EMERGENCY RELATED

1. DR.IRSHAD AHMED
SENIOR RESIDENT
DEPARTMENT OF
EMERGENCY MEDICINE
PESIMSR
KUPPAM

2. HISTORY OF TOXICOLOGY
• The term poison was first used to describe a potion or draught that was
prepared with deadly ingredients around 1225 AD
• The earliest poisons consisted of plant extracts, animal venoms, and
minerals
• They were used for hunting, waging war, and sanctioned and unsanctioned
executions
• Poison is any substance (liquid, solid, or gas) that is harmful to the body
when ingested, inhaled, injected or absorbed through the skin
• Poisoning is contact with a substance that results in toxicity
• Ebers papyrus, an ancient Egyptian text is first documented books of
toxicology

3. The term toxicology is derived from the Greek terms toxikos (“bow”) and
toxikon (“poison into which arrow heads are dipped”)
 Medical toxicology as a medical
subspeciality started shortly after
World War II
 Toxicology is a branch of medicine
that deals with the detection &
treatment of poisoning
 Mathieu Joseph Bonaventure
Orfila (1787–1853), Spanish
toxicologist and chemist who is
generally regarded as the Father of
Modern Toxicology

4.  Poisons Information Services made their first appearance in the
Netherlands in 1949
 In India first National Poisons Information Centre at the All India
Institute of Medical Sciences, New Delhi in December, 1994
 A full-fledged Poison Control Centre with poison information service
Amrita Institute of Medical Sciences and Research, Cochin, Kerala in
July 2003

5. TYPES OF POISONING
 DELIBERATE: (intentional)-Suicide or Homicide
 ACCIDENTAL: (unintentional)
 Dosage error
 Environmental: plants, food
 Venomous stings/bites
 Industrial exposures.
 Ingestion is the most common route of exposure(77%), followed by
dermal, inhalation, & ophthalmic routes

6.  A poisoned patient can present to ED in many ways.
 Broadly, there are 4 types:
Fulminant: produced by a massive dose. Death occurs very rapidly
sometimes without preceding symptoms
Acute: produced by a single dose/ several small doses taken in a
short period
Chronic: produced by small doses taken over a long period
Sub-acute: characterized by mixed features of acute & chronic
poisoning

7.  Mofenson and Greensher
coined the term
toxidromes to describe the
groups of signs and
symptoms that consistently
result from particular toxins
 These syndromes best
described by a combination
of the vital signs and
clinically apparent end-
organ manifestations

8. HISTORY IN POISONED PATIENT
WHAT: Description of the toxin
Product names (brand, generic, chemical), ingredients along with their
concentrations.
Bring the container to the hospital with patient
HOW MUCH: determine as accurately as possible. It is better to
overestimate than underestimate

9.  WHEN: time lapse between exposure & the onset of symptoms
 PERIOD OF EXPOSURE: first use/ chronic user
 PROGRESSION OF SYMPTOMS: to assess the need for immediate
life support, the prognosis & the type of intervention needed
 INTERVENTIONS DONE BEFORE: traditional home remedies may
be harmful
 Medical history
 Underlying diseases
 Concurrent drug therapy

10. In most of the cases, the poisoned pt presents with one or more of the
following non-specific features:
 Impairment of consciousness
 Respiratory/cardiovascular depression
 Dehydration due to vomiting/diarrhoea
 Hypothermia
 Convulsions
 Cardiac arrhythmias

11. TELL-TALE SIGNS
 Sudden unexplained loss of
concioussness or illness
 Smell of particular toxin on the
patient
 Chemical products are evident
at the victims scene
 Drugs are on or around the
victim
 A syringe is in or next to victim
 Warning signs of gases &
chemicals are at/around the
location
 Victim is conscious & tells either
they have been poisoned

12. DIAGNOSTIC ODOURS
ODOUR SUBSTANCE
Acetone( apple -like) Chloroform, ethanol, isopropanol,
lacquer
Acrid(pear-like) Chloral hydrate, paraldehyde
Bitter almond cyanide
Burnt rope Marijuana(cannabis)
Coal gas Carbon monoxide
Disinfectant(hospital odour) Carbolic acid, creosote
garlicky Arsenic, dimethylsulfoxide,
organophosphorus
mothballs Camphor, naphthaline
Musty(fishy) Aluminium phosphide, zinc phosphide
Rotten egg Carbon di sulfide, disulfiram,NAC
Shoe polish nitrobenzine
vinegar Acetic acid
wintergreen Methyl salicylate

13. VITAL SIGNS
 Vital signs play an important role beyond assessing and
monitoring the overall status of a patient because they
frequently provide valuable physiologic clues to the
toxicologic etiology and severity of an illness
 The vital signs also are a valuable parameter, which are
used to assess and monitor a patient’s response to
supportive treatment and antidotal therapy

14. CARDIAC SIGNS
Tachycardia &
Normotension
Tachycardia &
Hypotension
Tachycardia &
Hypertension
Bradycardia &
Hypotension
Bradycardia &
Hypertension
Antihistamines,
caffeine,
cannabis,
lomotil
(atropine
&
diphenoxylate),
thyroxine
Carbon
monoxide,
cyanide,
phenothiazine
theophylline
Amphetamines
cocaine,
phencyclidine,
phenyl
propanolamine
Clonidine,
levodopa,
MAOIs,
organophospha
tes,
opiates,
tricyclic
antidepressants
Phenylpropanol
amine

15. TOXIC RESPIRATORY SIGNS
Failure of
Respiratory Centre
Failure of Respiratory
muscles
Tachypnea
Anti Depressants Neuromuscular Blocking
Agents
Salicylates
Anti Psychotics Organophosphates Sympathomimetics
Ethanol Snake Bite Pulmonary Irritants
Opiates Shellfish Poisoning Cyanide , Hydrogen Sulfide
Sedatives Strychnine Epinephrine,
Methyl Xanthines
Nicotine

16. TEMPERATURE
 Hypothermia and hyperthermia are common manifestations
of toxicity
 Xenobiotics induced life-threatening hyperthermia from any
cause may lead to extensive rhabdomyolysis, myoglobinuric
kidney failure, and direct liver and brain injury and must
therefore be identified and corrected immediately
 Hypothermia impairs the metabolism of many xenobiotics,
leading to unpredictable delayed and/or prolonged toxicologic
effects when the patient is warmed

17. GRADING THE SEVERITY OF CNS INTOXICATION
GRADE FEATURES GRADE FEATURES
0 Asleep, but can be aroused --- ---
1 Semi-comatose, withdraws
from painful stimuli, reflexes
Intact
1 Restlessness,
irritability, insomnia,
tremors,
hyperreflexia,
sweating, mydriasis
2 Comatose, doesn’t withdraw
from painful stimuli, reflexes
intact
2 Confusion,
hypotension,
tachyphoea,
tachycardia,
extrasystoles
3 Comatose, most reflexes lost,
no depression of CVS or RS
3 Delirium, mania.
Arrythmia,
hyperreflexia
4 Comatose, reflexes absent,
respiratory & or circulatory
failure
4 Convulsions, coma &
circulatory collapse
DEPRESSANTS STIMULANTS

18. Common clusters of features that can be diagnostic
Feature cluster Likely poisons
Coma, hypertonia, hyper-reflexia, extensor
plantar responses,
myoclonus, strabismus,
mydriasis, sinus tachycardia
Tricyclic antidepressants, less
commonly antihistamines,
orphenadrine
Coma, hypotonia,
hyporeflexia, plantar
responses flexor or
non-elicitable, hypotension
Barbiturates, benzodiazepines
and alcohol combinations.
Severe tricyclic antidepressant
poisoning
Coma, miosis, reduced
respiratory rate
Opioid analgesics
Nausea, vomiting, tinnitus,
deafness, sweating,
hyperventilation,
vasodilatation, metabolic
acidosis
Salicylates

19. Clusters continued;
Feature cluster Likely poisons
Restlessness, agitation,
mydriasis, anxiety, tremor,
tachycardia, convulsions,
arrhythmias
Sympathomimetics
Hyperthermia, tachycardia,
delirium, agitation,
mydriasis
Ecstasy (MDMA),
amphetamines, cathinones
Blindness (usually with
other features)
Quinine, methanol
Miosis, hypersalivation,
bronchorrhoea
Organophosphorus and
carbamate insecticides, nerve
agents

20. SYSTEMIC MANIFESTATIONS
• Ingested and absorbed toxins generally cause systemic symptoms
• Caustics and corrosive liquids damage mainly the mucous membranes
of the gastrointestinal (GI) tract, causing stomatitis, enteritis, or
perforation
• Some toxins (eg, alcohol, hydrocarbons) cause characteristic breath
odors
• Skin contact with toxins can cause various acute cutaneous symptoms
(eg, rashes, pain, blistering); chronic exposure may cause dermatitis
• Inhaled toxins cause symptoms of upper airway injury if they are
water-soluble (eg, chlorine, ammonia) and symptoms of lower airway
injury and non cardiogenic pulmonary edema if they are less water-
soluble (eg, phosgene)

21.  Inhalation of carbon monoxide, cyanide, or hydrogen sulfide gas can cause
organ ischemia or cardiac or respiratory arrest
 Eye contact with toxins (solid, liquid, or vapor) may damage the cornea,
sclera, and lens, causing eye pain, redness, and loss of vision
 Some substances (eg, cocaine, phencyclidine, amphetamine) can cause
severe agitation, which can result in hyperthermia, acidosis, &
rhabdomyolysis
INTESTINAL SIGNS:
 Cramps- Arsenic, Lead, Thallium, Organophosphates
 Diarrhea- Antimicrobials, Arsenic, Iron, Boric acid
 Constipation- Lead, Narcotics, Botulism
 Hematemesis- aminophylline, corrosives, iron, salicylates

22.  Muscle fasciculation- organophosphates, theophylline
 Muscle rigidity- cyclic antidepressants, PCP, phenothiazines,
haloperidol
 Paresthesia- cocaine, PCP, MSG
 Altered behaviour- LSD, PCP, amphetamines, cocaine,
alcohol, anticholinergics, camphor
 Peripheral neuropathy- lead, arsenic, mercury,
organophosphates

23. MIOSIS MYDRIASIS NYSTAGMUS
BARBITURATES ALCOHOL ALCOHOL
BENZODIAZEPINES AMPHETAMINES BARBITURATES
CAFFEINE ANTIHISTAMINES CARBAMAZEPINE
CARBAMATES CARBON MONOXIDE PHENCYCLIDINE
CARBOLIC ACID COCAINE PHENYTOIN
METHYL DOPA CYANIDE
CLONIDINE DATURA(ATROPINE)
NICOTINE EPHEDRINE
OPIATES
ORGANOPHOSPHATES
PARASYMPATHOMIMETICS
DRUGS/POISONS PRODUCING PUPILLARY CHANGES

24. Toxic ophthalmological manifestations
Feature Cause
DIPLOPIA BARBITURATES, CANNABIS, ETHANOL,
OPIATES, PHENYTOIN, TETRACYCLINE,
VITAMIN A
BLURRED VISION ALCOHOL, ANTICHOLINERGICS,
BOTULISM, ETHANOL, LITHIUM, MAOIS,
METHANOL
ALTERED COLOUR PERCEPTION CANNABIS, CO, DIGITALIS,
HYDROCARBONS, IBUPROFEN, NALIDIXIC
ACID
CORNEAL DEPOSITS CHLOROQUINE, VITAMIN D
OCULOGYRIC CRISIS PHENOTHIAZINES, BUTYROPHENONES,
METOCLOPRAMIDE
OPTIC NEURITIS
CHLOROQUINE, DIGITALIS, DISULFIRAM,
ERGOT, HEAVY METALS, METHANOL,
PENICILLAMINE, QUININE

25. DERMAL MANIFESTATIONS
POISON/DRUG FEATURE POISON/DRUG FEATURE
Dature, atropine Dry, hot skin Heroin,barbiturate
s, morphine,
phencyclidine
Needle marks
OP, salicylates,
arsenic, LSD, CO
Profuse sweating Bromides, iodides,
phenytoin
Acne, brown
colour
Carbon monoxide Cherry pink colour arsenic Rain-drop
pigmentation
cyanide Brick-red colour Chlorinated
hydrocarbons
Eczematous
dermatitis
Barbiturates, CO,
imipramine,
methadone,
nitrazepam
blisters Chloroquine,
busulfan,
clofazimine
Dark
pigmentation
warfarin Petechiae &
purpuric spots
Bromides, iodides,
salicylates
Erythema
nodosum
ACUTE CHRONIC

26. Poisons for which emergency measurement of plasma or serum
concentration is essential:
 Carboxyhaemoglobin
 Digoxin
 Ethanol
 Ethylene and diethylene glycol
 Iron
 Lithium
 Methanol
 Paracetamol
 Salicylate
 Theophylline
 Valproate

27. INSPECTION OF BLOOD :
 Chocolate-coloured blood indicates methaemoglobinaemia, caused by
abuse (inhalation or ingestion) of organic nitrites such as isobutyl
nitrite or drugs such as dapsone
 Pink plasma suggests haemolytic poisons (e.g. sodium chlorate)
 Brown plasma suggests the presence of circulating myoglobin
secondary to rhabdomyolysis
INSPECTION OF URINE:
 Brown discolouration of the urine suggests presence of haemoglobin (
intravascular haemolysis) or myoglobin secondary to rhabdomyolysis
 Crystals can be prominent after ingestion of ethylene glycol or an
overdose of primidone

28. Non-toxicological investigations
Serum Sodium Hyponatraemia in MDMA poisoning
Serum Potassium Hypokalaemia in theophylline poisoning;
hyperkalaemia in digoxin poisoning, rhabdomyolysis, haemolysis
Plasma
Creatinine
Renal failure in ethylene and diethylene glycol poisoning
Blood Sugars Hypoglycaemia in insulin and severe untreated paracetamol
poisoning, hypoglycaemia and hyperglycaemia in salicylate poisoning
Serum Calcium Hypocalcaemia in ethylene glycol poisoning
Serum
Phosphate
Hypophosphataemia in paracetamol Induced renal tubular damage
Serum AST/ALT Serum ALT/ASTactivities e.g. increased in paracetamol poisoning
Acid Base
Disturbance
Metabolic Acidosis, Metabolic Alkalosis, Respiratory Acidosis
Red Blood Cell
Cholinesterase
Activity
OP insecticide and nerve agent poisoning
Whole Blood
Methhemoglobin
Nitrite poisoning

29. RADIOGRAPHY:
 Some enteric coated or
sustained-release drug
formulations can be seen on
plain abdominal radiographs

30. A) Ingested packets of illicit substances may
be discernible on a plain radiograph, but CT
or MRI is more reliably able to detect such
objects.
B) CT or MRI can also be useful in confirming
the extent of corrosive damage, particularly
of the oesophagus.
 Radiology is helpful in diagnosing
complications of poisoning, such as
aspiration pneumonia, non-cardiogenic
pulmonary oedema (salicylates),
bronchiolitis obliterans (nitrogen oxides),
ARDS or pulmonary fibrosis (paraquat).

31. ECG:
 Routine ECG is of limited diagnostic value, although it should be
recorded in those who have ingested potentially cardiotoxic drugs
 Sinus tachycardia with prolongation of PR & QRS interval in
unconscious patient: TCA
 QT prolongation: quetiapine, terfenadine, quinine

32.  Resuscitation is the first priority in any poisoned patient
 After resuscitation, a structured risk assessment is used to
identify patients who may benefit from an antidote,
decontamination or enhanced elimination techniques