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Camphor poisoning in children

Camphor poisoning in children
Literature review current through: Jan 2024.
This topic last updated: Jun 05, 2023.

INTRODUCTION — Camphor is an essential oil originally derived from the camphor tree, Cinnamomum camphora, but now primarily produced from turpentine [1]. It is a terpenoid, which is a large family of naturally occurring hydrocarbons. Pediatric overdose of camphor can cause refractory seizures. Despite this potential for serious toxicity, camphor-containing products remain widely available.

This topic will discuss the clinical features, diagnosis and management of camphor poisoning in children. The approach to pediatric poisoning caused by over-the-counter (OTC) cough medications is discussed separately. (See "Over-the-counter cough and cold preparations: Approach to pediatric poisoning", section on 'Approach'.)

EPIDEMIOLOGY — Approximately 9000 to 11,000 camphor exposures are reported to United States poison control centers annually [2-5]. Exploratory ingestion of camphor-containing products by children younger than six years of age is most common, accounting for about 80 percent of exposures. Rarely, excessive topical exposure by a caregiver has been described [6,7]. Although the majority of exposures result in minor or no toxicity, refractory seizures can occur. (See 'Clinical features' below.)

PHARMACOLOGY AND TOXICITY — Camphor is marketed for topical use for cough suppression, nasal decongestion, cold sore ointments, muscle liniments, and rubefacients (table 1) [1]. Preparations for treatment of cough and cold symptoms in children typically advise application of a thick layer to the chest or throat three to four times daily [8]. Camphorated liquid for use in vaporizers is also available. Despite significant potential for toxicity, camphor products remain widely available. (See 'Clinical features' below.)

Formulations — In the United States, the concentration of over-the-counter (OTC) camphor products is limited to 11 percent (table 1). Products from some foreign countries are unregulated and may not be labeled including solid camphor for religious ceremonies and pest control and liquid camphor for dermal and inhalational use [6,7]. In Middle East traditional medicine, camphor has been used as an aphrodisiac [9].

Mechanism of action — Research in animal models suggests that the transient receptor potential vanilloid (TRPV)1 channel and the transient receptor potential ankyrin (TRPA)1 channel may be important in mediating cough and that camphor may desensitize these channels [10].

Limited evidence in children suggests that camphor, in combination with menthol and eucalyptus oil (Vick’s Vaporub) may improve some symptoms in children with viral upper respiratory tract infections. As an example, in a trial of 138 children with cough and cold symptoms for several days, Vick’s vaporub significantly decreased parental report of cough severity and the child’s ability to sleep on the first night of use when compared to unmedicated petrolatum or no treatment [11]. Adverse effects, primarily mild irritation of the skin, nose or eyes, was reported in 46 percent of the children receiving the camphor product compared with 2 to 6 percent of patients receiving petrolatum or no treatment. This study received support from the manufacturer.

In overdose, neurotoxicity is manifested by agitation and seizures soon after exposure. The mechanism of this action is unclear.

Pharmacokinetics — Camphor is lipophilic and well-absorbed through the skin and mucous membranes, especially in young infants. Gastrointestinal absorption is rapid with an onset of action of toxic effects within 5 to 20 minutes and a peak effect at 90 minutes [1,12]. The volume of distribution is 2 to 4 L/Kg and protein binding is 61 percent. The half-life in an adult volunteer ranged from approximately 90 to 170 minutes [13].

Toxic amount — Expert consensus suggests emergency evaluation for any child exposed to doses >30 mg/kg [12]. Seizures are unlikely to occur at doses less than 10 mg/kg [1].

Based upon case reports, the ingested toxic dose of camphor is considered to be approximately 500 mg or approximately 30 to 50 mg/kg (eg, equivalent to 5 mL [one swallow] of 10 percent topical camphor and 10 mL [two swallows] of 5 percent topical camphor).

Death due to refractory seizures or respiratory failure has been reported at ingested doses of 780 mg to over 1 g (>60 mg/kg) [12,14-17].

Toxicity from topical absorption of camphor is less common than from ingestion but has been described after application of unlabeled camphor oil in a four month old infant [7] and copious application of a labeled topical ointment hourly for 10 hours in a three year old child [6].

CLINICAL FEATURES — Key findings of camphor poisoning include:

History of oral ingestion or topical exposure to a camphor-containing product

Strong medicinal smell on the breath or if a topical exposure, on the skin

Oropharyngeal irritation, such as burning or stinging

Nausea, vomiting, and abdominal pain [9]

Seizures which may be the first sign of exposure [14]

Other central nervous system effects, including agitation, confusion, myoclonus, hyperreflexia, lethargy, and/or coma

Rarely, patients have experienced delirium and altered mental status lasting up to seven days after ingestion [18]

Additional studies are determined by the degree of toxicity as follows:

Patients with altered mental status or seizures warrant measurement of rapid blood glucose, serum sodium, and serum or blood calcium

Patients with prolonged altered mental status or focal neurologic findings warrant neuroimaging.

DIAGNOSIS — The diagnosis of camphor poisoning is based upon the typical clinical findings. History of camphor exposure is particularly important because many caregivers may be unaware of the dangers of camphor and not mention its use when seeking medical care [6]. Thus, the clinician should directly question parents regarding camphor exposure when clinical findings are suggestive (eg, seizures of unknown cause), especially in communities or cultures where camphor is frequently used as a cold remedy.

Laboratory studies for diagnostic purposes are not typically helpful. Camphor can be detected in both blood and urine, but testing is generally reserved for forensic cases because these studies are not readily available at most health care facilities and results do not correlate with the clinical course [1]. Other nonspecific laboratory findings include leukocytosis, proteinuria, and transient elevation in hepatic transaminases [19-22].

DIFFERENTIAL DIAGNOSIS — There are many causes of seizures that deserve consideration when evaluating the patient with suspected camphor intoxication.

Toxicological causes of seizures are extensive and include, but are not limited to the following toxins (table 2):

Sympathomimetics (eg, amphetamine)

Bupropion

Tramadol

Cyclic antidepressants

Anticholinergic agents

Antihistamines (eg, diphenhydramine, hydroxyzine)

Salicylates

Isoniazid

Methylxanthines (eg, theophylline or caffeine)

Organophosphates

Toxidromes, physical findings characteristic for specific toxins, can be helpful for determining the cause of seizure for many of these agents, including sympathomimetics, anticholinergic agents, and organophosphates (table 3). In addition to anticholinergic findings, cyclic antidepressants will often cause a constellation of symptoms other than seizures, including central nervous system (CNS) depression, hypotension, and widened QRS on EKG. (See "Tricyclic antidepressant poisoning", section on 'Clinical features'.)

Seizures caused by isoniazid are typically refractory to standard seizure treatment and usually respond only to treatment with pyridoxine. A history of a family member being treated for tuberculosis or travel to an endemic region may be a helpful clue. (See "Isoniazid (INH) poisoning", section on 'Clinical features of acute toxicity'.)

Unlike camphor, acute methylxanthine toxicity typically results in significant tachycardia and tachyarrhythmias, tachypnea, and hypokalemia. (See "Theophylline poisoning", section on 'Clinical features of overdose'.)

Some common medical causes of status epilepticus and differentiating features from camphor poisoning include (see "Clinical features and complications of status epilepticus in children", section on 'Causes'):

Hypoglycemia – Low rapid blood sugar (see "Causes of hypoglycemia in infants and children")

Electrolyte imbalance (eg, hyponatremia or hypocalcemia) – Low serum sodium or calcium (see "Etiology of hypocalcemia in infants and children")

Central nervous system infection (eg, meningitis or encephalitis) – Fever and/or meningismus

Intracranial mass lesion – Suggested by signs of increased intracranial pressure (eg, morning headache with vomiting, papilledema, and/or focal neurologic deficits)

Traumatic brain injury, especially abusive head trauma – Abusive head trauma may present with intracranial injury (eg, subdural hematoma) without an appropriate mechanism by history, retinal hemorrhages, skin bruising, and/or fractures (see "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children", section on 'Clinical features')

MANAGEMENT — Recommendations for the care of children with camphor exposure are derived from case reports and expert consensus [1,12]. Treatment of camphor poisoning is primarily supportive with special attention to management of seizures.

Decontamination — Any camphor-containing medicine that is on the skin should be removed using soap and lukewarm water. Hot water should not be used to prevent local vasodilation and increased absorption. Core temperature should be monitored during skin decontamination to avoid hypothermia.

Because camphor is rapidly absorbed from the stomach and has the potential for causing sudden altered mental status and seizures soon after ingestion and based upon case reports and expert consensus, we suggest that children who ingest camphor not receive activated charcoal [12]. Furthermore, gastric emptying with syrup of ipecac is contraindicated.

Asymptomatic — Asymptomatic patients and those children with only mild oropharyngeal or gastrointestinal irritation should be observed for a minimum of four hours. These patients warrant a bag and mask at the bedside and continuous monitoring of heart rate, respiratory rate, and pulse oximetry. The greatest risk for seizures is within the first two hours after ingestion. Patients who remain asymptomatic at four to six hours after exposure can be discharged to home.

Seizures — Seizures caused by camphor poisoning typically occur soon after ingestion and can be brief. Treatment is warranted for patients with active seizures on arrival to the emergency department or if seizures recur. Benzodiazepines (eg, lorazepam) are the first line treatment with repeat doses as necessary as shown in the table (table 4). If seizures are not controlled by appropriate doses of benzodiazepines, a second anticonvulsant agent such as phenobarbital should be administered. Other second-line agents, such as phenytoin or fosphenytoin, are unlikely to be effective in toxin-induced seizures.

Although unusual following camphor poisoning, patients with refractory status epilepticus should receive further pharmacologic therapy based upon the patient’s hemodynamic status, which is presented in the algorithm (algorithm 1) and reviewed elsewhere. (See "Management of convulsive status epilepticus in children", section on 'Refractory status epilepticus'.)

Children who develop seizures after camphor exposure warrant hospitalization. Once initial seizures are controlled most children fully recover and do not require seizure prophylaxis.

Extracorporeal removal (eg, hemodialysis or charcoal hemoperfusion) has not been shown to improve clinical outcomes in serious poisoned patients [1,12]. Hemodialysis is unlikely to remove a significant amount of camphor given its high volume of distribution and degree of protein binding.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)

SUMMARY AND RECOMMENDATIONS

Formulations Camphor, a terpenoid hydrocarbon, is marketed for topical use for cough and nasal decongestion, cold sores, and muscle or joint pain (table 1). (See 'Formulations' above.)

Toxic amount – Expert consensus suggests emergency evaluation for any child exposed to doses >30 mg/kg. Seizures are unlikely to occur at doses less than 10 mg/kg. (See 'Toxic amount' above.)

Clinical features – Important findings of camphor poisoning consist of ingestion or dermal exposure to a camphor-containing product, oropharyngeal and/or gastrointestinal irritation, and seizures. Although most pediatric exposures result in no or minimal symptoms, refractory seizures can occur. (See 'Clinical features' above.)

Diagnosis – The diagnosis of camphor poisoning is based upon clinical findings. History of camphor exposure is particularly important because many caregivers may be unaware of the dangers of camphor and not mention its use when seeking medical care. (See 'Diagnosis' above.)

Differential diagnosis – The differential diagnosis of camphor poisoning includes toxicologic and other medical causes of refractory seizures. (See 'Differential diagnosis' above.)

Management

Decontamination – Removal of any camphor-containing medication from the skin using soap and lukewarm water. (See 'Decontamination' above.)

In a child who ingests camphor, we suggest to not administer activated charcoal (Grade 2C). Furthermore, gastric emptying with syrup of ipecac is contraindicated. (See 'Decontamination' above.)

Asymptomatic patients – A child who has no symptoms or only mild oropharyngeal or gastrointestinal irritation should be observed for a minimum of four hours. The greatest risk for seizures is within the first two hours after ingestion. (See 'Asymptomatic' above.)

Seizures – Benzodiazepines (eg, lorazepam) are the first line treatment for seizures with repeat doses as necessary as shown in the table (table 4). If seizures are not controlled by appropriate doses of benzodiazepines, a second anticonvulsant agent such as phenobarbital should be administered. (See 'Seizures' above.)

Refractory status epilepticus – Patients with refractory status epilepticus should receive further pharmacologic therapy based upon the patient’s hemodynamic status, which is presented in the algorithm (algorithm 1) and reviewed elsewhere. (See 'Seizures' above and "Management of convulsive status epilepticus in children", section on 'Refractory status epilepticus'.)

Specialist consultation – Consultation with a regional poison control center is encouraged for all symptomatic overdoses. Contact information for poison centers is provided above. (See 'Additional resources' above.)

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