[Radiotherapy and spinal toxicity: News and perspectives]. / Radiothérapie et toxicité médullaire : actualités et perspectives.

Radiation-induced myelopathy is a devastating late effect of radiotherapy. Fortunately, this late effect is exceptional. The clinical presentation of radiation myelopathy is aspecific, typically occurring between 6 to 24 months after radiotherapy, and radiation-induced myelopathy remains a diagnosis of exclusion. Magnetic resonance imaging is the most commonly used imaging tool. Radiation oncologists must be extremely cautious to the spinal cord dose, particularly in stereotactic radiotherapy and reirradiation. Conventionally, a maximum dose of 50Gy is tolerated in normofractionated radiotherapy (1.8 to 2Gy per fraction). Repeat radiotherapies lead to consider cumulative doses above this recommendation to offer individualized reirradiation. Several factors increase the risk of radiation-induced myelopathy, such as concomitant or neurotoxic chemotherapy. The development of predictive algorithms to prevent the risk of radiation-induced myelopathy is promising. However, radiotherapy prescription should be cautious, regarding to ALARA principle (as low as reasonably achievable). As the advent of immunotherapy has improved patient survival data and the concept of oligometastatic cancer is increasing in daily practice, stereotactic treatments and reirradiations will be increasingly frequent indications. Predict the risk of radiation-induced myelopathy is therefore a major issue in the following years, and remains a daily challenge for radiation oncologists.

Peripherally inserted central catheter placement in patients with coagulation disorders: A retrospective analysis.

OBJECTIVE: To assess the safety of peripherally inserted central venous catheter (PICC) placement in patients with altered and uncorrected coagulation parameters or receiving antiplatelet therapy. MATERIALS AND METHODS: Medical charts of all patients with major primary and secondary hemostasis disorders, combined hemostasis disorders or on antiplatelet therapy and who had undergone non-tunneled PICC placement from December 2009 to December 2013, were retrospectively reviewed. A hemostatic disorder was defined as a platelet count (PC)≤50×10(9)/L, an international normalized ratio (INR) ≥ 2, or an activated partial thromboplastin time (aPTT)≥66s, alone or in combination. Underlying hemostasis disorders were not corrected and antiplatelet therapy was not interrupted before PICC placement in any patient. 4, and 5-Fr single and dual lumen PICCs were used. RESULTS: A total of 378 PICCs were placed in 271 patients (180 men and 91 women; mean age=62±13.4years; range, 18-93 years)) with coagulation disorders. Eighty-nine (23%) PICCs were placed in patients who were receiving antiplatelet therapy (aspirin, clopidogrel, rivaroxaban). Thrombocytopenia was noted in 269PICC placements (71%). Among these patients, 23 had disseminated intravascular coagulation. Prolonged INR and aPTT were observed in 42 procedures (11.1%). PICC placement was achieved in all patients, with a mean number of 1.14 attempts. Peripheral venous access was obtained through the basilic and the brachial vein respectively in 295 (79.1%) and 83 (20.9%) of patients. The placements were performed by residents and fellows in 108 (28.5%) and 270 (71.5%) procedures, respectively. No early or late complications were reported after any procedure. No accidental puncture of the brachial artery occurred. CONCLUSION: In patients with severe primary and secondary hemostasis disorders, combined hemostasis disorders or on antiplatelet therapy, PICC placement is a feasible and safe procedure and does not require correction of coagulation parameters or discontinuation of antiplatelet therapy.

Gadolinium enhancement in brain magnetic resonance imaging in progressive multifocal leukoencephalopathy after natalizumab monotherapy: is it really atypical?

Progressive multifocal leukoencephalopathy (PML) generally occurs in patients with impaired cellular immunity. Monoclonal antibodies also predispose the patient to PML as they depress the immune system. PML was classically characterized by a lack of inflammation and absence of gadolinium enhancement. However, gadolinium enhancement of PML lesions was first described in HIV-positive patients under therapy. We present a case of gadolinium enhanced PML lesions occuring after natalizumab monotherapy of a relapsing multiple sclerosis. Radiologists must be aware of this particular feature, as confirmation of the diagnostic of PML becomes more challenging. Namely, distinction between starting PML and multiple sclerosis enhanced additional active lesion is difficult and diagnosis must be established by combined analysis of full clinical evolution, brain MRI scans, and polymerase chain reaction of cerebrospinal fluid.