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 Table of Contents  
Year : 2020  |  Volume : 7  |  Issue : 1  |  Page : 32-34

Nerve conduction study as a diagnostic tool in atypical presentation of accidental organophosphorus poisoning

1 Department of Physiology, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, India
2 Department of Anatomy, Government Medical College, Vidisha, Madhya Pradesh, India

Date of Submission17-Oct-2019
Date of Acceptance27-May-2020
Date of Web Publication18-Aug-2020

Correspondence Address:
Dr. Santosh L Wakode
Department of Physiology, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJAMR.IJAMR_125_19

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Poisoning with organophosphorus (OP) compounds is a worldwide phenomenon. However, atypical presentation of OP toxicity, particularly when there is a paucity of muscarinic manifestations, can be a diagnostic challenge. We report a patient with atypical symptoms where exposure to OP poison was not clearly determined. Motor nerve conduction studies done to rule out acute motor neuropathy revealed that a single supramaximal stimulus-evoked repetitive compound motor action potentials. As this finding is the earliest and most sensitive indicator of acetylcholine esterase inhibition, OP poisoning was suspected. Decreased plasma acetylcholinesterase levels confirmed the diagnosis. The patient recovered completely with treatment. Although the diagnostic hallmark of OP poisoning is a reduction in serum and red blood cell cholinesterase activity, clinicians should be alert to recognize evidence of neuromuscular transmission failure seen on nerve conduction study to diagnose atypical or concealed cases of OP poisoning.

Keywords: Acetylcholinesterase, action potential, atypical, nerve conduction, organophosphorus

How to cite this article:
Wakode SL, Wakode NS, Bose S. Nerve conduction study as a diagnostic tool in atypical presentation of accidental organophosphorus poisoning. Int J Adv Med Health Res 2020;7:32-4

How to cite this URL:
Wakode SL, Wakode NS, Bose S. Nerve conduction study as a diagnostic tool in atypical presentation of accidental organophosphorus poisoning. Int J Adv Med Health Res [serial online] 2020 [cited 2023 Apr 2];7:32-4. Available from: https://www.ijamhrjournal.org/text.asp?2020/7/1/32/292395

  Introduction Top

Organophosphorus (OP) compounds are widely used as insecticides in rural areas, and poisoning with OP compounds is a worldwide phenomenon. Toxicity due to OP compound may be intentional or accidental. Among agricultural workers in the less developed world, OP poisoning due to accidental exposure to agricultural pesticides is common.[1] OP toxicity includes irreversible inhibition of acetylcholine esterase leading to the accumulation of acetylcholine at cholinergic synapses. This accumulation leads to weakness and fasciculation of the muscles. Clinical manifestation of acute OP poisoning can be a muscarinic syndrome, nicotinic syndrome, central nervous system (CNS) syndrome or OP-induced delayed polyneuropathy. Nerve conduction study (NCS) can be used to evaluate and characterize neuromuscular transmission disorders seen in OP poisoning.[1],[2] Plasma cholinesterase or erythrocyte cholinesterase estimation is done to assess the severity of OP poisoning.[3]

Atypical presentations of OP toxicity, particularly when there is a paucity of muscarinic manifestations could be a diagnostic challenge. We report a patient with an atypical clinical presentation of accidental OP exposure from an unknown source to emphasize the diagnostic relevance of nerve conduction abnormality.

  Case Report Top

A 20-year-old male patient was presented to a private clinic with a history of two bouts of vomiting and one episode of loose stools during the previous night, followed by mild weakness since that morning. The previous evening, he had gone to a neighboring village for a religious festival celebration and partook in a community dinner. On his arrival in the clinic, general physical examination and vitals were stable, and hence he was treated for food poisoning with antiemetic, antacid, and oral rehydration salts solution. The following day, he returned to the clinic with a history of generalized weakness, which was more pronounced in the lower limbs during clinical examination with mild difficulty in walking. The Medical research council (MRC) muscle power grade was 4/5, proximally in the lower limbs. His complete blood counts and blood chemistry revealed mild hypokalemia (3.1 mmol/L) as the only abnormality. He was admitted to the hospital and was treated for hypokalemia with intravenous fluids and oral potassium. On the 3rd day, his weakness had progressed, and he developed marked difficulty in walking and getting up. On examination, the patient was conscious and oriented; his skin was moist; heart rate was 90 beats per minute, blood pressure was 120/80 mm Hg; and respiratory rate was 18/min. His MRC muscle power grade was 2/5 proximally, 3/5 distally in the lower limbs, and 3/5 for both proximal and distal muscles in the upper limbs. Plantar reflex was flexor, deep-tendon reflexes were absent, and there was no sensory loss. There was no cranial nerve palsy; pupils were normally reacting; urinary and bowel function were normal. The patient had areflexic symmetrical pure motor quadriparesis and normal electrolytes.

The differential diagnosis of such pure motor areflexic paralysis is potentially long encompassing myelopathies, polyneuropathies, neuromuscular junction transmission disorders such as myasthenia gravis, botulism, neurotoxic snake envenomation, and myopathies. Therefore, the patient's history was reviewed, and a detailed interview was done. It was revealed that on his way back to home, it started raining, and hence he took a shortcut through farmlands with standing crops. However, this additional revelation by the patient was not sufficient to either confirm or refute any of the diagnostic possibilities under consideration.

Because of the acute onset of progressive weakness without bladder involvement, Guillain–Barre syndrome was suspected, and a NCS was advised. Motor nerve conduction studies revealed that a single supramaximal stimulus-evoked repetitive compound motor action potentials (CMAP) [Figure 1].
Figure 1: Characteristic nerve conduction study findings showing single supramaximal electrical stimulus-induced repetitive response depicted by arrows. (a) Median nerve (b) Peroneal nerve, (c) Ulnar nerve

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Distal motor latency and conduction velocity were normal, as were sensory nerve conduction, f-waves, and H-reflex. Spontaneous firing of single evoked CMAP is the earliest and most sensitive indicator of acetylcholine esterase inhibition. Hence, a diagnostic possibility of OP poisoning was considered. A detailed history and questioning of parents and relatives did not suggest either suicidal or accidental exposure to OP compounds. All the other individuals who had food in the community dinner did not manifest any symptoms similar to that of the patient and were asymptomatic. To rule out endplate dysfunction, plasma acetylcholine esterase was estimated. A value of 604 units (normal value 5000–9000 units) was consistent with the diagnosis of OP poisoning. The patient was shifted to the intensive care unit and was treated as a case of OP poisoning with predominant nicotinic symptoms. Intravenous pralidoxime was used; atropine was not given as there were no obvious muscarinic symptoms. The patient was discharged after complete recovery.

  Discussion Top

The diagnosis of OP poisoning is primarily based on a history of exposure and characteristic signs of cholinergic overdose. However, a history of exposure may not be evident, as in the present case.[4] OP compounds are commonly used in agricultural products, including insecticides. They are rapidly absorbed by all routes of exposure, including dermal, respiratory, and gastrointestinal, and inhibit the enzyme acetylcholinesterase resulting in excess cholinergic stimulation at the neuromuscular junction and CNS.[3] In our patient, the exposure and absorption were probably through the skin or mucus membranes. He walked though the farms which had been recently sprayed with insecticides and thereby possibly exposed himself to OP compound. OP poisoning can result in cholinergic stimulation at nicotinic and muscarinic receptor sites. Muscarinic manifestation can be diarrhea, urination, miosis, bronchospasm, lacrimation, salivation, and emesis; a few patients may show signs of sympathetic stimulation.[5],[6] Nicotinic manifestation at the neuromuscular junction may result in fasciculations, muscle weakness, and occasional paralysis. Commonly described CNS manifestations include agitation, confusion, and coma. The patient described in this report had an atypical clinical presentation with a paucity of muscarinic symptoms.[5],[7] Rapidity of onset of symptoms in OP poisoning depends on the dose, route, and potency of the compound. It may vary from minutes in cases of massive ingestion to several days, if the agent is highly fat-soluble,[8] owing to its storage and slow release from the liver and fat.

In the present case, the early and most sensitive indicator of acetylcholine esterase inhibition was a single supramaximal stimulus-induced repetitive CMAPs demonstrated on NCS. The repetitive action of excess of acetylcholine at the motor endplate is responsible for this type of findings on NCS.[1] In nicotinic syndrome, there is a failure of transmission at the neuromuscular junction, and electrodiagnostic studies of neuromuscular transmission can be utilized to characterize and evaluate this disorder. Electrodiagnostic findings can be a single supramaximal stimulus-induced repetitive response, a decrement-increment response to high frequency (30 Hz) repetitive nerve stimulation (RNS), or a decremental response to high frequency (30 Hz) RNS.[1] The decrement-increment response represents a depolarization type of neuromuscular blockade.[9] Decremental response to high rate RNS represents the desensitization type of neuromuscular blockade,[10] and it correlates with the presence of the clinically recognizable intermediate syndrome. In addition to the demonstration of repetitive CMAP response to single supramaximal stimulation, the disappearance of this phenomenon to high-frequency RNS or exercise test can be seen in many symptomatic cases.[2] Therefore, these additional parameters should be included while performing NCS in suspected cases of OP poisoning. However, high-frequency RNS or exercise testing was not done in our patient in view of poor patient tolerance, and it is one of the limitations of our report.

Although the diagnostic hallmark of OP poisoning is a reduction in serum and red blood cell cholinesterase activity (50% or greater decrease in the activity below normal values), clinicians must be aware of the utility of NCS in diagnosing OP poisoning.[9],[11] The timing of NCS and proper interpretation of findings can be very useful in the diagnosis of atypical, accidental, or concealed cases of OP poisoning, and clinicians should be alert to detect evidence of neuromuscular transmission failure on NCS findings, which could be of medicolegal importance as well.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Singh G, Khurana D. Neurology of acute organophosphate poisoning. Neurol India 2009;57:119-25.  Back to cited text no. 1
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Singh G, Khurana D, Avasthi G, Mahajan R, Soni RK. The spectrum and clinical correlates of electrodiagnostic abnormalities in acute organophosphorus poisoning: A study of 55 patients. Neurol India 1998;46:28-35.  Back to cited text no. 2
van Heel W, Hachimi-Idrissi S. Accidental organophosphate insecticide intoxication in children: A reminder. Int J Emerg Med 2011;4:32.  Back to cited text no. 3
Kaur I, Jayashree K, Hiranandani M, Singhi SC. Severe organophosphate poisoning in a neonate. Indian Pediatr 1996;33:517-9.  Back to cited text no. 4
Teke E, Sungurtekin H, Sahiner T, Atalay H, Gur S. Organophosphate poisoning case with atypical clinical survey and magnetic resonance imaging findings. J Neurol Neurosurg Psychiatry 2004;75:936-7.  Back to cited text no. 5
Ghosh S. Atypical manifestations of organophosphorus poisoning following subcutaneous injection of Dichlorvos with suicidal intention. Indian J Crit Care Med 2014;18:244-6.  Back to cited text no. 6
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Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.  Back to cited text no. 7
Davies JE, Barquet A, Freed VH, Haque R, Morgade C, Sonneborn RE, et al. Human pesticide poisonings by a fat-soluble organophosphate insecticide. Arch Environ Health 1975;30:608-13.  Back to cited text no. 8
Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome. N Engl J Med 1987;316:761-3.  Back to cited text no. 9
Maselli RA, Leung C. Analysis of anticholinesterase-induced neuromuscular transmission failure. Muscle Nerve 1993;16:548-53.  Back to cited text no. 10
Karami-Mohajeri S, Nikfar S, Abdollahi M. A systematic review on the nerve-muscle electrophysiology in human organophosphorus pesticide exposure. Hum Exp Toxicol 2014;33:92-102.  Back to cited text no. 11


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