Tarek Abuelem, David Dornbos III and Adam Arthur
David Dornbos III, Jocelyn Morin, Joshua R. Watson and Jonathan Pindrik
Osteomyelitis of the spine with associated spinal epidural abscess represents an uncommon entity in the pediatric population, requiring prompt evaluation and diagnosis to prevent neurological compromise. Cat scratch disease, caused by the pathogen Bartonella henselae, encompasses a wide spectrum of clinical presentations; however, an association with osteomyelitis and epidural abscess has been reported in only 4 other instances in the literature. The authors report a rare case of multifocal thoracic osteomyelitis with an epidural abscess in a patient with a biopsy-proven pathogen of cat scratch disease. A 5-year-old girl, who initially presented with vague constitutional symptoms, was diagnosed with cat scratch disease following biopsy of an inguinal lymph node. Despite appropriate antibiotics, she presented several weeks later with recurrent symptoms and back pain. Magnetic resonance imaging revealed 2 foci of osteomyelitis at T-8 and T-11 with an associated anterior epidural abscess from T-9 to T-12. Percutaneous image-guided vertebral biopsy revealed B. henselae by polymerase chain reaction analysis, and she was treated conservatively with doxycycline and rifampin with favorable clinical outcome.
David Dornbos III, Constantine L. Karras, Nicole Wenger, Blake Priddy, Patrick Youssef, Shahid M. Nimjee and Ciarán J. Powers
The utilization of the Pipeline embolization device (PED) has increased significantly since its inception and original approval for use in large, broad-necked aneurysms of the internal carotid artery. While microsurgical clipping and advances in endovascular techniques have improved overall efficacy in achieving complete occlusion, recurrences still occur, and the best modality for retreatment remains controversial. Despite its efficacy in this setting, the role of PED utilization in the setting of recurrent aneurysms has not yet been well defined. This study was designed to assess the safety and efficacy of PED in the recurrence of previously treated aneurysms.
The authors reviewed a total of 13 cases in which patients underwent secondary placement of a PED for aneurysm recurrence following prior treatment with another modality. The PEDs were used to treat aneurysm recurrence or residual following endovascular coiling in 7 cases, flow diversion in 2, and microsurgical clipping in 4. The mean time between initial treatment and retreatment with a PED was 28.1 months, 12 months, and 88.7 months, respectively. Clinical outcomes, including complications and modified Rankin Scale (mRS) scores, and angiographic evidence of complete occlusion were tabulated for each treatment group.
All PEDs were successfully placed without periprocedural complications. The rate of complete occlusion was 80% at 6 months after PED placement and 100% at 12 months in these patients who underwent PED placement following failed endovascular coiling; there were no adverse clinical sequelae at a mean follow-up of 26.1 months. In the 2 cases in which PEDs were placed for treatment of residual aneurysms following prior flow diversion, 1 patient demonstrated asymptomatic vessel occlusion at 6 months, and the other exhibited complete aneurysm occlusion at 12 months. In patients with aneurysm recurrence following prior microsurgical clipping, the rate of complete occlusion was 100% at 6 and 12 months, with no adverse sequelae noted at a mean clinical follow-up of 27.7 months.
The treatment of recurrent aneurysms with the PED following previous endovascular coiling, flow diversion, or microsurgical clipping is associated with a high rate of complete occlusion and minimal morbidity.
David Dornbos III, Christy Monson, CNP, Andrew Look, Kristin Huntoon, Luke G. F. Smith, Jeffrey R. Leonard, Sanjay S. Dhall and Eric A. Sribnick
While the Glasgow Coma Scale (GCS) has been effective in describing severity in traumatic brain injury (TBI), there is no current method for communicating the possible need for surgical intervention. This study utilizes a recently developed scoring system, the Surgical Intervention for Traumatic Injury (SITI) scale, which was developed to efficiently communicate the potential need for surgical decompression in adult patients with TBI. The objective of this study was to apply the SITI scale to a pediatric population to provide a tool to increase communication of possible surgical urgency.
The SITI scale uses both radiographic and clinical findings, including the GCS score on presentation, pupillary examination, and CT findings. To examine the scale in pediatric TBI, a neurotrauma database at a level 1 pediatric trauma center was retrospectively evaluated, and the SITI score for all patients with an admission diagnosis of TBI between 2010 and 2015 was calculated. The primary endpoint was operative intervention, defined as a craniotomy or craniectomy for decompression, performed within the first 24 hours of admission.
A total of 1524 patients met inclusion criteria for the study during the 5-year span: 1469 (96.4%) were managed nonoperatively and 55 (3.6%) patients underwent emergent operative intervention. The mean SITI score was 4.98 ± 0.31 for patients undergoing surgical intervention and 0.41 ± 0.02 for patients treated nonoperatively (p < 0.0001). The area under the receiver operating characteristic (AUROC) curve was used to examine the diagnostic accuracy of the SITI scale in this pediatric population and was found to be 0.98. Further evaluation of patients presenting with moderate to severe TBI revealed a mean SITI score of 5.51 ± 0.31 in 40 (15.3%) operative patients and 1.55 ± 0.02 in 221 (84.7%) nonoperative patients, with an AUROC curve of 0.95.
The SITI scale was designed to be a simple, objective communication tool regarding the potential need for surgical decompression after TBI. Application of this scale to a pediatric population reveals that the score correlated with the perceived need for emergent surgical intervention, further suggesting its potential utility in clinical practice.
Tetsuhiro Higashida, Christian W. Kreipke, José A. Rafols, Changya Peng, Steven Schafer, Patrick Schafer, Jamie Y. Ding, David Dornbos III, Xiaohua Li, Murali Guthikonda, Noreen F. Rossi and Yuchuan Ding
The present study investigated the role of hypoxia-inducible factor-1α (HIF-1α), aquaporin-4 (AQP-4), and matrix metalloproteinase-9 (MMP-9) in blood-brain barrier (BBB) permeability alterations and brain edema formation in a rodent traumatic brain injury (TBI) model.
The brains of adult male Sprague-Dawley rats (400–425 g) were injured using the Marmarou closed-head force impact model. Anti–AQP-4 antibody, minocycline (an inhibitor of MMP-9), or 2-methoxyestradiol (2ME2, an inhibitor of HIF-1α), was administered intravenously 30 minutes after injury. The rats were killed 24 hours after injury and their brains were examined for protein expression, BBB permeability, and brain edema. Expression of HIF-1α, AQP-4, and MMP-9 as well as expression of the vascular basal lamina protein (laminin) and tight junction proteins (zona occludens-1 and occludin) was determined by Western blotting. Blood-brain barrier disruption was assessed by FITC-dextran extravasation, and brain edema was measured by the brain water content.
Significant (p < 0.05) edema and BBB extravasations were observed following TBI induction. Compared with sham-operated controls, the injured animals were found to have significantly (p < 0.05) enhanced expression of HIF-1α, AQP-4, and MMP-9, in addition to reduced amounts (p < 0.05) of laminin and tight junction proteins. Edema was significantly (p < 0.01) decreased after inhibition of AQP-4, MMP-9, or HIF-1α. While BBB permeability was significantly (p < 0.01) ameliorated after inhibition of either HIF-1α or MMP-9, it was not affected following inhibition of AQP-4. Inhibition of MMP reversed the loss of laminin (p < 0.01). Finally, while inhibition of HIF-1α significantly (p < 0.05) suppressed the expression of AQP-4 and MMP-9, such inhibition significantly (p < 0.05) increased the expression of laminin and tight junction proteins.
The data support the notion that HIF-1α plays a role in brain edema formation and BBB disruption via a molecular pathway cascade involving AQP-4 and MMP-9. Pharmacological blockade of this pathway in patients with TBI may provide a novel therapeutic strategy.