BHARATI VIDYAPEETH (DEEMDED TO BE UNIVERSITY),

COLLEGE OF NURSING,
PUNE

LESSON PLAN
ON
POISONING

SUPERVISED BY
MR.STAWAN CHOUGULE
CLINICAL INSTRUCTURE
MEDICAL SURGICAL DEPT
BVCON, PUNE

PRESENTED BY:
MS. LOMA R WAGHMARE
F.Y. MSC NURSING
BVCON, PUNE
TOPIC: POISONING
DATE OF PRACTICE TEACHING:

TIME:

NAME OF GROUP: S. Y. GNM (Nursing)

NAME OF THE EVALUATOR: MR. STAWAN CHOUGULE

OBJECTVES

General objectives:

At the end of the practice teaching the students will gain knowledge on poisoning and use it in clinical practice.

Specific objectives:

By the end of the class students will be able to

● Define poisoning

● List the emergency goal of poisoning

● Discuss the incidence and statistics of poisoning

● Explain the phases of poisoning

● Enlist the mode of absorption

● Enlist the types of poisoning

● Enumerate the clinical manifestation of poisoning

● discuss the assessment and diagnostic findings

● discuss the management of poisoning
● discuss the prevention of poisoning
● discuss the nursing management of poisoning
 METHOD

OBJECTIVES TIME CONTENT OF STUDENT AV AIDS EVALUATION

TEACHING ACTIVITY
1. define
1 min DEFINITION: Lecture & Listening Power Student
poisoning
-Any substance that when ingested, inhaled, absorbed, Discussion point defines the

applied to the skin, or produced within the body in presentati term poisoning

relatively small amounts, injures the body by its chemical on

action.

Poisoning is a condition or a process in which

an organism becomes chemically intoxicated by
an exogenous substance, usually by ingestion or external
exposure

The branch of medicine that deals with the detected and

treatment of poisons is known as toxicology.

EMERGENCY GOAL:

 To remove or inactivate the poison before it is

2. list the absorbed
emergency 2 min  To provide supportive care in maintaining vital
Students list
goal of organ systems Lecture &
the term
 poisoning  To administer a specific antidote to neutralize a Discussion Listening poisoning
specific poison
 To implement treatment that hastens the elimination
of the absorbed poison

INCIDENCE

- Poisoning represents the harmful effects on the

human body of accidental or intentional exposure to
toxic amounts of any substance.
- According to WHO data, in 2012 an estimated
193,460 people died worldwide from unintentional
3. Discuss the
poisoning. Of these deaths, 84% occurred in low-
incidence
and middle- income countries. Students
of
- In the same year, unintentional poisoning caused discuss the
poisoning 1 min Lecture
the loss of over 10.7 million population a year of incidence of

healthy life (disability adjusted life years, DALYs) Listening poisoning

 PHASES OF POISONING:

 Preclinical phase-some signs and symptoms may not

be evident during this phase; the priority is
decontamination
 Toxic phase-signs and symptoms and lab changes are
evident during this phase and guide treatment; the
emphasis is on shortening the duration of poisoning
and lessening the severity of toxicity
 Resolution phase-this phase encompasses peak
4. Explain
phases of toxicity to recovery; the goal is to shorten the duration
of toxicity. Students
poisoning
explain the
phases of

MODES OF ABSORPTION: Lecture & poisoning

Discussion
4 min  Ingestion Listening

 Inhalation

 Injection

 Splashing in to the eye

  Absorbed through the skin (Inuction)

 Insufflation (the act of blowing gas or a powder in to a

body cavity

TYPES OF POISONING:
5. Enlist the
mode of  Acids
Students enlist
absorption  Alkalies
the mode of
 Medication
absorption of
 Metal poisoning
poisoning
 Organophosphorous poisoning
 Petroleum products Lecture

 Oils
2 min Listening

ACIDS:

Nitric acids , H2SO4 , HCL , Carbolic acid , Acetic acid

ALKALIES:
6. Enlist the
Drain cleaners, Dishwashing – detergents, ammonia
types of Students enlist
poisoning Bleaches the types of
poisoning
MEDICATION:

Aspirin & Aspirin containing medications ,NSAIDS

Hallucinogen, Barbiturates, Alcohol (in homeo treatment :
spirit)
Lecture Chart
METAL POISONING: Iron, Copper, Cyanide, Lead
2 min Ethylene glycol Listening
and
OP POISONING:
observatio
Insecticides naphthalene, Pesticides, Opium, Castor oil , n
Mushroom, Tobacco, Cannabi

CLINICAL MANIFESTATION:

Sign and Symptoms may differ according to the type and mode of
poisoning. In general they include: Vomiting, Diarrhea, Upper
abdominal pain, Jaundice, Difficulty breathing,·
Palpitations, Skin rashes, decrease urine out put

Alarming Signs include:No breathing, Wheezy or noisy

 breathing, Pulse below 50, or above110 beats per minute,
irregular, or very weak, Non-reacting pupils, Loss of
consciousness, Continuous seizures, Temperature > 39°C
(mouth or rectum) or 38°C (armpit), Severe abdominal
tenderness, Anuria, Asterixis

ASSESSMENT AND DIAGNOSIS:

The diagnosis in a case of poisoning can be made from

the 1) History 2) Physical Examination 3) Laboratory
Evaluation and 4) Toxicological Screening

7. Enumerate
the clinical
1. History Students
manifestati
enumerate the
ons  Most important indicator of toxic ingestion. Careful
clinical
history regarding involved toxins, amount of drug
manifestations
and timing should be recorded.
 Information regarding prescription medication, over
the counter drugs and illicit substances of abuse
should be obtained.
 Friends, relatives and other involved healthcare
 providers should be questioned and medications Lecture Listening
identified.
3 min
 Medication found on or near the patient should be
examined and pharmacy on the medication label
should be called to determine the status of all
prescription medication.
2. Physical Examination
 Evaluation of Airway patency, Respiration,
 Circulation.
 Rapid assessment of mental status, temperature,

8. Discuss the pupil size, muscle tone, reflexes, skin and peristaltic

assessmen activity.
Students
t and 3. Labororatory evaluation
discuss the
diagnosis  Clinical laboratory data include assessment of the
assessment
of three gaps of toxicology9
and diagnosis
poisoning 1. The Anion gap
of poisoning
2. The osmolal gap
3. The arterial oxygen saturation gap.

Unexplained widening of the difference between calculated

and measured determination of these values raises the Lecture Listening
suspicion of toxic ingestion.

4. Toxicological Screening

It provides direct evidence of ingestions, but it rarely

impacts initial management and initial supportive
measures should never await results of such analysis. It is
used to

1) provides ground for treatment with specific antidote or

method for enhancing drug elimination and

2) also identifies drugs that should be quantified to guide

subsequent management. Also look for characteristic signs
of various kinds of poisoning while immediate treatment
measures are being started.

MANAGEMENT:
Treatment objectives include:

 To maintain normal vital signs

 To decontaminate the site of exposure
 To prevent and reduce absorption To enhance
elimination
 To relieve symptoms
 To prevent further organ damage or impairment
without delay

NON PHARMACHOLOGICAL TREATMENT:

- Ensure airways are patent

- Remove contaminated clothing, if necessary
- Wash chemical away from the skin with soap and a
lot of water
- If necessary Perform nasogastric aspiration if
airway is protected
- Carry out gastric lavage or aspiration within the first
1 hour after the event or later if it involves slow
release or highly toxic substances
- Detain the patient in the clinic or hospital for close
 and continuous observation, re-evaluation, and
supportive and symptomatic treatment Maintain and
continuously monitor vital signs

PHARMACHOLOGICAL MANAGEMENT:

Initial Management :

1. For hypoglycaemia Glucose, IV,25-50 ml of 50%

over 1-3 minutes  For opioid overdose Naloxone,
IV,  Adult= 0.4-2 mg, repeat every 2-3 minutes
(maximum of 10 mg)  Children= 10 micrograms/kg
stat, subsequent dose of 100 microgram/kg if no
response to initial dose Then,  Naloxone, SC or IM,
only if IV route is not feasible

List of anti-dotes:

9. Discuss the
manageme
nt of
poisoning
 Lecture Listening

INJESTED POISON & MANAGEMENT:

15
Swallowed poisons may be corrosive.  Corrosive
min
poisons include alkaline and acid agents that can cause
tissue destruction after coming in contact with mucus
membranes.

- Alkaline products:-Drain cleaners, toilet bowl

cleaners, bleach, non-phosphate detergents, oven
 cleaners, and button batteries
- Acid products:-Toilet bowl cleaners, pool cleaners,
metal cleaners, rust removers, and battery acid.
- Petroleum distillates/hydrocarbons, Kerosene ,

Turpentine
- Drug overdose
- Food poisoning
 Check and maintain ABC
 Take ECG.
 Assess neurologic status
 Give water and milk to drink for dilution of strong
acid and alkaline poison.
 Gastric emptying procedure:-  Syrup of Ipecac to
induce vomiting in the alert patient ( never use with
corrosive poison).  Gastric lavage for the obtunded
patient, gastric aspirate is saved and sent to the
laboratory for testing (toxicologic screens)
Activated charcoal administration (1g/Kg).
Cathartic, when appropriate Sorbitol (1-2 g/kg)
Sodium sulfate Magnesium citrate.
 If there is specific antidote then administer it as
early as possible.  If antidote is not available then
 remove the ingested material by adminitration of
charcoal, diureis, dialysis or hemoperfusion
 Hemoperfusion involves detoxification of the blood
by processing it through an extra corporeal circuit
and an adsorbent cartridge containig charcoal and
resin, after which clean blood is returned to the
patient.

INHALATION POISINING: (Carbon Monoxide

Poisoning)

Carbon monoxide poisoning may occur as a result of

industrial or household incidents or attempted suicide.

Carbon monoxide bound Hb called Carboxyhemoglobin,

does not transport O2. Carbon monoxide exerts its toxic
effect by binding to circulating Hb and thereby reducing the
O2 carrying capacity of the blood.

Hb absorbs Carbon monoxide 200 times more rapidly than

O2.

Clinical Manifestation: Headache, Muscular weakness

Palpitation, Dizziness, Confusion progress towards coma
Skin color blue, False reading of pulse oximetry

GOAL:

- To reverse cerebral and myocardial hypoxia

INTERVENTION:

- Carry the patient to fresh air immediately, open all

doors and windows
- Loosen all tight clothing
- Initiate CPR if required; administer 100% O2.
- Prevent chilling; wrap the patient in blanket.
- Keep the patient as quiet as possible.
- Do not give alcohol in any form or permit the patient
to smoke.
SKIN CONTAINMENT:

Skin contamination injuries from exposure to chemicals are

challenging because of the large number of possible
offending agents with diverse actions and metabolic
effects.

The severity of a chemical burn is determined by the

mechanism of action, the penetrating strength and
concentration, and the amount and duration of exposure of
the skin to the chemical

GOAL- prevent skin from exposure.

INTERVENTION: Wash the exposed skin thoroughly with

water.

NOTE- water should not be applied to burns from lye or

white phosphorous because of the potential for an
explosion or for deepening of the burn.  All evidence of
these chemicals should be brushed off the patient before
any flushing occurs.
Start with standard burn treatment according to size and
location of wound (antimicrobial treatment, debridement,
tetanus prophylaxis, antidote administration as prescribed)
Plastic surgery may be required for further management of
wound.

ORGANOPHOSPHATE POISONING (OPP):

Organophosphate (OP) compounds are a diverse group of

chemicals used in both domestic and industrial settings.

Pathophysiology:

 The primary mechanism of action of

organophosphate pesticides is inhibition of
acetylcholinesterase (AChE).
 AChE is an enzyme that degrades the
neurotransmitter acetylcholine (ACh) into choline
and acetic acid.
 ACh is found in the central and peripheral nervous
system, neuromuscular junctions, and red blood
 cells (RBCs).
 Organophosphates inactivate AChE by
phosphorelation.
 Once AChE has been inactivated, ACh accumulates
throughout the nervous system, resulting in
overstimulation of muscarinic and nicotinic
receptors.
 Clinical effects are manifested via activation of the
autonomic and central nervous systems and at
nicotinic receptors on skeletal muscle.
 Organophosphates can be absorbed cutaneously,
ingested, inhaled, or injected.
 Although most patients rapidly become
symptomatic, the onset and severity of symptoms
depend on the specific compound, amount, route of
exposure, and rate of metabolic degradation.

Signs & Symptoms:

Listening
Can be divided into 3 broad categories, including:
(1) muscarinic effects,

(2) nicotinic effects, and

(3) CNS effects.

MUSCARINIC:
SLUDGE

Salivation  Lacrimation  Urination  Diarrhea  GI upset

 Emesis

DUMBELS

 Diaphoresis and diarrhea  Urination  Miosis 

Bradycardia, bronchospasm  Emesis  Excess
Lacrimation  Salivation

NICOTINIC:

muscle fasciculations, cramping, weakness ,

diaphragmatic failure.

Autonomic nicotinic effects include hypertension

Tachycardia , mydriasis , pallor.

CNS EFFECT:

Anxiety, emotional lability, Restlessness,Confusion ,

ataxia , tremors , seizures ,coma.

TREATMENT:

 Airway control and adequate oxygenation are

paramount in organophosphate (OP) poisonings.
 Intubation may be necessary in cases of respiratory
distress due to laryngospasm, bronchospasm,
bronchorrhea, or seizures.
 Immediate aggressive use of atropine may eliminate
the need for intubation.
 Succinylcholine should be avoided because it is
degraded by acetylcholinesterase (AChE) and may
 result in prolonged paralysis.

MEDICATIONS:

The mainstays of medical therapy in organophosphate

(OP) poisoning include ATROPINE, pralidoxime , and
Lecture
diazepam.

Initial management must focus on adequate use of

atropine. Optimizing oxygenation prior to the use of
atropine is recommended to minimize the potential for
dysrhythmias.

Anticholinergic agents:These agents act as competitive

antagonists at the muscarinic cholinergic receptors in both
the central and the peripheral nervous system. These
agents do not affect nicotinic effects.

1. ATROPIN:
Adult  1-2 mg IV bolus, repeat q1-5min prn for
desire effects (drying of pulmonary secretions and
adequate oxygenation) Strongly consider doubling
each subsequent dose for rapid control of patients
 in severe respiratory distress
Pediatric  0.05 mg/kg IV, repeat q1-5min prn for
control of airway secretions Strongly consider
doubling each subsequent dose to rapidly stabilize
patients with severe respiratory distress

SNAKE BITE AND ITS MANAGEMENT:

EPIDIMIOLOGY:

Worldwide issue. While reliable data are hard to obtain, it

has been estimated that about 5 million snake-bites occur
each year, resulting in up to 2.5 million envenomings, at
least 100,000 deaths and around three times as many
amputations and other permanent disabilities.

In India :The peak incidence of snakebite cases is reported

during the paddy sowing and harvesting periods, June to
November. The common krait, Bunganrs caeruleus, is
regarded as the most dangerous species of venomous
snake in the Indian subcontinent.

National crime bureau of India has reported in Accidental

Deaths & Suicides in India 2015 that:- 8,554 deaths occur
because of snakebite in 2015 in India.

CLASSIFICATION:

In India, poisonous snakes belong to three broad families:

1. Elapidae: Cobras, Kraits

2. Viperidae: Vipers Russell’s viper, saw scaled viper Pit

viper

3. Hydrophidae: Sea Snakes

Poisonous snakes can be identified by their characteristic

morphology

Poisonous snakes belong to three Families on the basis of

poison secreted :

1. Elapidae : Neurotoxic

2. Viperidae : Vasculotoxic

3. Hydrophidae : Myotoxic
INITIALS TREATMENT:

R. = Reassure the patient. 70% of all snakebites are from

non- venomous species. Only 50% of bites by venomous
species actually envenomate the patient

I = Immobilise in the same way as a fractured limb.  Use

bandages or cloth to hold the splints, not to block the blood
supply or apply pressure. Do not apply any compression in
the form of tight ligatures, they don’t work and can be
dangerous!

G. H. = Get to Hospital Immediately. Traditional remedies

have NO PROVEN benefit in treating snakebite.

T= Tell the doctor of any systemic symptoms  such as

ptosis that manifest on the way to hospital

TREATMENT:

Patient Assessment Phase:

On arrival.

- Deal with any life threatening symptoms on

 presentation. i.e. Airway, Breathing and Circulation.
- If there is evidence of a bite, where the skin has
been broken, give Tetanus Toxoid  Routine use of
anti-biotic is not necessary, although it should be
considered if there is evidence of cellulitis or
necrosis
- Polyvalent antivenin is available in a lyophilized
form (as liquid antivenin is unstable at room
temperature).  Active against the four common
poisonous snakes in India – cobra, krait, Russel’s
viper and saw scaled viper (Echis).
- Average potency of the antiserum available is that 1
ml will neutralize  0.6mg cobra  0.45mg krait 
0.6mg Russel’s viper  0.45mg saw scaled viper
venom
- Reconstitution involves the addition of 10ml of
distilled water to an ampoule and shaking till the
solution is clear.  It should be administered
intravenously as early as possible. It is essential to
enquire about allergy (specially to horse serum). It
is well to be prepared for an anaphylactic reaction
 during the antivenin administration
- Standard High Dose: loading dose of 100ml
followed by 50ml every 6 hours till the clotting time
became normal.
- Low Dose:  The basis of low dose therapy is that
the venom is absorbed only gradually into the
systemic circulation and the low dose is sufficient to
neutralize the absorbed quantity of venom.  The
low dose is given over a longer period as absorption
of venom continues into the systemic circulation.
- Analgesics for pain – Tab Paracetamol
- Antibiotics for infection. The choice should cover for
anaerobic infection.
- Anti-tetanus prophylaxis
- Replacement of coagulation factors / platelets if
there is active significant bleeding or bleeding into a
vital organ
- Respiratory failure  Edrophonium / atropine 10mg /
0.6mg as a test  Neostigmine / atropine
0.5mg/0.6mg every 30 – 60 min
- Mechanical ventilation
 - Shock Treat as appropriate
- Renal Failure Dialysis:

Tight (Aterial) strangulation is not recommended:

 To be effective, these had to be applied around the

upper part of the limb, so tightly that the peripheral
pulse was occluded.
 This method was extremely painful and very
dangerous if the tourniquet was left on for too long
(more than about 40 minutes), as the limb might be
damaged by ischaemia- gangrenous limbs
 Confining this toxin in a smaller area, by use of
compression techniques creates a greater risk of
serious local damage.
 When the tourniquet is removed there is the
problem of the venom rapidly entering the system
and causing respiratory failure in the case of
neurotoxic bites
 The Rusell Viper’s venom contains pro-coagulant
enzymes which cause the blood to clot. In the small
space below the tourniquet the venom has a greater
chance of causing a clot. When the tourniquet is
 released the clot will rapidly enter the body and can
cause embolism and death.(Kevin Loria 2014)
 Lastly, there has been a great deal of research
showing that tourniquets DO NOT stop venom from
entering the body

PREVENTION:

Prevention strategies include

- locking up medicines and cleaners,

- reading labels on medicines and cleaners before
using or storing, and
- safely discarding unneeded medicines, herbal
supplements, and vitamins.

NURSING MANAGEMENT:

ASSESSMENT-

Assess the condition of patient.

Assess the type of poisoning

Assess the more injured area.

GOALS-  Early detection, early management and

prevention of complications

NURSING DIAGNOSIS:

 Ineffective breathing pattern related to the swelling

of the nasal mucosa wall as evidenced by:
shortness of breath, breath with the lips, there
rhinitis.
 Acute pain related to gastric irritation as evidenced
by: abdominal pain, looked grimacing while holding
stomach.
 Impaired skin integrity related to changes in
circulation as evidenced by: swelling and itching of
the skin and the nose, there are hives, urticaria.

INTERVENTION:

Ineffective breathing pattern related to the swelling of the

respiratory mucosa wall

- Assess the respiratory rate & depth

- Maintain patency of airway.
- Do ET intubation in case of laryngeal edema.
- Give comfortable position.
- Remove the cause of allergy.
- Give anti inflammatory drugs/antidote as prescribed
by doctor.

Acute pain

- Assess characteristics of pain.

- Stop patient from eating.
- Keep patient on NPO.
- Give IV fluids.
- Give activated charchol and cathartics as told by
doctor.

Impaired skin integrity related to changes in circulation

- Assess skin condition.

- Prevent the patient from exposure.
 - Wash the exposed area thoroughly with water.
- Do aseptic dressing .
- Apply antibiotic ointment as told by doctor.

CONCLUSION:

Thousands of deaths takes place every year because of

intentional poisoning among adults and unintentional
among children in our state. Many snake bites and even
deaths from snakebite are not recorded. One reason is
that many snake bite victims are treated not in hospitals
but by traditional healers. Some people who are bitten by
snakes or suspect or imagine that they have been bitten,
may develop quite striking symptoms and signs, even
when no venom has been injected. This results from an
understandable fear of the consequences of a real
venomous bite.
BIBLIOGRAPHY:

 Brunner & suddarth’s. Text book of medical surgical

nursing. 12th edition. Vol2. lippincott. 2017-2019
 www.who.org
10. Discuss the 1
prevention min
of
poisoning

11. Discuss
the 15
min
nursing
manage
ment of
poisoni
ng