Downloaded from emj.bmj.com on October 20, 2014 - Published by group.bmj.com
EMJ Online First, published on August 19, 2013 as 10.1136/emermed-2013-202908 Original article
Pyrethroid poisoning: features and predictors of atypical presentations Yong Sung Cha,1 Hyun Kim,1 Nam Hyub Cho,1 Woo Jin Jung,1 Yong Won Kim,1 Tae Hoon Kim,1 Oh Hyun Kim,1 Kyoung Chul Cha,1 Kang Hyun Lee,1 Sung Oh Hwang,1 Lewis S Nelson2 1
Department of Emergency Medicine, Wonju College of Medicine, Yonsei University, Wonju, Kangwon, Republic of Korea 2 New York University School of Medicine, New York, New York, USA Correspondence to Dr Hyun Kim, Department of Emergency Medicine, Wonju College of Medicine, Yonsei University, 162 Ilsandong, Wonju, Kangwon 220-701, Republic of Korea;
[email protected] Received 4 June 2013 Revised 11 July 2013 Accepted 18 July 2013
ABSTRACT Background Although pyrethroids are known for low toxicity to humans, clinical systemic characteristics of pyrethroid poisoning remain undefined. We investigated atypical presentations of pyrethroid poisoning and the predictors, among those readily assessed in the emergency department. Methods 59 pyrethroid poisoning cases that were diagnosed and treated at the emergency department of Wonju Severance Christian Hospital from September 2004 to December 2012 were retrospectively reviewed. Results Atypical presentations were seen in 22 patients (39.3%). Atypical presentations after pyrethroid poisoning included respiratory failure requiring ventilator care (10 patients, 17.9%), hypotension (systolic blood pressure 3.5 mmol/L.
INTRODUCTION
To cite: Cha YS, Kim H, Cho NH, et al. Emerg Med J Published Online First: [please include Day Month Year] doi:10.1136/emermed2013-202908
Pyrethrin insecticides extracted from the flower Chrysanthemum cinerariaefolium have been used in China since the 1st century AD1 and developed for commercial application by the 1800 s. Allethrin was the first pyrethroid identified in1949,2 since many pyrethroid-containing products have been used worldwide. Pyrethrin and pyrethroid prolong the activation of the neuronal voltage-dependent Na+ channel; by binding to the channel’s open state causing a prolonged depolarisation.3 4 The mammalian voltage-dependent sodium channel, unlike its insect counterpart, has many isoforms, which may help explain the relative resistance of mammals to
Cha YS, et al. EmergArticle Med J 2013;0:1–5. Copyright authordoi:10.1136/emermed-2013-202908 (or their employer) 2013.
pyrethroid insecticides,5 which are usually classified as types I and II and are about 2250 times more toxic to insects compared with mammals.2 6 Humans and other mammals rapidly metabolise pyrethroid compounds to non-toxic substances,6 making them a preferred and approved insecticide for household use. Although pyrethroids are widely used, reports of accidental and intentional poisoning due to pyrethroid compounds are common.7 8 Because the clinical characteristics for humans in systemic pyrethroid poisoning remain undefined, we investigated the general characteristics, clinical presentations, and the factors, among those readily assessed in the emergency department (ED), that can predict atypical presentations in patients poisoned with pyrethroid.
METHODS Study design and data This was an observational and retrospective study of pyrethroid poisonings that were diagnosed and treated at the ED of Wonju Severance Christian Hospital. Fifty-nine patients were diagnosed with pyrethroid poisoning from September 2004 to December 2012 in the ED of Wonju Severance Christian Hospital, Wonju College of Medicine, Yonsei University. From 2004 to 2012, the number of patients recruited in our hospital ED increased from 28 000 to 37 000 patients, annually. Exclusion criteria were age younger than 18 years (none of the patients screened) and coingestion of other drugs or poisons with the exception of alcohol. Three patients presented with combined pyrethroid and organophosphate poisoning, the latter confirmed by measurement of plasma pseudocholinesterase levels. Therefore, 56 patients were included in the study. Data were retrospectively collected from medical records and reviewed. Poisoning with pyrethroid was confirmed by patient or guardian statements and verification of the agent by an emergency physician who transcribed the bottle label into patient records. The following parameters were assessed: age, sex, cause of poisoning, the ingested amount of pyrethroid, coingestion with alcohol, elapsed time from ingestion to arrival at the ED, initial symptoms, initial mental status (Glasgow Coma Scale (GCS)) and initial vital signs. Ingested amount was defined as follows: ‘a little or a spoon’ was taken to be 5 cc, ‘a mouthful’ was presumed to be 25 cc, ‘a small cup’ was presumed to be 100 cc and
Produced by BMJ Publishing Group Ltd under licence.
1
Downloaded from emj.bmj.com on October 20, 2014 - Published by group.bmj.com
Original article ‘a bottle’ was presumed to be 300 cc.9 Arterial blood gas, serum lactate, complete blood count, and levels of electrolytes (sodium, potassium), blood urea nitrogen, creatine (Cr), aspartate aminotransferase (AST) and alanine aminotransferase were evaluated. ECG was obtained at the time of pyrethroid poisoning presentation. The corrected QT interval (QT) on the electrocardiogram (ECG) was calculated using Bazett’s formula. Prolonged QTc interval was defined as >440 ms.10 After pyrethroid ingestion, symptoms are usually limited to nausea, vomiting and abdominal pain.2 7 These mild symptoms of poisoning are defined as typical presentations. Atypical presentations are defined as patients with respiratory failure requiring mechanical ventilation, hypotension (systolic blood pressure 1.4 mg/dL), seizure, GCS
