6.5.2) PREVENTION OF ABSORPTION
A) ACTIVATED CHARCOAL 1) There have been few cases where large amounts of Toxicodendron species have been ingested. Activated charcoal would not be necessary for chewing on a stick or eating 1 or 2 berries. Activated charcoal may be beneficial in large toxicodendrol ingestions, although there is a paucity of clinical evidence. 2) Patients at risk for seizures or CNS depression should NOT be administered activated charcoal due to the risk of aspiration. 3) CHARCOAL ADMINISTRATION a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
4) CHARCOAL DOSE a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005). 1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
b) ADVERSE EFFECTS/CONTRAINDICATIONS 1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
6.5.3) TREATMENT
A) CORTICOSTEROID 1) Corticosteroids have been used to treat renal toxicity seen with poison oak (Devich et al, 1975).
2) There is very limited clinical evidence for both renal toxicity and for effectiveness of corticosteroid treatment.
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6.9.1) DECONTAMINATION
A) DERMAL DECONTAMINATION 1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). 2) Washing may only be useful if done in the first 5 minutes (Guin et al, 1989). 3) ALLERGEN PERSISTENCE a) The allergen is oily and nonvolatile and readily impregnates objects. Persistence of allergen permits spread by contaminated fingers, clothing, shoes, tools, animals, and sports and hunting equipment. b) The oleoresins responsible for dermatitis quickly become tissue-bound and washing the affected area 10 to 15 minutes after contact does little to remove the antigen. This is probably due to the alkyl and alkenyl catechols of the sap which bind tightly to the skin, and will not wash off. c) Immediate soaking of the exposed area in water is recommended, but is not always possible in the woods. The oleoresins involved are not very water soluble. 1) Immediate washing with soap and water, if possible, can reduce or eliminate the extent of exposure: a) Reference: Fisher, 1996
d) Soap and water will eventually remove or degrade the material, so all clothes should be laundered several times before wearing. 6.9.2) TREATMENT
A) SUPPORT 1) Symptomatic and supportive care is the mainstay for toxicodendrol toxicity; remove contaminated clothing and wash skin thoroughly with soap and water. Antihistamines and topical corticosteroids are the mainstay of treatment. 2) Topical and external prophylactic measures have centered on three primary areas: 1) Removal of the antigen by washing with soap and water or with organic solvents
2) Use of barrier creams
3) Detoxicants (oxidizing and complexing agents which may chemically inactivate the antigen)
3) WASHING: Removal of the antigen by washing with soap and water has shown to be ineffective once the antigen has become fixed to the skin, usually within 10 to 15 minutes. 4) AVOID topical antihistamines, benzocaine and zirconium, which may act as common sensitizers and cause exacerbation of symptoms (Lee & Arriola, 1999; Tanner, 2000). B) PROTECTANT, DERMATOLOGICAL 1) SUMMARY a) Kligman (1958) tested 34 different preparations over a 2 year period on a group of poison ivy sensitive patients and concluded that all of these substances were incapable of preventing the occurrence of dermatitis (Kligman, 1958). b) However, it was found that a barrier cream containing organoclay had shown some benefit in preventing or limiting an allergic response (Marks et al, 1995). c) ORGANOCLAY: Epstein (1985) evaluated an organoclay made by United Catalyst Inc (Louisville) in a double-blind, randomized study, and found it gave a 95.3% protection, as compared to 29.6% for bentonite, 37.9% for kaolin, and 32.9% for silicone. 1) CASE SERIES: In a single-blind, paired comparison randomized study of 211 individuals with a history of allergic contact dermatitis to poison ivy/oak, 5% quaternium-18 bentonite lotion significantly prevented or limited the production of an allergic response to experimentally produced urushiol (Marks et al, 1995). It is an organoclay material produced by reacting quaternium-18, a dimethyl dihydrogenated tallow quaternary ammonium compound, with bentonite (a natural hydrated colloidal aluminum silicate clay). Although the mechanism of action remains unknown, it is assumed that it acts as a physical barrier to prevent absorption of the allergen.
2) Quaternium-18 was found to be effective, nonirritating, nonsensitizing, and without toxic or allergic potential, but required the lotion be washed off then reapplied every 4 to 8 hours for ongoing protection (Tanner, 2000).
2) OTHER PRODUCTS/GENERALLY INEFFECTIVE a) Barrier creams have been of little use (Hardin, 1974). Many substances have been tried including alkaline peroxides (Gisbold, 1941), sodium perborate (Shelmire, 1944), tyrosinase (Sizer & Prokesch, 1945), exchange resins (Thurmon et al, 1955), chloramide (Sulzberger et al, 1946) and zirconium salts (Kligman, 1958).
b) Orchard et al (1986) tested several compounds as protectants. They found simple chemical nucleophiles and polyvinyl pyrrolidones (PBP) were not protective, but polyamine salts of linoleic acid dimers did have the ability to prevent dermatitis in some people (Orchard et al, 1987). The salts appeared to work as a barrier rather than as a chemical reactant. Further work needs to be done to evaluate the substances thoroughly.
c) PROTECTANT JEFFAMINS: Various polyoxypropylene amines of linoleic acid dimer (called "Jeffamins") have been tested as protectants. Dermatitis was totally prevented in 50% to 73% of subjects exposed to poison ivy extract for 48 hours. If the skin were washed 8 to 12 hours after sequential application of the Jeffamin and the poison ivy extract, 75% to 100% of test subjects were protected (Orchard et al, 1987).
d) ZIRCONIUM CONTAINING PRODUCTS/WITHDRAWN: Which usually also contain antihistamines were once thought to inactivate urushiol. Contradictory information concerning the efficacy of these agents and the documentation of zirconium sensitivity has led to withdrawal of these agents.
e) CHEMICAL DETOXICANTS are generally ineffective, in that they are unavailable at the site of the exposure, and are useless after the antigen has combined with the skin.
C) GENERAL TREATMENT 1) Application of cool compresses to the affected areas reduces itching, removes heat from the inflamed surfaces, and provides topical anesthesia. Compresses are also used to help dry the lesions, particularly in the presence of weeping or oozing edematous areas or areas with broken vesicles or bullae (Chapel, 1985). a) SOAKING AGENTS: Although tap water alone is effective, astringents such as Burows's solution (aluminum acetate) offers enough advantages to merit its routine use (Simons, 1986). When the dermatitis is widespread, potassium permanganate baths may be prescribed. Starch or oatmeal baths are also soothing (Chapel, 1985).
b) SOAPLESS SHOWERS: Several times a day may be effective in relieving itching. The water should be directed onto the affected areas until the resulting pleasant sensation subsides and any accumulated exudate has been washed away (Daniell, 1984). This treatment will decrease the risk of secondary infections by removing exudate which provides a culture medium for bacterial growth. Bathing with HOT water may mask symptoms but may increase the physiologic sequelae of vasodilation, erythema, and edema. Repeated exposure to very hot water may increase the itching (Tromovitch et al, 1984).
D) CORTICOSTEROID 1) CORTICOSTEROIDS: Are the mainstay of treatment. A topical steroid preparation is adequate for mild, localized cases while moderate to severe cases require treatment with a systemic steroid. a) TOPICAL: Mild dermatitis consisting of erythema, edema, and papules limited to a few anatomic regions can be banished with a topical steroid cream or lotion, e.g., hydrocortisone, triamcinolone, desoximetasone or fluocinonide (Chapel, 1985). Topical steroids are ineffective when used in the oozing, vesicular stages. 1) FREQUENCY: One study (Kaidbeg & Kligman, 1976) demonstrated an advantage of 3 times a day administration over once a day application, but other clinicians failed to show a similar advantage in a 6 times a day application (Roberts, 1985).
2) CREAM vs OINTMENT: Various studies have demonstrated that one form is better than another, but no consistent difference has been noted.
3) HYDROCORTISONE CREAM: Apply to affected areas of face or intertriginous regions in a thin film three times a day. In children, apply sparingly because of the greater susceptibility for adrenal suppression and Cushing's syndrome. Brand names include Cort-Dome(R), Hytone(R), Synacort(R), and Cortaid(R). OTC creams with hydrocortisone in strengths of 0.5% or less may not offer significant benefit (Guin et al, 1989).
4) DESOXIMETASONE: Used for mild dermatitis consisting of erythema, edema and papules limited to a few anatomic regions. For areas other than the face or intertriginous regions, a desoximetasone cream (0.25%) may be prescribed. It should be applied to the affected area in a thin film 3 times a day. Children should have this material applied sparingly because of greater susceptibility for adrenal suppression and Cushing's syndrome. Brand names include Topicort(R) and Topicort LP(R).
5) FLUOCINONIDE: A 0.05% cream may be applied for mild dermatitis. This should be applied to affected areas in a thin film three times a day with the amounts used in children applied sparingly because of greater susceptibility to adrenal suppression and Cushing's syndrome. Available forms include Lidex(R) and Lidex-E(R).
6) TRIAMCINOLONE: Another steroid cream that can be used is triamcinolone, in either a 0.025% or 0.1% concentration. It should be applied to the affected area in a thin film 3 times a day with the amount used in children reduced due to greater susceptibility to adrenal suppression and Cushing's syndrome. Available forms include Kenalog(R), Aristocort(R) and several generic preparations.
b) SYSTEMIC: Systemic steroids are useful for generalized involvement and for relief of symptoms and associated edema. Most patients with significant poison ivy did not respond to topical steroids but usually respond dramatically to oral steroids. 1) Indications for systemic steroids in the absence of contraindications, would be progressive lesions or pruritus unresponsive to topical therapy, intractable pruritus that interferes with sleep or daily activities, swelling of the face, genitalia, feet and/or ankles, widespread eruption described as greater than 25% of the body surface area, with patches of vesicles or bullae (Brodell & Williams, 1999). 2) DOSAGE : The dosage is determined by the severity of the dermatitis and the phase of the skin lesions. Because most cases will reach peak severity after about 3 to 5 days, the required dose may be minimal if the patient is started on systemic steroids after this time; however, if a patient is seen early in the course, dermatitis severity may progress beyond the effectiveness of the original treatment, and a higher initial dose is required (Simons, 1986). 3) DURATION OF THERAPY: Steroid therapy should be started and tapered over a period of at least 14 to 18 days. Shorter treatment periods, especially those under 1 week, often result in rebound flare of the hypersensitivity reaction, with eruption of new lesions when the drug is stopped (Simons, 1986). The patient should be instructed to complete the full course of medication even if the rash is completely subsided. 4) PREDNISONE a) Two-week tapered course (Oral): 60 mg/day for days 1 through 4; 50 mg/day on days 5 and 6; 40 mg/day on days 7 and 8; 30 mg/day on days 9 and 10; 20 mg/day on days 11 and 12; and 10 mg/day on days 13 and 14 (Brodell & Williams, 1999). This dosing schedule eliminates the possibility of severe rebound exacerbation of rash and pruritus (Ives & Tepper, 1991; Brodell & Williams, 1999; Lee & Arriola, 1999).
b) Three-week tapered course: 60 mg/day orally for the first week; 30 mg/day orally for the second week; 20 mg/day orally for the third week.
5) METHYLPREDNISOLONE a) A 6 day tapering course of oral methylprednisolone is often prescribed for treatment. There have been several anecdotal reports about flare-ups of the dermatitis several days after completion of the 6 day course (Ives & Tepper, 1991).
E) ANTIHISTAMINE 1) Most patients require an oral antihistamine (ie, diphenhydramine or hydroxyzine) for relief of pruritus (Chapel, 1985). 2) DIPHENHYDRAMINE a) ADULT: 25 to 50 mg orally every 4 to 6 hours; CHILD: 5 mg/kg/day orally in 4 divided doses with a maximum of 300 mg/day.
3) HYDROXYZINE a) ADULT: 25 mg orally 3 times a day or 4 times a day; CHILD: 2 mg/kg/day orally in 4 divided doses.
F) WOUND CARE 1) Large bullae can be aspirated aseptically with the roofs left intact (Chapel, 1985).
G) SECONDARY INFECTION 1) Secondary infections are relatively common following toxicodendron dermatitis.
2) Treat with antibiotics that have staphylococcus and streptococcus coverage.
H) PSYCHOLOGIC DESENSITIZATION THERAPY 1) LACK OF EFFECT a) SUMMARY: In general, hyposensitization is not considered an effective method based on its lengthy regimen, multiple side effects, and limited (6 to 10 months) effectiveness (Tanner, 2000). b) Oral hyposensitization has been tried with minimal success. Marks et al (1987) tried an orally administered mixture (1:1) of pentadecylcatechol and heptadecylcatechol diacetate without statistically significant hyposensitization. Most over-the-counter products have little or no active ingredients (Marks et al, 1987). This treatment is generally no longer recommended, and when used, is reserved for severely allergic cases of occupational exposure (Epstein, 1973; Block, 1973). c) DOSES: Prescription products must be ingested in large quantities over a period of time. Epstein et al (1981; 1974) showed hyposensitization could be done but it required oral doses of greater than 300 mg of urushiol ingested over a long period of time. It takes 3 to 6 months to develop a reduced sensitivity. d) SIDE EFFECTS: Pruritus and rashes may develop during treatment, as may other serious symptoms. e) DURATION: This hyposensitization immediately begins to deteriorate after the antigen is stopped. 1) Cashew nuts are in the same family as poison ivy and share similar allergens. Nineteen adults working in a cashew nut shell oil processing plant tested positive to poison ivy allergens. After working for several months, only 3 remained test positive, 2 minimally. This implies that hyposensitization occurred after handling the cashew nut shells (Reginella et al, 1989).
2) TOLERANCE INDUCTION a) Epstein et al (1981) tried to induce tolerance by giving IM injections of a poison ivy oil preparation weekly. Three to five years after the study, one-half of his group had become reactive even without being exposed to poison ivy. This method has not been very effective, and is currently not in use.
b) Hyposensitization and desensitization does occur in lacquer workers exposed to urushiol. In one study where 81.5% of all workers became sensitized, 55.2% of these became hyposensitized and 12.9% became desensitized. This change in sensitization was noted after daily exposures of about 1 month (Kawai et al, 1991).
3) POISON IVY EXTRACTS a) Should not be administered for treatment of the dermatitis. They are not considered useful and may actually exacerbate the irritation (Baer, 1990).
4) In a randomized, double-blind, paired comparison study of 10 adult volunteers, the jewel weed plant (extract and juice applied to urushiol exposed sites) was not found to be any more beneficial in the resolution of symptoms when compared to the control - plain water (Long et al, 1997). I) EXPERIMENTAL THERAPY 1) In a small pilot study (n=10), pentoxifylline, an agent known to suppress irritant and allergic contact dermatitis, was found to be beneficial in limiting patch-test reactivity to urushiol (Rietschel, 1995).
J) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate. |