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LATE NEUROLOGICAL SEQUELS AFTER ACUTE POISONING WITH DIMETHOATE

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Title: LATE NEUROLOGICAL SEQUELS AFTER ACUTE POISONING WITH DIMETHOATE


1
LATE NEUROLOGICAL SEQUELS AFTER ACUTE POISONING
WITH DIMETHOATE
  • Niko Bekarovski, B. Pavlovski, N.Popovski,
    I.Jurukov
  • Clinic of Toxicology and Urgent Internal Medicine
    Clinic Center - Skopje,
  • Republic of Macedonia

2
INTRODUCTION
  • There are large number of studies describing
    acute neurological effects after acute
    organophosphate poisoning, but there are only a
    limited number of studies describing the chronic
    neurological effects, after acute organophosphate
    poisoning.

3
AIM OF THE STUDY
  • Aim of this study is to show a case with late
    neurological sequels, develop one year after
    acute poisoning with organophosphate pesticide
    Dimethoate
  • ( Sistemin 40).

4
CASE REPORT
  • 63 year old male patient was admitted to the
    Clinic of Toxicology in Clinic Center Skopje,
    Republic of Macedonia, six hours after ingesting
    an unknown dose of the organophosphate Dimethoate
    in a suicide attempt. In the next few days
    developed bilateral hyporreflexia, positive
    Babinski, rigidity of all limbs, akinesia,
    tremor, that persisted even after total
    cardiopulmonary recovery (8th day) and
    normalization of plasma cholinesterase range
    (12th day).

5
  • Bradyphrenia, tremor and rigidity remained after
    two weeks of poisoning and therefore the
    diagnosis of Parkinsonism was suspected by
    neurologist, and treatment with Biperiden lactate
    (Akinetone) 2x5 mg. started I.V. After second
    injection, there was great improvement of all
    symptoms, especially on consciousness, mobility
    and speech. Four weeks latter, at 43rd day of
    poisoning, all signs disappeared and patient was
    discharge from the Clinic completely free of
    Parkinsonism. CT, EEG and EMG were normal.

6
  • One year later the patient was called to hospital
    and matched controls. We found a serious deficit
    in memory, decrease in vibrotactile sensitivity,
    as indicator for peripheral neuropathy, tremor
    and bilateral patellar hiporreflexia. EEG didn't
    show any pathological changes and EMG wasn't made
    because the patient didn't allow to make it.

7
DISCUSSION
  • Three large epidemiological studies have examined
    the chronic effects among patients poisoned by
    organophosphates. Savage et al studied 100
    patients, an average of nine years after
    poisoning. They found significant deficits among
    the cases on several cognitive tests of memory
    and abstraction but no differences on
    electroencephalography or neurological
    examination. Cases had worse reading ability than
    controls, and educational differences may have
    accounted for the results.

8
  • Rosenstock et al. and McConnell et al. studied 36
    men poisoned by organophosphates (mostly
    methamidaphos) who had been admitted two years
    earlier, as well as matched controls. They found
    several cognitive deficits in the poisoned
    subjects and a significant decrease in
    vibrotactile sensitivity, an indicator of
    peripheral neuropathy.

9
  • Finally, Steenland et al studied 128 men poisoned
    a mean of seven years earlier and 90 controls.
    Vibrotactile sensitivity and one cognitive test
    (sustained attention) were significantly worse in
    the poisoned men, and several tests showed
    deficits which increased with the severity of the
    poisoning. Nerve conduction tests and clinical
    neurological examination showed no differences

10
  • In summary, therefore, well-designed studies have
    shown chronic sub clinical damage to the central
    and peripheral nervous system among those
    previously poisoned by organophosphates. Studies
    of subjects with long-term low level exposures
    have been less consistent, but some have also
    shown sub clinical effects on the central and
    peripheral nervous system. Low response rates and
    possible selection biases have affected almost
    all studies but are unlikely to explain the
    observed effects indeed loss to follow up of
    more severely affected individuals may have
    caused some bias towards showing no effect

11
  • Differences between studies may be due to the
    different organophosphates. The observed
    peripheral effects are consistent with persistent
    delayed neuropathy induced by organophosphate.
    The mechanism by which chronic central nervous
    system effects might occur is unknown Duffy et
    al has observed persistent changes on
    electroencephalograms after high level exposure.

12
  • Clinical neurological examinations have given
    negative results in the subjects studied
    epidemiologically. The importance of the observed
    sub clinical effects on quality of life or day to
    day functioning may be minimal. The study
    subjects generally were not followed for long
    periods, and we do not know whether the observed
    sub clinical effects will diminish, persist, or
    get worse. This question is important in the
    light of the large number of people exposed and
    in the light of some case reports that suggest
    that more severe long term effects are possible.

13
CONCLUSSION
  • This case shown that all patients with acute
    organophosphate intoxication have to be
    monitoring few years after the poisoning,
    especially if there are any signs of neurological
    sequels during the acute phase.
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