Background?Baclofen (para-chlorophenyl-gamma-aminobutyric acid) is widely used for its therapeutic effect of providing muscle relaxation from the persistent muscle spasms and posturing often related to spinal and central nervous system injuries. However, baclofen is also a potent neuronal depressant which is most evident in cases of toxicity. In severe toxicity, respiratory failure and obtundation may occur. Case-diagnosis/treatment?We present the case of a neurologically devastated 16-year-old on chronic baclofen therapy for bilateral spastic cerebral palsy (Gross Motor Function Classification System level V) who presented with fever, leukocytosis, and hypotension. Initial management with fluid resuscitation and antimicrobials for presumed infection did initially improve the patient's mental status; however, he subsequently became comatose later during the same hospitalization. Comprehensive diagnostic studies and infectious work-up did not reveal an etiology. Upon further examination of history, acute kidney injury from chronic nonsteroidal use and complicated by vancomycin toxicity was suspected to cause acute baclofen toxicity. The patient underwent a single run of hemodialysis with resultant neurologic improvement and later laboratory-confirmed toxic baclofen levels. Conclusion?Clinicians should consider possible acute baclofen toxicity in patients with impaired renal function who present with neurologic depression. Respiratory failure and mechanical ventilation, with its associated intensive care costs and complications, may be avoided with prompt treatment using hemodialysis.

state of rats, and in the 7th day after poisoning, the lungs were taken and the lung tissue morphology were obererved by HE staining. The expression of PERK, P-elF2a, ATF4 were detected by immunohistochemistry, and the expression of GRP78, PDI, PERK, P-elF2a, ATF4 and CHOP protein were detected by western blotting in lung tissue.Then we did statistical analysis. Results: In the 7th day of acute PQ poisoning, HE staining of lung tissue exposed that there was a lot of inflammatory exudation in group B; the expression of GRP78, PDI, PERK, P-elF2a, ATF4 and CHOP protein were higher than that of the control group, with the difference statistically significant (P <0.05). There was basal expression of GRP78, PDI, PERK, P-elF2a, ATF4 and CHOP in the control group. The inflammatory response in Salubrinal treatment group was more serious than that of the exposure group, the expression of GRP78, PDI, PERK, P-elF2a, ATF4 and CHOP protein was increased, with the difference statistically significant (P <0.05). The degree of inflammation and protein expression in Sal (0.5mg/kg) treatment group was between Sal (1.0mg/kg) treatment group and the exposure group, with the difference statistically significant (P <0.05). Mortality: The mortality of group B,group C and group D were 54.0%, 70.0%, 88.0%; and the mortality of Sal (1.0mg/kg) treatment group was the highest,with the difference statistically significant (P <0.05). Conclusions: Acute PQ poisoning can enhance ERS, PERK-eIF2a-ATF4 signaling pathway and cause lung injury; Salubrinal can strengthen ERS, increase PERK-eIF2a-ATF4 signal transduction pathway and aggravate acute lung injury caused by PQ poisoning.