Organophosphate Toxicity Clinical Presentation
- Author: Kenneth D Katz, MD, FAAEM, ABMT; Chief Editor: Asim Tarabar, MD more...
Signs and symptoms of organophosphate poisoning can be divided into three broad categories: (1) muscarinic effects, (2) nicotinic effects, and (3) central nervous system (CNS) effects.
Mnemonic devices used to remember the muscarinic effects of organophosphates are SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset, emesis) and DUMBELS (diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; excess lacrimation; and salivation). Muscarinic effects by organ system include the following:
Cardiovascular - Bradycardia, hypotension
Respiratory - Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress
Gastrointestinal - Hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence
Genitourinary - Incontinence
Ocular - Blurred vision, miosis
Glands - Increased lacrimation, diaphoresis
Nicotinic signs and symptoms include muscle fasciculations, cramping, weakness, and diaphragmatic failure. Autonomic nicotinic effects include hypertension, tachycardia, mydriasis, and pallor.
CNS effects include the following:
Clinical presentation may vary, depending on the specific agent, exposure route, and amount. Symptoms are due to both muscarinic and nicotinic effects. Interestingly, a review of 31 children with organophosphate (OP) poisoning described that, in contrast to adults, the most common presentations were seizure and coma with relatively less muscarinic or nicotinic findings. The authors hypothesized the difference may be due to difficulty in detecting muscarinic findings in infants (eg, crying) and ingestion of contaminated produce instead of organophosphate directly.
Depressed respirations, bradycardia, and hypotension are possible findings. Alternatively, tachypnea, hypertension, and tachycardia are possible. Hypoxia should be monitored for with continuous pulse oximetry.
Three types of paralysis may result from organophosphate poisoning. Type I is described as acute paralysis secondary to continued depolarization at the neuromuscular junction.
Type II (intermediate syndrome) was first described in 1974 and is reported to develop 24-96 hours after resolution of acute organophosphate poisoning symptoms and to manifest commonly as paralysis and respiratory distress. This syndrome involves weakness of proximal muscle groups, neck, and trunk, with relative sparing of distal muscle groups. Cranial nerve palsies can also be observed.
Intermediate syndrome persists for 4-18 days, may require mechanical ventilation, and may be complicated by infections or cardiac arrhythmias. Although neuromuscular transmission defect and toxin-induced muscular instability were once thought to play a role, this syndrome may be due to suboptimal treatment.
Type III paralysis, or organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks after exposure to large doses of certain organophosphates and is due to inhibition of neuropathy target esterase. Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, and proximal muscle groups characterizes OPIDP. Recovery can take up to 12 months.[12, 11]
Other neurologic and neuropsychiatric effects
Neuropsychiatric effects of organophosphate poisoning include the following:
Chronic organophosphate-induced neuropsychiatric disorders
Extrapyramidal effects are characterized by dystonia, cogwheel rigidity, and parkinsonian features (basal ganglia impairment after recovery from acute toxicity). Other possible neurologic and/or psychological effects include Guillain-Barré–like syndrome and isolated bilateral recurrent laryngeal nerve palsy.
Organophosphate toxicity may affect other organ systems as follows:
Ophthalmic: Optic neuropathy, retinal degeneration, defective vertical smooth pursuit, myopia, and miosis (due to direct ocular exposure to organophosphates)
Ears: Ototoxicity is possible
Respiratory: Muscarinic, nicotinic, and central effects contribute to respiratory distress in acute and delayed organophosphate toxicity
Muscarinic effects: Bronchorrhea, bronchospasm, and laryngeal spasm, for instance, can lead to airway compromise; respiratory failure is the most life-threatening effect and requires immediate intervention
Nicotinic effects: These effects lead to weakness and paralysis of respiratory oropharyngeal muscles
Central effects: These effects can lead to respiratory paralysis
Cardiac rhythm abnormalities: Sinus tachycardia, sinus bradycardia, extrasystoles, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation (often a result of, or complicated by, severe hypoxia from respiratory distress) are possible
Other cardiovascular effects: Hypotension, hypertension, and noncardiogenic pulmonary edema are possible
Gastrointestinal manifestations: Nausea, vomiting, diarrhea, and abdominal pain may be some of the first symptoms to occur after organophosphate exposure
Genitourinary and/or endocrine effects: Urinary incontinence, hypoglycemia, or hyperglycemia is possible
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