Traumatic Shock

Military Medicine, Apr 2006 by Hardaway, Robert M

The association of shock with trauma has long been recognized. There are three types of shock, i.e., (1) hypovolemic or hemorrhagic shock, (2) traumatic shock, and (3) septic shock. The conditions and their treatments are described.

Introduction

The association of shock with trauma has been recognized since the 18th century. In 1731, Le Dran1 described a case of injury by a missile that led to a collapse of vital function, ending in death. He called it "secousse" (jar). In fact, shock was called "wound shock" until World War II. It has since been subdivided into hemorrhagic (hypovolemic), traumatic, and septic shock, all associated with war wounds. Shock can be defined as inadequate capillary perfusion, encompassing neurogenic, cardiogenic, and anaphylactic shock as well as other types.2 During the American Civil War, shock and hemorrhage were considered to be separate conditions. In the Army Surgeon General's report written in 1876,3 it was stated that "the collapse of bleeding resembles syncope as distinguished from shock. Rest in bed, opium, and warm fomentation constitute the treatment."

In World War I, traumatic shock was attributed to a "toxin" originating in dead or dying tissue.4 However, a toxin was never found. In the 1920s, Blalock5 "proved" that shock after trauma was attributable to blood loss into the tissues. He bluntly traumatized dogs' legs and measured the increase in volume of the legs. He estimated that the increase in weight of the legs (which consisted of extravasated blood in the tissues) showed enough blood volume loss to account for the shock produced. If this is true, however, why is the mortality rate of severely traumatized patients so high even if adequate blood volume has been achieved with intravenously administered fluids? According to the accepted classification scheme described by Trunkey,6 traumatic shock is considered a subset of hypovolemic shock but with features that make it more difficult to treat. It now seems likely that both a toxin and hypovolemia play roles in the development of traumatic shock.

Many trauma patients die with normal blood volume. In Vietnam, 153,303 wounded U.S. personnel were admitted to military hospitals.7 Approximately 3,000 died as a result of "shock," despite being adequately treated with intravenously administered fluids and appropriate surgical procedures.8 Something else must be involved besides blood volume loss. Death after trauma is often attributable to multiple-organ failure (MOF), especially acute respiratory distress syndrome. What is the etiology of MOF? Many metabolic changes occur after massive injury, the most important of which have been grouped together as the systemic inflammatory response syndrome, usually followed by a compensatory anti-inflammatory response syndrome.9 The inflammatory cytokines of the systemic inflammatory response syndrome can lead to cellular death and MOF if not adequately balanced by mediators of the compensatory antiinflammatory response syndrome. However, a number of antiinflammatory drugs have failed to alter the mortality rate in clinical trials, despite successes in the laboratory and in animal studies.10 Perhaps a more important change is the frequent onset of disseminated intravascular coagulation (DIC). DIC is rarely diagnosed in its early stages, because it is widely thought that bleeding, prolongation of prothrombin time and decreases in fibrinogen and platelet levels are signs of developing DIC. This is not true; these are late developments in DIC and appear only late in the disease. The only accurate tests for the presence of early DIC are increases in D dimer and fibrin split product levels.

What initiates DIC? It is widely accepted that endotoxin from the cell walls of Gram-negative bacteria induces thrombosis. This is undoubtedly true. However, there is a much more common factor that promotes clotting and is present in all cell walls (animal and bacterial). These cell walls are made up of a bilayer of phospholipids, with the inner layer differing from the outer in one important aspect. The external layer consists largely of choline-containing phospholipids, which are not thrombogenic. The internal layer, however, is composed of aminophospholipids, which are strongly thrombogenic.11 It has been shown that, when the cell wall is inverted or broken, as in "sickling" in sickle cell disease or in paroxysmal nocturnal hemoglobinuria or malaria, the inner layer is exposed to the systemic circulation and promotes coagulation.12 Cells, including red blood cells, may be broken because of trauma, heat, or cold, and the resulting exposure of their internal membranes can promote coagulation, including DIC. These microclots occlude the microcirculation of any and all organs and in turn may lead to MOF and acute respiratory distress syndrome.13

Types of Shock

On the basis of the above observations, the following is proposed. There are three types of shock, i.e., (1) hypovolemic or hemorrhagic shock, (2) traumatic shock, and (3) septic shock. They are separate and distinct, each with different etiology and treatment. Hypovolemic (hemorrhagic) shock is characterized by inadequate blood volume resulting from hemorrhage, dehydration, or loss of plasma because of burns or third spacing. "Pure" hemorrhagic shock involves little or no tissue damage. Its treatment is intravenously administered fluids (in appropriate volume and kind) and is very effective, provided hemorrhage can be controlled. Traumatic shock is characterized by severe tissue damage, such as multiple fractures, severe contusions, or burns. Its treatment is unsatisfactory, and mortality rates are high even if blood volume is brought to normal and the injury repaired. DIC is usually present. Treatment may involve administration of a thrombolytic agent, which lyses the microclots of DIC.13-20 Septic shock is attributable to infection with bacteria or viruses. Treatment is unsatisfactory in severe septic shock. Again, DIC is usually present. To date, treatments with antiendotoxin agents or drugs against cytokines and systemic inflammation have not been effective in saving lives in either traumatic or septic shock.