Sudden asphyxia caused by retropharyngeal hematoma after blunt thyrocervical artery injury

Background

Retropharyngeal hematomas are often associated with blunt cervical spine injury. Generally, they improve with conservative treatment; however, rarely, airway obstruction occurs due to delayed swelling of retropharyngeal hematoma.

Objectives

To report a case of sudden asphyxia due to retropharyngeal hematoma caused by blunt thyrocervical artery injury.

Case Report

A 30-year-old woman was admitted to the Emergency Department of Tokai University Hospital 4 h after injury in a motor vehicle collision. On arrival, she had severe dyspnea and neck swelling; thereafter, a 26-mm-thick retropharyngeal swelling was visualized on lateral cervical plain X-ray study, extending from C1 anterior vertebrae to mediastinum. Emergency intubation was performed for the asphyxia. Because extravasation of contrast agent was observed in the hematoma on emergency contrast-enhanced computed tomography (CT) scan, emergency angiography was performed, from which we diagnosed a hemorrhage from the right thyrocervical artery.

Conclusion

If a patient with a non-displaced cervical spine injury suffers airway obstruction due to retropharyngeal hematoma, vigorous hemorrhage from a thyrocervical artery injury should be considered as the cause, and emergency contrast-enhanced CT scan of the neck should be performed after emergent tracheal intubation.     

Priming by grepafloxacin on respiratory burst of human neutrophils: its possible mechanism

Grepafloxacin is a broad-spectrum fluoroquinolone derivative that has good tissue penetration. We demonstrated that grepafloxacin showed a priming effect on neutrophil respiratory burst, triggered by either a chemotactic factor N-formyl-methionyl-leucyl-phenylalanine (fMLP) or leukotriene B4 (LTB4), but not by the phorbol ester phorbol 12-myristate 13-acetate (PMA). The priming effect of grepafloxacin on fMLP-stimulated superoxide generation by human neutrophils correlated with the penetration of grepafloxacin into cells. Removal of extracellular grepafloxacin did not inhibit the priming effect on fMLP-stimulated superoxide generation. Furthermore, grepafloxacin induced the translocation of p47-phox and p67-phox to the membrane fraction of neutrophils, whereas tyrosine phosphorylation was hardly observed in neutrophils exposed to grepafloxacin. The priming effect of grepafloxacin on superoxide generation from neutrophils was not inhibited by treatment with pertussis toxin, a protein-tyrosine kinase inhibitor (ST-638) or a protein kinase C inhibitor (calphostin C), or chelation of extracellular calcium. Grepafloxacin did not change the fMLP receptor-binding properties. Taken together, these findings suggest that grepafloxacin evokes a priming effect on neutrophil superoxide generation intracellularly through the translocation of p47-phox and even p67-phox protein to the membrane fractions. GTP binding protein, protein-tyrosine phosphorylation and protein kinase C activation are not involved in the priming effect.     

Beta-galactosidase of ROSA26 mice is a useful marker for detecting the definitive erythropoiesis after stem cell transplantation

BACKGROUND: Hematopoietic reconstitution after stem cell transplantation has been analyzed by using stem cells of Ly5 congenic mice. However, the early erythropoiesis has never been analyzed because this marker is not expressed on all of the erythroid lineage cells. The transgenic mouse expressing beta-galactosidase (beta-gal) or green fluorescent protein (GFP) has been reported. Using these markers, we analyzed the early erythropoiesis after stem cell transplantation. METHODS: The beta-gal activity and GFP were examined in the hematopoietic cells of ROSA26 and GFP transgenic mice, respectively, by flow cytometry. The primitive hematopoietic stem cell fraction (Lin(-)c-kit(+)Sca-1(+)) in bone marrow (BM) cells of ROSA26 mice was transferred into lethally irradiated mice. The kinetics of hematopoietic reconstitution was analyzed in the BM and spleen after transplantation. RESULTS: The beta-gal activity, but not the GFP and Ly5, was detected in all of the erythroid (TER119+) cells. The beta-gal activity was also detected in the donor-derived myeloid (Mac-1+), B lymphoid (B220+), and T lymphoid (Thy-1+) cells in the BM and spleen after stem cell transplantation. The kinetics of the hematopoietic reconstitution demonstrated that early erythroid (TER119(low)CD71(med)) cells were developed in the BM and spleen within 2 days after transplantation before development of proerythroblasts (TER119(+)CD71(high)), and that massive erythropoiesis and myelopoiesis were observed in the spleen until 2 and 4 weeks after transplantation, respectively. Conclusions. The beta-gal of ROSA26 mice can be a useful marker to identify the donor-derived hematopoietic cells, including early erythroid cells, and the first major wave of erythropoiesis occurring in the spleen after stem cell transplantation.