Organophosphorus Intoxication

Khurana, Dheraj; Prabhakar, S.

doi:10.1001/archneur.57.4.600

Cited by 28 publications

(20 citation statements)

References 6 publications

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“…Sadly however, given the prevailing scenario at the time, World War II, Schrader's work was mainly oriented toward the synthesis of chemical warfare agents. [2,3] However, after the war, the pharmacological properties of these agents were published leading to the realization of their potential use as insecticides and pesticides. This eventually led to the development of many more new OP compounds and their main use as insecticides and pesticides worldwide.…”

Section: Historical Aspectsmentioning

confidence: 99%

“…[23] Extrapolating these results to human beings, the WHO-recommended dose of pralidoxime is 30 mg/kg bolus followed by 8 mg/kg/ hour infusion. [19] The other limiting aspect of these studies were: (1) the randomization and masking techniques were not adequately described in both the studies [33,34] and (2) in the latter study the intervention arm included patients with more severe poisoning which could explain the increased frequency of intermediate syndrome, ventilator requirement, and mortality in the intervention arm. [36] Discrepancies between the robust rationale for the use of oximes and the failure to demonstrate their efÞ cacy in clinical trials can be understood if the limitations of oxime action are appreciated.…”

Section: Role Of Cholinesterase Reactivationmentioning

confidence: 99%

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Neurology of acute organophosphate poisoning

2009

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Acute organophosphate (OP) poisoning is one of the most common poisonings in emergency medicine and toxicological practice in some of the less-developed nations in South Asia. Traditionally, OP poisoning comes under the domain of emergency physicians, internists, intensivists, and toxicologists. However, some of the complications following OP poisoning are neurological and involve neurologists. The pathophysiological basis for the clinical manifestations of OP poisoning is inactivation of the enzyme, acetylcholinesterase at the peripheral nicotinic and muscarinic and central nervous system (CNS) nerve terminals and junctions. Nicotinic manifestations occur in severe cases and late in the course; these comprise of fasciculations and neuromuscular paralysis. There is a good correlation between the electrophysiological abnormalities and the severity of the clinical manifestations. Neurophysiological abnormalities characteristic of nicotinic junctions (mainly neuromuscular junction) dysfunction include: (1) single, supramaximal electrical-stimulus-induced repetitive response/s, (2) decrement-increment response to high frequency (30 Hz) repetitive nerve stimulation (RNS), and (3) decremental response to high frequency (30 Hz) RNS. Atropine ameliorates muscarinic manifestations. Therapeutic agents that can ameliorate nicotinic manifestations, mainly neuromuscular, are oximes. However, the evidence for this effect is inconclusive. This may be due to the fact that there are several factors that determine the therapeutic effect of oximes. These factors include: The OP compound responsible for poisoning, duration of poisoning, severity of poisoning, and route of exposure. There is also a need to study the effect of oximes on the neurophysiological abnormalities.

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Section: Historical Aspectsmentioning

confidence: 99%

Section: Role Of Cholinesterase Reactivationmentioning

confidence: 99%

Neurology of acute organophosphate poisoning

2009

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“…For this reason Khurana and Prabhakar 13 suggested that this syndrome, although known as organophosphate-induced delayed polyneuropathy, is inappropriately labeled because pyramidal involvement is usually present; initially, peripheral nerve involvement predominates, while corticospinal tract signs evolve more slowly. Our patient showed hyperreflexia of the upper limbs, with signs of pyramidal tract involvement.…”

Section: Type 2 Syndrome (Intermediate Syndrome)mentioning

confidence: 99%

Organophosphate-induced delayed neuropathy: case report

Vasconcellos

Leite

Nascimento

2002

Arq. Neuro-Psiquiatr.

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-Organophosphate induced delayed neuropathy (OPIDN) is an uncommon clinical condition. It occurs in association with the ingestion of great amounts of organophosphate after the stimulation of cholinergic receptor. The clinical picture is characterized by a distal paresis in lower limbs associated with sensitive symptoms. Electrodiagnostic studies show a motor axonal neuropathy. Involvement of the central nervous system may occur. We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a Dichlorvos-based insecticide. Electrophysiological study was characterized by an axonal polyneuropathy pattern. Pyramidal tract dysfunction was observed later in upper limbs. Considering that both peripheral and central nervous systems are involved we believe that the more appropriated term would be organophosphate induced delayed neuropathy (OPIDN) instead of organophosphate induced delayed polyneuropathy (OPIDP).KEY WORDS: neuropathy, polyneuropathy, organophosphate. Neuropatia tardia por organofosforado: relato de casoRESUMO -A neuropatia tardia dos organofosforados (NTOF) é condição clinica incomum. Geralmente ocorre após a intoxicação aguda por organofosforados, seguindo-se a fase de hiperestimulação colinérgica. O quadro clínico é caracterizado por déficit motor distal nos membros inferiores associado a sintomas sensitivos. O estudo eletroneuromiográfico tem demonstrado padrão axonal motor na maioria dos casos. Podem ocorrer sinais de comprometimento do sistema nervoso central. Descrevemos o caso de uma paciente de 39 anos que ingeriu inseticida a base de Dichlorvos e quatorze dias após apresentou quadro de hiperestesia associado a paresia distal nos membros inferiores. Realizou eletroneuromiografia que se caracterizou por padrão compatível com polineuropatia axonal. Sinais piramidais, de aparecimento mais tardio, foram observados nos membros superiores. Diante do comprometimento do sistema nervoso periférico e central, também consideramos o termo neuropatia tardia por organofosforado (NTOF) mais adequado do que tão somente polineuropatia tardia por organofosforado (PTOF).

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“…Copious secretions may also occur in patients with bronchiectasis (usually purulent), endobronchial tuberculosis, and malignancies, especially in cases of bronchoalveolar carcinoma [1,2,3,4,5,6]. Intoxications of organophosphate, carbamate, and cyanide may also induce bronchorrhea [7,8,9]. …”

Section: Introductionmentioning

confidence: 99%

Bronchorrhea following Stroke

Sung¹,

Lee²,

Chu³

2011

Eur Neurol

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Background: Stroke-induced excessive bronchial secretion is not rare, but seldom discussed. This study emphasizes its recognition, pathophysiology and treatment. Methods: We prospectively collected data from 19 consecutive stroke patients with bronchorrhea who were admitted within 2 days of stroke onset. Results: Sixteen of them (84%) suffered from ischemic stroke, and 3 patients (16%) had hemorrhage. All of them had brainstem involvement, and 11 of them (58%) had localized lesions in the dorsal lateral medulla. In 15 patients (79%), copious secretion developed within 3 days after stroke onset. The frequency of expectoration was variable with fluctuation, and half of the patients (47%) had to spit every 2–5 min during its climax. The duration of increased secretion ranged from 4 days to over 2 months. Half of the patients (53%) received anticholinergic treatment, and the response was fair to good. Conclusions: Our data provide clinical evidence that stroke patients with dorsal medulla involvement might present with bronchorrhea which seemed to be mediated via a parasympathetic mechanism. This is a treatable disease, and early diagnosis and treatment may greatly reduce patients’ suffering, avoid antibiotics abuse, reduce the incidence of aspiration pneumonia, and shorten the length of hospitalization.

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Organophosphorus Intoxication

Cited by 28 publications

References 6 publications

Neurology of acute organophosphate poisoning

Neurology of acute organophosphate poisoning

Organophosphate-induced delayed neuropathy: case report

Bronchorrhea following Stroke

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