Temporary heal can possibly kill: A case series on Eucalyptus ingestion

Sangavi

Department of Emergency Medicine, Alwarpet, Chennai

Background

Eucalyptus oil is a traditional herbal medicine widely used for a number of common ailments. Genus – Eucalyptus – Myrtaceae family. Eucalyptuscitriodora (EC), Eucalyptus tereticornis (ET), and Eucalyptus globulus (EG)) The main constituent is monoterpenes and 1. 8 cineole, which constitute 70%of the content.  Eucalyptus oil taken from the eucalyptus tree (true eucalyptus oil) does not contain camphor. Cineole fraction of camphor laurel that is also used to manufacture eucalyptus oil. Like eucalyptus oil, camphor is also epileptogenic. Extreme toxicity following ingestion is well-documented, but public awareness is generally lacking. The toxic symptoms are rapid in onset, which include a burning sensation in the mouth and throat, abdominal pain, and spontaneous vomiting. The initial central nervous system (CNS) effects are giddiness, ataxia, and disorientation followed by loss of consciousness and convulsions occurring within 30 min.

Case presentation

Case 1

A 49 years female, known systemic hypertension, type 2 diabetes mellitus and hypothyroidism, presented to ER with alleged history of accidental ingestion of eucalyptus oil of approximately 10ml in her residence. After which she had 3 episodes of watery vomiting followed by 2 episodes of involuntary jerky movements involving all 4 limbs with uprolling of eyeballs, tongue bite and urinary incontinence.

On arrival

Patient in Ictus, RR – 28/ min, Spo2 – 66% RA B/L wheeze with harsh vesicular sounds heard, BP – 170/ 100 mmHg, HR – 128/ min, Temp: 98.6o F Tongue bite with bloody frothy secretions noted. ABG shows severe metabolic acidosis. Other biochemical parameters were with in normal limits.

Management

Patient was treated with injection lorazepam 4mg stat. High flow oxygen using NRBM, dual anti-epileptics loading dose given. In view of status epilepticus, she was intubated and connected to mechanical ventilator. Started on sodium bicarbonate infusion for severe metabolic acidosis. Patient was monitored in ICU. Patient GCS improved and extubated the very next day. MRI brain and EEG – Normal. Anti-epileptics weaned off slowly. Patient discharged without any anti-epileptics and was normal in repeat follow ups.

Case 2

A 26-year gentleman brought to ER with A/H/O Eucalyptus oil inhalation at home while taking steam inhalation in view of URI, following which patient had drowsiness, agitation, f/b stiffening of both upper and lower limb with tongue bite.

On arrival: to ER RR – 26/ min, Spo2 – 96% RA, mild wheeze+, GCS E3V4M5, Temp: 98.6o F, post ictal state. ABG shows severe metabolic acidosis. Other biochemical parameters were with in normal limits.

Management

Started on sodium bicarbonate infusion for severe metabolic acidosis. Patient was monitored in ICU.  Patient discharged without any anti-epileptics

Case 3

A 48-year gentleman known bronchial asthma presented to ER with sudden onset of jerky movements with tongue bite. History of fever with cough and expectoration for 2 days for which patient had done steam inhalation with eucalyptus oil 15mins before the onset of acute symptom.

On arrival: to ER Post ictal confusion, wheeze+/creps+, GCS E3V5M6 , Temp: 98.6o F, tongue bite+. ABG shows severe metabolic acidosis. Other biochemical parameters were with in normal limits.

Management

Started on sodium bicarbonate infusion. Nebulization done. Imaging and EEG- normal. patient was monitored. No further episodes of seizure. Acidosis corrected. Discharged without antiepileptics.

Case 4

A 58year gentleman known Old CVA presented to ER with sudden onset of jerky movements with tongue bite. History of fever with cough and expectoration for 5 days for which patient had done steam inhalation with eucalyptus oil approx 20min before the onset of acute symptom.

On arrival: to ER Post ictal confusion, wheeze+, GCS E3V5M6, Temp: 98.6o tongue bite+. Routine investigations were done. ABG shows metabolic acidosis. Other lab parameters were within normal limit.

Management

Nebulization done. Antiepileptics given. Since pt had background of old CVA other neurological assessment done. Patient was continuously monitored and discharged without antiepileptics.

Case 5

A 5year child with no known comorbidities presented to ER with sudden onset of jerky movements of all four limbs lasted for few seconds . H/O accidental ingestion of eucalyptus at home.

On arrival:  to ER child was crying, vitals stable, moving all four limbs, afebrile no any other issues. ABG was normal. Other blood investigations turned to be normal.

Management

Supportive treatment given. Child was monitored no any further complaints and discharged. Doing well in regular follow-ups.

Discussion

In 1788 Drs. Dennis Considen and John White used essential oil like Eucalyptus to treat respiratory problems in Australia (details/ further studies were still unknown). In 1790, it was planted first by Tipu sultan at Nandhi hills in Mysore. In 1898, the first case report of Eucalyptus oil induced seizure was reported from Kerala.

By this way practice of eucalyptus oil usage for upper respiratory tract infection has been commenced. Eucalyptus oil is a popular household product, commonly presented as an essential oil, medicinal product, cleaning product, inhalational/vaporiser fluid or topical preparation. It is available commercially in many forms like cough drops, liniments, toothpaste, mouth washes and cold preparation.

Eucalyptus oil is highly toxic. Small ingestions of pure oil (≥5 mL) can lead to severe symptoms. CNS depression and respiratory compromise are the main features of eucalyptus oil poisoning to monitor. The common side effects in children include depression in the level of consciousness, ataxia, seizures, and vomiting.

In a study by K. Jagadish Kumar et al, out of 109 children with Eucalyptus oil ingestion, 59% of them were symptomatic. Minor poisoning (ataxia, vomiting, and abdominal pain) was observed in 30%, moderate poisoning (Glasgow coma scale of 8–14) in 25% and major poisoning with coma (coma scale of 3–7) accounting for 4%.

Pharmacokinetics and Pharmacodynamics

Gastrointestinal absorption of eucalyptus appears to be rapid and may be enhanced by the intake of lipids and milk. Pulmonary absorption of eucalyptus oil is also possible with peak plasma levels observed reportedly at 18 min. Studies suggest the route of elimination for cineole or eucalyptol via urine Studies have determined a terminal half-life for cineole or eucalyptol approx. 7 hr.

Pathophysiology of Eucalyptus oil induced seizures

Neurological impact

Cineole can cross the blood-brain barrier and affect the central nervous system.

Neurotransmitter disruption

Cineole may disrupt the balance of neurotransmitters in the brain, particularly by affecting gamma-aminobutyric acid (GABA) and glutamate.

Excitotoxicity

The imbalance between GABA and glutamate can lead to a state of excitotoxicity, where excessive neuronal firing and hyperactivity occur.

Seizure threshold lowering

Excitotoxicity and neuronal hyperactivity can lower the seizure threshold in susceptible individuals.

Seizure onset

In individuals with a lowered seizure threshold, the imbalance in neurotransmitters and hyperexcitability of neurons can trigger seizures.

Seizure manifestation

Seizures may manifest in various forms, including tonic-clonic seizures, absence seizures, or focal seizures, depending on the specific brain regions affected.

Individual variability

The susceptibility to eucalyptus oil-induced seizures can vary among individuals. Factors such as dosage, individual sensitivities, and pre-existing neurological conditions play a role.

Poisoning dose

5ml–30ml. In adults, death is commonly seen after ingestion of 30 ml, but encountered after 4-5 ml.

  • 5ml – significant depression of consciousness.
  • 30ml – mortality.

Toxic symptoms include

Burning sensation in mouth and throat, Abdmonial pain, vomiting, CNS symptoms like giddiness, ataxia, disorientation, convulsions, unlike ingestion, inhalation results in faster onset of CNS symptoms due to direct CNS stimulation. (Usually within few minutes) Onset of symptoms 10–15 min

Grades of poisoning

  • Minor poisoning – GCS 15/15 with ataxia, vomiting, abdominal pain
  • Moderate poisoning- GCS 8-14,
  • Major poisoning- GCS 3-7

Management

  • ABCD approach
  • Supportive treatment
  • Correction of metabolic acidosis
  • Adequate maintenance of hemodynamic parameters
  • Antiepileptic’s
  • No role of gastric lavage and no specific antidote

Conclusion

All physicians should be aware of the toxic effects of eucalyptus oil, which is used often in daily life in India. As there is no specific antidote, supportive care in ER, including rapid correction of metabolic acidosis and adequate maintenance of hemodynamic parameters, will lead to a rapid recovery. Unlike ingestion, inhalation results in faster onset of CNS symptoms because inhaled volatile oils are known to reach the brain directly and stimulate the neurons.

Since EO is one of the common ailment medicine used in every household, as an Emergency Physician we should be aware of the atypical presentation and should be vigilant in eliciting proper history. In patients with unprovoked seizures after steam inhalation/URI, we have to suspect EO poisoning also. Literature review suggests these seizures do not recur and AED can be safely withheld after two weeks. Any individuals can be prone if they are exposed to upper limits. People with seizure disorder and seizure prone individual were high chances of getting toxicity.

Since there is no regulatory mechanism for native products at Present, the manufacture bottle has no statutory warning signs; it should be made mandatory to have warning signs mentioned in eucalyptus bottle as means of public awareness. The health hazard of eucalyptus oil must be made aware to public in order to prevent unnecessary complications.

Bibliography

  • Eucalyptus oil poisoning Jagadish kumar etal/ Toxicol2015- 109 cases ,  mortality zero
  • J Paediatr Child Health. 1993; 42 inhalational cases, mortality zero
  • Case series of eucalyptus oil induced seizures. Asian journal pf pharmeuctical research 2020- 4 ingestion cases, no mortality
  • Webb NJ, et al. Eucalyptus oil poisoning in childhood: 41 cases south-east Queensland. J Paediatr Child Health. 1993;29:368-71.
  • Patel S, Wiggins J. Eucalyptus oil poisoning. Arch Dis Child. 1980;55:405-6.
  • Flaman Z, et al. Unintentional exposure of young children to camphor and eucalyptus oils. Paediatr Child Health. 2001;6:80-3.
  • Kumar KJ, et al. Eucalyptus oil poisoning. Toxicol Int. 2015;22(1):170-1.
  • Dhakad AK, et al. Biological, medicinal and toxicological significance of eucalyptus leaf essential oil: a review. J Sci Food Agric. 2018;98(3):833-48.

Acknowledgement

For guiding me with the article, I would like to thank, Dr. Aslesha (Consultant & Clinical lead – Department of Emergency Medicine).

 

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