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Hypothermia and hemostasis in severe trauma: A new crossroads workshop report
Abstract
Objective:
The hypothermia and hemostasis in severe trauma (HYPOSTAT): a new crossroads workshop was convened to evaluate the interplay among hypothermia, hemostasis, and severe trauma/hemorrhage. Trauma is the major cause of death in young individuals in the United States, with uncontrolled hemorrhage representing the major cause of preventable deaths.
Data sources:
This workshop organized by the National Heart, Lung, and Blood Institute and the US Army Medical Research and Material Command as a forum for exchange of ideas among experts from diverse fields. The specific workshop goals were to (1) identify state-of-the-art and needs in knowledge of biology of hypothermia and hemostasis in the setting of significant traumatic injury; (2) provide an interdisciplinary forum to enhance knowledge regarding early detection of traumatic shock and monitoring of the level and effect of controlled hypothermia in severe trauma settings; and (3) identify future research directions of the role of therapeutic-oriented hypothermia and hemostasis in trauma with severe blood loss.
Study selection:
Not applicable.
Data extraction:
Expert opinion and literature review.
Conclusion:
This document provides a summary of the expert opinion and highlights the recommendations that came out of the discussions at this workshop to guide scientific efforts in basic, translational, and clinical research in this area.
... -У беременных женщин, рожениц и родильниц при массивной кровопотере рекомендуется согревать инфузионные растворы до 37-38°C (УДД -2, УУР -В) [148][149][150][151][152][153]. ...
... Комментарий. Даже незначительная гипотермия (<1,0°C), вызывает коагулопатию, значительно увеличивающую кровопотерю (на 16%) и относительный риск переливания препаратов крови (на 22%) [148,149]. Согревание вводимых внутривенно инфузионных растворов (как и пациента в целом) является неотъемлемой частью интенсивной терапии массивной кровопотери и геморрагического шока [152][153][154]. Аппараты для периоперационного подогрева инфузионных растворов вхо-дят в перечень оборудования родильного дома и перинатального центра 5 (151700 -Аппарат для онвекционного подогрева крови/инфузионных растворов, 151720 -Аппарат для конвекционного подогрева крови/инфузионных растворов, с высокой скоростью потока, 293820 -Аппарат для кондуктивного подогрева крови/инфузионных растворов, 293840 -Аппарат для кондуктивного подогрева крови/инфузионных растворов, с высокой скоростью потока). ...
The article presents recommendations for the diagnosis and intensive care of DIC syndrome in massive blood loss in obstetrics. Issues of clinical, laboratory and instrumental diagnostics of DIC-syndrome in massive blood loss in obstetrics, application of allogeneic blood components (erythrocytes, plasma, cryoprecipitate, platelets) and blood coagulation factors (factor Vlla, concentrate of prothrombin complex factors) are considered. The quality criteria of medical patients with DIC-syndrome in massive blood loss are presented.
... We did not evaluate another significant issue, which is the effect of hypothermia and rewarming on hemostasis. Nevertheless, induced hypothermia to ≥33 • C does not seem to be associated with altered hemostasis or increased bleeding (Alam et al., 2012;Mohr et al., 2013). Finally, hypothermia was rapidly induced, concomitantly to the development of shock, which is different from the slower development that occurs in clinical scenarios. ...
Background:
Rewarming is a recommended therapy during the resuscitation of hypothermic patients with hemorrhagic shock. In experimental models, however, it increases inflammatory response and mortality. Although microcirculation is potential target of inflammation, the microvascular effects of rewarming during the resuscitation of hemorrhagic shock have not been studied. Our goal was to assess the systemic and microcirculatory effects of an increase in core temperature (T°) during the retransfusion of hemorrhagic shock in sheep. Our hypothesis was that rewarming could hamper microcirculation.
Methods:
In anesthetized and mechanically ventilated sheep, we measured systemic, intestinal, and renal hemodynamics and oxygen transport. O2 consumption (VO2) and respiratory quotient were measured by indirect calorimetry. Cortical renal, intestinal villi and sublingual microcirculation were assessed by IDF-videomicroscopy. After basal measurements, hemorrhagic shock was induced and T° was reduced to ~33 °C. After 1 h of shock and hypothermia, blood was retransfused and Ringer lactate solution was administered to prevent arterial hypotension. In the control group (n = 12), T° was not modified, while in the intervention (rewarming) group, it was elevated ~3 °C. Measurements were repeated after 1 h.
Results:
During shock, both groups showed similar systemic and microvascular derangements. After retransfusion, VO2 remained decreased compared to baseline in both groups, but was lower in the control compared to the rewarming group. Perfused vascular density has a similar behavior in both groups. Compared to baseline, it remained reduced in peritubular (control vs. rewarming group, 13.8 [8.7-17.5] vs. 15.7 [10.1-17.9] mm/mm2, PNS) and villi capillaries (14.7 [13.6-16.8] vs. 16.3 [14.2-16.9] mm/mm2, PNS), and normalized in sublingual mucosa (19.1 [16.0-20.3] vs. 16.6 [14.7-17.2] mm/mm2, PNS).
Conclusions:
This is the first experimental study assessing the effect of rewarming on systemic, regional, and microcirculatory perfusion in hypothermic hemorrhagic shock. We found that a 3 °C increase in T° neither improved nor impaired the microvascular alterations that persisted after retransfusion. In addition, sublingual mucosa was less susceptible to reperfusion injury than villi and renal microcirculation.
... Although TH can be beneficial, harmful effects can occur (e.g., bleeding complications, in addition to those listed above). TH can affect hemostasis by inhibiting clotting factors and altering platelet function (Alam et al., 2012). We showed that prolonged hypothermia (HYPO) aggravates bleeding in the collagenase ICH model ( John et al., 2015). ...
Localized brain hypothermia (HYPO) can be achieved by infusing cold saline into the carotid artery of animals and patients. Studies suggest that HYPO improves behavioral and histological outcomes in focal ischemia models. Given that ischemic stroke and intracerebral hemorrhage (ICH) share pathophysiological overlap, we tested whether cold saline infusion is safe and neuroprotective when given during collagenase-induced ICH. Eighty-five adult male Sprague-Dawley rats were used. Experiment 1 investigated brain and body temperature changes associated with a cold saline infusion paradigm that was scaled from patients according to brain weight and blood volume (3 mL/20-minute infusion). Experiment 2 determined whether HYPO aggravated bleeding volume. Experiment 3 investigated if cerebral edema or elemental concentrations were altered by HYPO. We also collected core body temperature and activity data through telemetry. Experiment 4 investigated whether behavioral outcomes (e.g., skilled reaching) and tissue loss were influenced by HYPO. Our HYPO protocol decreased the ipsilateral striatal temperature by ∼0.20°C (p < 0.001), with no other effects. HYPO did not affect hematoma volume (p = 0.64), cerebral edema (p = 0.34), or elemental concentrations (p = 0.49) at 24 hours post-ICH. Although ICH caused persistent behavioral impairments, HYPO did not improve behavioral outcomes (measured by a neurological deficit scale, cylinder, and the staircase test; p > 0.05 for all). Brain tissue loss was not different between groups on day 28 post-ICH (p = 0.90). Although cold saline infusion appears to be safe in the acute post-ICH period, there was no evidence that this therapy improved outcome. However, our treatment protocol was relatively mild and additional interventions might help improve efficacy. Finally, our findings may also speak to the safety of this cooling approach in focal ischemia where hemorrhagic transformation is a risk; future studies on this issue are needed.
Objective
Induced hypothermia improves outcome in aortic arch surgery, neonatal neurointensive care, and transplant surgery for example. In contrast, spontaneous hypothermia has been associated with worse outcomes in patients suffering from hemorrhagic shock, mostly explained by its adverse effects on the coagulation system. We investigated if induced hypothermia would impair short-term survival in experimental aortic rupture with retroperitoneal bleeding.
Methods
Anesthetized pigs were randomized into 2 groups: hypothermia by peritoneal lavage of ice-cold Ringer’s acetate and external cooling ( n = 10) and normothermia ( n = 10). Aortic rupture with retroperitoneal bleeding was induced by endovascular means creating a 6 mm hole in the retroperitoneal portion of abdominal aorta. Survival (primary outcome), hemodynamics, and arterial blood gases including lactate were collected and analyzed up to 180 min after aortic rupture.
Results
The body temperature (mean ± standard deviation) in the hypothermic group was 31.5 ± 1.0 °C and 38.7 ± 0.4 °C in the normothermic group at the time for aortic rupture. Survival up to 180 min after the retroperitoneal bleeding was significantly higher in the hypothermic compared with the normothermic group ( P = 0.023).
Conclusions
Induced hypothermia did not impair survival in this experimental retroperitoneal aortic bleeding model in anesthetized pigs. This finding may indicate a minor role for the coagulation system in this type of bleeding.
To investigate the etiological characteristics of wound infection in severe trauma patients and logistic regression analysis of the influencing factors of infection. The 116 patients with severe trauma who were intervened in our hospital from 22 October 2017 to 9 September 2019 were selected as the subjects of this retrospective study and divided into a control group and an observation group according to whether they were infected or not, 58 cases each. Observe and compare the pathogenic characteristics (pathogen distribution and drug resistance) of the two groups of patients and logistic regression analysis of the influencing factors of infection. The gram‐positive bacteria in the observation group were mainly Staphylococcus aureus , accounting for 17.20%; the fungi were mainly Candida tropicalis , accounting for 17.20%; and the gram‐negative bacteria were mainly Acinetobacter baumannii , accounting for 20.39%; the control group was gram‐positive. The main bacteria are S. aureus , accounting for 8.60%; the fungi are mainly Candida albicans , accounting for 4.3%; and the gram‐negative bacteria, which are mainly Pseudomonas aeruginosa , accounting for 14.56%. Gram‐positive bacteria Enterococcus faecium , S. aureus , Enterococcus faecalis , Staphylococcus epidermidis . The highest drug resistance of other gram‐positive bacteria is penicillin and erythromycin at 85.00% and above. Fungi C. tropicalis , Candida parapsilosis , C. albicans , fluconazole and amphotericin B have the highest resistance to 80.00% and above. Gram‐negative bacteria A. baumannii , Ps. aeruginosa , Klebsiella pneumoniae , Escherichia coli , Proteus mirabilis , Enterobacter cloacae and other gram‐negative bacteria are the most resistant to ampicillin, and Piperacillin was 70.00% and above. The combined primary diseases of the two groups of patients, ventilator use ≧3 days, long‐term use of glucocorticoids, catheter use days ≧5 days, fever days ≧3 days and long‐term use of broad‐spectrum antimicrobial drugs, the difference is statistically significant academic significance ( p < 0.05). Logistic analysis showed that combined with underlying diseases, fever days ≥3 days, long‐term use of glucocorticoids and catheter use days ≥5 days are the influencing factors for the occurrence of wound infections in patients with severe trauma. Trauma patients are prone to wound infections, and there are many influencing factors. Close observation of patients should be strengthened. Effective prevention and control measures should be taken for related influencing factors to reduce the incidence of infection.
Perioperative coagulation disorders pose a serious risk of life-threatening complications. The article presents methodological recommendations of the Federation of Anesthesiologists and reanimatologists of Russian Federation for the perioperative management of patients with disorders of the hemostatic system, which summarizes aspects of both diagnosis and assessment, and intensive care of congenital and acquired disorders of the coagulation system in the perioperative period. The literature search focused on meta-analyses and randomized controlled trials, but also included registries, non-randomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. The principles of perioperative management of disseminated intravascular coagulation syndrome, hepatic, uremic, traumatic, septic coagulopathy, acquired thrombocytopenia and trobocytopathies, antiphospholipid syndrome, hemophilia A and B, von Willebrand disease and other pathologies are described. For each recommendation, the level of certainty of the evidence and the level of strength of the evidence are presented. The recommendations were developed by experts in the field of perioperative patient management for anesthesiologists and intensive care physicians as a help in making clinical decisions; the final decision for a particular patient is made by the attending physician.
The treatment of bone infections has always been difficult. The emergence of drug-resistant bacteria has led to a steady decline in the effectiveness of antibiotics. It is also especially important to fight bacterial infections while repairing bone defects and cleaning up dead bacteria to prevent biofilm formation. The development of biomedical materials has provided us with a research direction to address this issue. We aimed to review the current literature, and have summarized multifunctional antimicrobial materials that have long-lasting antimicrobial capabilities that promote angiogenesis, bone production, or “killing and releasing.” This review provides a comprehensive summary of the use of biomedical materials in the treatment of bone infections and a reference thereof, as well as encouragement to perform further research in this field.
Trauma patients present a unique challenge to anesthesiologists, since they require resource-intensive care, often complicated by pre-existing medical conditions. This fully revised new edition focuses on a broad spectrum of traumatic injuries and the procedures anesthesiologists perform to care for trauma patients perioperatively, surgically, and post-operatively. Special emphasis is given to assessment and treatment of co-existing disease, including surgical management of trauma patients with head, spine, orthopedic, cardiac, and burn injuries. Topics such as training for trauma (including use of simulation) and hypothermia in trauma are also covered. Six brand new chapters address pre-hospital and ED trauma management, imaging in trauma, surgical issues in head trauma and in abdominal trauma, anesthesia for oral and maxillofacial trauma, and prevention of injuries. The text is enhanced with numerous tables and 300 illustrations showcasing techniques of airway management, shock resuscitation, echocardiography and use of ultrasound for the performance of regional anesthesia in trauma.
Introduction:
Although hypothermia is independently associated with an increased mortality in trauma patients, it might be an effective therapeutic approach for otherwise lethal hemorrhage. The effect of hypothermia on microcirculation, however, has been poorly studied in this setting. Our goal was to characterize the effects of hypothermia on microcirculation in normal conditions and in severe hemorrhagic shock.
Methods:
In anesthetized and mechanically ventilated sheep, we measured cardiac output (CO), renal blood flow (RBF), and systemic and renal O2 consumption (VO2). Cortical renal, intestinal villi and sublingual microcirculation was assessed by IDF-videomicroscopy. After basal measurements, sheep were assigned to hypothermia (n = 12) and normothermia (n = 12) groups. Central temperature was reduced to ∼34°C and maintained at baseline in each group, respectively. Measurements were repeated after 1-h of hemodynamic stable conditions and 1-h of severe hemorrhagic shock.
Results:
In conditions of hemodynamic stability, the hypothermia group showed lower CO, RBF, and systemic and renal VO2 than the normothermia group. Red blood cell velocity was also lower in renal, villi, and sublingual microvascular beds (836 ± 195 vs. 1066 ± 162, 916 ± 105 vs. 1051 ± 41, and 970 ± 182 vs. 1102 ± 49 μm/s, respectively; P < 0.0001 for all). In hemorrhagic shock, most of the microvascular variables were similarly compromised in both groups. In hypo- and normothermia groups, the percentage of reduction in perfused vascular density was higher in renal than in intestinal and sublingual microcirculation (66 ± 31 vs. 31 ± 23 and 15 ± 15%, and 78 ± 26 vs. 32 ± 37 and 18 ± 21%, P < 0.01 for both).
Conclusions:
This is the first experimental study assessing the effect of systemic hypothermia on microcirculation in severe hemorrhagic shock. The main finding was that hypothermia did not hamper additionally the microcirculatory derangements induced by hemorrhagic shock. In addition, renal microcirculation was more susceptible to hemorrhagic shock than villi and sublingual microcirculation.
Background:
Tranexamic acid can reduce bleeding in patients undergoing elective surgery. We assessed the effects of early administration of a short course of tranexamic acid on death, vascular occlusive events, and the receipt of blood transfusion in trauma patients.
Methods:
This randomised controlled trial was undertaken in 274 hospitals in 40 countries. 20 211 adult trauma patients with, or at risk of, significant bleeding were randomly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min then infusion of 1 g over 8 h) or matching placebo. Randomisation was balanced by centre, with an allocation sequence based on a block size of eight, generated with a computer random number generator. Both participants and study staff (site investigators and trial coordinating centre staff) were masked to treatment allocation. The primary outcome was death in hospital within 4 weeks of injury, and was described with the following categories: bleeding, vascular occlusion (myocardial infarction, stroke and pulmonary embolism), multiorgan failure, head injury, and other. All analyses were by intention to treat. This study is registered as ISRCTN86750102, Clinicaltrials.govNCT00375258, and South African Clinical Trial RegisterDOH-27-0607-1919.
Findings:
10 096 patients were allocated to tranexamic acid and 10 115 to placebo, of whom 10 060 and 10 067, respectively, were analysed. All-cause mortality was significantly reduced with tranexamic acid (1463 [14.5%] tranexamic acid group vs 1613 [16.0%] placebo group; relative risk 0.91, 95% CI 0.85-0.97; p=0.0035). The risk of death due to bleeding was significantly reduced (489 [4.9%] vs 574 [5.7%]; relative risk 0.85, 95% CI 0.76-0.96; p=0.0077).
Interpretation:
Tranexamic acid safely reduced the risk of death in bleeding trauma patients in this study. On the basis of these results, tranexamic acid should be considered for use in bleeding trauma patients.
Funding:
UK NIHR Health Technology Assessment programme, Pfizer, BUPA Foundation, and J P Moulton Charitable Foundation.
Objective:
Recognizing the impact of the 1977 San Francisco study of trauma deaths in trauma care, our purpose was to reassess those findings in a contemporary trauma system.
Design:
Cross-sectional.
Material and methods:
All trauma deaths occurring in Denver City and County during 1992 were reviewed; data were obtained by cross-referencing four databases: paramedic trip reports, trauma registries, coroner autopsy reports and police reports.
Measurements and main results:
There were 289 postinjury fatalities; mean age was 36.8 +/- 1.2 years and mean Injury Severity Score (ISS) was 35.7 +/- 1.2. Predominant injury mechanisms were gunshot wounds in 121 (42%), motorvehicle accidents in 75 (38%) and falls in 23 (8%) cases. Seven (2%) individuals sustained lethal burns. Ninety eight (34%) deaths occurred in the pre-hospital setting. The remaining 191 (66%) patients were transported to the hospital. Of these, 154 (81%) died in the first 48 hours (acute), 11 (6%) within three to seven days (early) and 26 (14%) after seven days (late). Central nervous system injuries were the most frequent cause of death (42%), followed by exsanguination (39%) and organ failure (7%). While acute and early deaths were mostly due to the first two causes, organ failure was the most common cause of late death (61%).
Conclusions:
In comparison with the previous report, we observed similar injury mechanisms, demographics and causes of death. However, in our experience, there was an improved access to the medical system, greater proportion of late deaths due to brain injury and lack of the classic trimodal distribution.
Background: The purpose of this study was to identify the causes and time to death of all trauma victims who died at a level I trauma center during an 11-year period.Study Design: Autopsies were performed on all patients who died secondary to trauma. Retrospective review of these autopsies was carried out and appended to existing trauma registry data. Standard definitions were used to attribute the cause of death in each case. Preventable deaths were determined by a standardized peer review process.Results: Between January 1985 and December 1995, a total of 900 trauma patients died. This represented 7.3% of all major trauma admissions (12,320). Seventy percent of these patients died within the first 24 hours of admission. Thoracic vascular and central nervous system (CNS) injuries were the most common causes of death in the first hour after admission to the hospital. CNS injuries were the most common causes of death within the 72 deaths after admission. Acute inflammatory processes (multiple organ failure, acute respiratory distress syndrome, and pneumonia) and pulmonary emboli were the leading causes of death after the first 72 hours. Overall, 43.6% (393 of 900) of all trauma deaths were caused by CNS injuries, making this the most common cause of death in our study. The preventable death rate was 1%.Conclusions: The first 24 hours after trauma are the deadliest for these patients. Primary and secondary CNS injuries are the leading causes of death. Prevention, early identification, and treatment of potentially lethal injuries should remain the focus of those who treat trauma patients.