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Estimation of the Potential for Bioeffects
Published in Marvin C. Ziskin, Peter A. Lewin, Ultrasonic Exposimetry, 2020
It is important to recognize that these modeling efforts assume the existence of stabilized pockets of gas or free bubbles. Whether these exist in an in vivo setting is not clear. There is evidence that lung hemorrhage is developed in mice with the application of ultrasound with as low peak pressures as 1 to 2 MPa.34 This suggests that the alveoli may act as cavitation nuclei and that caution should be applied in cases where the ultrasound beam reaches lung tissue. It might be added that these experiments agreed well with the cavitation indices described earlier. However, attempts to generate kidney hemorrhage in mice following exposure to intense pulsed ultrasound gave fairly negative results.35 Peak positive pressures in the order of 9 to 10 MPa and negative pressure of 4 to 5 MPa at frequencies of 1.2 and 3.8 MHz were unable to generate unequivocal indications of extravasation in mouse kidneys. The implication that there were no nuclei available is strengthened by the observation that the same fields were able to drill a hole through an 8-mm slab of plaster of Paris in approximately 15 s. It is apparent that the availability in vivo of nuclei for cavitation requires additional experimentation for a more concrete picture of cavitation to be established.
Procoagulant Activity and Lung Disease
Published in Gary A. Levy, Edward H. Cole, Procoagulant Activity in Health and Disease, 2019
Harold A. Chapman, John S. Munger, David A. Waltz
The low-pressure physiology of the pulmonary vasculature coupled with potent reflex mechanisms for vasoconstriction and extensive extravascular procoagulant activity makes the development of diffuse lung hemorrhage unusual. Even in the setting of classical hemophilia (factor IX, factor VIII, or factor XI deficiency) pulmonary hemorrhage is rare.116 As pointed out recently by Drake and colleagues, the sites of bleeding in classical hemophilias are largely tissues with little or no subendothelial tissue factor expression, e.g., joints.19 The lung, as discussed, is lined with procoagulants in the extravascular compartments. The risk of pulmonary hemorrhage in thrombocytopenia (<50,000/cc), however, is appreciable, especially in the setting of leukemia with chemotherapy, where there is presumably also alveolar and endothelial cell damage.117 For reasons discussed above, platelets may act by multiple mechanisms to limit lung hemorrhage.
Biomechanical Perspective on Blast Injury Comorbid Brain and Somatic Trauma
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Mariusz. Ziejewski, Ghodrat. Karami
Earle et al. (2007) ran laboratory studies with pigs in order to model blast trauma to multiple organ systems. The researchers discharged a nail gun over the brain and then over the lungs. Results showed that lung hemorrhage occurred, characteristic of that in a human injury.
Dose- and dosage-dependent spectrum of respiratory toxicity of cypermethrin in rabbits
Published in Toxin Reviews, 2023
Latif Ahmad, Shafia Tahseen Gul, Xiaoxia Du, Riaz Hussain, Muhammad Rafiq Khanani, Shajeela Iram, Aziz Ur Rehman, Ahrar Khan
Detailed histopathological evaluation is vital for diagnosis (Melo et al.2019, Namdev et al. 2023, Zhong et al. 2023). Previously, studies reported changes in texture, consistency, and lung hemorrhage due to pyrethroids (Arafa et al.2015, Zheng et al.2021) those were also observed in the present study (Table 3; Figures 1–2). Diffuse alveolar damage in the acute phase accompanied edematous widening and inflamed alveolar septae. The plasma CFH increases due to lung injury causing pulmonary edema; cation sodium (Na+) and amiloride-sensitive epithelial Na + channels located on the apical membrane are critical to maintaining the epithelial fluid layer (Wynne et al.2017). The reduced or damaged surfactant can produce atelectasis and edema (Wang et al.2021). The red color observed in airway exudates indicates the presence of RBCs and hemolysis (Gaggar and Patel 2016).
Ultra-central lung tumors: safety and efficacy of protracted stereotactic body radiotherapy
Published in Acta Oncologica, 2021
Joyce E. Lodeweges, Peter S. N. van Rossum, Marcia M. T. J Bartels, Anne S. R. van Lindert, Jacqueline Pomp, Max Peters, Joost J. C. Verhoeff
Tekatli et al. suggested squamous cell histology, endobronchial involvement and anticoagulant use during radiotherapy as possible risk factors. Also, PTV Dmax above 123% of the prescription dose in all treatment plans was considered as possible contribution to the observed toxicity, leading to a modification of the institutional protocol with a permitted Dmax of 110% of the prescription dose instead of 140% [11]. The same risk factors for fatal hemorrhage were proposed by other previous studies, with the addition of the use of anti-vascular endothelial growth factor therapy (anti-VEGF) around the SBRT treatment [24,25]. In our series, 60% of patients with fatal bronchopulmonary hemorrhage used anticoagulant or antiplatelet drugs during SBRT, compared to 50% of patients who did not die of fatal hemorrhage. Also, two patients received the anti-VEGF therapy bevacizumab during and 2 months after SBRT of the lung, respectively. The latter patient died of bronchopulmonary hemorrhage, 6 months after initiation bevacizumab. In addition, Chaudhuri et al. reported that biopsy and bronchoscopy of the radiated main bronchus could increase the risk of lung hemorrhage [10]. This was the case in one of our patients who died of bronchopulmonary hemorrhage one month after she have had a biopsy of a necrotic patch in the irradiated bronchus.
Investigation of fibrinogen in early bleeding of patients with newly diagnosed acute promyelocytic leukemia
Published in Platelets, 2021
Tiantian Chu, Hong Wang, Xin Lv, Jiaqian Qi, Yaqiong Tang, Yi Fan, Huiying Qiu, Xiaowen Tang, Chengcheng Fu, Changgeng Ruan, Yue Han, De-Pei Wu
Follow-up ended on 22 June 2019, and the median follow-up time was 50.0 months (range, 0.07–87.3 months). Nine of 198 patients were lost to follow-up, so only 189 patients were included in the OS analysis. Fifteen patients died (7.6%), of whom 14 (7.1%) had severe hemorrhage, including six cases of brain hemorrhage and eight of lung hemorrhage. Twelve (6.1%) patients died within 30 days of admission. Univariate analysis showed that patients with moderate/severe bleeding had a worse 1-year OS than those with no/mild bleeding (p < .001) (Table III). Additionally, age ≥60 years (p < .001), PT >12.8 s (median value) (p = .008), intermediate/high risk group (p = .034), a CDSS score ≥5 (p < .001), and fibrinogen ≤1.6 combined with PT >12.8 s (p = .029) were significantly associated with a worse 1-year OS. Multivariate analysis identified moderate/severe bleeding (p = .018, OR: 6.5, 95% CI: 1.4–31.3) (Figure 2a), age ≥60 years (p = .001, OR: 71.4, 95% CI: 7.2–100.0) (Figure 2b), and a CDSS score ≥5 (p = .044, OR: 4.2, 95% CI: 1.0–16.6) (Figure 2c) as independent risk factors for 1-year OS. Moreover, patients with fibrinogen ≤1.6 g/L accompanied by PT >12.8 s had a significantly worse 1-year OS than those with fibrinogen ≤1.6 g/L combined with PT ≤12.8 s (p = .005, OR: 52.6, 95% CI: 3.3–100.0) (Figure 2d).