PLANT POISONING
Dr. Hisham Zein Alabdin
POISONOUS PLANTS
The active principles in most of these plants
are alkaloids but glycosides (digitales) and
resinous materials, as cannabis also exist.
The plant poisons have mainly remote action
after their absorption. The route of poisoning
is usually the oral one, so gastric lavage is
indicated . each plant poison has its specific
physiological antidote.
Atropine poisoning
Atropa belladonnas. Datura fastiosa, Datura
strammonium ( thorn apple),
 Plant contains ; atropine, hyoscine and
hyoscayamine. All parts of the plant contain the
active substance.
 Atropine has 2 actions:
1. central action causes stimulation of the CNS . In
large toxic doses it causes depression.
2. peripheral action anticholenergic: atropine
blocks nicotinic and muscarinic effects of
acetycholine.
Uses
A- Therapeutic:
o Pre- anesthetic.
o Antispasmodics.
o In the treatment of peptic ulcer.
o Ophthalmic use.
o Nocturnal enuresis
o Toxicological use: as antidote in phosphate esters,
digitalis, aconite poison.
B- Non therapeutic: by addicts.
Toxicokinetics
 Absorption : slowly absorbed from the gut.
Metabolism: is in the liver and muscle to
tropine tropic acid.
Excretion: is via the kidney in the urine, partly
unchanged and partly metabolized.
Pathophysiology
A- Central action:
stimulation followed by depression of CNS.
Except hyoscine has depressant action only.
B- Peripheral action:
By blocking the muscarinic action of
acetylcholine at the post ganglionic nerves
whether parasympathetic or sympathetic
(sweat glands)
Clinical picture
1- Central effects:
A- Stimulation phase:
1-Delirium ,disorientation, confusion, loss of short
term memory, talkativeness(acute toxic
psychosis).
2-Ataxia, in-coordination, hallucination(Lilliputian
type)
3-Occupational purposeless movements (picking
or grasping)
4- Tremors and convulsions.
B- Depressant phase: it follows pre-existing
stimulation phase . Patient is calm and falls
into sleep then into stupor and coma. The
respiration becomes slow and irregular. The
end result will be central asphyxia and death.
II- Peripheral effects:
1- Vital signs:
o Increased respiration.
o Increased blood pressure.
o Increased temperature up to atropine fever
resulting from anhydrosis.
o Rapid pulse and may be cardiac arrhythmia.
2- Diminished secretion:
o saliva
dryness of the mouth with
dysarthria and dysphagia.
o Sweat
dry skin
o GIT
constipation (decreased secretion and
motility)
o Urinary
oliguria and retention of urine
3- Blood vessels: Peripheral vasodilatation to
increase heat loss , leading to atropine flush
which may be misdiagnosed as scarlet fever.
4-Eye changes:
o Dilation and fixed pupils
blurred vision.
o Loss of accommodation due to cycloplegia
(ciliary muscle paralysis)
o Diplopia and photophobia
o Loss of light reflex.
• The eye symptoms may be the earliest ones,
thus the anticholinergic syndrome of
parasympathetic paralysis can be remembered
Blind as a Bat.
Red as a Beet.
Dry as a Bone.
Hot as a Hare.
Mad as a Hen.
Treatment
 Support respiration.
Control convulsion if present by diazepam.
Stop further absorption by inducing emesis or
by gastric lavage.
The physiological antidotes ( physostigmine,
pilocarpine.).
Treat hyperthermia by ice packs
IV fluids to maintain urine output
DIGITALIS (FOX GLOVE)
Uses:
 As cardiac tonic for cases of congestive heart
failure.
As diuretic.
As an anti-arrhythmic especially in atrial
flutter and. fibrillation as well as in paroxysmal
tachycardia
Toxicokinetics
• Digitalis preparations are rapidly absorbed
from the GIT and injection sites . Metabolism
takes place in the liver . Excretion is via the
renal route mainly, a small part in the bile (
enterohepatic circulation).
Pathophysiology
Digitalis toxicity is an exacerbation of the drug
Pharmacological actions:
 Positive inotropic action: it increases the
force and velocity of myocardial contraction
by increasing intracellular Ca++ . This increase
in the excitability and contractility of the atria
and ventricles may result in extrasystoles and
tachyarrhythmias.
 Negative chronotropic action: (rate) It
increases the vagal tone in the early stage
leading to decreased heart rate.
Negative dromotropic action: (conduction
velocity) It slows AV node conduction velocity
that can be depressed resulting in Saor AV
block.
 It increases the refractory periods of AV
node and depresses that of the atria and
ventricles, resulting in prolonged PR interval ,
AV block and shortened QT interval.
Alteration of impulse formation with
suppressant and excitatory effects.
Mechanism of action:
 Digitalis inhibit active transport of Na+ ,K+
across cell membranes by binding to the Na+ K+ ATP ase , and inhibiting Na+ - K+ pumps .
 The net result
 Increase extracellular potassium
 Increase intracellular sodium.
 Increase intracellular calcium
Predisposing factors
 Patient factor: (old age, myocardial infarction,
core pulmonale, renal failure.)
Electrolyte abnormalities: ( hypo and
hyperkalemia, hypomagnesemia, hyper and
hypocalcemia.)
 Drug interaction: (diuretics, antibiotics,
quinidine , reserpine.)
Clinical picture
 Asymptomatic period of several minutes to
several hours follows a single oral toxic dose. The
toxic effects include non cardiac and cardiac
effects
A- Non cardiac :
o GIT: may be the first complaints. (nausea,
vomiting, abduminal pain and diarrhea)
o CNS: headache, trigeminal neuralgia, confusion,
delirium, disorientation, drowsiness and
hallucination.
o Visual transient amblyopia, diplopia, blurring,
scotoma and abnormal colour vision including
yellow halos (xanthopsia).
o Endocrine : Gynecomastia.
o Allergic : Urticaria.
B- Cardiac:
Early slow full pulse (vagus) , with hypotension,
followed by any type of dysrhythmia (altration
in cardiac rate and rhythm):
o AV block.
o Atrial tachycardia with AV block.
o Sino-atrial block.
o Atrial flutter, fibrillation.
o Ventricular premature extrasystoles , flutter.
Digoxin toxicity
Acute
1- following acute
overdose
2- Usually young
3-normal heart
4-high digoxin level
5- K+ normal to high
6-AV conduction blocks
more common
7-Lessnon cardiac
manifestations
Chronic
Following long term
therapy
Usually elderly
Heart disease.
High digoxin or therapeutic
K+ normal to low
Various dysrhthmias
Non cardiac symptoms
prominent
MANAGEMENT
Investigations:
1-ECG:
o Prolonged PR interval
o Shortened QT interval
o ST segment depression, inverted T wave.
2- Laboratory :
o Electrolytes (K+ )
o Serum digoxin: toxic level is above 2ng/ml and
is above 25ng/ml for digitoxin.
Treatment
Stop drug administration.
 monitor the patient in an ICU.
Establishment of respiration.
Dicontamination.
Atropine sulphate 1-2mg IM for bradycardia.
Phenytoin or diphenyl hydantoin is the drug of
choice for tachyarrhythmia.
 Cholestyramine help excretion of digitalis
Determine electrolytes hourly and correct
electrolytes and acid base disturbances.
o For hypokalaemia: potassium chloride5g in
fruit juice every hour until ECG show
improvement or peaking of T wave.
o For hyperkalaemia : give 20 units of insulin
with 5% Dextrose.
o For hypocalcemia: avoid replacement
because intracellular calcium is very high.
 Antidotal therapy: Digoxin specific antibody
(Digibind ).They bind to the free digoxin and
increase the renal excretion of digoxin bound
to FAB fragment.
Indications for (DIGIBIND )
Hyperkalaemia (k + > 5 mEq/L).
 Bradyarrhythmias unresponsive to atropine.
High degree AV block.
Life threatenting ventricular tachycardia and
ventricular fibrillation.
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