Negative Splenic Angiography in Blunt Trauma: Does Embolization Affect Splenic Salvage?

Angioembolization in blunt splenic trauma is used to maximize splenic preservation. Superiority of prophylactic embolization over expectant management in patients with a negative splenic angiography (SA) is debated. We hypothesized that embolization in negative SA would be associated with splenic salvage. Of 83 patients undergoing SA, 30 (36%) had a negative SA. Embolization was performed in 23 (77%). Grade of injury, contrast extravasation (CE) on computed tomography (CT) or embolization were not associated with splenectomy. In 20 patients with either a high-grade injury or CE on CT, 17 (85%) underwent embolization with a failure rate of 24%. In the remaining 10 without high-risk features, 6 underwent embolization with a 0% splenectomy rate. Despite embolization, the failure rate of nonoperative management (NOM) remains significant in those with high-grade injury or CE on CT. A low threshold for early splenectomy after prophylactic embolization is needed.

Distal Pancreatic Necrosis After Splenic Angioembolization.

Pancreatic ischemia with necrosis is an extremely rare complication of splenic angioembolization (SAE). A 48-year-old male with a grade IV blunt splenic injury underwent angiography which demonstrated no active bleeding or pseudoaneurysm. Proximal SAE was performed. One week later, he developed severe sepsis. Repeat CT imaging showed nonperfusion of the distal pancreas, and laparotomy found necrosis of approximately 40% of the pancreas. Distal pancreatectomy and splenectomy were performed. He endured a prolonged hospital course with multiple complications. Clinicians should have a high index of suspicion for ischemic complications after SAE when sepsis develops.

Co-targeting myelin inhibitors and CSPGs markedly enhances regeneration of GDNF-stimulated, but not conditioning-lesioned, sensory axons into the spinal cord.

A major barrier to intraspinal regeneration after dorsal root (DR) injury is the DR entry zone (DREZ), the CNS/PNS interface. DR axons stop regenerating at the DREZ, even if regenerative capacity is increased by a nerve conditioning lesion. This potent blockade has long been attributed to myelin-associated inhibitors and (CSPGs), but incomplete lesions and conflicting reports have prevented conclusive agreement. Here, we evaluated DR regeneration in mice using novel strategies to facilitate complete lesions and analyses, selective tracing of proprioceptive and mechanoreceptive axons, and the first simultaneous targeting of Nogo/Reticulon-4, MAG, OMgp, CSPGs, and GDNF. Co-eliminating myelin inhibitors and CSPGs elicited regeneration of only a few conditioning-lesioned DR axons across the DREZ. Their absence, however, markedly and synergistically enhanced regeneration of GDNF-stimulated axons, highlighting the importance of sufficiently elevating intrinsic growth capacity. We also conclude that myelin inhibitors and CSPGs are not the primary mechanism stopping axons at the DREZ.