Landmarks for identifying the suprascapular foramen anteriorly: Application to anterior neurotization and decompressive procedures

BACKGROUND: Additional landmarks for identifying the suprascapular nerve at its entrance into the suprascapular foramen from an anterior approach would be useful to the surgeon. OBJECTIVE: To identify landmarks for the identification of this hidden site within an anterior approach. METHODS: In 8 adult cadavers (16 sides), lines were used to connect the superior angle of the scapula, the acromion, and the coracoid process tip thus creating an anatomic triangle. The suprascapular nerve\u27s entrance into the suprascapular foramen was documented regarding its position within this anatomical triangle. Depths from the skin surface and specifically from the medial-most point of the clavicular attachment of the trapezius to the suprascapular nerve\u27s entrance into the suprascapular foramen were measured using calipers and a ruler. The clavicle was then fractured and retracted superiorly to verify the position of the nerve\u27s entrance into the suprascapular foramen. RESULTS: From the trapezius, the nerve\u27s entrance into the foramen was 3 to 4.2 cm deep (mean, 3.5 cm). The mean distance from the tip of the corocoid process to the suprascapular foramen was 3.8 cm. The angle best used to approach the suprascapular foramen from the surface was 15° to 20°. CONCLUSION: Based on our study, an anterior suprascapular approach to the suprascapular nerve as it enters the suprascapular foramen can identify the most medial fibers of the trapezius attachment onto the clavicle and insert a finger at an angle of 15° to 20° laterally and advanced to an average depth of 3.5 cm

Microhemorrhage-associated tissue iron enhances the risk for Aspergillus fumigatus invasion in a mouse model of airway transplantation

Invasive pulmonary disease due to the mold Aspergillus fumigatus can be life-threatening in lung transplant recipients, but the risk factors remain poorly understood. To study this process, we used a tracheal allograft mouse model that recapitulates large airway changes observed in patients undergoing lung transplantation. We report that microhemorrhage-related iron content may be a major determinant of A. fumigatus invasion and, consequently, its virulence. Invasive growth was increased during progressive alloimmune-mediated graft rejection associated with high concentrations of ferric iron in the graft. The role of iron in A. fumigatus invasive growth was further confirmed by showing that this invasive phenotype was increased in tracheal transplants from donor mice lacking the hemochromatosis gene (Hfe(-/-)). The invasive phenotype was also increased in mouse syngrafts treated with topical iron solution and in allograft recipients receiving deferoxamine, a chelator that increases iron bioavailability to the mold. The invasive growth of the iron-intolerant A. fumigatus double-knockout mutant (Delta sreA/Delta cccA) was lower than that of the wild-type mold. Alloimmune-mediated microvascular damage and iron overload did not appear to impair the host's immune response. In human lung transplant recipients, positive staining for iron in lung transplant tissue was more commonly seen in endobronchial biopsy sections from transplanted airways than in biopsies from the patients' own airways. Collectively, these data identify iron as a major determinant of A. fumigatus invasive growth and a potential target to treat or prevent A. fumigatus infections in lung transplant patients