a) Most patients will do well with supportive care. Monitor vital signs and mental status. Treat hypotension with intravenous fluids, add vasopressors, if hypotension persists. Arrange for early (ideally within 24 hours) endoscopy for patients with concern for caustic GI injury. Treat bronchospasm with inhaled beta agonists and corticosteroids. Endotracheal intubation and mechanical ventilation may be needed in patients with significant CNS depression or respiratory distress.

a) Up to 50% of all initial histories are incorrect; a history should be obtained from several individuals, if possible. Important information to be obtained from a product includes the type of packaging, the amount in the package, and the surface area and duration of dermal exposure. Contact the product manufacturer or your local poison center to obtain more specific information about the chemical in question.

a) Perform serial examinations to determine whether the patient is improving or deteriorating. Perform a slit lamp exam and evaluate visual acuity in any patient with an eye exposure.

a) Remove contaminated clothing, wash exposed skin thoroughly with soap and water, and irrigate exposed eyes.

a) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.

a) VENTRICULAR DYSRHYTHMIAS/SUMMARY: Institute continuous cardiac monitoring, obtain an ECG, and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders. Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.

a) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

a) Aggressively treat and evaluate coma regardless of suspected cause. Intubate and ventilate as needed. Comatose patients should receive oxygen, naloxone, thiamine (adults), and either D50 or rapid determination of blood glucose. Check core temperature to evaluate for hypo- or hyperthermia. Consider evaluation for CNS lesion or infection with CT scan and lumbar puncture.

a) Very little is known about the risks of human exposure to the chemicals coded to this document. Every effort should be made to obtain information from the manufacturer (your local poison center can often assist with this). If possible, test the pH of the chemical to evaluate for potential caustic injury.

a) HOME CRITERIA: Patients who are asymptomatic or have minimal irritant symptoms after an inadvertent small dermal exposure can probably be observed at home.
b) OBSERVATION CRITERIA: Patients with systemic symptoms, those with large surface area exposures, or patients with more than minimal dermal or eye irritation should be referred to a healthcare facility for 6 to 8 hours of observation.
c) ADMISSION CRITERIA: Patients with severe dermal or eye injury, persistent symptoms or laboratory abnormalities should be admitted.
d) CONSULT CRITERIA: Consult a medical toxicologist or poison center for any patient with symptoms or a large exposure. Contact the product manufacturer for more information about the specific chemical in question. Consult a plastic surgeon for any patient with severe dermal burns that may require debridement or grafting.

a) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

a) Health care personnel should take precautions to avoid exposure to contaminated skin or clothing of the patient. Safety and health care personnel should refrain from entering a contaminated area in order to rescue or treat an individual unless appropriate protective equipment and rescue procedures are in use.

a) Immediate pain and erythema, with concentration and pH dependent destruction of the skin or eyes is evident with acid and alkali burns. First, second or third degree chemical burns may occur (Mathias, 1988). Other chemicals may also produce burns/corrosion.
b) Some burns may not become clinically apparent for several hours or days after exposure (e.g., hydrofluoric acid, nitrogen mustard, some organotins and alkalies). Severe damage may result without prompt treatment.
c) Refer to "ACIDS" or "CORROSIVES-ALKALINE" managements for further information.

a) Cutaneous changes and inflammation may develop as a result of acute or repeated exposure to a chemical. Symptoms may include: itching, erythema, swelling, and sloughing of the skin. Examples of causative agents include: lime, paints, oils, solvents, soaps, detergents, hypochlorite solutions, and fuels.

a) Irritation results from skin exposure to a phototoxic chemical which is activated by ultraviolet light. Symptoms may include: immediate redness and swelling upon skin exposure to the sun, with vesicle or bulla formation 2 to 3 hours later. A brown discoloration may be evident for months to years after exposure (Nethercott, 1990). Creosote, tars, psoralens, and plants are common causative agents.

a) Allergic contact dermatitis is a dermal response to an allergen in sensitized individuals. A vesicular dermatitis and eczema may develop at the site of contact with the allergen. The skin effects may mimic chronic irritant (non-allergic) dermatitis. History of exposure and skin testing (patch test) may aid in diagnosis.
b) Examples of causative agents include: epoxy resins, formaldehyde, paraphenylendiamine and other dyes, lacquers, acrylic monomers, nickel, chromium, platinum, plants, glutaraldehyde, thimerosal and penicillin (Epstein, 1994; Meding et al, 1994; Carmichael & Foulds, 1993) (Nethercott, 1990).

a) Immunologically mediated (IgE) or nonimmunologically mediated (histamine, other vasoactive substances) skin reactions may occur within seconds or minutes of exposure to certain substances. Edema, erythema, hives, and/or angioedema may be noted for several hours, and resolve upon discontinuation of exposure. Examples of causative agents include: shellfish, platinum salts, antibiotics, animal urine and saliva.

a) Exposure to agents such as liquid oxygen and liquid nitrogen can cause severe frostbite. As an injury of this kind occurs and progresses, the affected area of skin becomes red and then bluish red. There is burning pain in the affected area, then pain decreases, numbness occurs, and the area becomes waxy and pale due to ischemia (Zenz, 1988).

a) Cutaneous changes may occur as a result of repeated or prolonged exposure to a chemical. Drying and cracking of the skin, and increased risk of infection may result. Exposure to some chemicals under occlusion (e.g., hat band or belt) may result in vesicle formation. Solvents and other chemicals which cause skin defatting are more commonly associated with chronic dermatitis.

a) Structurally similar halogenated aromatic hydrocarbons have been associated with the development of unique, acneiform lesions. Although the brominated compounds tend to be more toxic, the term chloracne stems from the chlorinated version (Coenraads et al, 1994). Examples of chemicals associated with chloracne include polychlorinated dibenzofurans, polychlorinated dibenzodioxins, polychloronaphthalenes, and polychlorinated biphenyls (Emmett, 1984).
b) The histologic abnormalities in chloracne include follicular infundibular dilation, comedones, and follicular horny cysts. Acute chloracne exhibits squamous metaplasia of the sebaceous glands and lamellae of keratin-like material in its ducts. Although a biopsy is helpful in acute cases, the histopathologic changes in long standing cases are not specific for chloracne (Coenraads et al, 1994).

a) Oils, greases, coal tar pitch, creosote and other substances have been associated with the development of lesions similar to those observed in acne vulgaris (Emmett, 1984).

a) Scalds, contact with liquid metal or hot machinery, and flame are sources of thermal burns. The severity of a burn is related to the depth of burn and the extent of surface area involved. Thermal burns are categorized as first, second, or third degree, depending upon the layers of the skin injured (Brandt and Fratianne, 1994).

a) Intravenous injection of kerosene, naphtha, turpentine, gasoline, or hydrocarbon insecticides has resulted in febrile reactions, and local tissue inflammation.

a) A 12-lead electrocardiogram should be performed to evaluate for dysrhythmia, tachycardia, or interval prolongation.

a) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
b) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993).
c) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).

a) PERSONNEL PROTECTION: The person performing the procedure should be protected by wearing rubber gloves, disposable shoe covers, and a rubber apron.
b) Two separate water/detergent washes should be performed. Remove the patient's clothes and place them in specially marked plastic bags.
c) Studies performed with two separate water/detergent washes showed that as long as 6 hours postexposure, the first water/detergent wash removed only 50 to 70% of an organophosphate. When a second wash was done immediately after the first, only a 6 to 9% residue remained.
d) Any soap that is available can be used for decontamination. Wash all parts of the body including the hair and under the nails. The vomitus of a person who has ingested an organophosphate or carbamate insecticide should also be removed by decontamination if it is on the person's clothes or skin (Kulig et al, 1983).

a) The use of NEUTRALIZING AGENTS for acids and alkalis is NOT WARRANTED. The use of emollients such as vaseline or creams will make decontamination more difficult.

a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
c) WOUND DRESSING:
d) DRESSING CHANGES:
e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).

a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).

a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
c) The injured extremities should be elevated and should not be allowed to bear weight.
d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).