Oleander Intoxication Research Articles

Fatal poisoning by ingestion of a self-prepared oleander leaf infusion

An unusual case of poisoning by the ingestion of oleander leaves is reported. A 71 year old male laboratory technician committed suicide at home in this unusual manner. At the death scene a steel pan and other paraphernalia, used for the extraction of oleandrin and other cardiac glycosides from the leaves of the Nerium oleander plant were found.Toxicological investigations for oleandrin, oleandrigenin, neritaloside, and odoroside were performed by LC–MS/MS on all biological samples (peripheral blood, vitreous humor, urine, liver, gastric contents) and on the yellow infusion found at the death scene.In all samples, toxic levels of oleandrin were detected (blood 37.5 ng/mL, vitreous humor 12.6 ng/mL, urine 83.8 ng/mL, liver 205 ng/mg, gastric content 31.2 µg/mL, infusion 38.5 µg/mL). Qualitative results for oleandrigenin, neritaloside, and odoroside were obtained. Oleandrigenin was present in all tissue samples whereas neritaloside and odoroside were absent in the blood and vitreous humor but present in urine, liver, gastric content, and in the leaf brew.The purpose of this study was the identification of oleandrin and its congener oleandrigenin, detected in the vitreous humor. The blood/vitreous humor ratio was also calculated in order to assess of the likely time interval from ingestion to death. According to the toxicological results death was attributed to fatal arrhythmia due to oleander intoxication. The manner of death was classified as suicide through the ingestion of the infusion.

Experimental Nerium oleander poisoning in Balb/c mice and Wistar rat: comparative hepatotoxicity and nephrotoxicity effects based on biochemical and pathological studies

Abstract Objective Nerium oleander is a member of the Apocynaceae family. All parts of the plant are considered toxic and can poison livestock and humans. Method The present paper was carried out to compare the toxic effect of oral administration of N. oleander extract at single doses of 10, 12.5, 15 and 25 mg/kg body weight in Balb/c mice and Wistar rat. The toxicity of this plant was determined by measuring serum levels of ALT, AST, total protein, albumin, BUN and creatinine. Histopathological examination was performed on the liver and kidney. Results Significant differences were observed in the level of the ALT, AST, BUN and creatinine. Interestingly, the biochemical changes were more severe in AST in rats compared with mice (15–16 and 4–5 times compared to control, respectively). In comparison, the values of BUN in rats were higher compared with mice (2–2.5 and 1–1.5 times, respectively). In mice and in rat more sever toxic lesions were observed in the liver and kidney, respectively. Conclusion In conclusion, the biochemical and pathological results of the current study suggested that mice have more susceptibility to hepatotoxicity of N. oleander intoxication. But, rats show more susceptibility to nephrotoxicity of N. oleander poisoning.

Thevetia peruviana

Thevetia peruviana, a poisonous shrub of the Apocynaceae family, is commonly called bastard oleander, exile oleander, tiger apple, and lucky nut. The attractive yellow flower is the reason this plant is cultivated to beautify landscapes in the tropics and subtemperate regions. The toxic glycosides contained in the plant, highly concentrated in the roots and seeds, produce digoxin-like effects and act primarily by inhibiting the Na+-K+ ATPase enzyme in the cardiovascular system. Although this plant is popularly found in the Indian subcontinent, poisoning is chiefly reported from India and Sri Lanka.1Eddleston M. Ariaratnam C.A. Meyer W.P. et al.Epidemic of self-poisoning with seeds of the yellow oleander tree (Thevetia peruviana) in northern Sri Lanka.Trop Med Int Health. 1999; 4: 266-273Crossref PubMed Scopus (99) Google Scholar, 2Puvaneswaralingam S. Yellow oleander poisoning and suicide in Sri Lanka.Scott Univ Med J. 2012; 1 (Available from: http://sumj.dundee.ac.uk/data/uploads/epub-article/002-sumj.epub.pdf. Accessed August 4, 2015): 02Google Scholar, 3Bose T.K. Basu R.K. Biswas B. De J.N. Majumdar B.C. Datta S. Cardiovascular effects of yellow oleander ingestion.J Indian Med Assoc. 1999; 97: 407-410PubMed Google Scholar, 4Saraswat D.K. Garg P.K. Saraswat M. Rare poisoning with cerebra thevetia (yellow oleander). Review of 13 cases of suicidal attempt.J Assoc Physicians India. 1992; 40: 628-629PubMed Google Scholar Accidental poisoning occurs in children who mistakenly consume the fruit either in confusion for water chestnut or out of curiosity.4Saraswat D.K. Garg P.K. Saraswat M. Rare poisoning with cerebra thevetia (yellow oleander). Review of 13 cases of suicidal attempt.J Assoc Physicians India. 1992; 40: 628-629PubMed Google Scholar, 5Camphausen C. Haas N.A. Mattke A.C. Successful treatment of oleander intoxication (cardiac glycosides) with digoxin-specific Fab antibody fragments in a 7-year-old child: case report and review of literature.Z Kardiol. 2005; 94: 817-823Crossref PubMed Scopus (28) Google Scholar Mixing the dried plant parts in herbal tea has also resulted in accidental poisoning in adults.6Driggers D.A. Solbrig R. Steiner J.F. Swedberg J. Jewell G.S. Acute oleander poisoning—a suicide attempt in a geriatric patient.West J Med. 1989; 151: 660-662PubMed Google Scholar The entire plant is poisonous, and suicidal and homicidal poisoning is frequently reported with ingestion of its kernels and leaves. Knowledge of its toxicity among the locals has increased poisoning incidences from this plant, which has no specific antidote; however, it may be treated with a Fab-specific antibody in conjunction with gastric lavage using activated charcoal.5Camphausen C. Haas N.A. Mattke A.C. Successful treatment of oleander intoxication (cardiac glycosides) with digoxin-specific Fab antibody fragments in a 7-year-old child: case report and review of literature.Z Kardiol. 2005; 94: 817-823Crossref PubMed Scopus (28) Google Scholar

Oleander toxicosis in equids: 30 cases (1995–2010)

To determine clinical, laboratory analysis, and necropsy findings for equids with oleander toxicosis and to identify factors associated with outcome. Retrospective case series. 30 equids. Medical records of equids with detectable concentrations of oleandrin in serum, plasma, urine, or gastrointestinal fluid samples and equids that had not received cardiac glycoside drugs but had detectable concentrations of digoxin in serum were identified via a medical records database search. Descriptive statistics were calculated for medical history, physical examination, laboratory analysis, and necropsy variables. Logistic regression analysis was used to identify physical examination and laboratory analysis factors significantly associated with outcome. 3 of 30 (10.0%) equids died before or immediately after arrival at the hospital. Of the other 27 equids, 23 (85.2%) had gastrointestinal tract abnormalities, azotemia was detected for 19 (70.4%), and a cardiac arrhythmia was ausculted for 18 (66.7%). Mortality rate for all equids was 50.0%; mortality rate for hospitalized equids was 44.4%. The most common cause of death was cardiac dysfunction. Odds of survival to discharge from the hospital were lower for equids with cardiac arrhythmias versus those without arrhythmias and decreased with increasing Hct and serum glucose concentrations. Odds of survival increased with increasing serum chloride concentration and duration of hospitalization. Equids with oleander toxicosis frequently had simultaneous gastrointestinal tract, cardiac, and renal problems. Oleander intoxication should be a differential diagnosis for equids with colic in geographic areas where oleander is found, especially when azotemia or cardiac arrhythmias are detected concurrently.

Oleander intoxication in New World camelids: 12 cases (1995–2006)

To characterize the clinical and clinicopathologic effects and evaluate outcome associated with oleander toxicosis in New World camelids. Retrospective case series. 11 llamas and 1 alpaca. Medical records from a veterinary medical teaching hospital from January 1, 1995, to December 31, 2006, were reviewed. Records of all New World camelids that had detectable amounts of oleandrin in samples of serum, urine, or gastrointestinal fluid were included in the study. Descriptive statistics were used to evaluate the history, physical examination findings, clinicopathologic data, and outcome of affected camelids. 11 llamas and 1 alpaca met the inclusion criteria of the study. Either oleander plants were present where the camelids resided (n = 7) or oleander plant material was identified in the hay fed to the camelids (5). One llama was dead on arrival at the hospital, and another was euthanized upon admission because of financial concerns. Of the 10 treated camelids, 9 had evidence of acute renal failure, 7 had gastrointestinal signs, and 4 had cardiac dysrhythmias on initial evaluation. The overall mortality rate was 25%, but the mortality rate for the 10 camelids that were medically treated was 10%. In New World camelids, oleander intoxication was associated with a triad of clinical effects (ie, renal, gastrointestinal, and cardiovascular dysfunction). Oleander intoxication often represented a herd problem but carried a fair to good prognosis if treated promptly. Oleander toxicosis should be considered a differential diagnosis in sick camelids.

THE EFFECT OF MAGNESIUM SULFATE IN TREATMENT OF EXPERIMENTAL OLEANDER (NERIUM OLEANDER) POISONING IN SHEEP

The purpose of this study was evaluation of magnesium sulfate effect in treatment of acute oleander intoxication in sheep. Eleven young native sheep randomly divided into 2 groups, 6 sheep being allocated to the treatment group and 5 served as controls. Sheep of both groups were dosed with a lethal dose of 110mg/kg body weight of dried oleander leaves. In sheep of treatment group, following development of ventricular arrhythmias, magnesium sulfate was slowly administered intravenously with dose rate of 100mg/kg body weight. Clinical signs of toxicosis were developed within 30 -40 minutes after dosing of the plant. Serial electrocardiography revealed various abnormalities and arrhythmias of cardiac rhythm in sheep of control group. Animals of control group died within 4.5 to 12 hours (median 8.5 hours) after receiving the toxic material. Administration of magnesium sulfate in sheep of treatment group suppressed ventricular arrhythmias to benign ones or normal sinus rhythm but its effect was transient and persisted for 3 to 3.5 hours. Second injection of magnesium had same effect but there was no considerable therapeutic effect after third injection of the drug. Sheep of treatment group died within 18 to 34 hours (median 24.5 hours) after receiving the oleander. Statistical analysis revealed a highly significant difference in survival time between the control and the treatment groups (p<0.004). The results suggested that magnesium sulfate can be used as a complementary therapeutic agent for treatment of acute oleander toxicosis in farm animals.

Successful treatment of oleander intoxication (cardiac glycosides) with digoxin-specific Fab antibody fragments in a 7-year-old child

A 7-year-old girl presented six hours after ingestion of a yellow oleander seed (Thevetia peruviana) with severe emesis, change in colour vision and complete heart block. Initial treatment with phenytoin and isoprenalin infusion led to intermittent supraventricular and ventricular tachycardia. The patient was then treated with two intravenous doses of 190 mg of digoxin-specific Fab antibody fragments (Digibind). Subsequently the patient's rhythm reverted to sinus rhythm and the symptoms resolved within 2 hours. administration of digoxin-specific Fab antibody fragments in an otherwise healthy child after oleander intoxication is safe and without adverse reactions.

Determination of Oleandrin in Tissues and Biological Fluids by Liquid Chromatography−Electrospray Tandem Mass Spectrometry

A rapid LC-MS/MS method, using a triple-quadrupole/linear ion trap mass spectrometer, was developed for the quantitative determination of oleandrin in serum, urine, and tissue samples. Oleandrin, the major cardiac glycoside of oleander (Nerium oleander L.), was extracted from serum and urine samples with methylene chloride and from tissues with acetonitrile. The tissue extracts were cleaned up using Florisil solid-phase extraction columns. Six replicate fortifications of serum and urine at 0.001 microg/g (1 ppb) oleandrin gave average recoveries of 97% with 5% CV (relative standard deviation) and 107% with 7% CV, respectively. Six replicate fortifications of liver at 0.005 microg/g (5 ppb) oleandrin gave average recoveries of 98% with 6% CV. This is the first report of a positive mass spectrometric identification and quantitation of oleandrin in tissue samples from oleander intoxication cases. The sensitivity and specificity of the LC-MS/MS analysis enables it to be the method of choice for toxicological investigations of oleander poisoning.

Beneficial Effect of Digoxin-Specific Fab Antibody Fragments in Oleander Intoxication

A 24-year-old man presented to the emergency department with nausea, vomiting, abdominal pain, and an acute confusional state of 6 hours' duration. Ten hours before admission, he had ingested a mixture of orange juice and six ground leaves, later identified as Nerium oleander (common pink oleander) leaves. His blood pressure was 100/80 mm Hg, and his pulse rate was irregular at 40/min. He was disoriented and his speech was dysarthric. Twelve-lead electrocardiography revealed a complete atrioventricular block, with a nodal escape rhythm of 40/min and diffuse ST depression. The presumptive diagnosis of acute oleander intoxication was confirmed by the detection of digoxin (1.0 nmol/L [0.8 ng/mL]) on radioimmunoassay. Despite intensive therapy, the patient's hemodynamic condition deteriorated. His blood pressure decreased to 70/40 mm Hg; he became oliguric and nonresponsive to external stimuli; and his potassium concentration rose to 6.8 mmol/L. Eighteen hours after admission, an empiric 480-mg dose of digoxin-specific Fab antibody fragments was administered intravenously over 30 minutes. Within minutes of the initiation of immunotherapy, the patient woke up; his blood pressure rose to 90/50 mm Hg; and he regained a sinus rhythm of 68/min with a prolonged PR interval. His potassium concentration decreased to 5.1 mmol/L within 15 minutes and normalized within 1 hour of therapy initiation. One day later, the 1 degree atrioventricular block disappeared, but the ST depression persisted for an additional 6 days. The value of digoxin-specific Fab antibody fragments in the treatment of plant glycoside and, in particular, oleander intoxication is discussed.

Beneficial effect of digoxin-specific Fab antibody fragments in oleander intoxication

Beneficial effect of digoxin-specific Fab antibody fragments in oleander intoxication