CBRNE - Mustard Agents - Hd, Hn1-3, H

Sulfur mustard was first produced in 1822 but was not deployed on the battlefield until the First World War (WWI). During the Battle of Ypres, Belgium in July 1917, Germany was the first nation to deploy sulfur mustard-containing artillery shells on the battlefield against British and Canadian troops. The Allied Powers in WWI referred to this agent as HS (Hun Stoffe), later shortened to H. Pure distilled sulfur mustard was given the name HD (Distilled Hun). Other names included yellow cross (how it was identified on artillery shells), Yperite (after the location of first use), S-LOST (from Lommel and Steinkopf, German chemists who developed mass production of mustard), or Kampfstaff LOST (Kampfstaff = warfare agent).

Mustard holds the title “King of the War Gases” due to the large number of casualties that it inflicted. This name is somewhat of a misnomer as mustard is an aerosol, not a gas. It is primarily used as an area-denial tool and to incapacitate troops.[3, 4]

Use of mustard agents continued after WWI. During the 1930s, Italy dropped mustard-containing bombs and sprayed mustard from aircraft during its invasion of Ethiopia and Japan employed mustard during its invasion of China. During WWII, both Allied and Axis powers produced significant amounts of mustard, including nitrogen mustard (Hn), but it was never used on the battlefield.[3]  A significant mustard release  occurred in 1943 when German bombers struck an American munitions vessel carrying mustard in the Italian port of Bari, resulting in 617 casualties and 83 fatalities from mustard released into the air and water.[5]

Since WWII, the Middle East has been the primary location for use of mustard agents. Egypt used mustard against royalist forces during the Yemen Civil War (1963-1967).[3]  During the Iran-Iraq War (1980-1988), Iraq deployed mustard against Iranian troops and civilian targets, generating a large number of casualties.[6]  More recently, in 2015 and 2016, mustard agents have been used by both Syria and nonstate actors (ISIS) as part of the ongoing Syrian civil war.[7, 8, 9, 10]

In April 1997, the US ratified the Chemical Weapons Convention (CWC). Part of this treaty involves the destruction of US stockpiles of chemical and nerve agents, including mustard. Exposures to mustard still occur, largely due to accidental contact with discarded munitions or during disarming operations.[11, 12, 13]  Destruction of the US mustard stockpile is ongoing.[14]

Despite being referred to as gas, mustard agents are liquids at room temperature. Pure mustard is clear and odorless, while mustard with impurities is generally a yellow/brown oily liquid. The impurities give these agents the odor of mustard, garlic, or horseradish.[15]  

Persistence in the environment and level of vaporization depend on temperature. In more temperate climates, mustard agents vaporize slowly and may persist for a week. In desert climates, they vaporize rapidly and may persist for a day or more, depending on the extent of exposure. Rapid vaporization makes mustard more deadly in warmer climates.[16]  Mustard has a high freezing point (57°F) and must be mixed with other substances to lower its freezing point for use in winter environments.[4]  Sulfur mustard is 5.4 times heavier than air, leading to accumulation in low-lying area, which made it suitable for attacking trenches.[4, 16]

Mustard agents cause damage through multiple proposed mechanisms. Mustard agents are lipophilic and get absorbed rapidly through the skin. Once absorbed, they act primarily as alkylating agents that form highly reactive sulfonium (sulfur mustard) or imonium (nitrogen mustard) ions within minutes of absorption. These ions react with sulfhydryl and amino groups in proteins and DNA. Sulfur mustard alkylates purine bases (guanine and adenine) in DNA. This triggers the activation of cellular repair machinery, rapidly depleting cellular stores of nicotinamide adenine dinucleotide (NAD+). Depletion of NAD+ stores begins around 1 hour after exposure and peaks at 4 hours, leading to indirect inhibition of glycolysis and cellular necrosis.[16, 15, 17]  More recent studies indicate that sulfur mustard may also inhibit glycolysis directly.[18]  

Another proposed mechanism of mustard agents is a reaction with glutathione, causing its depletion and increasing cellular susceptibility to oxygen–free radical damage. Depletion of glutathione leads to the inactivation of sulfhydryl-containing enzymes, leading to the inability to control calcium homeostasis. Increases in intracellular calcium trigger the activation of cell death machinery, resulting in apoptosis. Depletion of glutathione also leads to lipid peroxidation, with formation of free radicals that damage cell membranes.[4]

The lethal dose of sulfur mustard in humans varies by route of exposure. The median lethal concentration for inhalation (LCt50) is 1500 mg-min/m3. The medial lethal dose (LD50) is 50mg/kg for cutaneous exposure and 0.7mg/kg for oral exposure.[19] The LD50 for cutaneous nitrogen mustard exposure in humans is 75 mg/kg.[19]

Battlefield concentrations in WWI were estimated to be between 19-33 mg/m3. Exposures at these concentrations for several minutes led to eye and skin injury. Exposures of 30-60 minutes resulted in severe respiratory injury and death.[16]  The majority of chemical casualties in WWI were caused by mustard (76-88%), with a mortality rate of 2-3%.[4]  Mortality rates in the Iran-Iraq War were 3-4%.[16]

After exposure to mustard agents, the onset of signs and symptoms follows a latent period. If decontamination does not occur immediately (1-2 min), mustard absorption in unprotected victims commences. The eyes, skin, and respiratory system are the three immediate targets of mustard agents, with the eyes being the most sensitive and the earliest to display symptoms. Gastrointestinal (GI) effects are also seen. Bone marrow suppression occurs later, increasing the risk of infection. Deaths occur from respiratory compromise and infection brought on by immunosuppression.

Ocular Effects

The eyes are the organ most sensitive to mustard exposure. The exposure threshold for signs and symptoms to occur is roughly 10 times lower for the eyes than for other organs, and the latency period is the shortest.[20]  The rapid metabolic rate of corneal cells, the presence of a thin mucosal layer, and tears covering the eye make it markedly susceptible to the effects of mustard.[21, 22]  The majority of victims exposed to mustard (75-90%) will develop ocular signs and symptoms.[20]  Most soldiers exposed to sulfur mustard in WWI initially had conjunctivitis, photophobia, and blepharospasm.[20]

The onset and severity of ocular effects are a function of exposure dose and duration. Damage can occur via exposure to mustard vapor or liquid. Eye irritation has been reported within minutes of exposure, but typically develops after 1 hour.[8, 22, 23]  At lower concentrations, conjunctivitis, a foreign body sensation (grittiness), and reddening develop, with progression towards more severe conjunctivitis, lacrimation, blepharospasm, blurred vision, periorbital edema, and corneal injury leading to decreased visual acuity.[22]  

Liquid mustard exposure to the eye by contact with droplets or by self-contamination causes the most severe damage, which can lead to severe corneal damage and loss of vision.[4]  Corneal ulcers develop within 48 hours and the cornea may take on an orange-peel appearance.[22]  Miosis, anterior uveitis, elevated intraocular pressure, and hemorrhages can also be seen.[22]  Severe corneal erosions can lead to Pseudomonas infection.[24]  Development of panophthalmitis can lead to loss of the eye.[4]

Time to recovery depends on the severity of the injury. Victims may be visually disabled for 10 days following exposure.[25] Recovery from mild injuries occurs within 1-2 weeks, and recovery from moderate injuries takes 6-12 weeks. Severe injuries can take months to heal, or may be permanent.[20, 22]

Cutaneous Effects

The concentration of mustard required to produce skin lesions depends on multiple factors. Hot, humid weather results in more severe lesions. Warm, moist areas of the body such as the axillae, antecubital fossa, neck, external genitalia, and perineum are the most susceptible to damage. Mustard liquid penetrates the skin faster than vapor, but both are absorbed rapidly. There is a latent period between exposure and the development of skin lesions.[4]

The earliest sign on physical examination is the development of erythema. This can occur anywhere from 1-24 hours following exposure, with the average being between 4-8 hours. Erythema is accompanied by pruritus or burning pain. Vesicles begin to develop 2-18 hours later and may continue to form for several days.[4]

This development of blisters/bullae is what gives mustard its namesake as a blistering/vesicating agent. The bullae that form are dome-shaped, thin-walled, superficial, translucent, and filled with a clear or straw-colored liquid that coagulates over time. These tend to form in warm, moist areas of the body. This liquid inside the blisters does not contain liquid mustard. The liquid contains thiodiglycol, a mustard metabolite, which can aid in diagnosis. Vapor exposure generally causes injury similar to first-degree (superficial) or second-degree (partial thickness) burns, while liquid penetrates deeper and causes findings similar to third-degree (full thickness) burns.[4]

Blister healing depends on the severity of the lesion. Erythema resolves within a few days, while more severe injuries may take weeks or months to resolve. Both hyperpigmentation and hypopigmentation of skin can follow. Transient hyperpigmentation followed by exfoliation was seen in both WWI and Iran-Iraq war mustard victims. Hypopigmentation can occur if melanocytes are destroyed. This can last months or become permanent.[4]

Respiratory Effects

Exposure to mustard vapor causes irritation and damage to the respiratory tract mucosa. Upper airway structures are affected first, with lower airway structures becoming involved as the concentration of mustard vapor increases. Inflammation can range from mild to severe, with injury becoming more apparent over several days.[4]

Signs and symptoms of irritation develop 4 to 6 hours after exposure. Mild exposure can lead to a dry hacking cough; chest tightness; dyspnea; wheezing; and hoarseness, which may progress to loss of voice. These manifestations will usually be seen if the patient has ocular effects from exposure.[4]

Higher-dose exposures result in earlier development of respiratory symptoms and deeper penetration into lower airways. Epithelial sloughing and pseudomembrane formation can cause upper and lower airway obstruction.[4, 26]  Bronchitis progressing to bronchopneumonia over the course of a few days contributes to mortality.[4, 5, 21, 27]  In WWI, bronchopneumonia was a leading cause of death for mustard causalities.[28]  Mustard vapor generally does not affect the lung parenchyma and pulmonary edema is not common.[4]

Gastrointestinal Effects

Nausea and vomiting commonly occur within a few hours after mustard exposure. These tend to develop around the time that skin lesions appear and are thought to be due to cholinergic effects of mustard, due its unpleasant odor, or a result of a stress reaction. Initial nausea and vomiting are usually transient and resolve in 24 hours.[28]  Nausea and vomiting occurring later (24-36 hrs post-exposure) can be a result of systemic cytotoxicity of mustard, with damage to the GI mucosa. Diarrhea and GI hemorrhage is not common.[4]  If present, GI bleeding has a poor prognosis.[4, 29]

Hematopoietic Effects

Suppression of bone marrow from systemic absorption of mustard leads to increased susceptibility to infection and subsequent mortality. In an animal model, changes to the bone marrow can be seen as early as 4 hours post exposure, with extensive damage within 24 hours.[30]  Initially masked by a reactive leukocytosis following chemical injury, leukopenia becomes evident by days 3-5 and reaches its nadir in 7-9 days.[26, 28]  Leukopenia < 200 cells/mm3 or a rapid decline in leukocytes in one day indicates a poor prognosis.[4, 26, 28]  Thrombocytopenia and anemia lag behind leukopenia.[4, 10]

Neurologic Effects

Central nervous system (CNS) effects are not a prominent feature of mustard exposure. Most CNS complaints were nonspecific in mustard-contaminated victims of the Iran-Iraq War.[4]  Chronic neuropathic pain may develop years later in areas of skin exposure to mustard.[31] Allodynia, stinging, burning, itching, and numbness can be aggravated by changes in temperature or exposure to sunlight.[31]

No clinically available laboratory test exists to identify or quantify mustard exposure. Mustard is biotransformed in tissues within minutes of exposure. Detection of mustard metabolites (thiodiglycol (TDG), thiodigylocol sulfoxide (TDG-sulfoxide), 1-methylsulfinyl-2-[2-(methylthio)ethylsulfonyl]ethane (MSMTESE), 1,1’-sulfonylbis[2-(methylsulfinyl)ethane (SBMSE), and 1,1’-sufonylbis[2-S-(N-acteylcyteinyl)ethane]) requires more advanced detection methods.[32]

Results of blood studies include the following:

• Complete blood count – Reactive leukocytosis occurs initially after chemical injury with leukopenia developing by day 3-5. Leukopenia < 200 cells/mm ³ is a poor prognostic sign. Thrombocytopenia and anemia follow due to bone marrow suppression.
• Metabolic panel – Electrolyte derangements can occur from nausea/vomiting. Acute kidney injury may occur from dehydration.

The US military, as well as state and local emergency responders, have the capability to detect mustard agents on the battlefield or at the sites of suspected mustard agent release in the civilian environment. This capacity is effectively accomplished through the use of specialized equipment such as chemical detection papers, chemical detection alarms, gas detection tubes, photometric detection, ion mobility spectroscopy, Raman spectroscopy, and portable gas chromatography–mass spectroscopy. Some specific examples include the following[33, 34, 35, 36] :

• M8 and M9 chemical detection paper
• Joint Chemical Agent Detector (JCAD)
• Improved chemical Agent Monitor (ICAM)
• M256A1 chemical agent detector kit
• M272 chemical agent water testing kit
• M22 automatic chemical agent detector and alarm
• M21 remote sensing alarm
• M90 chemical agent detector
• Joint Services Lightweight Standoff Chemical Agent Detector (JSLSCAD)
• M93A1 Fox Nuclear Biological and Chemical Reconnaissance System

Inhalation of mustard vapor causes chemical pneumonitis, which may progress to pneumonia. Serial chest x-rays are recommended to track progression. Chest computed tomography (CT) is more sensitive than chest x-rays in detecting chronic changes caused by mustard exposure.[37]

Initial care of patients contaminated with mustard agents should focus on removing the patient from the environment and initiating rapid decontamination procedures. Decontamination performed in the first 1-2 minutes following exposure is the most effective means of preventing injury as well as assisting to mitigate cross-contamination with others.[4] Decontamination helps to prevent further absorption and protect others involved in patient care from exposure.

Decontamination should be undertaken in the field, before transport to a medical facility. Providers attending contaminated patients should have protective masks, butyl rubber gloves (latex gloves are not adequate), and chemical protective overgarments. The Occupational Safety and Health Administration's (OSHA's) Hazardous Waste Operations and Emergency Response (HAZWOPER) standard (29 CFR 1910.120[q]) provides additional information for responding to hazardous substance releases, including blister agents.

The level of personal protective equipment (PPE) needed depends on the sites where first responders are operating.[38]

Level A PPE (maximal protection) is needed for scenes in which the identity of the chemical weapon is unknown or levels of the agent are above Immediately Dangerous to Life and Health (IDLH) limits. It comprises the following:

• Self-contained breathing apparatus (SCBA)
• Fully encapsulated chemically resistant suit
• Chemically resistant inner and outer gloves
• Chemically resistant boots

Level B PPE (highest level of respiratory protection, less skin protection) is indicated for decontamination zones above IDLH levels. It comprises the following:

• SCBA
• Chemically resistant suit
• Chemically resistant inner and outer gloves
• Chemically resistant boots
• SCBA

Level C PPE is indicated for decontamination zones with levels under IDLH. It comprises the following:

• Air purifier respirator (APR) or powered air purified respirator (PAPR)
• Chemically resistant suit
• Chemical-resistant inner and outer gloves
• Chemical resistant boots

Level D PPE is indicated for zones where the concentration of the contaminant is below the exposure limit (minimal protection). It consists of work clothing with minimal protection.

Unless carried out within 1-2 minutes, decontamination of victims exposed to mustard agents does not prevent subsequent blistering. After that brief window, decontamination still should be carried out, in order to prevent secondary contamination of first responders and medical personnel at treating facilities. The decontamination procedure is as follows:

• Remove all clothing, to decrease penetration into the skin; clothing acts as an occlusive dressing that increases absorption. Removed clothing should be bagged and left at the scene.
• Eyes should be flushed immediately with water or saline solution.
• Exposed skin and scalp can be decontaminated using Reactive Skin Decontamination Lotion (RSDL), which is a packaged sponge that helps wipe away chemical agents. This has replaced the military’s M291 skin decontamination kit and is now the preferred agent. If RSDL is unavailable, 0.5% aqueous hypochlorite solution can be used. ^[38]
• Following this, victims should be washed with soap and water.
• Transport decontaminated patients to a medical facility for further treatment.

There is no specific antidote or treatment regimen to reverse the effects of mustard agents. Care for exposed persons is supportive.

Treatment of Eye Exposure

Following irrigation, examine the eyes for corneal injury with fluorescein. Topical anesthetic can be applied for the initial exam but should not be used for continued pain relief. Use of topical anesthetics increases the risk of inadvertent corneal scarring, which can worsen infection. Instead, systemic narcotics should be used for pain control.[4]

Topical antibiotic ointment should be applied 3-4 times a day to reduce the risk of infection. Do not patch the eyes and do not allow the eyelids to stick together, as that can increase the risk of infection. Apply sterile petroleum jelly to lubricate and prevent sealing of the eyelids. In patients with mild injury (conjunctivitis), lubricating drops may provide pain relief. The efficacy of topical steroids has not been established, but these agents may be beneficial within the first 48 hours after injury.[4]

In patients with severe blepharospasm and photophobia, use cycloplegic eye drops (atropine or homatropine) three times a day for pain and to prevent adhesion formation. A darkened room or sunglasses may be helpful. All severe injuries require admission with emergent ophthalmologic evaluation.[4]

Treatment of Skin Exposure

Once all clothing has been removed and the patient has been decontaminated, evaluate the extent of erythema and blistering. Mild erythema does not require any specific treatment. Treat pruritis with calamine lotion, topical steroid creams, or silver sulfadiazine.[39]  Mild erythema does not require treatment.

There is no consensus on the treatment of blisters or bullae. If blisters or bullae have ruptured, debride the remaining material, clean the skin with sterile water or saline, and cover it with a sterile dressing.[39]  Chlorhexidine, povidone-iodine, and silver sulfadiazine can be utilized as disinfectants.[34]  Once the site is cleansed, apply topical antibiotic ointment to prevent infection. If infection occurs, treat with intravenous antibiotics. Control pain with narcotic analgesics. Ensure tetanus immunization is up to date.

Mustard injury to the skin is considered a chemical burn, which meets the criteria for referral to a burn center.[40]  Patients with more than mild erythema should be transferred for specialized care. Significant lesions may require skin grafting. Mustard injury is different from chemical burns and involves less fluid loss. Formulas for calculating fluid loss in thermal burns may overestimate fluid loss in mustard injury.[4]

Treatment of Respiratory Exposure

Mild respiratory symptoms (throat irritation, nonproductive cough, hoarseness) can be treated supportively. Nebulized saline or cough suppressants may be useful.[36]  Hypoxia should be treated with supplemental oxygen.

Patients in severe respiratory distress or with signs of airway compromise should be intubated early. The development of airway edema may make later attempts at intubation more difficult. Severe mustard injury can cause chemical pneumonitis similar to acute respiratory distress syndrome (ARDS), with bilateral infiltrates on chest imaging. A lung protective strategy for mechanical ventilation should be employed. Frequent suctioning of debris and secretions may be required. Bronchoscopy allows for direct visualization of airways and can assist with the clearance of debris.[4, 36]

Bronchodilators can help reduce bronchospasm. Albuterol/ipratropium bromide (Combivent Respimat, DuoNeb) should be administered. Greater efficacy has been seen using a combination of beta-2 agonists plus an anticholinergic agent in mustard exposures than using one agent alone.[37] Corticoteroids can be considered if the patient shows no response to bronchodilators.[4]

Pneumonia is a late complication of mustard exposure. It typically does not develop in the first few days. If pneumonia develops, begin antibiotic treatment.  

Treatment of Systemic Toxicity

Nausea/vomiting should be treated with antiemetics. If cholinergic symptoms are found, atropine should be used. Intravenous fluids should be given for dehydration and electrolytes repleted as necessary.  

Leukopenia increases susceptibility to infection and subsequent sepsis. If neutropenic fever develops, empiric antibiotic therapy should be initiated. Granulocyte colony-stimulating factor (G-CSF) has shown efficacy and should be considered if neutropenia develops.[41]

Thrombocytopenia and anemia lag behind leukopenia. If traumatic injuries are present, transfusion of platelets or red blood cells may be required.

Consultations include the following:

• Medical toxicology or local Poison Control Center for assistance in the management of chemical weapons exposures
• Medical intensive care unit for critically ill or intubated patients
• Ophthalmology for treatment of eye exposures
• Plastic surgery/burn specialists for care of cutaneous injury
• Dermatology for management of cutaneous injury  
• Hematology/oncology for assistance in managing pancytopenia

Chronic respiratory complications are the most common cause of long-term disability following mustard exposure. In a cohort of Iranian mustard victims, 42.5% developed chronic lung lesions and respiratory signs and symptoms.[42]  The most common respiratory effects are dyspnea, chronic cough, and sputum production.[37, 43]  Bronchiolitis, asthma, tracheobronchiomalacia, and airway stenosis (in severely-exposed patients) are the most common long-term conditions associated with exposure.[37]  Pulmonary function test results evolve from an obstructive pattern to a restrictive pattern over time.[43]

Chronic ocular complaints are the next most common complication. In a cohort of Iranian mustard victims, 39.3% developed chronic ocular issues.[44]  Chronic inflammation of the eyes may occur or delayed keratitis may develop.[22, 45]  Itching, burning, and photophobia are the three most common complaints, with conjunctivitis, peri-limbal hyperpigmentation, and vascular tortuosity being the three most common exam findings.[46]  Delayed keratitis involves an asymptomatic period after mustard exposure with abrupt recurrence of keratitis, corneal opacification, corneal ulceration, neovascularization, pain, decreased visual acuity, and vision loss.[22]  This delay can span from 1 to 40 years following exposure, with most cases occurring between 15 and 20 years post-exposure.[22, 24, 46, 47]  Delayed keratitis can happen unpredictably, with periods of exacerbation and remission.[24]  

Chronic dermal findings are also prevalent, affecting 24.5% of Iranian mustard victims.[44]  The most common complaints are itching and burning, with hyperpigmentation, erythematous papular rash, and dry skin being the most common physical exam findings.[46, 48] Hypopigmentation can also occur but is less common. Chronic skin findings are usually noted in the groin, back, thorax, abdomen, and axillary areas.[46]

The International Agency for Research on Cancer (IARC) has determined that there is sufficient evidence to classify sulfur mustard as a known human carcinogen (IARC Group 1) due to its alkylating effects on DNA. The strongest evidence exists for lung and laryngeal cancers, especially among occupational workers.[49]  Increased rates of cancers have been noted in acutely exposed Iranian war veterans, however, no specific type of cancer has been found to be statistically significant when compared with the general population.[42, 50]

Dermostyx (IB1) is a topical skin protectant (TSP) developed by the Israeli Defense Forces (IDF) to provide passive protection against percutaneous exposure to chemical agents, including sulfur mustard. When applied to the skin prior to exposure, this lotion forms a protective barrier that reduces the size and severity of skin lesions caused by vesicants, has an efficacy of 12 hours, has minimal side effects, and does not interfere with decontamination procedures.[51, 52]

The goals of pharmacotherapy are to neutralize toxicity, reduce morbidity, and prevent complications.

Class Summary

Instillation of long-acting cycloplegic agents can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

Homatropine (AK-Homatropine, Isopto-Homatropine)

Contains homatropine hydrobromide, which blocks action of certain parasympathetic nerves and cholinergic drugs; used in ophthalmology for mydriatic and cycloplegic effects; peripheral effects are much weaker than those of atropine; preferred to atropine for diagnostic purposes because its action is more rapid, less prolonged, and is controlled readily by physostigmine; effect is exerted in 15-30 min and passes off in 12-24 h; usually does not produce complete paralysis of accommodation in children.

Atropine ophthalmic (Isopto, Atropair, Atropisol)

For use as long-acting mydriatic and cycloplegic; most potent ophthalmic parasympatholytic available; by paralyzing sphincter pupillae muscle, helps dilate pupil; also paralyzes ciliary muscle; effect lasts 7-10 d; also indicated to decrease GI motility.

Class Summary

Thought to work centrally by suppressing conduction in vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.

Atropine IV/IM (Atropair, Isopto, Atropisol)

Acts at parasympathetic sites in smooth muscle and decreases GI motility.

Dosage may require reduction in elderly patients due to possible occurrence of cardiovascular and CNS adverse effects.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained burns.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia because of its 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 commonly is titrated until desired effect is obtained.

Meperidine (Demerol)

Narcotic analgesic with multiple actions similar to those of morphine; may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.

Hydrocodone bitartrate and acetaminophen (Vicodin ES)

Drug combination indicated for relief of moderate to severe pain.

Class Summary

Primary action is to decrease muscle tone in both small and large airways in the lungs, thus increasing airflow and ventilation. This category includes beta-adrenergic, methylxanthine, and anticholinergic medications.

Albuterol (Proventil, Ventolin)

Bronchodilator in reversible airway obstruction due to asthma; relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on heart rate.

Albuterol/ipratropium (Combivent Respimat)

Combination of albuterol, a beta2-adrenergic bronchodilator, and ipratropium, an anticholinergic (parasympatholytic) agent

Class Summary

Topical and ophthalmic antibiotics routinely are used for dermal and ocular burns, respectively. Injured tissues lose many of their protective mechanisms and are at increased risk of infection.

Class Summary

Used to induce active immunity against tetanus in selected patients.

Tetanus toxoid adsorbed or fluid

Immunizing agents of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.

Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product.

In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is mid thigh laterally.

Class Summary

Indicated for control of excessive cough.

Codeine/guaifenesin (Robitussin AC, Guiatuss AC, Mytussin AC, Brontex liq)

Treats minor cough resulting from bronchial and throat irritation.

Class Summary

Indicated for inflammation of skin.

Hydrocortisone 1% (Cortaid, Dermacort, Westcort)

Adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.