1. Background
Jatropha curcas is a common plant found all over the world. The name is derived from Greek (iatros = physician and trophe = nutrition), hence the common name physic nut [1] . The other common names are Jungle Erandi, Ratanjot, Bagranda, purging nut tree and Barbados nut tree [2] , also known as mbono kaburi in Swahili language and michakaburi in local language. Children are regularly exposed to toxic plants and usually poisoned when plants are mistaken for common, edible plants e.g., Jatropha curcas is often mistaken for nuts [3] [4] [5] [6] [7] . There are fewer datasets on paediatric poisoning from developing countries than from developed countries, likely due to underreporting of cases and lack of proper data management systems [8] . It’s even less reported and observed in our region. Gastrointestinal system manifestations are commonly reported, including vomiting, diarrhoea, and abdominal pain [9] .
We present a case report of a 5-year-old boy with acute neurological manifestation from Jatropha curcus poisoning from tertiary hospital in Northern Tanzania.
2. Case Presentation
A 5-year-old boy was referred to our hospital due to loss of consciousness for one hour and three episodes of convulsion. This child was well until 7 hrs prior to admission where he was found unconscious in the farm, after being reported by his brother to ingest fruits with black nuts of locally known as mchakaburi. His brother developed severe vomiting and recovered in a nearby health centre, but our patient was reported to have lost consciousness for almost one hour, and after regaining consciousness he was reported to develop one episode of tonic-clonic convulsion associated with tongue biting, followed by deep sleep. At the primary health centre he was given normal saline and Phenobarbitone then referred to our hospital. On arrival he developed two episodes of convulsions tonic-clonic in nature and was loaded with Diazepam and maintained with Phenobarbitone.
The fruits was brought by the parent and identified as Jatropha carcus (Figure 1). This was his very first admission, and was reported to have no any history of chronic illness or trauma.
Examination findings on admission, he was semiconscious with GCS of 8/15, normal posture, nutritionally well, no scalp swelling or bruises, no bleeding per
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Figure 1. Picture of the tree and nuts sent by parent of the child.
ENT, oxygen saturation 98% in room air. His temperature was 38˚C, respiratory rate was 31 breaths per minute, pulse rate of 140 beats per minute. His random blood glucose on admission was 7.2 mmol/l. On neurological examination he was semiconscious, with pinpointed pupils, no lateralization, negative signs of meningeal irritation and normal funduscopic findings.
Investigation findings
Blood workup showed a normal serum sodium level of 140 mmol/l, potassium of 4.35, mmol/l, urea of 2.43 mmol/l, serum creatinine of 36 µmol/l, slightly elevated AST 50 U/l and normal of ALT 25 U/l. He had leukocyte count of 11.90 × 109/L, haemoglobin of 10.7 g/dl, and platelets of 480 × 109/L Serology for HIV was negative.
Diagnosis and management
We reached a diagnosis of Herbal Neurotoxicity, differential diagnosis of meningitis. The child was started on maintenance IV fluids of 1400 mls of Ringers Lactate alternating with Dextrose Normal Saline (DNS), as maintenance since the child was kept nil per oral, empirical IV Ceftriaxone 900 mg 12 hourly due to clinical mimicry of meningitis, Diazepam loading of 5.4 mg IV if seizure reoccur and Phenobarbitone 60 mg nocte, and was nursed in lateral recumbent position in the paediatric intensive care unit to avoid risk of aspiration if he vomits. Urethral catheter was inserted with good urine output. Patient was planned for Brain CT scan to rule out any intracranial abnormality, but unfortunately due to financial constraints of the parents it was not done. Within the first 24 hours the child had marked improvement in terms of level of consciousness from 8/15 to 15/15, had no any vital instability, and could walk and eat by himself. On the second day he was transferred out to general ward, of which antibiotics were stopped and on the third day the child was discharged with no any marked neurological deficit.
3. Discussion
The seeds of J. curcas are toxic to both humans and animals excluding their use in foodstuffs. Despite its medicinal uses, the plant is toxic due to presence of toxalbumin called curcin, ricin and cyanic acid, related to ricinoleic acid. Ricin has been shown to exhibit both cardiotoxic and haemolytic effects. Though all parts of the plant are poisonous, seeds have the highest concentration of ricin and thus very poisonous [10] . Toxicity of the seed is attributed predominantly to the phorbol-type diterpene esters which they contain at high concentrations. Previous studies on leaves of this plant have investigated the isolation of flavonoids, sterols, polyprenols, besides saprophytic fungal activity, larvicidal activity, and molluscicidal activity [11] .
J. curcas seeds were shown to have inflammatory effect on study of mice and effects on the nervous system were founded as stereotypes and Straub tail [12] .
Although GI manifestation are commonly reported, it’s sometimes associated with neurological or cardiovascular signs, and hepatic or renal disorders; these were generally interpreted as complications of severe gastroenteritis, although direct toxic effects could not be formally excluded. In most cases, simple supportive measures were sufficient to ensure complete recovery within 24 - 48 hours [13] . May present also with features that resemble organophosphate poisoning, where in clinical setting may stand as an important differential diagnosis [14] . In our patient, he primarily presented with neurological manifestation which is rarely seen in this poisoning and has never been reported in our country.
Treatment is essentially symptomatic and supportive. In all cases of ingestion or suspected ingestion, if the child is conscious; induce emesis within 1 - 2 hours of ingestion with Ipecac syrup or perform gastric lavage. There is no specific antidote. Specific therapy may be indicated for haemorrhagic gastrointestinal damage, skeletal muscle and gastrointestinal spasm, excessive salivary secretions and haemoglobinuria. After substantial exposures to toxalbumin containing plants, minimum observation period of up to 8 hours is advised. IV fluids and electrolyte as necessary to restore and maintain fluid and electrolyte balance is to be given. Monitoring of renal functions and alkalinisation of urine is done to minimize effects of haemoglobinuria. Treatment of haemorrhagic gastro-intestinal damage is like that of peptic ulceration. Signs of central nervous system depression are looked for and assisted ventilation is initiated, if necessary [15] . In our patient we gave IV fluids and empirical antibiotics as CNS infection could not be ruled out and within 48hours he recovered.
Although most of the Jatropha curcas poisoning clinical manifestation are self-limiting, precaution and proper symptomatic approach has to be established as if left untreated can simply become life threatening to the victim.
4. Conclusion
Jatropha curcas poisoning is less reported in our region and our country in general. Worldwide neurological manifestation from this poison is also less reported. It can easily be confused with CNS infection which may be hard to diagnose due low socio economic status of our patients and also low resource setting which may not have diagnostics available. This is the first case report in our setup and country with neurological manifestation.
Consent
Verbal informed consent was obtained from the patient’s Father for publication for this case report.
Authors’ Contributions
MM, AS, RM and DNM conceptualised and prepared the manuscript PEM, FM, EK, AL, DNM, ZH, IM, ERM, NP, AI, LF, FM, BM and MJ reviewed the patient medical records. All authors have read and approved the final manuscript.
Acknowledgements
The authors would like to thank the child’s Father for permission to share her child’s medical history for educational purposes and publication.