Introduction
Background
Chemical burns are primarily divided into 2 groups: acid and alkali. In addition to the occupational hazards associated with industrial strength product use in the work place, a plethora of products are available and used by the general public. As with most environmental or toxicological exposures, knowing the specifics of the offending agent is key. Appropriate evaluation of chemical burns requires a complete assessment of the offending agent (composition, acid or alkali, concentration), type of exposure (inhalation, cutaneous, ocular, GI), duration of exposure, and other events or injuries associated with the chemical burn (explosion, fall, trauma).
Pathophysiology
Acids and alkalis cause injury via different mechanisms.
Acids produce coagulation necrosis by denaturing proteins upon tissue contact. An area of coagulation is formed and limits extension of injury. An exception is hydrofluoric acid, which produces a liquefaction necrosis similar to alkalis. Hydrofluoric acid is also unique in that it may rapidly penetrate the skin to the vasculature, allowing for rapid fluoride ion dissemination.1,2 The fluoride may then precipitate with calcium, causing life-threatening hypocalcemia and metastatic calcification.
Alkalis cause a liquefaction necrosis and are potentially much more dangerous than acid burns. Alkali agents liquefy tissue by denaturation of proteins and saponification of fats. In contrast to acids burns, in which tissue penetration is limited by the formation of a coagulum, alkali burns can continue to penetrate very deeply into tissue.
Frequency
United States
Accurate statistics are lacking. However, approximately 25,000-100,000 chemical burns are reported every year.
Mortality/Morbidity
- Chemical burns result in approximately 20 deaths per year, with a mortality rate of less than 1%.
- Morbidity, defined as severe toxicity, occurs in less than 1% of those exposed.
- Bleach is associated with severe toxicity in less than 1% of cases. Death is rare, although reports of fatalities have been anecdotally reported.
- Alkali exposures are high risk.
- Drain cleaners are associated with severe toxicity in 1-2% of cases, with a mortality rate of less than 0.1%.
- Caustic ingestions are high risk and may result in airway compromise.
- Ocular exposures are high risk.
Age
- Children and adults have similar exposure rates.
- Younger children tend to be accidentally exposed because of inadequate childproofing.
- Older children and young adults may be exposed because of impetuous behavior or experimentation.
Clinical
History
In patients with chemical burns, a careful physical examination is important; however, a thorough history usually helps determine how a patient should be treated.
- Type of exposure
- Determine the offending substance. Relying solely on patient history is insufficient. Obtain the substance's container, call the manufacturer, use a computerized poison index, and/or call your regional poison center.
- Determine whether the substance is acid, alkali, or chemical in composition, and ascertain the concentration.
- Determine whether the exposure was cutaneous, oral, GI, ocular, or inhalation.
- Time and duration of exposure
- Symptoms immediately after the injury (pain, burning, numbness, change in level of consciousness, respiratory distress, vital signs, oral discomfort or swelling, ocular discomfort, change in vision)
- Decontamination or life-saving measures provided at the scene
- Other injuries possibly resulting from a fall, explosion, or fire
- Preexisting medical conditions
Physical
- Airway
- Patients with oral or inhalation injury may experience significant edema or difficulty maintaining their airway and often require intubation.
- Particular attention should be paid to the presence of stridor, hoarseness, and oral swelling.
- Breathing: Patients may develop wheezing and labored breathing as a result of inhalation. Symptoms may range from discomfort and mild wheezing to respiratory failure requiring artificial ventilation.
- Circulation
- Assess circulation by determining perfusion to end organs, level of consciousness, skin color and temperature, capillary refill, and urinary output.
- Assess heart rate for appropriate rate and regularity.
- Disability: Perform a thorough neurologic evaluation to determine the presence and degree of deficit. Serial examinations are necessary to evaluate symptom progression or resolution.
- Environmental
- As with many environmental injuries, patients with chemical burns may be at risk for becoming hypothermic, with associated increased morbidity and mortality. Attention should be paid to maintaining normal temperature.
- Preventing further injury is also important. Wet or contaminated clothing should be removed, and the patient maintained warm and dry.
- Extremities: Close inspection of all extremities should be performed to rule out any other associated injuries.
- Special considerations
- Patients with oral or inhalation injury may experience significant swelling or difficulty maintaining their airway. Particular attention should be paid to the presence of drooling, stridor, hoarseness, and oral swelling. Intubation may be necessary.
- Oral burns are an underreported problem and may lead to severe contracture. Oral contractures can be divided into anterior, posterior, and total. Posterior oral contractures result from caustic ingestion and involve the posterior buccal mucosa, posterior tongue, retro-molar area and oro-pharynx. Total oral contractures typically result from caustic lye ingestion and involve the lips, tongue, oral cavity, and oro-pharyngeal mucosa.
- Seek, and document, the presence, size, and depth of cutaneous burns.
- Depths of burn classifications are superficial partial thickness, deep partial thickness, and full thickness. Depth determination involves describing the affected area's color, texture, and sensation.
- First-degree burn: Redness without change in texture and intact sensation denotes a superficial injury.
- Second-degree burn: Blister formation with or without denuding and pink to mildly pale tissue with intact sensation denotes deeper partial-thickness injury.
- Third-degree burn: Areas that are white, leathery, and insensate denote full-thickness injury.
- Determining extent of involvement requires an estimate of the affected body surface area. Special attention is also paid to injuries of the face, hands, feet, and genitalia. Circumferential injury should also be noted.
- Body surface area can be estimated by using a standard chart with the Rule of 9's. However, the Lund and Browder Chart provides a more accurate estimate in children.
- Most small injuries can be approximated using the size of the patient's palm. The entire palm, including the fingers, represents approximately 1% of total body surface area (TBSA).
- Oral or GI
- Oral or GI exposure may cause severe burns, particularly if the exposure is to a strong alkali.
- Early injury may be represented by redness, swelling, and pain. Patients breathe through an open mouth, drool, speak with a hoarse voice, or have stridor.
- Remember that alkali compounds result in liquefaction necrosis, with potential for ongoing deep tissue penetration. Severe precipitous airway edema or obstruction may result.
- Children who refuse to swallow their own saliva should be given particular attention. Risk of esophageal perforation and stricture is very real (although these are later complications and are not usually present when the patient is in the emergency department.)
- Ocular
- Patients with ocular exposure or complaints require detailed ophthalmologic evaluation. However, initial examination is deferred until adequate decontamination has occurred with copious amounts of saline (minimum of 0.5 h).
- Complete evaluation includes general appearance of the globe, conjunctiva, anterior chamber, and cornea with attention to redness, pallor, or opacification.
- Examine the eye for presence of foreign bodies.
- Verify pupillary and extraocular muscle function.
- pH testing should be performed before and after each set of irrigations and should be continued until the pH returns to the normal range (7-8).
- Stain with fluorescein to look for areas of increased uptake signifying corneal abrasion.
- A slit lamp examination may be useful. It allows for a more detailed examination of the cornea and anterior chamber, including the presence of a hyphema or hypopyon.
- Document the visual acuity of patients with ocular exposure or complaints. Documentation should include right eye and left eye individually, then vision with both eyes.
Causes
- Inadequate child-proofing
- Cleaning or caustic products are not stored out of reach of young children.
- Cleaning solutions or agents are stored in bottles other than the original container (eg, a potentially caustic solution in a soda pop bottle).
- Directions are not regarded or supplies are inappropriately mixed (eg, mixing bleach and ammonia products creates a noxious gas, which can precipitate acute bronchospasm and respiratory distress).
- Unintended exposures are caused by something breaking, exploding, or being squirted or sprayed.
- Common sources of acids
- Toilet bowl or drain cleaners may contain sulfuric or hydrochloric acid. They may also contain alkali.
- Automotive tire or metal cleaners and rust removers may contain hydrofluoric, sulfuric, or phosphoric acid.
- Engraving solution may contain hydrofluoric or nitric acid.
- Tile cleaners or glass etching may contain hydrofluoric acid.
- Battery fluid may contain sulfuric acid.
- Common sources of alkalis (bases)
- Drain or oven cleaners may contain sodium or potassium hydroxide.
- Cleaners and detergents may contain ammonia or any of the sodium or potassium polyphosphates.
- Household bleach or pool chlorination system or tablets may contain sodium or calcium hypochlorite.
- Cement, mortar, or plaster may contain calcium hydroxide or oxide.
- Denture cleaners or Clinitest tablets may contain sodium or potassium hydroxide.
- Dishwashing or clothing detergents may contain silicates or sodium carbonate.
- Toilet cleaners (lye) may contain potassium hydroxide or other strong alkali.
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References
Bertolini JC. Hydrofluoric acid: a review of toxicity. J Emerg Med. Mar-Apr 1992;10(2):163-8. [Medline].
Bjornhagen V, Hojer J, Karlson-Stiber C, et al. Hydrofluoric acid-induced burns and life-threatening systemic poisoning--favorable outcome after hemodialysis. J Toxicol Clin Toxicol. 2003;41(6):855-60. [Medline].
Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus [see comments]. N Engl J Med. Sep 6 1990;323(10):637-40. [Medline].
Ahsan S, Haupert M. Absence of esophageal injury in pediatric patients after hair relaxer ingestion. Arch Otolaryngol Head Neck Surg. Sep 1999;125(9):953-5. [Medline].
Baruchin AM, Jakim I, Rosenberg L, Nahlieli O. On burn injuries related to airbag deployment. Burns. Feb 1999;25(1):49-52. [Medline].
Bond SJ, Schnier GC, Sundine MJ, et al. Cutaneous burns caused by sulfuric acid drain cleaner. J Trauma. Mar 1998;44(3):523-6. [Medline].
Broto J, Asensio M, Jorro CS, et al. Conservative treatment of caustic esophageal injuries in children: 20 years of experience. Pediatr Surg Int. Jul 1999;15(5-6):323-5. [Medline].
Caravati EM. Acute hydrofluoric acid exposure. Am J Emerg Med. Mar 1988;6(2):143-50. [Medline].
Chung JY, Kowal-Vern A, Latenser BA, Lewis RW 2nd. Cement-Related Injuries: Review of a Series, the National Burn Repository, and the Prevailing Literature. J Burn Care Res. Oct 3 2007;[Medline].
Conner JC, Bebarta VS. Images in clinical medicine. White phosphorus dermal burns. N Engl J Med. Oct 11 2007;357(15):1530. [Medline].
Edlich RF, Farinholt HM, Winters KL, et al. Modern concepts of treatment and prevention of chemical injuries. J Long Term Eff Med Implants. 2005;15(3):303-18. [Medline].
Ein SH. Gastric tubes in children with caustic esophageal injury: a 32-year review. J Pediatr Surg. Sep 1998;33(9):1363-5. [Medline].
Fisher AA. Cement injuries: Part II. Cement burns resulting in necrotic ulcers due to kneeling on wet cement [news]. Cutis. Mar 1998;61(3):121. [Medline].
Friedman EM, Lovejoy FH Jr. The emergency management of caustic ingestions. Emerg Med Clin North Am. Feb 1984;2(1):77-86. [Medline].
Gallerani M, Bettoli V, Peron L, Manfredini R. Systemic and topical effects of intradermal hydrofluoric acid. Am J Emerg Med. Sep 1998;16(5):521-2. [Medline].
Hashem FK, Al Khayal Z. Oral burn contractures in children. Ann Plast Surg. Nov 2003;51(5):468-71. [Medline].
He J, Bazan NG, Bazan HE. Alkali-induced corneal stromal melting prevention by a novel platelet-activating factor receptor antagonist. Arch Ophthalmol. Jan 2006;124(1):70-8. [Medline].
Holmes RG, Chan DC, Singh BB. Chemical burn of the buccal mucosa. Am J Dent. Jun 2004;17(3):219-20. [Medline].
Homan CS, Singer AJ, Thomajan C, et al. Thermal characteristics of neutralization therapy and water dilution for strong acid ingestion: an in-vivo canine model. Acad Emerg Med. Apr 1998;5(4):286-92. [Medline].
Horgan N, McLoone E, Lannigan B, et al. Eye injuries in children: a new household risk. Lancet. Aug 13-19 2005;366(9485):547-8. [Medline].
Howell JM. Alkaline ingestions. Ann Emerg Med. Jul 1986;DA - 19860730(7):820-5. [Medline].
Hugh TB, Kelly MD. Corrosive ingestion and the surgeon [published erratum appears in J Am Coll Surg 2000 Jan;190(1):102]. J Am Coll Surg. Nov 1999;189(5):508-22. [Medline].
Jiaqi C, Zheng W, Jianjun G. Eyelid reconstruction with acellular human dermal allograft after chemical and thermal burns. Burns. Mar 2006;32(2):208-11. [Medline].
Karjoo M. Caustic ingestion and foreign bodies in the gastrointestinal system. Curr Opin Pediatr. Oct 1998;10(5):516-22. [Medline].
Karnak I, Tanyel FC, Buyukpamukcu N, Hicsonmez A. Combined use of steroid, antibiotics and early bougienage against stricture formation following caustic esophageal burns. J Cardiovasc Surg (Torino). Apr 1999;40(2):307-10. [Medline].
Kerstein MD, Schaffzin DM, Hughes WB. Acute management of exposure to liquid ammonia. Mil Med. Oct 2001;166(10):913-4. [Medline].
Kiristioglu I, Gurpinar A, Kilic N, et al. Is it necessary to perform an endoscopy after the ingestion of liquid household bleach in children? [letter]. Acta Paediatr. Feb 1999;88(2):233-4. [Medline].
Lusk PG. Chemical eye injuries in the workplace. Prevention and management. AAOHN J. Feb 1999;47(2):80-7; quiz 88-9. [Medline].
Makela JT, Laitinen S, Salo JA. Corrosion injury of the upper gastrointestinal tract after swallowing strong alkali. Eur J Surg. Aug 1998;164(8):575-80. [Medline].
Mannan A, Ghani S, Clarke A, et al. Psychosocial outcomes derived from an acid burned population in Bangladesh, and comparison with Western norms. Burns. Mar 2006;32(2):235-41. [Medline].
Mehta RK, Handfield-Jones S, Bracegirdle J. Cement dermatitis and chemical burns. Clin Exp Dermatol. Jun 2002;27(4):347-8. [Medline].
Mercer R. Three steps toward eye safety. Occup Health Saf. May 1999;68(5):107-8. [Medline].
Meredith JW, Kon ND, Thompson JN. Management of injuries from liquid lye ingestion. J Trauma. Aug 1988;28(8):1173-80. [Medline].
Moghadam BK, Gier R, Thurlow T. Extensive oral mucosal ulcerations caused by misuse of a commercial mouthwash. Cutis. Aug 1999;64(2):131-4. [Medline].
Nagel TR, Schunk JE. Using the hand to estimate the surface area of a burn in children. Pediatr Emerg Care. Aug 1997;13(4):254-5. [Medline].
Nordt SP, Molloy M, Ryan J, McQuillan RF. Burns from automobile airbags. J Emerg Med. Aug 2003;25(2):201-2. [Medline].
Ogawa M, Nakajima Y, Endo Y. Four cases of chemical burns thought to be caused by exposure to chromic acid mist. J Occup Health. Sep 2007;49(5):402-4. [Medline].
Ohtani M, Nishida N, Chiba T, et al. Pathological demonstration of rapid involvement into the subcutaneous tissue in a case of fatal hydrofluoric acid burns. Forensic Sci Int. Jan 17 2006;[Medline].
Pelclova D, Navratil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev. 2005;24(2):125-9. [Medline].
Penner GE. Acid ingestion: toxicology and treatment. Ann Emerg Med. Jul 1980;9(7):374-9. [Medline].
Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. Sep 15 2007;76(6):829-36. [Medline].
Ryan F, Witherow H, Mirza J, Ayliffe P. The oral implications of caustic soda ingestion in children. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Jan 2006;101(1):29-34. [Medline].
Saidinejad M, Burns MM. Ocular irrigant alternatives in pediatric emergency medicine. Pediatr Emerg Care. Jan 2005;21(1):23-6. [Medline].
Spoo J, Elsner P. Cement burns: a review 1960-2000. Contact Dermatitis. Aug 2001;45(2):68-71. [Medline].
Tamhane A, Vajpayee RB, Biswas NR, et al. Evaluation of amniotic membrane transplantation as an adjunct to medical therapy as compared with medical therapy alone in acute ocular burns. Ophthalmology. Nov 2005;112(11):1963-9. [Medline].
Tiras U, Erdeve O, Karabulut AA, et al. Debridement via collagenase application in two neonates. Pediatr Dermatol. Sep-Oct 2005;22(5):472-5. [Medline].
Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J. May 2005;22(5):359-61. [Medline]. [Full Text].
Vitello W, Kim M, Johnson RM, Miller S. Full-thickness burn to the hand from an automobile airbag. J Burn Care Rehabil. May-Jun 1999;20(3):212-5. [Medline].
Wallace KL, Pegg SP. Self-inflicted burn injuries: an 11-year retrospective study. J Burn Care Rehabil. Mar-Apr 1999;20(2):191-4; discussion 189-90. [Medline].
Wason S. The emergency management of caustic ingestions. J Emerg Med. 1985;2(3):175-82. [Medline].
Wasserman RL, Ginsburg CM. Caustic substance injuries. J Pediatr. Aug 1985;107(2):169-74. [Medline].
Wibbenmeyer LA, Morgan LJ, Robinson BK, et al. Our chemical burn experience: exposing the dangers of anhydrous ammonia. J Burn Care Rehabil. May-Jun 1999;20(3):226-31. [Medline].
Wirbelauer C. Management of the red eye for the primary care physician. Am J Med. Apr 2006;119(4):302-6. [Medline].
Woolf A, Shaw J. Childhood injuries from artificial nail primer cosmetic products. Arch Pediatr Adolesc Med. Jan 1998;152(1):41-6. [Medline].
Further Reading
Keywords
chemical burns, acid burns, alkali burns, base burns, caustic agents, caustic burns, inhalation burn, cutaneous burn, ocular burn, gastrointestinal burn, GI burn, coagulation necrosis, liquefaction necrosis, hypocalcemia, airway compromise, trauma, fall, edema, hypothermia, inhalation injury, respiratory distress
Overview: Burns, Chemical