Does CBD interact with Benadryl and other antihistamines?

Benadryl is the brand name for a substance known as diphenhydramine HCL. Diphenhydramine belongs to a class of medications called antihistamines. It can alleviate human allergy symptoms, but people also commonly use Benadryl for dogs experiencing allergic reactions.

Antihistamines work by blocking the activity of histamine, a substance in the body that causes allergic symptoms(1).

Diphenhydramine is used to alleviate symptoms, like red, itchy, irritated, and watery eyes, sneezing, and runny nose caused by allergies, hay fever, or the common cold. 

Diphenhydramine is also used to relieve coughs caused by minor throat or airway irritation. Moreover, diphenhydramine is used to prevent and treat motion sickness, and to treat insomnia (difficulty falling asleep or staying asleep)(2).

Can CBD Be Taken With Benadryl?

There is no known interaction between CBD (cannabidiol) and Benadryl. However, there is a potential risk when combining CBD and Benadryl, as both are metabolized (broken down) through the cytochrome P450 enzyme system.

Due to how Benadryl is metabolized, the concentrations of the drug could potentially increase when taken with CBD.

The CYP450 liver enzymes are responsible for metabolizing potentially toxic compounds, including over 60% of any over-the-counter or prescription drugs consumed.

Certain substances can affect processing times within this system, making drugs metabolize faster or slower than they would on their own.

Cannabidiol can inhibit the cytochrome P450 system’s ability to metabolize certain drugs, leading to an overall increase in processing times(3). 

Antihistamines use the cytochrome P450 enzyme system and can interact with CBD, as reiterated by authors Eileen Konieczny, RN, and Lauren Wilson, in their book, Healing with CBD(4).

According to an article written in August 2019 by Peter Grinspoon, MD, any medicine can have different effects on different people. 

For example, Benadryl, an antihistamine, makes some people sleepy yet can make others wide awake. Thus, it is not inconsistent for a particular medicine to cause a symptom in one person and to help alleviate it in another(5).

Until studies that specifically look at how CBD interacts with Benadryl are completed, talk with a doctor to make sure that there are no CBD drug interactions with other medications currently taken.

Can CBD Replace Benadryl?

There is no scientific study that recommends using CBD as a substitute for Benadryl. However, studies have shown that CBD possesses therapeutic characteristics that may help with symptoms of medical conditions for which Benadryl is indicated. 

These conditions include nausea, insomnia, mucus production, minor throat or airway irritation, and inflammation.

A review from the European Journal of Pharmacology established the potential of cannabis to limit or prevent nausea and vomiting from a wide range of causes(6). Results also demonstrated the crucial role of cannabinoids and their receptors in the regulation of nausea and vomiting.

A study from January 2019 looked at the role of CBD in anxiety and sleep, showing a positive correlation. The results, published in The Permanente Journal, indicated that individuals with anxiety or poor sleep experienced an improvement in both or either cases when taking CBD every day(7)

CBD has been shown to interact with the endocannabinoid system to reduce mucus production, as one review in Future Medicinal Chemistry indicated(8).

In another 2019 study, which was published in the European Journal of Pharmacology, scientists found that CBD helped to reduce airway inflammation and fibrosis in animal subjects that were experiencing an allergic asthmatic response(9).

Meanwhile, CBD’s potent anti-inflammatory properties were demonstrated in a 2018 study published in the Journal of Pharmacology and Experimental Therapeutics(10). CBD may also be useful in treating different types of chronic pain(11).

Conclusion

Benadryl has been used for many common symptoms and medical conditions. However, as with most pharmaceuticals, Benadryl use comes with side effects and health risks.

In a 2015 report published in JAMA Internal Medicine, researchers offered compelling evidence of a link between long-term use of Benadryl and dementia(12).

Meanwhile, studies have shown that CBD possesses therapeutic characteristics that may help with symptoms of medical conditions that Benadryl addresses. 

However, no scientific study recommends using CBD or any CBD products with Benadryl. Neither is there a study that promotes CBD as a substitute for Benadryl.

While CBD is generally safe, as the 2011 review in the Current Drug Safety Journal suggests, the long-term effects are yet to be examined further(13). 


  1. MedlinePlus. (2020, Feb 18).v Diphenhydramine. Retrieved from https://medlineplus.gov/druginfo/meds/a682539.html
  2. Ibid. 
  3. Pharmotech SA. CBD Drug Interactions. Retrieved from https://pharmotech.ch/cbd-drug-interactions/
  4. Eileen Konieczny and Lauren Wilson. Healing with CBD: How Cannabidiol Can Transform Your Health without the High (California: Ulysses Press, 2018). P46-47.
  5. Grinspoon, P. (2018, Aug 24). 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.
  6. Sharkey KA, Darmani NA, Parker LA. Regulation of nausea and vomiting by cannabinoids and the endocannabinoid system. Eur J Pharmacol. 2014;722:134–146. DOI:10.1016/j.ejphar.2013.09.068. 
  7. Shannon S, Lewis N, Lee H, Hughes S. Cannabidiol in Anxiety and Sleep: A Large Case Series. Perm J. 2019;23:18–041. doi:10.7812/TPP/18-041.
  8. Nagarkatti P, Pandey R, Rieder SA, Hegde VL, Nagarkatti M. Cannabinoids as novel anti-inflammatory drugs. Future Med Chem. 2009;1(7):1333–1349. DOI:10.4155/fmc.09.93.
  9. Vuolo F, Abreu SC, Michels M, et al. Cannabidiol reduces airway inflammation and fibrosis in experimental allergic asthma. Eur J Pharmacol. 2019;843:251–259. DOI:10.1016/j.ejphar.2018.11.029.
  10. 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.
  11. Grinspoon, P. (2018, Aug 24). 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.
  12. Gray SL, Anderson ML, Dublin S, et al. Cumulative Use of Strong Anticholinergics and Incident Dementia: A Prospective Cohort Study. JAMA Intern Med. 2015;175(3):401–407. doi:10.1001/jamainternmed.2014.7663. 
  13. Bergamaschi MM, Queiroz RH, Zuardi AW, Crippa JA. Safety and side effects of cannabidiol, a Cannabis sativa constituent. Curr Drug Saf. 2011 Sep 1;6(4):237-49.

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Camphor
1. NAME
1.1 Substance
1.2 Group
1.3 Synonyms
1.4 Identification numbers
1.4.1 CAS number
1.4.2 Other numbers
1.5 Brand names, Trade names
1.6 Manufacturers, Importers
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
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
3.3 Physical properties
3.3.1 Properties of the substance
3.3.2 Properties of the locally available formulation
3.4 Other characteristics
3.4.1 Shelf-life of the substance
3.4.2 Shelf-life of the locally available formulation
3.4.3 Storage conditions
3.4.4 Bioavailability
3.4.5 Specific properties and composition
4. USES
4.1 Indications
4.2 Therapeutic dosage
4.2.1 Adults
4.2.2 Children
4.3 Contraindications
5. ROUTES OF ENTRY
5.1 Oral
5.2 Inhalation
5.3 Dermal
5.4 Eye
5.5 Parenteral
5.6 Other
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 by route of exposure
7. 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
7.2.2 Relevant 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
8. TOXICOLOGICAL 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 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 Relevant laboratory analyses
10.2.1 Sample collection
10.2.2 Biomedical analysis
10.2.3 Toxicological analysis
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic/specific treatment
10.4 Decontamination
10.5 Elimination
10.6 Antidote treatment
10.6.1 Adults
10.6.2 Children
10.7 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
11.2 Internally extracted data on cases
11.3 Internal cases
12. Additional information
12.1 Availability of antidotes
12.2 Specific preventive measures
12.3 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

PHARMACEUTICALS
1. NAME
1.1 Substance
Camphor
1.2 Group
Rubefacient/counter-irritant
1.3 Synonyms
1,7,7-trimethyl bicyclo (2,2,1)-heptan-2-one
2-bornanone
2-camphanone
2-keto-1,7, 7-trimethylnorcamphane
2-oxo-bornane
alcanfor
camfora
camphor-natural
camphor-synthetic
formasa-camphor
Gum camphor
Japan camphor
l,7,7-trimethy1norcamphor
laurel camphor
matricaria camphor
root bark oil
spirit of camphor
tramfer
1.4 Identification numbers
1.4.1 CAS number
76-22-2
1.4.2 Other numbers
U.N. Number: 2717
1.5 Brand names, Trade names
Camphora synthetic tablets, camphora (see Section 4).
1.6 Manufacturers, Importers
NMD (Norwegian Medicinal Depot).
2. SUMMARY
2.1 Main risks and target organs
Central nervous system (CNS) and kidney: convulsions followed
by depression, and renal damage may occur after intake of
relatively small amounts of camphor may occur. The main risks
are apnoea, asystole, and severe post-convulsive coma. Toxic
effects appear after the ingestion of approximately 2 g
(lethal dose LD adults: 4 g; children: 1 g of pure camphor).
2.2 Summary of clinical effects
Clinical effects are: gastric irritation, colic, nausea,
vomiting, and diarrhoea; anxiety, excitement, delirium, and
epileptiform convulsions; apnoea and asystole. CNS depression
follows the excitatory phase, and may result in coma or,
rarely, death. Anuria may occur. The breath has the
characteristic odour of camphor.
2.3 Diagnosis
Poisoning by camphor is associated with an initial excitatory
phase, with vomiting, diarrhoea and excitement, followed by NS
depression and death. A characteristic odour of camphor is
present on the breath.

The symptoms may appear 5 to 90 min after ingestion depending

on the product ingested (solid or liquid). Oral and
epigastric burning sensations, nausea, and vomiting usually
occur early. The onset of convulsions may be sudden and
without warning, or may be preceded by confusion and
irritability, neuromuscular hyperactivity, and jerky movements
of the extremities.

Convulsions may be followed by coma, apnoea, and death.
Camphor is irritating to the eyes, skin and mucous membranes.

Blood and urine samples should be taken for routine analysis
and follow-up.

No specific laboratory analyses are indicated: camphor levels
are not clinically useful.

Camphor is recognized by its characteristic odour on the
patient’s breath.
2.4 First aid measures and management principles
Camphor induces convulsive states which may be life-
threatening and must be considered before attempting emesis or
gastric lavage.

If camphor has been ingested recently, and the condition of
the patient allows, perform gastric lavage with warm water (38°
C to 40 °C). If only small amounts have been ingested,
administer cathartics. Administration of vaseline oil
(laxative mineral oil) is controversial.

If camphor has been inhaled, remove patient from exposure,
administer fresh air or oxygen, and establish respiration.

If there has been external contact with camphor, wash skin
thoroughly with soap and water. Irrigate eyes with large
amounts of water.

Send patient immediately to hospital.

In case of severe poisoning:

Establish respiration if depressed – artificial respiration
may be necessary.

Treat convulsions (e.g., with diazepam).

With the airway protected (endotracheal intubation), gastric
lavage may be performed, followed by activated charcoal, and
then a saline cathartic.

Resin and charcoal haemoperfusion may be used in severe cases.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Camphor may be natural or synthetic. It occurs naturally in
the wood of the camphor tree (cinnamonum camphora), and is
xtracted by steam distillation and crystallization. Natural
camphor is dextrorotatory. Synthetic camphor may be made from

pinene which is converted into camphene by treatment with
acetic acid and nitrobenzene. Synthetic camphor is optically
inactive.
3.2 Chemical structure
C10H16O

Molecular Weight = 152.2
CH3

= O

H3C-C-CH3
3.3 Physical properties
3.3.1 Properties of the substance
Normal state at room temperature: solid,
translucent
crystals.

Colour: white crystals.

Odour: penetrating, aromatic.

There are dangers associated with the vapour, its dispersion,
and possible ignition. There is a moderate risk of fire if
camphor is exposed to heat or flame, but spontaneous
combustion does not occur.

Boiling point: 204 °C

Melting point: 176 to 180 °C

Sublimes appreciably at room temperature and normal
atmospheric pressure

Flash point: 65°C

Autoignition temperature: 466°C

Relative density: 0.99 (specific gravity)

Relative vapor density: 5.2

Vapour pressure: 20 PA at 20°C

Solubility in water: 0.125 g/100 m1 (25 °C)

Soluble in ethanol, ethylether, turpentine, and
essential oils

Explosive limits: 0.6 to 3.5 vol% in air

Relative molecular mass: 152.2.
3.3.2 Properties of the locally available formulation
No data available.
3.4 Other characteristics
3.4.1 Shelf-life of the substance

Five years.
3.4.2 Shelf-life of the locally available formulation
No data available.
3.4.3 Storage conditions
Store in airtight containers at a temperature not above
25°C.
3.4.4 Bioavailability
No data available.
3.4.5 Specific properties and composition
Strong aromatic odour.
4. USES
4.1 Indications
Camphor is used:

as a rubefacient
as a plasticizer for cellulose esters and ethers
in the manufacture of plastics (especially celluloid)
in lacquers and varnishes
in explosives and pyrotechnics
as a moth repellent
in the manufacture of cymene
as a preservative in pharmaceuticals and cosmetics.

When camphor is applied on the skin, it is analgesic. It is also
used in liniments as a counter-irritant in fibrositis, neuralgia,
and similar conditions.

In dermatology, when it is applied as lotion (0.1 to 3%), it is
an anti-pruritic and surface anaesthetic (when applied gently,
it creates a feeling of coolness).

In dentistry, it is prepared with parachlorophenol 35% (and 65%
camphor) and used as an antibacterial for infected root canals.

Taken internally, it is an irritant and carminative. It has been
used as a mild expectorant and to relieve griping (abdominal
discomfort) (this use is now discouraged because of toxicity).

Camphor was formerly administered as a solution in oil by
subcutaneous or intramuscular injection to act as a circulatory
and respiratory stimulant, but there is no evidence of its value
for this purpose (Reynolds, 1982).

According to the Dutch Information Medicamentorum (1986), camphor
is used:

For pruritus: lotion with 1 to 70 mg/g

For muscular pains: oil with 40 to 250 mg/g or alcohol solution
with 100 mg/ml

For colds: chest liniment, with 20 to 100 mg/g; nose ointment,
with 20 to 50 mg/g: nose drops/spray, with 0.15 mg/ml.

4.2 Therapeutic dosage

4.2.1 Adults
The dosage varies according to its uses (see section
4.1).
4.2.2 Children
The dosage varies according to different uses (see
section 4.1).
4.3 Contraindications
Internal use is discouraged because of its toxicity.

It is dangerous to place camphor into infants’ nostrils, since
it can cause instant collapse (Reynolds, 1982).

As with all rubefacients, it should not be applied to abraded,
irritated skin.
5. ROUTES OF ENTRY
5.1 Oral
Ingestion of camphor, camphorated oils, spirits, or other
preparations is the main route of poisoning.
5.2 Inhalation
Camphor fumes may be inhaled.
5.3 Dermal
Camphor liniments, spirits, or oil can be applied in excessive
amounts.
5.4 Eye
Splash or fumes may cause irritation.
5.5 Parenteral
Subcutaneous or intramuscular injections.
5.6 Other
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Camphor is readily and rapidly absorbed from the skin, and
gastrointestinal and respiratory tracts. Camphor in oil
solutions is absorbed slowly from subcutaneous or
intramuscular depots.
6.2 Distribution by route of exposure
After oral ingestion, peak blood levels are reached in 5 to 90
min. The high lipid solubility of camphor suggests that it
accumulates in adipose and other tissues. Camphor crosses the
placenta (Kresel, 1982), and has a large volume of
distribution.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Camphor is rapidly oxidized to campherols (2-hydroxycamphor
and 3-hydroxycamphor), and then conjugated in the liver to the
glucuronide form (Kresel, 1982). Camphor-related metabolites
are relatively fat-soluble and may accumulate in fatty tissue.
6.5 Elimination by route of exposure
Campherol conjugated to glucuronic acid is eliminated mainly
in the urine as an inactive compound (Kresel, 1982). Trace
amounts are eliminated by the lungs.
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
Camphor is a CNS stimulant whose effects range from mild

excitation to grand-mal convulsions or status
epilepticus. These effects result from excitation of
the cerebrum and lower structures of the CNS.

Gastric irritation, together with cortical and medullary
stimulation, frequently causes vomiting and diarrhoea.

It is not clear whether camphor toxicity is due to the
parent compound, a metabolite (secondary alcohols,
including borneol and isomers of hydroxy-camphor), or
both (Kresel, 1982).
7.1.2 Pharmacodynamics
Camphor is used exclusively because of its local
effects. When rubbed on the skin, it acts as a
rubefacient and causes localized vasodilatation
(mediated by way of an axon reflex), which gives
feelings of comfort and warmth.

As an anti-pruritic gent, when applied gently on the
skin, it may create a feeling of coolness, and a mild,
local anaesthetic effect, which may be followed by
numbness.

When ingested in small amounts, it creates feelings of
warmth and comfort in the stomach, but given in large
doses it acts as an irritant (Goodman et al 1985).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The probable oral lethal dose is 50 to 500
mg/kg. A dose of 2 g generally causes toxic
effects in adults. The potential lethal oral
dose in adults is 4 g pure camphor.
7.2.1.2 Children
The lethal dose for children is estimated to be
0.5 to 1.0 g (Siegel & Wason, 1986); for infants,
the oral LDLo is 70 mg/kg.
7.2.2 Relevant animal data

Species Route Effect Dose mg/kg

Rat Intraperitoneal LDLo 900

Mouse Intraperitoneal LD50 3000

Mouse Subcutaneous LDLo 2200

Dog Oral LDLo 800

Cat Intraperitoneal LDLo 400

Rabbit Oral LDLo 2000

Frog Subcutaneous LDLo 240

Guinea-pig Oral LDLo 1800

7.2.3 Relevant in vitro data
Not relevant.
7.3 Carcinogenicity
Carcinogenicity tests have been negative.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
Not mutagenic with the Ames test.
7.6 Interactions
Oils, alcohols, and fats promote gastrointestinal absorption.
Although vaseline oil has been used for gastric
decontamination, its use is controversial.
7.7 Main adverse effects
There have been reports of instant collapse in infants after
camphor has been applied to their nostrils (Reynolds, 1982).
8. TOXICOLOGICAL 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
General: Serum camphor levels are not
clinically useful.

A level of 15 mg/l within 20 minutes of
ingestion caused no symptoms.

A level of 19.5 microgram/l 7 h after ingestion
caused convulsions (Phelan,1976).
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
The symptoms that occur within 5 to 90 min after
ingestion are: oral and epigastric burning sensations,
nausea, vomiting and feeling of warmth.

Mydriasis and impairment of vision have been reported.

Other symptoms are: headache, confusion, vertigo,
excitement, restlessness, delirium, and hallucinations;
increased muscular excitability, tremors, and jerky
movements; epileptiform convulsions followed by
depression; convulsions sometimes occur early in cases
of poisoning and may be severe; coma; CNS depression may
at times be the primary clinical response.

Death results from respiratory failure or from status
epilepticus.
9.1.2 Inhalation
Inhalation of concentrations above 2 ppm irritates the
nose and throat (mucous membranes). Respiratory
depression and apnoea may occur. Very large exposures
will cause the same clinical features as ingestion.
9.1.3 Skin exposure
Camphor may be a skin irritant. Acute poisoning may
occur after skin absorption. (Symptoms may be the same
as those that occur after ingestion, see section 9.1.1).
9.1.4 Eye contact
Camphor may be somewhat irritating to the eyes, but no
serious injuries have been reported.
9.1.5 Parenteral exposure

Camphor was formerly used parenterally as a circulatory
and respiratory stimulant; therefore, there is a
theoretical possibility of overdose or
poisoning by the parenteral route (clinical features as
in section 9.1.1).
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Symptoms include viral illness, rapid neurological
deterioration, liver injury, prolonged prothrombin time,
and low blood glucose were observed in a 6-month-old
male child who received a total dose of 3 g/kg over a 5
month period (Jimenez et al 1983).
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
No data available.
9.3 Course, prognosis, cause of death
If the patient survives for 24 h, recovery is likely. Death
results from respiratory failure during a convulsion or from
status epilepticus, and may also result from exhaustion and
circulatory collapse. Death may occur during an early
convulsion or as late as 20 h after ingestion.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Peripheral circulatory collapse and shock have been
reported (Vasey & Karayannopoulus, 1972).
9.4.2 Respiratory
Respiratory depression and apnoea may occur. Death
usually results from post-convulsive respiratory
depression.

The odour of camphor may be detected on the breath.
9.4.3 Neurological
9.4.3.1 CNS
Seizures are characteristic of camphor toxicity
and may occur suddenly, even without previous
symptoms. Confusion, hallucinations, tremors,
agitation, and irritability can also be
observed. Convulsions may be followed by CNS
depression and coma.
9.4.3.2 Peripheral nervous system
There is neuromuscular hyperactivity.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Increased muscular activity and tremor
(Ellenhorn & Barceloux, 1988).
9.4.4 Gastrointestinal

Oral and epigastric burning sensations, nausea, and
vomiting usually occur shortly after ingestion.

Symptoms may be delayed for several hours if food is
present in the stomach (Ellenhorn & Barceloux, 1988).
9.4.5 Hepatic
Mild and transient hepatic derangement may occur with
elevation of serum concentrations of SGOT, ALAT, SGPT,
and lactic dehydrogenase.
9.4.6 Urinary
9.4.6.1 Renal
Urinary retention, albuminuria, and anuria have
been described (Smith & Margolis, 1954).
9.4.6.2 Other
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Camphor may be a skin irritant when applied in excessive
amounts or too vigorously.
9.4.9 Eye, ear, nose, throat: local effects
Eyes: Camphor is an eye irritant. Keratitis is
normally transient.

Ear: No data available (but camphor is probably
irritating).

Nose: Camphor irritates the nose at concentrations
above 2 ppm or when applied directly on mucous
membranes.

Throat: Camphor may irritate mucous membranes and cause
burning pain in the mouth or throat.
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
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
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Pregnancy: Camphor crosses the placenta and has been
implicated in fetal and neonatal death. It has been
used to induce abortions. Camphor poisoning during
pregnancy was reported in four cases and, in each case,
camphorated oil was mistaken for castor oil (Weiss &
Capalano, 1973). The topical use of camphorated oil in
pregnancy was not associated with teratogenic effects.

Breast feeding: no data available .
9.5 Other
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
If 10 mg/kg has been ingested and no symptoms appear within
4 h there is no need for hospital admission (Blodgett
Regional Poison Centre, 1987).

If 30 mg/kg have been ingested, the patient must be admitted
to hospital for gastric lavage if indicated (see section
10.4) (Geller et al 1984).

Establish respiration

Treat convulsions

Initiate gastric lavage only after airway has been
protected.

Do not induce vomiting

Administer activated charcoal and then a cathartic

Resin or charcoal haemoperfusion may be indicated in very
severe cases.
10.2 Relevant laboratory analyses
10.2.1 Sample collection
Blood and urine for biomedical analysis

Sample of the product for identification.
10.2.2 Biomedical analysis
Routine blood and urine analysis

In particular:

Hepatic transaminases and LDH

Albuminuria

EEG (Phelan, 1976).
10.2.3 Toxicological analysis
Tests for qualitative and quantitative determination
of camphor levels in serum/blood are generally not
available. They can be performed by gas
chromatography (Phelan, 1976).
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic/specific
treatment
Support respiratory and cardiovascular functions

Treat seizures with:

Diazepam IV

Adults: 5 to 10 mg initially, which may be repeated every
10 to 15 min to a maximum of 30 mg.

Children: 0.25 to 0.4 mg/kg up to a maximum of 5 mg in
children aged 30 days to 5 years, and a maximum of 10 mg in
children over 5 years old.

If seizures cannot be controlled or if they recur,
administer phenytoin or phenobarbital.

Phenytoin

Adults: 150 to 250 mg of phenytoin-sodium by slow
intravenous injection at a steady rate of not more than 50
mg/min. An additional 100 to 200 mg may be given 30 min
later if necessary (Reynolds, 1982).

Children: 5 mg/kg in one dose or divided into two doses
(Reynolds, 1982).

Phenytoin administered intravenously can prevent a relapse
into a convulsive state. It should be administered very
slowly in order to avoid cardiac arrhythmias.

Phenobarbital

Adults: initially 200 mg intramuscularly that can be
repeated after 6 h if necessary (Reynolds, 1982).

Children: initially 3 to 5 mg/kg intramuscularly (Reynolds,
1982).

Doubts have been expressed as to the efficacy of
henobarbitone by intramuscular injection in an emergency
because of the slowness of absorption.

Control renal function.
10.4 Decontamination
Ingestion

Camphor is a convulsant: do not induce vomiting. Gastric
lavage is contraindicated unless it is performed immediately
after ingestion or after the airway has been protected
(endotracheal intubation), and when the camphor ingested is
in solid form (Bozza-Marrubini et al 1987).

If the amount of ingested camphor is small, give a saline
cathartic.

Activated charcoal should be administered in the usual doses
of 30 to 100 g in adults and 15 to 30 g in children.

Saline carthartics are indicated a few minutes after
activated charcoal has been given, and should be stopped
when a charcoal stool appears.

Dose of sodium sulfate: 20 to 30 g in adults and 250 mg/kg
in children

Dose of sorbitol: 30 to 50 g orally in adults.

Eye contact

Keep eyelids apart using your finger and flush eyes with
large amounts of water for at least 15 min. Keratitis is
normally transient, but if it persists, an opthalmic
examination should be performed.

Skin contact

Wash exposed area very thoroughly with soap and water.
10.5 Elimination
Both lipid haemodialysis and resin haemoperfusion have been
helpful in lowering blood camphor concentrations (Kopelman
et al, 1979).

Aqueous haemodialysis is ineffective in removing camphor.
In one patient lipid dialysis with soyabean oil removed
camphor effectively, but it is not routinely recommended
(Ginn et al, 1968).

Amberlite resin haemoperfusion was used in 1 patient;
camphor was cleared from the blood and the patient had a
good recovery (Kopelman et al, 1979).

Charcoal haemoperfusion has proven effective (Mascie-Taylor
et al, 1981)
10.6 Antidote treatment
10.6.1 Adults
There is no specific antidote.
10.6.2 Children
There is no specific antidote.
10.7 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Camphor has occasionally been used in attempts to induce
abortion (Briggs et al 1965): it was detected in maternal
blood 15 min after ingestion, but not after 8 h. At
delivery 36 h later, however, it was present in the amniotic
fluid, the umbilical cord, and in the fetal blood. This
distribution might reflect immature hepatic glucuronic
conjugation in the fetus – a major detoxication process for
camphor in adults. The infant appeared viable at birth, but
failed to initiate respiration. Post-mortem examination
revealed severe atelectasis and CNS-necrosis (Gosselin et al,
1984).

A patient who ingested approximately 60 g of camphorated oil
(i.e., 12 g pure camphor) was successfully treated by lipid
haemodialysis (Ginn et al, 1968).

A 3 year-old girl swallowed 1 tablespoon of camphor-
containing salve and developed violent vomiting, convulsions,
and respiratory depression (Anon, 1975).

A 2-year-old girl swallowed 2 teaspoons of a camphor
preparation and had violent vomiting but no convulsions
(Anon, 1975).

A 19-month-old infant died after ingesting 1 g of a camphor
product; autopsy showed haemorrhage and brain cell
degeneration (Anon, 1975).

A man attempted suicide with 150 ml of camphorated oil, i.e.,
30 g pure camphor (the potential lethal dose in an adult is
4 g pure camphor). He had peripheral circulatory shock and
severe dehydration because of vomiting. Severe and
prolonged grand-mal attacks occurred. The patient was fit
and well 36 h after intensive treatment. This is one of the
largest camphor overdoses of camphor associated with
survival (Vasey & Karayannopoulus, 1972; Reynolds, 1982).

A 12-year-old boy given approximately 30 g camphorated oil
(20% camphor) developed coma and convulsions. After
treatment with diazepam, his condition improved, and he was
discharged from hospital on the 3rd day (Aronow & Spigiel,
1976).

A 33-year-old woman ingested 115 g camphorated oil (20%
camphor); she had several convulsions in hospital, but was
discharged after 4 days in the intensive care unit (Aronow &
Spigiel, 1976).

A 37-year-old man ingested 18 g pure camphor and developed
grand-mal seizures. He was treated by haemoperfusion; an
amberlite system was more effective than lipid dialysis in
extracting camphor from the blood (Kopelman et al, 1979).

A 19-year-old girl ingested 60 g camphorated oil (20%
camphor) and had grand-mal seizures; she was discharged from
hospital after 13 days of treatment (Kopelman et al, 1979).

A 15-year-old boy ingested 60 g camphorated oil (20%
camphor) and had grand-mal seizures; he was discharged from
hospital after 2 days of treatment (Kopelman et al, 1979).

A 61-year-old man ingested 60 g camphorated oil (20%
camphor) and developed status epilepticus and coma; after
treatment in hospital he fully recovered (Antman et al,
1978).

A 56-year-old woman ingested 12 ml camphorated oil (20%
camphor). She had nausea, vomiting, and convulsions. The
odour of camphor on her breath helped to diagnose her
condition. Lipid haemodialysis with soybean oil dialysate
was performed for 4 to 5 h and she recovered fully (Antman
et al, 1978).

A 6-month-old boy received a total dose of 3 g/kg camphor
over a 5-month period and developed clinical symptoms
consistent with a diagnosis of Reye’s syndrome (Jimenez et
al, 1983).

A 3-year-old girl ingested 7OO mg camphor from 1 tablespoon
of Vicks VapoRub (R). This product had also been placed in
her nostrils twice daily for 5 months. Grand-mal seizures
occurred 2 h after ingestion. Coma and respiratory
depression lasted 21 h. Full recovery ensued (Phelan,
1976).
11.2 Internally extracted data on cases
11.3 Internal cases
(to be added by PC using the monograph).
12. Additional information
12.1 Availability of antidotes
12.2 Specific preventive measures
Keep pharmaceutical preparations and moth-repellents out of
the reach of children and irresponsible people.

Label camphorated oil appropriately to avoid mistaking it
for castor oil and cough syrups.

Do not place camphor ointments into infants’ nostrils.

Do not use the rubefacient on abraded skin.

In the workplace, the maximum permissible atmospheric
concentration is 2 ppm.
12.3 Other
No data available.
13. REFERENCES
Abdernalden’s Handbuck der Biologischen Arbveitsmetoden (1935)
Vol 4, p l289 Leipzig, Germany.

Anon (1975) Camphor may do more harm than good. J Am Med Assoc
234: No 2, p l45.

Antman E, Jacob G, Volpe B, Finkel S & Savona M (1978) Camphor
Overdosage: therapeutic considerations. NY State J Med, 6: 896-
897.

Arena JM (197O) Poisoning. Toxicology, Symptoms, Treatments.
2nd Ed, p 73. Springfield, Illinois, CC Thomas.

Aronow R (1976). Camphor Poisoning. J Am Med Assoc, 235: l26O.

Aronow R & Spigiel RW (1976) Implications of Camphor Poisoning.
Drug Intelligence and Clinical Pharmacy, lO: 63l.

Baselt RC (1982) Disposition of toxic drugs and chemicals in
man. 2nd ed, pll2. California, Biomedical Publications.

Bozza-Marrubini ML, Ghezzi R, Ucelli P (1987) Intossicasioni
acute 2nd ed. Org Editoriale Medico Farmacentica Milano.

Briggs GG, Freeman RK & Yaffe SJ (1986) Drugs in pregnancy and
lactation. 2nd ed p 56c Baltimore, Williams & Wilkins.

“Documentation of Threshold Limit Values for Substances in
Workroom Air” (1971). Cincinnati, Ohio, Amer Conf of
Governmental Industrial Hygienists, Vol;3 p 37.

Dreisbach RH & Robertson WD (1987) Handbook of Poisoning. l2th
ed p 419 Connecticut, Appleton & Lange.

Dupeyron IP, Quattrocchi F, Castaing H & Fabiani P (1976) Child
poisoning after external application of a revulsive ointment.
Eur J Toxicol, 9: 3l3-32O.

Ellenhorn MJ, Barceloux DG (1988) Medical Toxicology – Diagnosis
and Treatment of Human Poisoning, 1st ed, New York, Elsevier.

Fuhner H (1932) Beitrage zer vergleichenden Pharmakologie I. Die
giftigen und t÷dlichen Gaben einiger substanzen fnr fr÷sche und
m_use. Nauynschmiedebergs Archir fnr Experimentelle Pathalogie
und Pharmacologie, 166: 443.

Geller RJ, Spyker DA, Garrettson LK & Rogol AD (1984) Camphor
toxicity. Development of a triage system. Vet Hum Toxicol,
(Suppl 2): 8-10.

Ginn HE, Anderson KE, Mercier RK, Stevens TW, Matter BJ (1968)
Camphor Intoxication Treated by Lipid Dialysis. J Am Med Assoc
2O3: 23O-23l.

Goodman LS, Gilman AG, Rall TW & Murad F (1985) Goodman and
Gilman’s The Pharmacological Basis of Therapeutics, 7th ed, New
York, Macmillan.

Gosselin RE, Hodge HC, Smith RP & Gleason MN (1984). Clinical
Toxicology of Commercial Products, 4th ed p 259 & p 84. USA,
Williams & Wilkins.

Grant WM (1986). Toxicology of the eye. 3rd ed Springfield, CC
Thomas.

Haddad LM & Winchester JF (1983). Clinical Management of
Poisoning and Drug Overdose, p 428-43l. Philadelphia, W.B
Saunders & Co.

Hawley, GG (1981). The Condensed Chemical Dictionary. 10th ed
New York, van Nostrand Reinhold Co.

Jimenez JF, Brown AL, Arnold WC (1983). Chronic camphor
ingestion mimicking Reye’s syndrome. Gastroenterology 84: 394-
398.

Kelly RC, Kopelman RC, Sunshine I (1976) A simple gas
chromatographic procedure for the determination of camphor in
plasma. J Anal Toxicol 3: 76.

Kopelman R, Miller S, Kelly RC & Sunshine I (1979). Camphor
Intoxication Treated by Resin Hemoperfusion. J Am Med Assoc 24l:
727-728.

Koppel C, Tenczer J, Schirop TH & Ibe K (1981). Camphor
poisoning. Abuse of camphor as a stimulant. Arch Toxicol 51:
101-106.

Kresel JJ (1982) Camphor. Clin Toxic Rev, 4(7): l.

Mascie-Taylor BH, Widdop B, Davison AM (1982) Camphor
intoxication treated by hemoperfusion. Postgrad Med J, 57: 725-
726.

Merck Index (1983) lOth ed p 238, (1983). New Jersey, Merck & Co
Inc.

Phelan WJ (1976) Camphor poisoning: over the counter dangers.
Pediatrics, 57: 427-43l.

Plunkett (1987) Handbook of Industrial Toxicology, 3rd ed p l64.
London Edward Arnold.

Poisindex, February 1988.

Proctor NH & Hughes JP (1978) Chemical Hazard of the Workplace,
p l43. Philadelphia, Lippincott.

Reynolds EF (ed) (1982). Martindale, The Extra Pharmacopoeia,
28th ed, p 35l. London, Pharmaceutical Press.

Sampson WL & Fernandez L (1939). Experimental convulsions in the
rat. J Pharmacol Exp Ther, 65: 275-280.

Sax NI (1977). Dangerous Properties of Industrial Materials. 6th
ed, p 625. New York, van Nostrand Reinhold.

Siegel E & Wason S (1986). Camphor toxicity. Pediatric Clinics
of North America, 33: 375-379.

Sittig M (1985). Handbook of Toxic and Hazardous Chemicals and
Carcinogens. 2nd ed New Jersey, Noyes.

Skoglund RR, Ware LL Jr, Schanberger JE (1977). Prolonged
seizures due to contact and inhalation exposure to camphor. A
case report. Clin Pediatr, l6: 9Ol-9O2.

Smith EG, Margolis G (1954). Camphor poisoning: anatomical and
pharmacological study. Report of a fatal case. Experimental
investigation of protective action of barbiturates. Am J Pathol,
3O: 857-868.

Thienes CH & Haley TJ (1972). Clinical Toxicology, 5th ed p l6.
Philadelphoa, Lea & Febiger.

Trestrail JH & Spartz EM (1977). Camphorated and castor oil
confusion and its toxic results. Clin Toxicol, ll: l5l-l58.

Vasey RH & Karayannopoulus SJ (1972). Camphorated oil. Brit Med,
1l2.

Weiss J, Capalano P (1973). Camphorated oil intoxication during
pregnancy. Pediatrics, 52: 7l3-74O.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Elsa Wickstrom
National Poison Center
P.O. Box 8189 DEP
0034 Oslo
Norway

Tel: 47-2-456063
Fax: 47-2-454374

Date: 29 February 1988.

Peer review: Hamilton, Canada, May 1989

See Also:
Camphor (UK PID)

INTOX Home Page

ACUTE DYSTONIA

DEFINITION

Dystonia is a brief or sustained muscle spasm, often with slow
abnormal movements. Although any muscle group may be involved, it
most commonly affects facial muscles (eyes, jaw, tongue).

TOXIC CAUSES

Numerous pharmaceutical agents are associated with acute dystonic
reactions. Important examples include:

Benzamides: metoclopramide
sulpiride
Butyrophenones: haloperidol
Chloroquine and hydroxychloroquine
Cocaine
Levodopa
Lithium
Phenothiazines, especially piperazine compounds:
trifluoperazine
perphenazine
fluphenazine
prochlorperazine
thiethylperazine

Serotonin syndrome and neuroleptic malignant syndrome are specific
toxic syndromes, associated with increased muscle tone, that
require specific management.

NON-TOXIC CAUSES

Degenerative: Spinocerebellar degeneration

Focal dystonias: Blepharospasm
Writer’s cramp

Infective: Encephalitis
Tetanus

Metabolic: Thyrotoxicosis
Wilson’s disease

Structural: Arterio-venous malformation
Cerebrovascular accident
Tumour

CLINICAL FEATURES

Onset of dystonia may occur up to 20 hours following the
administration of the causative agent.

Various types of dystonia, involving particular muscle groups have
been described:

Laryngeal dystonia – spasm of pharyngeal and laryngeal muscles
resulting in stridor.

Oculogyric crisis – spasm of extra-ocular muscles, forcing the
eyes into upward or lateral gaze.

Opisthotonus – spasm of all paravertebral muscles, forcing the
trunk and neck into hyperextension.

Retrocollis – spasm of paravertebral neck muscles, forcing the
neck into hyperextension.

Torticollis – spasm of lateral neck muscles, twisting the neck
to one side.

DIFFERENTIAL DIAGNOSIS

Catatonic states
Dyskinesias
Seizures (tonic phase)

RELEVANT INVESTIGATIONS

Usually, no specific investigations are required to evaluate acute
toxic dystonias. Where indicated, the following may be useful:

CPK
EEG or CT scan of head (to exclude seizures or central organic
lesions)
Toxicology screens
Urinalysis

TREATMENT

Dystonias may increase in severity after initial presentation and
therefore all patients should be treated. Initial treatment is
usually provided with a parenteral formulation, followed by oral
medication for 2 to 3 days to prevent recurrence. Milder forms can
be treated with oral medication alone.

Suggested agents include:

Benztropine 1 to 2 mg by intramuscular or intravenous injection
(0.02 mg/kg in children). This dose may be repeated in 10 minutes
if the response is incomplete and anticholinergic side effects have
not occurred. Follow with 1 mg (0.02 mg/kg in children) orally
every 12 hours for 2 days. Benztropine is not the agent of choice
in children less than 3 years of age.

Diphenhydramine 1 mg/kg intravenously or intramuscularly to a
maximum of 30 mg. This dose may be repeated in 30 minutes if the
response is incomplete and anticholinergic side effects have not
occurred. Follow with 25 mg (0.5 mg/kg in children) orally, every
6 hours for 2 days.

Diazepam 0.1 mg/kg by slow intravenous injection. This dose may
by repeated in 30 minutes if the response is incomplete and
excessive sedation has not occurred.

Procyclidine 5 to 10 mg (0.5 to 2 mg in children under 2 years
of age, 2 to 5 mg in children over 2 years of age) intramuscularly
or intravenously. This dose may be repeated after 20 minutes if
the response is incomplete. Follow with 2.5 mg orally every 8
hours for 2 days.

CLINICAL COURSE AND MONITORING

Patients should be observed until symptom free. Prior to
discharge, they should be instructed that recurrent dystonia can
occur for up to 48 hours. In this event, they should return for
medical evaluation. The clinical course may be prolonged in the
case of dystonic reactions following injection of depot
preparations.

LONG-TERM COMPLICATIONS

Unusual.

AUTHOR(S)/PEER REVIEW

Author: Robert Dowsett
Consultant Toxicologist
Departments of Clinical Pharmacology and Emergency
Medicine
Westmead Hospital
Westmead, NSW 2145
Australia

Peer Review: London, March 1998: P. Dargan, T. Della Puppa, L.
Murray, A. Nantel, M. Nicholls.

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