By

Dr. Safaa El-Shanawany

Professor of Forensic Medicine
& Clinical Toxicology
 RODENTICIDES

Learning Objectives:
 Define the nature of rodenticides
 Identify the major classes of rodenticides
 Recognize the pathophysiology of some rodenticides
 Describe signs and symptoms of their toxicity
 Assess severity of poisoning by different methods of investigations
 Treat rodenticide poisoning and specify antidotes
Use of rodenticides : to kill rodents and insects
Types: anticoagulant and non-anticoagulant.

Anticoagulant rodenticides

Coumarin derivatives Indandiones

Hydroxy C. 4-H.C.
e.g warfarin
Regular warfarins: Super warfarins:
Massive or repeated doses Single, small dose

Toxic Prolonged, powerful toxic

effect
Pathophysiology
1) Interference of activation of vit k-dependent factors: II, VII, IX, X

2) Direct capillary damage

1) , 2)  bleeding tendencies

Clinical picture

Onset: 8-12 hours  1-3 days

 Bleeding
Minor  life threatening
 Epistaxis - gums - hematomas –
 Hemoptysis - hematuria - vaginal bleeding
 GIT bleeding
 Intracranial hemorrhages.

Investigations
 Identify the type (box)
  P.T, INR
 Monitoring of P.T in long acting (super warfarins)
 CBC, blood grouping
  Vit K-dependent factors
 Rodenticide screening (RIA, HPLC, GC-MS)
 Treatment
1-A.B.C.

2-Decontamination:

 No emesis (Fear of hemorrhage)

 Gastric lavage then activated charcoal + cathartic esp. in

super warfarins.

3-Transfusion of fresh blood or fresh frozen plasma.

4-Vit K1 :

 1-5 mg in child, 5mg in adult s.c/oral.

 Action after several hours, may need blood transfusion first.

 Non anticoagulant rodenticides

They are more serious and may cause death as a result of single
ingestion. They are divided into three groups according to toxicity.

Highly toxic:
Arsenic, phosphorus, strychnine, thallium, and zinc phosphide.

Moderately toxic:
ANTU (α- naphthyl thiourea)

Low toxic:
Norbormide and red squill.
 Zinc phosphide

It is dark gray crystalline powder with rotten fish odor.

Pathophysiology:
Zinc phosphide reacts with water and hydrochloric
acid in the stomach producing phosphine gas which
causes systemic toxicity.
 Clinical picture:
GIT: Nausea, vomiting, abdominal pain ,
diarrhea, black in color.
Respiratory: Rotten fish odor of breath, chest
tightness, cough, dyspnea, crepitations,
pulmonary edema and subpleural
hemorrhage.
CVS: Hypotension, shock, arrhythmia
CNS: Ataxia, seizures,coma.
Hepatorenal toxicity
Others: Hypocalcemia, tetany, renal failure.
 Treatment:
1. A-B-C
2. Dilution with milk or starch then gastric lavage with
sodium bicarbonate to alkalinize the gastric
environment and decrease the conversion of phosphide
to phosphine.
3. Activated charcoal decreases absorption of phosphide.
4. Symptomatic treatment:
 Diazepam for seizures
 Ca gluconate or chloride I.V for tetany.
5. Ca Na2 EDTA: may have a role.
 STRYCHNINE
 It is a very bitter crystalline powder obtained by
crushing strychnous nux vomica seed.
 The active principles are mainly strychnine and
brucine, but strychnine is 20 times more potent.

Uses

Medical: Non medical:

Not used nowadays due Rodenticide & a common
to its toxic effects. Only adulterant of many street
as vermicide in veterinary drugs as cocaine and
medicine. marihuana.
 Circumstances of poisoning:
Accidental:
By accidental ingestion of rodenticides by children

Suicidal:
By pharmacists, medical personnel and agricultural workers.

Homicidal:
Is very rare due to its bitter taste and rapid action. Sporadic
cases do occur by giving the poison with alcohol or foods
which normally have a sour taste.
Pathophysiology:
It is a convulsing poison. Convulsions result from either:

Blocking of Enhancing of
inhibition. excitation.

 Strychnine mainly produces its effect by blocking of

inhibition, so any stimulus will pass to all motor cells.
 Strychnine competes with the neuro-transmitter glycine
(anti convulsing) for specific receptors (mainly in the spinal
cord, brain stem and thalamus).
 Strychnine opposes GABA (gamma amino butyric acid)
which produces inhibition at presynaptic sites.
 Clinical picture:
Symptoms begin 15 to 30 minutes after ingestion.
The patient is restless, apprehensive
Muscles stiffness especially back and neck

Tremors and twitches


Sudden onset of convulsions characterized by:

 Painful.
 Phasic (contraction followed by relaxation)
 Diffuse (all muscles of the body ).
 Symmetric (both sides of the body).
 Extensor thrust (extensor group of muscles being
stronger will predominate).
 The end result will be

Arched back position Contraction of muscles

(opisthotonus) i.e. of expression -----> bitter

hyperextension of smile expression

spines. (risus sardonicus).

Contraction of the
muscle of the jaw
(locked jaw).
 The abdominal and respiratory muscles are
involved in the generalized convulsions with

 Bulging of the eye balls.   Pulse

 Cyanosis  Consciousness is

  temperature retained till the end

  B.P with severe agony

The fit remains for 1-2 minutes

 Between convulsions

Complete muscle Profuse

relaxation sweating
typically occurs
Breathing
resumes

 The patient may fall asleep from exhaustion or will be

anxious about a recurrence of the attack, with a fear of
impending death.
 The relaxation phase remains for 5 - 15 minutes.
 Then another paroxysm will occur provoked by any
sudden sensory stimulus (auditory, visual).
 Death usually follows 4 or 5 of such convulsions.
Complications:

Complications of strychnine poisoning are due

to profound muscle spasms:

 Lactic acidosis

 Rhabdomyolysis

 Hyperthermia
 Diagnosis:
1.Circumstantial evidence
2.History of:
 Sudden appearance of the paroxysm in a healthy person.
 Negative history for any injury or disease and the attack is
directly related to the intake of medicine or ingestion of food or
drink.
3.Clinical diagnosis: occurrence of sudden, phasic, painful, diffuse,
symmetric, extensor thrust.
4.Laboratory diagnosis: by thin layer chromatography , even after
death as it resists putrefaction
Differential diagnosis:
From other causes of convulsions:
 Traumatic.
 Pathological (meningitis, epilepsy).
 Toxic e.g. organophosphorous and carbamate insecticides,
carbolic acid, oxalic acid poisoning ... etc.
 The most important D.D. is from tetanus by:

TETANUS STRYCHNINE
Injury Intake of drug • History
Gradual Sudden • Onset
Start in the jaw Generalized from the start • Convulsions
Absent as the convulsions are tonic Present and complete • Pause between attacks or
and the muscles remain rigid (relaxation)
Death within few days Fatal within ½ - 2 hours • Prognosis
-ve Strychnine • Chemical analysis
Tetanic bacilli -ve • Bacterial analysis
Treatment:
Strychnine antagonists
control convulsions and prevent asphyxia by

Diazepam Phenobarbital
Muscle
5 - 10 mg IV 5 mg/kg IV
relaxant

Could be repeated Every 5 min until convulsions Succinyl choline

every five minutes resolve. If no response within 10-50 mg IV.

up to five times. 20 min give the anesthetic dose

of Phenobarbital preceded by

intubations and artificial

ventilation.
 Prevent recurrence of convulsions

Keeping the patient in Put ear plugs keep him under

dark quiet room to observation of a
block the sensory reliable nurse.
stimuli
Respiratory support

Patent clear air Artificial respiration

way may be needed.

Decrease absorption

Gastric lavage using any alkaloid antidote.

(Preceded by endo tracheal intubations)