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INTRODUCTION: Most tumour-related pathological fractures occur in patients with bone metastases. However, in mostly younger patients, a pathological fracture can be due to both a benign or a malignant bone tumour. Making the correct diagnosis from among these two differential diagnoses is enormously important. If the tumour is malignant, treating the fracture inevitably leads to tumour cell contamination and can significantly worsen the oncological situation. The aim of this review article is firstly to provide the reader with diagnostic assistance in the case of suspected pathological fractures, and secondly to focus on the treatment of pathological fractures occurring with benign bone tumours. METHODS: This is a non-systematic review of the diagnosis and treatment of pathological fractures in benign bone tumours or tumour-like lesions, based on an electronic PubMed database search. We also present our own procedures, in particular for ruling out a malignant bone tumour. RESULTS AND DISCUSSION: Whenever a fracture occurs in the absence of sufficient traumatic force, the possibility of a pathological fracture should always be considered. As well as taking a general history for a possible primary tumour, it is particularly important to ask the patient whether they had any pain before the fracture occurred. If the findings from clinical examination or conventional radiological imaging give rise to suspicion of a pathological fracture, an MRI of the affected skeletal section with contrast medium should be carried out before commencing any fracture treatment. A CT scan is also helpful for accurately assessing bone destruction. If a malignant or locally aggressive benign bone tumour such as giant cell tumour (GCT) or aneurysmal bone cyst (ABC) cannot be definitively ruled out through imaging, a biopsy is essential. The bone biopsy must always be carried out on the assumption that the histological work-up will reveal a malignant bone tumour; it must therefore be performed according to strict oncological criteria. If the radiological diagnosis is unambiguous, e. g., a juvenile bone cyst (JBC) or a non-ossifying fibroma (NOF), conservative treatment of the fracture can be considered, depending on the location. In the presence of a locally aggressive benign bone tumour such as a GCT or ABC, curettage of the tumour must be carried out as well as treating the fracture. With GCT in particular, neoadjuvant therapy with denosumab prior to curettage and osteosynthesis or en bloc resection of the tumour should be considered, depending on the extent of the tumour. CONCLUSION: Pathological fractures, especially in younger patients, should not be overlooked. Only after a malignant or benign locally aggressive bone tumour has been definitively ruled out should fracture treatment be performed. In the presence of a locally aggressive bone tumour, as well as treating the fracture, it is usually necessary to perform curettage of the tumour - also en bloc resection, where applicable, in the case of a GCT. Depending on the location, benign, non-aggressive tumours can be treated conservatively if necessary.
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BACKGROUND: Coagulopathy following severe trauma contributes significantly to mortality. Impaired clotting factors have been observed in adult trauma patients, but in pediatric trauma victims their activity has not yet been investigated. METHODS: Sixteen pediatric trauma patients were evaluated according to the ISS and assigned to two cohorts. An additional control group (CO; n = 10) was formed. Routine coagulation parameters and the soluble clotting factors (F) were tested. Nonparametric data was analyzed using the Mann-Whitney U test. Results are reported as median and interquartile range. RESULTS: The ISS of severely (SI, n = 8) and mildly (MI, n = 8) injured children differed significantly (25 [19-28] vs. 5 [4-6]; p < 0.001). INR was elevated in the SI cohort only when compared to the CO (1.21 [1.04-1.58] vs. 0.96 [0.93-1.00]; p = 0.001). Differences between SI and MI were found for FII (67 [53-90] vs. 82 [76-114] %; p = 0.028), FV (76 [47-88] vs. 92 [82-99] %; p = 0.028), and FXIII (67 [62-87] vs. 90 [77-102] %; p = 0.021). Comparison of the SI with the CO (FII 122 [112-144] %; p < 0.001; FV 123 [100-142] %; p = 0.002; and FXIII 102 [79-115] %; p = 0.006) also revealed a reduction in the activity of these factors. Furthermore, fibrinogen (198 [80-242] vs. 296 [204-324] mg/dl; p = 0.034), FVII (71 [63-97] vs. 114 [100-152] %; p = 0.009), FIX (84 [67-103] vs. 110 [90-114] %; p = 0.043), and FX (70 [61-85] vs. 122 [96-140] %; p = 0.001) were reduced in the SI in comparison with the CO. Finally, FVIII was considerably, yet not significantly, increased in both patient cohorts (235 [91-320] % and 197 [164-238] %, respectively). CONCLUSIONS: This study proves that children suffer a depletion of clotting factors following severe injury which basically reflects the findings for adult trauma patients. Attempts to correct the impaired clotting factor activity could be based on a specific hemostatic therapy involving administration of coagulation factors. Nevertheless, therapeutic implications need to be investigated in future studies.
