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Poisoning

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Agents & syndromes
Elimination
Organ support
Severity

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

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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