After a traumatic injury, hemorrhage is responsible for over 35% of pre-hospital deaths and over 40% of deaths within the first 24 hours, second only to the rates of death due to severe central nervous system injury. A cascade of life-threatening medical problems can begin with severe hemorrhage, and many of these occur simultaneously: 1) hemorrhage, 2) impaired resuscitation, 3) shock, 4) inflammation and 5) coagulopathy (Fig. 1). The severity of each problem is commonly associated with the extent of overall blood loss. Low blood pressure due to blood loss indicates immediate complications, including the incidence of multiple organ failure and life-threatening infections.[2, 3]
Simple associations of trauma, hemorrhage, resuscitation, shock, inflammation and coagulopathy
Early trauma care focuses on minimizing hemorrhage and restoring circulation (resuscitation) effectively.
Mitigation of battlefield injury and hemorrhage is the highest priority of U.S. military trauma surgeons and researchers. There is no debate about the importance of hemorrhage control as a first-line measure by medics or emergency medicine personnel.
While extremity wounds are more amenable to compression to stop bleeding, 15% of Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) battle injuries are to the torso (chest, abdomen, pelvis and back), where compression cannot be applied. Noncompressible hemorrhage from truncal injury is the leading cause of potentially survivable deaths of American troops. Patients who have penetrating wounds to the trunk are at risk of severe injuries to major vessels, causing massive hemorrhage, and are most likely to die during the acute (emergency) phase of care. The control of bleeding and limitation of blood loss is the only way to avoid the problems associated with massive hemorrhage in trauma.
Currently, there is no active intervention for noncompressible hemorrhage available to military or civilian medics and physicians; however, research of noncompressible hemorrhage control methods may offer solutions that could save lives. A systemic drug that could be given intravenously to induce coagulation or a device that compresses or occludes the bleeding vessel are potential treatments of truncal hemorrhage that have promise.
Many people are familiar with the ABCs of resuscitation: airway, breathing and circulation. In a hemorrhage situation, resuscitation refers to the restoration of circulation after blood loss. Resuscitation is vital because restoration of blood volume and blood pressure is the main method for prevention of hemorrhagic shock (see below). Many resuscitation products have been tried and are dependent on the nature of the injury, the location of bleeding and the treatment situation. Products include colloids (dextran, gelatin, hetastarch); crystalloids (isotonic saline, lactated Ringer’s solution); and human plasma or plasma proteins such as albumin, blood transfusion with whole blood, hemoglobin-based oxygen carriers, and autotransfusion (the transfusion of the patient’s own exsanguinated blood after filtration to remove contaminants).
Some resuscitation fluids, including whole blood, promote an immune response, causing inflammation. In some cases, trauma, itself, promotes an immune response, and this can be either exacerbated or diminished by the resuscitation fluid. Reduction in the immune response is known to be associated with increased survival in critically ill patients, but more research is required in this arena to fully understand and control inflammation to save lives.
Current challenges in resuscitation are development of blood products such as freeze-dried blood or blood substitutes that can be used in austere environments, prediction of resuscitation requirements, development and selection of resuscitation fluids, control and monitoring of the immune response to resuscitation and trauma, and identification of optimal resuscitation blood pressure.
Hemorrhagic shock is a severe and life-threatening condition. Over 21% of military casualties are in shock upon admission, and over 25% require a blood transfusion. Shock occurs when loss of blood leads to a lack of oxygen to the tissues, causing a systemic build-up of acids. In an attempt to reverse the acid build-up, the patient begins to hyperventilate and, along with other physiological changes, blood pressure increases and blood diverts from the renal system to the heart, lungs and brain. These symptoms occur due to the cellular response to the lack of oxygen, and lead to further breakdown and malfunction of cells, prompting various responses in the circulatory system.
If the problem is not treated or rectified, the cellular response will promote the dysfunction or complete failure of the vital organs, and the patient will die. Prevention of severe hemorrhage, or resuscitation with novel or advanced physiological resuscitation fluids would diminish the onset of shock.
About 28% of patients with severe traumatic injury also have dysfunction in the process of coagulation (coagulopathy) when they arrive at the emergency department. This is often caused by dilution of the blood due to infusion of resuscitation products. Coagulopathy is associated with a 3.5- to 5-fold increase in mortality,[8, 9] and when combined with hypothermia and acidosis is known as the “lethal (or fatal) triad” because of the high likelihood of impending death.
Coagulopathy could be prevented or diminished with transfusion products that not only increase fluid/blood volume but closely resemble whole blood with component clotting factors. Methods to detect early signs of coagulopathy would aid in a timely response to limit exacerbation of coagulopathic symptoms.
Continued research on issues ranging from hemostasis to inflammation and organ dysfunction is required. With advances resulting from focused research programs, it seems likely that the rates of immediate death and late complications that lead to death will be decreased and outcomes improved for both soldiers with battlefield injuries and trauma victims in the civilian community.
1. Kauvar, D.S., Lefering, R., and Wade, C.E. (2006) Impact of hemorrhage on trauma outcome: an overview of epidemiology, clinical presentations, and therapeutic considerations. J Trauma 60, S3-11
2. Heckbert, S.R., Vedder, N.B., Hoffman, W., Winn, R.K., Hudson, L.D., Jurkovich, G.J., Copass, M.K., Harlan, J.M., Rice, C.L., and Maier, R.V. (1998) Outcome after hemorrhagic shock in trauma patients. J Trauma 45, 545-549
3. Franklin, G.A., Boaz, P.W., Spain, D.A., Lukan, J.K., Carrillo, E.H., and Richardson, J.D. (2000) Prehospital hypotension as a valid indicator of trauma team activation. J Trauma 48, 1034-1037; discussion 1037-1039
4. Eastridge, B. (2009) Joint Theater Trauma Registry Data. September 2001-February 2008.
5. Kelly, J.F., Ritenour, A.E., McLaughlin, D.F., Bagg, K.A., Apodaca, A.N., Mallak, C.T., Pearse, L., Lawnick, M.M., Champion, H.R., Wade, C.E., and Holcomb, J.B. (2008) Injury severity and causes of death from Operation Iraqi Freedom and Operation Enduring Freedom: 2003-2004 versus 2006. J Trauma 64, S21-26; discussion S26-27
6. Raghavan, M., Murray, H., and Kellum, J.A. (2006) Fluid resuscitation and immunomodulation in the critically ill. In Intensive Care Medicine (Vincent, J.-L., ed), 68-75, Springer
7. Eastridge, B. (2009) Joint Theater Trauma Registry Data. June 2006-November 2008.
8. MacLeod, J.B., Lynn, M., McKenney, M.G., Cohn, S.M., and Murtha, M. (2003) Early coagulopathy predicts mortality in trauma. J Trauma 55, 39-44
9. Brohi, K., Cohen, M.J., and Davenport, R.A. (2007) Acute coagulopathy of trauma: mechanism, identification and effect. Curr Opin Crit Care 13, 680-685