Objectives and Study: Cade oil is aromatic oil obtained from the branches and wood of Juniperus oxycedrus, common in the Mediterranean region and widely used in traditional medicine. This oil contains many chemical compounds with neurological, cardiac, renal, respiratory, hepatic, and gastrointestinal toxicity. Cade oil poisoning often requires intensive care admission due to the severity of the clinical picture. The objective of this study is to highlight the multiple manifestations found in the pediatric population due to cade oil exposure objectifying its significant toxicity. Methods: The authors report during this article a series of five cases of cade oil poisoning on pediatric patients hospitalized in the pediatric intensive care unit of El HARROUCHI hospital at the CHU Ibn Rochd in Casablanca during the period from 11/01/2022 to 12/07/2022. The patients have been exposed, a few hours before their admission, to an external cade oil application used by parents for therapeutic purposes. Main Findings: Our patients were aged from 1 month to 4 years, the average age was 1.5 years with a female predominance and a sex ratio of 1.5:1. The patients had no prior medical history, and the cade oil application was spontaneously declared by the parents of only 2 patients, 3 of them reported the use of it after the detection of the substance by the clinician. For all the cases, cade oil was applied to treat fever. All five (5) patients presented initial neurological signs. 3 of them were admitted to an acute consciousness disorder and the 2 other patients presented respectively a convulsive status epilepticus and generalized-onset seizure. We report respiratory symptoms in 4 cases ranging from a simple caught, rhinorrhea to severe respiratory distress. Three patients presented acute liver failure with very high transaminase levels associated with acute kidney failure. Two of them presented digestive symptoms such as abundant hematemesis, vomiting, and watery diarrhea. All patients received high doses of N acetylcysteine in their initial treatments. The evolution was unfavorable for 4 patients who developed a multiorgan failure, 3 of them died, with a good clinical improvement in the fifth patient after supportive and symptomatic treatment. Conclusion: Cade oil poisoning remains a very frequent situation in our context. Its toxicity is widely described in the literature. The increasing number of cases admitted, and the seriousness of the clinical picture require mass awareness among the population and the scientific community toward the use of medicinal plants.
Cade oil, also called “Katran”, remains one of the most used products in Moroccan folk medicine. This substance is readily available to the general population. Therefore, cade oil poisoning is far from being an exceptional situation in our context, justifying the large number of pediatric cases observed in a short period of time.
Cade oil mainly contains phenols (derivatives of guaiacol and cresol), a sesquiterpenoid (cadinene), and an Alcohol (carbinol) known for their significant toxicity. Frequently applied topically, and rarely ingested, the systemic passage of its chemical compounds often involves multi-visceral failure. Cade oil poisoning cases are characterized by polymorphic and severe clinical pictures.
During this article, we report a retrospective study involving 5 cases of cade oil poisoning admitted to the pediatric intensive care unit. The objective is to underscore the seriousness of clinical manifestations found during cade oil poisoning in pediatric patients to raise awareness in the scientific community about this deadly situation.
This was a retrospective descriptive study of 5 patients admitted to the pediatric intensive care unit of a tertiary care hospital Abderrahim El Harrouchi from November first, 2022, to December first, 2022, that have been exposed, less than 10 hours before their admission, to external cade oil application.
Data collected included first the symptoms leading to the use of cade oil, then the clinical, biological, and radiologic presentations including the therapeutics used for each patient, and, finally, the clinical evolution of each case.
Patients were aged from 1 month to 4 years, with no prior medical history (
The average age of our patients was 1.1 years with a female predominance and a sex ratio of 1.5:1. All of them had no prior medical history. In 3 cases, cade oil
| Patient | Gender | Age (months) | Past medical history | Time of use (Before admission) | Symptoms found before application | ||
|---|---|---|---|---|---|---|---|
| A | M | 11 | - | 8 H | Fever + rhinorrhea + sneezing + cough | ||
| B | F | 1 | - | 4 H | Fever + dyspnea + wheezing + diarrhea | ||
| C | M | 2 | - | 6 H | Fever + cough + wheezing + atopic dermatosis | ||
| D | F | 48 | - | 6 H | Fever + hemicorporal partial seizure | ||
| E | F | 5 | - | 6 H | Fever + rhinorrhea + dyspnea + seborrheic dermatisis | ||
| Patient | Chief complaint | Other symptoms reported | |||||
| A | Acute consciousness disorder | Abundant hematemesis + diarrhea | |||||
| B | Respiratory distress | Vomiting + diarrhea | |||||
| C | Respiratory distress associated with a generalized onset fever | - | |||||
| D | Convulsive status epilepticus | - | |||||
| E | Respiratory distress followed by acute consciousness disorder | - | |||||
was applied by parents, while for the 2 other patients, the application was done by grandparents. Two parents spontaneously declared the use of this substance, and the others recognized its use after its detection during the physical exam. In this series, all patients have been exposed to external application of cade oil which concerns the scalp, nostrils, and the sole of the foot.
Cade oil was used to treat a fever with neurological, respiratory symptoms (rhinorrhea, dyspnea, wheezing, cough, focal onset fever) (
In our series, neurological signs remain the first complaint motivating parents to consult, 60% of our patients presenting an acute consciousness disorder, the others reporting seizures. 40% of our patients presented a digestive symptom with hematemesis, vomiting and diarrhea.
All the patients were initially admitted to pediatric emergency service where the initial physical examination was performed.
Physical exam objected that all patients presented a pathological neurologic examination; 4 of them were unconscious, while one was found hypotonic and lethargic. On admission, acute respiratory distress was found in 60% of the cases. Respiratory examination was mainly abnormal. 60% of patients presented pathological auscultation and 80% of them had clinical respiratory distress signs. Only one patient was hemodynamically unstable on admission. Initially, fever was objectified in 3 patients, the 2 others were either apyretic or hypothermic.
| Patient | Vital signs | Neurological examination | Respiratory examination | General exam | |||
|---|---|---|---|---|---|---|---|
| BP | HR | RR | PO | ||||
| A | 50/30 | 150 | 50 | 78% | Comatose patient, GCS 07/15, SRP | PA: diffused bilateral crackles | Hypothermic, Mottled skin |
| B | 08/04 | 170 | 60 | 75% | obtunded, GCS 11/15, SRP | PA: diffused wheezing with fine crackles at right pulmonary apex. Intercostal and subcostal retraction, abdominal breathing Peripheral cyanosis | Apyretic |
| C | 80/40 | 190 | 68 | 85% | lethargic, hypotonic, SRP | PA: diffused bilateral wheezing with crackles Nasal flaring, intercostal and subcostal retraction. | Febrile at 38.5˚C Sunken fontanel and eyes, |
| D | 10/06 | 110 | 40 | 89% | Unconscious, GCS 08/15, SRP | PA: Normal | Febrile at 39.5˚C |
| E | 09/04 | 130 | 70% | Unconscious, GCS 08/15, SRP | PA: Normal Intercostal and subcostal retraction | Febrile at 38.9˚C | |
BP = blood pressure cmHg, HR = heart rate ppm, RR = Respiratory rate cpm, PO = pulse oximetry (on room air), GCS = Glasgow coma scale, SRP = symmetric and reactive pupils, PA = pulmonary auscultation.
The kidney function was evaluated by serum urea, creatinine levels, and calculated creatinine clearance. Muscle enzymes measured included the creatine kinase (CK) enzyme and lactate dehydrogenase (LDH). We used transaminases (alanine transaminase and aspartate transaminase) with bilirubin levels to evaluate liver function. The procalcitonin (PCT) and C-Reactive protein (CRP) were measured as a part of the infectious and inflammatory workup. Coagulation profile included Prothrombin time (TP), activated cephalin time/activated partial thromboplastin time (APTT) and fibrinogen assay. The results are reported in
60% of patients presented a hyperkaliemia with acute kidney failure and acute liver failure with high transaminases levels on admission. 80% of the cases presented an extensive rhabdomyolysis with very high muscles enzymes levels. Leukocytosis was reported in 4 cases while anemia was found in 2 patients. 2 patients had a disturbed coagulation profil with low prothrombin time and prolonged APTT. Gazometry (
The radiological examinations requested were guided by the initial symptomatology of each patient. In this series, all patients benefited from a chest X-ray and a computed tomography brain scan (without contrast).
| Patient | Electrolytes | Transaminases | Total bilirubin | Kidney function | Troponins | Muscle enzymes | CRP/PCT | ||
|---|---|---|---|---|---|---|---|---|---|
| A | Hyperkalemia Hyperphosphoremia | Normal | - | Altered | Normal | Elevated | Elevated 160/- | ||
| B | Hyperkalemia | Elevated 9N | Elevated | Altered | Elevated | Elevated | Elevated 120/7 | ||
| C | Normal | Normal | Normal | Normal | - | Normal | Elevated 80/1.4 | ||
| D | Normal | Elevated 3N | Elevated | Normal | Normal | Elevated | Negative | ||
| E | Hyperkalemia | Normal | Normal | Altered | Negative | Elevated | Negative | ||
| Patient | CBC (Complete Blood Count) | Coagulation profile | |||||||
| A | Normochromic normocytic anemia Leukocytosis with neutrophilia | disturbed | |||||||
| B | Leukocytosis with neutrophilia | Normal | |||||||
| C | Leukocytosis with lymphocytosis Thrombocytosis | Normal | |||||||
| D | Normal | normal | |||||||
| E | Hypochromic microcytic anemia Leukocytosis with neutrophilia Thrombocytopenia | disturbed | |||||||
N = normal, CRP (mg/L), PCT (ng/ml).
| Patient | pH | PaO2 | PCO2 | H C O 3 − | Ratio PaO2/FiO2 |
|---|---|---|---|---|---|
| A | 7.20 | 138 | 73 | 28 | 138 |
| B | - | - | - | - | - |
| C | - | - | - | - | - |
| D | 7.28 | 88 | 67 | 24 | 88 |
| E | 7.32 | 51 | 62 | 20 | 51 |
PaO2/PCO2: mmHg, HCO 3 − : mmol/l.
2 patients had a pathological brain scan, the first objectified a diffused cerebral edema while the other report intra parenchymal hematoma. The initial chest X-ray was pathological for all patients (
For patient D a complementary imaging was performed (Brain MRI with angiography sequences) revealing bilateral isolated cortical venous thrombosis.
Patient B had an abdominal ultrasound revealing a normal size liver, with regular contours and a hypoechoic echo structure with multiple echogenic spots creating a “starry sky” appearance suggesting acute hepatitis.
| Patient | Chest X-ray | Brain scan |
|---|---|---|
| A | Bilateral alveolar opacities | Diffused cerebral edema |
| B | Systematized right apical opacity with air bronchogram and a cardiomegaly | normal |
| C | Bilateral perihilar infiltrates | normal |
| D | Right basal alveolar opacity | Hyperdense parietal and frontal lesions (intra parenchymal hematoma) |
| E | Bilateral alveolar opacities | normal |
All patients received supportive and symptomatic treatment.
First, skin decontamination was performed using water and soap. Mechanical ventilation was required for 4 patients who presented a consciousness disorder with a Glasgow coma scale below 8 or severe respiratory distress.
Initially, 4 patients received deep sedation with anticonvulsant treatment (A, B, D, and E). Hemodynamic support was necessary for hemodynamically unstable patients using vasoactive drugs. We used high doses of N-acetyl cysteine for the first 3 days: 150 mg/kg as loading dose then 60 mg/kg/4hours. We then proceed to correction of hydro electrolytic and acid-basics disorders. None of our patients required hemodialysis considering the conservation of diuresis and the absence of dialysis emergencies. Probabilistic antibiotic therapy was initiated according to the suspected infectious site.
During their hospitalization, patients A, B and E developed a multiorgan failure leading to death despite the supportive treatment established.
The evolution of patient C was favorable with good clinical improvement, biological tests were normalized within 4 days, and the patient was transferred a week later to the pediatric department.
Patient D is still, to date, hospitalized in the pediatric intensive care unit dependent on mechanical ventilation.
Cade oil is aromatic oil obtained from the branches and wood of Juniperus oxycedrus.
Numerous studies have reported the beneficial virtues of the latter, in particular its antimicrobial activity tested in vitro [
As previously mentioned, this oil contains phenols, trierpene and etheric oils [
Phenol is considered as the most toxic compound in this list, responsible for most systemic effects observed during cade oil poisoning [
The latter is easily absorbed through the skin, lungs, and gastrointestinal tract, widely distributed, and mainly metabolized in the liver via glucuronidation, sulfonation, and oxidation by CYP450 2E1 isoenzyme [
Phenol toxicity can cause central nervous system excitation or depression responsible for neurological disorders ranging from coma to seizures [
Severe phenol poisonings may also result in cardiovascular instability to include Cardiac dysrhythmias [
We report that phenol and cresol intoxication can be responsible for respiratory failure with acute respiratory distress syndrome (ARDS) [
T. Hashimoto et al. [
Acute kidney injury was found in most reported cases of cade oil poisoning [
Other abnormalities have been reported during cade oil poisoning cases including a decrease in prothrombin time with increased APTT [
Hemolytic anemia, platelet, bleeding and clotting disorders were described following exposure to phenol [
Exposed skin decontamination is an important step in the management of cade oil poisoning cases, skin should be copiously irrigated with soap and water, however 70% isopropanol (a common formulation of rubbing alcohol) was reported to be superior to water or soap and water for decontamination of phenol [
N-Acetyl cysteine (NAC) is commonly used in acute hepatic failure, it provides cysteine, which is an essential precursor in glutathione production allowing to restitute glutathione reserve and neutralize free radicals, NAC by itself can binds to the toxic metabolites and eliminates free radicals [
Cade oil poisoning remains a very frequent situation in our context. The latter contains phenols known for their significant toxicity affecting multiple organs with life-threatening effects. Its high capacity of skin absorption in addition to the reduced skin surface in the pediatric population can lead to severe poisoning cases evolving, days later, to a multiorgan failure. The increasing number of cases admitted and the seriousness of clinical presentations should lead to the regulation of the use of these substances.
The case series was written by Anass Erragh and Salma Bellaftouh. References were provided by Salma Bellaftouh, Anas Erragh, Amine Afif and Karima Amenzoui, first reviewed by Professor Kaoutar ElFakhr, approved by Professor Ouissal Aissaoui, Professor Samira Kalouch and Professor Abdelaziz Chlilek. All the authors have read and agreed to the final manuscript.
No financial or non-financial benefits have been received or will be received from any party related directly or indirectly to the subject of this article.
Written informed consent was obtained from parents of the patients for publication of this case series and accompanying images.
Patients were diagnosed and treated according to national guidelines and agreements, our analysis looked retrospectively at outcomes of patients admitted, therefore, we did not seek ethical committee approval.
The authors declare no conflicts of interest regarding the publication of this paper.
Erragh, A., Bellaftouh, S., Afif, A., Amenzoui, K., ElFakhr, K., Aissaoui, O., Kalouch, S. and Chlilek, A. (2023) Cade Oil Poisoning: A Case Series. Case Reports in Clinical Medicine, 12, 159-167. https://doi.org/10.4236/crcm.2023.126022