INCIDENCE

Trauma complicates 7%–8% of pregnancies and is the leading cause of maternal death.¹ The incidence of significant maternal and fetal injury increases with gestational age, with slightly over 50% of injuries occurring in the third trimester.²

The most common mechanisms of injury for maternal trauma are motor vehicle collisions (MVCs) at 55%–70%, followed by assault at 12%–22%. In contrast, fetal death is a consequence of motor vehicle collisions in 82% of cases, followed by gunshot wounds (GSWs) in 6%, and falls in 3%.³

MECHANISM OF INJURY

Blunt Trauma

Blunt trauma is the leading cause of both maternal and fetal death and is usually a consequence of MVCs, assaults, or falls. Although mortality rates are similar for pregnant versus nonpregnant blunt trauma patients, with equivalent Injury Severity Scores (ISS), their patterns of injury are notably different. Pregnant patients injured in MVCs are more likely to sustain significant abdominal injuries and less likely to sustain head injuries than their nonpregnant counterparts. Splenic, hepatic, and retroperitoneal injuries occur more frequently in gravid trauma patients, due in part to the increased vascularity associated with pregnancy as well as to the displacement of the abdominal contents by the uterus. Up to 25% of pregnant blunt trauma patients sustain significant splenic or hepatic lacerations.⁴

Direct injury to the fetus from blunt trauma is rare (<1%). The leading cause of fetal mortality after blunt trauma is maternal mortality followed by placental abruption. Since the uterus is elastic and the placenta is not, sheering forces can result in placental abruption, even in otherwise minor blunt abdominal trauma. The estimated incidence of abruption is 2%–3% for minor trauma and up to 40% for severe blunt abdominal trauma. Uterine rupture occurs less commonly than placental abruption but increases in incidence with gestational age.³ Although uterine rupture is life-threatening to both the mother and the fetus, its diagnosis is often difficult, given the variable and sometimes subtle clinical presentation. The clinician must maintain a high index of suspicion for both placental abruption and uterine rupture in any patient with blunt abdominal trauma, especially in late gestation.

Penetrating Trauma

Penetrating trauma is usually the result of either GSWs or stabbing. This type of injury in pregnant patients is most often sustained at the hands of a spouse or intimate partner. Death rates for these injuries are actually decreased in pregnant patients compared with nonpregnant patients, owing to the protective effect for the mother of the gravid uterus. Unfortunately, the consequence to the fetus is a mortality rate of 71% for abdominal GSWs and 42% for abdominal stab wounds. It should also be noted that due to the upward displacement of intra-abdominal content by the uterus in pregnancy, upper quadrant abdominal stab wounds carry a high risk for small bowel injury in pregnant patients.^1,³

Intimate Partner Violence

Intimate partner violence (IPV) is not uncommon in pregnancy. Between 7.4% and 21% of pregnant patients reported physical abuse at the hands of an intimate partner and fully two-thirds reported an escalation of violence during pregnancy. Physically abused women have higher rates of miscarriage and low birth-weight infants than nonabused women. Battering during pregnancy is not only associated with an increase in the frequency of abuse but also with a threefold increase in risk of homicide compared with physically abused women who are not pregnant.⁵ Hence, intrapartum battering is a marker for a particularly violent and potentially lethal relationship.

PHYSIOLOGIC ALTERATIONS OF PREGNANCY

The extent of the anatomic and physiologic changes that occur during normal pregnancy is dependent on gestational age. During the first trimester, early changes are easily adapted to, so there is minimal functional alteration. By the third trimester, virtually every organ system has undergone change to compensate for the enlarged uterus and growing fetus. It is most important to remember that the presence of a fetus and the physical size of the abdomen are not the only aspects to consider when caring for the injured pregnant patient.

During the entire first trimester, the uterine size is small enough so that it remains relatively well protected by the bony pelvis. The earliest physiologic changes result from the presence of the placenta. Hormones released from the placenta include human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone, estrogen, adrenocorticotropic hormone (ACTH), and thyroid stimulating hormone (TSH). These hormones increase maternal insulin resistance and promote hyperglycemia. The subsequent increase in insulin and glucose levels translate into enhanced protein synthesis for the fetus. The reproductive hormones also inhibit gastrointestinal motility, which increases the potential for aspiration as early as 8–12 weeks gestation.

Increased levels of estrogen and progesterone, as well as of renin and aldosterone, lead to increased sodium resorption and plasma volume expansion beginning at about 10 weeks gestation. While heart rate, mean arterial pressure, and central venous pressure are not yet altered, the cardiac output may start to increase by 1–1.5 l/min (Table 1). Progesterone also promotes hypertrophy of the kidneys from 10 weeks gestation and leads to impaired gallbladder contraction and bile stasis. Beginning at the end of the first trimester, there may be an increase in gallstone formation.

Table 1 Cardiovascular Alterations during Pregnancy

During the second trimester, the uterus begins to rise out of the pelvis, and by 20 weeks, it may reach the umbilicus (Figure 1). Blood pressure falls by about 5–15 mm Hg and reaches its lowest level of the pregnancy. In traumatic maternal hemorrhage, placental blood flow is preferentially reduced, and 30% of maternal blood volume may be lost prior to signs of shock.⁶ The “supine hypotensive syndrome” is caused by compression of the inferior vena cava by the gravid uterus, decreasing venous blood return and thereby decreasing preload and cardiac output. Turning the mother left side down increases cardiac output by about 30% after 20 weeks gestation.⁷

Figure 1 The height of the uterine fundus relative to the abdominal wall.

(Courtesy of David Gens, MD.)

Third Trimester

By the 7th month, the pubic symphysis and sacroiliac joints widen. At approximately 36 weeks gestation, the uterus reaches its maximal height near the costal margins. Intraperitoneal structures are displaced cephalad and laterally.

During the third trimester, blood pressure returns to more normal levels and heart rate increases up to 20 beats per minute relative to the nonpregnant state. This physiologic tachycardia must be considered when evaluating the pregnant trauma patient. Pulmonary capillary wedge pressure and left ventricular function remain normal, while systemic and pulmonary vascular resistances are decreased.⁸

After 30 weeks gestation, plasma volume has increased 40%, accompanied by a 15% increase in red blood cell mass. This discrepancy leads to the “physiologic anemia of pregnancy.”⁹ Serum albumin declines by up to 30% because of this volume expansion. Benign physiologic pericardial effusion is more prevalent and may complicate the Focused Assessment with Sonography for Trauma (FAST). The decrease in colloid oncotic pressure may increase the risk for pulmonary edema. A hypercoagulable state is also induced because of an increase in nearly all coagulation factors, procoagulants and fibrinogen, and a reduction in fibrinolytic activity.¹⁰

Anatomic changes in the thorax include the diaphragm rising about 4 cm and the chest diameter increasing by 2 cm.¹¹ The most significant changes in respiratory function include an increase in minute ventilation by as much as 50%, mostly by an increase in tidal volume. Functional residual capacity decreases largely due to elevation of the diaphragm. A state of compensated respiratory alkalosis results in a chronic reduced PaCO₂ to approximately 30 mm Hg and reduced plasma bicarbonate level.¹²

The movement of gastrointestinal viscera cephalad is associated with a displacement of the gastroesophageal sphincter into the thorax. Placental release of gastrin augments the acid production of the stomach, making the risk for aspiration greatest at this time.

Uterine compression of the bladder and ureters results in a compensated hydronephrosis. The increase in blood volume and cardiac output is associated with increased renal blood flow of up to 80% and increased glomerular filtration rate of 50%. Blood urea nitrogen and serum creatinine are commonly reduced, but urine output volume does not significantly change.