Maternal Trauma and the Fetus
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How does trauma during pregnancy affects fetal morbidity and mortality?
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@laina Four factors in maternal trauma or surgery predict fetal morbidity and mortality—hypoxia, infection, drug effects, and preterm delivery. Fetal death can occur at any gestational age and usually results from fetal hypoxia. In particular, a decrease in maternal hematocrit greater than 50% and a decrease in maternal mean blood pressure of 20% or a maternal PaO2 less than 60 mm Hg (oxygen saturation < 90%) results in fetal hypoxia, acidosis, and compromise.
The most important surgical risk to the fetus is preterm delivery. Before 23 weeks' gestation, preterm delivery uniformly results in neonatal death. When delivery occurs at a hospital with a level 3 perinatal center, survival rates at 25, 26, 27, and 28 weeks' gestation is 60%, 70%, 80%, and 90%, respectively. Major long-term defects associated with delivery at 24, 25, 26, and 28 weeks occur in 70%, 50%, 40%, and 20% of neonates, respectively. After 28 weeks' gestation, intact survival rates improve more slowly.
An infant born at term is better off than an infant born preterm. The key gestational age breakpoints in fetal outcome appear to be 25, 28, 32, and 36 weeks' gestation. Birth at hospitals without expertise in high-risk obstetrics and neonatology is associated with a significantly higher risk of perinatal death and a doubling or tripling of long-term handicap. Taking into consideration the transport time, resources, and maternal condition, in-utero transport is preferable to delivery and neonatal transport in most cases.
The most likely cause of preterm labor in a trauma patient is abruptio placentae; however, other etiologies are possible and must be considered. Preterm labor may be the cause of abdominal pain or a consequence of nonobstetric disease, trauma, or infection. Diagnosis and treatment of preterm labor in pregnant patients are difficult perioperatively. Daily tomography has been shown to be accurate in the diagnosis of placental abruption and can help determine if a patient is at risk for fetal complications. Clear risks exist for preterm delivery; however, the intrauterine environment may not be ideal, and the treatment of preterm labor may exacerbate the effects of intra-abdominal disease. Before making a definitive diagnosis, consider the many obstetric conditions that pose greater fetal risk (eg, chorioamnionitis, abruptio placentae). These often mimic acute nonobstetric conditions.
Tocolysis in the presence of these diseases is not indicated. The cardiovascular effects of beta-adrenergic drugs (eg, terbutaline, ritodrine) can exacerbate those of sepsis (eg, vasodilatation, shock). For example, intravenous ritodrine poses a 5-10% risk of serious cardiopulmonary complications, such as pulmonary edema and significant subendocardial ischemia. Other tocolytic agents that involve calcium ion physiology (eg, magnesium sulfate, calcium channel blockers) have less significant, but still disturbing, cardiovascular effects in the presence of sepsis. Prostaglandin synthetase inhibitors (eg, indomethacin) are used cautiously for tocolysis because they mask the clinical signs of infection or cause maternal platelet dysfunction.
Keeping these problems in mind, the following management of preterm labor in trauma or after trauma surgery is suggested. First, uterine irritability is not considered labor until evidence of cervical effacement or dilatation exists. Prophylactic tocolysis is not indicated. Any decision to begin tocolysis requires demonstration of the following: cervical change, assurance that membranes have not ruptured via sterile examination using Nitrazine and fern tests, and the absence of the usual precautions against the use of tocolytics. Second, determine the presence of intrauterine disease by a thorough physical and ultrasonographic examination and, perhaps, amniocentesis.
Amniocentesis under ultrasonographic guidance has many advantages. Bacteria or sheets of leukocytes on a high-power microscopic examination of an unspun specimen suggest chorioamnionitis. Fetal lung maturity studies can be performed rapidly in most institutions. Keep in mind the risks associated with third trimester amniocentesis, including fetal trauma (1%), ruptured membranes (1-2%), and preterm labor (1-2%). If peritonitis is present, amniotic fluid contamination is a special concern. In the presence of peritonitis, do not allow amniocentesis to delay an exploratory laparotomy. Localized peritoneal contamination over the amniocentesis site cannot always be predicted. Perform amniocentesis away from points of tenderness. An uncomfortable but acceptable alternative is to perform a suprapubic tap through a full bladder under ultrasonographic guidance. This approach avoids the peritoneum.
Once the diagnostic test or surgery has been performed and the mother's cardiovascular status is stable, the decision of whether or not to inhibit labor can be made. Magnesium sulfate is the therapy of choice. The dose is 4 g in 250 mL of isotonic sodium chloride administered intravenously during a period of 15 minutes, followed by 2 g/h by electronically monitored intravenous drip. Monitor the fetus continuously throughout diagnosis and management. Aggressively diagnose and treat fetal distress. Continue magnesium sulfate for 12-24 hours after the operation. At that point, patients are weaned off the medication.
Anesthesia and the fetus
Surgeons, anesthesiologists, and patients have major concerns regarding the independent risk of anesthesia for surgical interventions common in maternal trauma. Conflicting data exist concerning the effect of first trimester anesthesia on the rate of spontaneous abortion. A consistent small increase in the likelihood of spontaneous abortion appears among women working in the operating room. However, the one-time exposure of a trauma patient may be different. Mazze and associates found no increase in spontaneous abortion among 3000 women who underwent first trimester surgery. However, Duncan and colleagues did report an increase. They stratified 2565 women who underwent anesthesia during pregnancy by type of anesthesia and surgery. They reported an increased risk of spontaneous abortion among patients undergoing general anesthesia (risk ratio = 1.58) and obstetric and gynecologic surgery in particular (risk ratio = 2.00).The major problem with retrospective studies on spontaneous abortion and general anesthesia is selection bias among cases and controls (selected for baseline rate of spontaneous abortion). The pathologic process that warranted surgery may have increased the patient's risk of spontaneous abortion. The selection of control patients may be biased by the timing and sensitivity of the pregnancy test. The risk of spontaneous abortion varies considerably by gestational age. The earlier the patient is tested, the higher the risk of spontaneous abortion. Most studies have not adequately matched patients by gestational age.
The sensitivity of pregnancy tests varies considerably (eg, serum human chorionic gonadotropin versus home urine pregnancy test). The period of greatest discordance between serum and urine pregnancy tests is 3-6 weeks after the first day of the last menstrual period, and this is also the period of greatest risk of spontaneous abortion after a positive test result. Most studies have not evaluated timing and technique of pregnancy diagnosis.
The lessons of the thalidomide and diethylstilbestrol tragedies raise concerns about teratogenic effects of anesthetic agents. Risk may be species-agent specific (eg, humans and thalidomide), or effects may be manifested years after exposure (eg, genital tract abnormalities and diethylstilbestrol). Many different anesthetic agents are used alone and in combination. Although many of the most common agents (eg, N20, diazepam [Valium], isoflurane) have demonstrated species-specific teratogenic risk, these results have been neither reproduced consistently nor easily translated to the human experience. Among 8000 women who underwent surgery during pregnancy, no increased incidence of congenital abnormalities in the offspring was demonstrated.
To a certain extent, the controversy concerning first trimester exposure to anesthesia is moot. Incidence of spontaneous abortion (15-20%) and congenital abnormalities (3-5% by 5 y) is high enough and the propensity of patients and physicians to attach blame is strong enough that elective surgery in the first 13 weeks after the first day of the last menstrual period is fraught with potential legal risk and psychological concerns.
After 13 weeks' gestation, the major organ systems of the fetus are developed. The risk of congenital malformation is minimal. Between 13 and 23 weeks' gestation, the uterus is less sensitive to the stimulating effects of surgery, and minimal risk of preterm labor exists. In addition, should a preterm delivery occur as the result of surgery, heroic methods, such as cesarean delivery, rarely are considered because no chance of neonatal survival exists. Therefore, if trauma surgery must be performed during pregnancy, the period between 13 and 23 weeks' gestation is optimal.
After 24 weeks' gestation, trauma surgery can produce 3 complications—supine hypotension, neurodevelopmental delay in the offspring, and preterm birth. After 16 weeks' gestation, when the uterus becomes an extra pelvic organ, the enlarging uterus has an increasing potential to obstruct return venous flow in the inferior vena cava when the pregnant woman is supine. In the late third trimester, symptomatic hypotension (characterized by syncope, nausea, and vomiting) occurs in 10% of healthy pregnant women. This risk is higher when the patient's cardiovascular system is challenged further by sepsis (eg, appendicitis), hypovolemia (eg, trauma), or sympathetic blockage (eg, epidural analgesia). After 16 weeks' gestation, place all patients undergoing surgery in the left lateral tilt position to reduce venous and arterial compression by the pregnant uterus.
A significant proportion of fetal neurodevelopment occurs in the third trimester. Insult through the primary disease process, surgical complications, anesthetic agents, or anesthetic management (eg, respiratory support) has the potential to affect neonatal and childhood neurodevelopment. Animal models have been used to investigate whether anesthetic agents can cause neurodevelopmental handicap. Exposure to local anesthetic or inhalation of anesthetics has been associated with neurodevelopmental deficits in rodents. Transfer to the human experience is fraught with error. The few studies that have been performed on children exposed to general anesthesia in utero have yielded conflicting data.
A provocative study by Hollenbeck and associates observed that scores on 1 of 3 standardized intelligence tests were lower among 4-year-old children who were exposed to anesthetics in utero compared with the scores of unexposed children of the same age (ie, 91 [± 15 SD] versus 108 [± 20 SD], respectively). [10] Human studies never will be able to rule out the possibility that the pathologic conditions that require surgery rather than the anesthetic agent or management may be the culprit in these neurologic deficits.
Fetal assessment
Fetal assessment in the recovery from trauma is always a concern for nonobstetricians. Severe traumatic injury increases fetal mortality and morbidity. However, minor injury in the first and second trimesters can also cause fetal demise, as well as premature delivery and low birth weight. [11]At any gestational age, documentation of a live fetus by fetal heart auscultation is appropriate; however, continuous fetal monitoring for fetal heart rate changes is appropriate only if an obstetrician is willing to act on the information (eg, a fetus >25 wk gestation or with no lethal anomalies). In the recovery period, as a patient's condition becomes stable and consciousness is regained, continuous fetal assessment can be changed to a combination of recording 10 fetal movements every 12 hours and a nonstress test twice a week. This scheme can be used until the patient has returned to the usual functional state but not necessarily for the duration of the pregnancy.
Similarly, uterine contraction monitoring is appropriate only if the documentation of contractions changes management. In the acute phase, continuous uterine contraction monitoring is appropriate after 20-22 weeks' gestation with a normally formed fetus. Serial cervical examinations are essential for the diagnosis of preterm labor. Withhold tocolytic therapy until cervical change has taken place. If no uterine irritability exists, the patient's condition has stabilized, and she can recognize and report fetal movement and contractions, then continuous uterine contraction monitoring can be replaced by maternal perception and patient education about the signs of preterm labor.