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PLANTS-LOBELINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) There are over 200 species of lobelia. They are found in North and South America, India, Europe, the Philippines, and Puerto Rico. These plants contain over 14 pyridine alkaloids and lobeline is the major alkaloid.

Specific Substances

    A) Lobelia berlandieri (Indian Pink)
    1) Synonyms: Indian Pink
    2) Mordilla (Mexico)
    Lobelia cardinalis (Cardinal Flower)
    1) Synonyms: Cardinal Flower
    2) Hog physic (rustic name)
    3) Scarlet lobelia
    4) Red lobelia
    5) Red-birds
    6) Indian pink
    Lobelia inflata (Indian Tobacco)
    1) Indian tobacco
    2) Indian weed
    3) asthma weed
    4) emetic herb
    5) eyebright
    6) vomitwort
    7) Tobacco indio (Spanish)
    8) tobacco indiano (Italian)
    9) lobelia
    10) pukeweed
    11) wild tobacco
    12) lobenlien kraut (German)
    13) lobeline enflee (French)
    14) Indianischer taka (German)
    15) emetic weed
    16) bladder podded lobelia
    17) bladder pod
    18) herba lobeliae (Latin)
    19) gagroot
    Lobelia laxiflora
    1) chilpantlazolli (Mexico)
    2) toxcuitlapulxochitl (Mexico)
    3) pipiloxochitl (Mexico)
    4) jarritos (Spanish)
    5) chilpanxochitl (Mexico)
    6) arretitos (Spanish)
    7) aretitos (Spanish)
    8) chilpanzochitl (Mexico)
    Lobelia nicotianaefolia
    1) adlabong (Philippines)
    2) lobelic (German)
    3) nal (Hindi, Bengali)
    4) nala (Sanscrit)
    5) nalasal (Hindi)
    6) post nila (Unani)
    7) tee (Nepalese)
    Lobelia portoricensis Urban
    1) tupa (Puerto Rico)
    2) Tupa portoriensis Vatke
    3) tupa assurgens
    Lobelia siphilitica
    1) (Great Lobelia)
    2) blue cardinal flower
    Lobelia tupa (Chile)
    1) tupa
    2) tobacco del diablo
    Lobeline
    1) 2-(6-(2-hydroxy-2-phenylethyl)-1-methyl-2
    2) -piperindinyl)-1-phenylthanone
    3) 2-(6-(beta-hydroxy-phenyethyl)-1-methyl-2
    4) -piperidinyl)-acetophenone
    5) Alpha-lobeline
    6) Lobelanidine
    7) Lobelanine
    8) Lobelia
    9) Lobelidine

Available Forms Sources

    A) FORMS
    1) Lobelia species: Although various lobeline containing plants are available as houseplants, poisoning is unusual unless the plants are used as an ingredient in an herbal preparation, or for abuse. The dried plant material has little activity (Lampe & McCann, 1985). Most human ingestions are the result of using Lobelia inflata as a medicinal agent. Accidental human ingestions are rare.
    2) The dried leaves and tops of L. inflata are used to make the "drug" lobelia (Tyler, 1993).
    3) Lobeline sulfate in a 2 mg tablet was available for use as an adjunct for smoking cessation. It was shown to be no more effective than placebo (Stead & Hughes, 2000) (Rapp & Olen, 1955). It has been removed from the market in the US. Brand names include: Bantron, Toban o-t-c.
    4) Four gram pellets of Lobelia cardinalis, Lobelia inflata, and Lobelia syphilitica are available (Redbook, 1996).
    B) USES
    1) SUMMARY: Lobeline was used medicinally as a spasmolytic, antiasthmatic, and emetic for years. Homeopathic physicians still may use the product, although because of its margin of safety, it is seldom if ever used by contemporary physicians.
    2) PSYCHOLOGICAL USES: Brewed as a tea to promote feelings of happiness, mental clarity and well being (Duke, 1985). Leaves and seed capsules have been chewed and produce giddiness, headaches, and generalized tremors (Spoerke, 1980).
    3) TOBACCO SUBSTITUTE: Smoked by individuals as a substitute for tobacco, in order to help stop smoking (Duke, 1985). It is not effective for this use (Jellin et al, 2000; Tyler, 1993).
    4) VARIOUS USES: Steeped as a tea, mixed as a poultice, and prepared as capsules to treat an exhaustive list of medical complaints (Duke, 1985). Seldom used today due to small therapeutic index (Jellin et al, 2000).
    5) SEXUALLY TRANSMITTED DISEASES: A decoction of the roots of Lobelia syphilitica was used by Native American Indians to treat venereal diseases (Heywood, 1993).
    6) Toothache: Juice pressed from the leaves of Lobelia tupa are used to treat toothache (Emboden, 1980).
    7) ANTIINFLAMMATORY: Piperidine alkaloids found in ethanol extracts of Lobelia laxiflora (L.) were successful in reducing inflammation in the carrageenan and cobra venom induced paw edema tests in mice. Inflammation reduction was found at 100 milligrams/kilogram. These agents were found to inhibit the complement system with a primary effect on classical complement pathways (Philipov et al, 1998).
    8) DRUG ADDICTION: There has been some reports of using lobeline for the treatment of psychostimulant abuse and addiction (Dwoskin & Crooks, 2002; Miller et al, 2007).
    9) Used externally with soothing barks and roots for some conditions (Meyer, 1981).
    10) Used by Native American Indians as a rapid, severe emetic and purgative; if not expelled, it could cause death (Lewis & Elvin-Lewis, 1977).
    11) Macerated roots of Lobelia nicotianaefolia have been topically applied in India to relieve the pain of scorpion stings (Lewis & Elvin-Lewis, 1977).
    12) It is considered an aphrodisiac (Lewis & Elvin-Lewis, 1977).
    13) Beta-amyrin palmitate, isolated from Lobelia inflata L. demonstrates antidepressant activity in mice (Sunarnas, 1992).
    14) Alpha-lobeline was investigated for use as a respiratory stimulant. The stimulatory effect was unreliable, and toxicity (vomiting, sneezing and respiratory disturbances) occurred (Norris & Weiss, 1927). It may still be used as a respiratory stimulant in horses where results have been reproducible (Marlin et al, 2000).
    15) Amphetamine Abuse: In mouse studies, it was found that lobeline redistributes the dopamine pools within the presynaptic terminal, therefore decreasing the amounts available for release by amphetamine. It was therefore suggested that lobeline might be an agent for treatment of amphetamine and other psychostimulant abuse (Miller et al, 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Lobeline, an alkaloid constituent of Lobelia inflata, has been used as a natural product in the treatment of asthma, bronchitis, and pneumonia. It has also been used as an aid in tobacco smoking cessation (its utility remains unproven) to help with withdrawal symptoms, and is commercially available in tablets and lozenges. It has recently been studied in animals as a potential aid in drug addiction and neurotoxicity by inhibiting the psychostimulant effects of amphetamines. Its earliest use was as a short-acting respiratory stimulant. Various lobeline containing species are also used as houseplants.
    B) PHARMACOLOGY: Lobelia is a primary stimulant and secondary depressant to autonomic ganglia. It acts as an agonist and antagonist at different nicotinic receptor subtypes. It also inhibits dopamine uptake and promotes dopamine release from presynaptic storage vesicles.
    C) TOXICOLOGY: Excessive nicotinic stimulation can cause vomiting, hypertension and tachycardia.
    D) EPIDEMIOLOGY: Exposure is not common and significant toxicity is very rare.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: The most common prominent symptoms include: nausea, vomiting, bradycardia, dizziness, tachycardia, a transient increase in blood pressure and respiratory rate, tremors and paresis. INFREQUENT: Hypothermia has been reported in one case. Throat irritation has also occurred following the use of tablets and pastilles that contain lobeline to relieve nicotine withdrawal. Old literature suggests that seizures and paralysis can occur, but this has not been described in recent literature. Exposure to the various lobeline plant species can produce dermatitis and mucous membrane irritation. Eye irritation has been reported following contact with the sap.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: Limited human data, severe toxicity has not been reported recently. In animal studies, it has many nicotine-like effects including tachycardia, hypertension, hypotension and bradycardia (usually transient).
    2) TOXICITY: Most human poisonings are the result of using Lobelia species as a medicinal agent or tobacco substitute NOT as a houseplant. Similar clinical events as reported with adverse effects would be anticipated following acute exposure. Severe poisoning has not been well documented but might include coma, weakness and paralysis that may lead to death secondary to respiratory paralysis.
    0.2.4) HEENT
    A) Sap from lobelia species may be irritating to the eyes. Dried foliage may irritate the nose like snuff. A tickling or choking sensation developed after intravenous administration.
    0.2.20) REPRODUCTIVE
    A) Likely unsafe, due at least in part, to emetic properties. At the time of this review, no reliable information was available to assess the potential effects of exposure to this agent during pregnancy or lactation in humans (Jellin et al, 2000).

Laboratory Monitoring

    A) Monitor vital signs.
    B) Monitor electrolytes and fluid status in patients that develop significant vomiting.
    C) Although laboratory measures exist to isolate these alkaloids, no therapeutic/toxic levels have been published.
    D) Monitor electrocardiogram, respiratory status, and neurologic status.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is primarily supportive and symptomatic. Monitor vital signs. Bradycardia and/or tachycardia may occur along with transient increases in blood pressure. Vomiting is common, administer intravenous fluids and antiemetics as needed. Persistent vital sign abnormalities, altered mental status, and seizures indicate a more severe poisoning.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is primarily symptomatic and supportive. Monitor vital signs. Atropine can be given for bradycardia if there is associated hypotension. Hypotension should be treated with intravenous fluids and then a vasopressor as needed. Hypertension is likely to be transient and does NOT usually require treatment. Consider therapy only if prolonged severe hypertension with end organ effects develops. Treat seizures with benzodiazepines.
    C) DECONTAMINATION
    1) PREHOSPITAL: GI decontamination is unlikely to be of benefit as spontaneous vomiting can occur following exposure and toxicity is limited.
    2) HOSPITAL: GI decontamination is generally not necessary as toxicity is limited. Consider activated charcoal only after exceedingly large ingestions if the patient is alert, not vomiting and can protect the airway.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary following a minor exposure. Patients with an altered mental status (ie, seizures) or significant respiratory depression may need orotracheal intubation and mechanical respiratory support, but this is very rare.
    E) ANTIDOTE
    1) No specific antidote exists for lobeline.
    F) ENHANCED ELIMINATION
    1) Efficacy of enhanced elimination techniques is unknown, but life threatening toxicity is rare.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: An asymptomatic child or a child with mild vomiting following a "taste" ingestion of plant material or who ingested one commercially prepared tablet can be monitored at home with adult supervision. An asymptomatic adult or an adult with mild vomiting that ingests more than one commercially prepared tablet or an extra dose can be monitored at home.
    2) OBSERVATION CRITERIA: Patients with CNS symptoms, persistent vomiting, those with deliberate abuse or self harm ingestions should be referred to a healthcare facility. Patients should be observed until symptoms of intoxication resolve.
    3) ADMISSION CRITERIA: Patients with persistent vital sign abnormalities, seizures, altered mental status, or respiratory insufficiency should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing severe poisonings or following a significant lobeline plant ingestion by a child.
    0.4.4) EYE EXPOSURE
    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).
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    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).

Range Of Toxicity

    A) TOXICITY: A toxic dose has not been established; poisoning is uncommon. Lobelia is less potent than nicotine but, otherwise similar in action.

Clinical Effects

Summary Of Exposure

    A) USES: Lobeline, an alkaloid constituent of Lobelia inflata, has been used as a natural product in the treatment of asthma, bronchitis, and pneumonia. It has also been used as an aid in tobacco smoking cessation (its utility remains unproven) to help with withdrawal symptoms, and is commercially available in tablets and lozenges. It has recently been studied in animals as a potential aid in drug addiction and neurotoxicity by inhibiting the psychostimulant effects of amphetamines. Its earliest use was as a short-acting respiratory stimulant. Various lobeline containing species are also used as houseplants.
    B) PHARMACOLOGY: Lobelia is a primary stimulant and secondary depressant to autonomic ganglia. It acts as an agonist and antagonist at different nicotinic receptor subtypes. It also inhibits dopamine uptake and promotes dopamine release from presynaptic storage vesicles.
    C) TOXICOLOGY: Excessive nicotinic stimulation can cause vomiting, hypertension and tachycardia.
    D) EPIDEMIOLOGY: Exposure is not common and significant toxicity is very rare.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: The most common prominent symptoms include: nausea, vomiting, bradycardia, dizziness, tachycardia, a transient increase in blood pressure and respiratory rate, tremors and paresis. INFREQUENT: Hypothermia has been reported in one case. Throat irritation has also occurred following the use of tablets and pastilles that contain lobeline to relieve nicotine withdrawal. Old literature suggests that seizures and paralysis can occur, but this has not been described in recent literature. Exposure to the various lobeline plant species can produce dermatitis and mucous membrane irritation. Eye irritation has been reported following contact with the sap.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: Limited human data, severe toxicity has not been reported recently. In animal studies, it has many nicotine-like effects including tachycardia, hypertension, hypotension and bradycardia (usually transient).
    2) TOXICITY: Most human poisonings are the result of using Lobelia species as a medicinal agent or tobacco substitute NOT as a houseplant. Similar clinical events as reported with adverse effects would be anticipated following acute exposure. Severe poisoning has not been well documented but might include coma, weakness and paralysis that may lead to death secondary to respiratory paralysis.

Vital Signs

    3.3.3) TEMPERATURE
    A) HYPOTHERMIA was reported in a human case (Kingsbury, 1964; Wright & Littauer, 1937).

Heent

    3.4.1) SUMMARY
    A) Sap from lobelia species may be irritating to the eyes. Dried foliage may irritate the nose like snuff. A tickling or choking sensation developed after intravenous administration.
    3.4.3) EYES
    A) BLINDNESS: The white milky "sap" of Lobelia philippinensis is said to be capable of producing blindness (Altschul, 1973), but case histories are lacking.
    3.4.5) NOSE
    A) NASAL DISCHARGE has been reported in ANIMAL ingestions (Kingsbury, 1964).
    B) IRRITATION: The dried foliage of Lobelia nicotinaefolia irritates the nose, like snuff (Behl et al, 1966).
    3.4.6) THROAT
    A) Tickling, a choking sensation, burning, pain, pressure, and a feeling of smoke in the throat was reported in subjects given less than 2 mg of lobeline intravenously. Symptoms were felt within seconds of administration (Raj et al, 1995).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH THERAPEUTIC USE
    a) Hypotension may occur in overdose (Tyler, 1993).
    B) HYPERTENSIVE EPISODE
    1) WITH THERAPEUTIC USE
    a) Hypertension which is transient, may occur soon after exposure.
    C) TACHYARRHYTHMIA
    1) WITH THERAPEUTIC USE
    a) Rapid, feeble pulse was reported (Kingsbury, 1964).
    b) Tachycardia may occur as a side effect of therapeutic use (Cada, 1997).
    D) BRADYCARDIA
    1) WITH THERAPEUTIC USE
    a) Reflex bradycardia was infrequent in subjects receiving intravenous lobeline (Raj et al, 1995).
    E) ATRIOVENTRICULAR BLOCK
    1) WITH THERAPEUTIC USE
    a) Extrasystoles, A-V block, and partial bundle branch block may be seen on electrocardiogram (Cada, 1997; Whitehead & Elliott, 1927).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) HYPOVENTILATION
    1) WITH THERAPEUTIC USE
    a) Small doses produce a transient (30 minute) increase in ventilation. Large doses significantly depress respiration and death has occurred from paralysis of the respiratory center. Cough, a feeling of pressure, pain and burning have also been reported.
    b) Lobeline poisoning is uncommon. In the event of severe poisoning, symptoms mignt include coma, weakness and paralysis that may lead to death secondary to respiratory paralysis (Nelson et al, 2007).
    c) Low doses dilate the bronchioles and increase respirations. Large doses significantly depress respirations. Death has occurred due to paralysis of respiratory centers (Cada, 1997).
    B) COUGH
    1) WITH THERAPEUTIC USE
    a) Cough has developed within seconds of the administration of intravenous lobeline (Raj et al, 1995).
    C) RESPIRATORY FAILURE
    1) WITH THERAPEUTIC USE
    a) Pressure in the upper chest, pain and burning, a feeling of suffocation and the feeling of smoke fumes in the chest occurred in subjects given less than 2 mg of intravenous lobeline (Raj et al, 1995).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH THERAPEUTIC USE
    a) Seizures have been reported (Norris & Weiss, 1927).
    B) DIZZINESS
    1) WITH THERAPEUTIC USE
    a) Dizziness has been reported after therapeutic use of lobeline sulfate (Cada, 1997).
    C) COMA
    1) WITH THERAPEUTIC USE
    a) Lobeline poisoning is uncommon. In the event of severe poisoning, symptoms might include coma, weakness and paralysis that may lead to death secondary to respiratory paralysis (Nelson et al, 2007).
    b) Coma has been reported (Kingsbury, 1964).
    D) PARALYSIS
    1) WITH THERAPEUTIC USE
    a) Medullary paralysis has been reported (Kingsbury, 1964).
    E) EUPHORIA
    1) WITH THERAPEUTIC USE
    a) Euphoria has been reported.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANIMAL STUDIES
    a) When tested in mice, lobeline at maximal effective dose, dependently produced motor impairment and decreased locomotor activity (Damaj et al, 1997).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH THERAPEUTIC USE
    a) Vomiting and nausea, belching, severe heartburn, and epigastric pain are frequent symptoms (Cada, 1997; Norris & Weiss, 1927).
    b) STINGING or a burning sensation in the mouth which may be delayed, has also been reported because of the acrid taste of the plant material (Wren, 1968; Duke, 1985).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SALIVA INCREASED
    a) Salivation has been reported in animal cases (Kingsbury, 1964).
    2) STOMATITIS ULCERATIVE
    a) Mouth ulcers have been reported in animal cases (Kingsbury, 1964).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) POISONING
    1) WITH THERAPEUTIC USE
    a) Lobeline is absorbed through the skin and can produce significant toxicity (Osol & Farrar, 1955).
    b) CASE REPORT: Death occurred in an 8-year-old who had the juice of leaves applied to his head (Osol & Farrar, 1955).
    B) DERMATITIS
    1) Various species of Lobelia have been known to cause dermatitis. This is true of the stems, leaves, and fruits (Mitchell & Rook, 1979; Woods, 1962).
    a) Lobelia inflata: The application of this plant to the skin may cause irritation (Piffard, 1881).
    b) Lobelia nicotinaefolia: This species has a milky, white latex that may cause dermatitis (Kapoor, 1990) (Altschul, 1973).
    c) Lobelia excelsa: The milky juice of this plant may produce an irritant dermatitis (Behl et al, 1966).
    C) EXCESSIVE SWEATING
    1) WITH THERAPEUTIC USE
    a) Sweating and cold sweats have been reported in humans (Kingsbury, 1964; Wright & Littauer, 1937).

Reproductive

    3.20.1) SUMMARY
    A) Likely unsafe, due at least in part, to emetic properties. At the time of this review, no reliable information was available to assess the potential effects of exposure to this agent during pregnancy or lactation in humans (Jellin et al, 2000).
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, little data were available to assess the potential teratogenic effects of exposure to this agent.

Genotoxicity

    A) Lobeline and ethanol are not clastogenic by themselves but when tested together in a mutagen-sensitivity assay of lymphoblastoid cells, genetic damage resulted (Brown et al, 1992).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs.
    B) Monitor electrolytes and fluid status in patients that develop significant vomiting.
    C) Although laboratory measures exist to isolate these alkaloids, no therapeutic/toxic levels have been published.
    D) Monitor electrocardiogram, respiratory status, and neurologic status.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Although laboratory measures exist to isolate the various alkaloids, no therapeutic/toxic levels have yet been published.
    2) Lobelia has not been shown to interact with any specific laboratory tests (Jellin et al, 2000).

Treatment

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 persistent vital sign abnormalities, seizures, altered mental status, or respiratory insufficiency should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) An asymptomatic child or a child with mild vomiting following a "taste" ingestion of plant material or who ingested one commercially prepared tablet can be monitored at home with adult supervision. An asymptomatic adult or an adult with mild vomiting that ingests more than one commercially prepared tablet or an extra dose can be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing severe poisonings or following a significant lobeline plant ingestion by a child.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with CNS symptoms, persistent vomiting, those with deliberate abuse or self harm ingestions should be referred to a healthcare facility. Patients should be observed until symptoms of intoxication resolve.

Monitoring

    A) Monitor vital signs.
    B) Monitor electrolytes and fluid status in patients that develop significant vomiting.
    C) Although laboratory measures exist to isolate these alkaloids, no therapeutic/toxic levels have been published.
    D) Monitor electrocardiogram, respiratory status, and neurologic status.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GI decontamination is unlikely to be of benefit as spontaneous vomiting can occur following exposure and toxicity is limited.
    6.5.2) PREVENTION OF ABSORPTION
    A) GI decontamination is generally not necessary as toxicity is limited. Consider activated charcoal only after exceedingly large ingestions if the patient is alert, not vomiting and can protect the airway.
    B) CHARCOAL ADMINISTRATION
    1) 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.
    C) CHARCOAL DOSE
    1) 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).
    a) 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).
    2) ADVERSE EFFECTS/CONTRAINDICATIONS
    a) 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.
    b) 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) SUPPORT
    1) Lobeline poisoning is uncommon. Treatment is symptomatic and supportive.
    2) Monitor vital signs and CNS function. Alterations in heart rate (bradycardia or tachycardia) and blood pressure (hypo- or hypertension) may develop; effects are likely to be transient and may not require intervention.
    3) Vomiting is common, administer intravenous fluids and antiemetics as necessary.
    B) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    C) HYPERTENSIVE EPISODE
    1) Hypertension is usually transient and does NOT require treatment. Consider therapy only if prolonged severe hypertension with end organ effects develops.
    2) Monitor vital signs regularly. For mild/moderate hypertension without evidence of end organ damage, pharmacologic intervention is generally not necessary. Sedative agents such as benzodiazepines may be helpful in treating hypertension and tachycardia in agitated patients, especially if a sympathomimetic agent is involved in the poisoning.
    3) For hypertensive emergencies (severe hypertension with evidence of end organ injury (CNS, cardiac, renal), or emergent need to lower mean arterial pressure 20% to 25% within one hour), sodium nitroprusside is preferred. Nitroglycerin and phentolamine are possible alternatives.
    4) SODIUM NITROPRUSSIDE/INDICATIONS
    a) Useful for emergent treatment of severe hypertension secondary to poisonings. Sodium nitroprusside has a rapid onset of action, a short duration of action and a half-life of about 2 minutes (Prod Info NITROPRESS(R) injection for IV infusion, 2007) that can allow accurate titration of blood pressure, as the hypertensive effects of drug overdoses are often short lived.
    5) SODIUM NITROPRUSSIDE/DOSE
    a) ADULT: Begin intravenous infusion at 0.1 microgram/kilogram/minute and titrate to desired effect; up to 10 micrograms/kilogram/minute may be required (American Heart Association, 2005). Frequent hemodynamic monitoring and administration by an infusion pump that ensures a precise flow rate is mandatory (Prod Info NITROPRESS(R) injection for IV infusion, 2007). PEDIATRIC: Initial: 0.5 to 1 microgram/kilogram/minute; titrate to effect up to 8 micrograms/kilogram/minute (Kleinman et al, 2010).
    6) SODIUM NITROPRUSSIDE/SOLUTION PREPARATION
    a) The reconstituted 50 mg solution must be further diluted in 250 to 1000 mL D5W to desired concentration (recommended 50 to 200 mcg/mL) (Prod Info NITROPRESS(R) injection, 2004). Prepare fresh every 24 hours; wrap in aluminum foil. Discard discolored solution (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    7) SODIUM NITROPRUSSIDE/MAJOR ADVERSE REACTIONS
    a) Severe hypotension; headaches, nausea, vomiting, abdominal cramps; thiocyanate or cyanide toxicity (generally from prolonged, high dose infusion); methemoglobinemia; lactic acidosis; chest pain or dysrhythmias (high doses) (Prod Info NITROPRESS(R) injection for IV infusion, 2007). The addition of 1 gram of sodium thiosulfate to each 100 milligrams of sodium nitroprusside for infusion may help to prevent cyanide toxicity in patients receiving prolonged or high dose infusions (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    8) SODIUM NITROPRUSSIDE/MONITORING PARAMETERS
    a) Monitor blood pressure every 30 to 60 seconds at onset of infusion; once stabilized, monitor every 5 minutes. Continuous blood pressure monitoring with an intra-arterial catheter is advised (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    D) BRADYCARDIA
    1) Bradycardia rarely requires treatment. If severe bradycardia results in hypotension administer atropine.
    2) ATROPINE/DOSE
    a) ADULT BRADYCARDIA: BOLUS: Give 0.5 milligram IV, repeat every 3 to 5 minutes, if bradycardia persists. Maximum: 3 milligrams (0.04 milligram/kilogram) intravenously is a fully vagolytic dose in most adults. Doses less than 0.5 milligram may cause paradoxical bradycardia in adults (Neumar et al, 2010).
    b) PEDIATRIC DOSE: As premedication for emergency intubation in specific situations (eg, giving succinylchoine to facilitate intubation), give 0.02 milligram/kilogram intravenously or intraosseously (0.04 to 0.06 mg/kg via endotracheal tube followed by several positive pressure breaths) repeat once, if needed (de Caen et al, 2015; Kleinman et al, 2010). MAXIMUM SINGLE DOSE: Children: 0.5 milligram; adolescent: 1 mg.
    1) There is no minimum dose (de Caen et al, 2015).
    2) MAXIMUM TOTAL DOSE: Children: 1 milligram; adolescents: 2 milligrams (Kleinman et al, 2010).
    E) TACHYARRHYTHMIA
    1) Tachycardia rarely requires treatment. If severe tachycardia results in hypotension or myocardial ischemia, consider the use of beta blocking agents. A short acting cardioselective agent such as esmolol is preferred.
    2) TACHYCARDIA SUMMARY
    a) Evaluate patient to be sure that tachycardia is not a physiologic response to dehydration, anemia, hypotension, fever, sepsis, or hypoxia. Sinus tachycardia does not generally require treatment unless hemodynamic compromise develops.
    b) If therapy is required, a short acting, cardioselective agent such as esmolol is generally preferred (Prod Info BREVIBLOC(TM) intravenous injection, 2012).
    c) ESMOLOL/ADULT LOADING DOSE
    1) Infuse 500 micrograms/kilogram (0.5 mg/kg) IV over 1 minute (Neumar et al, 2010).
    d) ESMOLOL/ADULT MAINTENANCE DOSE
    1) Follow loading dose with infusion of 50 mcg/kg per minute (0.05 mg/kg per minute) (Neumar et al, 2010).
    2) EVALUATION OF RESPONSE: If response is inadequate, infuse second loading bolus of 0.5 mg/kg over 1 minute and increase the maintenance infusion to 100 mcg/kg (0.1 mg/kg) per minute. Reevaluate therapeutic effect, increase in the same manner if required to a maximum infusion rate of 300 mcg/kg (0.3 mg/kg) per minute (Neumar et al, 2010).
    3) The manufacturer recommends that a maximum of 3 loading doses be used (Prod Info BREVIBLOC(TM) intravenous injection, 2012).
    4) END POINT OF THERAPY: As the desired heart rate or blood pressure is approached, omit loading dose and adjust maintenance infusion as required (Prod Info BREVIBLOC(TM) intravenous injection, 2012).
    e) CAUTION
    1) Esmolol is a short acting beta-adrenergic blocking agent with negative inotropic effects. Esmolol should be avoided in patients with asthma, obstructive airway disease, decompensated heart failure and pre-excited atrial fibrillation (wide complex irregular tachycardia) or atrial flutter (Neumar et al, 2010).
    F) SEIZURE
    1) Seizures may develop following a significant exposure. There are minimal reports of seizure activity with lobeline.
    2) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    3) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    4) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    5) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    6) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    7) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

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).
    6.8.2) TREATMENT
    A) SUPPORT
    1) No specific treatment is available.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    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).
    6.9.2) TREATMENT
    A) SUPPORT
    1) No specific treatment is available. Treat persistent symptoms symptomatically.
    2) There has been one report of dermal exposure resulting in systemic symptoms. For treatment, refer to the oral exposure treatment section.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) Efficacy of enhanced elimination techniques is unknown, but life threatening toxicity is rare.

Range Of Toxicity

Summary

    A) TOXICITY: A toxic dose has not been established; poisoning is uncommon. Lobelia is less potent than nicotine but, otherwise similar in action.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) As an adjunct for smoking cessation, doses of 8 milligrams of lobeline sulfate have been used. The usual recommended dose is 6 milligrams/day (Cada, 1997).
    2) Lobeline was used medicinally as a spasmolytic, antiasthmatic, and emetic for years. Homeopathic physicians still may use the product, however; due to its limited margin of safety, it is seldom if ever used by contemporary physicians. A common dose as an expectorant is 100 milligrams/day, but has ranged as high as 375 mg once a day to 820 milligrams three times a day. An extract is also available. The dose is 2 to 5 drops three to four times a day (Jellin et al, 2000).
    3) The leaves and above ground parts of L. nicotianaefolia are used in doses of 50 to 125 milligrams in adults (Kapoor, 1990).
    B) ROUTE OF ADMINISTRATION
    1) SUBCUTANEOUS - Recommended doses of Lobeline hydrochloride: 10 milligrams single dose, daily dose 20 milligrams, daily maximum dose of 50 milligrams (Osol & Farrar, 1955).
    2) INTRAVENOUS - single dose 3 milligrams, daily dose 6 to 10 milligrams, daily maximum dose 20 milligrams (Osol & Farrar, 1955).
    3) Usual doses of lobeline when used as herbal preparation may be as high as 100 milligrams (Spoerke, 1980).

Minimum Lethal Exposure

    A) CASE REPORTS
    1) Death was caused in an 8-year-old who had the juice of leaves applied to his head (Osol & Farrar, 1955).
    2) Fifty milligrams of the dried herb or 1 mL of the tincture have produced "alarming" symptoms (Spoerke, 1980).

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Lobelia is absorbed orally, by inhalation, and cutaneously (Osol & Farrar, 1955).
    B) Normal herbalist doses may produce bronchiole dilatation, but larger doses induce respiratory depression (Tyler, 1993).

Toxicologic Mechanism

    A) Lobelia is a primary stimulant and secondary depressant to autonomic ganglia. Lobelia has a stimulant effect on medullary centers, especially the emetic center and the respiratory center (Tyler, 1993) Gilman et al, 1990; (Marshall, 1928).
    B) In large doses, it has a curare-like paralyzing action. Lobelia has an action of 1/5 to 1/20 that of nicotine on the autonomic ganglia (Osol & Farrar, 1955).
    C) Lobeline activates vagal and spinal afferent nerves (Gilman et al, 1990).
    D) Lobelia is absorbed orally, by inhalation, and cutaneously (Osol & Farrar, 1955).
    E) Several low molecular weight cytostatic compounds have been isolated from Lobelia chinensis and are being investigated for anti-neoplastic properties (Santosa et al, 1986).
    F) Lobeline stimulates nicotinic receptors producing vasoconstriction and increased blood pressure (Lewis & Elvin-Lewis, 1977).
    G) BETA-AMYRIN PALMITATE (from Lobelia inflata L.) has demonstrated antidepressant activity in mice. The mechanism is speculated to be due to increased release of newly synthesized norepinephrine stores in the CNS (Sabarnes et al, 1993; Sabarnes et al, 1992).
    H) PORTORICIN is isolated from Lobelia portoricensis. It has been shown to stimulate the respiratory centers in animal models. It also blocks acetylcholine action on guinea pig and rabbit intestine at 1/200 the potency of lobeline (Melendez et al, 1967).

Physicochemical

Physical Characteristics

    A) Dried lobelia has an irritating odor.
    B) Lobelia first has an acrid, bitter taste which is followed by numbness.

Molecular Weight

    A) Not available

Animal Toxicology

Clinical Effects

    11.1.4) CAPRINE/GOAT
    A) Horses given rapid intravenous doses of 0.15, 0.2, 0.25, or 0.3 milligrams/kilogram of lobeline developed hyperpnea and tremor. Apnea of about 40 seconds was common after the lobeline-stimulated hyperpnea. Arterial pO2 (PaO2) was increased from a resting level of 104 mmHg to 146 mmHg. Peak flow rate, peak expired flow rate, and minute ventilation were also increased. The results of lobeline respiratory effects were highly reproducible (Marlin et al, 2000).
    11.1.6) FELINE/CAT
    A) When cats were injected subcutaneously with 0.5 to 5 milligrams of lobeline, violent vomiting occurred. Twitching of the ears appeared to be a regular symptom that occurred about 3 to 4 minutes after the injection.
    1) The twitching did not last long, usually less than a minute (Edmunds, 1904).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) CAT
    1) CASE REPORTS
    a) Five milligrams given intravenously to a cat caused struggling, vomiting, and dyspnea.
    b) One hundred milligrams caused death in forty minutes by respiratory paralysis (Edmunds, 1904; Dreser, 1889).
    c) A dose of 75 milligrams given subcutaneously to a 1250 gram cat produced violent panting in 20 seconds, extreme anxiety, and ear twitching for about a minute; this was followed by twitching and trembling that led to a violent seizure in six minutes.
    1) The seizure lasted about 20 seconds. Trembling continued between seizure attacks and the animal died 15 minutes post injection (Edmunds, 1904).
    d) One half to five milligrams of lobeline given to cats subcutaneously caused immediate violent vomiting from three to three and one half minutes after injection. This vomiting subsided until about 45 minutes post injection, when it occurred again (Edmunds, 1904).
    B) RABBIT
    1) Rabbits given 5 to 7 milligrams subcutaneously had moderate effects, producing mild slowing of the respiratory rate and difficulty in controlling its limbs (Edmunds, 1904).
    C) DOG
    1) One milligram given subcutaneously produced accelerated respirations, three milligrams produced a respiratory rate increase and vomiting within 15 minutes. Ten milligrams given to a large dog produced increased respirations and vomiting within 10 minutes (Edmunds, 1904).

References

General Bibliography

    1) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    2) American Heart Association: 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005; 112(24 Suppl):IV 1-203. Available from URL: http://circ.ahajournals.org/content/vol112/24_suppl/. As accessed 12/14/2005.
    3) Behl PN, Captain RM, & Bedi BMS: Skin-irritant and sensitizing plants found in India, PN Behl, New Delhi, India, 1966.
    4) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    5) Brown NM, Trizna Z, & Pathak S: Clastogenic interactions between lobeline sulfate and ethyl alcohol: a cytogenetic study. Anticancer Research 1992; 12:1467-1470.
    6) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    7) Cada DJ: Drugs Facts and Comparisons, St. Louis, MO, 1997.
    8) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    9) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    10) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    11) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    12) Damaj MI, Patrick GS, & Creasy KR: Pharmacology of lobeline, a nicotine receptor ligand. J Pharmacol Exp Ther 1997; 282(1):410-419.
    13) Dreser: Archiv fur experimentelle Pathologie und Pharmakologie 1889; 26:237.
    14) Duke JA: Handbook of Medicinal Herbs, CRC Press Inc, Boca Raton, FL, 1985.
    15) Dwoskin LP & Crooks PA: A novel mechanism of action and potential use for lobeline as a treatment for psychostimulant abuse. Biochem Pharmacol 2002; 63(2):89-98.
    16) Edmunds CW: On the action of lobeline. Am J Physiol 1904; 11:79-102.
    17) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    18) Emboden W: Narcotic Plants, MacMillian Publishing Co Inc, New York, NY, 1980.
    19) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    20) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    21) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    22) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    23) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    24) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    25) Jellin JM, Gregory P, & Batz F: Pharmacist's Letter/Prescriber's Letter Natural Medicines Comprehensive Database, Therapeutic Research Faculty, Stockton, CA, 2000, pp 677-678.
    26) Kapoor LD: CRC Handbook of Ayurvedic Medicinal Plants, CRC Press, Boca Raton, FL, 1990, pp 219.
    27) Kingsbury JM: Poisonous Plants of the United States and Canada, Prentice-Hall, Englewood Cliffs, NJ, 1964.
    28) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    29) Lampe KF & McCann MA: AMA Handbook of Poisonous and Injurious Plants, American Medical Association, Chicago, IL, 1985.
    30) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    31) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    32) Marlin DJ, Roberts CA, & Schroter RC: Respiratory responses of mature horses to intravenous lobeline bolus. Equine Vet J 2000; 32(3):200-207.
    33) Marshall WR: Alpha lobelin as a respiratory stimulant. Arch Int Med 1928; 42:180-188.
    34) Melendez EN, Carreras L, & Gijon JR: New alkaloid from Lobelia portoricensis Urban. J Pharm Sci 1967; 56:1677-1680.
    35) Miller DK, Lever JR, Rodvelt KR, et al: Lobeline, a potential pharmacotherapy for drug addiction, binds to mu opioid receptors and diminishes the effects of opioid receptor agonists. Drug Alcohol Depend 2007; 89(2-3):282-291.
    36) Miller FK, Crooks PA, & Teng L: Lobeline inhibits the neurochemical and behavioral effects of amphetamine. J Pharmacol Exp Ther 2001; 296(3):1023-1034.
    37) Mitchell J & Rook A: Botanical Dermatology, Greengrass Ltd, Vancouver, British Columbia, 1979.
    38) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    39) Nelson LS, Shih RD, & Balick MJ: Handbook of Poisonous and Injurious Plants, 2nd ed. Springer, New York, NY, 2007, pp -.
    40) Neumar RW , Otto CW , Link MS , et al: Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122(18 Suppl 3):S729-S767.
    41) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    42) Norris VH & Weiss S: The pharmacological and therapeutic properties of alpha-lobeline: A comparison of its action on the respiratory center with that of other respiratory stimulants. J Pharmacol 1927; 31:43-63.
    43) Osol A & Farrar G: The Dispensatory of the United States of America, 25th Ed, JB Lippincott, Philadelphia, PA, 1955.
    44) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    45) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    46) Philipov S, Istatkova R, & Ivanovska N: Phytochemical study and antiinflammatory properties of Lobelia laxiflora L. Z Naturforsch 1998; 53(5-6):311-317.
    47) Piffard HG: A treatise on the Materia Medica and Therapeutics of the Skin, Wm Wood and Co, New York, NY, 1881.
    48) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    49) Product Information: BREVIBLOC(TM) intravenous injection, esmolol HCl intravenous injection. Baxter Healthcare Corporation (per FDA), Deerfield, IL, 2012.
    50) Product Information: NITROPRESS(R) injection for IV infusion, Sodium Nitroprusside injection for IV infusion. Hospira, Inc., Lake Forest, IL, 2007.
    51) Product Information: NITROPRESS(R) injection, sodium nitroprusside injection. Hospira,Inc, Lake Forest, IL, 2004.
    52) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    53) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    54) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    55) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    56) Raj H, Singh VK, & Anand A: Sensory origin of lobeline-induced sensations: A correlative study in man and cat. J Physiol 1995; 48:235-246.
    57) Rapp GW & Olen AA: A critical evaluation of a lobeline based smoking deterrent. Am J Med Sci 1955; 230:9-14.
    58) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    59) Redbook: 1996 Drug Topics Redbook, Medical Economics, Montvale, NJ, 1996.
    60) Santosa MH, Herzog R, & Voelter W: Antitumor activity of the hot water extract of Lobelia chinensis. Planta Medica 1986; 52:555.
    61) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    62) Siegel RK: Herbal intoxication: psychoactive effects from herbal cigarettes, tea, and capsules. JAMA 1976; 236(5):473-476.
    63) Spoerke DG: Herbal Medications, Woodbridge Press Publishing Co, Santa Barbara, CA, 1980.
    64) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    65) Tyler VE: Chaparral: In: The Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies, 3rd ed, Pharmaceutical Products Press, NY, New York, NY, 1993.
    66) Whitehead RW & Elliott DC: Electrocardiographic studies of the action of alpha lobelia and epinephrine on the mammalian heart. JPET 1927; 31:145-175.
    67) Woods B: Irritant Plants. Trans St. John's Hosp Derm Soc 1962; 48:75.
    68) Wren RW: Potter's New Cyclopaedia of Botanical Drugs and Preparations. Re-edit by Wren RW, Potter & Clarke, Ltd, Health Science Press, Rustington, Sussex, 1968.
    69) Wright IS & Littauer D: Lobeline sulfate. Its pharmacology and use in the treatment of the tobacco habit. JAMA 1937; 109:649.
    70) de Caen AR, Berg MD, Chameides L, et al: Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132(18 Suppl 2):S526-S542.