CBRNE - Vesicants, Mustard - Hd, Hn1-3, H Clinical Presentation

  • Author: Daniel J Dire, MD, FACEP, FAAP, FAAEM; Chief Editor: Robert G Darling, MD, FACEP   more...
 
Updated: May 6, 2011
 

Physical

  • The clinical presentation of exposure to a vesicant depends on the route of administration and the agent used.
  • Moderate-to-severe liquid cutaneous, inhalational, or GI exposures cause systemic symptoms of nausea, vomiting, fever, malaise, and prostration.
    • Immediate bronchospasm and respiratory distress may occur.
    • Patients with severe exposures may also present with CNS symptoms (eg, CNS depression) and parasympathetic effects such as bradycardia and other dysrhythmias.
    • Hemoconcentration and hypovolemic shock may occur due to fluid shifts and losses or GI hemorrhaging.
  • The eyes are most sensitive and vulnerable to mustard. Ocular effects precede cutaneous manifestations and occur at lower concentrations (as low as 1/10th) than that required to affect the airways. HN causes more severe and earlier ocular lesions than HD.
    • Conjunctivitis follows an exposure time of approximately 1 hour to a concentration barely perceptible by odor that does not affect the skin or respiratory mucosa significantly.
    • After mild exposure, a latent period of 4-12 hours is followed by lacrimation, a sensation of grit in the eyes, conjunctival injection, and edema (palpebral and bulbar). Recovery requires 1-2 weeks.
    • In World War I, 75% of eye exposures were classified as mild conjunctivitis. In more modern times, conjunctivitides occurred in 85% of all Iranian casualties, with 8% sustaining long-term consequences;[3] 15% of Iranian soldiers developed delayed keratitis.[2] Delayed ocular symptoms follow a latent period of 1-40 years, and reduced symptoms are reported in cold climates.[4]
    • After heavy exposure, eye signs and symptoms appear after 0.5-3 hours, and severe lesions may appear. Blepharospasm is common.
    • A steamy haziness of the cornea or an orange-peel roughening of the cornea may occur. Spotty hemorrhagic discolorations of the iris may be observed. Temporary blindness is common, but permanent blindness is rare.
    • Mild corneal involvement demonstrates corneal erosions with fluorescein staining. Superficial corneal scarring and vascularization or iritis may occur.
    • With severe corneal involvement, dense corneal opacification with deep ulceration and vascularization occurs. Local necrosis of the cornea may rupture the globe. Panophthalmitis may occur and result in eye loss if appropriate therapy is not instituted.
    • Recovery from the ocular effects, especially with corneal involvement, may take months.
    • Delayed ocular manifestations may occur abruptly from 1-40 years after exposure.[3] They exacerbate and remit in an unpredictable fashion.
  • Severity of cutaneous effects of mustard and the rapidity with which they develop are influenced by the degree of exposure and the weather. Hot, humid weather results in more severe lesions. Warm, moist areas, such as the perineum, external genitalia, axillae, antecubital fossae, and neck, are most susceptible.
    • The latent period from contact with liquid or vapor exposures is usually 6-12 hours but may be as short as 1/2 hour when the weather is hot and humid. The effects appear more rapidly from liquid agent than from vapor.
    • The initial cutaneous effect is erythema, resembling sunburn. Slight skin edema may occur with mild exposures, but in severe burns, edema is greater. Vapor exposures may not cause skin lesions. Systemic symptoms such as malaise, vomiting, and fever may develop approximately at onset of erythema.
    • Intense cutaneous pruritus is common, may last for several days, and may persist after healing.
    • Erythema is followed by vesication as a result of liquefaction necrosis in the epidermal basal cell keratinocytes. The stratum corneum remains intact. Separation of the epidermis from the dermis occurs.[2] A liquid droplet with 10 mcg of mustard produces vesication. Vesicles are more concentrated in warm, moist areas such as the groin and axilla. Vesicles and bullae may be painful and are filled with yellow transudate that tends to coagulate. This fluid does not contain mustard and is not a risk to contacts.[3] Reabsorption of the fluids takes place in approximately 1 week if the vesicles or bullae do not rupture. If rupture occurs, the burn is considered an open wound and is susceptible to secondary infection. Spontaneous healing occurs slowly with little scar formation.
    • Exposed areas of skin may (20% of patients) develop a persistent brown pigmentation except at the site of actual vesication, where a temporary depigmentation is seen.[3] The rate of healing typically is 1-2 weeks for facial lesions and up to 2-4 weeks or longer for other areas of the skin. Secondary infection may increase the severity of the lesions and delay healing. Skin lesions are more severe in light-skinned, younger, and female patients.[2]
    • Arsenical vesicants such as phenyldichloroarsine (PD) or chlorovinyldichloroarsine (L) often are mixed with mustard agents for chemical warfare weapons. When mixed as such, the resulting skin lesions are not more severe than either agent alone but tend to confuse and make the specific diagnosis difficult.
  • A longer latent period (4-24 h) may occur before the onset of respiratory symptoms. In patients with eye symptoms, expect the development of respiratory effects. Inhalation of mustard vapors may damage the laryngeal and tracheobronchial mucosa. Single exposure to a low concentration of vapor does not cause significant injury. Extreme, repeated, or chronic exposures may lead to the development of pulmonary fibrosis, chronic bronchitis, and bronchiectasis.
    • Respiratory effects develop slowly and reach maximal severity in several days. Symptoms begin in the upper airways and progress to the lower airways. Early symptoms begin with hoarseness, sneezing, rhinorrhea, sore throat, and loss of voice. This is followed by a cough, which subsequently becomes productive. Fever, dyspnea, chest tightness, rhonchi, and wet crackles may develop. Mild symptoms last 1-2 weeks. Recovery is slow, and coughing may persist for 1 or more months.
    • Moderate acute exposure leads to mucous membrane hyperemia, edema, and necrosis. Profuse, thin, mucopurulent rhinorrhea occurs; sinusitis may develop later. Mucosal findings range from small discrete ulcerations to extensive sloughing.
    • Pharyngitis usually appears 1-3 days after inhaling mustard vapors and may occur with nasal involvement in mouth breathers. The palate, uvula, tonsils, and pharynx are hyperemic and edematous. Multiple whitish ulcerations appear, varying in size according to severity of exposure. Laryngeal involvement resembles that of the pharynx. Edema and necrosis may lead to airway obstruction. Hoarseness, which almost always is present, may last 3-6 weeks or longer.
    • Severe inhalation exposures lead to a diphtherialike pseudomembrane, which may form a cast of the tracheobronchial tree. Mechanical obstruction from pseudomembrane formation and laryngospasm may cause death in the first 24 hours. Mild patchy pulmonary edema and focal atelectasis occur. Chemical pneumonitis may appear after the first 24 hours. Hemorrhagic pulmonary edema is not common and occurs only with severe damage. Symptoms resemble acute respiratory distress syndrome. Suppurative bacterial bronchitis and bronchopneumonia are frequent complications (particularly with Pseudomonas) 36-48 hours after exposure;[3] the latter is responsible for almost all deaths from vapor exposure.
    • In World War I, early mortality occurred in slightly more than 2% of US troops exposed to mustard and was caused almost entirely by pulmonary complications. Approximately 10% of the Iranian casualties treated in western European hospitals during the Iran-Iraq War developed progressive stenosis of the tracheobronchial tree.
    • Respiratory symptoms can occur 15 years after exposure in a previously asymptomatic individual.[3]
  • Liquid mustard ingestion leads to gastrointestinal mucosal necrosis and hemorrhage. Severe gastrointestinal (GI) effects from mustard poisoning are relatively infrequent.
    • Initial symptoms include nausea, vomiting, painful diarrhea, and prostration.
    • Vomiting and bloody diarrhea beginning days after a high-dose exposure imply a poor prognosis.
  • With systemic absorption of near lethal doses, hematopoietic and lymphatic tissue injuries occur, resulting in myelosuppression (leukopenia, thrombocytopenia, and anemia).
    • Bone marrow suppression may be evident by 4 hours postexposure.
    • High mortality rates were seen in Iran-Iraq war veterans who had an absolute neutrophil count < 200 cells/mm3.[2]
    • The thymus, spleen, and lymph nodes may involute rapidly. The development of shock, thrombocytopenia, leukopenia, and hemorrhagic diathesis are grave prognostic signs. Bone marrow failure resulting in fulminant sepsis and bleeding is the most frequent cause of late deaths from mustard exposure.
  • Neuropathic symptoms may persist years after exposure.[2]
    • Chronic pain at the sites of cutaneous injury may be due to the destruction of nerve fibers and receptor.
    • Symptoms include allodynia, paresthesias, stinging, burning, and itching, which may be aggravated by sunlight exposure or shifts in ambient temperature.
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Contributor Information and Disclosures
Author

Daniel J Dire, MD, FACEP, FAAP, FAAEM  Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Specialty Editor Board

Fred Henretig, MD  Director, Section of Clinical Toxicology, Professor, Medical Director, Delaware Valley Regional Poison Control Center, Departments of Emergency Medicine and Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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

Robert G Darling, MD, FACEP  Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

References

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  3. Wattana M, Bey T. Mustard gas or sulfur mustard: an old chemical agent as a new terrorist threat. Prehosp Disaster Med. Jan-Feb 2009;24(1):19-29; discussion 30-1. [Medline].

  4. Lagali N, Fagerholm P. Delayed mustard gas keratitis: clinical course and in vivo confocal microscopy findings. Cornea. May 2009;28(4):458-62. [Medline].

  5. Eisenkraft A, Krivoy A, Vidan A, Robenshtok E, Hourvitz A, Dushnitsky T. Phase I study of a topical skin protectant against chemical warfare agents. Mil Med. Jan 2009;174(1):47-52. [Medline].

  6. Doi M, Hattori N, Yokoyama A, Onari Y, Kanehara M, Masuda K, et al. Effect of mustard gas exposure on incidence of lung cancer: a longitudinal study. Am J Epidemiol. Mar 15 2011;173(6):659-66. [Medline].

  7. Headquarters, Department of the Army. Field Manual 8-285, Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries. Washington, DC: Dec 22 1995.

  8. Iyriboz Y. A recent exposure to mustard gas in the United States: clinical findings of a cohort (n = 247) 6 years after exposure. MedGenMed. 2004;6(4):4. [Medline]. [Full Text].

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  10. Morad Y, Banin E, Averbukh E, Berenshtein E, Obolensky A, Chevion M. Treatment of ocular tissues exposed to nitrogen mustard: beneficial effect of zinc desferrioxamine combined with steroids. Invest Ophthalmol Vis Sci. May 2005;46(5):1640-6. [Medline].

  11. Pons P, Dart RC. Chemical incidents in the emergency department: if and when. Ann Emerg Med. Aug 1999;34(2):223-5. [Medline].

  12. Richter MN, Wachtlin J, Bechrakis NE, Hoffmann F. Keratoplasty after mustard gas injury: clinical outcome and histology. Cornea. May 2006;25(4):467-9. [Medline].

  13. Saladi RN, Smith E, Persaud AN. Mustard: a potential agent of chemical warfare and terrorism. Clin Exp Dermatol. Jan 2006;31(1):1-5. [Medline].

  14. Smith KJ, Hurst CG, Moeller RB, et al. Sulfur mustard: its continuing threat as a chemical warfare agent, the cutaneous lesions induced, progress in understanding its mechanism of action, its long-term health effects, and new developments for protection and therapy. J Am Acad Dermatol. May 1995;32(5 Pt 1):765-76. [Medline].

  15. US Army Medical Research Institute of Chemical Defense. Medical Management of Chemical Casualties Handbook. 3rd ed. Aug 1999.

 
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