402

Indian J. Anaesth. 2003; 47 (5) : 402-411

INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

402

POISONING
Dr. Indu A. Chadha
Introduction
Parcelsus over 400 years ago stated, All substances
are poisons, there is none which is not a poison. The
right dose differentiates a poison and a remedy.1,2 The
safety of a chemical is defined as therapeutic index or
ratio, which is LD50/ED50.

Poisons are classified as according to the mode of

action2,4 as:1. Corrosive Poisons: These are highly active irritants
which produce both inflammation and ulceration of
tissues. This group consists of strong acids and alkalis.
2.

Epidemiology
Over 5 million people are treated in USA every
year on exposure to drugs. Only about 5% require
hospitalization. Over all mortality rate is low, only 0.03%
of all exposures, but 1-3% in suicidal cases. Acute
poisoning accounts for 2-3% of all admissions to hospital
in India. High incidence in the community reflects cases
of availability of insecticides and pesticides and also stress
of modern lifestyle. Insecticides, vegetable poisons,
aluminum phosphide, alcohol, hypnotics and sedatives are
the major poisons en- countered in India. In rural areas,
Insecticides, pesticides and vegetable poison, predominate
whereas in cities and towns it is sedatives or other drug
overdosage. The figures are much higher in India and are
increasing day by day.2,4
Poison is defined as a substance which when
administered, inhaled or swallowed is capable of acting
deleteriously on the body. It is defined also as a medicine
in a toxic dose.1,2 Poisoning also refers to the development
of dose related adverse effects following exposure to
chemicals/ drugs / xenobiotics.
This may be Suicidal, Homicidal, Stupefying and
Accidental.

Irritant poisons: These produce symptoms of pain

in the abdomen, vomiting and purging.
A . Inorganic poisons
Metallic Arsenic, antimony, mercury, lead and
copper
Non Metallic - Phosphorus, chlorine, bromine
and iodine
B. Organic Poisons Vegetable Castor oil
Animal Snakes, scorpions, spiders.
C. Mechanical Poisons
Powder glass, diamond dust.

3.

Neurotic Poisons : - These chiefly act on the central

nervous system. Symptoms usually consist of
headache, drowsiness, giddiness, delirium, stupor,
coma, and convulsion.
a. Cerebral Poisons Opium, alcohol, sedatives,
hypnotics, Anaesthetics.
b. Spinal Poison Strychnine.
c. Peripheral Curare.

4.

Cardiac Poisons Digitalis, tobacco.

5.

Asphyxiants Coal gas, CO, CO2 and war gases.

6.

Miscellaneous Analgesics, antipyretics,

tranquillizers, antidepressants.

1.

Suicidal poisons are Potassium Cyanide, Opium,

Barbiturates, Organophosphates (insecticides).

2.

Homicidal poisons are Arsenic, Antimony, Aconite,

and Thallium.

Mechanisms of action of poisons are 1, 2, 4

1. Local action-Poisons act directly on the tissues and
cause corrosion, irritation and inflammation.

3.

Stupefying poisons are: Dhatura, Belladonnas.

2.

Professor
Department of Anaesthesiology
B J Medical College and Civil Hospital
Asarwa, Ahmedabad - 380016
Correspond to :
E-mail : chadhaindu@hotmail.com.

Remote action-As the poison gets absorbed

systemically, it produces both specific CNS, spinal
cord, cardiac and nonspecific shock.

Poisons And The Oxygen Pathway2,3 :

Most of the poisonings involve the oxygen pathway,
from the inspired air to cellular respiration. The effects
and the poisons involved are given in (Table 1).

CHADHA : POISONING

403

Factors modifying the action of poisons1,2,4:

1. Dose-As a general rule small dose usually produce
no toxic effects, whereas large doses produce toxic
effects on the body. Some individuals also exhibit
phenomena like idiosyncrasy, allergy and synergism.
The presentations are different with single or chronic
exposure and with frequency of exposure.
2.

3.

4.

Form of poison (a) Physical state- Gases and

vapours act more quickly than fluid poisons because
they are absorbed immediately. Fluid poisons act
faster than solid ones. (b) Chemical combinationSome substances in certain combination become inert
like AgNO3 and Hydrochloric acid, and certain other
combinations becomes poisonous like lead carbonate
and copper sulphide. (c) Mechanical combinationThe action of a poison is considerably altered when
combined mechanically with inert substances.
Method of administration -A poison acts most rapidly
when inhaled in gaseous or vapours form or when
injected I.V. followed by I.M./S.C. and least rapidly
when swallowed
Condition of the body - (a) Age- Children is more
susceptible than adults to toxins. In old age poisons
have greater effects. (b) Sleep and intoxication-The
bodily functions are lowest during sleep, so the
poisons are absorbed slowly during sleep.

Table - 1 : Some major causes of blockade of the oxygen

pathway due to poisoning with mechanisms.
Cause

Mechanism

Effect

Asphyxiant gases (e.g. butane,

methane, carbon dioxide,
nitrogen)

Hypoxic gas mixture

Reduced inspired
oxygen fraction (FIO2)

Respiratory depression
(e.g. opioids, barbiturates,
other sedatives and hypnotics.

Failure of ventilation Reduced alveolar

(type II respiratory
oxygen tension (PAO2)
failure)

Respiratory muscle disorders:

Failure of oxygen
paralysis (e.g.organophosphates, transfer (type I
botulinus toxin) or spasm
respiratory failure)
(e.g.strychnine,phencyclidine)
Aspiration pneumonitis
Adult respiratory distress
syndrome (paraquat)

Reduced arterial
oxygen tension (PaO2)

Carboxyhaemoglobin
(carbon monoxide)
Methaemoglobin
(e.g.nitrites) Haemolysis
(e.g.arsine, stibine)

Loss of functioning
haemoglobin

Reduced arterial
oxygen content(CaO2)

Myocardial depressants
(e.g.b-blockers, tricyclic
antidepressants,
dextropropoxyphene)

Reduced cardiac
output

Chemical asphyxiants
(cyanide, hydrogen sulphide)

Block of cytochrome
enzyme chain

Fate of poisons in the body1,2,4,5:

Greater part of a poison is lost by vomiting and
diarrhea. After absorption the poison is dealt with in one
of the several ways. Most frequently the poison undergoes
biotransformation in the liver. The main route of excretion
of the poison or its end products is the urinary tract. Other
routes are bile ducts, sweat glands, saliva, mucus and
lungs. Epidermis, hair and nails retain inorganic poisons
like Arsenic. Bony skeleton holds substances like lead and
radioactive metals.
Any patient showing the clinical features shown in
(Table 2) should be considered for toxic ingestion6.
Table - 2 : Clinical features mandating consideration of
toxic ingestion.

Past history of drug overdose

or substance abuse

Aspiration

Suicidal ideation or prior suicide attempt

Bronchospasm

History of other psychiatric illness

Liver failure

Agitation

Renal failure

Stupor or coma

Hyper / hypothermia

Delirium or confusion

Rhabdomyolysis

Seizures

Osmolal gap

Muscles rigidity

Anion gap acidosis

Dystonia

Oxygen saturation gap

Cardiopulmonary arrest

Hyper / hypoglycemia

Unexplained cardiac arrhythmia

Hyper / hyponatremia

Hyper / hypotension

Hyper / hypokalemia

Ventilatory failure

Polypharmacy

Diagnosis of poisoning3,4,7,8,9 :
The diagnosis in a case of poisoning can be
made from the 1) History 2) Physical Examination
3) Labororatory Evaluation and 4) Toxicological Screening
1. History

Most important indicator of toxic ingestion5. Careful

history regarding involved toxins, amount of drug
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
identified.4,7

Reduced tissue
oxygen delivery(QO2)

Reduced tissue
oxygen consumption
(VO2) causing failure
of oxidative metabolism.

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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

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.4,7

Table - 3 : Level of consciousness (Reed Coma Scale).

Stage

Conscious
level

Pain
response

Reflexes

Respiration

Circulation

Asleep

Normal

Normal

Normal

Normal

Evaluation of Airway patency, Respiration,

Circulation.

Coma

Decreased

Normal

Normal

Normal

Coma

None

Normal

Normal

Normal

Rapid assessment of mental status, temperature, pupil

size, muscle tone, reflexes, skin and peristaltic
activity.

*Coma

None

None

Normal

Normal

+ Coma

None

None

Abnormal

Abnormal

2. Physical Examination3,4,6,9

Separate patients into two groups9 1) Depressed Status

2) Agitated Status

Drugs causing the depressed status are

sympatholytics like adrenergic blockers, anti- arrhythmics,
anti-hypertensive, anti-psychotics, cyclic antidepressant;
Cholinergics like nicotine, carbamates, organophosphates,
physostigmine, pilocarpine; Sedative-hypnotics like
alcohols, barbiturates, benzodiazepines; Narcotics like
analgesics, anti-diarrheal agents; and others like CO,
cyanide, H2S, hypoglycemic agents, lithium and salicylates.
Drugs causing an agitated status are sympathomimetics like adrenergic agonists, amphetamines, caffeine,
cocaine, ergot alkaloids, MAO inhibitors, theophylline;
Anticholinnergics like anti-histamines anti-parkinsonian
drugs, anti-psychotics, anti-spasmodics, cyclic
antidepressant, cyclobenzaprine; Drug withdrawal like a
blockers, clonidine, ethanol, opioids, sedatives-hypnotics;
Hallucinogens like LSD, marijuana, mescaline,
phencyclidine; and others like thyroid hormones.

Pupillary size and reaction to light, with the patients

physiological status gives a rapid clue regarding
dominant ingestion.
Pinpoint pupils with
agitation

- Phencyclidine
intoxication

Pinpoint pupils with

lethargy

- Narcotic overdose.

Dilated pupils not reacting - Anticholinergic

to light intoxication
Dilated pupils reacting
to light

- Cocaine intoxication

Level of coma of all poisoned patients should be

assessed and recorded according to the REED COMA
SCALE (Table 3)

* Patients in stages 3 and 4 require intubation and placement in an intensive care unit.
+ Patients in stage 4 need intervention to sustain life.

Look for muscle and motor movement. Muscle

rigidity with hyperthermia is characteristic of
neuroleptic malignant syndrome, malignant
hyperthermia and black widow spider bite.9

2. Labororatory evaluation
Clinical laboratory data include assessment of the
three gaps of toxicology9
1.

The Anion gap

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 suspicion of toxic ingestion.
1. Anion Gap: refers to the difference between
measured Cations and measured Anions
AG = [Na+] - [Cl-] [HCO3-]
Normal Value = 12 4 meqL-1
The presence of anion gap indicates that there are
more unmeasured anions than cations, since total serum
cations equals total serum anions. Unmeasured cations
include K+, Mg++ and Ca++ totaling about 11 meqL-1.
under normal conditions, and the concentration of
unmeasured anions including protein (mainly albumin),
sulfates, phosphates and organic acids, is about 23 meqL-1.
The anion gap falls by 2.3 meqL-1 for every l gmL-1
decrease in plasma albumin concentration.9,10,11,12,13
2. Osmolal gap: (measured calculated osmolality)
Certain drugs and toxins of low molecular weight
produce a discrepancy between measured and calculated
plasma osmolality, commonly referred to as the osmolal
gap. (osmolal gap equals measured minus calculated
osmolarity). Normal Plasma Osmolality=285295 mosmlL-1.
and is calculated as:

CHADHA : POISONING

Calculated osmolality =2[Na+] + [BUN]/2.8 +

[Glucose]/18 + [ethanol] /4.6 Where Na+(in mmolL-1) is
multiplied by 2 to account for anions(Cl- and HCO-) and
BUN and glucose are divided by 2.8 and 18 to convert
mgdL-1 to mmolL-1 and ethanol is divided by 4.6.14,15,16
3.

Oxygen saturation gap: Toxins associated with an

elevated arterial oxygen saturation gap [>5%
difference between saturation calculated from ABG
determination and saturation measured by
co-oximetery] including carbon monoxide and
methemoglobin. These toxins interfere with oxygen
binding to haemoglobin and thereby significantly
decrease oxygen content without lowering PaO2. It is
important to note that Oxygen saturation measured
by pulse oximetry is also falsely high in the setting
of these toxins.

H2S and cyanide interfere with cellular utilization

of oxygen leading to an abnormally high venous oxygen
saturation or arterilization of venous blood.

405

Obtain serum electrolytes, BUN, Blood glucose and

serum osmolality.
Calculate anion and osmolal gaps.
Obtain ECG, look for widened QRS, and QT intervals
and AV block.
Obtain CXR to look for pulmonary edema or inflates.
Obtain Abdominal X-Ray to look for radio opaque
pills.17
Obtain urine for toxicological screening and routine
analysis. Look for calcium oxalate crystals.
Pregnancy test in women of child bearing age.

Laboratory assessment may be helpful in differential

diagnosis of the poisoning (Fig. 1)
4. Toxicological Screening18,19
It provides direct evidence of ingestions, but it rarely
impacts initial management and initial supportive measures
should never await results of such analysis.

Fig. 1 : Differential diagnosis of poisoning based on the results of routine

laboratory tests. Dashed lines indicate the possible pathway.

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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

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.

serum electrolyte and blood glucose measurements

and tests of hepatic and renal function.
D.

1. Give glucose, 50ml of a 50% solution (25g

glucose) IV over 3-4 minutes.

Also look for characteristic signs of various kinds

of poisoning while immediate treatment measures are being
started.

2. Give Naloxone, 0.4 2 mg I.V. If patients

response is weak or if narcotic overdose is
suspected, give repeated doses of 2 mg every
1-2 min up to a total of 10-20 mg. Patients
responding to naloxone must be observed for at
least 3 hours after the last dose of naloxone.

Management of Poisoning
Treatment goals include support of vital signs,
prevention of further poison absorption, enhancement of
poison elimination administration of specific antidotes and
prevention of reexposure.4,6,8,20,21 Majority of poisoned
patient require only supportive treatment.4,8,20 (TAB IV)

3. If Alcoholism or Malnutrition is suspected, give

thiamine, 100mg I.V/I.M. The level of
consciousness of all intoxicated patients should be
assessed and the time of assessment should be
recorded.

Initial Therapy
Immediate management of life threatening conditions
in victims of poisoning with coma, seizures or marked air
way obstruction should be as follows.3,4,8,20,21,23 :
A.

Begin supplemental oxygen 5-10 lts. by nasal

prongs or mask.

If the patient has no gag reflex, intubate the trachea

with a cuffed endotracheal tube as soon as possible
to a) protect the airway b) facilitate oxygenation
and ventilation c) helps removal of secretions.

Indications for endotracheal intubation

1. Patients in coma or with markedly depressed
gag reflex.
2. Awake patient with normal gag reflex
3. Lethargic patient with fluctuating mental status
and a variable gag reflex.

Choice of Intubation technique3,4,21,22,23:

Orotracheal intubation : This technique is useful
for the comatose patients, since it is rapid and the location
of E.T. tube can be verified by direct vision.
Nasotracheal intubation. This technique is useful
in the agitated patient. It doesnt require jaw relaxation
and has the advantage of not requiring neck manipulation
in a patient who may have cervical spine injury.
B.
C.

4. Give Flumazenil, 0.2-0.5 mg. I.V. repeated

every 30 sec. upto 3 mg. in case of suspected
benzodiazepine poisoning.

Keep Airway open: Establish and maintain an

adequate airway and ventilation.

Obtain Arterial Blood Gas measurements: to

determine adequacy of ventilation and perfusion.
Gain Intravenous Access: Insert a 18G peripheral or
central line and draw blood for complete blood count,

Treat Coma (COMA COCKTAIL)21,22,23,24,25,26

E.

Maintain Circulation: Restore the intravascular volume

by intravenous infusion of crystalloids.
If the administration of more than 20-30 mlKg-1 of
crystalloid solution and usual doses of dopamine
(5-15 mgkg-1min-1) fail to restore blood pressure, insert
a pulmonary artery catheter to obtain pressure reading
and help guide further with fluids and pressor agents.

F.

Treat Seizures: Give diazepam 0.1 to 0.2 mgKg-1

IV over 1-2 minutes. Followed by Phenobarbital
15 mgkg-1 IV if there is no response to diazepam.

G.

Start ECG monitoring

Obtain 12 lead ECG.
Note the rate rhythm, presence of arrhythmias and
PR, QRS and QT intervals.

H.

Perform Gastric lavage: Collect sample for future

toxicological analysis if required

I.

Search for associated Illness:

Look for cause of coma or seizures
Look for a) head trauma b) haemorrhage or shock c)
infection d) metabolic discorders e) hypothermia and
f) hyperthermia

J.

Document: The available history and the level of

coma before ambulance personnel, relatives etc. leave
the hospital.

CHADHA : POISONING

407

Table - 4 : Fundmentals of poisoning management.

1

SUPPORTIVE CARE
Airway protection

Oxygenation / Ventilation

Treatment of arrhythmia
Hemodynamic support

Treatment of Arrythmia

Correction of metabolic
derangements

Correction of metabolic
derangements

Prevention of secondary
complications

PREVENTION OF FURTHER POISON ABSORPTION

Gastrointestinal decontamination

Induced emesisGastric lavage

Decontamination of other sites

Eye decontamination

Activated charcoal

Skin decontamination

Whole bowel irrigation

Body cavity decontamination

Catharsis
Dilution
Endoscopic/surgical removal
3

ENHANCEMENT OF POISON ELIMINATION

Multidose activated charcoal

Forced diuresis

Extracorporeal removal
Peritoneal dialysis

Alteration of pH

Hemodialysis

Chelation

Hemoperfusion /hemofiltration

Exchange transfusion

Hyperbaric oxygenation

Neutralization by antibodies

Metabolic antagonism

Neutralization by chemical binding

Physiologic antagonism

Adult education

Notification of regulatory
agencies

Child proofing

Psychiatric referral

ADMINISTRATION OF ANTIDOTES

PREVENTION OF REEXPOSURE

Prevention of further drug absorption4,6,21,22

Inhaled Poisons

Remove the patient from the source of the poison.

Give oxygen by mask(CN poisoning)

Inhalation of water aerosol may dilute inhaled irritant

in the nasopharynx.

Check for hoarseness and singed nasal hairs.

Be alert for delayed development of upper airway

obstruction and pulmonary edema.
Contaminated Eyes

Wash the Eyes with the copious amounts of plain

water or (hang a bottle of 500-1000 ml of NS) above
the patient and dribble the solution slowly into the
corner of the eye through the I.V tubing.

Check the tears with pH paper after the eyes have

been washed to make sure that all toxic material has
been removed.

A careful eye examination is done following irrigation.

Contaminated skin

Wash the skin immediately with plenty of water and

dilute soap solution.

Discard contaminated clothes in a marked plastic bag.

Organophosphate compounds are well absorbed
through the skin and are difficult to remove.27
Ingested Poisons
a. Emesis is recommended for emergency treatment of
drugs not adsorbed by activated charcoal. It is induced
with syrup of Ipecac. Dose is 15ml orally for children
(5-10 ml for 6m-1yr) and 30ml for adults. Give
2-3 glasses of plain water following this. This induces
the vomiting within 20-30 min. and can be repeated
after 30 min. The vomitus should be inspected for
remnants of pills or toxic substances, its appearance
and odor should be noted. Apomorphine is a parenteral
emetic, and can be used with caution because of its
CNS and cardiac side effects Do not induce emesis
in a comatose patients.
Contraindications to the induction of emesis are
Caustic (alkali) or corrosive (acid) ingestion.
Agents that rapidly produce coma or convulsions in
less then 30 min. and may predispose to aspiration
during emesis.
Prior significant vomiting.
In infants less than 6 months of age.
In foreign bodies.
-

Absence of bowel sounds.

b.

Gastric Lavage: It is done a) after suspected serious

ingestion when attempt to induce emesis fail and
b) when patients are uncooperative or lethargic, or
when gag reflex is markedly depressed. Place the
patient in left lateral decubitus position with head
down. It is performed with a large bore [36F]
nasogastric tube. Use tap water or saline at body
temperature in 250ml increments and continue lavage
until fluid returns clear. Airway must be protected if
gag reflex is depressed.

c.

Activated Charcoal 4,6,21,22,28: It has powerful

adsorption capacity and is given orally or via gastric
tube. It irreversibly binds the drugs within the bowel
and reduces the blood concentration by reducing drug
absorption and by creating a negative diffusion
gradient between the gut lumen and blood (gastrointestinal dialysis).The dose of activated charcoal is
1gmKg-1 orally with a minimum of 15 gm. The usual
dose is 60-70 gm. It can be mixed with 4 parts of
water and given every 4 hourly as long the bowel

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INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

sounds are present. It is used for most poisons accept

alcohol, potassium, Fe and Li.

(a) Weak acids such as salicylate and phenobarbital

are more fully ionized in basic solutions, so that
alkalinizing the urine may serve to trap them in
the tubular lumen, thus increasing excretion of
the drug in the urine.

Contraindication to the use of activated charcoal21,22,28

a) It should not be given before, concomitantly or just
after ipecac because it may absorb the ipecac and
interfere with its emetic properties
b)

It should not be given before, concomitantly or just

after oral antidotes unless proved not to interfere
significantly with their absorption.

c)

It does not effectively adsorb caustic and corrosive

and may produce vomiting or stick to the mucosa of
oesophagus or stomach and may look like burn on
endoscopy

d)

It should not be given if no bowel sounds are present.

e)

Activated charcoal is a stool marker, indicating that

the toxin has passed through the GIT and no further
significant absorption from the original ingestion will
occur

d.

Catharsis: Cathartic salts (disodium phosphate,

magnesium citrate and sulphate, sodium sulphate) or
saccharide (mannitol, sorbital), promote the rectal
evacuation of gastrointestinal contents. The dose of
sorbitol is 1-2 gkg-1.Their aim is to prevent
constipation following charcoal administration. They
are contraindicated in corrosive poisonings and
pre-existing diarrhea.

e.

Whole bowel irrigation: It is performed by

administering a bowel cleansing solution containing
electrolytes and polyethylene glycol orally or by
gastric tube at a rate of 0.5 Lhr-1 in children and
2Lhr-1 in adults until rectal effluent is clear. The
patient must be in sitting position. It is useful in
patients who have ingested foreign bodies, packets
of illicit drugs, slow releasing or enteric coated
medicines or heavy metals. It is contraindicated in
patients with bowel obstruction, ileus, haemodynamic
instability, and compromised unprotected airway.

(b) Weak bases such as amphetamines, strychnine

and phencyclidine are more ionized in acid
medium; acidification of urine has been proposed
to enhance their removal.
Contraindication to forced diuresis includes severe
CHF, cerebral failure and pulmonary oedoma.
(2) Extra Corporeal Removal of Toxins29:
(a) Hemodialysis : During haemodialysis, toxin is
removed from the blood into a dialysate solution
across a semipermeable membrane. The toxin must
be relatively water soluble and not highly protein
bound. It should have a small volume of
distribution and slow rate of intrinsic elimination
(a long t ). It is effective in removing methanol
ethylene glycol, salicylates and lithium. It is
also of value in correcting pH and electrolyte
imbalances especially in anuric patients.
Criteria for potential dialyzalibility includea) water solubility b) low molecular weight
c) protein binding d)volume of distribution and
e) intrinsic clearance of the substance. Complications of haemodialysis include intravenous
access complications, hypophosphatemia, alkalemia,
disequilibrium syndrome and hypotension.
(b)

Peritoneal Dialysis: Peritoneal Dialysis is only

1/8-1/4 as efficient as haemodialysis and is not a
preferred method.

c)

Hemoperfusion6: is defined as direct contact of blood

with a sorbant system. In hemoperfusion, blood is
pumped through a column of adsorbent material
(charcoal or resin) and returned to the patients
circulation. Vascular access similar to that for
hemodialysis is required. The kinetic conditions are
the same as in hemodialysis. It is commonly associated
with thrombocytopenia. It will not correct pH or
electrolyte imbalance.

d)

Hemofilteration6: Hemofilteration is potentially useful

method for removal of substances with a large Vd
slow inter compartmental transfer and vivid tissue
transfer. Arteriovenous (CAVH) or venovenous
(CVVH) methods are used.

Enhancement of the Absorbed drug 3,4,5,6,20,21:

The decision to use measures to enhance drug
elimination should be based on a rational understanding of
drug properties and the clinical condition of the patient.
The various methods are:
(1)

Diuresis and pH manipulations: Since many toxins

are weak acids or bases, they can be ionized in
solutions of varying pH. In the Ionized state, they
are less likely to cross cell membranes and their
reabsorption by renal tubular epithelium is decreased.

CHADHA : POISONING

409

Table - 5 : Commonly used antidotes in poisonings

Poison

Antidote

Dosage regimen

Anticholinergic
agents

Physostigmine

2 mg iv over 5 minutes, continue

with an infusion of 4-6 mg
hourly (adult dose)

Anticholinesterases

Atropine

1-2 mg i.v.repeated 2-4mg every

5-10 min. or atropine drip

Anticoagulants
(warfarin type)

Vitamin K

2-5 mg iv adult,
0.4 mg/kg child

Organophosphates

Atropine
Pralidoxime

2 mg iv (IM or SC in less
severely poisoned patients)
followed by further two doses at
5-10 minutes interval until full
atropinisation.
1 gm iv (in 100 ml saline over
30 mins) repeated every 4 hours
for 24 hours in severe cases.

Benzodiazepines

Narcotic analgesics

Carbon monoxide

Cyanide

Methaemoglobin

Paracetamol

Acetaminophen

Flumazenil

Naloxone

Initially 0.2 mg IV over 30

seconds. Further doses of 0.5 mg
can be given over 30 seconds at
60 seconds interval to a total
dose of 3 mg.
0.8-1.2 mg i.v. (children 0.2 mg)
Repeat if respiratory depression
not reversed within 1-2 mins.

Oxygen
(normobaric or
hyperbaric)

Administer as high as inspired

oxygen as possible until
carboxyhaemoglobin
concentration falls below 5% hyperbaric oxygen in severe cases.

Dicobalt edentate

300 mg iv over 3 minutes

Sodium nitrite

10 ml of 30% iv over
10 minutes

Sodium
thiosulphate

50 ml of 25% solution in over

10 minutes

Hydroxocobalamin

May be upto 4 gm I.V.

Oxygen

Administer inspired oxygen

till clinical recovery occurs.

Methylene blue

0.2 mlkg-1 of 1% solution. Slowly

I.V. over 5 mins. Repeated as
necessary upto 6 mgkg-1.

Ascorbic acid

1 g/24 hours I.V. or orally

Acetylcysteine

300 mgkg-1 over 16 hours

Methionine

2.5 gm orally every 4 hours for

12 hours.

n-acetylcysteine

140 mgKg-1 orally followed by

70 mgKg-1 every 4 hrly for 17
doses or 6 doses if no
hepatotoxicity

Poison

Antidote

Dosage regimen

Thallium

Berlin blue

250 mgkg-1 per day in divided

doses till thallium level is < 10
mgL-1 in blood and urine.

Ethylene Glycol

Ethanol

Dose given should be sufficient

to maintain plasma ethanol levels
at 1-2 gL-1.

Methanol

Ethanol

Dose given should be sufficient

to maintain plasma ethanol
levels at 1-2 gL-1.

b-Blockers

Glucagon
Isophrenaline

5 mg iv over 1 minute followed

by an infusion of 1-10 mgh-1
10-50 mgmin-1 I.V

Digoxin and
Digitoxin

Fab antibody
fragments

Dose should match estimated

dose of ingested digoxin.

Ca channel
Blockers

CaCl2, Ca gluconate

10 ml of 10% CaCl2 or30 ml of

10% Ca gluconate over 2 min. or
Continous infusion of Ca Cl2
0.2 mlKg-1hr-1-10mlKg-1hr-1

Hydroflouric acid

Calcium gluconate

For burns: calcium gluconate

(10%) 0.25-0.5 mmolkg-1, upto
25 mmolkg-1

Heavy metals
(lead, mercury,
arsenic)

DMSA (2,3
dimercaptosuccinic
acid)

30 mgkg-1 8 hourly for 5 days

then 20 mgkg-1 12 hourly for
14 days.

DMPS (Sodium
2,3-dimercaptopropane sulphonate)

Chronic: 100 mg 3 times a day.

Acute: 250 mg every 4 hours
for 24 hours then 250 mg every
6 hours for the next 24 hours.

Sodium calcium
edentate

Upto 40 mgkg-1 twice daily by

iv infusion repeated every
48 hours until level falls below
toxic levels.

Dimercaprol

Mercury: 2.5-3 mgkg-1 deep IM

injection 4-hourly for 2 days,
2-4 times on third day. 1-2 times
for upto 10 days.

Pencillamine

Lead: 0.5-1.5 g per day orally

for 1-2 months or until lead
levels falls below toxic level.

Iron salts.

Desferrioxamine

In severe iron poisoning

(> 90 mmolL-1) upto 15 mgkg-1
per hour reduced to keep the total
iv dose under 80 mgkg-1 in each
24 hours.

Coral snake
Rattlesnake bite

Anti-venom

Loading dose 1mgKg-1 upto

100 mg. Antivenum is diluted in
1000 ml of saline for adults or
20 ml for children.

410

Antidotes3,6:
An antidote is any substance that increases the mean
lethal dose of a toxin, or that can favourably affect the
toxic effects of a poison. The specific antidotes for various
poisons and their dose schedule are given in Table 5.
Supportive care
The goal of Supportive therapy is to maintain
physiologic homeostasis until detoxification is accomplished
and to prevent and treat secondary complications.
Respiratory Complications - are the commonest
cause of death after acute poisoning and immediate
management must be given priority to airway ventilation
and prevention of aspiration. Hypoventilation, hypoxia and
pulmonary oedema should be treated. Treatment consists
of O2, fluid restriction diuretics, mechanical ventilation
with PEEP, dialysis.
Cardiovascular complications - include hypotension,
cardiac arrhythmias and cardiac arrest. Treatment should
be on the lines of peripheral perfusion and maintenance of
myocardial function.
Renal Failure - may be due to tubular necrosis
because of hypotension hypoxia or direct effect of poison
on tubular cells. Haemoglobinuria or myoglobinuria may
further precipitate renal failure. Patient should be
catheterized to maintain a urine output of 0.5 mlkg-1hr-1
with volume resuscitation or dopamine infusion
(2-4 gmkg-1min-1).
Neurological complications - include depression of
consciousness level, seizures, cerebral oedema and
peripheral nerve injuries as a result of prolonged pressure.
Therapy consists of correction of ABG and metabolic
abnormalities and hypotension, reduction in intracranial
pressure, hyperventilation, elevation of head and fluid
restriction. Seizures may be because of metabolic
disturbances and cerebral hypoxia and direct toxic effect.
Treatment by I.V. diazepam / phenobarbitone or infusion
of thiopentone.
Hypothermia - should be treated by passive
rewarming, I.V. fluid warming, and warm water humidifier
in artificial ventilation. Temperature should be monitored
centrally via oesophagus or nasopharynx and ECG should
be monitored for arrhythmias.
Hyperthermia - may occur with tricyclic
antidepressant cocaine or amphetamine etc. Active cooling
with sedation, paralysis and ventilation may be required to
control core temperature.
Metabloic complications - The concentration of
urea and electrolytes and blood glucose, ABG should be

INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

checked routinely. Sodium bicarbonate may be needed if

PH falls below 7.1
Hematemesis - can be produced by caustics,
corrosives, iron, mercury, arsenic, lithium, phosphorous,
fluoride mushroom, plant poison and organophosphates.
The therapy consists of iced saline lavage, fluid and blood
replacement antacids H2 blockers may be used.
Hepatic and gastrointestinal complications Gastric stasis may occur in comatose patients or in
anticholinergic or opioid poisoned patient. Early
decompression with ryles tube and stress ulcer prophylaxis
may be used.
Indications for ICU admission
The usual disposition of an admitted poisoned patient
is the medical intensive core unit or a cardiac monitored
unit on the general medical ward. Risk factors that predict
the need for ICU admission are:1. PaCo2 > 45 mm Hg
2. The need for incubation
3. Seizures
4. QRS duration 0.12 s
5. 2nd / 3rd degree AV block
6. Cardiac Arrhythmias
7. Systolic blood pressure < 80 mmHg
8. Unresponsiveness to verbal stimuli
9. Need for emergency dialysis or hemoperfusion
10. Progressive metabolic acidosis
11. Cyclic antidepressant and phenothiazine overdose with
signs of anticholinergic cardiac toxicity
12. Severe hyperkalemia
13. Wide alterations in body temperature
14. Need for continuous infusion of naloxone
Volatile substance abuse (solvent abuse, glue
sniffing). This cause 150 deaths/year in UK. The main
substance abuse is toluene, a constituent of impact adhesives
and butane in lighter fuels. The main cause of death is
either a direct effect causing ventricular fibrillation,
hypotension, respiratory depression or aspiration of vomit.
Butane inhalation can cause hypoxia due to asphyxiant
effect. Management consists of resuscitation, oxygenation
and treatment of arrhythmias by b blockers.
Drug Couriers, body packers smuggle the drugs
(usually heroin, cocaine or amphetamine) by bodily
concealment. This can be by swallowing condoms, plastic
bags, vials of drug or by rectal or vaginal concealment.
The leakage results in severe toxicity. The patient has
history of recent plane journey. Abdominal X-ray may
reveal the diagnosis. Heroin toxicity may be treated by

CHADHA : POISONING

naloxone. Surgical removal may be the only way to prevent

worsening toxicity
Poisons unit and its role
The poisons information centre was first installed
on a national scale in Netherlands in 1949. Now most of
the nations have established centres on similar lines.
The functions of these central units are two fold:
1. To collect and make available information on the
constituents of household, agriculture and industrial
chemicals as well as drugs.
2.

To advise by telephone on the management of an

individual poisoning case. In addition, many units
have the facility for the estimation of plasma and
urine concentrations of a wide range of poisons and
to conduct screening tests.

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