Poisoning with Juniperus oxycedrus (Cade Oil): About a Case at the A4 Intensive Care Unit of the HASSAN II University Hospital in Fez
- 1. Unit of Toxicology, University Hospital Hassan II, Fez, Morocco
Abstract
Cade oil is a product extracted from the branches and wood of Juniperus oxycedrus. It contains etheric oils, triterpene and phenols.
Used widely in traditional Moroccan medicine with a high frequency of serious poisoning, especially in young children. We report here the case of an elderly subject victim of ingestion of cade oil, admitted in a state of neurological, renal and hepatic instability, successfully placed under resuscitation measures.
Citation
Mugisha A, Salaheddine S, Naoufil H, Nabil K (2024) Childhood Poisoning with Juniperus oxycedrus (Cade Oil): About a Case at the A4 Intensive Care Unit of the HASSAN II University Hospital in Fez. JSM Clin Case Rep 12(2): 1240.
INTRODUCTION
Cade oil (Guetran) often used by “Ferraga” can cause serious or even fatal accidents [1].
This oil obtained by dry distillation from branches of Juniperus oxycedrus (Mediterranean species) is used locally for skin conditions (psoriasis and eczema) and as an antiparasitic and antiseptic.
Poisoning is most often of iatrogenic origin, resulting from ingestion of a large quantity or prolonged and extensive skin application, especially in infants and newborns [2].
It contains etheric oils, triterpene and phenols. Phenol remains the most toxic component and probably responsible for the majority of systemic symptoms observed during poisoning [3].
After ingestion of cade oil by a subject, they may then present a clinical picture due to the “mixture” between the underlying pathology for which they are taking it, and the picture of intoxication or infection.
Description and chemical composition
Cade oil is a thick and homogeneous liquid, black in color and with a particular strong and empyreumatic odor.
Cade oil dissolves completely in different organic solvents (ether, crystalline acetic acid, benzene, chloroform, etc.).
It contains 17 to 26% phenols, including 12% guaiacol, cadinene, and other carbides, an alcohol, cadinol. Its antiseptic and antiparasitic properties are universally known and attributed to phenols [4].
What are the properties of cade oil?
Cade oil is considered to be:
• Antibacterial and digestive antiseptic: cade oil can stop the development of certain bacteria responsible for itchy skin;
• Anti-inflammatory: it calms rashes and reactions of the skin;
• Healing: cade oil can be found in many creams, soaps or shower gels intended for sensitive skin;
• Repellent, due to its smell, cade oil helps keep away summer insects but also those living around horses and sheep;
• Relaxing.
Its field of application was wide because it could be prescribed for the treatment of pulmonary diseases as well as for dental pain or certain eye diseases. It was also used internally, as part of the treatment of cholelithiasis, chronic nephritis but especially as an antihelmintic, in children who had a verminous condition [5-7].
CASE REPRESENTATION
Clinical observation
Identify: This is a 64-year-old patient, originally from and living in Fez.
Medical background
• Concept of psychosis put under treatment in 2015 with poor compliance (mystical theme, hypochondriac according to relatives) ·
• Chronic smoker says he quit more than 3 years ago ·
• Concept of consumption of plants and herbs for therapeutic purposes
• No concept of hypertension or underlying diabetes
• No known nephropathy
The history of the illness dates back to 4 days before his admission where the patient took cade oil in a context of acute diarrhea, the patient had consulted a “traditional healer” who applied cade oil on the neck, torso and back of the patient without any immediate skin reactions being reported. The patient was also asked to ingest 3 large spoons of cade oil daily. The clinical picture was complicated by the onset of vigilance disorders, as well as abnormal bilateral movements, motivating his loved ones to consult the emergency room of the Fes University Hospital Center.
Note that the family found a 50ml bottle near the patient with half consumed?
Physical examination: Vital parameters: HR: 88 bpm FR: 20cycle/min BP 16/10cm Temperature: 36.9°C, Dextro at 3g/dl
Performing an EKG: without anomalies
Anti-poison center contacted: monitoring of respiratory, neurological, hepatic and renal failures with carrying out a troponin.
Neurological examination: patient with a GCS of 14 confused with incoherent speech at times, non-aggressive and agitated at times. no meningeal stiffness, having presented myoclonus of the right hemibody with a spasm of the left hemiface with reduced muscular strength of the left hemibody but osteotendinous reflexes still present but reduced on the left side.
Brain MRI instead of a CT scan (to avoid a worsening of tubular necrosis) was carried out showing the presence of a right temporo-occipital cortical hypersignal as well as the posterior part of the thalamus (pulvinar Sign) which flashes in diffusion in favor of a status epilepticus
*Presence of a rounded hypointense lesion on T2* which may be related to a cavernoma (which could be the cause of its cortical irritation)
Thus, the patient was immediately admitted to the A4 intensive care unit
• Patient initially treated as status epilepticus on Gardenal loading dose and maintenance then put on Lamictal 25mg: 1 tab/day for 2 weeks, then 1 tab*2/day for 2 weeks, then 2 tabs in the morning and 1 tab in the evening for 2 weeks then lamictal 50mg: 1 tab*2/d
• Urbanyl 10mg: 1 tab*3/d for 7 days then 1-1/2-1 for 7 days then 1-0-1 for 7 days then 1/2-0-1 for 7 days then 1/2-0 -1/2 for 7d then 0-0-1/2 pdt 7d then stop
Psychiatric examination: finds a stable patient on the psychomotor level, disoriented in time and space, familiar contact, playfulness continuous court speech at normal pace with multiple responses alongside, ideas of overestimation and grandeur, no delirium detected during this examination the patient denies perceptual disturbances insight.
CAT: An organic origin was implicated given the patient’s picture and the patient was put on risperidone 1 mg in the evening + valium 10 mg 3 times a day
The biological assessment showed
• On the hematological level: Hb 15 PLQ 267000 TP correct TCA iso GB 18750 CRP 115
• Rhabdomyolysis assessment: CPK 2733 CPKMB 61
• Liver function: ASAT 52 ALAT 27 GGT 27 PAL 108
• Kidney function: Urea 1.44 Creatinine 18
• Drug assessment (Toxicology): returned in favor THC + Barbiturates positive in urine
A measurement of arterial blood gases showed a pH of 7.23, alkaline reserves of 12mmol/L, pCO2 of 35 mmHg, PaO2 of 115 mmHg and lactate level of 2.79 mmol/L Na 135 K 4.8 Hb 12
EVOLUTION
During the rest of his stay: Patient remained stable on the hemodynamic and respiratory level, calm GCS 14 but still confused, afebrile with an improving inflammatory assessment.
Therapeutically: Rehydration, Basic ration, thromboprophylaxis, gastric protection, lamictal, urbanyl, valium, Augmentin.
In total, this is a patient, 64 years old with psychosis with poor therapeutic compliance admitted to the A4 Multipurpose Intensive Care Department of the HASSAN II University Hospital in Fez, in a case of cade oil intoxication in whom the evolution was marked by a clinical-biological improvement, the patient was discharged and transferred to the Psychiatry department for further treatment.
DISCUSSION
Cade oil intoxication causes cardiovascular, neurological, renal and respiratory problems. Phenol remains the most toxic component and probably responsible for the majority of systemic symptoms observed during poisoning. Its absorption is rapid, its metabolism is essentially hepatic. Its renal and hepatic toxicity is well known [8]. Systemic toxicity is multivisceral and could be explained by the formation of cytotoxic metabolites. The hydroxylation of phenols produces semiquinone radicals whose oxidation leads to the formation of toxic free radicals when the quantity ingested exceeds the hepatic conjugation capacities [9].
According to Christiansen and Klaman et al. [10], cardiac, renal and hepatic toxicities are well known [11,12] following phenol toxicity. Hashimoto et al. [13], observed elevations in aminotransferases (AST 10,450 IU/L, ALT 8,990 IU/L), LDH (15,580 IU/L) and CK (170 IU/L) after 24 h of ingestion of approximately 70 mL of a 50% solution of cresol, in a 26-year-old woman who was initially asymptomatic.
An alteration of the central and peripheral nervous system such as involuntary movements, headache, hypotonia, mental confusion and then myoclonic or convulsive coma has been reported in several cases of phenol poisoning [14-16].
Hepatic cytolysis by centrilobular necrosis, which is linked to the formation of semi-quinone radicals, has been observed in several cases of phenol poisoning [13]. Renal tubular necrosis is due to both direct cytotoxicity, hemodynamic disorders and the precipitation of hemoglobin and myoglobins in the tubules.
Wu et al. [13], reported that acute renal failure (urea 49 mg/ dL, creatinine 9.8 mg/dL), mild gastrointestinal toxicity and pneumonia occurred following intentional ingestion of 150 g of cresol in a 44 year old man.
Koruk et al., reported acute renal failure (urea = 1.14 g/L, serum creatinine = 4.7 mg/dL) in a subject who took one tablespoon of cade oil to treat nephrolithiasis [14]. Multi-visceral damage is accompanied by metabolic acidosis and sometimes, consumption coagulopathy [16]. Lung damage can range from pneumonia to acute lung edema and can appear when applied to the skin or taken orally.
Toxic doses of phenol cause initial hypertension, followed by a marked drop in blood pressure. This is mainly due to depression of the central vasomotor system leading to a loss of vasoconstrictor tone, but also to a reduction in cardiac output secondary to a direct effect of phenol on the myocardium [17].
Christiansen and Klaman et al. [10], reported that hypotension can progress to cardiovascular shock.
Juniperus oxycedrus contains ethereal oils, a tripene (cadinene resin) and phenols (guaiacol and cresol derivatives). Phenol causes severe hypotension, hypothermia, tachypnea, and tachycardia [18-20].
On a biological level, the elevation of muscle enzymes is often significant, it is due to caustic digestive lesions, clonic movements and direct cytotoxicity. Treatment requires early emergency care and often in an intensive care unit.
CONCLUSION
Juniperus oxycedrus contains phenol which has potentially fatal effects: corrosive, cardiac, neurological, hemolytic, pulmonary and renal. Hence the interest in mentioning it when faced with any picture of multi-visceral failure.
REFERENCES
3. Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975; 55: 871-876.
5. JC. Amoric Skin absorption and toxic accidents of local treatments in children. Rev Fr Allergol Immunol Clin. 2000.
6. Hamba A. Cadier and cade oil (Juniperus oxycedrus L. and Pix Cadi). (PhD Thesis in Pharmacy). Montpellier.
9. Bismuth C, Baud F, Garnier R. Clinical toxicology. Paris: Flam-marion; 2000.
10. Poison Control Center, Refik Saydam H?fz?ss?hha Hygiene Institute, Ankara, Turkey.
18. Esin Ozyilkan, P?nar Kaya, Dilsen Colak, Omer Donderici. Department of Internal Medicine, Ankara Training and Education Hospital, Ankara, Turkey Y?ld?r?m Cesaretli.
19. https://santejeunes.ma/intoxication-a-lhuile-de-cade-katrane/
20. www.capm.ma
