it is a pro - insecticide that forms cl 303268 that uncouples oxidative phosphorylation within the mitochondria . consequently , chlorfenapyr inhibits adenosine triphosphate ( atp ) production , causing cellular death and the death of the target organism . chlorfenapyr has not been studied extensively , but its toxicity to humans is very high . some fatal cases of chlorfenapyr poisoning by oral ingestion have been reported in the medical literature . however , fatality case from small amount of chlorfenapyr ingestion has not been reported . here , we present a fatal case caused by delayed chlorfenapyr toxicity , even though only a small amount was ingested . a 41-year - old woman was transferred from a rural hospital to our emergency department for further evaluation and management , following pesticide poisoning . she had ingested a mouthful ( estimated 20 ml ) of pesticide during a suicide attempt approximately 2 weeks earlier . however , she showed no symptoms immediately after ingesting the pesticide ; therefore , she continued in her daily activities . her symptoms worsened . by the time she was referred to our hospital , she was drowsy and had mild fever . she denied coingesting other toxic substances ; however , she did not remember the pesticide class or trade name . upon examination , her vital signs were as follows : blood pressure , 98/50 mm hg ; heart rate , 86/min ; respiratory rate , 17/min ; and body temperature , 37.6c . she exhibited a slight drowsiness , and her glasgow coma scale ( gcs ) rating was 14 . there were no abnormalities in her initial electrocardiogram , blood gas analysis , or chest radiograph . her hemoglobin ( hb ) was 11.7 g / dl , her white blood cell ( wbc ) count was 6830/mm , and a platelet count of 198000/mm . her renal function and serum electrolyte tests were normal , but other laboratory results showed high levels of serum creatinine kinase ( ck ) ( 3081 the emergency department managed this patient by providing supportive care , including intravenous fluid hydration and urine alkalinization . we were able to exclude the possibility of central nervous system ( cns ) infection , because we had already performed brain computed tomography ( ct ) and a lumbar puncture . the brain ct scan showed diffuse cerebral swelling with low density lesions in the white matter throughout the brain [ figure 1 ] . however , the patient 's cerebrospinal fluid ( csf ) pressure was normal and the lumbar puncture was unremarkable . a brain computed tomography scan shows diffuse cerebral swelling with low - density lesions in the white matter throughout the brain on the following morning , 20 h after admission , the patient suddenly exhibited a high fever , diaphoresis , and an altered mental state . her vital signs were as follows : blood pressure , 150/90 mm hg ; heart rate , 98/min ; respiratory rate , 28/min ; and body temperature , 40.7c . a tracheal intubation was performed and a mechanical ventilator was applied to maintain her airway and support ventilation . following these measures , we investigated her brain ct follow - up scan for sudden mental changes and her chest / abdomen ct scan for a high fever . the follow - up brain ct scan showed no significant change and we could not find any infection foci in the chest / abdominal ct scan . soon afterward , she showed signs of sudden cardiac arrest . advanced cardiac life support was performed for 30 min , but she finally expired , approximately 2 weeks after ingesting a small amount of chlorfenapyr . the symptoms and signs of chlorfenapyr toxicity include nausea , vomiting , fever , diaphoresis , tachypnea , rhabdomyolysis , and mental state changes . tharaknath et al . , reported that a similar fatality presented delayed adverse neurological effects ten days after chlorfenapyr ingestion and kwon et al . , reported symptoms approximately 2 weeks after chlorfenapyr ingestion . in both cases , the patients presented brain and spinal cord magnetic resonance imaging ( mris ) demonstrating the demyelination of the cns . this delayed toxicity was also observed in our case ; however , we could not conduct a brain mri because of institutional circumstances . we assume that chlorfenapyr poisoning has a latent period related to the formation of the active toxic product from this pro - insecticide . in our case , after the patient died , her husband found the pesticide bottle and informed us . we had prescribed antipyretics , such as nonsteroidal anti - inflammatory drugs and acetaminophen , to control a high fever , but the fever could not be controlled . thermoregulation is conducted by hypothalamic regulation of the sympathetic nervous system and by mitochondrial oxidative phosphorylation . nonshivering thermogenesis occurs in brown adipose tissue and it primarily uncouples oxidative phosphorylation through the activity of a group of mitochondrial proteins known as uncoupling proteins . chlorfenapyr seems to affect the inhibition and uncoupling of oxidative phosphorylation in the mitochondria . because of this uncoupled system , atp production from glucose is lacking , and this deficiency can cause severe damage to the skeletal muscle , retina , and other parts of the nervous system with high - energy requirements . endo et al . , reported that 8 patients out of 24 chlorfenapyr poisoning cases died . in addition to toxicity from oral ingestion , there was one case of death from chlorfenapyr vapor exposure . because of these findings , we believe that chlorfenapyr is highly toxic to humans , and the use of chlorfenapyr may need to be restricted in the same way that paraquat is controlled . we have described a fatal chlorfenapyr poisoning case that included a latent period accompanying delayed toxicity , even though only a mouthful of chlorfenapyr was ingested . based on this observation , patients with chlorfenapyr poisoning should be carefully observed for several weeks after ingestion , even when small amounts of chlorfenapyr are ingested and no toxic symptoms are present .
chlorfenapyr has been used worldwide for agricultural pest control since 1995 . despite its widespread use , 
 acute human poisoning data are insufficient ; only a small number of fatalities from chlorfenapyr poisoning have been reported . 
 the signs and symptoms of chlorfenapyr toxicity include nausea , vomiting , fever , rhabdomyolysis , among others . 
 in addition , central nervous system effects in association with delayed toxicity have also been observed . 
 here , we detail a fatality resulting from delayed chlorfenapyr toxicity following the ingestion of a small amount of pesticide .