A patient with clove oil intoxication.
A 67-year-old man, with a history of hypertension and alcohol abuse, was seen at the emergency department of our hospital. The patient had been found by his wife, unable to speak and confused. At the emergency department his blood pressure was 163/79 mmHg, pulse rate 82 beats/ minute and central body temperature 34[degrees]C with warm extremities. The Glascow Coma Score was E1M3V1, pupils were equal in size and responsive to light. There was no nuchal rigidity. Hyper-reactive symmetrical reflexes were seen and he had a Babinski on the left and a dubious Babinski on the right. Physical examination of heart and lungs was unremarkable. Laboratory results showed: pH 7.24, pC[O.sub.2] 41.25 mmHg, HC[O.sub.3]-17.2 mmol/l, p[O.sub.2] 84 mmHg, base excess -9.8 mmol/l, chloride 103 mmol/l, lactic acid 5.7 mmol/l, alcohol 1.62% and an osmolality of 334 mOsm/kg. Cerebrospinal fluid was drawn via lumbar puncture and showed no abnormalities. The patient was intubated and a computed tomography scan of the brain was performed. Apart from some old small ischaemic lesions, no abnormalities were seen. From the emergency department he was transferred to our intensive care unit, where thiamine and fluids (NaCl 0.9%) were administered. The laboratory abnormalities resolved over time. Ten hours after admission, the patient was fully awake and could be extubated. He had recovered completely and was discharged from the intensive care unit after one day. On repeated neurological examination the Babinski signs had also resolved.
This patient had used a clove oil solution of 81% eugenol and some alcohol for toothache. He also uses pure clove oil, combined with alcohol, to anaesthetise his fish to trim their fins at home. The patient's neurological symptoms and laboratory abnormalities can be explained by intoxication as a result of this highly concentrated clove oil and ethanol. The clove oil used had a concentration of 881 mg/ml, about a thousand times higher than the clove oil which is sold for dental pain. At doses greater than 0.25 ml per litre of water, it results in anaesthesia and subsequent death of fish when dissolved in ethanol (4).
The chemical structure of eugenol is similar to that of capsaicin. Like capsaicin, the mechanism of action is thought to be through vanilloid receptor I antagonism. However, affinity towards the gamma-amino butyric acid receptor has also been demonstrated. Eugenol and isoeugenol can each cause neurologic depression and coma in rodents when used in high concentrations. Dallmeier et al described eugenol-induced side-effects related to depressant activity on the central nervous system such as sedation, reduction of convulsion threshold and hypothermia. Concerning its local-anaesthetic properties, eugenol is pharmacologically characterised as a direct blocker of voltage-dependent Na+ channels (5).
The local analgesic effects of eugenol are well accepted in human dentistry. When mixed with zinc oxide, a resin is obtained which has antimicrobial, anti-inflammatory, local-anaesthetic and analgesic properties (6). But clove oil poisoning is rare and only a few cases have been reported. In children, a high anion gap acidosis and fulminant hepatic failure, depression of the central nervous system, coma, renal failure and disseminated intravascular coagulation have been found (1).
In humans, the presence of a toxic compound may be suspected indirectly by the demonstration of an osmolar gap between the measured and calculated plasma osmolality. The measured plasma osmolality will exceed the calculated plasma osmolality. The high osmolar gap in our patient (334 mOsm/kg measured vs 302 mOsm/kg calculated) with an unexplained high anion gap metabolic acidosis was suggestive of the presence of a toxic compound. In retrospect, the neurological symptoms, the high anion gap metabolic acidosis and the osmolar gap could all be explained by the combined eugenol and alcohol intoxication.
B. A. DYRBYE
Amsterdam, The Netherlands
(1.) Brown SA, Biggerstaff J, Savidge GF. Disseminated intravascular coagulation and hepatocellular necrosis due to clove oil. Blood Coagul Fibrinolysis 1992; 3:665-668.
(2.) Lane BW, Ellenhorn MH, Hulbert TV, McCarron M. Clove oil ingestion in an infant. Hum Exp Toxicol 1991; 10:291-291.
(3.) Kirsch CM, Yenokida GG, Jensen WA, Wendland R, Suh H, Bourgault M. Non-cardiogenic pulmonary oedema due to the intravenous administration of clove oil. Thorax 1990; 45:235-236.
(4.) Gladden JN, Brainard BM, Shelton JL, Camus AC, Divers SJ. Evaluation of isoeugenol for anesthesia in koi carp (Cyprinus carpio). Am J Vet Res 2010; 71:859-866.
(5.) Dallmeier K, Carlini EA. Anesthetic, hypothermic, myorelaxant and anticonvulsant effects of synthetic eugenol derivatives and natural analogues. Pharmacology 1981; 22:113-127.
(6.) Meryon SD, Johnson SG, Smith AJ. Eugenol release and the cytotoxicity of different zinc oxide-eugenol combinations. J Dent 1988; 16:66-70.
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|Author:||Dyrbye, B.A.; Dubois, L.; Vink, R.; Horn, J.|
|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Case study|
|Date:||Mar 1, 2012|
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