Trauma in the Gravid Patient

Published on 22/03/2015 by admin

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Last modified 22/03/2015

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162 Trauma in the Gravid Patient

Trauma is the most common nonobstetric cause of death in pregnant women, accounting for 46% of maternal deaths.1 In the United States, 5% to 7% of all pregnancies are complicated by some form of traumatic injury.2 The most common mechanisms of blunt trauma are motor vehicle accidents (55%-70%), assaults (11%-21%) and falls (9%-22%).3,4 Penetrating trauma and burns are less common in most communities. The risk of trauma to the fetus increases as pregnancy progresses and the size of the uterus and fetus increases. The most common causes of fetal death are maternal hemorrhagic shock, abruptio placentae, and uterine rupture. A common maternal injury that results in fetal death is pelvic fracture, frequently leading to fetal skull fracture and intracranial injury. However, even relatively minor injuries to the mother can be devastating to the unborn child.5

The major causes of death from trauma (i.e., head injury and hemorrhage) are similar in gravid and nongravid patients. Patterns of injury are generally the same, based upon mechanism of injury. Hepatic and splenic injuries remain common, though gastrointestinal injuries are less common as the pregnancy progresses and the uterus enlarges.6

The outcome from trauma for the mother and fetus is dependent upon multiple factors, including gestational age of the fetus and the mechanism and severity of injury. The largest contributor to fetal mortality is gestational age less than 28 weeks.5 Scorpio et al.7 found in gravid victims of mostly blunt trauma (80% motor vehicle crashes) that injury severity score and admission serum bicarbonate level were the only independent factors that predicted fetal demise. The serum bicarbonate or base deficit may be important markers of occult hypoperfusion in trauma victims, though serum bicarbonate is normally decreased late in pregnancy. El Kady et al.5 and Schiff et al.8 reported that while the actual injury severity score was not predictive of fetal outcomes, maternal and fetal mortality were highest with internal injuries to the thorax, abdomen, and pelvis. The critical factor for the fetus is the extent to which trauma disrupts normal uterine and fetal physiology. Fetal demise occurs in up to 80% of gravid patients who develop hemorrhagic shock. In addition, however, even minor injuries to the mother can result in abruptio placentae or fetal demise.5 In one study of interpersonal violence as a cause of trauma in pregnancy, 5 of 8 women with fetal losses had no apparent physical injury.9

Any female patient of child-bearing potential could be pregnant at the time of injury. Screening (beta-human choriogonadotropin) should therefore be routine during the initial assessment of the patient. Recognition that a “second” patient is present is essential for the care of both mother and fetus. Optimal management of the pregnant trauma victim is the best way to optimize outcome for the fetus: “save the mother, save the fetus.” To manage the gravid patient, the traumatologist or intensivist must have an understanding of fetal and maternal physiology, as well as the specific complications of trauma that are unique to these patients. Early obstetric consultation should be obtained. If delivery of a viable fetus is imminent, neonatology consultation may also be needed.

image Fetal Physiology

During the first week after conception, the conceptus has not yet implanted in the uterus, making it relatively resistant to injury. Soon thereafter, the blastocyst begins implantation and the placenta begins to develop. The embryo attaches to the uterus via anchoring villi. The placenta is not as elastic as the myometrium, potentially leading to shear stresses and disruption of these villi (particularly if intraamniotic fluid pressure is increased) when force is applied to the uterus. The resulting abruptio placentae rapidly leads to fetal hypoxemia, acidosis, and death.

On the positive side, amniotic fluid is a cushion for the fetus, but the fetus may still suffer injury as a result of rapid compression, deceleration, or contrecoup injury. Late in pregnancy, however, the head of the fetus is typically in the pelvis. Pelvic fractures may lead to fetal skull fracture and brain injury.4

Adequate oxygen delivery to the fetus is critical during pregnancy. Blood flow to the uterus decreases proportionally as maternal systemic blood pressure decreases. In addition, as the mother becomes hypovolemic, peripheral vasoconstriction can further decrease uterine circulation. The placenta is exquisitely sensitive to catecholamines. The ability of the fetus to withstand changes in uterine blood flow and/or oxygenation is variable. The fetus can redistribute blood flow to the most vulnerable organs, the brain and heart, but this response (the “diving reflex”) is limited. Decreased placental blood flow quickly leads to fetal distress.

image Anatomic and Physiologic Changes Associated with Pregnancy

The gravid patient undergoes a multitude of anatomic and physiologic changes to accommodate the developing fetus. Theses changes have a significant impact upon anatomic injury patterns and the response to injury.

From a respiratory standpoint, maternal tidal volume increases by as much as 40%, causing respiratory alkalosis. Renal compensation maintains a normal arterial pH. The diaphragms are elevated, decreasing functional residual capacity and risking intraabdominal placement of chest tubes. The gravid patient has little respiratory reserve and desaturates quickly.

From a cardiovascular standpoint, heart rate increases by 15 to 20 beats per minute by the third trimester. During the second trimester, both systolic and diastolic blood pressure decrease by about 15 mm Hg, then increase to normal levels during the third trimester. By the 10th week of pregnancy, cardiac output increases by 1 to 1.5 L/min due to increased plasma volume and decreased peripheral resistance.

Maternal blood volume increases by nearly 50% by 28 weeks. Red cell mass does not increase proportionally, leading to the “anemia of pregnancy.” Normal hematocrit late in pregnancy is 31% to 35%. A mild leukocytosis (up to 18,000 cells/mL) occurs during the second trimester. Coagulation factors and fibrinogen levels increase while plasminogen activator levels decrease during pregnancy, leading to an increased risk of thromboembolism. Trauma to the gravid uterus can lead to release of thromboplastic factors (e.g., amniotic fluid) which can cause disseminated intravascular coagulation (DIC). Serum albumin levels decrease to 2.2 to 2.8 gm/dL.

Decreased gastric motility and cephalad displacement of the abdominal contents predispose women to gastroesophageal reflux and aspiration. Gallbladder function is also impaired, increasing risk of stone formation.

The abdominal examination of gravid women is complicated by cephalad displacement of the abdominal contents by the enlarging uterus. The urinary bladder is displaced upward out of the pelvis, and the ureters become dilated after the 10th week of gestation.

During pregnancy, the uterus increases in size from 70 to 1100 g, taking on an intraabdominal position after 12 weeks, increasing risk of direct trauma. At 20 weeks, the fundus reaches the umbilicus. By 34 to 36 weeks, it reaches the costal margin. Uterine blood flow increases to 10 times normal. One of the most important consequences of the anatomic changes during the latter half of pregnancy is that the uterus can occlude the inferior vena cava when the patient is in the supine position (supine hypotension syndrome), leading to hypotension from decreased venous return. Positioning the patient with the right side of the torso elevated can increase cardiac output by up to 25%. The pelvis of the gravid female has relaxed ligaments, causing gait instability and risk of falls. In addition, venous engorgement in the pelvis increases risk of severe hemorrhage.

From an endocrine standpoint, the hormones of pregnancy (placental lactogen, progesterone, estrogen, parathormone, and calcitonin) lead to insulin resistance and diabetes of pregnancy, decreased lower esophageal sphincter pressure, decreased gastric emptying, and increased calcium absorption. The pituitary gland is increased in size by 135% with increased blood flow demands. Hemorrhagic shock can lead to necrosis of the gland and pituitary insufficiency (Sheehan’s syndrome). Preeclampsia (triad of hypertension, proteinuria, and peripheral edema) can increase risk of intracranial hemorrhage or seizures. Subsequent neurologic findings may mimic head injury.

image Initial Assessment and Resuscitation

Optimal care of the mother will maximize the chances for survival of the fetus. Resuscitation of the gravid patient should follow guidelines for the nongravid patient. Given the exquisite sensitivity of the placenta and fetus to hypoperfusion and hypoxemia, supplemental oxygen and intravenous fluids should be administered early, even before extrication if possible, particularly since the latter may be delayed by anatomic factors. There is no indication for fetal assessment in the field. Use of the pneumatic antishock garment for stabilization of fractures or control of hemorrhage is contraindicated because the resulting increase in intraabdominal pressure can further decrease venous return in the gravid patient.

Prehospital protocols and interhospital transfer arrangements must account for management of a pregnant trauma victim. The optimal receiving facility should have obstetric and neonatology consultants available, even if it is not the closest trauma center.

The airway of the gravid patient is at risk because of the tendency toward gastroesophageal reflux and aspiration. In addition, the vocal cords are frequently edematous. Ventilation of the gravid patient late in pregnancy may be impeded by the enlarged uterus and cephalad positioning of the abdominal contents. Functional residual capacity may be significantly reduced, leading to more rapid decompensation, particularly with chest trauma.

Because of the increased blood volume late in pregnancy, the mother may not show signs of hypovolemia, given the same blood loss (up to 1500 mL) as a nongravid patient. Uterine perfusion, however, may still be compromised. Uterine blood flow may decrease by up to 30% before the mother demonstrates clinical signs of shock. Aggressive volume replacement is necessary to assure adequate uterine blood flow. Blood transfusions should be administered per standard guidelines, but the mother’s Rh-antigen status must be considered. If it is unknown, Rh-negative blood should be administered. Invasive hemodynamic monitoring should be considered early during resuscitation to assure adequate volume resuscitation.

To prevent the supine hypotensive syndrome, beyond 20 weeks of gestation, patients should be placed in the left lateral decubitus position to relieve the pressure of the uterus from the inferior vena cava. The uterus can also be manually displaced to the left. If the patient is immobilized on a long board before spinal injury is ruled out, the entire board can be tilted 15 degrees with a wedge. Vasopressors, which are very rarely indicated in trauma patients, should be avoided unless absolutely necessary because of the risk of decreasing uterine blood flow.

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