Does CBD work for coughs, and if so, how?

Coughing is a reflex that keeps the throat and airways clear. While it can be annoying, coughing helps the body protect and heal itself. 

Coughs may either be acute or chronic. Acute coughs often begin suddenly and last no more than 2 or 3 weeks. Acute coughs are the kind that one often gets with a cold, flu, or acute bronchitis (1).

Chronic coughs may last longer than 2 or 3 weeks and causes vary. Causes of chronic coughs may include:

  • Asthma
  • Allergies
  • COPD (chronic obstructive pulmonary disease)
  • Chronic bronchitis
  • GERD (gastroesophageal reflux disease)
  • Smoking
  • Throat disorders, like croup in young children

Water can help ease coughing, whether one drinks it or add it to the air with a steamy shower or vaporizer. 

For a cold or the flu, antihistamines may work better than non-prescription cough medicines. Note that cough medicines are not recommended for children under four years old. For children over four, use caution and read labels carefully (2). 

Why Some People Are Taking CBD for Cough

Some people are using cannabis as a natural alternative treatment for cough symptoms. 

CBD for Congestion

The plant’s anti-inflammatory properties have been shown to help individuals cope with symptoms, like sore throat, sinus pain, and body aches. 

Nasal congestion may be one of the most annoying and uncomfortable cold symptoms. 

When the virus attacks the nasal passage, it causes it to swell up and overproduce mucus. This overproduction of mucus clogs sinuses causing pain and pressure.

Decongestants help relieve nasal stuffiness by narrowing blood vessels and reducing swelling in the nose. However, decongestants can increase blood pressure (3). 

Meanwhile, CBD may also act as a decongestant by helping reduce inflammation, providing relief from the pressure and sinus drips. 

Unlike other decongestants, CBD does not cause concern for those with cardiovascular issues. 

Data from a study even showed that acute administration of CBD reduces resting blood pressure and blood pressure due to stress (4).

An anti-inflammatory, CBD may help open up the sinus passages and increase ease of breathing, although research is not conclusive.

Targeting the inflammation, CBD may help calm the membranes that line the nasal passages, decreasing congestion and opening up those airways.

A study showed the mechanism by which CBD inhibits inflammatory and neuropathic pain (5). 

CBD’s potent anti-inflammatory properties were also demonstrated in a 2018 study published in the Journal of Pharmacology and Experimental Therapeutics (6). 

Meanwhile, CBD may act as an analgesic, relieving pain. A study published in Therapeutics and Clinical Risk Management showed how employing cannabinoids, such as THC and CBD, helped in the management of difficult-to-treat pain (7).

CBD may offer an option for treating different types of chronic pain (8)

CBD for Bacterial Infections

CBD has natural antibacterial properties that may help fight against secondary bacterial infections that can develop from the cold and flu. 

A study showed the antibacterial characteristics of delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) (9).

Another study, conducted in 2019 by researchers from the University of Queensland, showed CBD might be a capable fighter against bacterial infections (10). 

CBD for Fevers

A fever may develop as the body fights a viral infection, like the common cold. A fever is also a sign of inflammation. 

Cannabinoids could play a role in inhibiting the progression of a fever caused by a virus (11).

If the fever is part of a more substantial inflammatory reaction, the use of CBD oil can trigger an anti-inflammatory response through its action in the body’s endocannabinoid system.

Data from a review published in Cannabis and Cannabinoid Research in 2020 overwhelmingly support the concept that CBD is immunosuppressive (12).

CBD’s potential as an immune suppressor means it may have positive effects when the immune system becomes hyperactive or weakened.

Hemp oil has antiproliferative effects, as indicated in a 2017 study published in Frontiers in Pharmacology (13). The findings demonstrated that CBD might help stop cell growth of foreign organisms, like the cold virus. 

When the immune system launches its attack on a virus, it causes an inflammatory response that produces flu or cold-like symptoms. 

While the body uses its endocannabinoids to moderate the immune response, it is not always capable of controlling the inflammatory process. 

Cannabinoids in cannabis plants help by providing the natural endocannabinoid mechanism with a much-needed boost. 

Moreover, constant use of these cannabinoids, found in full-spectrum CBD extracts, may help the body protect itself against a future attack.

CBD for Relaxing Muscles

CBD oil may not only provide anti-inflammatory effects, as studies have shown. CBD may help with relaxing the muscles as well.

CBD’s potential muscle-relaxant qualities may be of interest to those suffering from a persistent cough. CBD oil may reduce the inflamed airway and relax the muscles to reduce coughing. 

Through the mechanism by which CBD works with the endocannabinoid system, CBD is useful in treating muscle pain by calming excessively-contracting muscles. 

This mechanism is explained in a 2013 study published in the Rambam Maimonides Medical Journal (14).

Also, CBD may help reduce muscle spasms, a feature of neuropathic damage which often manifests in painful, uncontrolled muscle twitches (15).

Conclusion

CBD hemp oil may be available in different forms of CBD products, such as tincture, vape juice, or lozenges.

CBD is generally well-tolerated with a good safety profile, says the World Health Organization (WHO) (16). 

Studies have shown that some of CBD’s purported therapeutic benefits may be useful in treating some of the causes and symptoms of cough.

However, note that more longitudinal research is needed, as the results from previous studies are not conclusive. Also, the long-term side effects of CBD use are still unknown.

Thus, before using CBD oil for cough as an adjunct therapy or for treating symptoms of medical conditions linked to cough, make sure to consult with a doctor experienced in cannabis use for advice.


  1. MedlinePlus. (2016, March 18). Cough. Retrieved from https://medlineplus.gov/cough.html.
  2. Ibid. 
  3. Sheps S. (2019, July 20). High blood pressure and cold remedies: Which are safe? Retrieved from https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/expert-answers/high-blood-pressure/faq-20058281.
  4. Jadoon KA, Tan GD, O’Sullivan SE. A single dose of cannabidiol reduces blood pressure in healthy volunteers in a randomized crossover study. JCI Insight. 2017;2(12):e93760. Published 2017 Jun 15. DOIi:10.1172/jci.insight.93760.
  5. Xiong W, Cui T, Cheng K, et al. Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors. J Exp Med. 2012;209(6):1121–1134. DOI:10.1084/jem.20120242.
  6. Petrosino S et al. Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis. Journal of Pharmacology and Experimental Therapeutics June 2018, 365 (3) 652-663; DOI: https://doi.org/10.1124/jpet.117.244368.
  7. Russo EB. Cannabinoids in the management of difficult to treat pain. Ther Clin Risk Manag. 2008;4(1):245–259. DOI:10.2147/tcrm.s1928.
  8. Grinspoon, P. (2019, Aug 27). Cannabidiol (CBD) — what we know and what we don’t. Retrieved from https://www.health.harvard.edu/blog/cannabidiol-cbd-what-we-know-and-what-we-dont-2018082414476.
  9. Van Klingeren B, Ten Ham M. Antibacterial activity of delta9-tetrahydrocannabinol and cannabidiol. Antonie Van Leeuwenhoek. 1976;42(1-2):9–12. DOI:10.1007/bf00399444.
  10. The University of Queensland. (2019, June 24). Cannabis compound could be powerful new antibiotic. Retrieved from https://imb.uq.edu.au/article/2019/06/cannabis-compound-could-be-powerful-new-antibiotic.
  11. Benamar K, Yondorf M, Meissler JJ, et al. A novel role of cannabinoids: implication in the fever induced by bacterial lipopolysaccharide. J Pharmacol Exp Ther. 2007;320(3):1127–1133. DOI:10.1124/jpet.106.113159.
  12. Nichols J and Kaplan B. Immune Responses Regulated by Cannabidiol. Cannabis and Cannabinoid ResearchVol. 5, No. 1. 27 Feb 2020. https://doi.org/10.1089/can.2018.0073.
  13. Morales P, Reggio PH, Jagerovic N. An Overview on Medicinal Chemistry of Synthetic and Natural Derivatives of Cannabidiol. Front Pharmacol. 2017;8:422. Published 2017 Jun 28. DOI:10.3389/fphar.2017.00422. 
  14. Fine, P. and Rosenfeld, M. (2013). The Endocannabinoid System, Cannabinoids, and Pain. Rambam Maimonides Medical Journal, 4(4). 
  15. NINDS. (2018, Aug). Peripheral Neuropathy Fact Sheet. Retrieved from https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Peripheral-Neuropathy-Fact-Sheet.
  16. WHO. Expert Committee on Drug Dependence. (2017, Nov 6-10). Cannabidiol (CBD). Retrieved from https://www.who.int/medicines/access/controlled-substances/5.2_CBD.pdf

More Info

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Dextromethorphan

  1. NAME

1.1 Substance

1.2 Group

1.3 Synonyms

1.4 Identification numbers

1.4.1 CAS

1.4.2 Other numbers

1.5 Brand names/trade names:

1.6 Manufacturers and importers:

  1. SUMMARY

2.1 Main risks and target organs

2.2 Summary of clinical effects

2.3 Diagnosis

2.4 First aid measures and management principles

  1. PHYSICO-CHEMICAL PROPERTIES

3.1 Origin of the substance

3.2 Chemical structure

3.3 Physical properties

3.3.1 Colour

3.3.2 State/form

3.3.3 Description

3.4 Other characteristics

3.4.1 Shelf-life of the substance

3.4.2 Storage conditions

  1. USES

4.1 Indications

4.1.1 Indications

4.1.2 Description

4.2 Therapeutic dosages

4.2.1 Adults

4.2.1 Children

4.3 Contraindications

  1. ROUTES OF EXPOSURE

5.1 Oral

5.2 Inhalation

5.3 Dermal

5.4 Eye

5.5 Parental

5.6 Others

  1. KINETICS

6.1 Absorption by route of exposure

6.2 Distribution by route of exposure

6.3 Biological half-life by route of exposure

6.4 Metabolism

6.5 Elimination by route of exposure

  1. PHARMACOLOGY AND TOXICOLOGY

7.1 Mode of action

7.1.1 Toxicodynamics

7.1.2 Pharmacodynamics

7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

7.2.1.2 Children

7.2.3 Animal data

7.2.3 Relevant in-vitro data

7.3 Carcinogenicity:

7.4 Teratogenicity

7.5 Mutagenicity

7.6 Interactions

7.7 Main adverse effects

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

8.1 Material sampling plan

8.1.1 Sampling and specimen collection

8.1.1.1 Toxicological analyses

8.1.1.2 Biomedical analyses

8.1.1.3 Arterial blood gas analysis

8.1.1.4 Haematological analyses

8.1.1.5 Other (unspecified) analyses

8.1.2 Storage of laboratory samples and specimens

8.1.2.1 Toxicological analyses

8.1.2.2 Biomedical analyses

8.1.2.3 Arterial blood gas analysis

8.1.2.4 Haematological analyses

8.1.2.5 Other (unspecified) analyses

8.1.3 Transport of laboratory samples and specimens

8.1.3.1 Toxicological analyses

8.1.3.2 Biomedical analyses

8.1.3.3 Arterial blood gas analysis

8.1.3.4 Haematological analyses

8.1.3.5 Other (unspecified) analyses

8.2 Toxicological Analyses and Their Interpretation

8.2.1 Tests on toxic ingredient(s) of material

8.2.1.1 Simple Qualitative Test(s)

8.2.1.2 Advanced Qualitative Confirmation Test(s)

8.2.1.3 Simple Quantitative Method(s)

8.2.1.4 Advanced Quantitative Method(s)

8.2.2 Tests for biological specimens

8.2.2.1 Simple Qualitative Test(s)

8.2.2.2 Advanced Qualitative Confirmation Test(s)

8.2.2.3 Simple Quantitative Method(s)

8.2.2.4 Advanced Quantitative Method(s)

8.2.2.5 Other Dedicated Method(s)

8.2.3 Interpretation of toxicological analyses

8.3 Biomedical investigations and their interpretation

8.3.1 Biochemical analysis

8.3.1.1 Blood, plasma or serum

8.3.1.2 Urine

8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses

8.3.3 Haematological analyses

8.3.4 Interpretation of biomedical investigations

8.4 Other biomedical (diagnostic) investigations and their interpretation

8.5 Overall interpretation of all toxicological analyses and toxicological investigations

  1. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

9.1.2 Inhalation

9.1.3 Skin exposure

9.1.4 Eye contact

9.1.5 Parenteral exposure.

9.1.6 Other

9.2 Chronic Poisoning

9.2.1 Ingestion

9.2.2 Inhalation

9.2.3 Skin contact

9.2.4 Eye contact

9.2.5 Parental exposure

9.2.6 Other

9.3 Course, prognosis, cause of death:

9.4 Systematic description of clinical effects:

9.4.1 Cardiovascular

9.4.2 Respiratory

9.4.3 Neurologic

9.4.3.1 Central nervous system (CNS)

9.4.3.2 Peripheral nervous system

9.4.3.3 Autonomic

9.4.3.4 Skeletal and smooth muscle

9.4.4 Gastrointestinal

9.4.5 Hepatic

9.4.6 Urinary

9.4.6.1 Renal

9.4.6.2 Others

9.4.7 Endocrine and reproductive systems

9.4.8 Dermatologic

9.4.9 Eye, ear, throat: local effects

9.4.10 Hematological

9.4.11 Immunologic

9.4.12 Metabolic

9.4.12.1 Acid-base disturbances

9.4.12.2 Fluid and electrolyte disturbances

9.4.12.3 Others

9.4.13 Allergic reactions

9.4.14 Other clinical effects

9.4.15 Special risks

9.5 Others

  1. MANAGEMENT

10.1 General principles

10.2 Life supportive procedures and symptomatic treatment

10.3 Decontamination

10.4 Enhancd elimination

10.5 Antidote

10.5.1 Adults

10.5.2 Children

10.6 Management discussion

  1. ILLUSTRATIVE CASES

11.1 Case report from the literature

  1. ADDITIONAL INFORMATION

12.1 Specific preventive measures

12.2 Other

  1. REFERENCES
  2. AUTHOR(S), REVIEWER(S) DATES (INCLUDING EACH UPDATING), COMPLETE ADDRESSES

 

DEXTROMETHORPHAN

 

International Programme on Chemical Safety

Poisons Information Monograph 179

Pharmaceutical

 

  1. NAME

 

1.1  Substance

 

Dextromethorphan

 

1.2  Group

 

Cough and cold preparations (R05)/

Antitussives, excl. combinations with expectorants

(R05D)/ Opium alkaloids and derivatives (R05D A)

 

1.3  Synonyms

 

Dextromethorphan hydrobromide monohydrate;

dextromethorphani hydrobromidum;

demorphan hydrobromide

 

1.4  Identification numbers

 

1.4.1  CAS

 

125-69-9 (anhydrous)

 

1.4.2  Other numbers

 

CAS: 6700-34-1 (monohydrate)

 

1.5  Brand names/trade names:

 

Polistirex Extended Release suspension.

 

1.6  Manufacturers and importers:

 

To be completed by each centre using the mongraph.

 

  1. SUMMARY

 

2.1  Main risks and target organs

 

The main risks associated with dextromethorphan are

ataxia, central nervous system (CNS) stimulation, dizziness,

lethargy and psychotic behavior. Less frequently with large

doses seizures and respiratory depression can occur. Nausea,

vomiting, constipation and tachycardia may occur. The main

target organ is the central nervous system (CNS).

 

2.2  Summary of clinical effects

 

Central nervous system effects include ataxia,

drowsiness, vertigo and rarely coma. CNS stimulation may be

observed. Restlessness, increased muscle tone with body

rigidity have been reported. With extremely large ingestions

respiratory depression can occur. Gastrointestinal effects

include nausea, vomiting, constipation and dry mouth. Urinary

retention may be seen. Dextromethorphan abuse has been

described and produces euphoria, CNS stimulation, visual

and/or auditory hallucinations. There does not appear to be

any evidence of dependence of the morphine type.

The possibility of bromide poisoning should be considered in

the long term abuser.

 

2.3  Diagnosis

 

Diagnosis of dextromethorphan toxicity is primarily

based on the history of an ingestion of dextromethorphan or

dextromethorphan containing products. The presence of

dextromethorphan may be confirmed by qualitative

determination of the drug in urine.

 

2.4  First aid measures and management principles

 

Assess and support airway, respiration and

cardiovascular function if needed. Gastric decontamination is

recommended for recent ingestions of more than 10 mg/kg.

Seizures and/or CNS depression have occurred within 30

minutes of ingesting dextromethorphan.

 

ACTIVATED CHARCOAL/CATHARTIC.

Activated charcoal may be given alone or with a cathartic

such as sorbitol or magnesium citrate even though at this

time there is no data concerning the adsorption or clinical

efficacy of activated charcoal in the treatment of

dextromethorphan ingestions.

 

GASTRIC LAVAGE followed by activated charcoal may be

indicated for the treatment of recent large ingestions, or in

patients who are comatose or at risk of convulsing.  NALOXONE

may be of benefit to reverse the respiratory and CNS effects

of dextromethorphan although its efficacy is yet to be

adequately determined.

 

  1. PHYSICO-CHEMICAL PROPERTIES

 

3.1  Origin of the substance

 

Dextromethorphan is a synthetic compound.

Dextromethorphan has been abused and is claimed to be habit

forming but has not been reported to produce physical

dependence (Ellenhorn & Barceloux 1988). It is not a

substitute for opiates in dependent individuals.

 

3.2  Chemical structure

 

Chemical name:

Dextromethorphan is 3 Methoxy-17-methylmorphinan monohydrate,

which is the d isomer of levophenol, a codeine analogue and

opioid analgesic.

 

Molecular formula: (Dextromethorphan Hydrobromide):

C18H25NO.HBr.H2O

 

Molecular weight 370.3

 

3.3  Physical properties

 

3.3.1  Colour

 

White

 

3.3.2  State/form

 

Solid-crystals

Solid-powder

 

3.3.3  Description

 

Odourless verging on a faint odour. Solubility

in water 1.5 g/100 mL at 25 C.

Soluble 1 in 10 of ethanol.

Practically insoluble in ether.

Freely soluble in chloroform.

pH of a 1% aqueous solution 5.2 to 6.5 (Budavari,

1996).

 

3.4  Other characteristics

 

3.4.1  Shelf-life of the substance

 

No information available.

 

3.4.2  Storage conditions

 

Powder should be preserved in air-tight

containers and solutions stored in light-resistant

containers (USP National Formulary).

 

Lozenges: store between 15 and 30 degrees C in well

closed containers.

Syrup USP: Store between 15 and 30 degrees C in light,

resistant container, protected from freezing.

 

  1. USES

 

4.1  Indications

 

4.1.1  Indications

 

Cough/cold preparation

Antitussive (not with expectorant);

cough/cold

Opioid;

antitussive

 

4.1.2  Description

 

Antitussive.

 

4.2  Therapeutic dosages

 

4.2.1  Adults

 

Oral doses of 10 to 20 mg every four hours or

30 mg every 6 to 8 hours not to exceed 120 mg

daily.

 

Long-acting preparations: 60 mg twice a day.

 

4.2.1  Children

 

Children aged 6 to 12 years may be given 5 to

10 mg every 4 hours or 15 mg every six to eight hours,

not to exceed 60 mg daily.

 

Children aged 2 to 6 years 2.5 to 5.0 mg every 4 hours

or 7.5 mg every 6 to 8 hours not to exceed 30 mg

daily.

The recommended dose in a child is 1 mg/kg/day to 2

mg/kg/day given in three to four divided doses (Benitz

& Tatro, 1988).

Dextromethorphan is not generally recommended in

children less than two years of age unless under

medical supervision (USPC, 1991).

 

Long-acting preparations: children aged 6 to 12 years

30 mg twice a day and children aged 2 to 6 years 15 mg

twice a day (AHFS, 1992).

 

4.3  Contraindications

 

Dextromethorphan should not be administered in patients

taking selective serotonin reuptake inhibitors (eg

fluoxetine, paroxetine) (Skop et al., 1994) and monoamine

 

oxidase inhibitors (Rivers & Horner, 1970). This may produce

a life threatening serotonergic syndrome which consists of:

restlessness, sweating, hypertension, hyperthermia, tremor,

myoclonus and seizures.

 

Dextromethorphan may be associated with histamine release and

should not be used in atopic children. Dextromethorphan

should not be taken for persistent or chronic cough (e.g.

with smoking, emphysema, asthma) or when coughing is

accompanied by excessive secretions, unless directed by a

physician (AHFS, 1992).

Alcohol and CNS depressants should be avoided with

dextromethorphan.

 

  1. ROUTES OF EXPOSURE

 

5.1  Oral

 

Dextromethorphan is usually taken orally.

It has been abused orally.

 

5.2  Inhalation

 

Dextromethorphan has been sniffed in the abuse setting.

 

5.3  Dermal

 

No data available

 

5.4  Eye

 

No data available

 

5.5  Parental

 

No data available

 

5.6  Others

 

No data available

 

  1. KINETICS

 

6.1  Absorption by route of exposure

 

Dextromethorphan is well absorbed from the

gastrointestinal tract with maximum serum level occurring at

2.5 hours (Barnhart et al., 1979).  Peak concentration of the

major metabolite dextrorphan) was 1.6  to 1.7 hours (Silvasti

et al., 1987).  Onset of effect is rapid, often beginning 15

to 30 minutes after oral ingestion (Pender & Parks, 1991).

 

Peak levels for sustained release products generally occur

about 6 hours after ingestion (Amsel, 1981) although

absorption may be erratic.

 

6.2  Distribution by route of exposure

 

There is no information about the volume of distribution

in humans. In dogs, the volume of distribution is reported to

range from 5.0 to 6.4 L/Kg (Baselt & Cravey, 1989).

 

6.3  Biological half-life by route of exposure

 

The half life of the parent compound is approximately 2

to 4 hours in people with normal metabolism.

 

6.4  Metabolism

 

There is a clear first pass metabolism and it is

generally assumed that the therapeutic activity is primarily

due to its active metabolite, dextrophan (Silvasti et al.,

1987; Baselt & Cravey, 1982).

Genetic polymorphism has profound effects on its metabolism

(Hildebrand et al 1989).  Dextromethorphan undergoes

polymorphic metabolism depending on variation in cytochrome

P-450 enzyme phenotype. The specific cytochrome P-450 enzyme

is P450 2D6(CYP2D6) (Schadel et al., 1995).

Fast metabolizers constitute about 84% of the population.

After a 30 mg dose plasma levels are less than 5 ng/mL four

hours postingestion (Woodworth et al., 1987). Intermediate

metabolizers constitute about 6.8% of the population. After

an oral dose of 30 mg plasma levels are 10 to 20 ng/mL at 4

hours and less than 5 ng/mL at 24 hours postingestion

(Woodworth et al., 1987).  Poor metabolizers constitute 5% to

10% of the Caucasian population. The ratio of metabolite to

parent drug in 8 hour urine sample is less than 10 to 1 after

a 15 mg dose (Hildebrand et al., 1989).  After an oral dose

of 30 mg plasma levels are greater than 10 ng/mL at 4 hours

and greater than 5 ng/mL at 24 hours (Woodworth et al.,

1987).

It is metabolized in the liver by extensive metabolizers to

dextrorphan. Dextrorphan is itself an active antitussive

compound (Baselt & Cravey, 1982). Only small amounts are

formed in poor metabolizers (Kupfer, 1986).  Less than 15% of

the dose form minor metabolites including D-methoxymorphinane

and D-hydroxmorphinane (Kupfer, 1986).

 

6.5  Elimination by route of exposure

 

Dextromethorphan and its metabolites are excreted via

the   kidney. Depending on the metabolism phenotype up to 11%

may be excreted unchanged or up to 100% as demethylated

 

conjugated morphinan compounds (Hildebrand, 1989).  In the

first 24 hours after dosing, less than 0.1% is eliminated in

the faeces (Baselt & Cravey, 1989).

 

  1. PHARMACOLOGY AND TOXICOLOGY

 

7.1  Mode of action

 

7.1.1  Toxicodynamics

 

The toxicodynamic actions of dextromethorphan

are not completely defined. Dextromethorphan enhances

serotonin activity by inhibiting the reuptake of

serotonin (Kramei et al., 1992; Bem & Peck, 1992)

Specific non-opioid dextromethorphan binding sites are

present in the central nervous system (CNS) which

mediate the antitussive effects, separate from codeine

and other opioids (Hardman et al., 1996).

Dextromethorphan and dextrorphan both affect the NMDA

receptor (Carpenter et al., 1988; Reynolds, 1993).

 

7.1.2  Pharmacodynamics

 

The antitussive effects of dextromethorphan and

the metabolite dextrorphan are secondary to binding in

the CNS at non-opioid receptors. Dextromethorphan does

not have analgesic or addictive properties, although

abuse and dependence have been described(Hardman et

al, 1996). One of the major metabolites, dextrorphan

has cough suppressant activity.

 

7.2  Toxicity

 

7.2.1  Human data

 

7.2.1.1  Adults

 

Coma was reported in an adult who

ingested 720 mg over 36 hours (Schneider,

1991).  Rated as lethal at oral doses of 50

to 500 mg/kg (Gosselin, 1981).

Death has been reported after overdose in two

cases but quantity was uncertain (Rammer et

al., 1988).

Long-acting products: adults have tolerated

up to 960 mg/day with minor adverse effects

(Walker and Hunt, 1989).

Abuse: Has been used for abuse. Orally in

doses of 300 mg to 1800 mg in adults it can

cause intoxication with hyperexcitability,

visual and/or auditory hallucinations (Dodds

& Revai, 1967; Orrell & Campbell, 1986). It

 

has been reported that sniffing 0.25 g two to

three times a day over 2 to 3 months produced

euphoria and restlessness for up to 2 hours

followed by dizziness, nausea, depression and

fatigue (Fleming, 1986).

Chronic effects: It should be noted that

dextromethorphan is marketed as the

hydrobromide and can produce bromide toxicity

with chronic use.

Dextromethorphan has been abused at doses of

2160 to 2880 mg daily for up to five years

producing hallucinations, euphoria,

disorientation, insomnia and nausea.

Withdrawal produced dysphoria and craving for

the drug (Wolf and Caravati 1995).

 

7.2.1.2  Children

 

Toxicity may be variable in

children. Ingestion of as little as 17 mg/Kg

has resulted in signs and symptoms of

toxicity.  At this dosage range some children

have shown no symptoms whilst others have

shown ataxia, stupor, transient fever,

lethargy or nystagmus (Versie et al., 1962;

Katona & Wason, 1986). Seizures have been

reported.

Long-acting products may be more toxic in

children, producing prolonged CNS depression

at 10 mg/kg (Devlin, 1985).

 

7.2.3  Animal data

 

LD 50 in mice 165 mg/kg

LD 50 in rats 350 mg/kg (Gosselin, 1981)

LD 50 in mice 39 mg/Kg (Benson, 1953)

 

7.2.3  Relevant in-vitro data

 

No data available

 

7.3  Carcinogenicity:

 

No data available

 

7.4  Teratogenicity

 

There was no association between dextromethorphan and

malformations (Heinonen et al., 1977). Dextromethorphan is

generally considered safe to use during pregnancy (Berkowitz

et al., 1981).

 

7.5  Mutagenicity

 

No data available

 

7.6  Interactions

 

Concomitant use of monoamine oxidase inhibitors has

caused toxicity leading to death (Rivers & Horner, 1970;

Hansten, 1989).

Not to be taken with serotonin re-uptake inhibitors

(Skop et al., 1994)

Alcohol and drugs causing CNS depression should be avoided

when taking dextromethorphan.

 

7.7  Main adverse effects

 

Adverse effects are very uncommon with therapeutic doses.

Infrequent adverse effects include dizziness, drowsiness,

nausea, vomiting and stomach ache (USPC, 1989).

 

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

 

8.1  Material sampling plan

 

8.1.1  Sampling and specimen collection

 

8.1.1.1  Toxicological analyses

 

8.1.1.2  Biomedical analyses

 

8.1.1.3  Arterial blood gas analysis

 

8.1.1.4  Haematological analyses

 

8.1.1.5  Other (unspecified) analyses

 

8.1.2  Storage of laboratory samples and specimens

 

8.1.2.1  Toxicological analyses

 

8.1.2.2  Biomedical analyses

 

8.1.2.3  Arterial blood gas analysis

 

8.1.2.4  Haematological analyses

 

8.1.2.5  Other (unspecified) analyses

 

8.1.3  Transport of laboratory samples and specimens

 

8.1.3.1  Toxicological analyses

 

8.1.3.2  Biomedical analyses

 

8.1.3.3  Arterial blood gas analysis

 

8.1.3.4  Haematological analyses

 

8.1.3.5  Other (unspecified) analyses

 

8.2  Toxicological Analyses and Their Interpretation

 

8.2.1  Tests on toxic ingredient(s) of material

 

8.2.1.1  Simple Qualitative Test(s)

 

8.2.1.2  Advanced Qualitative Confirmation Test(s)

 

8.2.1.3  Simple Quantitative Method(s)

 

8.2.1.4  Advanced Quantitative Method(s)

 

8.2.2  Tests for biological specimens

 

8.2.2.1  Simple Qualitative Test(s)

 

8.2.2.2  Advanced Qualitative Confirmation Test(s)

 

8.2.2.3  Simple Quantitative Method(s)

 

8.2.2.4  Advanced Quantitative Method(s)

 

8.2.2.5  Other Dedicated Method(s)

 

8.2.3  Interpretation of toxicological analyses

 

8.3  Biomedical investigations and their interpretation

 

8.3.1  Biochemical analysis

 

8.3.1.1  Blood, plasma or serum

 

“Basic analyses”

“Dedicated analyses”

“Optional analyses”

 

8.3.1.2  Urine

 

“Basic analyses”

“Dedicated analyses”

“Optional analyses”

 

8.3.1.3  Other fluids

 

8.3.2  Arterial blood gas analyses

 

8.3.3  Haematological analyses

 

“Basic analyses”

“Dedicated analyses”

“Optional analyses”

 

8.3.4  Interpretation of biomedical investigations

 

8.4  Other biomedical (diagnostic) investigations and their

interpretation

 

8.5  Overall interpretation of all toxicological analyses and

toxicological investigations

 

Monitoring dextromethorphan serum levels is not useful

clinically in the overdose situation because a correlation

between levels and clinical effects has yet to be determined

(Walker & Hunt, 1989). However plasma levels may be measured

to determine metabolizer phenotype.  The presence of

dextromethorphan may be confirmed by qualitative

determination of the drug in urine or serum.

 

Plasma dextromethorphan concentrations have not been

correlated with clinical toxicity. Monitoring concentrations

of dextromethorphan, therefore, would not be useful

(Ellenhorn & Barceloux, 1983; Walker & Hunt, 1989) Plasma

dextromethorphan concentrations are used to determine hepatic

metabolism phenotype.

 

Sample collection

If required arterial blood for blood gasses.

 

Biomedical analysis

Arterial blood gasses to determine the degree of ventilatory

depression.

 

Toxicological analysis

The presence of dextromethorphan may be confirmed by

qualitative determination of the drug in urine or blood, see

Section 8. Plasma levels may be used to determine metabolizer

phenotype.

 

  1. CLINICAL EFFECTS

 

9.1  Acute poisoning

 

9.1.1  Ingestion

 

Oral ingestion is the most common route of

acute poisoning. The most common clinical effects

involve the central nervous system (CNS).

Neurologic: drowsiness, lethargy, ataxia, nystagmus,

CNS stimulation, vertigo, coma, psychosis and

hyperreflexia (Cetaruk & Aaron, 1995; Wolfe &

 

Caravati, 1995; Devlin et al., 1985; Shaul et al.,

1977; Schneider et al., 1991).

Seizures have been reported within 30 minutes of

ingestion.

Respiration: Respiratory depression has been noted

(Katona and Wason, 1986; Shaul et al., 1977).

Cardiovascular: Long-acting preparations may cause

tachycardia (Devlin et al.,  1985).

Gastrointestinal: Nausea, vomiting (Versie at al.,

1962) constipation and dry mouth may occur.

Eye: Mydriasis, miosis and nystagmus may be seen.

Genitourinary: Retention of urine may be seen.

Skin: Urticaria was noted after ingestion of a long-

acting preparation in a child (Devlin et al.,

1985).

Long-acting preparations: With 10 mg/Kg or more taken

orally ataxia, lethargy, nystagmus and tachycardia

have been reported.

 

9.1.2  Inhalation

 

No data available.

 

9.1.3  Skin exposure

 

No data available.

 

9.1.4  Eye contact

 

No data available.

 

9.1.5  Parenteral exposure.

 

No data available

 

9.1.6  Other

 

No data available.

 

9.2  Chronic Poisoning

 

9.2.1  Ingestion

 

The daily abuse of oral dextromethorphan has

been described as causing hallucinations (visual and

auditory), dyspnea, floating and flying sensations,

and increased perception (Wolfe & Caravati, 1995).

Central nervous system (CNS) stimulation has also been

reported (Dodds & Revai, 1967; Orrell & Campbell,

1986). When the drug was stopped no withdrawal

symptoms were noted, however, craving for

dextromethorphan continued.

 

It should be noted that dextromethorphan may be

marketed as the hydrobromide salt and can produce

bromide toxicity with chronic use.

 

9.2.2  Inhalation

 

No data available.

 

9.2.3  Skin contact

 

No data available

 

9.2.4  Eye contact

 

No data available

 

9.2.5  Parental exposure

 

No data available

 

9.2.6  Other

 

It has been reported that sniffing 0.25 g two

to three times a day over 2 to 3 months produced

euphoria and restlessness for up to 2 hours followed

by dizziness, nausea, depression and fatigue (Fleming,

1986).  This patient did not demonstrate withdrawal

symptoms on cessation but did complain of continuing

craving for dextromethorphan.

 

9.3  Course, prognosis, cause of death:

 

Following overdose of short acting dextromethorphan

patients may become clumsy, hyperkinetic and ataxic a few

hours after the ingestion. There may be vomiting, drowsiness,

dizziness, blurred vision, nystagmus, and visual and auditory

hallucinations. Later unsteadiness and unstable gait are

observed with truncal ataxia. In severe cases, shallow

respirations, urinary retention, stupor, or coma may

supervene, especially if high doses of alcohol have been

ingested. The prognosis for recovery is good (Ellenhorn &

Barceloux, 1988).

Following ingestion of long acting dextromethorphan symptoms

of over use in children include urticaria, restlessness,

lethargy, nystagmus, ataxia, tachycardia and blood pressure

elevation. This may require admission to an intensive care

unit. Long acting preparations may produce a higher rate of

toxic symptoms in children than short-acting

dextromethorphan. There does not appear to be a correlation

between the amount of long-acting dextromethorphan ingested

and the severity of symptoms (Ellenhorn & Barceloux,

1988).

 

9.4  Systematic description of clinical effects:

 

9.4.1  Cardiovascular

 

Long-acting preparations may cause tachycardia

(Devlin et al., 1985).  No reports of chronic effects

were found in the literature.

 

9.4.2  Respiratory

 

Respiratory depression has been noted following

large doses (Katona and Wason, 1986; Shaul et al.,

1977). No reports of chronic effects were found in the

literature.

 

9.4.3  Neurologic

 

9.4.3.1  Central nervous system (CNS)

 

In acute overdose ataxia, drowsiness

(Devlin et al., 1985; Shaul et al., 1977)

vertigo and coma (Schneider et al.,

1991).

CNS stimulation may be noted.  Restlessness,

increased muscle tone with body rigidity have

been reported (Benson et al., 1953).

Seizures have been reported within 30 minutes

of ingestion.

In the abuse situation it can cause CNS

stimulation and visual and/or auditory

hallucinations (Dodds & Revai, 1967; Orrell &

Campbell, 1986). It has been reported that

sniffing 0.25 g two to three times a day over

2 to 3 months produced euphoria and

restlessness for up to 2 hours followed by

dizziness, nausea, depression and fatigue

(Fleming, 1986).

Cognitive deterioration resulting from

prolonged abuse has been reported (Hinsberger

et al., 1994).

 

9.4.3.2  Peripheral nervous system

 

No data available

 

9.4.3.3  Autonomic

 

No data available

 

9.4.3.4  Skeletal and smooth muscle

 

No data available

 

9.4.4  Gastrointestinal

 

After acute overdose nausea, vomiting (Versie

et al., 1962), constipation and dry mouth may occur.

No chronic effects were found.

 

9.4.5  Hepatic

 

No data available.

 

9.4.6  Urinary

 

9.4.6.1  Renal

 

No data available.

 

9.4.6.2  Others

 

Urinary retention has been seen.

 

9.4.7  Endocrine and reproductive systems

 

No data available.

 

9.4.8  Dermatologic

 

Urticaria was reported in a child after acute

overdose of a long-acting preparation (Devlin et

al.,1985).

 

9.4.9  Eye, ear, throat: local effects

 

After acute overdose mydriasis or miosis

(Schneider et al.,  1991) and nystagmus (Katona &

Wason, 1986; Devlin et al., 1985) may be noted.

Nystagmus may persist from 7 to 8 hours with long-

acting preparations (Devlin et al., 1985). No chronic

effects were found.

 

9.4.10 Hematological

 

No data available.

 

9.4.11 Immunologic

 

No data available.

 

9.4.12 Metabolic

 

9.4.12.1 Acid-base disturbances

 

No data available.

 

9.4.12.2 Fluid and electrolyte disturbances

 

No data available.

 

9.4.12.3 Others

 

No data available.

 

9.4.13 Allergic reactions

 

A cutaneous lesion consistent with a fixed-

drug reaction was reported after ingestion over 2 to 3

weeks in therapeutic doses (Stubb & Reitamo,

1990).

 

9.4.14 Other clinical effects

 

No data available.

 

9.4.15 Special risks

 

Pregnancy:

Ingesting dextromethorphan during the first trimester

demonstrated no association between the drug and

malformations (Heinonen, 1989).  Dextromethorphan is

generally considered safe during pregnancy (Berkowitz,

1981).

 

Breast feeding:

No data available.

 

Enzyme deficiencies:

No data available.

 

Serotonergic Syndrome (see 4.3)

 

9.5  Others

 

Dextromethorphan has been used for abuse however there

were no withdrawal symptoms on cessation but there was a

continued craving for the drug.

 

  1. MANAGEMENT

 

10.1 General principles

 

Assess and support airway, ventilation, and

circulation. Naloxone may antagonize respiratory depression.

Gastric decontamination is recommended for recent ingestions

of more than 10 mg/kg of dextromethorphan.  Patients with

respiratory depression may require admission to an intensive

care unit. Others can be observed in the emergency facility

for 4 to 6 hours and then discharged. A small number of

patients with minor symptoms (such as ataxia or restlessness)

 

may be sent home under careful supervision. (Ellenhorn &

Barceloux, 1988) Children who have ingested a long-acting

preparation should be hospitalized.

 

10.2 Life supportive procedures and symptomatic treatment

 

Assess and support airway, ventilation, and

circulation. Naloxone may antagonize respiratory depression.

Patients with respiratory depression may require admission to

an intensive care unit. Other patients can be observed in the

emergency facility for 4 to 6 hours and then discharged.

Patients with minor symptoms (such as ataxia or restlessness)

may be sent home under supervision. (Ellenhorn & Barceloux,

1988) Children who have ingested a long-acting preparation

should be hospitalized for 24 observation.

 

10.3 Decontamination

 

Gastric decontamination is recommended for a recent

ingestion of more than 10 mg/kg. Seizures and/or central

nervous system (CNS) depression have occurred within 30

minutes of ingesting dextromethorphan.

 

GASTRIC LAVAGE followed by activated charcoal may be used

within 1 to 2 hours of ingestion and may be indicated in

recent large ingestions or in patients who are comatose or at

risk of convulsing. Gastric lavage in a comatose patient

should be preceded by intubation.

 

ACTIVATED CHARCOAL/CATHARTIC. Activated charcoal may be given

alone or with a cathartic such as sorbitol or magnesium

citrate, even though at this time there is no data concerning

the adsorption of dextromethorphan by charcoal.

Because there is no data concerning the adsorption of

dextromethorphan by charcoal if routine gastric emptying is

omitted the patient may receive inadequate treatment if

charcoal alone is used. A reasonable approach might be to

consider gastric lavage in patients ingesting more than 10

mg/Kg of dextromethorphan, those with clinical features of

overdose, or those where the time and quantity of ingestion

is unknown.

The optimum dose of activated charcoal has not been

established, but as a guide 1 g to 2 g/kg of activated

charcoal is recommended, particularly in infants. The adult

dose may therefore be 30 g to 100 g and the dose in children

15 g to 30 g.  If a patient vomits the dose it may be

repeated.  Do not use charcoal tablets or universal antidote

as a substitute for activated charcoal.

 

WHOLE BOWEL LAVAGE. If a long-acting dextromethorphan

preparation has been ingested whole bowel lavage may be

considered.

 

CATHARTIC. A saline cathartic or sorbitol may be administered

with the first dose of activated charcoal or it may be given

separately.  Although there is little evidence to support the

use of cathartics (McNamara, 1988; Stewart, 1983) their use

would seem logical to shorten transit time and avoid the

constipation caused by charcoal. Repeated doses of cathartics

is not recommended especially in children. If the dose is

repeated this should be done with extreme caution.

 

10.4 Enhancd elimination

 

There is no information currently available on the

effectiveness of forced diuresis, alkalinization,

acidification, haemoperfusion, or dialysis for the treatment

of dextromethorphan overdose.  The use of these methods of

potentially increasing drug elimination are not recommended

for the treatment of dextromethorphan poisonings.

 

10.5 Antidote

 

10.5.1 Adults

 

NALOXONE may be of benefit to reverse the

respiratory and CNS effects of dextromethorphan.

Although there have been reports concerning the

response to naloxone (Katona & Wason, 1986; Shaul et

al, 1977), in most cases improvement in, and

resolution of, neurologic symptoms occurred over three

to eight hours after naloxone administration, and this

may represent the natural course of dextromethorphan

toxicity rather than a response to naloxone

(Pender,1991).  There is currently no evidence which

suggests significant efficacy associated with naloxone

administration (Wolfe & Caravati, 1995).

 

10.5.2 Children

 

No data available.

 

10.6 Management discussion

 

Many references still recommend the use of Ipecac to

induce emesis in dextromethorphan overdose.  However there

have been reports of seizures following overdose and thus

this monograph does not advocate the induction of emesis.

Also, most dextromethorphan ingestions are the liquid

formulation which are most likely absorbed quickly. Emesis

may thus be ineffective and contraindicated due to rapid CNS

depression, and may delay the administration of activated

charcoal. Charcoal has been recommended without reports

proving or disproving its efficacy. However it is commonly

 

used for dextromethorphan overdose and is likely to be

effective and safe. Research on this matter would determine

if this is so.

Further information is required before naloxone can be

accepted as an antidote for dextromethorphan toxicity.  The

cases presented to date do not support reversal of

dextromethorphan toxicity by naloxone. This is supported by

the pharmacology of dextromethorphan (Wolfe & Caravati, 1995;

Hardman et al., 1996).

 

  1. ILLUSTRATIVE CASES

 

11.1 Case report from the literature

 

Case 1

A 41 year old female ingested 720 mg of dextromethorphan over

a 36 hour period. She presented lethargic and responding only

to painful stimuli. Respirations were shallow and sporadic,

pupils pinpoint and minimally reactive to light. Because of

her decreased level of consciousness and miosis, 1 mg of

naloxone intravenous (IV) was administered with some

improvement of consciousness. An additional 2 mg naloxone was

administered with further improvement and ultimate return to

normal mental status. Serum samples showed dextromethorphan

level of 100 ng/mL (Schneider et al., 1991).

 

Case 2

A report is given of two young adults who died after overdose

of dextromethorphan. How much was taken is uncertain (Rammer

at al 1988).

 

Case 3

A 23 year old male presented with psychosis after an acute

overdose of dextromethorphan. He demonstrated

hyperexcitability and hallucinations which he compared to his

experience with LSD.(Dodds & Revai, 1967).

 

Case 4

A 26 year old female took approximately 60ml of a cough

medicine containing dextromethorphan about six hours after

ingesting 30 mg of phenelzine (Nardil). Thirty minutes later

she felt nauseated, dizzy and collapsed. Within one hour she

was brought to the hospital unconscious with rigid

extremities and fixed, dilated pupils.  She was severely

hypotensive with a systolic blood pressure that did not rise

above 70 mm of mercury and a temperature that ranged from

42°C to 42.2°C. Despite vasopressors, anti-arrhythmics and

adrenaline, approximately four hours after arriving at the

hospital she had a cardiac arrest and died (Rivers & Horner,

1970).

 

Case 5

An 11 week old infant was given inappropriate doses of a

dextromethorphan/guaifenesin mixture over a period of 24

hours. Doses were more frequent and larger than those

recommended, but the exact amount was unable to be

determined.  The infant was alert and noted to be

hyperexcitable with intermittent periods of extremity

stiffening and cutaneous mottling.  He was given naloxone 0.1

mg/Kg intravenously.  Within 30 minutes of the naloxone he

was noted to be calmer and within two hours all signs had

resolved (Pender & Parks, 1991).

 

Case 6

A 3 year old boy ingested an unknown amount of

dextromethorphan and presented with lethargy, somnolence,

ataxia and nystagmus. Vital signs were normal, and

respirations adequate. He awoke after he was given

intravenous naloxone (0.4 mg).  Twenty five grams of charcoal

was given and during the next three hours his condition

steadily improved and he was discharged (Katona & Wason,

1986).

 

  1. ADDITIONAL INFORMATION

 

12.1 Specific preventive measures

 

Dextromethorphan must not be used with monoamine

oxidase inhibitors (MAOIs) since death has occurred.

Dextromethorphan should not be used with other CNS

depressants.

Dextromethorphan should not be used with serotonin re-uptake

inhibitors.

Care should be taken that dextromethorphan is not given in

overdose, especially to children.

Medicines containing dextromethorphan are best store in child

resistant containers.

Dextromethorphan has been abused and care should be taken not

to supply it to susceptible individuals.

 

12.2 Other

 

No data available.

 

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USP (1991) Drug information for the Health Care Professional, 11th

ed, Vol 1. US Pharmacoepial Convention, Inc, Rockville,

Maryland.

 

Versie R, Noirfalise A, Neven M et al. (1962) Toxicite et

metabolisme du 3 methoxy-N-methyl morphinane (Romilar) chez

l’infant. Ann Med Leg 42:561-565.

 

Walker FO, Hunt VP (1989) An open label trial of dextromethorphan

in Huntington’s Disease. Clin Neuropharmacol 12:322-330.

 

Watson WA, Cremer K, Chapman (1986) Gastrointestinal obstruction

associated with multiple dose activated charcoal. J Emerg Med

4:407-410.

 

Wolfe TR, Caravati ME (1995) Massive Dextromethorphan Ingestion

and Abuse. Am J Emerg Med 13;174-176.

 

Woodworth JR, Dennis SRK, Moore L et al (1987) The polymorphic

metabolism of dextromethorphan. J Clin Pharmacol 27:139-143

 

  1. AUTHOR(S), REVIEWER(S) DATES (INCLUDING EACH UPDATING), COMPLETE

ADDRESSES

Author: Jim Magarey

Poisons Information Centre

Royal Childrens Hospital

 

Date of writing: 1992

Updated by same author August 1996

Peer review: Dr. A.N.P. van Heijst, August 1996

Dr. W. Watson August, 1996

PIM review group: Intox 9, September, 1996, Cardif, Wales

Editor: Dr M. Ruse (August, 1997)

Abrus precatorius L.

  1. NAME

1.1 Scientific name

1.2 Family

1.3 Common name(s)

  1. SUMMARY

2.1 Main risks and target organs

2.2 Summary of clinical effects

2.3 Diagnosis

2.4 First-aid measures and management principles

2.5 Poisonous parts

2.6 Main toxins

  1. CHARACTERISTICS

3.1 Description of the plant

3.1.1 Special identification features

3.1.2 Habitat

3.1.3 Distribution

3.2 Poisonous parts of the plant

3.3 The toxin(s)

3.3.1 Name(s)

3.3.2 Description, chemical structure, stability

3.3.3 Other physico-chemical characteristics

3.4 Other chemical contents of the plant

  1. USES/CIRCUMSTANCES OF POISONING

4.1 Uses

4.2 High risk circumstances

4.3 High risk geographical areas

  1. ROUTES OF ENTRY

5.1 Oral

5.2 Inhalation

5.3 Dermal

5.4 Eye

5.5 Parenteral

5.6 Others

  1. KINETICS

6.1 Absorption by route of exposure

6.2 Distribution by route of exposure

6.3 Biological half-life by route of exposure

6.4 Metabolism

6.5 Elimination by route of exposure

  1. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY

7.1 Mode of action

7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

7.2.1.2 Children

7.2.2 Animal data

7.2.3 Relevant in vitro data

7.3 Carcinogenicity

7.4 Teratogenicity

7.5 Mutagenicity

7.6 Interactions

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

8.1 Material sampling plan

8.1.1 Sampling and specimen collection

8.1.1.1 Toxicological analyses

8.1.1.2 Biomedical analyses

8.1.1.3 Arterial blood gas analysis

8.1.1.4 Haematological analyses

8.1.1.5 Other (unspecified) analyses

8.1.2 Storage of laboratory samples and specimens

8.1.2.1 Toxicological analyses

8.1.2.2 Biomedical analyses

8.1.2.3 Arterial blood gas analysis

8.1.2.4 Haematological analyses

8.1.2.5 Other (unspecified) analyses

8.1.3 Transport of laboratory samples and specimens

8.1.3.1 Toxicological analyses

8.1.3.2 Biomedical analyses

8.1.3.3 Arterial blood gas analysis

8.1.3.4 Haematological analyses

8.1.3.5 Other (unspecified) analyses

8.2 Toxicological Analyses and Their Interpretation

8.2.1 Tests on toxic ingredient(s) of material

8.2.1.1 Simple Qualitative Test(s)

8.2.1.2 Advanced Qualitative Confirmation Test(s)

8.2.1.3 Simple Quantitative Method(s)

8.2.1.4 Advanced Quantitative Method(s)

8.2.2 Tests for biological specimens

8.2.2.1 Simple Qualitative Test(s)

8.2.2.2 Advanced Qualitative Confirmation Test(s)

8.2.2.3 Simple Quantitative Method(s)

8.2.2.4 Advanced Quantitative Method(s)

8.2.2.5 Other Dedicated Method(s)

8.2.3 Interpretation of toxicological analyses

8.3 Biomedical investigations and their interpretation

8.3.1 Biochemical analysis

8.3.1.1 Blood, plasma or serum

8.3.1.2 Urine

8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses

8.3.3 Haematological analyses

8.3.4 Interpretation of biomedical investigations

8.4 Other biomedical (diagnostic) investigations and their interpretation

8.5 Overall Interpretation of all toxicological analyses and toxicological investigations

8.6 References

  1. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

9.1.2 Inhalation

9.1.3 Skin exposure

9.1.4 Eye contact

9.1.5 Parenteral exposure

9.1.6 Other

9.2 Chronic poisoning

9.2.1 Ingestion

9.2.2 Inhalation

9.2.3 Skin exposure

9.2.4 Eye contact

9.2.5 Parenteral exposure

9.2.6 Other

9.3 Course, prognosis, cause of death

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

9.4.2 Respiratory

9.4.3 Neurological

9.4.3.1 CNS

9.4.3.2 Peripheral nervous system

9.4.3.3 Autonomic nervous system

9.4.3.4 Skeletal and smooth muscle

9.4.4 Gastrointestinal

9.4.5 Hepatic

9.4.6 Urinary

9.4.6.1 Renal

9.4.6.2 Others

9.4.7 Endocrine and reproductive systems

9.4.8 Dermatological

9.4.9 Eye, ears, nose, throat: local effects

9.4.10 Haematological

9.4.11 Immunological

9.4.12 Metabolic

9.4.12.1 Acid base disturbances

9.4.12.2 Fluid and electrolyte disturbances

9.4.12.3 Others

9.4.13 Allergic reactions

9.4.14 Other clinical effects

9.4.15 Special risks

9.5 Others

9.6 Summary

  1. MANAGEMENT

10.1 General principles

10.2 Relevant laboratory analyses and other investigations

10.2.1 Sample collection

10.2.2 Biomedical analysis

10.2.3 Toxicological/toxinological analysis

10.2.4 Other investigations

10.3 Life supportive procedures and symptomatic treatment

10.4 Decontamination

10.5 Elimination

10.6 Antidote/antitoxin treatment

10.6.1 Adults

10.6.2 Children

10.7 Management discussion

  1. ILLUSTRATIVE CASES

11.1 Case reports from literature

11.2 Internally extracted data on cases

11.3 Internal cases

  1. ADDITIONAL INFORMATION

12.1 Availability of antidotes/antitoxins

12.2 Specific preventive measures

12.3 Other

  1. REFERENCES

13.1 Clinical and toxicological

13.2 Botanical

  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

POISONOUS PLANTS

  1. NAME

1.1 Scientific name

Abrus precatorius L.

1.2 Family

Leguminosae

1.3 Common name(s)

Abrus seed

Aivoeiro

Arraccu-mitim

Buddhist rosary bead

Carolina muida

Crabs eye

Deadly crab’s eye

Indian bead

Indian liquorice

Jequirite

Jequirity Bean

Jumble beads

Juquiriti

Lucky bean

Prayer beads

Precatory bean

Rosary beads

Rosary Pea

Ruti

Tentos da America

Tentos dos mundos

Weather plant

Wild liquorice

  1. SUMMARY

2.1 Main risks and target organs

The main risk is the severe gastroenteritis leading to

dehydration and shock.

Ingested seeds can affect the gastrointestinal tract, the

liver, spleen, kidney, and the lymphatic system.  Infusion of

seed extracts can cause eye damage after contact.

2.2 Summary of clinical effects

The early features of toxicity are burning of the mouth and

oesophagus, and severe gastroenteritis with vomiting,

haematemesis, diarrhoea, melaena, and abdominal pain.  Later,

drowsiness, disorientation, weakness, stupor, convulsions,

shock, cyanosis, retinal haemorrhages, haematuria, and

oliguria can occur.  Contact with the eyes can cause

conjunctivitis and even blindness.

2.3 Diagnosis

Diagnosis is made by the presence of the typical

manifestations following ingestion:  gastroenteritis with risk

of dehydration, haematemesis and melaena.  Drowsiness and

convulsions may occur.

Toxicological analysis of body fluids for the poison is not

helpful.

Plant material, seeds or remnants of seeds, vomitus, and

gastric aspirate should be collected in clean bottles for

identification.

2.4 First-aid measures and management principles

First-aid measures: Remove all seed particles from the mouth.

Induce vomiting and save it for identification.  Ensure that

the patient’s airway is clear and that there is adequate

ventilation.

Do not induce vomiting if the patient is semi-conscious or is

at risk of having convulsions.  If the eyes are contaminated,

wash eyes with running water for ten minutes.  Medical

attention is essential if the seeds were ingested, or if the

eyes were contaminated.  Collect remaining seeds or plant

material or remnants of seeds for identification.

Management principles: induce emesis or perform gastric

lavage.  Supportive measures include parenteral fluids and

electrolytes.  Keep the patient in hospital for several days

because severe symptoms can develop some time after ingestion.

2.5 Poisonous parts

The most poisonous parts of the plant involved in poisoning

are the small, scarlet seeds, that have a black eye at the

hilum.

2.6 Main toxins

The main toxin is abrin, which is concentrated in the seeds.

  1. CHARACTERISTICS

3.1 Description of the plant

3.1.1 Special identification features

Abrus precatorius is a slender, perennial climber that

twines around  trees, shrubs, and hedges.  It has no

special organs of attachment.  Leaves are glabrous with

long internodes.  It has a slender branch and a

cylindrical wrinkled stem with a smooth-textured brown

bark.  Leaves alternate compound paripinnate with

stipules.  Each leaf has a midrib from 5 to 10 cm long.

It bears from 20 to 24 or more leaflets, each of which

is about 1.2 to 1.8 cm long, oblong and obtuse.  It is

blunt at both ends, glabrous on top and slightly hairy

below.  Flowers are small and pale violet in colour with

a short stalk, arranged in clusters.  The ovary has a

marginal placentation.

The fruit, which is a pod, is flat, oblong and truncate-

shaped with a sharp deflexed beak is about 3 to 4.5 cm

long, 1.2 cm wide, and silky-textured.  The pod curls

back when opened to reveal pendulous seeds.  Each fruit

contains from 3 to 5 oval-shaped seeds, about 0.6 cm.

They are usually bright scarlet in colour with a smooth,

glossy texture, and a black patch on top.

3.1.2 Habitat

Abrus precatorius is a wild plant that grows best in

fairly dry regions at low elevations.

3.1.3 Distribution

It grows in tropical climates such as India, Sri Lanka,

Thailand, the Philippine Islands, South China, tropical

Africa and the West Indies.  It also grows in all

tropical or subtropical areas.

3.2 Poisonous parts of the plant

The most poisonous part of the plant is the seed. It is 0.6 cm

long (although length may vary), and oval-shaped. It is

usually bright scarlet, and has a jet-black spot surrounding

the hilum which is the point of attachment.  The seed coat, or

testa, is smooth and glossy and becomes hard when the seed

matures.

3.3 The toxin(s)

3.3.1 Name(s)

Abrin, which consists of abrus agglutinin, and toxic

lectins abrins [a] to [d] are the five toxic

glycoproteins found in the seeds (Budavari, 1989).

3.3.2 Description, chemical structure, stability

Five glycoproteins have been purified from the seeds.

They are abrus agglutinin (a haemagglutinin) and the

toxic principles abrins [a] to [d].

Abrus agglutinin is a tetramer with a molecular weight

of 134,900. It is non-toxic to animal cells and a potent

haemagglutinator.

Abrins a through d (molecular weight: 63,000 – 67,000)

are composed of two disulphide-linked polypeptide

chains. The larger sub-unit, which is the neutral B-

chain has a molecular weight of approximately 35,000.

The other sub-unit an acidic A-chain has a molecular

weight of approximately 30,000 (Windholz, 1983; Budavari,

1989).

Stability: Pure abrin is a yellowish-white amorphous

powder. The toxic portion is heat-stable to incubation

at 60°C for 30 minutes. At 80°C most of the toxicity is

lost in 30 minutes (Budavari, 1989).

3.3.3 Other physico-chemical characteristics

Pure abrin is a yellowish-white amorphous powder. Abrin

is soluble in sodium chloride solutions, usually with

turbidity (Budavari, 1989).

3.4 Other chemical contents of the plant

The seeds also contain an amino acid known as abrine (N-methyl-

L-tryptophan), glycyrrhizin and a lipolytic enzyme.

The roots, stems, and leaves also contain glycyrrhizin

(Windholz, 1983).

  1. USES/CIRCUMSTANCES OF POISONING

4.1 Uses

Children are attracted by the brightly-coloured seeds.

In some countries theyplay with them and in school use

them in their handiwork and to count.  Necklaces and

other ornaments made from the seeds are worn by both

children and adults.

The seeds were also used to treat diabetes and chronic

nephritis.

The plant is also used in some traditional medicine to

treat scratches and sores, and wounds caused by dogs,

cats, and mice, and is also used with other ingredients

to treat leucoderma.  The leaves are used for their anti-

suppurative properties.  They are ground with lime and

applied on acne sores, boils, and abscesses.  The plant

is also traditionally used to treat tetanus, and to

prevent rabies.  Various African tribes use powdered

seeds as oral contraceptives (Watt & Breyer, 1962).

Boiled seeds of Abrus precatorius are eaten in certain

parts of India (Rajaram& Janardhanan, 1992).

4.2 High risk circumstances

Children are attracted to the brightly-coloured seeds and may

chew, suck, or swallow them.  Because of the hard and

relatively impermeable coat of the mature seeds, they are

considerably less toxic if swallowed whole.  They are more

dangerous when the seeds are chewed or sucked because the

toxic elements in the seeds are extracted and mixed with

enzymes.  Immature seeds are also poisonous if ingested

because of their soft and easily broken coat.  When the seeds

are used as ornaments, such as necklaces, holes are drilled in

the seeds, which allows contact between the intestinal

secretions and the core of the seed resulting in absorption of

the toxic ingredients.

Another reported circumstance is the drinking of beverages

where seeds from a necklace have been soaked (Jouglard, 1977).

If swallowed, these seeds easily cause poisoning.

4.3 High risk geographical areas

The high-risk areas are the dry regions and lowland tropical

areas although necklaces are sold in many countries.

  1. ROUTES OF ENTRY

5.1 Oral

Abrus precatorius mature or immature seeds are chewed or

ingested.

5.2 Inhalation

Unknown.

5.3 Dermal

Unknown.

5.4 Eye

Cold preparations made from soaking the seeds have been used

to treat trachoma and corneal opacities (Hart, 1963).

5.5 Parenteral

Subcutaneous injections from dried infusions made from the

seeds have been used to poison livestock and human beings in

India (Hart, 1963).

5.6 Others

Unknown.

  1. KINETICS

6.1 Absorption by route of exposure

Abrin is very stable in the gastrointestinal tract, from where

it is slowly absorbed.  It is considerably less toxic after

oral administration than after parenteral injection Gunsolus,

1955).

6.2 Distribution by route of exposure

Abrin is widely distributed in tissues.

6.3 Biological half-life by route of exposure

Unknown.

6.4 Metabolism

Unknown.

6.5 Elimination by route of exposure

Unknown.

  1. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY

7.1 Mode of action

Abrin exerts its toxic action by attaching itself to the cell

membranes.  Abrin’s toxic effect is due to its direct action

on the  parenchymal cells (e.g., liver and kidney cells) and

red blood cells (Hart, 1963).

Both subunits from which abrins [a] through [d] are made up

are required for its toxic effects.

The larger subunit, the B chain (haptomere) binds to the

galactosyl-terminated receptors on the cell membrane, which is

a prerequisite for the entry of the other subunit, the A chain

(effectomere).  This inactivates the ribosomes, arrests

protein synthesis, and causes cell death (Stirpe & Barbieri,

1986).  The A-chain attacks the 60S subunit of the ribosomes

and by cutting out elongation factor EF2, stops protein

synthesis (Frahne & Pfander, 1983).

Abrus agglutinin agglutinates the red blood cells by combining

with the cell stroma (Hart, 1963).

7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

One seed well masticated can cause fatal

poisoning (Budavari, 1989).

7.2.1.2 Children

One seed well masticated can cause fatal

poisoning (Budavari, 1989).

7.2.2 Animal data

Abrin’s toxicity has been tested in different animals

with widely  divergent results. The lethal dose for

animals is about 0.01 mg/kg body weight (Gunsolus,

1955).  The intra-peritoneal LD50 value in mice is 0.02

mg/kg body weight (Budavari, 1983). The intravenous

minimal lethal dose of abrin in mice is 0.7

micrograms/kg (Ellenhorn, 1988). Simpson et al. report

that 2 ounces of seeds are fatal to horses, but that

cows, goats and dogs are more resistant.  The symptoms

reported are anorexia, violent vomiting, lassitude,

chills, and incoordination.  Severe gastroenteritis is

also common in animals (Gosselin, 1984).

7.2.3 Relevant in vitro data

No data available.

7.3 Carcinogenicity

Unknown.

7.4 Teratogenicity

Unknown.

7.5 Mutagenicity

Unknown.

7.6 Interactions

Unknown.

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

8.1 Material sampling plan

8.1.1 Sampling and specimen collection

8.1.1.1 Toxicological analyses

8.1.1.2 Biomedical analyses

8.1.1.3 Arterial blood gas analysis

8.1.1.4 Haematological analyses

8.1.1.5 Other (unspecified) analyses

8.1.2 Storage of laboratory samples and specimens

8.1.2.1 Toxicological analyses

8.1.2.2 Biomedical analyses

8.1.2.3 Arterial blood gas analysis

8.1.2.4 Haematological analyses

8.1.2.5 Other (unspecified) analyses

8.1.3 Transport of laboratory samples and specimens

8.1.3.1 Toxicological analyses

8.1.3.2 Biomedical analyses

8.1.3.3 Arterial blood gas analysis

8.1.3.4 Haematological analyses

8.1.3.5 Other (unspecified) analyses

8.2 Toxicological Analyses and Their Interpretation

8.2.1 Tests on toxic ingredient(s) of material

8.2.1.1 Simple Qualitative Test(s)

8.2.1.2 Advanced Qualitative Confirmation Test(s)

8.2.1.3 Simple Quantitative Method(s)

8.2.1.4 Advanced Quantitative Method(s)

8.2.2 Tests for biological specimens

8.2.2.1 Simple Qualitative Test(s)

8.2.2.2 Advanced Qualitative Confirmation Test(s)

8.2.2.3 Simple Quantitative Method(s)

8.2.2.4 Advanced Quantitative Method(s)

8.2.2.5 Other Dedicated Method(s)

8.2.3 Interpretation of toxicological analyses

8.3 Biomedical investigations and their interpretation

8.3.1 Biochemical analysis

8.3.1.1 Blood, plasma or serum

8.3.1.2 Urine

8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses

8.3.3 Haematological analyses

8.3.4 Interpretation of biomedical investigations

8.4 Other biomedical (diagnostic) investigations and their

interpretation

8.5 Overall Interpretation of all toxicological analyses and

toxicological investigations

8.6 References

  1. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

Symptoms and signs can occur after a latent period that

ranges from a few hours to several days.  They include a

burning sensation in the mouth, dysphagia, nausea,

vomiting, bloody diarrhoea, and abdominal cramps.

Drowsiness, disorientation, convulsions, cyanosis,

stupor, circulatory failure, retinal haemorrhages,

haematuria and oliguria may occur.

9.1.2 Inhalation

Unknown.

9.1.3 Skin exposure

Unknown.

9.1.4 Eye contact

Eye irritation leads to a dose-related reaction ranging

from mild conjunctivitis to a severe damage (Hart,

1963).

9.1.5 Parenteral exposure

The clinical effects after intravenous and subcutaneous

administration are similar to ingestion but

gastrointestinal symptoms are lesser.  There is severe

inflammation at the injection site.

9.1.6 Other

Unknown.

9.2 Chronic poisoning

9.2.1 Ingestion

Unknown.

9.2.2 Inhalation

Unknown.

9.2.3 Skin exposure

Unknown.

9.2.4 Eye contact

Unknown.

9.2.5 Parenteral exposure

Unknown.

9.2.6 Other

Unknown.

9.3 Course, prognosis, cause of death

The major symptoms of poisoning are acute gastroenteritis with

nausea, vomiting and diarrhoea leading to dehydration,

convulsions, and shock.  Dehydration, as  well as direct

toxicity on the kidneys, could result in oliguria that might

progress to death in uraemia.

The fatality rate is approximately 5%.

Reported fatalities occurred after a 3 to 4 day course

characterized by persistent gastroenteritis (Ellenhorn, 1988).

Death may occur up to 14 days after poisoning from uraemia

(Dreisbach & Robertson, 1987).

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

There is no direct effect on the heart.

 

Shock, hypotension, and tachycardia may occur after

prolonged vomiting and diarrhoea.

9.4.2 Respiratory

Cyanosis secondary to hypotension and shock may be seen.

9.4.3 Neurological

9.4.3.1 CNS

Drowsiness, convulsions, hallucinations, and

trembling of the hands.

9.4.3.2 Peripheral nervous system

Unknown.

9.4.3.3 Autonomic nervous system

Unknown.

9.4.3.4 Skeletal and smooth muscle

Unknown.

9.4.4 Gastrointestinal

Because of abrin’s irritant action, severe

gastroenteritis with nausea, vomiting, diarrhoea,

dysphagia and abdominal cramps may occur.  Nausea and

vomiting are due to direct irritation of the gastric

mucosa.  Erosion of  the intestinal mucosa can cause

haematemesis and melaena.

9.4.5 Hepatic

The necrotizing action of the toxin causes liver damage.

Serum levels of liver cell enzymes, i.e., aspartate-

transferase (AST), alanine-transferase (ALT), and lactic

dehydrogenase (LDH) are markedly increased.  The serum

bilirubin level is elevated indicating progression of

the lesions.  Hypoglycaemia may occur.

9.4.6 Urinary

9.4.6.1 Renal

Oliguria and anuria may result from prolonged

hypotension, but may also be due to acute renal

failure as a result of focal degeneration of the

tubular cells.  Blocking of the tubules with

haemoglobin from haemolysed red cells may also

contribute to renal failure.

9.4.6.2 Others

Unknown.

9.4.7 Endocrine and reproductive systems

Unknown.

9.4.8 Dermatological

Skin contact may cause irritation and dermatitis.

9.4.9 Eye, ears, nose, throat:  local effects

Eye: Retinal haemorrhages can appear early in the course

of intoxication. The patient may complain of impaired

vision that is caused by changes in the retina.  Eye

contact can cause severe swelling and reddening of the

ocular conjunctiva.

Ear, nose, throat: Irritation of the throat may occur

after ingestion.

9.4.10 Haematological

Abrus agglutinin causes haemagglutination and

haemolysis by its direct effect on red cells.  Blood

loss may also occur because of haemorrhages in the

gastrointestinal tract.

9.4.11 Immunological

Unknown.

9.4.12 Metabolic

9.4.12.1 Acid base disturbances

Prolonged vomiting may cause alkalosis.  Shock

is likely to lead to acidosis.  Acidosis can

also occur from renal failure.

9.4.12.2 Fluid and electrolyte disturbances

Vomiting, diarrhoea, and haemorrhages lead to

 

loss of fluids and electrolytes, thus causing

lethargy, muscle weakness, cardiac

dysrhythmias, and muscle cramps.

9.4.12.3 Others

Liver damage may cause hypoglycaemia.

9.4.13 Allergic reactions

Unknown.

9.4.14 Other clinical effects

Unknown.

9.4.15 Special risks

Unknown.

9.5 Others

9.6 Summary

  1. MANAGEMENT

10.1 General principles

The management of poisoning cases is mainly symptomatic and

supportive.  Induced emesis or gastric lavage are usually

indicated (if the conditions of the patient allow the

procedures) to remove the seeds from the stomach.  Fluid and

electrolyte imbalances should be carefully monitored and

corrected.

10.2 Relevant laboratory analyses and other investigations

10.2.1 Sample collection

Collect the seeds or any other plant material for

identification, also collect the vomitus or gastric

contents in a clean jar.  Seeds may be identified if

vomitus is put inside a transparent plastic bag.

10.2.2 Biomedical analysis

Full blood count, liver profile, serum electrolytes

blood gases, blood urea and creatinine are the

essential analyses.  Urinalysis may reveal the

presence of protein, red blood cells, haemoglobin,

and casts.

10.2.3 Toxicological/toxinological analysis

No simple analyses are available in practice.

10.2.4 Other investigations

May be indicated according to the patient’s

condition.

10.3 Life supportive procedures and symptomatic treatment

Make a proper assessment of airway, breathing, circulation

and neurological status of the patient.

Monitor vital signs.

Maintain a clear airway. Administer oxygen if the patient is

in shock.

Monitor acid base balance, and fluid and electrolyte

balance.

Give adequate oral fluids by mouth, if possible.  If the

patient is unable to swallow, administer intravenous fluids

and electrolytes, according to the severity of the symptoms

and the results of serum electrolyte analysis.  Correct

metabolic acidosis if present.

Fluid loss may lead to hypovolaemic shock with hypotension.

If the intravenous fluid therapy does not raise the blood

pressure, insert a central venous pressure line and give

plasma or dextran to expand the intravascular volume. If

hypotension still persists consider administration of

dopamine or dobutamine in a continuous infusion.

No cases of severe haemolysis have been reported.  However,

if significant haemolysis occurs, and if kidney function is

normal, maintain the urine output at over 100 ml/hour with

alkaline fluids.

If anuria persists after receiving fluid replacement,

consider the possibility of dialysis.

If convulsions occur, administer anti-convulsant drugs

(diazepam, intravenously or intrarectally in paediatric

emergencies).

Demulcents may relieve oropharyngeal and gastric irritation.

10.4 Decontamination

Emesis with syrup of ipecacuanha is the best way to remove

the seeds or pieces of plant from the stomach unless

contraindications to induced emesis exist or orpharyngeal

oedema is present.

If emesis induction is not possible, gastric lavage may be

performed if the condition of the patient allows it.  If the

patient is obtunded, convulsing or comatose, insert an oro-

or naso-gastric tube and lavage after endotracheal

intubation.

Cathartics should not be used because they can aggravate

diarrhoea and fluid loss.

In case of eye exposure, irrigate eyes with copious amounts

of water or saline.

10.5 Elimination

No method has proved to be beneficial.

10.6 Antidote/antitoxin treatment

10.6.1 Adults

There is no specific antidote available.

An anti-serum used to be supplied under the name of

“anti-abrin” or “jequiritol” (Gunsolus, 1955) but is

no longer available.

10.6.2 Children

There is no specific antidote available.

An anti-serum used to be supplied under the name of

“anti-abrin” or “jequiritol” (Gunsolus, 1955) but is

no longer available.

10.7 Management discussion

Gastric lavage may be difficult to perform and may not be

successful if the size of the seeds is large.  Induction of

emesis may be preferred.

A cathartic can be administered to accelerate intestinal

transit in cases where entire seeds have been recently

ingested and no clinical features of poisoning are present.

Cathartics are contraindicated in the symptomatic patient.

Magnesium sulphate should be avoided when gastrointestinal

irritation is present because it may be absorbed

systemically.

  1. ILLUSTRATIVE CASES

11.1 Case reports from literature

Adults: Some investigators have reported that abrin is

poorly absorbed from the intestine.  However, there have

been reports of severe, sublethal toxicity in adults after

ingestion of only one-half to two seeds (Hart, 1963).

A 37-year-old man was severely poisoned after ingesting half

a seed (Gunsolus, 1955).

A 19-year-old girl died after she was treated for trachoma

with jequirity infusions (Gunsolus, 1955).

An adult, who homogenized 20 seeds in a blender and a

portion of the mixture died (Davis, 1978).

Children: Deaths in children have been reported in Florida,

USA, in 1949, 1958 and 1962 after ingestion of one or more

seeds.  In 1955, two seeds caused severe but non-fatal

poisoning (Hart, 1963).  In Missouri, USA, a child who

ingested exactly one-half seed was immediately made forced

to vomit.  The remainder of the swallowed half seed, whose

coat was broken, was found in the vomitus.  He was  treated

immediately and did not develop any symptoms (Kinamore,

1980).  In most of the cases, the quantity of the seed

ingested has been described as the potentially lethal dose

in children.

11.2 Internally extracted data on cases

To be added by the centre.

11.3 Internal cases

To be added by the centre.

  1. ADDITIONAL INFORMATION

12.1 Availability of antidotes/antitoxins

No antidotes are available at present.

12.2 Specific preventive measures

Do not allow children to play with seeds of Abrus

precatorius.

Keep seeds or ornaments made out of seeds away from

children.

Do not grow Abrus precatorius plants in home gardens

Educate older children and the public of the dangers of

ingesting seeds.

12.3 Other

No data available.

  1. REFERENCES

13.1 Clinical and toxicological

Budavari S ed. (1989) The Merck Index: an encyclopedia of

chemicals, drugs, and biologicals, 10th ed. Rahway, New

Jersey, Merck and Co., Inc.

Davis JH (1978)  Abrus precatorius (rosary pea).  The most

common lethal plant poison. Journal of Florida Medical

Association, 65: 189-191.

Dreisbach RH & Robinson WO eds. (1987)  Handbook of

Poisoning: Prevention, Diagnosis & Treatment, Los Altos,

California, Appleton and Lange. p 497.

Ellenhorn MJ & Barceloux DG. eds (1988). Medical Toxicology.

New York, Elsevier Science Publishing Company, Inc. 1224-

Gosselin RE, Smith RP, & Hodge HC (1984) ed. Clinical

Toxicology of Commercial Products, Baltimore/London,

Williams & Wilkins.

Gunsolus JM (1955).  Toxicity of Jequirity beans.  J Amer

Med Assoc, 157: 779.

Hart M (1963).  Jequirity bean Poisoning.  N Engl J Med,

268: 885-886.

Hoehne FC (1978). Plantaxe substancias vegetais toxicase

medicinais. Sao Paulo, Novos Horizontes, 355p

Jouglard J (1977).  Intoxications d’origine vegetale In:

Encycl. Med. Chir.; Intoxication Paris, Editions Techniques,

16065 A-10-A-20.

Kinamore PA, Jager RW, De Castro FJ, & Peck KO (1980).

Abrus & Ricinus Ingestion:  Management of three cases.

Clinical Toxicology, 17(3): 401-405.

Kunkel DB (1983).  Poisonous Plants in: Haddad LM &

Winchester JF.  ed. Clinical Management of Poisoning & Drug

Overdosage, Canada, W.B. Saunders Company. pp 1012.

Lampe KF (1976).  Changes in therapy in Abrus precatorius &

Ricinus communis poisoning suggested by recent studies in

their mechanism of Toxicity.  Clinical Toxicology, 9(1): 21.

Lin JY, Tserng, KY, Chen CC, Lin LT, & Tung TC (1970).

Abrin & Ricin:  New Anti-tumour Substances.  Nature, 227:

292 – 293.

Reynolds JEF, ed (1982) Martindale, The Extra Pharmacopoeia,

28th ed. London, Pharmaceutical Press, p 2025

Rajaram N & Janardhanan K (1992)  The chemical composition

and nutritional potential of the tribal pulse, Abrus

precatorius L.  Plant Foods Hum Nutr, 42(4): 285-290.

Schvartsman S (1979) Plantas venenosas.  Sao Paulo, Sarvier.

Stripe F & Barbieri L (1986).  Symposium:  Molecular

Mechanisms of Toxicity, Toxic Lectins from Plants.  Human

Toxicology, 5(2): 108-109.

Windholz M. ed (1983) The Merck Index: an encyclopedia of

chemicals, drugs, and biologicals, 10th ed. Rahway, New

Jersey, Merck and Co., Inc.

13.2 Botanical

Frohne D & Pfander HJ (1983) ed. A Colour Atlas of Poisonous

Plants, Germany, Wolfe Publishing Ltd. pp 291.

  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE

ADDRESS(ES)

Author:   Dr Ravindra Fernando

National Poisons Information Centre

Date:     September 1988

Reviewer: Dr A. Furtado Rahde

Poisons Control Centre

Date:     November 1988

Peer Review:   London, United Kingdom, March 1990

Update:   Dr R. Fernando, London, United Kingdom, June 1993

Review:   IPCS, May 1994

 

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