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    Poisoning: Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition)

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    lia lykim
    Organophosphate poisoning is a major public health issue worldwide, resulting in 200,000 deaths each year mostly from ingestion with suicidal intent. The acute toxicity of organophosphates is due to the inhibition of the enzyme acetylcholinesterase, resulting in accumulation of acetylcholine at nerve endings and neuromuscular junctions. Clinical features of acute exposure range from mild symptoms like headache to severe poisoning causing coma, respiratory failure, and hypotension. Treatment involves maintaining a clear airway, giving atropine until atropinization is achieved, and administering pralidoxime within 4 hours to reactivate acetylcholinesterase before enzyme inactivation occurs.

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    Poisoning: Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition)

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    lia lykim
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    Organophosphate poisoning is a major public health issue worldwide, resulting in 200,000 deaths each year mostly from ingestion with suicidal intent. The acute toxicity of organophosphates is due to the inhibition of the enzyme acetylcholinesterase, resulting in accumulation of acetylcholine at nerve endings and neuromuscular junctions. Clinical features of acute exposure range from mild symptoms like headache to severe poisoning causing coma, respiratory failure, and hypotension. Treatment involves maintaining a clear airway, giving atropine until atropinization is achieved, and administering pralidoxime within 4 hours to reactivate acetylcholinesterase before enzyme inactivation occurs.

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    Poisoning

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    Organophosphate poisoning is a major public health issue worldwide, resulting in 200,000 deaths each year mostly from ingestion with suicidal intent. The acute toxicity of organophosphates is due to the inhibition of the enzyme acetylcholinesterase, resulting in accumulation of acetylcholine at nerve endings and neuromuscular junctions. Clinical features of acute exposure range from mild symptoms like headache to severe poisoning causing coma, respiratory failure, and hypotension. Treatment involves maintaining a clear airway, giving atropine until atropinization is achieved, and administering pralidoxime within 4 hours to reactivate acetylcholinesterase before enzyme inactivation occurs.

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    48 views2 pages

    Poisoning: Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition)

    Uploaded by

    lia lykim
    Organophosphate poisoning is a major public health issue worldwide, resulting in 200,000 deaths each year mostly from ingestion with suicidal intent. The acute toxicity of organophosphates is due to the inhibition of the enzyme acetylcholinesterase, resulting in accumulation of acetylcholine at nerve endings and neuromuscular junctions. Clinical features of acute exposure range from mild symptoms like headache to severe poisoning causing coma, respiratory failure, and hypotension. Treatment involves maintaining a clear airway, giving atropine until atropinization is achieved, and administering pralidoxime within 4 hours to reactivate acetylcholinesterase before enzyme inactivation occurs.

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    Poisoning

    James W. Dear, in Clinical Biochemistry: Metabolic and Clinical


    Aspects (Third Edition), 2014
    Organophosphates
    Organophosphate poisoning is a major public health issue worldwide
    resulting in 200 000 deaths each year. Most of these occur through
    ingestion with suicidal intent. In developed countries, however, the
    number of poisonings is low and deaths are very rare. The most
    serious poisoning occurs by ingestion; cutaneous absorption and
    inhalation of sprays rarely cause serious toxicity.
    Toxicity
    The acute toxicity of these compounds is due to the inhibition of the
    enzyme acetylcholinesterase by phosphorylation, resulting in an
    accumulation of acetylcholine at postganglionic parasympathetic
    nerve endings (muscarinic receptors), parasympathetic ganglia
    (nicotinic receptors) and neuromuscular junctions (nicotinic receptors).
    All the organophosphates inhibit both red cell acetylcholinesterase
    and plasma cholinesterase (pseudocholinesterase) and this provides
    the basis for biological monitoring of toxicity (red cell measurements
    being preferred for acute toxicity). For monitoring of occupational
    exposure, regular measurement of plasma cholinesterase activity
    should be carried out: a reduction of the pre-employment value by
    30% indicates excessive exposure and the worker should be removed
    from exposure pending recovery of enzyme activity.
    Phosphorylated acetylcholinesterase is relatively stable, which means
    that the features of poisoning may persist longer than the presence of
    the organophosphate in the bloodstream. Spontaneous reactivation of
    the enzyme depends mainly on the chemical structure of the
    organophosphate. Exposure to compounds such as
    dimethylphosphates and dimethylphosphorothioates leads to
    dealkylation of the enzyme (a process referred to as ‘ageing’), which
    makes the enzyme inaccessible to reactivation, either spontaneously
    or by administration of reactivating agents such as pralidoxime. In
    poisoning by carbamates, the affected acetylcholinesterase
    undergoes rapid spontaneous reactivation.
    Clinical features and management
    Early symptoms of acute exposure to organophosphates are non-
    specific but lead on to more characteristic features. In mild-to-
    moderate poisoning there may be headache, blurred vision, miosis,
    excessive salivation, lacrimation, sweating, wheezing and lethargy.
    The patient should be kept under observation for at least 24 h. Severe
    poisoning may cause coma, convulsions, respiratory muscle paralysis,
    bradycardia and hypotension.
    The first step is to maintain a clear airway and ensure adequate
    ventilation, after which atropine should be given until atropinization is
    achieved, that is, the heart rate is > 80/min, secretions are inhibited or
    pupils are enlarged.
    Pralidoxime (a specific cholinesterase reactivator) should ideally be
    started within 4 h of exposure. In patients who present late to hospital,
    enzyme inactivation becomes less reversible and pralidoxime is
    unlikely to have any effect if given after 24–36 h.
    The patient may relapse after apparent recovery, as a result of an
    acute myopathy that is distinct from the acute toxicity or the delayed
    neuropathy that may occur after several weeks. This has been called
    the ‘intermediate syndrome’.

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