oleander poisoning

26
Oleander Poisoning Dr. Shatdal Chaudhary MD Assistant Professor Department of Internal Medicine, BPKIHS, Dharan

Upload: dr-shatdal-chaudhary

Post on 15-Nov-2014

182 views

Category:

Documents


7 download

DESCRIPTION

It is for undergraduate medical students.

TRANSCRIPT

Page 1: Oleander Poisoning

Oleander Poisoning

Dr. Shatdal Chaudhary MDAssistant Professor

Department of Internal Medicine, BPKIHS, Dharan

Page 2: Oleander Poisoning

case

• 32 yr female came to ER on 14/2/2066– Multiple episodes of vomiting– H/o ingestion of 4 oleander seed after family dispute

• Admitted in CCU

• Developed sinus bradycardia and first degree heart block

• Treated with atropine infusion and discharged on day 7

Page 3: Oleander Poisoning

Oleander• Also known as Kaner

• Wide spread in Nepal and India.

• Flowers are used as offerings in the temples

Page 4: Oleander Poisoning

• Can be used for

– Suicide

– Accidental poisoning especially in children

– Abortion

– Cattle poison

Page 5: Oleander Poisoning

• In Sri Lanka- – In some areas up to 40% of suicidal poisoning

cases are now linked to oleander seeds.– annual incidence of >150 per 100 000.– mortality rate of about 10%.– results in about 2000 deaths each year.

• Accidental oleander poisoning occurs throughout the tropics and subtropics

• oleander caused 27%of the paediatric plant poisonings in Australia

Page 6: Oleander Poisoning

• There are two varieties

– Nerium oleander- Common, pink or white Oleander– Thevetia peruviana- Yellow Oleander

All the parts are poisonous

Page 7: Oleander Poisoning

White Oleander (Nerium oleander)

• The active principle is nerin• It consisting of three glycosides

– Neriodorin: Acts on heart similar to digitalis

– Neriodorein: cause muscular twitching and tetanic spasms

– Karabin: Affect heart as well as cause muscular spasms.

Toxic effects last for 3-6 days.

Page 8: Oleander Poisoning
Page 9: Oleander Poisoning
Page 10: Oleander Poisoning
Page 11: Oleander Poisoning
Page 12: Oleander Poisoning

Clinical Features

Local, Gastrointestinal, Cardiac, Neurological• Vomiting, Pain abdomen, salivation and

restlessness.• Difficulty in swallowing and lock jaw• Muscular twitching, tetanic spasm• Pulse- slow various Brady arrhythmias, SVT

with various degree of AV block.• Heart failure, comaFatal Dose: • about 15 grams of roots, 5-15 leaves

– can kill an adults in about 24 hrs

Page 13: Oleander Poisoning

Yellow Oleander (Cerbera Thevetia)

• Contains at least eight different cardiac glycosides, including Thevetin A, Thevetin B, thevetoxin, neriifolin, peruvoside and ruvoside.

– Thevetin B- Acts like strychnine– Thevetin A- acts like digitalis– Thevotoxin-

• acts like digitalis• Less toxic than thevetin• Presents in kernels of the seeds

Page 14: Oleander Poisoning
Page 15: Oleander Poisoning
Page 16: Oleander Poisoning
Page 17: Oleander Poisoning
Page 18: Oleander Poisoning

Clinical Features

• seeds are usually eaten as whole or in chunks . • Large variation in the amount of absorption of cardio

active toxins from a seed• the number of seeds ingested does not always

correlate with the degree of toxicity • Burning sensation in the mouth, dryness of the

throat, vomiting, diarrhoea• Fragments of seeds can be seen in the stomach

contents

Page 19: Oleander Poisoning

• Dizziness, tetanic convulsions • Various Brady arrhythemia are can be seen ranging

sinus bradycardia to various degree heart block.• sudden cardiac death can occur due to ventricular

fibrillation or cardiac asystole

Fatal dose:8-10 seeds

15-20 grams of roots

5-15 leaves

Page 20: Oleander Poisoning

Treatment

• Continuous ECG monitoring for at least 24 h is necessary to detect arrhythmias

• longer monitoring in patients with severe poisoning. • Correct dehydration with iv fluids• Correct electrolyte imbalance

– Hypokalemia / hyperkalemia both must be corrected.

• Hyperkalemia is best treated with insulin-dextrose infusion.

• Antiemetics to control severe vomiting.• Gastric decontamination by the use of single dose

and multiple doses of activated charcoal

Page 21: Oleander Poisoning

Activated CharcoalRationale• activated charcoal prevent the initial absorption of

the toxic glycosides, but also prevent toxin reabsorption

• After absorption into the systemic circulation, cardiac glycosides are secreted into the gut lumen from the systemic circulation.

• In the gut, activated charcoal binds the secreted glycoside and encourages further secretion, and helps in glycoside excretion.

Page 22: Oleander Poisoning

Activated Charcoal 50 g of activated charcoal every 6 h for 3 days or sterile

water as placebo. 201 patients received multiple-dose activated charcoal and

200 placebo. There were fewer deaths in the treatment group (five [2·5%]

vs 16 [8%]; percentage difference 5·5%; 95% CI 0·6–10·3; p=0·025),

Multiple-dose activated charcoal is effective in reducing deaths and life-threatening cardiac arrhythmias after yellow oleander poisoning and should be considered in all patients.

Treatment of patients who had yellow oleander poisoning with multiple doses of activated charcoal over 72 h reduced the death rate by 69%.

M Eddleston et al. Lancet 2003; 361: 1935–38

Page 23: Oleander Poisoning

Atropine

• IV Atropine three 2 mg intravenous boluses at 5–10 min intervals, or infusions of 12 mg/h for:

a) sinus bradycardia <50 per min

b) sinus bradycardia <60 per min and low systolic blood pressure

c) All other bradyarrhythmias

Page 24: Oleander Poisoning

Bradyarrhythmias.

• Adrenaline, Noradrenaline, isoprenaline

• Tachyarrhythmias- iv lignocaine

• Temporary cardiac pacing

Page 25: Oleander Poisoning

Digoxin-specific Fab antibody Fragments

• 66 patients who presented to hospital with a serious cardiac arrhythmia were randomised to receive either 1200 mg of anti-digoxin Fab or placebo.

• 34 patients received anti-digoxin Fab and 32• received placebo. • The presenting arrhythmia had resolved completely

after 2 h in 15 antibody-treated patients and two controls (p<0·001); 24 patients and five controls, respectively, were in sinus rhythm at 8 h (p<0·001).

M Eddleston and D A Warrell et al. Lancet 2000; 355: 967–72

Page 26: Oleander Poisoning

The End