MOBILE VIEW  | 

SANDALWOOD OIL

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Sandalwood oil is the volatile oil distilled by steam from the dried heartwood of Santalum album (L.) (Osal & Farrar, 1955).
    B) This oil is a common fragrance used in creams, detergents, lotions, soaps, incenses, and a flavoring in food. When used in foods, the average concentration is 0.001% (Duke, 1985).

Specific Substances

    1) Oil Santal or Santal Oil
    2) Santalol
    3) Oleum Santali
    4) East Indian Sandalwood Oil
    5) Arheol
    6) Australian Sandalwood Oil (Eucarya spicata)
    7) West Indian Sandalwood Oil (Amyris balsamifera)
    8) AUSTRALIAN SANDALWOOD OIL
    9) EUCARYA SPICATA
    10) OIL SANTAL

Available Forms Sources

    A) SOURCES
    1) Sandalwood oil is a volatile oil from the dried hardwood of Santalum album L. Commercial sandalwood oil is comprised of about 90% alpha and beta santalol and about 2% to 4% santal oil esters. Alpha and beta santalol are sesquiterpene alcohols used in perfumes, soaps, and detergents. Australian sandalwood oil (Eucarya spicata) contains sesquiterpene alcohols known as fusanols (Osal & Ferrar, 1955; (DerMarderosian, 1993).
    2) Santalum album (yellow sandalwood) is an evergreen parasitic tree indigenous to the mountains of India and the Malay archipelago. It is cultivated for wood and sandalwood oil in India (Osal & Ferrar, 1955).
    3) The yield of sandalwood oil (via steam distillation) is about 2.5% (Osal & Farrar, 1955) to 5.7% (Sharma & Singh, 1987).
    B) USES
    1) Sandalwood is used in the perfume industry. It has been used medicinally since the 15th century.
    2) Formerly used medicinally to treat dysuria and gonorrheal cystitis and urethritis (Osal & Farrar, 1955).
    3) In traditional medicine, sandalwood has been used for a variety of disorders which have included headache, stomachache and urogenital disorders (DerMarderosian, 1993). It has also been used topically as an antiseptic and astringent; however, studies are lacking to support its reported effects.
    4) Currently, the oil is most often used as a popular fragrance with minimal use as a medicinal agent (DerMarderosian, 1993).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) SOURCE: Sandalwood oil is a volatile oil from the dried hardwood of Santalum album L. Sandalwood oil is obtained from the coarsely powered hardwood of a small evergreen tree native to cultivation in tropical Asia (ie, India, Sr Lanka, Malaysia, Indonesia, and Taiwan).
    B) USES: Sandalwood oil is used as a fragrance in many soaps, detergents, cosmetics, aromatherapy and fragrances. It is also used as a flavoring agent in various food products (eg, beverages, baked goods, frozen desserts and candy). In Chinese medicine, it has been used to treat stomach pains, vomiting and gonorrhea. Currently, the oil is most often used as a popular fragrance with minimal use as a medicinal agent. The oil also purportedly has antiviral activity against HSV-1 and 2; antibacterial activity against Helicobacter pylori; alpha-santalol has relaxing and sedative effects.
    C) PHARMACOLOGY: Commercial sandalwood oil is comprised of about 90% alpha and beta santalol and about 2% to 4% santal oil esters.
    D) TOXICOLOGY: Most essential oils including sandalwood can cause mucous membrane irritation. Aspiration is a risk from both the essential oil and from hydrocarbons or emulsifiers that are added to commercial products.
    E) EPIDEMIOLOGY: Exposure can occur but serious toxicity has not been reported with sandalwood oil. The most serious anticipated effect would be related to aspiration.
    F) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: Adverse clinical effects are not anticipated with therapeutic doses. Possible side effects can include dermatitis, itching of the skin and GI distress. Drug interactions have not been reported.
    G) WITH POISONING/EXPOSURE
    1) OVERDOSE: MILD TO MODERATE TOXICITY: There is minimal published information regarding human toxicity associated with sandalwood exposure. Anticipated effects may be similar to other essential oils and include mucous membrane irritation or numbness, gastrointestinal irritation, and dermal irritation. Ocular exposure may cause irritation, erythema, pain and possible chemical conjunctivitis. SEVERE TOXICITY: CNS depression, seizures, and coma may develop. Aspiration can cause severe pneumonitis. Rare severe events may include respiratory depression, bradycardia, and hypotension.

Laboratory Monitoring

    A) It is not anticipated that any laboratory studies are needed following ingestion of sandalwood oil used as a flavoring agent; monitoring may be indicated following an intentional or inadvertent ingestion of commercial products.
    B) Monitor vital signs and mental status.
    C) Monitor pulse oximetry and/or arterial blood gases and obtain a chest radiograph in patients with pulmonary signs or symptoms.
    D) Monitor creatine kinase (CK) and renal function in patients with prolonged seizures or coma.
    E) Routine laboratory studies are not indicated and should be obtained as needed in symptomatic or at risk patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) There is limited overdose information for sandalwood oil. Treatment is symptomatic and supportive. It is not anticipated that flavoring agents containing sandalwood oil would cause toxicity. Toxicity may develop from commercial products. Like other essential oils, treatment is based on the potential risk of aspiration or CNS effects following ingestion.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Following a significant ingestion of sandalwood oil, monitor for CNS depression and respiratory depression or distress. Treat hypotension with IV fluids. Add vasopressors, if hypotension persists. Treat seizures with benzodiazepines and barbiturates, or propofol if seizures persist or recur. RESPIRATORY: If pulmonary aspiration is known or suspected, monitor ABGs and pulse oximetry, obtain chest radiograph.
    C) DECONTAMINATION
    1) PREHOSPITAL: INGESTION: Gastrointestinal decontamination is not recommended because of the risk of aspiration following ingestion of commercial products containing sandalwood oil. DERMAL: Remove contaminated clothing and wash exposed skin with soap and water. OCULAR: Irrigate exposed eyes.
    2) HOSPITAL: INGESTION: Gastrointestinal decontamination is not recommended because of the risk of aspiration following ingestion of commercial products containing sandalwood oil. DERMAL: Remove contaminated clothing and wash exposed skin with soap and water. OCULAR: Irrigate exposed eyes.
    D) AIRWAY MANAGEMENT
    1) Airway support is unlikely to be necessary following a minor "taste" ingestion. Patients with a significant or unknown ingestion may be at risk to develop significant CNS or respiratory depression or aspiration and may require airway support including endotracheal intubation and mechanical ventilation.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) There is no strong evidence for the use of extracorporeal methods of elimination for volatile oils such as sandalwood.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with small ("taste") inadvertent exposures who have minimal symptoms (mild gastrointestinal upset or mucous irritation) may be managed at home.
    2) OBSERVATION CRITERIA: Patients with more than mild symptoms and those with deliberate or large ingestions should be sent to a healthcare facility. Patients who have remained asymptomatic for a period of 6 to hours following an ingestion can be release from observation. Patients should be observed in a medical facility until free of symptoms.
    3) ADMISSION CRITERIA: All patients who have developed severe gastrointestinal, pulmonary, or neurologic effects of poisoning should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist for assistance with medical management in patients with severe toxicity or in whom the diagnosis is unclear.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: A specific toxic dose has not been established. DAILY CONSUMPTION: The calculated individual consumption of sandalwood oil (found in various foods as a flavoring agent) is 0.0074 mg/kg day.

Summary Of Exposure

    A) SOURCE: Sandalwood oil is a volatile oil from the dried hardwood of Santalum album L. Sandalwood oil is obtained from the coarsely powered hardwood of a small evergreen tree native to cultivation in tropical Asia (ie, India, Sr Lanka, Malaysia, Indonesia, and Taiwan).
    B) USES: Sandalwood oil is used as a fragrance in many soaps, detergents, cosmetics, aromatherapy and fragrances. It is also used as a flavoring agent in various food products (eg, beverages, baked goods, frozen desserts and candy). In Chinese medicine, it has been used to treat stomach pains, vomiting and gonorrhea. Currently, the oil is most often used as a popular fragrance with minimal use as a medicinal agent. The oil also purportedly has antiviral activity against HSV-1 and 2; antibacterial activity against Helicobacter pylori; alpha-santalol has relaxing and sedative effects.
    C) PHARMACOLOGY: Commercial sandalwood oil is comprised of about 90% alpha and beta santalol and about 2% to 4% santal oil esters.
    D) TOXICOLOGY: Most essential oils including sandalwood can cause mucous membrane irritation. Aspiration is a risk from both the essential oil and from hydrocarbons or emulsifiers that are added to commercial products.
    E) EPIDEMIOLOGY: Exposure can occur but serious toxicity has not been reported with sandalwood oil. The most serious anticipated effect would be related to aspiration.
    F) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: Adverse clinical effects are not anticipated with therapeutic doses. Possible side effects can include dermatitis, itching of the skin and GI distress. Drug interactions have not been reported.
    G) WITH POISONING/EXPOSURE
    1) OVERDOSE: MILD TO MODERATE TOXICITY: There is minimal published information regarding human toxicity associated with sandalwood exposure. Anticipated effects may be similar to other essential oils and include mucous membrane irritation or numbness, gastrointestinal irritation, and dermal irritation. Ocular exposure may cause irritation, erythema, pain and possible chemical conjunctivitis. SEVERE TOXICITY: CNS depression, seizures, and coma may develop. Aspiration can cause severe pneumonitis. Rare severe events may include respiratory depression, bradycardia, and hypotension.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Essential oils can be irritating to the eye and produce erythema and pain.
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) MUCOUS MEMBRANE IRRITATION: Generally, essential oils are irritants, and can cause a burning sensation the mouth, chest and stomach following ingestion.

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PULMONARY ASPIRATION
    1) WITH POISONING/EXPOSURE
    a) As with other essential oils, patients may be at risk to develop aspiration following ingestion of commercial products containing sandalwood oil. This risk may be due to the oil itself and/or from the hydrocarbons or emulsifiers that are added to many products.
    B) DECREASED RESPIRATORY FUNCTION
    1) WITH POISONING/EXPOSURE
    a) As with other essential oils, patients that intentionally or inadvertently (ie, a child) ingest commercial products containing sandalwood oil may be at risk to develop tachypnea, dyspnea, wheezing, hypoxia secondary to aspiration.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Effects may be extremely variable depending on the amount, type, and concentration of an essential oil. CNS effects have included ataxia, drowsiness, and coma with other essential oils.
    b) ONSET: CNS depression may have a rapid onset; however, there are currently no reports to evaluate this clinical effect with sandalwood oil.
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) As with other essential oils seizure activity may develop following ingestion of a commercial product containing sandalwood oil. Currently, there are no reports of seizure activity with sandalwood oil exposure.
    b) OTHER ESSENTIAL OILS: Between 1976 and 1981, 8 cases of toxicity involving essential oils (eg, sage, hyssop, thuja, and cedar leaves) resulting in seizure activity were reported to the Poison Control Center in Marseille, France. In 7 cases the essential oil was ingested for supposed therapeutic reasons; one case involved occupational exposure through pipetting. Recurrent seizures were observed in most cases. Neurologic investigation ruled out organic causes for the seizures in 6 cases but 2 patients had been on long-term anticonvulsant therapy. The seizure activity resolved spontaneously in 6 cases. In 2 cases, intensive respiratory care and anticonvulsant treatment was required (Millet et al, 1981).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) EXCESSIVE SALIVATION
    1) Increased salivation may be noted.
    B) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may be seen (Osal & Farrar, 1955). Heartburn, epigastric and oral pain, nausea, vomiting, and abdominal pain may occur after ingestion.
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea may occur. The fats, waxes, and oil could contribute to the diarrhea.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Sandalwood oil may produce a feeling of warmth and a burning sensation which may lead to blisters.
    B) PHOTOSENSITIVITY
    1) WITH POISONING/EXPOSURE
    a) Photosensitivity has also been reported (Starke, 1967) but not been confirmed with patch testing.
    C) DERMATITIS
    1) WITH THERAPEUTIC USE
    a) The oil may cause dermatitis in sensitive individuals (Burdock & Carabin, 2008; Leung, 1980).
    b) West Indian Sandalwood oil (from Amyris balsamifera) has caused contact sensitivity (Gougerot & Delzant, 1940). A case of erythematous, hyperpigmented, scaly plaque on the forehead and fissured fingertips was reported and confirmed by patch testing (Sharma & Singh, 1987).
    c) Allergic dermatitis occurred in a Gujarati woman following the use of "chandan" (sandalwood) bindi (a paste used by women in India to designate their marital status). Patch testing to bindi was positive (Tewary & Ahmed, 2006).
    d) A 63-year-old man developed depigmented contact dermatitis due to incense exposure. Patching testing with multiple allergens was performed and 10% sandalwood oil was positive (Burdock & Carabin, 2008).
    e) FRAGRANCE CONTACT DERMATITIS: In a study of 167 individuals, the prevalence of an allergy to a fragrance mix containing sandalwood oil was 6.6% and 1.8% of individuals had an irritation reaction (Burdock & Carabin, 2008).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Sandalwood oil is irritating to rabbit and mouse skin (Duke, 1985; Burdock & Carabin, 2008).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) It is not anticipated that any laboratory studies are needed following ingestion of sandalwood oil used as a flavoring agent; monitoring may be indicated following an intentional or inadvertent ingestion of commercial products.
    B) Monitor vital signs and mental status.
    C) Monitor pulse oximetry and/or arterial blood gases and obtain a chest radiograph in patients with pulmonary signs or symptoms.
    D) Monitor creatine kinase (CK) and renal function in patients with prolonged seizures or coma.
    E) Routine laboratory studies are not indicated and should be obtained as needed in symptomatic or at risk patients.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) All patients who have developed severe gastrointestinal, pulmonary, or neurologic effects of poisoning should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with small ("taste") inadvertent exposures who have minimal symptoms (mild gastrointestinal upset or mucous irritation) may be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist for assistance with medical management in patients with severe toxicity or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with more than mild symptoms and those with deliberate or large ingestions should be sent to a healthcare facility. Patients who have remained asymptomatic for a period of 6 to hours following an ingestion can be release from observation. Patients should be observed in a medical facility until free of symptoms.

Monitoring

    A) It is not anticipated that any laboratory studies are needed following ingestion of sandalwood oil used as a flavoring agent; monitoring may be indicated following an intentional or inadvertent ingestion of commercial products.
    B) Monitor vital signs and mental status.
    C) Monitor pulse oximetry and/or arterial blood gases and obtain a chest radiograph in patients with pulmonary signs or symptoms.
    D) Monitor creatine kinase (CK) and renal function in patients with prolonged seizures or coma.
    E) Routine laboratory studies are not indicated and should be obtained as needed in symptomatic or at risk patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital decontamination is not recommended because of the risk of aspiration following ingestion of commercial products containing sandalwood oil.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Gastrointestinal decontamination is not recommended because of the risk of aspiration. It may be considered if the airway can be protected, the patient is not vomiting and ingestion is recent.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) There is no overdose information for sandalwood oil. Treatment is symptomatic and supportive. It is not anticipated that flavoring agents containing sandalwood oil would cause toxicity. Toxicity may develop from commercial products. Like other essential oils, treatment is based on the potential risk of aspiration or CNS effects following ingestion.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Following a significant ingestion of sandalwood oil, monitor for CNS depression and respiratory depression or distress. Treat hypotension with IV fluids. Add vasopressors, if hypotension persists. Treat seizures with benzodiazepines and barbiturates, or propofol if seizures persist or recur. RESPIRATORY: If pulmonary aspiration is known or suspected, monitor ABGs and pulse oximetry, obtain chest radiograph.
    B) MONITORING OF PATIENT
    1) It is not anticipated that any laboratory studies are needed following ingestion of sandalwood oil used as a flavoring agent; monitoring may be indicated following an intentional or inadvertent ingestion of a commercial product.
    2) Monitor vital signs and mental status.
    3) Monitor pulse oximetry and/or arterial blood gases and obtain a chest radiograph in patients with pulmonary signs or symptoms.
    4) Monitor creatine kinase (CK) and renal function in patients with prolonged seizures or coma.
    5) Routine laboratory studies are not indicated and should be obtained as needed in symptomatic or at risk patients.
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) SUMMARY
    1) There is no strong evidence for the use of extracorporeal methods of elimination for volatile oils such as sandalwood.

Summary

    A) TOXICITY: A specific toxic dose has not been established. DAILY CONSUMPTION: The calculated individual consumption of sandalwood oil (found in various foods as a flavoring agent) is 0.0074 mg/kg day.

Therapeutic Dose

    7.2.1) ADULT
    A) CONSUMPTION
    1) DAILY CONSUMPTION: The calculated individual consumption of sandalwood oil (found in various foods as a flavoring agent) is 0.0074 mg/kg day (Burdock & Carabin, 2008).
    B) HISTORICAL
    1) Sandalwood has been used medicinally since the 15th century. Doses of 0.3 to 1 mL 3 or 4 times a day, were used to treat dysuria, gonorrheal urethritis, and cystitis (Sollmann, 1957).

Minimum Lethal Exposure

    A) SUMMARY
    1) A minimum lethal dose has not been established.

Maximum Tolerated Exposure

    A) SUMMARY
    1) A specific toxic dose has not been established.
    B) ANIMAL DATA
    1) RATS: The acute oral toxicity (LD50) sandalwood oil in rats is reportedly 5.58 g/kg of body weight, and the acute oral LD50 of major constituent of sandalwood oil, alpha-santalol, was 3.8 g/kg (Burdock & Carabin, 2008).
    2) RABBITS: The acute dermal toxicity (LD50) of sandalwood oil in rabbits was reportedly greater that 5 g/kg of body weight and the acute oral LD50 of major constituent of sandalwood oil, alpha-santalol, was greater than 5 g/kg (Burdock & Carabin, 2008).

Pharmacologic Mechanism

    A) Sandalwood has a weak antibacterial action, which has not been supported by clinical studies (DerMarderosian, 1993). Its phenol coefficient against the typhoid bacillus is under 0.1 (Rideal & Richardson, 1931).
    B) DMBA and TPA provided a maximum of 67% and 96% decrease in papilloma incidence and multiplicity, respectively. Sandalwood pretreated mice showed a significant decrease in ODC activity. No significant differences in weight gain were noted between the groups. The authors concluded that sandalwood oil could be an effective chemopreventive agent against chemically induced skin cancer (Dwivedi and Abu-Ghazaleh, 1997; Dwivedi and Zhang, 1999). Using the same protocol as Dwivedi and Zhang (1999), Kim et al. (2006) investigated the antitumor activity of three isolates sandalwood oil (neolignans, see Kim et al., 2005) and found that the percentage of tumor-bearing mice was reduced to 33.4–46.7%, even at 15 weeks (control).

Physical Characteristics

    A) Sandalwood oil has a peculiar faint persistent aromatic odor and an unpleasant spicy taste.
    1) Sandalwood oil has been habitually adulterated with castor oil and other fixed oils including oil of cedar. The hydrocarbon fraction contains 9 components.
    B) East Indian sandalwood oil is a slightly viscid pale yellow liquid. It has a strong persistent warm woody odor and a characteristic taste of sandalwood oil (HSDB , 2000).

Molecular Weight

    A) Varies

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