Oleander Poisoning

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OLEANDER POISONING ANBU

Transcript of Oleander Poisoning

Page 1: Oleander Poisoning

OLEANDER POISONING

ANBU

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OLEANDER Also known as Kaner Wide spread in Nepal and India. Flowers are used as offerings in the temples Can be used for

Suicide Accidental poisoning especially in children Abortion Cattle poison

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OLEANDER VARIETIES Nerium oleander- Common, pink or

white Oleander Thevetia peruviana- Yellow Oleander All the parts are poisonous

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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.

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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

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FATAL DOSE White oleander

about 15 grams of roots, 5-15 leaves can kill an adults in about 24 hrs

Yellow Oleander 8-10 seeds 15-20 grams of roots 5-15 leaves

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CLINICAL FEATURES Vomiting, Pain abdomen, salivation and restlessness. Difficulty in swallowing and lock jaw Muscular twitching, tetanic spasm Pulse- slow Brady arrhythmias, SVT with various degree

of AV block. Heart failure, coma

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ACTION OF ACTIVE PRINCIPLE

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POTASSIUM EFFECTS Hyperkalaemia is a feature of poisoning, due to

inhibition of the Na+/K+ ATPase. Causes hyperpolarisation of cardiac tissue, enhancing AV block.

Pre-existing hypokalaemia also inhibits the ATPase & enhances myocardial automaticity, increasing the risk of glycoside induced dysrhythmias

Effect of hypokalaemia may be in part due to reduced competition at the ATPase binding site

Hypokalaemia <2.5 mmol/L slows the Na pump, exacerbating glycoside induced pump inhibition.

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MANAGEMENT OF POISONING Available options

Anti-digoxin/digitoxin Fab Activated charcoal Anti-arrhythmics – lidocaine & phenytoin Atropine & pacemakers Correction of electrolyte abnormalities Correction of hyperkalaemia

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DIGOXIN SPECIFIC AB FRAGMENT Empirical dose

Acute posioning- 2-5 vials Chronic poisoning -10-20 vials Each vial contains 38 mg of Fab , that binds 0.5

mg of digoxin

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ACTIVATED CHARCOAL 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.

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50 g (1g/kg) of activated charcoal every 6 h for 3 days (maximum dose 100g)

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.

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ATROPINE IV Atropine three 2 mg intravenous boluses

at 5–10 min intervals, or infusions of 12 mg/h for: sinus bradycardia <50 per min sinus bradycardia <60 per min and low systolic

blood pressure All other bradyarrhythmias

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Phenytoin/lidocaine – depress automaticity, while not depressing AV node conduction.Phenytoin reported to terminate digoxin-induced SVTs.

Temporary pacemaker – to increase heart rate, but cannot prevent ‘stone heart’. Also insertion of pacemaker may trigger VF in sensitive heart. Now not recommended where Fab is available.

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CORRECTION OF ELECTROLYTE DISTRURBANCE Hypokalaemia exacerbates cardiac glycoside toxicity

therefore replace K+.However, in acute self-poisoning (not acute on chronic), hypokalaemia is uncommon.

Hypokalemia is corrected by giving insulin-dextrose infusion

Hypomagnesaemia. Serum [Mg2+] is not related to severity in oleander poisoning. However, low [Mg2+] will make replacing K+ difficult.

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SYMPTOMS OF POISONING Cardiac dysrhythmias 100%

Nausea 100% Vomiting 100% Weakness 88% Fatigue 86% Diarrhoea 80% Dizziness 67% Abdominal Pain 59% Visual Symptoms 36% Headache 34% Sweating 20% Confusion 19% Fever and/or Chills 5% Anxiety 3% Abnormal Dreams 3%