various types of poisoning

1. Prepared By-
Ms. Anshu
M.Sc Nursing
KGMU Institute of Nursing

2.  A poison is any substance that, when ingested,
inhaled, absorbed, applied to skin, or produced
within the body in relatively small amounts,
injures the body by its chemical action.
 The branch of medicine that deals with the
detection and treatment of poisons is known as
toxicology.

3.  Poisoning represents the harmful effects on the
human body of accidental or intentional
exposure to toxic amounts of any substance.

4. According to WHO data, in 2012
an estimated 193,460 people died worldwide from
unintentional poisoning.
Of these deaths, 84% occurred in low- and middle-
income countries.
 In the same year, unintentional poisoning caused the
loss of over 10.7 million population a year of healthy
life (disability adjusted life years, DALYs).

5.  Acute pesticide poisoning is one of the most
common causes of intentional deaths worldwide
 IN INDIA
 National crime bureau of India has reported in
Accidental Deaths & Suicides in India 2015 that:-
26,173 died of poisoning in year 2015

6.  Ingestion
 Inhalation
 Injection
 Absorption

7. The effect of poisoning may be :-
 Local
 systemic or
 both
It may occur immediately or several hours or
even days after the exposure.

8.  · Chemicals
 · Household e.g. bleach, kerosene
 · Industrial e.g. methanol, ethylene glycol, cyanide,
arsenic
 · Pesticides e.g. organophosphates, organochlorines
(e.g. DDT), rat poison
 · Therapeutic drug overdose e.g. paracetamol, aspirin,
iron tablets, nifedipine, phenobarbitone
 · Toxic plants e.g. poisonous mushrooms, toxic herbal
preparations
 · Bites and stings of venomous animals e.g. snakes,
scorpions, bees, spiders, aquatic animals

9.  · Vomiting
 · Diarrhoea
 · Upper abdominal pain
 · Jaundice
 · Difficulty breathing
 · Palpitations
 Skin rashes
 Scanty urine

10.  · Fever
 · Vomiting
 · Diarrhoea
 · Dehydration
 · Jaundice
 · Tongue discolouration
 · Unusual fetor (smell on breath)
 · Changes in breathing rate or regularity
 · Changes in pulse rate or regularity
 · Skin lesions
 · Abdominal tenderness
 · Changes in pupil size (small or enlarged)
 · Seizures

11.  · 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

12.  · TLC
 · BUN and creatinine
 Electrolyte levels
 · Liver function tests
 · Fasting blood glucose
 · Toxicological analysis of identified substance or
tissue samples (e.g. gastric aspirate)

13. Treatment objectives
 · 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

14.  · 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

15.  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

16. Initial Management
 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

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

22. 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.

23.  Petroleum distillates/hydrocarbons
 Kerosene
 Turpentine
 Drug overdose
 Food poisoning

24.  Check and maintain ABC.
 Take ECG.
 Assess neurologic status
 Give water and milk to drink for dilution of strong
acid and alkaline poison.

25. 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.

26.  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.

27.  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.

28. 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.

30.  Headache
 Muscular weakness
 Palpitation
 Dizziness
 Confusion progress towards coma
 Skin color blue
 False reading of pulseoximetry

31.  GOAL-
To reverse cerebral and myocardial hypoxia

32.  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.

33.  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.

34.  GOAL- prevent skin from exposure.

35.  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.

36.  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.

38.  Organophosphate (OP) compounds are a diverse
group of chemicals used in both domestic and
industrial settings.
38

39.  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.

40.  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.
40

41.  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.

42. Can be divided into 3 broad categories,
including:
 (1) muscarinic effects,
 (2) nicotinic effects, and
 (3) CNS effects.

43. SLUDGE
 Salivation
 Lacrimation
 Urination
 Diarrhea
 GI upset
 Emesis

44. DUMBELS
 Diaphoresis and diarrhea
 Urination
 Miosis
 Bradycardia, bronchospasm
 Emesis
 Excess Lacrimation
 Salivation

45.  muscle fasciculations
 cramping, weakness
 diaphragmatic failure.
Autonomic nicotinic effects
 include hypertension
 Tachycardia
 mydriasis
 pallor.

46.  Anxiety
 emotional lability
 Restlessness
 Confusion
 ataxia
 tremors
 seizures
 coma.

47.  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.

48.  The mainstays of medical therapy in
organophosphate (OP) poisoning include
ATROPINE, pralidoxime , and 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.

49.  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.

50.  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

52.  WORLDWIDE
 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.

53.  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.

54.  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

55.  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.

56. Poisonous snakes belong to three Families on the
basis of poison secreted :
 1. Elapidae : Neurotoxic
2. Viperidae : Vasculotoxic
3. Hydrophidae : Myotoxic

61.  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.

62.  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

63.  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).

64. 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

65.  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

67.  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.

68.  Analgesics for pain – Tab PCM
 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

69.  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

70. 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.

71.  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

72. 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

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

74. 1. 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.

75.  Assess characteristics of pain.
 Stop patient from eating.
 Keep patient on NPO.
 Give IV fluids.
 Give activated charchol and cathartics as told by
doctor.

76. 3. 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.

77.  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.

78.  Brunner & suddarth’s. Text book of medical
surgical nursing. 12th edition. Vol2. lippincott.
2017-2019
 www.who.org