Hemorrhagic Shock Review Article Text

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published: 30 june 2004 i read with interest the review by prof. The treatment of hemorrhagic shock is addressed in the review, and mention is made of the main goals: to stop the source of hemorrhage and to restore the circulating volume. Conserving blood products, on the grounds of cost, restricted availability and their pathophysiological effects, is becoming a necessary shift in the approach to these difficult patients and was not touched upon in the review. There have been clear advances in recent years in developing other strategies to aggressively stem the flow. Damage control surgery in trauma and embolization are certainly useful tools in the control of bleeding. Pharmacological manipulation of the coagulation system is a rapidly expanding field of research. Activated recombinant factor vii factor viia is a hemostatic agent originally developed for the hemophilia population, but it is emerging as a very effective way of treating uncontrolled hemorrhage in patients without pre existing factor deficiencies.

A heterogeneous case series of major hemorrhage was reported last year, in which 80% of the cases given factor viia responded with complete or partial cessation of bleeding 2 . Data from the trauma environment with massive bleeding suggest a useful role for factor viia 3 , and further studies are ongoing. We agree that conservation of blood and blood products is not just an economic concern, but it is necessary to protect a limited resource and to prevent untoward effects of such products. Our sections on hypertonic saline and the use of blood substitutes were meant to address this issue directly. We limited our discussion to a general discussion of hemorrhagic shock and did not specifically address surgical approaches to the control of bleeding. 'damage control' and packing is a valid concept in the treatment of severely injured patients with hemorrhage 4 . This approach was frequently used in battlefields, and has become more popular in civilian injury as a method for preventing death from coagulopathy and hypothermia in the operating room.

The use of radiological embolization as a technique to control ongoing hemorrhage from solid organs such as the spleen and the liver has also supplemented its use in pelvic hemorrhage. This technique is not necessarily an ideal therapy for patients who are in shock. We agree that pharmacological manipulation may be an adjunct to good surgical practice. There are anecdotal reports on the use of activated recombinant factor vii to control bleeding in trauma patients, as well as in numerous other patient populations who do not have hemophilia. The unencumbered use of this extremely expensive treatment has led to the loss of millions of dollars in uncompensated care and occasional significant complications.

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The present status of this potentially important addition to the armamentarium is under investigation. Prospective studies need to be performed to establish efficacy and criteria for use before we embark on this new approach. published: 2 april 2004 this review addresses the pathophysiology and treatment of hemorrhagic shock – a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. The primary goals are to stop the bleeding and to restore circulating blood volume. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. A hemoglobin level of 7–8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia.

However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.

Blood loss estimated blood volume hemorrhage oxygen consumption oxygen delivery shock transfusion life threatening decreases in blood pressure often are associated with a state of shock – a condition in which tissue perfusion is not capable of sustaining aerobic metabolism. Shock can be produced by decreases in cardiac output cardiogenic , by sepsis distributive , or by decreases in intravascular volume hypovolemic. The latter may be caused by dehydration from vomiting or diarrhea, by severe environmental fluid losses, or by rapid and substantial loss of blood. A less common form of shock cytopathic may occur when the mitochondria are incapable of producing the energy required to sustain cellular function 1 . Agents that interfere with oxidative phosphorylation, such as cyanide, carbon monoxide and rotenone, can produce this type of shock. Hemorrhage is a medical emergency that is frequently encountered by physicians in emergency rooms, operating rooms, and intensive care units.

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Significant loss of intravascular volume may lead sequentially to hemodynamic instability, decreased tissue perfusion, cellular hypoxia, organ damage, and death. This review addresses the pathophysiology and treatment of hypovolemic shock produced by hemorrhage, which is also known as hemorrhagic shock. The average adult blood volume represents 7% of body weight or 70 ml/kg of body weight 2 . Children have ebvs of 8–9% of body weight, with infants having an ebv as high as 9–10% of their total body weight 3 . doi: 10.1186/2110 5820 3 1 received: 25 september 2012 accepted: 1 december 2012 published: 12 january 2013 managing trauma patients with hemorrhagic shock is complex and difficult. Despite our knowledge of the pathophysiology of hemorrhagic shock in trauma patients that we have accumulated during recent decades, the mortality rate of these patients remains high.

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In the acute phase of hemorrhage, the therapeutic priority is to stop the bleeding as quickly as possible. As long as this bleeding is uncontrolled, the physician must maintain oxygen delivery to limit tissue hypoxia, inflammation, and organ dysfunction. This process involves fluid resuscitation, the use of vasopressors, and blood transfusion to prevent or correct acute coagulopathy of trauma. To move forward, we need to establish optimal therapeutic approaches with clear objectives for fluid resuscitation, blood pressure, and hemoglobin levels to guide resuscitation and limit the risk of fluid overload and transfusion. Trauma hemorrhagic shock fluid resuscitation vasopressors acute coagulopathy of trauma hemorrhage remains the major cause of preventable death after trauma 1 . In the acute phase of hemorrhage, the physician’s therapeutic priority is to stop the bleeding as quickly as possible.

Hemorrhagic shock is a pathologic state in which intravascular volume and oxygen delivery are impaired. As long as this bleeding is not controlled, the physician must maintain oxygen delivery to limit tissue hypoxia, inflammation, and organ dysfunction. This procedure involves fluid resuscitation, use of vasopressors, and blood transfusion to prevent or correct traumatic coagulopathy. However, the optimal resuscitative strategy is controversial: choice of fluid for resuscitation, the target of hemodynamic goals for hemorrhage control, and the optimal prevention of traumatic coagulopathy are questions that remain. This review focuses on new insights into resuscitative strategies in traumatic hemorrhagic shock. Fluid resuscitation is the first therapeutic intervention in traumatic hemorrhagic shock. There is no proof in the literature that supports the superiority of one type of fluid over another type of fluid in trauma patients.

The most important dual advantage that colloids have over crystalloids is that colloids can induce a more rapid and persistent plasma expansion because of a larger increase in oncotic pressure, and they can quickly achieve circulatory goals. Although crystalloids are cheaper, research findings have shown no survival benefit when colloids are administered. However, resuscitation with large volumes of crystalloids has been associated with tissue edema, an increased incidence of abdominal compartment syndrome 2 , and hyperchloremic metabolic acidosis 3 . The safe study demonstrated that albumin administration was safe for fluid resuscitation for intensive care unit icu patients and that there was no difference in the mortality rate of patients who were treated with albumin and saline 4 . In a subgroup of trauma patients, the investigators observed a positive trend in benefit for saline use over albumin use. This difference in the relative risk of death was due to the greater number of patients, who had trauma and an associated brain injury and who died after random assignment to the albumin treated group as opposed to the saline treated group.

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