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PLANT POISONS
Every
thing is
poisonous, only the
amount differentiates a
poison from a remedy.
Types of Poisoning
 Accidental
 Intentional-Suicidal,
the
Medicinal
Raw plant, tea made from
plant
Mechanisms
Toxic to
CVS: e.g oleander
CNS:e.g Datura
Blood: e.g Abrus
Liver: e.g Mushrooms
Kidney:e.g Cleistanthus
General issues
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Proper identification of plant is key to prognosis,
therapy and preventing unnecessary treatment
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Majority of plant poisoning needs supportive
management
Treatment
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Terminating further exposure
Dilution with cool fluids may relieve irritating
sensation or disagreeable taste
Gentle cleansing with soap and water in peri oral
and dermal exposures
No role for induced emesis with ipecac
Gastric lavage
Role of activated charcoal
No role for cathartics and whole bowel irrigation
CARDIOVASCULAR TOXINS
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Thevetia nerifolia-yellow oleander
Nerium oleander-pink oleander
Digitalis purpurae
Digitalis lanata
Cleistanthus collinus-oduvanthalai
Poisoning
calotropis
OLEANDER
OLEANDER SEEDS
PINK OLEANDER
OLEANDER POISONING
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All parts of the plant are poisonous.
Peruvoside, cerebrin and thevetin –active
components.
Ingestion of more than 2 seeds is toxic. as seeds
contain more glycosides than other parts
MECHANISM OF TOXICITY
Inhibition of Na+/K+-ATPase pump leading to
overall increase in intracellular Na+ ions and
secondary increase in intracellular Ca+ levels
 Partly vagotonic action
 SA node, AV node and conduction system are
involved.
 Form of focal toxic myocarditis
[Lymphocyte infiltration of the conduction system]
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CLINICAL FEATURES
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On ingestion ,burning sensation, abdominal pain
nausea ,vomiting ,diarrhea ,also dizziness and
numbness in oral and perioral region
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Most important cardio toxic effects are sinus
bradycardia, varying degrees of heart block,
ventricular ectopics, ventricular tachycardia which
can be fatal.
INCIDENCE OF HEART BLOCK IN
GGH
25
20
15
10
5
0
SINUS
IST DEGREE
COMPLETE
BRADYCARDIA HEART BLOCK HEART BLOCK
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Acute hemolysis occurs due to inhalation of
oleander blossoms.
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Dermal route of exposure can cause local
irritation and inflammation, unconsciousness and
convulsions .
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Hyperkalemia occurs due to acute toxicity.
Hypoxia and metabolic acidosis are potential
complications
MONITORING
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Rate
Pulse rate
E.C.G
Serum potassium
Blood urea
Serum creatinine
Arterial blood gas analysis
MANAGEMENT
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If patient arrives within 4 hrs of ingestion, and the
patient has no convulsions and fully conscious,
perform gastric lavage.
Take care of ABC and stabilize
Activated charcoal and cholestyramine to decrease
absorption.
Treatment of hyperkalemia and arrhythmias
Fab fragments
MANAGEMENT OF
CARDIOTOXICITY
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Atropine 0.6 mg ,Orciprenaline 10mg to maintain
HR around 80/mt.
T-wave inversion and ST depression due to toxic
myocarditis corrected over a period of 3-4 hrs with
the above regimen.
Sodium bicarbonate 50 ml iv 6th hourly if ABG
shows acidosis.
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Monitor heart rhythm for at least 5 days.
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If the heart rate persists below 30/mt after all
these regimen put the patient on temporary
pacemaker.
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Do not treat asymptomatic Ventricular premature
beats, if symptomatic use lignocaine 1mg/kg iv
every 5-10 minutes.
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Forced alkaline diuresis .has no role in the
management .
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Peritoneal dialysis, hemodialysis, hemoperfusion
do not increase the elimination of cardiac
glycosides because of large volume of distribution
ODUVANTHALAI POISONING
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Cleistanthus collinus
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Second most common suicidal plant poison in
rural south India after oleander poisoning.
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Poison preferred by young women.
Pathogenesis
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Cleistanthus collinus is an extremely toxic plant
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It is known by various names in different parts of
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poison.
India viz., Oduvanthalai / Nillipalai in Tamilnadu
and Pondicherry, Kadishe in Andhra pradesh,
Karlajuri in West Bengal and Garari in the Hindi
speaking belt.
All parts of the plant are poisonous.
Cleistanthin A and B are the toxins of Cleistanthus
collinus
They are diphyllin glycosides which produce
cardiac arrhythmias, urinary potassium wasting,
hypoxia, metabolic acidosis and hypotension.
MECHANISM OF TOXICITY
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Inhibition of Na+K+ATPase
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The cause of hypokalemia remains enigmatic.
Pathogenesis
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Hypokalemic metabolic acidosis, hypotension and
hypoxia have been described in this poisoning.
Cases have been reported where dRTA, distributive
shock and ARDS identified in patients, explaining
the above findings
CLINICAL FEATURES
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ECG abnormalities :Bradycardia, Varying degrees
of heart Blocks
Hypokalemia : Severe hypokalaemia
Severe non anion gap metabolic acidosis
Increased urinary K+ excretion
Increased urine anion gap
MONITIORING
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E.C.G
Serum potassium
Heart rate
Blood pressure
Respiratory rate
QTc –USEFUL PROGNOSTIC INDEX
Management
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Correct hypokalemia by i.v KCL AT A RATE OF
NOT MORE THAN 40 meq/l
Bradycardia corrected with atropine
0. 6mg/Orciprenaline 10mg.
If the heart rate is less than 30/mt, temporary
Trans venous pacing may be instituted
Calotropis
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Calotropis is used as a traditional medicinal plant
with unique properties
Traditionally alotropis is used alone or with other
medicinals to treat common disease such as fevers,
rheumatism, indigestion, cough, cold, eczema,
asthma, elephantiasis, nausea, vomiting, diarrhea
According to Ayurveda, dried whole plant is a good
tonic, expectorant,, and anthelmintic. The dried
root bark is a substitute for ipecacuanha.
The powdered root used in asthama, bronchitis,
and dyspepsia.
Calotropis
Toxicity
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Signs Acrid taste usually limits ingestion.
Exposure of the skin or mucous membranes to
the latex may result in vesicle formation.
Keratoconjunctivitis will result if the cornea is
exposed.
Ingestion of significant quantities will result in
ECG abnormalities.
Treatment
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Wash the exposed tissue with plenty of warm
water and soap.
Flush the eyes with sterile saline or water for 15
minutes.
If cardiac abnormalities are seen, manage
according to ECG assessment
AUTONOMIC NERVOUS
SYSTEM TOXINS
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DATURA STRAMONIUM
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ATROPA BELLADONA
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HYOSCYAMUS NIGER
DATURA STRAMONIUM
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All parts of the plant are poisonous. Seeds are
considered to be the most noxious.
The alkaloids are scopalamine and hyoscyamine or
atropine both have anticholinergic effects.
Mostly accidental ingestion by children.
Also used to induce hallucinations.
Contact with leaves/flowers-dermatitis
Fruit containing the Seed
CLINICAL FEATURES
DATURA
PERIPHERAL ANTICHOLINERGIC
CENTRAL ANTICHOLINERGIC
PERIPHERAL
ANTICHOLINERGIC
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Tachycardia
Dry flushed skin
Dilated pupils
Hyperpyrexia
Urinary retention
Hypertension/hypotension
CENTRAL ANTICHOLINERGIC
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Disorientation
Agitation
Muscle in coordination
Ataxia
Visual/auditory hallucinations
Severe toxicity can result in seizures, respiratory
Failure & cardiovascular collapse.
Investigations
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Detection of Atropine by
 Radio
immuno assay
 Gas chromatography
 Mass spectrometry
 Thin layer chromatography
 Liquid chromatography
MANAGEMENT
Supportive care
 Airway
 Circulation
 Gastric lavage (due to inhibition of peristalsis,
seeds may remain in stomach for up to 24 hrs).
 Activated charcoal-50g every 4 hrs and magnesium
sulphate 30g every 4 hrs
MANAGEMENT
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Hypotension: IVF, Dopamine
Convulsions & agitation: :IV Diazepam 10 -20mg
over 30-60minutes not to exceed 3mg/kg over
24hrs
Not to use chlorpromazine for controlling
agitation, Hyperactivity, disorientation
Severe Hyperthermia: Sedation, Paralysis and
active cooling
Careful use of physostigmine to counteract CNS
anticholinergic syndrome.
PHYSOSTIGMINE USE
To be used only if definitely known
 Dosage:
1-2 mg IV slowly repeated every 10 min. should not
exceed 4 mg in 30 min period
 Watch for seizure activity, bradycardia, heart
blocks, and asystole
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INDICATIONS OF
PHYSOSTIGMINE
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Pronounced hallucinations and agitation
Supraventricular arrthymias and ventricular
arrthymias with hemo dynamic instability
Seizures unresponsive to standard anticonvulsants
Toxalbumins (Ricin, Abrin)
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Both differ in appearance and taxonomy but both
toxins are similar structurally and functionally
Synonyms:
 Ricinus communis: castor bean
 Abrus: jequirity, Indian bead, rosaeary pea
Toxic parts: All parts especially seeds
Abrus -Seeds
Ricinus Plant
Ricinus - Seeds
Clinical Presentation
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Oral: Gastro intestinal upset
- vomiting, diarrhoea, abdominal pain, GI leeding,
Abnormal LFT and RFT, Hematuria,
acrocyanosis, Shock, Dehydration, hemolysis
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Parenteral: Not well documented but toxicity is
very severe
Management
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Activated charcoal
Aggressive fluid resuscitation
Other supportive care
Cathartics not indicated
Extracorporeal elimination not useful
Mushroom Poisoning
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Fatalities resulting from mushroom ingestion are
due to Amatoxins
They are octapeptides and are heat-stable,
insoluble in water, and not destroyed by drying. At
least 5 subtypes of amatoxins exist; alpha and beta
amatoxins are the most significant subtypes.
Alpha amatoxin inhibits RNA polymerase II,
which ultimately leads to cell death.
Clinical features
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Initial latent and asymptomatic period of 6-12
hours
Abdominal cramping, vomiting, and profuse
watery diarrhea (rice water, cholera like) occur.
Leading to severe dehydration and circulatory
collapse.
The patient appears to have improved clinically,
ongoing liver damage occurs as indicated by
laboratory abnormalities (elevation of serum
aminotransferase levels, prothrombin time). This
stage may last as long as 2-3 days.
Hepatic and renal injury become clinically
apparent and may progress to fulminant hepatic
failure in the third phase. Death may occur in 3-7
Lab Investigations
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LFT
prothrombin time (PT) (most reliable indicator for
severity of poisoning) ,Enzyme and bilirubin levels
Complete blood count (CBC)
Electrolytes, BUN, and creatinine levels
(dehydration from vomiting and diarrhea)
Glucose level (monitor very closely with hepatic
failure)
Urinalysis (hematuria and proteinuria signifying
renal involvement)
Amylase/lipase level (pancreatitis)
Urinary amanitin analysis
Other Specific Tests
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Maixner test :
Place a drop of liquid expressed from the mushroom on lignincontaining paper (ie, paper derived from wood pulp, such as newspaper
but not filter paper). After the drop has dried, place a drop of 10-12 N
HCl on the spot. The appearance of a blue color within several
minutes suggests the presence of amatoxins.
A delayed appearance of a blue color suggests that amatoxin is present
but in lower concentrations.
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Gastric contents are not suitable for this test.
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An experienced mycologist may analyze and identify spores in gastric
contents
Management
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Reduction of amatoxin absorption
- Gastric lavage, Activated charcoal
Aggressive management of fluid and electrolyte
imbalance.
Vitamin K (if coagulopathy is present)
N-acetylcysteine
Colchicine containing plants
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Colchicine is the drug of choice to relieve acute attacks of
gout and familial Mediterranean fever
At present there is renewed interest in the use of colchicine
as a possible cure for cancer-related diseases
Among the Indian medicinal plants, Colchicum luteum and
the seeds of Iphigenia contain alkaloid, chiefly colchicine,
to the extent of about 0.25% and 0.9%
These plants are not available in sufficient quantities to
warrant any commercial utilization
Tubers of six different species of Gloriosa, viz., Gloriosa
superba, Gloriosa rothchildiana, Gloriosa planti, Gloriosa
lutea, Gloriosa casuariana and Gloriosa vuchuria, also
contains colchicine
Colchicum luteum
Gloriosa superba (glory lily)
Gloriosa superba (glory lily)
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Gloriosa superba (glory lily) poisoning has been
reported from Sri Lanka and south India
The plant contains the alkaloids colchicine and
gloriosine.
Colchicine has antimitotic properties and causes
vomiting and severe diarrhoea, dehydration,
haemodynamic instability, renal failure and
eventually multiorgan failure.
Colchicum autumnale (meadow saffron) also
contains colchicine.
It appears to be a rare cause of poisoning in many
countries
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Antibodies against colchicine have been developed
in France for the management of acute poisoning
with the drug form of colchicine.
Animal studies have shown good efficacy.
Anti-colchicine antibody fragments are not in
commercial production.
If they could be made available at a price
affordable to local health systems, they might
make a significant difference in the management
of G. superba and C. autumnale poisoning.