Temporal Profile of Central and Peripheral Neuromuscular features of acute Organophosphorus poisoning: A Prospective Observational Clinical Study

Nirmal Raj, Francis (2015) Temporal Profile of Central and Peripheral Neuromuscular features of acute Organophosphorus poisoning: A Prospective Observational Clinical Study. Masters thesis, Christian Medical College, Vellore.


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INTRODUCTION: Deliberate self-harm is one of the most common problems we encounter in our community. Poisoning is one of the common methods of deliberate self-harm in the world. Poisoning by organophosphorus compound consumption is common among developing countries such as India and Srilanka. Organophosphorus poisoning can occur by deliberate ingestion or accidental exposure to skin or by ingestion. Morbidity and mortality associated with organophosphorus poisoning is due to development of intermediate syndrome which develops 3 days after the consumption. But currently there are no effective ways of predicting the development of intermediate syndrome in patients who present with organophosphorus poisoning. Predicting the most common complication of organophosphorus poisoning can help in managing the patient better with accurate triaging of patients to the ICU or to ward. Organophosphorus induced Encephalopathy has been described in patients with organophosphorus poisoning, both as an early as well as delayed manifestation. But the relationship between the central encephalopathic manifestations and peripheral neuromuscular manifestations have not been studied in detail. In our study we propose to develop a clinical scoring tool to predict the development of intermediate syndrome in patients who present with organophosphorus poisoning and describe the temporal profile of central and peripheral neurological manifestations of organophosphorus poisoning. OBJECTIVES: 1. To assess the utility of a clinical scoring system at admission to predict the development of Intermediate syndrome in patients with acute Organophosphorus poisoning. 2. To describe and correlate the central (encephalopathic) and peripheral neuromuscular features (Type 1 and Type II [Intermediate syndrome]) and their temporal profile in acute Organophosphorus poisoning. MATERIALS AND METHODS: Type of study: This is an observational study conducted between November 2013 to August 2014. Sample Size: The sample size calculation is based on previous studies done on Intermediate Syndrome and organophosphorus poisoning. The incidence of Intermediate syndrome in Organophosphorus poisoning is 37 % based on the study done by Dr. Lovely et.al in our institution in 2010. With an anticipated odd’s ratio of 4 and the study is powered to detect 80% difference and 5 % level of significance the sample was calculated to be 169. Proportion of the disease : 0.375, Anticipated odd’s ratio : 4, Power of the study(1-beta)% : 80, Alpha Error : 5, Multiple correlation coefficient : 0.41, Sample size : 169. Since the study involves detailed clinical examination with daily neurological examinations and electrophysiological studies, it was decided to keep a feasible sample size of 80 in this study. METHODS: The study participants were enrolled from the accident and emergency department, Christian Medical college who satisfied the following inclusion criteria. Inclusion criteria: 1. Age above 15 years. 2. Patients with history of consumption of organophosphorous pesticide poisoning. 3. Patients presenting within 72 hours after consumption of organophosphorous compound. Case Ascertainment: 1. Patients who present with alleged history of organophosphorous poisoning with an identified compound. 2. Patients who present with alleged history of organophosphorous poisoning with typical toxidrome, and low butylcholinesterase levels. 3. Patients who present without an alleged history of poisoning but with typical toxidrome of OP poisoning and low butylcholinesterase levels. CONCLUSION: 1. The Incidence of Intermediate syndrome observed in this study is 33.3%. 2. The risk factors for the development of intermediate syndrome identified in this study were: neck muscle weakness at admission (OR -7.87;CI – 1.86 - 33.4), sensorium assessed by Glasgow coma scale (OR - 1.38;CI – 0.36 -5.43) and severity of poisoning assessed by Namba scale(OR – 1.78;CI - 0.3 - 12.8). We have also observed that the type of compound, WHO class do not influence the occurrence of intermediate syndrome. The observations seen in our study suggests that the most important determinant of intermediate syndrome is the poison load, acetylcholinesterase inhibition and the resulting severity of poisoning. 3. Based on the risk factor analysis we propose a scoring system to predict the occurrence of Intermediate syndrome with sensorium assessed by Glasgow coma scale (maximum score – 2), Severity of poisoning assessed by Namba scale(maximum score – 3), type of compound(maximum score – 2), WHO class of compound(maximum score – 2) and neck muscle weakness(maximum score – 4). A score of < 8 is associated with a low risk of development of intermediate syndrome (area under the curve of 0.784 and sensitivity and specificity of 79% and 72% respectively). The positive predictive value negative predictive values were 56% and 92% respectively. The prediction score can be used to screen patients in accident and emergency to triage patients who can be shifted to the ward and discharged earlier and those who require intensive care. 4. Three patterns of muscle paralysis were identified in this study. About half the patients did not develop any muscle paralysis. 20.5% developed early paralysis (Type I paralysis); 33.3% developed early paralysis that persisted beyond 72 hours (Type I and Type II paralysis continuum); 4 (5.1%) patients developed new onset weakness after 72 hours (pure Type II paralysis). The only distinguishing features between Type I and Type II paralysis were the severity of weakness and the duration of weakness which were greater in Type II paralysis. These results support the concept of a Type I Type II paralysis continuum. 5. Early encephalopathy was seen in 23 patients (29.5%) and delayed encephalopathy, that is low sensorium developing after 72 hours after consumption or persisting low sensorium beyond 72 hours, was seen in 4 patients (5%). Patients who had developed delayed encephalopathy had low sensorium at admission, hence we have observed the early and delayed encephalopathy to be a spectrum disorder. 6. Three patterns of the relationship between encephalopathy and muscle weakness were observed in our study. In the early phase of severe poisoning, most patients have encephalopathy and muscle weakness. In the first pattern, encephalopathy and muscle weakness both recover in 72 hours (13%). In the second pattern, encephalopathy recovers but the muscle weakness persists (13% of patients). In third pattern which occurred in 4(5%) patients encephalopathy and muscle weakness persist for > 72 hours and recover together. The results suggest that encephalopathy and muscle weakness are closely inter-related phenomena both in early paralysis (Type I paralysis) and delayed paralysis (Type II paralysis/intermediate syndrome). Based on the results we suggest that the delayed encephalopathy be referred to as intermediateencephalopathy syndrome rather than Delayed organophosphate encephalopathy (DOPE). Although patients with persistent encephalopathy require prolonged ventilation, the neurological recovery and prognosis is good.

Item Type: Thesis (Masters)
Uncontrolled Keywords: Temporal Profile ; Central and Peripheral Neuromuscular features ; acute Organophosphorus poisoning ; Prospective Observational Clinical study.
Subjects: MEDICAL > General Medicine
Depositing User: Punitha K
Date Deposited: 18 May 2018 18:57
Last Modified: 18 May 2018 18:57
URI: http://repository-tnmgrmu.ac.in/id/eprint/7963

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