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PLANTS-DERMATITIS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management deals with a general approach to plant dermatitis and dermatologic response due to various plant exposures. Allergic skin reactions to plants and their products account for 4% to 10% of all visits to dermatology clinics. For more specific information regarding some of the plants discussed in this management, please refer to the following: PLANTS-PSORALENS or PLANTS-TOXICODENDROL.
    B) The mechanism involved can include: mechanical irritation, primary chemical irritants, contact allergens, and photosensitizing agents.
    C) Some plants may produce systemic, as well as dermatologic responses. Please refer to the specific plant data, or another management.

Specific Substances

    A) MECHANICAL IRRITATION
    1) Dieffenbachia sp (dumbcane)
    2) Philodendron sp
    3) Brassia sp
    4) Urtica sp (stinging nettles)
    PRIMARY CHEMICAL IRRITATION
    1) Urtica sp (stinging nettles)
    2) Hippomane mancinella (manchineel, manzanillo)
    3) Agave sp
    4) Clemattis sp
    ALLERGENS
    1) Toxicodendron sp (poison ivy, poison oak, poison sumac)
    2) Mangifera indica (mango)
    3) Anacardium occidentale (cashew)
    4) Cotinius coggygria (smoke tree)
    PHOTOTOXINS
    1) Ficus carica (fig)
    2) Agrimonia eupatoria (agrimony)
    3) Pastinaca sativa (parsnip)
    ALLERGENIC PLANT PRODUCTS
    1) Bergamot oil
    2) Balsam of peru
    3) Cassia oil
    4) Citrus oil
    5) Colophony
    6) Costus oil
    7) Laurel oil
    8) Oak moss oil
    9) Dermatitis, plants
    CHEMICAL ALLERGENS (found in plants)
    1) Cinnamic aldehyde
    2) Coniferyl benzoate
    3) Citral
    4) Delta-3-carene
    5) Abietic acid
    6) Costunolide
    7) Atranorin
    BLACK-EYED SUSANS
    1) Rudbeckia spp.
    PRAIRIE CONEFLOWER
    1) Ratibida columnifera
    YELLOW CONEFLOWER
    1) Ratibidia pinnata

Available Forms Sources

    A) SOURCES
    1) The Toxicodendron plants are the most commonly known as poison ivy, poison oak and poison sumac.
    2) Nettles (Urtica species) and various Euphorbia species (crown of thorns, poinsettia) are capable of producing dermatitis.
    3) Allergic skin reactions to plants and their products account for 4% to 10% of all visits to dermatology clinics (Epstein, 1987).
    4) Particularly sensitive individuals may develop dermatitis following exposure to lumber and various oils in citrus fruits (Senear, 1933; Mitchel & Rook, 1979) and to tree pollen (Millikan, 1980).
    5) PHYTOPHOTODERMATITIS: Requires exposure to ultraviolet light A in wave lengths 320 to 380 NM. A partial list of causative plants includes (Mandalia et al, 2008; Hipkin, 1991):
    1) Achillea millefolium
    2) Anthemis cotula
    3) Dictamnus albus
    4) Ficus carica L. (fig tree sap)
    5) Heracleum mantegazzianum
    6) Heracleum sphondylium
    7) Pastinaca satina
    8) Psoralea bituminosa
    9) Ruta chalepensis
    10) Ruta graveolens
    11) Skimmia species
    6) Exposures may result from plant products or a derivative, or plant materials may be transferred to chairs, clothing, or pets. Dermatitis may occur secondary to mites or insects that infect the plant. Even some dried plants may cause a reaction (Burrall, 1989).
    7) Plants may contain several potential sensitizers (Burrall, 1989):
    1) ALLERGENIC PLANT PRODUCTS
    a) Balsam of peru
    b) Bergamot oil
    c) Cassia oil
    d) Citrus oil
    e) Colophony
    f) Costus oil
    g) Laurel oil
    h) Oak moss oil
    2) CHEMICAL ALLERGENS (FOUND IN PLANTS)
    a) Abietic acid
    b) Atranorin
    c) Cinnamic aldehyde
    d) Citral
    e) Coniferyl benzoate
    f) Costunolide
    g) Delta-3-carene

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) SOURCES: Toxicodendron plants frequently produce dermatitis, and are commonly known as poison ivy, poison oak and poison sumac. Nettles (Urtica species) and various Euphorbia species (crown of thorns, poinsettia) are capable of producing dermatitis. Allergic skin reactions to plants and their products account for 4% to 10% of all visits to dermatology clinics. This management deals with a general approach to plant dermatitis and dermatologic response due to various plant exposures. For more specific information regarding some of the plants discussed in this management, please refer to the following: PLANTS-PSORALENS or PLANTS-TOXICODENDROL.
    B) TOXICOLOGY: Plant-induced dermatitis can be divided into four major categories based on mechanism of toxicity. Many exposures involve combinations of more than one mechanism. The majority of these cases are self-limiting and disappear within 14 to 21 days.
    1) ALLERGIC REACTION: This is a true sensitization (type IV hypersensitivity reaction) of an individual to the particular allergen contained in the plant. After the first exposure, the patient usually has a 5 to 7 day latency period before the immunological sensitization develops. Subsequent exposure results in allergic contact dermatitis.
    2) CHEMICAL IRRITATION: This is not an allergic response, but rather the direct effect of a particular chemical contained in the plant.
    3) MECHANICAL TRAUMA: It may occur following exposure to the sharpened thorns, barbs, and so forth of various plants.
    4) PHOTODERMATITIS: It occurs following exposure to some plants and their various oils that react in such a way to make the skin sensitive to sunlight.
    C) EPIDEMIOLOGY: Exposure is common, but severe symptoms are rare.
    D) WITH POISONING/EXPOSURE
    1) ALLERGIC REACTION: Allergic contact dermatitis usually presents with pruritus and vesiculation of varying degrees. The affected area may be erythematous, edematous, and develop large bullae; weeping and crusting may be present. Upon healing, these lesions may become thickened, fissured and sometimes pigmented.
    2) CHEMICAL IRRITATION: Symptoms are usually seen within 24 hours of exposure and usually consist of erythema, pruritus, and burning. Vesicle formation occurs in moderate to severe exposures, and frequently appears in linear streaks as a result of brushing the skin against the plant.
    3) MECHANICAL TRAUMA: Infection or chronic changes may occur in the skin if a portion of a plant has become imbedded under the surface of the skin.
    4) PHOTODERMATITIS: Erythema occurs in most cases, followed by vesicles which coalesce to form large blisters. Hyperpigmentation is a late finding in some individuals and appears somewhat dose-dependent; the effects are related to a stimulation in melanin production.

Laboratory Monitoring

    A) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    B) Patches and skin testing may be useful in the differential diagnosis of allergic reaction and chemical irritation in the outpatient setting.
    C) Monitor patients for clinical signs of infection.

Treatment Overview

    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive; patients may only require observation. CHEMICAL IRRITATION: After thorough decontamination, topical emollients and/or corticosteroids may assist in resolution of dermatitis. Oral or IM diphenhydramine may decrease pruritic symptoms. MECHANICAL TRAUMA: Remove any foreign bodies. Observe for infection. ALLERGIC REACTION: Identification of the specific agent involved and confirmation by patch testing or skin testing may make it possible to perform desensitization therapy. The development of systemic symptoms is rare. Oral antihistamines and topical or oral corticosteroids should be used for symptomatic relief.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Evaluate for life-threatening allergic reactions and anaphylaxis.
    3) DECONTAMINATION
    a) Remove the patient from the site of exposure; all thorns, stickers, prickles, and other foreign bodies should be removed. Remove contaminated clothing and wash exposed area thoroughly with soap and water. Exposed clothing should be washed before being worn again. The clothes may also need to be brushed.
    4) AIRWAY MANAGEMENT
    a) Endotracheal intubation and mechanical ventilation may be required in patients with severe allergic reactions, but this is extremely rare.
    5) ANTIDOTE
    a) None.
    6) ACUTE ALLERGIC REACTION
    a) Systemic allergic reactions are extremely rare. MILD TO MODERATE EFFECTS: Monitor airway. Administer antihistamines with or without inhaled beta agonists, corticosteroids or epinephrine. SEVERE EFFECTS: Administer oxygen, aggressive airway management may be necessary. Administer antihistamines, epinephrine, corticosteroids as needed. Treatment includes IV fluids and ECG monitoring.
    7) PATIENT DISPOSITION
    a) HOME CRITERIA: Patients with mild symptoms may be monitored at home.
    b) OBSERVATION CRITERIA: Patients with severe symptoms should be referred to a healthcare facility for evaluation/observation.
    c) ADMISSION CRITERIA: Patients with severe symptoms (eg, anaphylaxis) should be admitted.
    d) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing a patient with severe symptoms or if the diagnosis is unclear.
    8) PITFALLS
    a) The patient may have been exposed to other more toxic plants.
    9) DIFFERENTIAL DIAGNOSIS
    a) The differential diagnosis is primarily allergic/hypersensitivity reactions.

Range Of Toxicity

    A) TOXICITY: There is no specific toxic dose. Toxicity is variable. The extent of reaction is related to the amount and duration of direct contact. Toxic exposure is usually due to direct or indirect contact with offending plant. Some individuals may develop severe allergic reactions. Most isolated dermal exposures do not result in significant toxicity, but irritation of ocular, oral, or upper airway tissue can have serious consequences.

Clinical Effects

Summary Of Exposure

    A) SOURCES: Toxicodendron plants frequently produce dermatitis, and are commonly known as poison ivy, poison oak and poison sumac. Nettles (Urtica species) and various Euphorbia species (crown of thorns, poinsettia) are capable of producing dermatitis. Allergic skin reactions to plants and their products account for 4% to 10% of all visits to dermatology clinics. This management deals with a general approach to plant dermatitis and dermatologic response due to various plant exposures. For more specific information regarding some of the plants discussed in this management, please refer to the following: PLANTS-PSORALENS or PLANTS-TOXICODENDROL.
    B) TOXICOLOGY: Plant-induced dermatitis can be divided into four major categories based on mechanism of toxicity. Many exposures involve combinations of more than one mechanism. The majority of these cases are self-limiting and disappear within 14 to 21 days.
    1) ALLERGIC REACTION: This is a true sensitization (type IV hypersensitivity reaction) of an individual to the particular allergen contained in the plant. After the first exposure, the patient usually has a 5 to 7 day latency period before the immunological sensitization develops. Subsequent exposure results in allergic contact dermatitis.
    2) CHEMICAL IRRITATION: This is not an allergic response, but rather the direct effect of a particular chemical contained in the plant.
    3) MECHANICAL TRAUMA: It may occur following exposure to the sharpened thorns, barbs, and so forth of various plants.
    4) PHOTODERMATITIS: It occurs following exposure to some plants and their various oils that react in such a way to make the skin sensitive to sunlight.
    C) EPIDEMIOLOGY: Exposure is common, but severe symptoms are rare.
    D) WITH POISONING/EXPOSURE
    1) ALLERGIC REACTION: Allergic contact dermatitis usually presents with pruritus and vesiculation of varying degrees. The affected area may be erythematous, edematous, and develop large bullae; weeping and crusting may be present. Upon healing, these lesions may become thickened, fissured and sometimes pigmented.
    2) CHEMICAL IRRITATION: Symptoms are usually seen within 24 hours of exposure and usually consist of erythema, pruritus, and burning. Vesicle formation occurs in moderate to severe exposures, and frequently appears in linear streaks as a result of brushing the skin against the plant.
    3) MECHANICAL TRAUMA: Infection or chronic changes may occur in the skin if a portion of a plant has become imbedded under the surface of the skin.
    4) PHOTODERMATITIS: Erythema occurs in most cases, followed by vesicles which coalesce to form large blisters. Hyperpigmentation is a late finding in some individuals and appears somewhat dose-dependent; the effects are related to a stimulation in melanin production.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) HYPERSENSITIVITY REACTION
    1) WITH POISONING/EXPOSURE
    a) An allergic reaction is a true sensitization of an individual to the particular allergen contained in that plant.
    1) After the first exposure, the patient usually has a 5 to 7 day latency period before the immunological sensitization develops. Symptoms manifest upon subsequent exposures.
    2) Allergic contact dermatitis usually presents with pruritus and vesiculation of varying degrees. The affected area may be erythematous, edematous, and develop large bullae, weeping and crusting may be present (Bruynzeel et al, 1998).
    3) Upon healing, these lesions may become thickened, fissured and sometimes pigmented.
    4) Airborne contact dermatitis (from Parthenium hysterophorus) is a cause of considerable morbidity in India (Srinivas et al, 1991).
    5) SPECIES: Allergic reactions are common from the Compositae family (De Corres, 1984; Guin & Skidmore, 1987; Menz & Winkelmann, 1987; Srinivas et al, 1991; Bruneton, 1999).
    a) Compositae family: In humans, sesquiterpenoid lactones are responsible for producing allergic contact dermatitis. Some examples are reported in vegetables (i.e., artichoke {cynaropicrine} or endive {lactucopicrin}), with ornamentals (i.e., chrysanthemum {arteglasin} or inula {alantolactone}) and with some medicinals (i.e., arnica {helenalin, carabron}, Roman chamomile {nobilin} or products derived from them and sunflower {niveusin- and dihydroniveusin-type derivatives}). Most often these dermal reactions are due to occupational exposure (Bruneton, 1999).
    b) In North America, the genus Toxicodendron (e.g., sumac species) are responsible for allergic cutaneous reactions and commonly known as: poison ivy (T. radicans) native to northeastern United States; western poison oak (T. diversiloba), and eastern poison oak (T. quercifolium); poison sumac (T. vernix) found in the eastern half of the US and abundant in Florida; and T. rydbergii. Onset of symptoms is usually 2 to 4 days.
    1) All of these species contain some percent of unsaturated 3-n-pentadecylcatechins and their 3-n-heptadecyl homologs. They can produce allergic reactions because the alkenylphenols traverse the external layers of the skin and are subsequently oxidized to electrophilic quinones capable of reacting with the nucleophilic groups of proteins (Bruneton, 1999). See PLANTS-TOXICODENDROL management for further information.
    c) Primula obconica is a common source of allergic reactions in Europe and reactions are becoming more frequent here in the United States (Epstein, 1990; Apted, 1988).
    d) Tulip fingers is the diagnostic term for the allergic contact dermatitis associated with the handling of tulip bulbs. Tulip fingers is a frequent occupational problem among workers in the tulip industry. Typically presenting with erythematous, dry, scaling plaques on the fingertips and periungually, with painful fissures, and dystrophic nails (Gette & Marks, 1990).
    e) Thapsia garganica L, a perennial herbaceous plant found in North Africa, contains thapsigargin and thapsigargicine which are histamine liberator substances; thapsigargin is also a potent stimulator of mast cell degranulation (Bahri & Makhlouf, 2001).
    B) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) CHEMICAL IRRITATION: Not an allergic response, but rather a direct effect of a particular chemical contained in the plant.
    1) Symptoms are usually seen within 24 hours of exposure and usually consist of erythema, pruritus, and burning. Vesicle formation occurs in moderate to severe exposures and frequently appears in linear streaks as a result of brushing the skin against the plant (Burrall, 1989).
    2) The majority of cases of primary irritant contact dermatitis may be traced to three plant families, namely the Euphorbiaceae (spurges), Brassicaceae (mustards), and the Ranunculaceae (buttercups) (Epstein, 1987), but citrus fruits also are commonly involved (Mitchel & Rook, 1979).
    3) NETTLES: Urtica species have special injector cells that produce rapid development of short-lived wheals followed by itching, burning sensation, and possible prolonged (12 hours) paresthesias, which persist after the visible reaction is gone (Kulze & Greaves, 1988).
    C) PHOTOSENSITIVITY
    1) WITH POISONING/EXPOSURE
    a) PHOTODERMATITIS may occur following exposure to some plants and their various oils that react in such a way to make the skin sensitive to sunlight (Rook, 1962). Reactions may be photoallergic or phototoxic (Epstein, 1987). The diagnosis can be readily confused with other possible causes, such as allergic dermatitis, purpura, impetigo, fungal infection or even child abuse (ie, traces left on the skin appear as the result of abuse) (Bruneton, 1999).
    b) Phototoxic reactions occur following contact with plants that contain phototoxic chemicals, such as psoralens found in limes and parsnips. Onset of toxic reactions occur within hours, but only to skin sites that have been in contact with the plant and exposed to the sun (Burrall, 1989).
    c) SUMMARY: In many occupational exposures of photodermatitis, the two main families of plants responsible are the APIACEAE (Umbelliferae) and the RUTACEAE (Baxter et al, 2000).
    1) Photosensitizing Apiaceae are species that contain furanocoumarins (ie, psoralens, bergapten, xanthotoxin, and related derivatives). When exposed to sunlight these species causes a phototoxic dermatitis of variable intensity, which can range from erythema to blisters and vesicles on the exposed area (e.g., back of hands, wrists, forearms, and lower legs). Excessive pigmentation usually occurs several days after exposure (Bruneton, 1999).
    2) INCIDENCE: Phototoxic reaction is relatively common and has occurred in numerous plant species: parsnip (Pastinaca sativa L.), celery, parsley, carrots, angelica, lovage (levisticum officinale), and hogweed (Heracleum sphondylium L.) (Bruneton, 1999; Baxter et al, 2000). In warmer climates, the MORACEAE (figs) and LEGUMINOSAE (pea) may also produce symptoms (Mandalia et al, 2008; Baxter et al, 2000).
    3) Other Apiaceae (eg, Ammi majus L.) can cause primary photosensitization in animals and some birds (Bruneton, 1999).
    d) FIG TREE SAP (Moraceae family): Two children developed phytophotodermatitis after playing with fig tree branches while playing outside. The branches had been stripped bare of their bark. The older child played with the branches while in a swimming pool. About 12 hours after exposure, both children experienced a burning sensation and erythema of the skin. Vesicles were visible over the affected areas within 48 hours. Treatment was sought and superficial partial thickness burns (2% total body surface area in the 8 year-old boy and 5% total body surface area in the 10-year-old girl) were treated with simple nonadherent dressings. Large bullae were observed 6 days after exposure in both children. The wounds gradually healed over eight weeks. Persistent hyperpigmentation to the affected areas was successfully treated with topical steroids and avoidance of sun exposure (Mandalia et al, 2008).
    e) RUTACEAE
    1) The family Rutaceae (over 150 genera) are mainly found in tropical geographic area of the world; mainly arborescent and have secretory pockets (i.e. Citrus). The main reaction caused by this family is dermatological; Rutaceae are rich in photosensitizing furanocoumarins (e.g., bergapten), and may cause phototoxic injury (Bruneton, 1999). Reactions may occur due to contact with the plant or with the products produced (i.e., essential oils, cosmetics) by the plant following exposure of the skin to sunlight. Generally, humidity worsens the response.
    2) COMMON: Erythema in most cases; followed by vesicles which coalesce to form large blisters. Hyperpigmentation is a late finding in some individuals and appears somewhat dose-dependent; the effects are related to a stimulation in melanin production (Bruneton, 1999).
    3) SPECIES IMPLICATED: Species used for the production of fruits or essential oils are likely to produce photodermatosis; especially in children. Lemons, limes, bergamot (ingredient found in perfumes and tanning lotions) and contact with some ornamentals (ie, fraxinella) (Bruneton, 1999).
    D) REACTION TO THORN AND/OR SPINE IN SKIN
    1) WITH POISONING/EXPOSURE
    a) MECHANICAL TRAUMA may occur following exposure to the sharpened thorns or barbs on various plants. Infection or chronic changes may occur in the skin if a portion of a plant has become imbedded under the surface of the skin. There is potential for bacterial or fungal inoculation and infection in this situation.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    B) Patches and skin testing may be useful in the differential diagnosis of allergic reaction and chemical irritation in the outpatient setting.
    C) Monitor patients for clinical signs of infection.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) DERMAL
    a) Although not applicable in the emergency setting, patch and skin testing can be useful in the differential diagnosis of allergic reaction and chemical irritation in the outpatient setting (Epstein, 1990).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.5) DISPOSITION/DERMAL EXPOSURE
    6.3.5.1) ADMISSION CRITERIA/DERMAL
    A) Patients with severe symptoms (eg, anaphylaxis) should be admitted.
    6.3.5.2) HOME CRITERIA/DERMAL
    A) Patients with mild symptoms may be monitored at home.
    6.3.5.3) CONSULT CRITERIA/DERMAL
    A) Consult a poison center or medical toxicologist for assistance in managing a patient with severe symptoms or if the diagnosis is unclear.
    6.3.5.5) OBSERVATION CRITERIA/DERMAL
    A) Patients with severe symptoms should be referred to a healthcare facility for evaluation/observation.

Monitoring

    A) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    B) Patches and skin testing may be useful in the differential diagnosis of allergic reaction and chemical irritation in the outpatient setting.
    C) Monitor patients for clinical signs of infection.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Remove the patient from site of exposure; all thorns, stickers, prickles, and other foreign bodies should be removed. Remove contaminated clothing and wash exposed area thoroughly with soap and water. Exposed clothing should be washed before being worn again. The clothes may also need to be brushed.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) Remove patient from the site of exposure; all thorns, stickers, prickles, and other foreign bodies should be removed. Remove contaminated clothing and wash exposed area thoroughly with soap and water. Exposed clothing should be washed before being worn again. They may also need to be brushed.
    6.9.2) TREATMENT
    A) MONITORING OF PATIENT
    1) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    2) Patches and skin testing may be useful in the differential diagnosis of allergic reaction and chemical irritation in the outpatient setting.
    3) Monitor patients for clinical signs of infection.
    B) ACUTE ALLERGIC REACTION
    1) Identification of the specific agent involved and confirmation by patch testing or skin testing may make it possible to perform desensitization therapy. The development of systemic symptoms is rare.
    2) Oral and topical corticosteroids, diphenhydramine, and other symptomatic care may be useful in decreasing the degree of symptoms.
    3) In India, two cases of persistent airborne contact dermatitis (due to Parthenium hysterophorus) were successfully treated with a combination of azathioprine 100 mg daily and either steroids or psoralen photochemotherapy (Srinivas et al, 1991).
    C) ANAPHYLAXIS
    1) SUMMARY
    a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.
    2) BRONCHOSPASM
    a) ALBUTEROL
    1) ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007). CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 mg/kg (up to 10 mg) every 1 to 4 hours as needed, or 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    3) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm.
    b) PREDNISONE: ADULT: 40 to 80 milligrams/day. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 to 2 divided doses divided twice daily (National Heart,Lung,and Blood Institute, 2007).
    4) MILD CASES
    a) DIPHENHYDRAMINE
    1) SUMMARY: Oral diphenhydramine, as well as other H1 antihistamines can be used as indicated (Lieberman et al, 2010).
    2) ADULT: 50 milligrams orally, or 10 to 50 mg intravenously at a rate not to exceed 25 mg/min or may be given by deep intramuscular injection. A total of 100 mg may be administered if needed. Maximum daily dosage is 400 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    3) CHILD: 5 mg/kg/24 hours or 150 mg/m(2)/24 hours. Divided into 4 doses, administered intravenously at a rate not exceeding 25 mg/min or by deep intramuscular injection. Maximum daily dosage is 300 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    5) MODERATE CASES
    a) EPINEPHRINE: INJECTABLE SOLUTION: It should be administered early in patients by IM injection. Using a 1:1000 (1 mg/mL) solution of epinephrine. Initial Dose: 0.01 mg/kg intramuscularly with a maximum dose of 0.5 mg in adults and 0.3 mg in children. The dose may be repeated every 5 to 15 minutes, if no clinical improvement. Most patients respond to 1 or 2 doses (Nowak & Macias, 2014).
    6) SEVERE CASES
    a) EPINEPHRINE
    1) INTRAVENOUS BOLUS: ADULT: 1 mg intravenously as a 1:10,000 (0.1 mg/mL) solution; CHILD: 0.01 mL/kg intravenously to a maximum single dose of 1 mg given as a 1:10,000 (0.1 mg/mL) solution. It can be repeated every 3 to 5 minutes as needed. The dose can also be given by the intraosseous route if IV access cannot be established (Lieberman et al, 2015). ALTERNATIVE ROUTE: ENDOTRACHEAL ADMINISTRATION: If IV/IO access is unavailable. DOSE: ADULT: Administer 2 to 2.5 mg of 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube. CHILD: DOSE: 0.1 mg/kg to a maximum of 2.5 mg administered as a 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube (Lieberman et al, 2015).
    2) INTRAVENOUS INFUSION: Intravenous administration may be considered in patients poorly responsive to IM or SubQ epinephrine. An epinephrine infusion may be prepared by adding 1 mg (1 mL of 1:1000 (1 mg/mL) solution) to 250 mL D5W, yielding a concentration of 4 mcg/mL, and infuse this solution IV at a rate of 1 mcg/min to 10 mcg/min (maximum rate). CHILD: A dosage of 0.01 mg/kg (0.1 mL/kg of a 1:10,000 (0.1 mg/mL) solution up to 10 mcg/min (maximum dose 0.3 mg) is recommended for children (Lieberman et al, 2010). Careful titration of a continuous infusion of IV epinephrine, based on the severity of the reaction, along with a crystalloid infusion can be considered in the treatment of anaphylactic shock. It appears to be a reasonable alternative to IV boluses, if the patient is not in cardiac arrest (Vanden Hoek,TL,et al).
    7) AIRWAY MANAGEMENT
    a) OXYGEN: 5 to 10 liters/minute via high flow mask.
    b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
    c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction (Vanden Hoek,TL,et al).
    d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
    e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
    f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    8) MONITORING
    a) CARDIAC MONITOR: All complicated cases.
    b) IV ACCESS: Routine in all complicated cases.
    9) HYPOTENSION
    a) If hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 L/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.
    1) VASOPRESSORS: Should be used in refractory cases unresponsive to repeated doses of epinephrine and after vigorous intravenous crystalloid rehydration (Lieberman et al, 2010).
    2) DOPAMINE: Initial Dose: 2 to 20 micrograms/kilogram/minute intravenously; titrate to maintain systolic blood pressure greater than 90 mm Hg (Lieberman et al, 2010).
    10) H1 and H2 ANTIHISTAMINES
    a) SUMMARY: Antihistamines are second-line therapy and are used as supportive therapy and should not be used in place of epinephrine (Lieberman et al, 2010).
    1) DIPHENHYDRAMINE: ADULT: 25 to 50 milligrams via a slow intravenous infusion or IM. PEDIATRIC: 1 milligram/kilogram via slow intravenous infusion or IM up to 50 mg in children (Lieberman et al, 2010).
    b) RANITIDINE: ADULT: 1 mg/kg parenterally; CHILD: 12.5 to 50 mg parenterally. If the intravenous route is used, ranitidine should be infused over 10 to 15 minutes or diluted in 5% dextrose to a volume of 20 mL and injected over 5 minutes (Lieberman et al, 2010).
    c) Oral diphenhydramine, as well as other H1 antihistamines, can also be used as indicated (Lieberman et al, 2010).
    11) DYSRHYTHMIAS
    a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TL,et al). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.
    12) OTHER THERAPIES
    a) There have been a few reports of patients with anaphylaxis, with or without cardiac arrest, that have responded to vasopressin therapy that did not respond to standard therapy. Although there are no randomized controlled trials, other alternative vasoactive therapies (ie, vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in patients in cardiac arrest secondary to anaphylaxis that do not respond to epinephrine (Vanden Hoek,TL,et al).
    D) IRRITATION SYMPTOM
    1) DECONTAMINATION of the skin with soap and water and a soft sponge or washcloth will prevent exacerbation of symptoms.
    2) SCRATCHING: Discourage the patient from scratching the affected area until it has been thoroughly washed; scratching the affected area and then an unaffected area may transport the irritant chemical and produce symptoms on previously unexposed areas of the body.
    3) CORTICOSTEROIDS: Topical corticosteroids may assist in resolution of dermatitis and oral or IM diphenhydramine may decrease the pruritic response. Symptoms usually resolve within 1 to 2 days.
    E) PHOTODERMATITIS
    1) Identification of the toxic substance and avoidance is probably the most significant factor. Treatment is symptomatic and supportive. Cold compresses and topical corticosteroids are the primary therapy. Hyperpigmentation may, however, last for a considerable period of time and is not known to be amenable to current therapy. Symptoms usually subside in a few weeks. In children, traces on the skin may be mistaken for child abuse and may complicate the diagnosis (Bruneton, 1999).
    F) WOUND CARE
    1) Decontamination of the skin surface and removal of obvious barbs or thorns is of primary importance. Infection may occur following introduction of fungus or bacteria. Debridement of lesions is usually not necessary initially, however, following significant infection, removal of foreign bodies may be the only way to relieve the condition.

Abstracts

Case Reports

    A) ACUTE EFFECTS: In India, the plant Parthenium hysterophorus (a member of the Compositae family) has caused a considerable number of cases of airborne contact dermatitis. The resultant dermatitis is often difficult to manage and persistent with features suggestive of a photosensitivity. Two difficult cases were treated successfully with a combination of azathioprine 100 mg daily and either steroids or psoralen photochemotherapy (Srinivas et al, 1991).

Range Of Toxicity

Summary

    A) TOXICITY: There is no specific toxic dose. Toxicity is variable. The extent of reaction is related to the amount and duration of direct contact. Toxic exposure is usually due to direct or indirect contact with offending plant. Some individuals may develop severe allergic reactions. Most isolated dermal exposures do not result in significant toxicity, but irritation of ocular, oral, or upper airway tissue can have serious consequences.

Maximum Tolerated Exposure

    A) There is no specific toxic dose. Toxicity is variable. The extent of reaction is related to the amount and duration of direct contact. Toxic exposure is usually due to direct or indirect contact with offending plant. Some individuals may develop severe allergic reactions. Most isolated dermal exposures do not result in significant toxicity, but irritation of ocular, oral, or upper airway tissue can have serious consequences.

Pharmacology Toxicology

Toxicologic Mechanism

    A) Plant dermatitis may be due to several causes. There are chemical irritants such as are found in the Euphorbiaceae, there are mechanical irritants like cactus needles, glochids, and rose thorns, and there are combinations of the two, such as with nettles.
    B) Plant dermatitis may also be due to sensitivity, allergic (Toxicodendron), and anaphylactic reactions.
    C) Various studies have shown an enzymatic basis for itching. This has been tested against various plant and animal irritants (Arthur & Shelley, 1955) Arthur & Shelly, 1955a).
    D) The stinging nettles, such as Urtica dioica, U. urens, and U. parviflora, have histamine, acetylcholine, and 5-hydroxytryptamine in special injector cells. Earlier studies which proposed formic and acetic acid as the mediators were incorrect (Kulze & Greaves, 1988).
    E) The initial step inducing an allergic contact dermatitis begins when the hapten and skin carrier protein form a covalent bond. The proteins are usually nucleophiles (electron-rich) containing amino, thiol, imidazole, or hydroxyl groups. Most plant haptens are electrophiles (electron-poor). The electrophilic haptens accept a protein nucleophile and form a complete antigen (Burrall, 1989).
    1) In the Toxicodendron spp., the alkenylphenols that transverse the external layers of the skin are subsequently oxidized to electrophilic quinones that are capable of reacting with the nucleophilic groups of proteins and become immunogenic which produces the allergic reaction (Bruneton, 1999).

References

General Bibliography

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