Introduction

Uncontrolled hemorrhage is the second leading cause of death in the civilian trauma setting [1] and the leading cause of preventable death during armed conflict [2,3]. Traditional methods of hemorrhage control in the prehospital setting were simple dressings, direct pressure, proximal arterial pressure points, elevation of bleeding extremities, and, as a last resort, a tourniquet. These measures are essentially the same as those used in antiquity [4]. Recent military and civilian experiences, as well as technological advances, have made new hemorrhage control tools available to both civilian and military out-of-hospital personnel.

Advances in civilian trauma care have often occurred secondary to military conflict. Because hemorrhage is the leading cause of potentially survivable death on the battlefield, researchers and physicians have focused intensely on prehospital management of severe hemorrhage. Within the past 10 years, significant advances have included several hemostatic dressings, ready-to-use tourniquets, and improved training in their use [5]. Some of these experiences have directly translated into saved lives in the civilian setting as well [6].

Death from compressible hemorrhage is rare in civilian settings [7], being, in most instances, entirely preventable with simple first aid measures [8]. Most civilian patients with severe hemorrhage can be rapidly transported to urban or suburban trauma centers while direct pressure is applied by a prehospital provider to an isolated injury. Hemorrhage control techniques commonly used by the military on the battlefield, such as tourniquets and advanced hemostatic agents, may have a role in EMS systems likely to encounter delayed patient transport, such as the rural and wilderness setting, prolonged extraction from a collapsed structure, enclosed space, or wrecked vehicle, and mass casualty incidents (MCI). This is particularly important in a scenario of mass shootings or deliberate bombings, where penetrating injury is the most common pattern and approximates battlefield situations.

Assessment

Traumatic hemorrhage is the acute loss of circulating blood volume as a result of injury [9]. Hemorrhage severity is largely predicated on the volume of blood lost before hemostatic control can be achieved. This volume will vary as a function of vessel defect, vessel size, type, and location. Large defects result in not only greater bleeding but also greater consumption of clotting factors and platelets, increasing the likelihood of coagulopathy. Brisk, pulsatile bleeding and the bright red hue of oxygenated blood identify arterial hemorrhage. Arterial bleeding control will require the application of pressure sufficient to overcome the systolic blood pressure and compress the muscular wall of the vessel. Constant pressure for 20 or more minutes may be required to stop arterial bleeding. Venous bleeding is non-pulsatile, may be brisk if the vessel is large, and may appear darker until exposed to oxygen. Venous bleeding will occlude at much lower pressures, will require less time to control, and is more amenable to the use of hemostatic agents than arterial bleeding. Capillary bleeding is usually much less brisk than arterial or venous bleeding due to the smaller size of the involved vessels but may be difficult to control if the patient has platelet dysfunction or clotting factor deficiency.

Diagnosis of hemorrhagic shock

Hemorrhagic shock is a failure of the cardiovascular system to deliver oxygen and nutrients to tissues due to blood loss and hypovolemia. Hemorrhagic shock recognition has often depended on abnormalities of vital signs, appearance of the skin, urine output, and mental status [10]. Although providing the basis of shock recognition and assessment, these metrics are limited by a number of important factors. Physiological response in patients on antihypertensives and other pharmacological agents is often blunted. Healthy patients in good physical condition may have sufficient physiological reserves to delay alterations in heart rate, blood pressure, and respiratory rate even with significant blood loss [11]. Urine output can rarely be assessed in the prehospital environment and mental status, while sensitive to hypotension due to blood loss, can be clouded by concomitant head trauma, intoxication, hypoglycemia, pain medications, or mental illness.

Alternative predictors of the severity of shock include the pulse pressure or shock index, both of which can be calculated from traditional vital signs. Pulse pressure is the difference between systolic and diastolic blood pressures. Use of pulse pressure in trauma is based on the principle that hemorrhage will increase the systemic vascular resistance, thus increasing diastolic pressure. At the same time, decreased preload will subsequently produce a reduction in systolic pressure. Narrowing of pulse pressure occurs before significant decreases in systolic blood pressure. Dynamic changes in pulse pressure have been used as a marker for cardiac output and volume status [12,13]. Shock index is calculated by dividing the heart rate by the systolic blood pressure and has been shown to be more sensitive than either of the vital signs alone. Shock index predicts shock states in multiple trauma patients and is predictive of complications once patients are admitted to the hospital [14]. It can also be adjusted to compensate for age-related differences in physiology, especially in the elderly [15].

Serum lactate measurements may identify hypoperfusion; however, this is a late finding and may not be useful in a prehospital setting [16,17]. Point-of-care testing of serum lactate, however, may be useful during long transports.

A novel method for measuring and diagnosing shock is tissue oxygen saturation (which can be measured peripherally); however, it is still undergoing evaluation. Early laboratory studies show it to be an earlier marker than standard vital signs [18,19]. Heart rate variability measurements are able to predict mortality but do not perform better than other common indices, and may not be the best for evaluation of hemorrhagic shock [20]. Sublingual capnography theoretically recognizes local tissue hypoxia and microcirculatory injury, but recent studies suggest it is not present earlier than standard vital signs [21].