Kyphoplasty in osteoporotic vertebral compression fractures - Guidelines and technical considerations

Osteoporotic vertebral compression fractures are a menace to the elderly generation causing diminished quality of life due to pain and deformity. At first, conservative treatment still is the method of choice. In case of resulting deformity, sintering and persistent pain vertebral cement augmentation techniques today are widely used. Open correction of resulting deformity by different types of osteotomies addresses sagittal balance, but has comparably high morbidity

ATLS® and damage control in spine trauma

Substantial inflammatory disturbances following major trauma have been found throughout the posttraumatic course of polytraumatized patients, which was confirmed in experimental models of trauma and in vitro settings. As a consequence, the principle of damage control surgery (DCS) has developed over the last two decades and has been successfully introduced in the treatment of severely injured patients. The aim of damage control surgery and orthopaedics (DCO) is to limit additional iatrogenic trauma in the vulnerable phase following major injury. Considering traumatic brain and acute lung injury, implants for quick stabilization like external fixators as well as decided surgical approaches with minimized potential for additional surgery-related impairment of the patient's immunologic state have been developed and used widely. It is obvious, that a similar approach should be undertaken in the case of spinal trauma in the polytraumatized patient. Yet, few data on damage control spine surgery are published to so far, controlled trials are missing and spinal injury is addressed only secondarily in the broadly used ATLS® polytrauma algorithm. This article reviews the literature on spine trauma assessment and treatment in the polytrauma setting, gives hints on how to assess the spine trauma patient regarding to the ATLS® protocol and recommendations on therapeutic strategies in spinal injury in the polytraumatized patient

Complications and safety aspects of kyphoplasty for osteoporotic vertebral fractures: a prospective follow-up study in 102 consecutive patients

<p>Abstract</p> <p>Background</p> <p>Kyphoplasty represents an established minimal-invasive method for correction and augmentation of osteoporotic vertebral fractures. Reliable data on perioperative and postoperative complications are lacking in the literature. The present study was designed to evaluate the incidence and patterns of perioperative complications in order to determine the safety of this procedure for patients undergoing kyphoplasty.</p> <p>Patients and Methods</p> <p>We prospectively enrolled 102 consecutive patients (82 women and 20 men; mean age 69) with 135 operatively treated fractured vertebrae who underwent a kyphoplasty between January 2004 to June 2006. Clinical and radiological follow-up was performed for up 6 months after surgery.</p> <p>Results</p> <p>Preoperative pain levels, as determined by the visual analogous scale (VAS) were 7.5 +/- 1.3. Postoperative pain levels were significantly reduced at day 1 after surgery (VAS 2.3 +/- 2.2) and at 6-month follow-up (VAS 1.4 +/- 0.9). Fresh vertebral fractures at adjacent levels were detected radiographically in 8 patients within 6 months. Two patients had a loss of reduction with subsequent sintering of the operated vertebrae and secondary spinal stenosis. Accidental cement extravasation was detected in 7 patients in the intraoperative radiographs. One patient developed a postoperative infected spondylitis at the operated level, which was treated by anterior corporectomy and 360 degrees fusion. Another patient developed a superficial wound infection which required surgical revision. Postoperative bleeding resulting in a subcutaneous haematoma evacuation was seen in one patient.</p> <p>Conclusion</p> <p>The data from the present study imply that percutaneous kyphoplasty can be associated with severe intra- and postoperative complications. This minimal-invasive surgical procedure should therefore be performed exclusively by spine surgeons who have the capability of managing perioperative complications.</p

Therapeutic options to prevent recurrence of an aggressive aneurysmatic bone cyst of the cervical spine of a 16 year old boy - a case report

The aneurysmatic bone cyst (ABC) is a benign primary bone tumour. If located in the cervical spine, its expansive growth and destructive behaviour may lead to instability and serious neurological impairment. We report a case of a 16-year-old boy with an aggressive ABC in the 7th cervical vertebra. Computertomographic and magnetic resonance imaging revealed the envelopment of the left 7th and 8th spinal nerve along with the anterior displacement of the left vertebral artery. The interdisciplinary surgical strategy consisted of a partially incomplete cyst resection, subtotal spondylectomy with posterior screw-and-rod fixation from C6-Th1, iliac crest bone grafting and anterior plating from C6-Th1. With regard to the high rate of recurrence after incomplete resection published in the recent literature, the patient was postoperatively treated by megavoltage radiotherapy with a total dose of 30Gy (daily dose of 1.8 Gy for 3 weeks). The clinical and radiographic follow-up showed complete recovery of all neurologic impairments and no signs of tumour recurrence at 3, 6 and 12 months after surgery. This case highlights diverse treatment regimens and shall outline the challenge and the problems of the interdisciplinary decision-making in adolescents presenting with ABC in high-demanding anatomical regions

Tumor necrosis factor-mediated inhibition of interleukin-18 in the brain: a clinical and experimental study in head-injured patients and in a murine model of closed head injury.

Tumor necrosis factor (TNF) and interleukin-(IL)-18 are important mediators of neuroinflammation after closed head injury (CHI). Both mediators have been previously found to be significantly elevated in the intracranial compartment after brain injury, both in patients as well as in experimental model systems. However, the interrelation and regulation of these crucial cytokines within the injured brain has not yet been investigated. The present study was designed to assess a potential regulation of intracranial IL-18 levels by TNF based on a clinical study in head-injured patients and an experimental model in mice. In the first part, we investigated the interrelationship between the daily TNF and IL-18 cerebrospinal fluid levels in 10 patients with severe CHI for up to 14 days after trauma. In the second part of the study, the potential TNF-dependent regulation of intracerebral IL-18 levels was further characterized in an experimental set-up in mice: (1) in a standardized model of CHI in TNF/lymphotoxin-α gene-deficient mice and wild-type (WT) littermates, and (2) by intracerebro-ventricular injection of mouse recombinant TNF in WT C57BL/6 mice. The results demonstrate an inverse correlation of intrathecal TNF and IL-18 levels in head-injured patients and a TNF-dependent inhibition of IL-18 after intracerebral injection in mice. These findings imply a potential new anti-inflammatory mechanism of TNF by attenuation of IL-18, thus confirming the proposed "dual" function of this cytokine in the pathophysiology of traumatic brain injury

Pitfalls and complications in the treatment of cervical spine fractures in patients with ankylosing spondylitis

Patients with ankylosing spondylitis are at significant risk for sustaining cervical spine injuries following trauma predisposed by kyphosis, stiffness and osteoporotic bone quality of the spine. The risk of sustaining neurological deficits in this patient population is higher than average. The present review article provides an outline on the specific injury patterns in the cervical spine, diagnostic algorithms and specific treatment modalities dictated by the underlying disease in patients with ankylosing spondylitis. An emphasis is placed on the risks and complication patterns in the treatment of these rare, but challenging injuries

Trauma induces apoptosis in human thoracolumbar intervertebral discs

BACKGROUND: Vertebral fractures resulting from high energy trauma often comprise the risk of posttraumatic degenerative changes in the affected intervertebral discs (IVD). Particularly in conservatively treated patients, or in cases after implant removal of an exclusively posterior stabilization, consecutive disc degeneration and the associated functional losing of the spinal segment clearly represent detrimental treatment results. In this regard, apoptosis of IVD cells has been suggested to be involved in the critical changes of the extracellular matrix. METHODS: To investigate whether fractures of the vertebrae induce apoptosis in the affected IVD, disc tissue from patients (n = 17) undergoing open reduction and internal fixation of thoracolumbar spine fractures were analysed in regards to caspase activity, apoptosis-receptor expression levels and gene expression of apoptosis-regulating proteins such as Bax and Bcl-2. Healthy IVD tissue (n = 3) obtained from patients undergoing surgical resection of adjacent vertebrae were used as control samples. RESULTS: In contrast to healthy control IVD tissues, samples from traumatic thoracolumbar IVD showed positive TUNEL staining and a significant increase of caspase-3/7 activity. Interestingly, analyses of the initiator caspase-8 and -9 revealed significantly increased activation levels compared to control values, suggesting the coexistent activation of both the extrinsic (receptor-mediated) and intrinsic (mitochondria-mediated) apoptosis pathway. Accordingly, expression levels of the Fas receptor (FasR) mRNA were significantly increased. Although the TNF receptor I (TNFR I) was only slightly upregulated, corresponding TNFα from trauma IVD presented significantly increased mRNA expression values. Furthermore, traumatic IVD cells demonstrated significantly reduced expression of the mitochondria-bound anti-apoptotic Bcl-2, thereby maintaining baseline transcriptional levels of the pro-apoptotic Bax protein when compared to control IVD cells. CONCLUSION: Our data suggest that thoracolumbar fractures induce early caspase-dependent apoptosis in IVD cells of the affected intervertebral disc, in part, by downregulation of the anti-apoptotic protein Bcl-2 (intrinsic apoptosis pathway), as well as signalling via the death receptor complex (TNFR I and FasR)

Inflammation and Apoptosis in human thoracolumbar intervertebral discs following spine trauma

GesamthabilitationsschriftEin zentrales Problem nach Frakturen im Bereich der thorakolumbalen Wirbelsäule ist der sowohl nach konservativer als auch nach operativer Behandlung im Verlauf auftretende Korrekturverlust, der nicht nur im betroffenen Wirbelkörper, sondern vor allem in den angrenzenden Bandscheiben stattfindet. Aus Untersuchungen der Degeneration von Bandscheiben ist bekannt, dass beim Prozess der Degeneration sowohl eine lokale Entzündungsreaktion als auch Apoptose eine zentrale Rolle spielt. Damit stellte sich die Frage, ob auch in einmaliges und schweres Trauma, welches zu Frakturen der an die Bandscheibe angrenzenden Wirbel führt, in der Lage ist, zu intradiskalen Veränderungen zu führen, wie sie aus degenerativen Bandscheiben bekannt sind. Zur Beantwortung dieser Fragestellung wurden Bandscheiben von Patienten mit Wirbelkörperfrakturen, welche im Rahmen der operativen Versorgung ohnehin entnommen werden mussten, auf posttraumatische inflammatorische Reaktionen (Migration von Entzündungszellen, Aktivierung der Komplementkaskade) und auf Apoptose und deren Aktivierungswege hin untersucht. Als Vergleichsgruppe wurden operativ zu versorgende Patienten mit degenerativ bedingten Pathologien der Wirbelsäule und als Kontrollgruppe gesunde Bandscheiben von Patienten, bei denen der angrenzende Wirbelkörper entfernt werden musste, verwendet. Dabei konnten in Bandscheiben aus der Traumagruppe regelmässig CD66-positive neutrophile Granulozyten, T-Lymphozyten (CD3-positive- und Perforin-positive zytotoxische-T-Lymphozyten) und Makrophagen (CD68-positive und CD163-positive Makrophagen) ebenso wie zentrale Mediatoren der Komplementkaskade (C3c, C5b und der MAC/C5b-9) nachgewiesen werden. Ebenso konnte regelhaft die Caspase- vermittelte Apoptose ortständiger intradiskaler Zellen in der Traumagruppe nachgewiesen werden. Die Analyse der Pathways der Apoptose zeigte eine Aktivierung über den intrinsischen mitochondrial vermittelten Weg und Hinweise für eine Aktivierung über den extrinsischen Rezeptor vermittelten Weg. Die vorliegenden Ergebnisse zeigen, dass in Bandscheiben, die an frakturierte Wirbelkörper angrenzen, eine posttraumatischen Entzündungsreaktion ausgelöst und Apoptose hervorgerufen wird. Es kommt zur Migration einer Reihe verschiedener Entzündungszellen und zur Aktivierung von Bestandteilen der Komplementkaskade. Weiterhin lässt sich Caspase vermittelte Apoptose sowohl über den extrinsischen (Rezeptor vermittelt) als auch über den intrinsischen (mitochondrial vermittelt) Weg aktiviert, nachweisen. Damit konnte erstmalig gezeigt werden, dass ein einmaliges und schweres Trauma zu intradiskalen inflammatorischen Reaktionen und zur Apoptose intradiskaler Zellen führt.In the follow up of both conservatively treated or surgically stabilized thoracolumbar spine fractures consecutive loss of reduction remains a key concern. Correlating to the scale of fracture, the resulting deformity is further determined by the condition and functionality of its adjacent intervertebral discs. Previous studies from degenerative disc diseases have reported that the disc degenerating process not only involves local inflammation, but also significant apoptotic induced changes of the cellular matrix. Therefore, the hypothesis was to investigate whether a single traumatic incident causing fracture of the spine was capable of mounting intradiscal changes, otherwise related to degenerating discs. Adjacent intervertebral discs from patients with a spine fracture were resected within the procedure of surgical stabilization and analyzed in regard to posttraumatic inflammation (migration of inflammatory cells, complement activation) and apoptosis-related changes. Discs from patients with degenerative spinal disorders were analysed for comparison. The control group consisted of healthy discs from patients where resection of the pathologic vertebral body was necessitated. Trauma specimens continuously presented with CD66+ neutrophils, CD3+ and perforin-positive cytotoxic T lymphocytes, as well as CD68+ and CD163+ macrophages. Furthermore, analyses from traumatic discs demonstrated significant increases of key complement-associated mediators including C3c, C5b and the MAC/C5b-9 complex. These data were complemented by significant increases of caspase-3 induced apoptosis of intervertebral disc cells. Continuing analyses of the apoptotic pathways in traumatic discs revealed a significant activation of the intrinsic apoptosis signalling cascade and, in part, the extrinsic receptor-mediated apoptotic sequence. In conclusion, these data indicate, for the first time in human samples, that trauma induces inflammation and apoptosis in intervertebral disc cells adjacent to the fractured vertebra. Respectively, trauma-induced inflammation is characterized by migration of diverse inflammatory cells and activation of components involved in the complement cascade. Along with the caspase- dependent activation of both the extrinsic (receptor-mediated) and intrinsic (mitochondria-mediated) apoptotic signalling pathway it may thus be suggested, that such trauma-induced intradiscal changes may alter the functional integrity of the extracellular matrix and promote disc degeneration