Venous Thoracic Outlet Syndrome with an Upper Extremity Deep Vein Thrombosis Caused by a Dislocated Clavicle Fracture: A Case Report.

BACKGROUND Clavicle fractures are a relatively common injury, and are not problematic when occurring alone. Venous thoracic outlet syndrome (TOS) is generally caused by compression of the subclavian vein between the first rib and oblique muscles, and is often complicated by the presence of upper extremities deep vein thrombosis (UEDVT). Herein, we present a case of venous TOS complicated with UEDVT due to a dislocated clavicle fracture. CASE REPORT A 29-year-old man was injured in a motorcycle accident. The patient's right clavicle was fractured, and the distal part of the fracture had dislocated into his right thorax. Contrast-enhanced computed tomography showed an obstruction of the subclavian vein by the dislocated clavicle and thrombus on the distal side of the obstruction. Anticoagulant therapy was not indicated because of other injuries, such as traumatic subarachnoid hemorrhage. No vena cava filter was placed in the superior vena cava owing to the relatively low volume of the thrombus. Alternatively, intermittent pneumatic compression to the right forearm was initiated. On day 6, surgical reduction of the clavicle was performed. The thrombus remained after the reduction. The patient received anticoagulation therapy with heparin followed by oral anticoagulants. The patient was discharged without any complications of UEDVT or bleeding. CONCLUSIONS Venous TOS with UEDVT caused by trauma is rare. Anticoagulation therapy, pneumatic limb compression, and vena cava filter placement should be considered according to the degree of the obstruction and other associated injuries.

Complement Activation in Human Sepsis is Related to Sepsis-Induced Disseminated Intravascular Coagulation.

INTRODUCTION: In human sepsis, little is known about the relationships between complement activation and the clinical characteristics of sepsis, including disseminated intravascular coagulation (DIC), interventions, and prognosis. PATIENTS AND METHODS: Adult patients with sepsis admitted from November 2016 to December 2018 were included. We used the plasma levels of soluble C5b-9 (SC5b-9) as a marker of complement activation. We compared the clinical characteristics and complement components between patients with and without DIC. We also compared the clinical characteristics and each DIC parameter across quartile groups for the SC5b-9 value. RESULTS: Forty-nine sepsis patients were eligible. Thirty-four patients developed DIC, and eight patients died. The median (interquartile range) SC5b-9 value was 342 (261-501) ng/mL. Compared with patients without DIC, patients with DIC showed lower C3 levels (mean, 95.7 vs. 70.4 mg/dL, P < 0.01) and higher SC5b-9 levels (median, 287 vs. 400 ng/mL, P = 0.01). Patients were stratified by SC5b-9 quartile (ng/mL: low: < 260, moderate: 260-342, high: 343-501, highest: > 501). The mean Sequential Organ Failure Assessment score varied across these groups (P = 0.02). In the high and highest groups, many more patients received vasopressors and developed DIC. In the highest group, the coagulation parameters were severe, and thrombocytopenia was prolonged. In-hospital mortality tended to be high (33%) in the highest group. CONCLUSIONS: The degree of complement activation is related to DIC, severity, intensive interventions, and mortality. Further studies are needed to confirm the usefulness of SC5b-9 for stratifying sepsis patients.