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PLANTS-LUPINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Lupine, a member of the legume family, is a pea-like plant cultivated all over the world. It is a source of protein used for animal feed. Selective breeding of the plants have developed strains used as human food. There are hundreds of species of lupine which contain various concentrations of quinolizidine and piperidine alkaloids.

Specific Substances

    A) GENERAL
    1) Lupin
    2) Lupanine
    3) Sparteine
    DOMESTIC ("Sweet" or "Semi-sweet")
    1) Lupinus albus
    2) Lupinus angustifolius
    3) Lupinus luteus
    4) Lupinus mutabilis
    5) Lupinus polyphyllus
    QUINOLIZIDINE ALKALOIDS
    1) Cytisus
    2) Laburnum
    3) Lupinus
    4) Sophora
    5) Thermopsis
    TERATOGENS
    1) L. caudatus
    2) L. sericeus
    3) L. laxiflorus
    4) L. formosus (piperidine alkaloid)
    ORNAMENTAL
    1) Lupine Texensis Hook
    2) (Bluebonnet flower)

Available Forms Sources

    A) SOURCES
    1) SUMMARY
    a) There are hundreds of species of lupine which contain various concentrations of quinolizidine and piperidine alkaloids.
    2) DOMESTIC LUPINES
    a) DOMESTIC ("Sweet" or "Semi-sweet")
    1) These plant species are extensively bred to be low in alkaloid content, and do not have the characteristic "bitter" taste associated with toxicity (Panter et al, 1999). Whole seeds contain 34% to 35% protein, L. albus contains 13% oil (80% oleic and linoleic acids). The alkaloid content in L. albus "sweet" seeds was 0.02% (Yanez et al, 1983).
    3) QUINOLIZIDINE ALKALOIDS
    a) Over 150 quinolizidine alkaloids have been identified from the Leguminosae family (Panter et al, 1999).
    B) USES
    1) Lupine seeds/beans (Lupinus albus, Lupinus mutablis, and other species) have been traditionally used as animal feed. Some species are now used for human consumption. These species have been selectively bred for lower alkaloid content, and are referred to as "sweet" or "semisweet" lupines.
    a) Lupine seeds are consumed in the Middle East, Spain, and southern Europe as an appetizer (Ballester et al, 1980; Marquez et al, 1991).
    b) By selectively breeding and debittering the seeds to be more palatable for human consumption, the seeds have been safely used in breads, pasta, cookies, milk substitutes, and other foods (Ballester et al, 1980) (Zaror et al, 1990) (Hefle et al; 1994).
    c) Repeated soaking of the beans in water results in a debittering process that allows the alkaloids to be released from the beans and dispersed in the water. After the debittering process, the concentration of alkaloids from the European high-alkaloid plants ("bitter lupins") is approximately 500 mg/kg (Litkey & Dailey, 2007).
    d) Although not clinically indicated (Diaz et al, 1990), lupine seeds were used by one individual as an herbal therapy in the treatment of diabetes mellitus (Tsiodras et al, 1999).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Lupines are often classified as either bitter or sweet. Bitter lupines, such as the lupini beans consumed in Europe, have high concentrations of alkaloids (mainly sparteine), which make them bitter to taste. A debittering process is required before consumption. Sweet lupines, such as those grown in Western Australia, have low levels of alkaloids (mainly lupanine).
    B) USES: Lupine seeds/beans (Lupinus albus, Lupinus mutablis, and other species) have been traditionally used as animal feed. Some lupine species are grown for their aesthetic properties. The Texas state flower (Bluebonnet) is a wild lupine. Some species are now used for human consumption. These species have been selectively bred for lower alkaloid content, and are referred to as "sweet" or "semisweet" lupines. Lupine seeds are consumed in the Middle East, Spain, and southern Europe as an appetizer and are a good source of protein.
    C) EPIDEMIOLOGY: Exposure has occurred. Severe toxicity is uncommon and dependent on the amount of alkaloid ingested.
    D) TOXICOLOGY: Bitter lupine seeds contain quinolizidine and piperidine alkaloids, and may cause significant toxicity. Two alkaloids in particular that are potentially toxic are sparteine and lupanine.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EXPOSURE: Weakness, dizziness, blurred vision, and loss of coordination may develop in patients with anticholinergic effects after acute exposure. Dysrhythmias were reported in a patient after ingestion of lupine seed extract ("debittering solution"). Nausea and vomiting have been reported following ingestion. Anaphylaxis was reported in a child after ingestion of lupine seed fortified flour.
    2) CHRONIC EXPOSURE: Chronic ingestion of lupine has resulted in permanent neurotoxic effects. Motor neuron disease has been reported after chronic use.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: At the time of this review, there are limited reports of adverse events associated with lupine seed ingestion. Not all lupine species are poisonous. Of those that cause illness, toxicity is generally dependent on the concentration of toxic alkaloid.
    0.2.20) REPRODUCTIVE
    A) Red cell aplasia, vascular anomaly and skeletal dysplasia were found in a child born of a woman who ingested goat milk contaminated with lupine alkaloid.
    B) Milk from animals fed with lupines may induce toxic effects in both animals and humans.

Laboratory Monitoring

    A) Monitor for anticholinergic effects following acute ingestion.
    B) Monitor neurological function following acute or chronic exposure to lupine.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) Treatment is SYMPTOMATIC and SUPPORTIVE.

Range Of Toxicity

    A) TOXICITY: Not all species are poisonous. Toxicity is dependent on the plant's alkaloid concentration. The lethal dose of lupanine is 100 mg/kg, with 10 g of seeds capable of releasing 100 mg of lupanine. Several case reports of self-limiting, anticholinergic toxicity have occurred following ingestion of lupine seed extract. A child developed mild anticholinergic toxicity following the ingestion of approximately 10 home-prepared lupine beans.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Lupines are often classified as either bitter or sweet. Bitter lupines, such as the lupini beans consumed in Europe, have high concentrations of alkaloids (mainly sparteine), which make them bitter to taste. A debittering process is required before consumption. Sweet lupines, such as those grown in Western Australia, have low levels of alkaloids (mainly lupanine).
    B) USES: Lupine seeds/beans (Lupinus albus, Lupinus mutablis, and other species) have been traditionally used as animal feed. Some lupine species are grown for their aesthetic properties. The Texas state flower (Bluebonnet) is a wild lupine. Some species are now used for human consumption. These species have been selectively bred for lower alkaloid content, and are referred to as "sweet" or "semisweet" lupines. Lupine seeds are consumed in the Middle East, Spain, and southern Europe as an appetizer and are a good source of protein.
    C) EPIDEMIOLOGY: Exposure has occurred. Severe toxicity is uncommon and dependent on the amount of alkaloid ingested.
    D) TOXICOLOGY: Bitter lupine seeds contain quinolizidine and piperidine alkaloids, and may cause significant toxicity. Two alkaloids in particular that are potentially toxic are sparteine and lupanine.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EXPOSURE: Weakness, dizziness, blurred vision, and loss of coordination may develop in patients with anticholinergic effects after acute exposure. Dysrhythmias were reported in a patient after ingestion of lupine seed extract ("debittering solution"). Nausea and vomiting have been reported following ingestion. Anaphylaxis was reported in a child after ingestion of lupine seed fortified flour.
    2) CHRONIC EXPOSURE: Chronic ingestion of lupine has resulted in permanent neurotoxic effects. Motor neuron disease has been reported after chronic use.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: At the time of this review, there are limited reports of adverse events associated with lupine seed ingestion. Not all lupine species are poisonous. Of those that cause illness, toxicity is generally dependent on the concentration of toxic alkaloid.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CASE REPORT/PEDIATRIC: A 6-year-old girl ingested approximately 10 lupine beans that were prepared at home and developed nausea, headache, blurry vision and photophobia about 30 minutes after ingestion. Upon admission, tachycardia (120 bpm), dry mucous membranes, and mydriasis were observed but cardiovascular and respiratory function were normal. The mother acknowledged that the beans were still bitter (even after soaking for 2 to 3 days) because the child liked the bitter taste. The child recovered spontaneously within 12 hours and was discharged the following day with no further symptoms (Daverio et al, 2014).
    2) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth, facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).
    3) CASE REPORT: A 51-year-old woman developed anticholinergic toxicity, which included weakness, anxiety, dry mouth, mydriasis and ptosis after ingesting lupine seeds. Her symptoms resolved within 12 hours without any therapy (Di Grande et al, 2004).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 19-year-old man developed an anticholinergic syndrome, which included mydriasis, urinary retention, dry mouth, and sinus tachycardia with extrasystoles. A holter monitor indicated supraventricular tachycardia and trigemny. Symptoms appeared after drinking half a liter of debittering water (boiled water used to detoxify the seeds) (Marquez et al, 1991). The extrasystoles resolved within 48 hours. Analysis of blood and urine were positive for alkaloids, one of which was identified as lupanine. All symptoms resolved without intervention.
    B) TACHYARRHYTHMIA
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth, facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).
    b) CASE REPORT: Anticholinergic effects which included sinus tachycardia and mydriasis were reported after ingestion of a glass of extract made from lupine beans in a 72-year-old diabetic woman (Tsiodras et al, 1999). The extract was taken for its purported ability to lower blood sugar. Symptoms resolved within 12 hours of ingestion with no intervention. Gas-chromatography of the extract found primarily oxo-sparteine and sparteine.
    C) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth, facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) DIZZINESS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A woman developed dizziness and lack of coordination after ingesting improperly prepared lupine seeds purchased from a grocery store in Canada. Elaborate cooking instructions, intended to remove any toxins, were not followed. The author noted that when cooking directions were followed precisely, 1 gram of lupine alkaloids were removed from 100 grams of seeds (Smith, 1987).
    B) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth, facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).
    b) CASE REPORT: A 72-year-old woman ingested lupine seed extract as a home remedy for diabetes mellitus and developed anticholinergic toxicity (Tsiodras et al, 1999). The patient complained of weakness and blurred vision, and on physical exam exhibited mydriasis, with minimal pupil response and sinus tachycardia. The patient was discharged after 24 hours of observation and felt completely well after 3 days.
    c) CASE REPORT: A 51-year-old woman developed anticholinergic toxicity, which included weakness, anxiety, dry mouth, mydriasis and ptosis after ingesting lupine seeds. Her symptoms resolved within 12 hours without any therapy (Di Grande et al, 2004).
    C) HEADACHE
    1) WITH THERAPEUTIC USE
    a) CASE REPORT/PEDIATRIC: A 6-year-old girl ingested approximately 10 lupine beans that were prepared at home and developed nausea, headache, blurry vision and photophobia about 30 minutes after ingestion. Upon admission, tachycardia (120 bpm), dry mucous membranes, and mydriasis were observed but cardiovascular and respiratory function were normal. The mother acknowledged that the beans were still bitter (even after soaking for 2 to 3 days) because the child liked the bitter taste. The child recovered spontaneously within 12 hours and was discharged the following day with no further symptoms (Daverio et al, 2014).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 72-year-old woman experienced nausea, vomiting, and anticholinergic toxicity after ingesting a glass of debittering extract (a boiling method used to detoxify lupine seeds) as a home remedy for diabetes mellitus. Twelve hours after her exposure she had improved and was in her normal state of health 3 days after ingestion (Tsiodras et al, 1999).
    b) CASE REPORT/PEDIATRIC: A 6-year-old girl ingested approximately 10 lupine beans that were prepared at home and developed nausea, headache, blurry vision and photophobia about 30 minutes after ingestion. Upon admission, tachycardia (120 bpm), dry mucous membranes, and mydriasis were observed but cardiovascular and respiratory function were normal. The mother acknowledged that the beans were still bitter (even after soaking for 2 to 3 days) because the child liked the bitter taste. The child recovered spontaneously within 12 hours and was discharged the following day with no further symptoms (Daverio et al, 2014).
    B) APTYALISM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth , facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).
    b) CASE REPORT: A 51-year-old woman developed anticholinergic toxicity, which included weakness, anxiety, dry mouth, mydriasis and ptosis after ingesting lupine seeds. Her symptoms resolved within 12 hours without any therapy (Di Grande et al, 2004).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GASTROINTESTINAL DISORDER
    a) Lupinosis is a mycotoxicosis that effects livestock and is produced by the fungus Phomopsis leptostromiformis that grows on the lupine plant. It causes anorexia, constipation, jaundice, and depression in animals who ingest the contaminated plants (Panter et al, 1999; Tsiodras et al, 1999). It is generally limited to grazing that occurs on plants in Australia.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) FLUSHING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 46-year-old woman ingested lupini beans and presented to the ED approximately 4 hours later with anticholinergic symptoms including blurry vision, dry mouth, facial flushing, agitation, and confusion. Vital signs of the patient indicated tachycardia (120 bpm), and hypertension (171/103 mmHg). Over the next several hours, the patient's symptoms spontaneously resolved (Litkey & Dailey, 2007).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH THERAPEUTIC USE
    a) CHRONIC TOXICITY
    1) CASE REPORT: A 28-year-old woman developed spasticity and amyotrophy possibly as a result of lupine seed toxicity. The patient experienced progressive difficulty in performing fine motor tasks such as knitting and writing, and increasing symptoms of dystonia, dysarthria, diffuse hyperreflexia, weakness, dysphagia, and fasciculations. After more than a year of symptoms, the patient stated that she had been consuming approximately 3 g of lupine seeds monthly for 8 years. Two months after discontinuing the lupine seeds, dysphagia and fasciculations had improved. Almost 2 years later, however, the patient continued to have residual neurological effects, which included pyramidal signs, limb weakness, and amyotrophy of the extremities (Agid et al, 1988).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ANAPHYLAXIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT/PEDIATRIC: A 5-year-old girl with a history of peanut allergy developed urticaria and angioedema after consuming pasta that was fortified with sweet lupine seed flour. The authors sought to further study the effects of lupine seeds and conducted allergy testing in 7 volunteers with peanut allergy. In 4 of the 7 subjects, RAST test showed IgE binding to lupine-fortified extract, and skin prick tests were positive in 5 of the 7 subjects, indicating partial cross-reactivity and sensitivity to lupine seeds in peanut sensitive patients (Hefle et al, 1994).
    b) CASE REPORT/ADULT: A 36-year-old woman with a past medical history of legume-sensitivity, but no peanut allergy, developed anaphylaxis (ie, immediate throat swelling, dyspnea, chest tightness) after ingesting 3 lupine seeds for the first time. She previously developed palmar itching erythema and facial angioedema 4 years earlier after ingestion of chickpea. Testing demonstrated an IgE-mediated mechanism (ie, positive skin prick test for lupine, assay for specific IgE antibodies were positive for all legumes except green bean, and an ELISA assay was designed for specific IgE to legumes and found antibodies to lupine, chickpea, white bean and lentil). The authors concluded that clinical cross reactivity progressed in this patient (Matheu et al, 1999).
    2) WITH POISONING/EXPOSURE
    a) CASE SERIES/OCCUPATIONAL: In a small cross-sectional study of 7 laboratory workers, inhalation of lupine seed flour (LSF) produced allergy-related symptoms (respiratory symptoms, ocular itching, rhinorrhea, chest tightness, dyspnea and wheezing) following exposure in 3 individuals. Skin prick tests with LSF were positive in all 3 and lupine-specific IgE antibodies were detected in 2 of the workers. The authors suggested that lupine should be considered a potential sensitizing agent by inhalation (Crespo et al, 2001).

Reproductive

    3.20.1) SUMMARY
    A) Red cell aplasia, vascular anomaly and skeletal dysplasia were found in a child born of a woman who ingested goat milk contaminated with lupine alkaloid.
    B) Milk from animals fed with lupines may induce toxic effects in both animals and humans.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) HUMAN EXPOSURE - Red cell aplasia, vascular anomaly and skeletal dysplasia were found in a child born of a woman who ingested goat milk contaminated with lupine alkaloid. The skeletal abnormalities were similar to those of crooked calf disease (foreshortening of the forearms, radial deviation of the hands, no thumbs, ulna bowing). The child had severe anemia at birth. At 5 years of age, the child still requires packed red cell transfusions monthly. The mother's primary milk source was from goats. These goats had several spontaneously aborted fetuses noted to have skeletal abnormalities similar to crooked calf disease. A pregnant dog fed milk from these goats also had pups with these abnormalities. Lupines were found in the goat's pasture (Ortega & Lazerson, 1987).
    B) ANIMAL STUDIES
    1) Panter et al (1999) postulated that lupine exposure during gestation can result in decreased fetal movement in mammals and may play a role in the congenital defects observed.
    a) The following potential causes for defects found in cattle are suggested below:
    1) Alkaloid-induced reduction in fetal movement related to skeletal contracture malformation and cleft palate in animals.
    2) Abnormal alignment in utero resulted from a lack of movement.
    3) Mechanical interference by the tongue caused cleft palate at a crucial time of closure.
    4) Spinal and rib cage abnormalities resulted from malpositioning in utero.
    2) Anagyrine, a quinolizidine alkaloid, is responsible for the teratogenic effects observed in livestock following ingestion of certain species of lupines (Panter et al, 1999).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) ANIMAL STUDIES
    1) Milk from animals fed with lupines may induce toxic effects in both animals and humans (Tsiodras et al, 1999).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor for anticholinergic effects following acute ingestion.
    B) Monitor neurological function following acute or chronic exposure to lupine.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) VITAL SIGNS
    1) Monitor temperature, heart rate, and blood pressure as indicated.
    C) URINALYSIS
    1) Monitor urine output and fluid status.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Obtain a baseline ECG and institute continuous cardiac monitoring in patients with anticholinergic effects.

Methods

    A) CHROMATOGRAPHY
    1) Hatzold et al (1983) studied the composition of Lupine mutabilis using high resolution capillary gas-liquid chromatography and capillary-GLC mass spectrometry.
    2) A gas chromatography/mass spectrometry (GC/MS) method was used by Smith (1987) to determine the amount of alkaloid present in lupine seeds.
    3) Marquez et al (1991) and Tsiodras et al (1999) described the use of GC/MS to identify the specific alkaloid present in serum, urine, and lupine extract (debittering solution) during toxicological analyses.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor for anticholinergic effects following acute ingestion.
    B) Monitor neurological function following acute or chronic exposure to lupine.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) 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.
    2) 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).
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) SUPPORT
    1) In a limited number of cases, anticholinergic toxicity has been reported (Marquez et al, 1991; Tsiodras et al, 1999) following lupine seed ingestion that was improperly prepared or ingestion of the debittering solution. These cases were managed with SYMPTOMATIC and SUPPORTIVE care. At the time of this review, administration of physostigmine, has not been necessary.
    2) Refer to the "ANTICHOLINERGIC POISONING" management for further information as indicated.
    B) MONITORING OF PATIENT
    1) Monitor heart rate and blood pressure in all patients. Obtain a baseline ECG as indicated in symptomatic patients
    2) Monitor neurological and gastrointestinal function.
    3) Monitor urinary output.
    C) TACHYARRHYTHMIA
    1) Obtain a baseline ECG and continuous cardiac monitoring as indicated. In several case reports of lupine-induced sinus tachycardia the effects were self-limiting and required no intervention (Marquez et al, 1991; Tsiodras et al, 1999).
    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).
    D) PHYSOSTIGMINE
    1) PHYSOSTIGMINE/INDICATIONS
    a) Physostigmine is indicated to reverse the CNS effects caused by clinical or toxic dosages of agents capable of producing anticholinergic syndrome; however, long lasting reversal of anticholinergic signs and symptoms is generally not achieved because of the relatively short duration of action of physostigmine (45 to 60 minutes) (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008). It is most often used diagnostically to distinguish anticholinergic delirium from other causes of altered mental status (Frascogna, 2007; Shannon, 1998).
    b) Physostigmine should not be used in patients with suspected tricyclic antidepressant overdose, or an ECG suggestive of tricyclic antidepressant overdose (eg, QRS widening). In the setting of tricyclic antidepressant overdose, use of physostigmine has precipitated seizures and intractable cardiac arrest (Stewart, 1979; Newton, 1975; Pentel & Peterson, 1980; Frascogna, 2007).
    2) DOSE
    a) ADULT: BOLUS: 2 mg IV at slow controlled rate, no more than 1 mg/min. May repeat doses at intervals of 10 to 30 min, if severe symptoms recur (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008). INFUSION: For patients with prolonged anticholinergic delirium, a continuous infusion of physostigmine may be considered. Starting dose is 2 mg/hr, titrate to effect (Eyer et al, 2008)
    b) CHILD: 0.02 mg/kg by slow IV injection, at a rate no more than 0.5 mg/minute. Repeat dosage at 5 to 10 minute intervals as long as the toxic effect persists and there is no sign of cholinergic effects. MAXIMUM DOSAGE: 2 mg total (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    c) AVAILABILITY: Physostigmine salicylate is available in 2 mL ampules, each mL containing 1 mg of physostigmine salicylate in a vehicle containing sodium metabisulfite 0.1%, benzyl alcohol 2%, and water (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    3) CAUTIONS
    a) Relative contraindications to the use of physostigmine are asthma, gangrene, diabetes, cardiovascular disease, intestinal or urogenital tract mechanical obstruction, peripheral vascular disease, cardiac conduction defects, atrioventricular block, and in patients receiving choline esters and depolarizing neuromuscular blocking agents (decamethonium, succinylcholine). It may cause anaphylactic symptoms and life-threatening or less severe asthmatic episodes in patients with sulfite sensitivity (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    b) Too rapid IV administration of physostigmine has resulted in bradycardia, hypersalivation leading to respiratory difficulties, and possible seizures (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008).
    4) ATROPINE FOR PHYSOSTIGMINE TOXICITY
    a) Atropine should be available to reverse life-threatening physostigmine-induced, toxic cholinergic effects (Prod Info physostigmine salicylate intravenous injection, intramuscular injection, 2008; Frascogna, 2007). Atropine may be given at half the dose of previously given physostigmine dose (Daunderer, 1980).
    E) ACUTE ALLERGIC REACTION
    1) Based on limited evidence, some individuals with peanut-sensitivity may be at risk for cross-reactivity to lupine seeds (Hefle et al, 1994). As part of the legume family, which can produce IgE mediated hypersensitivity, lupine seeds may cause an allergic response.
    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,TL,et al).
    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,TL,et al).
    d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
    e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
    f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    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,TL,et al). 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,TL,et al).

Range Of Toxicity

Summary

    A) TOXICITY: Not all species are poisonous. Toxicity is dependent on the plant's alkaloid concentration. The lethal dose of lupanine is 100 mg/kg, with 10 g of seeds capable of releasing 100 mg of lupanine. Several case reports of self-limiting, anticholinergic toxicity have occurred following ingestion of lupine seed extract. A child developed mild anticholinergic toxicity following the ingestion of approximately 10 home-prepared lupine beans.

Minimum Lethal Exposure

    A) SUMMARY
    1) The lethal dose of the alkaloid lupanine is 100 mg/kg, with 10 g of seeds capable of releasing 100 mg of lupanine. Therefore, the lethal dose of lupine seeds may be less than 10 g/kg if the alkaloids are not removed by cooking or other means (Smith, 1987; Hatzold et al, 1983).

Maximum Tolerated Exposure

    A) SUMMARY
    1) Lupines can be poisonous. Toxicity varies depending on the amount of quinolizidine and piperidine alkaloids present in the plant (Kim et al, 1982; Marquez et al, 1991; Tsiodras et al, 1999).
    2) Although over 12 quinolizidine alkaloids have been identified, sparteine and lupanine are the most widely studied (Yovo et al, 1984; Pothier et al, 1998). In a mouse study, sparteine, lupanine, and lupine extract caused similar toxicity: shaking, excitation, and convulsions (Pothier et al, 1998).
    3) Although both sparteine and lupanine have antimuscarinic effects, sparteine has a greater binding affinity to muscarinic receptors, while lupanine has greater affinity to nicotinic receptors (Pothier et al, 1998; Panter et al, 1999). Toxicity has been found to be greater in sparteine as compared to lupanine (Yovo et al, 1984; Pothier et al, 1998).
    B) CASE REPORTS
    1) Several cases of self-limiting, anticholinergic toxicity have been reported with the ingestion of "debittering extract" (a boiling method used to detoxify the seeds) (Marquez et al, 1991; Tsiodras et al, 1999).
    2) CASE REPORT/PEDIATRIC: A 6-year-old girl ingested approximately 10 lupine beans that were prepared at home and developed nausea, headache, blurry vision and photophobia about 30 minutes after ingestion. Upon admission, tachycardia (120 bpm), dry mucous membranes, and mydriasis were observed but cardiovascular and respiratory function were normal. The mother acknowledged that the beans were still bitter (even after soaking for 2 to 3 days) because the child liked the bitter taste. The child recovered spontaneously within 12 hours and was discharged the following day with no further symptoms (Daverio et al, 2014).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) Lupanine (as found in the L. albus species) References: (Yovo et al, 1994; RTECS, 2000)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 175 (154-197) mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 410 (341-492) mg/kg
    B) Sparteine (as found in the L. albus species) References: (Yovo et al, 1994; RTECS, 2000)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 36 (34-37) mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 220 (341-492) mg/kg
    C) Sparteine - References: (Yovo et al, 1994; RTECS, 2000)
    1) LD50- (SUBCUTANEOUS)MOUSE:
    a) 105 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 42 mg/kg
    3) LD50- (ORAL)RAT:
    a) 960 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) The Lupinus genus contains hundreds of species of lupine. Lupines are part of the legume family and are high in protein and other nutrients. The dietary fiber contained in lupines is mainly pectin material. Lupines contain various alkaloids in differing concentrations. The process of removing or decreasing the alkaloid content results in an end product known as "sweet" lupines, while lupines high in alkaloid content are described as "bitter" (Ballester et al, 1980; Hefle et al, 1994; Panter et al, 1999).
    B) Sparteine and lupanine are two of the prominent quinolizidine alkaloids found in lupine seeds in varying amounts depending on the species (Yovo et al, 1984; Panter et al, 1999). At the time of this review, there are limited data regarding the pharmacological effects of lupanine, but they are thought to be similar to sparteine (Yovo et al, 1984; Pothier et al, 1998). Yovo et al (1994) noted that chemically, sparteine and lupanine are similar in structure. They both comprise a bisquinolizidine nucleus with a ketone function for lupanine.
    C) Pharmacodynamically, both alkaloids have ganglioplegic, oxytocic, and cardiac properties (Yovo et al, 1994; (Pothier et al, 1998). Sparteine also has antihypertensive, central nervous system (depressant), diuretic, and local anesthetic effects (Pothier et al, 1998).

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) CATTLE
    1) SUMMARY
    a) In general, there is a wide variation of alkaloid content among lupine species. Typically, alkaloid content is high during early growth stages, decreasing through the flower stage and increasing in the seeds and pods. Thus, most losses to livestock occur under conditions where large amounts of pods are eaten.
    2) ACUTE TOXICITY
    a) In cattle, arthrogryposis, which can include scoliosis, torticollis, kyphosis, or cleft palate is one of the most frequently encountered malformations due to lupine exposure (Panter et al, 1999).
    b) Permanent and progressive osseous changes are characteristic in lupine exposure and result in load bearing stress.
    c) Critical time for gestational exposure is 40 to 70 days and up to 100 days to produce teratogenic effects.
    d) Anagyrine-containing lupines have caused birth defects only in cattle and not in sheep.
    e) The quinolizidine alkaloid anagyrine and the piperidine alkaloids ammodendrine, N-methyl ammodendrine and N-acetyl hystrine are believed to be responsible for the teratogenic effects in cattle.
    11.1.4) CAPRINE/GOAT
    A) GOAT
    1) Latifolius has been responsible for limb deformation in goats whose mothers ingested the plant during pregnancy (Panter et al, 1999).
    a) Critical time for gestational exposure is 35-40 days and up to 60 days to produce teratogenic effects.
    11.1.9) OVINE/SHEEP
    A) SHEEP
    1) A lupinosis (a mycotoxicosis caused by the fungus Phomopsis leptostromiformis) outbreak occurred among lambs grazing on a lupine pasture in Spain (Rodriguez et al, 1991). Symptoms included constipation, weakness, varying degrees of jaundice, depression, and anorexia. Variations in the degree of toxicity were noted, and believed to be related to the amount of lupine ingested. Laboratory analysis of hematocrit, glucose, and total protein were within normal limits. Liver examination was conducted on 2 lambs that died and the pathological changes included necrotic areas and fatty metamorphosis.
    11.1.10) PORCINE/SWINE
    A) SWINE
    1) Although less frequently reported, swine have been poisoned.
    11.1.13) OTHER
    A) OTHER
    1) DEER
    a) Although less frequently reported, deer have been poisoned.

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Treatment is SYMPTOMATIC and SUPPORTIVE.

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Treatment is SYMPTOMATIC and SUPPORTIVE.
    11.4.3) TREATMENT
    11.4.3.5) SUPPORTIVE CARE
    A) SUPPORTIVE CARE
    1) Treatment is SYMPTOMATIC and SUPPORTIVE.
    2) Monitor fluid and electrolyte status carefully.

References

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