TRAUMA IN PREGNANCY

Published on 10/03/2015 by admin

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Last modified 10/03/2015

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CHAPTER 77 TRAUMA IN PREGNANCY

The pregnant trauma patient presents significant challenges to the trauma surgeon. The physiologic changes in the mother during pregnancy represent both diagnostic and treatment dilemmas, while the need to treat two patients simultaneously may represent both clinical and emotional challenges for the trauma team.

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.

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.

Second Trimester

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

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.

DIAGNOSIS

Primary Survey

The initial evaluation of the pregnant trauma patient should include early consultation with the obstetrics service as well as neonatology if appropriate (>24 weeks gestation). The general principles of evaluation of trauma patients are similar to those of the nonpregnant patient and include initial focus on assessing and stabilizing maternal vital signs. These include the standard Advanced Trauma Life Support (ATLS) primary survey, which is then followed by a rapid and brief assessment of the fetus for viability. Because pressure from the pregnant uterus on the inferior vena cava can result in a decrease in cardiac return, an effort should be made to displace the uterus laterally in pregnant patients. This may be accomplished by tilting the backboard to the side or by manually displacing the uterus to the left side.

Indications for intubation in the pregnant trauma patient are similar to those in the nonpregnant patient, although aspiration risk is higher during pregnancy. It should be kept in mind, however, that the fetus will not tolerate hypoxemia as well as the mother, so supplemental oxygen should always be applied and oxygen saturation monitored in all pregnant patients.

Accurate assessment of maternal volume status may be complicated by the physiologic changes of pregnancy. Since the fetus will be compromised by even minor maternal hypovolemia, aggressive volume replacement should be undertaken. Vasopressors and inotropes may actually reduce maternal blood flow to the fetus and should not be used as a substitute for volume resuscitation in alleviating maternal hypotension. Immediate jeopardy of the mother’s life may occasionally necessitate the use of vasopressors or inotropes for circulatory support, but they should be used sparingly and discontinued as rapidly as possible.