Poisons Assessment ASSESSMENT
Common clusters of features that may be diagnostic Feature cluster
C
Coma, hypertonia, hyper-reflexia, extensor plantar responses, myoclonus, strabismus, mydriasis, sinus tachycardia
C
Coma, hypotonia, hyporeflexia, plantar responses flexor or non-elicitable, hypotension
C C Coma, miosis, reduced respiratory rate
Nausea, vomiting, tinnitus, deafness, sweating, hyperventilation, vasodilatation, metabolic acidosis
C
Restlessness, agitation, mydriasis, anxiety, tremor, tachycardia, convulsions, arrhythmias
Hyperthermia, tachycardia, delirium, agitation, mydriasis Blindness (usually with other features) C Miosis, hypersalivation, bronchorrhoea
C C Table 2
irreversible brain damage and the patient recovers fully. Acute dystonic movements (including acute torticollis, orolingual dyskinesias and oculogyric crises) also occur following exposure to metoclopramide10 or, less commonly, haloperidol, droperidol, prochlorperazine or trifluoperazine. Choreoathetosis has been reported as a rare presenting feature of poisoning with organo- phosphorus insecticides.11,12
Pupillary changes in poisoning
Inequality of the pupils is often found in poisoned patients. Widely dilated pupils that react poorly to light may be caused by poisons with anticholinergic actions (e.g. tricyclic antidepres- sants) or sympathomimetic effects (e.g. amfetamines), or which cause blindness (e.g. quinine, methanol). Miosis is usually caused by opioid analgesics or poisons with cholinergic or anti- cholinesterase actions (e.g. organophosphorus insecticides, nerve agents). The degree and speed of reaction of the pupils to light is of no clinical value.
Ocular movements
Strabismus, internuclear ophthalmoplegia and total external ophthalmoplegia have been described in acute poisoning, with impairment of consciousness caused by various drugs that act on the brain.13 Transient and variable strabismus (usually with the optic axes divergent in the horizontal plane) have been attributed to phenytoin, carbamazepine and tricyclic antidepressants. Dys- conjugate, roving eye movements may also be seen if both eyes are observed for a period of time, and occasionally there may be total external ophthalmoplegia, even in patients in whom consciousness is no more than minimally impaired. Dysconjugate eye movements may become apparent only
when the oculovestibular reflexes are examined using caloric stimuli, and have been reported in poisoning with tricyclic antidepressants, phenothiazines, benzodiazepines, barbiturates and ethanol. Instillation of ice-cold water into an ear should make both eyes turn to the irrigated side; failure of one eye to deviate suggests internuclear ophthalmoplegia and disturbed function of the medial longitudinal fasciculus.
MEDICINE 40:2 42 Africa Health 50 Loss of oculocephalic and oculovestibular reflexes
Loss of these reflexes is usually regarded as evidence of severe brain stem damage and brain death. In acute poisoning, however, such a conclusion is not justified. Overdose with car- bamazepine, phenytoin and tricyclic antidepressants can be associated with loss of these reflexes, but patients recover completely.
Visual impairment
Visual impairment is associated most commonly with quinine14,15 and methanol16 poisoning.
Trial of antidotes Naloxone
Administration of intravenous naloxone has been used to make a rapid clinical diagnosis of opioid poisoning; this approach depends on noticeable improvement in the patient’s clinical condition within 1e2 minutes. Naloxone has a low incidence of adverse reactions and its use is, therefore, justified particularly in those whose clinical presentation suggests inadequate ventilation caused by an opiate. In severe poisoning, an adequate dose of naloxone must be given to reverse toxicity to a clinically detectable extent; this is typically at least 1.2 mg of naloxone initially, followed by 2 mg if the response is only partial. If necessary, a naloxone infusion should be commenced.
Flumazenil Although flumazenil will reverse the respiratory and CNS depressant actions of a benzodiazepine, caution should be exercised in patients who have co-ingested a tricyclic antide- pressant and in those known to be epileptic, because seizures and arrythmias could be precipitated by its use.
Toxicological investigations
Measurement of the concentration of a specific poison in the blood, or toxicological screening of blood or urine, can be used to establish a diagnosis of poisoning.
2011 Published by Elsevier Ltd. July 2012
Likely poisons
Tricyclic antidepressants, antihistamines less commonly, orphenadrine
Barbiturates, benzodiazepines and alcohol combinations. Severe tricyclic antidepressant poisoning Opioid analgesics Salicylates
Sympathomimetics
Ecstasy (MDMA), amfetamines, cocaine Quinine, methanol
Organophosphorus and carbamate insecticides, nerve agents
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