Myristica fragrans Houtt.
| 1. NAME |
| 1.1 Scientific name |
| 1.2 Family |
| 1.3 Common name(s) and synonym(s) |
| 2. 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 |
| 3. 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 |
| 4. USES/CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstances |
| 4.3 High risk geographical areas |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. 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 and excretion |
| 7. TOXINOLOGY |
| 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 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. 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 |
| 9. 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 Central nervous system (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 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, 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 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote/antitoxin treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventative measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
MYRISTICA FRAGRANS
International Programme on Chemical Safety
Poisons Information Monograph 355
Plant
1. NAME
1.1 Scientific name
Myristica fragrans Houtt.
1.2 Family
Myristicaceae
1.3 Common name(s) and synonym(s)
mace (UK); muscadier (France); Muskatbaum
(Germany); myristica; nuez moscada (Uruguay, Spain);
nutmeg (UK); nutmeg tree (UK); nux moschata;
Myristica officinalis L.
2. SUMMARY
2.1 Main risks and target organs
-transient psychosis
-possibility of fatty liver and hepatic necrosis
-transient renal toxicity
-possible carcinogen and teratogen
-possibility of death occurring
2.2 Summary of clinical effects
Nutmeg intoxication resembles anticholinergic
intoxication, e.g. profuse sweating, flushed face, delirium,
dry throat etc. There is always an altered state of mind,
e.g. hallucinations, confusion and an impending sense of
doom. Clinical symptoms may be contradictory depending on
the length of time lapsed after ingesting the toxin.
Symptoms also vary according to the dose taken and the
variability between different samples of nutmegs.
2.3 Diagnosis
Blood: for electrolytes, liver enzymes and renal
function tests; plus urinalysis.
2.4 First-aid measures and management principles
Management
Treatment is symptomatic and supportive. The use of
cathartics, gastric lavage or ipecac may be beneficial if
they are not contraindicated. A sedative and anticonvulsant
may be administered to calm the patient and combat seizures
should they occur. A liquid diet high in protein and
carbohydrate, but low in fat, is recommended.
2.5 Poisonous parts
The seeds (nutmeg) and, to a lesser extent, the aril
(mace).
2.6 Main toxins
Myristicin and elemicin, but intoxication is not thought
to be due to these alone.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
M. fragrans is a spreading aromatic evergreen
tree usually growing to around 5 to 13 metres high,
occasionally 20 metres. The bark contains watery pink
or red sap. The pointed dark green leaves (5 to 15 cm
× 2 to 7 cm) are arranged alternately along the
branches and are borne on leaf stems about 1 cm long.
Upper leaf surfaces are shiny. Flowers are usually
single sexed; occasionally male and female flowers are
found on the same tree. Female flowers arise in
groups of 1 to 3; males in groups of 1 to 10. Flowers
are pale yellow, waxy, fleshy and bell-shaped. Male
flowers are 5 to 7 mm long; female flowers are up to
1 cm long. The fruits are fleshy, drooping, yellow,
smooth, 6 to 9 cm long with a longitudinal ridge.
When ripe, the succulent yellow fruit coat splits into
2 valves revealing a purplish-brown, shiny seed
(nutmeg) surrounded by a red aril (mace). Seeds
(nutmegs) are broadly ovoid (2 to 3 cm long), firm,
fleshy, whitish and transversed by red-brown veins.
When fresh, the aril (mace) is bright scarlet becoming
more horny, brittle and a yellowish-brown colour when
dried (Purseglove, 1968).
The tree does not flower until around 9 years old,
when it fruits; it can continue to do so for a further
75 years. The tree bears 2 to 3 crops a year. The
seeds (nutmegs) need 3 to 6 weeks to dry before they
are ready for use.
3.1.2 Habitat
Grows wild on rich volcanic soils in lowland
tropical rain forests. Its cultivation as a crop is
largely confined to islands in the hot, humid tropics
at altitudes up to 4,500 metres (Purseglove,
1968).
3.1.3 Distribution
Indigenous to the Moluccas and Banda Islands in
the South Pacific although it is seldom found truly
wild. It is now cultivated in tropical regions,
especially Indonesia, Grenada in the West Indies and
Sri Lanka (Purseglove, 1968; Bown, 1995).
3.2 Poisonous parts of the plant
Seeds (nutmegs) and to a lesser extent the aril
(mace).
Nutmeg oil:
Nutmeg oil is also known as oleum myristicae, ol. myrist.,
myristica oil, essence de muscade, atheririsches muskatol,
essencia de moscada and essencia de nuez moscada. It is a
volatile oil obtained by steam distillation from the seed.
It is a colourless or pale yellow liquid with an odour and
taste of nutmeg. It is scarcely distinguishable from the
volatile oil of mace and frequently no commercial distinction
is made between the two. There are two types of nutmeg oil,
mainly East Indian Nutmeg Oil and West Indian Nutmeg Oil.
The East Indian Nutmeg Oil has a weight of 0.885 to 0.915
g/mL and is soluble in 90% alcohol at a ratio of 1 part oil
to 3 parts alcohol. West Indian Nutmeg Oil has a weight of
0.86-0.88 g/mL and is soluble in 90% alcohol at a ratio of 1
part oil to 4 parts alcohol. Nutmeg oil should be stored in
a cool place in well filled airtight containers and protected
from light.
Nutmeg Butter:
Nutmeg butter, also known as balsam of nutmegs, oil of mace,
butter of mace, Banda soap and oleum myristicae expressum is
the fixed oil component of the seed (nutmeg). It accounts
for 25 to 40% of the nutmeg's weight and it is a solid at
room temperature. Sometimes it occurs in the form of
prismatic crystals. It is obtained by exposing the nuts to
hydraulic pressure and heat.
Pharmacologically active parts of the plant:
The most important part of the plant in terms of its
pharmacological activity and also in commerce, is of course
the dried kernel (seed), the nutmeg. Intoxication from the
use of the aril of the fruit (seed case), generally known as
mace, has also been reported, but only rarely. The oil of
nutmeg has also been used for medicinal purposes and it is
this fraction of the nutmeg which is strongly suspected of
harbouring the pharmacologically active components of
nutmeg.
3.3 The toxin(s)
No single component of the nutmeg has been identified as
responsible for all the symptoms seen during intoxication.
It is widely believed that myristicin is the major component
responsible, however, it alone cannot reproduce all the
symptoms. Shulgin (1966) suggests that myristicin and
elemicin may not be the active ingredients but they may be
metabolized in the body to 3-methoxy-4,5-methylenedioxy
amphetamine (MMDA) and elemicine, an ether analogous to
myristicin, 3,4,5-trimethoxy amphetamine (TMA).
3.3.1 Name(s)
Myristicin:
CAS number: 607-91-0
Molecular formula: C11H12O3
Molecular weight: 192.21
Elemicin:
CAS number: 487-11-6
Molecular formula: C12H16O3
Molecular weight: 208.26
(Harborne & Baxter, 1996).
3.3.2 Description, chemical structure, stability
Components of nutmeg
The major components in M. fragrans are terpenes,
terpene alcohols and phenolic ethers. The major
phenolic ether is myristicin (4-methoxy-6-(2-
propenyl)-1,3-benzadioxole) accompanied by safrole
(5-(2-propenyl)-3-benzodioxole) and eugenol methyl
ether (3,4,-dimethoxy-(2-propenyl)-benzene).
Myristicin accounts for about 2.12 to 2.88% of the
total weight of the nutmeg where as safrole accounts
for 0.27 to 0.39%. The volatile oil content of nutmeg
depends on the geographical origin and length of
storage. Chemical analysis has shown that even though
there is a real variability between the quality
(differences in composition) and quantity of nutmeg
oil from various samples of nutmegs oil accounts for
84 to 95% of the total aromatic fraction of the
volatile oil from all the samples tested. In the
samples, myristicin, safrole and elemicin accounted
for 3.86 to 12.7%, 0.53 to 3.42% and 0.02 to 2.36%,
respectively of the nutmeg oil samples. Early work on
myristicin used myristicin distilled from nutmeg oil.
It has been subsequently proven that myristicin
extracted from nutmeg via this method is not elemicin
free and therefore the effects reported may be due to
either substances found in the extract.
3.3.3 Other physico-chemical characteristics
No data available.
3.4 Other chemical contents of the plant
No data available.
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
Miscellaneous pharmaceutical product
Other therapeutic preparation
Food;
general
Beverage; general
4.1.2 Description
Medicinal:
Used as an anti-diarrhoea agent for patients with
medullary carcinoma of the thyroid. The effectiveness
of the treatment may be due to the inhibition of
prostaglandin synthesis in the mucosa and submucosa of
the colon. The dosage given was 9 tablespoons orally
per day but it may vary between patients to avoid
toxic symptoms.
Domestic:
Used as a spice in various dishes, as components of
teas and soft drinks or mixed in milk and alcohol.
Traditional and folk medicine:
It is widely used as a traditional medicine in the
Middle East and Asia.
In Western medicine nutmeg is sometimes used as a
stomachic, stimulant, carminative as well as for
intestinal catarrh and colic, to stimulate appetites,
to control flatulence, and it has a reputation as a
emmenagogue and abortifacient.
4.2 High risk circumstances
Abuse
Nutmeg has been known for its hallucinogenic properties for a
long time. Adults may abuse the hallucinogenic properties of
nutmeg. Children may be at high risk at home, since nutmeg
may be widely available as a cooking additive. In the course
of its use in traditional medicine, overdose may occur.
4.3 High risk geographical areas
No data available.
5. ROUTES OF EXPOSURE
5.1 Oral
This is the most common method of consuming nutmeg, be
it as a remedy, a spice or as a psychotropic drug.
5.2 Inhalation
Nutmeg is mixed with tobacco snuff in certain parts of
southern India. Intoxication through this method of
administration is reported to be the same as for intoxication
through oral administration, except that the onset of
symptoms is faster.
5.3 Dermal
No data available.
5.4 Eye
No data available.
5.5 Parenteral
Reported only in experimental animals. The effects are
reported to be the same as those when given orally.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
No detailed studies are available concerning the
absorption of the active principles involved in nutmeg
poisoning. Current literature states that when nutmeg powder
is administered orally, the toxic effects begin within 1 to
12 hours. The effects last generally for 24 hours but may
continue for as long as a week or more. When taken as a tea,
the reaction is reported to be immediate. Snuffing nutmeg is
reported to produce a reaction within 15 minutes.
6.2 Distribution by route of exposure
No data available.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
3,4,5,-trimethoxy amphetamine (TMA):
It has been postulated that elemicin, a major component in
nutmeg oil, could undergo oxidation of its oleficin side
chain in the same manner that the mentioned side chain in
safrole is also oxidized in the body. This would produce a
vinyl alcohol which could under go transamination to produce
TMA.
The potency of TMA is reported to be more than that of
mescaline as a psychotropic drug.
3-methoxy-4,5-methylenedioxy amphetamine (MMDA):
It has been proposed that myristicin may be metabolized in
the body to MMDA in a manner similar to the metabolism of
elimicin into TMA.
MMDA is reported to have a higher potency than TMA as a
psychotropic drug, that is, its potency is about three times
the potency of mescaline. It has almost the same properties
as TMA, being both hallucinogenic and permitting total recall
of the experience.
6.5 Elimination and excretion
No data available.
7. TOXINOLOGY
7.1 Mode of action
3,4,5,-trimethoxy amphetamine (TMA):
It has been postulated that elemicin, a major component in
nutmeg oil, could undergo oxidation of its oleficin side
chain in the same manner that the mentioned side chain in
safrole is also oxidized in the body. This would produce a
vinyl alcohol which could under go transamination to produce
TMA.
The potency of TMA is reported to be more than that or
mescaline as a psychotropic drug.
3-methoxy-4,5-methylenedioxy amphetamine (MMDA):
It has been proposed that myristicin may be metabolized in
the body to MMDA in a manner similar to the metabolism of
elimicin into TMA.
MMDA is reported to have a higher potency than TMA as a
psychotropic drug, that is, its potency is about three times
the potency of mescaline. It has almost the same properties
as TMA, being both hallucinogenic and permitting total recall
of the experience.
Nutmeg has monoamineoxidase inhibition properties (1963).
Nutmeg is also known to have anti-prostaglandin synthesis
effects.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The dose needed to induce
intoxication varies according to the quality
and length of storage of the nutmeg. 1 to 3
nutmegs (5 to 15 g) is reported as the toxic
dose (Haddad & Winchester, 1983).
7.2.1.2 Children
Death by nutmeg intoxication has
been reported by Cushny (Weil, 1964) in an 8-
year-old boy after consuming 2 nutmegs.
7.2.2 Relevant animal data
In cats, an oral dose of 24 mg nutmeg oil per
kg body weight was found to be lethal.
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
Safrole is a known mild hepatocarcinogen. Although
safrole itself is not carcinogenic, it is metabolized to form
1'-hydroxysafrole which is carcinogenic. Data are not
available on the carcinogenicity of nutmeg itself.
7.4 Teratogenicity
Verrett (Wulf et al., 1978) reports that myristicin may
be a strong teratogen.
7.5 Mutagenicity
No data available.
7.6 Interactions
Consideration should be given to possible nutmeg-ethanol
interaction since nutmeg has hallucinogenic and MAO
inhibition effects.
8. 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
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning:
9.1.1 Ingestion
In the toxic state, the patient first feels
excited and may have psychedelic hallucinations. This
is followed by a period of drowsiness, delirium and,
possibly, unconsciousness. Thirst has been reported.
Mental concentration may either be impaired or
enhanced; delirium with agitation, disorientation and
incoherence may develop. Prison inmates taking nutmeg
"trips" have compared it to alcohol, heroin and
marihuana and referred to it as making them feel
"high", relaxed and drowsy. Some reported a sleepy
feeling, others, restlessness and tense. Most
patients with accidental nutmeg intoxication
experience an impending sense of doom after the
initial excitation. The effects of nutmeg are most
often compared to those of marihuana. Although the
hallucinogenic effects of nutmeg are satisfactory, the
side effects often discourage its use as such an
agent. One reported case of nutmeg intoxication after
drinking nutmeg tea, states that the reaction is
immediate.
9.1.2 Inhalation
The effects by inhalation are generally similar
to those experienced via oral administration with the
exception that onset is faster by 15 minutes.
9.1.3 Skin exposure
No data available.
9.1.4 Eye contact
No data available.
9.1.5 Parenteral exposure
Parenteral exposure in animals has shown to
produce the same general effect as that of oral
exposure.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic poisoning by oral administration has
caused temporary (up to six months) psychosis in
prison inmates.
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
9.3 Course, prognosis, cause of death
Not all the symptoms listed below appear in every case
of poisoning. Contradicting symptoms may occur at different
times during the course of intoxication.
The subject initially feels excited, then drowsy before a
delirious state sets in. This is followed by a deep sleep.
During this period, cyanosis of the extremities and
convulsions may occur. Generally there is tachycardia and an
increase in blood pressure. Acidosis may set in because of
diarrhoea and vomiting which is usually present along with
various other gastrointestinal symptoms such as abdominal
cramps. The subject may or may not be hallucinating but
usually expresses a feeling of impending doom. Nutmeg
intoxication usually clears by itself within 24 hours,
however, it has been reported that psychosis may set in.
Transient renal toxicity has also been reported causing an
increase in albumin and non-protein nitrogen content in the
urine, returning to normal within 24 hours.
Nutmeg has been proven to cause fatty liver in cats which
have later died from the dose of nutmeg oil but, in the case
of humans, this is not clear since only one death has been
attributed to nutmeg toxicity: an 8-year-old boy who became
comatose and later died after ingesting two nutmegs.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Tachycardia.
Hypertension or hypotension may occur.
Chest pains or tightness in chest.
9.4.2 Respiratory
No data available.
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
Severe headaches.
Drowsiness several hours after taking nutmeg.
Fitful sleep/convulsions.
Hallucinations (predominantly visual). Colour
distortion may also occur.
Delirium.
Unconsciousness/coma.
Agitation.
Disorientation.
Incoherence.
Sedation.
Euphoria.
Concentration may be impaired or improved.
Excitation resembling that caused by
anticholinergic intoxication.
Florid paranoia.
Belligerence.
Vertigo.
Stupor.
Feeling of impending doom.
Sometimes unusual behaviour occurs during
intoxication such as hysteria and wild
trashing of limbs, and behaviour resembling
that of a snarling dog.
9.4.3.2 Peripheral nervous system
Initial stimulation after
administration.
Strong tingling in the fingers and toes
shortly after snuffing some nutmeg.
Numbness in hand and feet half an hour after
snuffing nutmeg.
Absent limb reflexes.
9.4.3.3 Autonomic nervous system
Profuse sweating several hours after
administration possibly reflecting
amphetamine-type reaction.
Absence of salivation.
9.4.3.4 Skeletal and smooth muscle
Muscular excitation several hours
after administration.
9.4.4 Gastrointestinal
Nausea.
Vomiting.
Diarrhoea.
Abdominal pain.
9.4.5 Hepatic
Hepatic necrosis in heavy poisoning.
Fatty degradation of liver.
9.4.6 Urinary
9.4.6.1 Renal
Transient renal toxicity producing
albuminuria. Non-protein nitrogen content in
urine which returns to normal within 24
hours.
9.4.6.2 Other
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Flushed skin.
9.4.9 Eye, ear, nose, throat: local effects
Eyes: A drawing sensation over the eyes after
snuffing.
Miosis (initially or it may not occur)
Mydriasis (occurs less often than miosis)
Throat: Epigastric pain
9.4.10 Haematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Acidosis may be attributed to
excessive diarrhoea and vomiting.
9.4.12.2 Fluid and electrolyte disturbances
Fluid and electrolyte disturbance
may develop because of diarrhoea and
vomiting.
9.4.12.3 Others
Hypothermia/hyperthermia.
9.4.13 Allergic reactions
Oedema of eyelids.
Possible elevation in body temperature.
Marked flushing and itching of face.
Allergic reactions tend to subside quickly.
9.4.14 Other clinical effects
Severe thirst.
9.4.15 Special risks
Nutmeg has been used as an abortifacient but
there are no confirmed clinical accounts.
9.5 Other
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Treatment is supportive. Decontamination procedures,
such as gastric lavage and cathartics, are theoretically
beneficial within the first few hours but be aware of any
contraindications before their administration. Syrup of
ipecac is not advisable because it may precipitate
convulsions. Milk or a demulcent may be given to alleviate
gastric irritation.
10.2 Life supportive procedures and symptomatic/specific treatment
Nasal oxygen may be administered to patients suffering
from vertigo. Barbiturates or diazepam may be given for
convulsions and analeptics such as chlorpromazine (25 mg
every 4 hours) for severe agitation. Sedatives should be
administered with caution since the patient goes through
alternating periods of delirium and lethargy. A liquid diet
is recommended, high in protein and carbohydrate and low in
fat. Wash eyes if they are physically contaminated by nutmeg
powder. Monitor cardiac function and blood pressure and
treat as necessary.
10.3 Decontamination
Decontamination procedures such as gastric lavage and
cathartics are theoretically beneficial within the first few
hours but be aware of any contraindications before their
administration. Syrup of ipecac is not advisable because it
may precipitate convulsions. Milk or a demulcent may be
given to alleviate gastric irritation.
10.4 Enhanced elimination
No data available.
10.5 Antidote/antitoxin treatment
10.5.1 Adults
No data available.
10.5.2 Children
No data available.
10.6 Management discussion
No data available.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Two male college students, 19 and 20 years of age, each
ingested 2 tablespoons (about 14 gm) of powdered nutmeg
suspended in a glass of milk to produce a sense of
exhilaration. Five hours later, rapid heart rates and
palpitations were noted and both complained of dry mouths and
thirst. Onlookers observed that one student became
hyperactive, agitated and talked incoherently. Their faces
were "red as beets". Nausea, vomiting and abdominal cramps
were absent. 60 hours were needed for full recovery.
A 37 year old woman drank a nutmeg tea at a party. The tea
consisted of two ground nutmegs in a glass of warm water.
She had flushed skin, rapid pulse, incoherent speech and felt
giddy after 4 hours. Her vision was disturbed and she had
hallucinations of faces laughing at her and monsters in the
bed trying to engulf her. Symptoms gradually diminished and
recovery made within 24 hours.
12. ADDITIONAL INFORMATION
12.1 Specific preventative measures
No information available.
12.2 Other
No information available
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: UKM
Kuala Lumpur
Malaysia
Date: April 1991
Peer Review: Singapore, November 1991
General edit and botanical review:
Christine Leon
Medical Toxicology Unit
Guy's & St Thomas Hospital Trust
c/o Royal Botanic Gardens, Kew
Richmond
Surrey
TW9 3AB
United Kingdom
Tel: +44 (0) 181 332 5702
Fax: +44 (0) 181 332 5768
e-mail: c.leon@rbgkew.org.uk
July 1997