Pregnancy Trauma
Background
The pregnant trauma patient presents a unique challenge because care must be provided for two patients—the mother and the fetus. Anatomic and physiologic changes in pregnancy can mask or mimic injury, making diagnosis of trauma-related problems difficult. Care of pregnant trauma patients with severe injuries often requires a multidisciplinary approach involving an emergency clinician, trauma surgeon, obstetrician, and neonatologist.
A 2013 systematic review on this topic noted that the available literature is characterized by severe limitations, including retrospective design, widely variable outcomes, and ascertainment bias. [1] The review did conclude that the major determinant of obstetrical outcomes after trauma is the severity of injury and that motor vehicle accidents and domestic violence/intimate partner violence are the most common mechanisms of traumatic injury during pregnancy, with substance abuse being a common accompaniment to these forms of trauma.
Pathophysiology
To evaluate the pregnant patient, the various physiologic changes that occur during pregnancy must be understood. Because balance and coordination are most adversely affected during the third trimester, the frequency of accidental injury is greatest during this period. Although the pregnant patient's blood pressure decreases during pregnancy, changes may not be as great as traditionally thought. Systolic blood pressure changes by only 2-4 mm Hg, while diastolic pressure decreases by 5-15 mm Hg in mid-trimester. In addition, the resting heart rate usually increases by only 10-15 beats per minute. Thus, tachycardia or hypotension in the pregnant trauma patient should not be attributed solely to the gravid state.
Physiologic anemia in pregnancy is due to a dilutional effect of plasma volume increasing by 50% but red blood cell volume increasing by only 18-30%. Thus, the average hematocrit level is 32-34% and is at its nadir around the 30th to 34th week of gestation. Because the average estimated blood loss is approximately 500 mL for a vaginal delivery and 1000 mL for a cesarean delivery, no change in hemodynamic parameters occurs because of these preemptive adaptations. The uterus, which grows from 70 g to 1000 g, enlarges into the peritoneal cavity after the 12th week of pregnancy. Although it now becomes more susceptible to injury, it also provides protection for other maternal abdominal organs such as the small bowel. The bladder is also moved into the abdomen by the uterus in the second and third trimesters, and the ureters become dilated (right > left). Gastrointestinal tract motility decreases.
Blood flow to the uterine arteries is normally maxillary vasodilated, so blood delivery to the uterus is maximal in the normal physiologic state. Maternal hypovolemia may result in vasoconstriction of the uterine vasculature. The third trimester fetus can adapt to a decrease in uterine blood flow and oxygen delivery by diverting blood distribution to the heart, brain, and adrenal glands. Because fetal hemoglobin has a greater affinity for oxygen than does adult hemoglobin, fetal oxygen consumption does not decrease until the delivery of oxygen is reduced by 50%. Thus, maternal shock may have a significant impact on the developing embryo/fetus.
Overview
Trauma caused by accidents and violence is a common and important complication of pregnancy, involving 5-20% of pregnancies. Recent studies demonstrate that trauma is more likely to cause maternal death than any other medical complication of pregnancy. The medical records of the Cook County Medical Examiner were reviewed for the years 1986-1989. Direct and indirect obstetric factors caused maternal deaths in 31.5% of 95 cases. Trauma caused maternal deaths in 46.5% of the 95 cases, and, of these traumatic death cases, 34% were due to accidents, 57% to homicide, and 9% to suicide. The following describes the percentage of traumatic maternal deaths caused by each mechanism of injury in this series.
Gunshot wounds 23%
Motor vehicle accidents 21%
Stab wounds 14%
Strangulation 14%
Blunt head injury 9%
Burns 7%
Falls 4%
Toxic exposure 4%
Drowning 2%
Iatrogenic injury 2%
Records of the New York City Medical Examiner from 1987-1991 identified women aged 15-44 years who were pregnant at the time of traumatic death. Homicide (63%), suicide (13%), motor vehicle accidents (12%), and drug overdoses (7%) accounted for the deaths, and 48% of the injury-related deaths were associated with recent substance use. The cause of maternal death in the emergency department was reviewed in the level I trauma center in Miami, Fla. Motor vehicle collisions was responsible for 72% mortality and penetrating trauma was responsible for a 19% of deaths reported. The use of seatbelts was associated with lower mortality. [1, 2]
Although the initial focus of management is always maternal stabilization, the approach to treating trauma is different in patients who are pregnant than in patients who are not pregnant. Unless the treating physician is aware of maternal physiologic adaptation to pregnancy, misdiagnosis and suboptimal treatment may ensue. On the other hand, a wide variety of obstetrical pathologies can obscure, confuse, and delay the diagnosis of intra-abdominal injury.
A central focus is balancing the health and well-being of the fetus against the mother's need for surgery. When a surgical intervention is chosen, the effect of surgery on the fetus and the pregnancy often is very difficult to discern from the effects caused by the pathologic process (eg, trauma) that created the need for surgery. A demonstrable increase in risk to the fetus occurs from surgery alone, and the risk appears to be greatest in the first and third trimesters. The concern for the fetus adds to complexity of diagnosis and management of trauma during pregnancy.
Maternal-Fetal Physiology
An understanding of normal maternal-fetal physiology is critical in the diagnosis, surgical management, and postoperative care of pregnant women who require major surgery or who have been injured. Normal clinical and laboratory findings in pregnant women would be suggestive of pathology in women who are not pregnant. The differentiation between normal physiology and pathology in these groups of women saves them from exposure to needless, and sometimes dangerous, diagnostic testing. Table 1 outlines the differences in laboratory values between pregnant and nonpregnant women.
Table 1. Changes in Laboratory Values During Pregnancy
Value Nonpregnant Pregnant
Chloride (mEq/L) 100-106 90-105
Bicarbonate (mEq/L) 24-30 17-22
PCO2 (mm Hg) 35-50 25-30
PO2 (mm Hg) 98-100 101-104
Table 2. Central Hemodynamics in Pregnancy
Hemodynamic Parameters Nonpregnant (± SD) Pregnant (± SD) Percent Change %
Heart rate (beats per min) 71 (10) 83 (10) +17
MAP (mm HG) 86.5 (7.5) 90.3 (5.8) NS*
Cardiac output (L/min) 4.3 (0.9) 6.2 (1.0) +43
SVR† (dyne sec/cm5) 1520 (520) 1210 (266) -21
LVSWI‡ (g m/m2) 41 (8) 48 (6) NS
Central venous pressure
(mm Hg) 3.7 (2.6) 3.6 (2.5) NS
PCWP (mm Hg) 6.3 (2.1) 7.5 (1.8) NS
COP (mm Hg) 20.8 (1.0) 18 (1.5) -14
‡ Left ventricular stroke work index
*Not significant
†Systemic vascular resistance
The specific organ system changes that lead to the variation in laboratory test results and cardiovascular parameters are described briefly in the following sections. These sections focus on physiologic changes relevant to the pregnant patient who is undergoing surgery or who has had a physical trauma.
Intravascular volume
The rapidly growing uteroplacental-fetal unit places a marked pressure on oxygen delivery. These demands are met by increasing oxygen carrying capacity (ie, blood volume), cardiac output, and minute ventilation. Total blood volume increases by 35-40%, and this increase in blood volume can help predict the normal adaptations in most organ systems. Plasma volume is the first component to respond to the new hormonal milieu of pregnancy. Plasma volume increases progressively from 5-7 weeks' gestation to a maximum volume of about 5000 mL at 32 weeks' gestation, an increase of 45% (about 1400 mL). This increase in plasma volume is more rapid than the increase in red cell mass. Red cell mass increases by about 350 mL by term, an increment of 25%. The greatest discrepancy between the increasing red cell mass and the increasing plasma volume occurs at 27-33 weeks' gestation; the hematocrit decreases during this period. A hematocrit less than 30% or a hemoglobin less than 10 g/dL is diagnostic of anemia.
Erythrocyte 2,3-diphosphoglycerate concentration increases during pregnancy, thus lowering the affinity of maternal hemoglobin for oxygen. This facilitates the dissociation of oxygen from hemoglobin as the blood passes through the intervillous space in the placenta. This process enhances the delivery of oxygen to the growing fetus. Pregnancy-induced decreases in colloid osmotic pressure (COP) place the gravid woman at greater risk of pulmonary edema. Colloid osmotic pressure describes the ability of large molecules (eg, proteins) to retain fluid in the intravascular (or interstitial) space. Their large size prevents their transfer across the semipermeable endothelial membrane and sets up an osmotic gradient.
Nonpregnant ambulatory patients have a mean COP value of 25 (± 2.5 standard deviation [SD]) mm Hg. In pregnancy, COP declines to about 22.5 (± 0.5 SD) mm Hg at term. After delivery (nadir at 6 h), COP drops to 15 (± 2 SD) mm Hg. The pulmonary capillary wedge pressure (PCWP) is a proxy for left ventricular cardiac function. When the COP-to-PCWP gradient is less than 4 mm Hg, a substantial risk for pulmonary edema exists. Preeclampsia reduces COP to 18 mm Hg antepartum and 14 mm Hg postpartum. The drop in COP in preeclampsia corresponds to the decrease in serum albumin that is associated with preeclampsia. The large transfusion (ie, 2-3 mL/1 mL blood loss) of crystalloid solutions in association with trauma or burns results in earlier onset of pulmonary edema in pregnant women and immediately postpartum.
The loss of circulating blood volume and hemorrhage are major physiologic challenges associated with trauma. The typical pregnant woman is young and healthy and can adapt to the challenge more easily than older women with chronic diseases such as ischemic heart disease, diabetes, or chronic hypertension. In healthy individuals with normal oxygen carrying capacity, the traditional signs of hemorrhage and adaptation do not become evident at rest until 15-20% (ie, 1200 mL) of total blood volume is lost. Pregnant women who are older (ie, >35 y) or who have underlying medical disease may manifest symptoms with less significant blood loss. Because pregnancy is associated with an increase in blood volume, the actual amount of blood loss that results in clinical signs of response is greater in pregnant women than in nonpregnant women.
Once 20-25% (ie, 1200-1500 mL) of blood volume is lost, systemic adaptation through sympathetic stimulation becomes apparent along with mild tachycardia (ie, 95-105 beats per min and peripheral vasoconstriction manifested as cold, pale extremities). Any decreases in blood pressure are mild, and mean arterial pressure (MAP) drops 10-15% (ie, MAP is 70-75 mm Hg). Moderate hemorrhage, 25-35% (ie, 1500-2000 mL) of blood volume, is associated with increasing evidence of sympathetic stimulation and the onset of tissue hypoxia, tachycardia (ie, 105-120 beats per min), MAP drop of 25-30% (ie, MAP is 50-60 mm Hg), restlessness, and oliguria (ie, < 0.5 mL/kg of actual weight). With severe hemorrhage (ie, >30% or >2000 mL loss of blood volume), hemorrhagic shock is manifest along with significant tissue hypoxia, tachycardia (ie, >120 beats per min), hypotension (ie, MAP < 50 mm Hg), altered consciousness, and anuria.
Fetal tolerance of maternal hemorrhage depends on the degree of maternal sympathetic response, the oxygen carrying capacity of the maternal blood, and maternal blood pressure. In the presence of an acute decrease in intravascular blood volume, progressive fetal acidosis occurs, with significant peripheral vasoconstriction, maternal tachycardia at rest and without pain (ie, >105 beats per minute), drop in MAP of 10-15% (or < 70 mm Hg), hematocrit less than 24%, or maternal oxygen saturation less than 92%. While maternal oxygenation requires adequate respiratory and cardiovascular function, the fetus relies entirely on cardiovascular function and placental transfer of oxygen. Understanding pregnancy changes in maternal cardiovascular physiology is critical to understanding the fetal response to trauma.
Cardiovascular physiology
Hypervolemia, increased cardiac output, and positional hypotension are the major changes and risks of pregnancy-induced adaptations of the cardiovascular system. In healthy pregnancies, oxygen consumption (VO2) is increased by a combination of increasing fetal metabolic requirements, maternal vasodilation, and arteriovenous shunting through the placenta. The full effects of vasodilation and arteriovenous shunting reach their maximum at 24-30 weeks' gestation, and a 30% reduction in both systolic and diastolic blood pressures is expected. Cardiac output rises rapidly until 30-32 weeks' gestation. This is accomplished by an increase in heart rate to 85 beats per minute and a lesser increase in stroke volume.
In the course of anesthesia, surgery, and postoperative recovery, the obstetrician, surgeon, and anesthesiologist monitor and manipulate critical physiologic variables, such as blood pressure, heart rate, cardiac output, hematocrit, PaO2, and PaCO2. Table 2, adapted from a study by Clark et al, depicts normal cardiovascular parameters in pregnant women.
In Clark et al's classic study, 10 healthy pregnant women consented to serial placement of a Swan-Ganz catheter and measurement of their cardiovascular parameters in a resting, nonanesthetized state. [3] These results are the values against which the values of critically ill pregnant women should be compared.
The maternal cardiovascular system plays a key role in utero-placental physiology. Familiarity with the maternal cardiovascular response to surgical hemorrhage, trauma, and sepsis is critical in understanding the complications resulting from these abdominal disorders and their treatment (eg, surgery, vasoactive drugs). Circulatory physiology in response to challenge in nonpregnant animals and humans has been well described.
In summary, tissue perfusion and aerobic tissue metabolism are a reflection of overall circulatory function. Oxygen delivery (DO2), defined as arterial oxygen content multiplied by cardiac index (CI), reflects circulatory function. VO2, defined as arteriovenous oxygen content difference multiplied by CI, reflects the sum of all oxidative metabolic reactions plus arteriovenous shunting. The production of metabolic acids, especially lactate, indicates a failure of the circulatory system (ie, DO2) to meet the oxygen needs (ie, VO2) of the tissue.
Patients with shock associated with hemorrhage or cardiac dysfunction have greatly reduced DO2 with moderately reduced VO2. Increased oxygen extraction is the principal compensatory reaction when tissue perfusion is limited by reduced DO2. In contrast, the increased VO2, which is provoked by increased metabolism from sepsis and trauma, is compensated by increased CI and DO2. Therapeutically, management is directed at maintaining levels of VO2 and DO2 within the reference range rather than focusing on a specific cardiac profile (eg, blood pressure, wedge pressure).
The way uterine arteries (ie, uterine blood flow) participate in the maternal compensatory response to hypovolemia and shock reflects fetal tolerance. Knowledge of uterine blood flow and response to hemorrhage, hypoxia, or vasoactive drugs is derived from data in anesthetized animal models, usually ovine. Data from animal experiments imply that the uterine vascular bed in pregnant organisms is a low-resistance system. The uterine vessels appear to be maximally dilated and, therefore, exhibit minimal autoregulation. More importantly, uterine blood flow reflects maternal arterial blood pressure in a linear fashion in pregnant organisms. When maternal blood volume is reduced by 30-35%, a minimal change in maternal mean arterial pressure occurs. As participants in the compensatory response, the uterine arteries constrict, and uterine blood flow is reduced by 10-20%.
Alpha-adrenergic compensatory vasoconstriction occurs in response to maternal hypoxia. Alpha-adrenergic blocking agents, such as phenoxybenzamine, limit this response. A decrease in uterine PaO2 from 70 to 55 mm Hg was associated in one study with a 16% reduction in uterine blood flow; a decrease in PaO2 from 96 to 28 mm Hg resulted in a 25% reduction in uterine blood flow.
These observations contribute considerable interpretative information to the clinician faced with a pregnant woman with an acute abdomen. Clinical evidence of alpha-adrenergic stimulation raises a concern regarding reduced uterine blood flow and subsequent fetal compromise, despite maternal blood pressures within the reference range. Alpha-adrenergic stimulation is manifested by marked peripheral vasoconstriction, cold and clammy extremities, a decrease in capillary refill in response to skin pressure, widened pulse pressure, decreased urinary output, and increased sweating.
In the third trimester, maternal position has a great impact on intravascular pressures and cardiac output. In the supine position, the uterus obstructs both the inferior vena cava and the aorta. Venous pressures in the lower leg can be as high as 20-25 mm Hg, and the caliber of the aortic lumen is reduced by 40%. Cardiac output in the supine position subsequently may be reduced as much as 25% compared with that in the left recumbent position. Approximately 10% of pregnant women in the third trimester have supine hypotensive syndrome, which is manifested by profound maternal hypotension and fetal hypoxia. Acute nausea is a common symptom. A key component in the treatment of a critically ill trauma patient is to place the patient with a left pelvic tilt via a wedge.
Respiratory physiology
Hormonal and mechanical changes (eg, enlarging uterus) combine to produce hyperventilation. Progesterone acts early to increase the respiratory rate by 15%. Minute ventilation and tidal volume are increased 50% and 40%, respectively. The relative hyperventilation is reflected by hypocapnia (ie, PaCO2 is 28-32 mm Hg). Anxiety and pain can cause a pregnant patient to increase her respiratory rate to the point of significant hypocapnia, which results in faintness and perioral numbness. A 5-minute episode of hyperventilation that drops the maternal PaCO2by 6 mm Hg results in a 4–mm Hg drop in fetal PaCO2 and, more importantly, a 3.5–mm Hg drop in fetal PaO2.
Baseline hyperventilation also reduces respiratory compensation for metabolic acidosis. Inhalation anesthesia has a more rapid onset in pregnant patients. After the first trimester, progressive anatomic changes reduce the functional residual capacity and residual volume by 20%. When these changes are coupled with an increase in oxygen consumption (15%), hypoventilation or apnea results in a more rapid onset of hypoxia. During pregnancy, the closing capacity is elevated in the first 48-72 hours after abdominal or thoracic surgery; the resultant arteriovenous shunting further hastens the onset of hypoxia.
Renal physiology
Changes in the cardiovascular system are reflected in the renal system. The 50% increase in blood volume during pregnancy results in an increased renal plasma flow and an increased glomerular filtration rate (GFR). As a result, an increase occurs in the excretion of metabolic products (eg, proteins, glucose) that may exceed the tubular reabsorption capability. In healthy pregnancy, BUN and creatinine levels are 10 mg/dL and 0.7 mg/dL, respectively. Glucosuria has been found on 2 or more occasions in 5-10% of women as a result of a reduction in the renal threshold between 140 and 160 mg/dL. Proteinuria levels as high as 300 mg/d are considered within the reference range. Hematuria is always abnormal during pregnancy.
Pregnancy-induced changes of the renal system include partial ureteral obstruction in the third trimester and increased glomerular clearance. A combination of smooth muscle relaxation by progesterone and compression by the enlarging uterus at the pelvic brim creates physiologic hydronephrosis of pregnancy. Changes occur before 12 weeks' gestation, and the obstruction is more pronounced on the right side. The anatomic changes revert to normal by 6 weeks postpartum. These normal changes must be recognized in the interpretation of intravenous pyelography during pregnancy and the puerperium.
While the exact pathophysiology is unknown, pregnant women are more susceptible to symptomatic urinary tract infections. The risk may be related to increased urinary stasis, or urinary human chorionic gonadotropin may enhance the attachment of pathologic organisms to the urinary mucosa. Approximately 5-10% of reproductive-aged women enter pregnancy with chronic, episodic, asymptomatic bacteriuria. If unidentified and untreated in the first trimester, asymptomatic bacteriuria leads to pyelonephritis in about one third of individuals. Because women who experience trauma often have Foley catheters, another risk factor for urinary tract infection, consider pyelonephritis when a trauma patient's fever spikes.
Coagulation physiology
Pulmonary embolism is a major cause of maternal death, and the pregnant (or immediately postpartum) woman is at increased risk. Obesity (ie, body mass index [BMI] >26) is an independent risk factor for deep venous thrombosis after trauma, and many women have a BMI greater than 26 in late pregnancy. In addition, changes in coagulation physiology place these patients at an even greater risk.
Thrombosis is more likely to occur in pregnancy because pregnant women have 2 of the components of Virchow triad, venous stasis and hypercoagulability. As occurs in the ureters, high progesterone levels relax the smooth muscle of maternal vasculature. A greater venous capacitance exists. The enlarged uterus compresses the vena cava and triples the venous pressure in the lower extremities (8-24 mm Hg).
Estrogen increases the hepatic production of coagulation factors, yielding a 30-50% increase in fibrinogen and factors VII, VIII, IX, and X. Fibrinolysis is decreased in the second and third trimesters. These changes increase the incidence of thrombophlebitis to 1:70.
Infection, general anesthesia, and surgery further exaggerate the risk when the third component of Virchow triad, vascular injury, is added. Postoperative bed rest increases the risk of stasis. Prevention is the cornerstone of management. Once high-risk patients are identified, prophylactic heparin (5000-7500 U q8-12h), intermittent pressure stockings, and early ambulation constitute standard therapy.
Gastrointestinal physiology
Nausea and vomiting are common in pregnancy. In the first half of pregnancy, as many as 70% of pregnant women experience nausea and 40% report episodes of vomiting. Incidence is reduced considerably in the second half of pregnancy, but 15-20% of patients report persistence of symptoms throughout their pregnancy.
The diagnosis of nausea and vomiting in pregnancy (ie, hyperemesis gravidarum) is a diagnosis of exclusion. Any patient with nausea and vomiting requires a history and physical examination performed in a timely and thorough manner. Gastroenteritis is the most common nonobstetric diagnosis, but hepatitis, pancreatitis, and pyelonephritis also are frequent. Nausea and vomiting may be a component of appendicitis, but anorexia and pain usually are prominent. In a patient with previous pelvic and/or abdominal surgery, pelvic inflammatory disease, or endometriosis, intestinal obstruction is a consideration. In this case, the physical examination is very important in diagnosis and management.
Abdominal distention, with or without ascitic fluid, is best determined by the location of areas of dullness when the patient is turned from side to side. Peristaltic sounds characteristic of an obstruction are high-pitched, tinkling, and with rushes. Absence of peristalsis sounds is an important sign, often indicating an ileus or the presence of intraperitoneal fluid, pus, or blood. Between these 2 extremes, wide variations in the type and quality of peristaltic sounds may be noted, but these differences usually are not important. When intestinal obstruction is suspected, abdominal x-ray films (ie, upright, flat plate, left lateral decubitus) are essential and should not be withheld for fear of fetal exposure to radiation.
Constipation is common in pregnancy because of the effects of progesterone on bowel mobility and the widespread use of hematinic agents; however, flatus always should be present. The combination of bedrest, pregnancy, iron supplements, and narcotics for pain after trauma during pregnancy poses an important management problem. Routine use of bulk stool softeners is recommended. Anorexia, constipation, and the failure to pass flatus are serious signs that could indicate appendicitis, bowel perforation, or intestinal obstruction. Diarrhea is seldom an indication of an acute surgical problem in the abdomen except as a symptom of recurrent ulcerative colitis.
Physiologic changes in the GI tract during pregnancy increase the risk of aspiration during surgery and anesthesia. Progesterone is a smooth muscle relaxant, and lower esophageal sphincter tone is decreased. One fourth of pregnant women have symptomatic lower esophageal reflux. Gastrin, the hormone that increases the volume of gastric secretion and lowers the pH of the stomach contents, increases considerably during pregnancy.
In addition, intragastric pressure is increased by the large uterus, the supine/lithotomy position, fundal pressure, and light anesthesia. Classic training has taught that approximately one fourth of pregnant women undergoing abdominal surgery after an overnight fast have gastric contents of sufficient volume and sufficiently low pH to place them at high risk of aspiration. More recent evidence demonstrates that pregnancy does not delay gastric emptying. Despite the latter finding, an 8-hour fast and metoclopramide or other histamine 2 (H2) antagonist should be prescribed as antacid prophylaxis before surgery.
When the patient is not allowed or cannot have oral intake, such as with prolonged ventilation, neurologic injury, and bowel injury, fetal intrauterine growth retardation may occur. Most patients with an acute abdomen are not permitted oral intake, at least for the acute phase, and intravenous dextrose and multivitamins are indicated. If a patient has had insufficient intake (ie, < 1500 kcal/d) for 72 hours, start parenteral nutrition.
If support is needed for less than 10 days, peripheral parenteral nutrition is indicated. An appropriate nutrient solution is the simultaneous use of 4.25% amino acid and 5% dextrose (1500 mL) with a fat emulsion (1500 mL of intralipid) through a Y-connector. This provides the patient with 3000 mL water, 64 g of protein, and 1950 calories in 24 hours. Electrolytes, trace elements, and vitamins can be added to the protein solution. If support is needed for more than 10 days or if a patient's condition is particularly severe, total parenteral nutrition through a central venous catheter is needed.
The specific problems of parenteral nutrition during pregnancy are the increased metabolic needs (ie, increase to 40 kcal/kg/d, increase in protein by 30-50 g/d). Hyperglycemia can be a greater risk because pregnancy usually is a diabetogenic state. Treat mean blood glucose levels consistently greater than 105 mg/dL with insulin. Pregnancy is a hyperlipidemic state, and some theoretic caution exists about the use of lipid solutions (eg, pancreatitis, preterm labor). However, hyperalimentation is a replacement rather than a supplementation, and this caution may not be applicable. The fetus is evaluated for growth and well-being. Nonstress tests are performed twice weekly, and serial ultrasonography for fetal growth should be obtained.
Central nervous system
Pregnancy critically changes the need for several anesthetic drugs. The requirement for halogenated anesthetics (ie, halothane) is reduced by 40% because of the increased minute volume. Serum pseudocholinesterase is decreased by 20% in late pregnancy; however, clinically significant increases in the duration of succinylcholine neuromuscular block are reported rarely. Venous distention increases the caliber of epidural veins. The dose of epidural anesthetic agents is reduced by 50%. The uterine vasculature is sensitive to alpha-adrenergic stimulation. Maternal stress response, maternal anxiety, or alpha-adrenergic vasopressors can result in fetal hypoxia and acidosis.
Maternal Trauma and the Fetus
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. [4] 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. [5] However, Duncan and colleagues did report an increase. [6] 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). [7] 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. [8]
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.
Special Maternal Issues
Abdominal pain and tenderness
Abdominal pain and/or tenderness in pregnant trauma patients raises the difficult question of whether the signs and symptoms are obstetric or nonobstetric in origin. After the first trimester of pregnancy, the most common confusing obstetric diagnoses are preterm labor, intra-amniotic infection, or abruptio placentae. Unfortunately, these complications may be the consequence of maternal trauma, rather than the cause of the abdominal pain and tenderness.
The differentiation between nonobstetric and obstetric causes is critical to management. The single most effective aid in diagnosis is an experienced obstetrician who has conducted a detailed history and physical examination. Subsequently, the results of serial pelvic examinations, electronic fetal monitoring, and ultrasonographic examinations are important in the diagnosis and management.
In selected cases, amniocentesis may provide useful information concerning amniotic fluid character (eg, bloody, meconium stained), infection (obtain Gram stain and culture), and fetal lung maturity studies. When ultrasonography is not helpful, perform radiographic examinations in a calculated and focused manner. The fetal risks of diagnostic radiographs are minimal compared with the potential risk associated with delayed diagnosis or misdiagnosis of an acute abdomen.
When pain is present, careful analysis of the location, type, intensity, and radiation is essential. Pain may be generalized or may be confined to the lower, middle, or upper abdomen. Generalized pain, when associated with rebound tenderness and guarding, is suggestive of severe irritation of the peritoneum, as found in pancreatitis, ruptured viscus, severe infection, or intra-abdominal hemorrhage. The presence of generalized pain and rebound tenderness subsequent to pain localized to one part of the abdomen suggests relatively sudden rupture of an organ, cyst, abscess, or tumor. With the rare exception of pancreatitis, early surgical exploration may be life saving for a mother and fetus. Central lower abdominal pain suggests a uterine origin.
Preterm labor may be the source or a consequence of the acute process. In either case, signs and symptoms of preterm labor must be evaluated. Preterm labor often is associated with one or more of the following signs or symptoms: waxing and waning central abdominal pain (similar to menstrual cramps), pelvic fullness, back pain, anterior thigh pain, groin pain, change in vaginal discharge, tenderness, urinary urgency, and vaginal bleeding or spotting. The diagnosis of preterm labor is based on evidence of effacement and dilation of the cervix. After confirmation of intact membranes and normal placental position, serial cervical examinations can be used to help diagnose preterm labor. The diagnosis of preterm labor is based on the presence of 3 contractions in 20 minutes plus cervical change or a cervix that is 2 cm dilated and less than 1 cm in length.
Steady central lower abdominal pain, especially when accompanied by point tenderness, is suggestive of an accident related to the uterus, such as uterine injury, torsion or infarction of a leiomyoma, abruptio placentae, or chorioamnionitis, each of which may be accompanied by localized tenderness or rebound tenderness. In rare cases, urinary disorders (eg, cystitis) can cause pain levels sufficient to be confused with more serious and acute intra-abdominal problems.
Lateralized lower abdominal pain suggests an adnexal problem such as infection, torsion, rupture, or hemorrhage. The pain caused by ovarian disease often radiates to the anterior thigh. Extraperitoneal causes of lateralized pain include the intense, colicky pain of a ureteral stone, which may radiate to the groin or labia. The pain of pyelonephritis may be abdominal but is more often prominent in the flank area. Intraperitoneal causes include appendicitis on the right side. The pain may be higher than usual because of the upward displacement of the appendix by the growing uterus. As a result of displacement, the classic spread of pain from the umbilical area to the right lower quadrant of the abdomen may be absent in appendicitis.
Other rare causes of right lower abdominal pain include regional enteritis, diverticulitis of the cecum, and volvulus. Pain in the left lower abdomen may be due to disorders of the descending and sigmoid colon, such as ulcerative colitis, diverticulitis, or volvulus of the sigmoid.
Incidental ovarian mass
An exploratory laparotomy for trauma in an undiagnosed pregnancy brings many young women under the care of general surgeons unfamiliar with obstetric problems. Often, these are women in the first trimester, and unilateral ovarian enlargement is apparent. In most cases, this is a corpus luteum. Not infrequently, the corpus luteum shows minimal bleeding. Conservative management always should be practiced. Oophorectomy rarely is indicated in pregnancy unless the tumor is large (ie, >10 cm), solid, or exhibits signs of malignancy. Unless significant hemorrhage has occurred, do not perform oophorectomy for a bleeding corpus luteum cyst.
Incidental resection of a corpus luteum cyst at the time of laparotomy for other diseases should be discouraged because removal can cause spontaneous abortion. The corpus luteum is essential for hormonal (progesterone) support of the pregnancy until the placenta can support itself. The corpus luteum is indispensable until approximately 7 weeks' gestation. From 7-9 weeks' gestation, the placenta becomes the source for progesterone. Luteectomy before 9 weeks' gestation results in spontaneous abortion; however, luteectomy occasionally is necessary. In these cases, 100 mg/d of progesterone administered intramuscularly is essential for pregnancy support until 9 weeks' gestation.
Ill-advised ovarian biopsy or cystectomy may cause infertility. Ovarian surgery has a 35% incidence of iatrogenic postoperative adhesions. Incidence of subsequent infertility is hard to determine, but it may be as high as 5-10%. When ovarian surgery is indicated, careful surgical technique is critical to reduce the risk of adhesions. These techniques include the use of fine (ie, 4-0 to 6-0) nonreactive absorbable sutures, atraumatic tissue handling, excellent hemostasis, and avoidance of tissue dehydration.
The use of adjunctive procedures to decrease adhesions has been suggested. The most popular are the instillation of 50-100 mL of 32% dextran and administration of systemic steroids and antihistamines after surgery. Theoretically, these procedures work by inhibiting contact adhesions and the inflammatory response. Unfortunately, well-designed prospective studies are needed to define their efficacy in pregnancy. In addition, the risks to the fetus presented by the use of dextran, steroids, and antihistamines are not well defined.
Blunt Trauma
Blunt trauma is a common denominator to many injuries during pregnancy. [9, 10, 11]Motor vehicle accidents are a common source of blunt trauma. Crosby reviewed 441 pregnant women involved in automobile collisions. [9] Collisions were divided into the categories of minor or severe. When minor damage occurred to the vehicle, only 3 of 233 victims experienced injury and no placental separation occurred. When the damage to the vehicle was severe, 15 of 208 pregnant women (ie, 7.2%) died, and 25 of the 193 survivors (ie, 13.5%) had major injury. An analysis of 1.46 million patients from The National Trauma Data Bank (from 2001-2005) found that pregnant women have lower mortality rates when compared with women of similar age groups who sustained equivalent injuries. [12] A series from North Carolina demonstrated 12.6 automobile accidents per 1000 pregnant women. The 18-24-year-old pregnant patient was at greatest risk, especially between weeks 20 and 27. [13]
Fetal death after 12 weeks' gestation occurred in 14 of 176 women (ie, 8%) surviving a severe collision. [14] Except for cases of maternal death, first trimester loss could not be explained by trauma. The most common causes of fetal death after 12 weeks' gestation were maternal death, abruptio placentae, and maternal shock. Abruptio placentae occurred in 3.4% of pregnant women involved in severe accidents.
Despite the recommendations ofpublic health officials and obstetricians, the lay public, and, occasionally, misinformed physicians, raise the concern that use of restraints (eg, seat belts) in motor vehicles increases the likelihood of injury during a collision. Wolfe and coworkers provided scientific support for the public health recommendations for women to use 3-point restraints in motor vehicles. [15]
Low birth weight (odds ratio = 1.9 [95% confidence intervals = 1.2, 2.9]) and delivery within 48 hours (odds ratio = 2.3 [95% confidence intervals = 1.1, 4.8) were more common among 1349 unrestrained pregnant women (>20 wk gestation) than among 1243 restrained pregnant women. [15] Regardless of the source or severity of trauma, the mother and her fetus benefit most by knowledge, planning, and protocols that reflect the physiologic differences between pregnant and nonpregnant women and the special needs of the vulnerable fetus.
The following treatment guidelines are recommended. A pregnant trauma patient should be observed in a hospital equipped to diagnose and manage obstetric and neonatal emergencies. Transport the injured mother on her left side to avoid supine hypotension. Obtain a brief description of the severity of the accident and status of the patient from the ambulance attendant. Focus a brief physical examination on central nervous system function (neck injury), vital signs, chest wall motion, and movement of extremities.
At this point, perform diagnostic and monitoring studies. Before and during the screening physical examination, one or more large-bore intravenous catheters (16- to 18-gauge) are placed peripherally. If intra-abdominal trauma is suspected or if the patient is unconscious, place a central venous pressure line. Ringer lactate (2 mL/1 mL estimated blood loss) is transfused in a rapid fashion. The rate of subsequent transfusion is dependent on maternal vital signs and rate of continued blood loss. In most cases, early blood transfusion is preferable to massive crystalloid transfusion.
Obtain a complete bloodcount, urinalysis, serum electrolyte level, and blood for typing and cross-match. Administer tetanus toxoid (0.5 mL) to all patients. Perform endotracheal intubation on all patients in respiratory failure or who are unconscious. Place a 3-way Foley catheter in the bladder to monitor hourly urinary output and to identify hematuria. Insert a nasogastric tube to establish the integrity of the upper GI tract and to empty the stomach of its contents. In pregnancies after 24 weeks' gestation, apply an external fetal monitor as soon as possible. The presence of fetal heart accelerations (ie, 2 accelerations of more than 15 beats per min for >15 s) is a good sign. During the placement of lines and monitors, obtain a more complete history and perform a complete physical examination.
Monitor the patient's vital signs frequently and have a trained attendant with her at all times, including when she is taken for diagnostic radiographic studies. Young healthy patients maintain their cardiovascular status to a pointafter which shock develops very quickly. Radiographic and obstetric ultrasonographic studies are important. No ordinarily indicated radiographic examination should be avoided during pregnancy. Irradiation of the fetus poses little risk compared with the dangers of undiagnosed maternal trauma. Focus standard studies on areas of injury.
