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

Updated: Jan 02, 2018
  • Author: Daniel J Dire, MD, FACEP, FAAP, FAAEM; Chief Editor: Zygmunt F Dembek, PhD, MPH, MS, LHD  more...
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Presentation

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 gastrointestinal (GI) exposures cause systemic symptoms of nausea, vomiting, fever, malaise, and prostration. Other effects are as follows:

  • Immediate bronchospasm and respiratory distress may occur

  • Patients with severe exposures may also present with central nervous system (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

Ocular effects

The eyes are most sensitive and vulnerable to mustard. Ocular effects precede cutaneous manifestations and occur at lower concentrations (as low as one tenth) than that required to affect the airways. Nitrogen mustard (HN) causes more severe and earlier ocular lesions than sulfur mustard (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). [20] 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 [6] ; 15% of Iranian soldiers developed delayed keratitis. [4] Delayed ocular symptoms follow a latent period of 1-40 years, and reduced symptoms are reported in cold climates. [7]

After heavy exposure, eye signs and symptoms appear after 0.5-3 hours, and severe lesions may appear. Blepharospasm is common. [20]

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. [6] They exacerbate and remit in an unpredictable fashion.

Cutaneous effects

The 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. [4] 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. [6]

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. [6] 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. [4]

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.

Respiratory effects

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; [6] 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. [6]

Gastrointestinal effects

Liquid mustard ingestion leads to GI mucosal necrosis and hemorrhage. Severe 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.

Hematopoietic and lymphatic effects

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. [4] See the Absolute Neutrophil Count calculator.

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.

Neurologic effects

Neuropathic symptoms may persist years after exposure. [4] 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. These may be aggravated by sunlight exposure or shifts in ambient temperature.