Diagnostic Imaging Approach to Solitary Bone Lesions.

Radiologists frequently encounter solitary bone lesions in daily practice. The interpreting radiologist has the onus to determine the level of suspicion and appropriate next-step recommendations to aid in timely healthcare decisions. Lesion imaging characteristics in conjunction with patient history and demographics ultimately determine if a bone lesion is benign. Lesions that cannot be confidently disregarded as benign and clinically insignificant require further evaluation through additional imaging, tissue sampling, or both. We review a diagnostic imaging approach to solitary bone lesions with case examples that detail real-world thought processes for interpretations and practical next-step recommendations.

Atypical Causes of Dyspnea: A Review of Neuromuscular and Chest Wall Disorders that Compromise Ventilation.

Dyspnea is a common presenting symptom among patients with cardiopulmonary diseases. However, several neuromuscular and chest wall conditions are often overlooked and under-recognized causes of dyspnea. These disorders frequently adversely affect the structure and function of the ventilatory pump (diaphragm, accessory muscles of ventilation) and can precipitate respiratory failure despite normal lung parenchyma. Weakened musculature impairs clearance of airway secretions leading to aspiration and pneumonia, further compromising respiratory function. Radiologists should be aware of the pathophysiology and imaging manifestations of these conditions and might suggest them to be causes of dyspnea which otherwise may not have been considered by referring clinicians.

Misplaced tracheoesophageal voice prosthesis: A case of foreign body aspiration.

Foreign body aspiration (FBA) is a rare, but potentially fatal condition frequently seen in the emergency department. Bronchoscopy plays a major role in its diagnosis and treatment. In patients with laryngectomy, the strategies for airway maintenance and foreign body retrieval are limited. We describe management of a patient with laryngectomy presenting with aspiration of a tracheoesophageal voice prosthesis (TEP). The TEP was not initially seen in chest radiography; however, computed tomography showed it within the right lower bronchus. Successful extraction of the TEP was achieved through bronchoscopy with forceps and retrieval basket. Otolaryngology placed a larger TEP and secured it with sutures. TEP migration is rare, but represents a risk for FBA. Initial imaging in the emergency department can be misleading, requiring a high degree of suspicion, as the TEP device may not be seen in standard chest radiography. Flexible bronchoscopy under moderate sedation in conjunction with forceps and retrieval basket may be appropriate for treatment of FBA in patients with laryngectomy and can be performed in the emergency department, preventing hospital admission.

RGS4 inhibits angiotensin II signaling and macrophage localization during renal reperfusion injury independent of vasospasm.

Vascular inflammation is a major contributor to the severity of acute kidney injury. In the context of vasospasm-independent reperfusion injury we studied the potential anti-inflammatory role of the Gα-related RGS protein, RGS4. Transgenic RGS4 mice were resistant to 25 min injury, although post-ischemic renal arteriolar diameter was equal to the wild type early after injury. A 10 min unilateral injury was performed to study reperfusion without vasospasm. Eighteen hours after injury, blood flow was decreased in the inner cortex of wild-type mice with preservation of tubular architecture. Angiotensin II levels in the kidneys of wild-type and transgenic mice were elevated in a sub-vasoconstrictive range 12 and 18 h after injury. Angiotensin II stimulated pre-glomerular vascular smooth muscle cells (VSMCs) to secrete the macrophage chemoattractant RANTES, a process decreased by angiotensin II R2 (AT2) inhibition. However, RANTES increased when RGS4 expression was suppressed implicating Gα protein activation in an AT2-RGS4-dependent pathway. RGS4 function, specific to VSMC, was tested in a conditional VSMC-specific RGS4 knockout showing high macrophage density by T2 MRI compared with transgenic and non-transgenic mice after the 10 min injury. Arteriolar diameter of this knockout was unchanged at successive time points after injury. Thus, RGS4 expression, specific to renal VSMC, inhibits angiotensin II-mediated cytokine signaling and macrophage recruitment during reperfusion, distinct from vasomotor regulation.