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General management
- history. Note history from patient may be unreliable and history should
also be obtained from friends
- consider toxicology in any comatose patient in whom history, examination and
biochemical analysis do not yield a diagnosis. Collect samples of gastric
content, serum, plasma (in lithium heparin and in fluoride) and urine, ideally
before administration of any drugs
- urea, creatinine, electrolytes, glucose, complete blood count, arterial
blood gas, serum osmolality
- in unconscious patients suspect brain damage if the history of poisoning is
unsatisfactory or if the depth of coma does not improve within 12 hrs
Clinical manifestations
- aetiology of poisoning can usually be narrowed to a few possibilities bases
on physical findings and a few simple tests
- mental status and vital signs provide the most useful information:
Excited
- CNS stimulation with increased vital signs
- sympathomimetics eg amphetamines, cocaine,
monoamine oxidase inhibitors, bronchodilators,
catecholamine analogues. Vital sign changes usually > mental changes
- anti-cholinergics eg antihistamines, tricyclics
(early, mild). Associated with hot dry flushed skin, decreased/absent bowel
sounds, urinary retention. Other causes of excited state usually associated with
pallor, sweating and increased bowel or bladder activity. Mydriasis most
pronounced in anti-cholinergic poisoning (although is a feature of all causes of
depressed picture). Associated with minimal response to light or accomodation
- hallucinogens eg LSD/tryptamine derivatives, marijuana, mescaline/amphetamine
derivatives, psilocybin mushrooms, phencyclidine. Mental sign changes > vital
sign changes
- withdrawal syndromes: beta blockers, clonidine, ethanol, tricyclics,
sedative-hypnotics
Depressed
- CNS depression with decreased vital signs
- sympatholytics eg alpha and beta blockers, ACE
inhibitors, calcium channel blockers, tricyclics
(late, severe), digoxin, neuroleptics.
Tend to cause marked CVS changes with normal respiration and relatively clear
sensorium
- cholinergics eg carbamate/organophosphate
insecticides, nicotine, physostigmine. Cause all degrees of physiological
depression but can usually be distinguished from other causes by presence of
SLUDGE: salivation, lacrimation, urination, defaecation, gastrointestinal cramps
and emesis. Skin pale and sweaty while in other causes of physiological
depression skin usually warm and dry
- opioids. CNS and respiratory depression with little CVS change. Similar
picture with sedative-hypnotics
- sedative-hynotics eg alcohol, barbiturates, benzodiazepines
Discordants
- some systems depressed while others stimulated
- asphyxiants eg cytochrome oxidase inhibitors, irritant gases,
methaemoglobinaemia, oxidative phosphorylation inhibitor herbicides
- increased anion gap metabolic acidosis eg alcohol, ethylene
glycol
- membrane active drugs eg anti-arrhythmics, tricyclics
(late, severe), lithium, neuroleptics,
quinine, heavy metals
- CNS syndromes: disulfiram, dystonic reactions, isoniazid, volatile substances
of abuse
Normal
- agents with slow absorption, slow distribution or active metabolites and
those that inhibit metabolism
- sometimes agents listed under excited or depressed categories may cause
discordance between mental and vital signs if they have activity that is
selective for a receptor subtype, results in a compensatory or opposing
autonomic response or is dose related eg hypotension may be accompanied by
tachycardia if due to alpha blocker, beta2 agonist or vasodilator
- degree of severity also gives clues to cause. In excited patient marked vital
signs
Investigations
- acid-base, anion gap
- serum osmolality
- ketones
- glucose
- electrolytes, urea, creatinine
- ECG
Treatment
Immediate measures
- airway. If necessary intubate patient, including those with marginally
adequate protective reflexes who require gastric lavage
- breathing. Assess ventilation and gas exchange. Look for evidence of gastric
aspiration, toxic gases or foreign substances
- circulation. IV access early. Assess peripheral circulation and begin
resuscitation if required. ECG and BP monitoring
- collect samples for toxicology
- document history from patient, relatives and ambulance staff
- examine thoroughly for associated injuries, medical conditions which may have
precipitated the overdose or which may produce coma
Measures to limit absorption
- usefulness of gastric lavage not clear
- indicated within 4 hrs of serious poisoning (ie patient comatose) with any of
the commonly ingested poisons. Should also be considered in any seriously
poisoned patient up to 12 hr after ingestion of poisons which delay gastric
emptying (eg tricyclics and aspirin)
Activated charcoal
- irreversibly binds drugs within bowel and by decreasing the diffusable
fraction within the bowel increases the gradient across the gut mucosa and thus
may increase excretion of drug. ? repeated administration effective in
reducing drug levels.
- of demonstrable benefit after poisoning with several commonly ingested drugs
including aspirin and paracetamol.
- absorptive capacity varies widely between different chemicals. Small, highly
ionized molecules of inorganic compounds (eg acids, alkalis, electrolytes, salts
of arsenic, cyanide, lithium and iron) not significantly absorbed
- recommended dose ³ 10 x weight of ingested
chemical or as much as possible if chemical dose is unknown. Maximum single dose
usually limited to 1-2 g/kg body weight due to volume constraints
- may be associated with serious pulmonary consequences if aspirated and may
cause GI obstruction, nausea, vomiting, abdominal cramps, diarrhoea and
constipation
- some preparations mixed with sorbitol as a cathartic
- equal or superior to ipecac followed by charcoal in awake overdose patients,
to gastric lavage and charcoal in obtunded patients, particularly those who
present >1h after OD and in awake patients with paracetamol OD
Measures to enhance elimination
- < 5% merit treatment with specific measures to increase elimination
- forced diuresis should only be considered for those patients in whom
toxicological analysis has demonstrated the presence in the blood of a toxic
agent in sufficient amount to cause severe poisoning
- brisk diuresis maintains a small concentration gradient between the renal
tubular fluid and the renal capillary bed, thus minimizing tubular reabsorption
of toxins
- manipulation of pH may further decrease tubular reabsorption of toxins by
ensuring that they remain mainly in the ionized form. Thus for weak acids (eg
salicylates and barbiturates) forced alkaline diuresis is most effective while
for weak bases (eg phencyclidine) forced acid diuresis more appropriate.
Ineffective fore drugs which are strongly protein bound (eg tricyclics) or which
have a large apparent volume of distribution (eg paracetamol, tricyclics)
- haemodialysis
- haemoperfusion
Supportive measures
Antidotes
© Charles Gomersall December 1999, June 2003
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