Poisoning & Envenomation

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...................................................................Toxicology................................................................
Poisoning
• Poisoning is injury or death due to swallowing, inhaling, touching or injecting various drugs,
chemicals, venoms or gases.
Poisoning Chemicals
   
Agricultural and industrial chemicals Drugs and health care products Biological Poisons Radiation
(plant & animal sources)
Agricultural chemicals  Pesticides Insecticides, herbicides, fungicides, fumigants, and rodenticides.
Insecticides Organophosphates (e.g. malathion, parathion), Carbamates (ecarbaryl, carbofuran, methomyl),
chlorinated hydrocarbons, DDT, methoxychlor, chlordecone (Kepone), insecticides from plants (e.g. pyrethrins)
Industrial chemicals  Hydrocarbons (gasoline, toluene, xylene, hexanes, n-hexane, heptane), Chlorinated
hydrocarbons (chloroform, carbon tetrachloride, methylene chloride, and others), Alcohols (methanol, ethanol),
Aldehydes, Ketones, Esters, Aromatic amines and nitro compounds, Anhydrides and isocyanates, Metals,
Corrosives (acids and alkalies), Miscellaneous inorganic compounds, Air pollutants (SO2, NO, NO2, O3, CO)
Drugs and health care products Painkillers (aspirin, sodium salicylate, acetaminophen, morphine),
Tranquilizers and sleeping pills (benzodiazepines, barbiturates), Nasal decongestants, Nasal decongestants,
Cough medicine, Antiseptics, Vitamins and iron pills, Antidepressants, Drugs of abuse, Cardiovascular drugs,
Therapeutics for asthma.
Biological Poisons  Microbial toxins (By bacteria, blue-green algae, dinoflagellates, golden-brown algae),
Phytotoxins (poisons produced by plants), Zootoxins (poisons produced by animals)
Radiation  Ionizing radiation: Particulate (Alpha particles, beta particles, neutrons, and positrons),
Eletromagnetic (e.g., X rays, gamma rays),
Nonionizing radiation: Electromagnetic waves (ultraviolet light, infrared radiation, microwaves,
and radio waves)
Organophosphorus (OP) compound poisoning:
Q.1- Clinical features and management of Organophosphorus compound poisoning.
[3] My/Jn 2013, 2012, 2010, Winter 2012, Nov/Dec 2010, 2008, Jn/Jl 2006, Dec. 2005
Q.2- Organophosphorus compound poisoning. [3] Summer 2016

• Most common cause of acute poisoning in India.

• Organophosphorus compounds:
Nerve agents: Insecticides:
• G agents: sarin, tabun, soman Dimethyl compounds Diethyl compounds
• V agents: VX, VE • Dichlorvos • Chlorpyrifos
• Novichok agents • Fenthion • Diazinon
• Malathion • Parathion-ethyl
• Methamidophos • Quinalphos
• Organophosphates are acetylcholinesterase inhibitors
• Mode of intoxication: Through ingestion or inhalation or dermal absorption.
• Mechanism of OP Toxicity:
OP compound  Inhibits AChE  No degradation of ACh  Acetylcholine (ACh)
(by phosphorylation) (Accumulation of ACh in synapses & NMJ)

Cognitive function Neuronal network function  ACh signalling  Overstimulation of ACh receptors
  (Muscarinic and nicotinic receptors)
Cardiovascular dysregulation Respiratory distress/arrest
(Acetylcholine (ACh)= a naturally occurring neurotransmitter)
• Excessive accumulation of acetylcholine (ACh) at the neuromuscular junctions and synapses
causes symptoms of both muscarinic and nicotinic toxicity. (These include cramps, increased
salivation, lacrimation, muscular weakness, paralysis, muscular fasciculation, diarrhea, and blurry vision.)
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Clinical Features:
1. Acute cholinergic phase (Due to ACh excess at the synapses):
Muscarinic receptor action:
• Gastrointestinal: • Genitourinary: • Respiratory:
− Increased salivation, − Urinary incontinence − Rhinorrhea,
− Nausea, • Cardiovascular: − Stridor,
− Vomiting, − Bradycardia (80%), − Bronchospasm,
− Abdominal pain, diarrhea, − Hypotension − Bronchorrhea,
− Fecal incontinence − Cough
• Skin: • Ocular:
− Flushing, − Diplopia
− Diaphoresis (Sweating) − Lacrimation,
− Cyanosis − Miosis
Nicotinic manifestations:
• Muscle: • Eyes:
− Fasciculations − Mydriasis
− Paralysis
CNS Manifestations:
• Anxiety, • Tremors, • Confusion,
• Restlessness, • Convulsions • Coma.
• Weakness
2. Intermediate syndrome (IMS): • Weakness of neck muscles, • Proximal & respiratory muscle
Due to lack of early use of oximes, • Decreased deep tendon reflexes, weakness or paralysis
release of OP from adipose tissue, • Cranial nerve abnormalities, • Respiratory failure
& NMJ dysfunction.
(1 to 4 days after exposure)
3. Organophosphate-induced • Cramping muscle pain in the lower • Shuffling gait
Delayed Neuropathy (OPIDN): limbs • Foot and wrist drop
Due to degeneration of long • Distal numbness • Wasting,
myelinated nerve fibers • Paraesthesia in the distal upper • DTR reduced/absent,
(1 to 3 weeks after acute OP exposure) and lower limbs • Pyramidal tract signs absent.
Diagnosis/Investigations:
• Clinical examination: pulse, Respiratory rate, Pin point pupil, basal crept, sweating,
Kerosene like smell in mouth
• Laboratory:
− Plasma cholinesterase levels   50% of normal (20-61 ukat/L)
− Red cell cholinesterase   50% of normal (20-46 ukat/L)
− ECG  Prolonged QTc and sinus tachycardia
− Arterial blood gas (ABG) Hypoxemia
Management:
General Measures: Specific Measures:
• Remove the patient from site of exposure and • Atropine: the main antidote (antagonizes muscarinic
wash the skin with soap and water. effect of ACh)
• Make patients to lie down in the left lateral position: − Dose: 2-3 mg intravenously
With head lower than the feet. − After 5 minutes, check pulse, BP, chest crepitations
• Maintain airway, breathing, circulation (Aim: Pulse  80bpm, SBP  80mm Hg, clear chest,
• Oxygenation Pupils no longer pinpoint, Dry axillae)
• Endotracheal Intubation (In respiratory distress) − If target endpoints are not met, double the atropine
• Gastric lavage (in case of ingestion) dose every 5 minutes till the target endpoints are
• Eye exposure should be irrigated with copious achieved. Then @10-20% of total initial dose/hr.
amount of normal saline. • Pralidoxime (2-PAM) (a cholinesterase reactivator):
• Activated charcoal (orally) at a dose of 1-2 g/kg Dose: 30 mg/kg iv initially over 20 minutes followed
• Benzodiazepines for convulsions by a constant infusion at 9 mg/kg/ hour for 12-24 hrs.
For Carbamate poisoning also above will be the same.
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Acute Barbiturate poisoning and Diazepam poisoning:
Q.3- Treatment of acute barbiturate poisoning. [3] My/Jn2007
Q.4- Management of barbiturate poisoning. [3] Nov/Dec 2006
Q.5- Describe clinical picture and management of a case of diazepam poisoning.
• Sedative-hypnotics causing CNS depression (Depressant drug)
• M/c barbiturates: Amobarbital (for insomnia), Butalbital (for migraines & tension headaches),
Methohexital (for anaesthesia), Pentobarbital (for Pre- anaesthesia), Phenobarbital (for seizures),
Primidone (to prevent convulsion), Secobarbital (for insomnia).
• Barbiturate overdose is acute barbiturate poisoning.
Mechanism of Action:
Barbiturate  Bind to GABA receptors  Prolong the opening of chloride channel  Inhibiting excitable cells
Diazepam of the CNS
Clinical Features:
• Slurred speech. • Constricted pupils
• Incoordination and unsteady gait. • Hypotension
• Impaired attention or memory. • Pulmonary oedema
• Impaired consciousness (from stupor to coma). • Cardiac arrest
• Nystagmus and decreased reflexes. • Hypothermia
• Respiratory depression.
• Bullous skin lesions
Investigations:
• Complete blood count (CBC).
• Arterial blood gas (ABG).
• Blood glucose, electrolytes.
• ECG.
• Toxicology screen.
Management:
General Measures: Specific Measures:
• Endotracheal intubation and ventilator support • Haemodialysis
(In respiratory distress) • Alkaline diuresis
• Gastric lavage (for gastrointestinal decontamination) • Flumazenil (a benzodiazepine antagonist): 0.2 mg IV
• Activated charcoal (orally) at a dose of 1-2 g/kg 2-4 over 30 seconds. Further doses of 0.5 mg at every
hourly 60 seconds up to a total of 5 mg.
• IV fluids.
Q.6- Digoxin Toxicity. [3] Nov/Dec 2008
Digoxin Toxicity:
• Digoxin comes from the foxgloves plant known as Digitalis lanata.
• Digoxin is used to treat atrial fibrillation, atrial flutter, and heart failure.
• Digoxin toxicity, also known as digoxin poisoning, is a type of poisoning that occurs in people
who take too much of the medication digoxin or eat plants such as foxglove that contain a
similar substance.
• Normal digoxin serum levels (0.5-2 ng/mL) & digoxin serum levels  2 ng/mL  Toxicity
• Fatal doses of digoxin: 10 mg or more in healthy adults, or 4 mg (or more than 0.1 mg/kg) in
healthy children.
Mechanism of toxicity:
Digoxin (Overdose)   Na/K - ATPase   Na (Intracellular)  Ca2 (Intracellular)
(Na-K Pump) ( Na/Caexchanger)
 
Hyperkalemia Cellular damage & uncontrolled release of neurotransmitters
 Vagus nerve  Vagal tone   Conduction through SA and AV nodes  Arrhythmia
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Risk Factors:
• Hypokalemia (m/c trigger) • Hypercalcemia
• Hypothyroidism/hyperthyroidism • Alkalosis
• Advanced age • Hypoxemia
• MI • Acidosis
• Renal insufficiency • Drugs (Diuretics, Amiodarone, -blockers, Benzodiazepines,
• Hypomagnesemia Calcium channel blockers, Macrolide antibiotics, Propylthiouracil,
Amphotericin)
Clinical Features:
• Headache, • Altered colour perception (yellow-green discoloration)
• Generalized malaise • Photophobia,
• Nausea and vomiting • Photopsia
• Insomnia • Diminished visual acuity
• Altered mental status • Arrhythmias (range of arrhythmias)
• Abdominal pain • Sinus Bradycardias
• Hyperkalemia • Tachyarrhythmias (Supraventricular tachycardia, Slow ventricular
response, atrial tachycardia)
Investigations:
• UEC (urea and electrolytes tests – Kidney function test)
• Serum digoxin concentration,
• Serum potassium concentration,
• Creatinine,
• BUN
• Screening paracetamol level
• ECG
Management:
General Measures: Specific Measures:
• Resuscitation • Digoxin immune Fab (Digibind)  Antidote (1st line)
• Oxygenation (10 vials for adults and five vials for children IV)
• IV fluids ( Hydration & electrolyte correction) • -blockers (for Supraventricular tachycardia)
• Cardiac monitoring • Phenytoin (to suppress ventricular automaticity)
• Activated charcoal (in acute ingestion within 2 hours) • lidocaine (to suppress ventricular automaticity)
• Atropine (for bradycardia)
Q.7- Corrosive poisoning. [3] Oct 2002
Corrosive poisoning:
• A corrosive is a substance that fixes, destroys and erodes the surface with which it comes
into contact. [Caustic substances with pH less than two or more than 12 are especially destructive.]
Corrosive poisons:
1. Mineral acids (H2SO4, HNO3, HCl)
2. Organic acid (Oxalic acid, Carbolic acid, Acetic acid, Salicylic acid)
3. Vegetable acid (Hydrocyanic acid)
4. Alkalis (caustic soda-NaOH, caustic potash-KOH, rubidium hydroxide, Ca(OH)2)
Mechanism of action of corrosives:
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[Alkalis produce liquefaction necrosis while mineral acids produce coagulation necrosis.]
Clinical features:
Type of corrosive poison: General symptoms: Signs:
Corrosive Acids • Burning sensations and pain (mouth, • Tongue: Swollen or shrivelled, & black
throat, oesophagus, stomach) • Chalky white teeth (in H2SO4 case)
• Intense thirst & yellowish teeth (in HNO3 case)
• Dysphagia, • Whitish plaques in the oral cavity
• Retching • Laryngospasm
• Hematemesis • Mediastinitis
• Anxiety • Sunken eyes with dilated pupils
• Hyper salivation • Hypocalcemia,
• Pharyngeal pain • Hyperkalemia,
• Retrosternal chest and stomach pains • Renal injury,
• Vomiting (bloody vomitus) • Hemoglobinemia
• Hemoglobinuria
• Ulceration, bleeding, sloughing &
perforation of the stomach or
oesophagus
• Metabolic acidosis
• Scanty urine with corrosive acids
Alkalies • Burning pain in the mouth, • Metabolic alkalosis
oesophagus and stomach (retrosternal • Tetany
and epigastric pain) • Chemical burns on the mucosa of the
• Erythema and vesicle formation oral cavity.
• Nausea & vomiting • Stricture (oesophageal)
• Chest pain • Oesophageal and pharyngeal oedema
• Coughing, • Pyloric stenosis
• Drooling, • Mediatinitis and peritonitis
• Dysphagia, • Ulceration or whitish plaques in the
• Vomiting (bloody vomitus), oral cavity, palatal mucosa and
• Dyspnea pharynx.
• Hyper salivation • Tachycardia,
• Bronchoconstriction • Tachypnea,
• Pulmonary oedema • Abdominal tenderness,
• Chemical pneumonitis • Hypotension
Investigations:
• Saliva test for pH • Chest X-ray • CT scan (water soluble contrast)
• CBC • Kidney, Ureter, and Bladder X-ray • Endoscopy
• Arterial blood gas (ABG) test • Urine test • Cine Oesophagography
Treatment/ Management:
Gastric lavage, activated charcoal and emetics are contraindicated.
Acids: Alkalies:
• Standard resuscitation if required • Standard resuscitation if required
• Protection of airway • Protection of airway
• Ice (to relieve thirst) & IV fluids (for fluid loss) • Ice (to relieve thirst) & IV fluids (for fluid loss)
• Immediate dilution with water or milk (5ml/kg) • Acetic acid, citric acid mixed with large quantity of
• Intravenous (IV) proton-pump inhibitors (PPIs) water to neutralize alkali
• H2-blockers • Immediate dilution with water or milk (5ml/kg)
• Laparotomy (in gastric perforation & peritonitis), • Xylocaine viscous & analgesics (to relieve pain)
Gastrotomy, & Tracheostomy (as per case) • Sucralfate (1mg/6hrs) – a demulcent
• Xylocaine viscous & analgesics (to relieve pain) • Calcium gluconate IV (for tetany)
• Sucralfate (1mg/6hrs) • Broad spectrum antibiotics (Ampicillin 1g IV/6 hourly)
• Broad spectrum antibiotics (Ampicillin 1g IV/6 hourly) • Corticosteroids (to prevent oesophageal stricture)
• Prednisolone 60mg/day to prevent strictures & shock (Prednisolone 60mg/day)
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Alcohol poisoning:
Q.8- Clinical features and treatment of Methanol poisoning. [3] Winter 2013, My/Jn 2009
Q.9- Discuss the hazards of chronic alcoholism.
Q.10- Describe the role of alcohol in the causation of different clinical syndromes. Give the treatment
in brief of any one of them.
• Ethanol (ethyl alcohol, grain alcohol, drinking alcohol, or simply alcohol) (Formula: CH3CH2OH)
• Methanol (methyl alcohol, wood spirit, CH3OH)  varnishes, industrial solvents, windshield washers etc.
• Alcohol Poisoning: Alcohol poisoning can occur when the body’s ability to process and clear
alcohol is outpaced by the rate at which alcohol is consumed, at which point vital physical
processes may stop working properly.
Mechanism:
• The Chemical Breakdown of Alcohol in the human body:

• Alcoholic drink  Alcohol in bloodstream  Ethanol molecule in brain GABA  Calming effect
mesolimbic pathway (Relaxing)
[Dopamine release in the NAc shell  Feeling of pleasure & urge to drink more
 Endorphins release  Soothing, euphoric effect, sense of pleasure and well-being]
• Small dose of alcohol gives pleasure but continued drinking/higher dose of alcohol results in
physical symptoms such as slurred speech, blurred vision, lack of control, slower reaction
time, impaired judgment, confusion, troubled walking or standing.
Cause: Binge drinking (consuming 5 or more drinks for men & 4 or more drinks for women).
Clinical Features:
Symptoms: Signs:
• Strong alcohol odour • Low body temperature
• Nausea and vomiting • Bluish or pale skin
• Throwing up • Damp or clammy skin
• Severe dizziness • Seizures
• Headache • Slow responses (such as gag reflex)
• Dehydration • Very slow/ irregular heartbeat
• Increased urination (involuntary urination) • Low BP
• Asphyxia, impaired breathing • Slow breathing ( 8 breaths/minute), Long pauses
• Trouble staying awake between breaths (≥ 10 seconds)
• Hypothermia • Slurred speech
• Mood and behaviour changes • Blood alcohol level (BAC): 0.30% to 0.40%:
• Severe confusion (euphoria: 0.03 - 0.12, excitement: 0.09 - 0.25,
• Poor coordination or stumbling confusion: 0.18 - 0.30, stupor: 0.25 and 0.40)
Treatment/Management:
• keep the patient warm with a jacket or • A urinary catheter if patient become incontinent
blanket • Haloperidol (parenterally)
• Monitoring breathing • Psychological counselling
• Oxygen therapy • Disulfiram (to prevent patient from drinking)
• IV fluids • Naltrexone (to prevent and reduce the urge to drink) or
• Hemodialysis (if required) Vivitrol IV
• Lifestyle change • Acamprosate (to combat alcohol cravings)
• Gene therapy • IV thiamine
• Gastrolavage & activated charcoal within 2 hrs • Metadoxine 300–900 mg i.v. or reduced glutathione 600 mg
• Stomach pumping (to rid the body of excess i.v. or S-adenosylmethionine 400 mg i.v. to reduce the BAC
alcohol) and acetaldehyde concentrations.
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Hazards of chronic alcoholism:
• Alcohol use disorder (AUD)  A person continues to consume alcohol despite adverse health.
• Alcohol psychosis (alcohol hallucinosis)
• Liver disease  Alcohol-related fatty liver disease, Alcohol-related hepatitis, Liver fibrosis, Cirrhosis
• Pancreatitis
• Cancer  mouth and throat, voice box, oesophagus, colon and rectum, liver, breast
• Ulcers and gastrointestinal problems
• Immune system dysfunction
• Brain damage and accidents
• Iron deficiency anemia
• Osteoporosis
• Heart and cardiovascular diseases
• Significant social and economic losses to individuals and society.
• Mental and behavioural disorders
• Death and disability early in life
• Clinical Syndromes: Fetal alcohol syndrome (FAS), Korsakoff Syndrome, Alcohol
dependence Syndrome

Methanol (methyl alcohol) poisoning:

Common names: Carbinol, Methyl alcohol, Wood alcohol
Mechanism of Toxicity:
• Methanol is extremely poisonous. (lethal dose 30 to 240 mL or 1 g/kg)
• Oral ingestion of illicit or adulterated liquors or as ethanol substitution causes methanol
poisoning. [Ingestion of as little as 4–10 mL of methanol in adults may cause permanent damage.]
• Toxicity is due to its breakdown by ADH into metabolites formaldehyde and formic acid.
Clinical features:
• Neurological: headache, dizziness, agitation, acute mania, amnesia, decreased level of
consciousness including coma, and seizure.
• Gastrointestinal: Nausea, vomiting, lack of an appetite (anorexia), severe abdominal pain,
gastrointestinal bleeding (hemorrhage), diarrhea, liver function abnormalities, and
inflammation of the pancreas (pancreatitis).
• Ophthalmologic: visual disturbances, blurred vision, sensitivity to light (photophobia), visual
hallucinations (misty vision, skin over the eyes, snowstorm, dancing spots, flashes), partial to total loss
of vision, and rarely eye pain.
• Other: Rapid breathing, myocardial depression, bradycardia, shock, anuria, hematuria
electrolyte imbalances
Investigations/Diagnosis:
• Serum methanol levels. • Renal function tests and liver function tests.
• Arterial blood gas (ABG) • CT scan of the brain
Management:
General Measures: Specific Measures:
• Sodium bicarbonate infusion (to correct acidosis) • Fomepizole (4-methylpyrazole)  blocks alcohol
• Gastric lavage (within 1 hour of ingestion) dehydrogenase
• Control of seizures. • Hemodialysis
• IV fluids • Ethanol therapy  blocks alcohol dehydrogenase
• Oxygen • Folinic acid (leucovorin)  increasing the rate of
• Ventilation degradation of formic acid to carbon dioxide
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Q.10- Kerosene Poisoning. [3] Winter2021
Kerosene Poisoning:
• Kerosene is an oil (a derivative of petroleum) used as a fuel for lamps, as well as heating and
cooking.
• Kerosene uses: lamp fuel, cooking fuel, paints, pesticides,
• Accidental kerosene ingestion  Poisoning
• Fatal Dose: kerosene – 15 to 30ml, petrol – 10 ml
Clinical Features:

• Burning and associated pain in the mouth, throat, • Low blood pressure
and food-pipe • Respiratory effort
• Dyspnea • Rib cage retractions
• Tachypnoea • Cough
• Throat swelling & pain • Fever
• Vision loss (ocular poisoning) • Grunting
• Abdominal pain (may be cramping) • Cyanosis
• Bloody stools • Abdominal Distension
• Burns of the oesophagus (food pipe) • Pneumonia
• Nausea & Vomiting (possibly with blood) • Arrhythmias
• Headache and lethargy
• Euphoria
• Tinnitus
• Drowsiness
• Convulsions (seizures)
• Coma
Diagnosis:
• History of ingestion
• Chest X-ray  Ill defined, patchy densities in the perihilar area and midlungfields
• Blood and urine tests
• Sputum culture  To rule out bacterial pneumonia
• Arterial Blood Gas Analysis (to assess ventilation and acid base status)
• Bronchoscopy
• ECG
• Endoscopy
Management:
• Induced emesis, gastric lavage and activated charcoal are contraindicated.
• Stabilization of the airways
• Endotracheal intubation
• Mechanical ventilation (if required)
• Supplemental oxygen
• Salbutamol [Selective -2 adrenergic agonist (to dilate air passages in the lungs)]
• Gastric aspiration (within 1 hour)
• Antibiotics (penicillin G and Kanamycin) to prevent secondary infection.
− Levofloxacin (500 mg/day, slow infusion over 60-minute period)
− Ceftriaxone (1-2 g/day)
• IV fluids (for dehydration)
• IV paracetamol (for fever)
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Forced alkaline diuresis:
• Forced diuresis involves administration of diuretic agents and isotonic saline to increase
glomerular filtration rate and urine flow. When combined with bicarbonate infusion, it is
referred to as forced alkaline diuresis.
• It is used for eliminating toxins.
• GOAL: Alkalinise the urine and maintain a urine volume of  6 ml/min ( 300 ml./hr)
• It is efficient only in poisons with the following properties:
− Substances excreted mainly by kidneys.
− Substances with low volume distribution.
− Substances with low protein binding.
•Types:
1- Fluid Diuresis
2- Osmotic Diuresis: mannitol 10%, which is excreted by renal tubules
• In the first hour fluid infused contain:
− 500 ml 5% dextrose
− 500 ml bicarbonate 1.4%
− 500 ml dextrose 5%
# Potassium chloride should be added to keep serum potassium above 3.5 mmol/l. A diuretic like furosemide
is given 20 mg intravenously
# Administer 1.5-2.0 litres of i.v. fluids per hour to maintain urine volume greater than 500 ml per hour. Than
500 ml per hour.
# Urine pH should be maintained between 7.5 and 8.5.
# Several such cycles may be repeated till patient becomes conscious.

Carbon dioxide (CO2) narcosis/ Hypercarbia: [3] Summer 2016

• CO2 is a regulator of blood pH (Normal pH: 7.35 - 7.45).
• Carbon dioxide (CO2) narcosis is a condition that develops when excessive CO2 is present in
the bloodstream, leading to a depressed level of consciousness.
• CO2 narcosis is a condition of confusion, tremors, convulsions and possible coma that may
occur if blood levels of CO2 increases to ≥ 70mm Hg (Normal pressure = 40mm Hg)
[Carbon dioxide is a narcotic gas capable of depressing awareness to the degree of total loss of consciousness.]
• Etiology:
− Decreased minute ventilation,
− Increased physiologic dead space,
− Increased carbon dioxide production (Due to COPD, sleep apnea, toxins, pulmonary embolism. an infection,
illness, or trauma. cystic fibrosis)
[In the human body, carbon dioxide is formed intracellularly as a by-product of metabolism.
C6H12O6 (glucose)  6O2  6CO2 + 6H2O]
• Driving mechanism: acute hypercapnia (high levels of carbon dioxide in the blood) {It is caused due
to respiratory problems, excessive metabolism, or more rarely, from breathing in too much CO2}
Normal range of CO2 in blood: 20 to 29 millimoles per liter (mmol/L)
Hypercapnia is defined as the Partial pressure of CO2  42 mm Hg.
• Clinical features:
• Dyspnea (Shortness of breath). • Flushed skin • Coma
• Tachypnea (Rapid breathing) • Increased blood pressure • Dilation of blood vessels in the skin
• Headaches. • Muscle twitches • Panic attack
• Dizziness • Paranoia. • Respiratory failure
• Fatigue • Depression. • Papilledema
• Disorientation. • Seizures. • Tachycardia
• Confusion or altered mental state. • Fainting
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Investigations:
• Chest X-ray. • Toxicology screen,
• Blood pH, • Thyroid function tests,
• ABG analysis, • Pulse oximetry,
• CBC, • Pulmonary function tests
Management:
• Securing airway, breathing and circulation • Bronchodilators and steroids for COPD
• Non-invasive ventilation patients
• Oxygen therapy • Naloxone for opiate overdose,
• Endotracheal intubation followed by • Antibiotics,
mechanical ventilation • H1 and H2 blockers
• Esophageal balloon • Corticosteroids, and epinephrine
• Correction of the hypercapnia • Lifestyle changes
• Treatment of underlying cause
Food Poisoning: [3] Summer 2017
• Food poisoning, a type of foodborne illness, caused by food contaminated with bacteria,
viruses, parasites or toxins.
Etiology:
• Toxic food (poisonous mushrooms, toxic fish, etc.)
• Contamination of food:
− By environmental factors (industrial effluents  toxic fish, fecal contamination  infection of oysters by
Salmonella)
− By chemical agents (adulteration, accidental)
− By Microbial agents (bacteria, viruses, protozoa etc.): m/c Campylobacter, others are Salmonella,
Escherichia coli, Vibrio cholerae, Clostridium botulinum (Botulism), Bacillus cereus, Staphylococcus aureus,
Norovirus and Listeria
− By preformed toxins contaminating the food articles.
• Allergy to the food materials/food ingredients
• Inadequate cooking of food
Clinical features:
• Nausea • Weakness
• Vomiting • Dizziness
• Headache • Loss of appetite
• Diarrhoea that may contain blood or mucus • Fever
• Stomach cramps and abdominal pain • Muscle ache
• Excessive thirst or dry mouth, little or no • Chill
urination • Double vision
Investigations:
• Stool culture  To detect disease causing microbes. • Chemical analysis of suspected food sample/
• Urine culture ruminants for toxins/ toxic content if any
• Vomitus culture  To detect disease causing • Serological test of blood for antibody titre
microbes. • ELISA to detect viral antigen in stool
• PCR to determine the viral genome
Management/Treatment:
• Sucking ice chips and oral rehydration drink — to replace lost fluids (mild cases)
• IV fluids and electrolytes
• Antidiarrheal agents (codeine phosphate, loperamide)
• Antibiotics (As per sensitivity report of culture)
• Probiotics (to restore the balance of good bacteria in the intestine)
• Anti-allergy agents (Atropine for mushroom poisoning, Diphenhydramine and cimetidine for fish poisoning)
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Paracetamol (acetaminophen) poisoning:
• Maximum recommended daily dose is 4 gm in adults.
• Toxicity: Doses  10g or  200 mg/kg (whichever is less) within 24 hours.
• Severe liver toxicity: Doses  350 mg/kg
Mechanism:

Clinical features:
Phase/Stage Symptoms: Signs:
Phase1 24hrs • Nausea & Vomiting • Pallor • ALT & AST
• Anorexia • Malaise (After 12 hrs.)
• Diarrhea • Vomiting
• Loss of appetite • Sweating
Phase2: 24-72hrs • Nausea & Vomiting • Tachycardia • Bilirubin
• Anorexia • Hypotension • BUN
• Diarrhea • Hepatomegaly • Prolonged PT
• Oliguria • ALT & AST • Creatinine
• Upper abdominal pain
Phase3: 3-4 days • Phase1 symptoms • Peak hepatotoxicity • Encephalopathy
• GI upset & GI bleeding (AST 20000 IU) • ALT & AST
• Confusion • Jaundice • Bilirubin
• Lethargy • Hypoglycemia • BUN
• Bleeding • Creatinine
• Hyperammonemia • Uremia
Phase4: 4-21 days Upon survival of critical illness in phase 3: complete resolution of symptoms and
complete resolution of organ failure
Investigations:
• History of taking paracetamol
• Serum concentration of paracetamol and evaluation of toxicity using Rumack Matthew
nomogram.
• Liver function tests
• Kidney function test (GFR)
• Electrolytes
• CBC
• Coagulation factors
• Arterial blood gas and ammonia
Management/ Treatment:
• Gastric lavage. • Methionine 12 gm orally 4th hourly, to a total
• Activated charcoal of four doses (alternative to NAC)
• Antidote: N-acetylcysteine (NAC) IV/Orally • Antiemetics (Metoclopramide or Ondansetron)
(shall be given within 10 hours of overdose) • IV fluids
[Oral regimen  140 mg/kg stat followed by 17 doses • Lactulose for hepatic encephalopathy
of 70 mg/kg given every 4 hours.] • Hemodialysis for renal failure
• Transfusions prn (platelets/plasma for coagulopathy; • Liver Transplantation
pRBC if anemia from GIB)
 12
Miscellaneous Poisoning:
Substance Clinical features Management
Opiate / Opioid • Decreased conscious level. • CPR
(heroin, morphine, methadone, • Decreased respiration. • Maintenance of airway.
codeine, pethidine, dihydrocodeine • Decreased bowel sounds. • Supplementary high-flow oxygen.
and dextropropoxyphene) • Decreased pupil size (pinpoint • Endotracheal intubation and
pupils). ventilatory support if required.
• Respiratory depression. • Antidote: Naloxone IV bolus
• Hypotension (0.8–2 mg) at every 2 minutes
• ARDS • IV fluids
• Hypothermia
• Discoloured lips or fingernails
Datura stramonium • Drunken gait • Gastric lavage with potassium
(Road side poison) • Dry mouth, throat & skin permanganate solution or 5% tannic
• Dysphagia acid solution.
• Burning pain in the stomach • Activated charcoal
• Decreased GI motility • Antidote: Physostigmine
• Giddiness (@1-4mg/1-2hrs as required) or
• Ataxia Neostigmine (@2.5mg iv /3hours
• Flushed face
• Diplopia
• Dilated pupils
• Reddening of the conjunctiva
• Delirium
• Drowsiness
• Nausea & vomiting
Lead • Abdominal pain • Prevention of further exposure
• Microcytic anaemia with • Measurement of blood lead
basophilic stippling concentration, CBC, blood smear,
• Headache and encephalopathy urea and electrolytes, LFT, Ca tests
• Motor neuropathy • Abdominal X-ray in children to
• Nephrotoxicity detect pica
• Hypertension • Bone X-ray for ‘lead lines’
• Hypocalcaemia • Chelation therapy with DMSA or
sodium calcium edetate
Cyanide • Dizziness • Gastric lavage.
• Shock • Activated charcoal.
• Hypotension and bradycardia • Antidotes:
• Dyspnoea, − Dicobalt edetate
• Cyanosis − Hydroxocobalamin
• Anxiety − Sodium nitrite
• Headache − Sodium thiosulphate
• Delirium
• Convulsions,
• Coma
• Fixed dilated pupils
• Vomiting
• Lactic acidosis
 13
Zink Phosphide Poisoning: [3] Summer 2017
• Black powdered rodenticides and fumigants.
• Mechanism of Toxicity:
Zinc phosphide  Gastric acid (stomach)  Phosphine gas (pulmonary and gastrointestinal toxicant)
Absorption of Phosphine in stomach  Systemic toxicity  Cellular hypoxia  Multi organ dysfunction
Clinical Features:
Symptoms: Signs:
• Severe gastrointestinal disturbances • ARDS and respiratory failure
(nausea, vomiting, and diarrhea) • Tachycardia
• Chest tightness • Metabolic acidosis
• Cough and breathlessness • Electrolyte disturbances
• Tremor • Hypoglycaemia
• Paraesthesiae • Hypotension
• Convulsions • Myocarditis  Cardiac failure
• Liver cell necrosis
• Renal failure
• Leucopenia.
• Lung injury
• Coma
Diagnosis:
• Detecting phosphine in the exhaled air or stomach aspirate by using silver nitrate-
impregnated strip or gas chromatography.
Management:
• Gastric lavage with KMnO4 (1:10000) or with magnesium sulphate (MgSO4)
• Activated charcoal (orally or through nasogastric tube)  adsorb phosphine in GIT
• Antacids or H2 blockers  burning pain (stomach), absorption of phosphine
• Sodium bicarbonate infusion  Metabolic acidosis correction
[Note: Aluminium phosphide poisoning will be same as zinc phosphide poisoning]
Bioterrorism: [3] Summer3013
• Intentional release or dissemination of biological agents (bacteria, viruses, insects, toxins)
• Spreading of the agents by air, water, food.
• Single case of a disease caused by an uncommon agent (e.g. smallpox, inhalational or
cutaneous anthrax, pneumonic plague)
• Large numbers of persons with similar diseases
• Large number of persons with unexplained deaths
• High morbidity and mortality in association with a common disease
• Failure of patients with a common disease to respond to usual therapy
• Unusual, atypical or genetically engineered strain of an agent
• Agent resistant to most antibiotics
• Disease with an unusual geographic distribution
• Sudden increase in occurrence of a disease, otherwise stable (e.g. plague, tularemia)
• Atypical disease transmission through aerosols or water
• Unusual illness that affects a large population
• Unusual pattern of death or illness among animals
• Simultaneous clusters of similar illness in non-contiguous areas
 14
Envenomation:
Q.1- Discuss the clinical features, investigations, complications and treatment of snake bite.
[8] Summer 2014
Q.2- Management of neurotoxic snake bite. [3] Summer 2019
Q.3- Management of vasculotoxic snake bite. [3] Winter 2017
Q.4- Management of poisonous snake bite. [3] Winter 2015
Q.5- Management of neuro-paralytic snake bite. [3] Winter 2018, 2017, My/Jn 2013, 2009, 2008
Q.6- Snakebite – Clinical features and treatment. [3] Winter 2012
Q.7- Describe clinical features and management of effective poisonous snake bite. [3] Jl/Ag 2005
Classification of Poisonous Snakes:
1. Elapidae (neurotoxic): 2. Viperidae (vasculotoxic): 3. Hydrophidae (myotoxic):
• Common cobra (Nag or kalsap or • Pitiless vipers: • About 20 types of Sea snakes
Naja naja) − (a) Russell’s viper m/c
• King cobra (Raj nag or Naja − (b) Sawscaled viper m/c
hannah or Naja bungarus) m/c • Pit vipers:
• Krait: − (a) Pit viper - crotalidae and
− (a) Common krait or Bungarus − (b) Common green pit viper.
caeruleus m/c
− (b) Banded krait or Bungarus
fasciatus
− (c) Coral snake
− (d) Tiger snake
− (e) Mambas and
− (f ) Death adder.
Differences between poisonous and non-poisonous snakes:
Poisonous: Non-poisonous:
• In upper jaw two large hollow fangs are present • All the teeth (small hooked teeth) in the upper jaw
along with small hooked teeth. are uniform.
• Triangular and broad head • Elongated and oval shaped head
• Vertical slit-like elliptical pupil  • Round pupil
• Flat or cylindrical tail • Cylindrical or blunt tail
• Ventral scales: Large and cover the belly region • Ventral scales: Small or large but not cover the
completely belly region completely
• Head scales: Small or large • Head scales: Large shield
• Dorsal scales: Smaller (hexagonal in krait) • Dorsal scales: Large, not in hexagonal shape
• Colour: Bright • Colour: Not bright (bright in python, sand boa)
• Teeth mark: • Teeth mark:

Composition of Snake Venoms:

• Hemorrhagins  Vascular leakage and bleeding • Cardiotoxins  Myocarditis, reduce cardiac output
• Procoagulants  Activate clotting factors • Neurotoxins  Inhibit nerve impulses
• Proteolytic enzymes  Local tissue necrosis, • Myotoxins  Local tissue necrosis, rhabdomyolysis
coagulation defects, and organ damage.
 15
Snake Bite:
Clinical features:
Elapid bite (neurotoxic bite): Viperid bite (vasculotoxic bite): Hydrophid bite (myotoxic bite):
Local Manifestations: Local Manifestations: Local Manifestations:
• Fang marks, burning pain, • Fang marks, Rapid swelling at • Fang marks, local swelling & pain
swelling and discoloration, bite site, discoloration, blister
serosanguineous discharge. formation, bleeding from bite site,
pain
Systemic features: Systemic features: Systemic features:
• Preparalytic stage: • Generalized bleeding: • Muscle weakness, Muscle pain &
− Vomiting − Epistaxis Stiffness
− Headache − Hemoptysis • Rhabdomyolysis Myoglobinuria
− Giddiness − Hematemesis • Renal failure
− Weakness − Bleeding gums
− Lethargy − Hematuria,
• Paralytic stage: − Malena,
− Ptosis − Hemorrhagic areas over skin and
− Ophthalmoplegia mucosa
− Drowsiness • Asymmetrical pupils
− Dysarthria • Intracranial bleed
− Dysphagia • Hypotension
− Convulsion • Low back pain
− Bulbar paralysis • Muscle pain: Rhabdomyolysis
− Respiratory failure • Parotid swelling
− Intercostal muscle paralysis • Conjunctival edema
− Stomach pain • Subconjunctival hemorrhage
− Submucosal hemorrhage in • Idiopathic systemic capillary leak
stomach syndrome (ISCLS)
− Neck muscle weakness • Hypoalbuminemia
− Death • Renal failure
• Hypopituitarism and cardiotoxicity
Investigations:
• Bedside 20-minute whole blood clotting test (20-WBCT)  Incoagulable blood at 20 minutes
indicates systemic envenomation
• CBC:
− Total leucocyte count  20,000/mm3  Severe envenomation
− Anemia (Low Hb)
• Serum creatinine
• Serum amylase
• Creatine phosphokinase (CPK).
• Blood coagulation profile
[Prothrombin time (PT), fibrinogen degradation product (FDP) and fibrinogen level]
• LFT (Albumin, total protein, ALP- alkaline phosphatase, ALT, AST, Bilirubin, LD - lactate dehydrogenase)
• Arterial blood gas (ABG)  Amount of O2 & CO2, pH of blood
• Electrolytes
• Urine examination (For proteinuria, myoglobinuria, RBCs, RBC casts)
• ECG  Arrhythmias
• Troponin test   Troponin  Myocardial damage
• Quantitative D-dimer test  Venom-induced consumption coagulopathy (VICC)   2.5 mg/L
(Within 2 hours of snakebite)
• Specific snake venom antigens may be detected in wound aspirates and body fluids.
 16
Management/ Treatment of snake bite:
1. First aid: RIGHT approach  R = Reassure the patient
I = Immobilize in the same way as a fractured limb.
GH = Get to Hospital immediately.
T = Tell the physician about any systemic symptoms that
develop on the way to hospital (e.g., ptosis)
2. Hospital management:
2.1- Antivenom Treatment
• Administration of anti-snake venom (ASV) as IV injection or infusion @ 2 mL/minute or ASV
dilute 5–10 mL/kg body weight of normal saline or 5% dextrose and infused over 1 hour.
[In mild cases, 5 vial (50 mL); in moderate cases, 5–10 vials; and in severe cases, 10–20 vial.]
• Additional infusion containing 5–10 vials are infused until progression of swelling ceased and
systemic symptoms are disappeared.
• In vasculotoxic or hemotoxic envenomation: ASV every 6 hours until coagulation (WBCT) is
restored.
• In neuroparalytic or neurotoxic envenomation: Initial dose of ASV 10 vials stat as infusion to
be followed by 2nd dose of 10 vials if no improvement within 1st hour (total 20 vials).
• In case of any hypersensitivity reaction/ anaphylaxis:
− Adrenaline injection (epinephrine) 0.5-1.0 ml subcutaneous (S.C.)  May be repeated
− Chlorpheniramine maleate (antihistamine) 10mg IV
− Hydrocortisone 100mg IV
2.2- Supportive Measures
• Monitoring of blood pressure, heart rate, respiration, coagulation, renal, and neurological
status.
• Injection tetanus toxoid 0.5 cc IM (supportive measure)
• IV fluids for hypotension and shock (supportive measure)
• Fresh whole blood or fresh frozen plasma, dopamine and hydrocortisone for hypotension and
shock.
• Neostigmine 1 mg IV stat  atropine 1 mg IV (for neuromuscular paralysis) and it is to be
repeated every half hourly.
• Artificial ventilation for respiratory paralysis.
• Surgical debridement for local necrosis and skin grafting.
• Antibiotics (Augmentin  metronidazole iv) to address local infection.
Complications:
• Compartment syndrome • Capillary leak syndrome
• Paralysis • Sepsis
• Vision impairment • Bronchospasm
• Limb loss (by amputation) • Aspiration pneumonia
• Gangrene • Cellulitis
• Cardiac damage • Necrosis
• Acute respiratory distress syndrome • Necrotizing fasciitis
• Renal failure • Coagulopathy
• Acute myocardial infarction
Indications for Antivenom:
Evidence of systemic envenomation Evidence of severe local envenomation
• Neurotoxicity • Persistent hypotension • Local tissue destruction
• Coagulopathy • Renal failure • Swelling
• Rhabdomyolysis • Pain
 17
Q.8- Scorpion sting. [3] Winter 2014, 2020
Scorpion stings:

• Black scorpions (Palamnaeus) and red scorpions (Mesobuthus)...m/c...(Red one is most danger)
• The glands in the terminal segment of the tail produce venom that is injected by a stinger.
• Scorpion venoms contain neurotoxins which stimulate synaptic sodium and potassium
channels with release of catecholamines and acetylcholine.
Clinical Features:
Local Features:
• Severe local pain radiating throughout the affected dermatome.
• Redness and swelling at the site of the sting
Systemic Features:
Cholinergic symptoms: Adrenergic features:
• Restlessness & anxiety • Convulsions
• Vomiting • Intracranial hemorrhage
• Increased gastrointestinal motility • Hypertension
• Profuse sweating • Tachycardia
• Hyper-salivation • Chest discomfort
• Pupillary constriction • Cold extremities
• Bronchoconstriction • Myocardial failure
• Increased secretion of lacrimal • Pulmonary edema
• Sensation of tongue thickening
• Dysphagia
• Bradycardia
• Hypotension
• Priapism
Other symptoms:
• Myocarditis or Ischemia (is shown by ECG)
• Vanillylmandelic acid (VMA) in urine
• Cardiac enzymes
Treatment:
• Immobilize the limb and apply a tourniquet above the sting
• Pack sting in ice, and incise and use suction, and wash with weak solution of ammonia,
borax or potassium permanganate
• Local anesthetic (0.1% lignocaine) for severe local pain
• NSAIDs and opiates for relieving pain.
• Selective 1-adrenergic blockers (prazosin 0.25-0.5 mg every 4-6 hours) for hypertension
and pulmonary edema
• Intravenous metoprolol or esmolol for tachycardia
• Monitor for cardiac rhythm, conduction disturbances and oxygen saturation.
• Dopamine infusion for hypotension.
• Calcium gluconate IV to control local swelling
• Barbiturate to reduce convulsions
• Atropine to prevent pulmonary edema
 18

Comprehensive evaluation of the envenomed patient: