Abstract Introduction Clot in transit (CIT) is a rare, life threatening form of venous thromboembolism (VTE) involving a mobile right-heart thrombus en-route to the pulmonary arteries. Cirrhosis increases VTE risk by approximately twofold. We describe a case of CIT masquerading as sepsis in a cirrhotic patient, underscoring the need for prompt evaluation and management. Case Presentation A 53-year-old female with cirrhosis of unknown etiology and recurrent ascites who presented with weakness, lightheadedness, and abdominal distention. Blood pressure was 77/46 mm Hg with a heart rate of 95. Laboratory studies showed a leukocytosis (WBC 11.7 × 109/L) and elevated lactate (4.3 mmol/L) with normal coagulation studies. Diagnostic paracentesis revealed 253 nucleated white cells. During critical care evaluation the patient became unresponsive and required cardiopulmonary resuscitation. Return of spontaneous circulation was briefly achieved, and bedside echocardiography demonstrated a large clot in transit within the right ventricle. Given her comorbidities, the family declined thrombolytic therapy, and the patient subsequently expired. Discussion Clot in transit refers to a mobile thrombus, temporarily lodged within the right heart chambers en-route to the pulmonary arteries. This phenomenon represents a critical, life-threatening stage of VTE carrying a mortality rate of 29-45%. Echocardiography is the primary diagnostic modality, revealing a free-floating or partially adherent mass within the right heart. Mortality in patients with a clot in transit is significantly higher than in those with pulmonary embolism alone, primarily due to the risk of acute hemodynamic collapse. Prompt diagnosis with point-of-care ultrasound or echocardiography is therefore essential. Management includes systemic anticoagulation, thrombolysis, catheter-directed thrombectomy, or surgical embolectomy, dictated by patient stability, comorbidities, and clot morphology. In this case, a relative hypercoagulable state likely contributed to thrombus formation, despite normal standard coagulation tests. This paradox may be explained by decreased synthesis of hepatic clotting factors in conjunction with elevated endothelial derived factors such as factors VIII and von Willebrand factor. While cirrhotic patients have a 2.6 fold increased risk of sepsis and hypotension compared to those without liver disease, alternative causes of hypotension, such as thromboembolic events, must be considered. This rare presentation of clot in transit underscores the importance of maintaining a high index of suspicion for thromboembolic complications in patients with advanced liver disease. Conclusion Clot in transit should be considered in cirrhotic patients with unexplained hypotension. Early echocardiographic evaluation is essential to distinguish clot in transit from sepsis and guide life saving therapy. This abstract is funded by: None
Singh et al. (Fri,) studied this question.