Survival benefits of interventional radiology and surgical teams collaboration during primary trauma surveys: a single-centre retrospective cohort study.

BACKGROUND: A team approach is essential for effective trauma management. Close collaboration between interventional radiologists and surgeons during the initial management of trauma patients is important for prompt and accurate trauma care. This study aimed to determine whether trauma patients benefit from close collaboration between interventional radiology (IR) and surgical teams during the primary trauma survey. METHODS: A retrospective observational study was conducted between 2014 and 2021 at a single institution. Patients were assigned to an embolization group (EG), a surgery group (SG), or a combination group (CG) according to their treatment. The primary and secondary outcomes were survival at hospital discharge compared with the probability of survival (Ps) and the time course of treatment. RESULTS: The analysis included 197 patients, consisting of 135 men and 62 women, with a median age of 56 [IQR, 38-72] years and an injury severity score of 20 [10-29]. The EG, SG, and CG included 114, 48, and 35 patients, respectively. Differences in organ injury patterns were observed between the three groups. In-hospital survival rates in all three groups were higher than the Ps. In particular, the survival rate in the CG was 15.5% higher than the Ps (95% CI: 7.5-23.6%; p < 0.001). In the CG, the median time for starting the initial procedure was 53 [37-79] min and the procedure times for IR and surgery were 48 [29-72] min and 63 [35-94] min, respectively. Those times were significantly shorter among three groups. CONCLUSION: Close collaboration between IR and surgical teams, including the primary survey, improves the survival of severe trauma patients who require both IR procedures and surgeries by improving appropriate treatment selection and reducing the time process.

Senescence in brain pericytes attenuates blood-brain barrier function in vitro: A comparison of serially passaged and isolated pericytes from aged rat brains.

Aging is associated with the dysfunction of the blood-brain barrier (BBB), which comprises brain microvessel endothelial cells (BMECs), astrocytes, and pericytes. Pericytes are present at intervals along the walls of the brain capillaries and play a key role in maintaining BBB integrity. Accumulation of senescent cells and the senescence-associated secretory phenotype (SASP) in the brain facilitate the development of age-related neurodegenerative diseases with BBB dysfunction. However, the ability of pericytes to support BBB integrity and their correlation with cellular senescence or aging remain unknown. Here, we investigated cellular senescence in pericytes focusing on its impact on BBB function using BBB models comprising intact BMECs co-cultured with senescent pericytes, which were obtained through a serial passage or isolated from 18-month-old rats. To assess BBB function, transendothelial electrical resistance (TEER) and permeability of sodium fluorescein (Na-F) were studied. Both serially passaged pericytes (in passage 4, 7, and 10) and aged pericytes isolated from 18-month-old rats showed decreased TEER and enhanced permeability of BMECs to Na-F compared to that of normal pericytes (passage 2 or young). Furthermore, serially passaged and aged pericytes showed characteristic features of cellular senescence, including increased ß-galactosidase activity, cell cycle arrest, enhanced expression of mRNA, and SASP factors. However, the senescence-induced mRNA expression profile of pericyte markers varied between serially passaged and aged pericytes. Hence, in vitro serial passages and isolation from naturally aged rodents differently influenced genetic and biochemical features of senescent brain pericytes. We conclude that senescent brain pericytes can induce BBB dysfunction and those isolated from aged rodents retain the senescence-specific properties. Our findings provide an alternative tool to investigate the senescence in brain pericytes in vitro.

Bortezomib Increased Vascular Permeability by Decreasing Cell-Cell Junction Molecules in Human Pulmonary Microvascular Endothelial Cells.

Bortezomib (BTZ), a chemotherapeutic drug used to treat multiple myeloma, induces life-threatening side effects, including severe pulmonary toxicity. However, the mechanisms underlying these effects remain unclear. The objectives of this study were to (1) investigate whether BTZ influences vascular permeability and (2) clarify the effect of BTZ on the expression of molecules associated with cell-cell junctions using human pulmonary microvascular endothelial cells in vitro. Clinically relevant concentrations of BTZ induced limited cytotoxicity and increased the permeability of human pulmonary microvascular endothelial cell monolayers. BTZ decreased the protein expression of claudin-5, occludin, and VE-cadherin but not that of ZO-1 and ß-catenin. Additionally, BTZ decreased the mRNA expression of claudin-5, occludin, ZO-1, VE-cadherin, and ß-catenin. Our results suggest that BTZ increases the vascular permeability of the pulmonary microvascular endothelium by downregulating cell-cell junction molecules, particularly claudin-5, occludin, and VE-cadherin.

Levetiracetam Suppresses the Infiltration of Neutrophils and Monocytes and Downregulates Many Inflammatory Cytokines during Epileptogenesis in Pilocarpine-Induced Status Epilepticus Mice.

Acute brain inflammation after status epilepticus (SE) is involved in blood-brain barrier (BBB) dysfunction and brain edema, which cause the development of post-SE symptomatic epilepsy. Using pilocarpine-induced SE mice, we previously reported that treatment with levetiracetam (LEV) after SE suppresses increased expression levels of proinflammatory mediators during epileptogenesis and prevents the development of spontaneous recurrent seizures. However, it remains unclear how LEV suppresses neuroinflammation after SE. In this study, we demonstrated that LEV suppressed the infiltration of CD11b+CD45high cells into the brain after SE. CD11b+CD45high cells appeared in the hippocampus between 1 and 4 days after SE and contained Ly6G+Ly6C+ and Ly6G-Ly6C+ cells. Ly6G+Ly6C+ cells expressed higher levels of proinflammatory cytokines such as IL-1ß and TNFα suggesting that these cells were inflammatory neutrophils. Depletion of peripheral Ly6G+Ly6C+ cells prior to SE by anti-Ly6G antibody (NIMP-R14) treatment completely suppressed the infiltration of Ly6G+Ly6C+ cells into the brain. Proteome analysis revealed the downregulation of a variety of inflammatory cytokines, which exhibited increased expression in the post-SE hippocampus. These results suggest that Ly6G+Ly6C+ neutrophils are involved in the induction of acute brain inflammation after SE. The proteome expression profile of the hippocampus treated with LEV after SE was similar to that after NIMP-R14 treatment. Therefore, LEV may prevent acute brain inflammation after SE by suppressing inflammatory neutrophil infiltration.

Testosterone deficiency promotes the development of pulmonary emphysema in orchiectomized mice exposed to elastase.

Testosterone deficiency is commonly observed in male patients with chronic obstructive pulmonary disease (COPD), which is characterized by chronic inflammation of the airways and pulmonary emphysema. Although clinical trials have indicated that testosterone replacement therapy can improve respiratory function in patients with COPD, the role of testosterone in the pathogenesis of COPD remains unclear. The aim of this study was to explore the effect of testosterone deficiency on the development of pulmonary emphysema in orchiectomized (ORX) mice exposed to porcine pancreatic elastase (PPE). ORX mice developed more severe emphysematous changes 21 d after PPE inhalation than non-ORX mice. Testosterone propionate supplementation significantly reduced PPE-induced emphysematous changes in ORX mice. PPE exposure also increased the number of neutrophils and T cells in bronchoalveolar lavage fluid (BALF) of mice that had undergone ORX and sham surgery. T cell counts were significantly higher in the BALF of ORX mice than of sham mice. Testosterone supplementation reduced the infiltration of T cells into BALF and alleviated emphysematous changes in the lungs of ORX mice. Our findings suggest that testosterone, a male-specific hormone, may suppress the development of pulmonary emphysema through the regulation of T cell-mediated immunity.

Usefulness of virtual parenchymal perfusion software visualizing embolized areas to determine optimal catheter position in superselective conventional transarterial chemoembolization for hepatocellular carcinoma.

AIM: To determine the optimal catheter position during superselective conventional transarterial chemoembolization (cTACE) for hepatocellular carcinoma (HCC) using virtual parenchymal perfusion software. METHODS: Patients who had newly developed HCC nodules ≤6 cm and five or fewer lesions were eligible. The virtual catheter tip was placed on a tumor-feeder identified by TACE guidance software using cone-beam computed tomography during hepatic arteriography to minimize the virtual embolized area (VEA), including the tumor with a safety margin. Conventional transarterial chemoembolization was then carried out at the same position. The VEA and real embolized area where iodized oil was retained on cone-beam computed tomography after cTACE were compared using the dice similarity coefficient, linear regression analysis, and mean surface distance. Technical success of cTACE and therapeutic effects by the modified Response Evaluation Criteria in Solid Tumors were also evaluated. RESULTS: Ninety-one tumors in 56 patients were embolized. The mean dice similarity coefficient values in 80 VEAs and real embolized areas were 0.78 ± 0.01. Both volumes were well correlated (r = 0.957, p < 0.001) with a mean surface distance of 2.78 ± 2.11 mm. Eighty-four (92.3%) tumors were embolized with a safety margin. Regarding the early response of 82 tumors, complete response was achieved in 72 (87.8%), partial response in six (7.3%), and stable disease in four (4.9%). Regarding responses of 81 tumors during the follow-up (mean, 20 ± 4.9 months), complete response was maintained in 62 (76.5%), whereas 19 (23.5%), including six that were incompletely embolized, locally progressed. CONCLUSION: Virtual parenchymal perfusion software can determine the optimal catheter position in superselective cTACE.

Monomeric α-synuclein induces blood-brain barrier dysfunction through activated brain pericytes releasing inflammatory mediators in vitro.

Blood-brain barrier (BBB) disruption is often mediated by neuroinflammation, and occurs during various neurodegenerative diseases including Parkinson's disease (PD). PD is characterized by loss of dopaminergic neurons and aggregated α-synuclein protein in inclusions known as Lewy bodies. Misfolded α-synuclein has been implicated in neurodegeneration and neuroinflammation through activation of microglia and astrocytes. Pericytes are a key cellular regulator of the BBB, although it is not known if they participate in α-synuclein-associated PD pathology. Here, we investigated the impact of pericytes on BBB integrity in response to α-synuclein using rat brain endothelial cells (RBECs) co-cultured with rat brain pericytes (RBEC/pericyte co-culture). In RBEC/pericyte co-cultures, α-synuclein added to the abluminal chamber (where pericytes were grown) significantly increased RBEC permeability to sodium fluorescein. In contrast, it had no marked effect when added to the luminal chamber. In the absence of pericytes, both luminal and abluminal addition of α-synuclein failed to affect permeability of the RBEC monolayer. α-Synuclein did not self-assemble in culture media within 24 h, suggesting that monomeric α-synuclein can disrupt the BBB by interacting with pericytes. We found that in response to α-synuclein, pericytes, but not RBECs, released interleukin (IL)-1ß, IL-6, monocyte chemotactic protein (MCP)-1, tumor necrosis factor (TNF)-α, and matrix metalloproteinase-9 (MMP-9). α-Synuclein did not affect platelet-derived growth factor (PDGF)-BB release from RBECs and PDGF receptor-ß expression in pericytes. These results suggest that pericytes are more sensitive to monomeric α-synuclein than RBECs regarding release of various inflammatory cytokines/chemokines and MMP-9. Thus, monomeric α-synuclein-activated pericytes may contribute to BBB breakdown in patients with PD.

Feeding-produced subchronic high plasma levels of uric acid improve behavioral dysfunction in 6-hydroxydopamine-induced mouse model of Parkinson's disease.

The development of Parkinson's disease (PD) involves the degeneration of dopaminergic neurons caused by oxidative stress. Accumulating clinical evidence indicates that high blood levels of uric acid (UA), an intrinsic antioxidative substance, are associated with reduced risk of PD. However, this hypothesis has not been confirmed by in-vivo experiments. The present study investigated the effects of UA on behavioral abnormalities in the development of PD. We used unilateral 6-hydroxydopamine-lesioned mice, which were fed on a diet containing 1% UA and 2.5% potassium oxonate (an uricase inhibitor) to induce hyperuricemia. A significant elevation in UA levels was found in groups that were fed a UA diet. The 6-hydroxydopamine-lesioned mice showed impaired rotarod performance and increased apomorphine-induced contralateral rotations. These behavioral abnormalities were significantly reversed by feeding a UA diet for 1 week before and 5 weeks after surgery (subchronic hyperuricemia). These behavioral improvements occurred in parallel with recovery of tyrosine hydroxylase protein levels in the lesioned striatal side. The present study with a dietary hyperuricemia mice model confirms that UA exerts a neuroprotective effect on dopaminergic neuronal loss, improving motor dysfunction and ameliorating PD development.

CT Findings of Thoracic Paravertebral Lesions in IgG4-Related Disease.

OBJECTIVE. The objective of our study was to characterize the CT findings of IgG4-related paravertebral lesions. MATERIALS AND METHODS. We selected cases of IgG4-related paravertebral lesions that satisfied two inclusion criteria: first, lesions in patients with IgG4-related disease diagnosed by a multidisciplinary approach between April 2007 and June 2018; and, second, patients who had soft-tissue lesions in paravertebral regions on CT images. We added one case of an IgG4-related paravertebral lesion diagnosed pathologically in 2003. Finally, the study consisted of 30 patients (25 men and five women; median age, 69.5 years). We retrospectively evaluated the CT findings of the paravertebral lesions. RESULTS. A total of 31 paravertebral lesions were identified in 30 patients. All lesions were located around thoracic vertebrae, particularly the lower thoracic regions (n = 30). Twenty-six lesions (84%) involved two or more vertebrae in a row. The right side of vertebrae was predominantly affected in all cases except one (30/31 lesions). Radiologically, the paravertebral lesions were characterized as a bandlike, demarcated soft-tissue mass (mean maximum thickness, 8.7 mm) with homogeneous enhancement on late phase images of contrast-enhanced CT. All patients had IgG4-related lesions at other sites. Histologically, paravertebral lesions showed sclerosing inflammation consisting of diffuse lymphoplasmacytic infiltrations with many IgG4-positive plasma cells and irregular fibrosis. CONCLUSION. IgG4-related paravertebral lesions occur mainly in the right side of the lower thoracic vertebrae and present as a homogeneously enhanced bandlike mass corresponding to plasma cell-rich sclerosing inflammation.

Oncostatin M-induced blood-brain barrier impairment is due to prolonged activation of STAT3 signaling in vitro.

Oncostatin M (OSM) is a member of the interleukin (IL)-6 family cytokines. We previously demonstrated that OSM induces blood-brain barrier (BBB) impairment. However, functional characterization of IL-6 family cytokines in BBB regulation and the cytokine-related intracellular signaling pathway remain unclear. In this study, we demonstrate that among IL-6 family cytokines, including IL-6 and leukemia inhibitory factor (LIF), OSM is the most potent molecule for inducing BBB dysfunction via prolonged activation of signal transducer and activator of transcription (STAT) 3 following Janus-activated kinase (JAK) activation. OSM but not IL-6 and LIF (100 ng/mL for 24 hours) markedly produced increased sodium fluorescein permeability and decreased transendothelial electrical resistance in rat brain endothelial cell (RBEC) monolayers. This OSM-induced BBB dysfunction was accompanied by decreased levels of claudin-5 expression in RBECs, which were ameliorated by JAK inhibitor. We examined the time-course of STAT3 phosphorylation in RBECs treated with OSM, IL-6, and LIF. OSM upregulated STAT3 phosphorylation levels during a 24 hours period with a peak at 10 minutes. While IL-6 and LIF transiently increased phosphorylated STAT3 at 10 minutes after addition, this phosphorylation decreased during the period from 1 to 24 hours after addition. These findings suggest that OSM-induced sustained increases in STAT3 phosphorylation levels largely contribute to BBB impairment. Thus, elevated OSM levels and activation of brain endothelial JAK/STAT3 signaling pathway under pathological conditions should be considered as a possible hallmark for induction and development of BBB impairment.

Initial inferior vena cava diameter predicts massive transfusion requirements in blunt trauma patients: A retrospective cohort study.

OBJECTIVES: The inferior vena cava (IVC) diameter is associated with shock and increased mortality in trauma patients. However, there are no reports examining the association between the IVC diameter and massive transfusion (MT) requirements in trauma patients. The aim of this study was to evaluate the association between IVC diameter and MT requirements in patients with blunt trauma. METHODS: We retrospectively reviewed all patients who were consecutively hospitalized with blunt trauma (Injury Severity Score [ISS] ≥16) between from November 1, 2011 to March 30, 2016. Univariate and multivariate analyzes were performed to identify the independent predictors of MT (defined as >10units of red cell concentrate transfusions within 24h of admission). Receiver operating characteristic curve and the area under the curve (AUC) were estimated. RESULTS: Of the 222 patients included in this study, MT occurred in 22.5% patients. On multiple regression analysis, IVC diameter [Odds ratio (OR), 0.88; 95% confidence interval (CI), 0.80-0.96; p<0.01], fibrin degradation product (FDP; OR, 1.01; 95% CI, 1.00-1.01; p<0.01), and fibrinogen level (OR, 0.99; 95% CI, 0.98-1.00; p<0.01) were strong predictors of MT. IVC diameter demonstrated moderate accuracy (AUC, 0.74; cutoff level, 13.0mm; sensitivity, 67%; specificity, 73%). Combined cutoff levels of FDP <80.5µg/ml, fibrinogen ≥165mg/dl, and IVC diameter ≥13mm could also determine how unnecessary a MT was with 100% accuracy. CONCLUSIONS: Initial IVC diameter is a predictor of MT in blunt trauma patients.

Fewer REBOA complications with smaller devices and partial occlusion: evidence from a multicentre registry in Japan.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) performed by emergency physicians has been gaining acceptance as a less invasive technique than resuscitative thoracotomy. OBJECTIVE: To evaluate access-related complications and duration of occlusions during REBOA. METHODS: Patients with haemorrhagic shock requiring REBOA, from 18 hospitals in Japan, included in the DIRECT-IABO Registry were studied. REBOA-related characteristics were compared between non-survivors and survivors at 24 hours. 24-Hour survivors were categorised into groups with small (≤8 Fr), large (≥9 Fr) or unusual sheaths (oversized or multiple) to assess the relationship between the sheath size and complications. Haemodynamic response, occlusion duration and outcomes were compared between groups with partial and complete REBOA. RESULTS: Between August 2011 and December 2015, 142 adults undergoing REBOA were analysed. REBOA procedures were predominantly (94%) performed by emergency medicine (EM) physicians. The median duration of the small sheath (n=53) was 19 hours compared with 7.5 hours for the larger sheaths (P=0.025). Smaller sheaths were more likely to be removed using external manual compression (96% vs 45%, P<0.001). One case of a common femoral artery thrombus (large group) and two cases of amputation (unusual group) were identified. Partial REBOA was carried out in more cases (n=78) and resulted in a better haemodynamic response than complete REBOA (improvement in haemodynamics, 92% vs 70%, P=0.004; achievement of stability, 78% vs 51%, P=0.007) and allowed longer occlusion duration (median 58 vs 33 min, P=0.041). No statistically significant difference in 24-hour or 30-day survival was found between partial and complete REBOA. CONCLUSION: In Japan, EM physicians undertake the majority of REBOA procedures. Smaller sheaths appear to have fewer complications despite relatively prolonged placement and require external compression on removal. Although REBOA is a rarely performed procedure, partial REBOA, which may extend the occlusion duration without a reduction in survival, is used more commonly in Japan.

The novel heart-specific RING finger protein 207 is involved in energy metabolism in cardiomyocytes.

A failing heart shows severe energy insufficiency, and it is presumed that this energy shortage plays a critical role in the development of cardiac dysfunction. However, little is known about the mechanisms that cause energy metabolic alterations in the failing heart. Here, we show that the novel RING-finger protein 207 (RNF207), which is specifically expressed in the heart, plays a role in cardiac energy metabolism. Depletion of RNF207 in neonatal rat cardiomyocytes (NRCs) leads to a reduced cellular concentration of adenosine triphosphate (ATP) and mitochondrial dysfunction. Consistent with this result, we observed here that the expression of RNF207 was significantly reduced in mice with common cardiac diseases including heart failure. Intriguingly, proteomic approaches revealed that RNF207 interacts with the voltage-dependent anion channel (VDAC), which is considered to be a key regulator of mitochondria function, as an RNF207-interacting protein. Our findings indicate that RNF207 is involved in ATP production by cardiomyocytes, suggesting that RNF207 plays an important role in the development of heart failure.

Characteristics of physical activity in patients with critical limb ischemia.

[Purpose] The purpose of this study was to evaluate the amount of physical activity of the patients with critical limb ischemia consecutively in order to clarify the characteristics of physical activity of critical limb ischemia. [Subjects and Methods] Twelve patients who were eligible for the 2 months of consecutive evaluation of the amount of physical activity were enrolled in the study (men: 11; woman: 1; mean age: 64.4 [range: 44-80]). A pedometer with an accelerometer was used for the measurement of the number of steps walked as an index of the amount of physical activity. Participants were asked to lead a regular life and no instruction was given as to the number of steps. [Results] The average number of daily steps walked was 2,323 steps (range: 404-6,505). There was no clear tendency in the number of amputation site-specific steps walked. There was also no correlation between the number of steps walked and age as well as the maximum strength of the knee-extension muscle, skin perfusion pressure of the sole and the dorsum, and QOL scores. [Conclusion] The number of steps walked of the patients with critical limb ischemia was remarkably low and no significant association with health-related QOL.

Brain pericyte-derived soluble factors enhance insulin sensitivity in GT1-7 hypothalamic neurons.

Insulin signaling in the hypothalamus plays an important role in food intake and glucose homeostasis. Hypothalamic neuronal functions are modulated by glial cells; these form an extensive network connecting the neurons and cerebral vasculature, known as the neurovascular unit (NVU). Brain pericytes are periendothelial accessory structures of the blood-brain barrier and integral members of the NVU. However, the interaction between pericytes and neurons is largely unexplored. Here, we investigate whether brain pericytes could affect hypothalamic neuronal insulin signaling. Our immunohistochemical observations demonstrated the existence of pericytes in the mouse hypothalamus, exhibiting immunoreactivity of platelet-derived growth factor receptor ß (a pericyte marker), and laminin, a basal lamina marker. We then exposed a murine hypothalamic neuronal cell line, GT1-7, to conditioned medium obtained from primary cultures of rat brain pericytes. Pericyte-conditioned medium (PCM), but not astrocyte- or aortic smooth muscle cell-conditioned medium, increased the insulin-stimulated phosphorylation of Akt in GT1-7 cells in a concentration-dependent manner. PCM also enhanced insulin-stimulated tyrosine phosphorylation of insulin receptor ß without changing its expression or localization in cytosolic or plasma membrane fractions. These results suggest that pericytes, rather than astrocytes, increase insulin sensitivity in hypothalamic neurons by releasing soluble factors under physiological conditions in the NVU.

Nifedipine prevents sodium caprate-induced barrier dysfunction in human epidermal keratinocyte cultures.

Tight junctions (TJs) of the epidermis play an important role in maintaining the epidermal barrier. TJ breakdown is associated with skin problems, such as wrinkles and transepidermal water loss (TEWL). Clinical studies have reported that topical nifedipine is effective in reducing the depth of wrinkles and improving TEWL. However, it remains unknown whether nifedipine influences the TJ function in the epidermis. In the present study, we investigated the effect of nifedipine on epidermal barrier dysfunction in normal human epidermal keratinocytes (NHEKs) treated with sodium caprate (C10), a TJ inhibitor. Nifedipine reversed the C10-decreased transepithelial electrical resistance values as a measure of disruption of the epidermal barrier. Immunocytochemical observations revealed that nifedipine improved the C10-induced irregular arrangement of claudin-1, a key protein in TJs. Taken together, these findings suggest that nifedipine prevents epidermal barrier dysfunction, at least in part, by reconstituting the irregular claudin-1 localization at TJs in C10-treated NHEKs.

A Case Study of Non-specialist Disease Management Using Teladoc Health Support: A Case Report.

In Japan, there is a shortage of emergency medicine specialists, often leading non-specialists (physicians who treat conditions outside their area of specialty) to handle cases outside their expertise, which can cause challenges and necessitate specialist support. Starting from December 2023, the St. Marianna University Hospital, which has emergency medicine specialists, began offering overnight emergency outpatient support to Kawasaki Municipal Tama Hospital using the Teladoc HEALTH Mini Cart telemedicine device (Teladoc Health, Inc., CA, USA). The case involved a 44-year-old male with a history of peritonsillar abscess and incisional drainage presented with pharyngeal pain. The treating physician at the Kawasaki Municipal Tama Hospital and a neurologist (the supported physician) examined the patient at 9 PM. An enlarged right tonsil was noted, and a peritonsillar abscess was suspected, prompting a contrast-enhanced CT scan. The results confirmed a 1 cm right peritonsillar abscess. Faced with the decision to transfer the patient to a higher medical facility, the supported physician consulted with the support physician through a Teladoc HEALTH Mini Cart. The St. Marianna University Hospital's emergency physician (supporting physician) used the Teladoc HEALTH Mini Cart to assess the patient's overall condition, blood tests, and CT images and advise on antibiotic treatment. A visit to the ear, nose, and throat expert (ENT) the following day was considered sufficient. The supported physician received feedback that the use of the Teladoc HEALTH Mini Cart reduced the burden of nighttime transfers for otolaryngological conditions, which can take several hours. This finding suggests that remote medical support can affect Japan's emergency medical system.

Transcatheter Arterial Embolization for Blunt Splenic Injury With Resuscitative Endovascular Balloon Occlusion of the Aorta: The Significance of Early Involvement of Radiologists.

Splenectomy is a common procedure for managing splenic injury in patients with unstable vital signs. Transcatheter arterial embolization (TAE) has emerged as a limited alternative to splenectomy, although the role of TAE can be expanded upon the stabilization of vital signs. The current case report discusses a man in his 50s, in shock after a motor vehicle accident, who was successfully stabilized using resuscitative endovascular balloon occlusion of the aorta (REBOA), followed by splenic artery embolization (SAE) instead of splenectomy, with early involvement of diagnostic and interventional radiologists from the initial stage of care. We also discuss the difficulties of SAE under REBOA and the significance of the early involvement of radiologists in trauma care.

Predictors and pathways of in-hospital mortality in active vascular contrast extravasation detected on abdominopelvic CT.

OBJECTIVES: This study aimed to identify factors influencing in-hospital mortality in adult patients with active vascular contrast extravasation (AVCE) on abdominopelvic computed tomography (CT). METHODS: All consecutive patients with AVCE detected on CT between January 2019 and May 2022 were retrospectively included. Their data were compared through uni- and multivariable analyses between patients with and without in-hospital mortality. Path analysis was utilized to clarify the relationships among factors affecting mortality. RESULTS: There were 272 patients (60.2 ± 19.4 years, 150 men) included, of whom 70 experienced in-hospital mortality. Multivariable analysis revealed nonsurgery, chronic kidney disease (CKD) stage 4-5 or dialysis, prolonged partial thromboplastin time (PTT), minimum AVCE length > 8 mm, and a lower rate of packed red cell (PRC) transfusion were identified as independent predictors of in-hospital mortality (p = 0.005-0.048). Path analysis demonstrated direct influences of CKD4-5 or dialysis, prolonged PTT, and minimum AVCE length on mortality (coefficients 0.525-0.616; p = 0.009 to < 0.001). PRC transfusion impacted mortality through nonsurgery (coefficient 0.798, p = 0.003) and intensive care unit (ICU) admission (coefficients 0.025, p = 0.016), leading to subsequent death. Three AVCE spaces (free, loose, and tight) defined on CT were not directly associated with in-hospital mortality. CONCLUSION: In adults with AVCE on CT, AVCE size had a direct independent influence on mortality, highlighting the critical role of radiologists in detecting and characterizing this finding. Additionally, CKD4-5 or dialysis and prolonged PTT also directly influenced mortality, while the lower rate of PRC transfusion impacted mortality through nonsurgery and ICU admission. CLINICAL RELEVANCE STATEMENT: In patients with active vascular contrast extravasation (AVCE) on abdominopelvic CT, larger AVCE directly increased in-hospital mortality. Radiologists' detection and characterization of this finding is crucial, along with recognizing factors like CKD4-5, dialysis, and prolonged PTT to improve patient outcomes. KEY POINTS: Several factors independently predicted in-hospital mortality in patients with abdominopelvic AVCE. Extravasation length > 8 mm was the only imaging marker predictive of in-hospital mortality. Non-imaging factors correlated with in-hospital mortality, and PRC transfusion impacted mortality through nonsurgery and ICU admission pathways.