Ammonia Toxicity Medication

  • Author: Steven Issley, MD, FRCPC; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Jun 27, 2011
 

Medication Summary

Management of toxic exposure to ammonia is largely supportive, and medical therapy is directed at hypoxia, bronchospasm, acute lung injury (ALI), hypovolemia, and burns of the skin and eyes.

Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures.

Although antibiotics and corticosteroids are often used in the acute treatment of patients with inhalation injury, neither has been shown to improve outcome and many believe that corticosteroids may actually increase morbidity. Corticosteroids are recommended to treat bronchospasm in patients with underlying reactive airways disease and acute inhalation injury or for chronic respiratory complications that follow an acute inhalation injury. Patients experiencing signs of airway edema after caustic exposure may benefit from IV administration of dexamethasone (adults: 10 mg; children: 0.6 mg/kg up to 10 mg max).

Use of steroids for the treatment of caustic injuries after caustic ingestion is still very controversial. Intravenous corticosteroids and antibiotics administration can be considered in symptomatic patients following ammonia ingestion with grade IIb (near-circumferential) caustic injuries. Presumably, corticosteroids are administered in order to decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries. Antibiotics are given because of increased risk of mediastinitis associated with full-thickness esophageal alkaline corrosive burns and steroid use. Although controlled animal studies do support the use of these therapies, no well-controlled human trials have been performed; thus, corticosteroids and antibiotics should be administered in consultation with a GI specialist and surgeon.

If steroids are administered, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 weeks followed by gradual tapering. If antibiotics are administered, a broad-spectrum antibiotic (eg, second-generation cephalosporins) is appropriate.

The decision to continue or stop corticosteroid and antibiotic therapy is based on endoscopic findings. Discontinue steroid and antibiotic therapies for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation. Furthermore, patients with severe transmural burns are at risk for stricture formation, but steroid therapy will not alter their risk. Thus, antibiotic therapy alone is recommended for this group to diminish their risk of mediastinitis. Patients with extensive superficial ulceration or deep discrete or circumferential ulcerations are at risk for stricture formation and may benefit from steroid administration. Consider administering corticosteroids and antibiotics to this group of patients.

Next

Bronchodilators

Class Summary

Bronchodilators selectively stimulate beta 2-adrenergic receptors of the bronchial tree and lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

Albuterol, salbutamol (Proventil, Ventolin)

 

Beta 2-agonist is used for the treatment of bronchospasm. Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility.

Previous
Next

Diuretics

Class Summary

Are sometimes considered for the treatment of acute lung injury (ALI). However, positive end-expiratory pressure (PEEP) may be much more useful than diuretics for optimizing oxygenation because ALI is secondary to alveolar capillary injury, not excess fluid. Nonetheless, a trial of diuretics can be considered in patients with evidence of concomitant fluid overload.

Furosemide (Lasix)

 

Loop diuretic; inhibits sodium chloride reabsorption in the ascending loop of Henle. Administer IV because this allows for superior potency and a higher peak concentration, despite an increased incidence of adverse effects, particularly ototoxicity (rare).

Previous
Next

Antibiotics

Class Summary

Although expensive, topical Silvadene has antipseudomonal properties in addition to coverage for most gram-positive organisms.

For eye exposures, antibiotic eye preparations will reduce risk of infection secondary to tissue injury.

Silver sulfadiazine 1% (Silvadene)

 

Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria including yeast.

Wash burn before application to remove previously applied agent.

Not for ophthalmic and facial use.

Other products may be used instead of silver sulfadiazine for partial thickness burns; these include TransCyte, Acticoat, or Biobrane.

Ciprofloxacin ophthalmic (Ciloxan)

 

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and growth.

Neomycin 5% is described in much of the literature on ammonia-related eye injury; however, newer broad-spectrum antibiotics have fewer adverse effects

Erythromycin ophthalmic (E-Mycin)

 

Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections

Previous
Next

Anticholinergic agents

Class Summary

Induces cycloplegia by blocking the body's parasympathetic (cholinergic) effects in the eye. This is beneficial to prevent ciliary spasm. Should be used in consultation with the ophthalmology service.

Cyclopentolate (AK-Pentolate)

 

Blocks muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation, thus causing mydriasis and cycloplegia.

Induces mydriasis in 30-60 min and cycloplegia in 25-75 min; these effects last up to 24 hours

Homatropine (Isopto Homatropine)

 

Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Induces mydriasis in 10-30 min and cycloplegia in 30-90 min; these effects last up to 48 h.

Tropicamide (Mydriacyl)

 

Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulation

Previous
Next

Corticosteroids

Class Summary

Decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, may potentiate infection. Should be administered only in consultation with the ophthalmology service.

Prednisolone ophthalmic (Pred Forte)

 

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Note that ophthalmologic steroids are controversial; discuss their use with ophthalmology. Also, steroid-antibiotic combination may be useful.

Fluorometholone (FML)

 

Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability

Rimexolone (Vexol)

 

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Previous
Next

Local anesthetics

Class Summary

Used primarily for pain relief. Duration of action is relatively short-lived, limiting usefulness of local anesthetics outside of the hospital or clinic setting.

Proparacaine 0.5% (Alcaine)

 

Has rapid onset of anesthesia that begins within 13-30 sec after instillation. However, has short duration of action of about 15-20 min.

Least irritating of all topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.

Onset of action occurs within 20 s of application.

Anesthetic effect may last up to 10-15 min

Previous
Proceed to Follow-up
 
 
Contributor Information and Disclosures
Author

Steven Issley, MD, FRCPC  Attending Physician, Trauma Team Leader, Department of Emergency Medicine, Hotel Dieu Grace Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Eddy S Lang, MDCM, CCFP(EM), CSPQ  Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Edmond A Hooker II, MD, DrPH, FAAEM  Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, 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.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References
  1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol (Phila). Dec 2010;48(10):979-1178. [Medline].

  2. Watson WA, Litovitz TL, Rodgers GC. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2003;21(5):353-421. [Medline].

  3. de la Hoz RE, Schlueter DP, Rom WN. Chronic lung disease secondary to ammonia inhalation injury: a report on three cases. Am J Ind Med. 1996;29(2):209-14. [Medline].

  4. Caplin M. Ammonia-gas poisoning: 47 cases in a London shelter. Lancet. 1941;2:958-61.

  5. Eduard W, Pearce N, Douwes J. Chronic bronchitis, COPD, and lung function in farmers: the role of biological agents. Chest. Sep 2009;136(3):716-25. [Medline].

  6. Klein J, Olson KR, McKinney HE. Caustic injury from household ammonia. Am J Emerg Med. Jul 1985;3(4):320. [Medline].

  7. Close LG, Catlin FI, Cohn AM. Acute and chronic effects of ammonia burns on the respiratory tract. Arch Otolaryngol. Mar 1980;106(3):151-8. [Medline].

  8. Arwood R, Hammond J, Ward GG. Ammonia inhalation. J Trauma. May 1985;25(5):444-7. [Medline].

  9. Montague TJ, Macneil AR. Mass ammonia inhalation. Chest. Apr 1980;77(4):496-8. [Medline]. [Full Text].

  10. Pascuzzi TA, Storrow AB. Mass casualties from acute inhalation of chloramine gas. Military Medicine. Feb 1998;163(2):102-4. [Medline].

  11. Am J Respir Crit Care Med. Respiratory health hazards in agriculture. Am J Respir Crit Care Med. Nov 1998;158(5 Pt 2):S1-S76. [Medline].

  12. Birken GA, Fabri PJ, Carey LC. Acute ammonia intoxication complicating multiple trauma. J Trauma. Sep 1981;21(9):820-2. [Medline].

  13. Burgess JL, Pappas GP, Robertson WO. Hazardous materials incidents: the Washington Poison Center experience and approach to exposure assessment. J Occup Environ Med. Aug 1997;39(8):760-6. [Medline].

  14. do Pico GA. Hazardous exposure and lung disease among farm workers. Clin Chest Med. Jun 1992;13(2):311-28. [Medline].

  15. do Pico GA. Toxic fume inhalation. In: Bone RC, Dantzker DR, eds. Pulmonary and Critical Care Medicine. St Louis: Mosby-Year Book; 1998:N5-1- N5-16.

  16. Respiratory tract irritants. In: Ellenhorn MJ, Schonwald S, Ordog G, eds. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore: Lippincott, Williams & Wilkins; 1996:1519-25.

  17. Flury KE, Dines DE, Rodarte JR, Rodgers R. Airway obstruction due to inhalation of ammonia. Mayo Clin Proc. Jun 1983;58(6):389-93. [Medline].

  18. Goldfrank LR. Toxicological imaging, ophthalmologic principle, occupational and environmental toxics. In: Goldfrank's Toxicologic Emergencies. 5th ed. Norwalk, Conn: Appleton & Lange; 1994:127, 368-9, 1183-1280.

  19. Haddad LM, Winchester JF, eds. Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia: WB Saunders Co; 1990.

  20. Klein JD, Olson KR. Caustic injury from household ammonia, too. J Pediatr. Feb 1986;108(2):328. [Medline].

  21. Leung CM, Foo CL. Mass ammonia inhalational burns--experience in the management of 12 patients. Ann Acad Med Singapore. Sep 1992;21(5):624-9. [Medline].

  22. O'Kane GJ. Inhalation of ammonia vapour. A report on the management of eight patients during the acute stages. Anaesthesia. 38(12):1208-13. [Medline].

  23. Perry GF Jr. Occupational medicine forum. J Occup Med. Oct 1994;36(10):1061-3. [Medline].

  24. Rakel RE, ed. Caustics and corrosives. In: Conn's Current Therapy 2000. ed. Philadelphia: WB Saunders Co; 1999:1224-5.

  25. Reisz GR, Gammon RS. Toxic pneumonitis from mixing household cleaners. Chest. Jan 1986;89(1):49-52. [Medline].

  26. Rosenstock L. Acute inhalational injury. In: Textbook of Clinical Occupational and Environmental Medicine. Philadelphia: WB Saunders Co; 1994:236-7.

  27. Shenoi R. Chemical Warfare Agents. Clin Ped Emerg Med. 2002;3:239-247.

  28. Sotiropoulos G, Kilaghbian T, Dougherty W, Henderson SO. Cold injury from pressurized liquid ammonia: a report of two cases. J Emerg Med. May-Jun 1998;16(3):409-12. [Medline].

  29. Swotinsky RB, Chase KH. Health effects of exposure to ammonia: scant information. Am J Ind Med. 1990;17(4):515-21. [Medline].

  30. Weiner AL, Bayer MC. Inhalation: gases with immediate toxicity. In: Ford: Clinical Toxicology. 2001:679.

Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.