Surgical treatment and anticoagulant therapy for liver injury due to cardiopulmonary resuscitation with lethal pulmonary embolization: A case report.

INTRODUCTION: Cardiopulmonary resuscitation (CPR) can sometimes induce organ injury, however, such an occurrence is rare. We herein report a case of liver injury due to CPR with life-threatening pulmonary embolization (PE) that required the patient to undergo surgical hemostasis and antithrombotic therapy. PRESENTATION OF CASE: A woman in her 70s fell off her bicycle. She suffered cardiopulmonary arrest and underwent CPR. She was diagnosed with PE and underwent catheter treatment and anticoagulant therapy; however, her blood pressure did not increase. Contrast-enhanced computed tomography revealed injury to the liver and inferior phrenic artery. Hemostasis could not be completely achieved by transcatheter arterial embolization alone. She was therefore transferred to our hospital and underwent damage control surgery (DCS). Definitive surgery (DS) performed 33 h after DCS showed right hepatic subcapsular hematoma and left hepatic subcapsular hematoma. We cut away the capsules and removed the hematomas. There were lacerations and oozing under the capsule in the left lobe. We sutured the laceration. At 72 h after undergoing DS, antithrombotic therapy was started. On day 19, the patient was discharged home by herself without any neurological damage. DISCUSSION: For a case of liver injury due to CPR with life-threatening PE, treatment with both hemostasis and antithrombotic therapy should be performed. Antithrombotic therapy was started appropriately in this case by accurately identifying the liver laceration and suturing it. CONCLUSION: Hemostasis following both DCS and DS with appropriate anticoagulant therapy was effective for the management of liver injury due to CPR with life-threatening PE.

A case of hemorrhagic shock due to intercostal artery injury that occurred during initial trauma care with multiple displaced rib fractures and traumatic head injury.

Rib fractures can cause injury to some organs. We herein report a case of hemorrhagic shock due to intercostal artery injury that occurred during initial trauma care (ITC) treated by resuscitative thoracotomy (RT) and transcatheter arterial embolization (TAE) with multiple displaced rib fractures (RFs) and traumatic head injury (THI). A man in his 50s who was injured in a traffic accident was transferred to our institution by helicopter for emergency medical treatment. He underwent left thoracic drainage on site. On admission, he was diagnosed with multiple RF, THI, pelvic fracture and right humerus fracture. His D-dimer and fibrin degradation products (FDP) level were extremely elevated. However, contrast enhance CT (CECT) revealed no extravasation. At 2 h after arrival, massive hemorrhaging from his thoracic tube suddenly occurred and his blood pressure decreased to approximately 40s mmHg. CECT performed after volume resuscitation and massive transfusion revealed extravasation from the intercostal artery. Because his blood pressure could not be maintained by massive transfusion, we performed RT and TAE followed by RT. He then received intensive care and several surgical procedures were performed, including craniotomy for removal of hematoma, rib fixation and humerus fixation. He was transferred to another hospital for rehabilitation on day 63, with a GCS of 15. Hemorrhagic shock due to intercostal artery injury may occur at any time from arrival in cases with displaced RF, especially when complicated by THI.

Cas9-AAV6 gene correction of beta-globin in autologous HSCs improves sickle cell disease erythropoiesis in mice.

CRISPR/Cas9-mediated beta-globin (HBB) gene correction of sickle cell disease (SCD) patient-derived hematopoietic stem cells (HSCs) in combination with autologous transplantation represents a recent paradigm in gene therapy. Although several Cas9-based HBB-correction approaches have been proposed, functional correction of in vivo erythropoiesis has not been investigated previously. Here, we use a humanized globin-cluster SCD mouse model to study Cas9-AAV6-mediated HBB-correction in functional HSCs within the context of autologous transplantation. We discover that long-term multipotent HSCs can be gene corrected ex vivo and stable hemoglobin-A production can be achieved in vivo from HBB-corrected HSCs following autologous transplantation. We observe a direct correlation between increased HBB-corrected myeloid chimerism and normalized in vivo red blood cell (RBC) features, but even low levels of chimerism resulted in robust hemoglobin-A levels. Moreover, this study offers a platform for gene editing of mouse HSCs for both basic and translational research.

Increased expression of membrane TNF-alpha on activated peripheral CD8+ T cells in systemic lupus erythematosus.

Membrane TNF-alpha is a precursor form of soluble TNF-alpha and exerts pro-inflammatory functions in a cell-to-cell contact manner. We showed that membrane TNF-alpha is induced upon activation on the cell surface of CD4+ T cells and CD8+ T cells. In patients with systemic lupus erythematosus (SLE), the percentage of membrane TNF-alpha-bearing CD8+ T cells (41.5+/-12.3%) was significantly higher compared with those of healthy controls (26.7+/-3.9%) (p=0.007) or patients with rheumatoid arthritis (29.8+/-15.4%) (p=0.038). Membrane TNF-alpha-bearing CD8+ T cells from SLE patients displayed cytotoxic activity against L929 cells. It is possible that membrane TNF-alpha may be involved in the increased apoptosis and the generation of autoantigens in SLE.