Shock (Augusta, Ga.)最新文献

{"title":"Irisin Protects Against LPS-Stressed Cardiac Damage Through Inhibiting Inflammation, Apoptosis, and Pyroptosis.","authors":"Qian Li,&nbsp;Mingming Zhang,&nbsp;Ying Zhao,&nbsp;Maolong Dong","doi":"10.1097/SHK.0000000000001775","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001775","url":null,"abstract":"<p><strong>Abstract: </strong>Septic cardiac dysfunction remains a clinical problem due to its high morbidity and mortality. Uncontrolled cell death and excessive inflammatory response are closely related to sepsis-induced cardiac dysfunction. Irisin has been found to play cardioprotective roles in sepsis. However, there is enough uncertainty in the mechanism of irisin-mediated cardioprotection. We hypothesized that irisin may ameliorate myocardial dysfunction via reducing cardiac apoptosis, pyroptosis, and inflammation during LPS-induced sepsis. Mice were subjected to LPS with or without irisin treatment. After stimuli of LPS, the function of myocardium was distinctly impaired, which was closely related to increased level of apoptosis (decreased expression of Bcl-2 and elevated expression of Caspase-3 and Bax), pyroptosis (increased expression of Caspase1, NLR family pyrin domain containing 3 (NLRP3), and gasdermin D) and inflammatory mediators (increased level of IL-1β, TNF-α, and IL-6). This process is consistent with increased toll-like receptor 4 (TLR4)/nuclear factor-kappa B signal, apoptotic signal, and NLRP3-mediated pyroptotic signal. Activation of apoptosis and pyroptosis enhanced the expression of proinflammatory cytokines and further exacerbated septic myocardial damage. However, irisin can inhibit the expression of TLR4 and its downstream signaling molecules and also lower the level of apoptosis and pyroptosis. Besides, similar results were also found in vitro model of LPS-induced H9c2 cardiomyocyte injury. In general, irisin suppressed inflammation, apoptosis, and pyroptosis by blocking the TLR4 and NLRP3 inflammasome signalings to mitigate myocardial dysfunction in sepsis.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"1009-1018"},"PeriodicalIF":3.1,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39733651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time to Hemorrhage Control in a Hybrid ER System: Is It Time to Change?","authors":"Danielle Tatum,&nbsp;Bruno Pereira,&nbsp;Bryan Cotton,&nbsp;Mansoor Khan,&nbsp;Megan Brenner,&nbsp;Paula Ferrada,&nbsp;Tal Hörer,&nbsp;David Kauvar,&nbsp;Andrew Kirkpatrick,&nbsp;Carlos Ordonez,&nbsp;Artai Pirouzram,&nbsp;Derek Roberts,&nbsp;Juan Duchesne","doi":"10.1097/SHK.0000000000001539","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001539","url":null,"abstract":"<p><strong>Abstract: </strong>Time to hemorrhage control is critical, as mortality in patients with severe hemorrhage that arrive to trauma centers with sign of life remains over 40%. Prompt identification and management of severe hemorrhage is paramount to reducing mortality. In traditional US trauma systems, the early hospital course of a severely hemorrhaging patient typically proceeds from the trauma resuscitation bay to the operating room or angiography suite with a potential stop for radiological imaging. This protracted journey can prove fatal as it consumes valuable minutes. In contrast to the current US system is a newly developed and increasingly adopted system in Japan called the hybrid emergency room system (HERS). The hybrid ER is equipped to allow resuscitation, imaging, and damage control intervention to occur in the ER without the need to transport the patient to a subsequent destination. The HERS is relatively new and remains restricted to a small number of institutions, limiting the ability to robustly examine impact(s) on patient outcomes. Even if proven to yield superior outcomes, there are significant obstacles to adopting the HERS in the US. Challenges such as the high cost of building and implementing a HER system, return on investment, and the significant differences between the US and Japan in terms of physician training, trauma center, and reimbursement schemes may render the hybrid ER system to be unfeasible in most current trauma centers. Barriers aside, the Japanese hybrid ER system remains the most novel recent advancement in the quest to reduce potentially preventable mortality from hemorrhage.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"16-21"},"PeriodicalIF":3.1,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37765143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulatory Trauma: A Paradigm for Understanding the Role of Endovascular Therapy in Hemorrhage Control.","authors":"Juan Duchesne,&nbsp;Sharven Taghavi,&nbsp;Mansoor Khan,&nbsp;Bruno Perreira,&nbsp;Bryan Cotton,&nbsp;Megan Brenner,&nbsp;Paula Ferrada,&nbsp;Tal Horer,&nbsp;David Kauvar,&nbsp;Andrew Kirkpatrick,&nbsp;Carlos Ordoñez,&nbsp;Artai Priouzram,&nbsp;Derek Roberts","doi":"10.1097/SHK.0000000000001513","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001513","url":null,"abstract":"<p><strong>Abstract: </strong>The pathophysiology of traumatic hemorrhage is a phenomenon of vascular disruption and the symptom of bleeding represents one or more vascular injuries. In the Circulatory Trauma paradigm traumatic hemorrhage is viewed as injury to the circulatory system and suggests the underlying basis for endovascular hemorrhage control techniques. The question \"Where is the patient bleeding?\" is replaced by \"Which blood vessels are disrupted?\" and stopping bleeding becomes a matter of selective vessel access and vascular flow control. Control of traumatic hemorrhage has traditionally been performed via external access to the end organ that is bleeding followed by the application of direct pressure, packing, or clamping and repair of directly affected blood vessels. In the circulatory trauma paradigm, bleeding is seen as disruption to vessels which may be accessed internally, from within the vascular system. A variety of endovascular treatments such as balloon occlusion, embolization, or stent grafting can be used to control hemorrhage throughout the body. This narrative review presents a brief overview of the current role of endovascular therapy in the management of circulatory trauma. The authors draw on their personal experience combined with the last decade of published experiences with the use of endovascular techniques in trauma and present general recommendations for their evolving use. The focus of the review is on the use of endovascular techniques as specific vascular treatments using the circulatory trauma paradigm.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"22-29"},"PeriodicalIF":3.1,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39906353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemorrhagic Shock and Resuscitation Causes Glycocalyx Shedding and Endothelial Oxidative Stress Preferentially in the Lung and Intestinal Vasculature.","authors":"Sarah Abdullah,&nbsp;Mardeen Karim,&nbsp;Mark Legendre,&nbsp;Laura Rodriguez,&nbsp;Jessica Friedman,&nbsp;Aaron Cotton-Betteridge,&nbsp;Robert Drury,&nbsp;Jacob Packer,&nbsp;Chrissy Guidry,&nbsp;Juan Duchesne,&nbsp;Sharven Taghavi,&nbsp;Olan Jackson-Weaver","doi":"10.1097/SHK.0000000000001764","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001764","url":null,"abstract":"<p><strong>Introduction: </strong>Hemorrhagic shock has recently been shown to cause shedding of a carbohydrate surface layer of endothelial cells known as the glycocalyx. This shedding of the glycocalyx is thought to be a mediator of the coagulopathy seen in trauma patients. Clinical studies have demonstrated increases in shed glycocalyx in the blood after trauma, and animal studies have measured glycocalyx disruption in blood vessels in the lung, skeletal muscle, and mesentery. However, no study has measured glycocalyx disruption across a wide range of vascular beds to quantify the primary locations of this shedding.</p><p><strong>Methods: </strong>In the present study, we used a rat model of hemorrhagic shock and resuscitation to more comprehensively assess glycocalyx disruption across a range of organs. Glycocalyx disruption was assessed by fluorescent-labeled wheat germ agglutinin or syndecan-1 antibody staining in flash frozen tissue.</p><p><strong>Results: </strong>We found that our model did elicit glycocalyx shedding, as assessed by an increase in plasma syndecan-1 levels. In tissue sections, we found that the greatest glycocalyx disruption occurred in vessels in the lung and intestine. Shedding to a lesser extent was observed in vessels of the brain, heart, and skeletal muscle. Liver vessel glycocalyx was unaffected, and kidney vessels, including the glomerular capillaries, displayed an increase in glycocalyx. We also measured reactive oxygen species (ROS) in the endothelial cells from these organs, and found that the greatest increase in ROS occurred in the two beds with the greatest glycocalyx shedding, the lungs, and intestine. We also detected fibrin deposition in lung vessels following hemorrhage-resuscitation.</p><p><strong>Conclusions: </strong>We conclude that the endothelium in the lungs and intestine are particularly susceptible to the oxidative stress of hemorrhage-resuscitation, as well as the resulting glycocalyx disruption. Thus, these two vessel beds may be important drivers of coagulopathy in trauma patients.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"803-812"},"PeriodicalIF":3.1,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39182463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What's New in Shock, November 2021?","authors":"Mark G Clemens","doi":"10.1097/SHK.0000000000001874","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001874","url":null,"abstract":"","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"655-657"},"PeriodicalIF":3.1,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39520319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Converting Asystole From Initial Shockable ECG Rhythm Before Extracorporeal Cardiopulmonary Resuscitation and Outcome.","authors":"Keisuke Maeda,&nbsp;Akihiko Inoue,&nbsp;Yasuhiro Kuroda,&nbsp;Fumiya Inoue,&nbsp;Masafumi Suga,&nbsp;Shinichi Ijuin,&nbsp;Soichiro Kai,&nbsp;Tokito Koga,&nbsp;Nobuaki Igarashi,&nbsp;Shigenari Matsuyama,&nbsp;Tetsunori Kawase,&nbsp;Satoshi Ishihara,&nbsp;Hiroshi Naitou,&nbsp;Shinichi Nakayama","doi":"10.1097/SHK.0000000000001727","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001727","url":null,"abstract":"<p><strong>Background: </strong>Initial electrocardiogram (ECG) rhythm is a predictor of outcomes in out-of-hospital cardiac arrest (OHCA) in patients receiving extracorporeal cardiopulmonary resuscitation (ECPR). However, ECG rhythm often changes before ECPR, and the consequence of this change remains unclear. This study aimed to assess the relationship between the conversion of ECG rhythm from initial shockable rhythm before ECPR and mortality.</p><p><strong>Patients and methods: </strong>This was a retrospective cohort study of OHCA patients with initial shockable rhythm who underwent ECPR between January 2010 and September 2020. Patients were classified into two groups: asystole (patients whose ECG rhythm converted to asystole at any time before initiating ECPR) and non-asystole (patients whose ECG rhythm did not convert to asystole at any time before initiating ECPR) groups. The primary outcome was in-hospital mortality.</p><p><strong>Results: </strong>A total of 102 patients were included in the study; in-hospital mortality rate was 46.1% (n = 47) and 76 (74.5%) patients had unfavorable neurological outcomes (Cerebral Performance Category: 3-5). There were 33 and 69 patients in the asystole and non-asystole groups, respectively. The mortality rates in the asystole and non-asystole groups were 69.7% and 34.8%, respectively (P = 0.001). On multivariable analysis, the asystole group showed a significant association with mortality (odds ratio, 5.42; 95% confidence interval, 2.11-15.36; P < 0.001).</p><p><strong>Conclusion: </strong>Conversion to asystole before ECPR at any time in patients with OHCA is associated with mortality in patients with an initial shockable ECG rhythm.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"701-708"},"PeriodicalIF":3.1,"publicationDate":"2021-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39520286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncertain Clinical Effect of Polymyxin B Hemoperfusion in Patients with Septic Acute Kidney Injury Requiring Continuous Renal Replacement Therapy.","authors":"Jong Min Lee,&nbsp;Seung Don Baek,&nbsp;Tae Hyun Kim,&nbsp;Hwa Ran Jeon,&nbsp;Jin Hee Han,&nbsp;Jai Won Chang","doi":"10.1097/SHK.0000000000001752","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001752","url":null,"abstract":"<p><strong>Abstract: </strong>Polymyxin B hemoperfusion (PMX-HP) may improve the clinical outcomes of patients with sepsis and gram-negative bacteremia by reducing endotoxin levels. However, the recent studies with the variable degree of renal support have shown that the improvement of survival rate by PMX-HP remains unclear in such patients. Therefore, we investigated whether the addition of PMX-HP to continuous renal replacement therapy (CRRT) could improve the survival rate than CRRT alone. This study included 231 patients with sepsis undergoing CRRT alone or PMX-HP with CRRT. Primary outcomes were 28-day and 90-day all-cause mortality. Urine output, ventilator support, and Sequential Organ Failure Assessment (SOFA) score were not significantly different between the two groups. Crude 28-day and 90-day mortality rates were higher in the PMX-HP with CRRT group than in the CRRT-alone group. To correct for disease severity, propensity score (PS) matching was performed with acute respiratory distress syndrome, mechanical ventilation support, extracorporeal membrane oxygenation, infection source (abdomen), age, inotropic score, SOFA score, C-reactive protein, and procalcitonin levels. Sixty-six PS-matched pairs revealed significantly higher 28-day and 90-day mortality rates in the PMX-HP with CRRT group than in the CRRT-alone group. Considering the mortality rates after PS matching, the additional use of PMX-HP does not improve the clinical outcomes of patients with sepsis and acute kidney injury requiring CRRT.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"551-556"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25390064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wearable Patch Heart Rate Variability Is an Early Marker of Systemic Inflammation During Experimental Human Endotoxemia.","authors":"Mats Koeneman,&nbsp;Rebecca Koch,&nbsp;Harry van Goor,&nbsp;Peter Pickkers,&nbsp;Matthijs Kox,&nbsp;Sebastian Bredie","doi":"10.1097/SHK.0000000000001827","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001827","url":null,"abstract":"<p><strong>Introduction: </strong>Early diagnosis and treatment can reduce the risk of organ failure and mortality in systemic inflammatory conditions. Heart rate variability (HRV) has potential for early identification of the onset of systemic inflammation, as it may detect changes in sympathetic nervous system activity resulting from the developing inflammatory response before clinical signs appear. With the use of new methodologies, we investigated the onset and kinetics of HRV changes as well as several inflammatory parameters and symptoms during experimental human endotoxemia, a model of systemic inflammation in humans in vivo.</p><p><strong>Patients and methods: </strong>Healthy volunteers were intravenously administered LPS (n = 15) or placebo (n = 15). HRV was determined using a wireless wearable device, and parameters low to high frequency (LF:HF) ratio, root mean square of the successive differences (RMSSD), and standard deviation of normal-to-normal R-R intervals (SDNN)were calculated through 1-min-rolling 6-min windows. Plasma cytokine levels and flu-like symptoms and vital signs were serially assessed.</p><p><strong>Results: </strong>The increase in LF:HF ratio, reflecting sympathetic predominance, was more pronounced in the LPS group compared to the placebo group, with the difference becoming statistically significant 65 min following LPS administration (1.63 [1.42-1.83] vs. 1.28 [1.11-1.44], P = 0.005). Significant between-group differences in RMSSD and SDNN were observed from 127 to 140 min post-LPS administration onwards, respectively. Plasma cytokine levels showed significant between-group differences staring 60 min post-LPS. For symptom score, heart rate, temperature, and diastolic blood pressure, significant differences compared with the placebo group were observed at 90, 118, 120, and 124 min post-LPS, respectively.</p><p><strong>Conclusion: </strong>In a controlled human model of systemic inflammation, elevations in the LF:HF ratio followed very shortly after elevations in plasma cytokine levels and preceded onset of flu-like symptoms and alterations in vital signs. HRV may represent a promising non-invasive tool for early detection of a developing systemic inflammatory response.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"537-543"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39028145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen Enhances the Microvascular Reactivity Through RhoA-ROCK Pathway in Female Mice During Hemorrhagic Shock.","authors":"Yun-Xue Yue,&nbsp;Jia-Yi Zhai,&nbsp;Hui-Bo Du,&nbsp;Li-Na Jiang,&nbsp;Li-Min Zhang,&nbsp;Chen Wang,&nbsp;Zhen-Ao Zhao,&nbsp;Chun-Hui Zhang,&nbsp;Zi-Gang Zhao","doi":"10.1097/SHK.0000000000001776","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001776","url":null,"abstract":"<p><strong>Abstract: </strong>Vascular hypo-reactivity plays a critical role inducing organ injury during hemorrhagic shock. 17β-estradiol (E2) can induce vasodilation to increase blood flow in various vascular beds. This study observed whether E2 can restore vascular hypo-reactivity induced by hemorrhagic shock, and whether E2 effects are associated with RhoA-Rho kinase (ROCK)-myosin light chain kinase phosphatase (MLCP) pathway. The hemorrhagic shock model (40 ± 2 mm Hg for 1 h, resuscitation for 4 h) was established in ovary intact sham operation (OVI), ovariectomized (OVX), and OVX plus E2 supplement female mice. Intestinal microvascular loop was used to assess blood flow in vivo, mRNA expression and vascular reactivity in vitro. Hemorrhagic shock significantly reduced norepinephrine microvascular reactivity. Decreased microvascular reactivity was exacerbated by OVX and reversed by E2 supplement. U-46619 (RhoA agonist) increased microvascular reactivity, and C3 transferase (an ADP ribosyl transferase that selectively induces RhoA ribosylation) or Y-27632 (ROCK inhibitor) inhibited sham mice microvascular reactivity. Similarly, U-46619 increased microvascular reactivity in OVI and OVX mice following hemorrhagic shock, which was abolished by Y-27632 or concomitant incubation of okadaic acid (OA) (MLCP inhibitor) and Y-27632. In OVX plus E2 supplement mice with hemorrhagic shock, Y-27632 inhibited microvascular reactivity, which was abolished by concomitant U-46619 application. Lastly, hemorrhagic shock remarkably decreased intestinal loop blood flow, RhoA and ROCK mRNA expressions in vascular tissues in OVX females, but not in OVI females, which were reversed by E2 supplement. These results indicate that estrogen improves microvascular reactivity during hemorrhagic shock, and RhoA-ROCK signaling pathway may mediate E2 effects.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"611-620"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25520940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen as a Safe Therapeutic Adjunct in Reducing the Inflammatory Storm in Trauma Hemorrhagic Shock Patients.","authors":"Dablu Lal Gupta, Shrestha Tiwari, Tej Prakash Sinha, Kapil Dev Soni, Sagar Galwankar, Subodh Kumar, D N Rao, Sanjeev Bhoi","doi":"10.1097/SHK.0000000000001779","DOIUrl":"10.1097/SHK.0000000000001779","url":null,"abstract":"<p><strong>Abstract: </strong>Trauma is a major cause of death and disability throughout the world. It is a leading cause of death with or without sepsis in about 50% of patients. Limited therapeutic options are available besides definitive care with a mortality benefit. Preclinical studies have demonstrated the mortality benefit of estrogen in trauma hemorrhagic shock (THS). Based on encouraging results from preclinical studies, we hypothesized that early administration of estrogen in male THS patients may reduce the inflammatory storm, prevent sepsis-associated problems, and subsequently reduce mortality. The authors studied the safety of early administration of estrogen as a therapeutic adjunct in the emergency department (ED) and its effects on the inflammatory storm, prevention of sepsis, and mortality during the intensive care unit stay. Forty THS patients were recruited. THS patients were divided into experimental and placebo control groups based on the estrogen administration in the ED. Serum levels of cytokines and immune cells were measured at different time points on days 0, 3, 7, and 14 in both groups of THS patients. The experimental group received intravenous estrogen (25 mg) at a single time point in the ED beside standard of care as per advanced trauma life support guidelines. Patients did not develop any major or minor adverse events and showed favorable clinical outcomes in the experimental group. The levels of T regulatory cells, monocytes, and systemic cytokines significantly reduced and showed a balanced inflammatory response in THS patients who received estrogen.In conclusion, this preliminary study showed that intravenous estrogen therapy is safe and reduced the inflammatory insult due to trauma hemorrhagic shock. It may protect THS patients from sepsis-associated complications. Future clinical trials are required to study the efficacy and mechanistic pathway.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"514-521"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25599388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}