When does intraoperative 3D-imaging play a role in transpedicular C2 screw placement?

INTRODUCTION: The stabilization of an atlantoaxial (C1-C2) instability is demanding due to a complex atlantoaxial anatomy with proximity to the spinal cord, a variable run of the vertebral artery (VA) and narrow C2 pedicles. We perfomed the Goel & Harms fusion in combination with an intraoperative 3D imaging to ensure correct screw placement in the C2 pedicle. We hypothesized, that narrow C2 pedicles lead to a higher malposition rate of screws by perforation of the pedicle wall. The purpose of this study was to describe a certain pedicle size, under which the perforation rate rises. PATIENTS AND METHODS: In this retrospective study, all patients (n=30) were operated in the Goel & Harms technique. The isthmus height and pedicle diameter of C2 were measured. The achieved screw position in C2 was evaluated according to Gertzbein & Robbin classification (GRGr). RESULTS: A statistically significant correlation was found between the pedicles size (isthmus height/pedicle diameter) and the achieved GRGr for the right (p=0.002/p=0.03) and left side (p=0.018/p=0.008). The ROC analysis yielded a Cut Off value for the pedicle size to distinguish between an intact or perforated pedicle wall (GRGr 1 or ≥2). The Cut-Off value was identified for the isthmus height (right 6.1mm, left 5.4mm) and for the pedicle diameter (6.6mm both sides). CONCLUSION: The hypothesis, that narrow pedicles lead to a higher perforation rate of the pedicle wall, can be accepted. Pedicles of <6.6mm turned out to be a risk factor for a perforation of the pedicle wall (GRGr 2 or higher). Intraoperative 3D imaging is a feasible tool to confirm optimal screw position, which becomes even more important in cases with thin pedicles. The rising risk of VA injury in these cases support the additional use of navigation.

Current concepts review: Fractures of the patella.

Fractures of the patella account for about 1% of all skeletal injuries and can lead to profound impairment due to its crucial function in the extensor mechanism of the knee. Diagnosis is based on the injury mechanism, physical examination and radiological findings. While the clinical diagnosis is often distinct, there are numerous treatment options available. The type of treatment as well as the optimum timing of surgical intervention depends on the underlying fracture type, the associated soft tissue damage, patient factors (i.e. age, bone quality, activity level and compliance) and the stability of the extensor mechanism. Regardless of the treatment method an early rehabilitation is recommended in order to avoid contractures of the knee joint capsule and cartilage degeneration. For non-displaced and dislocated non-comminuted transverse patellar fractures (2-part) modified anterior tension band wiring is the treatment of choice and can be combined - due to its biomechanical superiority - with cannulated screw fixation. In severe comminuted fractures, open reduction and fixation with small fragment screws or new angular stable plates for anatomic restoration of the retropatellar surface and extension mechanism results in best outcome. Additional circular cerclage wiring using either typical metal cerclage wires or resorbable PDS/non-resorbable FiberWires increases fixation stability and decreases risk for re-dislocation. Distal avulsion fractures should be fixed with small fragment screws and should be protected by a transtibial McLaughlin cerclage. Partial or complete patellectomy should be regarded only as a very rare salvage operation due to its severe functional impairment.

Temporal profile of inflammatory response to fracture and hemorrhagic shock: Proposal of a novel long-term survival murine multiple trauma model.

Hemorrhagic shock (hS) interacts with the posttraumatic immune response and fracture healing in multiple trauma. Due to the lack of a long-term survival multiple trauma animal models, no standardized analysis of fracture healing referring the impact of multiple trauma on fracture healing was performed. We propose a new long-term survival (21 days) murine multiple trauma model combining hS (microsurgical cannulation of carotid artery, withdrawl of blood and continuously blood pressure measurement), femoral (osteotomy/external fixation) and tibial fracture (3-point bending technique/antegrade nail). The posttraumatic immune response was measured via IL-6, sIL-6R ELISA. The hS was investigated via macrohemodynamics, blood gas analysis, wet-dry lung ration and histologic analysis of the shock organs. We proposed a new murine long-term survival (21 days) multiple trauma model mimicking clinical relevant injury patterns and previously published human posttraumatic immune response. Based on blood gas analysis and histologic analysis of shock organs we characterized and standardized our murine multiple trauma model. Furthermore, we revealed hemorrhagic shock as a causative factor that triggers sIL-6R formation underscoring the fundamental pathophysiologic role of the transsignaling mechanism in multiple trauma.

Are pentraxin 3 and transsignaling early markers for immunologic injury severity in polytrauma? A pilot study.

BACKGROUND: Inflammatory-related conditions and organ failure (OF) lead to late trauma mortality. Cytokine profiles can predict adverse events and mortality, potentially guiding treatment strategies (damage control surgery versus early total care). However, the specific cytokines to predict the clinical course in polytraumatized patients are not fully identified. QUESTIONS/PURPOSES: We investigated the early pentraxin 3 (PTX3), IL-6, soluble IL-6 receptor (sIL-6R), and transsignaling ratio (TSR) in polytraumatized patients to estimate immunologic injury severity and predict OF and survival. METHODS: We prospectively followed 58 patients with severe polytrauma, six patients with minor trauma, and 10 healthy volunteers. The mean Injury Severity Score (ISS) was 43 points and the mean Hannover Polytrauma Score (PTS) was 59 points, with a consequently high mortality rate (30%). Twenty-seven of the 58 polytraumatized patients (46%) developed OF, 67% systemic inflammatory response syndrome, and 38% sepsis. RESULTS: Mean sIL-6R concentrations in polytrauma initially were low. Mean PTX3 concentrations were high and peaked at 24 hours. The mean TSR peaked at 6 hours; at that time, the mean value was higher for nonsurvivors. PTX3 concentrations at admission were associated with injury severity calculated by ISS and PTS. Higher PTX3 serum concentrations 24 hours after admission correlated with lower probability for survival. CONCLUSIONS: PTX3, sIL-6R, and TSR were early markers for posttraumatic inflammatory status, OF, injury severity, and TSR for survival after polytrauma. The temporal profile of PTX3 and TSR might be used to anticipate the total injury severity and the clinical course and thereby guide decision making in polytraumatized patients.

Diagnostic and prognostic potential of differentially expressed miRNAs between metastatic and non-metastatic renal cell carcinoma at the time of nephrectomy.

BACKGROUND: MicroRNAs are promising diagnostic and prognostic biomarkers in oncology. We aimed to evaluate the prognostic potential of selected microRNAs in primary clear cell renal cell carcinomas (ccRCC) as predictors of tumor recurrence after radical nephrectomy. METHODS: miR-122, miR-141, miR-155, miR-184, miR-200c, miR-210, miR-224, and miR-514, validated as differentially expressed in a previous study, were measured by RT-PCR in matched malignant and non-malignant tumor samples after nephrectomy from 111 patients (89 without, 22 with metastases) and clinicopathological and outcome data were collected. Non-parametric statistical tests, receiver-operating characteristics, Kaplan-Meier-, and univariate as well as multivariate Cox regression analyses were performed. RESULTS: Downregulation of miR-141/-184/-200c/-514 and upregulation of miR-122/-155/-210/-224 were not different between samples of non-metastatic and metastatic tumors except for miR-122 and miR-514. miR-514 was further downregulated in metastatic compared with non-metastatic tumors while the upregulation of miR-122 was significantly reduced in metastatic carcinomas. All miRNAs were suitable to discriminate malignant from non-malignant tissue. miR-122 and miR-514 were significantly related to the recurrence risk but only miR-514 provided independent prognostic information in the final model including relevant clinicopathological variables. CONCLUSIONS: MiR-122 and miR-514 play a role in tumor recurrence after nephrectomy. Expression of miR-514 was particularly downregulated in primary metastatic tumor and those that recur and might be a suitable adjunct marker for predicting tumor recurrence.

Identification of metastamirs as metastasis-associated microRNAs in clear cell renal cell carcinomas.

MicroRNAs (miRNAs) play a pivotal role in cancerogenesis and cancer progression, but their specific role in the metastasis of clear cell renal cell carcinomas (ccRCC) is still limited. Based on microRNA microarray analyses from normal and cancerous samples of ccRCC specimens and from bone metastases of ccRCC patients, we identified a set of 57 differentially expressed microRNAs between these three sample groups of ccRCC. A selected panel of 33 miRNAs was subsequently validated by RT-qPCR on total 57 samples. Then, 30 of the 33 examined miRNAs were confirmed to be deregulated. A stepwise down-regulation of miRNA expression from normal, over primary tumor to metastatic tissue samples, was found to be typical. A total of 23 miRNAs (miR-10b/-19a/-19b/-20a/-29a/-29b/-29c/-100/-101/-126/-127/-130/-141/-143/-145/-148a/-192/-194/-200c/-210/-215/-370/-514) were down-regulated in metastatic tissue samples compared with normal tissue. This down-regulated expression in metastatic tissue in comparison with primary tumor tissue was also present in 21 miRNAs. In cell culture experiments with 5-aza-2'-deoxycytidine and trichostatin A, epigenetic modifications were shown as one reason of this down-regulation. The altered miRNA profiles, comprising newly identified metastasis-associated miRNAs, termed metastamir and the predicted miRNA-target interactions together with the significant correlations of miRNAs that were either lost or newly appeared in the studied sample groups, afford a solid basis for further functional analyses of individual miRNAs in RCC metastatic progression.

Overall distribution of trauma-related deaths in Berlin 2010: advancement or stagnation of German trauma management?

BACKGROUND: Trauma is the leading cause of death among children, adolescents, and young adults. The latest data from the German Trauma Registry reveals a constant decrease in trauma mortality, indicating that 11.6 % of all trauma patients in 2010 died in hospital. Notably, trauma casualties dying before admission to hospital have not been systematically surveyed and analyzed in Germany. METHODS: We conducted a prospective observational study of all traumatic deaths in Berlin, recording demographic data, trauma mechanisms, and causes/localization and time of death after trauma. Inclusion criteria were all deaths following trauma from 1 January 2010 to 31 December 2010. RESULTS: A total of 440 trauma fatalities were included in this study, with a mortality rate of 13/100,000 inhabitants; 78.6 % were blunt injuries, and fall from a height >3 m (32.7 %) was the leading trauma mechanism. 32.5 % died immediately, 23.9 % died within 60 min, 7.7 % died within 1-4 h, 16.8 % died within 4-48 h, 11.1 % died <1 week later, and 8 % died >1 week after trauma. The predominant causes of death were polytrauma (45.7 %), sTBI (38 %), exsanguination (9.5 %), and thoracic trauma (3.2 %). Death occurred on-scene in 58.7 % of these cases, in the intensive care unit in 33.2 %, and in 2.7 % of the cases, in the emergency department, the operating room, and the ward, respectively. CONCLUSIONS: Polytrauma is the leading cause of death, followed by severe traumatic brain injury (sTBI). The temporal analysis of traumatic death indicates a shift from the classic "trimodal" distribution to a new "bimodal" distribution. Besides advances in road safety, prevention programs and improvement in trauma management-especially the pre-hospital phase-have the potential to significantly improve the survival rate after trauma.

Microcirculatory sequelae of the rotator cuff after antegrade nailing in proximal humerus fracture.

INTRODUCTION: Antegrade nailing allows a stable fixation and, thus, an early functional after treatment in proximal humerus fractures. Since the surgical procedure in antegrade humeral nailing requires a split of the supraspinatus tendon, the question arises whether the surgical approach causes microcirculatory dysfunction of the tendon. MATERIALS AND METHODS: A total of 15 consecutive patients suffering from proximal humerus fractures were enrolled. During the implantation of an antegrade humerus nail, microvascular perfusion of the supraspinatus tendon was directly visualized after the exposition and stabilization of the fracture using the OPS-imaging technique. RESULTS: Immediately after exposure, the nutritive perfusion showed physiological values of tendon microcirculation. After implanting antegrade humeral nails, the perfusion of the supraspinatus tendon reduced markedly. Capillary width was unaffected by the surgical procedure. CONCLUSION: The trauma leading to proximal humerus fracture causes no fundamental impairment of nutritive perfusion of the rotator cuff. Whereas the implantation of an antegrade humerus nail, which necessarily includes a splitting of the rotator cuff, nearly halves the functional capillary density of the supraspinatus tendon. Even though this effect seems to be reversible, the surgical dissection of the supraspinatus tendon should be performed in a soft tissue sparing way.

Angular stable anterior plating following thoracolumbar corpectomy reveals superior segmental stability compared to conventional polyaxial plate fixation.

STUDY DESIGN: Biomechanical in vitro testing of primary and secondary stability in 12 human thoracolumbar spinal specimens using a spine simulator. OBJECTIVE: In a corpectomy model anterior plate systems were investigated for their ability to restore spinal stability particularly focusing on the influence of angular stability, bone mineral density (BMD) and failure mode. SUMMARY OF BACKGROUND DATA: The concept of isolated anterior column reconstruction following thoracolumbar fractures using newly developed minimally invasive spine surgical techniques has attracted major clinical interest. In analogy to angular stable plate systems in long bone fixation the application of locking plates to the spine is aimed to limit loss of reduction and to improve stability. METHODS: Twelve human spinal specimens (Th11-L3) were tested in a 6-degree-of-freedom spine simulator under pure moments of 7.5 Nm to investigate primary and secondary stiffness of 2 different anterior reconstruction options: (1) Synex II cage and MACS TL polyaxial anterior plating system, (2) Synex II cage and ArcoFix angular stable anterior plating system. An increasing 4-step cyclic loading model was included. RESULTS: The angular stable plate system showed superior stability compared to the nonangular system in axial rotation and lateral bending. Flexion/extension loading demonstrated no difference between the systems in range of motion. A positive correlation between BMD and the number of load cycles until failure for the nonangular stable system (R2 = 0.90) was found. Different failure modes were investigated for the plating systems. The MACS system showed loosening at the connection between screw and plate inducing tilting under flexural load and final failure. The ArcoFix system revealed increased stability under cyclic loading and failed by parallel sintering to the endplate. CONCLUSION: Anterior angular stable fixation showed higher primary and secondary stability following thoracolumbar corpectomy. In specimens with lower BMD the use of angular stable systems substantially increased stability. Angular stable systems, however, differ in the way of construct failure.

Initial intramuscular perfusion pressure predicts early skeletal muscle function following isolated tibial fractures.

BACKGROUND: The severity of associated soft tissue trauma in complex injuries of the extremities guides fracture treatment and decisively determines patient's prognosis. Trauma-induced microvascular dysfunction and increased tissue pressure is known to trigger secondary soft tissue damage and seems to adversely affect skeletal muscle function. METHODS: 20 patients with isolated tibial fractures were included. Blood pressure and compartment pressure (anterior and deep posterior compartment) were measured continuously up to 24 hours. Corresponding perfusion pressure was calculated. After 4 and 12 weeks isokinetic muscle peak torque and mean power of the ankle joint in dorsal and plantar flexion were measured using a Biodex dynamometer. RESULTS: A significant inverse correlation between the anterior perfusion pressure at 24 hours and deficit in dorsiflexion at 4 weeks was found for both, the peak torque (R = -0.83; p < 0.01) and the mean power (R = -0.84; p < 0.01). The posterior perfusion pressure at 24 h and the plantar flexion after 4 weeks in both, peak torque (R = -0.73, p = or < 0.05) and mean power (R = -0.7, p = or < 0.05) displayed a significant correlation. CONCLUSION: The functional relationship between the decrease in intramuscular perfusion pressures and muscle performance in the early rehabilitation period indicate a causative and prognostic role of early posttraumatic microcirculatory derangements and skeletal muscle function. Therapeutic concepts aimed at effective muscle recovery, early rehabilitation, and decreased secondary tissue damage, should consider the maintenance of an adequate intramuscular perfusion pressure.

Biomechanical, microvascular, and cellular factors promote muscle and bone regeneration.

It is becoming clear that the long-term outcome of complex bone injuries benefits from approaches that selectively target biomechanical, vascular, and cellular pathways. The typically held view of either biological or mechanical aspects of healing is oversimplified and does not correspond to clinical reality. The fundamental mechanisms of soft tissue regeneration most likely hold the key to understanding healing response.

Local cooling restores microcirculatory hemodynamics after closed soft-tissue trauma in rats.

BACKGROUND: Severe closed soft-tissue injury (CSTI) results in progressively developing microvascular dysfunction and local inflammation. Cooling reduces swelling, pain, cellular oxygen demand, and metabolic activity. However, effects of cooling on posttraumatic microcirculation are not yet fully understood. Thus, we assessed effects of local cooling on microcirculation, regional inflammatory response including leukocyte-endothelial cell interaction, and edema formation after CSTI. METHODS: Standardized CSTI was induced by means of controlled impact injury in the left tibial compartment of 14 male Sprague-Dawley rats. Rats were assigned to four groups (n = 7 per group) as follows: group I, no trauma/no cooling; group II, no trauma/20 minutes of cooling; group III, 1.5 hours posttrauma/no cooling; and group IV, 1.5 hours posttrauma/20 minutes of cooling. RESULTS: CSTI resulted in a significant decrease in functional capillary density, a marked increase in microvascular permeability, and granulocyte infiltration (HIS48) as revealed by intravital microscopy and immunohistochemistry of the left extensor digitorum longus muscle. After 20 minutes of local cooling, these microvascular derangements were restored to the level of controls (group I). Edema (extensor digitorum longus muscle wet-to-dry weight ratio) was less pronounced compared with noncooling conditions (group III). Immunoreactivity for HIS48 (neutrophilic granulocytes) in injured rats subjected to local cooling (group IV) was markedly decreased compared with noncooling conditions (group III). CONCLUSION: These results provide in vivo evidence that cooling affords protection of posttraumatic microcirculation through sustained inhibition of microvascular and endothelial dysfunction leading to less granulocyte-dependent inflammation and skeletal muscle edema. Local cooling appears to reduce propagation of acute microvascular injury, preventing leukocyte-dependent tissue destruction and escalation of secondary tissue damage after musculoskeletal soft-tissue trauma.

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation.

Microcirculatory disturbances are an initial causative determinant in hepatic ischemia/reperfusion injury. The aim of this study was to assess sinusoidal perfusion during human liver transplantation using orthogonal polarization spectral imaging and to evaluate the significance of intraoperative microcirculation for early postoperative graft function. Hepatic microcirculation was measured in 27 recipients undergoing full-size liver transplantation and compared to a group of 32 healthy living-related liver donors. The microvascular parameters were correlated with postoperative aspartate aminotransferase and bilirubin levels. Hepatic perfusion following liver transplantation was found to be significantly decreased when compared with the control group. Volumetric blood flow within the individual sinusoids increased due to sinusoidal dilatation and enhanced flow velocity. Regression analysis of postoperative aspartate aminotransferase and bilirubin with microvascular parameters revealed significant correlations. The extent of volumetric blood flow increased within the first 30 minutes after reperfusion and showed a significant correlation with postoperative aspartate aminotransferase release and bilirubin elimination. In conclusion, postischemic hepatic microvascular perfusion was analyzed in vivo, demonstrating significant microvascular impairment during liver transplantation. Sinusoidal hyperperfusion appears to confer protection against postischemic liver injury, as given by the correlation with aspartate aminotransferase and bilirubin levels. Thus, these findings may have therapeutic importance with respect to mechanisms mediating postischemic reactive hyperemia.

In vivo imaging of human pancreatic microcirculation and pancreatic tissue injury in clinical pancreas transplantation.

Pancreatitis remains to be a major complication following clinical pancreas transplantation. We performed orthogonal polarized spectral (OPS) imaging for direct in vivo visualization and quantification of human pancreatic microcirculation in six healthy donors for living donor liver transplantation and 13 patients undergoing simultaneous pancreas-kidney transplantation. We further determined the impact of microvascular dysfunction during early reperfusion on pancreatic graft injury. Exocrine and endocrine pancreatic impairment was determined by analysis of serum lipase, amylase and C-peptide levels. Compared to normal pancreas in liver donors (homogeneous acinar perfusion) functional capillary density (FCD) and capillary red blood flow velocity of reperfused grafts were significantly decreased. Elevated CRP concentrations on day 2 post-transplant and serum lipase and amylase levels determined on days 4-5 significantly correlated with microvascular dysfunction during the first 30 min of graft reperfusion. Post-transplant serum C-peptide also correlated significantly with pancreatic capillary perfusion. OPS imaging allows to intra-operatively assess physiologic pancreatic microcirculation and to determine microcirculatory impairment during early graft reperfusion. This impairment correlated with the manifestation of post-transplant dysfunction of both exocrine and endocrine pancreatic tissue. OPS imaging may be used clinically to determine the efficacy of interventions, aiming at attenuating microcirculatory impairment during the acute post-transplant reperfusion phase.

Acute effects of N-acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats.

Trauma-induced microcirculatory dysfunction, formation of free radicals and decreased endothelial release of nitric oxide (NO) contribute to evolving tissue damage following skeletal muscle injury. Administration of N-acetylcysteine (NAC) known to scavenge free radicals and generate NO is considered a valuable therapeutic approach. Thus, the objective of this study was to quantitatively analyze the acute effects of NAC on skeletal muscle microcirculation and leukocyte-endothelial cell interaction following severe standardized closed soft tissue injury (CSTI). Severe CSTI was induced in the hindlimbs of 14 male anesthetized Sprague-Dawley rats using the controlled impact injury technique. Rats were randomly assigned (n = 7) to high-dose intravenous infusion of NAC (400 mg/kg body weight) or isovolemic normal saline (NS). Non-injured, sham-operated animals (n = 7) were subjected to the same surgical procedures but did not receive any additional fluid. Creatin kinase (CK) activity was assessed at baseline, 1 h before and 2 h following posttraumatic NAC or NS infusion. Microcirculation of the extensor digitorum longus (EDL) muscle was analyzed using intravital microscopy and Laser-Doppler flowmetry (LDF). Edema index (EI) was calculated by measuring the EDL wet-to-dry weight ratio (EI=injured/contralateral limb). EDL-muscles were analyzed for desmin immunoreactivity and granulocyte infiltration. Microvascular deteriorations observed following NS-infusion were effectively reversed by NAC: Functional capillary density was restored to levels found in sham-operated animals and leukocyte adherence was significantly (p < 0.05) reduced compared to the NS group. NAC significantly (p < 0.05) increased erythrocyte flux determined by Laser-Doppler flowmetry. Posttraumatic serum CK levels and EI were significantly (p < 0.05) decreased by NAC. During the posttraumatic acute phase, single infusion of NAC markedly reduced posttraumatic microvascular dysfunction, attenuated both leukocyte adherence and tissue infiltration. NAC also decreased CSTI-induced edema formation and myonecrosis as reflected by attenuated serum CK levels and attenuated loss of desmin immunoreactivity. NAC may serve as an effective therapeutic strategy by supporting microvascular blood supply and tissue viability in the early posttraumatic period. Additional studies aimed at long-term analysis and investigation of injury severity--or dosage dependency are needed.

The delay of rearterialization after initial portal reperfusion in living donor liver transplantation significantly determines the development of microvascular graft dysfunction.

BACKGROUND/AIMS: Graft reperfusion in liver transplantation is usually performed by initial portal reperfusion (IPR) and delayed rearterialization. Its influence on graft microcirculation is unknown. This study aimed to assess sinusoidal perfusion in dependence to this reperfusion technique during human living-donor liver transplantation. METHODS: Hepatic microcirculation was measured both in the donor and the recipient (n=14) by using the orthogonal polarization spectral imaging technique. By using initial portal reperfusion, the mean time interval between portal venous and hepatic arterial reperfusion was 27.7+/-13.3 min. RESULTS: Hepatic nutritive perfusion, as given by the functional sinusoidal density and the volumetric blood flow, was found significantly decreased during portal reperfusion when compared to baseline. Rearterialization resulted in hyperperfusion of individual sinusoids at a decreased density of the sinusoidal network. Interestingly, the time interval between portal venous and hepatic arterial reperfusion significantly correlated with the changes of the liver grafts' microcirculation. CONCLUSIONS: The study indicates graft microcirculatory dysfunction as a major determinant of postischemic liver injury. Moreover, microvascular impairment was significantly influenced by the interval between portal venous and hepatic arterial reperfusion, which suggests the reinforcement of the pathomechanism of injury involving hypoxia and rapid graft rewarming due to initial portal reperfusion.

Immediate microcirculatory derangements in skeletal muscle and periosteum after closed tibial fracture.

BACKGROUND: Severe musculoskeletal soft tissue injury sustained after a closed fracture to the extremities significantly influences bone healing and determines the patient's prognosis. The present study was aimed at quantitatively assessing immediate microcirculatory changes in skeletal muscle and periosteum after standardized closed fracture. METHODS: Standardized closed fracture of the left tibia in isoflurane-anesthetized Sprague-Dawley rats (n = 14) was induced using a modified weight-drop technique. The left extensor digitorum longus (EDL) muscle (n = 7) and tibial periosteum (n = 7) were surgically exposed for in vivo fluorescence microscopy 15 minutes after fracture. Nonfractured rats (n = 14) served as controls. EDL muscle edema was determined by the ratio of wet to dry weight (EDL water content). RESULTS: Closed tibial fracture resulted in a significant reduction of functional capillary density, red blood cell velocity, and volumetric blood flow in both EDL muscle and periosteum. Microvascular diameter, leukocyte adherence, and macromolecular leakage were markedly increased, indicating trauma-induced inflammation and endothelial disintegration. EDL muscle edema was found increased significantly after fracture. CONCLUSION: This model permits for the first time direct in vivo visualization and quantification of fracture-induced microhemodynamic changes and cellular interactions within the surrounding soft tissue. It demonstrates that even simple fractures lead to profound microcirculatory disturbances in skeletal muscle and periosteum, and also at sites remote from the diaphyseal fracture site. It provides a useful approach for the development of therapeutic strategies to counteract fracture-induced microvascular dysfunction.

Mild cervical spine trauma showing symptomatic calcified cervical disc herniation in a child: a case report.

STUDY DESIGN: A case study was conducted. OBJECTIVE: A child with a previously unknown calcified cervical disc herniation experienced acute myelopathy after minor cervical trauma. SUMMARY AND BACKGROUND DATA: Calcified cervical intervertebral disc herniations are rare in children. Although these herniations typically pursue a benign course and respond to conservative treatment, surgical removal of the disc may become necessary if spinal cord compression becomes symptomatic. METHODS: After a minor traumatic event, a 12-year-old boy with an underlying calcified cervical disc herniation at C3-C4 experienced progressive myelopathy requiring anterior discectomy and intervertebral fusion. RESULTS: After the progression of myelopathy over a 3-week period, an anterior discectomy and fusion with autologous tricortical iliac bone graft was performed at C3-C4. Histologic analysis showed a calcified disc herniation. CONCLUSION: In the presence of a large, calcified cervical disc herniation, mild cervical trauma may result in the onset of severe spastic myelopathy warranting surgical correction.