Original Article

Acute oleander poisoning: A study of clinical profile

from a tertiary care center in South India
Gunasekaran Karthik1, Ramya Iyadurai1, Ravikar Ralph1, Vijay Prakash1,
K. P. Prabhakar Abhilash2, Sowmya Sathyendra1, O. C Abraham1,
Catherine Truman3, Alex Reginald2
Departments of 1General Medicine, 2Emergency Medicine, and 3Pharmacy, Christian Medical College, Vellore, Tamil Nadu,
India

A bstract
Introduction: Yellow oleander (Thevetia peruviana), which belongs to the Apocyanaceae family, is a common shrub seen
throughout the tropics. All parts of the plant contain high concentrations of cardiac glycosides which are toxic to cardiac muscle
and the autonomic nervous system. Here, we describe the clinical profile of patients with oleander poisoning and their outcomes.
Methods and Materials: This retrospective study was conducted over a period of 12 months (March 2016 to February 2017). The
data was extracted from the inpatient electronic medical records. Adult patients with a diagnosis of acute yellow oleander poisoning
were included in the study. Descriptive statistics were obtained for all variables in the study and appropriate statistical tests were
employed to ascertain their significance. Results: The study comprised 30 patients aged 30.77 ± 12.31 (mean ± SD) who presented
at 12.29 ± 8.48 hours after consumption of yellow oleander. Vomiting (80%) was the most common presenting symptom. Metabolic
abnormalities at presentation included hyperchloremia in 22 patients and metabolic acidosis (bicarbonate <24 mmol/L) in 29 patients.
Fifteen (50%) patients had abnormal ECG, of which second‑degree AV block was the commonest ECG abnormality seen in 4 (13.3%).
Fifteen (50%) patients had transvenous temporary pacemaker insertion (TPI). Having a TPI significantly prolonged the duration
of hospital stay (OR 1.85, 95% CI 1.06–3.21, P 0.03). The mortality in the cohort was 2 (6.7%). Conclusion: In patients with yellow
oleander poisoning, dyselectrolytemia with ECG abnormalities was common. TPI prolonged the duration of hospital stay. Further
studies are required to know the indication for and to ascertain the effect of temporary pacing on survival.

Keywords: Deliberate self‑harm, oleander, plant poison, temporary pace maker

Introduction including neriifolin, thevetin A, thevetin B, oleandrin, and other

unidentified substances.[4]
Yellow oleander (Thevetia peruviana), which belongs to the
Apocyanaceae family, is a common shrub seen throughout the Ingestion of yellow oleander (Thevetia peruviana) results in clinical
tropics. Deliberate self‑harm by consumption of this plant is symptoms similar to those of digitalis toxicity.[5,6] Common
a common toxicological emergency in South Asian countries, symptoms include nausea, vomiting, abdominal pain, diarrhea,
especially in India and Sri Lanka.[1‑3] Ingestion of any part of this dysrhythmias, and restlessness. A common electrolyte abnormality
plant is toxic, as all parts contains a variety of cardiac glycosides is hyperkalemia. Cardiac toxicity, due to the cardiac glycosides, is a
Address for correspondence: Dr. Ramya Iyadurai, common life‑threatening clinical manifestation. Patients may develop
Department of Medicine, Christian Medical College, bradycardia with atrioventricular (AV) block, atrial tachycardias,
Vellore ‑ 632 004, Tamil Nadu, India. ventricular tachycardia including bidirectional ventricular tachycardia,
E‑mail: iramya@cmcvellore.ac.in
Received: 07-08-2019 Revised: 12-12-2019
This is an open access journal, and articles are distributed under the terms of the Creative
Accepted: 16-12-2019 Published: 28-01-2020 Commons Attribution‑NonCommercial‑ShareAlike 4.0 License, which allows others to
remix, tweak, and build upon the work non‑commercially, as long as appropriate credit is
Access this article online given and the new creations are licensed under the identical terms.
Quick Response Code:
Website:
For reprints contact: reprints@medknow.com
www.jfmpc.com

How to cite this article: Karthik G, Iyadurai R, Ralph R, Prakash V,

DOI: Abhilash KP, Sathyendra S, et al. Acute oleander poisoning: A study of
10.4103/jfmpc.jfmpc_632_19 clinical profile from a tertiary care center in South India. J Family Med
Prim Care 2020;9:136-40.

© 2020 Journal of Family Medicine and Primary Care | Published by Wolters Kluwer ‑ Medknow 136
 Karthik, et al.: A study of clinical profile of oleander poisoning from South India

and ventricular fibrillation. Cardiogenic shock with myocardial The outcomes of interest were ECG findings, shock, electrolyte
depression can also occur. The arrhythmogenic effects of the cardiac abnormalities, duration of hospital stay, and mortality.
glycosides are caused due to a combination of the direct effects of
the toxin on the myocardium and the conducting system of the heart Ethical approval and funding
and the neurally mediated increases in autonomic activity.
This retrospective study protocol was approved by the
Institutional Ethics Review Board (IRB NO: 10923), Christian
Cardiac glycosides exert various direct cardiotoxic effects through
Medical College, Vellore, India. In this study, data was collected
a variety of mediators such as histamine, nitric oxide, leukotrienes,
endothelin, angiotensin, and superoxide radicals. Increased from the hospital inpatient electronic medical records and
central sympathomimetic activity on the heart also plays an the collected information was anonymized.
important role in the development of cardiac arrhythmias in
patients with cardiac glycoside poisoning. Hence, the use of Statistical analysis
parasympathetic system blockade with atropine, or the use of Descriptive statistics were employed for all the variables in the
β‑adrenergic agonists, may result in tachyarrhythmias. study. Categorical and continuous variables were compared
for outcome using the Fisher’s exact test and student t‑test,
In most cases, clinical management of poisoning, by yellow respectively. All continuous data were expressed as mean with
oleander (T. peruviana), involves administration of activated standard deviation (SD) unless the data was not normally
charcoal and supportive care including temporary pacemaker distributed. A P value of <0·05 was considered statistically
insertion. This study aimed to describe the clinical profile and significant. Statistical analysis was done using Statistical Package
outcomes among patients with yellow oleander poisoning for Social Sciences for Windows (SPSS Inc. Released 2007,
requiring admission to a tertiary care center in South India.
version 16.0. Chicago).

Patients and Methods

Table 1: Demographic, symptoms, and laboratory
Patients and setting parameters of patients with oleander poisoning (n‑30)
Adult patients with a diagnosis of yellow oleander poisoning, Characteristics Number (n) Value
between March 2016 and February 2017, requiring admission to a Demographic
Age, mean (SD) years 30 30.77 (12.31)
medical ward, the Medical ICU, or high dependency unit (HDU)
Gender ratio (Female: Male) 30 21: 9
of a tertiary care teaching hospital in India were included in
Number of seeds consumed, Median (IQR) 27 4 (3‑5)
the study. The patients were identified from the Emergency Symptoms (n)
Department (ED) database and the data was extracted from Vomiting 30 24 (80%)
inpatient electronic medical records. Nausea 30 11 (36.7%)
Giddiness 30 17 (56.7%)
A diagnosis of yellow oleander poisoning was made when a Diarrhea 30 2 (6.7%)
patient presented with an alleged history of consumption of Laboratory parameters
yellow oleander seeds and exhibited clinical symptoms of yellow Potassium, mean (SD) m mol/L 30 4.11 (0.65)
oleander toxicity. Magnesium, mean (SD) mg/dL 17 1.86±0.30
Chloride, mean (SD) m mol/L 28 112.14±3.77
A detailed history of the number of seeds consumed, time of Random blood sugar, mean (SD) mEq/L 30 115.53±61.69
Calcium, mean (SD) mg % 9 8.86±0.69
consumption, time of presentation to hospital, and any form
Phosphorus, mean (SD) mg % 9 2.97±0.68
of treatment given prior to presenting to the hospital were
Creatinine, mean (SD) mg % 30 0.79±0.27
documented. The results of routine blood tests were noted Bicarbonate, mean (SD) m mol/L 30 19.23±3.07
including complete blood count, liver function tests, renal function
tests, and electrolytes. Heart rate, ST‑T changes, and rhythm
abnormalities from the baseline electrocardiogram (ECG) were Table 2: ECG changes in patients with oleander
also noted. The severity of illness at admission using the Acute poisoning (n-30)
Physiology and Chronic Health Evaluation II (APACHE‑II) Characteristics Value n (%)
score was documented. Normal ECG 15 (50)
Sinus bradycardia 3 (10)
Patient management and outcome parameters First degree AV block 1 (3.3)
Second degree AV block 4 (13.3)
All patients were managed with supportive therapy including fluid
Third degree AV block 1 (3.3)
resuscitation, correction of dyselectrolytaemia, hemodynamic
T wave abnormality 3 (10)
support, mechanical ventilation, renal replacement therapy as Sinus arrhythmia 2 (6.7)
indicated, and temporary pacemaker insertion as decided by the RBBB 1 (3.3)
treating physician. AV- Atrioventricular block, RBBB- Right bundle branch block

Journal of Family Medicine and Primary Care 137 Volume 9 : Issue 1 : January 2020
 Karthik, et al.: A study of clinical profile of oleander poisoning from South India

Table 3: Comparing patients with and without TPI in oleander poisoning (n‑30)
Characteristics With TPI (Mean±SD) Without TPI (Mean±SD) OR 95% CI P
APACHE II score 5.40±3.35 5.2±6.47 1.01 0.87-1.16 0.91
Time of presentation, minutes 709.00±469.08 790.00±596.53 1.00 0.99-1.001 0.67
Number of seeds consumed 5.93±7.11 4.38±1.98 1.07 0.88-1.31 0.48
Heart rate, beats/min 61.27±23.11 81.33±20.40 0.96 0.92-0.99 0.03
Potassium, mmol/L 4.39±0.54 3.84±0.66 5.32 1.12-25.25 0.03
Bicarbonate, mmol/L 19.87±2.06 18.60±3.79 1.17 0.88-1.54 0.27
Chloride, mmol/L 112.14±3.74 110.00±3.62 1.21 0.93-1.57 0.16
Duration of stay in days 6.53±1.96 3.67±1.84 2.20 1.26-3.84 0.005
APACHE‑ Acute Physiology and Chronic Health Evaluation

Table 4: Multivariate logistic regression analysis of hospital stay was 4.00 ± 1.85 and 5.10 ± 2.37 days, respectively.
factors associated with TPI in oleander poisoning Of the 15 patients who received TPI, 13 (86.7%) patients had
Variable Odds ratio 95% confidence interval P abnormal ECG findings of whom 10 (66.7%) patients presented
Duration of stay, days 1.85 1.06‑3.21 0.03 with bradycardia. The mean ± SD duration of hospital stay
Heart rate, beats/min 0.97 0.93‑1.01 0.19 in patients with TPI and without TPI was 6.53 ± 1.96 and
Potassium, mmol/L 1.74 0.25‑12.03 0.57 3.67 ± 1.84 days, respectively (P value <0.001) [Table 3]. The
overall hospital mortality was 2 (6.7%).
Results
Discussion
Baseline characteristics
Yellow oleander poisoning is a common form of plant poisoning in
Baseline characteristics are summarized in Table 1. The study South Asia. All parts of the plant are poisonous, especially the seeds
comprised 30 patients aged 30.77 ± 12.31 (mean ± SD) who and leaves. Deliberate self‑harm by consuming yellow oleander
presented at 12.29 ± 8.48 hours after consumption of yellow seeds is common in young women. The number of seeds consumed
oleander. The number of seeds consumed by patients ranged in our study was not associated with increased mortality, which is
from 2 to 30 seeds with a median of four seeds and there was similar to the findings of Bose et al.[1] In our study, gastrointestinal
no association between the quantity of seeds consumed and toxicity was a common presenting symptom including vomiting
mortality (p value 0.548). Twenty six (86.7%) patients received and nausea. Common electrolyte abnormalities in our study at
treatment in a primary or secondary level hospital prior to admission were hyperchloremia and metabolic acidosis.
presentation of which 22 (73.3%) patients received gastric lavage,
four (13.3%) patients received atropine, and two (6.7%) patients Fifteen (50%) of the patients had abnormal ECG findings
received activated charcoal. On presentation at our hospital, with Mobitz type II AV conduction block, a rare finding in
24 (80%) patients received gastric lavage, 15 (50%) patients isolated digoxin poisoning,[7] being the commonest rhythm
received TPI, and nine (27%) patients were treated with intravenous abnormality, which is consistent with other studies on oleander
magnesium and oral activated charcoal. Vomiting (80%) was the poisoning.[1,2,8] The myocardial effects of these compounds
most common symptom followed by giddiness in 17 (56.7%) are attributable to increased intracellular concentrations of
and nausea in 11 (36.7%). Admission APACHE‑II score was Ca2+ and Na+ resulting from inhibition of the transmembrane
5.30 ± 5.06(mean ± SD). Metabolic abnormalities at presentation Na+/K+ATPase pump.[9]
included hyperchloremia in 22 (78.5%) patients and metabolic
acidosis (bicarbonate <24 mmol/L) in 29 (96.6%) patients. Management of yellow oleander poisoning is essentially supportive,
The serum potassium and magnesium levels were 4.11 ± 0.65, comprising aggressive fluid resuscitation and correction of
1.86 ± 0.30 (mean ± SD) mmol/L, respectively [Table 1]. dyselectrolytemia.[10,11] Evidence for specific management exists
for use of multidose activated charcoal (MDAC) and digoxin
ECG parameters specific antibody fragments. MDAC acts by two mechanisms:
ECG parameters are summarized in Table 2. Fifteen (50%) it prevents absorption of cardiac glycoside and it causes
patients had abnormal ECG at admission of which the interruption of enterohepatic circulation of cardiac glycosides
commonest ECG abnormality was second‑degree AV block facilitating gastric elimination.[10,12] Clinical trials have not shown
seen in four (13.3%) patients followed by sinus bradycardia and consistent benefit for the use of MDAC. In a clinical trial by De
T wave abnormality in three (10%) patients each. Silva et al.,[13] use of MDAC at a dose of 50 grams every six hours
for 72 hours caused a significant reduction in mortality, as well
Outcomes as decreasing the occurrence of life‑threatening arrhythmias. In
Five (16.7%) patients presented with shock and one patient another major trial by Eddleston et al., consisting of 1647 patients,
required intensive care. The mean ± SD duration of TPI and use of MDAC did not show a mortality benefit.[14]

Journal of Family Medicine and Primary Care 138 Volume 9 : Issue 1 : January 2020
 Karthik, et al.: A study of clinical profile of oleander poisoning from South India

Digoxin specific antibody fragments are specific for neutralizing References

the cardiac glycosides.[10,11] These fragments have been found to
1. Bose TK, Basu RK, Biswas B, De JN, Majumdar BC, Datta S.
successfully reverse the occurrence of cardiac arrhythmias with
Cardiovascular effects of yellow oleander ingestion. J Indian
resultant decrease in mortality.[15‑17] Clinical dose finding studies Med Assoc 1999;97:407‑10.
have agreed upon a single dose of 1200 mg.[16,17] However, its 2. Eddleston M, Ariaratnam CA, Meyer WP, Perera G,
use is precluded in developing nations due to its nonavailability Kularatne AM, Attapattu S, et al. Epidemic of self‑poisoning
and high cost.[18] Hemodialysis and hemoperfusion have not with seeds of the yellow oleander tree (Thevetia peruviana)
demonstrated any mortality benefit.[19] in northern Sri Lanka. Trop Med Int Health TM IH
1999;4:266‑73.
3. Eddleston M, Sheriff MH, Hawton K. Deliberate self harm in
There have been no clinical trials evaluating the effect of Sri Lanka: An overlooked tragedy in the developing world.
temporary pacemaker insertion on survival, as they would be BMJ 1998;317:133‑5.
ethically difficult to perform. Temporary cardiac pacing is the 4. Langford SD, Boor PJ. Oleander toxicity: An examination
usual treatment for a patient with a heart rate below 40 beats per of human and animal toxic exposures. Toxicology
minute, with any form of sick sinus syndrome or heart block. 1996;109:1‑13.
However, there are no current guidelines on the indication for 5. Saravanapavananthan N, Ganeshamoorthy J. Yellow
oleander poisoning‑‑A study of 170 cases. Forensic Sci Int
temporary pacemaker insertion in yellow oleander poisoning.
1988;36:247‑50.
The proportion of patients requiring TPI in our study (50%) 6. Demiryürek AT, Demiryürek S. Cardiotoxicity of digitalis
is higher than in earlier studies (6%).[20] This is probably due to glycosides: Roles of autonomic pathways, autacoids and
selection bias as patient recruitment, unlike earlier studies, was ion channels. Auton Autacoid Pharmacol 2005;25:35‑52.
from a tertiary care center. Patients with abnormal ECG finding 7. Kelly RA, Smith TW. Recognition and management of
and bradycardia were more likely to receive TPI. The mortality digitalis toxicity. Am J Cardiol 1992;69:108G‑18G.
in our cohort was 6.7%, which is similar to other studies.[5,21,22] 8. Tripathi S, Hariharan U, Doval J, Meshram P. Management
TPI did not have added mortality benefit in our study and it of plant cardiac glycoside poisoning. Res Opin Anesth
Intensive Care 2017;4:90‑2.
prolonged the duration of hospital stay [Tables 3 and 4]. This
9. Smith TW, Antman EM, Friedman PL, Blatt CM, Marsh JD.
reiterates the need for the development of guidelines on the
Digitalis glycosides: Mechanisms and manifestations of
use of TPI in yellow oleander poisoning. In developing nations, toxicity. Part I. Prog Cardiovasc Dis 1984;26:413‑58.
where availability and cost constraints preclude the use of digoxin 10. Rajapakse S. Management of yellow oleander poisoning.
antibody fragments cautious monitoring, early aggressive fluid Clin Toxicol 2009;47:206‑12.
resuscitation, correction of dyselectrolytemia with prompt 11. Eddleston M, Warrell DA. Management of acute yellow
identification of appropriate candidates for TPI could decrease oleander poisoning. QJM Mon J Assoc Physicians
the morbidity yellow oleander poisoning. 1999;92:483‑5.
12. Ibañez C, Carcas AJ, Frias J, Abad F. Activated charcoal
Acute poisoning with oleander is a common rural problem; increases digoxin elimination in patients. Int J Cardiol
assessment of severity at the primary care level and triage of 1995;48:27‑30.
patients with severe toxicity to higher centers for temporary pace 13. de Silva HA, Fonseka MMD, Pathmeswaran A, Alahakone DGS,
Ratnatilake GA, Gunatilake SB, et al. Multiple‑dose activated
maker, imitation of multidose activated charcoal by the primary
charcoal for treatment of yellow oleander poisoning:
care physician can be lifesaving. A single‑blind, randomised, placebo‑controlled trial. Lancet
Lond Engl 2003;361:1935‑8.
Conclusion 14. Eddleston M, Juszczak E, Buckley NA, Senarathna L,
Mohamed F, Dissanayake W, et al. Multiple‑dose activated
Yellow oleander poisoning leads to significant morbidity in South charcoal in acute self‑poisoning: A randomised controlled
India. Dyselectrolytemia with ECG abnormalities were common trial. Lancet Lond Engl 2008;371:579‑87.
in these patients. TPI prolonged the duration of hospital stay. 15. Woolf AD, Wenger TL, Smith TW, Lovejoy FH. Results
Further studies are required to develop guidelines on the use of of multicenter studies of digoxin‑specific antibody
fragments in managing digitalis intoxication in
TPI in yellow oleander poisoning.
the pediatric population. Am J Emerg Med
1991;9 (2 Suppl 1):16‑20.
Financial support and sponsorship 16. Smith TW, Haber E, Yeatman L, Butler VP. Reversal of
The study was approved by Institutional Ethics Review advanced digoxin intoxication with Fab fragments of
Board (IRB NO: 10923). The authors received no financial digoxin‑specific antibodies. N Engl J Med 1976;294:797‑800.
support for the research, authorship, and/or publication of 17. Smith TW. Review of clinical experience with digoxin
this article. immune Fab (ovine). Am J Emerg Med 1991;9 (2 Suppl 1):1‑6.
18. Eddleston M, Senarathna L, Mohamed F, Buckley N,
Juszczak E, Sheriff MHR, et al. Deaths due to absence of an
Conflict of interest affordable antitoxin for plant poisoning. Lancet Lond Engl
There is no conflict of interest. 2003;362:1041‑4.

Journal of Family Medicine and Primary Care 139 Volume 9 : Issue 1 : January 2020
 Karthik, et al.: A study of clinical profile of oleander poisoning from South India

19. Gilfrich HJ, Okonek S, Manns M, Schuster CJ. Digoxin and Rajakanthan K, Rajapakse S, et al. Acute yellow
digitoxin elimination in man by charcoal hemoperfusion. oleander (Thevetia peruviana) poisoning: Cardiac
Klin Wochenschr 1978;56:1179‑83. arrhythmias, electrolyte disturbances, and serum cardiac
20. Fonseka MMD, Seneviratne SL, de Silva CE, Gunatilake SB, glycoside concentrations on presentation to hospital. Heart
de Silva HJ. Yellow oleander poisoning in Sri Lanka: 2000;83:301‑6.
Outcome in a secondary care hospital. Hum Exp Toxicol 22. Lokesh S, Arunkumar R. A clinical study of 30 cases of acute
2002;21:293‑5. yellow oleander poisoning. Journal of current trends in
21. Eddleston M, Ariaratnam C, Sjostrom L, Jayalath S, clinical medicine and Laboratory biochemistry 2013;1:29-31.

Journal of Family Medicine and Primary Care 140 Volume 9 : Issue 1 : January 2020