5% of patients also undergoing an esophagectomy concurrently. Left colon transplants were used in 258 (76.7%) patients. Early postoperative complications occurred in 89 patients and included pneumothorax/hematopneumothorax (13.09%), cervical anastomotic leakage (9.2%), transplant necrosis (2.38%), and abdominal anastomotic leakage (0.89%). Late postoperative complications occurred in 47 patients and included cervical anastomotic strictures (4.46%), thoracic outlet compression (2.08%), bowel obstruction (1.49%), and peptic colon ulceration (1.19%). Long-term follow up (1 to 30 years post-transplant, median 14.3 years) in 285 patients (84.82%) indicated good functional results in 233 patients (81.75%) (Knezevic et al, 2007).

1) RECOMMENDATIONS: Dietary recommendations depend on the degree of damage as assessed by early endoscopy (Dilawari, 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) One 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) 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).

1) BRONCHOSPASM SUMMARY
2) ALBUTEROL/ADULT DOSE
3) ALBUTEROL/PEDIATRIC DOSE
4) ALBUTEROL/CAUTIONS
5) CORTICOSTEROIDS

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

1) Upper airway tissue damage or swelling may cause airway compromise.
2) Endotracheal intubation or creation of a surgical airway could be required in severe cases.

1) In rabbits, treatment with isoproterenol and aminophylline significantly reduced the increased pulmonary artery pressure, vascular permeability, and fluid-flux associated with hydrochloric acid injury (Mizus et al, 1985).

1) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
2) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993).
3) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).

1) CORNEAL DAMAGE
2) EVALUATION
3) MEDICAL FACILITY IRRIGATION
4) MINOR INJURY
5) SEVERE INJURY
6) SURGICAL THERAPY

1) Immediately remove all potentially contaminated clothing and jewelry and irrigate the exposed area with copious amounts of water. A physician should examine the area if any irritation or pain persists.
2) The time to irrigation appears to be the most significant factor in determining burn depth. Studies in rats have shown that the degree of skin damage is less when washing occurs before the subcutaneous pH reaches its minimum value but this may be achieved within minutes (Flammiger & Maibach, 2006).
3) A study in rats burned with various concentrations of sulfuric acid showed that skin injury was less severe and mortality was lower when the skin was irrigated with water rather than rendered inert by neutralization with 5% sodium bicarbonate (Davidson, 1927).

1) Treat dermal irritation or burns with standard topical therapy. Patients who develop dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
2) Severe burns may require surgical consultation for debridement.

a) Acute inhalation may cause alterations in pulmonary function and respiration but results of various studies have differed and may depend on such factors as particle size, relative humidity, temperature, etc.
b) The lowest published toxic concentration by inhalation in humans was 3 mg/m(3) exposure over 24 weeks (RTECS , 1988).
c) In 15 subjects exposed to concentrations ranging from 0.35 to 0.5 mg/m(3) (mass medium diameter 1 micron) for 15 minutes, respiratory rate increased by 30% over controls, maximum inspiratory and expiratory flow rates decreased by approximately 20%, and tidal volume increased by about 28%. At 5 mg/m(3) there was a decrease in minute volume and prolongation of the expiratory phase of the respiratory cycle (Amdur et al, 1952).
d) No major changes in several parameters of pulmonary function (forced vital capacity maneuvers, lung volumes, maximum voluntary ventilation, Raw, TGV and helium-oxygen FVC) were seen in 11 subjects exposed to 0 to 939 mcg/m(3) particulate sulfuric acid with a mass medium diameter of 0.90 to 0.93 micron for 2 hours with alternating 20-minute periods of rest and exercise. FEV(1.0) was significantly decreased at the highest dose level but was not considered to be physiologically significant (Horvath et al, 1982).
e) No significant differences in pulmonary function were seen in 28 normal human subjects exposed to 100 mcg/m(3) of sulfuric acid 0.1 to 0.3 microns particle size for 4 hours; parameters examined were FVC, FEV(1), FEV(3), FRC, Raw and SBNER (Kerr et al, 1981).
f) Sulfuric acid mist at 100 mcg/m(3), ten-fold lower than the TLV, may produce bronchoconstriction in asthmatics (Hackney et al, 1985).
g) Sulfuric acid mist at 1000 mcg/m(3) potentiated the bronchoconstriction provoked by subthreshold levels of carbachol in 14 normal and 17 asthmatic subjects; at 100 mcg/m(3) sulfuric acid no potentiation was seen (Utell et al, 1984).
h) Aris et al (1991) varied aerosolized sulfuric acid particle size as well as relative humidity and was unable to provoke significant bronchoconstriction in normal and mildly asthmatic subjects.
i) Sulfuric acid aerosol at 0 to 1520 mcg/m(3)/0.9 micron mass median particle diameter for 1 hour with intermittent exercise did not affect pulmonary function or airway reactivity to methacholine in 21 healthy volunteers; 21 asthmatics showed significant increases in irritation and reduced pulmonary function but no significant changes in airway reactivity at 1060 and 1520 mcg/m(3) (Avol et al, 1988).
j) Sulfuric acid at 1000 mcg/m(3)/0.8 micron aerodynamic diameter inhaled for 16 minutes produced significant reductions in specific airway resistance (SGaw) and FEV(1) in 17 asthmatic subjects; 450 mcg/m(3) reduced SGaw and no significant change in airway function was seen at 100 mcg/m(3) (Utell et al, 1983).
k) Sulfuric acid aerosol at concentrations up to 1000 mcg/m(3)/0.1 micron mean aerodynamic diameter did not alter lung volumes, distribution of ventilation, ear oximetry, dynamic mechanics of breathing, oscillation mechanics of chest-lung system, pulmonary capillary blood flow, diffusing capacity, oxygen consumption, or pulmonary tissue volume in normal and asthmatic adults.
l) Respiration in dogs was not affected by sulfuric acid up to 4 mg/m(3) for 4 hours; sheep exposed up to 14 mg/m(3) for 20 minutes or 4 mg/m(3) for 4 hours had no alteration in tracheal mucous velocity (Sackner et al, 1978).
m) No effect of exposure to sulfuric acid at 100 mcg/m(3)/0.5 micron mean mass diameter was seen in the following biochemical parameters in the blood of 20 subjects exposed for 4 hours/day for 2 days while at rest or in 17 subjects exposed for 4 hours for 1 day while exercising: serum glutathione, red blood cell glutathione reductase, lysozyme, serum glutamic oxaloacetic acid transaminase, serum vitamin E, 2,3-diphosphoglycerate (Chaney, 1980a).

a) SUMMARY
b) PEDIATRIC
c) ADULT

a) Exposure of skin or eyes can produce deep burns.
b) Only about 12% of patients admitted to one burn unit suffered chemical burns. Of these sulfuric acid was the most common. Such injuries are rare (5%) in children, with most being occupational (Dominic, 1987).
c) A common cause of eye injuries from sulfuric acid is splashing of battery acid while working on car batteries. Of 93 cases most involved the conjunctiva, followed by injuries to the cornea; however, damage to the lids, anterior chamber, and retina were also seen (Holekamp & Becker, 1977).
d) Sulfuric acid may be used as a punishment or a form of humiliation in some countries like Bangladesh, where throwing acid on people is not uncommon. Victims frequently do no seek immediate care or perform immediate decontamination and burns are often fatal or severely disfiguring (Faga et al, 2000).
e) CASE REPORT: A 16-month-old girl suffered extensive burns on the skin when she knocked over a bottle of commercial drain cleaner containing sulfuric acid. Necrosis was into the dermis layer. After some skin grafting the remaining burns re-epithelialized and by 4 months there was little scar formation (Dominic, 1987).

a) Inhalation may cause etching or erosion of teeth at exposures lower than the TLV. Reduced pulmonary function (FVC) may occur. There may be some increased risk for lung cancer.
b) Occupational exposure to sulfuric acid has been associated with higher incidence of upper respiratory cancer, especially laryngeal cancer: in 50 confirmed cases there was an approximately 4-fold increased risk among highly exposed individuals relative to matched controls(Soskolne et al, 1984).
c) In a mortality study of 1165 workers exposed to sulfuric acid and other acid mists in steel-pickling operations, there was a 64% increase in deaths from lung cancer when compared with United States cancer death rates. An even higher increase of 124% was seen in persons exposed to other acid mists. A similar increase was seen in other steel workers exposed to other acids (Beaumont et al, 1987). The increased risk of death from lung cancer could not be attributed to sulfuric acid alone.
d) No increase in deaths from lung cancer was observed in American steel mill pickling workers (7 deaths versus 8 expected), but the sample size was very small (Redmond et al, 1981).
e) Of thirty-three workers in manufacture of batteries who were exposed to 12 to 35 mg/m(3) sulfuric acid (well above the TLV), 11 suffered from asthmatic bronchitis or chronic bronchitis and there was a reduction in vital capacity at the end of the shift compared to the beginning of the shift. However, these changes were not statistically different from those in a matched control group. There was a significant decrease in FEV(1), and dental lesions were seen in 21 out of 33 exposed workers (El-Sadik et al, 1972).
f) There was a slight excess of respiratory disease in 31 men working in the Forming department of an electric accumulator factory and exposed to an average of 1.4 mg/m(3) sulfuric acid. FEV(1) and FVC changes during the shift were not significantly different from those in controls (Williams, 1970).
g) In 225 workers in lead acid battery plants who were exposed to greater than 1 mg/m(3) of sulfuric acid, there was no significant evidence of acute symptoms or reduction in pulmonary function during the shift in a study by NIOSH (Gamble et al, 1984a).
h) In a related NIOSH study, 248 workers showed no significant cough, phlegm, dyspnea, or wheezing and no significant reduction of FEV(1), peak flow, FEF(50) or FEF (75) with exposure to acid. FVC was significantly reduced in the high-exposure group as a whole, but not when exposure was analyzed as a continuous variable. Erosion or etching of teeth was about 4 times greater than expected in the high-exposure group; etching occurred as early as 4 months of exposure to 0.23 mg/m(3) sulfuric acid, well below the TLV (Gamble, 1984b).

a) Many case reports of even relatively low volume sulfuric acid ingestion describe life-threatening sequelae including upper gastrointestinal hemorrhage, necrosis and stricture necessitating surgical correction (Penner, 1980; Jelenko, 1974; Zamir et al, 1985).

a) IARC Group 1: Ccarcinogenic to humans; strong inorganic acid mists containing sulfuric acid (IARC, 1992).
b) ACGIH has designated sulfuric acid contained in strong inorganic mists as an A2, Suspected Human Carcinogen (ACGIH, 2001).
c) NTP lists strong inorganic acid mists containing sulfuric acid as known human carcinogens in the Report on Carcinogens (RoC), 9th edition (NTP , 2001).
d) MAK: Category 4 (Substances with carcinogenic potential for which genotoxicity plays no or at most a minor role. No significant contribution to human cancer risk is expected, provided the MAK value is observed) (ACGIH, 2002a).

a) Adopted Value

1) Listed as: Sulfuric acid
2) REL:
3) IDLH:

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Sulfuric acid
2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Sulfuric acid
5) MAK (DFG, 2002): Category 4 ; Listed as: Sulfuric acid
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Strong Inorganic Acid Mists Containing Sulfuric Acid

1) Listed as: Sulfuric acid
2) Table Z-1 for Sulfuric acid:

1) LD50- (ORAL)RAT:
2) TCLo- (INHALATION)HUMAN:
3) TCLo- (INHALATION)RAT: