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To:
Journal of PRACTICAL NEUROLOGY Letters
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Case report does not report sufficient data to support a diagnosis of fatal organophosphorus poisoni
Triphasic effects of organophosphate poisoning, Is it an over simplification?
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Michael Eddleston, Doctor University of Oxford, Tissa Wijeratne, Lakshman Karalliedde, Mike Hurrell, Andrew Dawson
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eddlestonm{at}eureka.lk Michael Eddleston, et al.
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Dear Editor, We note the report of an unusual organophosphorus (OP) pesticide poisoning published in your journal [1]. However, from the data presented, we are not convinced that the patient’s death can be attributed to OP poisoning. Furthermore, we do not believe that this report can be used to expand the spectrum of syndromes seen following OP poisoning. There was no history of ingestion of an OP. In addition, no quantitative data was presented on the amount of thiometon that was detected in blood or urine, so it is not possible to decide whether it reflected environmental exposure or acute self-poisoning. No mention is made of the presence of pesticide solvents in the stomach. The butyrylcholinesterase (pseudo-cholinesterase) levels are not particularly low – even mildly symptomatic poisoning with chlorpyrifos, for example, results in values around zero. The mild reduction seen here could have resulted from a variety of non-toxicological acute illnesses [2]. The patient’s clinical features do not suggest OP poisoning [3]. The authors report that their “patient did not show the well defined neurological syndromes”, including the “acute cholinergic crisis”. However, later in the discussion, they write that “Another clue for organophosphate intoxication of the patient was typical reversible cholinergic signs with atropine administration such as improving bradycardia.” The normal blood pressure and a heart rate of 62 in a 31-yr-old man means little – heart rates can be low, normal, or high in significant OP poisoning [3]. The only muscarinic features reported are tracheal secretion and miosis, with no mention of other common signs such as bronchospasm, bronchorrhoea, incontinence, and sweating [3[. The raised temperature on admission is unexpected – hypothermia is usual. Clinical features of acute OP poisoning are not focal, typically involving widespread involvement of autonomic ganglia, CNS and neuromuscular junction [3]. This patient had a focal feature (deviation of the left eye) that is consistent with a brain stem lesion seen on MRI. Bilateral positive Babinski signs and increased deep tendon reflexes are uncommon in OP poisoning [3]. Only T2 MRI imaging sequences are reported. The wedge-shaped T2 hyperintensities in the cerebellar grey and white matter are more suggestive of a stroke than poisoning. Further information could be gained from reporting other MRI sequences or the results of a CT head. Other diagnoses need to be excluded before a diagnosis of OP poisoning with atypical neurology can be accepted. An allergy history is important since people with bee allergy can have severe reactions to Royal Bee Jelly [4]. The raised temperature and white cell count, and focal neurological signs are consistent with infective or inflammatory processes in the CNS. The T2 hyperintensity in the central midbrain /pontine region is compatible with infarction, pontine myelinolysis, or haemorrhage. Fundamentally, it is difficult to exclude any of these pathologies without the results of a post-mortem. We agree with Teke et al that OP pesticide poisoning is a major problem in rural areas of the developing world. However, in few places is it responsible for “nearly half” of acute poisoning admissions.5 The case fatality also varies widely,5 being dependent on the locally common OPs, the level of ICU facilities available for treatment, and the number of patients who survive to hospital admission. It is not possible to report a case fatality that is accurate for all parts of the world where OP pesticide poisoning is a problem. References (1). 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 Psych 2004;75:936-7. (2). Karalliedde L, Edwards P, Marrs TC. Variables influencing the toxic response to organophosphates in humans. Food Chem Toxicol 2003;41:1- 13. (3). Ballantyne B, Marrs TC. Overview of the biological and clinical aspects of organophosphates and carbamates. In: Clinical and experimental toxicology of organophosphates and carbamates, 0 edn. Oxford, Butterworth heinemann, 1992:3-14. (4). Thien FC. Asthma and anaphylaxis induced by royal jelly. Clin Exp Allergy 1996;26:216-22. (5). Eddleston M. Patterns and problems of deliberate self-poisoning in the developing world. Q J Med 2000;93:715-31. |
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Tissa Wijeratne, Senior Registrar in Neurology Department of Neurology, Christchurch Hospital, Christchurch,New Zealand
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tissa{at}ausdoctors.net Tissa Wijeratne
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Dear Editor We read with interest the letter by Teke et al,[1] which described a case of organophosphate (OP) poisoning with atypical features and also the magnetic resonance imaging (MRI) findings. The number of acute pesticide poisoning is estimated at three million a year world wide, resulting in over 200,000 deaths.[2,3] In a survey of deaths due to acute poisoning in the District of Kandy , Sri Lanka from 1967 to 1987 , the agent in 77% of the instance was a pesticide mainly OP.[4] Teke et al. described the triphasic effects of OP poisoning in humans as acute cholinergic crisis, intermediate syndrome and delayed polyneuropathy.[1] This is probably an over simplification of the neurological effects of OP poisoning. Cranial nerve palsies in intermediate syndrome were well described by Senanayake and Karalliadde in their original paper (8 patients among the original description of their ten patients with intermediate syndrome) and all of these patients had flexor plantar response.[5] Three patients were described with bilateral recurrent laryngeal palsies after successful treatment of OP poisoning.[6] The OP insecticide which caused poisoning in these patients is known to cause delayed neurological effects .It is postulated that the mechanism of recurrent laryngeal palsy is same as organophosphate induced delayed polyneuropathy. Case reports of opsoclonus, cerebellar ataxia, atypical ocular bobbing, and choreo –athetosis, extra pyramidal manifestation has been described secondary to OP poisoning.[7-12] 95% of the OP poisoning occurs in the developing world [3] where MRI is not available in majority of the centres. References 1.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;75:936-939 2.World Health Organization. Public health impact of pesticide use in agriculture.Geneva;WHO,1990 3.Jeyaratnam J. Pesticide poisoning : major global health problem. World Health Statistics Quarterly 1990;43:139-144 4.Senanayake N, Peiris H. Mortality due to poisoning in a developing agricultural country; trends over 20 years. Human and Experimental Toxicology 1995,14:808-811 5. Senanayake N, Karalliadde L. Neurotoxic effects of oraganophosphorus insecticide: an intermediate syndrome. N Engl J Med 1987;316:761-3 6.de Silva HJ, Sanmuganathan PS, Senanayake N. Isolated bilateral recurrent laryngeal paralysis : a delayed complication of organophosphorus poisoning . Human and Experimental Toxicology 1994;13:171-173 7.Pullicina P, Aquillana J.Opsoclonus in organophosphate poisoning . Archives of Neurology 1989;46:704-705 8.Michotte A, Van Dijck l,Maes V, D’Haenen H. Ataxia as the only delayed neurotoxic manifestation of organophosphate poisoning. European Neurology 1989;29:23-26 9.Hata S, Bernstein E, Davis L. Atypical ocular bobbing in acute organophosphorus poisoning. Archives of Neurology 1986;43:185-186 10. Joubert J.,Joubert PH, van der Spuy M, van Graan E. Acute organophosphate poisoning presenting with choreo – athetosis. Clinical Toxicology 1984;22:187-191 11. Senanayake N, Sanmuganathan PS. Extrapyramidal manifestations complicating organophosphorus insecticide poisoning. Human and Experimental Toxicology 1995;14:600-604 12.Davis KL, Yesavage JA, Berger PA. Possible organophosphate induced parkinsonism. Journal of Nervous and Mental Disease 1978;166:222-225 |
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