Arterial embolization of an extrapleural hematoma from a dislocated fracture of the lumbar spine: a case report

<p>Abstract</p> <p>Background</p> <p>We present a report of a blunt-trauma patient who developed an atypical extrapleural hematoma with hemodynamic instability following a dislocation fracture of the first lumbar vertebra. We successfully treated her with arterial embolization (AE) of the lumbar and intercostal arteries.</p> <p>Case report</p> <p>The patient, a 74-year-old woman, was injured in a traffic accident. At the scene of the accident, she was found to be alert, and her hemodynamic condition was stable. She arrived at our hospital complaining of lumbago. A thoracoabdominal computed tomography (CT) scan with contrast enhancement showed a dislocation fracture of the first lumbar vertebra along with paravertebral and retroperitoneal hematomas. Therefore, we managed the patient conservatively with bed rest. However, 3 h after admission, her blood pressure suddenly decreased. A repeated thoracoabdominal CT scan showed enlargement of the right retroperitoneal hematoma with extravasation of the contrast medium into the right extrapleural space. Angiography was immediately performed, showing extravasation of the contrast media from the right intercostal (Th12) and lumbar arteries (L1). After arterial embolization (AE) with gelatin-sponge particles, extravasation of the contrast medium ceased, and the patient's hemodynamic condition stabilized without massive fluid resuscitation.</p> <p>Conclusion</p> <p>The extrapleural hematoma reduced in size after AE, and almost disappeared on the 14^thday of hospitalization. The lumbar spinal fracture was successfully repaired on day 16, and the patient was kept in the hospital to recuperate. We believe that AE is effective for the management of intractable bleeding following fractures of the spine.</p

Arterial embolization in patients with grade-4 blunt renal trauma: evaluation of the glomerular filtration rates by dynamic scintigraphy with 99mTechnetium-diethylene triamine pentacetic acid

<p>Abstract</p> <p>Background</p> <p>High-grade blunt renal trauma has been treated by arterial embolization (AE). However, it is unknown whether AE preserves renal function, because conventional renal function tests reflect total renal function and not the function of the injured kidney alone. Dynamic scintigraphy can assess differential renal function.</p> <p>Methods</p> <p>We performed AE in 17 patients with grade-4 blunt renal trauma and determined their serum creatinine (sCr) level and glomerular filtration rate (GFR; estimated by dynamic scintigraphy) after 3 months. In 4 patients with low GFR of the injured kidney (<20 ml·min^-1·1.73 m^-2), the GFR and sCr were measured again at 6 months. Data are presented as median and interquartile range (25th, 75th percentile).</p> <p>Results</p> <p>The median GFR of the injured kidney, total GFR, and median sCr at 3 months were 29.3 (23.7, 35.3) and 96.8 (79.1, 102.6) ml·min^-1·1.73 m^-2and 0.6 (0.5, 0.7) mg/dl, respectively. In the patients with low GFR (ml·min^-1·1.73 m^-2), the median GFR of the injured kidney, total GFR, and median sCr (mg/dl) were 16.2 (15.7, 16.3), 68.7 (61.1, 71.6), and 0.7 (0.7, 0.9), respectively, at 3 months and 34.5 (29.2, 37.0), 90.9 (79.1, 98.8), and 0.7 (0.7, 0.8), respectively, at 6 months.</p> <p>Conclusions</p> <p>The function of the injured kidney was preserved in all patients, indicating the efficacy of AE for the treatment of grade-4 blunt renal trauma.</p

Genome-Scale CRISPR/Cas9 Screening Reveals Squalene Epoxidase as a Susceptibility Factor for Cytotoxicity of Malformin A1

Malformin A1 (MA1) is a fungus-produced cyclic pentapeptide. MA1 exhibits teratogenicity to plants, fibrinolysis-enhancing activity, and cytotoxicity to mammalian cells. To clarify the cytotoxic mechanism of MA1, we screened for the genes involved in the cytotoxicity of MA1 in monocytoid U937 cells by using a CRISPR/Cas9-based genome-wide knockout library. Screening was performed by positive selection for cells that were resistant to MA1 treatment, and single guide RNAs (sgRNAs) integrated into MA1-resistant cells were analyzed by high-throughput sequencing. As a result of the evaluation of sgRNAs that were enriched in MA1-resistant cells, SQLE, which encodes squalene epoxidase, was identified as a candidate gene. SQLE-depleted U937 cells were viable in the presence of MA1, and squalene epoxidase inhibitor conferred MA1 resistance to wild-type cells. These results indicate that squalene epoxidase is implicated in the cytotoxicity of MA1. This finding represents a new insight into applications of MA1 for treating ischemic diseases

Current strategy for hollow viscus injury with active bleeding: A case report

Despite rapid advancements in medical technologies, the use of interventional radiology in a patient with hemodynamic instability or hollow viscus injury remains controversial. Here, we discuss important aspects regarding the use of interventional radiology for such patients. A 74-year-old Japanese male climber was injured following a 10 m fall. On admission, his systolic blood pressure was 40 mmHg. He had disturbance of consciousness and mild upper abdominal pain without peritoneal irritation. Focused assessment sonography for trauma indicated massive hemorrhage in the intra-abdominal cavity. Plain radiographs revealed hemopneumothorax with right-side rib fractures. Thoracostomy to the right thoracic cavity and massive transfusion were immediately performed. Consequently, a sheath catheter was inserted into the common femoral artery for interventional radiology. His systolic blood pressure increased to 80 mmHg owing to rapid transfusion. In the computed tomography scan room, based on computed tomography findings, we judged that it was possible to achieve hemostasis by interventional radiology. The time from hospital admission to entering the angiography suite was 38 min. Transcatheter arterial embolization for hemorrhage control was performed without complications. Following transcatheter arterial embolization, he was admitted to the intensive care unit. All injuries could be treated conservatively without surgery. His post-interventional course was uneventful, and he recovered completely after rehabilitation. Hemorrhage control using interventional radiology should be assessed as a first-line treatment, even in hemodynamically unstable patients having a hollow viscus injury with active bleeding, without obvious findings that indicate surgical repair

Optimal compressive force accelerates osteoclastogenesis in RAW264.7 cells

Mechanical stress produced by orthodontic forces is a factor in the remodeling of periodontal ligaments (PDLs) and alveolar bone. It has been reported that the expression of a number of cytokines associated with osteoclastogenesis is upregulated when compressive forces act on osteoblasts and PDL cells. The present study investigated the effects of compressive forces on the formation of osteoclasts from the macrophage cell line RAW264.7. Compressive forces on osteoclasts were exerted using layers of 3, 5, 7, 9 or 14 glass cover slips on the 4th day of culture for 24 h. The number of osteoclasts was determined by counting the number of cells positive for tartrate-resistant acid phosphatase staining. Osteoclastogenesis advanced rapidly on days four and five. The number of osteoclasts with >8 nuclei peaked when the force of 7 slips was applied, which was therefore regarded as the optimal compressive force. Alterations in the expression of osteoclast-associated genes are associated with changes in the differentiation and fusion of macrophages in response to compressive forces; therefore, osteoclast-associated genes were assessed by reverse transcription quantitative polymerase chain reaction in the present study. The mRNA expression of osteoclast-associated genes increased significantly after 3 h of optimal compression, whereas mRNA expression increased after 24 h in the control group. These findings suggested that osteoclastogenesis of macrophages was accelerated when an optimal compressive force was applied

Release from optimal compressive force suppresses osteoclast differentiation

Bone remodeling is an important factor in orthodontic tooth movement. During orthodontic treatment, osteoclasts are subjected to various mechanical stimuli, and this promotes or inhibits osteoclast differentiation and fusion. It has been previously reported that the release from tensile force induces osteoclast differentiation. However, little is known about how release from compressive force affects osteoclasts. The present study investigated the effects of release from compressive force on osteoclasts. The number of tartrate-resistant acid phosphatase (TRAP) -positive multinucleated osteoclasts derived from RAW264.7 cells was counted, and gene expression associated with osteoclast differentiation and fusion in response to release from compressive force was evaluated by reverse transcription-quantitative polymerase chain reaction. Osteoclast number was increased by optimal compressive force application. On release from this force, osteoclast differentiation and fusion were suppressed. mRNA expression of NFATc1 was inhibited for 6 h subsequent to release from compressive force. mRNA expression of the other osteoclast-specific genes, TRAP, RANK, matrix metalloproteinase-9, cathepsin-K, chloride channel 7, ATPase H+ transporting vacuolar proton pump member I, dendritic cell-specific transmembrane protein and osteoclast stimulatory transmembrane protein (OC-STAMP) was significantly inhibited at 3 h following release from compressive force compared with control cells. These findings suggest that release from optimal compressive force suppresses osteoclast differentiation and fusion, which may be important for developing orthodontic treatments