Semi-quantitative evaluation of chest computed tomography for coronavirus disease 2019 in a critical care unit: A case-control study.

The spread of abnormal opacity on chest computed tomography (CT) has been reported as a predictor of coronavirus disease 2019 (COVID-19) severity; however, the relationship between CT findings and prognosis in patients with severe COVID-19 remains unclear. The objective of this study was to evaluate the extent of abnormal opacity on chest CT and its association with prognosis in patients with COVID-19 in a critical care medical center, using a simple semi-quantitative method. This single-center case-control study included patients diagnosed with severe COVID-19 pneumonia who were admitted to a critical care center. The diagnosis of COVID-19 was based on positive results of a reverse transcription polymerase chain reaction test. All patients underwent non-contrast whole-body CT upon admission. Six representative axial chest CT images were selected for each patient to evaluate the extent of lung lesions. The percentage of the area involved in the representative CT images was visually assessed by 2 radiologists and scored on 4-point scale to obtain the bedside CT score, which was compared between patients who survived and those who died using the Mann-Whitney U test. A total of 63 patients were included in this study: 51 survived and 12 died after intensive treatment. The inter-rater reliability of bedside scores between the 2 radiologists was acceptable. The median bedside CT score of the survival group was 12.5 and that of the mortality group was 16.5; the difference between the 2 groups was statistically significant. The degree of opacity can be easily scored using representative CT images in patients with severe COVID-19 pneumonia, without sophisticated software. A greater extent of abnormal opacity is associated with poorer prognosis. Predicting the prognosis of patients with severe COVID-19 could facilitate prompt and appropriate treatment.

[Nonischemic Priapism Following Brachytherapy : A Case Report and a Review].

We report a case of nonischemic priapism following brachytherapy. A 63-year-old man presented 22 days after brachytherapy for prostate cancer. He suffered painless sustained incomplete erection for a few days. The patient was diagnosed with nonischemic priapism by cavernosal blood gas analysis. Right internal pudendal arteriography showed blood pooling in the cavernosum caused by arteriovenous fistula. Selective arterial embolization with gelatin sponge particles was performed and detumescence achieved. To our knowledge,this is the first case of high flow priapism caused by brachytherapy for prostate cancer. In addition,we reviewed the mechanism of high flow priapism.

Pulmonary tumor thrombotic microangiopathy caused by prostate carcinoma.

Pulmonary tumor thrombotic microangiopathy (PTTM) is a fatal malignancy-related condition that involves rapidly progressing hypoxia and pulmonary hypertension. We report a case of PTTM caused by prostate carcinoma, which was diagnosed before autopsy in an 81-year-old man. Computed tomography showed diffuse ground-glass opacities, consolidation, and small nodules in the peripheral regions of the lung. Autopsy showed adenocarcinoma cells embolizing small pulmonary arteries with fibrocellular intimal proliferation, which was consistent with PTTM caused by prostate carcinoma.

In vivo evaluation of irinotecan-loaded QuadraSphere microspheres for use in chemoembolization of VX2 liver tumors.

PURPOSE: To investigate the pharmacokinetics and chemoembolization efficacy of irinotecan-loaded QuadraSphere microspheres (QSMs) in a rabbit VX2 liver tumor model. MATERIALS AND METHODS: Fourteen rabbits with VX2 liver tumors were divided into two groups. In the irinotecan-loaded QSM group (n = 7), 3 mg of QSMs (30-60 µm) containing 12 mg of irinotecan (0.6 mL; 20 mg/mL) were injected into the left hepatic artery. In the control group (hepatic arterial infusion [HAI] and QSMs; n = 7), 3 mg of QSMs suspended in ioxaglic acid were injected following a bolus injection of 0.6 mL of irinotecan solution (20 mg/mL). Sequential irinotecan, SN-38, and SN-38G concentration changes were measured in plasma within 24 hours and at 1 week and in tissues at 1 week. The VX2 tumor growth rates at 1 and 2 weeks were calculated from computed tomographic images. RESULTS: All rabbits underwent successful embolization. Plasma irinotecan, SN-38, and SN-38G concentrations in the irinotecan-loaded QSM group showed significantly sustained release compared with the control group (P = .01). Compared with the control group, the irinotecan-loaded QSM group had significantly higher irinotecan concentration in liver tumors (P = .03) and a tendency toward higher SN-38 concentration in liver tumors (P = .29). The SN-38G tissue concentrations were below the limits of quantification. The tumor growth rate was significantly lower and the tumor necrosis rate significantly higher in the irinotecan-loaded QSM group (P = .02 and P = .01, respectively). CONCLUSION: Chemoembolization via irinotecan-loaded QSMs more effectively suppresses tumor growth than chemoembolization with unloaded QSMs after HAI. A clinical feasibility study is warranted.

Embolic effects of transcatheter mesenteric arterial embolization with microspheres on the small bowel in a dog model.

PURPOSE: To determine the arterial distribution and ischemic effects of various particle sizes after transcatheter embolization of the small bowel in a dog model. MATERIALS AND METHODS: In 10 dogs, selective microsphere embolization was performed in six branches of the superior mesenteric artery. Microspheres were allocated into three size ranges (100-300 µm, 300-500 µm, and 500-700 µm) and four volume concentrations (0.625%, 1.25%, 2.5%, and 5%). For each size and volume concentration, embolization was performed of five branches at the origin of the last arcade. The distribution of microspheres and the range of ischemic changes of mucosa were evaluated histologically. Angiograms were categorized into two groups: group A, only the vasa recta nonopacified; group B, the last arcade or more proximal branches nonopacified. RESULTS: Microspheres sized 100-300 µm penetrated into intramural arteries and 500-700 µm microspheres mainly blocked arteries in the mesentery. There was a significant difference among three sizes in terms of the locations within the vasculature (P < .0001). The larger volume and the smaller size resulted in more ischemia. The range of ischemic changes among three sizes and among four volume concentrations was significantly different (P = .004 and P < .0001, respectively). The range of ischemic changes with 500-700 µm microspheres in group B was significantly greater than in group A (0% in group A vs 83% in group B, P = .001). CONCLUSIONS: In a dog model, embolization of the small bowel limited to the vasa recta with the use if 500-700 µm microspheres reduced the range of ischemic changes.

Initial experience with use of hydrogel microcoils in embolization of pulmonary arteriovenous malformations.

The purpose of this study is to describe our initial experience with embolization of pulmonary arteriovenous malformations (PAVMs) using hydrogel microcoils. The technical and radiological outcomes were retrospectively reviewed in seven patients with nine simple-type PAVMs (median feeder size 4 mm, range 3-6 mm) who underwent embolization. Hydrogel microcoils were mainly used, and detachable bare microcoils were combined as needed to occlude the terminal feeding artery just before the sac. Of a total of 43 microcoils, 30 (69.8%) hydrogel microcoils were deployed in eight PAVMs with the median number 3.5 (range 2 to 6) per lesion. All hydrogel microcoils were successfully deployed without microcatheter stuck or malposition. In the remaining one small PAVM, only soft bare microcoils were used, however, resulting in recanalization requiring additional coils in the second session. The venous sac was substantially shrunk in all lesions treated with hydrogel microcoils with the median size reduction rate 95.0% (range 81.8% to 99.0%) during the median follow-up period 10 months (range 6 to 18 months). In conclusion, hydrogel microcoils were safely and effectively applied for occluding PAVMs with relatively small feeders.

Current status of embolic agents for liver tumor embolization.

Gelatin sponge and polyvinyl alcohol particles have been the most popular particulate embolic agents for transarterial chemoembolization (TACE) of liver tumors. Over the last decade, calibrated microspheres have been introduced and increasingly used in liver tumor embolization in Western countries. In addition, drug-eluting beads (DEB) have been introduced for sustained local drug release. Such long-awaited spherical embolic agents will be introduced in Japan in the near future. The advantages of these microspheres are that particles are uniform in size and shape, and easy to inject through a microcatheter. They can travel distally to vessels corresponding to the particle size; in other words, the occlusion level can be predicted according to the particle size chosen. Thus, new bland microspheres and DEB may bring a significant advancement to embolization for primary liver tumors as well as hepatic metastases from various cancers. However, at this point, the published data suggests that both conventional TACE and DEB-TACE are equally effective for treatment of unresectable hepatocellular carcinoma, when patients are carefully selected. Therefore, indication, patient selection, and embolization techniques will be essential in order to individually adapt newer embolic agents based on oncological, anatomical and technical considerations.

Carvedilol blocks cardiac KATP and KG but not IK1 channels by acting at the bundle-crossing regions.

We examined the effects of carvedilol on cardiac inwardly rectifying K(+) (Kir) channels, i.e., ATP-sensitive (K(ATP)), G-protein-activated (K(G)) and background (I(K1)) Kir channels. We found that carvedilol effectively inhibits K(ATP) and K(G), but not I(K1) channels. Carvedilol inhibits K(ATP) channels reconstituted in HEK293 cells with Kir6.2 lacking the C-terminal 26 amino acids (Kir6.2DeltaC26), suggesting that carvedilol acts in the channel pore. A sequence comparison of the three channels revealed that a cysteine residue, C166, in the inner helix of Kir6.2 is conserved in both Kir6.xs (K(ATP)) and Kir3.xs (K(G)), but not in Kir2.xs (I(K1)). The mutation of this residue (C166A) made Kir6.2DeltaC26 resistant to the drug. Homology modeling and docking simulation suggested that interaction between carvedilol and the pore could be located at the cytosolic portion of the inner helix (bundle-crossing region) containing C166. This study shows that carvedilol blocks specific groups of Kir channels by interacting with the bundle-crossing region.