Clinical Pearls & Morning Reports
Published January 24, 2018
Signs and symptoms of hemorrhagic shock, especially from occult sources of bleeding, are often subtle. In most patients, robust compensatory mechanisms render hypotension an insensitive indicator of shock until more than 30% of the patient’s blood volume has been lost. More subtle clinical cues indicative of shock include anxiety, tachypnea, a weak peripheral pulse, and cool extremities with pale or mottled skin. Read the latest NEJM Review Article here.
Q: Is there evidence to support the training of bystanders in tourniquet application?
A: New evidence indicates that tourniquet application proximal to sites of hemorrhage in the extremities saves lives without risking amputation or extremity dysfunction, if the patient is rapidly transported to a hospital where definitive care can be provided. On the basis of this evidence, a public education program has been initiated by the American College of Surgeons and several partner organizations to train bystanders on tourniquet application and other hemorrhage-control measures. Guidelines for providing first aid and prehospital care now endorse tourniquet application when direct pressure is ineffective or impractical.
Q: Is it ever beneficial to delay fluid resuscitation in cases of severe hemorrhage?
A: Delaying resuscitation (i.e., withholding intravenous fluid until the moment of definitive hemostasis), improves survival among patients with penetrating trauma to the torso who receive care in an urban trauma center, probably because this approach averts dilutional coagulopathy.
A: Hemorrhage induces profound changes in the vascular endothelium throughout the body. At the site of hemorrhage, the endothelium and blood act synergistically to promote thrombus formation. However, the mounting oxygen debt and the catecholamine surge eventually induce a so-called endotheliopathy through systemic shedding of the protective glycocalyx barrier. With hemorrhage and shock, both adaptive and maladaptive changes occur in the blood. At the site of hemorrhage, the clotting cascade and platelets are activated, forming a hemostatic plug. Remote from the site of hemorrhage, fibrinolytic activity increases, presumably to prevent microvascular thrombosis. However, excess plasmin activity and autoheparinization from glycocalyx shedding can result in pathologic hyperfibrinolysis and diffuse coagulopathy. Conversely, nearly half of patients with trauma have a hypercoagulable phenotype of fibrinolysis shutdown. Depleted platelet numbers, decreased platelet margination due to anemia, and reduced platelet activity also contribute to coagulopathy and increased mortality. Iatrogenic factors can further exacerbate coagulopathy in patients with active bleeding. Overzealous resuscitation with crystalloid dilutes the oxygen-carrying capacity and clotting factor concentrations. Infusion of cold fluids exacerbates the heat lost from hemorrhage, depleted energy stores, and environmental exposure and leads to decreased function of the enzymes in the clotting cascade. Finally, overadministration of acidic crystalloid solutions worsens the acidosis caused by hypoperfusion and impairs the function of clotting factors, resulting in a “bloody vicious cycle” of coagulopathy, hypothermia, and acidosis.
A: Patients with purely abdominal or pelvic bleeding from any source may benefit from endovascular occlusion of the aorta as a temporizing measure to slow hemorrhage. This approach, termed resuscitative endovascular balloon occlusion of the aorta (REBOA), lowers the perfusion pressure to distal sites of severe hemorrhage, increases afterload, and redistributes the remaining blood volume preferentially to the heart and brain. REBOA reduces intraoperative mortality among patients with ruptured abdominal aortic aneurysm and is being evaluated in two prospective studies for patients with trauma. REBOA has also been used for severe gastrointestinal bleeding and peripartum hemorrhage.