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Open surgical repair (OSR) of descending and thoracoabdominal aortic aneurysms carries risks of mortality and major complications. Patients with connective tissue disorders (CTD) are younger and require safe, efficient treatment with long-term durability. This study provides current outcome data to help inform treatment decisions.All OSRs of descending thoracic aortic aneurysm (DTAA) or thoracoabdominal aortic aneurysm (TAAA) from January 2011 to July 2021 were included in a retrospective cohort study. Primary outcome measures were early and follow-up mortality and reintervention. Secondary outcome measures were major complications. Kaplan-Meier methods were used to estimate reintervention-free survival.A total of 26 OSRs (7 DTAA, 19 TAAA) were performed in 23 patients: 20 (77%) Marfan and 6 (23%) Loeys-Dietz syndrome; median age 43 years. Aortic dissection was present in 100% and 3/26 (12%) were urgent. Early mortality was 1/26 (3.8%). No patient suffered spinal cord ischemia, stroke, vocal cord paralysis, or re-exploration for bleeding. The transient respiratory failure occurred in 19% (5/26) and transient renal replacement therapy in 15% (4/26). Renal function normalized in all patients within 3 months. During follow-up (median 4.6, range 0-11 years) there were no deaths and only one re-intervention on a previously operated aortic segment, resulting in 92% reintervention-free survival at 5 years.In dedicated units, open surgical DTAA and TAAA repair in patients with CTD can be performed with a very low risk of death, severe complications and, late re-intervention. For CTD patients with reasonable risk, OSR should remain the first line of treatment.

INTRODUCTION Platelets are critical for hemostasis, and a low platelet count predicts mortality in trauma. The role of platelet dysfunction in severe traumatic hemorrhage and coagulopathy needs to be further defined. The aim of this study was to evaluate the platelet function in a new model of experimental traumatic hemorrhage. MATERIAL AND METHODS New Zealand white rabbits (n = 10) were subjected to tracheostomy and trauma laparotomy, and then bilateral femur fractures with 40% hemorrhage of their estimated blood volume. Arterial blood gases, standard coagulation tests, mean platelet volume, platelet aggregation using impedance aggregometry with agonist collagen, arachidonic acid (ASPI), and adenosine diphosphate (ADP), rotational thromboelastometry, and fibrinogen binding of platelets were analyzed using flow cytometry. RESULTS After traumatic hemorrhage, there was a significant physiological response with a rise in lactate (P < .001) and a decrease in base excess (P < .001) and temperature (P < .001). Platelet count decreased from a mean of 244x109/L to 94 x109/L (P = .004) and the mean platelet volume increased from 5.1fL to 6.1fL (P = .002). Impedance aggregometry with the agonist collagen, ASPI, and ADP was all significantly decreased after hemorrhage (P = .007). However, there was an increased fibrinogen binding of ADP-activated platelets after traumatic hemorrhage analyzed by flow cytometry (P < .05). CONCLUSIONS This traumatic hemorrhage model presents two parallel pathophysiological responses of platelets; platelet consumption as evidenced by a significant decrease in platelet count and aggregation, and platelet hyperreactivity as shown by a higher mean platelet volume and enhanced platelet fibrinogen binding. Further studies are needed to characterize these different aspects of platelet function in severe traumatic hemorrhage.