Updated: Jan 10, 2008
Acids are defined as proton donors (H+), and bases are defined as proton acceptors (OH-). Bases also are known as alkalies. Both acids and bases can be defined as caustics, which cause significant tissue damage on contact. The strength of an acid is defined by how easily it gives up the proton; the strength of a base is determined by how avidly it binds the proton. The strength of acids and bases is defined by using the pH scale, which ranges from 1-14 and is logarithmic. A strong acid has a pH of 1, and a strong base has a pH of 14. A pH of 7 is neutral.
Most acids produce a coagulation necrosis by denaturing proteins, forming a coagulum (eg, eschar) that limits the penetration of the acid. Bases typically produce a more severe injury known as liquefaction necrosis. This involves denaturing of proteins as well as saponification of fats, which does not limit tissue penetration. Hydrofluoric acid is somewhat different from other acids in that it produces a liquefaction necrosis.
The severity of the burn is related to a number of factors, including the pH of the agent, the concentration of the agent, the length of the contact time, the volume of the offending agent, and the physical form of the agent. The ingestion of solid pellets of alkaline substances results in prolonged contact time in the stomach, thus, more severe burns. In addition, concentrated forms of some acids and bases generate significant heat when diluted, resulting in thermal and caustic injury.
The long-term effect of caustic dermal burns is scarring, and, depending on the site of the burn, scarring can be significant. Ocular burns can result in opacification of the cornea and complete loss of vision. Esophageal and gastric burns can result in stricture formation.
In 2005, the American Association of Poison Control Centers (AAPCC) reported 26,300 cases of exposures to acidic substances, 40,800 cases of exposures to alkaline substances, 23,300 cases of peroxide exposures, and 59,500 cases of bleach exposures. During that time, 1,532 cases of exposure to phenols or phenol products were reported.1 Chemical injuries account for 2-6% of burn center admissions.2
Worldwide, corrosive substances are commonly used for chemical assault. The most common substances used are lye and sulfuric acid.3
In the 2005 report of the American Association of Poison Control Centers, exposures to acids and acid-containing products and chemicals resulted in 9 deaths, 129 cases of major toxicity, and 2380 cases of moderate toxicity. Exposures to alkali products and chemicals resulted in 8 deaths, 226 cases of major toxicity, and 3615 cases of moderate toxicity. Exposures to peroxides resulted in 1 death, 5 cases of major toxicity, and 108 cases of moderate toxicity. Exposures to bleaches and chlorite-containing products resulted in 8 deaths, 82 cases of major toxicity, and 2862 cases of moderate toxicity. Exposures to phenol-containing products resulted in 1 death, 5 cases of major toxicity, and 108 cases of moderate toxicity.1
Assaults with caustic chemicals worldwide are more likely to occur against women.3
Adults and children are nearly equally exposed to chemical burns.
A large number of industrial and commercial products contain potentially toxic concentrations of acids, bases, or other chemicals that can cause burns. Some of the more common products are listed as follows:
| Burns, Ocular | CBRNE - Vesicants, Mustard: Hd, Hn1-3, H |
| CBRNE - Chemical Decontamination | CBRNE - Vesicants, Organic Arsenicals: L, ED,
MD, PD, HL |
| CBRNE - Chemical Warfare Agents | Hazmat |
| CBRNE - Incendiary Agents, Magnesium and
Thermite | Toxicity, Caustic Ingestions |
| CBRNE - Incendiary Agents, White
Phosphorus |
Prompt wound irrigation is the most critical aspect in preventing the extent of dermal burns from exposure to caustic substances. Animal studies have shown that irrigation of both acid exposures and alkaline exposures within several minutes decreases the pH change in the skin and the extent of dermal injury. A burn center case series found that patients who received irrigation within 10 minutes had a 5-fold decrease in full-thickness injury and a 2-fold decrease in length of hospital stay.7
The first priority in treatment is to ensure complete removal of the offending agent. Thorough decontamination is key. Adequate irrigation is difficult to define and depends on the amount of exposure and the agent involved. Using litmus paper to measure the pH of the affected area or the irrigating solution is helpful. Complete removal and neutralization of concentrated acids and alkalis may require several hours of irrigation. Tap water is adequate for irrigation. Low-pressure irrigation is desired; high pressures may exacerbate the tissue injury.7,8,9,10
Medications have a limited role in the treatment of most chemical burns. Topical antibiotic therapy is usually recommended for dermal and ocular burns. Calcium or magnesium salts are used for hydrofluoric acid burns. Pain medications are important for subsequent burn care.
Steroid therapy is controversial for caustic ingestions but may be helpful for treating upper airway inflammation. No evidence indicates that steroid therapy decreases incidence of stricture formation. Steroids may predispose the patient to infection and may mask signs of perforation. There has been some use of aloe products on mild burns; however, currently, no definitive information on their use for chemical burns is available.17,15
Nonsteroidal anti-inflammatory agents do provide some degree of pain relief for mild burns by inhibition of prostaglandin mediators. These have not been evaluated for chemical burns and should be avoided in all cases of GI burns from ingestions.
After decontamination is performed on patients with chemical burns affecting a significant portion of the body, administer standard IV fluid and narcotic therapy as used for thermal burns. For additional information, see the Burns, Thermal article.
Topical and ophthalmic antibiotics are routinely used for dermal and ocular burns, respectively. The injured tissues lose many of their protective mechanisms and are at increased risk of infection.
Used topically for dermal burns and useful in the prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast.
Apply qd/bid to a thickness of 1/16th inch; continually cover burned area; remove all previous medication before applying each new dose
<2 years: Do not administer
>2 years: Apply topically as in adults
Reduces effectiveness of proteolytic enzymes
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Patients with G-6-PD deficiency and renal insufficiency
Use prophylactically to prevent infections following ocular burns. Ointment has a very low incidence of allergic reactions. Other possible agents include polymyxin B, bacitracin, and ciprofloxacin solutions.
Apply to affected eye topically tid/qid
Apply as in adults
None reported
Documented hypersensitivity; viral, mycobacterial, and fungal infections of the eye; patients using steroid combinations after uncomplicated removal of a foreign body from the cornea
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Do not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection (take appropriate measures if superinfection occurs)
Used topically for dermal burns and useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast. Preferable for face and visible areas.
Apply 1/16th-inch thickness bid/tid; continually cover burned area; remove all previous medication before applying each new dose
Apply as in adults
None reported
Documented hypersensitivity; epithelial herpes simplex keratitis, mycobacterial, and fungal infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in treating extensive burns (>20% body surface area) because absorption of neomycin is possible and may cause nephrotoxicity and ototoxicity; prolonged use may result in overgrowth of nonsusceptible organisms
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained injuries to the eye.
Morphine is recommended in the ED. For outpatient treatment, combinations of hydrocodone or oxycodone and acetaminophen are usually sufficient. Codeine is not recommended.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are most commonly used for the relief of mild to moderate pain. Although effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen is usually the DOC for initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.
DOC for narcotic analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Morphine sulfate administered IV may be dosed in a number of ways and is commonly titrated until the desired effect is obtained.
During the ED treatment of the acute burn, use IV (preferred) or IM for moderate or severe pain.
5-10 mg IV as loading dose; followed by 4-6 mg IV q10-15min prn
0.05-0.2 mg/kg IV/IM q2-4h; may need to titrate as in adults
Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; respiratory depression; potentially compromised airway with uncertain rapid airway control; nausea; emesis; constipation; urinary retention
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Drug combination indicated for the relief of moderate to severe pain. DOC for aspirin-hypersensitive patients.
Formulations of oxycodone/acetaminophen are available as follows:
Tylox-5/500
Percocet-5/325
Percocet-7.5/500
Percocet-10/650
1-2 tab or cap PO q4-6h prn pain
Products containing more than 500 mg of acetaminophen/tab should only be prescribed one tab per dose
0.05-0.15 mg/kg/dose oxycodone PO; not to exceed 5 mg/dose of oxycodone q4-6h prn
Phenothiazines may decrease analgesic effects of this medication; toxicity increases with coadministration of either CNS depressants or tricyclic antidepressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Duration of action may increase in elderly persons; be aware of total daily dose of acetaminophen patient is receiving; do not exceed 4,000 mg/d of acetaminophen; higher doses may cause liver toxicity
Drug combination for outpatient use and indicated for the relief of moderate-to-severe pain.
Formulations of hydrocodone/acetaminophen are available as follows: Vicodin-5/500, ES-7.5/750, HP-10/600 Lorcet-10/650, Plus-7.5/650 Lortab-2.5/500, 5/500, 7.5/500, 10/500 Norco-10/325.
Typical elixirs contain 2.5 mg hydrocodone and 167 mg/mL acetaminophen.
1-2 tab or cap PO q4-6h prn for pain
Products containing more than 500 mg of acetaminophen/tab should only be prescribed one tab per dose
0.3 mL/kg q4h provides 10 mg/kg of acetaminophen and 0.15 mg/kg of hydrocodone
0.5 mL/kg q4h provides 16 mg/kg of acetaminophen and 0.25 mg/kg of hydrocodone
Coadministration with phenothiazines may decrease analgesic effects; toxicity increases with CNS depressants or tricyclic antidepressants
Documented hypersensitivity; elevated intracranial pressure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Withhold for drowsiness; hepatic toxicity may occur in overdose; use Norco or a product that does not contain acetaminophen in patients with a history of severe hepatic disease; may cause constipation and stomach upset; caution in severe renal or hepatic dysfunction
Usually the DOC for the treatment of mild to moderate pain, if no contraindications exist.
Inhibits inflammatory reactions and pain by decreasing activity of the enzyme cyclooxygenase, resulting in the inhibition of prostaglandin synthesis.
Useful for outpatient oral use where nonsedating drugs are preferred. Also has the advantage of an anti-inflammatory effect.
400-600-800 mg PO, approximately 100 mg/h (eg, 400 mg PO q4h, 600 mg q6h)
5-10 mg/kg PO q4-6h
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Used for the relief of mild to moderate pain and inflammation.
Initially administer small dosages to patients with a small body size, the elderly, and those with renal or liver disease.
When administering this medication, doses higher than 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 14 years: 0.1–1 mg/kg PO q6-8h
>14 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Used for relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of enzyme cyclooxygenase, resulting in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg PO q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
These agents can help remove offending substances from the skin and minimize their caustic effects.
Used as an aid in removing phenol or cresols. Desired agent is PEG 400 mixed 50:50 in water. Most hospitals are not likely to have this product. If not available, use bowel-cleansing products containing PEG.
Use liberally to remove phenol or cresols; may need to wipe off with gauze soaked in PEG solution
Apply as in adults
None reported for this indication
Documented hypersensitivity to PEG
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Be cautious on large surface areas of denuded skin; may cause metabolic acidosis or hypocalcemia; phenol may also cause metabolic acidosis if large surface area is involved
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acid burns, base burns, corrosive ingestion, caustic burn, caustic chemical burn, esophageal burn, sulfuric acid, nitric acid, hydrofluoric acid, hydrochloric acid, muriatic acid, phosphoric acid, acetic acid, formic acid, chloroacetic acid, monochloroacetic acid, dichloroacetic acid, trichloroacetic acid, phenol, cresol, sodium hydroxide, potassium hydroxide, calcium hydroxide, calcium oxide, lime, ammonia, phosphate, chlorate, white phosphorus, vesicants, chromate, potassium dichromate, chromic acid, peroxides, hydrogen peroxide, bleach, potassium permanganate
Robert D Cox, MD, PhD, Professor, Department of Emergency Medicine, Associate Professor, Department of Pharmacology and Toxicology, University of Mississippi Medical Center; Medical Director, Mississippi Regional Poison Control Center
Robert D Cox, MD, PhD is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology
Disclosure: Nothing to disclose.
Jerry Balentine, DO, Professor of Emergency Medicine, New York College of Osteopathic Medicine; Senior Vice President, Chief Medical Officer, Medical Director, Attending Physician in Department of Emergency Medicine, Saint Barnabas Hospital
Jerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine
Disclosure: Nothing to disclose.
John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.
Jon Mark Hirshon, MD, MPH, Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine
Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting
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