Skip to Main Content

++

INTRODUCTION

++

The authors have no financial interests to disclose.

++

INCIDENCE

++

The risk of maternal death in the United States has decreased nearly 99% during the twentieth century—from 850 maternal deaths per 100,000 live births in 1900 to 7.5 in 1982. However, since the 1980s, this rate has remained relatively unchanged.1 Trauma is the leading cause of nonobstetric maternal death,2 comprising 6% to 7% of all fatalities.3 Motor vehicle accidents are the most common cause of injury, followed by falls and assaults.2 Young maternal age, nonwhite ethnicity, substance and alcohol abuse, and domestic violence have been identified as risk factors for obstetric trauma.4,5

++

HEMORRHAGIC SHOCK IN PREGNANCY

++

During pregnancy, hemorrhage is difficult to reliably assess by conventional clinical parameters. Normal indicators of early shock, such as narrowed pulse pressure typically seen with 15% to 25% blood volume loss, are diminished due to progesterone-induced peripheral vasodilation. Additionally, classic signs such as tachycardia that are commonly seen with a 25% to 40% loss of blood volume may already exist during normal pregnancy; healthy parturients may exhibit a 40% increase in heart rate above prepregnancy baseline.

++

Plasma volume expansion begins as early as the sixth week of pregnancy,6 peaking at 48% above baseline during the third trimester,7 thereby causing a dilutional anemia. This could lead to a misinterpretation if a low hemoglobin or hematocrit was to be assessed as a lone value. For this reason, hemoglobin or hematocrit should be followed only as a trend during assessment and treatment of maternal trauma and injuries.8 Pregnancy is associated with a hypercoagulable state, characterized by an elevation of certain coagulation factors, accelerated coagulation, and fibrinolysis.9 However, the substantial blood loss along with further dilution of coagulation factors and platelets that can occur with aggressive fluid resuscitation and transfusion of packed red blood cells (PRBCs) may disrupt clotting activities, resulting in coagulopathy. Even in the absence of obstetric complications, such as uterine hypotonia, abruptio placentae, and placenta previa, parturients have an increased background incidence of hypofibrinogenemia and elevated fibrin split products (FSPs).8 In the setting of trauma, rapid degradation of fibrin results in hypofibrinogenemia and elevated FSP levels, which can disrupt platelet function and further exacerbate coagulopathy during trauma resuscitation. This has been defined as “acute trauma coagulopathy.”10 Finally, the underlying coagulation abnormalities and tissue injuries that may occur during trauma and/or delivery predispose parturients to develop disseminated intravascular coagulation (DIC), a consumptive process of coagulation factors and platelets.11

++

Healthy pregnant women typically have good cardiovascular reserve and may not need full resuscitative measures until an excess of 30% blood volume is lost.12 When a blood transfusion is warranted during pregnancy, there are some unique considerations. Fetal-maternal hemorrhage occurs in up to 30% of traumas; therefore, most experts recommend that all Rh-negative women receive Rho(D) ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.