Clinical features of organophosphate poisoning: A review of different classification systems and approaches

Abstract

Purpose:The typical toxidrome in organophosphate (OP) poisoning comprises of the Salivation, Lacrimation, Urination, Defecation, Gastric cramps, Emesis (SLUDGE) symptoms. However, several other manifestations are described. We review the spectrum of symptoms and signs in OP poisoning as well as the different approaches to clinical features in these patients.Materials and Methods:Articles were obtained by electronic search of PubMed® between 1966 and April 2014 using the search terms organophosphorus compounds or phosphoric acid esters AND poison or poisoning AND manifestations.Results:Of the 5026 articles on OP poisoning, 2584 articles pertained to human poisoning; 452 articles focusing on clinical manifestations in human OP poisoning were retrieved for detailed evaluation. In addition to the traditional approach of symptoms and signs of OP poisoning as peripheral (muscarinic, nicotinic) and central nervous system receptor stimulation, symptoms were alternatively approached using a time-based classification. In this, symptom onset was categorized as acute (within 24-h), delayed (24-h to 2-week) or late (beyond 2-week). Although most symptoms occur with minutes or hours following acute exposure, delayed onset symptoms occurring after a period of minimal or mild symptoms, may impact treatment and timing of the discharge following acute exposure. Symptoms and signs were also viewed as an organ specific as cardiovascular, respiratory or neurological manifestations. An organ specific approach enables focused management of individual organ dysfunction that may vary with different OP compounds.Conclusions:Different approaches to the symptoms and signs in OP poisoning may better our understanding of the underlying mechanism that in turn may assist with the management of acutely poisoned patients.

Application of hemoperfusion in severe acute organophosphorus pesticide poisoning

“…This decreases cholinesterase activity; results in the accumulation of a large amount of acetylcholine in the body; leads to overexpression of cholinesterase receptors in the autonomic nervous system, central nervous system, and synapses of the neuromuscular junction; and gives rise to a series of clinical symptoms. Furthermore, dyspnea can appear suddenly in patients, especially in cases of type II respiration failure, which is the main cause of death (11,12). Intermediate syndrome can appear during the recovery from cholinergic crisis for patients with moderate or severe AOPP (13).…”

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

“…Acute OP exposures that inhibit AChE enzyme activity by 80–90% precipitate cholinergic crisis via overstimulation of the nervous system leading to respiratory failure, flaccid paralysis, decreased blood pressure, parasympathetic discharge, and even death. For reviews on acute OP exposure (see Sullivan and Blose, 1992; Singh and Sharma, 2000; Peter et al, 2014). The effects of developmental, prolonged, and chronic exposures to OPs are less clear, however.…”

Sex-Specific Neurotoxic Effects of Organophosphate Pesticides Across the Life Course

“…This acute neurotoxicity is well characterized and is mediated by inhibition of acetylcholinesterase (AChE), the enzyme that inactivates the neurotransmitter acetylcholine after its release at the cholinergic synapse (see [18] for review). This results in massive accumulation of acetylcholine at the synaptic cleft, excessive stimulation, and subsequently widespread impairment of all the physiological functions controlled by the cholinergic system (e.g.…”