Most patients with self-poisoning

require only general care

and support of the vital systems

PRINCIPLES OF MANAGEMENT

. 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 poison-induced 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 Positive-Pressure 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 < 35°C

Covered with a 'space blanket' and, if

Given intravenous and intragastric fluids at normal body temperature.

Inspired gases warmed to 37°C• 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