Abstract
Autonomic dysfunction after chronic low level exposure to organophosphorus (OP) pesticides has been consistently reported in the literature, but not following a single acute overdose. In order to study autonomic function after an acute OP overdose, sixty-six overdose patients were compared to 70 matched controls. Assessment of autonomic function was done by heart rate response to standing, deep breathing (HR-DB) and Valsalva manoeuvre; blood pressure (BP) response to standing and sustained hand grip; amplitude and latency of sympathetic skin response (SSR); pupil size and post-void urine volume. The patients were assessed one and six weeks after the exposure. The number of patients who showed abnormal autonomic function compared to standard cut-off values did not show statistically significantly difference from that of controls by Chi-Square test. When compared to the controls at one week the only significant differences consistent with autonomic dysfunction were change of diastolic BP 3 min after standing, HR-DB, SSR-Amplitude, SSR-Latency, post-void urine volume and size of the pupil. At 6 weeks significant recovery of autonomic function was observed and only HR-DB was decreased to a minor degree, −5 beats/min [95%CI 2–8]. This study provides good evidence for the lack of long term autonomic dysfunction following acute exposure to OP pesticides.
Highlights
Acute pesticide poisoning is a major health problem especially in developing countries
The current study did not reveal persistent autonomic dysfunction following acute single ingestion of OP compared to the matched controls
Autonomic function in farm workers has been looked in to, there were no studies that looked at autonomic function following acute OP exposure
Summary
Acute pesticide poisoning is a major health problem especially in developing countries. In Sri Lanka, the majority of poisoning cases are self inflicted [1]. Organophosphorus (OP) pesticides compounds were involved in 76% of pesticide poisoning [1,2]. OP leads to four well defined neurological syndromes, namely acute cholinergic crisis, intermediate syndrome, OP induced delayed polyneuropathy (OPIDN) and chronic OP induced neuropsychiatric disorders (COPIND) [3]. The acute cholinergic crisis reflects the acute inhibition of neuronal acetylcholine esterase (AChE). The mechanisms behind the other syndromes are less well defined
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