PRINCIPLES OF

MANAGEMENT

Most patients
with selfpoisoning
require only
general care
and support of
the vital
systems

For a few
drugs,
additional
therapy is
required.

Management strategy in acute

poisoning
Provide supportive treatment.
Is the use of an antidote appropriate?
Is it appropriate to attempt to reduce poison
absorption?
Is it appropriate to perform toxicological
investigations?
Will non toxicological investigations assist?
Should urine alkalinization, multiple-dose
activated charcoal, or haemodialysis be
employed to increase poison elimination?

Toxicological Investigations
Timed blood sample.
The determination of the concentrations
drugs will be valuable in management
and sometimes in medicolegal cases.
Drug screens on blood and urine are
occasionally indicated in severely
poisoned patients in whom the cause of
coma is unknown

Agents for which emergency measurement of

blood concentrations is appropriate
Aspirin (salicylate)
Digoxin
Ethanol (in monitoring treatment of ethylene
glycol and methanol poisoning)
Ethylene glycol
Iron
Lithium (NB: Do not use a lithium heparin tube!)
Methanol
Paracetamol
Paraquat
Quinine
Theophylline

Non-toxicological investigations
Routine investigations detection of poisoninduced hypokalaemia, hyperkalaemia,
hypoglycaemia, hyperglycaemia and hepatic
renal failure or of acid-base disturbances.
Measurement of carboxyhaemoglobin,
methaemoglobin and RBC cholinesterase
poisoning due to carbon monoxide,
methaemoglobin-inducing agents such as
nitrites, and organophosphorus insecticides and
nerve agents.

Relevant non-toxicological investigations

Serum sodium (e.g. hyponatraemia in MDMA* poisoning) and potassium (e.g.

hypokalaemia in theophylline poisoning and hyperkalaemia in digoxin poisoning)
concentrations
Serum creatinine concentration (e.g. renal failure in ethylene glycol poisoning)
Acid-base disturbances, including metabolic acidosis
Blood glucose concentration (e.g. hypoglycaemia in insulin poisoning or
hyperglycaemia in salicylate poisoning)
Serum calcium concentration (e.g. hypocalcaemia in ethylene glycol poisoning)
Liver function (e.g. in paracetamol poisoning)
Serum phosphate (e.g. hypophosphataemia in paracetamol-induced renal tubular
damage)
Serum creatine kinase (rhabdomyolysis)
Carboxyhaemoglobin concentration (in carbon monoxide poisoning)
Methaemoglobinaemia (e.g. in nitrite poisoning)
RBC cholinesterase activity (e.g. organophosphorus insecticide and nerve agent
poisoning)
ECG(e.g. wide QRS in tricyclic antidepressant poisoning)
Xray for ingestion/injection of radiopaque substances

*MDMA,3,4-methylenedioxy-methamfetamine(Ecstasy)

Some poisons inducing metabolic acidosis

Carbon monoxide
Cocaine
Cyanide
Ethanol
Ethylene glycol
Iron
Methanol
Paracetamol
Salicylates
Tricyclic antidepressants

CARE OF THE UNCONSCIOUS

PATIENT
Lateral position with the lower leg straight and the
upper leg flexed reduce the risk of aspiration.
A clear air passage.
Nursing care of the mouth and pressure areas
should be instituted.
Immediate catheterization of the bladder
unnecessary.
Insertion of a venous cannula is usual,
Administration of intravenous fluids unnecessary,
unless unconscious >12 hours or hypotensive.

Respiratory support
Respiratory depression oropharyngeal
airway + O2
Loss of the cough or gag reflex
Intubation
If ventilation remains inadequate after
intubation Intermittent PositivePressure Ventilation (IPPV)

Cardiovascular support
Marked hypotension Volume expansion
with saline, gelatins or etherified starches
(e.g. hetastarch, hexastarch)
Guided by monitoring CVP & Urine output
(aiming for 35-50 mL/h)
Arrhythmias or shock ECG monitoring.
Known arrhythmogenic factors hypoxia,
acidosis and hypokalaemia should be
corrected.

Other problems
Body temperature
Hypothermia - a rectal temperature < 35C
Covered with a 'space blanket' and, if
Given intravenous and intragastric fluids at
normal body temperature.
Inspired gases warmed to 37C
Hyperthermia can develop with CNS stimulant
ingestion.
Removal of clothing and sponging with tepid
water will promote evaporation.

Rhabdomyolysis
Pressure necrosis in drug-induced coma,
Complication of MDMA abuse in the
absence of coma.
At risk of developing:
1. Renal failure from myoglobinaemia,
particularly if they are hypovolaemic and
have an acidosis,
2. Wrist or ankle drop from the development
of a compartment syndrome.

Convulsions
Poisoning due to tricyclic antidepressants,
mefenamic acid or opioids.
Usually short-lived
If prolonged diazepam 10-20 mg i.v.
Persistent controlled rapidly prevent
severe hypoxia, brain damage and
laryngeal trauma.
If diazepam ineffective loading dose of
phenytoin (15 mg/kg) i.v not more than 50
mg/min, with blood pressure and ECG
monitoring.

Stress ulceration and bleeding

Medication to prevent stress ulceration of
the stomach should be started on
admission in all patients who are
unconscious and require intensive care.
An H2- receptor antagonist or a proton
pump inhibitor should be administered
intravenously