Introduction: Posterior mediastinal hematoma (PMH) is a rare complication of anti-coagulation (AC) use. We present a complex case of a patient with a sub-massive pulmonary embolism (PE) whose care was complicated by PMH causing airway obstruction following thrombectomy. Case: A 60-year-old male with a history of prostate cancer in remission presented after a syncopal event. On admission, he was afebrile, mildly tachycardic (100bpm), normotensive (135/91), with no oxygen requirement. Laboratory data showed high sensitivity troponin 244 ng/L and BNP 82 pg/ml. CTPA revealed a saddle PE with right heart strain (PESI score 100). He was initiated on anticoagulation and underwent successful mechanical thrombectomy using a Penumbra aspiration catheter. He had acute respiratory failure later that evening, necessitating intubation. Repeat CTPA showed increased clot burden and new onset PMH (Figure 1). Of note, his AC was continued due to clot burden. A repeat thrombectomy was performed using the FlowTriever System Device (Inari Medical, Irvine, CA). Despite this intervention, he continued to struggle with extubation, and a new stridor was noted. Bronchoscopy revealed external compression of proximal trachea correlating with the PMH location. He was deemed too high risk for evacuation of the PMH. Therefore, he underwent tracheostomy to bypass the area of compression. This subsequently allowed for successful extubation. Discussion: While thrombectomy can cause iatrogenic bleeding, no bleeding was seen on the post-procedure angiogram in our patient. Thus, these findings are attributed to PMH. PMH has been reported 6 times in literature (table 1), one associated with PE. Management options include hematoma evacuation or holding AC and performing serial follow up imaging. Our patient did not undergo evacuation of hematoma, and a tracheostomy was used instead to bypass the obstruction. This highlights the need to individualize management of these complex patients.

Introduction: Cardiac necrotizing soft tissue infections (NSTI) have been scarcely reported in the literature. We present a rare case of a disseminated NSTI with myocardial involvement secondary to embolic phenomena from emphysematous infective endocarditis (IE). Case presentation: 73-year-old female on dialysis with atrial fibrillation and diabetes mellitus was transferred for multifocal strokes evidenced on magnetic resonance imaging. Presented with leukocytosis, lactic acidosis, acute liver failure, and right upper extremity (RUE) NSTI. She was started on antibiotics and vasopressors and taken emergently to the operating room for RUE amputation. Following surgery, an electrocardiogram revealed anterior STEMI. Bedside transthoracic echocardiogram noted a severely reduced ejection fraction and a mitral valve vegetation. Computed tomography of head and chest revealed pneumomyocardium, portal venous gas, and pneumocephalus. Blood cultures revealed growth of Clostridium perfringens. With severe multi-organ failure and a poor prognosis, comfort care was elected, and the patient expired. Figures: A: RUQ subcutaneous gas. B: Chest wall gas. C: pneumocephalus. D: pneumomyocardium. E: MV vegetation. Discussion: Septic embolization is a devastating sequela of IE. Vegetations > 1cm have increased embolic potential and all-cause mortality. The most common site of embolization is the central nervous system; however, coronary embolization can also occur. Clostridial endocarditis is rare, despite being documented as the first cause of anaerobic IE. Mortality rate of clostridial NSTI and shock exceeds 50%. Source control and rapid identification of infection are paramount for treatment success. A multidisciplinary approach should be employed when treating Clostridial infections, specifically endocarditis. Our case highlights the need for prompt recognition of IE and the interplay of multimodal imaging in the diagnosis of disseminated infection.

Introduction: Pocket hematoma is a feared complication of cardiac implantable electronic device (CIED) placement. About half the patients undergoing the procedure are on anticoagulation with consequent increased frequency of device-pocket hematoma. The risk of hematoma is variable based on the type of anticoagulation therapy. The purpose of this study was to compare the risk of device-hematoma in patients on interrupted novel oral anticoagulants (NOAC) versus uninterrupted vitamin K antagonists (VKA) during the peri-operative period. Methods: We performed a meta-analysis using electronic literature search to retrieve studies with CIED surgery on uninterrupted VKA versus interrupted NOAC (range 12-96 hours). Primary outcome of interest was pocket-hematoma. Outcomes were pooled under random-effects meta-analyses and reported as risk ratios (RRs) and 95% CIs. 5 studies with low heterogeneity (I 2 =14%), 4 observational and 1 post-hoc analysis of a randomized trial, were included. 1002 patients NOAC group=376 and VKA group=626 were followed for 4-6 weeks. Results: Baseline characteristics were similar, mean age 71 years and 71% male across both groups. There was no significant difference in endpoints: pocket hematoma (major and minor) {RR 0.74 (0.43-1.29), P=0.29}; major hematoma {RR 0.53 (0.24-1.19), P=0.13}; hematomas with new implants {RR 0.82 (0.46-1.48), P=0.51}; hematomas with generator changes {RR 1.90 (0.84-4.31), P=0.12}; hematomas with device-upgrade {RR 0.41 (0.15-1.07), P=0.07}; major bleed {RR 0.18 (0.03-1.09), P=0.06}; pericardial effusion {RR 1.01 (0.13-8.19), P=0.67}(Fig 1). One study reported peri-implantation infection (n=4/311 NOAC, n=2/467 VKA). One patient out of all 5 studies had systemic thromboembolism in each group (1/837 NOAC, 1/1000 VKA). Conclusion: Interrupted NOAC use is not associated with a higher risk of pocket hematoma compared to uninterrupted VKA after CIED placement.

No abstract