Management Of Hemorrhagic Shock Research Articles

Low-Titer O-Positive Whole Blood: Lessons From the Battlefield for Civilian Rural Hospitals.

Low-titer O-positive whole blood was used extensively by the military during operations in Iraq and Afghanistan. Studies have consistently shown that this therapy is feasible, safe, and effective in the management of hemorrhagic shock in trauma patients, and it is now the standard of care across the US military Joint Trauma System. The military's success in using low-titer O-positive whole blood has renewed the practice in the civilian setting, with recent research confirming its safety and efficacy. In a few short years, use of this treatment for hemorrhagic shock has expanded to more than 80 US level I and level II trauma centers. However, its use is still relatively rare in the rural hospital setting. This article describes the benefits for patients, staff members, and the overall trauma system of using low-titer O-positive whole blood in rural hospitals.

A case report of a bleeding case after removal of chest drain after lung surgery.

Postoperative bleeding after lobectomy is relatively rare. By analyzing and discussing the case history and management of hemorrhagic shock caused by chest tube removal after lobectomy, we can achieve the purpose of preventing postoperative bleeding after thoracic surgery and reducing postoperative complications, which can help avoid the risk of second surgery, shorten the patient's hospital stay, reduce the cost of medical care, and improve the patient's quality of life. A case of bleeding from tube removal after lobectomy. The bleeding from chest drain removal on the 3rd day after thoracoscopic lobectomy resulted in hemorrhagic shock, which was stopped by thoracoscopic exploration again under active antishock, and there was no recurrence of bleeding after the operation, and the patient was discharged from the hospital after chest drain removal. Enhanced computed tomography of the chest revealed a space-occupying lesion in the middle lobe of the right lung. Thoracoscopy was performed again on the condition of active anti-shock. On the third day after thoracoscopic lobectomy, the patient underwent removal of the chest drain and subsequently experienced hemorrhagic shock. Given the necessity of maintaining anti-shock measures, the patient was subjected to a second thoracoscopic exploration with the objective of halting the hemorrhage. Following this procedure, the patient did not present with any further episodes of bleeding. Subsequently, a new chest drain was placed, and once the drainage flow had diminished to an acceptable level, the chest drain was removed. The patient subsequently made a full recovery and was discharged from the hospital. Even if the safely inserted drain tube is removed, the thoracic surgeon must be aware of possible vascular bleeding.

ARTERIAL DIAMETER VARIATIONS AS A NEW INDEX FOR STROKE VOLUME ASSESSMENT: AN EXPERIMENTAL STUDY ON A CONTROLLED HEMORRHAGIC SHOCK MODEL IN PIGLETS.

Background: The assessment of cardiac output (CO) is a major challenge during shock. The criterion standard for CO evaluation is transpulmonary thermodilution, which is an invasive technique. Speckle tracking is an automatized method of analyzing tissue motion using echography. This tool can be used to monitor pulsed arterial diameter variations with low interobserver variability. An experimental model of controlled hemorrhagic shock allows for multiple CO variations. The main aim of this study is to show the correlation between the femoral arterial diameter variations (fADVs) and the stroke volume (SV) measured by thermodilution during hemorrhagic shock management and the resuscitation of anesthetized piglets. The secondary objective is to explore the respective correlations between SV and subaortic time-velocity index, abdominal aorta ADV, carotid ADV, and subclavian ADV. Methods : Piglets were bled until mean arterial pressure reached 40 mm Hg. Controlled hemorrhage was maintained for 30 minutes before randomizing the piglets to three resuscitation groups-the fluid-filling group (reanimated with saline solution only), NEph group (norepinephrine + saline solution), and Eph group (epinephrin + saline solution). Speckle tracking, echocardiographic, and hemodynamic measures were performed at different stages of the protocol. Results : Thirteen piglets were recruited and included for statistical analysis. Of all the piglets, 164 fADV measures were attempted and 160 were successful (98%). The correlation coefficient between fADV and SV was 0.71 (95% confidence interval [CI], 0.62 to 0.78; P < 0.01). The correlation coefficient between SV and abdominal aorta ADV, subclavian ADV, and carotid ADV was 0.30 (95% CI, 0.13 to 0.46; P < 0.01), 0.56 (95% CI, 0.45 to 0.66, P < 0.01), and 0.15 (95% CI, -0.01 to 0.30, P = 0.06), respectively. Conclusions : In this hemorrhagic shock model using piglets, fADV was strongly correlated with SV.

Management of Hemorrhagic Shock: Physiology Approach, Timing and Strategies

Hemorrhagic shock (HS) management is based on a timely, rapid, definitive source control of bleeding/s and on blood loss replacement. Stopping the hemorrhage from progressing from any named and visible vessel is the main stem fundamental praxis of efficacy and effectiveness and an essential, obligatory, life-saving step. Blood loss replacement serves the purpose of preventing ischemia/reperfusion toxemia and optimizing tissue oxygenation and microcirculation dynamics. The "physiological classification of HS" dictates the timely management and suits the 'titrated hypotensive resuscitation' tactics and the 'damage control surgery' strategy. In any hypotensive but not yet critical shock, the body's response to a fluid load test determines the cut-off point between compensation and progression between the time for adopting conservative treatment and preparing for surgery or rushing to the theater for rapid bleeding source control. Up to 20% of the total blood volume is given to refill the unstressed venous return volume. In any critical level of shock where, ab initio, the patient manifests signs indicating critical physiology and impending cardiac arrest or cardiovascular accident, the balance between the life-saving reflexes stretched to the maximum and the insufficient distal perfusion (blood, oxygen, and substrates) remains in a liable and delicate equilibrium, susceptible to any minimal change or interfering variable. In a cardiac arrest by exsanguination, the core of the physiological issue remains the rapid restoration of a sufficient venous return, allowing the heart to pump it back into systemic circulation either by open massage via sternotomy or anterolateral thoracotomy or spontaneously after aorta clamping in the chest or in the abdomen at the epigastrium under extracorporeal resuscitation and induced hypothermia. This is the only way to prevent ischemic damage to the brain and the heart. This is accomplishable rapidly and efficiently only by a direct approach, which is a crush laparotomy if the bleeding is coming from an abdominal +/- lower limb site or rapid sternotomy/anterolateral thoracotomy if the bleeding is coming from a chest +/- upper limbs site. Without first stopping the bleeding and refilling the heart, any further exercise is doomed to failure. Direct source control via laparotomy/thoracotomy, with the concomitant or soon following venous refilling, are the two essential, initial life-saving steps.

A simple and novel equation to estimate the degree of bleeding in haemorrhagic shock: mathematical derivation and preliminary in vivo validation.

Determining blood loss [100% – RBV (%)] is challenging in the management of haemorrhagic shock. We derived an equation estimating RBV (%) via serial haematocrits (Hct1, Hct2) by fixing infused crystalloid fluid volume (N) as [0.015 × body weight (g)]. Then, we validated it in vivo. Mathematically, the following estimation equation was derived: RBV (%) = 24k / [(Hct1 / Hct2) – 1]. For validation, non-ongoing haemorrhagic shock was induced in Sprague–Dawley rats by withdrawing 20.0%–60.0% of their total blood volume (TBV) in 5.0% intervals (n = 9). Hct1 was checked after 10 min and normal saline N cc was infused over 10 min. Hct2 was checked five minutes later. We applied a linear equation to explain RBV (%) with 1 / [(Hct1 / Hct2) – 1]. Seven rats losing 30.0%–60.0% of their TBV suffered shock persistently. For them, RBV (%) was updated as 5.67 / [(Hct1 / Hct2) – 1] + 32.8 (95% confidence interval [CI] of the slope: 3.14–8.21, p = 0.002, R2 = 0.87). On a Bland-Altman plot, the difference between the estimated and actual RBV was 0.00 ± 4.03%; the 95% CIs of the limits of agreements were included within the pre-determined criterion of validation (< 20%). For rats suffering from persistent, non-ongoing haemorrhagic shock, we derived and validated a simple equation estimating RBV (%). This enables the calculation of blood loss via information on serial haematocrits under a fixed N. Clinical validation is required before utilisation for emergency care of haemorrhagic shock.

Can blood loss be assessed by echocardiography? An experimental study on a controlled hemorrhagic shock model in piglets.

Assessment of the volemic loss is a major challenge during the management of hemorrhagic shock. Echocardiography is an increasingly used noninvasive tool for hemodynamic assessment. In mechanically ventilated patients, some studies suggest that respiratory variations of mean subaortic time-velocity integral (∆VTI) would be predictive of fluid filling response. An experimental model of controlled hemorrhagic shock provides a precise approach to study correlation between blood volume and cardiac ultrasonographic parameters. The main objective was to analyze the ∆VTI changes during hemorrhage in an anesthetized-piglet model of controlled hemorrhagic shock. The secondary objective was to evaluate ∆VTI during the resuscitation process after hemorrhage and other echocardiographic parameters changes during the whole protocol. Twenty-four anesthetized and ventilated piglets were bled until mean arterial pressure reached 40 mm Hg. Controlled hemorrhage was maintained for 30 minutes before randomizing the piglets to two resuscitation groups: fluid filling group resuscitated with saline solution and noradrenaline group resuscitated with saline solution and noradrenaline. Echocardiography and hemodynamic measures, including pulsed pressure variations (PPV), were performed at different stages of the protocol. The correlation coefficient between ΔVTI and PPV with the volume of bleeding during the hemorrhagic phase were respectively 0.24 (95% confidence interval, 0.08-0.39; p < 0.01) and 0.57 (95% CI, 0.44-0.67; p < 0.01). Two parameters had a moderate correlation coefficient with hemorrhage volume (over 0.5): mean subaortic time-velocity index (VTI) and mitral annulus diastolic tissular velocity (E'). In this hemorrhagic shock model, ΔVTI had a low correlation with the volume of bleeding, but VTI and E' had a correlation with blood volume comparable to that of PPV.

The Pathophysiology and Management of Hemorrhagic Shock in the Polytrauma Patient.

The recognition and management of life-threatening hemorrhage in the polytrauma patient poses several challenges to prehospital rescue personnel and hospital providers. First, identification of acute blood loss and the magnitude of lost volume after torso injury may not be readily apparent in the field. Because of the expression of highly effective physiological mechanisms that compensate for a sudden decrease in circulatory volume, a polytrauma patient with a significant blood loss may appear normal during examination by first responders. Consequently, for every polytrauma victim with a significant mechanism of injury we assume substantial blood loss has occurred and life-threatening hemorrhage is progressing until we can prove the contrary. Second, a decision to begin damage control resuscitation (DCR), a costly, highly complex, and potentially dangerous intervention must often be reached with little time and without sufficient clinical information about the intended recipient. Whether to begin DCR in the prehospital phase remains controversial. Furthermore, DCR executed imperfectly has the potential to worsen serious derangements including acidosis, coagulopathy, and profound homeostatic imbalances that DCR is designed to correct. Additionally, transfusion of large amounts of homologous blood during DCR potentially disrupts immune and inflammatory systems, which may induce severe systemic autoinflammatory disease in the aftermath of DCR. Third, controversy remains over the composition of components that are transfused during DCR. For practical reasons, unmatched liquid plasma or freeze-dried plasma is transfused now more commonly than ABO-matched fresh frozen plasma. Low-titer type O whole blood may prove safer than red cell components, although maintaining an inventory of whole blood for possible massive transfusion during DCR creates significant challenges for blood banks. Lastly, as the primary principle of management of life-threatening hemorrhage is surgical or angiographic control of bleeding, DCR must not eclipse these definitive interventions.

Biological Connection of Psychological Stress and Polytrauma under Intensive Care: The Role of Oxytocin and Hydrogen Sulfide.

This paper explored the potential mediating role of hydrogen sulfide (H2S) and the oxytocin (OT) systems in hemorrhagic shock (HS) and/or traumatic brain injury (TBI). Morbidity and mortality after trauma mainly depend on the presence of HS and/or TBI. Rapid “repayment of the O2 debt” and prevention of brain tissue hypoxia are cornerstones of the management of both HS and TBI. Restoring tissue perfusion, however, generates an ischemia/reperfusion (I/R) injury due to the formation of reactive oxygen (ROS) and nitrogen (RNS) species. Moreover, pre-existing-medical-conditions (PEMC’s) can aggravate the occurrence and severity of complications after trauma. In addition to the “classic” chronic diseases (of cardiovascular or metabolic origin), there is growing awareness of psychological PEMC’s, e.g., early life stress (ELS) increases the predisposition to develop post-traumatic-stress-disorder (PTSD) and trauma patients with TBI show a significantly higher incidence of PTSD than patients without TBI. In fact, ELS is known to contribute to the developmental origins of cardiovascular disease. The neurotransmitter H2S is not only essential for the neuroendocrine stress response, but is also a promising therapeutic target in the prevention of chronic diseases induced by ELS. The neuroendocrine hormone OT has fundamental importance for brain development and social behavior, and, thus, is implicated in resilience or vulnerability to traumatic events. OT and H2S have been shown to interact in physical and psychological trauma and could, thus, be therapeutic targets to mitigate the acute post-traumatic effects of chronic PEMC’s. OT and H2S both share anti-inflammatory, anti-oxidant, and vasoactive properties; through the reperfusion injury salvage kinase (RISK) pathway, where their signaling mechanisms converge, they act via the regulation of nitric oxide (NO).

Extra Anatomical Bypass for Common Femoral Artery Pseudoaneurysm following Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)

Background: Improvements in the instrumentation and guidelines for the use of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) has increased the use of it as an adjunct in managing haemorrhagic shock. REBOA-related complications continue to be assessed and described.&#x0D; Methods: We describe a case of a femoral artery pseudoaneurysm within an infected groin wound after REBOA usage in a 25-year-old male after several bouts of sepsis and complications related to the initial penetrating injury and associated ICU stay.&#x0D; Results: An extra-anatomical external iliac-to-superficial femoral artery bypass was performed using a 6mm polytetrafluoroethylene graft to treat the FAP successfully.&#x0D; Conclusion:&#x0D; REBOA is a well described adjunct in the management of haemorrhagic shock. The immediate and delayed complications should be not overlooked. Deviations from the expected postoperative course should be promptly recognised and managed by a clinician with appropriate expertise.&#x0D; &#x0D; &#x0D;

The History of Hemorrhagic Shock and Damage Control Resuscitation.

The understanding and management of hemorrhagic shock have evolved significantly over the last 400years. Injured patients in shock mandate immediate surgeon involvement. Every graduating surgical resident and every surgeon taking trauma call should thoroughly understand the concepts of damage control resuscitation and be prepared to care for these patients. This review seeks to revisit the history of hemorrhagic shock and the evolution of damage control resuscitation.

Anesthetic management of a patient with hollow viscus perforation due to blunt abdominal trauma with grade IV hemorrhagic shock

Hemorrhagic shock is a form of hypovolemic shock in which severe blood loss leads to inadequate oxygen delivery at the cellular level. Death from hemorrhage represents a substantial global problem, with more than 60,000 deaths per year in the United States and an estimated 1.9 million deaths per year worldwide, 1.5 million of which result from physical trauma. This case report aims to stress the need of handling cases of hemorrhagic shock in accordance with damage control protocol.&#x0D; Hemorrhagic shock management using permissive hypotension management, bleeding control, massive transfusion protocol (MTP), minimal crystalloid therapy, and adjuvant therapy is the best approach to get optimal outcome to prevent triad of death. In this case, the application of damage control resuscitation has not been fully implemented because of several constraints.&#x0D; Key words: Hemorrhage; Hemorrhagic shock; Permissive hypotension; Massive Transfusion Protocol; MTP; Resuscitation; Damage control&#x0D; Citation: Pohan DK, Sudjud RW, Kurniawan MB, Ramila HN. Anesthetic management on patient with hollow viscus perforation due to blunt abdominal trauma with grade IV hemorrhagic shock. Anaesth. pain intensive care 2021;25(2):217-221. DOI: 10.35975/apic.v25i2.1474&#x0D; Received: 11 January 2021, Reviewed: 15 January 2021, Accepted: 16 February 2021

Whole blood for blood loss: hemostatic resuscitation in damage control.

Hemorrhagic shock and its complications are a major cause of death among trauma patients. The management of hemorrhagic shock using a damage control resuscitation strategy has been shown to decrease mortality and improve patient outcomes. One of the components of damage control resuscitation is hemostatic resuscitation, which involves the replacement of lost blood volume with components such as packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets in a 1:1:1:1 ratio. However, this is a strategy that is not applicable in many parts of Latin America and other low-and-middle-income countries throughout the world, where there is a lack of well-equipped blood banks and an insufficient availability of blood products. To overcome these barriers, we propose the use of cold fresh whole blood for hemostatic resuscitation in exsanguinating patients. Over 6 years of experience in Ecuador has shown that resuscitation with cold fresh whole blood has similar outcomes and a similar safety profile compared to resuscitation with hemocomponents. Whole blood confers many advantages over component therapy including, but not limited to the transfusion of blood with a physiologic ratio of components, ease of transport and transfusion, less volume of anticoagulants and additives transfused to the patient, and exposure to fewer donors. Whole blood is a tool with reemerging potential that can be implemented in civilian trauma centers with optimal results and less technical demand.

Evaluation and management of haemorrhagic shock in polytrauma: Clinical practice guidelines

Haemorrhagic shock is the most common preventable cause of early mortality in polytrauma patients. Road traffic injuries are the most common cause for polytrauma and most commonly include orthopaedic injuries. Hence, orthopaedic trainees and junior orthopaedic surgeons need to be well aware of evaluation and management of haemorrhagic shock in the multiple injured patient. The present narrative review discusses evaluation and current principles in management of haemorrhagic shock in a polytrauma patient. A classification system for haemorrhagic shock based on ATLS guidelines has been described along with novel use of colour coding to facilitate better and effective use of the classification. A treatment algorithm has also been presented for quick reference. The emphasis is to avoid overloading with crystalloid fluids, replacing with blood and blood products (Balanced resuscitation), permissive hypotension, prevent and acutely treat lethal conditions such as hypothermia, acidosis and coagulopathy. The management of haemorrhagic shock in polytrauma patient is quite challenging and require a detailed knowledge of its management. An arbitrary and haphazard management of these patients may lead to severe complications. We have mentioned the broad principles of management of hypovolemic shock in a polytrauma patient.

Immune response in fluid therapy with crystalloids of different ratios or colloid for rats in haemorrhagic shock

This study investigated the association between different ratios of balanced salt based-crystalloid (PLASMA SOLUTION-A [CJ HealthCare, Seoul, Korea]) (the ratios of crystalloid for blood loss, 1:1, 1:2 and 1:3) or balanced salt-based colloid (VOLULYTE 6% [Fresenius Kabi, Germany]) (the ratio of colloid for blood loss, 1:1) to restore blood loss and immune response in rats with haemorrhagic shock. About 50% of total estimated blood volume was removed after anaesthesia. The fluid was administered for resuscitation after exsanguination, according to the type of fluid and the ratios of exsanguinated volume and fluid volume for resuscitation. After sacrifice, expression of immune cells in blood and tissues was evaluated. Histological analyses and syndecan-1 immunohistochemistry assays were performed on tissues. Endothelial damage according to syndecan-1 and cytokine levels in blood was also assessed. Fluid resuscitation with same, two-fold, or three-fold volumes of crystalloid, or same volume of colloid, to treat haemorrhagic shock in rats resulted in a similar increase in blood pressure. The expression of neutrophils in blood decreased significantly after colloid administration, compared to before exsanguination. Syndecan-1 expression increased after exsanguination and fluid resuscitation in all groups, without any significant difference. In conclusion, same volume of balanced salt-based crystalloid for blood loss was enough to restore BP at the choice of fluid for the management of haemorrhagic shock in the rats, compared with different ratios of crystalloid or same volume of colloid, on the aspect of immune response.

Therapeutic effect of mesenchymal stromal cells in acute kidney injury after hemorrhagic shock

Background & Aim Hemorrhagic shock (HS) is an absolute hypovolemia and an abnormality of the circulatory system secondary to a sudden and significant extravascular blood loss. At the cellular level, the imbalance between systemic oxygen delivery and consumption lead to a transition from aerobic to anaerobic metabolism, lactic acid, inorganic phosphates and oxygen radicals start to accumulate. Release of damage-associated molecular patterns triggers a systemic inflammatory response. As ATP supplies decrease, cellular homeostasis ultimately fails leading to cell death. Among organ failures, acute kidney injury (AKI) affects up to 50% of the patients, is responsible for high morbidity. AKI following HS management is only symptomatic and no etiologic treatment is available. Mesenchymal Stromal Cells (MSC) are multipotent cells found in a large number of adult tissues and used in clinical cell therapy for immunomodulation and tissue repair. Many studies have highlighted their immunomodulatory, anti-apoptotic/anti-oxidative stress or stimulation of endogenous regenerative process by direct contact or by secreting bioactive molecules. Our objective was to evaluate the effect of an early MSC therapy after HS to prevent the onset of AKI. Methods, Results & Conclusion We have developed in vivo HS model. Sprague Dawley rats are subjected to 1h30 of HS at a fixed Mean Arterial Pressure of 35mmHg, followed by resuscitation and retransfusion of spoliated blood. Rat Bone Marrow MSC are intravenously administered at the beginning of the resuscitation phase. Blood gases, lactate and blood glucose are measured at the end of each experimental phase. Biological, histological and transcript analyses are performed at sacrifice, 6h after the end of hemorrhagic phase. Plasma markers indicating AKI (urea, creatinine, cystatin C) increased 6 hours after hemorrhage. The administration of MSC tends to decrease all these markers. Histological scoring of kidney injury and KIM-1 immunostaining (biomarker of tubule injury) are increased in hemorrhagic animals and also shows a tendency to decrease in MSC treated group. Finally, the mRNA levels of IFNγ, IL1β and IL10 increase with hemorrhage and tends to decrease with MSC treatment. Jointly, CD11b/c cell phenotyping in rat blood seems expressed increase activations markers. In conclusion our preliminary results suggest that MSC could prevent kidney damage induced by hemorrhagic shock. Hemorrhagic shock (HS) is an absolute hypovolemia and an abnormality of the circulatory system secondary to a sudden and significant extravascular blood loss. At the cellular level, the imbalance between systemic oxygen delivery and consumption lead to a transition from aerobic to anaerobic metabolism, lactic acid, inorganic phosphates and oxygen radicals start to accumulate. Release of damage-associated molecular patterns triggers a systemic inflammatory response. As ATP supplies decrease, cellular homeostasis ultimately fails leading to cell death. Among organ failures, acute kidney injury (AKI) affects up to 50% of the patients, is responsible for high morbidity. AKI following HS management is only symptomatic and no etiologic treatment is available. Mesenchymal Stromal Cells (MSC) are multipotent cells found in a large number of adult tissues and used in clinical cell therapy for immunomodulation and tissue repair. Many studies have highlighted their immunomodulatory, anti-apoptotic/anti-oxidative stress or stimulation of endogenous regenerative process by direct contact or by secreting bioactive molecules. Our objective was to evaluate the effect of an early MSC therapy after HS to prevent the onset of AKI. We have developed in vivo HS model. Sprague Dawley rats are subjected to 1h30 of HS at a fixed Mean Arterial Pressure of 35mmHg, followed by resuscitation and retransfusion of spoliated blood. Rat Bone Marrow MSC are intravenously administered at the beginning of the resuscitation phase. Blood gases, lactate and blood glucose are measured at the end of each experimental phase. Biological, histological and transcript analyses are performed at sacrifice, 6h after the end of hemorrhagic phase. Plasma markers indicating AKI (urea, creatinine, cystatin C) increased 6 hours after hemorrhage. The administration of MSC tends to decrease all these markers. Histological scoring of kidney injury and KIM-1 immunostaining (biomarker of tubule injury) are increased in hemorrhagic animals and also shows a tendency to decrease in MSC treated group. Finally, the mRNA levels of IFNγ, IL1β and IL10 increase with hemorrhage and tends to decrease with MSC treatment. Jointly, CD11b/c cell phenotyping in rat blood seems expressed increase activations markers. In conclusion our preliminary results suggest that MSC could prevent kidney damage induced by hemorrhagic shock.

An extracellular cold-inducible RNA-binding protein-derived small peptide targeting triggering receptor expressed on myeloid cells-1 attenuates hemorrhagic shock.

Extracellular cold-inducible RNA-binding protein (eCIRP) is a damage-associated molecular pattern, which is released into the circulation after hemorrhagic shock (HS). Recently, we discovered that triggering receptor expressed on myeloid cells-1 (TREM-1) serves as a new receptor of eCIRP to exaggerate inflammation. Here, we hypothesize that by inhibiting the interaction between eCIRP and TREM-1 with the use of a novel short peptide derived from human eCIRP known as M3, we can inhibit the inflammatory response and acute lung injury in HS. Hemorrhagic shock was induced using C57BL/6 mice by cannulating both femoral arteries. One femoral artery was used for removal of blood while the other was used for continuous monitoring of mean arterial blood pressure. The mean arterial pressure of 25 mm Hg to 30 mm Hg was maintained for 90 minutes, followed by a resuscitation phase of 30 minutes with 1 mL of normal saline. The treatment group was given 10 mg/kg of M3 during the resuscitation phase. Four hours after resuscitation, serum and lungs were collected and analyzed for various injury and inflammatory markers by using colorimetry, real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. There was an increase in the serum levels of tissue injury markers (alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase) as well as cytokines (TNF-α and IL-6) when comparing the vehicle group versus the sham group. This increase was significantly inhibited in the M3-treated group. The mRNA expression of proinflammatory cytokines TNF-α, IL-6, and IL-1β and the chemokines MIP-2 and KC in lungs was significantly increased in the vehicle-treated HS mice, while their expression was significantly decreased in M3-treated HS mice. Finally, M3 treatment significantly decreased the lung injury score compared with vehicle-treated HS mice. The novel eCIRP-derived TREM-1 antagonist (M3) can be a potential therapeutic adjunct in the management of hemorrhagic shock.

Vertebral Heart Score: A Useful Parameter in Determination of Resuscitation Endpoint in Dogs with Hemorrhagic Shock

BACKGROUND: GReliable prediction of patient response to fluid resuscitation is a crucial issue in the management of hemorrhagic shock. OBJECTIVES: This study was designed to investigate vertebral heart score (VHS) variation in fluid resuscitation of hemorrhagic shock patients and the feasibility of this method in determining resuscitation endpoint. METHODS: VHS values were assessed using previously published standard method in left to right lateral view. After induction of anesthesia (control assessments), hemorrhagic shock was induced by blood withdrawal to a mean arterial pressure of 40 to 50 mmHg within 30 minutes and then maintained in hypovolemic situation for an additional 30 minutes (second and third stages of assessments). Afterward, the dogs were randomly assigned to two groups which received 20 ml/kg lactated Ringer’s solution or 5 ml/kg Hydroxyethyl starch, in four consecutive 15 minute intervals (fourth stage of assessments). One hour after the last resuscitation step, final radiographic assessments were performed. RESUTLS: Hemorrhagic shock caused significant decrease in VHS values to a mean of 7.7 vertebrae (P<0.05). Following the fluid resuscitation VHS increased and returned to pre-shock values in both groups. CONCLUSIONS: This study confirms that the breed-specific VHS assessment can be a useful method in monitoring of patient’s response to fluid therapy and determination of resuscitation endpoint in dogs with hemorrhagic shock.

Permissive Hypotension: What’s New in Fluid Resuscitation in the Management of Hemorrhagic Shock?

Permissive Hypotension: What’s New in Fluid Resuscitation in the Management of Hemorrhagic Shock?

Controlled hypotension versus normotensive resuscitation strategy for people with ruptured abdominal aortic aneurysm.

An abdominal aortic aneurysm (AAA) is the pathological enlargement of the aorta and can develop in both men and women. Progressive aneurysm enlargement can lead to rupture. The rupture of an AAA is frequently fatal and accounts for the death from haemorrhagic shock of at least 45 people per 100,000 population. The outcome of people with ruptured AAA varies among countries and healthcare systems, with mortality ranging from 53% to 90%. Definitive treatment for ruptured AAA includes open surgery or endovascular repair. The management of haemorrhagic shock is crucial for the person's outcome and aims to restore organ perfusion and systolic blood pressure above 100 mmHg through immediate and aggressive fluid replacement. This rapid fluid replacement is known as the normotensive resuscitation strategy. However, evidence suggests that infusing large volumes of cold fluid causes dilutional and hypothermic coagulopathy. The association of these factors may exacerbate bleeding, resulting in a 'lethal triad' of hypothermia, acidaemia, and coagulopathy. An alternative to the normotensive resuscitation strategy is the controlled (permissive) hypotension resuscitation strategy, with a target systolic blood pressure of 50 mmHg to 100 mmHg. The principle of controlled or hypotensive resuscitation has been used in some management protocols for endovascular repair of ruptured AAA. It may be beneficial in preventing blood loss by avoiding the clot disruption caused by the rapid increase in systolic blood pressure; avoiding dilution of clotting factors, platelets and fibrinogen; and by avoiding the temperature decrease that inhibits enzyme activity involved in platelet and clotting factor function. This is an update of a review first published in 2016. To compare the effects of controlled (permissive) hypotension resuscitation and normotensive resuscitation strategies for people with ruptured AAA. The Cochrane Vascular Information Specialist searched the Specialised Register (August 2017), the Cochrane Register of Studies (CENTRAL (2017, Issue 7)) and EMBASE (August 2017). The Cochrane Vascular Information Specialist also searched clinical trials databases (August 2017) for details of ongoing or unpublished studies. We sought all published and unpublished randomised controlled trial (RCTs) that compared controlled hypotension and normotensive resuscitation strategies for the management of shock in patients with ruptured abdominal aortic aneurysms. Two review authors independently assessed identified studies for potential inclusion in the review. We used standard methodological procedures in accordance with the Cochrane Handbook for Systematic Review of Interventions. We identified no RCTs that met the inclusion criteria. We found no RCTs that compared controlled hypotension and normotensive resuscitation strategies in the management of haemorrhagic shock in patients with ruptured abdominal aortic aneurysm that assessed mortality, presence of coagulopathy, intensive care unit length of stay, and the presence of myocardial infarct and renal failure. High quality studies that evaluate the best strategy for managing haemorrhagic shock in ruptured abdominal aortic aneurysms are required.

Resuscitative endovascular balloon occlusion of the aorta performed by emergency physicians for traumatic hemorrhagic shock: a case series from Japanese emergency rooms

BackgroundResuscitative endovascular balloon occlusion of the aorta (REBOA), which has been increasingly used for the management of hemorrhagic shock, is a less invasive strategy for the management of patients with very severe hemorrhage. However, its effectiveness remains controversial.MethodsThis retrospective case series included trauma patients who underwent REBOA for hemorrhagic shock due to trauma in four Japanese tertiary care emergency centers from January 2013 to March 2017. Patients in cardiac arrest at the time of REBOA and those who underwent REBOA for nontraumatic causes during the study period were excluded.ResultsA total of 24 patients underwent REBOA during the study period. The median age was 52 years (interquartile range (IQR) 36.5–62.5), 17 (70.8%) of the patients were male, and 23 (95.8%) had blunt trauma. The 24-h survival was 50% (n = 12), and the in-hospital survival rate was 41.7% (10/24). In all cases, REBOA was performed in emergency rooms by emergency physicians without fluoroscopic guidance. Complications of REBOA were mesenteric ischemia (n = 1, 4.2%), ischemia of the lower extremities (n = 1, 4.2%), and placement of REBOA in thoracic aortic injury (n = 3, 12.5%).ConclusionsREBOA can be an effective and feasible tool for controlling massive hemorrhage due to trauma. However, caution should be exercised regarding complications including placement of REBOA in aortic injury and limb ischemia in cases where REBOA is performed in an emergency department setting with minimal or no support from trauma surgeons.