ABSTRACT
INTRODUCTION: Central airway stenosis is a life-threating requiring immediate medical intervention. There are several options for treating central airway stenosis, including rigid bronchoscopy, bronchoscopic high-power laser therapy, high-frequency electric needle knife, and balloon-expanding stents. However, interventional techniques may be unavailable in an emergent situation or at smaller local hospitals. In this case report, we publicly demonstrate for the first time that a tracheal intubation catheter may be applied as a temporary alternative to interventional bronchoscopic treatment. PATIENT CONCERNS: A 72-year old male patient was admitted with a 1-year history of intermittent dyspnea, which was exacerbated for one day. One day prior to admission to our hospital, the patient presented with cyanosis due to an exacerbation of dyspnea.A tracheotomy was performed and the patient had been carrying a tracheotomy cannula for 6 months. DIAGNOSIS: The ventilator alarm indicated high airway resistance and the nurses were unable to insert the suction pipes into the airway. Immediate fiberoptic bronchoscopy showed diffuse edema and stenosis of the inferior tracheal airways. INTERVENTIONS: Tracheal intubation was used to temporarily replace the tracheotomy cannula, which successfully expanded the narrowed airways. OUTCOMES: The blood oxygen saturation returned to normal, and dyspnea was quickly relieved. CONCLUSION: In emergent situations, tracheal intubation catheters may be used in patients with post-tracheotomy central airway stenosis, not only for surviving the most dangerous phase but for also prolonging the survival time for further treatments.
Subject(s)
Airway Obstruction/therapy , Intubation, Intratracheal/methods , Tracheal Stenosis/therapy , Tracheotomy/adverse effects , Aged , Humans , MaleABSTRACT
Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline. Hematoxylin-eosin staining showed that most hippocampal cells were contracted and nucleoli had disappeared in the paraquat group. Fewer cells in the hippocampus were concentrated and nucleoli had disappeared in the ulinastatin group. Western blot assay showed that expressions of GRP78 and cleaved-caspase-3 were significantly lower in the ulinastatin group than in the paraquat group. Immunohistochemical findings showed that CHOP immunoreactivity was significantly lower in the ulinastatin group than in the paraquat group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining showed that the number of apoptotic cells was reduced in the paraquat and ulinastatin groups. These data confirmed that endoplasmic reticular stress can be induced by acute paraquat poisoning. Ulinastatin can effectively inhibit this stress as well as cell apoptosis, thereby exerting a neuroprotective effect.
