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PLANTS-POINSETTIA

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Poinsettia is a member of the Euphorbiaceae family and a common household plant sold in the western world prior to the Christmas season. In warmer climates it may also be grown outdoors. It was discovered in Mexico and brought into the United States by our first minister to Mexico, Dr. Joel R. Poinsett (Jackson, 1986).

Specific Substances

    1) Euphorbia pulcherrima
    2) Christmas Star
    3) Christmas Flower
    4) Painted Leaf
    5) Lobster Plant
    6) Mexican Flameleaf
    7) Flor de Pascua
    8) Poinsettia pulcherrima (Grah)
    9) Euphorbia poinsettis (Buist)
    10) Annual poinsettia
    11) Easter Flower
    12) Mexican Flame Tree
    13) Flor de Nochebuena
    14) Papagallo
    15) Star of Bethlehem
    16) Flower of the Nativity

Available Forms Sources

    A) USES
    1) The Euphorbiaceae are used frequently in folk medicine (e.g., Phyllanthus spp., Croton spp.), but are NOT a source of any therapeutics. Some species may have an antiviral component (e.g., Homalanthus nutans) (Bruneton, 1999).
    2) Aztecs used the bracts of this plant as a glactopoietic and abortive agent (Dominguez et al, 1967). Poultices are made from the leaves to treat skin infections (Neal, 1948).
    3) An ethanolic extract of the plant is thought to have insecticidal properties (Rao, 1956), but others have shown the extracts to be without antibiotic activity (Karel & Roach, 1951; Watt & Breyer-Brandwijk, 1962).
    4) In the South China area, poinsettia is used to poison fish (Watt & Breyer-Brandwijk, 1962).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Poinsettia is a member of the Euphorbiaceae family and a common household plant. In warmer climates it may also be grown outdoors. There are over 300 genera and about 8,000 species found worldwide, except the Antarctica. They may grow as trees or bushes, vines or succulents and often produce latex.
    B) EPIDEMIOLOGY: Exposure can occur. Most exposures are related to the poinsettia plant (Euphorbia pulcherrima). Most cases can be managed at home.
    C) TOXINS: The toxin can differ depending on the species; however, complex diterpene esters (eg, phorbol esters) and mitogenic lectins are often present. The poinsettia plant does NOT contain irritant diterpenes. Some species may contain a milky latex; poinsettia has cross reactivity with latex.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL EVENTS: In most cases, exposure to poinsettia plants will cause little reaction. Irritation is the primary effect, which may manifest itself as mild skin irritation, nausea, vomiting or diarrhea. Vomiting is self-limited and seldom severe enough to require fluid or electrolyte replacement. Ocular exposure may cause irritant keratoconjunctivitis.
    2) ANAPHYLAXIS: Two infants with a history of atopic eczema and latex allergy developed anaphylaxis following inadvertent dermal exposure to the leaves of a poinsettia plant.
    0.2.4) HEENT
    A) Unlike other Euphorbiaceae, poinsettia does NOT appear to cause strong ocular irritation. Animal tests have shown little effect when the latex has been instilled into the eyes (Bruneton, 1999).
    0.2.14) DERMATOLOGIC
    A) There is some controversy as to whether poinsettia is a primary irritant. Effects have been shown in animals, and primary skin irritation is possible in humans. Poinsettia is not as irritating as other members of the Euphorbiaceae family.

Laboratory Monitoring

    A) There are no routine laboratory studies required. Vomiting is NOT expected to be extensive as to warrant monitoring of fluids and/or electrolytes.
    B) DERMAL: Patch testing may help diagnose allergic contact dermatitis in individuals with skin reactions.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Patients may only require observation. INGESTION: Inadvertent ingestion of plant material usually produces mild or limited vomiting. Fluid and electrolyte replacement is unlikely to be necessary. DERMAL: Remove contaminated clothing as necessary; clean the exposed area thoroughly with soap and water. If pruritus develops once the skin has been cleansed, oral or IM diphenhydramine may decrease pruritic symptoms. ALLERGIC REACTION: The development of systemic symptoms following poinsettia exposure is rare. Young children with a history of latex allergy may be more at risk to develop symptoms following contact with the plant.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Although not anticipated in most cases, evaluate for life-threatening allergic reactions and anaphylaxis.
    C) DECONTAMINATION
    1) INGESTION: Gastrointestinal decontamination is usually not necessary since the plant usually produces no symptoms or mild, limited vomiting.
    2) DERMAL: Remove contaminated clothing as necessary; wash exposed skin with soap and water.
    D) ANTIDOTE
    1) There is no known antidote.
    E) ACUTE ALLERGIC REACTION
    1) 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.
    F) ENHANCED ELIMINATION
    1) No studies have addressed the utilization of enhanced elimination techniques following oral exposure to poinsettia, but are unlikely to be necessary.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild symptoms may be monitored at home.
    2) OBSERVATION CRITERIA: Patients with severe symptoms should be referred to a healthcare facility for evaluation/observation.
    3) ADMISSION CRITERIA: Patients with severe symptoms (eg, anaphylaxis) should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing a patient with severe symptoms or if the diagnosis is unclear.
    H) PITFALLS
    1) The patient may have been exposed to other more toxic plants.
    I) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis is primarily allergic/hypersensitivity reactions.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

    A) TOXICITY: A toxic dose has not been established. Most exposures where a leaf or two has been ingested do not result in significant symptoms, with nausea and vomiting occurring in a small percentage of cases. Historically, there has been one death of a child following exposure; however, the accuracy of that case has been disputed. ANIMAL DATA: Animals who have ingested over 25 g/kg have had little or no clinical effect.

Summary Of Exposure

    A) BACKGROUND: Poinsettia is a member of the Euphorbiaceae family and a common household plant. In warmer climates it may also be grown outdoors. There are over 300 genera and about 8,000 species found worldwide, except the Antarctica. They may grow as trees or bushes, vines or succulents and often produce latex.
    B) EPIDEMIOLOGY: Exposure can occur. Most exposures are related to the poinsettia plant (Euphorbia pulcherrima). Most cases can be managed at home.
    C) TOXINS: The toxin can differ depending on the species; however, complex diterpene esters (eg, phorbol esters) and mitogenic lectins are often present. The poinsettia plant does NOT contain irritant diterpenes. Some species may contain a milky latex; poinsettia has cross reactivity with latex.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL EVENTS: In most cases, exposure to poinsettia plants will cause little reaction. Irritation is the primary effect, which may manifest itself as mild skin irritation, nausea, vomiting or diarrhea. Vomiting is self-limited and seldom severe enough to require fluid or electrolyte replacement. Ocular exposure may cause irritant keratoconjunctivitis.
    2) ANAPHYLAXIS: Two infants with a history of atopic eczema and latex allergy developed anaphylaxis following inadvertent dermal exposure to the leaves of a poinsettia plant.

Heent

    3.4.1) SUMMARY
    A) Unlike other Euphorbiaceae, poinsettia does NOT appear to cause strong ocular irritation. Animal tests have shown little effect when the latex has been instilled into the eyes (Bruneton, 1999).
    3.4.3) EYES
    A) LACK OF EFFECT/ANIMAL DATA: No damage to the cornea, iris, or conjunctiva was reported in rat eyes instilled with poinsettia latex (Winek et al, 1978).
    3.4.6) THROAT
    A) ORAL MUCOSAL EFFECTS: An 8-month-old child was seen in an emergency department shortly after chewing on a poinsettia leaf. Burns, described as a white area on the buccal mucosa at the corners of the mouth, were observed (Edwards, 1983). The plant was said not to have been sprayed with any chemical; the soil did contain a plant food.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting occasionally occurs after ingestion (Edwards, 1965). Edwards (1983) reported that 2 of 10 patients who called concerning poinsettia ingestion experienced vomiting. Of the 228 cases reported to the National Clearinghouse for Poison Control Centers in 1973, only 14 developed symptoms, which were primarily described as nausea and vomiting (Bruneton, 1999).

Dermatologic

    3.14.1) SUMMARY
    A) There is some controversy as to whether poinsettia is a primary irritant. Effects have been shown in animals, and primary skin irritation is possible in humans. Poinsettia is not as irritating as other members of the Euphorbiaceae family.
    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Allergic contact dermatitis may develop in susceptible individuals exposed to the latex of the plant. Symptoms may include erythema, pruritus, papules or vesicles, and eczema (D'Arcy, 1974; Santucci et al, 1985). Positive patch testing has been done (Santucci et al, 1985).
    b) CASE REPORT: A 66-year-old man developed irritation of the wrist, progressing over the next 3 to 5 days to erythema, edema, papules and vesicles involving the hands, arms, chest, shoulders and thighs. The condition lasted more than 10 days. The man had cut and bundled 1 to 2 meter tall red and white poinsettias in a greenhouse for 1.5 hours. The plants were not treated with herbicides or pesticides. The delayed onset suggested allergic hypersensitivity (D'Arcy, 1974).
    B) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Several references report that the latex from these plants are primary irritants (Rock, 1920; Francis & Southcott, 1967; Morton, 1958; Aplin, 1966), while others have tested poinsettia and found no irritancy (Kinghorn & Evans, 1975) (Mitchell & Rook, 1974).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Studies in rabbits showed a mild irritating action when a poinsettia suspension in water was applied to the skin. When an aqueous suspension was applied to the skin daily, in both occluded and nonoccluded test rabbits, moderate to severe irritation was noted (Winek et al, 1978).
    b) A study of 60 species of the genus Euphorbia conducted on mouse ears to determine irritant activity indicated that the poinsettia contains NO detectable quantities of toxic diterpenes and that based on the model used NO irritant action; 90% of other species were positive (Bruneton, 1999).
    2) PHOTOSENSITIVITY REACTION
    a) When the denuded backs of guinea pigs were treated with a poinsettia suspension, then ultraviolet light, a photosensitivity reaction was seen (Winek et al, 1978).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ANAPHYLAXIS
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: The latex of some of the Euphorbia species are poisonous (Nelson et al, 2007). Poinsettia has cross reactivity with latex (Kimata, 2007).
    b) Two infants with a history of atopic eczema and latex allergy developed anaphylaxis following inadvertent dermal exposure to the leaves of a poinsettia plant. In the first case, a 2-month-old with atopic eczema since birth was noted to develop wheezing after being bottle-fed using a rubber latex nipple and the symptoms improved after feeding. One day, the infant touched the leaves of a poinsettia and shortly afterwards he developed wheezing and became unconscious. He was treated with dexamethasone and recovered. In the second case, an 8-month-old female developed atopic eczema at 2 months and was also bottle fed using a latex rubber nipple. After touching the leaves of a poinsettia, she became unconscious and was successfully treated with dexamethasone. Both infants were positive for a latex allergy; ectopic eczema improved significantly once all latex products were avoided (Kimata, 2007).
    1) A follow-up study of infants admitted to the hospital for allergy screening was conducted. It was found that all infants with atopic eczema and a latex allergy were also allergic to poinsettia leaves while none of the infants with atopic eczema without a latex allergy developed an allergic reaction to poinsettia leaves

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) There are no routine laboratory studies required. Vomiting is NOT expected to be extensive as to warrant monitoring of fluids and/or electrolytes.
    B) DERMAL: Patch testing may help diagnose allergic contact dermatitis in individuals with skin reactions.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) There are no routine laboratory studies required. Vomiting is NOT expected to be extensive as to warrant monitoring of fluids and/or electrolytes.
    4.1.4) OTHER
    A) OTHER
    1) DERMAL
    a) PATCH TESTING may help diagnose allergic contact dermatitis in individuals with skin reactions.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe symptoms (eg, anaphylaxis) should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild symptoms may be monitored at home.
    B) An analysis of the outcomes of 3068 poinsettia exposures documented in the 1992 American Association of Poison Control Centers Toxic Exposure surveillance system reported that about 92% of exposures resulted in nontoxic outcomes. One case had a moderate adverse effect and approximately 96% of exposures were managed at home (Krenzelok EP, Provost FJ & Jacobsen TD et al, 1995).
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing a patient with severe symptoms or if the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with severe symptoms should be referred to a healthcare facility for evaluation/observation.

Monitoring

    A) There are no routine laboratory studies required. Vomiting is NOT expected to be extensive as to warrant monitoring of fluids and/or electrolytes.
    B) DERMAL: Patch testing may help diagnose allergic contact dermatitis in individuals with skin reactions.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Gastrointestinal decontamination is usually not necessary since the plant usually produces no symptoms or mild, limited vomiting.
    6.5.2) PREVENTION OF ABSORPTION
    A) Gastric decontamination is usually not necessary since the plant usually produces no symptoms or mild, limited vomiting.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Patients may only require observation. INGESTION: Inadvertent ingestion of plant material usually produces mild or limited vomiting. Fluid and electrolyte replacement is unlikely to be necessary. DERMAL: Remove contaminated clothing as necessary; clean the exposed area thoroughly with soap and water. If pruritus develops once the skin has been cleansed, oral or IM diphenhydramine may decrease pruritic symptoms. ALLERGIC REACTION: The development of systemic symptoms following poinsettia exposure is rare. Young children with a history of latex allergy may be more at risk to develop symptoms following contact with the plant.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Although not anticipated in most cases, evaluate for life-threatening allergic reactions and anaphylaxis.
    B) MONITORING OF PATIENT
    1) There are no routine laboratory studies required. Vomiting is NOT expected to be extensive as to warrant monitoring of fluids and/or electrolytes.
    2) Following dermal exposure, monitor site for possible adverse skin reaction. Patch testing may help diagnose allergic contact dermatitis in individuals with persistent skin reactions.
    C) IRRITATION SYMPTOM
    1) Decontaminate the skin with soap and water and a soft sponge or washcloth.
    2) 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.
    D) ANAPHYLAXIS
    1) Although rare, individuals, in particular young children, that are allergic to latex may develop a hypersensitivity or an allergic reaction following exposure (ie, touching the leaves) to a poinsettia (Euphorbia pulcherrima) plant. Poinsettia has cross reactivity with latex (Kimata, 2007).
    2) 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.
    3) 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).
    4) 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).
    5) 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).
    6) 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).
    7) 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,TLet al,null).
    8) 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,TLet al,null).
    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).
    9) MONITORING
    a) CARDIAC MONITOR: All complicated cases.
    b) IV ACCESS: Routine in all complicated cases.
    10) 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).
    11) 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).
    12) DYSRHYTHMIAS
    a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TLet al,null). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.
    13) 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,TLet al,null).

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) SUMMARY
    1) No studies have addressed the utilization of enhanced elimination techniques following oral exposure to poinsettia, but are unlikely to be necessary.

Summary

    A) TOXICITY: A toxic dose has not been established. Most exposures where a leaf or two has been ingested do not result in significant symptoms, with nausea and vomiting occurring in a small percentage of cases. Historically, there has been one death of a child following exposure; however, the accuracy of that case has been disputed. ANIMAL DATA: Animals who have ingested over 25 g/kg have had little or no clinical effect.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) There has been one death of a child reported in Hawaii (1918) (Arnold, 1944; Rock, 1920). There is considerable doubt as to the accuracy of the case history of this exposure (Bruneton, 1999).

Maximum Tolerated Exposure

    A) SIGNIFICANCE OF EXPOSURE
    1) Although the common poinsettia is a member of the Euphorbiaceae family, the expected effects from this plant are minimal. There are a few cases of nausea, vomiting, and irritation of the skin, mouth, and throat, but cases develop few if any symptoms (Dominquez et al, 1967) (der Mardersoian & Roja, 1979) (Runyon, 1980; Stone & Collins, 1971) (Winek et al, 1978).
    2) A study done at the New Jersey Poison Information Center reported that 91% of cases in a 3-year period developed no symptoms, 5% had minor symptoms, and 4% had symptoms which may or may not have been related to the plant. Nausea and vomiting occurred in 0.02% of cases, rash in 0.0028%, and sneezing in 0.0028% (Klug et al, 1990).
    3) An analysis of the outcomes of 3068 poinsettia exposures documented in the 1992 American Association of Poison Control Centers Toxic Exposure surveillance system reported that about 92% of exposures resulted in nontoxic outcomes. One case had a moderate adverse effect and approximately 96% of exposures were managed at home (Krenzelok EP, Provost FJ & Jacobsen TD et al, 1995).
    B) CASE REPORTS
    1) Two infants with a history of atopic eczema and latex allergy developed anaphylaxis following inadvertent dermal exposure to the leaves of a poinsettia plant. In the first case, a 2-month-old with atopic eczema since birth was noted to develop wheezing after being bottle-fed using a rubber latex nipple and the symptoms improved after feeding. One day, the infant touched the leaves of a poinsettia and shortly afterwards he developed wheezing and became unconscious. He was treated with dexamethasone and recovered. In the second case, an 8-month-old female developed atopic eczema at 2 months and was also bottle fed using a latex rubber nipple. After touching the leaves of a poinsettia, she became unconscious and was successfully treated with dexamethasone. Both infants were positive for a latex allergy; ectopic eczema improved significantly once all latex products were avoided (Kimata, 2007).
    a) A follow-up study of infants admitted to the hospital for allergy screening was conducted. It was found that all infants with atopic eczema and a latex allergy were also allergic to poinsettia leaves while none of the infants with atopic eczema without a latex allergy developed an allergic reaction to poinsettia leaves
    C) ANIMAL DATA
    1) Winek et al (1978) evaluated the poinsettia in rats, and concluded it was nontoxic based on their experiments. They extrapolated their data and reported that a 50 pound child would have to ingest almost 1.25 pounds (500 to 600) of leaves to surpass experimental doses given to animals.
    2) Rats given doses as high as 50 g/kg of a homogenate of leaves, bracts, or flowers of poinsettia experienced no mortality (Stone & Collins, 1971).
    3) Runyon (1980) gave rats 14 g/kg and found no gastrointestinal toxicity. One group did develop increase thyroid weight, but the relationship to the poinsettia ingestion was unknown.
    4) Rats given up to 25 grams/kilogram of body weight did not develop overt signs of toxicity, and none died. Necropsies of animals given an exaggerated dose (8 to 8.8 grams per day) for 5 days did not shown any gross pathology or histology (Winek et al, 1978).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (ORAL)RAT:
    a) >25 g/kg (RTECS, 2001)

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) Photosensitization, skin irritation, and diarrhea were mentioned as symptoms reported by Schmultz (1968).
    11.1.3) CANINE/DOG
    A) In a survey of calls to the Hennepin Regional Poison Center in 1985 to 1988, 3 of 15 dogs who ingested poinsettia experienced vomiting and diarrhea (one dog had eaten an entire plant) (Hornfeldt, 1989).
    11.1.6) FELINE/CAT
    A) In a survey of calls to the Hennepin Regional Poison Center in 1985 to 1988, only 1 of the 51 cats that ingested poinsettia showed signs of toxicosis (salivation); follow-up was not available on all animals (Hornfeldt, 1989).
    11.1.7) ICHTHYOID/FISH
    A) Poinsettia is said to be a fish poison in the South China area (Watt & Breyer-Brandwijk, 1962).

Continuing Care

    11.4.3) TREATMENT
    11.4.3.5) SUPPORTIVE CARE
    A) Based on a chart review of domestic animal (cats and dogs) exposures to poinsettia, it appears to cause only gastrointestinal irritation (i.e., vomiting, diarrhea)in some cases, and aggressive treatment is probably NOT necessary (Hornfeldt, 1989).

General Bibliography

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