Common poisonings encountered in clinical practice

1. COMMON
POISONINGS
CAPT NAJEEB MEMON

2. INTRODUCTION
What is a poison?
• Any substance that on introduction into the living body or on
bringing into contact with any part thereof will produce ill
effects or death by its local or systemic action or both.
Paracelsus, a Swiss chemist of the sixteen century has rightly
said that, there is no substance in this world that is not a poison.
It all depends on the dose and the mode of administration

3. STATUTES ON DRUGS/POISONS IN
INDIA
Drugs And Cosmetic Act (1940): defines
• Drug
• Cosmetic
• Manufacture in relation to any drug
• Misbranded drugs
• Adulterated drugs
• Spurious drugs
Related Legal Provisions:
• Sec 176, 177, 201, 202, 269-278, 284, 299, 300, 304 A,
324, 326 & 329 of IPC

4. FACTORS MODIFYING THE
ACTION OF POISONS
• Quantity
• Physical Form
• Chemical Form
• Concentration/Dilution
• Route of Administration
• Cumulative Action of the Poison
• Drug Interactions
• Condition of the Stomach
• Condition of the body
• Age, sex, tolerance, conditions surrounding the person, etc.

5. CLASSIFICATION OF POISONS ON
THE BASIS OF MODE OF ACTION
Corrosives
Strong Acids
(Organic/
Inorganic)
Eg. Sulphuric,
Hydrochloric,
Carbolic,
Oxalic, Acetic
Strong
Alkalies
Eg. Hydrates
& Carbonates
of Sod; Pot;
Ammonia, etc
Irritants
Non Metallic/
Metallic
Organic
(Vegetable/
Animal
poisons)
Mechannical
Neurotoxic
Central
(Somniferous,
Inebriants,,
Deliriants)
Spinal
Peripheral
Cardiotoxic
Acotine,
Digitalis, etc
Asphyxiants
Irrespirable
Gases
Eg. CO, CO2,
H2S
Cyanides

6. OVERVIEW
• Corrosives Poisoning
• Snake Envenomation
• Organophosphorus Poisoning (OP Poisoning)
• Sedatives Poisoning

8. CORROSIVES
Acids:
• Eg: Hydrochloric acid, Sulphuric acid, Acetic acid, Sod perchlorate
• MOA: Coagulation Necrosis
Alkalis:
• Eg: NaOH, KOH
• More dangerous
• MOA: Liquefaction Necrosis
Complications:
• Strictures or Perforations
• Metabolic Acidosis

9. CORROSIVES
Symptoms:
• Dysphagia, Retrosternal chest pain, Stomach pain, Dysphonia
Signs:
• Hypersalivation, Ulceration, Oedema, Whitish plaques, Contact bleed
Pathophysiology
• Hours: Small vessel thrombosis/injury
• Days: Inflammation, Bacterial invasion, Granulation tissue
• Weeks: Collagen deposition (healing), Tissue fibrosis (strictures)
Severity
• 1°: Mucosal oedema, Erythema
• 2°: Deep ulcers, Strictures
• 3°: Perforations

10. CORROSIVES
Management:
• Approach: To avoid perforation/stenosis
• Treatment of choice: Oesophagogastroduodenoscopy
• Milk & Ice cold water can be used (COntroversial)
• Sucralfate may help
• Gastric lavage, induced vomiting & charcoal are contraindicated
• Perforation: Immediate Sx
• Neutralisation: Not recommended
• Antibiotics: Can be used (Controversial)
• Strictures: Stents, NG tube, Intra luminal dialation
(>6 wks)

11. CORROSIVES
Nutrition*
<IIA:
• TPN: < 48 hrs, Liquid diet: 48 hrs – 10th day, Soft diet:
onwards
>IIB:
• “Oesophageal rest” for 10 days/NPO + Feeding Jejunostomy
*Based on Kendall’s endoscopic classification of post
corrosive injuries
• IA: Erythema, Odema
• IIA: Sup erosions
• IIB: Circumferential ulcers
• III: Deep grey/black ulcers
• IV: Perforation

12. CARBOLIC ACID/PHENOL
POISONING
• Corrosive aromatic hydrocarbon used as a
disinfectant
• Obtained from Coal Tar
• Has a characteristic odour, the so called “Phenolic
Odour”
• Household phenol contains 5% phenol in water
• Absorption can be the result of cutaneous exposure,
inhalation of its vapours & ingestion
• Fatal Dose: 10-15 gm
• Fatal Period: Death may occur within a few hours
due to resp failure and a few days due to renal
involvement

13. CARBOLIC ACID/PHENOL
POISONING
Clinical Features:
• Known as “Carbolism”
• Skin exposure: Burning sensation followed by tingling,
numbness & anaesthesia. A white opaque eschar is
produced that falls off in a few days leaving a brown stain
• Inhalation of vapours: Laryngeal & pulm oedema, respiratory
tract irritation and pneumonia
• Ingestion: Extensive local corrosions, pain, nausea, vomiting,
sweating and diarrhea. Systemic manifestations develop
after 5 to 30 minutes post ingestion or post dermal
application, and may produce nausea, vomiting, lethargy or
coma, hypotension, tachycardia or bradycardia,
dysrhythmias, seizures, acidosis, hemolysis,
methemoglobinemia & shock.

14. CARBOLIC ACID/PHENOL
POISONING
• Renal failure may occur. Urine contains traces of free
carbolic acid and its metabolised products, causing the
urine to turn into dark smoky green colour on standing
(due to oxidising of these products). Urine is scanty
and contains albumin & blood casts. All these findings
are grouped together as “Carboluria”
Diagnosis:
• Urine may show RBC’s, proteins & casts
• On adding a few drops of 10% ferric chloride to urine turns it to
violet or blue colour indicating the presence of phenolic
compounds
• Urine containing carbolic acid also reduces Benedict & Fehling
solution

15. CARBOLIC ACID/PHENOL
POISONING
Management:
• Establish vascular access
• Decontaminate the skin with extensive irrigation using soap
solution, water or undiluted polyethylene glycol
• Ingestion: Avoid emesis, alcohol and oral mineral oil and dilution,
because they may increase absorption. Gastric lavage is usually
not recommended. Immediate administration of olive oil and
activated charcoal by small bore nasogastric tube is necessary.
• 100% O2 administration
• Intubate and assisted ventilation might be reqd
• IVF and ionotropes for shock, lidocaine for arrhythmias &
lorazepam for seizures
• 1 to 2 mEq/kg of soda bicarb for metabolic acidosis
• Immediately decontaminate the eyes with copious amounts of tepid
water for at least 15 minutes

16. SNAKE
ENVENOMATION
All venomous snakes in India can be divided into:
Poisonous Snakes
Colubridae
Elapidae:
Eg. Cobra, Krait,
Coral & Mamba
Colubrinae:
Pit Viper & Rattle
snake
Hydrophidae:
Sea snakes
Viperidae True Vipers

17. POISONOUS & NON
POISONOUS SNAKE

18. SNAKE
ENVENOMATION
Classification of Venoms (Mixed features
commonly seen):
• Neurotoxic: All elapids
• Vasculotoxic: Vipers
• Myotoxic: Sea snakes
Neurotoxins are rapidly absorbed whereas
Vasculotoxins are taken up relatively slow through
lymphatics

19. SNAKE
ENVENOMATION
Snake Fatal dose in
human
Avg dose
per bite
Avg fatal
period
Indian Cobra 12 mg 60 mg 8 hrs
Common
Krait
6 mg 20 mg 18 hrs
Russell’s
Viper
15 mg 63 mg 4 days
Saw Scaled
Viper
8 mg 13-40 mg 41 days

20. SNAKE
ENVENOMATION
Clinical Features:
• Swelling & bruising of the bitten area results from increased
vascular permeability. Tissue necrosis near the site of the bite is
caused by myotoxic and cytolytic factors
• Ischaemia from thrombocytosis or a tight tourniquet may be seen.
Hypotension & shock due to hypovolaemia, vasodialatation and
myocardial dysfunction
• Some snake venoms activate the clotting cascade while others
degrade fibrinogen directly or via endogenous plasminogens
• Acute renal tubular necrosis may be caused by severe
hypotension, DIC, direct nephrotoxic effect and myoglobinuria
secondary to generalised rhambdomyolysis

21. SNAKE
ENVENOMATION

22. ASSESSMENT OF
SEVERITY OF
ENVENOMATION
No envenomation Absence of local or systemic
reactions, fang marks(+/−)
Mild envenomation Fang marks (+), moderate pain,
minimal local edema (0–15 ce),
erythema (+), ecchymosis(+/−), no
systemic reactions
Moderate envenomation Fang marks (+), moderate pain,
minimal local edema (0–15 ce),
erythema (+), ecchymosis (+/−), no
systemic reactions
Severe envenomation Fang marks (+), moderate pain,
minimal local edema (0–15 ce),
erythema (+), ecchymosis
(+/−), no systemic reactions

23. SNAKE
ENVENOMATION
• Presumptive Diagnosis:
• Vipers: Local envenomation + Bleeding/Clotting
disturbance
• Cobras: Local envenomation + Neurotoxicity
(Paralysis)
• Kraits: Minimum Local envenomation + Neurotoxicity
• Sea Snakes: Minimum Local envenomation +
Neuro/Muscle toxicity (Paralysis)
AKI, Shock, Rhabdomyolysis, Chemosis can occur in either

24. SNAKE
ENVENOMATION
Pre Hosp Care
• Immediately rush to hosp
• Try to click a picture of the snake for identification
• No incision, suction, tourniquet or ice at the bite
area. DO NOT USE TOURNIQUETS
• Immobilisation

25. SNAKE
ENVENOMATION
Hosp Care
• Assess ABC
• Assess state of level of consciousness
• CPR if required
• Oxygen
• Large bore IV canula
• IV Fluids
• Specific Treatment after History and physical examination
• Pain Management –Paracetamol/Tramadol
• Specific treatment as per complication
• Surgical intervention
• Blood tests: Routine hematological tests, coagulation profie (every
6 hrs)

26. SNAKE
ENVENOMATION
• Suspected Rhamdomyolysis: Creatine Kinase, Urine:
RBC’s/Myoglobin
• Vasopressors if unresponsive
• Fresh frozen plasma
• Cryoprecipitate (fibrinogen, Factor VIII),
• Fresh whole blood,
• Platelet concentrate.
• Broad spectrum antibiotics
• Prophylaxis against tetanus and gangrene
• Surgical debridement if required/Mechanical
• Ventilation/Dialysis

27. ROLE OF NEOSTIGMINE
AND ATROPINE
• Neostigmine test should be performed by
administering 0.5–2 mg IV and if neurological
improvement occurs, it should be continued 1/2
hourly over next 8 hours.
• Measure Single breath count
• Give Inj. Neostigmine 1.5 mg i.m. & Inj. Atropine 0.6
mg i.v. infusion oveer 8 hrs
• Repeat Single breath count every 10 mis for 1 hr
• If improving give Inj. Neostigmine 0.5 mg i.v. every
30 minutes until recovery, if no improvement
discontinue neostigmine

28. ASV ADMINISTRATION
• Either by slow intravenous injection at a rate of 2 ml/min or by
intravenous infusion (antivenom diluted in 5–10 ml/kg body weight
in NS and infused over 1 h). All patients should be strictly
observed for an hour for development of any anaphylactic
reaction
Dose:
• 1 ASV vial neutralizes the 6 mg of snake venom
• Each ml of Antisnake venom antiserum neutralizes not less than
the following quantities of standard venoms
• Cobra 0.60 mg
• Common Krait 0.45 mg
• Russell’s Viper 0.60 mg
• Saw-Scaled Viper 0.45 mg

29. INDICATION FOR ANTI
SNAKE VENOM
Evidence of systemic toxicity
• Heamodynamic instability
• Respiratory instability
• Hypotension
• Neurological complications
• Clinically significant bleeding
• Abnormal coagulation studies
• Progressive soft tissue swelling
• Passage of dark brown urine
• Snake identified as venomous

30. ORGANOPHOSPHORUS
POISONING
5 Lac deaths worldwide yearly, 60% self harm
• Highly Toxic: Tetraethyl Pyrophosphate & Parathion
• Int. Toxic: Coumaphos, Chlorpyriphos & Trichlorfon
• Low Toxic: Malathion, Diazinon & Dichlorovas
MOA: Inhibit AChE so the action of ACh prolongs at NM
junction resulting in:
• Muscarinic receptors: affecting pupils, bronchial muscles, salivary
and sweat glands, urinary bladder
• Nicotinic receptors: which causes twitching of eyelid, tongue and
facial muscles
• CNS stimulation: causes headache, restlessness, tremors. May
even lead to convulsions, coma and death

31. SIGNS AND
SYMPTOMS
• With massive ingestion or inhalation symptoms
might begin as early as within 5 min
• Involuntary muscles and secretory glands are
affected first followed by voluntary muscles
followed by vital centres in brain
• Respiratory signs include dyspnoea,
bronchoconstriction, increased bronchial
secretions, pulmonary edema
• G.I signs include anorexia, increased salivation,
abdominal cramps, diarrhoea

32. SIGNS AND
SYMPTOMS
• Miosis, increased lacrimation,blurred vision, urinary
incontinence
• Cardiovascular signs include bradycardia (may
sometime cause tachycardia also), conduction
blocks, arrhythmia and hypotension
• Muscular weakness ,fasciculation ,cramps may
occur as nicotinic effects
• CNS manifestation includes headache,
restlessness, tremors, drowsiness ,confusion
,convulsions may even lead to coma
• Very rarely chromolachryorrhoea (red tears) may
occur

33. CHOLINERGIC
TOXIDROME

34. INTERMEDIATE
SYNDROME
In around 20% of cases after 1-4 days, muscle
weakness and paralysis occurs
These occur after the signs and symptoms of
acute cholinergic syndrome is no longer
obvious
The characteristic feature of this syndrome is
weakness of the muscles of respiration and
proximal limb muscles. Other features include
motor cranial nerve palsies
Diagnosis can be made by 30Hz rapid nerve
stimulation test which shows a decremental

35. CHRONIC SEQUELAE
Delayed sequelae: Delayed peripheral neuropathy can
occur one to 5 weeks after exposure. It begins with
paraesthesias and cramps in the calves, followed by
weakness and foot drop and may progress to a flaccid
paralysis resembling GBS . The disease may progress
for 2-3 months
Cause of death: Respiratory muscle paralysis,
respiratory arrest due to respiratory centre failure or
intense bronchoconstriction and very rarely due to
arrhythmia

36. DIAGNOSIS
• Heparinised blood should be collected for cholinesterase
determination. Serum is separated and both are
refrigerated.
• RBC cholinesterase level less than 50% of normal
indicates poisoning
• Plasma cholinesterase is more sensitive and will fall
more rapidly and before that of red cells. Thus if the
plasma cholinesterase level is low and RBCs
cholinesterase levels are relatively unchanged , indicates
that amount of exposure is less and if both are low
indicates high amount of exposure
• In treated cases the plasma value approach to normal in
7-10 days

37. MANAGEMENT
• Remove from exposure
• ABC+O2+Position (Lat decubitus+Head Low)
• Check vitals every 5 mins, chest auscultation
• Inj. Atropine 1-3 mg bolus
• Once the patient is stable and signs of full atropinisation have
appeared start an infusion of atropine giving every hour 10% -
20% of the total dose needed to stabilize the patient, this
should be continued for at least 24 hrs maintaining the signs
of atropinisation.
• Inj. 2-Pralidoxime (PAM) 30mg/kg or 2g bolus dose followed
by an infusion dose of 8mg/kg/hr. They are given up till the
patient is clinically well and atropine has not been needed for
12-24 hrs

38. MANAGEMENT
• Assess response every 5 mins (HR>80/min,
SBP>80 mmHg, Chest Clear)
• Antibiotics to prevent pulm infections
• Glycopyrrolate can be considered in patients at
risk for recurrent symptoms (after initial
atropinization) but who are developing central
anticholinergic delirium or agitation
• Sedatives & AED’s for seizures

39. BARBITURATE
POISONING
• Non selective CNS depressants
• Derivatives of Barbituric acid
• Can poduce effects ranging fro sedation &
reduction of anxiety to unconsciousness &
death from resp & cardiovascular failure
• Used as sedatives, hypnotics, pre-op sedation
& for seizure disorders

40. BARBITURATE
POISONING
MOA:
• Potent enzyme inducer
• Precipitate acute attacks of Porphyria
• Tolerance & dependence can occur
Bind to GABA
receptors
Prolong the
opening of
Chloride
channels
Inhibit the
excitable cells
of CNS
Direct CNS
depression

41. CLINICAL FEATURES
• Stupor or coma, areflexia.
• Peripheral circulatory collapse.
• Weak & rapid pulse, Hypotension
• Cold clammy skin.
• Slow or rapid & shallow breathing.
• Pupils constricted & reacting to light initially but subsequently
develops paralytic dilatation.
• Nystagmus, Slurred speech, Hallucinations, Hypotonia
• Atelectasis.
• Pulmonary edema, Resp depression
• Bronchopneumonia
• AKI

42. MANAGEMENT
PROTOCOL
Hospitalisation
• Immediately take the pt to the
nearest hosp
Support Vitals Functions
• ABC
• Vitals monitoring
Prevent Further Absorption
• Emesis
• Gastric Lavage
• Activated charcoal & catharsis

43. MANAGEMENT
PROTOCOL
Increase Elimination of the Drug
• Forced diuresis
• Alkalinization of urine.
• Prophylactic antibiotic.
• Peritoneal dialysis.
• Hemodialysis.
• Hemoperfusion
Other Measures
• Psychiatric after care

44. BENZODIAZEPINE
POISONING
• Anxiolytic & hypnotic agents
• Wide therapeutic index
• Safest of all sedative drugs
• Used in the management of:
• Anxiety disorders
• Seizure disorders
• Insomnia
• Movement disorders (Adjunctive therapy)
• Mania (Adjunctive therapy)

45. BENZODIAZEPINES
Hypnotic
Diazepam
Alprazolam
Flurazepam
Nitrazepam
Antianxiety
Diazepam
Alprazolam
Lorazepam
Chlordiazepox
ide
Anticonvulsants
Diazepam
Lorazepam
Clobazam
Clonazepam

46. MECHANISM OF
ACTION
Stimulating GABA (b) receptors
Opening up the chloride ion channel in the receptor
complex
Increased conductance of chloride ion across the
nerve cell membrane
Lowers the potential diff across int & ext of cell
Blocking the ability of the cell to conduct nerve
impulses

47. CLINICAL FEATURES
Mild:
• Drowsiness, Ataxia, Weakness
Mod to Severe:
• Vertigo, slurred speech, nystagmus, partial ptosis, lethargy,
hypotension, respiratory depression, coma (stage 1 & 2 )
• Coma Stage 1: Responsive to painful stimuli
but not to verbal or tactile stimuli, no
disturbance in respiration or BP
• Coma Stage 2: Unconscious, not responsive to
painful stimuli, no disturbance in respiration or
BP

48. MANAGEMENT
Life supportive procedures & symptomatic/
specific treatment:
• Airway , breathing & circulation
• Intravenous fluid administration
• Endotracheal intubation
• Assisted ventilation
• Supplemental oxygen
• Decontamination:
• Stomach wash within 6-12 hrs
• Activated charcoal
• Emesis is contraindicated
• IVF
• Ionotrpes

49. MANAGEMENT
Antidote treatment: Flumazenil
• Reverses the coma induced by benzodiazepines by
competitive antagonism
• Complete reversal of benzodiazepine effect with a total slow
iv dose of 1mg.
• Administered in a series of smaller doses beginning with 0.2
mg & progressively increasing by 0.1- 0.2 mg every minute
until a cumulative total dose of 3.5 mg is reached.
• Resedation occurs within ½ hr – 2 hrs

50. REFERENCES
Guidelines for management of Snake bite in SE Asia: WHO
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of Acute
Organophosphorus Poisoning
Krishan Vij. Carbolic Acid Toxicity Treatment & Management. Text Book Of Forensic
Medicine & Toxicology, 6th Edition
Chibishev A, Pereska Z, Chibisheva V, Simonovska N. Corrosive poisoning in adults
Pillay VV.Acute Barbiturate Poisoning, Snake Bite management. Text Book Of
Forensic Medicine And Toxicology, 14th Edition
Gossel TA. Corrosive Poisoning & Management. Principles Of Clinical Toxicology, 2nd
Edition
Rang HP, Dale MM.Toxic Effects of Barbiturates & Benzodiazepines. Principles Of
Clinical Toxicology, 5th Edition
Tripathi KD. Classification of Benzodiazepines & Barbiturates. Essentials Of Medical
Pharmacology, 6th Edition
Images: Internet

51. DISCUSSION
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